Lange Radiology of The Chest Diseases

Radiology
of Chest Diseases
Sebastian Lange, MD
Professor and Chairman
Department of Radiology
Knappschaftshospital
Recklinghausen
Germany
Geraldine Walsh, MRCP, FRCR, FRANZCR

Consultant Radiologist
Department of Radiology
Royal Berkshire Hospital
Reading
United Kingdom
With a contribution by Michael Montag
Third edition, fully revised and updated
1118 illustrations
35 tables
BIBLIOTECA U.M.F . IASI
~I 1111111 ~I~ 11111

BARCOD: 1181272388
Thieme
Stuttgart· New York
IX
Table of Contents
1 Examination Technique and Normal Findings
Radiographic Examination. . . . . . . . . . . . . . . . . . . . . . . 2 Vascular System . .... . ...... . ... .... . . . .... . . 20

Frontal Chest Radiograph . . . . . . . . . . . . . . . . . . . . . 2 The Mediastinum .. ... .... ... ... .... . ....... . 24
Lateral Chest Radiograph . . ...... . .. .......... 3 Conventional Tomography .. .... . ........ ... ... . 25
Oblique Views ...... ... ........... .... ... . ... 3 Computed Tomography ..... .. .. ... .. .. . .... .. .. 28
Apical Lordotic View ...... . .... . . . .... ....... 4 Radionuclide Imaging . . .. .......... ... .. .. . .. ... 38
Fluoroscopy .. ............. .... ...... . .. ..... 4 Lung Scintigraphy . . . . . . . . . . . . . . . . . . . . . . . . . . .. 38
Scatter-Reduction Grids ... .... ... . ... . ... .... 4 Myocardial Perfusion Scintigraphy . . ..... . . .. . 39
The Normal Chest Radiograph ... .... . .. . . .... . .. 5 Positron Emission Tomography (PET)
Structures of the Chest Wall . . . . . . . . . . . . . . . . . . 5 and PET-CT .... . . . . .... . . . . .. . . . . .. . . . ... . . .. 41
Diaphragm ... ...... .... ..... ... .. ...... . ... . 9 Ultrasound ... ... ..... .... . . . . . .. . . . .. .... .. . . . . 42
Pleura ... . . . ......... . . ...... .... . .. . . ....... 9 Pulmonary Angiography ..... .. ..... .. . ....... . . 42
Lung Parenchyma ... . . . . . . . . . . .. . .. . . . . . . . . . . 16 Bronchography . ..... ... ... . . .. . ........ . .. .. . . . 45
Tracheobronchial System . . .. . .. .. . . . . . . . . . ... 18 Magnetic Resonance Imaging. . . . . . ... . . . . .. . . .. . 47
2 Malformations 50
Bronchopulmonary Sequestrations . . . . . . . . . . . . . .. 50 Congenital Bronchial Atresia. . . . . . . . . . . . . . . . . . . . . 60

Hypogenetic Lung Syndrome Vascular Malformations ... . . . . . .. . . . . ... . . . . .. . . 61
(Scimitar Syndrome) .......... .... .... . ... . ... .. 53 Pulmonary Arte riovenous Malformations
Bronchogenic Cysts .... . .. .... . .. . ........ . ..... 54 (AVM ) . .... ... .......... . . . . ...... ... .... .. .. 61
Congenital Cystic Adenomatoid Malformation of Partial Anomalous Pulmonary Venous Drainage
the Lung (CCAM) ..... .... ............ .... .. .. . . 56 (PAPVD ) . ........ .. ...... ........... . .. .. ... . 61
Pulmonary Agenesis, Aplasia, and Hypoplasia .... 57 Hypoplasia and Atresia of the Pulmonary
Congenital Lobar Emphysema .... ..... . . ........ 59 Artery...... . . .... ..... .............. ... ..... 62
3 Infection and Inflammatory Disorders 64
Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 64 Echinococciasis .. .. . .......... . .... ..... . .... 89

Lung Abscess and Septic Pulmonary Emboli ...... 69 Paragonimiasis . . . ........ ...... .. ... . .. ... .. 90
Pulmonary Tuberculosis. . . . . . . . . . . . . . . . . . . . . . . .. 72 Ascariasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 90
Fungal Diseases of the Lung ... ...... .... . ... . . . . 80 Strongyloidiasis and Ankylostomiasis . . .. ..... 91
Candidiasis . ............ .... ..... . ... . .. . . ... 80 Sarcoidosis .. ..... ...... ... ..... ......... .. . . ... 91
Aspergillosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81 Idiopathic Interstitial Pneumonias .. ... ... .... 95
Histoplasmosis ..... ..... .... . ... . .. .... . . . .. 84 Acquired Immunodeficiency Syndrome . . . . . . . . . .. 97
Coccidioidomycosis ... . .... . .... . . .... ....... 84 Infections . . . . ...... . ....... . . .. .. ..... .. .. . . 97
Actinomycosis ... . ........... . ........ . . ..... 85 Intrathoracic Malignancy . . . . . . . . . . . . . . . . . . . . . 98
Nocardiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 85 Lymphoproliferative Disorders. . . . . . . . . . . . . . . . 99
Cryptococcosis (Torulosis) . . .. ..... . . . . . . . . . .. 86 Autoimmune Disorders/Connective Tissue
Parasitic Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86 Diseases. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 100
Amebiasis . ............ .... ..... . ..... ..... .. 86 Systemic Lupus Erythematosus .. .... . . ... . ... 100
Toxoplasmosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 87 Rheumatoid Arthritis. . . . . . . . . . . . . . . . . . . . . . . .. 100
Pneumocystis Jiroveci Pneumonia Progressive Systemic Sclerosis (PSS ) . . ..... ... 101
(Previously Known as Pneumocystis Carinii Sjogren Syndrome . .. .. . ............... . .. ... 102
Pneumonia-PCP) . ..... ....... ..... .......... 87 Dermatomyositis . .... . . . ... . . .. .. . . . . ... . . .. 102
Schistosomiasis . ... . . . . . . . . . . . . . . . . . . . . . . . . .. 88 Ankylosing Spondylitis (AS ) ............. .. ... 102
X Table of Contents
Wegener Gra nulomatosis (WG ) ......... . . . ... 103 Pulmonary Eosinophilia 8 Thol
Allergic Angiitis and Granu lomatosis (Eosinophilic Lung Disease) . . .. .. .. . .... . ... . . .. . 106
(Ch urg- Strauss Di sease) .. . . . .. . .. .. . . ..... . . . 103 Radiation-Induced Lung Disease .. .. .. . .. . . . . .... 107 Chest W;
Antiglomerular Basement Membrane Disease Drug-Induced Lung Disease. . . . . . . . .. . .. . . . . .. . .. 108 Rib Fr
(AGBMD) . .. . ... . .. .... ...... . ....... .. . . .. .. 105 Stern;
Idiopathic Pulmonary Hemosiderosis (l PH ) ... . 105 Verte
Su bCl
Pleural II
4 Chronic Obstructive Pulmonary Disease PneUJ
Hem(
and Diseases of the Airways 110
Pulmoni
Pulm
Emphysema .. ..... ...... ....... . ... . . .. ... . . .. . 110 Cellular Bronchiolitis ......................... 122 Pulm
Other Forms of Emphysema ......... . .. .. ....... 114 Constrictive Bronchiolitis .............. . ...... 123
Cicatricial Emphysema ....................... 114 Swyer - james-Macleod Syndrome .. . ...... . ... 123
Bullous Emphysema . . ... ... .. .... .. ..... . .. . 115 Organizing Pneumonia/Cryptogenic Organizing
Compensatory Emphysema ..... . . . .... • . . .... 115 Pneumonia (also known as Bronchiolitis 9 Dis!
Chronic Bronchitis . . ................ .. . . .. ...... 116 Obliterans Organizing Pneumonia) .. . .... .. ... 124
Bronchiectasis .. . . . . . . . . . . . . . . . . . . . . . .. . .. .. . . . . 117 Bronchial Asthma . .. .. ....... .. ...... . .. . .. .. ... 125 Disease,
Bronchiolitis-Small Airway Disease ..... . . . ..... . . 122 Pleural
Pneum(
Pleural
5 Inhalational lung Diseases and Pneumoconioses 126 Fibre
Pleu
Pleural
Foreign Body Aspiration . . . . . . . . . . . . . . . . . . . . . . . .. 126 Other Inorganic Pneumoconioses ..... .. . , . , .. 144
Pneumoconiosis ........ ... ............ .. .. .. ... 128 Extrinsic Allergic Alveolitis (EAA)J
Pneumoconioses Due to Inorganic Dusts .. .. . .. . . 136 Hypersensitivity pneumonitis . . . . . . . . . . . . . . . . . . .. 145
Silicosis .. . .. .. . ..... .. . .. ........... . .. .. ... 136 Inhalation of Toxic Gases and Fumes ... . .. . . . .. .. 147
Coal-Worker's Pneumoconiosis (CWP) ... . .... 140
Asbestos-Induced Pleural Changes and
Asbestosis . .. .. .. . .. ....... .. . ............... 140
10 R,
Carl
Can
6 Tumors and Tumor-like lesions of the lung 149 Congel
Can
The Solitary Pulmonary Nodule (SPN) .. .... .. .... 149 Pulmonary Metastases .. . .. . .. . . .. . . ... .... .. . . . 172 PUll
Benign Tumors of the Lung. . . . . . . . . . . . . . . . . . . . . . 150 Lymphoma ............................. ... .... . 178 Con
Pulmonary Hamartom a .. .......... . ......... 151 Primary Pulmonary Lymphoma ......... . .... . 181 Coa
Carcinoid, Mucoepidermoid, and Adenoid AIDS- Related Lymphoma ........ . .. . ... . .... . 181 Con
Cystic Carcinoma ............. . .. . ....... .. . . 152 Lymphomatoid Granulomatosis .... . .. . ...... . 181 a Lf
Langerhans Cell Histiocytosis (LCH ) . . .... . .. .. 154 Treated Lymphoma ......................... . 181 Atri
Bronchial Carcinoma ................ .. ...... .. .. 157 Ver
PaO
Tot
(TA
7 Pulmonary Hypertension and Edema 183 COl
aR
Pulmonary Hypertension . .. .... . . . . . . .. . . .. . . . .. 183 Cardiac Defects with a Left-to-Right Sh unt .... 193 Tet
Precapillary Pulmonary Hypertension ........ . ... 184 Pulmonary Hypertension Due to Alveolar Unl
Primary Pulmo nary Hypertension. . . . . . . . . . . .. 184 Hypoventila tio n .. . . .... ...... .. . . .. .. .. . ... . 194 Ve!
Acute Pulmonary Embolism (PE) and Chronic Postcapillary Pulmonary Hypertension .. . . ... . .. . 195 Eb!
Thromboembolic Pulmonary Pulmonary Veno-Occlusive Disease ........... 195 Acquil
Hyperte nsion (CfEPH) .................. . .. ... 187 Pulmonary Congestion and Edema .. . . .. . . . . . .. . . 195
Table of Contents XI
8 Thoracic Trauma 200

106
107 Chest Wall Injuries . ..... . .... . . ...... . ..... . ... . 200 Pulmonary Atelectasis . . ...... . . ..... . • . ..... . 207
108 Rib Fractures . .. . . ......... . . ....• . ..... . .... 200 Pneumonia in the Trauma Patient . ..... . .... .. 207
Sternal Fractures . ................ . ......... . . 200 Tracheobronchial Rupture . .. . ... . . . .. .. ...... 207
Vertebral Fractures . ........... . . . . . ... . . . .... 201 Pulmonary Torsion . .. ... . ........ . . . . . . . ..... 207
Subcutaneous Emphysema .. ... . ... .. . . . ..... 202 Adu lt Respiratory Distress
Pleural Injuries ...................... .. ......... 203 Syndrome (S hock Lung, Da Nang Syndrome,
Pneumothorax . ................. . . . . ... . ..... 203 Stiff Lung Syndrome, Oxygen Lung, Tran sfusion
Hemothorax ...................... . .. . . .... .. 205 Lung) ... . ...... . .... . . . .... . .. . ............. 208
110
Pulmonary Parenchymal Trauma .. ............... 205 Mediastinal Injuries ............................. 210
Pulmonary Contusion ..... . .................. 205 Pneumomediastinum .......... .......... . ... 210
122 Pulmonary Hematomata and Pneumatoceles . . 206 Traumatic Aortic and Great Vessel Injury . .. . .. 211
123 Traumatic Diaphragmatic Rupture ...... ......... 212
123
izing
9 Diseases of the Pleura, Diaphragm, and Chest Wall 214
124
125 Diseases of the Pleura ........... . .... .. ...... . .. 214 Diseases of the Diaphragm ..... ... . ..... . . .. .... 228
Pleural Effusion .. . ........ . ....... . .. . .. . . . . .... 214 Diaphragmatic Paralysis . ..........• . ...... . ..... 229
Pneumothorax ........ ..... . ... . .. . .. ... .. . .... . 220 Subphrenic Abscess .............. • •. ...... .. .... 229
Pleural Thickening and Fibrothorax . . . .. . ........ 222 Diaphragmatic Hernia . .... .. .. . .. . . .. . ...... .... 23 1
126 Fibrothorax and Asbestos -Induced Diffuse Bochdalek Hern ia ........ .. . ..• • .. . ..• • . . .... 231
Pleural Thickening ................. ...... . .. . 224 Morgagni Hernia . ............. ... . . .. . . . ... . . 232
Pleural Mesothelioma . ......... . ...... . ....... .. 225 Hiatus Hernia . ..... . . . .' .. . . . .... . ...... . ... . . 232
144
Tumors of the Diaphragm ...... . . .... . . .. . .... .. 234
145
Diseases of the Chest Wall ....... .. ..... ... ... . . 234
147
10 Radiology of Cardiac Disease 240
Cardiac Size .... . .. . ..... . .. . . .. . . ...... . .. . . 240 Ca rdiac Failure ............................... 255
Cardiac Contour ....................... . .... . 240 Ischem ic Heart Disease (IH D) and Myocardial
149 Congenital Heart Disease . . ...................... 243 Infarction (MI) . .... ........ .. . . . ....... . .... . 256
Cardiac Anomalies without a Shunt .. ......... 243 Ca rdiomyopathi es ............................ 261
172 Pul monary Stenosis ................... . .. . . .. 243 Acq uired Va lvular Heart Disease .. ...... . ... .. 262
178 Congenital Aortic Stenosis ... ................. 244 Mitral Stenosi s ....................... .•.. .... 262
181 Coarctation of the Aorta . ........ . .. ....... ... 244 Mitral Regurgitation . . .. . . . ........ . .. • . ..... 263
181 Congenital Cardiac Anomalies Associated with Aortic Stenosis . .......... .. .... .. ...... .. .... 267
181 a Left-to-Right Shunt ......................... 247 Aortic Regurgitation . ............ .. ...... . .... 268
181 Atrial Septal Defect .......... .. .............. 248 Multivalvular Disease . . .... . .. . . .. . .. . .. ..... 268
Ve ntricular Septal Defect ..................... 250 Hyperte nsive Heart Disease . . ...... . ...... . .. 269
Patent Ductus Arteriosus . . . . . .... . ....... .... 250 Cardiac Neoplasms ........................... 269
Total Anomalous Pulmonary Venous Drainage Imaging the Heart Post~lntervention and Surgery. 269
(TAPVD) . . . ....... . ............... . . .. . .. .... 251 Cardiac Pacemake rs .......................... 269
183
Congenital Cardiac Anoma li es associated w ith Coronary Artery Bypass Craft (CABC) Surgery . 270
a Right-to-Left Shu nt ......................... 253 Corona ry Stents .............................. 271
193 Tetralogy of Fallot ........................... 253 Pericardial Disease . . . ........... . ............. .. 272
Uncorrected Transposition of the Great Pericardia I Effusion .......................... 272
...... 194 Vesse ls ...................................... 254 Prostheti c Heart Valves ....................... 272
195 Ebstein Anoma ly . ....... . .. . .. . .... . .... . .. .. 254 Constrictive Pericarditis . . . . . . . ..... .... . . .. . . 272
195 Acquired Heart Disease . .. . .... .. .. . .... . .. . .. . . 255 Pericardial Cysts and Diverticula ...... . .. . .... 273
195
XII Table of Contents
11 Diseases of the Mediastinum 274 1 I

Mediastinal Displacement .......... ' .. .. . . ... .. 274 Ao rtic Ectasia ..............• . ..... . . ......... 278
Air in the Mediastinum ...................•. . .... 274 Ao rtitis ................... " . . ....• . ... .. ... . 284
Air in the Eso phagus and Sto mach ... . . • .. .. . . 274 Mediastinal Hematoma .. .. ... .. ... . .. . . .. .... 284
Pneumomediastinum .................. • _.... 274 Neoplastic Mediastinal Widening ................ 285
Non-Neoplastic Mediastinal Widening ... . . • ...... 276 The Thymus ................................. 288
Acute Mediastinitis ...................• .. . ... 276 Mediastinal Lym ph Node Enlargement ........ 290
Indic
Diseases of the Thoracic Aorta ............ •...... 276 Primary Mediastina l Tumors: Benign Te ratoma
amir
Chronic Mediastinitis ....... . . .. •. ... , . . . .... 276 a nd Ma li gnant Germ Cell Tumors ............. 290
crite
Aortic Anomalies ........ • .....• •• ..... • . .... 276 Neurogenic Tumors .......................... 291
thor.
6-1(
the I
12 High-Resolution!Thin-Section IT Patterns in Pulmonary Disease 293 the
angi
Ground-Glass Opacification-Consolidation .... 293 Decreased Lung Attenuation and Cystic Lung nanl
Multifocal Peribronchial Consolidati on ........ 294 Change ...................................... 297 th e
Pulmonary Nodules .......................... 295 Inhomogeneou s-Mosaic Lung Attenuation ... . . 299
Intra- and Interlobul ar Septal Thickening and Use
Reticu lar Pa ttern ............................. 296 and
logi
acq
13 Radiographic Signs and Differential Diagnosis tho
301
su p
cap
1. The Opaque Hemithorax ... . ............ . .... 301 7. Linear Shadowing .. ........................ 324
2. lobar and Segmental OpaCification ........... 304 8. Reticular Shadowing ........................ 328 sur
3. Opacification which does not Conform to 9. Cavitating Lung Lesions .. ...... , ... .. .... , .. 332 fu r
Anatomic Boundaries . . ................... . .. 3 10 10. Ring Shadows and Cystic Lung Disease ....... 334 me
In homogeneous a nd Regionally Confluent Air 11 . Pulmonary Hypertransradiancy .,' ........ , .. 337 ti g
Space Opacification .. .. ........... .. ......... 3 10 12. Hilar Enlargement ........ , ........ , ...... ,' 341 (VI
Bilatera l Sym metric Hazy Opacifi cation ....... 312 13. Intrathoracic Calcifications .. . " .. ".", ... " 344
en
4. Opacification involving the Upper Zone and/or Pulmonary Calcifications ....... , .. . . ...... . .. 345 ml
Apicomediastinal Angle ................. . .... 315 Tracheobronchial Calcifica tions .....•........ , 347 no
5. lower lung and Cardiophrenic Angle Lymph Node Ca lcification .................... 348
Opacification "', . . , .. , ', . . " ... " . . " .. • , .. . 318 Ple ura l Ca lcifications .............. .. . . . . . .... 348 Re
6. Pulmonary Nodules ...... ... ............ . .... 320 n
th
di
14 Thoracic Intervention
r
349
Biopsy ......................................... 349 Coil Embolization of Pulmonary Arteriovenous

Drainage ............. . .... ... ...... .... . . .. .... 350 Malformations ...... , .... , ... , ....... , , ......... 354
Foreign Body Retrieval-Extraction ..... . . • • , .. ... . 35 1 Coil Embolization of Pulmonary Artery False
Bronchial Artery Embolization ...... . .. ... .. . .... 352 Aneurysms ..................................... 355
Reference list 357
Index 369
1
274 1 Examination Technique and Normal Findings

...... 278
. ..... 284
...... 284
.... .. 285
...... 288
...... 290
Indication and radiation exposure: All radiographic ex- Detect: A methodical approach is important in image in-
toma
aminations should be medically indicated, and stricter terpretation. In evaluation of the chest radiograph, the
290
criteria should be applied in selecting patients for heart size. shape and contour, mediastinalJhilar contour
291
thorac ic cr-which gives a radiation dose in the range of and widening/s ize, the lungs, pleura, bony and soft
6- 10 mSv-than for standard chest radiograph s where tissue structures of the chest wall should be systemati-
the dosage is much lower at 0.02-0.05 mSv. In addition, cally assessed. Review areas include the ap ices, costoph-
293 the ri sk of side effects from contrast agents used in CT, renic angles. retrocardiac lung. and posterior medi-
angiography, radionuclide imaging. and magnetic reso- astinum.
19 nan ce imaging (MRI ) should always be weighed against
297 the expected gain in diagnostic information. Describe and Discuss: If a pulmonary abnormali ty is de-
299 tected. it may be assigned to one of the radiographic pat-
Use of imaging studies: The fronta l pos teroanterior (PA) terns in Chapter 13.
and lateral chest radiographs constitute the basic radio-
logic examination of the thorax. Radiographs should be Differentia l diagnosis: Good results have been achieved
acquired at full inspiration in the upright position, al- with the "gamut approach" (Reeder and Felson 2003 ).
301 tho ugh in sick or debilitated pati ents supine or semi- Just as a musician deliberately strikes each note while
supine anteroposterior (AP) views at functional residual practicing scales on a piano. every possible interpreta-
capacity may be the only option, tion of a pattern should be considered when reading an
324 Plain radiographic findings together with the pre- image. At the very least, the reader should consider the
328 sumptive clinical diagnosis w ill determine the need for various main disease ca tego ries. These include congeni-
..... 332 further imaging studies. In current clinical practice, the tal malformations. inflammatory disorders, chronic ob-
... 334 most commonly requested second -line imaging inves- structive pulmonary di sease (CO PD ), inhalational dis-
.... . 337 eases and pneumoconioses. neoplasia, vascu lar dis-
tiga tion s are CT. ventilation-perfusion scintigraphy
..... 341 (VQS ), and ultrasound. Magnetic reso nance imaging in- orders, and trauma .
..... 344
creasingly is being used in cardiac/myocardial assess-
..... 345 Decide: The ultimate goal of imaging is to make a defini-
ment. and angiography continues to playa role in diag-
..... 347 tive diagnosis. The clinical data frequently are important
nosis as well as intervention .
..... 348 in making a definitive diagnosis. Sometimes. however,
... .. 348 this is not possible and the radiologist can do no more
Reading: Meticulous image interpretation is important.
The "five D's" provide an effective strategy for reading all than offer a differe nti al diagnosis in which diagnoses are
thoracic imagi ng procedures: detect, describe. discuss. listed in order of probability. In this case cytology/his-
differential diagnosis , and decide. tology may be required to make a definitive diagnosis.
349
The five D's for reading thoracic images Disease categories that should be considered in making
s Detect a differential diagnosis (acronym: Victim)
Describe Vascular disease
..... 354
Discuss Inflammation
Differential diagnosis Cancer and other tumors
.... 355 Decide Trauma
Inhalational disease
Malformation
357
369
Radiographic Examination
a
The patient wea rs a short lead apro n. The upper

Frontal Chest Radiograph bo rder of the cassette is at the level of (7, and 35 x 35 to
40 x 40 cm size film is used, depending on patient size.
The upright patient positio ns his ante ri or chest against The roentgen beam is colli mated late rally on the skin
the fil m cassette (Fig. 1.1 a, b ). The dorsa l aspects of the surface over the lower ribs and is centered on the fourt h
hands are placed on the hips, and the shou lde rs are thoracic vertebra (T4),
ro lled forward to project the scapulae ou tside the lungs. The radiograph is take n at full inspi rati on using, fo r
For better support, weak patients may place their arms example, a film-foc us distance (FFD) of 185 cm and ex-
around the cassette sta nd. posure parameters of approximate ly 125 kV, 5 rnA, or
automatic exposure control.
The AP projection is usefu l for imagi ng sick patients
(Fig, 1.1 c, d), Bedridden patients are filmed in the supine
posit ion, and inte rnal rotation of the sho ulders aids in
separating the scapulae (Fig. 1.1 e ).
Characterist ics of a technically acceptabl e fro ntal chest

ra diog ra ph:
The spinous process of T3 is projected midway be- e
tween the sternoclavicular joints. indicati ng the ab-
se nce of chest rotation.
The med ial borders of the scapu lae project outside the
rib cage or touch the lateral aspects of the ribs.
The t horax is complete ly imaged if the lary nx and both
costophrenic angles are vis ible.
The degree of inspi ration is adequate if t he dome of the
diaphragm projects caudal to the posterior part of the
9th rib.
Exposure time is appropriate if the hea rt. d iaphragm,
and large pu lmonary vessels are sharply defined.
Overexpos ure is excluded if vascu lar shadows can be
seen in the lung periphery.
Unde rexposure is excluded if the large r lower lobe :es- :J
sels and the t h oraci~ vertebrae still are visib le t hrough
the cardiac silhouette.
The technical parameters recommended for chest rad io-

graphs are listed in Table 1.1 .
Table 1.1 Techn ical parameters for chest rad iographs (Zimmer
and Zimmer-Brassy 1992)
Technical specifications Grid technique,

wa ll cassette holder
Automatic exposure control:

• PA Side chamber
• Lateral Central chamber
Film format 40 x 40 (30 x 40, 35 x 35)
Film-screen system Film speed 400 (200)
Focus-film distance 150-200 em
Kilovoltage 1l0- 150kV
Exposure:
• PA <20ms
Fig. 1.1 a- e Chest rad iographs in PA and AP projections. a , b • Lateral <40ms Fi~
Sta nding PA radiograph. c, d Sitting AP radiograph. e Supine AP Scatter reduction grid r/2(8) ra,
radiograph. gr
Radiographic Examinat ion 3
lateral Chest Radiograph

b
The patient, wea ring a lead apron. stand s sideways

le upper against the cassette with arms raised. The roentgen
15 x 35 to beam is centered approximately 10 em caudal to the ax-
:ient size. illa (Fig. 1.2a, b).
the skin The radiograph is taken at full inspiration using film
he fourth size 30 x 40 or 35 x 35 cm. A FFD of 185 cm and settings
of 125 kV, approximately 8 rnA, or automatic exposure
Jsing, for control are appropriate.
1and ex- Debilitated patients are radiographed in the sitting
5 rnA, or position (Fig,1.2c, d ) or, if necessary, in the lateral decu-
bitus position with the head supported, the arms drawn
; patients forward and upward, and the legs slightly flexed to im-
ne supine prove stability (Fig. 1.20).
rs aids in
Criteria for a t echnically acceptable lateral chest radio·
graph:
The entire lung is visible.
chest
The view is not rotated if the right and left posterior
e- c d rib margi ns are superimposed.
lb- The arms are not superimposed on pu lmonary struc-
tures.
je the The image is not overexposed if the pulmona ry ves:
elsJ
in the retrocardiac space are well defined.
d both
The image is not underexposed if the large pulmonary
~ of the vesse ls are vis ibl e through the card iac silhouette.
)f the
3.gm,
Oblique Views
n be
The patient is rotated in the frontal plane to approxi-
~e ~;~- I mately 45° with either the right (right anterior oblique
ro~ or "fencer" position; Fig. 1.3 a) or left anterior chest wa ll
(left anterior oblique or "boxer" position; Fig. 1.3 b) in
est rad io-
15 (Zimmer
) x 35)
0)
>-
o
Fig.l.2a-e lateral chest radiographs. a, b Standing lateral Fig. 1.3a. b Oblique chest radiographs. a Right anterior oblique
radiograph. c, d Sitting lateral radiograph. e Supine lateral radio- (fencer) position, b left anterior oblique (boxer) position.
graph.
4 1 Exa mination Tech nique and Normal Findings
contact with the cassette. The depth of inspiration, film Fluoroscopy

size, FFD, and exposure parameters are the same as for
the PA view.
Fluoroscopy is used occasionally today and is a valuable
adjunct to the chest radiograph. It analyzes dynamic
processes and facilitates localization of pathologic
Apical Lordotic View changes but it has a much lower spatial resolution than
the chest radiograph.
The patient stands about 4 cm from the chest stand and Fluoroscopy is performed using an AP or PA beam at
arches the upper body backward until the shoulders maximum shutter aperture. This permits comparison of
tou ch the cassette. A FFD of 100 cm and 35-45" of the respiratory movements of the diaphragm and chest
cephalad tube angulation are appropriate. The beam is wall on both sides. The patient should breathe deeply,
centered on the manubrium sterni (Fig. 1.4). cough, blow his nose, and expire against a closed glottis
A technically acceptable image shows the lung apices to raise intrathoracic pressure (ValsaJva maneuver). Fi -
projected clear of the sca pulae. nally. the patient attempts to inha le with the nostrils
pinched shut: this lowers intrathoracic pressure (Milller
maneuver). Sniffing is important since it elicits pure dia- Fig.
phragmatic motion and can thus magnify any asym- deer
soft
metric or paradoxical motion.
The above-described su pplementary chest views to-
b gether with fluoroscopy are used less frequently as cr
becomes the mainstream second line imaging investiga-
tion in the assessment of thoracic disease.
Fig.
line~
Scatter-Reduction Grids
Grids are used to reduce scatter radiation, which de- • I

grades contrast in radiographic images.
Two main types are available:
Focused moving grids, which are used on a Bucky
table. The strips in the grid are aligned to match the
divergence of the primary beam (Fig. 1.5 a). Because the
· (
grid moves during the exposure, grid lines do not appear

in the final image. There are two main sources of expo-
Fig. 1.4a. b Apical lordotic views. a Standing, b supine. sure errors with this type of grid system:
Th
• b •,, c
,,
,, The
,
,,
,,
,, ··
(Fig
(
• I
• I
• r
4 ---,-, ;
are
2 app
ord.
5 3
Fig.l.5a-c Scatter-reduction grids. The strips of the grid converge toward the roentgen focus (a). A defocused grid (b) leads to
underexposure of the lateral areas. An off-center grid (c) leads to asymmetrical exposure (modified from laubenberger 1980).
The Normal Chest Radiograph 5
valuable
dynamic
3thologic
tion than
. beam at
arison of
Ind chest
e deeply.
ed glottis
uver). Fi-
~ nostrils
e (Muller
pure dia- Fig. 1.6 Asymmetrical exposure due to a tilted grid. Note the
decreased lucency of the lung and "haziness " of the bones and
1Y asym-
soft tissues on the left side.
views ro-
Itly as CT
nvestiga-
Fig. 1.7 Stationary grid for bedside radiog raphy. Vertical grid
li nes are visible on the image.
• Defocused grid. If the necessary focus ing distance is Stationary grids with para llel strips are used for bedside
vhich de- not maintained between the grid and X-ray tube. the radiography. Often it is difficu lt to position the patient as
lateral portions of the image w ill be underexposed desired, and it is not unusual to work with a tilted grid.
(Fig. 1.5 b). This also causes asymmetrical film exposure because the
a Bucky • Off-center grid. If the central ray is not aimed at the strips at one ed ge are aligned with the beam divergence
narch the center of the grid (due to a poorly adjusted collima- while the strips at the other edge are not (Fig. 1.7 ). When
cause the tor. for example). the film will be asymmetrica lly ex- an image made with a stationary grid is examined
.ot appear posed (Figs. 1.5 c. 1.6). closely (e.g.. with a magnifying lens), grid lines always
:; of expo- can be seen.
The Normal Chest Radiograph
The chest radiograph requires a systematic evaluation Structures of the Chest Wall
(Figs. 1.8 and 1.9 ) in which the
• chest wa ll,
• diaphragm, • Thoracic Skeleton
• pleura,
• lungs, and The thoracic ske leton comprises the ribs, vertebral
• mediastinum column, scapulae, clavicles, and sternum.
are identified, analyzed, and described. To reinforce thi s Ribs

approach. these regions will be considered in the above
order. The posterior aspects of the ribs have an almost horizon-
tal orientation, and they then extend obliquely forward
from superolateral to inferomedial to the costochondral
(b) leads to junction. Rib cartilages are not visible on chest radio-
1980). graphs except in the elderly when carti lage calcification
Fig. 1.8 PA chest radiograph. Fig. 1.

1 Trachea 1 T
2 Right main bronchus 2 P
3 Left main bronchus 3 A
4 Scapula 4 R
5 Clavicle 5 L,
6 Manubrium sternum 6 L,
7 Azygos vein 7 R
8 Aortic arch 8 A
9 Left pulmonary artery 9 5
10 Upper left cardiac border. left atria l appendage 10 R
11 Lower left cardiac border, left ventricle v
12 Right atrium 11
13 Lower lobe arteries v
14 Lateral costophrenic angle 12 C
15 Breast shadow 13 T
14 If
Fig. 1.9 l atera l chest radiograph.

1 Trachea
2 Pretracheal vascular bundle
3 Aortic arch
4 Right upper lobe bronchus
5 left upper lobe bronchus
6 Left pulmonary artery
7 Right pulmonary artery in pretracheal vascular oval
8 Axi llary fold
9 Scapu la
10 Right posterior costophrenic ang le (right hemidiaphragm
visible as far as the sternum)
11 Left posterior costophrenic ang le (left hemidiaphragm
visible as far as the cardiac silhouette)
12 Gastric bubble
13 Transverse colon
14 Inferior vena cava
may be present. The dorsal aspects of the ribs appear Sternum Axilla
denser because they have an alm ost circular anatomic
cross section. while the ventra l aspects are flatter and On the frontal radiograph, only the ma nubrium, part of The al
therefore more radiolucent. The ribs may have a sli ghtly the body of the sternum, and the sternoclavicular articu- co ncal
ill-defined inferior border due to thinning of the bone at lations are delineated. The lateral view defi nes the corti- the lu
the subcostal sulcus. cal outlines and the synchondrosis between the manu- third (
On the latera l view, the posterior rib segments pro- brium and body (Louis' angle). The normal ste rnum the ax
ject behind the vertebral bodies while the lateral por- shows a slight degree of anterior convexity. In the "fun-
tions appear as faint bands running obliquely forward ne l chest" deformity (pectus excavatum), the sternum is Clavic
and downward. convex posteriorly and projects behind the anterior rib
margins. In "pigeon chest" (pectus carinatum), the ster- This n
Vertebral Column num is bowed forward, showing an exaggera ted anterior the c1;
convexity. x- ray
The vertebral col umn should be vis ible through the car-
diac silhouette on a we ll-exposed frontal radiograph. Stern!
The vertebra l bodies, pedicles, spinous and transverse • Soft Tissues of the Chest Wall
processes may be iden tified. On the latera l view, the su- The sl
perior and inferior articular processes may be identified. The soft t issues form the co ntour of the chest wa ll. They vertic.
also may project ove r the intrathoracic organs as opaci- fined
Scapula ties and interface lines (Figs. 1.10 and 1.11 ), camp.
The medial and lateral borders, the inferior angle, the Skin Folds Supra
spine, and the coracoid process of the sca pula may be
identified on the frontal chest radiograph. On the lateral Skin folds are especially prominent on supine radio- Visibl(
view, the scapulae project onto the vertebral column as graphs of cachectic patients. They may form linear pears
dense vertical bands; their connection with the raised opacities and should not be mistaken for a the el i
upper arms usually can be appreciated. pneumothorax. tingui
Clavicles Breast Shadow Juguli
The clavicles extend hori zontally from the acromio- The breast shadows decrease the lu cency of the lower In thir
clavicular joints laterally to the sternoclavicular joints lu ng zones. Nipple shadows may mimic small pulmo- sharp
medially. They are projected over the lung apices on the nary nodules and may be quite asymmetrical in appear- inaU·
fronta l radiograph. A notch formed by the insertion of ance. widen
the costoclavicular ligament often is seen inferiorly at
the sternal end of the clavicle (rhomboid fossa ), Uppel
The I;
upper
and ri
~---- Jugularfossa tours :
. -i~~~~~~~!P!~~- , r - -- - - Companion shadow
of clavicle
Floor of Dia~
supraclavicular fossa
Posterior __
Anterior The d
axillary fold
thora>.
indivi(
phragl
.-- -+- Nipple the lu
Breast viewa
te rior
phragl
In deE
Fig.1.10 Axillary folds: posterior Fig.1. 11 Soft-tissue shadows of the chest wa ll.
axi llary fold (white arrow), anterior caudal
axillary fold (arrowhead), apex of diophl
axilla (black arrow). aphrai
The Norma l Chest Rad iograph 9
Axillary Folds
n, part of Th e anterior and posterior axillary fold s have caudally

aT articu- concave contours. and the ir interface may project over
the corti- the lung. occasionally mimicking a pneumothorax. A
]e manu- third caudally concave shadow represe nting the apex of
sternum the axilla sometimes may be seen in thin patients.
the "fun-
ternum is Clavicula r Companion Shadows
Iterior rib
, the ste r- This narrow soft-tiss ue stripe along the upper border of
d anterior the clavicle represents soft tissue that is tangential to the
x-ray beam (Fig. 1.12).
Ste rno cleidomasto id Muscle

Fig.1 .12 Companion shadow of the clavicle (tangential projec-
The sternocleidomastoid muscle appears as an almost tion of the skin over the clavicle) and the vertical shadow of the
Nail. They vertical soft-tissue opacity in the neck. It has a we ll -de- sternocleidomastoid mu scle.
; as opaci- fined late ral border, and it merges inferiorly with the
companion shadow of the clavicle.
The right hemidiaphragm may lie up to 4 cm cranial
to the left hemidiaphragm. The cauda l surface of the dia-
Supraclavicular Fossa phragm is not visible unless it is outlined on the left by
the gastri c bubble or on th e right by air between the live r
ine radio- Visible only in thin pati ents, the supraclavicular fossa ap-
and diaphragm, as can occur in both pneumoperi-
rm linear pears as a th in hori zo ntal line projected above or below
toneum and colonic interposition (Ch ilaiditi syndrome).
n for a the clavicle. It extends laterally beyond the lung, thus dis-
Individual muscle slips may give the smooth contour
tinguish ing it froman ap ical pneumothorax(see Fig. 1.11 ).
of the diaphragm a scalloped or serrated appearance in
the lateral cos tophrenic angle. This normal variant may
Jugular Fossa be especially pronounced in emphysema.
the lowe r If the d istance between the lowe r border of the lung
In thin patients, both sternocleidoma stoid muscles have
and the gastric air bubble is more than 1 cm, a patho-
,II pulmo- sharp medial borders and their contours unite inferiorly
logic process such as a subpulmonic effusion should be
in appear- in a U-shaped configuration. This may sometimes mimic
suspected. Thi s sign is especially valuable in the lateral
widening of the trachea.
projection.
Several features can be used to differentiate the left
Upper Arms and right hemidiaphragms, On the lateral chest rad io-
graph, the left hemidiaphragm is usually lower anteri-
The latera l radi ograph projects the soft ti ssues of the
orly and higher posteriorly with the gastric bubb le lying
upper arm over the anteroapical lung. Usually the left
inferiorly. Its contour extends anteriorly only to the
and right upper arm s can both be seen and their con-
posterior border of the ca rdiac sil houette. The ri ght
a J tours are continuous with the posteri or axi llary fo ld.
hemidiaphragm is usually higher anteriorly and lower
shadow posteriorly. Its contour may be traced throughout its
posteroanterior course from the posterior costophrenic
Diaphragm angle forward to the sternum (Fig. 1.13 ),
Jlar fossa
The diaphragm form s the inferior boundary of the

tho rax. It is slightly curved towards the lu ng. In norma l Pleura
individuals, the angle between the chest wall and dia-
phragm is acute in inspiration. These angles border on
the lung, so they are clearly visible late rally in the PA • Anatomy and Physiology
view and posteriorly in the lateral view (lateral and pos-
terior costophrenic angles). The angle between the dia- The pleura co nsist of two laye rs. The parieta l pleura li nes
ph ragm and heart (cardiophrenic angle) is usually acute. the chest cavity and is fu sed w ith the chest wa ll, d ia-
In deep inspiration, the diaphragm moves sufficient ly phragm, and mediastinum. The visceral pleura invests
caudad to all ow visibility of the 10th rib in the right ca r- the surface of the lung and merge s with the parietal
diophrenic angle. During expiration, the dome of the di- pleura at the hi lum, A capi llary space containing a film of
aphragm moves upward by approxi mately 3-7 cm. fluid permits relative motion between the two layers.
10 1 Examination Te chnique and Normal Findings
Apposition of th e pleural leaves is made possible by

Sharp costophrenic
a nega tive pressure w ithin the pleural cavity (approxi-
angle
mate ly -S em H20); this counteracts the elastic recoil
of the pulmonary interstitium. Because of the intrinsic
we ight of the lung, this partial vacuum is greater in
the apical region than at the base (Pare and Frase r
1983).
Negative pressure is important in keep ing the lungs
inflated. Serum inflow would tend to equalize thi s pres-
sure were it not for the low protein content of the pleural
fluid and the oncotic "suction" of the adjacent capillary
Respiratory left blood, which tend s to draw flu id from the pleu ral space.
excursion 3-7 em hemidiaphragm Negative press ure is maintained eve n though approx i-
up to 4 em lower
than the right
mately 100 mL of fluid fl ows from the parietal pleura to
the visceral pleura eac h day. This is possible because of
the unequal hydrostatic pressures in the chest wall and
pulmonary ca pillaries (Fig. 1.14).
Fig.
and
• Radiographic Anatomy con
file
row
The peri pulmonary pleu ra invests the surface of the t he
lung, and the inte rlobar pleura lines the fi ssures be-
tween the lobes. Rad iographically, the peripulmonary
pleura appears only as an interface between the lung
and soft ti ss ues. The inte rl obar pleura wh ich comprises cos
the fissures, on the other hand. often is directly vis ible as wa'
a ha irline shadow.
Pe ripulmonary Pleura
AI
- Right leaflet usually hig her than the left leaflet A dense stripe 0.5 mm in width may occasionally be fro )
- Right leaflet extends anteriorly to sternum see n in the area where the lung abuts the chest wa ll, dia-
-left leaflet extends to posterio r heart border Thi
- Ga stric bubble lies below the left leaflet
phragm. and mediastinum. This st ripe does not repre- gra
sent the pleura; it is a visua l artifact caused by the col- po~
Fig.l.13 Radiographic appea ran ce of the diaphragm. lateral inhibition or stimulation of retina l receptors
(Mac h effect; Fig. 1. 15). This is easily co nfirmed by cove r-
Ap
ing the lung wi th a piece of paper next to the st ripe and
noting that the stripe is go ne (Fig. 1.16). Ani
The peripu imonary pleura has seve ral rad iographi- bUI
cally distinct compone nts (Coussement and Butori 1978; viel
Parietal Visceral Fig, 1.17 ). sup
pleura pleu ra
shG
Space Compa nion Shadow of the Second Rib par
The apical pleura appears in profil e as a stripe. 2 mm in

Osmot ic -34 - 34
pressure + 8 + 8 width, at the inferior border of the posterior aspect of
the second rib (Fig. 1.18). On
in I
Hydrostatic Companion Shadow of the Latera l Chest Wall ten
pressure +35 +16 the
The pleural line, if see n tangentially, usua lly is smooth pie
but occasionally bulges into th e intercostal spaces, phr
Net creating a scalloped co ntour. In obese patients an extra-
pressure + 9 - 10
pleural fat stripe, severa l mi ll imete rs in width. may be
visible between the inne r surface of the ribs and the lung
Fig.1, 14 Hydrostat ic and oncotic pressu re in t he pleu ral layers edge ; th is should not be confused with pleura l thicken-
(from Muller and Fraser 2001). ing or a small pleural effu sion. Occasiona lly the sub-
ssible by
approxi-
tic recoil
intrinsic
feater in
ld Fraser
'he lungs
:his pres-
le pleural
capillary
ral space.
approxi-
c
Densitometric
profile
L
1
L 2
L
pleura to
~cause of
wall and
Human
perception
1- 1- -t
Fig. l.15a-c The Mach effect. The contour of the aorta on a chest radiograph (a) appears to be accompanied by a dark stripe (a rrow),
and the paraverte bral space ap pea rs to be bou nded by a brig ht stripe (arrowhead). These are optical ill usions due to accentuation of
contrast in the human retina . Whe n two homogeneous areas of different brightness are apposed (1 in c), the actual de nsito metric pro-
file (top row in c) is not perceived. Instead, the bright area appears even brighter while the da rk area a ppea rs somewha t darker (bottom
row in c). If the bright area darkens toward the boundary, the contrast appears to be accentuated o nly in the dark area (2 in b and c). If
:e of the the dark area gradually lig htens toward the bo undary, a bright edge will be perce ived (3 in b and c).
sures be-
Lllmonary
the lung
:omprises costal muscle fibers elevate the pleura, producing a
visible as wavy contour (see Fig. 1.16).
Basal Pleural Reflection
A line may be seen passing medially and horizontally

onally be from the deepest point of the lateral costophrenic angle.
wall, dia- This is seen particularly well on overexposed radio-
lot repre- graphs. It corresponds to the pleural reflection at the
'y the col- posterior costophrenic angle.
receptors
I by cover-
Apical Pleural Cap
stripe and
Anteriorly the lung extends to the level of the clavicle,
liographi- but posteriorly it projects more superiorly. On the lateral
Itori 1978; view, the soft-tissue shadow of the upper arm usually is
superimposed usually on the lung apex. However, if the
shoulders are lowered, the lung apex with its accom-
panying pleural shadow may be seen.
~,2mm in
Posterior Pleural Stripe
aspect of
On the lateral view, the posterior pleural stripe is visible
in profile along the posterior ribs. The pleural stripe ex-
Nail tends inferiorly to the posterior costophrenic angle and
the diaphragmatic reflection. On the lateral view, the
is smooth pleural line can help in identifying right and left dia-
al spaces, phragmatic leaflets (see Fig. 1.13).
5 an extra-
ch, may be
Id the lung
Fig. 1.16 An apparent bright stripe is perce ived at the bou nd ary
al thicken- between t he lu ng and soft tissue as a result of the Mach effect
V the sub- (see Fig. 1.15).
J
12 1 Examination Te chnique an d Normal Findings
_.,
--------.. Azygo
~~.<y
Anterior superior The rig
pleural junction line
and fo
stripe supenor Retrotracheal Azygoeso- Para-aortic azygos
- -- pleural pleural stripe phageal - - _ stripe pleural
~ Juncti on Ime o
stnpe ---- VIII - - Paraverte bra I course
~ stflpe
a ~ b c
ParaVE
Posterior superior ---.",._ r-'-~y':::;a...~ The pc
Anteriors uperior
·~----· l~l~~~;~~~
___ __ ,+
lateral
Intercostal
tangen
Para tracheal stripe bulges ible str
Apical widening seen (
by inno minate vein proces:
Extrapleu ra l hemat!
fat stripe
(in obese patients) side, t t
Retrosternal
stripe half thl
Su bcostal
muscle stripe
Para-a
Basal Posterior
pleural stripe (in muscu lar patients)
widening by Thi s a,
epica rdial fat
Diaphragmatic Compa
muscle slips re vea l ~
d • border
tiveM;
pa ralle
Fi9.1.17a-e Pleural reflection s (from Heitzman 1993, Meschan 1981).
tis sues
su its ir
a whitl
pleural borde r is smoother beca use of the interposed
heart. In the basal part of the retrosternal stripe. epi- Right
cardial fat frequently di splaces the left anterior lung
border from the chest wa ll, producing a triangu lar retro- This cc
sternal opacity (cardiac incisure). the t ra
due to
ve in. 1
Posterior Superior Pleural Junction Line
exceed
The pleura sweeps medially from both sides as a con- perior
tinuation of the companion shadow of the 2nd rib, compu
unites at the level of the T3/4 interve rtebral space, then tra che,
passes as a vertical stripe to the aortic arch. This creates will d
Fig. 1.18 The companion shadow of the second rib corresponds a V-shaped shadow that corresponds to the posterior Fig. 1.1
to the lung apex or the boundary between air and soft tissue. The pleural reflection (see Figs. 1.17 d , 1.19). It is composed of
catheter position defines the course of the subclavian vein. Retrol
four layers of pleura and corres ponds to the co urse of the
superior intercostal ve ins.
On thl
poster
Retrosternal Stripe Anterior Superior Pleural Junction Line
3mm
On the lateral view, the retrosternal stripe is relatively This pleural renection corresponds to the cou rse of the
wide superiorly behind the manubrium. He re, t he bra- innominate and su bclavian veins. It form s a V-shaped
chiocephalic vein is interposed between the lung and configuration. the limbs of which originate from the in-
ste rnum. The stripe is narrower in its midportion. where ferior margins of the sternoclavicular joints. They course
the right and left anterior lung borders may be differe n- caudally, medially, and, on uniting, slant to the left. The
tiated. The right pleura protrude s into the intercostal anterior junction line complex extends inferio rly to the Fig. 1.21
spaces and thus has a wavy contour; it is frequently pro- heart and encompasses the pote nti al space of the ante- lateral!
jected over the body of the sternum, The left anterior rior mediastinum (see Figs, 1.17 e, 1. 19). and the
The Normal Chest Rad iograp h 13
Azygoesophageal Stripe
The right lung extends in front of the vertebral column

and fo rms the azygoeso phageal recess, It borders the
azygos vein and the esophagus and forms a mediastinal
pleural stripe in a paramed ian location, paralleli ng the
)ral course of the esophagus (see Figs. 1.17 e, 1.20),
Paravertebral Stripe
The posterior parts of the lungs are contiguous to the

lateral aspects of the vertebral bodies. Pleura seen in
tangent to the roentgen beam in this region forms a vis-
ible stripe on the left side. On the ri ght side, the stripe is
seen only if it is widened by aging or pathologic
processes such as degenerative osteophyte formation,
hematoma, or tumor (see Figs. 1.1S a, 1.17 e ). On the left
tients) side. the paravertebral stripe can reach a width equal to
half the diameter of the descend ing aorta.
Para-aortic Stripe
pe
Irpatients) Fig. 1.19 The posterior pleural reflection (- posterior superior
This accompanies the descending aorta on the left side. pleural junction line. arrows) and anterior pleural reflect ion
Comparison of the paravertebral and para -aortic stripes (= ante rior superior pleural junction line, arrowheads).
latic
reveals an interesting visual phenomenon : The aortic
" border to the lung is a convex arch; th is produces a nega-
tive Mach effect. resulting in an apparently darker stripe
paralleli ng t he desce nding aorta. The paravertebra l soft
tissues have a concave bou ndary with the lung; this re-
sults in a positive Mach effect creating the impression of
a white border stripe (Figs. 1.1Sa, 1.17 e, 1.20).
Iterposed
ripe, epi- Right Paratracheal Stripe
riar lung
(Iar retra- This corresponds to the mediastinal pleura l refl ection on
the tracheal wall. The inferior widening of the stripe is
due to the horizonta lly orientated arch of the azygos
ve in. The width of the paratrachea l stripe should not
exceed 4 mm. It frequently is superimposed on the su-
as a can- perior vena cava. A well-exposed view. conventional or
2nd rib, computed tomography (CT) wi ll demonstrate the para-
lace, then
lis creates
posterior
nposed of
lfse afthe
tracheal stripe. azygos ve in. and superior vena cava and
will determine the true width of this stripe (see
Fi g. I.17 e).
Retrotracheal Stripe
-
On the lateral radiograph, th is stripe blend s with the
posterio r border of the trachea and should not exceed
3 mm in width (see Fig. l.17d ),
rse of (he
V-sha ped
)m (he in-
ley course
e left. The
)fly to the Fig.1.20 The azygoesophageal stripe (black arrow). the left
'the ante- lateral esophageal wall with air in the esophagus (white arrow),
and the para-aortic stripe (arrowhead).
Interlobar Fissures
Two layers of visceral pleura separate the pulmonary

lobes and, occasionally, the segments. These duplica-
tions are visible when a significant segment is imaged in
profile. The following are frequently seen on the chest
radiograph:
Major (Oblique) Fissures
Very occasionally. a tenting of the diaphragmatic pleura

is seen on the PA chest radiograph; this corresponds to
the caudal end of the major fissure. On the lateral view.
the major fissures are seen as fine linear shadows that
course obliquely in an anteroinferior direction (Fig. 1.21 ).
The union of the right horizontal fissure with the ob-
lique fissure may help to distinguish between the right
and left oblique fissures. In addition, the left oblique fis-
sure usually runs more vertically than the right. The a
major fissures merge with the ipsilateral diaphragmatic
leaflets allowing further distinction between right and
left sides (see Fig. 1.13 ).
Minor (Horizontal) Fissure

Fig. 1.21 Right and left obliq ue fissures (lower black arrow),
In the right midzone. there is a fissure between the
horizontal fissure (upper black arrow). and left accessory fissure
(white arrow). upper and middle lobes extending to, but not crossing
the hilar shadow (Fig. 1.22). Occasionally this line is ac-
companied by a seco nd. parallel stripe representing a
second section of the horizontal fissure seen in tangent
to the x-ray beam. On the lateral view, the minor fissure
appears as a horizontal line extending anteriorly from
the major fissure to the sternum (see Fig, 1,21),
Azygos Lobe Fissure
The azygos vein normally runs medial to the right lung.

In 0.5 % of the population, it has a more lateral course Fig.
and descends along a fi ss ure in the upper lobe. This
forms a curvilinear shadow in the right upper zone
a
which has the shape of an inverted comma (Figs. 1.23,
1.24), The azygos fissure contains four layers of pleura.
Cardiac Lobe
In 10% of the population, the mediobasal segment of the

right lower lobe is separated from the other basal seg-
ments. On the PA view, this inferior accessory fissure is E
seen as a line lateral to the cardiophrenic sulcus (see 7
Fig. 1.22). 8,9
10
Other Accessory Fissures 11
12
In 6 %of the population, the apical segment of the lower 13
b lobe is separated from the basal segments by an acces-
Fig. 1.22a. b Horizontal fissu re and cardiac lobe. sory fissure. On the lateral view, this is seen as a horizon-
tal line extending from the oblique fissure to the poste-
Fig. 1
rior chest wall. Other unusual accessory lobes and fis - lese!
sures are illustrated in Figures 1.25 and 1.26.
The Normal Chest Radiog rap h 15
Ji monary
duplica-
maged in
the chest
tic pleura
lponds to
eral view,
lows that
:Fig.l .2l ).
b
th the ob-
the right
)lique fis-
eight. The
lragmatic
• Fig . 1. 23a , b Azygos lobe .
right and
Four pleural layers

..1\- I~ZVQOS lobe
ween the Azygos vein ------fIJ

t crossing
line is ac- Parieta l pleura
~sent in g a
.n tangent Visceral pleura
lOr fissure
iorly from
).
Embryonic state Normal development Development of anomalous azygos lobe

right lung.
Fig.1. 24 Development of an azygos lobe (from Meschan 1981).
'raJ course
lobe. This
pper zone
(Figs. 1.23, 1 Horizontal fissure of right lung
of pleura. 1a Horizontal fissure of left lung
2 Oblique fissure 4
3 Fissure of azygos lobe
4 Fissures 51 and 52
ne nt of the 5 Fissure between 56 and
basal seg- 1.
the basa l segments
y fissure is 6 Boundary of 57
;ulcus (see 7 Fissures 51 and 53
8,9 Fissures 52 and 53 5
10 Fissures 54a and S4b 11
ft he lower 13 Fissures 59 and 510
b
of an acces-
; a hori zon-
the poste-
Fig. 1. 25 a-c Interloba r and accessory fissures. a PA view of right lu ng. b Lateral view of right lung. c l ateral view of left lung (from W.
,es and fis- Teschendorf 1975).
L
\
Fig. 1.26 lateral views of the interlobar fissures. Note the typical Fig. 1.27 Landmarks for identifying lung zones. 1 Apex, 2 upper
propeller shape of the oblique fissure. formed by the costal mar- lone, 3 midzone. 4 lower zone.
gin (solid line) and the mediastinal margin (broken line) (from H.
Uthgenannt, Linear opacities. In: W. Teschendorf 1975).
lung Parenchyma
The frontal chest radiograph di splays the lungs as they

lie to either side of the mediastinum. For orientation
purposes, the lungs may be divided into upper, middle,
and lower zones by two horizontal lines drawn through
the upper and lower borders of the hilum (Fig, 1,27). The
ap ical subdivision of the uppe r zone (lung apex) lies su-
perior to the clavicle.
The lungs may also be divided into central (pe rihilar )
and peripheral (subpleural ) regions. The latter is the 4-
cm wide parenchymal zone at the periphery of the lobes
that is devoid of radiologically visible vessels (Fig. 1.28).
Subdivision of the lungs into upper, middle, and
Fig. 1, 28 Subdivision of t he lungs into 1 hilum . 2 central or peri- lower zones is possible when the topography is known
hilar region, and 3 peripheral region.
(Fig. 1.29). However, accurate subdivision and lesion lo-
calization are possible only when all ofthe interlobar fis-
sures are vis ible.
The basic unit of gas exchange, the alveolus, is radio-
logically invisible because of its minute size. The human
lung contains approximately 300 million alveo li ar-
ranged like clusters of grapes around the dichotomously
branching bronchial tree. The diameter of the alveolar
wall capillaries is just sufficient to allow passage of
erythrocytes. The alveolar wa ll consists of flattened
epithelial cells (type I pneumocytes ) and granular type II
pneumocytes. Type I pneumocytes line the alveolus and
o Upper lobe
are apposed to the endothelial cells of the alveolar wall
capillaries. Granular pneumocytes, usually five to eight
in number, lie between epithelial cell s and produce sur-
Prim
• Right middle lobe factant. This phospholipid reduces surface tension A pr

within the alveolus and allows expansion (Muller and lung.
ITII1 lower lobe Fraser 2001 ). tory
The alveol i toget her with the bronchioles, nerve s, and mal i
Fig. 1.29 Projection of the lobar boundaries in the PA radio- blood vessels are the functional units of the lu ng BecaJ
graph (from Bohlig 1975). (Fig. 1.30): ible (
Fig. 1.30 Branching pattern of the

o Site of bronchiectasis bronchial t ree (Meschan).
B Bronchi
I l lobular bronch ioles
T Terminal bronchioles
1- 4 Respi ratory bronchioles
D Alveolar ducts
At Atrium
5 Alveolar sac
Mi llimeter
region
Secondary
lobule
x, 2 upper
o Site of o Site of centri- 0 Site of panlobular

bronchia l ectasia lobular emphysema emphysema
:s as they
'ientation
Fig. 1.31 The secondary pulmo nary
r, middle,
lobul e. The lobu lar bronchiole and artery
.1 through enter th e lobule centra lly. and peripherally
Respirato~
1.27). The bronchioles ~s;;;;;;~;;;;;;;;;;r~~;;~l nterlobular septum the interlobula r veins course wit hin the in-
xl lies su- terlobu lar septa. The lobular bronchiole
branches into term inal bronchioles, which
aerate the acini. The term ina l bronchi oles
.perihi lar) give rise to respiratory bronchioles wh ich
r is the 4- supp ly t he primary lobu les (Schinz 1983).
' the lobes Acinus
(Fig. 1.28).
ddle, and
~~~~~Li~and
, alveolar
duct
is known
lesion 10-
"lobar fis-
Terminal
S, is radio- bronchioles
'he human
llveoli ar-
otomously Lobular
.~~----~------ arte~
Ie alveolar Interlobular
;Jassage of vein -Iff--------- Lobular bronchiole
f flattened
ulartype II
.veolus and
veolar wall
ve to eight Primary Lobule Acinus
~od uce sur-
ce tension A primary lobule is the smallest fun ctional unit of the An acinus consists of all structures distal to the terminal
Muller and lung. It comprises all the structures distal to a respira- bronchiole, including vessels, nerves, and connective
tory bronchiole induding the 16 to 40 a lveoli. The nor- ti ssue. It has a diameter of 4 to 8 mm and conta ins ap-
nerves, and mal adult has approximately 23 million primary lobules. proximately 10 to 20 primary lobules. Mull er and Fraser
f the lung Because of their small size, primary lobules are not vis- (2001 ) describe the acin us as the fun ctional unit in
ible on chest radiographs (Fig. 1.31 ), which perfusion and ve ntilatio n are coord inated. When
18 1 Exa m ination Technique and No rmal Finding s
Fig. 1.32a. b Pulm onary hemor-

rhage during percuta neous fine Rj~
needle aspiration (FNA) of a pulmo-
nary mass (a). The resulting pulm o-
(
nary opa cification has an u a cina r~
pattern (b).
a ...._ _ _ _- - ' = _ . -- 1 b
infiltrated. the acinus appears rad iologica lly as an iII-de- id enti fied by their characteristic radiogra phic appear-
fin ed opacity approxim ately 0.5 em in diamete r (acinar ances (see Figs, 1.26, 1.33),
shadows ). Peribron chiolar infiltration or co nso lid ation
may have a similar radiograph ic appea rance and thus Pasl
may mimi c acinar shadowing (Rau 1980; see Figs. 1.31,
1.32 ).
Tracheobronchial System
Second a ry Lobul e
Th e second ary lobule is th e smallest structural unit of

lung parenchym a that is surround ed by a connective
Th e bro nchi fo rm a syste m of di chotomous branch ing
channels that conduct air to the alveo li and gas-ex-
cha nge surfaces. Inhal ed gases mu st pass through an
ave rage of 14 bro nchia l di visions (8-25 ) before reaching Ant.
(
tissue septum. Heitzman (1993 ) descri bes it as the the a lveoli.
principa l physiologic functional unit of the lung. It co n- The walls of the trachea and main bro nchi are rein-
tains 3-12 acini and measures 1.0-2.5 em in diameter. fo rced by incomplete cartil age rings w hich preve nt
W hen th e connective tiss ue se pta between secondary luminal co llapse. In the segmenta l bro nchi, thi s rein -
lobules (i, e, in terlobu lar septa) become abnormally fo rce ment dw indles to irregular ca rtilage plates that be-
thi cke ned, they are visib le on both the chest radiograph come smaller and less numerous in the subsegme ntal
(Kerley lines) and on hi gh-resoluti on CT (HRCT) images and small er bronchi. The bro nchiolar walls are devoid of
(see Fig 1.48 ). Normal in terl obu lar septa occasionally cartilage.
may be seen on HRCf images in the periphera l sub- The tracheobronchial system has a mu cosal lin ing
pleural lung. that sec retes approx im ately 10 to 100 mL of mu cus daily.
Covering the mucosa are myriad ci liated ce lls that beat
Lung Se gm e nts rhythmi ca lly in the directio n of the oro pharynx and
mouth (mu cociliary esca lator), helping to remove in -
These are 10 func tionally autonomou s bronchovascular haled foreign bodi es and irritants from th e lung.
and bro nchopulmonary units on each side. They are Only th e trachea, main and lobar bronchi ca n be iden-
wedge shaped wi th their apices directe d toward th e hi la. tified o n the chest radiograph. Thei r lumina appea r as
When they are infiltrated or ate lecta tic, they produce radi olu ce nt bands or, w hen see n end -on, as elliptica l and
characteristi c appearan ces (Fig. 1.33 ). Occasiona lly, circular luce ncies outlined by the fa int linear dens ity of
some of th ese segments may be se parated from the res t the bro nchia l wall.
of th e lung by accessory fi ssures (see Fig. 1.25 ).
Trachea
Lobes
On the frontal chest radiog raph, the trachea appears as a
The right lung is divided into three lobes, the left lung broad, lu cent band traversing the medi al part of the su-
into two lobes, and all are separated from one anoth er by perior med iasti num. Its wa lls are parall el, and the car-
in te rloba r fi ss ures lined by two laye rs of vi scera l pleura. ti lage rings produce a slight scall opi ng o f its contour. The Fig. 1.
In 50 to 70 % of cases, the interlobar fi ssures are in- left lowe r tracheal wa ll is usually ind ented by the aorti c
complete. Lobar consolidatio n and ate lectasis ca n be arch, and rarely th e right border is inde nted by the azy-
The Norm al Chest Ra diograph 19
hemor-
IS fine
Right Left Right Left
fa pulmo-
ng pulmo-
~adnar~
Upper lobe Lower lobe
l!J~
Apica l segment RUL (1 ) Apicoposterior segment LUL
Apical Segment (6) Apical Segment
hic appear-
tJs
Postenor seg ment RUL (2) Apicoposterior segment LUL
s branching
and gas-ex-
through an
ore reaching
chi are rei n-

Laterobasa l Segment (9)
(J CJ a~ w
lich preve nt
li this rein-
a;es that be-
ubsegmental
:lfe devoid of
ucosal lining Middle lobe

. mucus daily. Lingula (7) Mediobasal segment
, lis that beat Cardiac segment
pharynx and
) remove in-
, lung.
i can be iden-
Jna appea r as
. elliptical and
\\ n
O ~ \J ~
~a r density of
Posterobasalsegment(lO)
a appears as a
Jart of the su-
: and the car-
Medial segment (4) Inferior segmen t (5) Consolidation • Atelectasis
:~ contour. The Fig.1.33 Pulmona ry segments.

j by the aortic
ed by the azy-
Vascular System
• Anatomy and Physiology

.>''4 0
~
--,---
~
---
The lung has a dual blood supply with pa rti al co m-
munication between the two systems: the pulmonary
and the bronchial arterial systems.
The pulmonary system includes the pulmonary arter-
~ ies, the peri alveo lar capillaries, and the pulmonary
veins. All blood pumped from the right heart enters this
Fig. 1.34 Radiographically visible bronchi. The lateral projection system, is arterialized in the pulmonary ca pillaries. and
gives an en-face view of the right and left upper lobe bronchi. In
the PA projection. the anterior seg mental bronchus of the upper
then is pumped through the left hea rt into the syste mi c Fig.
lobe is occasionally seen end-on, adjacent to the seg mental circulation. fo ld
artery. The bronchial syste m has a predominantly nutritive
function. The paired bronch ial arteries arise from the de-
.""
scending aorta and accompany the bronchi along their
gas vein. On the lateral projection, the trachea appears course. In the perihilar regions. the blood drains via
as a lucent band in the upper mediastinum that passes bronchial ve ins into the azygos-hemiazygos system. In
caudally and posteriorly at a slightly oblique angle. the peripheral lung, the bronchial arte ri es open into the
perialveolar capi llary network creating an anastomosis
Tracheal Bifurcation between the two vascular netwo rks.
Functionally. the pulmonary vascu lar system re-
At the bifurcation, the trachea divides dichotomo usly sembles the systemic venous system with pressures of 5
into the main bronchi w hich extend obliquely in- to 20 mmHg. This is significantly lower than in the sys-
ferolaterally. This division is symmetrical up to the age temic arteries, in part because the pulmonary vesse ls are
of about 15 years, when the right main bronchus gains a highly compliant (Fig. 1.35 ).
more vertical orientation. Thi s explains why aspiration In a normal resting adu lt, blood nows through the
occurs more frequently on the right side. The angle ofbi- lungs at a rate of approximately 5 L/min. Only about 25 %
furcation is 55 to 70' in adults: an angle greater than 90' of the lung capillaries are perfused in this resting state.
is considered pathologic. When cardiac output increases during exercise. addi-
tional capillaries are recruited and the major vessels di-
Upper Lobe Bronchi late. There is only a slight concomitant increase in pul-
monary artery pressures (see Fig. 1.35 ).
On the fronta l projection, they arise from the main The com pliance of the pulmonary vessels is also re-
bronchi in an almost horizontal pl ane; the origin of th e sponsible for the normal orthostatic perfusion gradi ent
ri ght upper lobe bronchus is slightly superior to that of (orthostatic caudalization ) that exists in the lungs. In the
the left upper lobe bronchus. On the lateral view, the upright position and on deep in spiration, there is an in-
upper lobe bronchi may be seen end-on as elliptica l lu- creasing perfusion gradient from lung apex to base. This
cencies below the tracheal band. The more superiorl y is manifest radiographically as more dilated vascular
lying right upper lobe bronchus is seen inconsistent ly; shadows in the basal zones. Since the hydrostatic pres-
the more inferior left upper lobe bronchus is clearly de- sure is somewhat higher at the base than at the apex, it
marcated by the lower lobe artery arching over it (see causes greater dilatation of the basa l vessels. On expira-
Figs. 1.9, 1.34). tion, the basal vessels are compressed by the intrinsic
we ight of the lung, and the hydrostatic pressure effect is
Bronchus Intermedius and Lower Lobe Bronchi eliminated (Figs. 1.36- 1.39).
In pathologic conditions which give rise to pulmo-
On the right side, the main bronchus continues distally nary venous hypertension, the normal orthostatic perfu-
as the bronchus intermedius and then as the right lower sion gradient is lost, and perfusion may be directed pref-
lobe bronchus after giving bra nches to the right upper erentially to the upper zones.
and middle lobes, respective ly. The left main bronchus
divides into the upper and lower lobe bronchi. and the
left lower lobe bronchus descends caudally and rather
more steeply than on the ri ght side. On the fronta l chest
radiograph, these bronchi are usually but not invariably
visible as rad iolucent bands. On the right side, the lower
lobe artery lies lateral to the bronchus.
Card iac output (l/min)

25
• • Q/Vol
20 •••
••
15 ~
•
rtial com- I
10
••
?ulmonary
5 ••
nary arte r-
Base Apex
pul mona ry i i
enters this 15 30 45 Ppa (mmHg)
10 20 30cm
\laries, and
1e systemic Fig. 1.35 Compl iance of th e pulmonary vascu lar system. A five- Fig.l.38 Effect of degree of lung expansion on the distribution
fold increase in the cardiac output from 5 to 24l/min causes only of pulmonary blood flow. In the upright position and in inspira-
a two-fold increase in the mean pulmonary artery pressure (Pp.a) ' t ion, blood flow increases from apex to base. In the supine posi-
:Iy nutritive tion and in expiration, the apical and basal flows equalize. Blood
rom the de- flow per unit lun g volume (Q/Vol) is shown on the ordinate (Fuchs
along their and Voegeli 1973). Up right inspiratio n (solid line), upright expira-
I drains via tion or supine pos it ion (broken line).
5 system. In
pen into the
anastomosis
Fig. 1.36 The ~waterfall" model of the
system re- Dista nce pulmonary circulation . In the erect posi-
ressures of 5 tion and in deep inspiration, the apical
vessels are collapsed while the basal ves-
n in the sys- sels are dilated. The basal blood supply
-:y vessels are depends on the arteriovenous pressure
difference. Blood flow in the midzo ne is
through the determined by the arterial-alveolar pres-
sure grad ient. Hence the flow at that leve l
oly about 25 % is not regulated by the a-v pressure differ-
resting state. ence, just as t he flow across the rim of a
<ereise, addi - waterfa ll is independent of the height of
or vessels di- the waterfall . Ppa pulmonary arterial pres-
:rease in pul- sure, PA alveolar pressure, Pp~ pu lm onary
venous pressure (Fuchs and Voegeli 1973).
jels is also fe- Zone 3

lsion gradie nt
Blood flow
e lungs. In the
there is an in-
JX to base. This
lated vascular
drostatic pres- Fig. 1.37 a-c Gravitational effects on t he
at the apex. it lung. a Pulmonary pressure-volume
:els. On expira- 100 curve. Due to t he weight of the lung. in-
ly the intrinsic %TC trapleural pressure has a higher negative
value at the lung apex than at the lung
-essure effect is base. This resu lts in greater lung expan-
80
sion and larger volume of the alveoli in
rise to pulmo- the apical and upper zones. b Nonlinearity
thostatic perfu- ~
60 of the pressure-volume curve m ea ns t hat
E greater pressure is needed to inflate the
Ie directed pref- 0
"0 apical alveoli since they already are
> 40 great ly expanded. Because of this, in-
'"c
.3
-2 spired air is distribu ted predom inantly to
the basa l segments. c A suspended coil
20
spring is somewhat analogous to the
lung: pulling on the bottom of the spring
0 will cause relatively greater expansion of
0 -10 - 20 -30cm Hp the lower segments than the upper seg-
• b c ments. TC - total capacity (Fuchs and
Voegeli 1973).
Fig. 1.39 a. b Inspiratory and ex-

piratory radiographs. Note the
decrease in thoracic size on expira-
tion, the appa rent widening of the
•
cardiac sil houette . th e apparent
mediastinal widening. and the com- Th,
pression of the basal pu lmonary
ing
vessels.
stn
IYIT
fair
ove
dis!
all'
(Fi!
Arl
Th,
ve i
lob
bes
gra
its
w it
t hi!
chil
b
The Norma l Chest Radiograph 23
, and ex- bronchial tree is vis ible only to the level of the segmental
:e the • Radiographic Anatomy of the Vascular bronchi on chest radiographs, the prese nce of an adj a-
on expira-
ing of the
System ce nt bro nchus is usefu l only for ide ntifyi ng larger after-
)parent ies.
d the com- The pulmonary vascula ture is respo nsible fo r the branch-
monary ing linear markings see n on chest rad iographs. Other Origin of the Pulmonary Arteries
structures such as the bronchi al wa lls, bronchi al vesse ls,
lymphatic vessels, and interstitium are too small or too The pulmonary arterial bifurcation occurs at a more
fa in t to be visible. Small vessel shadows appea r as an cra nial level than th e entry of the pulmonary veins into
overlapping network of branches in w hich arteri es are in- th e left atrium. Thi s accou nts for the steep descending
distingui shable from veins. However, several feat ures co urse of the lower lobe arte ri es and the almost horizon-
all ow differentiation betwee n larger arte ries and ve ins tal course of th e lowe r lobe ve ins. The ve ins may be rec-
(Figs. 1.40, 1.41 ). ognized by the fact that their shadows cross the lowe r
lobe artery, whi ch in turn is ide ntifi ed by its typical
Arteries and Veins course and pe ri bro nchial positio n. Co nversely, in the
upper zo nes, the ve ins lie latera l to the arteries and have
The pulmonary arteri es accompany the bro nchi; the a more ve rtica l orie ntation.
veins do not. Thus, a vascu lar shadow acco mpanying a
lobar bronchus represents an artery. This re lati onship is Pulmonary Veins
best ap preciated on conventio nal and computed tomo-
graphi c images. When seen end on, a bronchus and The lower lobe ve ins en ter the left atri um anterior to the
its accompanying artery rese mble a pair of spectacles bro nchi, w hil e t he lowe r lobe a rteries lie posterio rly. The
with one opaque lens (see Fig. 1.41 ). Felso n (1973 ) call ed retroca rdi ac vascul ar bundl e is always clearly visible on
this the "semino ma" pattern in refe rence to the or- the latera l projection: its ante rio r compo nents are vei ns.
chi dectomy necessitated by that disease. Si nce t he its posterior com pone nts are arteri es.
Fig. 1.40 Vascular bundles in the lateral p rojection.

Pretracheal vascular band
(innominate artery and
brachiocepha lic veins)
Left pulmonary
Pretracheal vascular
artery and lower
ova l (right pulmonary
lobe artery
artery and confluence
of the upper lobe veins)
Retrocardiac
vascular bundle
(veins anterior.
arteries posterior) Conus pulmonalis
Fig. 1.41 Vascular bundles in the PA projection.
Apical vascu lar bu ndle

(arteries are med ial to veins)
Arteries are
always para bronchial
Veins cross
lower lobe arteries
Main Pulmonary Artery apica l vascular bundle. On the right. they frequently
cross the lower lobe artery at the level of the horizontal
On the lateral view, the main pulmonary artery lies su- fissure. On the lateral view, the upper lobe veins follow
perior to the upper cardiac shadow and exte nds to the an anteroposte rior course, are projected onto the card iac Be
trachea in an anteriorly convex arch. On the PA view, silhouette. and converge toward the left atrium. To- th
fro
the main pulmonary artery is visible only when it gethe r with the right pulmonary a rtery. they may form a be
forms a border along the upper left cardiac outline. large pretracheal oval shadow.
This may be due to slight right anterior rotation of the
chest (cardiac waist) or may occur as a normal variant
in young females.
The Mediastinum
Right Pulmonary Artery
The med iastinum lies between the lungs and is bounded
From its origin, the right pulmonary artery runs horizon- superiorly by the thoracic inl et. posteriorly by the verte-
tally to the right side. passing anterior to the airway. On bral column, anteriorly by the sternum, and inferiorly by
the lateral view. it appears as a pretracheal ell iptical the diaphragm. It is customary to subdivide the med i-
shadow. Pulmonary arterial and venous branches astinum into anterior, middle, and posterior compart-
frequently are superim posed on one another, giving the ments (Fig. 1.42 ). This subdi vis ion is useful. since certain
appearance of radiating branches. The horizontal lim b disease processes predominate in specific compart-
cannot be seen on the PA view, but its branches form ments.
most of the right hilar shadow: the upper pole by the On the frontal view, the mediastinum appears as a
upper lobe segmental arteries. and the mid and lowe r central shadow in which the air-fi lled lumina of the tra-
hilum by the interlobar and lower lobe arteries. chea and main bronchi may be identified. The
esophageal lumen may occasionally be visible because
Left Pulmonary Artery of swallowed air or contrast medium. A ca lcified aortic
wall may be visible in older patients. Other mediastinal
Shortly after its origin at the bifurcation. the left pulmo- structures can be identified only at sites w here they
nary artery divides anterior to the left ma in bronchus border the adjacent lung.
into the upper lobe artery, which passes superiorly, and On the frontal view, the right mediastinal border is
the lower lobe artery, which initially accompanies the formed by the brachiocephalic (innominate) vesse ls and
left main bronchus and then courses inferiorly with the more inferiorly by the superior vena cava, the hori zontal
lower lobe bronchus. Thus. the upper pole of the hilum is limb of the azygos vein. and the right atrium. The left
fo rmed by the left pulmonary and left upper lobe arter- mediastinal border is formed from above downward by
. T
ies while the mid and lower hilum are formed mainly by the brachiocephalic vessels. left subclavian artery. the
Conv
the lower lobe artery. Overall. the hilar point lies more aortic knuckle. the pulmonary artery. the left atrial ap-
toda)
superio rly on the left side than on the right side. The pendage. and th e left ve ntricle. On both sides. epicard ial
secti.
more distal lower lobe artery may lie adjacent to or be fat pads may occupy and obliterate the cardiop hrenic
grapl
superimposed on the cardiac silhouette. On the lateral angles. Tt
view, the left main bronchus appears as a lucent circle or A well-exposed radiograph also demonstrates the
speci
ring shadow, and as the lower lobe artery arches over it, characte ristic pleural stripes (see Fig. 1.20). including the
is ao
a characteristic shadow is formed. para-aortic and paraspinai lines and the azygoe- tube
sophageal stripe. plan<
Lower Lobe Veins On the lateral radiograph. the air-filled trachea may plan,
be seen descend ing within the mediastinal shadow. The tissUt
These vesse ls drain the lower lobes and pass to the left anterior contour of the mediastinum is formed inferiorly
H
atrium as hori zontal vascu lar shadows. Easily recog- by the right ventricle where it lies adjacent to the lower tiona
nized on PA tomograms. they appear on the chest radio- sternum. More superiorly, the right ventricular outflow may !
graph as linea r shadows which cross the steeply de- tract, the anterior border of the ascending aorta, and the ta ine
scending arteries. On the latera l view, the veins form the pretracheal band of brachiocephalic vessels form the size
anterior portion of the retrocardiac vascu lar bundle. Oc- anterior mediastinal contour. The retrosternal space is ca n b
casiona lly, individual pulmonary veins may be identified the triangular lucent area separating the vascu lar plain
as they run medially to enter the left atrium. shadows and the sternum.
phy ~
The posterior cardiac border is formed by the left
graph
Upper Lobe Veins atrium as it merges imperceptibly with the left ventricle. 0.6 s.
The triangu lar densi ty occupying the angle between the
ing fil
These veins drain the upper lobes and lingula and pass posterior cardiac border and the diaphragm corresponds taneo
inferomedially to enter the left atrium. In the upper to the inferior vena cava.
zones, they comprise the latera l vascular shadows of the
Conventional Tomography 25
,quently Fig. 1.42 Mediastinal compa rtments

"M iddle mediastinum
M
(Meschan 1981).
Jrizontal
1S follow ( Posterior border
Boundary line separating of the pleura
e cardiac
the posterior cardiac border
ium. To- from the anterior tracheal
lY form a border
"Poste ri or ~
~--I --7- media stinum
bounded
:he verte-
eriorly by
:he medi-
compart-
ce certain
compart-
fears as a
of the tra-
fied. The
.e because
fled aortic
lediastinai
!here they
I border is
Conventional Tomography
lesseis and
horizontal
11. The left • Technique
Nnward by
artery, the Conventional tomography is used much less frequently
t atrial ap- today due to increasing availability and use of cross-
t epicardial sectional imaging and particularly of computed tomo-
-diophrenic graphy.
The purpose of tomography is to demonstrate
.strates the specific body planes free of superimposed shadows. This
.eluding the is accomplished by simultaneous motion of the X-ray
le azygoe- tube and cassette around a fulcrum which lies in the
plane of interest (Figs. 1.43 and 1.44), Only objects in the
rachea may plane of interest appear in focu s; the motion blurs out
;hadow. The ti ssues which lie outside this focal plane.
,d inferiorly The sitting position is most appropriate for conven-
to the lower tiona l tomography, but supine and lateral positions also
liar outflow may be used. When possible, tomograms should be ob- A BC C B A
)rta, and the tained in two projections using a sufficiently large film ~
·Is form the size (24 x 30 or even 35 x 35 cm ), Unnecessary exposures Motion of cassette
'na1 space is can be avoided by determining the plane of interest from
he vascular plain radiographs. For thoracic studies, linear tomogra- Fig.1 .43 Conventio nal tomography. When the X-ray tube and
cassette are moved simultaneously in opposite directions, only
phy with craniocaudal motion is recommended. A tomo- the structures in the plane of interest are in focus. Detai l of ob-
I by the left graphic angle of 30 to 40· w ith exposure parameters of jects outside the focal plane are blu rred.
eft ventricl e. 0.6 s, 110 kV, and 8-20 mAs is appropriate. A compensat-
between the ing filter should be mounted nea r the tube for the simul-
corresponds taneous imaging of hilar and pulmonary structures.
a c
b d
Fig.l.44a-e Chest tomograms. 1 Trachea 11
a AP tomogram 10 em 2 Aortic arch 12 Lir
b AP tomogram 12 em 3 Main bronchus 13 Sy
c AP tomogram 14 em 4 Lower lobe artery 14 Ric
d l ateral tomogram 5 em left of midline 5 Apical lower lobe segmental bronchus 15 ul
e l ateral tomogram 7 em left of medial plane 6 lower lobe bronchus 16 Ac
7 Laterobasal veins 17 Ar
8 Upper lobe vein 18 An
9 Azygos vein
10 Pulmonary artery
Conventional Tomography 27
d e
11 Upper lobe bronchus 19 Venous conflue nce
12 Ungular bronchus 20 Apical lower lobe seg menta l bronchus and artery
13 Systemic venous confluence at right atrium 21 Posterobasallower lobe segmenta l bronchus and artery
14 Right midd le lobe bronchus 22 Anterobasal lowe r lobe segmental bronchus and artery
15 Upper lobe artery 23 Anterior upper lobe segmental bronchus and artery
16 Aorta 24 laterobasa l lower lobe segmenta l bronchus and artery
17 Anterior upper lobe segmental artery 25 lower lobe vein
18 Anterior upper lobe segmental bronchus
28 1 Examination Te chniqu e and No rmal Findings
computed Tomography dos

dos
• Technique All cr examinations initially require acquisition of a

preliminary AP scout view from w hich the cranial and •
CT data are acquired by passing a collimated beam caudal limits of the study are determined. The standard Co r.
through a transverse section of the patient's body. The cr examination is acquired at fu ll inspiration though pia.
emergent beam then is measured by a semicircular array supplem entary data acquired in expiration may be use- sur)
of detectors. During data acquisition, both the X-ray tube fu l. particularly in the investigation of sma ll airway dis- easl
and detector array rotate around the patient so that the ease. Contrast medium is infused preferably into an an- ass!
plane of interest is scanned from all directions. This tecubital vein during the examination (e. g .. 100- 140 mL (Sci
gives a large number of attenuation va lues (e.g., of approximately 300 mg iodine/mL. 3-4.5 mL/sec. 15-
400000). which then are recorded and processed by a 25 s delay). Reconstructed images usually are disp layed imc
computer to produce a digital image of the re levant at standard mediastinal (window width/center = 350/ age
plane (Fig. 1.45). 40) and lung (window w idth/ce nter = 1500/-700) w in- por
dow settings. tha
of r
Incrementa l a tior
t iar
Early generation Cf scanners used an incremental or ESC
single-slice technique in which one axial image was ac- reSI
quired during a breath- hold. The CT table then adva nced
up to 10 millimeters and a second image was acquired. qUe
hav
Helical and Multidetecto r a pia,
beE
He li cal Cf involves acquis ition of a vo lumetric data set nar
through th e anatomic region of interest during a si ngle eml
breath-hold. There is continuous patient movement calc
with simultaneous sca nning by a constantly rotating sco
gantry and detector system. Initial helical CT systems wh
employed a single detector but technology has advanced n ur
rapidly and today. 4. 16. and 64 mu lti-detector row CT nat
systems (M DCT) are in clinical use. 199
MOCf systems allow increasingly faster image acqui-
sition over any given craniocaudal distance (z axis) in a sial
single breath- hold. Hence. with increasing numbers of bre
detectors, collimation is decreased leading to improved are
spatial resolution. Coronal and sagittal reformatted im- 140
ages and three-dimensiona l (3 ~ ) reconstructio ns may 0.6
be acquired from thi s vo lumetric data set and evaluation SSC
of the former in particular is becoming routine in inter-
pretation of CT stud ies (Fig. 1.46 a-c). dur
pia
High-Re solution a are
a ne
HRCf acqui ring 1-2 mm collimation images at 10-
15 mm inte rval s and employing a high frequency recon- tha
struction algorithm was the sta ndard CT techn ique for ves
eva luation of diffuse parenchymal lung di sease for many to .
years. The advent of MDCT allows reconstruction of ass
these "high-resolution" images from the volumetric data w it
set and this now is an option if a "global" examination of mo
the thorax is required. However, when lung parenchy- be
mal evaluation only is required , the traditional HRCT acu
Fig. 1.45 Basic principle of computed tomography (Wegener technique sti ll is appropriate and this noncontiguous soc
1992). image acquisition gives a considerably lower radiation et c
Computed Tomography 29
dose (1.5-2 mSv) than standard helical /MDCT where the

dose is in the order of 6-10 mSv.
sition of a • Computed Tomography in Cardiology

ranial and
e standard Conventional coronary angiography remains essentia l in
on though planning and guiding catheter-based intervention and
lay be use- surgery in patients with significant coronary artery dis-
lirway disease. However, CT shows considerable promise in the
into an an- assessment of asymptomatic and early-stage disease
00-140 m L (Schoen hagen et al. 2004).
nL/sec. 15- The complex cyclical motion of the heart requ ires an
, displayed imaging modality with high tempora l resolution and im-
lter = 3501 ages need to be referenced to the cardiac cycle. The tem - ~"-_~_ a
-700) win- poral resolution of conventional angiography is 10 msec,
that of electron-beam CT (EBCT) is 50-100 msec and that
of MDCT is 50-300 msec. Therefo re. CT image acquisi-
tion should be during the phase of minimal cardiac mo-
tion. i. e .. late d iastole. MDCT has the advantages over
'emental or EBCT of a higher signal-to-noise ratio and higher spatial
age was ac- resolution.
~n advanced Noncontrast CT is used for coronary artery calcium
:1S acquired. quantification. Coronary artery calcium scores at EBCT
have been shown to correlate with total atherosclerotic
plaque (both calcified and nonca lcified) and also have
been shown to have a predictive value for future coro-
tric data set nary events (Secci et al. 1997). MDCT recently has
ring a single emerged as an alternative to EBCT for coronary artery
: movement calcium assessment (Becker et al. 2001). The traditional
otly rotating scoring method has been the Agatston scoring system,
CT systems which gives a calcium score based on maximum CT
las advanced number and area of calcium (Agatston et al. 1990). Alter-
ector row cr natives include vo lume and mass scoring (Ca ll ister et al.
1998. Detrano et al. 1995 ). b
image acqui- MDCT coronary angiography allows three-dimen-
~ (z axis) in a sional/volumetric scanning ofthe entire heart in a single
~ numbers of breath-hold. Typical imaging parameters for 16 MDCT
~ to improved are 16 x 0.75 mm collimation, 0.42-sec rotation time,
ormatted im - 140 kVp. and 400-500 mAs and for 64 MDCT are 64 x
Ifuctions may 0.6 mm co ll imation, 0.33-sec rotation time, 120 kVp,
Ind evaluation 850 mAs.
utine in inter- Data are gated retrospectively to reconstruct images
during the diasto lic phase of the cycle. Curved multi-
planar reformats along the axes of the coronary arteries
are possible as are maximum intensity projection (MIP)
and volume-rendered reconstructions.
mges at 10- While the temporal reso lution of MDCT is less than
·quency recon- that of conventional angiography. it has the advantage of
technique for vessel-wall and plaque depiction in addition to its ability
sease for many to assess luminal dimensions. Therefore, MDCT allows
onstruction of assessment of calcified and noncalcified plaque together
'olumetric data with changes in vessel architecture including arterial re-
~xamination of modeling. This is significant as noncalcified plaque may
ung parenchy- be more unstable and prone to rupture giving rise to
c
,ditional HRCT acute coronary events. Positive remodeling also is as-
Fig. 1.46 Axial image (a) from a volumetric MDCT study with
noncontiguous sociated with acute coronary syndromes (Schoenhagen coronal (b) and sagittal(c) reformats.
ower radiation et al. 2000. Yamagishi et al. 2000 ).
crossing the section ob liquely wi ll produce oval or el-

• CT of the Normal lung liptical rings and shadows. Since the thickness of the a
bronchial wa ll is only about 1/6 to 1/10 of its luminal Acinus 0.1
Volumetric cr in the thorax performed on MDcr gives diameter, bronchi are vis ible on ly to about the ir 8th boundary
collimation of 1.5-3 mm and all ows for much better res- division, or to the junction of the central and periph-
olution of pulmonary parenchyma l structures than was eral hal ves of the lung. Vessels, on the other hand,
possible when incremental cr with 8-10 mm collima- may be traced as far as their 16th division, or to about
tion images were acquired as standard practice. When 1 em from the pleural surface (Fig. 1.47 ).
1- 1.5 mm collimation noncontiguous HRCf images are • The pulmonary veins appear as branched structures
acquired, excellent visua li zation of lung parenchymal unattended by an airway. Since arteries in the outer
Acinar art
detail is also possible. half of the pulmonary lobe can no longer be iden- rarely visi
The vis ibility of a structure depends, in part, on at- tified by their accompanying bronchi, vei ns are ind is- from plel
tenuation differences between it and adjacent struc- tinguishabl e from arteries in the lung periphery.
tures. For example, an interlobular septum with an ana- • In tertobutar septa: The secondary lobule is sur-
tomical thickness of only 0.1 mm will be imaged on ly if it rounded by interlobular connective tissue septa
intersects the plane of section at right angles; it will not w hich form a polyhedral network com pletely per-
be detected if it is para llel to the section. Th is is because meating the lu ng parenchyma. These septa are we ll
the perpendicular septum w ill occupy a much greater developed in the peripheral portions of the lung, and Fig.1 .48a.
proportion of the voxel. increasing its average radio- they are best appreciated in the antero lateral and dia- structures
graphic density. phragmati c regions. Septa in the perihilar lung are in-
The following structures are vis ible in healthy sub- visible unless they are pathologically thickened due
jects (Naidich 1991 ): to edema, in filtration, or fibrosis. Portions of the
• The bronchovascular bundle is co mposed of bronchi, septa may show small nodular densities w hich repre- travel
arteries, and their associated con nective tissue. An sent vei ns cou rsing through the periphery of the positi
artery and bronchus always follow a para ll el course lobule. minel
and have equal outer diameters, which taper towards • The secondary pulmonary lobule usually can be iden- t he h
the lung periphery as the airways and vessels ramify tified in the peripheral lung on ly by its surrounding sha rp
into progressively smaller channels. A bundle run- connective tissue septum. The lobular arte ry at the cr. Th
ning perpe ndicular to the cr sect ion will appear as a center of the lobu le appea rs as a punctate or comma- tion,
round soft-tissue density adjacent to an air-contain- shaped structure on thin sectio n cr (Fig. 1.48). ally n
ing ring. A bundle in the plane of the cr section will • The fissures are less than 0.4 mm thick and frequently the al
appear as branching arterial streaks accom panied by are visible on today's thin co llim ation cr studi es . to 2 J
the tubu lar lines of the bronchial wa ll. A bundle They are visible in thicker sections only if they some
thrau
a sha:
ciate(
Fig. 1.47 li mits of thin section CT for de- sagitt
lineation of normal bronchovascular struc- • PteUli
tures. Normal bronchi are not visible in the
tissU(
peripheral lung due to their narrow walls.
whereas arteries and veins can be traced given
300 flm peripherally to the subpleu ral lung (Engler eas il)
visible to 1982).
8th division
Not visible
300~m
4--+ visible to
8th division
Not visible
computed Tomography 31
oval or el- l em
a
less of the
its luminal Acinus 0.6- 1 cm,
t their 8th boundarync
nd periph- Interlob ular septum 0.1 mm,
ther hand, rarely visible
or to about ,',
structures
0;;;:-- Visceral
n the outer Acinar artery 0.5 mm, pleura
~r be iden- rarely visible 3-5 mm 0. 1 mm
IS are indis- from pleura or septum
·iphery.
lie is sur- lobu lar artery 1.0 mm,
ssue septa visible 5- 10 mm from
lletely per- pleura or septum
)ta are well
le lung, and Fig. 1.48a, b The secondary pulmonary lobul e. Note the punctate, y-shaped, or v-shaped appearance of the lobula r artery. Other
structures are occasionally visible (Naidich 1999).
~ral and dia-
lung are in-
ickened due
ions of the
IoJhich repre- traverse the section at almost a right angle, but the pleura, the parietal pleura, the very thin extrapleural
hery of the position of the major fi ss ures can be indirectly deter- fat stripe, the endothoracic fascia, the internal inter-
mined by noting the adjacent relative avascularity of costal muscle, the intercostal fat, and the ribs
can be iden- the lung (Fig. 1.49). The major fissures appear as (Fig. 1.50). Given the obliquity of the ribs in the lateral
surrounding sharp lines of soft-ti ss ue density on high- resolution portion of the chest, axial CT scanning can demon-
utery at the CT. The minor fissure runs parallel to the plane of sec- strate the boundary between the lung and intercostal
e or comma- tion, so even on high-resolution CT its position usu- space. This boundary is marked by the narrow inter-
,.1.48 ). ally must be inferred from the relative avascularity in costal stripe, which consists of pleura, fascia, and the
ld frequently the adjacent lung. However, on these thin sections (1 internal intercostal muscle and contrasts sharply
I CT studies. to 2 mm ) the minor fissure, which usually has a with the intercostal fat. Posteriorly, the pleura and
only if they somewhat superiorly convex shape, may pass endothoracic fascia lie on the paravertebral fat and
through the section two or more times, appearing as appear as a very fin e stripe called the paravertebral
a sharp, wavy line. The fi ss ures may be readily appre- line. Pleura in close proximity to a rib can be iden-
ciated on reformatted images particularly in the tified only if it is pathologically thickened.
ion CT for de- sagittal plane.
lascuiar struc- • Pleura: Unlike the fi ssure s, the pleura borders on soft
)t visible in the tissue structures at the lung-chest wall interface and, • Normal Findings-a Thorax
narrow walls,
given its width (0.2 to 0.4 mm ), is not demonstrated
an be traced
allung (Engler easily by a. The chest wall comprises the visceral (See Figs. 1.49,1.51-1.55).
l(
11
Fig
NOi
a
A'
p,
b,
M
be
Ac
'"
be
l'
b2
Fig.
Tra
Bif
Computed Tomograp hy 33
<l Fig. 1.49 Computed tomography (CT) 12 Upper lobe artery

, Left subclavian artery 13 lower lobe artery
2 Right subclavian artery 14 Pulmonary veins
3 Right carotid artery 15 left atrium
4 Innominat e Artery 16 Right atrium
5 Left carotid artery 17 Right ventricle
6 Subclavian vein 18 left vent ricle
7 Superior vena cava 19 Left anterior descending coronary artery
8 Thoracic aorta (with atherosclerotic calcif ication)
9 Main pul monary artery 20 Esophagus
,a Right pulmonary artery 21 Trachea
11 l eft pulmonary artery 22 Tracheal bifurcation
• b
Lung
Visceral pleura
Parietal pleura
Subpleu ral fat
~~;~~;~~;;~~~~~~:::::=
.
£ndothoracic fascia
Intercostal fat
(with nerve and vessel)
Internal intercostal muscle
External intercostal muscle
Fig. 1.50 a. b The Mpleural stripe,M consisting of both pleural layers and t he int rat horacic fascia, shows soft-tissue attenuation on CT.
Note also t he intercostal fat stripe wit h it s vessels and t he intercostal muscles (Naidich 1999) .
lateral basal
bronchus U C'---_ M""" basal bronchus
Fig. 1.51 a- c Branching pattern of the right ma in bronchus. B1 Apical segmental bronchus RUL
Tra Trachea B2 Posterior segment al bronchus RUL
Bif Bifurcation Fig. 1.51 d-i I>
34 1 Examination Technique and No rmal Findings
b.
"
"
p
b
•b
Fig. 1.S1 d-i Branching pattern of the rig ht main bronch us. 84 Segmental bronchus to medial seg ment RML
Tra Trachea 85 Segmental bronchus to lateral segment RML
Bif Bifurcation 86 Apica l segmental bronchus to RlL
RMB Right main bronchus 87 Medial basal (cardiac) segmental bronchus RLl
UlB Upper lobe bronchus 88 Anterior basal segmental bronchus Rll
MLB Middle lobe bronchus 89 lateral basa l segmental bronchus Rll
lLB Lower lobe bronchus 810 Posterior basa l segment al bronchus Rll
B1 Apical segmental bronchus RUL RUl Right upper lobe
82 Posterior segmental bronchus RUl RMl Right middle lobe
83 Anterior segmental bronchus RUL RlL Right lower lobe
Fig.1. 52 Branching pattern of the left main bronchus. I>

UlB Upper lobe bronchus
l lB l ower lobe bronchus
Eso Esophagus
LI N Ungular bronchus
81/82 Apicoposterior bronchus
83 Anterior bronchus
84 Superior lin gular bronchus
85 Inferior lingular bronchus
86 Api ca l segmental bronchus
87 Medial basal bronchus
88 Anterior basal bronchus
89 l ateral basal bronchus
810 Posterior basal bronchus
Computed Tomography 35
Apical
segmental
bronchus lLl
chus. t>
10 Fig. 1.54 Schem atic representation of segmental lung

anatomy.
<l Fig. 1.53 a-f a CT 3D reconstruction of bronchial

anatomy, b virtual bronchoscopy at the level of the
bifurcation, c-f sagittal sections through the lung
(c = right lateral. d - right pa ramedian, e - left para-
median, f - left latera l).
, Apical segment upper lobe
2 Posterior segment upper lobe
3 Anterior segment upper lobe
4 Medial segment RM L or superior segment lingula
5 lateral segment RMl or inferior segment lingu la
6 Apical segment lower lobe
7 Cardiac or mediobasal segment
8 Anterobasal segment
9 laterobasal segment
10 Posterobasal segment
Fig. 1.55
computed Tomography 37
] 4
mental lung
ronchial
vel of the
:he lung
= left para-
ment lingula
nent lingula
Fig.1.55 Axial CT images through the thorax showing lobar and segmental lung anatomy.
Radionudide Imaging
Radionuclide imaging docu ments the distribution of a Ve ntilation Scintigraphy

radionuclide-Iabeled pharmaceutical within the body
with emitted radioactivity recorded by a gamma Gases or aeroso ls may be used to eva luate lung ventila-
camera. tion. Gases used include xenon ( 133 Xe and 127Xe) and
krypton (K r 81 m ). Shortcomings associated with these
agents include expense, low gamma ray energy, and ina-
bility to all ow six-v iew ventilation and consequently.
Lung Scintigraphy aerosols are wide ly used in cl in ical practice. Tc 99 m-di-
ethylenetriaminepentaacetic acid (DTPA) is the most
Fig.
Radionuclide lung imaging documents the regiona l dis- widely used aerosol. The patient breathes through a face nar)
tribut ion of pulmonary blood now (pe rfusion scanning) mask until the count is sufficiently high for imaging.
and of alveolar ventilation (ventilation scanning). Venti- When aerosols are used, Tc 99 m is the radionuclide for
lation-perfusion scintigraphy still plays a significant ro le both ve ntilation and perfusion studies and simultaneous
in investigation of pulmonary embolism particularly in image acquisition is not feasible. The ventilation study
young adults with a normal chest rad iograph. Ventila- usually is performed first. as aeroso l particles are cleaned
tion scintigraphy may also be helpful in evaluating the through the alveolar membrane relatively quickly.
activity and coordination of the ciliary appa ratus of the When assess ing ventilation only. delayed images may
bronchial mucosa (mucociliary escalato r: Fig 1.56). provide info rmation on radionuclide clearance from the
lungs and thus on the regional activ ity of the mucocil i-
Perfusion Scintigraphy ary system (see Fig. l.56 ).
a
The supine patient perform s a series of deep inspira- Ventilation-Perfusion Scintigraphy
tions, then technetiu m (Tc 99 m)-Iabeled albumin mi-
crospheres or macroaggregates are injected into the an- Comparison of ventilation and perfusion images allows
tecubital vein (Fig. 1.57 ). These albumin particles with a identification of unmatched perfusion defects (Fig. 1.5S).
diameter of 10 to 40 ~m , lodge in the pulmonary vascu- A probabi li ty score for pulmonary embolism then is
lar bed, embolizing about 1 of every 10000 capillaries. possible based on VQS and chest radiographic findings.
Fig. 1.56a, b Scintigraphic evaluation of

mucociliary transport. a Normal study. 1
b Chronic obstructive pulmonary disease bl
(COPD) with patchy central depos ition of
tracer.
(_ swallowed radionuclide appearing in the
bowel).
Rad
doCi
a a nd
neti
E
tion
~
pota
leve
cell.
ce ll ~
out.
ther
b advc:
15 min p.i. 60 min p.i. dosE
Radionuclide Imaging 39
1
19 ventila-
0 .......:...,,-
127Xe) and
Nith these
;y, and ina- ~
Isequently, a b
[c 99 m-di-
the most Fig . 1.57 a, b Principle of perfusion scintigraphy. a Radiolabeled microparticies injected intravenously are trapped within the pulmo-
Jugh a face nary capillaries. b Gamma camera imaging of distribution of radioactivity.
)f imaging.
nuclide for
nultaneous Fig.1 .58a. b a Ventilation (10 mCi
Ition study 133Xe) and b perfusion scans (4 mCi
99mTc-MAP) in patient with pulmonary
are cleaned embol ism. Images show characteristic
ickly. pattern of multiple unmatched perfu-
mages may sion defects with normal ventilation
ce from the study.
e mucociJi-
a
lages allows
ts (Fig. 1.58).
ism then is
lie findings.
3\uation of
II study.
Iry disease b
position of 5-20 s 70-100 s 300-400 s
)earing in the
Isonitrile compounds such as hexakis-2-methoxyi-

Myocardial Perfusion Scintigraphy sobutylisonitrile (HMIBI) bound to Tc 99 m may also be
used. These have the advantage of higher gamma energy.
Radionuclide imaging of the myocardium (Fig. 1.59) However, there is no redistribution and rest imaging re-
documents the extent and distribution of both ischemic quires a second injection.
and infarcted myocardium. Both thallium-201 and tech- Norma l scintigraphic studies show a re latively homo-
netium-99 may be used for myocardial scintigraphy. geneous distribution of radionuclide throughout the
Both agents are administered by intravenous injec- myocardium. Regions of decreased activity signify areas
tion. of dim inished blood now.
When Thallium-201 is used, it activates the sodium- Radionuclide uptake by myocardial cells is deter-
potassium ATPase enzyme system at the cell membrane mined during exercise or pharmacological stress and
level and this t ransports the isotope into the myocardial then at rest. Approximately 100 MBq of thallium-201
cell. Following initial uptake of 201 -TI in myocardial chloride or 240 MBq of Tc 99 m- HM IBI are injected in-
cells, redistribution occurs with thallium being washed travenously during exercise, and image acquisition
out of cells into the vascular compartment from which it begins immediately. Gamma camera equipment with
then is available for re-extraction. 201-TI has the dis- SPECT capability is routinely used. The distribution of
advantage of low gamma radiation and high rad iation tracer uptake by the myocardium is documented. Rest
dose to the kidneys. images are acqu ired approximately 30 minutes later.
40 1 Examination Technique and No rmal Findings
3
3
2
a b c
STRESS a
E(On
S RHT L
P
T
T
REST
'"F
STRESS
b
8 RH T R
~:::>~
E 'HF X
REST
b
Fig. 1
dim
STRESS as tl
crea
S;\L stre:
~q In g rit~
T BRSE T
REST cam
tion
Tl a'
Fig. l. S9 a-c Norm al myocardial perfusion study. During exer- lei t o the m itral va lve plane, b vertical long axis, c horizontal long ocal
cise or pharmacologic stress, thallium-201 is distributed hom o- axis . The examination subsequently is repeated at rest (a,. b,. cd.
geneously throughout the left vent ricu lar myocardium with sub- Both exercise/stress and resting thalli um stud ies show homo-
sequen t imaging in th ree perpendicular planes: a Short axis paral- ge neous uptake with no areas of decreased perfusion.
Po
Image analysis allows diffe rentiation of infa rcted my- mia/infarction. Reve rsible ischemia shows decreased (PI
oca rdium from regions of reversible ischemia. An area of tracer activity during stress but reverts to normal on the
decreased tracer activity which is present on both stre ss rest images. Th is occurs because a stenosed coro nary PET
and resting images usua lly indicates irreversi ble ische- artery may allow normal perfusion at rest. but perfu sion a liz
Ultrasound 41
a
-
b c
Fig.l.60 Axial (a), coronal (b) and sagittal (c) images from a normal l8FOG- PET study
diminishes relative to normal myocardium during stress (Fig. 1.60a-c). 18F fluorodeoxyglucose (FOG) is the most
as the stenosed vessel cannot allow the physiologic infrequently used radiopharmaceutical in clinical PET im-
crease in blood flow which normally is seen during aging. This glucose analogue is transported across cell
stress and exercise. membranes by glucose transporter proteins, is phospho-
"Hibernating" myocardium retains its cellular inte- rylated and with the exception of the liver. becomes
grity but blood flow is reduced so significantly that it trapped metabolically, Malignant cells are associated
cannot sustain the high energy requirement of contrac- with an increased glycolytic rate, PET has become increas-
tion. Rest-redistribution-reinjection protocols with 201 - ingly important in oncologic imaging and relies on imag-
TI attempt to distinguish hibernating from infarcted my- ing the distribution of FOG which shows increased accu-
lorizontallong ocardium (Hossein et al. 1999). mulation in neoplastic lesions relative to normal tissue.
iest (al. bl , CI)' 18F degrades to 1802 , a positron, and a neutron. The
:; show homo- neutron travels a short distance in the human body typi-
Isian. cally less than 1 mm for 18F. Once mostofits energy is lost,
Positron Emission Tomography
the neutron annihilates with a nearby electron and two
IS decreased
(PET) and PET-CT photons. each having energy of 511 keY. are produced.
ormal on the These photons leave the site of annihilation in opposite
0
jed coronary PET is a molecular imaging technique which allows visu - directions and travel at 180 to each other. They sub-
Jut perfusion alization of both physiologic and pathologic processes sequently reach the detector ring surrounding the body.
Simultaneous detection of two 511-keV photons in two Patients having PET/PET-a studies are required to
detectors in the ring indicates that an annihilation has oc- fast for 4-6 hours and are asked to avoid caffeinated and
curred somewhere along the column co nnecting the two alcoholic beverages. Blood glucose is measured prior to
detectors, and this event is recorded as a coincidence. injection and a normal blood glucose level is preferable.
PET-Cf is a unique combination of cross-sectional Administration of insulin to diabetic pa tients for gl ucose
anatomy provided by a and metabolic information pro- control is co ntroversial as it may exaggerate phys iologic
vided by PET. Both are acqui red during a single exami na- uptake in muscles. Strenuous activity should be avoided
tion and are fused. This com bined modality study all ows before and after injection as it too may lead to increased
accurate localization of increased FOG activi ty to specific muscle uptake of FOG (Ka poor et al. 2004).
anatomical locations.
Ultrasound
The role of ultrasound in the thorax is limited to evalua- and circumscribed pleural lesions are so lid or fluid and if
tion of the soft tissues of the chest wall and the patho- subacute/chronic effusions have become locu lated.
logica lly distended pleural space. The large impeda nce Wh il e ultrasou nd plays a limited role in chest imag-
difference betwee n the soft tissues and the aerated lung ing. echocardi ography plays a very major role in evalua-
prevents so nograph ic visua lization of the pulmonary tion of the heart. but a disc uss ion of this modality is be-
parenchyma. Pleu ral effusions are visuali zed eas ily w ith yond the scope of thi s text.
sonography. It also is possible to determine if chest-wall
Pulmonary Angiography
Advances in a technology and particu larly the develop- patients with pulmonary hypertens ion and in the eval-
ment ofa pulmonary angiography have led to a marked uation of pulmonary stenoses and malformations.
decrease in the use of co nventional pulmonary angiog- Accurate morta lity and morbidity figures for pu lm o-
raphy. Traditionally. it was regarded as the "gold stan- nary angiography were difficu lt to determine. w ith so me
dard" for investigation of pulmonary embolism. It in- series reporting morta li ty ra tes of 0.5 to 1.0 % (Mi lls
volved a transfemoral approach using the Seldinger 1980. PIOPED Study 1990). while in others there were no
technique (Fig. 1.61) with an initial test injection exclud- deaths (Cheely 1981 ).
ing the presence of thrombus in the right hea rt and main
pulm onary artery and allowing progression to selective
pulmonary artery injections (see Fig. 1.62 ). • Normal Findings
Today its use is largely co nfined to specialist centers
where it continues to be used in the assessment of some See Figures 1.62 and 1.63.
2 4
Fig. 1.61 Percutaneous arterial catheterization using the Seldinger technique . b

Pulmonary Angiography 43
Jired to Fig. 1.62a. b Normal pulmonary

.ted and angiogram. a Arterial phase .
b Venous phase.
prior to
,fe,able.
glucose
'sioiogic
avoided
lCreased
lid and if
tted.
~st imag-
n evalua-
lity is be-
! the evai-
ions.
or pulmo-
with some
.0 % (Mills
re were no
-
b
44 1 Examination Techniqu e and Normal Findings
Fig.l.63a-d Pulmonary vessels (from

Uthgenannt: li near densities. In: W. Teschendorf: Bro
Rontgenologische Differentialdiagnostik. Vol. 111,
5th ed. Stuttgart: Thieme 1975).
Arteries (circled numbers):
1 Apical segmental artery, 1 a apical branch,
1 b anterior branch
Bronc
2 Posterior segmental artery; 2 a apical of th,
branch, 2 b lateral branch rep la,
3 Anterior segmental artery; 3 a lateral most
branch, 3 b anterior branch
4 lateral artery of right middle lobe and su-
perior lingular artery of left upper lobe; 4 a
posterior branch. 4 b anterior branch
5 Medial artery of right middle lobe and infe-
rior Ji ngular artery of left upper lobe; 5 a su-
perior bra nch. 5 b infe rior branch
6 Api ca l or superior artery of lower lobe; 6 a
medial branch. 6b superior branch, 6c
lateral branch
7 Mediobasallower lobe artery with anterior
and posterior branches
8 Anterobasal lower lobe artery; 8 a lateral
branch, 8 b basal branch
9 laterobasallower lobe artery; 9 a lateral
branch, 9 b basal branch lat
a
1 Posterobasa llower lobe artery; lO a (m
laterobasal branch, 1 ab mediobasaJ branch,
10 c posterior branch Med
Veins (noncircled numbers) (mid
1 Apical vein of upper lobe; 1 a apical branch
(between 5 1 a and 5 1 b), 1 b anterior
bra nch (between 5 1 band 53 b)
2 Posterior vein of uppe r lo be; 2 a apical
bran ch (between 5 1 a and S 2 a), 2 b A
posterior branch (between 5 2 a and 5 2 b), (I
2 c intermed iate branch (between 5 2 band
5 3 a), lateral branch (between 5 3 a and
53 b), interlobar branch (interlobar
subpleural S 2 a)
3 Anterior vein of upper lobe; 3 a superior
branch (between 5 3 b1 and 5 3 b2) , 3 b
a
c d inferior branch (between 5 3 b2 and 5 4 b),
3 c (left side only) lateral branch (between
53 a and S4a)
4 lateral vein of right middle lobe; 4a posterior branch (be-
tween 5 4 a and 5 4 b). 4 b anterior branch (between 5 4 band Apico
5 5 a) and superior lingu lar vein of left upper lobe; 4 a poste- (uppe
rior branch (between 5 4 a and 5 5 b). 4 b anterior branch (be-
tween 5 4b and 5 5)
S Medial vein of right midd le lobe; Sa superior branch (be-
tween 5 5 a and 5 S b). 5 b inferior branch (interlobar sub-
pleura l branch in 5 S b) and inferior lingular vein of left upper
lobe; S a superior branch (between 5 5 a and S 5 b). 5 b infe-
rior branch (between 5 5 band 5 5 b2)
6 Apical or superior vein of lower lobe; 6 a medial branch (be- SuperiQ
tween 5 6a and 5 10). 6 b superior branch (between 5 6 band (lower I
S 6c. and betwee n 5 6b1 and 5 6b2). 6c lateral branch (be-
tween 5 6c and S8a)
7 Mediobasal vein of lower lobe ; 7 a anterior branch (between
5 7 a and 5 7 b) . 7 b posterior branch (between 5 7 band 5
lOb)
8 Anterobasal vein of lower lobe; 8 a lateral branch (between 5
8a and 5 8 b). 8 b basal branch (between 5 8 b. 5 7 a and 5 9b) p,
9 laterobasal vein of lower lobe; 9 a lateral branch (between 5 (I,
9 a and 5 9 b). 9 b basal branch (between 5 9 band 5 10 a)
10 Posterobasal vein of lower lobe; 10 a latera l branch (between c ~ __
5 lOa and 5 lOb). lOb medial branch (between 5 lac and 5
lOb)
Bronchography 45
hendorf:
Bronchography
)1.1/ 1,
ranch, Bronchography trad itionally has bee n used in evaluation • Normal Findings
of the airways. CT ± flexibl e bronchography ha s largely
replaced this procedu re which is no longer availab le at See Figures 1.64 and 1.65.
most institutions.
nd suo
Jbe; 4 a
h
nd infe·
~; Sa suo
Posterior Superior
Ibe; 6a lobe)
6c
3nterior Anterior
(upper lobe)
~
ateral
3teral
Lateral
3
(middle IObe)I...:;~~~~~
11 branch,
Medial
(middle lobe)
II branch
·rior
)ical Posterobasal
Anterobasal
2b (lower lobe)
(lower lobe)
ld S 2b),
5 2 band (lower lobe)
a and Apical
lr (upper lobe)
perior
2),3b a L -________________________________--'
b
ld S 4b),
between
Fig. l .64 a-c Normal lateral bronchogram (from Meschan
1981).
Apicoposterior
(upper lobe)
Superior
Superior ;;:-=~~or( lingula)
(lower lobe)
Posterobasal
(lower lobe)
laterobasal
c L -__________________~(lo
~w ~e~r~lo~b~e~
) ______________~
M,
Apical
(upper lobe)
MR
con
phy
teri
fie l.
net
mo
Anterior (upper lobe) _G"",( As
em:
a
g ra.
lateral (m iddle be,
t his
of i
Medial I
(middle lobe) wal
mel
Anterobasal to (
(lower lobe)
l aterobasa l Posterobasal
(lower lobe) {lower lobe)
a L-__________________________________ ~
b
Posterobasal
(lower lobe)
C L-__________________________________ ~
d
Fig. l .65 a-d Normal PA bronchogram (from Meschan 1981).

c
Fi g . .
Magnetic Resonance Imaging 47
Magnetic Resonance Imaging
MRI yields multi plana r cross-sectional images (i. e., • Normal Findings
coronal, sagittal, and axia l), as does computed tomogra-
phy, but MRI allows fo r a greater degree of tissue charac- See Figures 1.66 and 1.67.
terization. When exposed to a strong external magnetic
field, ti ssue protons realign along the plane of t he mag-
netic gradient. From this position, they can be denected • Cardiac MRI
momentarily by app lying a radio frequency (RF) pulse.
As they return to the ir o riginal alignment, the protons MRI has eme rged as a valuable tool in evaluation of the
emit a faint electromagnetic signal which is detected by heart. It allows accurate evaluation of ventricular func-
a "receiving" radiofrequ ency coil. With suitable tion and cardiac valve motion and allows for excell ent
grad ients along the magneti c field, signal detection ca n depiction of cardiac and vascular anatomy in congenital
be confined to a preselected body plane. Processing of heart disease. CMR also shows considerable promise in
this data then yields a cross-sectional image of the plane the field of myocardia l first-pass perfusion and viability
of interest (Stark and Bradley 1999 ). imaging.
MRI is sometimes useful in the assessment of chest- CMR pulse sequences may be divided into dark/black
wall and diaphragmatic lesions and, in selected cases, blood and bright blood sequences. Black blood se-
media stinal pathology. It remains significantly inferior quences include standard spin echo (S E), breath-hold
to CT for evaluation of the pulmonary paren chyma. turbo or fast s pin echo (TSE and FSE) and half Fourier
• b
d
Fig. 1.66 a-d Coronal (a, c) and sagitta l (b. d) MR images.
48 1 Examination Techn ique and Normal f indings
turbo Sl
double-
cardiac
Brigl
(GRE ) ,
These a
gional v
space tl
Single 5
include
• b GRE sec
elude tr
c d
e f
9 h
Fig. 1.67 a-i Axial MR images
2 Left common carotid artery
4 Left subclavian artery
6 Trachea
7 left brachiocephalic vein
9 Innominate artery
,0 Aortic arch
11 Superior vena cava
12 Ascending aorta
13 Main pulmonary artery
16 Descend ing aorta
18 Right/left mai n bronchus
20 left atrium
21 Right atriu m
22 Right ventricle
23 Left ventricle
Magnetic Resonance Imaging 49
turbo spin echo with double inversion recovery (HASTE, exce llent contrast between myocardium and blood pool
double-IR TSE/FSE). These allow exce llent depiction of (Poustchi-Am in et al. 2003 ).
cardiac anatomy. Myocardial perfusion can be eva luated w ith
Bright blood sequences are gradient recalled echo gado linium-e nhanced dynamic "first pass" rest and
(G RE ) sequences and cine GRE is particularly useful. stress studies, the latter du ring admini stration of a phar-
These all ow evaluation of ventricular function and re- macologic stress agent such as adenosine. Delayed imag-
gional wall motion. GRE imaging using the segmented k- ing postgadolinium administration allows detection of
space technique and cardiac gati ng allows multi phase regional myocardial hyperenhance ment indicative of
single sli ce or multislice single phase modes. Examples nonviable tissue. Dobutamine may also be used as a
include TurboFLASH. fast SPGR. and TFE/FFE. Newer fast pharmacologic stress agent when resulting ve ntricular
GRE sequences with completely refocused gradients in- wall motion abnormalities may be assessed.
clude true FISP. balanced FFE, and FIESTA and these give
50
w ith the
2 Malformations ta l thora
Accesso
Like an f
ow n pl,
bronchu
Pulmonary malformations are rare and frequently as- • Bronchopulmonary anoma li es include pulmonary the tracl
sociated w ith extrapulmo na ry anomalies. age nesis and hypoplasia, bronchia l atresia, broncho-
Three main categories are recognized: genic cysts, co ngenital cystic ad enomatoid malfor-
• Combined lung and va scular anomalies include bron- mations. and congenita l loba r emphysema. • Clin
chopulmonary sequestrations and hypoge netic lung • Vascular malformations include pulmonary arteri-
(scim itar) sy ndrome. ovenous malfo rmations and anomalous pulmonary Fifty per
venou s drainage (Zylak et aJ. 2002 ). first 6 m
dyspnea
co nge nil
Intra l
Bronchopulmonary Sequestrations co ug h al
of patier
20 yea rs
• Pathology also may have an intradiaphragmatic, mediastinal, or
intra-abdominal position. Ext ralobar sequestrations
Bronchopulmonary sequestrations represe nt areas of have a systemic arterial supply from branche s of the • Rad
nonfunctioning lung ti ssue that do not communicate aorta and a systemic venous d rainage to the azygos veins
with the tracheobronchial tree and have a systemic or inferior vena cava. Associated anomalies including di- • Che s
arterial blood supply. Embryo logically. pu lmonary aphragmatic hernia and bronchoge nic cyst may be pre-
sequestrations are due to anomalous ve ntral budding sent in up to 60 % of cases. The c~
from the foregut or tracheobronchial tree. Occasionally. seques tI
they have a fistulou s connection to the esophagus or Intralobar Seque stratio n angular
stomach. Sequestrations are class ifi ed as extra- or in- base. lnl
tra lobar in type. Intra lobar sequestration s usua lly have a systemic arte- peara no
ria l supply and pulmonary venous drainage. Sixty per- opacity.
Extra lobar Se que stration ce nt of intraloba r sequestrations are left-sided and they of pn eUl
invo lve the lower lobes in 98 %of cases. While extralobar hyperlu,
Extralobar malformations constitute 25 % of seq uestra- sequestration is accepted as a congenital anoma ly, sub- jace nt bJ
tion s. They are discrete accessory lobes of nonaerated sta ntial evidence suggests that in tral obar sequestratio ns cyst ic m
lung invested within their own pleural covering (Rosado may have an acquired origin. Reports of intralobar ma tion
de Christensen et aJ. 1993). They are located most com- sequ estrations in infants are virtually abse nt and as- ve rtebrc
monly betwee n the lower lobe and the diaphragm. They sociated anoma li es are relatively unco mmon compared rect dial
• Sone
Extralob
and ech
infected
• Com
CT findi
tra lobar
Hom ogeneous oval opacity Un ilocular or Aortogra phy Bronchography ge neous
in the vertebrophrenic angle. multilocular
seen in
Intra lobar sequestrations are cystic lesion Intralobar: Extrolobor: Opacification of
occasionally air-filled due to following - Shared pleura with - Separate pleura bronchial tree spares decreasl
collateral air drift perforation adjacent normal lung - Systemic venous sequestered segment tralobar
- Pulmonary venous drainage to azygos to collal
drainage vein and vena cava fibrou s
Fig . 2.1 Pulmonary sequestratio ns. lun g (Sc
Bronchopul monary Seq uestrations 51
with their prevalence in associ ation with othe r congeni-

tal thoracic anoma lies (Stocker 1986. Frazier et al. 1997 ).
Accessory Lung
Like an extralobar sequestration, accessory lung ha s its

own pleural covering. It also ha s a rudimentary
bronchus, which may be patent and co mmunicate with
;>ulmonary the trachea, the trachea l bifurcation, or the eso phagus.
I, broncho-
lid malfor-
3. • Clinical Features
ary arteri -
pulmonary Fifty perce nt of extralobar sequestrations present in the a
first 6 months of infancy. Cli nical manifestations incl ude
dyspnea and cyanosis. The frequent association of other
congenital anoma lies al so may lead to their detection.
Intralobar sequestrations present with productive
cough and recurrent episodes of pneumonia. Up to 50 %
of patients w ill have become symptomatic by the age of
20 yea rs.
Iiasti nal. or
luestration s
ches of the • Radiologic Findings
lZygOS vei ns
neluding di- • Chest Radiogra ph
:nay be pre-
The characteristi c appearance of an extralobar
sequestration is that of a we ll-defined round, oval, or tri - b
angular opacity located posteromed ially at the lung
base. Intralobar sequestrations are more va riable in ap-
stemic arte- pearance. Findings include a well-defined homogeneous
e. Sixty per- opacity, so litary pulmonary nodule, recurre nt ep isodes
led and they of pneumonic consolidation, and an area of pulmonary
Ie extra lobar hype rl ucency. Infecti on with fi stula fo rmation to an ad-
lomaly. subjacent bronchus may lead to formation of a multilocular
questrations cystic mass with air-fl uid levels. Th is "cystic" tran sfo r-
)f intralobar mation of an in itia lly homogeneous mass in the left
ient and as- ve rtebrophrenic angle is strongly suggestive of the cor-
)n compared rect diagnosis (Fig. 2.1 ).
• Sonography
Extralobar sequestrations may appear homogeneous c
and echogenic. If an intralobar sequestration becomes Fig. 2.2 a-c Intralobar seq uestration. Axia l CT image (a) shows a
lobulated mass with a surrounding rim of decrea sed lung at-
infected, a mu lticystic mass may be seen. tenuation in the left lower lobe. Maximum int ensity projection
(M IP) reconstructions from CTA study show t he systemi c arte rial
supply from the t horacic aorta (b) and pu lm onary venous
• Compute d Tomography (a)
drainage t o the left atrium (c).
CT findings include a solid mass in both intra- and ex-
tralobar sequestrations. In addition, an area of homo- Occasionally, a foca l area of decreased lung attenua-
Iphy geneous consolidation or a complex cystic mass may be tion in the lower lobes may be the only pare nchymal
seen in the intralobar variant. A peripheral zone of manifestation of intraloba r sequestration (Ikezoe et al.
nof decreased lung attenuation is sometimes seen in in- 1990).
:!e spares
( segment tralobar sequestrations (Fig. 2.2) and ha s bee n attributed Dedicated thin-colli mation helica l CT w ith in-
to collateral air drift through the incomplete. partially travenous contrast medium allows demon stration of the
fibrous boundary between sequestrated and normal syste mic arterial supply and pulmona ry/systemic
lung (Scu lly et al. 1981 ). ve nous drainage (Fig. 2.3 )
52 2 Malformations
en
tiga
phy
phy
Hy
• Fig. 2.3 a, b Int ralobar sequestration. CT shows a large area of decreased attenuation in t he left lower lobe with a small central tubu lar
b
. 1
opacity (a). Shaded surface display (550) 3D reconstruction demonstrates t he systemic arterial supp ly and pulmonary venous drainage
(b). Hyp
the
righ
Fig.2.4a - ( Intralobar sequ estration. CT shows a partly cystic co m
lung lesion (a) which is su pplied by a branch of the aorta and
drained by pulmonary venous branches as seen at angiography
deri
(b. c). Pulmonary arteries (white) and pulmonary veins (black) as syst
seen on DSA study (c). anOi
lun ~
cava
for 1
feet!
and
bror
Fig. 21
b and tI
vein
uppe l
Hypogenetic Lung Syndrome (Scimitar Syndrome) 53
Angiography sequestration from the thoracic aorta in 70 % of cases,

from the abdominal aorta in 20%, and from an inter-
cr has become the imaging modality of choice in inves- costal artery in 5 % (Ranniger and Valvassori 1964). An
tigation of sequestrations, and conventional angiogra- intralobar sequestration drains to the pulmonary veins;
phy now is performed much less frequently. Aortogra- an extralobar sequestration drains to the vena cava,
phy demon strates a systemic arterial supply to the hemiazygos vein. azygos vein, or portal vein (Fig. 2.4).
Hypogenetic Lung Syndrome (Scimitar Syndrome)
b
!ntral tubular • Clinical Features Clinically, patients may be asymptomatic or may
ous drainage suffe r from recurrent infections. A significant left-to-
Hypogenetic lung syndrome almost always is seen on right shunt may give rise to exertional dyspnea.
the right side. The right lung is hypoplastic, and both the
right bronchial tree and pulmonary vessels show in-
partly cystic complete development. The hypoplastic lung therefore • Radiologic Findings
he aorta and derives a significant proportion of its perfusion from the
angiography
~ins (black) as
systemic circulation via branches of the aorta. The The chest radiograph may show a small right lung and
anomalous pulmonary vein runs inferiorly through the cardiac dextroposition. The "scimitar" vein descend s
lung before curving medially to enter the inferior vena vertically and then curves medially to join the IVC
cava (IVC ): it has the shape of a scimitar, thus accounting (Fig. 2.5 ). CT confirms the diagnosis and shows the scim-
for the name of the syndrome. Congenital cardiac de- itar vein draining to the IVC (Fig. 2.6) and the hypoplastic
fects, usually septal defects, are present in 25 % of cases, right pulmonary artery. It also may demon strate as-
and some patients also have bronchiectasis and tracheo- sociated bronchiectasis and tracheobronchial anoma-
bronchial anomalies. lies.
Fig. 2.Sa, b Scimita r syndrome. The right lung is hypoplastic

c and the re is ipsilateral cardiac disp laceme nt. The right lower lobe
vein drains to the vena cava (scimitar pattern), and the right
upper lo be vein drains to the azygos vein. b
54 2 Malformations
a b
Fig.2 .
• R.
Fig . 2.6a-c Scimitar CXR and CT. Chest radiograph (a) shows • Ch
scimitar vein. Axial CT images (b and c) show vein traversing the
c right lower lo be and draining into the inferior vena cava. Two-I
lobes.
t04 Cl
have
shadD
Bronchogenic Cysts The f'::
place~
ME
maSSE
• Pathology Mediastinal Cysts bronc
(Fig. 2
Both bronchogenic cysts and bronchopulmonary Bronchogenic cysts were described as mediastinal in 86,
sequestrations embryologically are due to abnormal 77. and 65% of cases (Dee 1995. 5t-Georges 1991. Reed Co
ventral budding from the foregut or tracheobronchial 1974. Di Lorenzo 1989 ). Most can be differentiated from
tree. However, in sequestration, there is subsequent in- esophageal duplications and enterogenic mediastinal GUSt
duction of mesenchyme to form lung parenchyma. cysts only by pathologic examination. The bronchogenic ble a1
Bronchogenic cysts result from a failure in this induction cyst is the most common congenital cyst of the medi- 1995).
process. Most bronchogenic cysts arise within the mediastinum.
astinum or at the hilum; the remainder are intrapulmo- Ma
nary (Dee 1995c. Reed 1974).
• Clinical Features The M
Intrapulmonary Cysts scribe,
Bronchogenic cysts may be an incidental radiographic 1993).
The central type of cyst occurs in the perihilar lung, is finding in young adults. They become symptomatic if low T
lined by respiratory epithelium, and contains viscous complicated by infection. Occasionally, a ten sion cyst with t
mucoid material. Peripheral lung cysts are usually multi- develops through a check-valve mechanism and results be hy
locular and, when extensive, may be indistingu ishable in respiratory impairment (Fig. 2.7). queno
from congenital honeycomb lung. to hen
Bronchogenic Cysts 55
•
!-"'-_-I b
Infection Drainage Tension cyst
Fig.2.7 Bronchogenic cyst.
• Radiologic Findings
Jh (al shows • Chest Radiograph

raversing the
cava. Two-thirds of intrapulmonary cysts occur in the lower
Fig .2.8 Multiple bronchogenic cysts . There is an air-fluid level
lobes, appearing as we ll -defined homoge neous masses 2 in one cyst due to secondary infection.
to 4 em in diameter. Mural calcification is rare. Cysts that
have discha rged the ir contents appear as th in ring
shadows, which may contain an air-fluid level (Fig, 2.8 ).
The rare te nsion cysts form a large air co ll ection that d is-
places adjacent normal structures (Fig. 2.9),
Mediastinal cysts are smooth , round, homoge neous
masses located adjacent to the trachea. carina. or main
bronchi. They may compress the trachea or esophagus
(Fig. 2,10),
stinal in 86,
1991, Reed Computed Tomography
ltiated from
mediastinal CT usua lly demo nstrates a nonenhancing ma ss of varia-
'onchogenic ble attenuation molded to adjacent structures (Dee
f the medi- 1995 ). Mura l calcification occasionally is see n.
The MRI appearance of bronchogenic cysts ha s been de-

scribed (Barakos 1989, Naidich 1988, Pa lmer 1991, Suen
'adiographic 1993 ). MRI signal intensity may be si milar to wate r with
lptomatic if low T1 and high T2 values. Bronchoge nic cysts fi ll ed
:ension cyst with blood, cholesterol, or proteinaceous materia l will
I and results be hyperintense on both Tl - and T2-we ighted se-
quences. Nonhomogeneous signal intensity may be due Fig.2.9 Tension cyst in the left lower lobe. Earlier studies
to hemorrhagic complications. showed a round homogeneous mass progressing to a small cyst.
Bronchoge nic Cyst s 55
b
Infection Drai nage Tension cyst
Fig. 2.7 Bronchogenic cyst .
Jh (a) shows • Chest Radiograph

raversing the
cava. Two-third s of intrapulmonary cysts occ ur in th e lower
Fig. 2.8 Mu ltiple bronchog enic cyst s. There is an air-flu id leve l
lobes, appearing as well-defined homoge neo us masses 2 in one cyst due to secondary infect ion .
to 4 cm in diameter. Mural calcificati on is rare. Cysts that
have discharged thei r contents appea r as th in ring
shad ows, which may contai n an air-fluid level (Fig. 2.8).
The rare te nsion cysts form a large air collection that di s-
places adjacent normal st ructures (Fig. 2.9).
Mediastinal cysts are smooth, round, homoge neous
masses located adjacent to the trachea, ca rina, or main
bronchi. They may compress the trachea or esophagus
(Fig. 2.10).
.stinal in 86,
1991, Reed Computed Tomography
ltiated from
mediastinal CT usua lly demo nstrates a none nhanci ng mass of varia-
ronchogeni c ble atten uation molded to adj acent structures (Dee
)f the medi- 1995). Mural calcification occasionally is seen.
The MRI ap pearance of bro nchogenic cysts has bee n de-

scribed (Barakos 1989, Na id ich 1988, Pal mer 1991, Suen
radiographic 1993 ). MRI signa l intensity may be sim il ar to water with
nptomatic if low T1 and high T2 values. Bronchogenic cysts filled
tension cyst with blood, cholestero l. or prote inaceo us material will
1 and results be hyperintense on both T1 - and T2-we ighted se-
quences. Nonhomogeneo us signal in te nsity may be due Fig.2.9 Tension cyst in t he left lower lobe. Ea rlier studies
to hemorrhagic compli cations. showed a round homogeneo us mass progressi ng to a sma ll cyst.
56 2 Malformations
SO
fn
fel
ph
ab
pa
Fig
aPI
b mE
Fig. 2.10a, b Bronchogenic cyst. The chest radiog raph (a)

shows a round, sharply circumscribed mass in the rig ht tracheo-
bronchial angle. CT shows a round para tracheal mass of water at-
a tenuation (b).
Congenital Cystic Adenomatoid Malformation of the lung (CCAM)
• Pathology • Clinical Features
Thi s hamartomatous lesion accounts for 25 %of all con- Seventy to eighty percent of cases present in the
genital pulmonary anomalies. It comprises fibrou s neonatal period with symptoms of cough and dyspnea.
tissue. smooth muscle. and back-to-back bronchiolar Approximately 10 %of cases present after the first yea r of
and duct-like structures of varying size. Cartilage is ab- life. usually w ith recurrent respira tory infections ( Dee a
sent. Thi s interconnecting system of clefts and cav iti es 1995 ).
communicates with the adjacent parenchyma through
the pores of Kahn. This permits collateral air drift and
may account for the expansile nature of these lesions. • Radiologic Findings Pl
Congenital cystic adenomatoid malformati on is
classified into three types based on findings at micro- Type 1 ((AM is the most common (75%). and the chest
sco py. radiograph may show an air- fill ed multicystic lesion
• Type 1 ((AM contains large cysts lined by ciliated
co lumnar epithelium.
w ith at least one dominant cyst greater than 2 cm in
diameter. This produces local mass effect with di splace- •
• Multiple smaller cysts lined by columnar/cuboidal ment of adjacent pulmonary and media stinal structure s Thl
epithelium are found in type 11 ((AM. These have an (Figs.2.11. 2. 12 ). There frequently is a degree of con- nOl
association wi th other extrapulmonary co ngenital tra latera l pulmonary hypoplasia. The size of the lesion •
anomalies including renal agenesis. may vary considerably on se rial studi es, and intercur-
• Type 111 ((AM contains bronchiolar and cleft-like re nt mucus retention may produce granular and patchy •
structu res which are lined by low cuboidal epi- opacities. Type 11 ((AM is co mposed of smaller. more
thelium. uniform cysts. while type III lesions are solid masses
co mposed of bronehoalveolar mi erocysts ( Berroeal et al.
Both type II and III lesions are associated with a poor 2003 ).
• II
prognos is.
Pul mona ry Age nesis. Apl asia. and Hypopl as ia 57
Antenatal sonographi c diagnosis is poss ib le, and a

solid or cysti c intrathoracic mass may be seen. The re is
frequently associated polyhydramnios and hydro ps
fetal is (Dee 1995 ).
The d ifferential diagnosis incl udes conge nita l di a-
phragm atic hernia. This is associated with a "scaphoid"
abdome n. w hereas in ((AM the abdo mi na l bowe l gas
pattern is normal.
Fig. 2.11 Conge nital cyst ic adenomatoid ma lformati on (CCAM) . [>

appearing as a hyperinflated cyst ic les ion with vascular displace-
b ment.
)graph (a)
ht trachea-
)f water at-
M)
Fig . 2.12 a, b Congenita l cystic adenomatoid malformat ion.

Chest radiograph (a ) shows increased left lung volume with me-
!It in the
d iast ina l d isplacement to the right side and a patte rn of cystic
I dyspnea. change and patchy opacifica t ion in t he left lower zone. CT shows
rstyear of cystic transformation of t he lower lo be with decreased vascula rity
:ions (Dee a (b).
Pulmonary Agenesis, AplaSia, and Hypoplasia

I the chest
stie lesion
In 2em in • Pathology • Clinical Features
1 displace-
structures Th ree degrees of severity are recogn ized in this failure of Pri mary unilateral hypoplasia in the abse nce of sc imitar
~e of con- normal lung developme nt (Fig. 2. 13 ). syndrome is rare (Dee 1995 ). Patie nts may be asympto-
the lesion • Pulmonary agenesis, in w hich the lung and all as- matic. though affected child ren fre que ntly are prone to
j intercur- sociated structures are abse nt. bro nchopulmonary infections. So me patie nts may have
md patchy • Pulmonary aplasia, in w hi ch the lung parenchyma is associated extrapulmonary anom alies.
311eT, more absent but the re is a rud ime ntary mai n bro nchus
lid masses which terminates blindly (Fig. 2. 14).
:rocal et al. • Unilateral pulmona ry hy poplasia. in w hi ch a no rmally
formed main bro nchu s terminates in a small, rudi-
menta ry lung w ith malformed lobes.
58 2 Malformations
Agenesis Aplasia Hypoplasia

Con
• Pa
Conge:
chroni
Ca u se~
a chec
The et
varian
numb<
Absent main bronchus Rudimenta ry Small lung showing cystic tran sformation valved
main bronchus
rig ht l
1991 )1
Fig.2 .13 Congenital development an omalies of the lung.
ThE
1995 ).
ease (I
• eli
PatienJ
nasis i
later n
In the
an opa
b to the
perluo
Fig. 2.14 a, b Left lung ap lasia. The stump of the left main a nd tl
bronchus is opacified at bro nchography (a). Left -sided media sti- tralate
• nal displacement and right lung hyperinflation are seen (b). inc rea~
copy).
strate \
find ing
• Radiologic Findings Pulmonary angiography shows large-caliber vessels a tensi
in the opposite lung with an absent or rud imentary
The affected hemithorax is small with narrow inter- vascu lar syste m on the affected side.
costal spaces, an elevated hemidia phragm, and medi-
astinal displacement to the ipsil atera l side. The con-
tralaterallung shows compe nsatory hyperinflation with • Differential Diagnosis
posterobasal and anteroapicai herniation towards the
affected sid e. The diffe rential diagnosis includes pneumonectomy.
CT confi rms pu lm ona ry hypoplasia and accurate ly congenita l ate lectasis. lobar em physema, diaphragmatic
defines the extent of the herniation. The presence of a hernia, fibrothorax, and Macleod syndrome.
main bronchus serves to distingui sh pu lmonary aplasia
from agenesis. although thi s distinction clinically is un-
important.
Fig.2. 1E
Congenital Lobar Emphysema 59
Congenital Lobar Emphysema
• Pathology
Congenital lobar emphysema (CLE ) is characterized by
chronic hyperinflation of a lobe o r one of its seg ments.
Causes include congenital bronchi al stenosis producing
a check-valve obstruction and local mucous plugging.
The etiology is unclear in 50 % of cases. A polyalveo lar
variant of CLE also may occur, and in these cases the
number of alveo li is increased. The left upper lobe is in-
volved in 50%. the right midd le lobe in 24 %. and the
right upper lobe in 18 % of cases (All en 1966. Kennedy
1991) (Fig. 2.15 ).
The lower lobes are involved in only 2 %of cases (Dee
1995). There is an association w ith congen ital hea rt di s-
ease (Hendren 1966).
Fig.2.15 Congenital loba r emphysema: left upper lobe (50 %),
right middle lobe (24 X). rig ht upper lobe (18 %). Radiographs
• Clinical Features show localized hyperlucency with displacement of adjacent bron-
chovascular bundles.
Patients present with tachypnea. tac hyca rdi a. and cya-
nosis in the first 2 to 4 weeks of life. In rare instances, a
later man ifestation may occur.
In th e first week of life. the affected lob e may present as
an opaque mass due to retention of amn iotic fluid di stal
b to th e obstruction. Later, the affected hemithorax is hy-
perlu ce nt, the ipsilateral hemidiap hragm is depressed,
~ left main and the mediastinum is shifted towards the con-
d mediasti- tra lateral side. The degree of mediasti na l di splace ment
en (b). increases in expiration (medi astinal flutter on fluoros-
copy). Conven tional and co mputed tomogra phy demon-
strate vascular markings in the hype rtra nsradi ant lung, a
find ing that excludes the prese nce of a pne um otho rax or
ler vessels a tension cyst (Figs. 2.16.2.17 ).
jimentary
.onectomy,
Ihragmatic
Fig.2.16 Tracheal bronchu s. Fig.2.17 Congenital lobar emphysema of the right upper lobe
with bronchial displacement and crowdi ng.
60 2 Malformations
Congenital Bronchial Atresia Va
Congenital bronchial atresia frequently involves a collate ral air drift. The most common site is the api-
Pu
segmental bronchus, and its functional effects usually coposterior segmental bronchus of the left upper lobe
are mild. The postatretic bronchi are structura lly normal, (Fig. 2.18). Mi
although they may be ectatic and mucus filled (muco-
cele, mucoid impaction ). The alveoli are aerated through
• Radiologic Findings •
The chest rad iograph shows an elongated. partially Can
branched ce ntra l opacity representing the mucocele. ma~
The affected lung segment may be hyperinflated and due

this combined with a degree of hypoperfu sion results in ca n
hypertransradiancy. Son
Ventila tion and perfusion scintigraphy confirm the ab- t he
sence of ventilation and diminished perfusion to the af- bu t
fected segment. rno:
Helical computed tomography w ith reformats and
three-dimensional reconstructions clearly depicts the
mucocele. the focally decreased lung attenu ation. and
the hypo perfusion (Fig. 2.19 ).
•
ThE
mu
<l Fig. 2. 18 Bronchial atresia. The affected segment shows some zon
degree of hyperinflation due to collateral air drift. fluc
(Fig
,. agil
Avr
th e
lesi
are
dift
(Re
a b
Fig. 2. 19a. b Bronchial atresia. Axial CT image (a) shows decreased attenuation in the right upper lobe with a central tu bular branch-
ing structure. SSD 3D reconstruction-posterior view (b) of pulmonary vasculature shows paucity of vessels to right upper lobe.
•
Fig.
is ir
rna,
Vascular Malformations 61
Vascular Malformations
the api- Pulmonary Arteriovenous

.per lobe
Malformations (AVM)
• Clinical Features
partially Congenital pulmonary arteriovenolls malformations

nucocele. may lead to cyanosis, polycythemia, and finger clubbing
ated and due to the presence of a right-to-Ieft shunt. Hemoptysis,
results in ca rdiac failure, and paradoxica l emboli are uncommon.
Some 50 % of patients also have te langiectasia involving
m the ab- the buccal mucosa (Rendu- Osler-Weber telangiectasia ),
but only 15 % of patients wi th Osle r's di sease have pul- - Lobulated mass Arteriography
to the af- - Feeding and draining - Convoluted vascular
monary AVMs. vessels masses
llats and - Early opacification of
,picts the large-ca liber vein
Ition , and • Radiologic Findings
Fig.2.20 Pulmonary arteriovenous malformations (AVMs).
The chest radiograph frequentl y shows solitary (70 %) or
mu ltipl e (30 %) well-circumscribed nodules in the lower
hows some zones (Fig. 2.20 ). These show active pulsations on
fluorosco py. Conventional pulmonary angiography Partial Anomalous Pulmonary
(Fig, 2,21) has now been replaced by he lical CT as the im- Venous Drainage (PAPVD)
aging moda lity of choice in the detection of pu lmonary
AVMs. CT angiography (CTA) is also usefu l in the pre-
therapeutic evaluation of the angioarchitecture of these • Clinical Featu res
lesions as the number and orientation of feeding vessels
are the most important factors in determining technical Partial anomalous pulmonary venous drainage gives rise
difficulty and duration of the em bolizati on proced ure to a left-to-right shun t. PAPVDs are classified as supra-
(Remy-Jardin et al. 1999). cardiac, cardiac, infradiaphragmati c, and mixed in type.
2r lobe.
•
Fig. 2.21 a, b large AVM leh lower lobe. Angiographic cathete r
is in the left lower lobar artery. There is early opacification of a
markedly dilated left lower lobe vei n. b
62 2 Malformations
A large shunt vo lume may result in right ventricular

fai lure.
Scimitar syndrome is a specific examp le ofPAPVD but
with an associated lung bud anomaly.
Occasionally. an anomalous vein is seen on the chest

radiograph. These are recognized increasingly com-
monly at cr and may involve the left upper lobe with
drainage of a vertical vein to the brachiocephaJic vein
(Alder et al. 1973) and the right upper lobe with dra inage
of a right superior pulmonary ve in to the azygos ve in
(Thorsen et al. 1990). Ca reful evaluation of the cr study.
however. is required to distinguish a persistent left su-
perior vena cava (5VC ) draining to the coronary sinus Fig . 2.24
from left uppe r lobe PAPVD. The diagnosis may also be
confirmed at angiography (Figs. 2.22. 2.23).
Hypoplasia and Atresia

of the Pulmonary Artery
Fig.2.22 Anomalous venous drainage. Contrast material in-
jected into the pulmonary artery opacifies the superior vena cava The pu lmonary artery may be absent or atretic just past
through a large-caliber left upper lobe vein (the aorta is also its origin. This entity is more commonly right-s ided and
opacified). when left-s ided, there is an association with congenital
cardiovascular anomalies. The affected lung and hilum
are decreased in size and intrapulmonary vessels are
decreased markedly in size and are systemic.
• Fig. 2.23 a, bAnomalous drainage of right lower lobe vein to the right atrium. The pulmonary angiogram is equivocal (a), but the
b
anomalous dra inage is confirmed by retrograde opacification of the vein from the right atrium (b).
Vascular Malformations 63
:ntricular • Rad iolog ic Findings
~PV Dbut The chest radiograph shows a hypertransradiant lung

w hich is reduced in size (Figs. 2.24, 2.25). There is no air
trapping in contrast to the Macleod syndrome of ac-
quired constrictive bronchiolitis with secondary arterial
hypoplasia.
Radionuclide perfusion sc intigraphy demonstrates
the chest ventilation with no perfusion. CTA or MRI will confirm
gly com- the diagnosis.
.obe with
lalic vein
I drainage
- Small hypertransradiant
ygos vein hemithorax with no vascular markings
IT study, - Herniation of cont ralatera l lu ng
1t left su-
lary sinus Fig. 2.24 Pul monary artery at resia.
'y al so be
Fig.2.25 Congenita l hypoplasia of

t he right pu lmonary artery. Chest
rad iograph shows hypertransradi-
ancy of the rig ht lu ng with de-
creased vascularity. No air t rapping
was seen on t he expiratory view.
c just past
·sided and
:ongenital
,nd hilum
'essels are
b
,I (aJ, but the
64
3 Infection and Inflammatory Disorders
Pneumonia
Pneumonia is an infectious pu lmonary process that may

be caused by bacteria. mycoplasma, viruses. and other
microorganisms. It is characterized by inflammatory ex- Confirm the pre sum ptive cli ni ca l diagnosis; t hi s Fig
frequent ly ca n be accomp lished with frontal and late ral
udate in both the alveoli and inte rstitium. Dete rmina-
chest radiographs.
tion of the causative organism by sputum bacteriol ogy
or immunoserology may be helpful in initia tion of ther- Id entify underlying predisposing fa ctors such as m.
bronchiecras is and bronchial neoplasia.
apy. So me textbooks classify pneumonias accordi ng to te l
the causative orga ni sm (M urray 2000 ). However, give n Monitor the rad iologic progression and reso lutio n of
fill
disease.
the si milarity of the clinical manifestations and radio- no
graphic findings produced by different organisms. we Detect complications such as cav ita tio n, abscess for:a-J ga
t ion, and development of empyema (Fig. 3.1).
shall focus our discu ss ion on their morphologic features. flu
al.
• Pathology Inl
Morphologic class ification distingu ishes between lobar Int

pneumonia, bronchopneumonia, and interstitial pneu- fra
monia. This classification depend s on the nature and ex- ga
tent of inflammatory exudate in the alveoli and the ree
degree of interstitial infiltration. th,
ph
Lobar Pneumonia sui
int
Loba r pneu moni a is an a lveolar or airspace conso lida- of
tion in w hich the causative organisms are inhaled. On lot
reaching the alveoli, they proliferate and spread rapidly
through the pores of Kahn across segmental bound-
aries until the entire lobe is invo lved. In lobar pneu-
monia there is re lative sparing of the bronchi and in-
•
terstitium. eli
The class ic progression of lobar pneumonia through pa'
e the stages of co nges tion (i ntra-a lveolar ede ma), red sta
hepatization (e rythrocyte exud atio n), yellow hepatiza- rali
tion (leukocyte exudation ), gray hepati zatio n (fi brinous ca~
cha nge), and eventual lysis is rarely seen today, Effective tit{
antibioti c therapy also has led to a marked decrease in be
the incidence of lobar pneumonia. cui
ba,
Bronchopneumonia (Lobular Pneumonia)
9
Bronchopneumonia is acquired by inhalat ion o r, less
commonly, by hematogenous spread of the causative or-
•
ganis m. On reach ing the terminal and resp ira tory Th,
Fig. 3.1 Possible evolution of right upper lobar pneumonia.
bronchioles, the organ isms precipitate an inflammatory ma
a, b, c Complete resolution. a , d. e Abscess formation with sub-
sequent scarring and pleural thickening. a, f. 9 Pneumonia pro- reaction w hich then sp reads to adjacent alveoli. Further tur
gressing to bronchiectasis (from Bohlig). extension through the pores of Ka hn res ults in involve- ( Fit
Pneumonia 65
Lobar pneumonia: Bronchopneumonia: Int erstitial pneumonia:

Lobar and/or segmental consolidation coalescing areas of consolidation reticu lar pattern in a
with air bronchogram and in a predominantly basal dist ribution predominantly central distribution
accompanying pleural effusion
Fig.3.2 Radiog raphic patterns of pneumonia.

eral
ment of the entire secondary lobule. Bronchopneumonia Plain Chest Radiograph

tends to be multifocal and patchy in distribution, the in-
filtrated lobules being interspersed between areas of lobar Pneumonia
normally aerated lung. The most common causative or- In classic lobar or segmental pneumonia, the radio-
:J ganisms are Staphylococcus aureus, Haemophilus in-

fluenzae, Pseudomonas species, and anaerobes (Webb et
al. 1992).
graphic features are characteristic with homogeneous
opacification of the involved lobes or segments
(Figs. 3.3- 3.5 ), Segments often are incompletely
opacified, and this makes their location difficult to de-
Interstitial Pneumonia termine except when the shadowing extends to a well-
defined pleural /fissural margin. Patent bronchi within
1 lobar Inflammatory infiltration of the connective tissue homogeneous consolidation appear as linear branching
pneu- framework of the lung is characteristic. Causative or- lucencies or, when seen end on, as rounded lucencies
md ex- ganisms include Mycoplasma, Rickettsia, and viruses. On (air bronchogram ). The volume of the affected segments
nd the reaching the bronchial wall via the airways, they destroy may be diminished because of inflammatory narrowing
the ciliated epithelium, with resulting edema and lym- of the airways and decreased surfactant production.
phocytic infiltration of the bronchial mucosa. There is Classic lobar pneumonia, caused by Streptococcus pneu-
subsequent spread of the inflammatory process to the moniae in 95 %of cases, is extremely rare today. Segmen-
interlobular septa. There also is lymphocytic infiltration tal opacification, however, is quite common and very
lsolida- of the peribronchial alveoli and this appears similar to often represents confluent multifocal consolidation.
led. On lobular pneumonia.
rapidly Bronchopneumonia
bound- In bronchopneumonia, the radiologic pattern is that of
. pneu- • Clinical Features multiple, ill-defined, confluent, nodular opacities, which
and in- represent multiple secondary lobules filled with inflam-
Clinical manifestations include pyrexia, pleuritic chest matory exudate (Figs. 3.6, 3.7), The nonhomogeneous
hrough pain, and cough productive of serous, purulent, or blood- pattern of ventilated and consolidated lobules results in
,a), red stained sputum. Auscultatory findings of fine bubbling a sponge- like pattern. Focal air trapping within second-
~patiza rales correlate with radiographic change in only 40 % of ary lobules due to check-valve obstruction of bronchi-
brinous cases. Leucocytosis with left shift and elevated antibody oles may also contribute to this appearance. Poor aera-
ffective titers also may be present. Bacteriological diagnosis may tion of the infected lung may lead to basal opaque bands
~ease in be possible from sputum analysis with Gram stain and similar to discoid atelectasis.
culture: serology may yield the diagnosis in atypical
bacterial and viral pneumonia. Interstitial Pneumonia
Inflammatory infiltration of the bronchial wall and in-
terlobular septa leads to formation of linear and reticular
or, less • Radiologic Findings opacities most marked in the perihilar lung. Simul-
ltive or- taneously, focally confluent shadows are found which
piratory The pathomorphologic classification of pneumonias represent inflammatory exudate in the peribronchiolar
lmatory may also be used to characterize their radiographic fea- alveoli (Fig. 3.8).
Further tures, although differentiation is not always possible
involve- (Fig. 3.2).
66 3 Infection and Inflammatory Disorders
a b
Fig. 3. 3 a. b Pneumonia in the lateral segment of the right rior boundary at the major fissure (b). Patient presented clinically
middle lobe: homogeneous consolidation with a sharp boundary with pyrexia, productive cough, and leukocytosis.
anterosuperiorly at the minor fissure (a ) and a well-defined poste-
a b a
Fig. 3.4 a, b left lower lobe pneumonia. Patchy consolidation is seen to obl iterate the posterior aspect of t he left hemidiaphragm in Fig
the lateral view. an
Pn eumonia 67
Fig. 3.Sa, b lingular

pneumonia. Note the
posterior boundary of
the major fissure (a), t he
indistinct cardiac out-
line, and the translucent
costophrenic angle (b).
There may be associated
consolidation of the
anterior segment of t he
left upper lobe.
a b
b
:d clinically
b b
japhragm in Fig. 3.6a. b Bronchopne umonia. Diffuse reticulonodular shadowing is seen in t he rig ht lower zone. Radiograph taken after 10 days of
ant ibiotic therapy shows complete resolution of change.
68 3 Infection and Inflammatory Disorde rs
Fig. 3. 7 a, b Postict al
aspirat ion pneumonia s
(a) wit h clearing of
(
consolidation on
follow-u p radiograph !
taken 8 weeks later !
following prolonged
antibiotic t he rapy (b).
• b
• L..__
b
Fig. 3.8a, b Interstitial pneumonia. Radiog raph shows increased perihilar linear markings in a patient who presented with cough,
fever, hoarseness, and elevat ed mycoplasma anti body t iters .
Parapn eumonic Pleural Effu sion

computed Tomography (CT)
Pleural fluid usually collects adjacent to lobar pneu- cr is ra re ly used in the investigati on of communi ty-ac-
monia and causes homogeneous opacification of the quired bacterial pneumonia; the di agnosis is usually
pleura l space. The effusion may form a spind le-shaped based on clinical and plain radi ographic findings.
mass within the interl obar fi ssure, or it may be free ly However. cr accurately demonstrates the exte nt of th e
mobile and gravitate to the costophreni c sulcus, ca using pneu monia and all ows for ea rlier detection than the
blunting of the costoph re nic angle. plain radiograph. It al so demonst rates co mp li cations
such as pulmonary abscess formation and development
of e mpyema.
Lung Abscess and Septic Pulmonary Emboli 69
)ostictal Thin section /h igh resolution Cf (HRCf) find ings are that is below the resolution of Cf or partial filling of the
umonia similar to those found on the chest radiograph and in- alveoli.
19 of clude homogeneous consolidation with air broncho- Air space nodules range from 3 to 10 mm in diameter
on
ograph grams. Other manifestations of air space filling include and probably represent peribronchioiar consolidation
later ground-glass opacification and air space nodules. (Webb 1989, Murata 1986). They tend to be centrilobular
onged Ground-glass opacification refers to a "hazy" in - in distribution but may spread and coalesce to give more
apy (b). crease in lung attenuation that does not obscure of pul- extensive areas of patchy consolidation.
monary vessels. It may indicate interstitial thickening
Lung Abscess and Septic Pulmonary Emboli
A lung abscess is a circumscribed area of inflammation

with purulent liquefaction (Fig. 3.9). It may progress
rapidly and erode into an adjacent bronchus or into the Cavity with an air-fluid
pleura. In this era of antibiotic therapy, abscess forma- level within an area
of consolidated
tion has become much less common though it remains a lung. Accom-
serious complication of pneumonia with reported mor- panying pleural
tality rates of 20-50%, effusion or
empyema
Goals of Diagnostic Imaging:

Detect abscess formation: this frequently is eviden t on
the chest radiograph but CT may allow earlie r detection
and help to distinguish abscess from empyema forma-
tion.
Detect predisposing factors such as aspirated foreign I
material, bronchial stenos is, and obstructio n. ~
Fig.3.9 Lung abscess .
• Pathology
Staphylococcal or Klebsiella pneumonia may be compli-
cated by abscess formation. Abscesses also develop as a
result of aspiration, as a complication of infarction,
bronchiectasis, or distal to bronchial obstruction.
Multiple abscesses may also be a manifestation of
septic lung emboli; this may be seen in the setting of a
nidus of infection elsewhere (Fig. 3.10). Right-sided
bacterial endocarditis including tricuspid valve infection
b
in intravenous drug users, infected venous catheters,
lith cough.
and bacterial pharyngitis/tonsillitis in the setting of
Lemierre syndrome are recognized causes of septic pul-
monary embolism (Fig. 3.11,3.12).
The yellowish, purulent focus of the abscess is sur-
rounded by a seropurulent exudate in the surrounding
alveoli. In favorable cases the pus is expectorated and
IUnity-ac- the process heals by scarring. In other cases residual Fig.3 .10 Septic pulmonary emboli resultin g fro m systemic sep-
is usually cavities persist and may become co lonized by Aspergillus sis in pyelonephritis.
findings. Jumigatus or other organisms. In severe cases the ab-
ent of the scess may rupture into the pleural cavity, leading to for-
than the mation of a pyopneumothorax.
plications In children, the residual lung cavity may hyperinflate
'elopment via a check-valve mechanism, resulting in a pneumato-
cele which usually resolves in 4-6 weeks.
70 3 Infection and Inflammatory Disord ers
a
a b c
Fig. 3. 11 a-c Multiple foci of pulmonary consolidation. some of which show cavitation. Patient had an epi sode of acute tonsi llit is with
systemic sepsis.
posterobasal segments of the lower lobes are most com-

mon ly involved (see Fig. 3.9).
Radiologic progression may be quite rapid. Rupture of
an abscess into a draining bronchus produces a cavity
with an air-fluid level (Fig. 3.13,3.14). Multiple cav ities
develop ing w ithin consolidated lung is known as
necrotizing pneumonia.
Computed Tomography
c
cr all ows earlier detection of abscess formation within
areas of pu lmonary conso li dation than does th e stand-
Fi g.3 .12 Pneumonia with lung abscess formation in in- ard chest radiograph. cr is also superio r in defining the
t ravenous drug user. CT shows predominantly rig ht-sided con-
solidation with areas of abscess formation. relationship of the process to the pleura l cavi ty, and the
fo ll owing features may help in differentiation from
empyem a:
• Clinical Features Empyema te nds to be lenti cular in shape, and the
angle of interface with the chest wall is usually obtuse. A
Symptomatology resemb les that of acute pneumonia lung abscess is usua lly spherical and produces an acute
w ith fever, ri gors, cough productive of purulent sputum. angle with the chest wall.
and leucocytosis. Patients with diabetes mellitus, alco- Empye ma fluid lies between thickened parietal and
holism, and immunocompromised individuals are at in- viscera l pleura (the spl it pleura sign; Fig. 3.15). This
creased risk of developing lung abscess. pleural t hickening is relatively smooth in contrast to the
wall of an abscess, wh ich may be thickened , quite ir-
regular, and co ntain locules of gas. Lung adjacent to an
• Radiologic Findings empyema is compressed with pu lmonary vasc ular dis-
placement. A lung abscess is associated w ith destruction
of pu lmonary pa renchyma.
Plain Chest Rad iograph
Most abscesses arise within areas of pneumonic con-
so li dation and are ma rked by the development of a di s-
crete area of low density necrosi s and cavitation. The
a
Fig.3.1
Lung Abscess and Septic Pulmonary Emboli 71
Fig. 3. 13 a- d Lung
abscess (a, c) with
resolution after
11 weeks' therapy
(b. d). Radiograph a
showed consolidation
with possible cavita-
tion. (T (c) confirms
the presence of an
abscess.
a b
5i\litis with
cst com-
lpture of
a cavity
~ cavities
tOwn as
c ..IIIIIId
n within
Ie stand -
ining the
. and the
on fro m
and the
)btuse. A
an acute
ietal and
15). This
lSt to the
Quite ir-
~nt to an
:ular dis-
struction
a b
Fig. 3. 14a, b Postpneumonic lung abscess with an air- fluid level. Causative organism: staphylococcus.
Fig.3. 15 CT shows large right-sided empyema with Msplit

pleura~ sign .
Pulmonary Tuberculosis
Tuberculosis is an infectious disease which may affect The incide nce and prevalence of tuberculosis has al-
any organ but shows a definite predilection for the ways remained high in endemic regions and is the lead-
lungs. In 95 % of cases the causative organ ism is My- ing cause of death in patients with AIDS in developing
co bacterium tuberculosis human us. A less common strain countries.
is Mycobacterium bavis. Atypica l mycobacteria such as The main factor determining whether tubercu lous in-
M. kansasii and M. balnei occur only sporadically. The infecti on progresses to di sease is the immune competence
cidence of another atypical mycobacterial infection, my- of the indi vid ual (Murray 1996). Today the di sease most
cobacterium avium complex (MAC ), increased markedly commonly is found in persons whose immune status is
in th e 19805 and 19905 mainly due to the increasing com promised by old age, alcohol abuse, diabetes melli-
number of patients with acquired immunodeficien cy tus, steroid therapy, or AIDS. There is also a relatively
syndrome (AIDS ) and dep leted helper T-Iymphocyte high incidence in certain ethnic groups, many of whom
CD4 co unts (see p.97). have recently immigrated to Western Europe and North
In 1900, tuberculosis was still a worldwide epidemic America.
with a mortality rate of approx imately 250 per 100000 Tuberculosis is classically divided into primary and
per year. Effective antituberculous therapy and better postprimary disease (Fig. 3.16). Some controversy exists
socioeconomic conditions have substantially reduced as to whether the latter represents reactivation or rein-
the incidence and prevalence of tuberculosis, with a re- fection (McAdams et al. 1995). Primary tubercu losis oc-
sulting decline in mortality rates. Mortali ty rates in Ger- curs in those not previously ex posed to M. tuberculosis, is
many are less than 3 per 100000 pe r year. In the United frequently asymptomatic, and the refore is not detected
States, 1800 tube rculosis-related deaths are reported cl ini ca lly. Postprimary or "cavitating" tubercu losis oc-
each year, corresponding to a morta li ty rate of less than curs in prev iously sensitized individ uals: before the ad-
1 per 100000 per year. The re was a steady decl ine in the vent of antitube rculosis chemotherapy, it was frequently
incidence of tubercu losis in ind ustrialized countries fata l (ga l/oping consumption ). Today, fibroci rrhotic end-
during the second half of the 20th ce ntury until the mid stage disease with severe ventilatory impairment may
1980s. In Germany, the incidence had fa llen from 174 lead to eventual death from decompensated cor pul-
new cases per 100000 in 1942 to less than 32 new cases mona le. Fig.
per 100000 population in 1994 (1994 Report of the The frontal chest radiograph remai ns the initial imag-
German Central Committee on Tuberculosis Control). ing investigation in tube rculosis. Some studies have em-
However, in th e late 19805 and early 1990s, this
downward trend reversed, due mainly to the increasing
phasized the ro le of high-resolution cr, particularly in
the detection of endobronchial spread (Lee 1991 , 1m et
f9I ~
numbers of cases in patients with AIDS (1m 1995 ). In the al. 1993, Hatipoglu et al. 1996), Bacteriological diagnosis fe
United States, there were approximately 20000 new is made from detection of acid-fast bac illi (AFB) in A
cases in 1985 ; this had increased to more than 25000 sputum, gastric was hings, pleural nuid and, in patients
new cases by 1990. More rece ntly, the resurge nce of proceeding to bronchosco py, from bronchoalveo lar lav- "
si
tubercu losis in Western countries has also been at- age (BAL) fluid. Newer immunologic and nucl eic acid- lit
tributed to immigration and the development of multi- based techniques are also emerging (Furin and Johnson D
drug-resistant disease (MDR-TB; Faustini et al. 2006). 2005 ). Ci
Pulmonary Tuberculosis 73
lith ~sp l it
Primary tuberculosis Postprimary tuberculosis
Primary complex Dissem ination Organ tuberculosis
Primary complex - Assmann foc us

- Caseous pneumonia
- Simo n focus (usually
!
(caseous pneumonia + - Productive tuberculosis
lymphadenitis) heals by scarring)
(tubercle, tuberculoma)
;is has al-

the lead-
,veloping
[Ulous in-
mpetenee
!-
- Tubercu lous hilar lymph Miliary tuberculosis - Cavitating lesions in tuberculosis
~ase most - Disseminated acinonodu lar foci
node enlargement in children (discrete miliary tuberculosis,
~ status is - Epitubercu losis Landouzy tuberculous sepsis) - Lobula r caseous pneumonia
tes melli- Tuberculous empyema
relatively
of whom
md North
mary and
~rsy exists
In or rein-
Heals by scarring
:ulosis oe- (in 95% of cases)
'rcu/osis, is
t detected Exudative tubercu lo us effusion - Pleura l thickening
ulos is oe- - Fibrotic cavity
Ire the ad- Hematogenous dissemination to - Fibrocirrhotic tuberculosis
urogenital tract, spine, adrenal glands, (cicatricia l emphysema,
frequently bronchiectasis, vascular
liver, choroid plexus, meninges, etc
hotic end- distortion, pulmonary
ment may herniation)
j cor pul- - Cor pulmonale
Fig .3.16 Pu lmona ry tubercu losis.
litial imag-
5 have em- Goals of Diagnostic Imaging:
• Pathology
:ieularly in Adequate screening programs to detect early disease par-
1991, 1m et ticularly in high risk groups. In Germany, 30 % of new in- The German pathologist K. E. Ranke identified three
I diagnosis fections are detected in this way. stages in the evolution of tuberculosis. In modern no-
i (AFB) in Accurate interpretation of radiographic abnormalities menclature, the last two Ranke stages are included in
in patients with a re lative ly low thresho ld for sugge sting tuberculo- the postprimary phase (Table 3,1 and Fig. 3.16).
veolar lav- sis in the differential diagnosis.
lcleic acid- Monitoring the response to therapy with serial imaging.
ld Johnson Detecting the sequelae of healed tuberculosis such ;s
catricial emphysema, bronchiectasis, and cor pUlm~
~- I
Table 3.1 Stages of pulmonary tuberculosis (from Doerr, quative necrosis. also termed caseous necrosis due to its
Schmidt, Schmincke) grayish-yell ow appearance. There is surrounding gran u-
lation tissue rich in lymphocytes, epitheloid cells, and
A. Primary stage
Primary pulmonary focus (Chon focu s) and regional Iymph- Langerhans giant cells. Spread of tubercle via the lym-
adenitis = primary comp lex (dumbbe ll-shaped consolidation phatics leads to a specific hil ar lymphadenitis. In the
as described by K. E. Ranke) great majority of cases, th is primary complex (Ghon
B. Postprimary st age focus + regiona l lym phaden itis) heals with fibrosis and
l. Dissemination may calcify. Large infected lymph nodes may compress
,. Early dissemination the bronchi, particularly the right middle lobe bronchus,
a) Simon foci
b) Miliary tuberculosis
with resulting dista l atelectasis; this occurs almost ex-
c) Rarely in immunocompromised hosts: acute tuber- clusively in children (epituberculosis). In the severely
culous sepsis (Landouzy) immunoco mpromised patient, caseous lymphadenitis
2. Late dissemination may erode into an airway resulting in tuberculous dis-
a) Subapical acinonodular disseminated foci
semination through primary endobronchial spread.
b) Coarse granular dissemination (Aschoff-Puhl focus)
c) Early infraclavicular consolidation (Assmann-
Redeker-Simon) Hematogenous Dissemination
II. Isolated organ tuberculosis
1. Nodulation, fibrocirrhosis, cavitation Myco bacte ria entering the blood from the primary com-
2. Reticular lymphangitis
plex may become disseminated to numerous extrapul-
monary sites (urogenital system. bones. meninges,
adrena ls, bowel, etc. ).
• Miliary tuberculosis: Hematogenous dissemi nation a
appears as myriad small nodules (millet seeds)
throughout the lung but displaying an upper zone
predominance. These fine nodu les are tubercles with
a core of caseous necrosis and surrounding granula-
tion tissue. Discrete miliary tubercu losis. character-
Distribution of focus
ized by fewer nodu les, is associated wit h less seve re
deg rees of immunocompro mise. Disse minated
tuberculosis with multiorgan involvement is as-
sociated with a high mortality rate.
• The most frequent pulmonary manifestation of he-
matogenous di sse mination is the appearance of a
solitary tuberculous focus at the lung apex (the Simon
focus, Assmann infiltrate, subapical acinonodular
focus ). This predilection for the upper lobes is due to
the hi gher t issue oxygen tension and relatively low
perfusion in this region.
• Exudative pleurisy: Bacilli invade the pleura where
they form tubercles; this is associated with develop-
Distribution of cavities ment of a pleural effusion rich in lymphocytes.
b
Postprimary Organ Tuberculosis
This form of postprimary tubercu losis is characterized cu le

by cavitati ng lesions in the upper lobes or in the apica l ing
segme nts of the lower lobes (Fig.3. 17). Rupture of a latil
parenchymal focus into an adjacent airway and sub- • Cay
Fig.3. 17 Frequency distribution of tuberculous lesions by lung sequent endobronchial sp read may lead to extensive SiOli
segment s (Doerr 1983).
pu lmonary involve ment. soci
• Exudative tuberculosis is cha racterized by a lobular, tub.
caseous pneumonia with relatively few epithelioid cast:
Primary Complex cells. Coalescence may occur to form larger foci of bro~
caseous pneumonia. • Fibr
Inha led tubercle bacilli initially evoke a focal, non- • Productive tuberculosis is characterized by well-de- pro(
specific subpleu ral alveo li tis w hi ch converts to a tuber- fined soli d nodules, 1-2 mm in diameter and rich in coni
culosis-specific inflammatory focu s in about 10 days epithelioid cells; these corres pond to the size of the lead
(Ghon focu s). The latter is characterized by central colli- primary lobule. If the immune res ponse is weak. brOl
.
Ie to its Fig. 3.18a, b Acute prima ry co m-

granu- plex. The hazy infilt rate in the right
uppe r lobe. lym phatic stranding .
lls, and
a nd lymphadenitis fo rm a dumb-
Ie Iym- bell-shaped config uratio n.
In the
(Chon
Isis and
mpress
Dnchus,
IDst ex-
everely
ldenitis
)Us dis-
'ad.
ry com-
<trapul-
~ninges,
lination
seeds )
•
er zone
les with • Clinical Features
~ranula
aracter- Primary tuberculosis usually is asymptomatic. Occasion-
s severe ally, low-grade pyrexia with night sweats, coughing, an-
llinated orexia, and erythema nodosum develop. With progres-
is as- sive postprimary tuberculosis, the above clinical manife-
stations are present together with hemoptysis and dysp-
" of he- nea. The tuberculin skin test is positive, and acid -fast
Ke of a bacilli may be detected in the sputum, gastric washings,
e Simon pleural and bronchoalveolar lavage fluid.
Inodular
is due to
,ely low • Radiologic Findings
a where
Chest Radiograph
levelop-
es. Primary tuberculosis is rarely detected on the chest
radiograph. Positive radiographic findings are present in
only about 20 % of children with a positive tuberculin
larger foci may develop (acinonodular form ). Tuber- skin test:
Icterized culomas measuring 1-3 cm in diameter and compris- • The Chon Jocus is a circumscribed, small, peripheral
1e apical ing a caseous core surrounded by a mantle of granu- area of consolidation.
ure of a lation tissue are also found. • Hifar and mediastinal Lymphadenitis presents as hilar
md sub- • Cavitating tuberculosis: Cavitation results from ero- enlargement and mediastinal widening. Occasion-
~xtensive sion of enlarging tubercles into the airway and as- ally, Iymphangitic stranding connecting the primary
sociated liquefaction of caseous materiaL In active focus with the hilar lymphadenitis forms a dumbbell-
I lobular, tuberculosis, the wall of the cavity contains infectious shaped opacity. This represents the primary complex
lithelioid caseous material. Eventually, the cavity becomes fi- (Fig. 3.18).
'[ foci of brosed and may even acquire an epithelial lining. • A segmental opacity may be due to segmental atelec-
• Fibrocirrhotic tuberculosis, in which the tuberculous tasis distal to bronchial compression by enlarged
well-de- process heals by fibrosis, is associated with fibrous lymph nodes (epituberculosis).
ld rich in contraction and distortion of the lung architecture • The calcified healed primary complex is a frequent in-
ze of the leading to cicatricial emphysema and traction cidental finding on chest radiographs and has no
is weak, bronchiectasis. clinical significance (Fig. 3.19).
Hematogenous Dissemination
• Miliary tuberculosis exhibits a finely mottled nodular
pattern resulting from summation of individual
nodule s. The profusion of the mottling increases in an
apicobasaJ direction. Occasionally. in advanced cases,
miliary tuberculosis may produce a coarse granular
or "snowstorm" pattern due to coalescence of the
nodules (Fig. 3.20).
• Exudative tuberculous pleuritis radiographically re-
sem bles other effusions (Fig. 3.21).
Postprimary/secondary pulmonary tuberculosis produces

a spectrum of radiographic manifestations; exudative,
productive, cavitary, and fibrotic changes frequently
occur simultaneously. Because of the predilection for the
ap ical and posterior segments of the upper lobe and the
apical segment of the lower lobe, parenchymal changes
in these regions in the co rrect clinical setting should
arouse suspicion of tuberculosis.
• Exudative/productive tuberculosis manifests as a reas
of confluent consolidation, or more discrete areas of
nodular opacification may be seen. Fine nodular
opacities may indicate bronch iolar involvement and
endobronchial spread (Fig. 3.22).
• Tuberculomas form as pulmonary nodules or masses,
0.5-4 cm in diameter. They have smooth margins and
a predilection for the upper zones (Fig. 3.23). In 80 % Fig. :
of cases, conventional or computed tomography will ture
Fig.3. 19 Calcjfied primary complex, considered a normal in-
cidental finding. show small satellite les ions and calcifications.
• Fig. 3.20 a, b Miliary tuberculosis wit h fine nodular shadowing throug hout both lungs .
b
...
Pulmonary Tubercul osis 77
nodular
Idividual
ses in an
;:-d cases,
granular
e of the
cally re-
Jroduces
<udative,
equently
a
Ifl for the
, and the
changes
5 should
as areas
areas of
nodular
:lent and
~ masses,
~g ins and
). In 80 % Fig.3.21 Tuberculous pleural effusion. Mycobacteria were cul- Fig . 3.22a, b Tuberculosis. Plain radiog ra ph (a) shows bilateral
tured from the lymphocyte-rich pleural aspirate. reticu lonodular shadowing. CT (b) shows featu res of endo-
lphy will
bronchia l spread .
1S.
Fig.3.23 Multiple tubercu lomas.
'nv.
Bl8UOTEcA U.M.F. lAS,
eo.. W--- 56)/?
b
Fig.3. 24 Exudative cavitating

tuberculosis with areas of caseous
pneumonia and liquefaction.
Fig.3. 25 Fibrocirrhotic pulmonary •

tubercu losis. Upper lobe destruction
and fibrosis are associated with
elevatio n of the hila a nd compen-
satory emphysema in the lower
zones.
Co
cr
•
ng Fig . 3.26 Tuberculous pleural thickeni ng

:lseous and fibroci rrh otic pulmonary change.
ulmonary • Tuberculous cavities are 5-10 em in diameter and re- tor of active disease (Fig.3.27 ) as "hea led" cavities
lest ruction sult from caseous necrosis of tuberculous pneumonia may persist after antitube rculous therapy (Webb et
Iwith
'ompen-
with subsequent expectoration of the contents. Cavi- al. 1992).
lower ties frequently are comb ined with di sse minated aci - • Endobronchial spread: Features of endobronchial
nar shadows due to endobronchial spread. Coales- spread are detected by HRCT in up to 98 %of cases (1m
cence of the latter may occur (Fig. 3.24). 1993 ). These include centrilobular nodules or linear
• Radiologic manifestations of fibrotic tuberculosis in- structures, "tree- in- bud" branching linea r structures
clude apical pleural thickening, parenchymal sca r- and poorly defined nodules (Fig. 3.27). Ce ntrilobular
ring. calcification, and fibrotic bands radiating from nodules and tree-in-bud lin ea r structures represent
the hilum to the apex. Cranial migration/e levation of caseating material with in the terminal and respi ra-
hilar structures indicates fibrou s contraction; even- tory bronchi oles (1m 1993 ). Poorly defin ed nodules
tually parac icatricial emphysema. bronchiectasis. and probably represent peribronchiolar inflammation
bronchovascular distortion may ensue (Fig. 3.25). A (1m 1993, Webb et al. 1992 ).
thick pleural peel may e ncase the residual lung and • Miliary tuberculosis: HRCT images show fine nodules
lead to thoracic defo rmity with kyphoscoliosis that are di stributed uniformly throughout the lungs
(Fig. 3.26). (Fig. 3.27). These may be sharply or poorly defined
and range in size from 1 to 4 mm in diameter (O h
1994). These nodules a re distributed randomly
Computed Tomography
throughout the secondary lobule in co ntrast to the
cr manifesta tions of tuberculosi s includ e: centrilobular nodules of endobronchial spread.
• Cavitation: HRCT has been shown to be superior to • Fibrocirrhotic tuberculosis: Findings indi cating chron-
the ches t radiograph in demonstrating cavitation, ic parenchymal change inclu de fibrotic band s, bron-
particularly in cases complicated by fibrosis and ar- chovascular distortion, and cicatricial emp hyse ma
chitectural di stortio n (1 m 1993, Naidich et al. 1984). (Fig. 3.27).
Cavitation is frequently, but not invari ably, an indica-
P
tl
d
Fig. 3.27 a-d (T appearances of tuberculosis. a Features of ac- fluent poorly defi ned nodul es . c CT shows bilateral fine nodular
o
tive postprimary tuberculosis with cavitating lesion in apical seg- shadowing consistent with military TB . d (T shows "healed " cav- t;
ment of left lower lobe and adjacent nodular shadowing in api- ity with fibrosis in left upper lobe but with evidence of reactivated b
coposterior segment of left up per lobe. b Tubercu losis with fea- disease with cavitation and features of endo bronchia l spread in G
tures of endob ronchial spread including ce ntrilobular nodules . right upper lobe. al
branching linear structures (tree-in-bud appea rance). and con-
•
A
Fungal Diseases of the lung S(
di
10
la
Fungal disease of the lung may be classified as endemic The clinical symptoms and radiographi c findings of
m
or opportunistic. these diseases usually resemble those of bacterial pneu-
m
Endemic fungal diseases are caused by pat hogeni c monia. Thin section/high reso lution cr, in some cases,
sc
fungi in an immunocompete nt individual. They include may be helpful in sugges ting the diagnosis. Definitive di -
agnosis, however, is depe ndent on ide ntifi catio n of the
g<
histoplasmosis, coccidioidomycosis, blastomycosis, and
su
sporotrichosis. These infections are endemic in the U.S., fungus at microscopy.
Africa, and Asia and are seen sporadically in Europe as a p'
(P
result of foreign trave l.
all
Opportunistic fungal infection (aspergillosis, candidia-
sis ) is caused by sapro phytic fungi , which usually are
Candidiasis
present in the oral mucosa and become pathoge nic in
the immunocompromised host. These pneu momycoses
• Clinical Features A
have been encountered more freque ntly since the ad-
vent of an tibiotics and chemotherapy. However, the
overall incidence of pulmonary fungal infections re-
Candida albicans is part of the normal human microbial As
mains low.
flora of the oral cavity. Pulmonary cand idiasis occu rs tOI
only in the immunocompromised individ ual. Tn
Fungal Diseases olthe Lung 81
Fig.3.28 Candida pneumonia in a

leukemic patient on chemotherapy.
who presented with oral candidiasis .
The right upper lobe continued to
show patchy consolidation for sev-
eral weeks. and two smaller cavitat·
ing foci developed on the left side.
Pulmonary candidiasis should be suspected in the

presence of a pneumonia that is refractory to standard
therapy or in the immun ocompromised host with florid
d
oral or esophageal candidiasis. The diagnosis may be es-
ne nodular
ealed" cav-
tablished by demonstration of candida in transbronchial
reactivated biopsy specimens. Sputum analysis is of no value be-
II spread in cause of the ubiquitous nature of the organism (Geary et
al. 1980).
A wide spectrum of radiographic findings has been de-

scribed in candida pneumonia. Appearances may be in-
distinguishable from that of bacterial pneumonia with
lobar or segmental consolidation (Fig. 3.28). Diffuse bi- Fig.3.29 Pulmonary candidiasis may present as lobar pneu·
lateral alveolar or mixed alveolar-interstitial shadowing monia, interstitial pneumonia, or bronchopneumonia with cavi-
indings of may be seen (Buff et al. 1982; Fig. 3.29). Candida pneu- tation.
~rial pneu-
monia may present as multiple small pulmonary ab-
lme cases, scesses; these may be randomly distributed if hemato- cavity. The following are recognized manifestations of
finitive di- genous spread has occurred or peri bronchiolar when re- aspergillosis.
lion of the sulting from aspiration (M UlIer 1990). A miliary-nodular Primary invasive aspergillosis develops when mas-
pattern has been described in pulmonary candidiasis sive amounts of fungal spores are inhaled, usually from
(Pagani 1981). and diffuse pulmonary hemorrhage is cereal dust. The hosts have normal immunity.
also recognized as a manifestation (MUlIer 1991). Secondary angioinvasive aspergillosis occurs as an
opportunistic infection in patients with severe debilitat-
ing illness, particularly leukemia and lymphoma, or in
those undergoing prolonged therapy. Pathologically, this
Aspergillosis disease is characterized by mycotic vascular invasion,
thrombosis, and hemorrhagic infarction with sub-
1 microbial Aspergillus jumigatus, A. jlavus, and A. niger are ubiqui- sequent necrosis and cavitation. Invasive aspergi llosis is
asis occurs tous and flourish in substances such as cereal grains. associated with a mortality of 60 to 70%, and, in sur-
They also constitute part of the ftora of the healthy oral vivors, there is a 50% recurrence rate.
82 3 Infeclion and Innammatory Disorders
The initial chest radiograph may be normal. Multiple

foci of consolidation may be present; these are
frequently rounded in shape and probably represe nt in-
farcted parenchyma (Hruban et al. 1987 ). The charac-
teristic "air crescent" sign develops late in the course of
the disease and usually is associated with a recovering
neutrophil count. It is seen in approximately 40 % of
cases and is associated with improved survival rates.
Computed tomography shows characteristic findings
that strongly suggest the diagnosis early in the course of
the disease (Kuhlman et al. 1988 and 1987 ). In ea rly inva-
sive aspergillosis, a "halo" of ground-glass opacification
surrounds dense parenchymal foci (Fig. 3.30, Fig. 3.31). a
This represents a rim of hemorrhage or coagulation
necrosis su rrounding an area of infarction (H ruban et al.
Fig.3.30 Angiocentric invasive aspergillosis, confirmed at au-
1987). The halo sign precedes the air crescent sign
topsy.
(Fig.3.32 ) by up to 2 weeks (Kuhlman et al. 1987).
Magnetic resonance imaging may also be helpful in
early diagnosis of invasive aspergillosis (Herold 1989).
On standard Tl-weighted spin echo sequences, rounded
consolidations have a target appearance with a hypoint-
Fig.3
ense center and hype rintense rim: the rim enhances on bronc
administration of intravenous gadolinium. (oid i
Invasive aspergillosis of the airways: Aspergillosis
centered on the airways accounts for 14-34 % of cases
(Orr 1978, Young 1970 ) and also occurs in immunocom-
promised patients. Diagnosis is based on the presence of
organisms deep to the basement membrane. cr findings
include lobar consolidation, bilateral peribronchial con-
solidation, ground-glass attenuation, and centrilobular
nodules less than 5 mm in diameter (Logan 1994).
Fig. 3.31 Angiocentric invasive aspergillosis-early-stage dis- Allergic bronchopulmonary aspergillosis (ABPA ) rep-
ease with multiple areas of nodular consolidation som e of which resents a hypersensitivity reaction, usually in asthmat-
have a rim of ground-glass opacification highly suggestive of in- ics, and manifestations include asthma, blood
vasive fungal infection. eosinophilia, precipitating antibodies to Aspergillus and
elevated IgE titers. Pathologically, myce lial plugs
develop in the proximal airways (Gefter et al. 1981 ), but,
in contrast to invasive aspergillosis of the airways, tissue
invasion is minimal or absent (Glimp and Bayer 1981 ).
The chest radiograph shows transient infiltrates in a
lobar, segmental, or subsegmental distribution which
predominantly involve the upper lobes. Atelectasis is Fig. 3.~
cupyin
less common, occurring in 3-46 % of cases (Gefter et al.
1981, Malo et al. 1977 ). Bronchoceles also are a
frequent radiographic manifestation of ABPA; these
vary in shape but classically prese nt a "gloved-finger"
appearance. The lung distal to the bronchocele is threat
aerated by collateral air drift. Eventually, central 1973"
bronchiectasis involving the inner two-thirds of the Th.
bronchial tree and showing an upper lobe predomi- opacit
nance may develop (Fig. 3.33 a, b). cresce
Fig.3. 32 Angiocentric invasive aspergillosis- recovery phase. Aspergilloma is the most co mmon form of aspergillo- mycetl
Bilateral multifocal rounded consolidation with Mair crescents~
sis.lt occurs in hosts with normal immunity, and the fun- pleura
visible on the right side.
gus colonizes preexisting cavities (cysts, tuberculous indica
cavities, cystic bronchiectasis) and forms a fungus ball. 1974).
This may erode the cavity wall both mechanically and a
through enzymatic action and lead to hemoptysis: this tenuat
occurs in 50-80% of cases and may occasionally be life cavity
Fungal Diseases of the lung 83
~ultiple
~se are
'sent in-
charac-
)urse of
:overing
40 % of
rates.
findings
Gurse of
fly inva-
ification
'ig. 3.31). a
gulation
Jan et al.
ent sign
m
elpful in
Id 1989).
rounded
hypoint- Fig. 3. 33 a, b Allergic bronchopulmonary aspergillosis. Varicose
ances on bronchiectasis is seen in both upper lobes (a) with extensive mu-
coid impaction in the apical segment of the right lower lobe (b). b
ergillosis
of cases
unOCOffi-
esence of
f findings
:hial (00-
trilobular
94).
BPA) rep-
asthmat-
l. blood
gil/us and
ial plugs
981). but.
:1YS, tissue
er 1981).
:rates in a
on which
Fig.3.34 Conventional tomogram shows an aspergilloma oc- Fig.3.35 CT of aspergilloma in an emphyse matous bulla. The
lectasis is
cupying an old tuberculous cavity. wall of the cavity is thickened due to recurrent episodes of inflam-
efter et al. mation. The aspergilloma is partially ca lcified.
so are a
PA; these
'ed-finger"
:hocele is threatening (Faulkner et al. 1978. Freundlich and Israel ma ss may be demonstrated by image acquisition in the
y. central 1973.Jewkes et al. 1983 ). prone position. The mycetoma has a characteristic
'ds of the The chest radiograph shows a round. homoge neous sponge-like appearance and contains multiple foci of air
predomi- opacity which is mobile wi thin the cavi ty. A circular or (Armstrong et al. 1995. Roberts et al. 1987 ).
crescent-shaped air space may be vis ible between the ABPA may be diagnosed by microscopic detection of
aspergillo- mycetoma and the cavity wa ll (Fig. 3.34). l ocalized Aspergillus mycelia in the bronchial aspirate. Aspergil-
nd the fun - pleural thickening may be see n adjacent to the cavity. lorna may be largely a rad iologic diagnosis. Both trans-
uberculous indica ting superimpose d aspergillus infection (Libshitz bronchial and open lung bi opsy may be haza rdous in the
ungus ball. 1974). immunocompromised with bone marrow suppression.
nically and cr will show the myceto ma of inhomogeneous at- Sputum analysis has no va lue because the sputum con-
ptysis; this tenuation and the surrounding crescent of air within the tain s nonpathogenic fungi.
.ally be life cav ity (Figs. 3.35. 3.36). The mobility of the intracavitary
Histoplasmosis
Histoplasmosis is a fungal infection that occurs mainly

in North America. Except for an endemic region in
northern Italy, it occurs only sporadically in Europe. Pul-
monary changes caused by Histoplasma capsula tum are
comparable to tuberculosis in both primary and postpri-
mary phases of deve lopment.
Acute histoplasmosis develops as a result of airborne
primary in fection. An incubation period of 2 weeks
precedes the onset of pyrexia. malaise, dys pnea, produc-
tive cough, and hemoptysis; this infection may also ru n
an asymptomatic co urse.
• The chest radiograph s hows multiple, ill-defined

areas of consolidation throughout both lungs. There
is accompanying hil ar and mediastinal lymphade-
nopathy (Fig. 3.37). These pneumonic conso lidations
heal. leaving residual pulmonary gran ul omata that
undergo central calcification to produce a target pat-
tern (Co nnell and Muhm 1976; Fig. 3.38). When
granulomata are multiple, calcification occurs in up
to 75 %of cases, but only 25 %of sol itary granulo mata
w ill calcify.
• Chronic progressive histoplasmosis is the consequence Ch,
of reactivation and has a poor prognosis. Progressive va n
cavitation with fibrosis may progress to comp lete
lung destruction.
Fig. 3. 36a. b Aspergilioma.
Ac
Coccidioidomycosis
•
• Clinical Features Acti
fun!
Coccidioidomycosis is endemic in the southwestern hun
United States. It usually is asymptomatic and only the ies.
coccidioidin skin test is positive with elevated comp le- the
ment fi xati on. In those w ho become symptomatic, lunf
manifestati ons include severe pneumonia, pulmonary tatil
cavitation, pleurisy, and pericarditis. The development vas i
of pulmonary fibrosis represents end-stage disease
(Bayer 1981, McGa han et al. 1981 ).
•
Acute: Chronic: • Radiologic Findings The
- Exudative infiltrate - Hilar calcification nant
- Histoplasmoma - Target calcification The chest radiograph shows pneumonic consolidation solid
-lymphadenitis of histoplasmoma and pulmonary nodules (coccidioidomas ) that occa- esoR
- Fibrosis
sionally cav itate. In disseminated coccidioidomycosis, enm
Fig.3. 37 Histoplasmosis. there is a generalized micronodular pattern (Fig. 3.39). tissu
Fungal Diseases of the Lung 85
Fig.3. 38 Histoplasmosis . Dissemi-

nated. calcified granulomas were
found in a North America n male
who had a history of histoplasmosis
20 years earlier.
·s mainly
·egion in
-ope. Pul-
!atum are
j postpri-
.- airborne
. 2 weeks
3., produc-
y also run
iII-defined
ngs. There
.ymphade-
50lidations
)mata that
target pat-
lS). When
:curs in up
·anulomata
)nsequence Changes of pulmonary fibros is a re associated w ith ad-

Progressive vanced disease.
a complete
Actinomycosis
Actinomyces israelii is intermediate between mycelial

fung i and bacteria and is a co mmon sapro phyte in th e
Duthwestern human mouth, especially in the presence of dental car-
md only the ies. This is a relatively rare di sease entity and involves
Ited comple- the cervicofacial region, the intestinal tract, and the
ymptomatic, lung. In the thorax, manifestations include chronic cav i- Fig.3.39 Coccidioidomycosis: coccidioidomas. cavitation. bron-
tating pneumonia, pleural empyema, and chest wa ll in- chopneumonia. pleural involvement. and wid espread micro-
., pulmonary granu lomas. Pulmonary fibrosis is present in end-stage disease.
:levelopment vasion (Fig. 3.40).
tage di sease
• Radiologic Findings Nocardiosis

The chest radiograph shows nonsegmental, predomi -
nantly peripheral consolidation that may cavitate. Con- Nocardia asteroides is a ubiquitous aerobic saprophyte
solidation typically crosses interlobar fi ssures. Pleuro- found in the soil. It is a weakly acid-fast bacil lus, w hich,
consolidation
esophageal and pleuropulmonary fi stul ae , pleural after inha lation, may infect the lung sporadically.
s) that occa-
lioidomycosis, empyema, rib osteomyelitis, and innammatory soft Pulmonary nocardiosis may be similar to actinomycosis
,rn (Fig. 3.39). tissue masses of the chest wa ll may deve lop. in its radiographic appearance. Single or multiple
•
Ir
ti
CI
T
(I
•
Fig.3.40 Actinomycosis: consolidation with abscess formation, Fig. 3.41 Cryptococcosis: tumor-like masses with liquefaction, Ir
pleural empyema, osteo myelitis. chest wall abscess. subpleural granulomas, and bronchopneumonia. Ie
p
st
parenchymal abscesses frequently are seen, and pleural in immunocompromised hosts. The chest radiograph P
involvement is also common. There is an increased inci- shows small, subpleural granulomas, foci of bronchop- VI
dence of nocardiosis in the immunocompromised. in neumonia, and round masses (torulomas ). which may c(
AIDS. and in alveolar proteinosis. cavitate (Fig. 3.41 ). p'
Other mycoses like North and So uth American blasto- al
mycosis, sporotrichosis, and mucormycosis are ex-
tremely rare and present radiologically as nonspecific
Cryptococcosis (Torulosis) pneumonic infiltrates. Diagnosis is based on demon stra-
tion of the fungu s in ti ssue, smear, or culture.
•
Cryptococcosis results from inhalation; the spo res of R,
Cryptococcus neoformans are found in dust and excreta 01
(e. g., pigeon droppings) and cause pulmonary infection hi
Fr
Parasitic Infections P
(I
C
Parasitic infections are most prevalent in Asia, Africa, Amebiasis
Sout h America, and the Mediterranean basin. The causa-
tive organisms are protozoa (ameba, toxoplasma, ) and
helminths (echinococcus, schistosomes, ascarids, etc. ). • Clinical Features
•
Pr
They induce hyperse nsitivity reactions in the lungs w ith d,
formation of an eosinophilic "Loefner" infiltrate. Para- Amebae are found worldwide but are endemic in the
Mediterranean region. They are ingested in conta mi -
P'
sites may colonize the lungs and form cysts, granu lo- cr
mata, and abscesses. Radiographic abnormalities to- nated food and initially induce colitis (amebic dy- th
gether with blood eos inophilia should raise the suspi- sentery). They reach the liver via the bloodstream and 6C
cion of a parasitic pulmonary infection. Diagnosis is conform hepatic abscesses. which may extend through the th
firmed by identification of parasites in the sputum, stool. diaphragm to infect the lung. Direct hematogenous AI
and urine, and if necessary by biopsy and histological spread from the liver to the lung is rare. Clinical manife- Sa
assessment. stations include cough. blood eosinophilia, and expec- to
toration of bile when a hepatobron chial fistula is present m
(Meng 1994). to
co
it
an
Parasitic Infections 87
In 95 %of cases, the chest radiograph shows opacifica-

tion of the right lower hemithorax due to pneumonic
consolidation and an accompanying pleural effusion.
The initially ill-defined infiltrate may form an abscess
(Fig. 3.42).
Toxoplasmosis
• Clinical Features /
.- -."
I Usually due to spread of liver
uefaction, Infestation with Toxoplasma gondii is common but rarely abscess through the diaphragm
leads to disease. Congenital toxoplasmosis due to trans- \.- -"
placental infection is the most im portant form and pre-

sents with encephalitis and chorioretinitis. Adult toxo- Fig.3 .42 Amebia sis (amebic abscess): pleural effu sion. basal
pneumonia with cavitation.
diograph plasmosis is relatively uncommon except in patients
:onchop- with AIDS, in whom it is the most common cause of focal
lich may central nervous system lesions. In the HIV-negative
population, it manifests as lymphaden itis and occasion-
ill bias to- ally as interstitial pneumonia.
are ex-
nspecific
monstra- • Radiologic Findings
Radiographs show focal reticular, linear, and ill-defined

opacities resembling acute viral pneumonia. Associated
hilar lymph node enlargement is frequent (M Uller and
Fraser 2001; Fig. 3.43).
Pneumocystis Jiroveci Pneumonia

(Previously Known as Pneumocystis
Fig.3.43 Toxoplasmosis: interstitial pneumonia, hilar lymph-
Carinii Pneumonia-PCP) adenopathy.
Pneumocystis jiroveci/carinii pneumonia was originally alveolar-capillary membrane, and filling of the alveoli
described in premature infants. In adults, it is a frequent with eosinophilic exudate occurs. Concomitant activa-
lie in the pathogen in the immunocompromised. The marked in- tion of macrophages and plasma cells in the interstitium
contami- crease in the incidence of PCP has largely resulted from results in an interst itial pneumonitis (Ku hlman 1996).
lebic dy- the acquired immunodeficiency syndrome ep idemic; In HIV-positive patients. the preferred method of di-
ream and 60-70 % of patients with AIDS will develop PCP. and in agnosis is induced sputum samples proceeding to bron-
rough the the 1990s. it was the most frequent index disease for choalveolar lavage when necessary. Transbronchial bi-
1togenous AIDS in industrialized countries (40 %) (Kuhlman 1996. opsy is avoided because of the associated high mortality
11 manife- Safrin 1993. Naidich and McGuinness 1991 ).It continues and risk of pneumothorax in these patients. In patients
ld expec- to be a significant cause of morbidity in HIV/AIDS and without AIDS. transbronchial or open lung biopsy is ap-
is present more recent studies have indicated that it is second only propriate (Geary et al. 1980. Kuhlman 1996).
to bacterial pneumonia in the etiology of pulmonary
complications (Ben ito Hernandez et al. 2005 ).
Initial growth of pneumocystis is in the alveoli where
it becomes attached to Type 1 pneumocytes. Damage
and death of these cells destroys the integrity of the
• Radiologic Findings proportion of cases, thickened interlobular septa are

found in association with ground-glass opacification
(Bergin et al. 1990). Progression to diffuse homogeneous
Chest Radiograph groun d-glass opacification with spa ring of the sub-
The initial chest radiograph may be normal , but in 80% pleural lung may occur (Ku hlman 1990, Scott 1991 ).
of cases it shows diffuse, bilateral, granular, or reticular Recent years have seen a cha nge in the pulmonary
infiltrates (Ku hlman 1996, Safrin 1993, Naidich et al. manifestations of pneumocystis infection. Cystic lung
1991, Goodman 1991, Delorenzo et al. 1987). These may disease. spontaneous pneumothorax, and an upper lobe
involve the perihi lar and lower zo nes or have an upper distribution of opacification are now seen more
lobe distribution. Progress ion to diffu se air space con- frequently (Figs. 3.45, 3 .46). In the past, these were usu-
solidation may occur. Hilar lymph node enlargement ally associated with aerosolized pentamidine prophy-
and pleural effusions are unusual. laxis but this ha s now been largely replaced by more ef-
fective chemoprophylaxis (Boiselle et al. 1999 ).
Computed Tomography
Fig .
In acute PCP, the commonest HRCT finding is bilateral Schistosomiasis zor
grou nd-glass opacification. Less commonly, a mosaic ad\
pattern with scattered foci of parenchymal involvement
interspersed with normal lung is found (Fig. 3.44). In a • Clinical Features
Schistosomiasis hematobium is endemic in North Africa,

Schistosoma mansoni in South America and the Carib-
bean, and Schistosomajaponicum in Japan. Cercariae, the
infective larvae, penetrate the skin, en ter the cap illaries,
and migrate through the systemic venous syste m to the
right heart. From there they enter the pulmonary circu-
lation and subsequently the system ic arterial system to
reach the live r, kidneys, and urinary bladder. Diagnosis is
based on identification of Schistosoma eggs in the stoo l
and urine .
Fig.3.44 Pneumocystis pneumonia. Ground-glass opacification The chest radiograp h shows transient pulmonary infil-
involving both upper lobes. Some inhomogeneity is seen anteri- trates representing an eosinophilic Loeffler-type pneu-
orly with sparing of scattered secondary pulmonary lobules. monia which is associated with passage of the larvae a
thl
asi
inc
pu
(
Ec
•
Hy
an,
TO(
hal
Fig . 3.45a,b Pneumocystis infection in a renal transplant Spl
patient. Extensive ground-glass opacification/consolidation, invol
a terstitial t hickening, and some cystic change are seen. flu
Parasitic Infections 89
Ita are
icati on
~neous
e sub-
l1).
nonary
clung
er lobe
more
re usu-
,rophy-
lOre ef-
Acute: Chronic:
eosi nophilic pulmonary
infiltrate hypertension
Fi g.3.46 Cystic lung disease in AIDS. CT through the upper Fig.3.47 Schistosomiasis.
zones shows extensive bilatera l Kcystic" change in a patient with
advanced AIDS.
I Africa,
• Carib-
'iae, the
.ilI aries.
o to the
y circu-
stem to
~ no s i s is
he stool
.ry iofil-
e pn eu-
e larvae • b
through the pulmonary capillaries. Occasionally the par-

asites lodge in the precapillary pulmonary arterioles and
incite an obstructive endarteriti s leading eve ntually to
pulmonary hypertension and chron ic cor pulmonale
(Waldman 2001; Fig. 3.47).
c d
Fig. 3.48 a-d Hydati d cysts in the left lower lobe and right liver
of a 15-year-old Turkish male.
Echinococciasis
• Clinical Features the liver aod lung. These are surrounded by a fibrotic
capsule contributed by the host tissue (pericyst).
b Hydatid disease is ende mi c in the Mediterranea n bas in
and Africa. Humans ingest the ova of the dog tapewo rm
Taenia echinococcus in co ntaminated food. The larvae • Radiologic Findings
hatch in the intestine w ith subsequ ent hematogenous
transplant spread to the live r. Pulmonary, ce rebral , and bone in- The chest radi ograph shows a so litary. smooth, round.
:lation. involvement occur in about 10 % of cases. Larvae form homogeneous ma ss ranging from 1 to 10 em in diameter
fluid-conta ining hyda tid cysts (e ndocyst and ectocyst) in (Fig. 3.48. 3.49). Multipl e pulmonary hydatid cysts are
Fig. 3.49a, b Hydatid cyst. Note • R,

the pericyst and the collapsed en-
docyst with subtle evidence of the
~water liIy~ sign . Radio:
to eo~
asth lT
sensit
Di.
stool 1
Stro
Ank
a b • CI
Stron,
occur
Eu rop
Paragonimiasis lungs
is ass(
in atol
• Cli n ica I Featu res itated
Infection with lung flukes of the genus Paragonimus is

widespread in Southea st Asia an d Central and South
•
America. The metacercariae are ingested in seafood, San
penetrate the bowel wa ll , reach the peritoneal cavity,
and pass through the diaphragm and pleura to enter the
lungs. The para sites live in the lungs for many yea rs, and
•
Round mass the presence of eggs in the sputum may provide a diag-
Sarcoi
nosis .
tosis. 1
nodes
Meniscus sign: Water lily sign: skin. e
air between th e ruptured hydatid • Radiologic Findings may b
lung capsule and membrane floating abnon
hydatid membrane within lung capsule. The che st radiograph shows Loem er-ty pe eosinophilic
cu lin s:
infil trates occasionally associated with pleural effusions.
levels.
Fig.3.50 Echinococciasis. Later. predomi nantly basal nodules and cysts are see n.
freque
Calcifi cation may occur in late cases.
airbor
Th,
rare. Occasionally a thin crescent of air is visible be- per 10
tween the ectocyst and pericyst (me niscus sign); this is Ascariasis co id os
an indication of ea rly rupture. later, follo w ing cys t rup- ingov,
ture, the chitin mem brane of the e ndocyst may co llapse deveic
and float on the resid ual fluid (water lily sign; Fig. 3.50 ). • Clinical Features Th,
Diagnosis is based o n occasional de monstration of node I
echinococcal sco li ces in the sputum and on serology or The roundworm Ascaris lumbricoides hominis occurs paren<
skin tests. throughout th e world in areas inhab ited by humans. The Diagnl
eggs are ingested with food. The larvae hatch in the lym ph
small in testine and reach the lung ca pillaries via the
lymphatics and bloodstream. where they penetrate the
alveo lar septa and are transported with bronchial secre- • Pa
ti ons to the pharynx. Subsequently they are swa ll owed
and reenter the intestine, where they mature into adu lt Granu
worms. This remarkab le migration of Ascaris lasts ap- lymph
proximately 2 weeks. se ptal.
1St.Note • Radiologic Findings
Ipsed en-
Ke of the
Radiographs show regional, confluent infiltrates similar
to eosinophilic Loeffler pneumonia. In atopic patients,
asthma may be precipitated and results from a hyper-
sensitivity reaction to the larvae (Fig. 3.51 ).
Diagnosis is based on identification of Ascaris in the
stool togethe r with a blood eosinophi lia.
Strongyloidiasis and
Ankylostomiasis
Fig. 3. 51 Asca riasis, strongyloidiasis, ankylostomatiasis: tran-
• Clinical Features sient eosinophilic infiltrates.
Strongyloides stercoralis and Ankylostoma duodenale

occur in warm, wet regions and inhabit warm mines in
Europe. The larvae penetrate the skin, pass through the
lungs and ente r the intestine. Passage through the lung severe than in ascariasis, but a massive Strongyloides in-
is associated with transient eosinophilic infiltrates, and, festation may be fatal. Miner's strongyloidiasis is an oc-
in atop ic individuals, asthmatic episodes may be precip- cupational disease. Diagnosis is made by identification
itated (Fig. 3.51 ), Clinical manifestations are usua lly less of the wo rm s in stool sa mpl es.
animus is
nd South
. seafood, Sarcoidosis
~al cavity,
enter the
years, and
de a diag- Sarcoidosis is a generali zed epitheli oid cell granu loma- these lesions are characterized by epithelioid cells, lan-
tosis. It frequently involves both the in trathoracic lymph ghans' giant cells, ca lcifying Schaumann bodies, and
nodes and the pulmonary parenchyma. The live r, spleen, "asteroid bodies." In contrast to tuberculosis, sarcoid
skin, eyes, bones, salivary glands, and other organs also granulomata do not caseate. However, they are indistin-
may be affected. Most patients have so me immunologic gu ishable from other nonspeCific granulomata such as
abnormalities: a positive Kveim test, a negative tuber- those occurring in fungal infections, berylliosis, and bru-
,sinophilic cu li n skin reaction, and e levated serum imm unoglobulin cellosis. These granu lomatous foci may heal or may pro-
effusions. levels. The etiology of sarcoidosis is unknown, but the gress to pulmonary fibrosis. The latter, in severe cases, is
i are see n.
frequency of pulmonary invo lvement may indicate an associated with restrictive ve ntilatory impairment and
airborne agent (M urray 2000). eventual cor pulmonale.
The incidence of sarcoidosis in Germany is 8-10 cases
per 100000 per yea r (Doerr 1983 ), In most cases, sa r-
coidosis ru ns a self-limiting course, sometimes extend- • Clinical Features
ing ove r several yea rs. However, pulmonary fibrosis wi ll
deve lop in 10 %-20 %of cases (Scadding 1970), Clinical presentation is variable. Ocula r symptoms such
The typical radiologic findings of bilateral hilar lymph as iridocyclitis or Heerfordt sy ndrome (uveoparotid
node enlarge ment (BHL) with or without pulmonary fever) may predom inate. Cervical, axillary, and
nis occurs parenchymal involvement may suggest the diagnosis. epitrochlear lymph node enlargeme nt and cutaneous le-
Imans. The Diagnosis may be established from transbronchial or sions (lu pus pernio) also occur. Lofgren syndro me, an
tch in the lymph node biopsy, acute form of sarcoidosis, is see n mainly in Scandinavia
.es via the and presents with fever, arthra lgia, and erythema nodo-
letrate the sum. It is found almost exclusively in females.
:hial secre- • Pathology Up to 50 % of cases are asymptomatic and are de-
swallowed tected incidentally on routine chest radiographs. Pulmo-
~ into adult Granulomata 1-2 mm in diameter are found in involved nary symptoms include dyspnea and dry cough. Restric-
is lasts ap- lymph nodes and along the peribronchovascular, para- tive ventilatory impairme nt may be evident on pulmo-
se ptal. and subpleural lymph vessels. Histologically, nary function tests.
The tuberculin skin test is negative. Seru m immuno- • Mediastinal lymph node enlargement. Mediastinal
globulin leve ls may be elevated and there is increased lymph node enlargement may lead to widening and
activity of angioten sin I converting enzyme (ACE). which lateral scalloping of the mediastinum, usually more
is released by activated macrophages. Bronchoalveolar pronounced on the right side. Subca rinal lymph node
lavage demonstrates an increase in activated T lympho- enlargement may cause splaying of the tracheal
cytes. Seventy-five percent of patients have a positive carina. In most cases of stage I sarcoidosis, pulmonary
Kve im test. i. e., a sarcoid nodule forms at the site of the granul omata are detecta ble histologically, but
subcutaneous inj ection of a saline suspension of sarcoid parenchymal change may not be evident radiologi-
granulomata. cally (M urray 2000). Stage I disease usually reso lves
spontaneously over a va ri able time period (3-24
months), but it may persist for many years or pro-
• Radiologic Findings gress to stage II disease.
Stage II (Miliary Stage)

Chest Radiograph
Whil e the stage I ade nopathies gradua lly regress, pul-
Three stages of the disease are desc ribed (Fig. 3.52): monary granulomas enlarge. Howeve r. lung involve-
ment is twice as frequent with simultaneous lymph
Stage I (Intrathoracic Adenopathy) node enlargement as in isolati on. Pulmonary parenchy-
• Bilateral hilar lymph node enlargement: The hilar mal disease is most pronounced in the mid zone and in
lymph nodes show bilateral sy mmetrical enlarge- the perihil ar regions. An interstitial pattern with reti-
ment. En larged hilar shadows are we ll-defi ned with eul onodular shadowing predominates (Figs. 3.54, 3.55).
scalloped lateral borders (Fig. 3.53 ). A thin stripe of Less co mmonly, acinar shadows up to 7 mm in diameter,
lung tissue is often visible between the hilar and me- segmental infiltrates, round masses, or atelectasis distal
diastinal contours; this is in contrast to lymphoma to obstruction by endobronchial granulomatous lesions
and bronchial carcinoma, which extend fro m the are seen. Today the diagnosis is usually es tablished by
hilum to the mediastinum without interru ption. analysis ofbronchoalveolar lavage fluid and by histologi-
• Unilateral hilar lym ph node enlargement and calcified cal confirmation from transbronchial biopsy.
lymph nodes are fou nd infrequently in sarcoidosis.
acco unting for less than 5 %of cases (Armstrong et a/.
1995).
Fig,3, 52 Sarcoidosis .
- . ",'
, '- ' ,
:~~F;}
.. '. :-'~- .
,.
. . . ....
"
Stage I Stage II
Bilateral hilar and Disseminated pulmonary
mediastinal lymph node granulomata, miliary
en largement or reticular pattern
a
Fig. 3
",
, ;,'
I
\ , '"\.
" "
, '
Stage III
/
,
I
'
" Fibrosis, cicatricial emphysema,
cor pulmonale, occasional cavitation
Sarcoidos is 93
diastinal Fig.3.53 Stage I sa rcoidosis with

fling and bilateral hilar lymph node enlarge-
ment. Clinical examination identified
Illy more
erythema nodosum.
1ph node
tracheal
IImonary
,Ily, but
'adiologi-
r resolves
)d (3-24
s or pro-
ress, pul-
involve-
us lymph
~arenchy
ne and in
with reti-
.54, 3.55 ).
diameter,
:asis distal
us lesions
)lished by
histo logi-
• Fig . 3.S4 a, b Stage 1/11 sarcoidosis: mediastinal and hilar lymph node enlargement with a reticulonodular pattern in the perihilar lung.
b
Stage III (Pulmonary Fibrosis)

Stage II di sease may progress to pulmonary fibrosis,
frequently without a discrete tra nsition between stages.
Linear opacities rad iate from the hila into the lung. Thi s
is accompanied by coarse reticular markings and a •
honeycomb pattern. These changes are most marked in
the mid and upper zones (Fig. 3.56). End-stage disease is
associated with paracicatriciai em physema, traction
bronchiectasi s, and eventual pulmonary hypertension
with cor pulmonale (Schermuly 1977).
Computed Tomography •
The characteristic fi ndings of bilateral hilar and paratra-
chea l lymp h node enl argement with or without pulmo-
nary change are seen in 60-70% of cases (We bb et al.
1992, Hille rdal et al. 1984, Scadding 1985).
Pulmonary parenchyma l features of sa rcoido sis in-
clude:
• Small well-defined nodules, 2-10 mm in diameter,
which are found in timately related to the para hilar
bron chi and vessels in the lobular core, w ithin the in-
terlobular septa, adjacent to the fissures and in the
subpl eural lung (Webb et al. 1992 ; Fig. 3.55). Patho-
logically, these nod ules represent coalescent granu-
lomata (Lynch 1989).
• Irregular or nodular thickening of bronchovascular
bundles and interlobular septa (Webb et al. 1992,
Dawson 1990).
Fig.3.S5 Sarcoidosis. Multiple nodules in a peribronchovascu- • Areas of ground-glass opacification may represent
lar distribution. Precarinal lymph node enlargement is also pre- active alveo litis (Lynch 1989) or wides pread in te rsti -
sent.
b
Fig. 3. 56 a, b Stage II/III sarcoidosis: Reticular shadowing and a honeycomb pattern.
Sarcoidosis 95
t ial granu lomata below the resolu tio n of HRCT. The

fibrosis, former is favored by reso lution of ground-glass
n stages. change following steroid therapy (Lynch 1989. Webb
L1ng. Thi s et al. 1992).
:s and a • Appea rances suggesting alveolar sarcoidosis occur in
larked in 4 to 27 % of cases (Wilson 1995 ). The typica l appear-
iisease is ance is of bilateral. poo rly defined opacities. periph-
traction era l in di stribution (Berkmen 1985. Rubinowitz et al.
~rtensio n 1974. Shigematsu et al. 1978: Fig. 3.57 ). Lesio ns may
also have a fine nodular pattern creating the appear-
ance of acinar rosettes (Ziskind 1963).
• Patchy air trapping at the level of the secondary
lobule in keepi ng w ith small-a irway di sease has been
I paratra- described (Gleeson et al. 1996). Images acq uired in
It pul mo- in sp iration show the affected parenchyma to be of
,bb et al. decreased attenuation relative to normal lung; this
resul ts in a mosaic pattern. Changes due to air trap-
,dosis in- ping are acce ntuated in expiration. Fig. 3.57 HRCT: Sarcoidosis. CT shows foci of alveolar opacifica-
• Developing fibrosis is associated with the appearance tion in a predominantly peripheral distribution (starburst pattern).
diameter, of irregular reti cular opac it ies, includ ing irregular

parahilar septal thickening. and these frequent ly are see n along
lin the in- the perihilar bronchovascular bundles (Webb et al. • Usual interstitial pneu monia
nd in the 1992). Ce ntral conglomerations along perih il ar ves- • Desquamative interstitia l pneumonia- respiratory
5). Patho- sels and bronchi and traction bronchi ectasis develop bronchiolitis in te rstitial lung di sease (DIP-RBILD )
nt granu- w ith progression. Changes tend to be most marked in • Acute interstitial pneum onia (AlP)
the upper lobes and central perihilar lung. • Nonspecifi c interstitial pneumonia (NS IP)
avascular
al. 1992. Radionuclide Imaging Usual Interstitial Pneumonia
represent In active disease, intense gallium uptake is frequently UIP is a di sease of middle-age d adu lts. Onset may be
d intersti- observed in the enlarged hilar and media stinal lym ph grad ual with dry cough and progressive dyspnea. Prog-
nodes. nosis is poor w ith reported mean survivals of 2.8-6 years
(Bjoraker et al. 1998. Ca rringto n et al. 1978).
UIP is characterized h isto logically by a variegated
pattern w ith foci of normal lung, interstitial ce llular in-
Idiopathic Interstitial Pneumonias
filtrates. and zones of active fibrosis.
The chest radiograph shows a reticular pattern pre-
The idiopathic interstitial pneumonias are a hetero- dominantly in a periphera l and subpleural distribution.
geneous group of lung di seases characterized by differ- HRCT shows a su bpl eura l and predominantly basal
ing degrees of interstitial and alveolar innammation and di stribution of intralobu lar se ptal thickening and honey-
fibrosi s. combing. Bronchovascular di stortion and traction
The initial Liebow classification in 1969 ( Liebow and bronchiectasis are seen (Fig. 3. 58 ). Areas of ground-glass
Carri ngton 1969) recogni zed five entities: opacification may renect patchy septal fibrosis rather
• Usual interstitial pneumonia (UJP) than active alveo li tis (N ishimura et al. 1992) and this
• Desquamative interstitial pneumonia (DIP ) corre lates with the re lative la ck of response of this entity
• Lymphocytic interstitia l pneumonia (LIP ) to steroid therapy. HRCT findin gs frequently are diagnos-
• Giant cell interstitial pneumon ia (G IP) tic to the extent that hi stologica l confirmation is not
• Bronchiolitis and interstitial pn eumonia (B IP ) conside red necessary.
GIP is now recognized as a pneumoco niosis and LIP is Desquamative Interstitial Pneumonia-Respiratory
accepted as a Iymphoproliferat ive di sorder. Bronchioli- Bronchiolitis Interstitial lung Disease
tis and interstitial pneumo nia subsequently termed
bronchiolitis obliterans organiz ing pneumonia (BOO P) Desquamative interstitial pneumonia was included in
and then organ izing pneumonia (OP) is now co nsidered Liebow's original class ifi cation and, for a period, was con-
a disease of small airways and airspaces and no longe r as side red by some to represent the early ce llular phase of
an interstitial pneumonia. UIP. This co ncept now has been largely abandoned (Rey-
b The current classifi ca tion recognizes the following nold s and Hansell 2000 ). Respiratory bronch iolitis (RB ) is
entities: an incidental finding in asymptomatic smokers and is
This is consistent with the concept of a spectrum of dis-

ease ranging from bronchiolocentric RB llD to more dif-
fuse involvement of the secondary lobule in DIP.
Nonspecific Interstitial Pneumonia
NSIP initially was used by Katzenstein and Fiorelli in

1994 to denote cases of interstitial pneumonia in which
histology did not co nform to any of the recognized pat-
terns. These cases were characterized histologically by
spatially uniform interstitial inflammation with a varia-
ble amount of fibrosis.
The concept of NSIP as a s pecific clinicopathologic
entity subsequently has begun to emerge. This is
Fig.3.58 Usual interstitial pneumonia: HRCT shows extensive
strengthe ned by the finding that the prognosis for hi sto-
honeycombing with traction bronchiectasis. logically proven NS IP is very much better than for VIP,
w ith a 10 year survival of 60 % versus 10 % (Nagai et aJ.
1998, Tukiainen et aJ. 1983 ). J
The chest radiograph is abnormal in over90 %of cases
but findings tend to be nonspecifi c (Reynold s and Han-
sell 2000).
Hartman et aJ. have described the HRCT findings in P
NSIP (Hartman et aJ. 2000). They described ground-glass fl
opacification (GGO) in 76 %. irregular linear opacities in (I
46 %, honeyco mbing in 30%, consolidation in 16 %, and h
nodular opacities in 14 %of cases and concluded that CT tl
findings in NSIP were variable. Howeve r. all studi es on b
NSIP suggest that it predominates in the mid to lower lung ti
zones and that GGO is the sa li ent feature (Lynch 2001 ). b
The differentiation ofNSIP from DIP is like ly to be less
important than di stinguishing either entity from UIP, d
Fig.3.59 Respiratory bronchiolitis- interstitia l lung disease.
since both NSIP and DIP tend to be steroid-res ponsive G
HRCT through the up per lobes shows extensive ground-glass and both have a much better prognos is than UIP. A
opacification in a heavy smoker. sl
Acute Interstitial Pneumonia H
ir
characterized by pigmented macro phages within the res- Acute interstitial pneumonia is rare and is characterized A
piratory bronchioles with minor peribronchiolar inflam- by sudden onset of severe and progressive dyspnea in
mation. In RBILD. the inflammatory change is more ex- previously fit individ uals with rapid progression to res- A
tensive and these individuals tend to be symptomatic piratory failure with requirement for mechanical venti- IT
with a restrictive pattern at pulmonary function tests. lation. Thi s is the interstitial pneumonia which equates m
DIP shows very significant histologic overlap with most closely to that described by Hamman and Rich, al- Iy
RBILD and 90 %of patients with DIP and RBILD are heavy though this syndrome may also have included some
smokers. This suggests a histologic spectrum of small cases of rapidly progressive UIP (Hollingsworth and
airways and parenchymal reaction s to cigarette smoke. Mark 2001 ). This essentially is the idiopathic form of
Both entities are characterized by the presence of intra- adult res piratory di stress syndrome (ARDS) and ha s Ir
alveolar macrophages but in DIP the distribution is more three di stinct histological stages. The se acute exudative.
diffuse and less bronchiolocentric than in RBILD. subacute proliferative (Fig. 3.60) and chronic fibrosing o
The chest radiograph may be normal, show a reti- stages are characterized by alveolar edema and hyaline cl
culonodular pattern or ground-glass opacification membrane formation progressing to fibroblast prolifera- Z(
sometimes with a nodular or granu lar texture (Reynolds tion but with little mature collagen formation.
and Hansell 2000). Both the chest radiograph and HRCT show a combina-
M
Heyneman et aJ. (1999) looked at HRCT findings in tion of bilateral symmetric air space consolidation.
respiratory bronchiolitis (RB), RBILD, and DIP. RBILD was ground-glass opacification. traction bronchiectasi s. and TI
characterized by centrilobular nodules (38 %), ground- architectural distortion most commonly in a mid to ty
glass opacification (50 %; Fig. 3.59), and a fine reticular lower lung zone distribution. johkoh et aJ. (1999) found cv
pattern (25 %). DIP was characterized by ground-glass that the ex tent of ground-gla ss opacification and trac- si
opacification (100 %) and a fin e reticular pattern (63 %). tion bronchiectasis increased with disease duration. fu
, Acquired Immunodeficiency Syndrome 97
m of dis- Fig.3.60 Biopsy-proven acute interstitial pneumonia. CT shows

more dif- a nonhomogeneous pattern of ground-glass opacification/con-
solidation with some intralobular septal thickening in a mid-lower
IP. zone distribution.
:iorelli in
in which
lized pat-
,ically by
h a varia -
tathologic
This is
for his to-
n for UIP.
agai et al.
Acquired Immunodeficiency Syndrome
%ofcases
and Han-
indings in Acquired immunodefi ciency sy ndrome (AIDS) res ults diologic manifestations of tuberculosis, however, de-
lund-glass from infection with the human immunodeficiency virus pend on the degree of host immune impairment. Classic
~acities in (HIV). Groups at high risk of expos ure indude the male features of postprimary organ tuberculosis including en-
16 %. and homosexual population, intravenous drug users, and, in dobronchial spread and cavitation are seen in the mildly
ed that cr the past. those in receipt of regular blood transfu sions or immunocompromised. Tuberculosis in advanced AIDS is
,tudies on blood produ cts (Abrams 1985. Bessen 1988). HIV- posi- frequently aggressive and manifestations may be those
lower lung rive individuals may remain healthy for several years of primary or miliary tuberculosis. Cavitation is unusual
h 2001). befo re the onset of AIDS. in the severely immunocompromised.
/to be less Since its recognition as a disease entity in the in - Mycobacterium avium complex is found in up to 20 %
from UIP. du striali zed world in the ea rly 1980s (Gottlieb 1981 a. of AIDS patients and is associated with severe degrees of
:esponsive Gottlieb 1981 b). the incide nce of both HIV positivity and immunocompromise. Pulmonary manifestations are
UIP. AIDS have increased quite dramatically but rates now less common than in infection with Mycobacterium
show a degree of stabilization in Western countries. tuberculosis. When present. they include pare nchymal
However, the spread of HIV infection has been alarming nodules, masses, and consolidation in association with
in developing countries, particularly in sub-Saharan mediasti nal lymph node enlargement (Hartman et al.
Iracteri zed Africa and Southeast Asia (Von Overbeck 2005 ). 1994).
iyspnea in Intrathoracic disease is common in patients with Mycobacterium tuberculosis and MAC are the or-
lion to res- AIDS and is associated with significant morbidity and ganisms most frequently responsible for mediastinal ad-
lical ve nti- mortality (Hartman et al. 1994). The main intrathoracic enopathy in AIDS (Kuhlman 1989. Sider 1993). These
ch equates manifestations of AIDS are infections, neo plasia, and nodes may have low-attenuation centers (Pastores 1993 )
ld Rich. al- Iymphoproliferative di sorders. with evidence of rim enhancement on iodinated con-
Ided some trast-enhanced images (Kuhlman 1996; Fig. 3.61 ).
worth and Many patients with AIDS now receive highly active
lie form of antiretroviral th erapy. This therapy leads to so me degree
;) and has
Infections of restoration of cell-mediated immunity. However, its
exudative, initiation has been re ported to be associated with tran-
c flbrosing Organisms causing intrathoracic infection in AIDS in- sient worsening of radiograph ic abnormalities in AIDS
\Od hyali ne clude bacteria. typical and aty pical mycobacteria. proto- patients with tuberculosis. New or increased pulmonary
;t prolifera- zoa, vi ruses, and fungi. parenchyma l disease. lymphadenopathy. and pleural ef-
on. fusions have been described (Fis hman et al. 1998).
a combina- Mycobacteria
lsolidation, Pneumocystis Jiroveci/Carinii Pneumonia
~ cta s i s, and There is increased susceptibility to infection with both
1 a mid to typica l and atypical myco bacteria. Mycobacterium tuber- See p.87
999) found culosis may cause disease in individuals in whom re-
nand trac- sistance to atypical mycobacteria, Pneumocystis, and
uration. fu nga l infections is preserved (Goedert et al. 1987). Ra-
Fungi Pi
larg'
Pulmonary fungal infection is usually a manifestation of
disseminated disease. Cryptococcosis is the most co m-
mon pulmonary fungal infection in AIDS and frequently
coexists with cryptococcal meningitis (Chuck 1989). In- lyn
trathoracic manifestations include mediastinal lymph
node enlargement, pleural effusion s, and foca l alveo lar
A nu
and diffuse reticulonodular shadow ing (Dee 1995 b.
AIDS
Chechan i and Kamhol z 1990. Katz et al. 1989).
So me infections, such as invasive aspergillosis. are
relatively rare in AIDS as the neu tro phil co unt is pre- Lyml
se rved. However, neutropenia resulting from AZT and
LIP i,
ganciclovir therapy occasionally may result in its
ers f
develo pment.
HIV-
1995
bran
Intrathoracic Malignancy plasr
liter.::
Kaposi Sarcoma ce nCI
deve
Kapos i sa rco ma is a common intrathoracic mali gnancy TI
in the pati ent w ith AIDS, occurring in approximately shad.
25 % of cases. It is found almost exclu sively in ho- w ith,
Fig. 3.61 Mycobacterium avium complex (MAC) infection in mosexual and bi sex ual men, suggesting a cofactor in the usual
patient with AIDS. Enlarged right paracardiac lymph node shows homo sexual population (Des Jarlais et al. 1987). and its
peripheral enha ncement with low density center. ham
incidence appea rs to be on the declin e. Pulmonary in- nodu
volvement develops in approximately 20 % of patients patte
with Kaposi sa rcoma (Kuhlman 1996. Meduri et al. 1986) scribl
and is rare in the absence of cutaneous lesion s. amet
Findings on the chest radiogra ph may be no nspecific, bronc
particularly as there frequen tly is coex isting opportunis- also !
tic infection (Dee 1995 b, Ognibene et al. 1985). Charac-
te ristic features on HRa are bilateral irregul ar nodules
MuC(
or areas of consolidation in a peribron chovasc ular di s-
(MAl
tribution (Figs. 3.62, 3.63, 3.64). Interlobular septal
thickening, lymph node enlargement, and pleural effu - MAll
sions are also co mmon (Hartman et al. 1994). in die
prim.
Lymphoma have
the t
Pulmonary lymphoma is the seco nd most common phoel
malignancy linked to HIV positivity (Dee 1995 b, Kapl an 1991,
Fig.3.62 Kaposi sarcoma in AIDS. CT shows multiple spiculate
masses of Kaposi sarcoma. Diagnosis was confirmed at autopsy.
et al. 1987). All types of lym phoma have an inc reased in- in tht
cidence in AIDS (Kuhlman 1996), and whil e non-Hodg- 5-6 n
kins lymphom a (N HL) constitutes an AIDS-defining ill- t ion.
ness, Hodgkin lymphoma does not (Dee 1995 b, Boring et
Viruses al. 1985). B cell non -Hodgkin ty pe is the most common Atyp;
AIDS-related lym phoma. These are aggressive tumors
Cytomegalovirus (CMV ) is ubiqu ito us in patients with w ith a predilection for extra nodal sites, incl uding the ALD i
AIDS. It may cause severe esophagiti s and colitis. All pulmonary parenchyma and the gastrointe stinal tract by a
viruses, especially CMV, are an infrequent cause ofpneu- (Kuhlman 1996, Sider et al. 1989, Ziegler et al. 1984). findi r
mania in AIDS. Radiographic manifestations include dif- AIDS-re lated lymphoma (ARL) uncommonly involves diamf
fuse parenchymal infiltration which may be indistin- the chest as a major site of disease. Blun t et al. (1995) opaci
guishable from noncardiogenic pulmonary edema. found this to be the case in 15 of 11 6 pati ents with ARL
Pleural effusions and adenopathy are absent. (12 %).In this series, pleu ral and intrapulmonary masses,
frequently periphe ra l and sometimes cavitating, were
the most frequent imaging finding.
Acqu ired Immunodeficiency Syndrome 99
Pleu ral effus ions and mediastinal lymph node en-

largement also we re common.
arion of
.st com-
,que ntly
)89).ln- lymphoproliferative Disorders
I lymph
alveolar A number of Iymphoproliferative disorders are found in
1995 b, AIDS. These include:
)sis. are
..
lymphocytic Interstitial Pneumonia
......
: is pre-
ill and LIP is an AIDS-defi ning index disease in child ren (Cent-
in its ers for Di sease Control 1985 ); such an association in ~----------------------
HIV-positive adults is controversial (McGuinness et al.
1995). Pathologically, there is infilt ration of the peri-
bronchial interstitium by polyclonal lymp hocytes,
plasma ce ll s, and immunoblasts. Alveolar air-space ob-
li teration may be due to distal atelectasis, and coa les-
cence of these areas of air-space obliteration may lead to
development of nodular masses (Dee 1995 b).
lignancy The chest radiograph may show diffuse reticul ar
<imately shadowing and reticulonodular infiltrates w ith or
I in ho- without patchy alveolar infil tration. These changes are
or in the usually most marked at the lung bases (Dee 1995 b, Old-
), and its ham 1989). In patients with HIV infection, however,
,nary in- nodular shadowing may predominate (Bragg 1994). CT
patients patterns in LIP in adu lt patients with AIDS have been de-
al. 1986) sc ribed (McGuin ness et al. 1995): nodul es 2-4 mm in di-
ameter were the predominant fi nding. Bronchiectasis,
lspecific, bronchiolectasis, and bronchial-wall th ickening were
)ortunis- also seen.
. Charac-
nodules Mucosa-Associated lymphoid Tissue lymphoma
ular dis- (MALTOMA)
r septal
Iral effu- MALTOMA is defined as multiple, small (less than 5 mm
in diameter) nodular infi ltrates of lymphoid cells with a b
primarily perib ron ch ial distribu tion. The lymphocytes Fig. 3.63 a, b Bacterial pneumonia in patient with AIDS (a). Le-
sions of Kaposi sarcoma are visible and show "tumor blush" on
have a proportion of atypical cells wh ich may infiltrate bronchial artery injection (b).
the bronchial epithelium in clusters to produce Iym-
common phoe pithe li al lesio ns (McGui nness et al. 1995, Harris
J, Kaplan 1991, Herbert et al. 1985 ). The predominant CT findings
eased in- in the se ri es by McGuinness et al. (1995) were nodu les
JIl-Hodg- 5-6 mm in diameter, in a peribronchovascular distribu-
lning ill- tion.
Boring et
common Atypical Lymphoproliferative Disorder (ALD)
= tumors
,ding the ALD is defined as diffuse infiltration of the interstitium
Inal tract by a mixed po pulation of atypical lymphoid ce lls. CT
1984). findings include parenchymal nodules 2-4 mm in
{involves diameter, air-s pace consolidation, and ground-glass
,I. (1995) opacification (McG uinness et al. 1995).
with ARL
y masses,
ing, were Fig.3.64 Kaposi sarcoma. CT shows multiple bilateral "fluffy"
nodules in a peribronchovascular distribution.
Autoimmune Disorders/Connective Tissue Diseases •

PI,
m,
Autoimmune disorders are pathologic processes in Pleural involvement is co mmon and the chest radiograph inl
which the immune system develops antibodies that may show bilateral pleural effusions or thickening, In the (Ti
react with endogenous tissues. Antibodies frequently lungs. there may be evide nce of acute lupus pneumoni- ne
can be detected in the patient's blood, There is usually tis, pulmonary edema, pulmonary vasculitis w ith to
multiorgan involvement. The collagen vascular diseases hemorrhage, interstitial pneumonia, and occasionally an ita
affect connective tissue, the ubiquity of which accounts organizing pneumonia. Some pulmonary parenchymal cu
for the varied clinical picture. changes may regress with steroid therapy. In advanced lar
Pulmonary manifestations are common and connec- di sease, there may be evidence of pulmonary fibrosis Ca
tive tissue disease-associated interstitial pneu monia w ith reticular and honeycomb shadowing (Fig, 3,65 ), an
may progress to fibrosis. Pleural inflammation, peri- The HRCffindings in SLE have been described (Fenlon pa
carditis, and myocarditis may also be see n. 1996). Interstitial changes including thickened inter-
lobular septa were present in 44 %of cases, while airway ha
changes of bronchiectasis and bronchial-wall thickening al.
were seen in 21 % of patients, Mediastinal lymph node
Systemic Lupus Erythematosus en large ment was also a frequent finding( 18 %). HRCf fea- be;
tures of interstitial and airway disease were frequently Sti
seen in asympto matic individuals with both normal
• Clinical Features Fi ~
chest radiographs and normal pulmonary function tests.
Systemic lupus erythematosus (SLE) is a chronic di sease
with acute exacerbations that primarily affects pre- PI
menopausal females. The principal manifestations are Rheumatoid Arthritis
polyarthritis, glomerulonephritis with nephrotic syn-
drome, pleurisy, and pancarditis. Clinical features of
pneumonitis and pulmonary fibrosis are unusual. al-
though pulmonary involvement may be demonstrated
• Clinical Features •
Th
hi stologically in 70% of patients (Baum 1974), Diagnosi s So me degree of pulmonary fibrosis is present hi stologi- rat
is based on detection of lupus (LE ) cells in the blood. ele- cally in th e majority of patients w ith rheumatoid ar- tra
vated serum antinuclear factor (AN F), anti double- thritis (RA), Approximately 20 % of all cases of pulmo- of
stranded DNA and anticardiolipin antibodies. nary fibrosis are attributed to rheumatoid disease (Cer- eli,
vantes-Perez et al. 1980), Most of these changes are sub- (G'
clinical. and positive radiographic findings may be ex- Re
• Radiologic Findings pected in only 1-2 % of cases. Other thoracic manifesta-
tions include intrapulmonary necrobiotic nodules,
Pleuropulmonary involve ment has been reported in SLE w hich hi stologically resemble subcutaneous rheuma-
with an incidence ranging from 7 to 100 %(Orens 1994), toid nodules. pleural and pericardial effusions (Fig, 3,66 ),
Fig.3.65 Lupus erythematosus. Frontal radio-

graph shows perihilar and basal linear shadow-
ing in a patient with SLE.
Fig
lo~
tiCl
Autoimmune Disorders/ Connective Ti ssue Diseases 101
Pleural effusion is the most common intrathoracic

manifestation of rh eumato id arthritis. HRCf may show
'graph interstiti al pneumonia with either a UIP or NSIP pattern
In the (Tanaka et al. 2004; Fig. 3.67 ). Occasionally. multiple
moni- necrobiotic nodules are present. They range from 3 mm
with to 7 em in diameter, are usually subpleural, and may cav-
311yan itate (Fig. 3.66 ). They are found in association with sub-
hymal cutaneous rheumato id nodules and may pursue a simi-
ranced lar course. A continuum exists from these lesio ns to the
ibrosis Caplan syndrome. The latter occurs in anthracos ilicosis
;5). and may rep resent a hype rsens it ivity react ion in a
~en l on patient wit h underlying rheumatoid disease.
inter- Bronchiectasis and changes of sma ll airway di sease
lirway Fig.3.66 Rheumatoid nodules with central necrosis (a). Pleural
have been described in patients w ith RA (Remy-Jard in et change is also present. Rheumatoid arthritis (b).
.<ening al. 1994. Tanaka et al. 2004).
1 node Small airway changes of centri lob ular nodul es and
CTfea- branch ing linear structures in RA may also be a manife-
uently station of follicular bronchiolitis (Howling et al. 1999;
lOrmai Fig. 3.68 ).
n tests.
Progressive Systemic Sclerosis (PSS)
The chest radiogra ph and HRCT may show characteristic
basal interstitial changes of in terstitial pneumonia
• Clinical Features (Fig. 3.69 ). It has been noted that inte rstitial pneumonia
fo und in association w ith systemi c sclerosis ha s a better
This collagen vasc ul ar disease leads to atrophy and indu- prognosis tha n "lone cryptogeni c fibrosing alveo litis"
;tologi- ration of the skin and scleros is of the gastrointestinal (Wells et al. 1994). It has been postulated tha t this may
oid ar- tract. Pulmona ry fibrosis is present histologically in 90 % be due to a NS IP-type entity bei ng co mmoner than UIP-
?ulmo- of cases. but no more than 20 % of these cases manifest type pneumonitis in these patien ts (Fig. 3.70 ).
e ((e r- clinical sympto ms and radiograph ic abnormalities Esophageal dysmotility with dilatation is also seen in
re sub- (Gu rtl er et al. 1979, Kauffmann et al. 1983a. Otto and PSS and may be associated with episodes of aspiration
be ex- Re inha rd 1970). pneumonia.
lifesta-
odules.
leuma-
l-3. 66 ).
radio-
adow-
Fig.3.67 "NSIP" pattern in rheumatoid arthritis. CT through the Fig.3.68 Follicular bronchiolitis in rheumatoid arthritis. HRCT
lower zones shows patchy ground-glass opacification with fine re- shows bronchial wa ll thickening with features of a Mcellular
ticular change and some traction bronchiectasis. bronchiolitis." Histology was consistent with follicular bronchioli-
tis .
Sjogren Syndrome eyte an

patient
Sjogre n syndro me (s icca syndrome) is characterized by

the triad of keratoconjunctivitis sicca, parotitiS sicea, and
polyarthritis. There is an association w ith LIP. HRIT find- Weg
ings include ground-glass opacification (Fig. 3.71), focal
areas of consolidation, ill-defined nodules, and pulmo- Wegen
nary cysts (Fig. 3.72: Hond a et al. 1999), giiti s a
airway
semina
Dermatomyositis Remee
g raph i!
ground
Fig.3.69 Interstitial pneumonia in patient with progressive sys- Mino et al. (1997) have described IT findings in po ly- coid-lil
temic sclerosis. HRCT shows bilateral ground-glass opacification, and dermatomyositis. These include consolida tion in a vasculi
consolidation, and some interstitial thickening.
subpleural and patchy distribution, ground-glass opaci- with in
fication, pa renchymal bands, and irregular bron- Dial
chova scula r thickening (Fig. 3.73), These we re seen to be frequel
reversible with corticostero id and immunosuppressant positiv
the rapy. test rni
Chest wa ll involvement with muscular weakness Tra(
may lead to restricted ve ntil ation. high n
renal f;
chemo
Ankylosing Spondylitis (AS) phospt
and m
giving
Upper lobe fib rosis and bullous emphysema are some- Fauci e
tim es found in associatio n w ith ankylos ing spondyliti s.
In chronic cases, radiographi c findings may be indi st in-
gui shable from healed postp rimary tuberculosi s. Cavita- • Ra!
tion may also occur, and the upper lobes may then be
co loni zed by aspe rgillus to form mycetoma ta . DiagnOSis Eighty·
Fig.3.70 Progressive systemic sclerosis: predominantly basal is faci lita ted by the typical rad iographic find ings in the develo
pulmonary fibrosis. axial skeleton and the occurrence of the IlUman leuko- their iI
pulmo]
man. F
seen (F
usuall)
rhage (
HR(
nodule
consoH
(Fig. 3:
ties n
Maskel
bronch
bronch
era l re
cases i
tial fib
we (F
Sub
import
Mayo,
Fig.3.71 Biopsy-proven lymphocytic interstitial pneumonia in Fig.3.72 Lymphocytic interstitial pneumonia in Sjogren syn-
Sjogren synd rome. HRCT through the lower lobes shows bilateral drome. HRCT shows scattered bilateral lung cysts. proxirr
groun d-glass opaCification with interlobular septal thickening. q ui red
Autoimmune Disorders/Connective Tissue Diseases 103
cyte antigen (HLA)-B27 antigen in approximately 90% of

patients with AS.
'fized by
icca, and
{Cf find-
Wegener Granulomatosis (WG)
11), focal
I pulmo- Wegener granulomatosis is classified as a form of an-
giitis and granulomatosis, It is characterized by upper
airway ulceration, cavitating pulmonary nodules, a dis-
seminated vasculitis, and glomerulonephritis (De-
Remee et al. 1980). Histologic findings include geo-
graphic basophilic necrosis, an inflammatory back- Fig,3.73 Dermatomyositis. diaphragmatic paralysis. discoid
ground with scattered giant celis, and absence of sar- atelectasis, and pulmonary fibrosis (rare).
in poly- coid-like granulomata. Eccentric mononuclear celi
tion in a vasculitis that may evolve into a necrotic granuloma
ss opaci- within the vessel wall is also found (Colby 1996),
Ir bron- Diagnosis may be made from biopsy, but findings are
een to be frequently those of nonspecific inflammatory change, A
Jpressant positive ANCA (antineutrophil cytoplasmic antibody)
test may then be helpful in establishing the diagnosis.
Neakness Traditionally, untreated WG was associated with a
high mortality, death occurring within months from
renal failure. The prognosis now is much improved and
chemotherapeutic regimes encompassing cyclo-
phosphamide together with steroid therapy can induce
and maintain remission in the majority of patients,
giving 5-year survival rates of 90 to 95 % (Wilson 1995,
Ire some- Fauci et al. 1983, Thurlbeck and Muller 1989).
)ondylitis,
~ indistin-
is, Cavita- • Radiologic Findings
y then be
Diagnosis Eighty-five to ninety percent of patients with WG will
ngs in the develop pulmonary involvement during the course of Fig, 3,74 Wegener Granulomatosis: pulmonary infiltrates, cavi-
Ian leuko- their illness (Wilson 1995, Maguire et al. 1978). Multiple tating masses, atelectasis, and subglottic tracheal stenosis.
pulmonary nodules with or without cavitation are com-
mon, Focal infiltrates, which may be fleeting, are also
seen (Fig. 3.74). Bilateral diffuse alveolar consolidation is
usually a manifestation of diffuse pulmonary hemor-
rhage (Fig.3.7Sa).
HRCf findings in WG include multiple pulmonary within the proximal trachea and associated thickening
nodules frequently cavitating (Fig. 3.76), diffuse bilateral and calcification of tracheal rings (Stein et al. 1986).
consolidation consistent with pulmonary hemorrhage Mainstem and lobar bronchial stenoses are also a feature
(Fig.3.7Sb), and pleurally based wedge-shaped opaci- of WG and may be demonstrated by multi-detector
ties resembling pulmonary infarcts (Wilson 1995, computed tomography (MDCT).
Maskell et al. 1993). Maskell found a high incidence of
bronchial abnormalities in WG; these included
bronchiectasis and bronchial-wall thickening. Periph-
eral reticular change was also seen in a percentage of Allergic Angiitis and Granulomato-
cases in this series, and the authors suggest that intersti- sis (Churg-Strauss Disease)
tial fibrosis may be part of the pathologic spectrum of
WG (Fig. 3.77).
Subglottic tracheal narrowing is an infrequent but • Clinical Features
important complication of WG (Wilson 1995), In the
Mayo series (McDonald et al. 1982) it was found in ap- Intrathoracic manifestations of this systemic necrotizing
Sjogren syn-
proximately 15 % of cases, and some 50 % of these re- vasculitis include bronchial asthma, recurrent pulmo-
quired tracheostomy, CT will show abnormal soft tissue nary infiltrates, and pleural and pericardial effusions. An
b
a
Fig. 3.7Sa. b Wegener's granulomatosis: Chest radiograph and Fig. ::
HRCT show bilateral airspace consolidation consistent with dif-
a fuse pulmonary hemorrhage.
An
associated peripheral blood eosinophilia invariably is ME
.'
present.
The disease may evolve in three stages; asthmatic,
eosinophilic, and vasculitic (Wilson 1995 ),
AGI
• Radiologic Findings glol
mOl
Radiographic changes are found in the eosinophilic and mel
vasculitic stages of disease, Chest radiographs may show clin
transient, recurrent nonsegmental infiltrates, accen- turi
tuated interstitial markings, and noncavitating pulmo- us u
nary nodules. Pleu ral effusions may be found in up to lint'
Fig.3.76 Wegener's granulomatosis: Consol idati on with cavita- 29% of cases (Lanham et al. 1984), and cardiomegaly bra
tion in left upper lobe with a thin-walled cavity in the apical seg- may result from pericarditis or myocarditis (Wilson
ment of the right lower lobe.
1995, Armstrong et al. 1995),
cr findings have been described. These include
ground-glass opacification and consolid ation, cen-
•
tril abu lar nodules. interlobu lar se ptal thickening, hilar Thl
and mediastinal lymph node enla rgement, pleu ral and or
pericardial effusions (Fig. 3.78), nal
Shi
of
thi
Fig. 3. 77
lobes in a
Wegener's granulomatosis: HRCT through the upper
patient with resolving pulmonary hemorrhage shows
•
multjfocal reticular shadowing with soft tissue stranding in the Th
left upper lobe. pu
reI
an
Autoimmune Disorders/Connective Tissue Diseases 105
b
• Fig. 3.78a. b Churg-Strauss disease. Pericardial and bilateral pleural effusions with anterobasal infiltrate in the right lu ng.
b
)graph and
It with dif·
Antiglomerular Basement
ariably is Membrane Disease (AGBMD)
lsthmatic,
AGBMD or Goodpasture sy ndrome is characte ri zed by

glomerulon ephritis. recurrent episodes of diffuse pul-
monary hemorrhage, and anti glomerular base ment
philic and membrane antibody. It usually affects young men with
may show clinical manifestations that include hemoptysis, hema-
~s, accen-
turia, renal failure, and arterial hypertension. Diagnosis
19 pulmo- usually is established by renal biopsy and detection of
jinupto linear deposits of IgG on glomerular basement mem-
diomegaly branes (M uller 1991 ). Fig. 3. 79 Antiglomerular basement membrane disease. Pulmo·
s (Wilson nary hemorrhage. hemosiderosis. and eventual fibrosis.
;e include • Radiologic Findings

:ion, cen-
ning, hilar The chest radiograph and HRCT show diffuse unilateral renal or immunologic abno rmality (Mu ller 1991 ). Dpen
leural and or bilateral alveolar shad owing consistent with pulmo- lung biopsy usually is required for diagnosis and shows
nary hemorrhage (Figs. 3.79 and 3.80). As the alveolar alveolar hemorrhage, hemosiderin-laden macrophages,
shad owing clears, it is replaced by an interstitial pattern and fraying of elastin fibers.
of irregular linear opacities and interlobu lar se ptal
thickening (Muller 1991 ).
Pulmonary parenchymal cha nges resemble those of

Idiopathic Pulmonary AGBMD (Fig. 3.79). Hilar and mediastinal lymph node
Hemosiderosis (IPH) enlargement have been reported in the childhood vari-
ant (Case Records of Massachusetts General Hospital
1988 ).
The eti ology of this disorder wh ich gives rise to episodic

pulm onary hemorrhage is unknown. A disease of child-
ren and young adults, )PH is characterized by anem ia
and pulmonary infiltrates but with no demonstrable
Fig.3 .80 Antiglomerular basement

membrane disease: confluent air-
space shadowing in t he right lower
lobe. Patie nt had presented clinically
with hemoptysis and ren~1 failure.
Pulmonary Eosinophilia (Eosinophilic lung Disease)
These di sorders are characterized by blood and tiss ue is associated with a bronchocentri c reaction, w hile the
eosi nophilia usua lly in association w ith an abnorma l pulmona ry eosinophilia associated with drugs and para-
chest radiograph. Eosi nophilic lung disease is usually sites te nd s to be angioce ntric.
classified according to etiology (Table 3.2). The pulmo- Known ca uses of pulmona ry eosinophilia are drugs.
na ry hi stologic res ponse depends on the route by w hich parasites, and fun gal spore s: see allergic bronchop ulmo-
the organ ism enters the lung. All ergic bronchopulmonary aspergillosis (p. 82). parasitic infections (p. 86). and
nary aspergillosis caused by inhalation of fungal spores drug-induced lung disease (p. 108).
In approx imate ly 25 % of cases. etiology is unknown
Table 3.2 Pulmonary eosinophilia (from Carrington and Reeder)
and these are labeled cryptogenic pulmonary eosino-
philia. Characteristic findings include a pulmonary eo-
Idiopathic eosinophilic pneumonia. acute si nophilic infiltrate. granuloma formation, and a vasc uli-
(loftier syndrome) tis. The individ ual di seases are classified accord ing to
• Chronic eosinophilic lung diseases of known etiology
the relative amounts of each pathological change
- Drug allergy (nitrofurantoin, penicillin, sulfonamides,
imipramine, PAS, didofenac, ibuprofen, aspirin, pheny- (Flowe r 1995). a
toin, cocaine. tamoxifen. bleomycin. methotrexate. Cryptogenic pulmonary eos inophilia may present in Fig. 3.8
etc.) acute or chronic forms: eosino~
- Asthm a
- Fungal allergy (bronchopulmonary aspergillosis,
candidiasis. coccidioidomycosis) Acute Eosinophilic Pneumonia
- Parasitic diseases (ascariasis, echinococciasis, strongy-
loidiasis . ankylostomiasis. tropical pulmonary
(liiftler Syndrome)
Rad
eosi nophilia, filariae, larva migrans. schistosomiasis) This disorder is characterized by nonpersistent, usua lly
- Collagen diseases (polyarteritis nodosa, Wegener
peripheral co nsoli dation (Figs. 3.81 and 3.82).
granulomatosis. antiglomerular basement membrane
disease. Churg-Strauss allergic granulomatosis. rheu- • Pa
matoid arthritis) Chronic Eosinophilic Pneumonia
- Eosinophilic leukemia
The rc
- Hodgkin's disease In chronic eosinophilic pneumo nia, the consolidation is
- Paraneoplasia (e. g .• in bronchial carcinoma) lung c
- Brucellosis
persistent lasting for fou r or more weeks and tends to be the Sl
quite extensive. In 50 % of cases the chest rad iograph capaci
Radiation-Induced Lung Disease 107
,asement shows nonsegmental airspace consolidation confined to

nt air-
the outerthird of the lung, the "photographic negative of
It lower
I clinically pulmonary edema" Uederlinic et al. 1988, Gaensler
failure. 1977). CT is usefu l in demonstrating the peripheral na-
tu re of the consolidation when the chest radiograph is
not characteristic (Flower 1995). Associated mediastinal
lymph node enlargement may be evident at cr in up to
50 %of cases (Mayo et al. 1989).
Fig . 3.81Laffler syndrome: transient pulmonary infiltrates with

blood eosinophilia.
while the
and para-
:lore drugs,
hopulrno-
J. 86), and
unknown
'Y eosino-
onary eo-
a vasculi-
:ording to
,I change
present in
• Fig.3.82 a. b Eosinophilic Loffler infiltrate. Scattered patchy infiltrates in the upper and midzones cleared within 1 week . Blood
b
eosinophilia was 42 %. Ascariasis was confirmed.
Radiation-Induced lung Disease

nt, usually
• Pathology cytes is reduced, and eventually this imbalance in cell

turnover becomes significant.
The rad iat ion dose required fo r treatment of primary Radiation pneumonitis occurs 1 to 6 months after
)lidation is lung cancer almost invariab ly causes some damage to commencing therapy and may eventua lly progress to fi-
tends to be the surrounding lung parenchyma. The reproductive brosis.
radiograph capacity of both capillary endothelial cells and pneumo-
Clinical manifestatio ns of acute radiation pneumonitis

include nonproductive cough, dyspnea, and malaise. The
erythrocyte sed imentation rate (ESR) is elevated, and
pulmonary function tests may show restrictive ventila-
tory impairment. Hypoxemia may be present in severe
cases .
Chest radiographs initially show homogeneous con-

solidation with an air bronchogram conforming to the a
shape of the radiation portal (Fig, 3.83). Pathologically, Fig.
these cha nges of pneumonitis represent thickening of
alveolar septa, hyperplasia, and desquamation of
pneumocytes, intra-alveolar exudate, endothelial cell
damage, and thrombus formation (Dee 1995a), Eventu-
ally, the opacities progress to reticular and linear
shadowing and finally to fibrosis with strea ky opacities
and loss of lung vo lume (Teates 1980). BOC
Cf is supe rior to the chest radiograph in detection of ass(
postirradiation lung change. Pneumonitis is manifest as arrf
consolidation of geographic di stribution (Bell et al. patl
1988). Transitio n to fibrosis is gradual and is character- tior
ized by fibrous bands, loss of volume, bronchovascular al. ;
Fig.3.83 Radiation pneumonitis. Radiograph 6 weeks postradi- distortion, and traction bronchiectasi s.
otherapy (56 Gy for bronchial carcinoma) shows densely con-
fluent consolidation with air bronchogram conforming to the
radiation portal.
Drug-Induced Lung Disease
A number of drugs may cause pulmonary change. The Pneumonitis and fibrosis are the most common type
following radiographic patterns are recognized: of drug-induced lung damage and frequently result from
administration of cytotoxic chemotherapy and, in partic-
Hypersensitivity Reactions ular, bleomycin (Figs3.84a, b) (Padley et al. 1992,
Kuhlman 1991, Lien et al. 1985 ). HRCT findings may be
Drugs may evoke a hypersensitivity reaction; thi s some- similar to those found in usual or nonspecific interstitial
times occurs in patients with a history of atopia. Onset of pneu moni a with a predominantly basal and su bpleural
symptoms may be acute, and the reaction is unrelated to distribution.
the cumulative dose. A peripheral eos inophilia may be
present in 40% of cases (Coope r and Matthey 1987 ). His- Adult Respiratory Distress Syndrome
tologically, hypersensitivity reactions are characterized
by pulmonary eosinophilia and alveoli tis. Methotrexate Pulmonary change may develop within days of
is frequently implicated in these reactions (Cooper and chemotherapy admini stration (Cooper and Matthey
Matthey 1987, Searles and McKendry 1987). 1987). One chemotherapeutic agent, in particular bleo-
The chest radiograph may show a diffuse interstitial mycin, has been implicated. HRCT shows diffuse alveolar
pattern, sometimes in association with airspace consolidation, w hich may have a dependent distribution
shadowing. These changes may regress w ithin days. (Padley et al. 1992), Drug- induced ARDS is associated
Ground-glass opacification is the most common HRCf with a better prognosis than ARDS of other etiology.
finding in hypersensitivity alveolitis (Pad ley et al. 1992 ).
Dru g-Induced Lung Disease 109
monitis
.i se. The
ed, and
ventila-
1 severe
us con-
5 to the a
ogically, Fig. 3.84 a, b Bleomycin-induced pneumonitis. CT shows patchy consolidation in a peripheral subpleural distribution.
'ning of
tion of
lial cell
Eventu- Organizing Pneumonia/Bronchiolitis Obliterans
I linear Organizing Pneumonia (BOOP) Bronchiolitis obli te rans has been described in asso-
Ipacities ciation with penici llamine therapy for rheumatoid ar-
BOOP-type reactions have been described particu larly in thritis (Ge ddes et al. 1977), although its ro le in develop-
:ction of associati on with amiodarone therapy for cardiac ment of pulmonary change is somewhat controversial.
nifest as arrhythmias and with nitrofurantoin. HRCf shows HRCT findings incl ud e bronchial-wall thickening and
11 et al. patchy, bilate ral ground-glass opacifi cation/consolida- areas of decreased lung attenuati on (Pad ley et al. 1992)
laracter- tion in a subpleural and peripheral distribution (Ellis et with air trapping in expiration.
vascular al. 2000),
"on type
iult from
n partic-
11. 1992,
; may be
Iterstitial
Ibpleura l
days of
Matthey
liar bleo-
! alveolar
tribution
ssociated
ology.
110
4 Chronic Obstructive Pulmonary Disease Dila

both a[
and Diseases of the Airways which .
in dial
more t
bullae.
The
to ecta
Chronic obstructive pulmo nary disease (COPO) is very Diseases of the airways are characteri zed by increased righ t v.
co mmon and has been reported as being seco nd only to airway res istance, sputum production, obstructive type ular de
arteriosclerosis as a ca use of disabili ty and absence from ve ntilatory impairment. and air trapping.
work (Heitzman 1993. Hafner et al. 1977). Diseases of the airways include:
COPD is characterized by increased airway resistance • Bronchiectasis • CHi
and obs tru ctive-ty pe ve ntilatory impairment. The te rm • Small airway di sease/bron chiolitis
has a stro ng corre lation w ith a smo king history and • Bronchial asthma Manife
encompasses two main disorde rs: oosis. l
• Emphysema is poss
• Chron ic bronchitis • "Pin
dYSI
ca l
chrc
• "Blu
Emphysema are
brOJ
Physic<
Emphysema is common in the elderly. Mild degrees of s hallo ~
Goals of Diagnostic Imaging:
emphysematous change are found in two-thirds of all Spi rom
Class ificatio n of emp hysema together with documenta-
autopsies wh ile more severe form s are prese nt in ap- tion of the distribution and seve rity of change. decrea~
proximate ly 10 % of cases (Otto 1976. Thurlbeck and a rterial
Detection of any coexisti ng pulmonary di seases t hat
Muller 1994). may complicate emphysema. bloater
The word emphysema means "lung overinflation" be rela"
Eva luation of regional perfusio n and venti lation diS:
tur-J
(emphyseill = to inHate ). We defin e this entity as "a bances with radionuclide ventilation/perfusion sc inti -
chron ic and irreversibl e dilatation of the ai rspaces di sta l graphy.
to the terminal bron chiol e with associated destruction
of the ir wa lls" (World Health Organ izatio n 1961 ).
Emphyse ma may lead to significant res piratory im-
pairment wi th re sulting dyspnea, cyanosis, and eventual • Pathology
cor pulmonale.
The classification of emphysema most commonly Destruction of alveolar septa reduces both the surface
used today is based on the anatom ical distribu tion of area availabl e for gas exc hange and the total cross-
lung destruction. This subdivision into three main sectional area of the pulmo nary vessels. This leads to in-
groups is as follows: ce ntrilobular (ce ntriacinar, proxi- creased vascu lar resistance and pulmonary hy perten-
mal acinar). panlobu lar (panacinar). and parase ptal (di s- sio n. A further pathophysiologic phenomenon is ventila- Cal
tal acinar ). This "patho logica l" classifi cation of emphy- tion-pe rfu sion mi smatch : in normal individuals the von
sema is useful as it co rrelates with findings on high -res- Eu ler-liljest rand reflex, also know n as hypoxic vasocon- -c
olution computed tomograp hy (HRCT ). stricti on, regulates regional pe rfu sion and matches it to d
In practice, the diagnos is of emphysema usua lly is ve ntilati on. In e mphysema, this control mechani sm is -p
-p
based o n the appropri ate clinical hi story. abnormal pul- lost and ve ry poorly ventil ated regions co ntinu e to be
a
monary function tests, reduced diffu sing ca pacity, and a perfu sed. This results in an effective venoarterial shunt -p
chest radiograp h showing pulmonary hyperinflation. w ith systemic arterial hypoxem ia. tl
Howeve r, as both sta ndard chest radiographs and pul- Mac roscopically. the lungs are large and hyperin- - T.
monary function tests are re latively insensitive to the Hated. Emphysematous change may be patchy in dis- 51
presence of early disease, HRCf is useful when there is tri bution and interspersed between areas of normal
diagnostic uncertainty (Webb et al. 1992 ). lung. The lungs do not co ll apse w hen the chest is opened
as elastic recoil is dimini shed. The d iaphragm is
depressed and hypertrophic. sagittally ori ented muscle
fibers may ind ent the surface of the liver. Fig. 4.1
Emphysema 111
Dilated confl uent airspaces result from destruction of • Radiologic Findings

both alveolar and lobular septa. They may form bullae,
which are air-containing cystic cavities greater than 1 cm Chest Radiograph
in diameter (bullous emphysema). Bullae occupying
more than one-third of the lung are known as giant Findings on the chest radiograph are secondary to pul-
bullae. monary hyperinflation with subsequent deformity and /
The resulting pulmona ry arterial hyperten sion leads or displacement of the chest wa ll, heart, and diaphragm.
to ectasia and sclerosis of the pulmonary arteries and There is also attenuation and disorgan ization of the pul-
!Creased right ventricular hypertrophy. Eventually. right ventric- monary vasculature w ith features of oligemia and pul-
ive type ular deco mpensation may su pervene (cor pulmonale). monary hypertens ion (Figs. 4.1 and 4.2 ).
• Barrel chest: Sagittal chest diameter is increased. the
posterior ribs have a horizontal orientation, and the
• Clinical Features intercostal spaces are widened.
• Diaphragmatic depression: Findings include flatten-
Manifestations of emphysema include dyspnea and cya- ing of the domes of the diaphragm and a costophrenic
nosis. Transitional forms are common but sometimes it angle of approximately 90" (so-called "pse udoblunt-
is possible to identify specific clinical patterns: ing"). On the lateral view, the diaphragm may show
• "Pink puffer": These indi vid ual s usually are thin and inferior convexity. Respiratory diaphragmatic excur-
dysp neic. However, they are not cyanosed and clini- sion is also restricted « 3 cm in emphysema vs. nor-
cal features indicating the presence of associated mal values of 5- 10 em).
chronic bronchitis are absent. • Small, vertically orientated cardiac shadow: In the pre-
• "Blue bloater": These are "heavy-set" individuals w ho sence of a re latively low diaphragm. the heart as-
are cyanosed and have co ncomitant chronic sumes a vert ical orientation and cardiothoracic ratio
bronchitis. decreases on the frontal radiogra ph. There may also
be a degree of left ventricular atrophy as left heart
Physica l exa mination reveals a barrel chest. relatively filling and left ventricular output sometimes are re-
shallow respirations. and hyperresonance to percussion. duced in patients with emphysema, especially in
enta- Spirometry shows increased FVC, diminished FEV1, and cases complicated by cor pulmonale.
decrea sed FEV1/FVC ratio. Blood gas analysis revea ls • Increased retrosternal space: On the lateral radio-
lat
arterial hypoxemia and hypercapnia particularly in blue graph, the retrosternal space is widened due to both
bloaters. Arterial oxygen and ca rbon dioxide levels may the increased sagittal diameter of the chest and the
be relative ly normal in pink puffers.
is,~:- I re lative ly "small" heart.
• Dilatation of the central pulmonary arteries: Increased
IO~ pulmonary vascu lar resistance and subsequent pul-
monary arterial hype rtension lead to dilatation of the
central pulmonary arteries. This is manifest as bi-
lateral symmetric hilar enlargement on the chest
radiograph.
~ surface
31 cross-
Ids to in-
.yperten-
-) ventila- Cardiopulmonary Pulmonary Hyperinflation
"vascular" changes
:; the von - Barrel chest
vasocon- - Central vascular - Widened intercostal
: hes it to dilatation spaces
tanism is - Pru ning of vessels - Horizontal ribs
- Peripheral vascular - Large retrosternal
me to be attenuation space
ial sh unt - Pulmonary hyper- - Increased antero-
transradiancy posterior diameter
hyperin- - Teardrop- - Flat, low diaphragm
shaped heart indented by muscle
.y in dis-
insertions
f normal - Blunted costophrenic ang le
s opened - Respiratory excursion <3 cm
lragm is
d muscle
Fig. 4.1 Pulmonary emphysema.
112 4 Chronic Obstructive Pulmonary Oisease and Oiseases of the Airways
a b
Fig. 4.2 a. b Classic radiographic appearance of pulmonary emphysema.
• Rapid tapering of pulmonary vessels: The dilated cen- emphysema frequently becomes apparent on the
tral vessels decrease markedly in caliber at the chest radiograph only when common disorders such
segmental level. This may occasionally give the ap- as pneumonia and pulmonary edema supervene
pearance of an "amputated hilum." (Fig. 4.3 ). Pneumonic consolidation and cardiogenic
• Attenuation of peripheral pulmonary vessels: The com- edema develop with relative sparing of regions of
bination of pulmonary hyperinflation together with avascularity. Therefore, emphysematous lung that is
attenuation of peripheral vessels results in increased devoid of capillaries tends to be spared. This results in
lucency in the lung periphery. nonhomogeneous, relatively coarse infiltration. Pul-
• Marker vessels: Emphysema is often focal in distribu- monary edema may be asymmetrical or localized de-
tion. In these cases, pulmonary blood flow will be re- pending on the distribution of emphysematous in-
volvement. Fig . 4.4
distributed to areas of relatively normal lung and re-
decreas
sult in regional vascular dilatation. In addition, pulmon.
emp hysematous bullae may compress adjacent nor- • Computed Tomography
mal lung and cause crowd ing. disp lacement, and
draping of vesse ls. These findings are best appre- Correlation between CT and spirometric data has been • Pan
ciated on conventional and computed tomography reported to be relatively poor (Miller 1989). HRCT, stru
(CT). however, is valuable in detection of early disease. It is em,
• Bullae: Thin-walled emphysematous spaces greater also possible to classify emphysema on the basis of find- cien
than 1 (m in diameter sometimes are visible on the ings on HRCT: is ar
chest radiograph. However, CT wi ll show these thin- • Centrilobular emphysema: Centrilobular emphysema seru
walled. air-fil led cysts much more convincingly. classically develops in the setting of chronic 20 %
• Increased bronchovascular markings: Emphysema bronchitis and shows a predilection for the upper low~
often is found in association with chron ic bronchitis. lobes. Alveolar destruction is mainly around the res- lung
Peribronchovascular fibrosis is found in the latter and piratory bronchioles at the center of the pulmonary gion
is manifest as tortuosity, poor definition, and acinus and therefore involves the center of the sec- Clini
segmentation of vascular shadows (increased pulmo- ondary pulmonary lobule (Webb et al. 1992 ). HRCT deca
nary markings, "dirty chest," Thurlbeck and Muller shows centrilobular area s of low attenuation, some- tion
1994). times several millimeters in diameter. These foci • Para.
• Atypical appearance of pneumonia and pulmonmy have imperceptible walls, which helps in differenti- with
edema: Emphysema may alter the radiographic ap- ating them from cysts, bronchiectasi s, and the pleu.
pearance of other pulmonary diseases. Conversely, honeycombing of pulmonary fibrosi s (Figs. 4.4, 4.5). unle!
Emphysema 113
Fig. 4.3 a, b Pulmonary edema in emphysema. Coarse reticular

shadowing is seen in the perihilar lung with sparing of areas of
• emphysemato us lung .
on the
~rs
such
pervene
liogenic
~i ons of
~ that is
~sults in
on. Pul-
ized de-
taus in-
Fig.4.4 Centril obu lar emphysema. HRCT shows areas of Fig.4.5 Centrilobular emphysema.
decreased lung attenuation lying centrally within the secondary
pulmonary lobule.
las been • Panlobular emphysema: This is characterized by de- • HRCT w ill show subpleural and perifissural bullae
). HRCT. struction of alveo li throughout the lobule. Pan lobular and a studies have show n a hi gh incidence of apical
ase. It is emphyse ma is associated with aI-antitryps in defi- parase ptal emp hyse ma in young adu lts presenting
; of find- ciency and has a pred il ection for the lower lobes. This w ith spontaneous pneumothorax (Lesur 1990).
is an auto soma l recess ive disease associated w ith low
physe ma se rum leve ls of aI-a ntitrYPsin. Homozygotes have Quantification of abnormally low lung a ttenuatio n due
chro nic 20 % of normal enzyme activity. This deficiency al- to e mphysema is poss ible with volumetric cr acq ui si-
Ie upper lows leucocyte proteases to attack and destroy the tion and three-d im e nsional reco nstructions using a
I the res- lung pa renc hyma with changes most marked in re- thresho ld for inspiratory studies of approximately
llmonary gions of maximal perfusion (i. e. the basa l zo nes). -900 Houn sfi eld units. This method ha s bee n reported
the sec- Cli nical presentation is most common in the fourth as show ing good corre lation with pulmonary func tion
2 ). HRCT decade of life. HRCT shows pan lobular low attenua- tests (Mergo e t al. 1998).
n, some- tion wh ich persists on expiratory views (Fig. 4.6 ).
lese foci • Paraseptal emphysema, a form of bullous e m physe ma
ifferenri- w ith a fam ilial tende ncy, is cha racterized by sub-
and the ple ural bullae (Fig. 4.7 ). It usually is asymptomatic
4.4,4.5). unless co mplicated by a spontaneous pneum othorax.
114 4 Chronic Obstructive Pulmonary Disease and Diseases of the Airways
a
Fig.,
Fig.4.6 Panlobular emphysema. HRCT image through the lower Fig.4.7 Paraseptal emphysema. righ1
zones shows panlobular emphysema with diffuse decreased lu ng
attenuation particu larly in the lef t lower lobe.
Other Forms of Emphysema
togethe r w ith bro nchi al narrow ing may lead to areas of

pulmonary hype rinflatio n. The most common causes of
Cicatricial Emphysema cicatri cial e mphyse ma a re fibrocirrhoti c tu be rculosis
and progre ss ive ma ss ive fi brosis in pneum oco niosis.
Cicatricial or "scar" emphyse ma is see n w hen areas of The chest rad iograph shows coarse reticula r shadow-
developing fibrosis retract and ca use di stortion of sur- ing, vascular di stortio n, and foci of increased lucency
rounding pulmonary pa renchyma. These retractile forces (Fig. 4.8).
Fig.4 .8 Cicatricial emphysema in a patient

with healed pulmonary tuberculosis and fi-
brothorax. Note the left upper lobe hernia-
tion and the absence of vascular markings in
the right lower lone.
Fig. ,
Bu
Bull
l en
Jargl
up t
nize
solit
The.
grei
lung
folic
grac
as Ie
crea
Other Forms of Emphysema 115
a b
Fig . 4.9a, b Localized bul lous emphysema . Axia l CT image and coronal reformat show change involving the posterior segment of the
right up per lobe.
o areas of
causes of
oerculosis
niosis.
r shadow-
d lucency
a patient
is and fi-
e hernia-
narkings in
Fig.4.10 Bullous emphysema. Fig.4. 11 larg e emphysematous bulla in the left lower lobe.
Bullae may beco me more vis ible on expirato ry views as

Bullous Emphysema they do not empty on expiration. cr will show the exact
vo lume of the bulla, defin e its relationship to surround -
Bullae are defined as air-contai ning spaces greater than ing structures, and demonstrate the extent and severity
1 em in diameter. but they may reach a co nsiderably of surrounding emphysematous change (Fig. 4. 11 ).
larger size (Muller and Fraser 2001 ). Giant bullae occupy
up to one-thi rd of tota l lung volume and may be recog-
nized by their space-occupying effect. Bullae may be
solitary or, whe n multiple, tend to occu r in clusters.
Compensatory Emphysema
Their predilection for the upper lobes may be due to
greater gravitational stres ses in that region. "Vanishing Compensatory emp hysema occurs as a physiologic re-
lung" is a form of bullous emphysema w hich deve lops sponse to adjace nt volume loss whether it is due to lobar
following recurrent episodes of bronchiti s and it may ate lectasis or lobectomy.
gradua lly lead to lobar or lung destru ctio n. Bullae appear The chest radiograph shows hyperlu ce nt areas with
as local, we ll-circumscribed, thin-walled lesions of in- attenuated vascu lar markings. There may be associated
creased lucency and absent vascularity (Figs. 4.9. 4.10). di splacement of interlobar fissu res and hil ar structures.
Chronic Bronchitis B
Chronic bronchitis is defined as increased sputum pro- bronchial and perivascular fibrosis (M Uller and Fraser B
duction for at least 3 months in each of two consecutive 2001 ). b
years. It therefore is a clinical diagnosis, but imaging is • Tramlines are parallel lines spaced approximately il
important in detection of coexisting conditions such as 3 mm apart. They probably represent bronchial wall s'
emphysema and bronchiectasis. thickening and are seen most clearly in the right d
paracardiac lung.
• Thick-walled ring shadows at the superior poles of the
• Pathology hila. These represent the anterior and posterior
segmental bronchi of the upper lobe. r
The mucus-secreting glands of the bronchial mucosa are • Transient. functional tracheal narrowing. Fluoroscopy
hypertrophied, hype rplastic, and secrete very viscous shows partial collapse of the tracheal lumen on
mucus. Inflammatory change is evident in both the forced expiration, coughing, or sniffing. Th is is at-
bronchial wall and surrounding peribronchial connec- tributed to inflammatory weaken ing of the tracheal
tive tissue. Severe bronchitis is associated with airway wall together with increased transmural pressure.
E
obstruction and development of emphysema. Eve ntually, this may lead to a fixed stenosis and a
f
saber-sheath trachea (coronal narrowing and sagittal
widening of the intrathoracic trachea, in w hich the
• Clinical Features ratio of coronal to sagittal dimensions is less than
0.6 ), The cervical trachea is not affected.
Clinical manifestations include dyspnea and cough pro-
ductive of mucoid sputum. Characteristically, an ob- HRa may show bronchial wall thickening, the presence
stru ctive pattern is seen on pulmonary function tests. of concomitant emp hyse ma, supe rimposed infective
consolidation, or development of bronchial neoplasia.
Ventilation-perfusion scin tigraphy shows nonhomo-
• Radiologic Findings geneous tracer di stribution due to ventilation-perfusion
mismatch. Inhaled radionuclide aerosols show delayed
The chest radiograph may be normal or may show the clearance from the airways due to destruction of the mu-
following changes (Fig. 4.12 ): cociliary escalator.
• Increased lung markings throughout both lungs. This
"dirty-chest" pattern is believed to be due to peri-
Radiography
jG
ronChograPhY
Spicules
'L- Mild generalized

~ ~ dilatation
- Jf\.~ Abruptcal;berchanges
Tramlines Scintigraphy
MDirty chest~
Ventilation-perfusion
mismatch
Fig.4.12 Chronic bronchitis: nonspecific radiographic features.

Bro nchiectasis 117
Bronchiectasis
and Fraser Bro nchiectasis refers to an irreversible dilatation of the Table 4.1 Etiologic classification of bronchiectasis (modified
bro nchial tree. Changes may be locali zed or widespread from Huzly 1973b)
'oximately in distribution. Bronchiectasis is associated w ith an ob- Congenital bronchiectasis
\Chial wa\l structive pattern on pul monary functio n tests and pre- • Bronchiectatic honeycomb lung : a dysgenetic anomaly in
the right disposes to recurrent episodes of bronchop neumon ia. which numerous dilated bronchi terminate blind ly in
fibrous tissue.
• Mounier- Kuhn tracheobronchomegaly: cystic dilatation of
loles of the Goals of Diagnostic Imaging: the tracheobronchia l t ree, tracheal diameter greater t han
posterior To estab lish the diagnosis: HRCT has rep laced broncho- 3 em, wavy outlines of trachea and large bronchi (tracheal
gra phy as t he investigation of choice in suspected diverticulosis); famil ial incidence, related to Ehlers- Da nlos
uoroscopy bro nchi ectasis. syndrome (Fig. 4.13 ).
lumen on To identify the presence of associated small a irway I • Kartagener syndrome: autosomal recessive disorder
marked by triad of bronchiect asis, situs inversus, and
This is at- cha nge. ~
chronic sinusitis .
1e tracheal • Ciliary dyskinesia syndrome: autosomal recessive disorder
I pressure. Bro nchiectasis may be seconda ry to early chil dhood in-
marked by impaired mucociliary clearance. sperm im-
losis and a mot ility, and bronchiectasis; often combined with
fection. Other causes are listed in Table4. 1. Today, w ith Kartagener syndrome.
md sagittal pro mpt antibiotic therapy and the avai lability of vac- • Turpin syndrome: thoracic malformation syndrome
which the ci nes aga inst measles and w hooping co ugh, there has characterized by megaesophagus, tracheoesophageal
5 less tha n fistula, rib deformity, and bronchiectasis.
bee n a marke d decline in the inc idence of bronch iecta-
• Cystic fibrosis: congenital glandular disorder with viscous
sis. Other sources sugges t that the true incidence of secret ions leading to bronchiectasis, cystic pancreatic fi-
bro nchiectasis may have been und erestimated in the brosis, meconium ileus, and abnormal electrolyte levels in
le presence past w hen diagnos is was based on findi ngs at broncho- sweat and saliva (Wood 1997).
d infective graphy. HRCf ha s revealed increasing numbers of mi ld • Alpha l-antitryps in deficiency syndrome: like congenital
1eopiasia. immunodeficiencies, pred isposes to recurrent infl amma-
cases (Webb et al. 1992). The inc idence of severe symp- tions leading to bronchiectasis.
nonhomo- tomatic bro nchi ectasis, however, certai nly appears to be
n-perfus ion on t he decl ine. Primary bronchiectasis
ow de layed • These are acquired in early childhood an d usually are sec-
ondary to bronchiolitis.
1 of the mu-
Secondary bronchiectasis
• Pathology • Postobstructive bronch iectas is: caused by inflammatory
bronchial st rictures, a slow-growing bronchial tumor, or
Bro nchi ectasis most co mmo nly occurs in t he post- scarring of the lung parenchyma .
e robasal seg ments of the lower lobes. The Reid Class ifi- • Toxic bronchiectasis: toxic gas inha lation may incite a
bronchiolitis leading to secondary bronchiectasis.
cati on (1950) ident ifies :
Cylindrical Bronchiectasis
The bro nchi show cylin drical dilatati on most marked Saccular Bronchiectasis
fro m the 6-lOth bronchial generations. They reta in a
smooth co ntou r, and they terminate ab ruptly w here the In saccular or cystic bronch iectasis, bronchial divisio ns
sma\ler bronchi and bronchi oles become plugged with are greatly reduced in number w ith only 3-5 bronchial
mucus. The bro nch ial tree, however, has a structurally generations rema ini ng. Medi um -sized bronchi termi-
normal branching pattern dividi ng into 17-20 genera- nate in clusters of cysti c cavities whic h may extend to
tions. the pleural surface. Sacc ular bro nchi ectasis is found
most co mmonly in older pati ents and may be associated
Varicose Bronchiectasis with a degree of prox imal bro nchial stenosis. Ove r 50 %
of these patie nts have histological evidence of an as-
The bronchial lumen shows irregul ar dilatation w ith a sociated constrictive bronchioli tis. Hemoptysis may be
"beaded" wall contour. There are only 3-11 ge nerati ons due to eros ion of inflammatory granulation tissue in the
of pate nt ai rways w ith obli terati on of the more distal peripheral bronchi or dilatation of bronchial arteries and
airways. bro nchop ulmonary anasto moses.
•
Fea
div
wit
infl
va r
alsi
•
Fin
sP'
of
•
•
b (
Fig. 4. 13 a-d Mounier-Kuhn tracheobronchomegaly character-

ized by tracheomega ly and bronchiectasis. Fi
Bronchiectasis 119
• Clinical Features • Parallel line shadows (tramlines ) represent t hick-

walled, cylind rically dilated bronchi.
Features of bronchiectasis detected in asymptomatic in- • Cystic cavities 1-3 cm in diameter: These ring
dividuals may not be signifi ca nt. However, most pat ients shadows. usually in clusters, correspond to areas of
with significant abnormality suffer recurrent episodes of saccular bronchi ectasis. Fluid levels are due to mucus
infectio n with purulent sputum and hemoptysis. In ad- and purulent exudate lying dependently within these
va nced disease, severe dyspnea and finge r clubbing may foca l dilatations of the airways.
also be present. • Areas of nodular shadowing may reflect associated
cellular bronchiolitis (see p. 122 )
• Regions of increased pulmonary trans radiancy may re-
• Radiologic Findings fl ect air trapping and indicate an associated constric-
tive bronchi olitis.
Findings on the chest radiograph frequently are non-
specific. The following feature s. however, are suggestive High resolution /thin collimation CT may show:
of bro nchiectasis (Figs. 4.14 and 4.15 ): • Cylindrical bronchiectasis: Dilated bronchi running in
• Coarse linea r shadowing probably represents peri- the plane of section have roughly parallel wa lls.
bro nchial fibrosis. Those bronc hi running perpendicular to the plane of
• Crowding of linear markings may represent sub- section are seen as ri ng shadows (Figs. 4.16, 4.17,
segmental atelectasis. 4.18):
Radiographic finding s
Tramlines Shadowing due to Ring sha dows in Pneumonic consolidation

chronic bronchitis saccular bronchiect asis and mucous plugging
c Bronchographic findings
Cylindrical bronchiectasis Varicose bronchiectasis Saccular bronchiectasis
Iy character-
Fig.4. 14 Radiog raphic appearances of bronchiectasis.
120 4 Chronic Obstructive Pulmonary Disease and Diseases of the Ai rways
• Fig.4.1Sa. b Radiograph in Kartagener syndrome shows increased peripheral and basal linear shadowing. Bronchography showed
b
cylindrical and saccular bronchiectasis. Situs inversus is also present.
Fig. 4."
Fig.4.16 Cylindrical bronchiectasis. Note the ~sjgnet ring" signs Fig.4. 17 CT image in patient with cystic fibrosi s shows wide-
and areas of air trapping consistent with a degree of associated spread bronchiectasis and sma ll right-s ided anterior pneumo-
Mconstrictive bronchiolitis." thorax.
- There is bro nchi al wa ll thicken ing. • Mucus-filled bronchi. These are easily recognized
- Bronchia l cross-sectional diameter is greater than w hen the lumen is partially fl uid-fill ed and the a
t hat of t he accompany ing artery, thus producing characteristic air-fl uid level is present. Dilated Fig.4.1
the classic "signet ring" sign. bronch i that are co mpletely fill ed w ith mucus (muco-
- These di lated bro nchi fail to taper as they reach celes ) may occas ionally resemb le vascular structures.
the lung periphery. Diffe rentiation is usua lly aided by observing that
• Cystic and varicose bronchiectases: Bronchi ru nning in these bronchi are considerab ly dilated re lative to ad-
Rad io
the pl ane of section have a beaded contour ("string of jacent vessels. The presence of surrounding ai r-fill ed,
cysts"). In the perih ilar regions, bronchiectatic air- dilated, th ick-walled bro nchi may also be he lpful. If VentiI
ways are sometimes crowded together due to adja- diagnostic difficulty persists. the n contrast-enhanced (parti.
cent pul mo nary atelectasis. On axial cr sections, th is images may be useful. due t(
gives rise to the so-called "bunch of grapes" pattern • Features of associated "sma ll airway" disease/bronchi- the co
(Figs. 4.19.4.20). olitis (see p. 122). iary e,
Bronchiectasis 121
b
.hy showed
Fig.4.18 Cylindrical bronchiectasis. Fig.4 .20 Saccular bronchiectasis.
lr pneuma-
ecognized
I and the a b
t. Dilated Fig. 4. 19 a, b Varicose bronchiectasis with bronchia l wall thickening and ~varicose" dilatation.
:us (muco-
5tructures.
rving that
rive to ad-
Rad ionuclide Scintigraphy
~ air-filled,
helpful. If Ventil ation sc intigraphy shows rad iolabeled aerosol
-en hanced (particle size 2 ~m) accu mul ating in the central bronchi
due to turbulence in the dilated airways. Clearance of
;e/bronchi- the collected particles from the airways via the mucocil-
iary escalator is delayed as the cilia have been destroyed.
Bronchiolitis-Small Airway Disease c.

Co
The current classification of bronchioliti s/s mall airway th.
disease includes:
Cellular Bronchiolitis na
• Cellular bronchiolitis bn
Wi
• Organizing pneumonia lal so known as bronchiolitis Cellular bronchioliti s comprises inflammatory ce ll s in
obliterans organizing pneumonia (BOOP) and crypto- the walls of the airways and exudate in the lumen. Th e
genic organizing pneumonia (COP)I commonest cause is acute infectious bronchiolitis. Thi s is
ve
• Constrictive bron chiolitis. seen most commonly in young children. Causative or-
(51
ganisms include respiratory sy ncytial virus (R5V ), ade- on
noviru s, and mycoplasma and this entity usually re- ca
solves without sequelae. Cellular bronchioliti s is bo
frequ ently seen in association with bronchial diseases gr
reo
and particularly with bronchiectasis. Other causes of
W'
cellular bronchiolitis include e ndobronchial spread of
tubercu losis (see p.303) and Japanese diffuse pan- th
bron chiolitis.
ca
The chest radiograph may show areas of nodular ea
shadowing. HRCT features include centrilobul ar nodules
and ce ntrilobular branching linear structures (the so-
called "tree-in-bud" appearance, Fig. 4.21 ).
Fig.4.21 Cellular bronchiolitis: HRCT image th rough the lower

zones shows bronchiectasis with centrilobular change consistent
with an associated cellu lar bronchiolitis.
Fig. 4.22 a-c Postinfectious bronchiolitis (a-c). Initial chest

rad iograph (a) shows bilateral pulmona ry consolidation more ex-
tensive on the right side. Patient represented some weeks later
with progressive dyspnea. Further ra diograph (b) shows resolu-
tion of consolidation but pulmonary hypertransradiancy on the c
right side. HRCT shows mosaic pattern of lung attenuation con- Fi
c sistent with air trapping (c). 10
Bronchiolitis-S mall Airways Disease 123
HRcr very occasionally may show "direct signs" of

Constrictive Bronchiolitis ce ntrilobular cha nge. However, "ind irect" signs are
much more freque nt and include (Figs. 4. 22.4.23 ):
Constrictive bronchiolitis is the pathologic correlate of • Mosaic lung attenuation on inspirati on
the clinical e ntity "bronchioli tis oblite ran s." Constrictive • Air trapping in expi ration
narrowing of the bronchioles by submu cosal a nd peri- • Associated ce ntral bronchial dilatation
bronchiolar fibrosis is seen and this leads to chronic air-
'ells in way obstruction.
This entity may be idiopathic or represe nt the irre-
,n. The
ve rsible sequel of childhood vira l/myco plasma infection
Swyer-james-Macleod Syndrome
This is
ive or- (see Swyer- james-Mcleod sy ndrom e). It may be sec-
). ade- ondary to toxic fume inhalation and is see n as a co mpli - This entity is believed to represent a variant of postinfec-
lly re- cation of both bone marrow and lung tran splantation. In tiou s constrictive bronchiolitis.
itis is bone marrow transplantation, it is a manifestati on of The chest radiograph may show unilateral hyperlu-
iseases graft-vs.- host di sease w hereas in lung tran splantation, it cency w ith attenuated vascu lar markings. The affected
.ses of reflects chronic rejection. There is also an association lung is small on inspiration but does not deflate nor-
ead of with rheumatoid arthritis and in the past pen icillam ine mally on expiration (air trapping. Fig. 4.24).
~ pan-
therapy has been implicated in its development. It is oc- Radionuclide imaging shows diminished pe rfu sion in
casio nally see n in the setting of inflam matory bowel di s- the affected lung.
odular ease (Ma hadeva et al. 2000).
odules
:he so-
~I chest
nore ex-
~ks later
5 resolu-
y on the d
ion con- Fig. 4. 23 a-d Cystic fibrosis. Dilated bronchial lum ina are partially filled with mucus. The mosaic pattern of lung attenuation in the
lower zones probably reflects air trapping.
Fig.4.24a, b Swyer- James-Macleod syndrome. Frontal radio-

graph (a ) shows a hypertran sradian t left lung with decreased
vascular markings. The perfusion study (b) shows absence of
radionuclide uptake in the affected lung. These changes had been
a known to exist for more than 30 years in this 42-year-old man.
High-resolution Cf: HRCf findings in Swye r-James-

Macleod syndrome have been described (Marti-Bonmati
1989. Moore et al. 1992) and include areas of decreased
attenuation. Changes may be unilateral. although, more
frequently, bilateral abnormalities are evident. These
tend to be patchy in distribution, giving a mosaic pat-
tern. Regions of low attenuation are interspersed with
areas of normal lung. Air trapping is seen on expiratory
images (Wilson 1995. Fig. 4.25a. b).
Associated bronchiectasis, central in distribution,
may be present.
•
Organizing Pneumonia/Cryptogenic
Organizing Pneumonia Bf
• (also known as Bronchiolitis
Obliterans Organizing Pneumonia)
Bri
Organizing pneumonia or cryptogenic organizing pneu- th.
monia represents an organizing pneumonia and a "pro- PS!
liferative" bronchiolitis. Pathologically. the bronchiolitis ve:
is characterized by epithelia l denudation with prolifera- lat
tion of granulation tissue polyps that contain charac-
teristic Masson inclusion bodies. This entity was also ch
known as BOOP. but rece ntly the re has been a tendency ha'
to abandon this term as it potentially may cause confu- co:
sion w ith the clinical entity of bronchiolitis ob literans 48
(see Constrictive Bronchiolitis. p. 123 ). pa
HRCf shows areas of consol ida tion and ground-glass an
b opacification in a peripheral subpleural distribution
Fig. 4.25a, b HRCT: Swyer- Jam es-Macleod synd rome. cr (Fig. 4. 26 ). The differential diagno sis includes infection. wi
image acquired in inspiration (a) shows mosaic pattern; areas of chronic eosinophilic pneumonia, bronchio loalveolar cell tio
low attenuation are interspersed with areas of normal lu ng. Cen- carcinoma, and pulmonary lymphoma. Occasionally the (LJ
tral bronchiectasis is also present. Image acquired in expiration "bronchiola r component" is visib le radiologically and
(b) shows air trapping.
this is characterized by small centrilobu lar nodules. wi
Bronchial Asthma 125
ltal radio-
decreased
bsence of
5 had been
old man.
r-James-
-Bonmati
ecreased
gh. more
1t. These
tsaic pat-
sed with
'<piratory _ _.... b
:ribution. Fig.4 .26a, b Organizing pneumonia (BOOP). HRCT images

through the lower zones show areas of ground glass opacification
a h and consolidation in a peripheral subpleural distribution.
genic
Bronchial Asthma
,nia)
Bronchial asthma is characterized by hyperreactivity of suspected in asthmatic patients (see Fig. 3.33) or to de-
ng pneu- the airways to a variety of all ergic. infectious, toxic. and tect emphyse ma in smokers w ith asthma. It may also be
d a "pro- psychic stimuli. There is airway inflammation and re- performed to exclude entities such as hype rsensitivity
nchiolitis versible obstruction, the la tte r responding to bronchodi- pneumonitis which may mimic asthma.
prolifera- lator therapy. The true prevalence of bronchiectasis in patients with
1 charac- Up to 75 % of all asthmatic patien ts have a normal ch ronic uncomplicated asthma remain s unclea r (Lynch
was al so chest radiograph (Simon and Pride 1973). Other studies 1998 ). Mild e levations in bronchoarterial ratio may be
tendency have described bronchi al wa ll thickening as the most seen in patients with asthm a but may be due to hypoxic
se confu- common plain radiogra phic findin g. being prese nt in vasoconstriction in areas of air trapping rather tha n tru e
lbliterans 48 % (Paga nin et al. 1992 ) to 71 % (Lyn ch et al. 1993 ) of bronchial dilatation. Bronchial wa ll thickening is seen in
patients. However, th is is a re latively nonspecific finding 16- 92 % of patients (Gre ni er et al. 1996. Paga nin et al.
Jnd-glass and may al so be seen in bronchitis. 1992 ) and probably reflects a combination of submu-
;tributi on Pulmonary hyperinflation may be seen in patients cosal thickening due to inflammation. thickening of the
infection. w ith asthma but it is unu sual to see marked hyperinfla- muscularis mucosae due to mu scle hype rtro phy and
'eolar cell tion in patients who do not have co-existing em physema peribronchial fibrosis. Mucoid impaction and decreased
mally the (Lynch 1998). lung attenuation may also be see n.
:ally and HRCf may be performed to detect bronchiectasis
jules. when ABPA (allergic bronchopulmonary aspergillosis ) is
126
5 Inhalational Lung Diseases and Pneumoconioses
Foreign Body Aspiration
Foreign body aspiration is typically seen in early chi ld- • Radiologic Findings
hood. Much less frequently. adu lts may inhale tooth
fragments or dental fillings. Aspirated foreign bodies • Chest Radiograph
usually pass down the right main bronchus. w hi ch has a
more vertical orientation than the left main bronchus. Radiopaque foreign bodies such as co ins, marbles, and
Radiographic features may indicate the prese nce and ID- teeth are visi ble on standard radiogra phs. Indi rect signs Fi
eation of the foreign body (Figs. 5.1.5.2). Th is can then indicating the presence of a nonopaque foreign body in-
be confirmed and removed at bronchoscopy or com- clude: (Figs. 5.3 and 5.4):
puted tomography (eT) may be performed prior to bron- • Unilateral pulmonary lu cency: This results from hy-
choscopy. perinflation due to a check-valve obstruction and
from reflex oligemia due to hypove ntilation.
• Mediastinal silift: Air trapp ing in the affected lung
• Clinical Features leads to mediastinal shift to the contralateral side in
expiration and a return to its normal position in in-
Aspiration material leads to tracheal /bronchial irritation sp iration.
with symptoms of cough and dyspnea. If the foreign • Lobar atelectasis and distal pneumonia develop when
body is not detected promptly, it becomes su rrounded bronchial obstruction persists for at least several
by fibrous tiss ue and patients then may be asympto- hours.
matic or have minimal symptoms for many yea rs.
a
Fi~
ph
H.
th
w:
Fig. 5.1 Swallowed and aspirated teeth. Fig.5.2 Aspirated pin.

Foreig n Body Aspiration 127
- Mediastinal shift
- Unilateral pulmonary lucency - Atelectasis
(poststenotic hyperinflation) - Recurrent bouts of pneumonia
- Only 10%of foreig n bodies are visible - Bronchiectasis
". and
t signs Fig.5.3 Foreign body aspiration.
ldy in-
1m hy-
m and
d lung
sid e in
Iin in-
I when
;everal
• Fig. S.4a. b Check-va lve obstruction in foreign body aspiration (a) with co ntralateral shift of the mediasti num to the right side in ex-
b
piration (b).
Computed Tomography
seen in cases of check-valve obstruction or atelectasis,
Helical cr w ill freque ntly all ow direct visuali zation of and pneumo nic consolidation may be prese nt if the in-
the fore ign body w ithin the airway. Regio nal air trapping ha led body leads to a high-g rade obstructi on.
within the lung di stal to the endobro nchial body may be
128 5 Inhalationallung Diseases and Pneumoconioses
Pneumoconiosis
socia ted w ith an increased risk of developing both

• Pathology and International Labor Office
bronch ial ca rci noma and mesothe li oma.
(ILO) Classification
Pneumoconioses are recognized as occupational dis-
eases if a pro bable li nk betwee n the occupation a nd t he
The pneumoco nioses are a gro up of lung diseases ca used
illness can be established. Thi s "probability" is based on
by inh alation of inorga ni c or orga nic d ust of ani mal or
the hi sto ry of expos ure. abnorm al pulmonary function
plant o rigin. Typica lly, chro nic environmental or domes-
tests. and appropriate fi ndi ngs o n imaging studi es. Lung
tic expos ure leads to disease afte r a variable nu mber of
biopsy is rarely necessa ry.
yea rs. Minute dust pa rticl es up to a max imum diameter
of 10 ~ m reach the alveoli d uring inspiration. There they
Goa ls of Diagnostic Imaging:
are phagocytosed by macro phages and are deposi ted in
Detectio n of pneumocon ios is i n "at- risk" i ndividuals.
the lung pare nchyma. La rger pa rticles are retai ned in the
Eva luation of the extent and severity of change and
uppe r respi ra tory trac t and are clea red by the mucocili-
particularly the presence of pu lmo nary fi bros is.
ary escalator.
Detectio n of complications including SilicotubercU I0
: iS j
In simple pneumoconi osis, the in haled d ust particles
and developmen t of neoplas ia.
do not cause a reaction in the pulmonary pa renchyma.
Foreign body reactions, however, are freq uent and res ult
in eve ntual fi brosis. Dust particles may a lso bind w ith The In te rnati onal Labor Office has es tablished sta ndard-
endogeno us protei ns: thi s co mplex then acts as an an- ized criteria for t he classification of pne umoconi oses
tigen and the resulting allergic infla mmatory response based on t he catego rization of pulmonary opaci ties on
may also progress to pulmonary fi brosis. Pare nchyma l the posteroanterior (PA) chest radi ograph (ILO 2000):
fib rosis is characterized by cicatricial emp hyse ma and a • Shape and size of individual opacities: Small round
restrictive pattern on pulmona ry function tests. An ac- o pacities are classified by size as p, q, or r. Small ir-
co mpanying chro nic bro nchitis is freq uent and resul ts in regul ar opacit ies are class ified as s, t, or u (fine, me-
a degree of obstructive ventilatory im pairme nt. In add i- dium , or coarse). Opacities grea ter t han 1 cm in
tio n, certain types of dust ca use specifi c types ofl ung indi ameter are categorized as A, B, or C on the bas is of
jury. Fo r exa mple, sili cosis may be associated with t heir combined diamete rs (Fig. 5.5 and Table 5. 1).
tuberc ul ous reactivation and asbestos exposure is as-
Table 5. 1 Pneumoconioses due to inorganic dusts (from Mathys 2001)
Syndrome Source of antigen Effects
Progressive pneumoconiosis due to silica-containing dust s, with relatively severe fibrosis:

Talcosis Chalk (magnesium, silicate), industriallu- 1. Changes similar to asbestosis but with sparing of the apices and
bricants, rubber products. Inhalation of costophrenic angles. 2. Confluence of nodules to give PMF-type
pure talc, talc in association with silica appearance. 3. Hilar lymph node enlargement .
(talcosiliosis), and talc in association with
asbestos fibers (talcoasbestosis).
Kaolinosis Aluminum silicate, porcelain, and Fibrosis due to the presence of quartz dust in kaolin.
(kaolin lung) ceramic industries.
Persistent pneumoconioses due to quartz-free dusts. with mild fibrosis:
Anthracosis Coal dust. coal mining, heaters. No cli nical effects or radiographic changes; black lungs seen at au-
topsy.
Siderosis Iron oxide, arc welders. silver polishers. Inert depOSits producing sma ll opacities. Nodular opacification
iron mining. characteristically involving the midzones and reversible on cessa-
tion of exposure. Silicosiderosis: pulmonary fibrosis.
Bauxite lung Alum inu m manufact uring, smelting of Emphysema and pulmonary fibrosis.
aluminum ore to produce corundum.
Aluminum Manufacture of explosives. Fine reticular and focal opacities. spontaneous pneumothorax.
lung
Berylliosis Aircraft manufacturi ng . Only 2 % of exposed workers develop berylliosis; acute form
manifest as alveolitis, chronic form is associated with generalized
granulomatous disease similar to sarcoidosis.
Hard-metal Tungsten, carbide, cobalt. titanium, Spectrum of change from bronchitis and bronchiolitis through to
lung disease vanadium. antimony. t in, steel tool subacute fibrosing alveolitis and giant cell interstitial pneumonia.
manufacturing.
p
Pneumoconiosis 129
r Sectio.--n_4___________ ___________--, Date of radiograph --,
~::: (:i:~::t;"mb" 1 1CD·CD ·1111I

Day Month Year
h Radiographic findings based on 2000 ILO Classification
;-
Radiographic quality D+ D! D! Du Dr D Lateral view available
Small opacities Profusion Zones Symbols

Ie 0 01' D '" D '" D y, DRU D LU
, ,
Rounded shape
D D r,
n
D y,
Size p
D DD
0 010 D '" D '" D RM D LM
n D"
,g 0 011 0 112 D ,/0 D 01- D RL D LL D hi
D at D ho
D w- D D '" D 01' DRU D LU
Irregular shape
, , '" D sx D id
D y,
at Size
...,
<
D DD"
0 010 D '" D '" D RM D LM
0 0/1 D 1/2
0 2/3
D Ol- D RL D LL D bu D ih
Mixed shapes
0 0/. 0 1/0 0 211 0 312 DRU D LU D ca D k!
J DO 0
D Ol,
010 0
0
Size
1/ 1
1/2
DA
D
0
212
213
0
0
313
31 +
DRM
D RL
D RU
D LM
D LL
D LU
D og
D '"
D me
D od
D co D pa
J- Large opacities o None DB D RM D LM D op D pb
DC D RL D LL D pi
D cv
Blunting of
costophrenic angle o None Side R D 'D D di D px
Id Wideninglthicknessl<3 mmlen face wideninglthickness/<3 mm/en face
r- Pleural thickening " D ' D' D D
,D' D' D D D RU D LU
D er D ..
D em D ,p
In
Diffuse
Lateral chest wall o None D' D' D' D' DRM D LM
,
~ D' D' DRL DLL D es Dtb
)f D' D'
•
~ ,
Wideninglthickness1<3 mmlen face wideninglthicllnessJ<3 mmlen face
R Site
Pleural thickening D' D' D D D' D' D D
Circumscribed
(plaque)
o None D' D' D' D' Diaphragm AD ' D
D' D' D' D' Chest wall D D
Pleural calcification Diaphragm "D ' D
o None "D 'D ChestwaJl D D
Ott", D D
Interpretation of occupational disease*)
o No evidence of notifiable disease
Definite evidence of not ifiable disease··j D Other abnonnalities
D Silicosis
D Asbestosis D Asbestos·induced laryngeal cancer
D Silicotuberculosis o ~ Asbestos-induced pleural disease

D Pleural or peritoneal mesothelioma
Lung cancer in a paUent with
D known Quartz dust-associated lung disease D Asbestos-induced lung C3llcer D Disease caused by ionizing radiation
Cause of occ u pational disease, additional findings, recommendations and/or obligatory measures (please print)
I
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I
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Fig.5. s
3683198456 •• ) Please oolify the Insurance carrier and the insured.
Radiogra phic interpretation form based on the ILO Classificat ion (see pp. 131-134 for coding and symbols).
--'
130 5 Inhalational Lung Diseases and Pneumoconioses
• Profusion of lesions in the pulmonary parenchyma Formal disability assessment by a specially trained
(number of small opacities per lung zone) is graded and approved physician is based strictly on use of stand-
on a scale of 0-3 (Fig. 5.5). ard reference radiographs, computer-interpretable data
• Reactive pleural, pericardiai, and hilar changes are de- sheets, and in some cases cr assessment. A simplified
scribed and coded. scheme based on overall impression of pulmonary in-
volvement has been adopted for clinical use. The pre·
The ILO provides three guidelines for interpreting radio- dominant type of opacity and the predominant grade of
grap hic findings: profusion are determined using the ILO verbal defi ni-
• Standard reference radiographs (e. g., Fig. 5.6). Classi- tions. For example. grade qq 2/2 refers to numerous
fication aided by standard refere nce radiographs round opaciti es. 1.5-3 mm in diameter. scattered
helps to minimize interobserver variability. throughout both lungs but not obscuring pulmonary
• Verbal definitions (see text pp. 131-134), vascular markings; qt 2{2 refers to the additional pre-
• Drawings and diagrams (Figs. 5.5- 5.9), These materi- sence of irregular opacities 1.5-3 mm in diameter. Thi s
als are the least reliable and should be used only to simplified scheme by definition precludes a detailed ac-
reinforce verbal descriptions and letter codes. count of all findings and, in particular, of regional varia-
ti ons in severity of change.
a b
PROFUSION SHAPE-$tU
I~o ••
:.td!oQ,..m,_c·"~·""~1
,.. o. ,.,.,..."'oc-... ,"O'USION
c
I ~ -~ (~) 3/ 3 u/ u
d
Fig. 5.6 Illustrative radiographs from the ILO reference series.
Pneumoconiosis 131
Fig. 5.7 Diagram ill ustrati ng pul mo na ry

opacity codes used in th e 'LO Classifica-
tion. RUZ = right upper zon e (see
pp. 131 -134, Fig. 2.10).
• •
qq • •
• •
qt
•
• •~
4- •
•
~
-I
tq 1-
't-,/
... .... •
tt f
"" :,'"
A
. +.+,
=1-5cm
B
' +-+
>5cm - up toRUZ
-
t
b
C
.+
Area>RUZ
Interpretive criteria (from Hering 2003 ) 3 Small irregu lar opacities: linear, reticular, or reti-
1 Radiograph quality: cu lonodula r opacities, w hich are classified accord ing
• + Good; to the ir widt h.
• +/- Acce ptable. with no technical defect li kely to • s smaller than 1.5 mm, fine, li near;
impa ir classificat ion of the rad iograph; • t 1.5-3 mm, mode rately coarse, still linear;
• +/-- Poor, with technical defects tha t lim it eval- • u 3-10 mm, coarse.
uation of the lung or pleura; 4 Profusion and location: Profusio n indicates the
• u Unreadable. degree of parenchyma l involvement relative to the
2 Small round opacities: well-defined nodular opaci- stan dard refe rence radiographs. It is described in
ties that are classified accord ing to the diameter of terms of the affected sid e an d one or more affected
the predominant type of opacity. lung zones, which are defined geometrically rathe r
• p smaller than 1.5 mm; than anatom ically. Profusion is classified on a four-
• q 1.5- 3 mm in diameter; point major category scale (from 0 to 3 ), with each
• r 3-10 mm in di amete r. major category d ivided into t hree pa rts, resulting in
d a 12-point scale:
132 5 Inhalational l ung Diseases and Pneumoconioses
Pleural abnormalities- Pleural ca lcification: Fig.s.8 Review of pleural opacity

(localized and diffuse pleural t hickeni ng): codes used in the 1980 ILO Classification
(see 6 below).
Chest wall
~I l xx
D
Exte nt: Width:

0"0 a-3-5m m
' - upto 1/ . b-S-10mm
2- 1/ 4-'12 c->lOmm
L::3_· ,->.:.'/.:'_-" L_ _ __"1 See Text! I Diaphrag m
x
Costophrenie angle: Other sites
I _____--.,J !I : \
• a
-0
0/- a/a 0/1

-0
* • B: One or more opacities larger than in category

• 1 1/0 1/ 1 1/2 A but whose combined diamete r does not
• 2 2/1 2/2 2/3 exceed the equiva lent of the right up per zone.
• 3 3/2 3/3 3/+ • C: One or more opacities larger t han Band
Examples: A rad iograph that definitely fits category whose combi ned diameters exceed the equiv-
2 whe n compared with ISO refe rence No.2 is alent area of the right upper zone.
class ified as 2/2. A study classified as 2/1 closely re- 6 Pleural th ickening: Pleural thickening is class ified as
sembles the No.2 refe rence rad iograph but category localized (p laque) or diffu se and both categories
1 was also considered in classify ing the radiograph. may coexist (Fig. 5.9). Each side is classified sepa-
This scheme ean be applied to the remai ning cate- rately.
gories in the same way. The pleura l width or plaque thickness is measured
La rge opacities: Thi s term is limi ted to opacities that from the inner ma rgin of t he chest wa ll to the sharp
are cons iste nt with pneumocon ios is. margin of the pleura/lung interface (a-c). Concomi-
• A: Thi s is a single opacity larger than 1 em but no tant or exclu sive "e n-face" pleural thickening is re-
more than 5 cm in diameter or mu ltiple opaci corded as be ing present (Y) 0 1' absent (N); its width
ties la rger than 1 em indiv idually but that do cannot be measured.
not exceed a total combined diameter of 5 cm.
Pneumoconiosis 133
Fig.5.9 Coding symbols used in the ILO
uiJ {j~
cation Classification (for key to symbols, see
aa di me
o\} 7 below).
at
o~~ ef
8~ pa
wlJ
ax
M...
. .
{'...
':. :
em
O~ pb
O~
bu
O~ es
~
:". ;." '. '
pi
tJ ~
ca
Cj ~ fr
~~ px
~~
cg
el i ~
hi
G~ ra
a~
en
~"'"
:'.:
.. :it ho
~ rp
G}(f
it
O~ O~ l8~
:. , ..
co id tb ~ .~
cp
G~ ih
O~ od
g~
cv
~~ kl
O~ od
CJ.\j
:ory • a 3-5 mm the right (R) or left (L) side and are reported as
• b 5-10mm being present (Y) or absent (N).
:one. • c >10mm The side and extent of pleural calcifications are re-
The maximum longitudinal extent of pleural thick- ported separately for each side, and their location is
luiv- ening is based on the chest wall length for Rand L categorized as chest wall, diaphragm, or "other"
from the lung apex to the costophrenic angle. This is (med iastinal and pericardial pleura):
;:od as determined individually for diffuse thickening or as • lOne or more calcifications with a tota l com-
the combined en-face or in-profile lengths of pleural bined length < 2 em.
plaques: • 2 One or more calcifications with a total com-
• 1 < 1/4 the total length from the apex to the co- bined length of 2-10 cm.
red stophrenic angle on one side. • 3 One or more ca lcifications with a tota l com-
;harp • 2 1/4 to 1/2 the total length from the apex to bined length> 10 cm.
)mi- the costophrenic angle on one side. 7 Symbols: obligatory. Thei r expansions should be in-
; re- • 3 > 1/2 the total length from the apex to the co- terpreted as if they were preceded by "suspected.
fidth stophrenic angle on one side. or "findings consistent with.
• Diaphragmatic plaques with obliteration of the • 0 None.
costophrenic angle are designated as being on • aa Atherosclerotic ao rta.
134 5 In halation a I lung Diseases and Pneumoconioses
• at Apical pleural th ickening. w hich provides a reproducible reference point. a nd

• ax Coalescence of sma ll opacities. ateq uidi stant leve ls above and below the carina us ing a
• bu Bulla, add itional info rmation on emphysema. 1- 2 mm slice thickness and two wi ndow setti ngs. such
• ca Lung cancer. as C/W = 50/400 and C/W = -500/1500 to 2000.
• cg Calcified granuloma. (2) Smooth, we ll-circumscribed rou nded opacities:
• en Calcification in small pneumoconiotic opaci- Well -defined nodula r opaciti es, which are coded ac-
ties. cord ing to the diameter of the predomi nant type:
• co Abnormality of cardiac size or shape. < 1.5 mm, al so termed micronodular (P); 1.5-3 mm (Q); I
• cp Cor pulmonale or pulmonary hypertens ion. and 3-10 mm (R). The predom inant size (P, Q, o r R) is
• cv Cavitation, liquefaction.
•
• ef
di Marked distortion of intratho ra cic structures.
Free pleural effu sion.
only ind icate d in the summation.
(3) Small, irregular. and/or linear opacities: Linear in-
terlobu lar septa l and intralobular no nseptal opacities
-
• em Emphysema. or a fo ca l centrilobular arrangeme nt in the acinus. Sub-
• es Eggs he ll calcification of hilar and/or med i- pleural curvili near lines represent a specific distribu-
asti nal lymph nodes. tion of intralobular structures. Parenchymal bands are
• fr Fractu red rib(s ). residual scars longer t ha n 2 em that are located in the
• hi En largement of hila r and/o r mediastinal peripheral lung and gene rally are in contact w ith t he
lymph nodes > 1.5- 2 em. pleura. If the images do not document conta ct w ith the
• ho Honeycomb lung. pleura. t he ba nds are classified as trans lobu lar.
• id III-defined diaphragmatic contour. (4) Other pa renchymal abnormal ities :
• ih III-defined ca rdiac co ntour. Inhomogeneous lung attenuation due to mosaic perfu-
• kl Ke rley lines (indicate in cases w ith a sus- s ion (MP) and gro und-glass opacifi cation (GGO ).
pected ca rdiac cause ). Honeycombing. Emphysema with a class ification of
• me Malignant mesothelioma of the pleura, peri - type (e. g., acinar, panlobula r. pa raseptal, or cicatricial )
cardium, or peritoneum. may be entered under Add iti onal Findings. Bullae are
• od Other significa nt di sease. des ignated by the symbol BU.
• pa Plate atelecta sis. (5) Large opac iti es:
• pb Parenchymal bands. Both pneumoco niotic and nonpneumoconiotic opacities
• pi Pleural thickening of a n interlobar fissure larger than 1 crn in diameter are coded. Distinct areas
(designate R/l side). of rounded atelectasis (RA) in contact w ith the pleura
•px Pneumothorax (a lso mark "er' if effusion is fall under the heading of viscera l- type pleural thicken-
also present ). ing combined w ith the sym bol RA.
• ra Rounded atelectasis. (6 ) Pleural abnormalities:
• rp Rheumatoid pneumoconiosis. Pleural changes may be parieta l o r visceral in type.
• tba Tuberculosis, active? Parietal change includes typical pleural pla ques. There
• tbu Tubercu los is, inactive? is no lowe r size limit; if pleural thicken ing is detectable
8 Comments: Comments may be added to t hi s sectio n by imaging, it shou ld be coded. "Viscera l" pleura l
to explain or descri be findings in greate r detail. The change described as "d iffuse pleural thickening," is
ILO Class ification by definition is based on the PA freq uently associated with subpleural fibrosi s. W hen
chest radiograph. Info rmation from othe r imaging this is identified. t hen additional info rmation should be
modalities ca n and s hould be reco rded in t hi s sec- give n on sma ll opacities and /or symbols should be
-
tion. added such as PB (parenchymal bands ) or RA. Changes
9 Conclusion: Fina lly, it is determined whethe r th ~ involvi ng the mediasti nal (M) and diaphragmatic (0 )
coded changes are consistent with an occupationa l pleura may also be coded. W = wall, M = mediastinum.
o r environmenta l cause of pulmonary d isea se. D = diaphragm.
(7) Symbols:
Symbo ls are an obligato ry emry and sho uld be inter-
preted as if they we re preceded by "suspected ... " o r
"find ings cons istent with ..." Capita l letters are used to
• a Classification
cr today plays an essential role in the diagnosis of

pneumocon ioses (Hering 2003 ). An in ternational work-
ing group has issued guid elin es for standardized classifi-
cation.
(8 ) Additional findings :
Find ings not covered in the interpretation form may be
added as descriptive e ntries.
:J
disting ui sh [hem from the symbol s in the ILO Class ifi -
cation of cr images (Fig. S.10):
Interpretive criteria.
( I ) Image qua lity:
Image quality is graded on a scale from 1 (good ) to 4
(unreadable ). The number of images may be limited in
screening and/or follow-up exami nations. If the study
is limi ted to six reference slices. they shou ld be ac-
Fj~
quired in the prone position: at the leve l of the cari na,
Pneumoconio sis 135
d CT classification
:;ing a Name,SSN CT number, date Quality Position
such Number of slices Ima in technique kV 1 Prone
Slice thickness Sin Ie-slice s iral mA 2 Supine
Window Mullislice Spiral seo 3
s: setting
!C- 4
CT finding 2001
n(QI:
II is
I.__ I~~~~~~~~~~J~~~~~~~~~~~~~~~~~~~~~~~'
I
I Is the radiograph negative? J No Yes I Symbols I
'
I -0--II
r in- rI M tf t Zones/Profusion I AX II
§
os requen
ties I NoYes size R L I I
.. Sub- I p - < 1.5 mm U 0 2 3 0 2 3 I BE I
bu- J Rounded opacities Q=1.5-3mm ,. M 0 2 3 0 2 3 I BR I
I (sharply circ umscribed) R'" > 3 -10 mm -,.,-- L 0 2 3 0 2 3 I I
s are jlNo l Yes l I IBu r
I the
the
I1___________________________________ _ _ _ ___ _ Total I
~~o~ _ _ _ J
CA o II
th the r---- - ---- -------------------------- - - - - --------- 00 I
! I I
Most frequent Zones / Profusion
I
lerfu-
I
I Irregular and/or
I linear opacities
Intralobular
Interlobular
No Yes _____ type
El u
M
0
9
R
2
2
3
3
0
0
L
2
2
J
3
I
I
cv
DI
I
II
IINO I Yesl L a 230 23

I DO I
I
of 1 EF I
I
'kia]) ~ 1_ __ _______________________________________ ~~ion_ _ _ _ JI
I: D- ES I
. are 3 r------ - ---------------- 'r- - - - -
I Nonhomogeneous 1II u 0 R2 3 0 L2 3 FP I
Ground glass FR
I opacity II M 0 2 J 0 2 J I
lacities
Ifeas
I I No
I
I Yes II
II
I Nein I Ja I L 0 2 J a 2 J I
I
HI I
leura I II DTotai I ME I
icken- '- ______________________ JL ____________ ___ __ ~f~ioo __ _ _ J MP I
r----- lr------------- - - ---- -- - ~
I
I Honeycombing U 0
R
2 3 0
L
2 J
II
II Emphysema u 0 1
R
2 J 0 1
liDO
2 J I PB II
>e. I M 0 2 3 0 2 3 II M 0 2 3 0 2 J I I
There II No I Yes I L 0 2 J a 2 3 II I Nein I Ja I L 0 2 3 a 2 J I RA I
I II I SC I
ectable
I
is
t__ ________ _ _____
r -- ------ - -------------- - ,I - - ------- -------------~
9l;~ ___ J:_______________g~u~~ ___: lB
ill
I
I
hen I Large ~L II I ___ J
wid be I opacities ~ u II Most frequent parenchymal finding I
)e :I No I Yes tfj ~ II I RO I IR I GG I He I EM I LO :
langes I II I
:(01
tinurn, rI No Yes
Most frequent
type
i :~""':~al;,;es W ~:~::, : : ~:=:§ ~RL Extent, thi~kness l

nter- ~ II NolYeslM ._. ____ M 0 2 3 0 2 3
," or -~ I _ ____ _____
~
0 _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _L_ _ _ _ _ _ _ _ _O
_ _a
_ b
_ _c_ _ Oa b
___ _ c
__ _lJ
lsed to 0.
r --- - --- -- -- ------ --- ---- ---- - --- - -- - ---- - - - - - - ----- ~
assifi- I Pleu.r~1 . Site I
I calCifications Iw I M I D I I
II I y~ I ______ _ __ ___ 1
ma: J No
Comments, summary
Date, Signature ,
I Date ISignature
Fig . 5.10 CT interpretation form based on the ILO Classification.
Pneumoconioses Due to Inorganic Dusts

Tt
fu
poxemia probably results from vent ilation-perfusion m
Silicosis mismatch. •
Individuals exposed to quartz dust are at significantly
Silicosis develops after prolonged exposure to quartz highe r risk for developing tuberculosis (silicotuberculo-
dust, usually over a period of10- 20 years. It primarily af- sis).ln men with silicosis, the relative risk has been esti-
fects sandblasters, miners of quartz-rich stone, and mated as 2.8 (Cowie 1994). The incide nce of ca rcinoma •
workers in the polishing, ceramic, and porcelain in- also ap pears to be increased and there are cases in which
du stries. Pulmonary fibrosis develops as a result of both bronchial ca rcinom a has been recogn ized as an occu-
foreign body reaction and hyperse nsitivity-type allergic pational disease in German workers' compensation pro-
response. Changes may progress even when exposu re ceedings. Very rigorous criteria are applied in these
has been discontinued. cases including close proximity of the ca rcinoma to the •
fibrosis, profusion grea ter than category 1/1 or "large
opacities."
• Pathology
Inhaled dust particles reach the alveo li, are phagocy- • Radiologic Findings
tosed by macrophages, and transported to the inter-
stiti um. Here the phagocytosed particles act as a nidus Plain Chest Radiograph
for further aggregation of macrophages and fibroblasts,
and a nodule of concentrically arranged collagen fibers Radiographic changes in silicosis may be classified into
develops. These silicotic nodules may coalesce and oc- four types although mixed patterns are common
cupy an entire seco ndary lobule and appear rad iographi- (Fig.5.ll,5.l2):
cally as round opacities. Associated interlobular and in- • Nodu les: Multiple, homogeneous, we ll-defined nod-
tralobular septal fibrosis produces reticular shadowing ules 1- 10 mm in di ameter may produce a "snow-
and thickened intra- and interlobular septal lines on the storm" appea rance in the uppe r and mid zones.
chest radiograph. Finally, the nodul es may coalesce to Nod ular calcification occurs in 20 % of cases
form large conglomerate fibrotic masses (progress ive (Fig.5.13. ).
massive fibrosis). • Diffuse fibrosis: Fibrosis produces a genera li zed in-
Mixed-dust silicoses are much more com mon than crease in linear and reticu la r markings. A honeycomb
pure silicosis. These pursue the same clinical course as pattern may be seen in advanced cases (Fig. 5.14).
the pathogenic agent is always silicon dioxide quartz • Lymph node enlargement showing an "eggshell" pat-
dust but sometimes show more gradual progression. The tern of calcification: There is hilar and mediastinal
tota l SiD, co ntent of healthy lungs is less than 0.2 g; in lymph node enlargement and these nodes show a pe-
silicosis it is increased by up to 100-fold, Quartz crystals ripheral, eggshell-like pattern of calcification in 5 %of a
are found on microscopic examination of histological cases (Fig. 5.15 ), This appearance is very suggestive of
specimens from sil icotic nodules or from invo lved silicosis although sa rcoidosis occasionally may pro-
lymph nodes, duce a similar appearance. Lymph node changes may
precede the developme nt of parenchyma l involve-
ment.
• Clinical Features • Progressive massive fibrosis (PMF) is characterized by
large, homogeneous opacities with radiating strands
Acute silicosis is rare and results from massive exposure (pseudopodia ) mainly involving the upper lobes.
to silica dust, usually in sand blasters. This disease is These conglomerate masses gradually sh rink over a
rapidly progressive and res piratory insufficiency period of years and migrate toward s the hilum
develops within months. The radi ology and histology of (Figs. 5,16), Occasionally the centers of these masses
acute silicosis resemble pulmonary alveolar proteinosis. may unde rgo autolytic degeneration but upper lobe
Chron ic silicosis is much more common. Patients are cavitation may also indicate tuberculous reactivation.
usually asymptomatic when radiographic cha nges ini- • Acute silicoproteinosis: Th is very ra re acute form of
tially become visible. Fibrosis with cicatricial emphy- pneu moconiosis is only seen with massive exposu re,
sema then develops gradually over a period of years usually in sandblasters. Radiograph s show decreased
and this is associated with increasing dyspnea pro- pulmonary luce ncy consistent with grou nd-glass
c
gress ing to cyanosis and eventual cor pulmonale. Pul- opacification and consolidation.
Fig.
monary function tests show a mixed patte rn with both in 1
obstructive and restrictive ventilatory impairment. Hy- diff
Pneumoconioses Due to Inorganic Dusts 137
Computed Tomography
Thin-secti on CT images (collimation 1-3 mm) are help-

ful in classification of pulmonary parenchymal abnor-
ion mality. cr features of silicosis include:
• Diffuse pUlmonary nodules 2- 5 mm in diamete r in a
ltly perilympha tic (subpleural , parase pta l, and ce n-
110- trilobular) distribution. These sometimes may ca lcify
sti- (Fig. 5.13b. Fig.5.17a).
-rna • Conglom erate masses in PMF: irregular in outline and
lich w ith fibroti c stranding radi ating in to the adjacen t
·cu- lung. These masses are frequ ently calcified and may
,ro- undergo central degeneration with cavitation
(Fig.5.1S). - Fibrosis: - Progressive massive fibrosis
ese - Peripheral "eggshell" with cavitation; fibrotic mass
the • Asymmetric nodules, conso lidation, or cavitation lymph node ca lcification mig rates toward the hilum
lrge should rai se the possibility of development of sili- over a period of years
cotuberculosis. - Coarse pulmonary nodularity
Fig.S. 11 Si licosis.
into
no n
,ad-
ow-
nes.
3.ses
in-
)mb
J.
pat-
:inal
pe-
%of • b
'eof
pro-
may
Ilve-
d by
lnds
,bes.
fer a
il um
Isses
lobe
tion.
n of
lure,
ased
.Iass c d
Fig.5. 12a- d Progression of sili cosis from sma ll type q nod ul es emp hyse ma. The 60-year-o ld coa l worker was retired due to ill
in 1959 (a, b) to larger type r nod ules (1965 c, d), and finally to health in 1959 due to exertional dyspnea. His symptoms pro-
diffuse fibrosis and conglomerate masses (1968 e, f) with apical gressed slowly over years. Fig. 5. 12e, f [>
'38 5 Inhalationallung Diseases and Pneumoconioses
e
Fig. S. 12 e, f
•
Fig
•
Fig.
Fig. 5. 13 a, b Silicosis: Chest rad iograph (a ) and CT (b) show pul-

b monary nodularity.
Pneumoconioses Due to Inorganic Du st s 139
a b
Fig. 5.14a, b Silicosis (t 3/3) with pulmonary fibrosis. Radiog raphs show reticulolinear interstitial shadowing.
a b
Fig. 5. 15 a, b Silicosis with eggshell calcificat ion of hilar and mediastinal lymph nodes.
lOW pul-
Fig.5.16 Silicosis (C. wd) with

progressive massive fibrosis. con-
fi rmed histologically by biopsy of
nodular masses. Incidental finding
of right-sid ed thyroid goiter is also
noted.
• Hilar and mediastinal lymph node enlargement which Coal-Worker's Pneumoconiosis

may show calcification (Fig. 5. 19, Fig. 5.17b).
(CWP)
• Acute silicoproteinosis: cr findings include bilateral
centril obu lar nodules of ground-glass opacification,
more diffuse patchy ground-glass opacification, and Coal-worker's pneumoconiosis results from exposure to
consolidation (Marchiori et aJ. 2001 ). "washed coal" which is almost free of silica. While histo-
logically it differs from silicosis, imaging findings are
Magnetic Resonance Imaging (MRI) similar with coa l macules manifest as nodular opacities
frequently centrilobular in distribution and sometimes
MRI may be useful in distinguish ing between the con- less well defined than the nodules seen in silicosis. Com-
glomerate masses of progressive massive fibrosi s and plicated CWP is manifest as conglomerate masses (pro-
bronchial carcinoma. PMF-associated soft ti ssue masses gressive massive fibrosis ).
tend to be hypointense on T2-weighted sequences
whe rea s bronchial neoplasms generally show T2 hyper-
intensity (Mats umoto et aJ. 1998 ).
Asbestos-Induced Pleural Changes
and Asbestosis
• PET
Lesions in PMF may show intense fluorod eoxyglucose Asbestos is a magnesium silicate fiber used in the pro-
(FDG) uptake and thus thi s may not be helpful in their cessing of insulation materials, textiles, paper, and plas-
differe ntiation from bronchial neoplasia (C hong et aJ. tic. Pulmonary parenchymal and pleural change usually
2006). becomes evident 10-20 years after initial exposure. The
diagnosis is based on a history of exposure, the detection
of asbestos fibers in the spu tum , and typica l radiologic
findings. Lung biopsy for histological confirmation is
ve ry rarely performed.
As bestos exposure is also associated with an in- a
creased risk of developing both bronchial carcinoma and
19
so
Fig. 5.17 a, b Sil icosis: CT shows pulmonary nodularity in a peri- t>

lymphatic distribution (a). When study is viewed at mediastinal
window (b), the re is bilateral hilar and mediastinal lymph node
enla rgement which show eggshell calcification. b
~ to
;to-
are
ties
nes
)m-
)ro- <I Fig.5.18 Silicotic masses of PMF in both upper zones with calci-
i:il1.::!E!ll:~Z};,..;...... fication and cicatricia l emphysema.
)ro-
\as-
ally
The
tio n
Jgic
n is
in- a b
and Fig. 5.19a, b Eggshell calcification of enlarged hilar and mediastinal lymph nodes in silicosis.
• Chest Radiograph
Ple ural invo lvement is frequently more co nspicuous
tha n the un de rlying pulmonary pa renchymal change on
the chest rad iograph (Fig. 5.20 ).
• Pleural plaques: Plaques for m on the pa ri etal pleura
and sites of predilecti on include the diaphragmati c
pleura and the mid to lower an terola teral he mi-
thorax. The re ten ds to be preservati on of the cos-
tophrenic sulcu s. Calcifica ti on of pleu ral plaques is
co mm on occurring in 60-80 %of cases (Fig. 5.21 ).
- Pleural plaques - Pulmonary fibrosis
- Pleural effusion (asbestosis) • Recurrent pleural effusion: Th is is a diagnosis of exclu-
- Calcified diaphragmatic - Pleural thickening with sion and may appear less than 10 yea rs after initial
pleural plaques obliteration of the exposure. It is unilateral in 90 % of cases, and recur-
costophrenic angle rent effu sions may be associated w ith a smooth rind
Fig. 5.20 Asbestos-induced pleural and pulmonary disease . of pleural thi ckening. In a few cases, as bestos fibers
may be detected in the pleu ral aspirate.
• Diffuse pleural thickening: Diffuse pleu ra l thi ckeni ng
res ults from thickening and fibrosis of the visceral
pleura with fusion to the parietal pleura often over a
malignant mesothelio ma. These neoplasms also occur wide area (Solomon 1991 ). Its prese nce is less specific a
afte r a latent period of seve ral yea rs and are recogni zed to as bestos expos ure than pleural plaque s as ex uda-
as occupational di seases. tive effusions and hemoth orax may also lead to dif-
fuse pleura l thickening and fi brosis.
• Pulm onary fibrosis: Reticul ar and linea r shadow ing is
• Pathology see n predomina ntly in the basal zo nes. Furthe r pro-
gress ion leads to a honeyco mb pattern with cicatri-
Only asbes tos fi be rs 20- 150 ~m in length ca n reach the cial e mphyse ma and tracti on bronchi ectasis. Nodules
lowe r resp iratory tract and cause di sease. On reaching and mass ive fi brosis are usually an indicator of mi xed
the bro nchioles and alveo li in the basa l zo nes. fibers are du st exposure. In contrast to pu re silicosis, howeve r,
phagocytosed and coa ted in a ferri tin protein ge l by this has a predi lecti on for the lower zones when see n
ma crophages (as bestos bodies). in association with asbestos exposure (Fig. 5.22).
Flat plaques of ex trapleu ra l fib ros is up to 10 em in di - • The "shaggy-heart" sign: Fibrosis of th e medi astin al
ameter form sy mmetrica lly on the diaphragmatic and pleura adj acent to irregul ar pulmonary fib rosis in the
costopari etal pleu ral surfa ces. Plaq ues tend to spare the paracardiac lung may prod uce an irregul ar cardi ac
apices and costophren ic sulci. Calcification is frequent. co ntour called the shaggy-heart sign.
Their pathoge nesis is unclea r but may res ul t fro m me- • Ill-defin ed diaphragma tic co ntour: Thicken ing of the
chani cal irritati on by asbestos fibers w hi ch perfora te the diaphragmatic pleura togethe r with contiguous pul-
vi scera l pleura. monary fibros is obli terates the di aphragmati c borde r.
Pul mo nary fi brosis is initially peri bro nchiolar and
then spreads along the peri bronc hovasc ula r an d septal Computed Tomography
co nnective ti ss ue. Fibrosis is most marked in the lowe r
zo nes with rela ti ve spari ng of the api ces. In contrast to High- resol ution CT in both the supine and prone posi- a
sil icosis. changes are diffuse a nd nod ules are not see n. tions (We bb et al. 1992, Aberl e 1988) or in the prone Fig
Fib rotic co ntraction leads to cica tricial emphysema with position (Friedm an 1990) has bee n advocated for pie
tracti on bro nchi ectasis and eve ntual honeyco mb lung. assessmen t of the lung bases. cr is superio r to the chest
radiogra ph in demonstra tion of early pleural a nd pul -
mona ry changes and images acquired with the pati ent
• Clinical Features in the supine position may well be adequ ate for assess-
ment.
Dys pnea a nd cya nosis may develop up to 20 yea rs after a feat ures include:
ini tia l exposure. Pulm onary functi on tests may show a • Pleural plaques: Parietal pleural plaques are sharply
mixed pattern of ve ntilato ry impairme nt with both re- demarca ted from th e adjacent lung and are
strictive and obstructive feat ures. Pulmonary diffusi ng freque ntly calcified.
capaci ty is red uced. Asbestos bodies so metimes may be • Diffuse pleural thickening typically invo lves the post- •
detected in the sputum. ero lateral hemith orax inferiorly. cr helps in differen-
uous
:e on
eura
latic
emi-
cas-
es is
J.
:clu -
.itia l
cur-
rind
be rs
ling b
eral Fig. 5. 21 a, b a Asbestosis and ca lcified pleural
er a plaques, which particularly involve the diaphragmatic
a pleura. b Magnified view.
:ific
Ida-
dif-
g is
lro-
.tri-
Jl es
xed
ver,
een
nal
the
iac
the
ul-
ler.
Isi- a b
,ne Fig . 5.22 a, b Asbestosis with asbestos-induced pleura l plaques. Radiograph shows increased reticular markings and laterobasal
for pleural plaques. Asbestos fibers were found in significant numbers in the lung at postmortem.
est
ul-
~ nt
3S-
tiation of diffuse pleural thickening from extrapleural are seen subjacent to areas of pleural change, and a
fat deposition. However, extrapleu ral fat deposition is distinctive arching of vessels and bronchi is seen as
lly frequently seen in association wi th diffuse pleural they enter the area of infolded lung ("comet tail" sign,
ICe thickening pro bably due to inward pleural retraction Figs 5.23, 5.24 a, b).
(Abe rl e and Balmes 1991). • Asbestosis: Dot- like opacities in the subpleu ral lung
it- • Rounded atelectasis appears as rounded juxta pleural may be the earliest CT fin di ng in patients w ith asbes-
n- opacities up to severa l centimeters in diameter. They tosis (Webb et al. 1992). These represe nt ce ntril obu-
'44 5 Inhalational Lung Diseases and Pneumoconioses
lar peribronchiolar fibrosis (Aki ra et aJ. 1990). Curvi- Exl
.
linear subpleural fines are beaded lines running paral-
lel to and a few millimeters beneath the pleural sur-
face (Fig. 5.25). They may re present confluent peri-
bronchiolar fibrosis involving the subpleural terminal (
bronchioles but are not specific for asbestosis (Pilate
et aJ. 1987 ). Later findings include irregular thicken- Orgc
ing of interlobular and intralobular septa progressing caus
to a honeycomb pattern with traction bronchiectasis. fung
• Parenchymal bands may represe nt thickening of reac
several marginating septa or fibrosis along the bron- of al
chovascular sheath (Ak ira et aJ. 1990). 1-51
they
bron
T
Fig.5. 23 Rounded atelectasis in a patient with known asbestos- Other Inorganic Pneumoconioses farm
induced benign pleural change. Note the comet-tail appearance
of blood vessels entering the atelectatic lung. semi
See Table 5.1. ble 5
dysp
expc
actir
ratio
expo
and
firm.
mYCf
sode
orati
socia
versi
A
of"h
This
affec
moni
(MA(
a sped
by rE
tropt
infec
wate
or a 1
as so
apy,
cessa
• R,
In ac
(so ml
seen !
(2-31
Fig. 5.24a. b Rounded atelectasis. (T shows right-sided pleural
thickening and calcification (a) with associated infolded lung (b).
stage
comp
Extrinsic Allergic Alveolitis (EAA)/Hypersensitivity Pneumonitis 145
lrvi- Extrinsic Allergic Alveolitis (EAA)fHypersensitivity pneumonitis

ual-
sur-
leri-
• Clinical Features Table 5.2 Extrinsic allergic alveolitis/hypersensitivity pneumoni-
tinal tis due to organic dusts (from Baum)
ilate
ken- Organic dusts from plants and an imals in isolation rarely Syndrome Source of Precipitins against
sing cause pulmonary disease. Dust particles mixed with antigen
asis. fungal antigens, however, may induce a hypersensitivity
reaction in the lung. Animal proteins, particularly those Farmer's lung Moldy hay Thermoactinomyces
~ of vulgaris
ron- of anima l origin, also may cause disease. Dust particles
1-5 11m in diameter enter the gas exchange unit where Bird fancier's lung Bird Fecal proteins
droppings
they produce a gran ul omatous response centered on the
bronchi oles and su rrounding alveoli. Bagassosis Bagasse (sug- Fungal spores.
arcane fiber) Thermoactinomyces
The classic example of organic pneumoconiosis is
vulgaris
farmer's lung. Its clinical and radiographic features re-
semble those of othe r known organic dust di seases (Ta- Mushroom Mushroom Micropolyspora faeni
worker's lung compost and vulgaris
ble 5.2). An acute illness with symptoms of dry cough,
dyspnea, fever, and malaise develops 4-12 hours after Cork worker"s lung Moldy cork Cork dust
(suberosis)
ex posure to moist hay conta min ated with thermophilic
actinomycetes. These sympto ms are usua lly of short du- Wood dust lung Moldy Cryptostroma corti-
(maple and poplar sawdust cale, C. graphium,
ration, lasti ng for 12-24 hou rs, but recur with repeated
bark, sequoiosis) C. altenaria
exposure. The temporal association between exposure
Cheese washer's Moldy cheese Penicillium casei
and sy mptoms suggests the diagnosis, which is con-
lung dust
firmed by detection of serum precipitins against actino-
mycetes. Subacute illness is cha racterized by acute epi- Malt worker's lung Moldy barley Aspergillus clavatus
sodes of dyspnea superimposed on a progressive deteri- Air conditioning Contaminated Molds
oration in lung function. The chronic form of EAA is as- alveolitis air humidifier
sociated with continuous low-grade ex posure and irre- Cereal worker's Infected Cereal beetle
versible pulmonary damage. lung cereal dust 5itophilus granarius
A numbe r of recent studi es have described the entity Numerous other diseases: hormone sniffer's lung (pituitrin in
of "hot-tub" lung (Aksamit 2003, Cappelluti et al. 2003). diabetes insipidus), coffee worker's lung, fishmeal worker's
lung. detergent worker's lung. paprika splitter's lung.
This entity appears to be related to hot tub/spa use and
affected individuals develop a hypersensitivity pneu-
monitis-type illness. Mycobacterium avium complex
(MAC) organisms have been isolated from both patient
specimens and the spa water with matching fingerprints
by restricted fragment length polymorphism and elec- High resolution a
trophoresis. Hot-tub use appears to lead to high levels of
infectious aerosols containing organ isms found in the In early disease, patchy bilateral gro und-glass opacifica-
wate r. Whether this entity refl ects an infective process tion may be seen (Fig. 5.260). Centrilobular poorly de-
or a true hypersensitivity pneumonitis is controversia l, fined nodules of ground-glass opacifi cation are also a
as some patients im prove only after antimicrobial ther- frequent finding. Air trapp ing ind icative of a constrictive
apy whil e others improve on corticosteroid therapy and bronchiolitis may be seen on expiratory images (Small
cessation of exposure. 1996, Figs. 5.2Gb, 5.270, b).
Findings in hot-tub lung have been described and in-
clude cent rilobular nodules, whi ch may be well or
• Radiologic Findings poorly defined and which most commonly were sym-
metric in distribution, and areas of ground-glass opacifi-
Chest Radiograph cation. Irregular linea r opacities are occasionally see n
(Hanak et al. 2005),
In acute and subacute di sease, a gene rali zed ha ziness
(sometimes described as gro und -glass change) may be
see n on the chest radiograp h. Small pulmonary nodules
(2-3 mm in di amete r) are a lso a common finding. End-
stage di sease is characterized by upper lobe fibrosis with
compensatory emphysema in the lower lobes.
a~
Fig. S.
tenua
a b
Inh
. c
Inhal
an ac
ederr
fendi
age i!
ies u
dustr
Envir
c d isting
Fig.S. 2Sa-d Asbestosis: CT images were acquired with the patient prone. Note the subpleural curvilinea r densities with reticular is oft,
change. traction bronchiectasis, and fibrotic bands.
• R;
The (
shade
rad ial
incre.
Table !
Am
Sulfu
Ozan
a """' b Nitric
Fig. S. 26a . b Extrinsic allergic alveolitis/Hypersensitivity pneumon itis: CT in inspiration (a) shows exte nsive ground-glass opacifica- Tofu
tion with areas of focal air trapping evident in expiration (b).
Inhalation ofToxic Gases and Fumes 147
.~
~ _ _ _ _ --d
Fig. 5.27 a, b Extrinsic allergic alveolitis/hypersensitivity pneumonitis: CT acqu ired in inspiration (a) shows a mosaic pattern of lung at-
t enuation with evidence of extensive air trapping in expiration (b). Hi stology from VATS biopsy was consist ent with EAA/HP.
Inhalation of Toxic Gases and Fumes
Inhalation of noxious gases and vapors may precipitate

an acute bro nchitis, acute bron chi olitis, or pulm ona ry
edema (Table 5.3). Solubility and permeabili ty of the of-
fend ing substances appear to determine w hether dam-
age is predom inantly bro nchial or alveolar. These injur-
ies usua lly res ult fro m accide nts in the chem ica l in-
dustry and changes are very often compl etely reversi ble.
Environmental air pollution (smog) exacerbates preex-
~ d
isting bronchial di sease although a ca usa tive association
is ofte n difficult to prove.
lar
Bronchit isl Airway change
Fig.s. 28 Inhalation of toxic gases and fumes.
The chest radi ograph may show increased inte rsti tia l
shadowi ng in acute bronchitis, pulmon ary hypertrans-
radiancy in constrictive bro nchio litis, o r features of
increased permeabi lity pulmonary edema (Fig. 5.28).
Table 5.3 Pulmonary changes due to inha lation of toxic gases and fumes (from Baum and Mathys)
Substance Source Site of action
Oxygen Respiration Alveoli

Chlorine gas Chemical and plasticS industry Bronchi > alveoli
Phosgene Chemica l and plast ics industry Alveoli > bronchi
Ammonia Refrigerators, fertilizers Bronchi> alveoli. Bronchiectasis with constrictive
bronchiol itis. Pulmonary edema in severe cases.
Sulfur dioxide Chemical indust ry, combustion of Bronchi> alveoli
sulfur-containing oils
Ozone Bleach industry, electriC arc welding Bronchi> alveoli
b Nitric oxide Explosives, silos, automobi le exhaust Bronchi> alveoli
fica- Toluylene isocyanate Manufact ure of polyurethane foam Bronch i
cr findings include features of bronchitis (see p.116).
bronchiectasis (see p.117 ). constrictive bronchiolitis
(see p.123). and pulmonary edema (see p.195 ) (Fig.
5.29).
Fig.5.29 Chlorine gas poisoning. This patient developed dysp-

nea and cough 4 hours after an occupational accident. HRCT
showed extensive ground-glass opacification with minor air trap-
ping.
149
p.116 ).
:hiolitis
6 Tumors and Tumor-like Lesions of the Lung
5) (Fig.
The Solitary Pulmonary Nodule (SPN)

Jed dysp-
nt. HRCT
Ir air trap-
A solitary pulmonary nodule is defined as a round or types D to F. Partly solid lesions co rrela ted w ith inter-
oval opacity less than 3 em in diameter w hich is sur- mediate grade Noguch i lesions (Aoki et aJ. 2000).
rounded completely by pulmonary parenchyma and is • Lesion measurement on serial studies. No cha nge in the
not associated with lym ph node enl argement, atelecta- size of a les ion over a period of 2 years has trad ition-
sis. or pneumonia (Midthun et aJ. 1993). ally been accepted as being co nsistent w ith a beni gn
Cytologic and /or histological eval ua tion is usually re- lesio n. This concept has been challenged by
quired to differentiate benign from malignant lesions. Yankelevitz and Henschke (1997 ) as substantial in-
However. the followi ng may also be he lpful in eva luation creases in the vo lu me particu larly of small nodules
of SPNs: may be missed on se rial radiographic assessment. cr
assessment includes standard in plane measu rements
on axial cr images. There. however, may be a signifi-
Les ion Size and Morphology
cant margin of error in the assess ment of minor
• CT densitometry: Central or lam inated calcification is changes (i. e .. less than 2 mm ) in the diameter of
see n in granu loma ta whi le a "popcorn" patte rn of cal- smalle r lesions. Th is is importa nt as a 1 mm increase
cification characteri stically is see n in hamartomata. in the di ameter of a 4 mm lesion equates to an in-
The presence of intra Ie siona I fat is also co nsidered di - crease in volume of approxi mate ly 100 %. Volumetric
agnostic of either a hamartoma or lipoma. Computed analysis of in terval growth ha s been shown to be
tomography (Cf) also allows differentiation of lesions much more accurate than in plane measurements in
of soft tissue attenuation (called solid les ions) from the assessme nt of indeterminate lesions (Yankelevitz
those of ground-glass attenuation (ca ll ed "onso /id le- and Henschke 2000). Howeve r. more recently Good-
sions ). Some nodules may co mprise a combination of man and colleagues have re ported a mean interscan
ground glass and soft tissue attenuation (call ed partly va riability of 13.1 % in vo lu metric measurements
solid lesions ). Henschke et aJ. evaluated the signifi - using a semi-automated vo lumetric nod ule sizi ng
cance of non solid and partly solid lesions within the package (Goodman et a J. 2006).
context of a lung cancer scree ning program in a high-
ri sk po pulation. They found an overall malignancy
"Functiona l" Assess m ent
rate of 34 %for partly solid/nonsolid les ions vs. 7 %for
so lid lesions. The malignan cy rate for partly solid le- • cr enhancement: Image acqui sition post intravenous
sions was 63 %and for non solid lesio ns was 18 %. His- injection of iodinated contrast mediu m may be of
tologica lly. nonsolid and partly so li d les ions we re value in differenti ating benign from malignant le-
predominantly bronch ioloalveolar ca rcinomas or sions. Helical vo lumetric IT images through the le-
adenoca rcinomas w ith bronchioloa lveolar features sion may be acquired 1 and 2 minutes post adminis-
(Henschke et aJ. 2002). Aoki et aJ. co rrelated les ion at- tration of contrast medium. Swe nso n et al. have
te nuation with growth rate (tumor doub ling time ) show n that enhancement of less than 15 Hounsfield
and the Noguchi classification of peripheral lung ade- units (HU ) has a se nsitivity of 98 %for be nign les ions
nocarcinoma (see Screening fo r Lung Cance r. p. 157). greater than 5 mm in diameter. However, the speci-
They found lesions of ground-glass atten uation ficity of thi s criterion was significantly lowe r at 58 %
showed slower growth (tumor doubling times of up as benign lesio ns may al so show sign ificant enhance-
to 24 months) and correlated w ith Noguchi types A ment (Swenson et a J. 2000).
and B les ions. Lesions of un iform soft tissue atten ua- • Positron emission tomography (PET). Ma lignant
tion (sol id lesio ns) show much more rap id growth nodules are associated w ith an increased metabolic
(tumor doubling times of3-4 months) and correlated rate and hence increased fluorodeoxyglucose (FDG )
hi stologically with the more aggressive Noguchi uptake on PET eva lu atio n. A number of studi es have
150 6 Tumors and Tumor-like Lesions ofthe Lung
shown sensitivities of 93-100 % and specificities of sources, unnecessary patient anxiety, and impo se a sig-
87-88 % for all nodules (Gupta et al. 1996, Bury et al. nificant radiation dose particularly in young patients. On
1996, Dewan et al. 1997 ). For lesions less than or evaluation of Early Lung Cancer Action Project (ELCAP)
equal to 15 mm in diameter, sensitivities of 80-83 % data, Henschke et al. found no lung cancers in patients in
and specificities of 95-100 % have been reported whom the largest noncalcified nodule was less than
(Dewan et al. 1997, Lowe et al. 1998 ). Benign innam- 5 mm in diameter on initial CT. Therefore, the re appears
matory lesions may give fal se-positive results and to be little point in short-term interval follow-up for
some neoplasms such as bronchioloalveolar carci- nodules less than 5 mm even in high risk patients.
noma and carcinoid tumors have low metabolic ac- Bearing in mind these conside rations, the Fleischner
tivity and may give false-negative results. Society has recently issued the following recommenda-
tions for nodules detected incidentally at nonscreening
Miles et al. correlated cr enhancement measurements CT in persons aged 35 years or older (MacMahon et al.
(standard ized perfusion value [SPV]) of pulmonary 2005):
nodules with the ir standardized uptake va lue (SUV) on • Lesions :s:: 4 mm:
PET and showed a positive correlation between the two - in a low-risk patient: no follow-up requi red;
values (Miles et al. 2001). - in a high-risk patient: follow-up CT at 12 months
and;
- if unchanged, no further follow-up needed.
Evaluation of CT-Detected Small Pulmonary
• lesions > 4-6 mm:
Nodules
- in a low-risk patient: follow-up CT at 12 months
In the past decade, detection of small pulmonary and if unchanged, no further follow- up required;
nodules has become routine on thin collimation helical - in a high-risk patient: initial follow-up CT at 6-
volumetric CT. Data from multi-detector CT (MDCT) stu- 12 months, then at 18-24 months if unchanged.
dies at 5 mm collimation indicate that approximate ly • Lesions > 6-8 mm:
50% of smokers over SO years of age will have at least - in a low-risk patient, initial CT follow-up at 6-
one visible nodule and another 10 % w ill develop a new 12 months, then at 18-24 months if no change;
nodule ove r a 12-month period (Swenson et al. 2002 ). - in a high-risk patient, initial CT follow-up at 3-
The clinical importance of these nodules appears to be 6 months, then at 9-12 and 24 months if no
very different from those detected on chest radiographs change.
and the vast majority are benign (MacMa hon et al. • Lesions > 8 mms:
2005 ). - in both low- and high -ri sk patients: follow-up CT
Studies suggest that less than 1 % of nodules which at 3, 9, and 24 months. CT enhancement, PET
are less than 5 mm in diameter found in patients assessment, and/or biopsy.
without a history of neoplasia will demonstrate malig-
nant behavior (Henschke et al. 2004, Swenson et al. longer follow-up intervals may be appropriate for non-
2003, Henschke et al. 1999). Therefore, regular CT fol- solid and partly solid les ion s given their slower growth
low-up of the se lesions may reflect poor use of re- rates and longer tumor doubling times.
Benign Tumors of the lung
Benign tumors account for just 2 %of pulmonary neo- • Helical volumetric cr through the central airways w ill
plasms. They may grow slow ly or remain unchanged for confirm these findings and wi ll show the degree of
several years (Table 6.1 ). extrabronchial extens ion of these lesions. Hi stologi-
Clinical manifestations and radiographic findings are cal confirmation from bronchoscopic biopsy with
determined by their location (Fig. 6.1). subsequent surgical resection of these tumors is usu-
p
• Central endobronchial lesions present with cough, ally feasible.
hemoptysis, distal pneumonic consolidation, wheez- • Peripheral parenchymal tumors are frequently asymp- H,
ing, and dyspnea. The chest radiograph may occasion- tomatic and these solitary pu lmonary nodules are III
ally show these endob ron ch ial lesions as filling de- often an incidental finding on chest radiographs. co
fects within the air-fi ll ed lobar and segmental pr
bronchi (Fig. 6.2 ). In some instances, branching linear w
opacities representing mucoceles distal to the ob-
structing lesion may be seen. p€
1 Benign Tumors ofthe Lung 151
~ a sig- Table 6. 1 WHO Classification of lung tumors (modified from

nts. On Scholman et al. 1991)
~ LCAP )
Benign Malignant
ents in
s than
I. Epithelial • Papillomas • Squamous cell
ppears tumors • Adenomas carcinoma
up for • (Dysplasias) • Small cell
s. • (Carcinoma in situ) carcinoma
• Adenocarcinoma
schner
• large cell
lenda- carcinoma
~en in g • Adenosquamous
1 et al. carcinoma
• Carcinoid tumor Central type:
• Bronchial gland - Endobronchial Peripheral type:
carcinoma filling defect - Pulmonary nodule
I: • Others - Distal pneumonia - Rarely: flocculent
lonths and atelectasis calcification
II. Non- • lipoma • Fibrosarcoma
- Distal pulmonary
epithelial • Fibroma • Neurofibro-
hyperinflation
(soft-tissue) • Neurofibroma sarcoma
tumors • lymphangioma • Hemangio-
Fig. 6.1 Benign tumors.
lOnths • Hemangioma sarcoma
Jired:
• leiomyoma • Leiomyosarcoma
at 6-
• Granular cell • Malignant
tumor hemangioperi-
ged. • Chondroma cytoma
III. Mesothelial (Benign) Malignant
at 6- tumors mesothelioma mesothelioma
Ige: IV. Miscel- • Clear cell tumor • Carcinosarcoma
at 3- laneous • Paraganglioma • Pulmonary
if no tumors • (Chemodectoma) blastoma
• Teratoma • Malignant
melanoma
• Mal ig nant
up cr lymphoma
:, PET • Others
V. Metastases
VI. Un-
. non- classified
'owth tumors
VII. Tumor-like • Hamartomas
lesions • lymphoprolifera-
tive processes
• ~TumorletsH
• Eosinophilic
granuloma
• ~Sclerosing he-
mangioma~
• Inflammatory
pseudotumor
• Others Fig.6.2 Fibroma appears as a round filting defect within the tra-
swill cheobronchial air column.
ee of
)Iogi·
with
: usu- Pulmonary Hamartoma inflamed and may be indistinguishable from bronchial
carcinoma at bronchoscopy (Ahn et al. 1994, Fig. 6.30, b).
ymp- Hamartomata account for SS %of benign and approxi-
s are mately 8 % of all pulmonary neoplasms. These tUl110rs
s. contain cartilage, connective tissue. fat. and muscle. Ap- • Radiologic Findings
prox im ately 80% are peripheral pulmonary nodules
while the remainder are central endobronchial lesions. The chest radiograph typ ically shows a well-circum-
Endobronchial lesions typically contain more fat than scribed , homogeneous nodule which usually is less than
pe ri pheral les ions (Caerte et al. 2002) but frequently are 4 cm in diameter. Flocculent or popcorn calcification is
152 6 Tumors and Tumor-like lesions ofthe lung
Table
Atlas,
TX
Tl
12
T3
T4
b Nl
Fig. 6.3a. b Endobronchial hamartoma. (T shows low density

N2
lesion possibly containing some foci of fat density with the left N3
ma in bronchus (a). There are features of a cellu lar bronchiolitis
within the left lower lobe distal to this lesion (b). Histology of re-
• sected specimen was consistent w ith a hamartoma .
b
Fig.6.4a, b Pulmonary hamartoma appears as a well-defined
• round lesion and contains fod of calcification .
visible in up to 15 %of cases (Figs. 6.4. 6.5 ). The presence

of intralesional fat is also considered diagnostic.
Carcinoid, Mucoepidermoid, and
Adenoid Cystic Carcinoma
Computed Tomography
The term "bronchial adenoma" in the past has been used
Because of the superior contrast reso lution orCT, fat and to describe a group of lesions that included carcinoid Fig.
calcium with in hamartomata are identified more easily. tumor, mucoepidermoid carcinoma, and adenoid cys tic noe
The prevale nce offat at CT has been reported to be from carcinoma. The 1977 histologic classification considers
5 to 50% (Erasmus et al. 2000). Fat is found in up to 50% carcinoid to be a separate entity while cylindroma or ad-
of lesions and may be localized or generalized within the enoid cystic carcinoma is classified with carcinoma of
lesion (S iegelman et al. 1986. Erasmus et al. 2000, the tracheal wall glands (Tables 6.1, 6.2).
Fig. 6.6 a-( ). Bronchial carcinoid encompasses a spectrum of his-
tology ranging from slow growing, loca lly infiltrative
tumors to metastasizing lesions. Carcinoids may be typi-
Fig
cal (KuJchitsky cell carcinoma [KCC) type 1) or atypical
lob
(KCC type 2): the latter has cellular and clinical features ane
Benign Tumors of the lung 153
Table 6. 2 TNM classification of bronchial carcinoma (UICC: TNM

Atlas, 2 nd ed. Berlin: Springer 1990)
TX Positive cytology
T1 :-;:; 3 em in greatest dimension
T2 > 3 em in greatest dimension. or extension to the
hilar region, or invasion of visceral pleura. or a tumor
that has caused partial atelectasis
T3 Extension to the chest wall, diaphragm, mediastinal
pleura. or pericardium, etc., or a tumor that has
caused complete atelectasis
T4 Invasion of the mediastinum, heart. great vessels,
trachea, esophagus, etc.. or the presence of malig-
nant pleural effusion
b Nl Metastasis to peribronchial or ipsilateral hilar lymph

nodes
N2 Metastasis to ipsilateral mediastinal lymph nodes
'nsity
, left N3 Metastasis to contralateral mediastinal lymph nodes,
iolitis scalene lymph nodes, or supraclavicular lymph nodes
Jf re-
a
b
fined
b
Jsed
loid Fig.6.S Pulmonary chondroma appears as a well-defined
(stic nodule with flocculent calcification.
ders
·ad-
a of
his-
Itive
ypi-
Fig. 6 .6 a-c Peripheral lung hamartoma. CT shows right upper t>
)ical lobe lesion with smooth contour (a ), central nidus of calcification
ures and surrounding rim of fat attenuation(b and c) c
154 6 Tumors and Tumor-Like Lesions of the Lung
Pm
cou
anc
in t
disl
•
Rad
sho
The
sho
6.9)
a b
COlT
Fig. 6.7 a, b Carcinoid tumor left lower lobe - (T images show left lower lobe lesion which contains multiple foci of calcification.
gre~
There is distal left lower lobe atelectasis. Histology of resected specimen was consistent with a typical carcinoid.
min
(Fig
intermediate between those of typical carcinoid and (

small ce ll carcinoma (KCC type 3). Approximate ly 15 %of
Langerhans Cell Histiocytosis (LCH)
typical and 50% of atyp ical carcinoids ultimately will Higl
metastasize (A rmstrong et al. 1995). Langerhans ce ll histiocytosis comprises three di sorders peri
Lesions distal to the level of the segmental bronchi that show histologic sim il arities. These are: upp,
are defined as peripheral carcinoids. Typical carcinoids 1. Letterer-Siwe disease, a fulminant multisystem his-
characte ri stica lly are centrally located vascular tumors tiocytosis of young children.
and may prese nt with hemoptysis. Conversely. atypical 2. Hand-Schuller-Chri stian disease. a chronic histio-
carcino ids tend to have a peripheral location and pre- cyti c disorder.
sentation with hemoptysis is unusual. 3. Eosinophilic granuloma of bone.
Isolated pulmonary involvement was first reported in

• Radiologic Findings 1951. Pulmonary Langerhans cell histiocytosis (PLCH) is
today seen predominantly in young adults and has a
Most bronchial carcinoids are found within the major smoking prevalence of 80-100 %. A much less common
bronchi. The chest radiograph may be normal in 10 %of assoc iati on w ith neoplasia including bronchial carci-
cases and then the diagnosis is estab li shed at bronchos- noma and Hodgkin's lymphoma has been described.
copy or following surgical resection of tumors initially The etiology of this condition remain s poorly under-
detected at CT (Armstrong et al. 1995 ). stood but it has been suggested that it may reflect an un-
In those cases w ith an abnormal chest radiograph. controlled immune response to an unknown exogenous
the tumor may be visible as a well-defined hilar or peri- antigen in which Langerhans cells may se rve as acces-
hilar mass. Partial or comp lete bronchial obstruction so ry cells in the activation ofT lymphocytes.
leads to distal atelectasis or pneumonic consolidation. Pathologically. multifocal peribronchiolar collections
Occasionally. collateral air drift maintains distal aeration of Langerhans cells together with macro phages, lym-
even in the presence of tota l airway obstruction. phocytes. plasma cells. and eosinophi ls are seen. These
Tumors in segmental bronchi may cause obstruction ce llular infiltrates are then replaced in a centripetal
with mucus retention in the distal airway; branching fashion by a fibroblastic proliferation which results in
bronchoceles then may be the dominant rad iographic the classic stellate lesions. Over time, the ce ll ular infil-
finding. Ten to twenty percent of carcinoids present as trate disappears leav ing behind fibrotic scars that are
peripheral pulmonary nodules or masses. surrounded by enlarged and distorted air spaces. Tem-
cr characteristically shows a spherical or ovoid poral heterogeneity is common ly seen both within the
nodule with a we ll-defined lobulated contour. Calcifica- pathologic specime n and within individ ual lesions
tion is not ofte n visible on the plain radiograph but is (Abbott et al. 2004).
seen on CT in up to 30 % of lesions. It is see n more com- Patients may present clinically wi th a nonproductive
monly in cent ral than in pe ripheral lesions and may be cough and dyspnea. Less commonly. presentation may
diffuse or punctate in type (Chong et al. 2006. Fig. 6.7 •. be with systemic symptoms of malaise and weight loss.
b ).
Benign Tumors ofthe Lung 155
Pneumothorax occu rs in up to 25 % of cases over the

course of the disease (Basset et al. 1978, Tazi et al. 2000)
and may account fo r initia l presentation.
Up to 25 %of cases ofPLCH may be asymptomatic and
in these cases, the diagnosi s may be due to incidentally
discovered rad iologic abnormalities .
.. :'.
.......: .... .
.,
Chest Radiograph
Radiographs during the early granulomatous stage may

show multiple small nodul es (1-10 mm in diameter).
These are bilateral and symmetrical in distribution and
show a predilection for the upper to mid zones (Figs. 6.8, Fig.6. 8 l angerhans cell histiocytosis presents initially with in-
terstitial nodularity and may progress to cystic change and fibro-
6.9). They give way to a coarse reticular pattern, honey-
b sis.
comb shadowing, and cystic change as the disease pro-
cification. gresses. The presence of extensive cystic change may
mimic bullous emphysema on the chest radiograph
(Fig.6.1Da ). ing of the lung bases. A combination of nodules and cys-
tic les ions has been described as the commonest pattern
Computed Tomography (Brauner et al. 1989, Fig. 6.11 ) and the probable progres-
.CH) sion of change on cr ha s been postulated to be from
High-resolution CT (HRCT) in early-stage di sease shows nodules through to cavitary nodules, thick-walled cysts,
jisorders peribronchial or peribronchiolar nodularity with an then thin-walled cysts, and finally co nfluent cysts. Given
upper to mid zone predominan ce and with relative spar- this progression of change, it has been suggested that
tern his-
c hi stio- Fig.6.9 langerhan s cell histiocy-

tosis-early-stage disease with ex-
tensive pulmonary nodularity.
lorted in
:PLCH ) is
nd has a
common
ia l ca rci-
ribed.
Iy under·
~ct an un-
Koge nous
as acces-
)lIections
ses, Iym-
en. These
,n tripetal
results in
ul ar infil-
: that are
ces. Tem-
lith in the
.I lesions
roductive
Ition may
' ight loss.
HRC
actil
freq
rath
and
1
mat
mor
pnel
guis
Fig. E
prav!
poor
Bn
Bror
epit!
a local
an d
spec
It
crea:
man.
gastl
tum(
have
In th
su rp.
(Bra!
lung
The'
cigar
,v
~
....
_ _ _ __ • __ Tt"'~l
c
carci
BI
pla sr
rate
DOPf
deatl
in th
main
Natk
early
tumc
rates
Serer
Fig .6.10a-d Advanced sta ge Langerhan s cell histiocytosis.
There is extensive pulmonary ~ cyst " formation with fibrosis most
large
advanced in the upper zo nes with moderate midzone change and have
d with relative sparing of the lung bases. Maya
Bronchial Carcinoma 157
HRCf may be useful in evaluating the histopathologic

activity of PLCH (So ler et al. 2000). Cystic lesions are
frequently round or ovoid in shape but may exhibit
rather bizarre configurations with bilobed, branching,
and cloverleaf shapes (Fig. 6.10b-d).
The differential diagnosis is from Iymphangiomyo-
matosis but this affects females and shows diffuse pul-
monary involvement. Cystic change in pneumocystis
pneumonia (see p.87) may occasionally be indistin-
guishable from cystic change in PLCH (We bb et al. 2001).
Fig.6. 11 Pulmonary langerhans cell histiocytosis. Histologically

proven pulmonary langerhans cell histiocytosis with areas of
poorly defined nodular opacification and early cyst formation.
Bronchial Carcinoma
Bronchial carcinoma arises from the bronchial 10000 subjects: In the screened group who underwent
epithelium, grows by local expansion, and infiltrates sputum analysis and chest radiography at 4-month in-
local lymphatic channels and vesse ls to give rise to local tervals, 62 %of detected carcinomas were still operable
and regional lymph node and distant metastases, re- and the calculated 5-year survival rate was 45 %. This
spectively. compares with resectable tumors in 28 %of the control
Its incidence in industrialized countries has in- group and a 5-year survival rate of just 19 %. This study
creased IO-fold since 1930 (M uller 1983) and in Ger- found chest radiographs were rewarding much more
many bronchial carcinoma is now second only to frequently than sputum cytology.
gastrointestinal malignancy as the most common organ Most other trial screening programs using chest
tumor. Since the mid 1980s. the incidence appears to radiographs and sputum cytology have failed to demon-
have plateaued in males but continues to rise in femal es. strate improved survival in the screened group and they
In the U.S. in 1988, the incidence of bronchial carcinoma have emphasized the difficulties in detection of early
surpassed that of breast carcinoma for the first time lung cancer on plain radiographs (Bragg 1994).
(Bragg 1994). It is estimated that approximately 85 %of A number of studies on CT screening for lung cancer
lung cancer may be attributable to cigarette smoki ng. have repo rted in the past decade:
The "rule of 20" states that in individuals who smoke 20 Henschke and colleagues reported the results of the
cigarettes per day for 20 years, the risk of bronchogenic Ea rly Lung Cancer Action Project in 1999 (Henschke et al.
ca rcinoma is increased 20-fold (Wynde r et al. 1977 ). 1999). This two-center study enrolled 1000 patients
Bronchial carcinoma is a particularly aggressive neo- more than 60 years of age with a smoking history of
c
plasm with a high mortality. The reported 5-year survival greater than 10 paCk-years. Initial screening CT was per-
rate in Germany in 1976 was only 2 % (Heilmann and formed at 10 mm collimation. The initial prevalence
Doppelfeld 1976). and it remains a major cause of cancer screen showed 1-6 non calcified nodules in 233 (23%) of
deaths (27 %) in both men and women overthe age of 35 participants. In 27 (2.7 %) of all participants. lung cancer
in the industrialized world. Current overall survival re- was detected (ca ncer prevalence rate of 2.7 %) and 23
mains poor with a lO-year survival of just 7 %in the u.s. (84%) of these neoplasms represented stage 1 di sease.
National Cancer Database report (Fry et al. 1999). The The initial incidence screen showed 26 new nodules, 10
early diagnosis and treatment of resectable nonsmall cell of which were malignant and nine of which were pri-
tumors offers some chance of cure with 5-year survival mary bronchial carcinoma giving a cancer incidence rate
rates of62-82 %(Fry et al. 1999. Mountain 1997 ). of 0.9 %.
More recently, Swenson et al. have reported the re-
sults of a 5-year prospective study on evaluation of a co-
Screening for Lung Cancer
hort at high risk of lung ca nce r with low-dose helical Cf
ytosis. Large prospective studies on radiographic screening (Swe nso n et al. 2005). They enrolled 1520 individuals
imost
have been co ndu cted in the U.S. (Fontana 1977 ). The more than 50 years of age with a smoking history greater
ge and
Mayo Foundation reported very favorable results in than 20 pack-years and residing within a so-ca lled "his-
158 6 Tumors and Tumor-Like Lesions ofthe Lung
toplasmosis belt." After five annual examinations, 3356 • Peripheral bronchial carcinoma (15-30 %) originates in A
uncalcified lung nodules had been detected in 1118 the mucosa of the smaller bronchi and in itially the ,
sp
(74 %) of participants. Sixty-eight cancers had been de- tumor may form a solitary pulmonary nodule. Periph- 100
tected in 66 participants. Thirty-one of these were prev- eral bronchial carcinoma arising in the subpleural •
90 --
alence cancers of which 42 % were adenocarcinomas, parenchyma may involve the pleura at an early stage.
19 % were adenocarcinomas with bronchioloalveolar Bronchial carcinoma arising at the lung apex (Pan -
80
characteristics. and 13 % were bronchio loalveolar carci- coast or superior sulcus tumor) may infiltrate the
noma, There were 35 noosmall cell incidence cancers, brachial plexus and the sympathetic trunk to produce 70
17 % of which were adenocarcinomas and 29 % were the typical syndromes of pain in the upper limb (Pan-
squamous cell carcinomas. Sixty-one percent of inci- coast syndrome ) and the Horner's triad, respectively. 60
dence cancers were stage 1 disease. • Diffuse, infiltrating, pneumonicfonns of lung concer al-
These studies suggest that screening cr allows detec- most always are bronchioalveolar in type. In 1977, they 50
tion of early-stage lung cance r but the detection rate of accounted for just 2.8 %of primary lung cancer. Their
benign nodules is high and it remains uncertain if early- relative incidence has increased considerably in the 40
stage detection represents a true stage shift or over diag- past three decades and now they may account for up to
nosis. 15 % of primary lung cancer (Armstrong et al. 1995, 3D
The U.s. National Lung Screening Trial by the U.s. Vincent et al. 1977, Auerbach and Garfinke l 1991 ).
20
National Cancer Institute is a randomized controlled
trial which aims to determine if there is a di sease- Tumor spread may initi ally be via the lymphatics to the 10
specific mortality benefit (Hillman and Schnall 2003). hilar, mediastinal, and supraclavicular lymph nodes. He-
Until this study is completed, it has been suggested that matogenous spread may a lso occur with metastatic 0
CT screening should only be performed in the setting of seeding to the brain, adrena ls, liver, and bones.
a clinical trial (Earnest et al. 2003, Stanley 2001 ). Bronchial carcinoma is classified histologically ac-
cording to World Health Organization guidelines (Ta- Table 6.3
Goals of Diagnostic Imaging. ble6.2).
Early diagnosis 0/ bronchial carcinoma. In everyday The most common histologic types are (Fig. 6.12 ): T: Prim.
TX p,
practice, most primary lung cancers are detected ini- • Small cell carcinoma has the most irrefutable associa-
b
tially on the chest radiograph. tion with cigarette/tobacco smoking. It is predomi-
TO N
Staging 0/ carcinoma: Some prelim inary information nantly a central tumor (90 %) but growth is mainly
may be derived from the chest radiograpfl. Tumor size, Tis C
along anatom ic tissue planes. Small cell carcinoma
ate lectasis, the presence of a pleural effusion. Mediasti- T1 T,
tends to metastasize early; systemic spread is present IT
nal and hilar changes may be visible (Bragg 1994). in two-thirds of cases at presentation. Small cell car- T2 TI
cr 0/ the thomx and upper abdomen is then performed cinoma is classified as limi ted or extensive. Surgical •
for further evaluation. Magnetic resonance imaging
(MRI) is useful in demonstrating neurovascular involve-
resection plays no role in its management with •
ment in Pancoast (superior sulcus ) tumor and in
chemotherapy ± radiotherapy forming the basis of •
assessment of extrathoracic spread in se lected in- treatment. •
T3 T,
stances (see Fig. 6.13). IT
pET-eTis useful in determining the presence and ex- The following histologic types co ll ectively are called IT
tent of regional lymph node and distant metastatic nonsmall cell lung carcinoma and in early-stage disease T4 T,
spread and now is routinely employed in cases of non- (stage I and II ± stage ilia ), su rgery offers the best chance b
sma ll cell lung carcinoma (NSCLC) being considered for of cure. The International Staging System developed by e
surgical resection. the Task Force on Lung Cancer of the American joint N: Regil
Identification 0/ predisposing/actors other than tobacco Committee on Cancer (AjCC) was introduced in 1986 NX R
smoking such as asbestos exposure. (Mountain 1986, Stitik 1990). The TNM (Tumor, Nodes, NO
Detection 0/ concomitant disease such as emPhYSem:0rJ Metastasis) classification defines the primary tumor (T), Nl N
congestive heart failure which may preclude or in- the presence of nodal disease (N), and of distant e
crease the risk of surgical resection. metastases (M) (Tables 6.2,6.3). This TNM classification N2 N
is used to define the stage of disease (Fig. 6.13, Table 6.4). N3 N
• Squamous cell carcinoma is most commonly a central n
tumor developing at the level of the lobar, segmental, M: Dist
• Pathology or subsegmenta) bronchi in 66 % of cases. These MX P
tumors frequently are lobulated and have a tendency MO ~
Classification of bronchial carcinoma by location may to cavitate. Squamous cell carcinoma arises peripher- Ml 0
have important imp lica tions for surgica l management: ally in one-third of cases.
1 Rare SU~
• Central bronchial carcinoma (75-80 %) has its origin in • Adenocarcinoma is the third most common histologic
claSSifiec
the lobar, segmental, or subsegmental bronchi. These type in Germany. In the United States, its incidence is 2 Most pie
tumors grow into the bronchial lumen along the peri- increas ing, and it may now be the most common cell sian are
bronchial lymphatics and through to the interstitium. type in females and in nonsmokers. Adenocarcinoma effu sion
Bronchial Carcinoma ' 59
tes in Autopsy Surgical Fig.6.12 Bar graphs indicate the hi stologic types of bronchial
specimens specimens carcinoma found at autopsy (MOnster Institute of Pathology,
y the n - 393 n - 740 1965-1975) and at surgical resection (from Hinson et al.).
Tiph- 100
%
eural
90
;tage.
~ Pan
80
, the
Iduce 70
(Pan-
ively. 60
'er al-
.they SO
Their
n the 40
upto
30
1995,
).
20
§ Adenocarcinoma
o the 10 D large-cell carcinoma
;. He- ~ Squamous cell carcinoma
CZl Small cell carcinoma
static 0
y ac-
. (Ta- Table 6.3 TNM clinical classification of bronchial carcinoma
2): T: Primary t umor

TX Primary tumor cannot be assessed, or tumor proven by the presence of malignant cells in sputum or bronchial washings
:ocia- but not visualized by imaging or bronchoscopy
lomi- TO No evidence of primary tumor
lainly Tis Carcinoma in situ
lorna T1 Tumor :s: 3 cm in greatest dimension, surrounded by lung or visceral pleura, without bronchoscopic evidence of invasion
esent more proximal than the lobar bronchus (1. e., not in the main bronchus)!
I car- T2 Tumor with any of the following features of size or extent:
rgical • > 3 cm in greatest dimension
with • Involves main bronchus, ~ 2 cm distal to the carina
iis of • Invades the visceral pleura
• Associated with atelectasis or obstructive pneumonitis that extends to the hilum but does not involve the entire lung
T3 Tumor of any size that directly invades any of the following: chest wall (including superior sulcus tumors), diaphragm,
mediastinal pleura, parietal pericardium; or tumor in the main bronchus < 2 cm distal to the carina 1 , but without involve-
:alled ment of the carina itself; or tumor associated with atelectasis or obstructive pneumonitis of the entire lung
sease T4 Tumor of any size that invades any of the following: mediastinum, heart, great vessels, trachea, esophagus, vertebral
lance body, or carina; or satellite tumor nodules within the lobe containing the primary tumor; or presence of malignant pleural
,d by effusion 2
Joint N: Regional lymph nodes
1986 NX Regional lymph nodes cannot be assessed
odes, NO No regional lymph node metastasis
" (T), N1 Metastasis of ipsilateral peribronchial and/or ipsilateral hilar lymph nodes, and intrapulmonary nodes involved by direct
lstant extension of the primary tumor
:ation N2 Metastasis to ipsilateral mediastinal and/or subcarinallymph node(s)
,6.4). N3 Metastasis to contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular lymph
!ntral node(s)
ental, M: Dist ant met ast asis
rhese MX Presence of distant metastasis cannot be assessed
lency MO No distant metastasis
pher- M1 Distant metastasis present
I Rare superficial tumors of any size with invasive components limited to the bronchial wall that extend proximal to the main bronchus are also
llogic classified as Tl .
nee is 1 Most pleural effusion s in lung cancer are ca used by the tumor. But the re are a few patients in who m serial cytologic examinations of the ple ural effu-
n cell sion are negative and the effusion is not bloody o r exudative. When the se finding s and the clinical evaluation exclude a tumor-related effusion , the
noma effusi on should not be scored as a malignant e ffu sion for staging purposes. and t he tumor should be classified as Tl, T2, or n .
160 6 Tumors and Tumor-Like Lesions ofthe Lung
i~
ti
a
p
o
b
n
tl
h
o
o
o
V
IJ
s
h
Atelectasis or obstructive pneumonia n
s
N1 N1 t
Peribronchial h
Atelectasis or
obstructive ci
pneumonia
affecting the
entire lung
." ~
a
t
n
a
g
~
s
a
• l
s
Jugular cervical r
Pleural effusion with negative cytology
lymph node metastasis s
(not supraclavicular)
Heart and N3 ---!-----__~<.'I0\ij

great vessels
Fig.6. 13 TNM classification of bronchial carcinoma (UICC: TNM Atlas. Berlin: Springer 1990).
Bronchial Carci nom a 161
is a peripheral tumor in 75% of cases w ith a predilec- Table 6.4 Staging of bronchial carcinoma
tion for the upper lobes. Initially. it was thought that
Occult carcinoma TX NO MO
adenocarcin om a had a predilection for regions of
Stage 0 Tis NO MO
parenchymal fibrosis (scar ca rcinomas). More re-
Stage IA Tl NO MO
cently. this concept has been challenged and it has
Stage IB T2 NO MO
bee n suggested that so me peripheral adenocarci-
noma s may induce a desmoplastic reaction to the
Stage IIA Tl Nl MO
tumor and form central fibro sis (Aoki et al. 2000). The Stage liB T2 Nl MO
hi stologic subtype of adenocarcinoma, bronchi- T3 NO MO
oloa lveo lar ca rcinoma grows mainly w ithin the alve- Stage iliA Tl. T2 N2 MO
oli respecting interstiti al boundaries. Bronchioalve- T3 Nl. N2 MO
olar ca rci noma may be unifocal or multifocal and Stagolll8 Any T N3 MO
w hen multifocal may produce alveolar cell ca rcinosis. T4 Any N MO
Immunohi stoche mical express ion of thyroid tran- Stage IV Any T Any N Ml
scription factor 1 (TIF1) has been show n to be a
highly specific marker for primary lung adenocarc i-
noma (Reis-Filho et al. 2000). TIF1 has also been
shown to be positive more frequently in peripheral
than in ce ntral primary lung adenocarcinoma (Sten- • Clinical Features
house et al. 2004). This therefore may be helpful in
disti nguis hing a peripheral primary lung ade nocarci- Patients are frequent ly asymptomatic until the di sease
noma from a so litary pulm onary metastasis. has reached an adva nced stage. Respiratory manifesta-
• Noguchi Classification: The Noguchi classifi cation of tions include cough w ith recurrent epi sodes of pneu-
adenoca rcin oma was pub li shed in 1995. Noguchi monia and hemoptysis. Systemic features of neoplasia
types A/B showed a "replaceme nt" growth pattern, including lethargy, cachex ia, anorex ia. eleva ted erythro-
no lymph node metastases and was associated w ith cyte sedi mentation ra te (ESR). and anemia indicate ad-
an exce ll ent prognosis. Type C comprised the lepidic vanced disease. Local invasion of extra pulmonary stru c-
growth pattern of types AlB but in add ition showed tures may lead to venous obstruction (s uperior vena
foci of fib roblastic proliferation. Types D- F repre- cava). dysphagia (esop hagus ). hoarseness (recu rrent
se nted "nonrepl ace ment" form s of adenocarcin oma laryngeal nerve). Horn er sy nd ro me (sympathetic trunk ),
and had a less favorable prognosis (Noguchi et al. and arm pain (brachial plexus).
1995). Distant metastases especially to the brain and skele-
• Large cell carci noma tend s to be a diagnosis of exclu - ton may also be the initial manifestat ion of bronchial
sion. Microscopically. these large cells with promi- carc inoma.
nent nucleoli lack features of squamous, ade no, or
small cell differenti ation.
162 6 Tumors and Tumo r-like l esions of the lung
• Radiologic Findings Bro,

Mas
• Chest Radiograph (Fig. 6.14): do ll
oeel
are;
Central bronchial carcinoma. dire
predominantly peribronchial growth
freq
sene
• F
b
a
a
n
Hilum of increased size

· o
[
5'
- Laterally convex hilar contour tl
and/or density - Soft tissue stranding radiating Carcinomatous
Predominantly endobronchial growth

from the hilum into the lung pleural involvement
"ti
tl
• C
tl
. :::.~ b
, .-
'A
P
"
S!
d
la
- Distal pulmonary hyperinflation Small hypertransradiant Decreased tracer uptake
- Paradoxical hilum sign lung (Fraser's sign) at perfusion scintigraphy
T.
d,
Invasive peripheral tumor tt
ti
• R,
in
lu
(t
P'
d,
..... fn
al
Atelectasis Distal - Bronchial stenosis or occlusion - Rib destruction re
pneumonia - Endobronchial filling defect - Superior vena caval compression • H
- Diaphragmatic paralysis and elevation
- Esophageal encasement nc
Peripheral bronchial carcinoma and narrowing st
ea
• Rigler notch sign
.=:.... .. ..
te
•
lit
••••
.....
~
~
Corona radiata -4
. ....
~
.
~.
~
~
~ .
....
•
Eccentric cavitation • !.I
••
e--- Pleural tail
l epidic growth pattern with alveolar opacification -
Fig. 6.
copiG
jected
Pulmonary nodule unifocal or multifocal lobar
the at
pleura
Fig.6.14 Radiographic signs of bronchial carcinoma. advan
Bronchial Stenosis/Occlusion
Most ce ntra l bronchial ca rcinomas exhib it either en-
dolumin al or transmural growth and bronchial stenosis/
occlusion with associated di stal parenchymal changes
are a common finding. Occasionally, bronchial stenosis is
directly visible on the chest rad iograph. Much more
frequently. the following indirect signs suggest the pre-
sence of a ce ntral obstructing les ion:
• Partial or complete atelectasis is a commo n finding in
bronchi al carci noma. Segments, lobes, or occasion-
ally an enti re lung no longer are aerated (Fig. 6. 15,
and see Fig. 6.24 ). There may be associated displace-
ment of the adjacent interlobar fissure, mediastinum,
or hemidiaph ragm.
• Distal pneumonia presents as lobar or segmental con-
so lidation w hi ch may resolve partially w ith antibiotic
therapy. In patie nts w ith appropriate risk factors and
recurrent or persistent pneumonia, further evalua-
tion with cr and/o r bronchoscopy to exclude a cen-
tral endobronchial tumor is me rited.
• Distal Ilyperinflation is unu sual and is seen in less
than 2 % of cases (Frase r and Pare 1983). Partial
bronch ial occl usion creates a check-valve obstruction
w ith inspiratory expansion and expiratory air trap-
ping. Hyperinflated lung is seen radiogra phically as a
region of hypertransradiancy and there may be as-
sociated displacement of neighboring structures. Me-
diastinal shift to the contralate ral sid e and an en-
larged contralateral hilum are additional features.
This hil ar enlarge ment, w hich may also result from
decreased perfusion on the sid e of the carcinoma, is
the "paradoxical hilum" sign. Unilateral hyperinfla-
tion is sometimes more obv ious on expiratory views
• Reflex oligem ia. Partial obstruction causes ventilatory
impairment eve n when the volume of the affected
lung is normal or increased. Hypoxic vasoco nstricti on
(the Eu ler Liljestrand reflex) then results in reduced
perfu sion. This is manifest radiogra phically as a
decrease in vesse l caliber. Oligemia may also resul t
from e ncasement and compression of the pulmonary
artery. Vesse l attenuation in the affected lung then
results in hypertransradiancy.
• Hilar mass. Growth of so me central bronch ial ca rci -
nomas is predom inantly peribronchial in the initial
stages (see Fig. 6.19). Th e chest rad iograph in these
cases may show a hilar mass. Ini tially the hilum is a l-
tered in co ntour and enlarged, then the mass may ob-
literate the lateral hilar co ncavity and finally normal
Fig. 6.15 left lower lobe atelectasis in a patient with bronchos-

copically confirmed carcinoma. Note the triangular opacity pro-
jected behind the heart and inability to visualize the left lower
lobar artery on the chest radiograph (a). CT images (b , c) show
the atelectatic III with visible air bronchograms and a small left
pleura l effusion. Changes are superimposed on a background of
advanced centrilobular emphysema.
164 6 Tumors and Tumor-Like Lesions olthe Lung
may
may
larly
Intral
The F
trati"
• UI
(F
• Oi
in'
th
tic
• Es
stt
ch
stl
• Ip~
Fig.6.16 Adenocarcinoma of the right lower lobe displaying a Fig.6.17 Multifocal bronchioloa lveolar carcinoma. There is also
ph
lepidic type growth pattern with radiographic evidence of pulmo- cardiac enlargement due to the presence of a malignant peri-
nary consolidation. Histology co nfirmed alveolar infiltration by cardial effusion. to l
carcinoma cells. pit
by
efF
nodules g reater than 1 cm may be missed due to supe r- tht
im position of normal structures. Whil e a specific diagno- prt
sis is not possible from radi ologic findings, the foll owi ng tio
features suggest a diagnosis of bronchial ca rci noma: st.
• Larger lesio ns are more likely to be malignant.
• Ill-defined margins are present in 85% of mali gnant Hema'
tum ors (Mulle r and Fraser 2001). Osteol
• The corona radiata co rresponds to radial stri ated sign if~
markings at the interface with lung parenchyma;
these represent centri fugal tumor spread along the COl
lymp ha tics.
• Notching of the contour, which represents the vascu- Heli ca
lar hilum of the tumor and is termed the "Rigler Furthe
notch" sign. cantin
• A cavitating les ion is typ ical of either primary ing stc
bronchial sq uamous cell carcino ma or a metastati c Thi
deposit from a squamous ce ll ca rci noma of uterine thorax
cervix or skin. uppe r
ment i
Pneumonic Form of Carcinoma The
Th is patte rn of disease appears as an ill-defined, patchy, 1. The
Fig.6. 18 Bronchioloalveolar carcinoma. There is a segment of
o r homogeneous co nsolid ati on in a segmental or non- deg
peri pheral consol idation in t he su bpleural lung anteriorly wit h an segme nta l distribution. An air aJveologra m and air bro n- Ima
area of "a lveolar" type opacification also seen in the right middle chogram may be seen (Figs. 6.16-6.18). Initially, this ap- ide!
lobe. pearance simulates an infective consolidation but lack of roa(
radiologic and /or clinical response to antibiotic therapy 2, The
shoul d lead to biopsy and diagnos is. Histologically, the Iym
hilar structures may beco me com pletely obscured. majority of these tumors are bronchi oloal veo lar ca rci- nod
Linear stran ding extending into the perihilar lung nomas or adenoca rcinoma with bronchio loalveolar side
may represent lymphatic infiltration with desmo- characteri stics. less
plastic reaction. east'
Mediastinal lymph Node Enlargement usin
Peripheral Pulmonary Nodule Bulky paratrachea l. tracheobronchial, and ao rtopulmo- erat
The size threshold for detection of small les ions on the nary lym ph nodes lead to w iden ing of the mediastinum port
chest radiog raph is 7 to 9 mm (Armstrongetal. 1995), but w hile large volume subca rinal lymph node en la rgement 199 ~
Bronchi al Carcinoma 165
may cause splaying of the carina. Mediastinal w ideni ng Table 6.5 Radiographic signs related to tumor histology (from
may be the first radiogra phic sign of lung cance r particu- Muller and Fraser: Diseases of the Chest. Philadelphia: Saunders
2001)
larly in small cell carcinoma (Ta ble 6.5).
Occult carcinoma Squa- Small Adeno- large
Intrathoracic Spread of Bronchial Carcinoma mous cell car- carci- cell car-
The following radiographic features suggest loca lly infil- cell carcinoma noma cinoma
n'ative carcinoma (Fig. 6.19): cinoma
• Upper lobe tumor with local chest wall invas ion
Hilar mass 40 % 78 % 18% 32 %
(Fig. 6.20).
Peripheral mass 27 % 29 % 71 % 59 %
• Diaphragmatic paralysis secondary to phrenic nerve
large mass (18 %) (26 %) ( 8 %) (41%)
involvement. The inspi ratory view shows elevation of (> 4em)
the ipsilateral hemidiaphragm and paradoxical mo- Apical Mass ( 3%) ( 2%) ( 1%) ( 4%)
tion is evident at fluoroscopy. Multiple masses ( 0%) (1%) ( 2.4 %) ( 2%)
• Esophagea l involvement: Dilatation proximal to a Atelectasis 36 % 17 % 10 % 13 %
ste notic segment may occasionally be visible on the Pneumonia 15% 22 % 15 % 23%
chest radiograph. A contrast swall ow w ill demon- Cavitation 7% 2% 4%
0%
strate the level and degree of obstruction.
Mediastinal 1% 13 % 2% 10 %
• Ipsilateral pleural effusion may signify malignant lymph nodes
o pleural involve ment and this is co nfirmed by cy-
'i-
tology of pleural aspirate plus or minu s percutaneous
pleural biopsy. Occasionally, lymphatic obstruction
by a cent ral bronchial carcinoma res ults in a pleural Rib destruction
effu sion and in these cases resol utio n is expec ted as
r- the tumor responds to thera py. Pleural effusion is
)- prese nt in approximately 15 % of cases at presenta-
19 tion and is found in over 50 % of patients at so me
stage during the course of their illness.
ot Hematogenous Spread of Bronchial Carcinoma

Osteolytic bone lesions and pathologic fractures may
ed signify hematogenous spread of disea se. - Superior vena
la: caval compression
he computed Tomography - Diaphragmatic paralysi s
- Esophageal stenosis
:u- Heli cal MDCT is today the standard imaging modality for
Fig.6.19 Intrathoracic spread of bronchial carcinoma.
ler further eva luation of suspected bronchial carcinoma. It
confirms the presence of tumor and allows initial imag-
try ing staging of disease.
.tic Thin collimation helical vo lumetric CT through the
ine thorax in the systemic arterial phase and through th e
upper abdomen in the portal venous phase of enhance-
ment is routinely acquired.
These allow assessment of:
:hy, 1. The primary tumor including its size and to some
an- degree, the exte nt of local invasion (Figs. 6. 21, 6.22).
on- Image acqui sition through the thorax accurately
ap- identifies airway involvement and may se rve as a
<of road map for the bronchoscopist (Figs. 6. 23, 6.24b, e).
apy 2. The presence and vo lume of hilar and mediastina l
the lymph node enlarge ment (Fi g. 6.25 a, b). Lymph
lrci- nodes greater than 10 mm in short axis are con-
olar sidered to be abnormal w hil e lymph nodes that are
less than thi s va lue are determined to be free of dis-
ease. However, the sensitivity and s pecificity of cr
using these size criteria has been shown to be mod-
ma- erate (Fig. 6.26). Metastatic involvement has been re-
lum ported in up to 21 % of "normal" nodes (Arita et al. Fig.6.20 Pancoast tumor. Squamous cell carcinoma in the right
nent 1995 ) and up to 40 % of enlarged nod es have bee n upper lobe with associated destruction of the third to fifth ribs.
166 6 Tumors and Tumor-like lesions of the lung
Fig . 6.21 a, b Right upper lobe bronchial carcinoma in a heavy

smoker (who was reluctant to part with his cigarettes even during
CTl). b
Fig.6.22 left upper lobe tumor with rib destruction and infiltra-
tion of subscapularis muscle.
b
Fig.6.
lobe t
a b c
Fig. 6. 23 a-c Endobronchia l tumor. CT demonstrat es soft tissue lesion t hat is partially obstructing the right lower lobe bronchus as it
branches into segme ntal bronchi. Confirmed at bronchoscopy.
Bronchia l Carci noma 167
iltra-
b c
Fig.6. 24a-c G: Bronchial carcinoma. Chest radiograph (a) shows left upper lobe atelectasis. CT shows occlusion of the left upper
lobe bronchus (b) and tumor infi ltration of the mediastinum (c) .
•as it
b
Fig. 6. 2Sa. b Bronchia l carcinoma w ith mediastinal lymph node metastases. CT (a) shows cavitating right hilar/lower lobe mass with
confluent pretracheallymph node mass (b).
shown to be disease free at sampling du ri ng bron-

Sensitivity
choscopy or mediastinoscopy (A ri ta et al. 1996).
1.0
3. Compression and invasion of mediastina l vascular
10mm structures may be identified. Gross mediastinal inva-
/'
5mm
sion can be id entified accurately by cr (Figs. 6.27-
0.8
15mm 6.31). However, neither cr nor MR I a ll ows accurate
20mm differentiation between direct invasion and si mple
co ntact between the tumor and the mediastinum
0.6 (Rendina et al. 1987. Martini et al. 1985. Glazer et al. b
1989). In fact. Glazer et al. found that when contact of
the tumor with the mediastinum was less than or
25mm
0.4 equal to 3 em, the arc of contact with the aorta was
less than 90 degrees and/or the fat plane with the
30mm mediastinum was preserved, the tumor was re-
sectable in 97 % of cases.
0.2
4. Thin collimation images may be reconstructed on a
(l-Specificity) high-resolution algorithm at lung windows and allow
0.2 0.4 0.6 0.8 1.0 for assessment of the presence of both pulmonary
0 metastases and lymphangitis careinomatosa.
1.0 0.8 0.6 0.4 0.2 0
Specificity 5. Hepatic and adrenal involvement may be identified
on images through the upper abdomen.
Fig.6.26 Lymph node metastases from nons ma ll-cell bronch ial 6. Reformatted images in the coro nal and sagittal
carcinoma: sensitivity and specificity of CT detection versus the planes when viewed at bone windows (WW • 2500.
transverse diameter of the lymph nodes. When a lymph node
diameter of 10 mm is used as the value for lymph node involve-
WW. 500) may demonstrate lytic skeletal metasta-
ment. the specificity is 70 % and the sensitivity is 95 %. When this ses.
is increased to 15 mm, the specificity rises to 95 % while the sensi-
tivity falls to 80%.
Fig. 6.28 a, b Bronchial carcinoma with superior vena caval t>

encasement. CT shows right upper lobe mass which is occludi ng
the right upper lobe bronchus (a). There is mediastina l invasion
w ith tumor encasement and extrinsic compression of the super-
ior vena cava (b). a
Bronchial Carcin oma 169
Fig. 6. 27 a-c Bronchial carcinoma with pulmonary venous

thrombosis. CT shows right upper lobe tumor (a). There is occlu-
sion of the fight superior pulmonary vein by probable tumor
b thrombus (b) and this extends proximally into the left atrium(c).
II
J,
.-
.1 I>
'9
on
,-
•
170 6 Tumors and Tum or-Like Lesions ofthe Lung
a b
Fig. 6.
Fig. 6.29 a, b Squamous cell carcinoma with cavitation and direct left atrial invasion.
Sc
Ultra.
site fl
ticul.::
an ell
• Ra
PatieJ
w ith
denet
a b bone
Fig. 6. 30 a, b Bronchial carcinoma with extensive confluent right hilar and mediastinal lymph node involvement.
of sk,
• Po
To
The p
the (
patiel
Ev,
been
natiol
bronc
and s
men a
son 0
porati
They
a b 91 % f,
Fig. 6.31 a-( Bronchial carcinoma with SVC encasement. Contrast medium injected into the right antecubital vein opacifies the azy- 77 %f,
gos vein via chest-wall collatera l veins and then opacifies the SVC inferior to the level of tumor encasement. ac(ur;
Fig. 6.31 c t> ofNS(
ity, sp
and f
were
COl
PETw
a
b Fig. G.31c
• Sonography
Ultrasound may be useful in determining the optimal

site for pl eural aspiration and percutaneous biopsy par-
ticularly in the presence of phrenic nerve paralysis and
an elevated hemidiaphragm.
b
Radionuclide Bone Scintigraphy
Patients with systemic features of malignancy. patients

with bone pain, and those with plain radiogra phic evi-
dence of osteolysis may be evaluated with radionuc1ide
bone scintigraphy to assess the extent and distribution
b
of skeletal involvement.
Positron Emission Tomography-Computed

Tomography (PET-CT)
The past decade has seen PET-CT being incorporated into

the diagnostic pathway in the imaging staging of
patients with nonsmall cell lung ca rcinoma (Fig. 6.32).
Evaluation of nodal stage: As described above. cr has
been shown to have substantial limitations in determi-
nation of local/regional lymph node involvement in
bronchial carcinoma. PET shows increased sensitivity
and specificity in determination of nodal stage. Owa-
mena et al. (1999) performed a meta-analytic compari-
son of FDG-PET and CT for mediastinal staging incor-
porating a number of studies performed in the 1990s.
They reported a se nsitivity of 79 % and a specificity of c
b 91 %for PET and a se nsitivity of 60 % and a specificity of Fig. 6.32 a-c Staging of Bronchial Carcinoma. Axial CT image
azy- 77% for cr. More rece ntly, Shim et al. have compared the (a) shows TljT2 tumor in left upper lobe. Axial (b) and coronal (c)
accuracy of PET-a and cr alone in preoperative staging images from staging PET study show increased FDG uptake in pri-
I> mary tumor but no evidence of hi lar or mediastinal lymph node
of NSCLC. For depiction of malignant nodes the sensitiv- or distant metastatic spread consistent with stage 1 disease.
ity, specificity, and accuracy of CT were 70, 69, and 69 %
and for integrated PET-cr, the corresponding values
were 85, 84, and 84% (Shim et al. 2005 b).
Combined Nand M staging: Marom et al. co mpared
PET with "conventional" imaging staging in 100 patients
172 6 Tumors and Tumor-like lesions ofthelung
with newly diagnosed bronchogenic carcinoma. Con-

ventional imaging staging comprised thoracic cr,
radionuclide bone scintigraphy, and Cf/M RI brain. They
showed an overall accu racy in staging of 83 %for PET and
of 65 % for co nvent ional imaging. Nine percent of
patients had metastases at PET not demonstrated on
co nventional imaging whereas 10 %suspected of meta-
static spread at conventional imaging were shown COf-
rectly by PET to have no Illetastases (Marom et al. 1999).
FOG PET ha s also been evaluated in the assessment of
patients who had completed treatment for NSCLC.
Patients with a positive PET study had a median survival
of 12 months whereas in patients w ith a negative study.
85 % were still alive at a median follow-up of 34 months
(Patz et al. 2000). a
Fig. 6.~
Magnetic Resonance Imaging dobra,

pulmo
Magnetic resonance imag ing plays a complementary
role to IT in selected instances.
Superior sulcus tumors: Magnetic resonance remains
the modality of choice for imaging superior sulcus
tumors. Extent of tumor invasion and neurovascular in-
volvement may be demonstrated (Fig. 6.33 a, b), and the
intrin sic co ntrast between the low intensity of the
tumor and the high intensity of fat on Tl-weighted
sequences is valuable.
The role of MRJ in assessment of chest wa ll invasion
a
at other sites remains more equ ivocal (Musset et al.
1986, Webb et al. 1991).
CNS involvement: Up to 40 % of patients with adeno-
ca rcinoma and mediastinal node involvement will have
eNS metastases, and magnetic resonance brain im ag ing
may be appropriate in this group.
Fig. 6.33 a, b MRI shows large right upper lobe tumor which is
involving the lower cords of the brachia l plexus (a). There is also
invasion and destruction of the upper thoracic vertebrae with spi-
b nal cord compression (b).
Pulmonary Metastases Fig. 6.3
Pulmonary metastases occur in 20 to 30% of all malig- noma. Endobronchial spread is unusual but sometimes • Dis
nancies (Weiss et al. 1973 ) and usually result from he- may be found in head and neck malignancies as well as sile
matogenous spread of tumor cells. Less commonly. they in renal and breast carcinoma (Fig. 6.34). Pulmonary flO(
result from lymphatic spread; this occurs most metastases may be classified according to their growth tef:
frequently with gastric, pancreatic. and breast carci- patte rn (Fig. 6.35): sea
Pulmonary Metastases 173
.I
I,
S
a b
Fig. 6. 34a. b Metastatic breast carcinoma: pulmonary and en- and posterior segmental bronchi to the right upper lobe with dis-
dobronchial metastases. Helica l CT images show bilat eral nodular tal lung atelectasis (a, b). Biopsies acquired at bronchoscopy
pulmonary meta stases (a ). There is also occlusion of the anterior showed metastatic breast carcinoma.
y
IS
IS
l-
ie
Ie
d
In
II.
'
: . '.
..
• •
••
• •• •
•
•
•
• • ••
•
•
••• ••
••
)- Coarse nodular pattern:
Ie Miliary pattern: primary tumor in oropharynx, MCannon bali pattern:
R
primary tumor in thyroid, lung, stomach, thyroid, or female primary tumor may be a sarcoma,
Ig carcinoma, seminoma, or renal
breast, or skeletal sarcoma genital tract; lymphosarcoma,
choriocarcinoma cell carcinoma
is
so
pi-
Pulmonary Lymphang itis:

primary tumor in t he breast, Pleural metastatic disease: Pneumonic and peribronchial pattern:
pancreas, or lung ; lymphoma primary tumor in the breast. primary tumor in th e esophagus,
or leukemia stomach, or unknown. lung . or breast
Most common cell type is
adenocarcinoma
Fig.6.35 Rad iographic features of intrathoracic metastases (from Meschan 1981).
les • Discrete pulmonary nodu les show a spherical expan- taneous growth. Some correlation may exist between
as sile type of growth. Metastatic de posits range from the primary tumo r and the pattern of metastases.
uy fine miliary nod ul es to mass lesio ns several ce ntime- • Pulmonary lymphangitis carcinomatosa (PLC ) is
/th ters in diameter. Multiple nod ules of uni for m size characterized by permeation of t he lymp hatics of the
sca ttered t hroughout both lungs suggest simul- pulmonary interstitium by tumor cells.
174 6 Tumors and Tumor-Like lesions olthe lung
• Pleural carcinomatosis may ca use massive pleural ef- plied by the pulmonary circulatio n. In pulmonary lym- stc
fusio n w ith or without neo plastic pleural thickening. phangitis carci nomatosa, stra nds of neop lastic cells cai
• Endobronchial spread. grow in the subpleu ral, septal, and peribronchovascu- re!
lar interstitium. There is an associated desmoplastic
reactio n whic h leads to decreased pulmonary compli-
• Pathology ance.
Different tumor types metastasize with varying

frequency (Table 6.6). Tumor ce lls are filte red by pulmo- • Clinical Features
nary capillaries and lymphatics. pro liferate and develop
into ex pansive ly growing sphe rical masses. Permeati on Pulmonary metastases may be asymptom atic or whe n
of the ca pillary wall with growth into the lymphatics. profuse may cause dysp nea. Pulmonary lymphangitis
small airways and a lveoli may occur. Histologically, ca rcino matosa may be associated with co ugh and
metastases show good co rrelation w ith the ce ll type of marked dyspnea. Pleural ca rcinomatosis frequently
the primary tumor, e. g., ossification is see n in yields a se rosa nguinous blood-stained effu sion contain-
metastases from osteogenic sarcoma. ing tumor ce lls.
Quint et al. eval uated the frequen cy of single lung
metastasis, bronchogeni c carcinoma, and benign les ions
in patients w ith a solitary pulmonary nodule and a • Radiographic Findings
known extrapulmonary neoplasm. In patients with car-
cinomas of the head and neck. bladder. breast. ce rvix. • Plain Chest Radiograph
bile ducts. esophagus, ovary, prostate, and stomach, a
SPN was more likely to represent a primary broncho- • Nodular metastases. These homogeneous nodul es are
geni c carcinoma than a metastatic deposit w hereas in usually smooth with we ll-defined margi ns
patients w ith melanoma, sarcoma, and testicular ca rci- (Figs. 6.36-6.38 ). Cavitation is unusual (4%) and oc-
noma, a SPN was more likely to refl ect a metastati c curs predominantly in squamou s cell metastases.
deposit (Quint et al. 2000). Calcifi ca ti on and ossifi cation are found in metastases
Perihilar metastases are supplied by the bronchial from chondro- and osteosarcom a, respectively. a
arteri al system w hile peripheral lung lesions are sup- • Pulmonary lymphangitis carcinomatosa is character-
ized by reticulolinear markings including Kerley A
and B lines. Associated loss of vo lume may result in a
small hemithorax. Pleural effu sion is present in 50 %
of cases. In metastatic breast carcinoma, pleu ra l and
Table 6.6 Incidence of pulmonary metastasis associated with pulmonary changes are ipsilateral to the breast pri-
various primary tumors (after Dahnert 2002) mary in two-thirds of cases, presumably resulting
from contiguous extensio n Uanower and Blennerh as-
Primary tumors accounting for _ % of pulmonary
sett 1971 . lange and Minck 1983).
metastases
Breast 22 • Pleural carcinomatosis: Radiographic findings include
Kidney 11 pleural effu sion w ith o r w ithou t neoplastic pleural
Heat and neck t umors 10 thickening. Pleural carcinomatos is is especially co m-
Colorectal carcinoma 9 mon in breast, bronchoge ni c, and gastro in testina l ad-
Uterus 6 enocarcinoma.
Pancreas 5 • Endobronchial metastases lead to distal atelectasis.
Ovary 5
Prostate 4 • Radionuclide Scintigraphy
Stomach 4
Thyroid scintigraphy: Metastases from we ll-differen-
Frequency with which primary tumors metastasize to the tiated thyroid carcinoma may conce ntrate radi oactive
lung
Kidney 75 iodine as does the primary tumor (Fig. 6.40).
Osteosarco ma 75
Choriocarcinoma 75 • Computed Tomography
Thyroid gland 65
Me lanoma 60 Discrete pulmonary nodules: cr is su pe rior to the chest
radiograph in demonstrating small pulmonary nodules.
Breast 55
These tend to have well-defined smooth contours and be
Prostate 40
more numerous in the mid to lower zo nes in keeping
Head and neck tumors 30
with hematogenous spread. Metastases from a squa-
Esophagus 20
mou s cell primary lesion may s how cavitation and meta-
m- static deposits from osteo- and chondrosarcoma typi - Pulmonary lymphangitis carcinomatosa: Thin colli-
,lis ca lly show ossification and chondroid-type ca lcification, mation/high-resolution cr is optimal for demonstra-
:u- respectively. tion of PLC. Findings include s mooth or beaded thick-
:tic
,Ii-
len
itis
nd
tly
in -
b
Fig. 6.36 a, b Pulmonary metastases appear as
:ue multiple small nodules in a patient with known
gastric carcinoma.
ins
)(-
,es.
ses
a
er-
' A
Fig. 6.37 ~Cannon ball" pattern of
na
pulmonary metastases from a
0% testicular teratocarcinoma .
.nd
Iri-
.ng
as-
Ide
.ral
m-
,d-
:n-
ive
est
les.
be
ing
ua-
·ta-
176 6 Tumors and Tumor-like Lesions of the Lung
Fig.6. 38 Very large pulmonary metastases from

a tibial fibrosarcoma.
L
b
a b
Fig. 6.39 a-c Pulmonary lymphangitis carcinomatosa (Ple): In -

creased reticular markings are seen in the mid and lower zones
with an associ ated pleural effusion (a). Radionuc1ide scintigraphy
shows some decrease in right pulmonary perfusion (b). HRCT (c) L
c
shows extensive interlobular sept al and centrilo hular thickeni ng
consistent with Ple. There is also sig nificant m ediastinal lymph Fig. 6.·
node enlargement. Patient had presented clinically with severe uJar th
c dyspnea . show ,
the Ie'
from
R
b
'.
.,'
:): In-
:ones
'aphy
:T (e) L R Fig. 6.41 a-c Pulmonary lympha ngitis carcinomatosa:
e image (a) shows interlobular septal and centrilobular thickening,
~n;ng
(mph Fig. 6.40 a-c Pulmonary nodules in a patient with known follic- features consistent with PLC. Multiple discrete nodular metas-
~vere
ular t hyroid ca rcinoma. ThyrOid scintigraphy (99mTc-MOP and 1311) ta ses are also present. Images viewed at mediastinal windows
show a solitary iodine-concentrating lesion in the parenchyma of show evidence of a pericardial effusion (b) and subcarinallymph
the left lung. node enlargement (c). Final diagnosis was "metastatic adeno-
carcinoma with unknown primary."
ening of the peribronchovascular and centri lobular in- Endobronchial metastases: Helical vo lumetric CT
terstitiu m and of t he interl obular septa (Fig. 6.39 and thro ugh the cen tral airways may show bronchial occlu-
Fig. 6.41 ). sion and di sta l ate lectasis/consolid ati on (see Fig. 6.34).
lymphoma
lym phoma represe nts a neo pl astic proliferation of lym - Table 6.7 Classjfjcation of Hodgkin and non-Hodgkin lym-
phoid ti ssue and accounts for app rox imately 2 % of all phomas
mali gnancies. Hodgkin disease (HO) shows a peak inci- Ann Arbor staging classification of Hodgkin and
dence in chi ldhood and in the 2nd and 3rd decades non-Hodgkin lymphoma
w hile non-Hodgkin lymphoma (N Hl ) is most co mmon Stage I Involvement of a single lymph node region
in the 5th to 7th decades. Intrathoracic involveme nt is Stage I e Involvement of a single extra lymphatic organ or
site (e. g., pulmonary nodule)
common with me di astinal adenopathy be ing fou nd in Stage II Involvement of two or more lymph node
67 to 84 %of patie nts w it h HD at in itial prese ntation. Ex- regions on the same side of the diaphragm
tra nodal disease in the pulmona ry pare nchyma is less Stage It e Localized involvement of an extra lymphatic
co mmon. Diagnos is and hi sto logical cl ass ification are organ or site and of one or more lymph node
regions on t he same side of the diaphragm
us ually based o n node bi opsy, bu t occasionally lung bi-
(e. g., including perihilar parenchymal invasion
opsy may yield the di agnosis. with ipsilateral lymphadenopathy and uni lateral
pleural effusion with hjla r lymphadenopathy)
Stage III Involvement of lymph node regions on both
Goals of Diagnostic Imaging: sides of the diaphragm
Initial staging of lymphoma. Stage III e Stage III, accompanied by localized involvement
of an extralymphatic organ or site
Monitoring radiologica l response to therapy, imagin:J Fig. €
Stage IV Diffuse involvement of one or more ext ralym-
co mplications of trea tment, and detecting evi dence of phatic organs or tissues (e. g., including multifo-
re lapse. cal lung involvement, bilateral effusion)
Histologic classification of Hodgkin disease (Rye classifica-
tion)
1. Lymphocyte predominant (paragranuloma), incidence 15%
2. Nodular sclerosing, incidence 40 % . I;
• Pathology 3. Mixed cell, incidence 30%
ql
4 . Lymphocyte depleted (Hodgkin sarcoma), incidence 15 %
HD is cha racte rized by lym phocyte proliferation and the la
WHO classification of non-Hodgkin lymphoma • 1'1
presence of Reed-Sternberg ce ll s. The Kiel classifi cation (I) low-gra de lymphomas (low risk)
is used in NHL. and further characteri zatio n is based on • B-ceillymphoma:
specific im munologic marke rs (Table 6.7). Lymphocytic lymphoma, CLl m
Immunocytic lymphoma (Waldenstrom disease) tt
Hairy cell leukemia fn
Marginal zone lymphoma
• Clinical Features Extranodal MALT B-ceillymphoma m
Follicle center lymphoma br
Pati ents may prese nt w ith cervical. axilla ry. or inguinal Mycosis fungoides, Sezary syndrome cr
(II) Aggressive lymphomas (int erm ediat e risk) m
lym ph node enlarge ment or w ith systemic man ifesta-
tions such as fever, lethargy, weight loss, and night • B-cell origin: br
Plasmacytoma
sweats. Occasio nally, massive med iastin al lymph node ta
Mantle cell lymphoma
en largement may lead to respiratory sym ptoms of Follicle center lymphoma
co ugh, dys pnea, and ret rosternal pai n. Diffuse large-cell B-cell lymphoma C,
Thymic B-Iarge cell lymphoma
High-grade B-ceillymphoma crfo
• T-cell origin:
• Radiologic Findings It ail e
Peripheral T-cell lymphoma
Angioimmunoblastic lymphoma med i,
Plain Chest Radiograph Angiocentric lymphoma ( Figs.
Anaplastic T-cell lymphoma pa rae
(III) Very aggressive lymphomas (high risk)
• M ediastinal and hila r ly mph node enla rgement: Para- frequi
• B-cell origin:
tracheal lym ph node e nlargement cau ses widen ing of Burkitt lymphoma conti:
t he superio r mediastin um (Figs. 6.42,6.430 ). On t he Plasma cell leukemia NHL.
latera l view, the superior retroste rnal space may be • T-cell origin:
Adult T-cell lymphoma
narrowed or obli terated by enla rged pretrachea l
Lymphoma 179
cr
:clu-
14).
Thoraci c lymph node enlargement:

- Bilateral mediastinal widening
- Sca lloped hilum
.•
, or
on
••
'fal
Pulmona ry infiltration:
- Nodular peribronchial
ent - Mi liary
fig.6.42 lymphoma .
/"
:ifo-
fica-
b
15%
lymph nodes. Hilar lymph node enlargement fre-
quently is bilateral and symmetrical w ith lobulated
lateral contours.
• Pulmonary parenchymal involvement in HD is usually
associated with mediastinal lymph node enlarge-
ment (Kaplan et al. 1987); in NHL. it may be found in
the absence of mediastinal change. Direct extension
from the hilum into the adjacent lung is most com-
mon and results in nodular shadowing around patent
bronchi in the perihilar lung. giv ing visible ai r bron-
chograms. Pulmonary involvement may also be
manifest as multiple nodules. which may have a peri-
bronchial distribution or ve ry occasionally may cavi-
tate.
Computed Tomography c
Fig.6.43 Non-Hodgkin lymphoma: Chest rad iog raph (a) shows
cr forms an integral part of initial staging of lymphoma. mediastinal widening. Thoracic CT (b) shows extensive confluent
It allows accurate assessment of the size and extent of lymph node enlargement in the su perior mediastinum with SVC
compression and with intravenous contrast medium within right
mediastinal and hilar lymph node enlargement
chest wall collateral vessels and within the azygos vein . Patient
(Figs. 6.43 b. 6.44. 6.45 a). All node groups except for the had clinical signs of SVC obstruction. Chest radiograph (c) one
paracardiac and posterior mediastinal nodes are more week later shows of a stent within the SVc.
frequently involved by HD than by NHL. Involvement by
co ntiguity is typically found in HD but may be absent in
NHL.
180 6 Tumors and Tumor-like Lesions ofthe Lung
Ly
from
ro lln(
freq u
b).
Prir
Thre!
• b c of PI
(prirr
Fig. 6.44a-c Hodgkin disease. CT demonstrates cervical, axillary, and mediastinal lymph node enlargement.
1. Lo
2. Hi
3. In
m
Low
socia
frequ
Iympi
pragl
2002
Tt
scri b.
creas
these
appe.
• Iymp
Fig. 6.45 a, b Non-Hodgkin Lymphoma: CT image at mediasti- shows nodular areas of opacification confirmed histologically to tribu'
nal windows (a ) shows precarinal, aortopulmonary, and left hilar reflect pulmonary parenchymal involvement. Hi
lymph node en largement. CT image viewed at lung windows (b)
with
tend ~
AID
See p
lyrr
Inclu:
sial a
• Fig.6 .46a, b Pulmonary involvement in recurrent low-g rade areas of nodular opaCification containing visible air broncho-
b vascu
erre;
follicular lymphoma. CT shows peribronchial infiltration and post- grams (b). tribUi
erior mediastinal lymph node enlargement (a) There are also
wa lle
Lymphoma 181
Lymphoma involving the lung by direct extension

from the hilum may be seen as soft-tissue nodu les sur-
rounding patent bronchi. Discrete pulmonary nodules
frequently have ill-defined borders (Figs. 6.45 b. 6.46 a.
b).
Primary Pulmonary Lymphoma
Three distinct entities are now covered by the definition

of primary pulmonary clonal lymphoid proli feration
(primary pulmonary lymphoma). These comprise:
1. Low-grade pulmonary 8-cell lymphoma.
2. High-grade pulmonary 8-cell lymphoma.
3. Inclusion of lymphomatoid granu lomatosis (LG ) re-
mains controversial.
Fig.6.47 Baltoma. (T shows areas of peripheral consolidation
with visible air bronchograms.
Low grade 8-cell lymphoma arises from mucosa-as-
sociated lymphoid tis sue (MALT) and is the most
frequent form of primary pulmonary lymphoma (MALT
lymphoma). It tends to be indolent. has an excelle nt
prognosis, and treatment is controversial (Cadranel et al.
2002).
The a findings in MALT lymphoma have been de-
scribed. These included nodular and linear areas of in-
Treated Lymphoma
creased attenuation and areas of consolidation. All of
these changes had their epicenter on the airway which cr is routinely used to assess response to therapy and for
appeared dilated. and they correlated histologically with regular follow-up of patients in remi ssion. It is also ap-
lymphomatous infiltration in a peribronchovascular dis- propriate for imaging complications of lymphoma ther-
Y to tribution (Wislez et al. 1999. Fig. 6.47). apy.
High grade B-ceJf lymphoma usually occurs in patients For radiation-induced complications, see p. 107.
with underlying immunodeficiency and its prognosis For complications of chemotherapy. see drug-in-
tends to be poor. duced lung disease. p. 108.
Indirect complications of therapy are frequently sec-
ondary to bone marrow suppression and steroid ther-
apy. Thrombocytopenia may give rise to hemorrhagic
AIDS-Related Lymphoma
complications including diffuse pulmonary hemorrhage.
Neutropenia and lymphopenia result in increased sus-
See p.98. ceptibility to infection. Bacterial pneumonia may
develop but these individuals are also at risk of develop-
ing opportunistic infections.
Lymphomatoid Granulomatosis
• Radionuclide Scintigraphy
Inclusion of lymphomatoid granulomatosis is controver- Gallium citrate (67Ga) has been advocated for diagnosis
sial and debate continues as to whether this reflects a and staging of both HD and NHL. but cautio n is required
b vasculitis or a neoplastic entity. Lee et al. have described in image interpretation as 67Ga is not particularly tumor
lCho- IT features in LG that include a peribronchovascular dis- specific.
tribution of nodules, coarse irregular opacities, thin-
walled cysts. and large masses (Lee et al. 2000). FOG PETIPET-CT
The role of PET/PET-a in lymphoma has been evaluated

and PET may play an important role in evaluation and
management of lymphoma (Kazama et al. 2005). Re-
sidual abnormality at a after completion of chemother-
apy is not uncommon. This may reflect either residual
di sease or necrotic/fibrotic tissue.
182 6 Tumors and Tumor-Like Lesions of the Lung
Schaefer et al. retrospectively compared coregistered and NHL after completion of therapy. They found that
FOG PET-CT to contrast-enhanced CT in staging and re- FOG-PET allowed stratifi cation of patients into those at 7
staging of both Hodgkin disease and high-grade non- low « 20 %) and those at high ( > 80 %) risk of recurrence
Hodgkin lymphoma. For lymph node involvement. PET- (Reinhardt et al. 2005 ).
CT had a sensitivity and specificity of 94 and 100 % vs. These and other studies show FOG-PET to be more ac-
values of88 and 86 %for CT. For organ involvement. PET- curate than CT in assessing residual disease and in iden-
CT had a sensitivity and specificy of88 and 100 %respec- tifying patients who require more intense therapy.
tively vs. values of 50 and 90 % for CT (Schaefer et al. However. post-treatment PET may not identify minimal
2004). residual disease and as it is not tumor-specific, it some-
Reinhardt et al. eval uated the role of FOG-PET in pre- times may be positive in benign conditions so clinical
dicting progression-free survival of patients with HD and imaging correlation is appropriate.
Pl
Pul
pul
res
cre
19~
70 .
ele'
fro·
Of;
rna
ble
•
~ Fl
to
a
gr
D,
si
0,
io
m
183
7 Pulmonary Hypertension and Edema
Pulmonary Hypertension
Pulmonary arterial hypertension is defined as a mea n Table 7.1 Classification of pulmonary hypertension
I pulmonary artery pressure of greater than 25 mmH g at

rest or greater than 30 mmHg during exercise with in-
creased pulmonary vascu lar resistance (Burke et al.
1991 ). Pulmonary artery pressures greater than
70 mmHg are consistent with severe hypertension.
Precapillary Causes
• Chronic thrombo-embolic disease (CTEPH). fat and para-
sitic pulmonary emboli.
• Secondary t o a longstanding left-to-right cardiac/vascu lar
shunt.
• Pulmonary parenchymal disease: COPD. Diffuse interstitial
Ohm's Law (P",-Pp, = R x I) indicates that chronic
pulmonary fibrosis.
elevation of pulmonary arteria l pressure (P,,) may result • Vasospasm due t o alveolar hypoventilation (muscular dys-
from increased blood fl ow (I), increased resistance (R), trophy, poliomyelitis. Pickwickian syndrome. Ondine curse
or an increase in pulmonary venous pressure (Ppv )' Pul- synd rome).
monary hypertension may therefore be due to (Ta- • Idiopathic: primary pulmonary hypertension (PPH)
ble 7.1): Postcapillary Causes
• In creased pulmonary vascular resistance (precapillary • Left ventricular failure.
• Mitral valve disease. Left atrial myxoma.
pulmonary hypertension) in longstanding ca rdi ac left- • Idiopathic: Pulmonary vena-occlusive disease (PVOD).
to-right shunt. chronic thromboembolic disease, pul-
monary parenchymal diseases including chron ic ob-
structive pulmonary disease (COPD ) and diffuse in-
terstitial pulmonary fibrosis, vasospasm secondary to • Pathology
alveolar hypoventilation, and may be idiopathic in
primary pulmonary hypertension (PPH ). 60-70 % of Changes seen in all form s of precapillary pulmonary hy-
the pulmonary vascu lar bed must be occluded befo re pertension include intimal cellular proliferation and me-
there is an appreciable increase in pressure. dial smooth muscle hypertrophy. These changes are
• Increased pulmonary venous pressure (postca pillary characteristically seen in the musc ular arteries. In add i-
pulmonary hypertension ) is usually seco ndary to ele- tion. plexiform lesions and necroti zing arteritis are see n
vated left atria l pressure and may be see n in left in primary pulmonary hypertension and in pulmonary
ventricu lar failure, mitral valve stenosis. longstand- hypertension secondary to a card iac shunt. A plexiform
ing left atria l myxoma, or may be idiopathic in pul- lesion is defined as a focal disruption in the internal e las-
monary vena-occlusive disease (PVOD ) (Table. 7.1), tic lamina of a muscular artery by a "glomeruloid" plexus
of endothelial channels which proceed to ramify into
Goals of Diagnostic Imaging: alveolar septal capillaries.
Identify imaging features of pulmonary hype rtens ion. Postcapill ary hypertension is characterized by venous
Further evaluation with echocardiography, computed medial hypertrophy and intimal proliferation with
tomography (Cf). magnetic resonance imaging (MRI), marked prominence of the venous internal elastic lamina
and right heart catheterization with pulmonary angio- (Frazier et al. 2000).
grap hy may then be appropriate.
Determine if it reflects pre- or postcapillary hyperten-
sion.
Determine if there is an underlying cause or if it is:
' d- J
ioparhic (i. e., primary pulmonary hypertensio n or pul-
All forms of pulmonary hyperte nsion are associated
monary veno-occlusive disease ).
with progressive dyspnea, which in advanced disease
may be severe and associated w ith cya nosis. Clinical
manifestations of right heart failure include periphe ral
edema. elevated jugular venous pressure, hepatomegaly,
and ascites.
184 7 Pulmonary Hypertension and Edema
Precapillary Pulmonary Hypertension
Primary Pulmonary Hypertension • Radiologic Findings
PPH is relatively rare. Its existence as a separate entity The pulmonary circu lation is a low-pressure system.
has on occasion been Queried by those who suggest that Th is results in part from the hi gh compliance of the pul-
it may result from clinically latent microemboli (S hin - monary vessels. An increase in pressure is associated
nick et al. 1974 a. b). Nevertheless. the fo ll owing appear with a radiologi cally appreciable increase in vesse l cali-
to justify its recogn ition: It shows a familial incidence be r (Fig. 7.2).
and primarily affects you ng to midd le-aged adults with The frontal chest radiograph shows central pulmo-
a 3-5: 1 female to male ratio. Acetylcho line infu sion has nary artery dilatation. Apparent promine nce of the pul-
been shown to reduce the pulmonary arterial pressure monary segment of the left heart contour results from
(Fishman and Pietra 1980). In the 1960s. clusters of cases vascular dilatation and from a degree of cardiac rotation
were reported in Germany, Austria. and Switzerland; associated with right ventricular hypertrophy. Chroni-
this was subsequently attributed to use of the appetite cally elevated pulmonary arterial pressure leads to right
suppressant Menoc il (Fig. 7.1). Evidence suggests that ve ntricular overload. Initial adaptation is with ventricu-
endothelial injury to small pulmonary arteries and arte- lar mu scular hypertrophy. but eve ntually the right ve n-
rioles with resu lting vasoconstriction may act as an in- tricle becomes dilated and right ventricular failure su-
Fig .
citing mechanism for PPH (Frazie r et al. 2000). pervenes. dial
Clinical features include dyspnea. chest pain. syn- On the lateral view, right ventricu lar dilatation may cha
cope. cya nosis. and right ventricula r (RV) failure. Elec- be associated with narrowing or obliteration of the ret-
trocardiograp hic (ECG) changes in advanced disea se are rosternal space. Pulmonary vascularity is variable.
those of cor pulmonale.
CT
Fig. 7.1 Primary pulmo- (Fi:
nary hypertension in a art
patient who had used ap- die
petite suppressants. AI
87
hYI
is
brc
fi ci
(Fi:
ter
na'
les
pa,
to\
(Fi
pu
tri
ch,
Preca pilla ry Pulmonary Hyperte nsion 185
E
E
.£
f•
i!'
•o
o
m.
ul- ~0- 30
..
ed 1:
.2
Ili-
j 20
10- 10
ul- '"
·0
'0
)m 10
on ~
E
ni- •
i5 oL-~-L~L-~-L~--L--L~
~h t
10 20 30 40 50 60 70 80 o
:u-
Pulmonary artery pressure in mmHg
~n
:iU-
Fig.7.2 Correlation of pulmonary arterial pressure with the
diameter of the right lower lobe pulmonary artery (from Mes-
chan: Analyse der R6ntgenbilder, vol. II . Stuttgart: Enke; 1981) .
• Computed Tomography
CT demonstrates central pulmonary artery dilata tion

(Figs. 7.30, 7.40 ). The diameter of th e main pulmonary
artery is measured at the level of the bifurcation perpen-
). dicular to th e long axis of the vessel (Naidich et al. 1999).
A diameter of > 29 mm demonstrates a sensitivity of
87 %and specificity of 89% for predi cti on of pulmonary
hypertension.
When a main pulmonary artery diameter of > 29 mm
is associated with an elevated segmenta l arterial/ b
bronchial ratio (i. e., > 1) in th ree offou r lobes, the speci-
ficity for pulmonary hypertension increases to 100 %
(Fig. 7.3 b) (Tan et al. 1998).
A main pulmonary artery to ascending aortic diame-
ter ratio of > 1 also has a strong correla tion with pulmo-
nary hypertension (PH ) particul arly in pati ents w ho are
less th an 50 yea rs of age (Ng et al. 1999).
There may be di latation of ri ght hea rt chambers and
paradoxical bowing of the interventric ular septum
towards the left ventricle may be seen in severe PH
(Fig. 7.3(, and see Fig. 7.17b).
High-resolution images through the lu ngs in severe
pulmonary hypertension sometimes show small cen-
tril obular nodu les that may refl ect the presence of
cholesterol gra nu lomata (Nolan et al. 1999, Fig.7.4b, c). c
Fig.7.3a-c Pulmonary hypertension: Axial CT image shows di-
latation of the main pulmonary artery (a). Arterial-bronchial
diameter ratio is increased in the right lower lobe (b). There is
marked dilatation of the right heart chambers (c). Subcutaneous
edema and ascites are consistent with right ventricular decom-
pensation (cor pulmonale).
• iii
MRI
ing
char
venl
latec
seer
two- "
of a'
arte
lun,
1
fusit
reee
se n ~
pati
aL.......... b
.bolil
Ven
\
non
F
(
Rigt
vase
atri;
(em
and
Ac
an
d
Pu
. 1
Pull
6S~
logi
c
nar:
caSt
ei th
late
suff
I
usu
Fig.7.4a-e Primary pulmonary hypertension. CT shows dilated pen
main pulmonary artery (a ). (T images at lung windows show no
lary
evidence of mosaic perfusion but some small nodular areas of
ground-glass density are see n perhaps reflecting cholesterol nee
granulomata (b, c). Ventilation/perfusion scintigraphy shows no infa
evidence of unmatched filling defect s (d . e). e lun)
Precapillary Pulmonary Hypertension 187
Magnetic Resonance Imaging from the periphery. Subsequent organization of smaller

infarcts leads to complete resolution or contracted scar
MRI shows features of pulmonary hypertension includ- formation. Pulmonary infarcts very occasionally may be-
ing central pulmonary artery dilatation, right heart come infected leading to abscess formation.
chamber dilatation. and paradoxica l bowing of the inter-
ventri cu lar septum. Abnormal intravascular signal re-
lated to slow flow within pulmonary arteries may be • Clinical Features
seen on ECG-gated spin echo sequences.
Velocity-encoded gradient echo sequences provide a Clin ical diagnosis of acute pulmonary embo lism may be
two-dimensional velocity map of a cross-sectional area difficult as the classic triad of sudden onset of chest pain,
ofa vessel and allow calculation of aortic and pulmonary dyspnea, and hemoptysis is present in only a minority of
artery flow as well as flow volumes to the right and left cases. Hypoxia may be found on arterial blood gas analy-
lungs. sis. Studies have reported both a high se nsitivity and
The role of combined magnetic resonan ce (MR) per- negative predictive value of D-dimer assay in investiga-
fusion and magnetic resonance angiography (MRA) has tion of acute PE in ambulant patients (Hogg et al. 2006.
rece ntly bee n evaluated by Nikolaou et al. who report a Hlavac et al. 2005). This test is less reliable in immobile
sensitivity of 90 % for this technique in differentiating hospitalized and pregnant patients.
patients with PPH from those with chronic thromboem- It is estimated that 1-5 % of patients with acute PE
bolic disease (Nikolaou et al. 2005). progress to CTEPH (Frazier et al. 2000). The incidence of
CTEPH is higher in females and lupus anticoagulant and
Ventilation-Perfusion Scintigraphy (VQS) anticardiolipin antibody may be positive.
Ventilation-perfusion scintigraphy is characteristically

normal or of low probability in PPH (Fig. 7.4d. e ). • Radiologic Findings
• Pulmonary Angiography/Right Heart • Chest Radiograph
Catheterization
The chest radiograph in acute PE may be normal or find-
Right heart catheterization reveals elevated pulmonary ings may be nonspecific, even in seve rely sympto matic
vascular resi sta nce with normal capillary wedge and left patients (Fig. 7.5).
atrial pressures. Pulmonary angiography shows dilated The posterobasal segments are sites of predilection
central vessels and a diffuse pattern of abruptly tapering for pulmonary thromboembolism because of the rela-
and pruned subsegmental vessels (Frazier et al. 2000). tively high proportion of pulmonary blood flow which
they receive. Conversely, only 10 %of emboli involve the
upper lobes.
Acute Pulmonary Embolism (PE) Features of acute pulmonary embolism without in/arc-
tion include:
and Chronic Thromboembolic • Local oligemia (the Westermark sign) with regional
Pulmonary Hypertension (QEPH) hyperlucency. This finding, in isolat ion on a single
chest radiograph is unreliable. Howeve r, its occu r-
rence as a new finding w hen previous rad iographs
• Pathology have been normal may be sign ificant (Fig. 7.6).
• Areas of discoid atelectasis. These probab ly result from
Pulmonary thromboembolism may be found in up to surfactant deficiency in the involved lung. On the
65% of autopsies, making it the most common patho- chest radiograph, discoid or plate atelectasis is see n
logic finding in hospitalized patients. Howeve r, pulmo- as intrapulmonary linear opacities 1-3 mm in thick-
nary emboli remain clinically silent in up to 80 % of ness and up to several centimeters in length. These
cases. An e mbolus within a pulmonary artery results in may extend to the pleura.
either a reduction or a cessation in distal perfusion. Col- • Elevation of the hemidiaphragm: This may result from
lateral flow from the bronchial arterial system is usually reflex splinting due to pleuritic pain but may also be
sufficie nt to maintain lung via bility. seco ndary to surfacta nt deficiency with a resultant
Pulmonary infarction develops in 10 to 15 % of cases reduction in pulmonary compliance.
usually when there is associated pulmonary ve nou s hy- • Pleural effusion, which may yield serosanguinous
pertension. It results from local hypoxia leading to capil- fluid.
lary damage, exudation , hemorrhage, and coagulat ion
necrosis. Macroscopic examination of the hemorrhagic Radiographic features of acute PE with infarction include:
infarct shows a firm, airless, livid dark-red segment of • Wedge-shaped or oval opacities (the Hampton hump;
lung. Pulmonary infarcts are revascularized gradually Hampton and Castleman 1940). This opacity typically
Ra
-
Perfusion scintigraphy
_,;0::- A nOJ
ii
:
.
~~il
.~.:..J'
":'iJ
I:'"l.'.\
i\",d
--.,,;1: "It.;<"l
"
... ..
pulm(
study
into t
occlw
Ventilation scintigraphy
fects.
Pu
that a
chest
rnonil
- Knuckle sign - Hampton's hump - "Melting - Vascular "pruning" (.1,)
- Westermark's sign - Pleural effusion icebe rg" sign - Intravascu lar filling defect (*) An
- Elevation of - Plate atelectasis -Infarct shadow lation
hemidiaphragm This i:
Fig.7.5 Pulmonary em bolism and infarction.
fusior
unma
w hen
(high
freqw
Co
(ontr
direct
numt
helicc
the (I
speeil
graph
mona
show
bali c
1995)
Fa
(M DC
Their
b subse
tion c
II stu!
Fig.7.6a, b Pulmonary embolism. Frontal chest radiograph this,
shows attenuated vascular markings in the left lower zone (West-
ermark's sig n) correlating with large perfusion defect at scintigra-
(Patel
a phy. En
hano:
tion,
opaci
In
appears 24 hours after the embolic event and usually • Infarcts that become infected may show a tran sient
throrr.
measures 3-5 em in diameter. The base of the wedge- increase in size and may cavitate. Superinfection also
the v(
shaped infarct abuts the visce ral pleura wh ile the delays resolution (Fig. 7.7).
clusio
rounded apex points toward s the hilum. Resolution • Pleural effusion that is usually hemorrhagic on aspira-
may (
of the opacity in 4-7 days suggests simple alveolar tion.
eval u
edema and hemorrhage. An opacity that regresses • Features of pulmonary hypertension in CTEPH may be
dictin
gradua lly over a period of 3-5 weeks indicates indistinguishable from radiographic findings in PH
boenc
parenchymal necrosis. Characteristically, these opaci- due to other causes (see p. 183 ).
tral tl
ties shrin k from the periphery and remain homo-
adeql
geneous (melting iceberg). This differs from the pat-
(Hein
tern in pneumonic consolidation which usually re-
solves from the center towards the periphery.
Precapillary Pulmonary Hypertension 189
Radionuclide Scintigraphy
A normal ventilation/perfusion study excludes acute

pulmonary embolism in up to 95 % of cases (PIOPED
study). However, only approximately 25 %of patients fall
into this category. Pulmonary emboli causing vascular
occlus ion may produce wedge-shaped perfusion de-
fects.
Pulmonary infarcts produce scintigraphic defects
that are larger than the corresponding opacities on the
chest radiograph, but definite differentiation from pneu-
monic consolidation is not possible.
An unmatched perfusion defect with a normal venti -
lation study is consistent with pulmonary embolism.
This is in co ntrast to the typical findings of matched per-
fusion and ventilation defects in emphysema. Multiple
unmatched perfusion defects at scintigraphy are seen
when multiple acute pulmonary emboli are present
(high probability study Fig.7.8.-d) and also are
frequently seen in CTEPH (Fig. 7.9 b, c).
computed Tomography
Contrast-enhanced helical and elec tron -beam CT allow

direct visualization of pulmonary emboli. In the 1990s, a
number of studies reported sensitivities for single-row Fig. 7.7 Pulmonary infarction with cavitation.
helical CT of greater than 90 %for detection of em boli in
the central (main, lobar, and segmental ) vessels with
specificities comparable to those for pulmonary angio-
graphy (Goodman et al. 1995, Remy-Jardin 1992 ). CT pul-
monary angiography (CTPA) using this technology was
shown to be less sensitive for detection of thromboem-
boli confined to subsegmental vessels (Goodman et al.
1995).
Four-, 16-, and now 64-slice multi-detector row CT
(MDCT) scanners are in widespread clinical use today.
Their improved spatial resolution together with their
subsecond gantry rotation times show improved detec-
• b
b
tion of em boli within subsegmental vessels. The PIOPED
II study is currently evaruating the accuracy of MDCT in
-aph thi s setting and should yield important information
lest-
gra- (Patel and Kaze rooni 2005 ).
Emboli appear as filling defects within contrast-en-
hanced vessels (Fig. 7.10). In cases of pulmonary infarc-
tion, peripheral wedge-shaped areas of pulmonary
opaci fication may be seen (Fig. 7.11).
In CTEPH, CT may directly visualize endotllelialized
ient c d
thromboemboli which tend to lie asymmetrically within
also
the vesse l lumen (Figs. 7.9., 7.12., b, 7.13.). Vascularoc- Fig. 7.8a-d Perfusion scintigraphy showing high probability of
elusions, changes in vessel caliber. and mural irregularity pulmonary emboli sm with mu ltiple perfusion defects seen bi-
lira- laterally. a Prone. b LLD. c supine , and d RLD.
may also be seen (Schwickert et al. 1993). He inrich et al.
evaluated the ro le of preoperative helical CTPA in pre-
; be
dicting surgical outcomes of post pulmonary throm -
PH
boendarterectomy. They found that the absence of cen-
tral thrombi at crPA was a significant risk factor for in-
adequate hemodynamic improvement postsurgery
(Heinrich et al. 2005).
a
Fig. :
fusic
b
Fig. 7.9 a-c Chronic thromboembolic disease. CT shows en-

dothelialized thrombus within t he left inferior pulmonary artery
(a). Ventilation-perfusion scintigraphy shows multiple un-
matched perfusion defects consistent wit h a high probability for
pulmonary embolism (b, c). c
a
Fig. 1
sian
pulm
C
mon
din I
pati(
puln
20 0 ~
F,
mail
ratio
ratio
righl
sio n~
A
<J Fig. 7olO Acute pulmonary embolism. CT shows bilatera l filling tenw
defects within the central pulmonary arteries. (Figs
Precapillary Pulmonary Hype rte nsion 191
r .- -
,
• fig. 7.11 a, b Pu lmonary infarction. Chest rad iograph and CT show a wedge·shaped opacity in the left lower lobe with concomitant ef-
fusion in a patient with a history of pelvic and lower extremity venous thrombosis.
b
• Fig. 7.l2a . b Chronic thromboembolic pulmonary hyperten- artery. Coronal reformat (b) shows a further large defect within
sion (CTEPH): Axial CT im age (a) shows dilatation of the central the interlobar artery.
pulmonary arteries and a filling defect within the right upper lobe
Dilated systemic collateral vessels and most co m- more common in PH secondary to vascu lar disease than
monly dilated bronchial arteries may be see n. Remy-Jar- in cases due to cardiac or lung di sease (Sherrick et al.
din et al. reported this finding to be more co mmon in 1997).
patients with CfEPH (73 %) than in those with primary
pulmonary hypertens ion (14 %) (Remy-Jardin et al. • Pulmonary Angiography
2005).
Features of PH including increased diamete r of the Pulmonary angiography has large ly been replaced by
main pulmonary artery, elevated arterial-bronchial crPA in the diagnosis of acute pulmonary embolism.
ratio, and increased pulmonary a rtery-ascending aortic Typical angiographic features include intralum inal
ratio may be see n. cr features of cor pu lmona le include filling defects with abrupt cutoff of the contrast column.
right heart dilatation, peripheral edema, pleura l effu- Equivocal signs include (1) reg ions of abse nt or delayed
sions, and ascites (see Fig.7.3e ). perfusion and (2 ) increased tortuos ity of subsegme nta l
At lu ng windows, cr may show a mosaic pattern oJat- arteries (Fig. 7.15).
tenuation as a sign of inhomogeneous lung perfusion Pulmonary angiography in CfEPH shows nonhomo-
(Figs. 7. 13 b. 7. 14 a ). This patte rn has been show n to be geneo us distribution of pulmonary vesse ls with abrupt
vascu
and if
Can
Shu
• (I
In th,
throu,
________ __ ______ __ When
~
~
~
E
~
~
~
b
nary t
syster
de feel
topu ll
Fig. 7.13 a, b CTEPH: CT image at mediastina l windows shows th e Ie
endothelialized thrombus within the dista l right main and inferior pulm(
pulmonary artery (a). CT at lung windows shows mosaic perfu· An el
a sion (b).
anom
or rigl
Be,
pul m(
preseJ
fig.7. 14a- c CTEPH: High-resolution CT shows inhomogeneous te nsio
lung attenuation consistent with mosaic perfusion (a). Pulmo- seeanl
nary angiography (b, c) shows vascu lar occlusions, rapid "cut·
spa nsl
offs, ~ and stenoses.
nary \
mona.
wards:
dia l h:
zation
fleet p
to VI,
musCl
refl ecl
a
1997,
In(
leads
ven tri
ve ntri
The al
on ini
exe rtil
cul ta t.
(PDA)
tures •
• Ra
b c
There
pulm(
(Fig. 7.
Precapillary Pulmona ry Hype rtension 193
vascula r cut-offs, ste notic and absent arterial segmen ts,

and in travascular webs and bands (Fig. 7.14b, c)
Cardiac Defects with a Left-to-Right

Shunt
In the normal individual, equal vo lumes of blood flow

through both the pulmonary and syste mi c circulation.
When a congenitalleft-to-right sh un t is present, pulmo-
b na ry bl ood fl ow w ill increase 3- to 6-fold relative to the
system ic circulation. W hen an atri al or ventricular se ptal
defect (V5D ), patent ductus arteriosus (PDA ), or aor-
topulmonary w indow is prese nt, blood is shunted from
th e left hea rt through the defect into the right hea rt or
pulmonary artery and is recirculated through the lung.
An effective left-to-right shunt is also prese nt with
anomalou s pulmonary ve nous drainage to the vena cava
or right hea rt.
Because of the co mpliance of the pulmonary vesse ls,
pulmonary arterial pressure is initially normal in the
presence of increased flo w. Pulmonary arte rial hyper-
tension eventually develops in un treated cases and is
secondary to scl erosis of pulmonary arterioles in re- f ig.7.15 Pulmonary angiogram shows a filling defect in the left
sponse to in creased flow, leading to increased pulmo- upper lobar artery and poststenotic vascu lar attenuation: find-
nary vascular resista nce. Pathologic changes in the pul- ings consistent with a pulmonary embolus.
monary vessels may be classified by the Heath and Ed-
wards's system. Grades I and II are cha racterized by me-
dial hype rtrophy, intimal proliferation, and "m usculari-
zation" of the pul monary arterioles; these changes re- thora but w ith shunt reversa l, pulmonary o ligemia
flect potentially reve rsible disease. By co ntrast, grades IV develops. The so-called "hilar dance" sign seen in the
to VI are cha racterized by plexiform lesions, aneurysmal past w he n fluoroscopy was performed routinely in these
muscular arteries, and sites of necrotizing arteritis that cases rep resents the vigoro us pulsations of the ce ntral
reflect seve re irreversible di sease (Katze nstein et al. pulmonary arteries. This phenomenon was best appre-
1997, Fra zier et al. 2000 ). ciated in the right lower lobe artery. In patent ductus
Increased pulmonary vascul ar res ista nce, in turn arteriosus, pulsation s are less conspic uou s as flow
leads to right ve ntri cu lar hypertrophy. and whe n right through the shu nt continues throughout the cycle.
ven tricular pressure eventua lly exceeds that of the left Echocardiography dete rm ines the level of the shun t
ven tricl e, the s hunt reverses (Eisenmenger reaction ). and provides estimation of both its vo lume and pulmo-
The age at w hich shunt reversal occurs depends in part nary arterial pressure.
on initial shunt vo lume. Prese nting symptoms include
exertional dyspnea and palpitations. Characteristic aus- computed Tomography
cultatory findings include systoli c (V5D) or continuou s
(PDA) murmurs. The e lectroca rd iog ram may show fea- CT may show features of pulmonary hypertension, right
tures of ri ght ve ntricu la r hypertro phy and stra in. heart dilatation ± cor pulmonale (Fig. 7. 17a, b). Linear
calcification may be evident within the central pu lmo-
nary arteries. In cases of patent ductus arterios is, mural
• Radiologic Findings calcifi cation and dilatation of the ductus may be see n
(Virmani et al. 1987).
c Chest Radiograph
There is ca rdio megaly of RV configuration. The ce ntral
pulmo nary vesse ls are dil ated and often tortuous MRI shows features of pulmonary hypertension and the
(Fig. 7.16). Ini tia lly there is associated pulmonary ple- site and size of the intracardiac shunt may be seen.
Fig.7.16 Atrial septal defect with a left-to-

right shunt characterized by central pulmo-
nary artery dilatation.
f
I
,
f
r
E
a b
i
Fig. 7. 17 a, b Eisenm enger's reaction : CT shows dilatation of the central pulmonary arteries (a). There is very marked right atrial and
C
ve ntricular dilatation with paradoxical bowing of the interventricular septum towa rd the left atrium (b).
(
• Cardiac Catheterization
Pulmonary Hypertension Due to f
Ca rdiac catheterization is performed in some cases if sur-
gical correcti on is still feasible before development of
Alveolar Hypoventilation
Eise nme nge r's reaction, particularly in older patients
with suspected conco mi tant ischemic heart disease. Pulmona ry hypoventilation results in a reflex hypoxic F
Right hea rt catheterization w ill reveal increased oxygen vasoconstriction of the pulmonary arterio les. A per- t
saturati on in the right heart chambers and will also siste nt reduction in ventilation results in gradual
document the level and size of the shunt. developme nt of pulmonary hyperte nsion. This may be "
s
due to the following: a
Postcapillary Pulmonary Hyperte nsion 195
)-
Ondine's Curse Syndrome soconstriction. There may be secondary loss of hyper-
capnic responsive ness in the respi ratory center. This
This refers to a congenital or postencephalitic hyposen- phe nomenon may also result from inspiratory muscle
sitivity of the respiratory center to CO 2 , These patients weakness due to poliomyelitis, muscular dystro phy,
inte rmittently "forget" to breathe. and diaphragmatic amyotro phic lateral scleros is, etc.
pacing is occasionally beneficial.
Chronic Hypercapnia Syndrome
Pickwickian Syndrome
Chronic alveolar hypoxia and hypercapnia resulting
This syndrome, also known as obstructive sleep apnea, is from perfusion ve ntilation mismatch due to bullous
associated with inspiratory pharyngeal co ll apse and e mphysema and chest wa ll deformity may induce a re-
produces snoring and upper airway obstruction, partic- fractory state in the respi ratory ce nter lead ing to further
ularly in obese patients. This in turn leads to hypoxic va- hy pove ntilation.
Postcapillary Pulmonary Hypertension
Pulmonary Veno-Occlusive Disease
Pulmonary veno-occlusive disease is a rare cause of pul-

monary hypertension. It may be difficult but it is impor-
tant to distinguish it from PPH as the vasod il ator therapy
used to treat PPH may be fatal in PVOD. The histologic
changes in PVOD include intravascular webs, recanal-
ized thrombosis, and intimal fibros is w ithin the pulmo-
nary veins. Proliferative lesions referred to as capilla ry
"hemangiomatosis" may also be present or this may re-
flect a distinct variant. In add ition to the changes see n in
precapillary hypertension, the capillary wedge pressure
is elevated in PVOD. Fig.7.18 Pulmonary veno-occlusive disease (PVOD): CT shows
Imaging studi es suggest the diagnosis when changes ground-glass opacification with some interlobular septal thicken-
of pulmonary hype rtension are see n in assoc iation w ith ing .
features of interstitia l edem a in the presence of a normal
left atrium (Frazie r et al. 2000). Reston et al. studi ed cr
findings in PVOD. They found that the presence of
ground-glass opac iti es parti cu larly in a centril obular
distribution. subpl eural septal thickening. and lymph
node enlarge ment were more common in PVOD (Reston
et al. 2004). The same group studied cr featu res which
b predict epop rostenol therapy failure and found similar
,nd CT features including the presence of ground-glass
opaci tie s, septal thickening, and pleural effu sion (Resto n
et al. 2002. Fig. 7.18).
Pulmonary Congestion and Edema
Ixic Pulmonary edema occurs when pulmonary venous re- marked increase in intravascular vo lume as pulmonary
'er- turn is impaired, primari ly in left ventricular failure and vessels are also very com pli ant. Later, an increase in
.ual mitral stenosis. The increased pulmonary venous pres- capillary pressure leads to fluid transudation into the in-
be sure is transmitted to the pulmonary arteries as va lves terstitium and alveolar airspaces. Acute pulmonary
are absent in the pulmonary circu lation. There is a edema is reversible, but chronic edema results in a
degree of interstitial fibrosis. Left ventricular impai r- In chronic pulmonary edema, fibroblasts produce
ment commonly results in pulmonary edema and there- collagen in the alveolar wa ll and interlobular septa. This
fore this is a common radi ologic diagnosis. The radiolo- increases the texture of the blood-engorged lung (red in-
gist's role includes recognition of pulmonary edema and duration ). Eventually, hemorrhage through the capillary
identification of prec ipitating factors such as va lvular wa lls and phagocytosis of red cells by macrophages re-
heart disease. Frontal and la teral chest radiographs are sults in "brown" induration.
usually adequate for imaging evalu ation. Although
radiographic signs of interstitial edema may precede
clinical symptoms in up to 30 % of cases, some of these • Clinical Features
features are relatively nonspecific and clinical correla-
tion is helpful when making the diagnosis. Clinical manifestations of co ngestive heart failure in-
clude cough productive of frothy blood-stained spu tum,
dyspnea, orthopnea, cya nosis, and periphe ral edema .
• Pathology Auscultatory findings include moi st rales or crackles.
At autopsy, acutely co ngested lungs are large, heavy, and

engo rged with blood. There is capillary dilatation, w hich • Radiologic Findings
may com press the alveoli.
Interstitial ede ma is most pronounced at the lung Plain Chest Radiograph
bases because of higher hydrostatic pressure in these
zones. This unequal gravitational distribution of edema Whi le florid pulmonary edema is easily recognized, in-
a lso leads to a red istribution in perfusion; this is also terpretation of the chest radiograph in the initial stages
evident on the chest radiograph. remains more controversial w ith Significant interob-
At least two factors account for flow red istribution to server variation. Plain rad iographic findings include:
the upper zo nes. First, basal edema redu ces compliance • Pulmonary vascular dilatation due to raised pulmo-
in the lower zones and the vessels can not expand nor- nary venous pressure a
mally during inspiration. Second, reduced pulmonary • Upper-zone redi stribution of blood flow
elasticity leads to hypoventilation, hypoxic vasoconstric- • Interstitial edema
tion (by the von Euler-Liljestrand reflex), and decreased • Alveolar edema
perfusion to the lower zones (see Figs, 1.36 and 1.37).
With further increases in left atrial and pulmonary The radiographic equivalents of these changes include
venous pressures, alveolar edema develops. Initially, (Fig. 7.19):
fluid -filled lobules are interspersed among normally • Dilated lobar and segmental vessels: Given the varia-
aerated lung, producing a radiographic pattern of tion in normal vessel caliber, dilatation is best eva l-
mottled opacification. As edema becomes more diffuse, uated on se rial radiogra phs. Widening of the inter-
homogenou s opacification is seen. lobar artery at the level of the bronchus intermedius
b
Fig
brc
- Dilated pulmonary artery - Upper zone redistribution •

- Increased vascular markings of blood flow
- ~Ha zy" hilum - Peribronchial cuffing
- Thickened interlobar fissure - Kerley A and B lines
- Basal alveolar edema - Perihilar alveolar edema
- III-defined basal vessels - Cardiomegaly
- Pleural effusion (butterfly edema)
- Elevation of the diaphragm - Pleural effusion
Fig.7.19 Pulmonary congestion and edema.

Postcapillary Pulmonary Hypertension 197
juce
This
jin-
lIary
5 re-
~ in-
tum,
ema.
~S.
1, in-
:ages
~rob
e:
Imo-
• c
:Iude
ra ria-
eval-
nter-
~dius
b d
Fig. 7.20a-d Radiographic features of pulmonary edema include dilated central pulmonary vessels with ill-defined borders (a). peri-
bronchial cuffing with Kerley A lines (c) and Kerley B lines (d). Changes resolved on anti-failure therapy (b).
to more than 18 mm is co nside red pathologic • Dilated perihilar vessels seen in cross sectio n: Dilated
(Fig. 7.20). segmental and subsegmental arteries running paral-
• Increased vascular markings: Dilatation of small, pre- lel to the x-ray bea m appear as round or ova l opaci-
vious ly indefinable vessels increases the number of ties.
radio logically visible vascular markings. Also, • Upper-zone redistribution of blood flow: In the normal
dec reased pulmonary compliance results in reduced individual standing upright, upper zone vessels are
lung volume. which in turn leads to crowding of sma ller in ca liber than those to the lowe r zones, the
vascular markings. apica l-to-basal cross-sectional ratio bei ng approxi-
mately 0.8. With now redistribution to the upper
ri or segmental bronchi to the upper lobes which ap- a

pear end on as thick-wall ed ring shadows (Fig. 7.20 ). e
• Fissural thickening: Subpleural edema thickens the in -
terlobar fissures, which become radiographically vis- The
ible if tangential to the beam. edel
• Septal lines correspond to thickened, edematous in- • C
terlobu lar septa. Kerley B lines are thin horizontal I;
lines approximately 10 mm in length and are usually • F
seen in the costophrenic angles. Kerley A lines are ap-
proximately 40 mm in length and rad iate from the n
hila into the adjacent lung (Fig. 7.20). I.
• Basal pulmonary edema: Co nfluent airspace shadows n
approximately 5 mm in diameter in dependent lung t
represent fluid-filled acini (Fig. 7.21 ). Radiographi - r
ca lly. these appearances may be difficult to distin- (
guish from bronchopneumonia. • E
• "Butterfly" distribution of pulmonary edema. Pulmo- (
·
nary edema is perihi lar/central in di stribution in ap- f
proximately 5 %of cases (Fig. 7.220. b ). This is the so-
ca ll ed butterfly or bat's wing pattern of edema. This
results from the racemous branching pattern of the (
perihilar arteries which tends to ra ise capillary pres- erf
sure. It is also assumed that the pumping action of lobl
Fig. 7.21 Confluent acinar shadowing in pulmonary edema. respiratory excursions enhances pulmonary lymph pen
flow; thi s effect is more pronounced in the lung pe- den
riphery than in the perihilar zone. ede
• Localized pulmonary edema: In patients with preex- rna)
lo nes, this ratio may increase to values in the range isting lung conditions such as emphysema, edema ac-
from 1 to 3. cumulates in well-perfused lung. The underlying lung
• Hilar haze: Peribronchovascular edema surround ing disease accounts for the atyp ical distribution of the • E
the hilar structures and extending into the lung edema. Ech
parenchyma may partially obscure the hilar contours • Chronic pulmonary edema may lead to some degree of low
resulting in a "hilar haze." interstitial fibrosis. Occasionally, multiple small a nd
• Peribronchial cUffing: The bronchial wall appears granulomata in the lung parenchyma result from carc
thickened as a result of mucosal and peribronchial in- capi llary hemorrhage and lead to miliary nodulation yah
terstitial edema. This is seen particularly in the ante- (hemosiderosis). These granul omata are most numer- sior
a b
Fig. 7.22 a, b Pulmonary edema complicating acute myocardial infarction. Butterfly pattern of edema and bilateral pleural effusion
are seen.
Postcapillary Pulmonary Hypertension 199
OllS in the lower zones and may show a degree of min-

eralization.
The follow ing frequently are associated with pulmonary

edema:
• Cardiomegaly usually represents left ventricular di-
latation.
• Pleural effusion, wh ich often is more pronounced on
the right than on the left side (Fig. 7.19). This phe-
nomenon has been attributed to the anatomica l en-
largement of the visceral pl eural surface area by the
middle lobe, res ulting in greater transudation, and to
the lymphatics in the right hemidiaphragm, which
normally drai n peritoneal fluid into the pleu ral cavity
(Light 1983).
• Elevation of the diaphragm: This is attributable to the
decrease in pulmonary compliance wh ich results
from interstitial edema.
Computed Tomography
CT features of interstitial edema include thickened inter-

lobular septa with ground-glass opac ifi cation in a de-
pendent or perihilar distribution. More confluent and
denser opacification is seen with progression to alveolar
edema (Fig. 7.23a, b). Pleural and pericardial effusions
may also be present. . . . . . ._ __
Fig.7.23a , b Pulmonary edema: CT images show patchy
Echocardiography ground-glass opacification, areas of confluent con solidation, and
some interlobular septal thickening.
Echocardiography assesses left ventricular function, al-
lowing estimation of left ventricular ejection fract ion
and thus helping in differentiation of cardiac and non-
cardiogenic edema. It also allows detection of card iac
valve dysfunction and the presence of a pericardial effu-
sion/pericardial tamponade.
b
n
200
8 Thoracic Trauma
In this, the age of motorized transport, road traffic acci- Multiple injuries are frequent but the following ana-
dents (RTAs) frequently result in nonpenetrati ng chest tomic classification is helpful:
injury, In Northern Europe. penetrating injuries from • Chest wall
gunshot and stab wounds are less common. Thoracic in- • Pleural
juries are important as they account for up to 50 % of • Pulmonary
trauma deaths (Wiot 1975 ). Imaging is initially with • Mediasti nal/vascular injury
chest radiographs proceeding in many cases to com- • Diaphragmatic injuries
puted tomography (CT) and less commonly to aortogra-
phy.
Chest Wall Injuries
articulations. There may be accompanying fractures

Rib Fractures through the lateral ribs (Fig. 8.1 ) and costal cartilages. Fir
When a large segment of the chest wall loses continuity
with the remainder of the bony thorax, there are para-
• Clinical Features doxical respiratory excursions that may cause Ii fe-
threatening ventilatory impairment (flail chest, Fig. 8.2).
Isolated rib fractures occur at sites of limited impact. Fractures through the 1st and 2nd or 11th and 12th
Wide impact injuries deform the chest wall over a large ribs are unusual but they are frequently complicated by
area and result in multiple rib fractures which most com- vascular (aortic. subclavian artery ) and visceral (liver,
monly occur posteriorly adjacent to the costotransve rse spleen, kidneys ) injury, respectively. Arch aortography
will demonstrate aortic and subclavian artery transec-
tion and helical cr now plays an important role in
patient selection for angiography. Upper abdominal
visceral injury is best evaluated with co ntrast-enhanced
CT of the abdomen.
Rib fractures may appear as radiolucent lines. step-
like contour deformities. or overriding bone fragments
on the chest radiograph (Fig. 8.3). Fractures of the costal
cartilages are not visible on standard radiographs and
are detected only when there is gross displacement
(Fig. 8.4). While isolated rib fractures may not be signifi-
cant. when they are present it is important to exclude as-
sociated pleural. vascular, and visceral injury and partic-
ularly pneumothorax.
Sternal Fractures Fi
Sternal fractures res ult from severe direct trauma such

as from a sudden forward thrust against the steering
wheel of a car during rapid deceleration of the vehicle. d
They sometimes are visible on the chest radiograph but ti
Fig. 8. 1 Rib fractures. Minor adjacent pleural thickening may be are imaged optimally with computed tomography. f,
due to a small hematoma. Kehdy et al. recently have described the utility of three- n
Chest Wa ll Injuries 201
la-
res
;es. Fig.8. 2 Flail chest in a patient with multiple rib fractures. Fig.8.3 Multiple rib fractures on the right side wit h
hemothorax.
ity
ra-
fe-
2).
!th Fracture of 1st and 2nd ribs
by (may be associated with
vascular injury)
fer,
,hy
ec-
in Ri b fracture
nal (lucent line,
oed step deform ity.
displacement ) Flail chest
ep-
nts
stal Costa l carti lage
fract ure (not visible
md on radiographs)
ent
lifi- Chondrosternal
as- dislocation
tic- Fracture of 11th and 12th ribs
(may be associated with hepatiC,
Vertebral fractu re, splenic, or renal injury)
widening of paravertebral st ripe
Fig.8.4 Fractures and dislocations of the bony thorax.
uch
~i n g
icle. dimensional cr reconstructions in diagnosis and eva lua-
Vertebral Fractures
but tion of ste rnal fractures (Kehdy et al. 2006). There is
phy. freque ntly an associated pneumo med iastinum, pneu- Thorac ic vertebra l body fractures usually result from hy-
ree- mothorax, or pulm onary co ntus ion (see Fig. 8.16 ). perflexion injuries.
202 8 Thoracic Trauma
degree of vertebral body fragment retropu lsion is im- I

pOitant to assess. On the fronta l radiograph, associated
paravertebral soft-tissue hematoma may cause a convex
lateral bulge of the pa ravertebral stripe.
CT of the thoracic spine with sagittal and coronal re-
fo rmatted images will define accurately the extent of
I
both bony and associated soft tissue injury. Magnetic
resonance imaging (M RI ) may be complementary to CT
when there is clinical evidence of spinal cord or periph-
I
eral nerve root injury,
I
r
I
Subcutaneous Emphysema
r
f
Subcutaneous chest wall emphysema occurs when in-
- Subcutaneous chest wa ll Pneumomediastinum t
emphysema trathoracic air leaks into the soft tissues. There is usually
s
- Cervical emphysema an associated pneumothorax or pneumomediastinum. A
- linear gas shadows within characteri stic subcutaneous crackling sensation is noted
pectoralis muscles on palpation.
r
Fig.8.S Pneumomediastinum and chest-wa ll emphysema.
(
• Radiologic Findings The chest radiograph shows vesicular or linear gas
t
shadows and there may be quite marked thickening of
The lateral chest rad iograph/lateral thoracic spine may the subcutaneous tissues. Characteri stically, air also
a
show vertebral body wedging. There may be a step-like spreads along the fibers of the pectoralis major muscle
a
deformity of the anterior vertebra l margin as the com- and produces fan-shaped linear lucencies overlying the
(
pressed spongiosa produces a line of sclerosis. The upper thorax (Figs. 8.5, 8.6 ).
Fig.8.6 Subcutaneous chest-wall and cervical •

emphysema. linear gas shadows outline fibers
of pectoralis major muscle.
•
Pleural Injuries 203
m- Pleural Injuries
ted
lex
re-
Pneumothorax • Clinical Features
of
~tic
A small pneumothorax may be asymptomatic but if it
CT
• Pathology occu pies more than 25 % of the hemithorax it may lead
,h-
to signifi cant pulmonary atelectasis with hypoxe mia
Air entering the pleural space resu lts in a and dyspnea. The hemithorax is hyperreso nant to per-
pneumothorax. Leakage is most com monly from t he cussion and on auscultation breathing sou nd s are
lung. A pleurocutaneous fi stula resulting from penetrat- dimini shed. Tension pneumotho rax is associated w ith
ing chest injury and a bronchopleural fi stula will also progress ively increasing chest pain, dyspnea, and cya no-
produce pneumothoraces. Traumatic bronchopleural sis.
fistulas usually result from nonpenetrati ng co mpressive
in-
trauma w ith sudd en elevation of intra-a lveolar pres-
Ily sure ; this leads to alveolar rupture and tearing of the
.A
visceral pleura. The negative intrapleu ral pressure then
:ed draws air into the pleural cavity. Sharp rib fragments • Chest Radiograph (Fig. 8.7 )
may also injure the pleura and resu lt in pneumothorax.
The elastic recoil of the lung may lead to ciosu re of When possible, an upright chest radiograph should be
pleural tea rs through relaxation atel ectasis. Occasion- acq uired. In seve rely traumatized patients, cross-table
ally, the visceral pleural flap may produce a check-valve lateral o r supine views only may be poss ible. On the
obstruction with air ente ring the pleura du ring inspira- frontal chest radiograph, the viscera l pleura is separated
~as
tion and air trappin g within the pleura during expira- from th e chest wall and becomes vis ible as a late rally
of
tion. Th is leads to a tension pneumothorax with medi- convex '· pleural line" that parallels the chest wa ll
.so
astinal di splace ment and compression of major vessels (Fig. 8.8). Pulmonary vascular ma rkings a re abse nt
:Ie
and the contralatera l lung. A tens ion pneumothorax lateral to this line. On both upright and decubitus views,
he
constitutes a medical emergency. intrapleural air is seen at the most superior paint in the
The follo w ing are relatively unu sual causes of a hemithorax except when locul ation from adh es ions is
pneumothorax; they, however, have important implica- present. Tension pneu motho rax is associated with
tions for patient manageme nt: co mplete pulmonary atelectasis. There is fla ttening of
• Bronchial rupture. The presence of pne umomedi- the ipsilateral hemidi aphragm, w ide ning of intercostal
: al
!fS
asti num, pneumothorax, and partial pulmonary spaces, and mediastinal shift to the contralateral side
atelectasis togethe r w ith fractures of the 1st to 3 rd (Fig. 8.9).
ribs should raise susp icion of bronchial rupture. The In the supine position, air tends to co ll ect ante ri orly.
diagnosis may be confirmed at bronchoscopy. Radiographic findings in anterior pneumothorax include
• Esophageal rupture is associated w ith hydrop- increased clarity of the mediastinal contours and co-
neumothorax and dys phagia. The diagnosis may be stop hre nic angle on the affected side. These signs
co nfirmed by upper gastrointestinal endoscopy or frequently are subtle and may not be detected in the
contrast swallow w ith wate r-soluble contrast me- patient with multiple trauma (Dee 1995 d). A number of
dium. studies have shown that only 40 to 50 % of
pneumothoraces are detected on supine radi ograph s in
If-~~+: 10cm
,.. 6em
Peripheral pneumothorax Hemo- Tension pneumothorax with Volume estimation

(hairline, no peripheral pneumothorax contralateral mediastinal 63 216 A
vascular markings) displacement - 3 • - - ,., 80%of lung volume
10 1000
Fig.8. 7 Pneumothorax.
the clinical setting of acute trauma (Wall 1983, Tocino

1984). Herr
Pleural aspiration is advocated by so me sources if the
volume of the pneumotho rax exceeds 25 % of the
hemithorax. if serial radiographs show a progressive in- • eli
crease in intrapleural air or if the pneumotho rax persists
for more than 1 week (Light 1983 ). Tension Blood
pneumothorax is life-threatening and requires immedi- pulmc
ate aspiration. volum
nary r
• Computed Tomography tends
rh age.
Computed tomogra phy is highly accu rate in detection of evacu,
pneumothoraces that may be missed on sup ine radio- volurr
graphs; se nsitivities of up to 100 % have been reported drain;
(Wall 1983. McGonigal 1990). The most supe rior images hour,
through the lung bases therefore sho uld be reviewed at
lung windows when CT abdomen is performed in
patients with suspected intra-abdominal visceral • Rc
trauma.
Fig.8. 8 Visceral pleural line in peripheral pneumothorax.
Ch
When
are th
lares
stoph
that i
Fig. 8.9 Tension pneumothorax supiol
with contralateral mediastinal dis·
placement.
Pull
Pulr
• el
Pulm,
intra-
TheSE
patiel
allow
read il
mild
usual
36ho
distn:
• R;
The (
segm
side
Pulmonary Parenchymal Trauma 205
diffuse homogeneous opacification of the hemithorax.

Hemothorax With smaller hemothoraces. superimposed pulmona ry
vascular markings may be visib le on the sup ine chest
rad iograph (so called hazy opacification). A hemop-
• Clinical Features neumothorax is frequently present.
If prompt aspi ration is not performed, the hematoma
Blood in the pleural cavity may be due to transec tion of becomes organized with subsequent development of
pulmonary, mediastinal, or intercostal vessels. La rge pleural thickening and fibrosis (fibrothorax ).
volumes of blood are unlikely to be secondary to pulmo-
nary parenchymal injury as the expand ing hemothorax Computed Tomography
tends to com press the lung and tamponade the hemor-
rhage. All except trivial hemotho races shoul d be In the setting of acute trauma. CT may show pleura l fluid
f evac uated to preve nt development of fi brothorax. If the of increased attenuation ( i. e., 30-40 Hounsfield units)
volume of the hematoma is more than 1500 mL o r if cons istent w ith the prese nce of intrapleura l blood and
j drainage from the chest tube is more than 100 mL per hemothorax. A fluid-fluid leve l may a lso be seen in sub-
s hour. tho racotomy may be ind icated (Light 1983 ). acute or in acute-an-subacute intrapleural hemorrhage.
.t CT may demonstrate an air-fluid leve l in hemo-/hy-
n dropneumothorax. Associated mediastinal, pulmonary
" • Radiologic Findings and overlyi ng chest wa ll injuries may be demonstrated.

Posttraumatic pleural effusio n may also be due to an
esophagopleural fistu la. to a chylothorax secondary to
Chest Radiograph
tho racic duct injury o r very ra rely. to a cerebrospinal
When the patient is in the upright position, appearances fluid ((SF) fistula from communication with the sub-
are those of a pleural coll ection/effus ion. Blood accumu- arachnoid space. Biochemical analysis of aspi rated
lates in the lower hemithorax and ob lite rates the co- pleural fluid. magnetic resonance (MR ) eva luation of the
sto ph renic angle forming a medially concave meniscus thoracic spine, and upper gastro- in testina l (GI ) contrast
that is continuous laterally with the chest wa ll. In t he studies may provide clarification.
supin e position. the posterior laye ring of blood leads to
Pulmonary Parenchymal Trauma
Pulmonary Contusion
Pulmonary contusion is cha racterized by inte rstitial and
in tra-alveolar hemorrhage, edema, and microatelectasis.
These changes most frequently are found in young
pat ients as their chest wall is more co mpli ant and this
allows the force of impact to be transm itted more
readi ly through to the lungs. Clinical presentation w ith
mild dyspnea. low-grade pyrexia. and hemoptysis is
usual. Dramatic deterioration may occu r w ith in
36 hours of injury with progression to adult resp iratory
distress syndro me (see Fig. 8. 15).
The chest radiograph shows patchy or confluent non-
segmental opacities w hich usually are ips il atera l to the Fig.8.10 Pulmonary contusion and le ft ·sided pne umothorax
side of impact (Figs. 8.10. 8. 11 ). Less commonly. con- with contralateral mediastinal displacem e nt.
Pulmonary Hematomata and Pul

Pneumatoceles
Bron
Blunt trauma may cause a shearing fo rce which leads to be d
a pulmonary parenchymal laceration. These lacerations matE
alter in sha pe due to the elastic recoil of the lung. They sis. E
then may form posttraumatic pneumatoceles which the (
may become filled with blood to form a pulmonary he-
matoma (Fig. 8.13).
Pm
The·
risk
In contrast to contusions, hematomata appear as oval,
fig. 8." Posttraumatic stenosis of the left lower lobe bronchus homogeneous, well-defined opacities (Fig. 8.14). Most foci I
with distal air trapping. (T shows decreased lung attenuation in chesl

left lower lobe 6 months after severe chest trauma. Bronchos-
hematomata regress within weeks but occasionally they
may persi st for months (vanishing tumor). ing'
copy revealed a cicatricial stricture.
Pulmonary pneumatoceles/cysts appear as unilocular
lung
oval ai r- filled cav ities w hi ch usually are located in the
peripheral subpleural lung. They may become radio-
. Tra
tralateral contusions are seen (contrecoup lesion). graphically vis ible some days after injury as contusions
Radiographic changes appea r within 6 hours of inju ry are beginning to resolve. Occasionally, they appear
and tend to regress within 2-4 days. cr shows patchy within 24 hours of injury, Pulmonary cysts typically col-
ground-glass opacification and air space consolidation lapse and resolve completely w ithin 4 months (M Oiler (
(Fig. 8.12). and Fraser 2001, Gullotta and Wenzl 1974),
Trac!
tratiJ
road
usua
nary
ofse
30%
(Gu e
with
• R
Diag
and i
• L(
• A
Feat,
60 t,
pner
b thor;
indie
pnel:
se no
patiE
1995
A.
Wh i'
traUl
Fig. 8. 12 a, b Pulmonary contusion following a rear-end colli- ruptl
a sion, marked by posterior distribution of pulmonary changes. nom
Pulmonary Parenchymal Trauma 207
Pulmonary Atelectasis
Bronchial obstruction resulting in dista l ate lectasis may

be due to an endobronch ial mucus plug or aspirated
to
material. Radiographs show segmental or lobar atelecta-
)S
sis. Bronchoscopy is indicated to visuali ze and remove
,y
the obstruction.
:h
e-
Pneumonia in the Trauma Patient

- Hemothorax Pulmonary
The unconscious patient with multiple injuries is at high - Pulmonary
parenchymal
risk of developing as pira tion pneu monia. In add ition, hematoma contusion
al.
foc i of pulm onary contu sion may become infected. The
,st
cflest radiograph may show confl uent airspace shadow- Fig. 8.13 Pu lmonary he matoma and contusion.
ey
ing which is found predominantly in the posterobasal
lung in cases of aspiration pneumonia.
ar
he
0-
ns Tracheobronchial Rupture
~ ar
)1-
ler • Clinical Features
Trachea l or bro nchial rupture may be caused by pene-
trating injury or severe blunt trauma in high-velocity
roa d traffi c acci dents. When due to blunt trauma, it is
usua lly associated with severe chest-wall and pulmo-
nary injury. Airway ruptu re occurs in a pproximately 3 %
of severely traumatized patients and is associated w ith a
30 % mortality rate mainly du e to associated injuries
(G uest 1977). Most tears are found in the major bronchi
wi thin 2 cm of the carina.
Fig .8.14 Pulmonary hematoma.

Diagnosis of trac heobronchial rupture may be difficult
and is frequently de layed. Radiologic features are due to : teristic sign of airway rupture is the "fall en lung" sign
• Leakage of ai r at the site of rupture (Kumpe et al. 1970). In the presence of a large
• Altered pulmonary ventilation distally (Dee 1995d ) pn eumothorax. the ate lectatic lung falls inferolaterally
from the hilum in cases of airway disruption. When the
Features of air lea kage include pneumothorax found in airway is intact, atelectasis is towards the hilum.
60 to 100 % of cases (Hood 1959. Taskinen 1989 ) and
pneumomediastinum. The coex istence of a pneumo-
b thorax and pneumomediastinum is a particularly strong
indicator of airway rupture. In add iti on. w hile a
Pulmonary Torsion
pneumothorax may res ul t fro m ri b frac tu res, the pre-
sence of a pneumomedia stinum in th e traumatized Torsio n of the lun g is very rare and most common ly oc-
pat ient is a more specifi c sign of airway di sruption (Dee cu rs in young children. The lung rotates 180· at the
1995 d ). hilum; the lung base then lies in the superior
Altered pulmonary ventilation results in ate lectasis. hemithorax wh il e the lung apex lies infe ri orly. In most
Whil e atelectasis is a common find ing in severely cases, the affected lung rap idly becomes atelectatic. Oc-
trau mati zed patients whe n associated w ith bronchial casionally. only one lobe undergoes torsion, producing
:olli- rupture it tends to be persistent and unrespons ive to an atypica l pattern of lobar atelectas is (MUlier and
s. norma l the rapeutic measures. An unusual but charac- Fraser 2001 ).
Adult Respiratory Distress • Radiologic Findings

Syndrome (Shock Lung. Da Nang
Chest Radiograph
Syndrome. Stiff Lung Syndrome.
Oxygen Lung. Transfusion Lung) Initially, the chest rad iograp h may be normal. From 12-
72 hours posttrauma, the chest radiograph shows loss of
vessel definition with bilateral, widespread patchy
Clinical manifestations of adult respiratory distress syn- opacification resembling noncardiogenic pulm~nary
drome (ARDS ) include severe dyspnea, a restrictive pat- edema. Later, there is progression to confluent opaCifica-
tern of ventilatory impairment due to decreased pulmo- tion with visible air bronchograms.
nary compliance, severe hypoxemia, and extensive air- There is usually good correlation between the radio-
space shadowing, which may progress to pulmonary fi- graphic severity of pulmonary change and the arterial
brosis. PO, (Hansell 1995). Intubation and mechanical ventila-
ARDS has a guarded prognosis with a mortality rate tion may lead to a transient radiographic improvement
of 50 to 70% (Kauffmann et al. 1983). In the traumati zed with subsequent further deterioration.
patient, ARDS may resu lt from hemorrhagic shock,
severe pulmonary contusion, or fat embolism. Septic
shock, acute pancreatitis, heroin overdose, disseminated • Computed Tomography
intravascular coagulation (Die). and transfusion reac- • The lungs may be normal in attenuation in early
tions may also result in ARDS. The pathogenesis is not ARDS. Ground -glass opacifi cation wh ich may pro-
fully understood but may be related to disseminated gress to dense consolidation is characteristically seen
thrombosis in the pulmonary capillaries, capillary mem- in the mid-to-Iower lung zones and in a dependent
brane permeability disturbances due to endotoxins such di stribution (Fig. 8.15).
as histamine, serotonin, and oxygen radicals, as well as • Ground-glass opacification and consolidation in as-
disturbances in surfactant production. Diagnosis is sOCIatIOn with traction bronchiolectasis and
based on the clinical history, radiographic findings, and bronch iectasis are seen with disease progression.
blood gas analysis. Severe degrees of res piratory com- These cha nges may progress to eventual lung honey-
promise are frequent and necessitate mechanical venti- combing. These findings correlate with some degree
lation. of fibroproliferative change.
• Ichikado eva luated the prognostic value of thin-sec-
tion cr findings in ARDS and found that cr abnor-
• Pathology malities indicative of fibroproliferative change were
predictive of a poor prognosis in patients with clini-
In acute ARDS, the lungs are heavy, red, and have a tense, cally early-stage disease (Ichikado et al. 2005).
rubbery consistency. Histologic examination shows pul- • Desai studied a abnormalities at long-term follow-
monary microthrombosis together with alveolar and in- up of ARDS survivors. A reticular pattern with a strik-
terstitial hemorrhage and edema. The pathology is that ing anterior distribution was the most prevalent find-
of diffuse alveolar damage (DAD ) and the following ing and was seen in 85 %of patients. The extent of this
stages have been described (Greene 1987): In the first pattern correlated indepe ndently with the total dura -
24 hours, there is capillary congestion, endothelial cell tion of mechanical ventilation but related most
swelling, and microatelectasis (s tage 1). There is fluid strongly to the duration of pressure-controlled in-
leakage into the interstitium and alveo li together with verse-ratio ventilation (Desai et al. 1999).
fibrin deposition and development of hyaline mem-
branes fro m day 2 through to day 5 (stage 2). Prolifera-
tion oftype II pneumocytes occurs from 5 to 7 days post-
injury and is associated with microvascular destruction
and progressive interstitial fibrosis (stage 3). Necrotizing
pneumonia with abscess formation supervenes in a
small proportion of cases.
e
Pulmonary Parenchyma l Trauma 209
12-
; of
:hy
ary
ca-
lio-
rial
ila-
ent
a b
lrly
)ro-
ee n
ent
as-
and
ion.
ley-
~ree
5ec-
10r-
ve re
lini-
ow-
:rik-
ind- c d
this
ura-
ilost
in-
Fig.8.15a-f Pulmonary contusion with progression to ARDS.

Chest radiographs taken on April 21 (a, b) show pulmonary con-
tusion on the right side at the site of impact. Chest radiograph on
June 1 (c) shows diffuse. bilateral. partially confluent airspace
shadOWing. Chest radiographs on June 11 (d, e) show progression
to a diffuse reticular pattern indicating some degree of fibro-
proljferative change . CT examination on June 1 (f) shows patchy,
e bilateral alveolar change in a dependent distribution.
210 8 ThoracicTrauma
transr
Mediastinal Injuries graph
whict
tinuO!
betw<
Pneumomediastinum • Radiologic Findings hemic
The chest radiograph shows gas bubbles and linear col-

cr
astim
• Clinical Features lections of air i~ the mediastinum. The combined equivi
parietal and visceral layers of the mediastinal pleura bronc
Pneumomediastinum is characterized by air within the may be elevated appearing as a hairline shadow running
connective tissue planes of the mediastinum. The most parallel to mediastinal structures and the heart. There is
common cause is traumatic rupture of alveoli with dis- frequently associated deep cervical and chest-wall
section of air along the bronchovascular interstitium and emphysema (Fig. 8.16). Tral
its forced entry into the mediastinal connective tissue by Dissection of air along tissue planes within the medi-
respiratory excursions. Less frequent but important astinum may be more obvious on the lateral radiograph Inju
causes include tracheobronchial and esophageal rupture (Dee 1995d), and with relatively small quantities of air,
and penetrating neck injuries. the only radiographic feature may be a band of hyper- Blunt
sociat,
relati . .
hemol
traum
isthml
sum.l
descer
volvec
ruptur
to the
Tw,
they h
tion a~
tained
mains
finitel)
(Fig. 11
• b • Ral
The chi
and a I
negati . .
chest r;
10 to ,
aortic i
Rad l
sence 0
- Diffl
tion
- Infe,
> 40
- Trac
side.
- Post~
of th
Fig. 8.16a~c Pneumomediastinum with sternal fractu re. Note - Leak
the separation of the mediastinal pleura from the left heart
border on the frontal radiograph (a, b) and the presence of air in hem
c the retrosternal region on the lateral view (c). the I
Mediastinal Injuries 211
transradiancy in the retrosternal space. Other radio-

graphic signs include air dissecting deep to the thymus,
wh ich is spec ific for pneumomediastinum, and the "con-
tinuous diaphragm" sign (Levin 1973) due to air tracking
between the inferior aspect of the heart and adjacent
hem id iaphragm.
cr is highly accurate in detecting pneumomedi-
:01- astinum and is of value when the chest radiograph is
,ed equivocal, particularly in cases of suspected tra cheo-
ura bronchial or esophagea l rupture (A rmstrong et al. 1995 ).
ing
e is
vall
- Widening of the superior mediastinum
Traumatic Aortic and Great Vessel - Widened paravertebral stripe consistent
,di- with posterior mediastinal hemorrhage
lph
Injury - Accompanying hemothorax
air,
)er- Blunt injury to the aorta or its major branches is as- Fig.8.17 Med iasti nal hemorrhage.
sociated with severe decelerating trauma and while a
relatively rare injury, is a common cause of mediastinal
hemorrhage. Ninety-five percent of aortic transactionsl
traumatic aortic injuries (TAl) occur in the region of the
isthmus usually at the leve l of the ligame ntum arterio-
sum. The mobile aortic arch is sheared off the more fixed
descending aorta at this site. The ascending aorta is in-
volved in 5% of cases (Lund ell 1985) and 1 % of partial
ruptures are fou nd in the descending aorta at a site distal
to the isthmus (Dee 1995 d).
Twenty percent of patients survive the first hour;
they have injuries which fall short of complete transec-
tion as the integrity of the adventitial layer is main-
tained. The ris k of progression to complete rupture re-
mains high with only 2 % of patients surviving inde-
finitely and developing chronic pseudoaneurysm
(Fig. 11.9).
b • Radiologic Findings
The chest radiograph is the initial screeni ng examination

and a normal radiograph has been reported to have a
negative predictive value of98%. However, an abnormal Fig.8 .18 Traumatic aortic injury. Axial CT image shows medi-
chest radiograph is a poor predictor of injury with only astinal hematoma and left-sided hemothorax and an intimal flap
10 to 20% of angiograms being positive for traumatic is noted within the proximal descending thoracic aorta.
aortic injury in this patient group (Sturm 1990).
Radiographic features (Fig. 8.17) resu lt from the pre-
sence of mediastinal hematoma and include: While aortography ha s remained the standard of refe r-
- Diffuse widening of the mediastinum with oblitera- ence for diagnosis of aortic trauma, convention al non-
tion of the aortic contour. Ilelical IT ha s allowed detection of periaortic hematoma
- Inferior displacement of the left main bronchus to and has a superior negative predictive value to the chest
> 40° below the horizontal. radiograph for exclusion of aortic injury (Morgan 1992.
- Tracheal and esophageal disp laceme nt to th e right Raptopoulos 1992 ). IT signs suggestive of TAl include
side. the presence of mediastinal hematoma, aortic contou r
- Posterior gravitation of bl ood may result in widen ing deformity, intimal flaps, intraluminal debris, pseudo-
of the paravertebral stripe. aneurysm. and pseudo-coarctation (Fig. 8.18). However.
~ote - Leakage into the left pleural cav ity results in it has been continued practice at many institutions to
eart
hemothorax and extra pleural blood extending over proceed to aortography in patients at high risk of TAl
lirin
the lung apices forms the cha racteristic apical "cap." w hen the CT study is negative.
The role orer in evaluation of thi s patient group may MOcr technology. They reported a sensitivity of 100 %.
have changed with the arrival ofsingJe-slice helical a in specificity of 40 %. positive predictive va lue (PPV ) of 15 %.
the early 1990s and of multi-detector row cr (MOcr) in and negative predictive va lue (NPV ) of 99 %. They con-
the late 1990s. This technology allows acquisition of a cluded that while sensitivity and NPV were excellen t,
"volumetric" data set in contradistinction to the "con- there were a high number of equivocal CT studies which
ventional" CT examination. Parker et al. evaluated the still necessitated subsequent aortography (Bruckner et
role of helical cr in the evaluation of TAl and found the al. 2006). Both of these studies suggest that if helicall
sensitivity and negative predictive value of cr to be MOcr is normal. it may be reasonable not to proceed to
equivalent to that of aortography at 100 % (Parker et al. aortography even in patients who have sustained signifi-
2001 ). More recently. Bruckner et al. have repo rted re- cant trauma and who are at high ri sk of TAl. Further stu-
sults of a retrospective analysis of all patients undergo- dies are needed to determine the accuracy ofMDCT par-
ing aortography for blunt aortic injury between 1997 ticularly 16- and 64-slice technology in intrinsic evalua-
and 2004 at their institution. CT in those patients eval- tion of the aorta in this setting.
uated in the final yea rs of the study was performed on
Traumatic Diaphragmatic Rupture

a
• Clinical Features herniations through left-sided tears. Tears of the right

Fig. f
hemidiaphragm frequently are associated w ith a pleural sholll
Diaphragmatic injuries occur in 0.8-8 % of patients after effus ion and may be demonstrated at sonography. mati.
blunt trauma. This injury was initially believed to be Helical IT has been shown to be more valuable than
more com mon on the left side but some have suggested conventional CT in the diagnosis of diaphragmatic injury
that both leaflets are affected with equal frequency (Jochum et al. 2002 ). A sensitivity of 71 %. specificity of
(Wa ldschmidt 1980). Traumatic diaphragmatic injury 100 %. and accuracies of 88 % for left-sided and 70 % for
remains a diagnostic challenge and the high frequency right-sided injuries have been reported for helical cr
of associated injury including pelvic fractures, thoracic (Shanmuganathan et al. 2000. Killeen et al. 1999) vs.
aortic injury, s plenic and hepatic lesions may distract at- sensitivities of 14-61 % and specificities of 76-99% for
tention from this lesion (Jochum et al. 2002, Mirvis et al. conventional cr (Gelman et al. 1991. Murray et al. 1996.
2000. Shanmugananthan et al. 2000). Imaging diagnosis Worthy et al. 1995).
of diaphragmatic injury is even more important today as cr signs of diaphragmatic injury include:
increasing numbers of splenic and hepatic injuries are • Direct discontinuity of the hemidiaphragm/diaphrag-
being treated conservatively. marie defect has been reported to have a sensitivity of
Intrathoracic herniation of bowel may occur soon 71-73% and appears to be the most sensitive sign
after trauma or may develop over a prolonged interval (Murray et al. 1996. Worthy et al. 1995 ).
(progressive diaphragmatic rupture). Unrecognized • Intrathoracic herniation of intra-abdominal contents
tears on the left side lead to hernias which have a partic- has been reported to have a sensitivity of 55 % and a
ular predisposition to stra ngulation (Flower 1992). specificity of 100 % (Murray et aJ. 1996).
• The "collar" sign is a waist-like constriction of the
herniating viscus at the site of diaphragmatic tear
• Radiologic Findings and has been reported to have a sensitivity of 36 %on
conventional and 63 % on helical cr (Murray et al.
It has been reported that initial chest radiographs allow 1996. Killeen et al. 1999).
diagnosis of 27-60 % of left-sided but just 17 % of right- • The "dependent viscera" sign. When a patient with a
sided injuries (Shanmuganathan et al. 1999). The chest ruptured hemidiaphragm lies in the supine position
radiograph may show localized contour deformity and for CT examination, the herniated visce ra are no
apparent elevation of the soft tissue-lung interface. longer supported posteriorly by the hemidiaphragm
More specific radiograp hic signs include in- and move to a dependent position against the poste-
trathoracic herniation of a hollow viscus including rior ribs. This sign was observed by Bergin in 90 %of
stomach, colon, and small intestine with or without positive cases (Bergin et al. 2001 ).
focal constriction of the viscus at the site of the tear (col-
lar sign [Fig. 8.19]) and visua li zat ion of a nasogastri c Magnetic resonance imaging with breath-hold acquisi-
tube above the diaphragm on the left side (Iochum et al. tions and its capacity for multiplanar image acquisition
2002). In the setting of acute trauma, associated rib frac- allows good visualization of the diaphragm but this is
tures and hemothorax are frequent. Upper gastro intesti- rarely possible in the setting of acute severe trauma.
nal contrast studies may demonstrate gastric/intestinal
Traumatic Diaphragmatic Rupture 213
%,
%,
n-
lt,
[h
et
11/
to
fi-
u-
!r-
Ia-
•
:ht
Fig.8. 19a, b Radiograph (a) and upper GI contrast study (b)
ral show herniation of part of the fundus of the stoma ch into a trau-
matic diaphragmatic defect. b
.an
Iry
of
for
cr
vs.
for
96,
'g-
of
ign
n15
da
the
ear
on
al.
h a
ion
no
.gm
;te-
~ of
tisi-
:ion
5 is
214
9 Diseases of the Pleura, Diaphragm, and Chest Wall • Path

Pleural,
composi'
• Pleun
of les
3 g/d
Diseases of the Pleura fai lUi
Ascit
myxf
• Pleur
Pleural Effusion tent
than
iden
cyte:
A pleura l effusion is a pathologic fluid collection w ithin Table 9. 2 Causes of pleural effusion
narr-
the pleural cavity. Normally 10- 15 mL of fluid is present
Vascular eff",
and this serves as a lubrica nt between the parietal and o Pulmonary infarction ary 1
viscera l pleural laye rs. Pleural effu sions may reach M Heart failure di sti
vo lumes orup to a few li ters and these large effusions re- o Constrictive pericarditis nanl
sult in com pression of the underlying lung, contralateral Inflammatory mal;
displacem ent of the med iastinum, and depression of the o Tuberculosis
logil
hemidiaphragm. M Para pneumonic effu sion (viral, mycoplasma, bacterial.
fungal) • Em}
o Collagen diseases (SLE. rheumatoid arthritis) lI SU;
Goals of Diagnostic Imaging o Postinfarction Dressler's syndrome Les~
Detection of the effusio n and differentiation from other o Whipple disease
mat
pathological pleural processes such as tumor and o Mediterranean fever
fibrous thickeni ng. The mobility of the nuid with pos- o Recurrent familial polyserositis • Hen
tura l change and its co mputed to mograp hy (Cf) at- sen
Neoplastic
ten uation value may he lp in d ifferentiation. M Bronchial carcinoma nan
Detection of underlying pulmonary. cardiac. and o lymphoma eaSt
abdo minal pathology incl uding pneumonia. bronchial o Metastatic pleural adenocarcinoma • Chy
ca rcinoma. pulmonary embolism, left ventricular o Mesothelioma sco
fa ilu re, and hepatic cirrhosis (Tables 9.1 and 9.2 ). Iatrogenic pie'
Furthe r eva luation of a pleural effusion may req Uir: J o Intrapleural infusion (e. g., due to faulty catheter place- n al
thoracentesis with biochemical, cytologic, and bacterio- ment)
M Postthoracotomy
is c
logic a nalysis of aspirates. Iyn
M Radiotherapy
Trau matic • Sili
o Hemothorax 801
o Esophageal rupture po~
o Chylothorax tra
Table 9.1 Etiology of pleural effu sion s in the u.s. (fro m R. W. Mediastinal lov
light Pleural Diseases, 1983) M Superior vena caval obstruction
M Aortic rupture
Heart failure 500000 o Esophageal fistula (e. g., carcinoma)
Bacterial pneumonia 300000 o Thoracic duct fi stula (fi lariasis, carcinoma ) • (I
M Ruptured dermoid cyst
Malignant tumors 200000
Effusi
• lung 60000 Subphrenic Abdominal
• Breast 50000 o Pancreatitis pleur
• lymphoma 40000 o Subphrenic abscess w ith
• Miscellaneous 50000 o Cirrhosis with ascites may
Thromboe m bolism 150000 o Meigs' syndrome (ascites associated with ovarian tumo r) soum
Viral pneumonia 100000 Miscellaneous
Hepatic cirrhosis with ascites 50000 o Asbestosis
Gastrointestina l disease (e. g., pancreatitis) 25000
o Nephrotic syndrome
o Myxedema
Collagen diseases 6000 o Uremia
Tuberculosis 2600 o Spontaneous pleural hemorrhage due to coagulopathy
Asbestosis 2000 o Congenital lymphedema (M ilroy)
Mesothelioma 450
M - diseases in which the chest radiograph generally shows other
changes besides pleu ra l effu sion. 0 • diseases in which pleural effu sion
may be the only radiographic fi nding (from light).
Diseases of the Pleura 215
Table 9.3 Causes of chylothorax (modified from Reeder and Fel-

• Pathology son 2003)
Pleural effusio ns may be classified according to their Traumatic
composition: Tumor invasion (bronchial carcinoma, mesothelioma,
• Pleural transudate: Clear fluid with a specific gravity Hodgkin's disease, etc.)
of less than 1.016 and a protein content of less than Filariasis
3 g/dL. The Pandy test is negative. Left ventricular left subclavian vein thrombosis
failure is the most common cause of a transudate. lymphangioma, Iymphangiomatosis, Iymphangioleio-
Ascites in hepatic cirrhosis, nephrotic syndrome. and myomatosis
myxedema may also cause transudative effusions. Iatrogenic (postthoracic surgery)
• Pleural exudate: An opaque fluid with a protein co n- Idiopathic
tent of more than 3 g/dL. a specific gravity of greater
than 1.016, and a positive Pandy test. The mi croscop ic
id entification of cellular elements such as granu lo-
cytes, lymphocytes, erythrocytes, and malignant cells
narrows the differential diagnosis. Parapneumonic X-ray beam
effusions are most common and are usually second-

ary to pulmonary infections. Tuberculous exudate is
distinguished by its high lymphocyte content. Malig-
III
nant pleural effusions are also exudates although
malignant cells may not always be detected on cyto-
logic evaluation.
• Empyema: This suppurative intrapleural exu date is
usually either parapneumonic or postpneumonic.
Less commo nly it may result from transdiap hrag-
matic extension of a liver abscess.
• Hemothorax: Bleeding into the pleural space may be
secondary to trauma, aortic rupture, or pleural malig-
nancy, Occasionally, it is seen in thromboembolic dis-
ease when complicated by pulmonary infarction.
• Chylothorax: A turbid, milky fluid co ntaining micro-
Thickness of
pleural effusion
~ll
traversed by
scopic chylomicrons is an un common cause of a the beam
pleural effusion. It may be seen in neoplastic and
traumatic fi stulae of the thoracic duct (Table 9.3 ) and Fig. 9.1 Pleural effusion on PA chest radiograph. The effusion
is also associated characteristically with pulmonary surrounds the entire lung base but it is visible as a meniscus only
when it is tangential to the x-ray beam (from Greene, Mcloud,
lymphangiomata sis (LAM). and Stark 1977).
• Bilious and cerebrospinal fluid (CSF) pleural effusions:
Both are extremely rare. Bilious effusions are seen
posthepatic and after diaphragmatic lacerations. A
traumatic fi stu la to the spinal suba rachno id space al- • Radiologic Findings
lows CSF to enter the pleural space.
• Chest Radiograph
• Clinical Features The shape of the effusion results from:

• The adhesive and co hesive forces between the pleura
Effusions are frequently asymptomatic but may cause and the effusion.
pleuritic chest pain and sp linting of the hemidiaphragm • Elastic recoil which decreases lun g volume while pre-
with decrea sed respiratory excursion. Large effusions serv ing its shape and proportions and especially.
may result in dyspnea. On auscultation, breathing • Gravity, which accounts for the dependent distribu-
lOr) sounds are diminished. tion of the effusion.
Pleural fluid is mobile and the refore its distribution is

position-dependent. This accounts for its varying radio-
graphic appearances (Figs. 9. 1-9.3 ).
'Y
Upright position:
• The lateral chest radiog raph shows homogeneous
other opacification of the posterior costophrenic angle w ith
fusion
216 9 Diseases of the Pleura, Diaphragm, and Chest Wall
( ~ r
\
Hyd
Upright (lateral
projection): > 150 ml
Upright (frontal
projection): >175-500 mL
Supine:
>500-1000 mL
lateral
decubitus: >5 ml
r
a
Fig.9.2 limits of detectability of pleural effusion (from Moskowitz 1973).

Fig. 9.4
a Sl
Aui
Sm.
th e
dec
effe
ang
• The
litel
g l e~
b 175
bee
di a ~
eau
liga
a Supin e
Effusio
theye,
Manife
• The
• Opa
• Cen
• Api!
zon.
In cont
vessels
d sions a
Lateral
Fl uid e
Fig. 9.3 a- d Chylothorax. Fluid layering dependently in the lung. pi
lateral decubitus view appears as a crescent-shaped opacity en- the mil
tering the minor fissure (b). On the supine view. the fluid causes
general haziness of the hemithorax (d). The etiology of the chy-
Post
lothorax was a Milroy-Trenaunay malformation of the lymphatic o f Auid
c vessels. (Maske
~I
Hydropneumothorax Loculated Subpulmonic Posteromediastinal
pleural effusion effusion effusion Inversion of the hem i-
diaphragm in the presence
of larg e effusion
I, a b c
Fig.9.4a- ( Variants of pleural effusion.
a superiorly concave meniscus. At least 100 mL of ("'band" thickness) is less than 1 cm. then the effusion is
fluid is present before an effusion becomes visible. small.
Smaller effusions collect between the diaphragm and
the undersurface of the lung and may only be seen on Atypical forms of pleural effusion (Figs. 9.4,9.5):
\ decubitus views. For clinical purposes, a significant • Loculated effusion: Adhesions between the visceral
effusion is excluded if both posterior costophrenic and parietal pleura resu lt in development of locu~
angles are clear. lated collections along the inner aspect of the chest
• The posteroanterior (PA) chest radiograph shows ob- wall. En face, they may appear as ill-defined round
literation of the costophrenic and cardiophrenic an- opacities but tangentially they produce a semicircu~
gles if the effusion is greater than approximately lar opacity whose margins form an obtuse angle with
175 mL. The meniscus is concave toward the lung and the chest wall. This helps to distinguish them from
becomes thinner superiorly. Opacification of the me- peripheral pulmonary tumors, which usually form an
diastinal pleural space is lower and less marked be- acute angle with the chest wall.
cause affusion of the pleural layers at the pulmonary o Inter/abareffusion (Figs. 9.6, 9.7): This may develop in
ligament. the minor or major fissures. Chest radiographs show
a biconvex, spherical, or ell iptical homogeneous
Supine position: opacity. An effusion in the right minor fi ssure should
Effusions are only visible on supine radiographs when be distinguished from right middle lobe atelectasis.
they exceed 500 mL. The following features help in differentiation:
- The effusion is biconvex whi le lobar atelectasis is
Manifestations include: flat or concave.
• The diaphragmatic contour is obscured - Only atelectasis obliterates the right cardiac
o Opacification of the lateral costophrenic angles bo rder and
• Generalized "haziness" of the hemithorax - Atelectasis obscures the interlobar fissure but an
• Apical caps may indicate pooli ng of fluid in the upper effusion preserves the contour of the fissure as a
zones linear structure in its peripheral portion.
Conventional tomography allows more accurate
In contrast to pneumon ia or atelectasis, the pulmonary differentiation based on the homogeneity of the effu-
vessels are well defined with small to moderate effusion versus the heterogeneity of atelectatic lung.
d sions and there is no evidence of an air bronchogram. However, today cr is usually performed when there
is diagnostic difficu lty.
Lateral decubitus position: • Posteromedial loculated effusion: The fluid column is
Fluid collects between the late ral chest wall and the higher and wider toward the mediastinum. This re~
I the lung, producing a band of opacification which may enter suits from volume loss in the lower lobe and thus
:y en- the minor fissure. lower lobe atelectasis is included in the differential
auses
~ chy-
Postmortem studies have shown that as little as 5 mL diagnosis.
lhatic of fluid may be detected on the lateral decubitus view • Subpulmonic effusion. Occasionally up to a liter of
(Moskowitz et al. 1973 ). If the depth of the effusion fluid may accumulate between the diaphragm and
• b
• Fig. 9 .7a, 1
post treatr
lung \
sons I
Radio
interf.
phrag
then ~
pulm(
Fig. 9.S a- c Ma lignant pleural effusion in breast carcinoma (a). the ir
Hydropneumothorax developed following thoracentesis (b). CT bubbl
shows viscera l pleura l thi ckening and fluid extendi ng into the tus viI
c major fissure (c). chest
• In ve~
inve r!
infere
Durin
Fig.9.6 Interlobar effusions. redu c
signif
matic
• Ultra
Most pi E
have a
pl eura a
partieu];
• Major fjssure • Minor fi ssure hypoech
1983). 0
part of tl
Thin
ally indi
septa w :
di ffi cult
b
a b
Fig. 9.7 a, b Fissural effusion appears as a round opacity in the minor fissure in a patient with congestive heart failure. Radiograph
post treatment shows minimal residual fissural thickening.
lung without spill into the costophrenic sulcus. Rea-

sons for this phenomenon are not fully understood.
Radi ographs show elevation of the lung-soft tissue
interfa ce or apparent elevation of the hemidia-
phragm. The "dome" has a relatively late ral pea k and
then shows a stee p lateral downslope. Whe n the sub-
pulmonic effusion is left-sided, the distance between
).
the inferior surface of the left lung and the gastric
T bubble measures more than 2 em. The lateral decubi-
e tus view will show fluid laye ring along the dependent
chest wa ll.
• Inversion afthe diaphragm: Large effusions may cause
inversion of the hemidiaphragm. Radiographs show
inferomedial displacement of gastric and colonic gas.
During inspiration. the diaphragm contracts and this
reduces the volume of the hemithorax. This leads to
significant dyspnea and paradoxical diaphragmatic
motion .
• Ultrasound
Fig.9.8 Ultrasound shows large anechoic pleural effusion
Most pl eural fluid collections are an- or hypoechoic and bordering echogenic linear hemidiaphragm.
have a sharp echogenic line delineating the visceral
pleura and lung. Occasionally. tumors of the chest wall.
particularly lymphoma and neurogenic tumors, are also empyema. hemothorax, and exudates caused by pleural
hypoecho ic and may be mistaken for fluid (Rosenberg malignancy (Mc Loud et al. 1991. Fig. 9.8).
1983). Diagnostic needle aspiration therefore may form
part of the evaluation when there is diagnostic difficulty. • Computed Tomography
Thin mobile strands of fibrin within the effusion usu-
ally indicate an exudate rich in protein. A profu sion of CT does not allow differentiation between tran sudates,
septa within a collection (honeycomb pattern ) predicts exudates. and chylous effusions (Naidich et al. 1984,
difficulties with tube drainage; thi s may be a feature of Rawk in et al. 1980). Acute intraple ura l hemorrhage may
be identified by the presence of a fluid-fluid level or be- MagnetiC Resonance Imaging (MRI)
cause of the high attenuatio n of the collection (McLoud
et al. 1991, Fig.9.3), Pleural fluid co llections cha racteristica lly have low T1- ,
and hi gh T2-signal intensity. While MRI does not allow >
different iation between exudates and tran sudates in
vivo (Davis et aL 1990), subacute and chronic hemor-
rhage may be recognized by the ir high signal intensity
on both Tl- and T2-weighted images (Tshcholakoff et al.
1978).
Pneumothorax r
• Pathology A pneumothorax may be traumatic, iatroge ni c, or

spo ntaneous in eti ology.
Pneumothorax is cha racterized by air in the pleural a
• Traumatic pneumothorax is described on p.203.
space and may result from a defect in the visceral pleura • Iatrogenic pneumothorax may res ult from trauma to Fig.9.S
that allows co mmunication between the pleural space the viscera l pleura during thoracentesis or during
and bronchoalveola r air. Transthoracic and transdia- cent ral venous line inse rtio n. Pneumothoraces are
phragmatic fistulae in patients w ith pre-existing
pneumoperi to ne um are less common causes of
also assoc iated w ith positive-pressure mechanical
ventilation.
r
pneumothorax. In most cases, the pleural tear closes • Spontaneous pneumothorax. A number of pulmonary
spontaneously due to a decrea se in lung volume. Oc- di seases lead to pleuropulmonary fi stulae (Table 9.4).
casionally, a check-valve mechanism may develop lead- Subp leu ral bullae are the most com mon ca use and
ing to a tensio n pneumothorax with severe pulmonary these are usually found at the ap ices. Spontaneous
atelectasis. media stinal shift. and life-threatenin g com- pneumothorax is mu ch more common in males than r
pression of media stinal vessels. in females; it is especially co mmon in tall, thin
patients. This probably reflects the increased gravi-
tational stress on the apices in the upright position.
Table 9.4 Causes of pneumothorax
Traumatic • Clinical Features

• Rib fracture Fig.9.1
• Stab wound Clinical manifestation s include pleuritic chest pain and tion dft
Iatrogenic dys pnea w hich are usually sudden in onset.

• Thoracentesis (e. g., subclavian catheter)
• Percutaneous lung biopsy
• Positive-pressure ventilation
• Tracheostomy
Spontaneous The di splaced visceral pleural line co urses paralle l to the
• Subpleural emphysematous bulla
chest wa ll. Pulmonary vascu lar markings are absent
• Pneumatocele
• "Cystic" lung disease(e. g., PLCH, AIDS-related cystic lung lateral to this hairline shadow (Figs.9.9-9.12 ). In the
disease) upri ght position, the intrapleural air accumulates at the
• Cystic fibrosis apex. In expiration, the relative volume ofthe pleural air
• Pneumonia with abscess formation coll ection to that of the underlying lung increases; ex-
Esophageal rupture piratory views therefore occasio nally are useful when
Pneumoperitoneum there is diagnostic difficu lty, Tension pneumothorax is
Pneumomediastinum associated with ipsilate ral pulmonary atelectasis and
co ntralatera l mediastinal shift.
a
Fig. 9.1
the left
Diseases althe Pleura 221
,
n
y
I.
" a b
Fig. 9.9a. b Spontaneous pneumothorax. There is left-sided pulmonary atelectasis but no evidence of mediastinal displacement.
:0
.g
·e
.1
15
.n
.n
i-
t.
Fig . 9. 10 Spont aneous pneumothorax with pulmonary "fixa-

tion" due to old apica l pleu ral thickening.
1e
nr
1e
1e
lir
x-
,n
is
1d
a b
Fig. 9. 11 a, b Pneumothorax on radiograph acquired with patient in supine position. Air collects inferiorly and defines the contour of
the left hemidiaphragm.
~~~ __________________J b
a
Fig. 9. 12 a. b Residual pneumothorax following closed pleural drainage.
Pleural Thickening and Fibrothorax
Pleural thicken ing is common and is usua lly a sequel of com pani on shadows of the lI pper ri bs (see Chapter 1,
pleura l in fl ammation. It may also be a delayed complica- p. 10) and from ext rapleurallinear rat deposition whi ch
tion of hemothorax , pl eural empyema, an d recurrent usually is bilateral, symmetrical, and located predomi-
pneumothorax. nantly alo ng the late ral chest wa ll.
Loca lized pleura l thickening is frequently fo und at the Fib ro us pleural plaqu es, an indicator of past asbestos
bases and resul ts in blu nting of the costo phrenic angles exposure, may have a ring or target configuration.
wit h te nting of the dia ph ragmatic pleu ra (Fig. 9.13). Plaques may undergo hya line transformati on, calcify, or
Fibrous pleural thickening is also co mmon in the apical ossify (Figs. 9.15,9.16,9.17 a). These geograph ical opaci-
pleural cupola where it may be secondary to tuberculo- ties commonl y invo lve the pleura of the antero latera l
sis or represe nt age-related cha nge. These "api ca l chest wa ll in the mi d-to- Iowe r zo nes and the diaphrag-
pleural caps" sometimes have a scalloped contour or ma tic pleura. Computed to mograp hy will define accu-
may show slight te nting towa rds the lung (Fig. 9.14). rate ly the location and exte nt of pleu ral plaque fo rma-
Pleural thickening should be distingui shed fro m the ti on (Fig. 9.17b).
Fig. 9. 13 Differentiation of pleural thickening from ef-

fusion on the lateral decubitus radiograph.
Pleural thickening
Pleural effusion
Patient in upright position Lateral decubitus

Fig.9.14 Apical pleural thickening.

The scalloped borders and tented
extension of the apical pleural cap
distinguish it from the companion
shadow of the second rib.
b Fig.9.15 Calcified pleural plaques

with Mholly leaf" appearance.
" 1.
hich
)mi-
:stos
tinn.
Y, or
laci-
te ral Fig.9.16 Asbestos-induced pleura l
plaques: Chest radiograph shows
Irag- bilateral calcified pleural plaque for-
.(CU- mation with involvement of the di-
~ma- aphragmatic pleura.
1 ef-
a b
Fig. 9. 17 a, b Asbestos-induced pleural plaques: Chest rad iograph (a) shows bilateral calcified pleural plaque. Axial CT image (b)
shows characteri stic distribution of plaque along anterolateral chest wall in mid-to-Iower zones.
Fig.9. 1
t he lef
Fibrothorax and Asbestos-Induced

Diffuse Pleural Thickening
Plel
Fibrothorax results from fibrous organization of a
hemothorax or em pye ma and is characte ri zed by forma-
tion of a pleural peel that may be up to several millime-
ters in thickness and w hich encases the lung. Calcifica- Ma lig
tion is frequ ent at the pulmonary interface. mon 1
Pulmonary encasement preve nts normal respiratory yeari
excursion and res ulting unilateral hy poventilation in- year i
duces reflex pulmona ry vasoco nstriction. This may be mon
visible on the chest rad iogra ph and may be confirmed by pears
radionllclide perfusion scintigrap hy. survi\
Fi brothorax may cause significant thoracic deformity sothe
and scoliosis as well as cicatricial emphysema w ith pul- asbes
monary arterial hypertension (Figs. 9.18,9,19), fibers
Diffuse pleural thickening may result from past partie
asbestos exposure w hen it may be bilateral and sym- fibers
metric (Fig. 9.20 ), See also Asbestos-Induced Pleural Dis-
ease, Chapter S, p. 140.
• Pi
Meso
and g
entin
aphr,;:
com i·
Fig.9.18 Fibrothorax with diffuse pleural thickening and ca lcifi- differ
cation at the pleura-lung interface.
may
ep ith
abun
in tYI
Diseases olthe Pleura 225
Fig.9. 19 Oleothorax with fibrin ball and calcified shell. Note also Fig.9. 20 Diffuse pleural thickening: CT shows bilateral diffuse
the left-sided pleural calcification. pleural thickening with associated lung infoldi ng in the left lower
lobe.
Pleural Mesothelioma
\
Malignant pleural mesothelioma is a re latively uncom- • Clinical Features

mon neoplasm w ith approximate ly 120 new cases per
year in Germany and approximately 500 new cases each The main clinical manifestations are chest pain includ-
1 year in the United States. However, it is the most com- ing referred pain localized to the shoulder. dyspnea.
mon primary pleural malignancy and its incidence ap- cough, and weight loss. Thoracentesis yields serous nuid
pears to be inc reasing. Prognos is is poor w ith an ave rage in 50% of cases and hemorrhagic fluid in the remainder
survival of only 8 months. The risk of developing me- of patients. In contrast to adenocarcinoma, the (EA titers
sothelioma is increased approximate ly 300-fold in are not increased but hyaluronic ac id content is
asbestos workers (Greene et al. 1977). Long thin asbestos markedly elevated.
fibers are probably the most tumorigeni c and the re is a
particularly strong associati on between crocidolite
fibers and developme nt of mesothelioma. • Radiologic Findings
Chest Radiograph
• Pathology
• Pleural effusion is the initial rad iograph ic finding in
Mesothe li oma usua lly arises in the lowe r hemi tho rax 80 % of cases. Drai nage may be associated with a re-
and grows along the pleural surface until it encases the sidual pneumothorax since the lung may be encased
enti re lung. Pulmonary parenchymal, chest-wa ll and di- and cannot re-ex pand.
aph ragmatic infiltration occurs. There is usually a co n- • Neoplastic pleural thickening: This encases the lung
comitant pleural effus ion. Histologic and cytologic and may have a smooth or lobulated contour
differentiation from metastatic pleu ral carcinomatosis (Fig. 9.21). It sometimes becomes visible following
may be difficult. Histologically. mesotheliomas may be thoracentesis and drainage of the effu sio n.
e pithelial w ith gland-like structures. mese nchymal with • Tumor nodule: Th is peripheral nodul e is in contact
abundant collage n formation, mixed or undiffere ntiated with the chest wall. A continuum ex ists between
in type, the epitheli al variant being most co mmon. nodular and lobulated tumor types (Fig. 9.2 2).
• Rib destruction, contralateral metastatic nodules. and
cardiac enla rgement signifying pericardial invasion are
occasionally features of advanced di sease.
Fig. 9. 21 Mesothelioma with dif-

fuse nodular pleural thickening in
the right hemithorax .
Computed Tomography and Magnetic

Resonance Imaging
Nodular pleural thickening of grea ter than 1 em in thick-

ness, involving the mediastinal pleura and form ing a cir-
cumfere ntial sheath around the lung, ind icates malig-
nant pleural disease (Leung 1990, Figs. 9.23, 9.24). The
MRI findings in malignant pl eural involve ment have
bee n described (Falaschi 1996). Malignant lesions were
found to be hyperintense to muscle on intermediate and
T2-weighted sequences in all cases.
An In ternationa l Staging System has bee n proposed
b
for malignant pleural mesothelioma (Rusch 1995. Patl et
al. 1996, Table 9.5). Fig
rig
Tammilehto et al. assessed pretrea tment CT in 88 m(
patients. They suggested that in clinical practice it is dif-
fi cult to differentiate tumor (T) from nodal involvement
(N) with CT due to the "unique plate-like growth pattern
of the tumor" (Tammilehto et al. 1995). Patl et al. eval-
uated CT and MRI findings in mesotheli oma a nd focused
on three anatomic regions: diaphragm, chest wall, and
st;
mediastinum. They found both modalities to have high
sensitivity but low specifiCity and a high accuracy in pre- (T
M
dicting resectability (Patl et al. 1992).
in l
fo
C1
Fig.9.22 Nodular pleural masses in mesothe lioma.

Diseases ofthe Pleura 227
Table 9.5 International staging system for diffuse malignant

pleural mesothelioma
T1 a Tumor limited to the ipsilatera l parieta l pleura, in-

cluding mediastinal and diaphragmatic pleura. No in-
volvement of the visceral pleura.
l1 b Tumor involving the ipsilateral parietal pleu ra , includ-
ing mediastinal and diaphragm atic pleura. Scattered
foci of tumor involving the viscera l pleura.
T2 Tumor involving the ipsilateral pleura surfaces with:
(1) Involvement of diaphragmatic muscle or (2) Con-
fluent viscera l pleural t umor (including the
fissures).
T3 Locally advanced but potentially resectable disease.
Involvement of all the ipsilateral pleural surfaces with
at least one of t he following: (1) Involvement of en-
dothoracic fascia, (2) extension into the mediastinal
fat, (3) solitary. com pletely resectable focus of tum or
extending into the soft tissues of the chest wall , (4)
nontransmural involvement of t he perica rdi um.
T4 Locally advanced technically unresectable tumor in-
volving all ipsi lateral pleural surfaces with at least
one of the following: (1) Diffuse extension into the
a chest wall ± associated rib destruction, (2) direct
t ransdiaphragmatic spread of tumor to the peri-
toneum, (3) direct extension to the contralateral
pleu ra, (4) direct extension to one or more mediasti-
nal organs, (5) direct extension t o the spi ne, (6)
tumor extending to the internal surface of t he peri-
card ium ± pericardial effusion or involving the myo-
cardium.
NO No regional lymph node metastases.

Nl Metastases to ipSilatera l bronchopulmona ry or hilar
lymph nodes.
N2 Metastases to subcarinal or ipsi lateral mediastinal
lymph nodes including ipsilateral intra mammary
lymph nodes .
N3 Metastases to contra latera l mediastinal, contralateral
internal mammary, ipsi- or contralateral supraclavicu-
lar lymph nodes.
MO No distant met astases.

Ml Distant metastases present.
b
Fig. 9.23 a, b Pleural mesothelioma: Axial CT images show
right-sided nodu lar pleural thickening with involvement of the
mediastinal pleura.
Heelan et al. compa red the accuracy ofCT with MR I in and multi-detector Cf (MDCf) with its capacity for mul -
staging of mesothelioma with reference to the TNM tiplanar reformats may fare bette r in this assessment.
(Tumor, Node, Metastasis) Staging System. They found These authors again emph asize the limitations of both
MR I supe rior to CT in assessing diaphragmatic invasio n, modalities in staging of mesothelioma and suggest that
invas ion of the endothoracic fascia, or so li tary resectable these are due to the co mplex unpredictable pattern of
foci of chest wa ll invasion. However, single-slice helical simultaneous local and regional sp read of this neoplas m
Cf was available only in the final months of their study (Heelan et al. 1999).
Diapt
Diap hral
nerve d~
the nerv·
bea com
adjacent
and low,
phragma
monic ef
Diapc
6 month:
gested tl
result fr
a b (Fig. 9. 26
Fig. 9. 24a, b Pleural mesothelioma: CT shows left-sided nodular pleural thickening with involvement of the superior aspect of the left
major fissure.
• Radi
The ehe51
• Eleva/
Diseases of the Diaphragm phrag
the Ie
inferit
• Cranic
stric
The fibromuscular diaphragm se parates the thorax from Table 9.6 Disorders of the diaphragm
crania
the abdome n (Fig. 9.25). Diaphragmatic dysfunction is
frequently a consequence of either thoracic or abdomi-
Bilateral depression secondary to pulmonary hyperinfla- • Parod
tion let m(
nal disease (Table 9.6). Primary diaph ragmatic • Emphysema crania
pathology is ra re. • Chronic severe asthma
• Bronchiolitis obliterans accen'
degre.
Unilateral depression
• Unilateral pulmonary hyperinflation (foreign body aspi ra-
excur!
tion) movel
• Tension pneumothorax • Dynor
Bilateral elevation the i
Blunting of the deere.
• Abdom inal causes (increased intra·abdominal fat in obes-
costophrenic angle
ity, ascites, hepatomegaly) the n<
• Restrictive ventilatory impairment
s ume ~
Unilateral elevation
• Intra-abdominal mass (hepatic tumor, splenomegaly, sub-
phrenic abscess, gastric or colonic distention)
• Decreased lung volume (atelectasis, hypoplasia)
• Di aphragmatic paralysis (eventration), phrenic nerve dam-
age
Focal contour abnormality
Subpl
Visible diaphragmatic muscle slips • Hernia (hiatus hernia, Morgagni hernia, Bochdalek hernia,
traumatic diaphragmatic rupture)
• Tumors of the diaphragm
Fig.9.25 Depression of the diaphragm. • Basal pleural tumor The sll bd
• Locu lated sub pulmonic effusion
• Partia l eventration (Fig. 9. 26)
toneal ca
fluid mig
Subdiaphragmatic air
effect of
• Pneumoperitoneum (Fig. 9.27)
• Chilaiditi syndrome (Fig. 9.28) phragmal
• Subphrenic abscess with gas-forming organisms ity. Subp
secondar;
duodenUi
Diseases olthe Diaphragm 229
Diaphragmatic Paralysis
Diaphragmatic paralysis is usually secondary to phrenic

nerve dysfunction: this may result from infiltration of
the nerve by bronchial or esophageal carcinoma or may
be a complication of cardiac surgery. Infections which lie
adjacent to the diaphragm including subphrenic abscess
and lower lobe pneumonia may also lead to redu ced dia-
phragmatic excursion. Radiographically, a large subpul-
monic effusion may simulate diaphragmatic elevation.
Diaphragmatic paralysis persisting for longer than
6 months lead s to muscular atrophy. It has been sug-
ges ted that idiopathic diaphragmatic eventration may
result from phrenic nerve palsy in early childhood
b (Fig. 9.26).
a
The chest radiograph (Fig. 9.29) may show:

• Elevation of the hemidiaphragm. The right hemidia-
phragm normally lies up to 4 em more cranial than
the left hemidiaphragm since the latter is displaced
inferiorly by the heart.
• Cranial displacement of abdominal contents. The ga-
stric bubble, hepatic and splenic flexures move
cranially.
• Paradoxical excursion. In in spiration, the healthy leaf~
let moves caudally while the paralyzed leaflet moves
cranially (so called "see~saw" phenomenon). This is b
accentuated by sniffing (Hitzenberg sniff test). A mild fjg. 9.26a, b Partial eventration of the left hemidiaphragm.
degree of paresis just delays the caudad inspiratory
excursion on the affected side ( pseudo~paradoxical
movement).
• Dynamic mediastinal shift. During abrupt inspiration,
the intrathoracic pressure on the normal side
decreases; this results in media stinal shift towards • Basal discoid atelectasis. The elevated hemidia-
the normal side. In expiration, the media stinum re~ phragm leads to compression of the lung bases with
sumes its midline position. crowding of pulmonary vessels and atelectasis.
Subphrenic Abscess
The subdiaphragmatic space acts as a sump for the peri- • Radiologic Findings
toneal cavity particularly on the right side. Peritoneal
fluid migrates here because of the intermittent suction The chest radiograph may show elevation of the hemidia-
effect of respiratory excursions and because transdia- phragm. A co ncomitant pleural effusion is present in
phragmatic lymphatic vessels drain the peritoneal cav- 80 %of cases and lung base atelectasis may be seen. Sub-
ity. Subphrenic abscess formation is most co mmonly phrenic air-fluid levels are seen in 30 % of cases. A medi-
secondary to hollow viscus perforation (appen dix. ally and caudally displaced gastric air bubble is also a
duodenum, and colon). feature of a left subphrenic collection.
230 9 Diseases ofthe Pleura, Diaphragm, and Chest Wall
Other causes of subdiaphragmatic gas include

pneumoperitoneum when signs are usually bilateral and p
p
Ch il aiditi's colonic interposition between the hemidia-
phragm and liver (Figs. 9.27,9.28).
Crov
Ultrasound demonstrates both the subphrenic collec- pulrT
tion and the associated pleural effusion.
Computed tomography shows the size and exact loca-
tion of the subphrenic collection and also demonstrates
associated pulmonary and pleural change. cr may also
demonstrate the primary intra-abdominal pathology.
Abscess formation is characterized by central low at-
tenuation with peripheral enhancement of the wa ll
which may be quite irregular in thickness. Following lo-
calization, percutaneous Cf-guided drainage may be
feasib le.
Diap
Fig.9.27 Pneumoperitoneum in patient postabdominal surgery.
Diaphrc
the lac,
Fig.9.28 Chilaiditi syndrome with hepatic orly at
flexure interposed between the liver and right througt
hemidiaphragm. Note co lonic haustra l mark-
atus (A
ings.
mayals
the thOi
The Boc
results I
diaphra
1 :3600
Milder I
patient~
tectable
in the I
tions ap
In p,
there is
ing pul
vasculal
ford 19!
poreal r
institutE
The (
within t
the coni
cally h'
pneuma
and an i
prognos
Comi
agnasis.
Diseases olthe Diaphragm 231
Fig.9.29 Diaphragmatic paralysis.

Paradoxical
respiratory ascent Mediastinal
shift
Crowding of basal
pulmonary vessels
Plate
atelectasis
o
/. Chilaiditi's
syndrome
Partial
II eventration
,-
e
Diaphragmatic Hernia
y.
Diaphragmatic hernias may be classified according to

the location of the defect. Herniation can occur anteri-
orly at the foramen of Morgagni, posterolaterally
through the Bochdalek foramen. or at the esophageal hi-
atus (Alford 1992 ). Traumatic diaphragmatic ruptures
may also result in herniation of abdominal contents into
the thorax (Fig. 9.30. see Chapter 8. p.212).
Bochdalek Hernia
The Bochdalek type of congenital diaphragmatic hernia

results from a defect in the posterolateral aspect of the
diaphragm. Large lesions are rare with an incidence of
1:3600 live births and 1 :2200 fetuses (Sa iduffin 1993 ).
Milder forms may be an incidental finding at CT in adult
patients. The Bochdalek hernia is sonogra phically de-
tectable in utero. Presentation with respiratory distress
in the neonatal period is common; delayed presenta-
tions are recognized (Berman 1988, Malone 1989).
In patients undergoing satisfactory surgical repair,
there is still an appreciable mortality due to accompany-
ing pulmonary hypoplasia and increased pulmonary
vascular resistance with persistent fetal circulation (Al-
ford 1992). These infants are candidates for extracor-
poreal membrane oxygenation (ECMO ), which may be
instituted before or after corrective surgery (Gross 1995 ).
The chest radiograph shows multiple loops of bowel Morgagni hernia
within the affected hemithorax with mediastinal shift to
the contralateral side. The abdominal radiograph class i- Fig.9.30 Diaphragmatic herniae (from Meschan 1981).
ca lly has a "scaphoid" appearance. A contralateral
pneumothorax, absence of contralateral aerated lung,
and an intrathoracic stomach are associated with a poor
prognosis (Saiduffin 1993. Fig. 9.31).
Computed tomography if required will confirm the di-
agnosis.
a a
Fig. 9.31 a- c Bochdalek hernia wi th herniation of the upper

pole of the right kidney.
posterior m ed iastinum or in the left lower hemithorax.

Morgagni Hernia Herniation may be reversible (sliding hernia) or may be
fixed by adhesions.
Loops of sma ll and large intestine or omentum may The chest radiograph may show a retrocardiac opacity b
hern iate into the thorax through the retrosternally ID- or appa rent elevation of the hemidiaphragm. An air- Fig.9.32c
eated sternocosta l trigone (the Laffey trigone), Right- fluid level is frequently see n within the herniated viscus
sided lesions are lO-times more common than left-sided and is highly suggestive of the correct diagnosis
herniations. (Figs. 9.33a, 9.34).
Gas-filled intestinal loops are projected over the ca r- Barium swallow wi ll confirm the diagnosis and
diac silho uette on the frontal chest radiograph. These are characteristically shows an hourglass constriction of the
seen to lie anteriorly on the late ral view (Fig. 9.32). stomach at the hernia l opening.
Compu ted tomography will establish the diagnosis Occasionally, a large hiatus hernia may be diffi cult to
and may be particularly helpful in cases where only distinguish from eventration of the hemid iaphragm.
omentum has herniated into the chest. Computed tomography may be helpful in these cases as
it defines the re lationship of the medial diaphragmatic
crus to the stomach (Fig. 9.33b, c). Hiatus hernia is a
frequent incidental finding at CT in the elderly.
Hiatus Hernia
Dilatation of the esophageal hiatus may result in partial Fig.9. 33a·

prolapse of the stomach into the chest to give a hiatus the cardiac
hern ia. The herniated viscus usually lies in either the thoracic a(
Diseases of the Diaphragm 233
a
a
,er
.x.
be b
tty b
ir- Fig. 9.32 a, b Morgagni hernia diagnosed on co ntrast enema.
:us
sis
nd
he
to
ffi.
as
tic
;a
Fig.9.33a-c large hiatus hernia. Note the mass projected over t>
the cardiac shadow (al and the displacement of the descending c
thoracic aorta (b, c).
234 9 Diseases of the Pleura. Diaphragm. and Chest Wall
a b
Fig. 9.34a, b Large hiatus herni a with an air-fluid level which is virtually diagnostic.
Tumors of the Diaphragm
Diaphragmatic tumors (both benign and malignant ) are these cases. Helical vol umetric computed tomography
rare and may be an incidental finding on the chest radio- with multi planar refo rmats and 3D reconstructions and
grap h. Histologic types include fibroma, lipoma, and sar- magnetic resonance imaging will demon strate tumor
coma. size. location, and degree of local infiltration. These
Benign tumors may mimic a localized eventration on modalities may also demon strate tum or tissue charac-
the chest radiograph. Malignant tumors are frequently teristics and lipoma, which occasionally may co ntain
associated with a pleural effusion (Wilso n 1992 ) and ul- calcium, may be ide ntified by its characteristic CT at-
trasound will demonstrate the tumor particularly well in tenuation values and MRJ signal characteristics.
Diseases of the Chest Wall
Evaluation of the bony thorax and soft tissues of the Examples include :
chest wall is important for the following reasons: • Barrel chest in emphysema.
• Chest wall abnormality may produce shadows that • Osteolytic destruction of ribs and vertebral bodies by a
are projected onto the lungs on the chest radiograph superior sulcus tumor and bronchial ca rcinoma at
and require differentiation from intrapulmonary le- other sites.
sio ns. A detailed review of the normal and abnormal • Rib osteomyelitis from extension of pulmonary and
bony thorax and chest wall is beyond the scope of this pleural actinomycosis.
text. The read er, however, is referred to figures (see • Rib notching in coarctation of the aorta.
Figs.9.35, 9.36) which review the principal radio- • Restrictive ve ntilatory impairment seco ndary to ky-
graphic findings. phoscoliosis.
• Pulmonary disease and cardiovascula r lesions may • Upper lobe fibrosis associated with anky los ing s pon-
lead to morphologic change in the chest wall and dylitis.
thoracic deformities may impair respiratory function Fig.9.36a
(Fi gs. 9.35-9.46). num onte
______________________________________________________D_is_e_a_se_s_o_f_th_e_c_h_e_s_t _W_a_II_______ "~
Fig.9.35 Variant con-
figurations of the bony
thorax.
Barrel chest Bell-shaped chest

(emphysema) (osteomalacia, rickets)
,phy
and Barrel chest Pectus excavatum Pectus carinatum
mor (emphysema) (funnel chest) (pigeon chest)
lese
rae-
ra in
. at-
and
) ky-
pon-
Fig. 9.36a, b Pectus excavatum. Note the projection of the ster-

num onto the lung/ mediastinum on the lateral view. b
Tuberculous spondylitis
Ivory vertebra
Endplate concavity in osteoporosis
Picture-f rame vertebra

(Paget disease)
Vertical striations
in hema ngioma
Ankylosing spondylitis
• Fig. 9.41
(calcification of longitudinal
ligament and an kylosis of
facet joints)
Fig.9.37 Rib notching due to a tortuous, dilated intercosta l ves-
sel in a patient with known coarctation of the aorta. Wedged vertebra
(fracture. congenital
deformity)
Fig.9. 39 Thoracic spine changes . I> '--_ _ __ _ _ __ __ _ _ _ _ _ _ _ _ _ _ _----'
Fig.9.38 Rib lesions and

anomalies.
Cervical rib Rib destruction in Pancoast tumor
Srb anomaly
Osteomyelitis
in actinomycosis
Bifid ri b
Osteolytic and
osteoblastic
Rib
fusion
Calcified vascular notching

costal cartilage
Fracture
Bony call us Paget disease

formation
Diseases of the Chest Wall 237
a b
Fig. 9.40 a, b Histologically confirmed aneurysmal bone cyst.
Fig. 9.41 Scoliosis with chest wall

deformity. Note the narrowed inter-
costal spaces on the concave side
of the cu rve.
Fig.9.42 left-sided thoracoplasty

and right-sided oleothorax in a
patient with a history of pulmonary
tubercu losis.
Fig.9.43 Pleural mesothelioma with chest wall invasion and rib

destruction.
Fig. g.t
rib anc
camp(
Diseases of th e Chest Wa ll 239
Fig. 9.44a. b Extrapleural lipoma: Chest radiograph (a ) shows

low density lesion lying on left lateral chest wall. CT (b) shows le-
sion to be of negative CT attenuation consistent with fat. appear-
a ance diagnostic of an extrapleural lipoma.
Fig . 9.46 Scapu lar osteosarcoma with di lated anterior chest wall
collateral vessels.
Fig.9 .45 Osteolytic metastasis from bronchial carcinoma with

rib and vertebral body dest ruction and with extradural soft tissue
component.
240
10 Radiology of Cardiac Disease
Posteroanterior (PA) and lateral chest radiographs taken lateral radiograph (Fig. 10.2) although today this has
in inspiration are standard for evaluation of ca rdiac size been superseded by echocardiographic assessment.
and contour. On the PA chest radiograph. the right car-
diomediastinal border is formed by the superior vena
cava (5VC) and the ri ght atrium; the left cardiomediasti-
nal border is formed by the aortic arch, main pulmonary
Cardiac Contour
arte ry. left atrial appendage. and left ventricle (LV ) (see
Fi gs. 1.8. 10.1 a ). Both conge nital and acquired cardiac disease are
On the late ra l projection, the right ventricle is in con- frequ e ntly associated with specific chamber hypertro-
tact with the lower sternum. More superiorly, the ante- phy or enlargement resulting in alteration in the shape
rior cardiac silhouette is formed by the right ve ntricular of the cardiac silhouette (Table 10.1 ).
outflow tract and pulmonary conus. The left atrium and
Fi g. l0.2a
left ventricle form the posterior cardiac contour (see Radiographic features in: TransversI
Figs. 1.9.10.1 b ). • Left ventricular enlargement (e. g. secondary to sys- CT ratio -
temic arte rial hypertension or aortic stenosis ) in - ter TID
clude: Al - aort
AR • aorl
- On the PA view transverse cardiac diameter is in-
Cardiac Size creased, the cardiac apex is rounded, and there is
l - care;
B - BU '
late ral convexity of the left heart border (aortic mea
While there is some variation in normal values, trans- configuration ).
verse cardiac diameter usually should not exceed the - On the lateral view, there is partial obliteration of
transverse diameter of one hemithorax or 50 % of the the retrocardiac space as the heart extends up to
widest transverse thoracic diameter. A more accurate 2 cm posterior to the inferior vena caval (IVe ) Ta ble 10.1
determination of cardiac volume may be made from the shadow (Figs. 10.3. lO.4c. d ). from Higg
Small ca
• Asthe
• Cache
• Em ph
• Restrj,
• Const
Normal-!
significal
• Aortic
• Arteri;
• Mitral
• Hyper
• Acute
• Some
large cal
• Norm;
in athl
• Bivent
• Dilatel
• Aortic
• Mitral
• Decon
a b • Conge
• Perica l
Fig. 10.1 a, b Normal cardiac anatomy on PA and lat eral chest radiograph s (from Klose et al. 1991)
Ao = Aorta Vci = Inferior vena cava
M
Tp - Proximal m ain pulmonary artery (" pulmonary t run k ) Vd - Right ventricle
Ap - Pulmonary art ery Vcs - Superior vena cava
Asin - l eft atrium Vsin - l eft ventricle
Ad ., Right atrium
10 Radiology of Cardiac Disease 241
,as
Ire
'0'
pe
a b
Fig. lO.2a, b Cardiac dimensions on the PA chest radiograph. T - transverse dimension of heart in axial plane
Transverse cardiac diameter T - TR + TL V >= relative cardiac volume
IS- (T ratio = transverse ca rdiac diameter/transverse thoracic diame- V = 0.4 x L x B x T

inter TID Normal ratio of cardiac volume to body surface area:
Al - aortic dimension to left of midline In women: 450-490 cmJ/m2
AR - aort ic dimension to right of midline (Al + AR - , .8-3.8 em) In men: 500-540 cm 3/m 2 (Amundsen 1959)
in- l = cardiac long axis measurement
! is B - au
+ SO perpendicular diagonal to L (maximum short axis
tic measurement through the heart)
of
to
Ie) Table 10.1 Conditions which may alter hea rt size (modified
from Higgins 1992)
Small cardiac silhouette:

• Asthenic body habitus
• Cachexia
• Emphysema (narrow, elongated heart)
• Restrictive cardiomyopathy
• Constrictive peri carditis
Normal-size cardiac silhouette despite the presence of
Significant lesions
• Aortic stenosis
• Arterial hypertension
• Mitral stenosis
• Hypertroph ic cardiomyopathy
• Acut e myocardial infarction
• Some congenita l heart lesions
large cardiac silhouette:
• Normal variant (e. g., physiologic LV hypertrophy
in ath letes)
• Biventricular decompensation
• Dilated cardiomyopathy
Fig.10.3 Chest radiograph in aortic stenosis. Note the rounded
• Aortic insufficiency cardiac apex, the left ventricular enlargement, and the post-
• Mitral insufficiency stenotic dilatation of the ascending aorta.
• Decompensated valvular stenoses
• Congenital ca rdiac anomalies
• Pericardial effusion (globular or triangular silhouette)
242 10 Radiology of Cardiac Disease
Fig. 1O.4a~g Cardiac chamber enlarge- • Right vel

ment (from Klose et al. 1991). arterial'
- Right
beror
parer
cardi,
the I.
part I
terist
the p,
- Right
frequ,
a c and c
• Left am,
elude:
- On th
social
cardic:
diac \
Congen
Left atrial enlargement Left ventricular enlargement

b (e.g., due to mitral stenosis) d (e.g., d ue to aortic stenosis)
Congenital (
population.
anomalies b
sions may n
The presenc
complex h
functional a
Cardiac {
their hemad
of a shunt.
Right atrial enlargement

e 9 (e.g .. due to
Cardiac
tricuspid regurgitation)
Cyanosis is
ventricular
pulmonary
heart diseas
and aortic \
group.
Pulmonafl
Right ventricular enlargement
(e.g., due to pulmonary stenosis)
• Clinical
Pulmonary v.
results from
formation of
size and posi
Congenital Heart Disease 243
• Right ventricular enlargement (e. g., due to pulmonary - The left atrium extends posteriorly as enlarge-
arterial hypertension ) include: ment becomes more marked and then its right
- Right ventricu lar change may be quite marked border may be projected within the cardiac sil-
before radiographic abnormalities become ap- houette (double "right heart border" sign).
parent. Right ventricu lar hypertrophy results in - The re may also be splaying of the carina to an
cardiac rotation with posterio r displacement of angle of greater than 90° as the left atrium extends
the left ventricle. The right ventricle then forms superiorly.
part of the left heart border and there is charac- - On the lateral view, there is narrowing of the ret-
teristically some "elevation" of the cardiac apex on rocardiac space as the left at rium enlarges posteri-
the PA view (Fig. lO.4e. f ). orly (Figs. 10.40, b, 10.31 ).
- Right ventricular hypertrophy and dilatation are • Right atrial enlargement (e. g.. due to tricuspid insuffi-
frequently associated w ith dilatation of the main ciency) include:
and central pulmonary arteries. - Prominence of the right card iac border.
• Left atrial enlargement (due to mitral stenosis) in- - The height of the atrial shadow exceeds 50 %of the
clude: distance between the diaphragm and aortic arch
- On the PA rad iograph. left atria l dilatation is as- (Higgins 1992, Fig. 10.4 g ).
sociated with prominence o r "fullness" of the left
cardiac border and obliteration of the normal ca r-
diac waist.
Congenital Heart Disease
Congenital cardiac anomalies occu r in 0.2 to 0.4 %of the valvu lar systoli c pressure gradient determines the sever-
population. There is a spectrum of severity with severe ity of symptoms; the most severe end of the spectrum
anomalies being incompatible w itl1 life w hil e other le- presents with right ventricul ar failure in infancy. "Su-
sions may not become symptomatic until late adult life. pravalvular" pulmonary stenosis is considered to be an ar-
The presence of multiple anomalies may give rise to teritis with segmental arterial stenos is. It is seen in
complex hemodynamic patterns with secondary Noonan's and W illiams' syndrome and in congenita l
functional and stru ctu ral cardiac adaptation. rubella. Subva lvular stenos is is frequently due to right
Cardiac anoma li es may be classified accordi ng to ve ntri cu lar outflow tract (RVOT ) hypertrophy and the
their hemodynamic effects, i. e., the presence or absence valve may be normal or dysmorphic in these patients
of a shunt. (Boxt et al. 2003 ).
Cardiac Anomalies without a Shunt
The cfl est radiograpfl may show characteristic post-
Cya nosis is absent but a degree of e ither right or left stenotic di latation of the main pu lmonary artery extend-
ventricular outflow obstruction is present. Isolated ing to involve the left pulmonary artery and resulting in
pulmonary valve stenos is (10-15 % of all congenital enlargement of the left hilum (Fig. 10.5). The heart is of
heart disease), coarctation of the aorta (COA) (5-9 %), "righ t ventricular" configuration with elevation, round-
and aortic valve ste nosis (3-7 %) are includ ed in this ing, and flattening of the cardiac apex. Pulmonary vascu-
group. lari ty is normal in most cases except in high-grade ste-
noses.
Echocardiograpfly: In moderate to severe stenosis,
Pulmonary Stenosis pulmonary va lve leaflets are thickened with evidence of
"doming" during systole. Poststenotic dilatation of the
main pulmonary artery is seen with sign ifi cant degrees
• Clinical Features of obstruction. Right ventricul ar anterior wall thickness
may be measured. Pulsed (PW) and contin uous wave
Pulmonary valve stenosis (PVS ) is usually congenital and (CW) Doppler allow estim ation of the systolic gradient
resu lts from fus ion and thickening of valve cusps with across the va lve. The right ventricular anterio r wall
formation of a diaphragm perforated by an orifi ce the thickness and the systolic gradient determine the need
size and position of w hich are quite variable. The trans- for surgical intervention (G rainge r 1992).
Chest radiograph: Features of left ventricula r hypertro-
phy and dilatation of the ascending aorta are seen only
in high-grad e ste nosis.
Echocardiography: Two-dimensional (2 0) echocardi -
ography shows the abnorma l va lve, a small va lve ring.
and a hypertrop hied. hyperdynamic left ventricle. CW
Doppler echocardiography allows est imation of the sys-
tolic grad ient across the valve.
Magnetic resonance imaging demonstrates a small
aortic annulus and abnormal di stributio n of the aortic
sinuses by the unseparated va lvular comm issures. The
valve leafl ets may be thickened and leaflet doming may a
be evid ent on gradient echo sequences. These sequences
also demon strate the systolic signal vo id jets of stenosis.
Left ventricular hypertrophy is freque nt.
Fig. 10.5 Congenital pu lmonary valve stenosis. Chest radio- When there is aortic regurgitation, associated post-
graph shows poststenotic dilatation of the main pulmonary stenotic dilatation of the ascending aorta and a degree of
artery and left hilar enlargement. left ventricle dilatation may be prese nt. GRE sequences
in these cases show diastolic jets of regurgitation (Boxt
et al. 2003 ).
The pressure gradient across the valve may be esti-
mated from the length of signal loss across the aorta
(Mitchell et al. 1989) or quantified using phase veloc ity
Magnetic resonance imaging (MRI) : Spin echo mapping (Kil ner et al. 1991).
sequences in patients with valvular stenosis show bulg- Left ventriculography and aortography confirm the
ing of the pulmonary valve, posts ten otic dilatation of the presence of left ventricula r outflow obstruction and
main pulmonary artery, and a degree of right ventricular when appropriate balloon valvotomy may be perFormed d
hypertrophy. The presence of associated tricuspid re- during catheterization.
gurgitation is va riable and is dependent on the degree of Left ve ntricul ar outflow obstruction may also be su-
RV hypertrophy. Gradient echo (GRE) seque nces show pravalvular and associated with infantile hypercalcemia
the systolic jet of signal void across the valve and allow or subva lvular due to fibromuscular hypertrophy of the
calculation of the seve rity of the ste nosis. left ventricular outfl ow tract.
Right-heart catheterization w ith right ventricular in-
jection confirms the diagnosis and demonstrates dom-
ing of the va lve cusps during systole. The right ve ntricle Coarctation of the Aorta
is heavily trabeculated and right ventricular pressures
are elevated considerably in severe stenosis.
Congenital Aortic Stenosis Medial hypertrophy and intimal proliferation within the
aorta lead to localized stenosis which becomes hemody- g
namically significant when it causes more than a 50% re-
• Clinical Features duction in the size of the lumen.
Two forms are recognized :
Childhood aortic valve disease encompasses a wide • Infantile (preductal) COA: In this form. the stenosis
spectrum of abnormalities of varying severity. Severely lies proximal to the ductus arteriosus whic h usually
dysplastic valves are associated with cardiac failure in is patent. This may result in a right-to-left shu nt with
the neonatal period, the so-called "criti ca l aortic steno- cyanosis in the lower half of the body (Fig. 10.6).
sis of the newborn." A congenital bicuspid aortic va lve is
the most frequent malformation of the aortic valve and
occurs in 0.9-2 % of all indi vidua ls at autopsy (Roberts
1970). These lesions do not usually beco me sympto-
matic until adult liFe and about one-third of these in-
dividuals eventually develop aortic ste nosis (Fenoglio et
al. 1977 ) either related to the structural abnormality or Fig.10.6a-k Schematic representation of congenital ca rdiac [>
secondary to an episode of bacterial endocarditis. anomalies (from Schinz et at. 1983).
rtro-
only
ardi-
ri ng.
. CW
, sys-
Coarctation of the aorta
lmall (preductal type)
lortic
. The Atrial septa l Atrial septa l
may • b defect with a left-to-right shunt c d~fect with a right-to-Ieft shunt
~ n ces
.lOS is.
post-
~ee
of
ences
(Boxt
~ esti-
aorta
loei ty
n the
1 and
lrmed d Ventricular septal defect
• Patent ductus arteriosus Aortopulmonary window
De su-
cemia
of the
Fig.10. 7 Coarctation of the aorta . Note

the left ventricular enlargement, the foca l
"notch" in the aorta giving a "reversed 3"
configuration (1) and the rib notching (2).
• Adult (postductal) COA: In postductal or adult coarcta- Con!

tion, systolic blood pressure in the upper limbs Ass(
exceeds that in the lower limbs by at least 20 mmHg.
The lower body is supplied by collateral vessels
ShUi
w hich usually have deve loped by late childhood.
Associated anomalies including bicuspid aortic valve The IT
and aberrant subclavian artery occur in up to 75% of ventri
cases. cardia
10-15
Less.
• Radiologic Findings dromf
anom,
Chest radiograph: Radiographic findings in coarctation Th,
include a high aortic arch with pre- and poststenotic di- (VSD)
latat ion (Figs. 10.7, 10.8). In the postductal type, rib also b
notching involving the 3rd to 8th ribs is due to pressure right
erosion by dilated intercostal collateral vessels. In the in- greall
fantile type, dilatation of the pulmonary vessels may in- leads
dicate the presence of a left-to-right shu nt. su ltin
Magnetic resonance imaging and aortography demon- pulm(
Fig. 10.8 Aortic coarctation: "Reversed r configuration of the strate the length and level of the coa rctation segment right
aorta is seen.
and the degree of arterial co llaterali zatio n present in pu
(Figs. 10.9, 10.10). The relationship of the origin of the pressl
subclav ian arteries to the stenotic segment is important leadir
to demon strate given the association with the aberrant Chapt
subclavian artery (Boxt et al. 2003). MRI also plays a role In(
in imagin g follow-up of patients after balloon dilatation remai
and repair of the coarctation . (reas(
Congenital Hea rt Disease 247
Fig.10.9 Coarctation of the aorta. A

,I catheter has been placed in the pulmonary
artery, and injected contrast medium has
). opacified the left atrium, left ventricle. and
aorta.
cta- Congenital Cardiac Anomalies

Tlbs Associated with a Left-to-Right
lHg.
sels
Shunt
}od.
alve The most common causes of a left-ta-right shunt are
~ of ventricular septal defects (VS D: 20-28 %of all conge ni tal
cardiac anoma li es, Fig. 10.11 ), atrial septal defects (ASD:
10-15 %), and patent ductu s arteriosus (PDA: 10-15%).
Less common anomalies include Lutembacher syn-
drom e (ASD combined w ith mitra l stenosis) and
anomalous pu lm onary ve nou s drainage (APVD).
tion The shunt may be at the atrial (ASD ), ve ntri cular
: di- (VSD), or arterial (PDA) leveL Oxygenated blood may
rib also be shunted from the pulmonary ve ins back into the
sure right atrium (APVD ). Recirculating blood vo lume may
ein- greatly exceed the circulating systemic vo lume: th is
yin- leads to overload of the pulmonary circulation with re-
sulting pulmonary arteriolar sclerosis and increased
]011- pulmonary vascular resistance. Thi s in turn induces
nent right ventricular hypertrophy causing further increases
sent in pulmonary arterial pressure. Eventually right heart
, the pressure may exceed that in the left heart cham bers Fig.10.10 MRI demonstrates aortic coarctation and dilated in-
'tant lead ing to shunt reversal (Eisenmenger reaction: see tercostal vessels inferior to the level of the aortic narrowing.
Tant Chapter 7, p. 194).
role Ind ividuals w ith congenital left-to-right shunts may
Ition remain asymptomatic for many years but are at in-
creased ri sk of endocarditis. Large shunts may be as-
Chest radiograph: When the pulmonary to systemic
shunt ratio is greater than 2:1, there is cardiomegaly
(Gra inge r and Donner 1992) and pulmonary plethora
(Higgins 1992). Other characteri stic features include in-
creased pulsation of dilated central pulmonary arteries
(hilar dance ) visible at fluoroscopy. The level of the
shunt ca nnot be determined from sta ndard radiographs
although certain characteristics of the cardiac silhouette
may give diagnostic clues (Fig, 10,12),
Atrial Septal Defect

a
Atrial septal defects are classified accordi ng to the site of
the communication (see Fig. 1O.6b. c):
• An ostium secu ndum or fossa ovaHs defect is situated
in the upper part of the septum posterior to the co ro-
nary sinus and superior to the tricuspid va lve. The
size of the defect is va riable, the mildest form being a
slit-like patency of the foramen ovale that normally
closes soon after birth. Significant shunts are usually a
greater than 2 cm in diameter. are not va lvular, and
Fig. 10
will transmit blood from the left to the right atrium. pletho
Ostium secundum defects account for 80 to 90 % of all
ASDs (Grainger and Donner 1992 ).
• An ostium primum defect involves the inferior part of
the septum and is the mild est form of endocardial
cush ion defect. An ostium primum defect together
w ith cleft leaflets of malformed tricuspid and mitral
valves represent incomplete persistence of the arteri-
oventricul ar canal. If a high VSD is also present. the
combina tion constitutes complete persistence of the
arte rioventri cular canal. There is mitral regurgitation
w ith left -to-right shunting of blood, The e levation of
right heart pressures results in gradua l development
of pulmonary hypertension.
• A sinus venosus defect is situated in the most super-
b ior part of the septum just inferior to the termination
Fig . 10.11 a, b Ventricular septal defect: Frontal and lateral of the superio r vena cava. This almost invariably is as-
chest radiographs show right ventricular dilatation and marked sociated w ith aberrant drainage of the right upper
pulmonary plethora. Echocardiography shows large VSD with left
lobe pulmonary vein into the inferior part of the SVc.
atrial and biventricular enlargement.
Sinus venosus defects account for 5 %of all ASDs.
a
Fig.l(
• Radiologic Findings m ona
sociated with marked symptomatology including im-
paired physical development in children. Characteristic Chest radiograph: If the shunt ratio is greater than 2: 1,
auscultatory findings include a pansystolic murmur in the re is usually cardiomegaly. There is dilatation of the
VSD and a continuous murmur in PDA. In advanced un- central pulmonary arteries and a variable degree of pul- costa
treated cases, signs of right heart failure (dilated neck monary plethora is present. The aortic arch may appear prim
ve ins, peripheral edema, and hepatomegaly ) may supe r- small, probably due to a degree of aortic rotation (Figs. M
vene. Cyanosis develops with reversal of the shunt. 10.13,10.14). has £
Echocardiography will demonstrate nearly all defects, ASDs
When a sign ifi cant shunt is prese nt, there is ev idence of
right ventricu lar dilatation w ith sys tolic anterior motion
of the interventricular septum. The four-chamber sub-
Congenital Heart Disea se 249
b
Fig. 10.12 a, b Atrial septal defect with a left-to-right shunt. Note the central pulmonary artery dilatation (1 and 2) and the pulmonary
plethora (3).
a
Fig . 10.13 a, b Ostium secundum defect. (a) Chest radiograph shows cardiomega ly. dilatation of the main pu lmonary artery, and pul-
monary edema. Radiograph 4 years after operative closure of the defect is almost normal (b).
costa l view will differe ntiate ostium secundum from of gado lin ium may help to demonstrate small er and less
primum defects (Grainger and Donner 1992). apparent shunts (Manning et al. 1992). GRE sequences
Magnetic resonance imaging: MRI in the axial plane allow determination of the direction of the shunt and
has 97 % sensitivity and 90 % specificity for detection of ve locity-encoded cine (VEe) images allow some estima-
ASDs (Diethelm et al. 1987). Intravenous administration tion of the volume of the shunt.
Fig.10. 14 Ostium primum defect with a circulat

left-to-right shunt. There is cardiomegaly,
is varia
centra l pulmonary artery dilatation, and
CroSS-51
pulmonary plethora.
gradier
Onl~
the shl
ally.pu
of inert'
to pres
Eisenrr.
pulmOi
arterial
• Ra.
The ch
shunt.
proxirr
tricie,
shunt
central
ripher;
standil
menge
pulmo
Tw(
atrial c
tion 0
showil
Ventricular Septal Defect cardiomegaly. dilated centra l pulmonary arteries, and during
pulmonary plethora. diastol
This is the most common congenital cardiac anomaly ac- Two-dimensional echocardiography will identify the of the
coun ti ng for 20-28 %of cases. Membranous defects are site of the defect. Left atrial and left ventricul ar dilata- 1992. ,
most common and occur in the upper posterior septum. tion will be ev id ent in moderate to large shun ts. PW Mo.
Defects in the muscular se ptum (ma ladi e de Roger ) may Doppler wi ll confirm the prese nce of a shunt and Dopp- or in t
be single or multiple. When multipl e. they may produce ler color flow mapping will identify the site. extent. and may d
a "Swiss cheese" pattern. Defects in the muscular sep- direction of the shunt (G rainger and Donner 1992. Ludo- no dat
tum are frequently quite small although the associated mirsky et al. 1986. Ortiz et al. 1985). MRI in
pan systolic murmur may be relatively loud. Magnetic resonance imaging allows diagnosis of and magn'
The magn itude of the shunt is roughly proportional determination of the size of a VSD. Large defects may be mayb
to the area of the defect. With defects smaller than read ily id entified on spin echo sequences as signal vo ids and Iii
0.5 cm 2, systolic muscle contractions are sufficient to to the left of the atrioventricular rings. Smaller more dis- AOI
maintain the interventricu lar pressure gradient. With tal and muscular VSDs may be difficult to demonstrate tic arc
larger defects, the right ventricle is subjected to systemic on spin echo sequences but the signa l vo id jet of the the pc
pressures with resul ting right ventricular hypertrophy. shunted blood on GRE seq uences may allow their detec-
Right ve ntricular hypertrophy and increasing pulmo- tion.
nary vascular resistance lead to a reduction in the Total
volume of the left-to-ri ght shunt and if untreated will in Drair
time lead to its reve rsal (Eisenmenger reaction, see Patent Ductus Arteriosus
Fig. 10.6 d ). In TAl
This communication between the concavity of the aortic eleme
arch and the superior aspect of the main pulmonary rare al
• Radiologic Findings artery constitutes an essential part of the fetal circula- diac r
tion and usually closes soon after birth. Persistence of when
The chest radiograph may be normal when just a small this tubular connection (patent ductus arteriosus ) per- TAl
defect is present. Larger defects are associated with the mits passage of blood from the higher- pressure ao rta • TYI
chara cteri stic features of a left-ta-right shunt including in to the pulmonary artery and through the pulmonary wil
a circulation thus creating a left-ta-right shunt. The defect

Iy, is variable in size but is seldom greater than 1 cm 2 in
I
cross-sectional area. An aortopulmonary pressure
gradient is maintained in the majority of cases.
Only the left heart chambers are enlarged initially as
the shunt does not involve the right ventricle. Eventu-
ally, pulmonary vascular resistance increases as a result
of increased pulmonary blood flow and this in turn leads
to pressure overload on the right heart (see Fig. 10.60).
Eisenmenger reaction with shunt reversal occurs when
pulmonary arterial pressure exceeds that of the systemic
arteria l circu lation.
The chest radiograph shows features of a left-to-right

shunt. The re is associated enlargement of structures
proximal to the shunt including the left atrium, left ven-
tricle, ascending aorta, and aortic arch (Fig. 10.15 ), If a
shunt reversal occurs (Eisenmenger reaction) then t he
central pulmonary arteries become more dilated and pe-
ripheral oligemia develops (Fig. 10.15 ). In cases of long-
standing severe pulmonary hyperte nsion with Eisen-
menger reaction, calcification (Fig. 10.16) of the dilated
pulmonary arteries and ductus may be see n.
Two-dimensional echocardiography will show left
atrial and left ventricular dilatation. PW Doppler eva lua-
tion of the pulmonary artery confirms the diagnosis
show ing normal forward flow from the pulmonary valve
and during systole with reversed flow from the bifurcation in
diastole. Dopp ler color flow mapping allows assessment
the of the overall size of the shunt (Grainger and Donner
ata- 1992, see Fig. 10.17 ).
PW Magnetic resonance imaging: Imaging in the coronal
lPp- or in the parasagittal right anterior oblique (RAO) plane
and may demonstrate the ductal communication. However,
Jdo- no data are avai lable on the se nsitivity and spec ifi city of
MRI in diagnosis of PDA (Soxt et al. 2003). Furthermore,
and magnetic resonance (MR) evaluation of th is anoma ly
y be may be limi ted in infants by the small size of the ductus
aids and limited MR spatial resolution.
dis- Aortography: Contrast medium injected into the aor-
:rate tic arch will demonstrate the patent ductus and opacify
the the pu lm onary arteries (Fig. 10.17).
~tec- b
Fig. 10.1Sa, b Patent du ctus arteriosus. Radiographs show car-
Total Anomalous Pulmonary Venous diomegaly, ma rked central pulmonary artery dilatation. and a di-
Drainage (TAPVD) lated aortic arch.
In TAPVD, pu lmonary venous drainage is to almost any

Jftic element of the sinus venosus system. This is a relatively cal vein which then drains to the brachiocephalic
lary rare anomaly accounting for approx im ately 2 %of all ca r- vein and su perior vena cava or with PVD to the azygos
'ula- diac malformations and is compatible w ith life on ly vein and then to the SVC.
e of when a coexisting atrial septal defect is present. • Type II: Anoma lous return at card iac level w ith
per- TAPVD may be classified into: drainage to the coronary sinus or right atrium.
orta • Type I: Supraca rdiac return is most common (55 %) • Type III: Infradiaphragmatic return w ith drainage to
my with pulmonary venous drainage (PVD ) to the verti- the portal system or inferior vena cava.
Fig.1O. 16a- f Cardiac calcifi cations. (a )

Calcifi ed mitral valve ring, PA and lateral
views. (b) Aortic (Ao) and mitra l (Mi) valve
calcification on lateral view. (e) Left ant erior
descending (LAD) coronary arte ry ca lcifica-
tion in the RAG projection. (d ) Calcificat ion
in left atrial w all, PA and lateral views. (e)
Pericardial calcification. PA and RAO projec-
t ion s. (f) Ca lcifi ed ventricular aneurysm, PA
view (from Meschan 198 1).
a
Fig. 10.1:
patent d
b
c
• Typ.
198i
• Ra(
Chest n
in to tw
res ista r
w ith 01
d ( o mme
• Typ,
a fi
conI
latec
to tI
is SE
• Typ.
and
• Typ.
e pre ~
Echoca
characl
unite il
In ty pe
to the ~
show (
In t
mo nstl
monar:
p hragr
1987 ).
See
Draina,
',-.
'jar
on
~(.
PA
• b
Fig. 10.17 a, b Patent ductus arteriosus. Contrast medium injection into the aortic arch opacifies the pulmonary arteries through the
patent ductus.
• Type IV: Drainage at multiple levels (Pearson et al. Congenital Cardiac Anomalies
1987 ). associated with a Right-to-left
Shunt
Congenital cardiac anomalies associated with a right-to-
Chest radiograph: Patients with TAPVD may be divided left shunt lead to central cyanosis. Tetralogy of Fallot is
into two groups: those with normal pulmonary vascular most common accounting for 10-15 % of all congenital
resistance and unobstructed venous return and those cardiac anomalies fallowed by transposition of the great
with obstructed venous return. The latter is found most vessels (5-9 %), tricuspid atresia (1.2-3 %), and the Ebstein
commonly in type III TAPVD. anomaly (0.23-1 %) (Klose et ai. 1991 ).
• Type I: The chest radiograph characteristically shows When an atrial or ventricular septal defect is com-
a figure-of-eight shaped mediastinum (snowman bined with pulmonary stenosis, the increased right heart
configuration): this represents the vertical vein, di- pressure leads to development of a right-to-Ieft shunt.
lated left brachiocephalic vein, and SVC. If drainage is Similarly. when an atrial septal defect is combined
to the azygos vein, this vein may then be dilated and with tricuspid stenosis or a hypoplastic right ventricle
is seen in the right superior mediastinum. (the Ebstein anomaly), right-to- Ieft shunting also occurs.
• Type II: The right cardiac contour may be abnormal Pulmonary flow is diminished relative to flow through
and this may be due to a dilated coronary sinus. the systemic circulation resulting in central cyanosis.
• Type III: There may be gross pulmonary edema in the
presence of a normal-sized heart.
Tetralogy of Fallot
EcilOcardiography: The four-chamber view shows the
characteristic features of TAPVD. The pulmonary veins Tetralogy of Fallot is characterized by infundibular pul-
unite in a venous confluence superior to the left atrium. monary stenosis. a high ventricular septal defect. and
In type I TAPVD, suprasternal views may show drainage aortic override of the ventricular septum. Right ventric-
to the SVc. In type II, a posterior four-chamber view may ular hypertrophy is a consequence of these features. The
show dilatation of the coronary sinus. degree of pulmonary stenosis determines the magni-
In type III, the subcostal parasagittal view will de- tude of the shunt and the severity of clinical symptoms
monstrate a descending vein originating from the pul- (see Fig. 10.69, h). Patients may undergo a palliative
monary venous confluence and passing through the dia- shunting procedure to improve pulmonary blood flow
phragm in close proximity to the aorta (Pearson et al. prior to complete repair with VSD closure and infun-
1987). dibulectomy. A Blalock-Taussig shunt connects the sub-
See also Partial Anomalous Pulmonary Venous clavian to the ipsilateral pulmonary artery, a Waterston
Drainage, Chapter 2, p.61 and Figs. 2.22, 2.23. shunt connects the ascending aorta to the right pulmo-
nary artery. and a Potts shunt connects the descending
aorta to the left pulmonary artery.
bination of atrioventricu lar concordance and ven- valve I(

triculoarterial discordance. The anteriorly displaced valve ri
aorta ari ses from the right ventricle whi le the pulmo- connec
nary artery originates from the left vent ricle. Thi s ad here;
creates two separate circulations which are intercon- regurgi
nected by a bidirectional shunt (usually an ASD, less assesse
commonly a VSD or PDA, see Fig. 10.6 i). uation
used f(
decrea~
• Radiologic Findings (Graing
Chest radiograph: Card iomegaly develops in the first

weeks of life and there is associated narrowing of the su-
perior mediastinal vascu lar pedicle due to superimposi-
tion of the pulmonary artery and aorta. These features
ACql
lead to an "egg-shaped" cardiac si lhouette. The lungs are
plethoric in uncorrected transposition.
Two-dimensional echocardiography in the parasternal
long- and short-ax is plane s shows the anteroposterior re-
Cardi
R
Fig.10.18 "Boot-shaped heart in Tetralogy of Fallot. versa l of the aorta and pulmonary artery. The apica l four-
chamber view all ows eva lua tion of the ventricular sep- Cardiac
tum and if a VSD is present, PWand color flow Doppler im- and is c
• Radiologic Findings aging will demonstrate the degree of shunting from the an adeq
rightto the left ventricle( Grainger and Donner 1992 b).
The chest radiograph shows pulmonary oli gemia. The Right heart catheterization: A contrast medium injec-
ca rdiac silhouette may appear normal or have a charac- tion into the right ventricle shows the morphological
teristic "coeur en sabot" appearance resembling a ri ght ventricle leading to the ao rtic valve w hich is sit-
wooden shoe depending on the severity of the right uated more superiorly than is normal and to the anteri-
ventricular outflow obstruction. The latter is caused by orly displaced aorta. A left ve ntri cular inj ection will de-
right ventricular hypertrophy with cardiac rotation and monstrate the left ventricle in continuity with the pul-
by a markedly concave pulmonary bay as the main pulmonary va lve wh ich lies more inferiorly than is normal
monary artery is hypoplastic (Fig. 10.18). (Grainger and Donner 1992b).
Two-dimensional echocordiography will demonstrate
the VSD. Long-axis parasternal views show the aortic
override and parasternal short axis and suprasternal Ebstein Anomaly
views aid in evaluation of the pulmonary valve. PW and co-
lor flow Doppler imaging show the degree of right-to-Ieft The malformed septal and posterior leaflets of the tri-
shunting through the VSD (G rainger and Donner 1992 b). cuspid va lve are disp laced infe riorly and attached to the
Magnetic resonance imaging will demonstrate fea- wa ll of the right ventricle. The proximal right ventric le
tures of the Tetralogy. In addition, MRI may playa valua- therefore is incorporated into the right atrium (atrial-
ble role post shunting in evaluation of shun t patency. ized ) but it contracts synchronously with the right ven-
Right heart catheterization: An injection into the right tricle. This di sordered function leads to impaired right
ventricle shows the VSD and the aortic override; these atrial emptying. An ASD or patent foramen ovale is pre-
are demonstrated optimally in the left anterior oblique se nt in 80 % of cases and produces a right- to-Ieft shunt
0
(60" LAO) projection. The right anterior oblique (30 RAO ) resulting in cyanosis.
projection is optimal for visualization of right ventricular
outflow obstruction which is usually severe. Infundibular
stenosis is most common be ing present in 70 % of cases. • Radiologic Findings
The pulmonary valve is stenosed in 60 % of patients
usually in assoc iation with infundibular ste nosis. The chest radiograph characteristica lly shows an en-
larged globular-shaped heart. Right atrial enla rge ment 350 -
accounts for the convex right lateral border while the 300 -
Uncorrected Transposition of the convex left border is formed in part by the right ven- W250 ·
-;; 200
Great Vessels tricle. The vascular pedicle in the superior mediastinum
§ 150
is narrow, the main pulmonary arteries are inco nspicu- g 100
Transposition of the great vessels is a cyanotic congeni - ous, and th ere is pulmonary oli gemia. 50 ~
tal heart anomaly which requires surgical correction Echocardiography: The ap ical four-chamber view o
read ily demonstrates displacement of the tricuspid
o 1
(arterial swi tch ) early in life. The term describes a co m-
Acquired Heart Disease 255
n- va lve leaflets in to the right ventricl e. The true tricuspid Right heart catheterization confirms the diagnosis.
,d valve ring and the abnormal origin of the leaflets may be Contrast medium injected into the right atrium demon-
0- connected by a band of echoes representing valve tissue strates displacement of the abno rma l tricuspid valve
lis adherent to the ventricular wall. The degree of tricuspid leaflets to the left of the midline. There is usually
n- regurgitation and of right-to-Ieft shunting may be delayed emptying of the right atrium with right-to- Ieft
~ss assessed with PW and color flow Doppler imaging. Eval- shunting of opacified blood through an ASD or patent
uation of the anterior cusp is important as this may be foramen ovale. Right ventricular injection demonstrates
used for "monocusp surgical repair," wh ich aims to the severity of tricuspid incompetence.
decrease the severity of tricuspid regurgitation
(Grainger and Donner 1992b).
rst
jU-
si- Acquired Heart Disease
res
"e
nal
re-
Cardiac Failure Left ventricular failure leads to pu lmonary edema
ur- w ith dyspnea and peripheral cyanosis. There is systemic
=p- Cardiac failure is common, particularly in the elderly, venous congestion with dilatation of neck veins, periph-
m- and is characterized by inability of the heart to maintain era l edema, hepatomegaly, and ascites in right ventricu-
the an adequate cardiac output (Fig. 10.19). lar failure. Biventricular failure is frequently present.
).
ee-
ical Fig.10.19 Left ventricular ejection fraction. Left:
sit- systole and diastole in cardiac failure. Right: sys·
tole and diastole in a normally functioning heart.
=ri-
de-
JUI-
mal
~ tTi-
l the
ride
rnal-
ven-
eight
pre-
hunt
en-
nent
! the
ven- E250 .. ·
•.
~~~ , r:'-,"-.:-,.=_ ~__ .~-
.......... " .- ....... E
--j-. ~.
r
- "1." 1, ",;. --
'"]1'1 ::I~
num ';"200 ". ",- ';"100
§ 150 - . .~ ... +- .. +--.. ~ ...... -_ ... [.. §
-+
?icu-
view
~ '~~ :.
o ~~~~~~~~~~~
,+r·'.;.'iT ~ SO
0o~~~~~~----~
o 100 200 300 400 500 600 700 800 200 400 600 800 1000
lSpid Time (ms) Time (ms)
Cardiac failure may be due to: ers of the ventricular wall and most common ly occur in
• Myocardial dysfunction: A number of factors includ- the anterolateral and apica l regions. False aneurysms
ing ischemia, inflammation. and metabolic disorders formed by endocard ial tissue protruding through de-
may impair the contractile function of the myo- fects in the myocardium usually involve the inferior
cardium. This leads to a decrease in the systoli c ejec- wall.
tion fraction of the ventricle.
• Hemodynamicfailure results from severe valvular dis-
ease and other factors that impose a pressure or • Radiologic Findings
volume overload on the heart. Ini tially. the myo-
cardium compensates with muscular hypertrophy.
The chest radiograph is usually normal in IH D in the ab-
Eventua lly, the myocardial mass outstrips the coro-
sence of left ventricular decompensation. Occasionally
nary arterial supply leading to myogenic dilatation coronary artery ca lcificatio n may be seen (Fig. 10.20).
and overt heart failure. Approximately 50 % of patients have a normal chest
• Cardiac failure due to severe arrhythmia: Arrhythm ias radiograph in the first 24 hours postmyocardial infarc-
disrupt the synchronization of atria l and ventricular tion. The remainder show pulmonary edema often with
function necessary for effective cardiac performance. a normal-sized cardiac silhouette. Pulmonary edema is a
an important prognostic indicator. The mortality rate in
• Radiologic Findings the first 30 days has been reported to be 5 % when
there is no ev idence of edema whereas the presence of
See Pulmonary Edema (Chapter 7, p.195 ). edema has been reported to be assoc iated with mortal-
ity rates approaching 80 % (Battler 1980). Many acute
complications of myocardial infarction are not vi sible
on radiographs but are frequent ly associated with pul-
Ischemic Heart Disease (IHD) and monary edema.
Myocardial Infarction (MI) In survivors of MI, a left ventricular aneurysm may
calcify and appear as a circumscribed bulge with curv il -
inear calcification on the chest radiograph (Fig. 10.21 a ).
Ischemic heart disease is a major cause of morbidity and Myocardial perfusion scintigraphy: Single photon
mortality in the industrialized wo rld . Autops ies have emission computed tomography (SPECl) using thallium
shown a 50 % incidence of significant coronary artery or technetium is currently the imaging modality most
disease in men aged 45-60 years. Known risk factors infrequently used for assessment of myocardial perfusion.
clude hypercholesterolemia, cigarette smok ing, arterial SPECl demonstrates perfusion defects as foca l areas of
hypertension, and diabetes mellitus. The clinical corre- decreased tracer uptake.
late of IHD is angina pectoris. Ischemic myocardium shows decreased tracer uptake
Atherosclerosis: There is initial deposition of during exercise when perfusion is insufficient to meet
cholesterol foci w ithin the intima of the coronary arter- the increased requirements of exercise: these defects re-
ies. This induces a circumscribed fibrous proliferation solve during rest/recovery.
with plaque formation and this may lead to narrowing of Areas of irrevers ible myocardial ischemia (i. e., infarc-
the vessel lumen. Plaques may calcify over time. tion ) show decreased tracer uptake during stress/exer-
However, it is becoming apparent that non calcified cise and these defects persist during recovery/rest
plaque may be more unstable and prone to rupture (Fig. 10.22).
giving rise to acute coronary events. c
IHD is the leading cause of myocardial infarction. Fig. 10.20
(a , b) sho'
Very occasionally, a coronary artery is occluded by em- • Computed Tomography (CT)
the right I
bolus or involved in arteritis. Occlusion leads to myo-
cardial ce ll necrosis in the territory of the affected vesse l. Nonelectrocardiographic (ECG)-gated Standard Helical
In acute myocardial infarction, death may result from a of the Thorax
acute left ventricular failure, arrhythm ias, ventricu lar Coronary artery calcification may be readily visible
rupture, septa l perforation, or papillary muscle rupture. (Figs. 10.20 b, c, 10.23) and shou ld alert the physician to Cl fil
In patients who survive, myocardial infarcts heal by fi- the possible presence of coronary artery disease. When dial thin
brosis. there is no relevant history of IHD or renal impairment, subendo
Dressler's syndrome with pericardial and pleural ef- these patients may benefit from cardiovascular risk traventri
fusions occasiona lly develops in the initial weeks post- assessment. ventricu
myocardial infarction; it is thought to represent an auto- Non-ECG-gated contrast-enhanced helical Cl of the and mya
immune response to tissue antigens released by dam- thorax (when performed for eva lu ation of acute chest traventri
aged myocardial cells. pain ) occaSionally may show decreased myocardial en- myocard
Late sequelae of myocardial infarction include left hancement in the distribution of the. occluded coronary aneurysl
ventricular aneurysms. True aneurysms involve all lay- artery in acute MI.
. in
ms
Je-
"ior
ab-
,lly
).
lest
He-
vith
a is
e in •
hen
, of
tal- b
:ute
ible
)ul-
my
:1Iil-
1 a).
)ton
ium
nost
;ion.
s of
take
neet
s re-
fa rc-
~xer-
Irest
c d
Fig.10.20 Right coronary artery aneurysm: Chest rad iographs the anterior atrioventricular sulcus. There is virtual occlusion of
(a, b) show an ovoid opacit y containing rim calcification overlying the vessel with ext ensive intraluminal thrombus. Marked LAD and
the right heart. CT shows a neurysmal right coronary artery within circumflex artery calcification are also noted (c, d).
ieal
sible
,10 to CT find ings in the patients post-M I include myocar- Dedicated ECG-gated Multi-Detector CT (MOCT) of the
Vhen dial th inning ± LV aneurysm format ion and areas of early Heart
nent. subendoca rdial decreased enhancement (Fig. 10.24 ). In- - Coro nary artery calcium scoring: see Chapter 1, p. 29.
risk traventricular thrombus may form with in areas of - MDCT coronary angiograp hy and myocardial perfu-
ventricu lar akinesia/aneurysms. Focal areas of endo- sion
If the and myocardial ca lcification may be seconda ry to old in-
chest traventricular thrombus (Fig.1O.25a. b) or represent For details of technique: see Chapter 1. p.29.
d en- myocard ial calc ifi cation w ithin a left ventricu lar
mary ane urysm (Fig. 10.21 b ) respectively.
Fig. 10.23
artery.
Fig. 10.21 a, b Chest radiograph and CT show marked thinning

and calcification of LV apical myocardium in a patient postmyo-
a card ial infarction.
Normal Ischemia Infarction
stRESS a
5 R"T l
E([)A
p 1
r
Ilr
REst a,
a
a
Fig. 10.2501
ning of my'
SlRESS b
history of a
ing " on COl
B IIIIT A
"::>P
S
E IHF •
E
"E5I b, MDCT in I
MDCT co
b mise in th
coro nary
Fig.10.22a- c Myocardial perfusion scintigraphy in reversible
tion of all
stRESS c ischemia and infarction. Left ventricular myocardial uptake of with this
APEX thallium during stress (a, b , c) and du ring recovery (a , . b, . (,) in motion, tl
S(y
~ A
three perpendicu lar planes of section. Homogeneous tracer up-
take during stress and at rest is seen in normal subject. In pat ient
with myocardial ischemia, focally decreased tracer uptake is seen
their tortl
(Schoenh;
1 lASE T blockerth
in the laterobasal wa ll of the left ventricle during stress but this
RUT c, reverses on images acquired during recovery. Focal defect in per- quali ty pa
c fusion is irreversible in myocardial infarction. artery (S h
Fig.10.23 Axial CT image shows heavily calcified left coronary Fig.1O.24 CT shows a crescent of subendocardial hypodensity
artery. within the LV freewall in a patient with a past history of myo-
cardial infarction.
g
,.
• b
fig. 10.25 a, b Left ventricular thrombus. Initial CT showed thin- the LV (a). Follow-up CT study acquired some weeks later postan-
ning of myocardium of left ventricular apex in patient with a past ticoagulation therapy shows resolution of thrombus with a thin
history of apical infarction. Hypodense thrombus is noted "float- crescent of calcium adherent to the apical endocardium (b).
ing" on contrast opacified blood with in this hypo kinetic area of
Moa in Assessment of Coronary Artery Disease Studies using 4-slice MDCT technology repo rt ade-
MDCT coronary angiography shows considerable pro- quate vis ualization of 60-70% of all coronary arterial
mise in the assessment of asymptomatic and early-stage segments with a se nsitivity and specificity of91 and 84%
corona ry artery disease. However, complete visualiza- for detection of stenoses in these adequately visualized
tion of all segments of the epicardial coronary arteries segme nts in one study (Achenbach et al. 2001). Studies
ble
of with this technique to date ha s been limited by cardiac performed using 16-slice MDCT re port improved visuali-
) in motion. the small size of the more distal vesse ls. and zation of vesse l segments with similar sensitivity and
up· their tortuous course through standard imaging planes speci ficity for detection of stenoses in adequately visual-
2nt (Schoen hagen et al. 2004). Premedication with beta ized segments to 4-slice MDCT (N ieman et al. 2002,
~en
blocker therapy has been show n to give improved image Ropers et al. 2003). We await data from studies per-
:his
)er- quality particularly in visuali zation of the right coronary formed on 64-slice MDCT and further advances in CT
arte ry (Shim et al. 2005 ). technology.
MOO in Acute Chest Pain/Myocardial Infardion visually or signal inte nsity curves may be assessed quan-
Ghersin et al. prospectively evaluated the role of 16-slice titative ly or semi-quantitatively (Wagner et al. 2003).
MDCf coronary angiography versus conventiona l angio- Prospective analyses w ith CMRI for the detection of
graphy in the setting of acute chest pain syndrome. coronary artery disease yie lded a sensitivity of92 % and
MDCT angiography was technically successful in 89% of specificity of 86 % using a 1-slice technique (AI-Saadi et
patients and in this group, 96.9 %of segments were visual. 2000) and correspo nding values of 94 and 83 % using
alized adequately. The sensitivity. specificity. positive a 5-slice technique (Nagel et al. 1999 ). These correspond
predictive value. negative predictive value. and accuracy favorably with results of SPECT.
of MDCT in these segme nts was 80. 89. 52. 97. and 87 %. Revascularization of seve rely dysfunctional but via-
respectively (Ghersin et al. 2006 ). ble myoca rdiu m may improve LV function an d long-
The improved spatial and tempora l reso lution of term survival. Augmentation of myoca rdial contractility
MDCT has also made possible assessment of myocardial on administration of a suitable pharmacologic stimulus
perfusion. MDCf angiographic data is acquired during such as dobutamine or absence of delayed myocardial
maximum enhancement of the coronary arte ries and hypere nhan cement on a postgadolinium study are con-
assessment of "first pass" myocardia l perfusion may be sisten t with myocardia l viability. The transmural extent
possible from the sa me data set. 1(0 et al. have rece ntly of viab ility may also be assessed w ith gadolinium-en-
evaluated myocardial enhancement patterns in patien ts hanced CMRI and this has importance in prediction of Fig. 10.:
disease
wi th acute myocardial infarction w ho had presented too improvemen t in LV function postreva scularization (Kim scend ir
late for thrombolysis on 2-phase contrast-e nhan ced et al. 2000).
ECG-gated MDCT. Subendocardial or tran smural perfu- Myocardial infarction by definition indicates myocyte
sion defects were seen in all but one patient on the early death and therefore nonviable myoca rdium. Acute MI
phase acquis ition. The pattern of myocardial enhance- may be hyperintense to normal myocardium on T2- Carc
ment. however, was quite variable on late phase images we ighted images. Thinning of the region of infarction
in 75 % of patients (Ko et al. 2006). may occur early with a resultant increase in the cir-
cumfere nt ial extent of the infarcted segment known as • (Ii
Cardiac Magnetic Resonance Imaging (CMRI) infarct expansion (Pirolo et al. 1986). Delayed hype ren-
han ce ment on postgadolinium sequences is consistent Cardio
Evaluation of myocardial perfusion and viability: Myo- w ith nonviable infarcted myoca rdium (Fig. 10.26). w hich
cardial perfusion may be evalua ted w ith gadol inium-en- fects. I
hanced dynamic first-pass rest and stress studies, the Coronary Angiography (ischel
latter during administration of a pharmacologic stress knowr
agent such as adenosine. Delayed imaging post- Coronary angiography curre ntly remains the go ld stand- seca ne
gado lin ium admin istration allows detection of regio nal ard of reference for diagnosis of IHD and remains th e inage nt~
myocardial hypere nh ancement indicative of nonviable vestigation of choice in patients consid ered to be at Cal
tissue. Dobutamine may al so be used as a pharmacologic mod erate to high ri sk of signifi ca nt coro nary arte ry dis- gro up.
stress agent with assess ment of resulting ventricular ease. Arte rial ste noses and occlusions are readily de- • Dil.
wa ll motion abnormalities. monstra ted and the severity of each stenosis may be for:
Differences in myocardial perfusion between rest and assessed (Fig. 10.27 ). In selected cases. it may be appro- lar
stress suggest areas of reversible ischemi a as w ith the priate to proceed to coronary angioplasty ± coronary tial
sci nti graphic technique. These changes can be analyzed stent insertion (see Fig. 10.45 ). eXE
pel
dio
• HYi
Th,
log
cel
inti
pre
fur
ing
an,
• Re~
pri
pal
sec
• b c vel
Fig. l0.26a- c Cardiac MR perfusion-viability study: Images show early (a) and late (b, c) hyperenhancement of nonviable myo-
ca rdiu m in area of myocard ial infarction.
Acq uired Heart Disease 261
In- Table 10.2 Classification of secondary card iomyopathies (from

13). Schettler, 1990)
of Myocarditis
.nd • Vi ruses: coxsackie virus A and B, echovirus, influenza,
et infectious mononucleosis, poliomyelitis, mumps, measles.
ing smallpox, varicella, psittacosis. lymphogranuloma
venereum, herpes simplex, cytomega lovirus, infectious
.od hepatitis, yellow fever
• Bacteria: diphtheria, seps is
• Protozoons: Trypanosoma cruz; (Chagas disease), toxoplas-
ng- mosis, amebiasis, malaria, leishmaniasis
ity • Parasites: trichinae, echinococcus, ascarids
• Spirochetes: syphilis, leptospiroSis
Ius
lial Collagen diseases
• Rheumatic fever
)n-
• Systemic lupus erythematosus
=nt • Dermatomyositis
=0-
of
• Fig .10. 27 Coronary angiogram in a patient with ischemic heart
• Scleroderma
• Ankylosing spondylitis
disease shows a high-grade stenosis in the left anterior de- • Rheumatoid arthritis
:im scending (LAD) artery.
Hyperimmune cardiomyopathies
yte • Drugs (e. g., penicill in . phenylbutazone, aureomycin, anti-
tubercu losis agents, reserpine)
MI • Postvaccination
T2- Cardiomyopathies • Dressler's syndrome
ion Toxic cardiomyopathies
cif- ! • Alcohol
I as • Clinical Features • Drug toxicity (e . g., cytostatic drugs. t ricyclic antidepres-
en- sants)
ent Cardiomyopathies are diseases of the myocardium • Uremia
• Carbon monoxide poisoning
w hich do not result from press ure ove rl oad (valvular de-
fects, hypertension, etc) or an inadequate blood supply Metabolic and endocrine disorders
(ischemic hea rt disease). The etiology is frequ ently un- • Hyperthyroidism
• Hypothyroidism
known (primary cardiomyopathy) but some cases are • Acromegaly
nd- secondary to exposure to toxic. infectious, or metabolic • Pheochromocytoma
in- agents (second ary cardiomyopathy, Table 10.2 ). • Diabetes mellitus
Cardiomyopathies are classified in to three main • Hemochromatosis
~ at
• Amyloidosis
jjs- groups: • Storage disease, lipid storage diseases, glycogen storage
de- • Dilated cardiomyopathy is by far the most common diseases
be form and is characteri zed by impairment in ventricu- Neuromuscular diseases
)ro- lar function with atrial and ventri cu la r di latation. Ini - • Friedreich ataxia
.ary tially. there is only "forward fai lure" w ith decreased • Myotonic muscular dystrophy
exercise tolerance. Eventua lly, there is frank deco m- • Progressive muscular dystrophy
pensa tion with pulmonary edema (co ngestive car- • Myasthenia gravis
diomyopathy), Neoplastic cardiomyopathies
• Hypertrophic obstructive cardiomyopathy (HOeM): • Primary and metastatic neoplasms
• lymphatic and myeloid leukemia
The re is ventricu lar wa ll thicken ing due to a hi sto-
logically demonstrable hypertrophy of myocardial Granulomatous cardiomyopathy
• Sarco idosis
ce lls. The resu ltant loss of ventricular diste nsibility
in terferes w ith diasto li c filling. Usually the re is di s- Cardiomyopathies due to physical causes
• Radiotherapy
proportion ate hypertrophy of the se ptum : thi s may
further narrow the left ve ntricula r outflow tract lead- • ECT
• Heat stroke
ing in about one-third of cases to mi tral regurgitation • Cardiac trauma
and left atrial dilatation. Puerperal cardiomyopathy
• Restrictive cardiomyopathy is a rare disorder due to
Nutritional disorders
primary endocardial fibrosis. Involve ment of the
• Beriberi
pap illary musdes and chordae tendineae leads to • Kwashiorkor
secondary valvul ar dysfunction. The decreased • Pellagra
ventricu lar diste nsibility impedes diastolic filling. • Scurvy
Tlyo-
Fig. 10.
Fig . 10.28a, b Dilated cardiomyopathy. There is card iomegaly
fuse th
a L.._ _ _ _ __ a
and features of pulmonary venous hypertens ion. Axial image
was nc
shows left ventricular dilatation.
Clinical man ifestations are usually those of ve ntri cu la r Acquired Valvular Heart Disease
impairment with impaired exerc ise tolerance, dyspnea, • Ri
and periphe ral ede ma. The p
Mitral Stenosis • Lel
cal
• Radiologic Findings Mitral stenos is is characterized by restricted opening of gr;
the m itral va lve as blood flows from the left atrium into up
The chest radiograph in dilated cardiomyopathy shows the left ventricle. It most commonly results from ca rdiac (m
card iomegaly with or without pulmonary edema and involvement in rheumatic fever with scarring and thick- cal
pleural effu sions (Fig. 10.28). In HaeM, the heart may be en ing of the valve cus ps and fus ion of the commissures. rae
normal in size and shape or features of left ve ntricular This red uces the opening area of the mitral orifice from sig
hypertrophy may be evident. In restrictive cardiomy- the normal 4-6 to 2.5 cm' (grade 1 stenos is), to 1 cm' • Fel
opathy. cardiac size is usually normal but there may be (grade 2), or to less than 1 cm' (grade 3). The increased up
right atria l en largement and diminished pulmonary pressure proximal to the stenosed va lve leads to: ai,
vascu lari ty due to reduced right ventricular output. • Dilatation of the left atriu m of
Echocardiography: There is ventricular di latation in • Right ventricular hypertrophy and eventual right ch
d il ated ca rdiomyopathy with uniform th inn ing of the heart failure with ventricu lar dilatation and tricuspid so,
myocardium. The left ventricu lar cavity is sma ll in insuffici ency du
HaeM pa rticu larly at end systole and left ve ntricular hy- • Rai sed pulmonary venous pressure w ith pulmonary • Ril
pertrophy is almost always presen t. Septal hypertrophy congestion and edema of
is most co mmon and is frequently g reater than 20 mm in pro
thickness (normal value is less than or equal to 12 mm), Clinically, there is frequently a hi story of streptococcal
Systolic anter ior motion of the anterior mitral valve leaf- infection (sore throat, scarl et fever ). Ca rdiac auscu lta- Echoc
let is cha racteristic of HOeM but is seen in a minority of tion reveals a loud first heart sou nd, a presystolic cre-
cases (Ra phae l and Gibson 1992),
• A
sce ndo murmur, and a mitral opening snap. There is • A
Compu ted tomography and magnetic resonance imag- frequently associated atrial fib rill ation (Fig. 10.30) which • Le
ing: CT and MRI findings in dilated card iomyopathy and increases the risk of systemic embol ization. Dyspnea on • Inl
HaeM are as described for echocardiography exertion may progress to rest ing dyspnea and orthop- • eo
(Figs. 10.28 b, 10.29). MRI may be helpful in distinguish- nea. The li ps may be cyanosed and the re may be reactive m:
ing restri ctive ca rdiomyopathy from constrictive peri- dilatation of the skin capilla ries (mitral Jacies). as'
card itis. Myocard ial thickening is seen in restrictive ca r- Eventually, there is right ventricu lar decompensation lal
diomyopathy particularly when it is associated with wi th pe ripheral edema, elevated jugular venous pres-
amyloidosis (Boe r et al. 1977). This condition is sure, and hepatomegaly. Magri
frequen tly comp li ca ted by m itral and tricuspid regu rgi - ec ho(
tation. wher
The ~
atrial
meas
Fig .1 0.29 Hypertrophic cardiomyopathy. There is marked dif- Fig.10.30 CT shows left atrial thrombus in a patient with atrial
Iy fuse thickening of the left ventricular myocardium. This patient fibrillation.
j' was normotensive and had no valvular heart disease.
• Radiologic Findings Spin echo sequences demonstrate thickening of the

valve leaflets, left atrial dilatation, and a small left ven-
The principal chest radiographic features are: tricle. GRE sequences allow estimation of the degree of
• Left atrial enlargement with narrowing of the retro- stenosis based on the size and extent of the abnormal
cardiac space at the atrial level on the lateral radio- flow jet during diastole in the left ventricle. VEC-MR al-
of graph. The frontal radiograph shows fullness of the lows calculation of the maximum velocity within the
to upper left cardiac border and a double contour sign stenotic jet and the pressure gradient can be calculated
ac (mitral configuration, Fig. 10.31 ).In the elderly, calcifI- using the modified Bernoulli equation (Heidenreich et
k- cation of the mitral annulus may be seen on the chest al. 1995).
~S.
radiograph but this does not signify the presence of Cardiac catheterization: Both the pulmonary capillary
significant valvular disease (Fig. 10.32). wedge pressure (during right heart catheterization) and
• Features of pulmonary venous hypertension with the pressure in the left ventricl e (left ventricular cathe-
upper-zone blood flow redistribution. Interstitial and terization) are measured and the transvalvular pressure
alveolar edema may develop w ith increasing degrees gradient can then be calculated. Left ventricular angio-
of pulmonary venous hypertension. Fine interstitial graphy demonstrates:
:ht change in long-standing disease after multiple epi- • Thickened valve cusps which bow into the left ven-
lid sodes of pulmonary edema sign ifies hemosiderosis tricle in the filling phase (diasto lic doming).
due to fibrous organization of minute hemorrhages. • A thin, turbulent jet of opacified blood entering
try • Right ventricular hypertrophy with an increased area the opacified left ventricle during diastole (wash-in
of sternal contact on the lateral chest radiograph and jet).
prominence of the pulmonary outflow tract.
cal
ta- Echocardiogrophy shows: Mitral Regurgitation
re- • A thickened mitral valve.
, is • A decrease in size of the mitral orifice. Mitral regurgitation/insufficiency is characterized by in-
ich • left atrial dilatation. complete closure of the mitral valve during systole al-
on • Increased ventricular inflow velocity. lowing blood to regurgitate from the left ventricle into
)p- • Continuous wave Doppler allows estimation of the the left atrium. It may be due to:
ive mitral diastolic flow ve locity at the apex, and the di- • Ruptured chordae tendineae or papillary muscle dys-
asto li c gradient across the valve may then be calcu- function following myocardial infarction.
ion lated. • Valvular scarring and contraction secondary to bacte-
es- rial or rheumatic endocarditis.
Magnetic resonance imaging may be useful when the • Stretching of the mitral valve ring (functional incom-
echocard iographic data are insufficient for diagnosis or petence).
when echo findings are inconsistent w ith clinical data.
The MR study, however, may be limited in patients with Mitral valve prolapse results from elongation of the
atrial fibrillation with the potential for erroneous chordae tendineae and mucoid degeneration of the leaf-
measurements (Didier 2003). lets; this all ows prolapse of the mitral valve into the left
Fig. 10.31 a-( Mitral stenosis. Note the full-

ness of the upper left heart border (dilated left
at rial appendage) (1). the "double right heart
contou rn configuration (2), the narrowing of
t he ret rocardiac space at the level of the
atri um (3), and the prom inent right ventricular
outflow tract /m ai n pulmonary artery (4). Con-
trast-enhanced CT shows marked left atrial di-
latation.
Fig. 10.33
tricular an
• Rad i
Th e chesl
atrium during ve ntricular systole. It m ay be present tradi stincti on to mitral stenosis, pulmonary venous hy- e nlargerr
without associ ated regurgitation. pertension te nds to occu r qu ite late in mi tra l regurgita- pe rte nsic
Regurgitatio n of blood during sys tole depends in part tion. gresses.
on th e pressure w ithin the left ve ntricle. The increased Cli nical manifestations in advanced disease incl ud e ca uses n::
vo lume of blood fl owing from the atrium to the ventricle pulmonary congestion with dyspnea on exe rtion and at left atria
in d ias tole and retluxi ng into the atri um du ring systo le rest. Ca rdiac auscultati on revea ls a dim inished first grea ter d
causes di latati on of both chambe rs. Howeve r, in co n- hea rt so und and a high-frequency pa nsystolic murmur. monary
ventricul
Fig.10.32 Mitral
annulus calcification.
Fig. 10.33 a, b Mitral regurgitation. Radiog raphs show biven-

tricular and left atrial enlargement. b
• Radiologic Findings small ; a promine nt aortic arch should raise suspicion of

coexisting aortic valve disease.
The chest radiograph shows left atrial and left ventricular
ly- enlargement (Figs. 10.33, 10.34). Pulmonary venous hy- Echocardiography:
ta- pertension and edema develop as the disease pro- • The mitral valves leaflets are thickened.
gresses. A useful rule of thumb is that mitral stenosi s • There may be dilatation of the valve ring.
Ide causes relatively severe pulmonary congestion and mild • The maximum diameter of the left atrium is greater
at left atrial dilatation while mitral insufficiency causes a than 40mm,
!fst greater degree of atrial dilatation with less marked pul- • Ruptured chordae tendinea e or papillary muscles ap-
ur. monary venous congestion (Fig. 10.35). Because left pear as additional echoes in the region of the mitral
ventricular output is decreased the aorta is usually va lve.
a b
Aortic
Aortic 51
of the a'
elude rh
fuses th
and aort
cation a
left vent
concent!
cardium
cham bel
ventriclf
c d arte rial
Fig.l0.34a-d Mitral regurgitation: Chest radiographs before (a. b) and 3 years postinsertion of mitral valve prosthesis (c, d). which ir
treated,
Clini(
The need for surgery is determined by the severity of normal individual but left ventricular inflow is increased wh ich is
symptom s, an ejection fraction of less than 60 % or a LV in mitral regurgitation. The difference between the two may bel
end-systolic dimension of greater than 45 mm as deter- values therefore corresponds to the vo lume of mitral re- but latel
mined by Doppler echoca rdiogra phy (Ca rabello and gurgitation (D idier 2003). sufficien
Crawford 1997). Cardiac catheterization: The left ventricu logram dis- put ). an<
Magnetic resonance imaging: Spin echo sequences tinguishes four grades of mitral incompetence:
will show altered cardiac morphology including left Grade I: Opacified blood regurgitates to the va lvular
atrial and ventricular dilatation. GRE sequences allow region of the left atrium. • Rad
assessment of the severity of mitral regurgitation based Gra de II : Contrast medium opacities the atrium, but
on the area of the signal void that arises from the mitral less than the ventricle. The (hes
valve. Mitral regurgitation may also be assessed with Grade III: Contrast medium opacities the atrium and stage or
VEC-MR imaging by comparing diastoli c flow across the ventricles equally. ximal as
mitral annulus with systoli c outflow across the ascend- Grade IV: Cont rast medium opacities the atrium and tion de\
ing aorta. These have virtually identical values in the the pulmonary veins. ventricu
Fig.10.35 Chest radiograph in combined mitral

valve disease. Note the "double right heart con-
tour" sign (1), pulmonary artery dilatation (2),
prominence of the atrial appendage (3), and left
ventricular dilatation (4). The aortic arch is rela-
tively small due to decreased LV output.
Aortic Stenosis
Aortic stenosis is characterized by insufficient open ing
of the aort ic valve during ventricular systole. Causes in-
clude rheumatic endocarditis which scars and partially
fuses the valve cusps. Congenital bicuspid aortic valve
and aortic sclerosis which leads to stiffening and calcifi-
cation of the valve may also lead to aortic stenosis. The
left ventricle initially adapts to the pressure overload by
concentric hypertrophy of the left ventricu lar myo-
cardium and this. whi le reducing the volume of the
chamber leads to little or no cardiomegaly. When the
ventricle reaches a critical muscle mass, it exceeds its
d arterial supply and undergoes myogenic dilatation
Wlli ch increases the overa ll size of the heart. If this is un -
treated, left ventri cular failure w ill eventually develop.
Clini ca lly. auscu ltation reveals a systo li c murmur
which is transmitted to the carotid arteries, The disease
'0 may be virtually asymptomatic in its compensated stage Fig.1O.36 Left ventricular dilatation in a patient with aortic ste-
but later produces angina pectoris (re lative corona ry in - nosis.
sufficiency ), syncopal attacks (decreased cardiac out-
s- put), and dyspnea (left heart failure ).
pulmonary venous hypertension and edema eventually

• Radiologic Findings supervene.
Jt Echocardiography shows disorgan ization of the va lve
The chest radiograph may be normal in the compensated cusps with replacement by highly reflective calcium. ON
ld stage or there may be poststenotic dilatation of the pro- Doppler allows estimation of peak systo lic pressure
ximal ascending aorta. Later the typical aortic configura- gradient across the valve.
tion develops w ith a rounded cardiac apex and left Magnetic resonance imaging: Spin echo sequences
ventricular enlargement (Figs. 10.3, 10.36). Features of may show a bicuspid valve, thickening and bulging of
the cusps, and dilatation of the ascending aorta. Cine • Radiologic Findings Hyper
GRE and VEC-MR allow assessment of the seve rity of the
stenosis based on the size and extent of the abnormal Chest radiograph: left ventricular enlargement with an
flow jet and the maximum velocity of the stenotic jet, re- Systemic
aortic configuration reflects adaptive dilatation rather
spectively. arterial t
than the myogenic decompensation seen in aortic steno-
Cardiac catheterization: Aortic valve calcification is predispo
sis. The degree of aortic dilatation may be more marked
seen on fluoroscopy_ There is partial opening of the aor- overload
than is seen in aortic stenosis. Left atrial enlargement,
tic valve during systole and a negative jet of nonopaque load eve
pulmonary venous hypertension, and edema develop
blood may be seen passing through the stenosed valve at ventricul
with increasing degrees of left ventricular failure.
aortography. tive core
Ec/lOcardiography demonstrates left ventricular hy-
genic dil
pertrophy and dilatation and allows evaluation of LV
eventual
function. It may demonstrate abnormality of aortic
Aortic Regurgitation cusps, lesions of the annulus, or dilatation of the aortic
root. Color Doppler flow-mapping allows semiquantita-
Aortic regurgitation/insufficiency is characterized by in- tive assessment of the severity of regurgitation based on
• Radi
complete closure of the valve during diastole allowing the measurement of regurgitant jet length and width.
blood to reenter the left ventricle. It may result from The ches
Magnetic resonance imaging: Spin echo sequences
rheumatic fever, bacterial endocarditis, or be due to syp- left vent
allow assessment of abnormal valve/valve ring mor-
hilitic aortitis. Acute AR may be due to aortic dissectio n (aortic (
phology and size and function of the left ventricle. GRE
with secondary involvement of the valve ring. shows ni
sequences demonstrate the regurgitant jet and with
Aortic regurgitation leads to increased end-diastolic the ven
VEC-MR allow calculation of the severity of the regurgi-
volume which in the initial compensated stage is not as- atheroscl
tation (Fig. 10.37 ).
sociated with an increase in end-diastolic pressure. In tuosity a
Cardiac catheterization and aortography: An injection
more advanced disease, the left ventricle fails and e nd- Echoo
of contrast medium into the ascending aorta allows
diastolic pressure rises. This in turn is associated with crease in
grading of the degree of reflux:
functional mitral incompetence, left atrial dilatation, uation of
Grade I: Reflu x into the perivalvular region of the left
and pulmonary venous congestion. is seen if
ventricle.
Cardiac auscultation reveals an early diastolic mur- Grade II: Opacification of the entire left ventricle.
mur, Blood pressure amplitude is increased (water-ham- Grade III: Virtua lly all the contrast medium regurgitates
mer pulse ). The decompensated stage presents with pal- into the ventricle. Cardic
pitations, tachycardia, and left ventricular failure. Grade IV: Regurgitated contrast medium is retained in
the left ventricle for several cardiac cycles.
Primary I
plasms r
pulmona
Multivalvular Disease
primary (
surgical E
Involvement of two valves, usually the aortic and mitral
teratrial ~
valves, is common in patients with acquired valvular
it may Ie
heart di sease. Trivalvular disease is uncommon and
hyperten,
four-valve involvement is extremely rare. In addition,
Other
functional incompetence of a second valve may develop
oma, myI
as a seco ndary feature in advanced disease; for example
very rare
in aortic stenosis, left ventricular dilatation leads to
stretching of the mitral valve ring and functional mitral
incompetence.
• Radiologic Findings Imagil

Chest radiograp/l: Changes usually reflect the hemOdy-
namic consequences of a combi nation of abnormalities
that are associated with individual valve dysfunction. Cardiac
There is frequently marked cardiomegaly and given the
frequent involvement of the mitral valve, left atrial di- Single-ch.
latation is a common findin g. trode in t.
Fig.10.37 Aortic regurgitation. GRE cine MRI demonstrates left
of device ~
ventricular enlargement and the regurgitant jet from the aortic (V), and if
valve into the left ventricle. trinsic rat
Imaging the Heart Post Intervention and Surgery 269
Hypertensive Heart Disease

1 an
Systemic arterial hypertension is defined as a resting
ther
arterial blood pressure exceeding 140/95-100 mmHg. It
~no
predisposes to atherosclerosis and leads to pressure
eked
overload of the left ventricle. Ini tially, this pressure over-
lent,
load evokes compensatory hypertrophy of th e left
elop
ventricular muscle (concentric hypertrophy ). Later rela-
tive corona ry insufficiency develops, leading to myo-
hy-
genic dilatation with decreased ventricular o utpu t and
f LV
eventual pulmonary edema.
)rtic
Jftic
tita-
don
tho
The chest radiograph is initially normal. Later, there is
flees left ventricu lar dilatation and a rounded cardiac apex
nOf-
(aortic configuration). The lateral chest radiograph
GRE
shows narrowing of the retrocardiac space at th e leve l of
with Fig. 10.38 left atrial myxoma . MRI demonstra tes hypointense
the ventricle (see Fig.1O.4c, d ). Coexisting aortic
Jrgi- lesion lying within the left atriu m adjace nt to the mitral valve.
atherosclerosis leads to thoracic aortic ectasia and tor-
tuos ity and intimal calcification.
:tion
Echocardiography and MRI will show a concentric in-
lows crease in left ventricular wall thickness and allow eval-
uation of ventricu lar function. Left ventricu lar dilatation
, left
is seen in decompensated hypertensive heart disease.
tates
Cardiac Neoplasms
:>d in
es.
Primary cardiac tumors are rare and most cardiac neo-
plasms resu lt from infiltration by adjacent malignant
pulmonary or mediastinal tumors. The most common
primary cardiac tumor is myxoma wh ich is amenable to
surgical excision. It most commonly ari ses from the in-
nitral
teratrial septum and grows within the left atrium where
vular it may lead to venous inflow stasis. pulmonary venous
and hypertension, and pulmonary edema (Fig. 10.38).
irion,
Other primary cardiac tumors including rhabdomy-
velop
oma, myosarcoma, liposarcoma, and fibrosarcoma are
.mple
very ra re ( Fig. 10.39). Fig. 10.39 Right ventricular rhabdomyoma.
ds to
nitTa!
Imaging the Heart Post-Intervention and Surgery

nody-
:llities
ction. Cardiac Pacemakers If the atrial im pulse is to be used as a trigger in
patients with AV block, a dual -chamber pacing system
'" the
ial di- Single-chambe r permanent pacemakers with an elec- w ith electrodes in both the ri ght atrium and right ven-
trode in the right ventricle (W I) are common, This type tricle (DDD ) may be inserted (Fig. 10.42).
of device senses the ventricle (V), stimulates it as needed
(V), and inhibits t he impulse ifi t senses a satisfactory in-
trinsic rate (I) (Figs. 10.40, 10.41 ),
• Rae
The ch,
rea ppn
sites of
Coron
Corona
balloon
oasis al
coronal
visua lil
10.45 ),
ECG
with 16
invasivf
Fig.10.40 Sing le-chamber pacemaker (WI) in a patient wit h Fig.10.42 Dual-chamber pacemaker (DOD) with atrial and
atrial fibrillation. ventricu lar lea ds. Defibrillator is also present.
Fig. 10.41 a, b Pacemaker in a patient with prosthetic aortic and

mitral valves . b
Coronary Artery Bypass Graft (CABG)

• Radiologic Findings Surgery
The chest radiograph docum ents the positio n of the A bypass graft (ve nous or in terna l mamma ry artery) is
pacemaker w ithi n the chest wall and the position of t he inte rposed between the aorta and coro nary artery in
electrodes within the card iac cham be rs. Fluoroscopy ca n patients with significant coronary arte ry stenoses or oc-
de monstrate a "floating e lectrode" w hen the electrode clusions.
tip loses its endoca rdi al attachme nt. a
Imag ing the Heart Post Interve nt ion an d Su rgery 271
The chest radiograph shows the cerclage w ires used to

reapproximate the sternotomy and surgica l clips at the
sites of bypass (Fig. 10.43).
Coronary Stents
Coronary artery stenoses are freq uently dilated w ith a

ball oo n-tipped catheter at corona ry angioplasty. Reste-
nosis at these sites may be preve nted by place ment of a
corona ry ste nt. The metalli c mesh of these stents can be
visuali zed on chest radiograp hs and at Cf (Figs. 10.44,
10.45 ).
ECG-ga ted MOCf co rona ry angiography parti cul arly
with 16- or 64-sli ce technology may be va luab le in non-
invas ive assessme nt of stent patency.
Fig.10.43 Sternal wires and bypass clips postcoronary artery
bypass grafting (CABG) surgery.
Fig.l0.44a. b Double
stent in LAO coronary
artery. Surface-ren-
dered 3D reconstruc-
tion (a) and maxi mu m
intensity image along
the course of the vessel
(b).
a b
Fig. 10.45a, b Left

coronary stent on chest
radiograph.
b
is
in
,c-
, L-_ _ _ _ _ _ _ _ _ __
b
Prosthetic Heart Valves • Rae

The earliest prosthetic va lve in clinical use was the Starr- Chest rc
Edwards ball-valve prosthesis (Fig. 10.46). A large num - ca rdial
ber of mechani cal va lves and bioprostheses are available diminis
today. Echo
The median sternotomy w ires, the mechanical valve diac fili i
prosthesis, or the metallic ring of a bioprosrhes is are vis- myocan
ible on the chest radiograph. pericarc
all ows E
ness is I
Com·
ening ±
PeriCi
Fig.10.46 Combined mitra l valve disease treated with a Starr-
Edwards ball-and-cage valve.
These fi
contact'
separate
municat
Pericardia I Disease most COl
Di ve rtiCl
velops tl
culou s), transudate (LV failure), hemorrhage (infarction, ings and
The pericardium envelops the heart and the origins of trauma ), or malignant invol vement of the pericardium.
the great vessels. Its visceral layer (epicardium ) is fused
w ith the myoca rdium and this glides on its parietal layer • Radi
(pericardium) during cardiac contraction. • Radiologic Findings
Chest raCi
Chest radiograph: There is cardiomegaly and the ca rdiac appear i
Pericardial Effusion silhouette is globular or triangular in shape. Pulmonary which ar
blood flow is often diminished due to co mpression of Echocr
the right heart chambers; gross card iomegaly in the ab- choic, fil
Pericardial effus ions greater than 200 mL in volume may se nce of pulmonary edema shou ld raise the suspicion of tively in <:
interfere with cardiac filling (cardiac tamponade ). Effu- a pericardial effusion. The lateral chest rad iograph oc-
sions may represent inflammatory exudate (e. g., tuber- casionally shows a double fat stripe as the interposed
pericardial stripe (soft-ti ssue density ) is widened by the
effusion.
Echocardiography, CT, and MRI all clearly demon-
strate the effusion, echocardiography being the most
frequently used modality in clinical practice (Fig. 10.47).
Constrictive Pericarditis Fig.1O.49a

tense conti
lnfiammation and fibrosis may lead to pericardial thick-

e ning and obliteration of the pericardial cavity. The
thickened pericardium, which may calcify, interferes
w ith dia stolic heart filling. These changes tend to have a
more profound effect on the right than the left heart
chambers resulting in systemic venou s congestion with
hepatomegaly, ascites, and peripheral edema.
Fig .10.47 Pericardial effusion. Axial CT image shows the effu-
sion separated from the myocardiu m by a hypodense layer of epi-
cardial fat.
Pericardial Disease 273
Chest radiograph: The heart is normal in size and peri-

cardial calcifi ca tion may be visible. Fluoroscopy shows
dim ini shed card iac pulsation.
Echocardiography and cine MRI show restricted car-
di ac filling and dim in ished cardiac pulsation. Absence of
myoca rdial thickening helps to di stingu ish co nstrictive
pericarditi s from restrictive ca rdiomyopathy. MRI also
allows estimation of pericardial thickness (normal thick-
ness is less than 4 mm ).
Computed tomography may show pe rica rdial thick-
ening ± ca lcification (Fig. 10.48).
Fig.10.48 Pericardial calcification in patient with clinical fea-

Pericardial Cysts and Diverticula tures of constrictive pericarditi s. Pleural thickening and lung in-
folding is an incidental finding.
These nu id- filled lesions li e in close prox imi ty to or in

co ntact w it h the pe rica rdium. W hile a pericard ial cyst is
separate from the perica rdium , a dive rticu lum com-
municates with the perica rdi al sac. Pericardia l cysts are
most co mmonly found in th e right ca rdiophrenic angle.
Diverticula tend to ari se from the pe rica rdiu m w hich en-
velops the right at rium. Both lesions a re inc id ental find-
ings an d have no pathologic sign ifi cance.
"
I.
Chest radiog raph: Both pericardial cysts and dive rticula

appear as smooth, well-defined, soft-tiss ue opacities
"ry w hich are contiguous with the cardiac silho uette.
of Echocardiography, cr, and MRI show thin-wa ll ed ane-
b- choic, fluid density or signa l intens ity lesions. res pec-
of tively in a cha racteristic paracardiac location (Fig. 10.49). a
~
,d
he
,n-
1St
7).
Fig.l0.49a, b Pericardial cyst. Sp in echo MR shows hyperin-

tense contents of the cyst. b
ck-
rhe
~res
Ie a
~a rt
lith
274
11 Diseases of the Mediastinum
The mediastinum is bordered anteriorly by the sternum, heart. esophagus. trachea. thyroid gland. thymus. major
posteriorly by the tho racic vertebral col umn. and later- nerves, and vascular structu res.
ally by the mediastinal pleura. Its contents include the
Mediastinal Displacement
Fig. 11
Complete media stina l displacement res ults in asym-

metric pulmonary expansion.
More locali zed mediastinal di sp lace ment results in
unilateral extension of a pleuropulmonary recess across
the midline. These localized displacements frequently
result from pulmonary atelectasis and usually involve
the anterior or posterior mediastinum (Fig. 11 .1).
Mediastinal displacement may be fixed when the
differential diagnosis includes:
• Scoliosis
• Fibrothorax/pl eural neoplasia
• Pulmonary atelectasis
• Pneumonectomy
Localized mediastinal air (pulmonary herniation.
or dynamic when there is mediastina l shift during the tracheal aircoJumn. intraesophageal air, hiatal hernia)
respiratory cycle and when the differential diagnosis in-
Fig. 11.1 Air in the mediastinum.
cludes:
• Tension pneumothorax
• Unilateral pulmonary hyperinflation (e.g .. due to for-
eign body aspiration)
• Unilateral diaphragmatic paralysiS
Air in the Mediastinum
Air in the Esophagus and Stomach Pneumomediastinum
Occasionally. swa llowed air may be identified within the Air from ruptured alveoli dissects along the peribron-
esophagus; it is recognized by visuali zation of the left chovascular connective tiss ue planes into the adjacent
esophageal wa ll separate from the azygoesophageal mediastinum (Figs. 11.2. 11.3). Alveolar rupture is usually
stripe. Megaesophagus, esophageal diverti cula. hiatu s a consequence of marked increases in intra-alveolar Freq
hernia, and communicating esophageal duplication press ure during mechanical ventilation, severe bouts of cuta ne(
cysts may also appear radiographically as air-containing co ughing. or acute exacerbations of asthma. Blunt chest pneum l
lesions. trauma w ith rupture of the esophagus or tracheo- venous
bronchial tree w ill also result in pneumomediastinum
(Table 11. 1 ).
Ai r in the Mediastinum 275
Table 11.1 Causes of pneumomediastinum
Traumatic Pulmonary contusion and pneumothorax

Bronchial ruptu re
Spontaneous Acute exacerbation of asthma
Pneumonia (especially in children)
Acute mediastinitis with gas-forming or-
ganisms
Spontaneous esophageal rupture (Boerhaave
jor syndrome)
Iatrogenic Tracheotomy
Positive-pressure ventilation
Pneumomediastinum
Fig.11.2 Pneumomediastinum.
Fig. 11.3 Pneumomediastinum . Air

column separates the visceral from
the parietal layers of the mediasti-
nal pleura.
lron-
Kent
ually
eolar Frequently. there is associated deep cervical and sub- • Radiologic Findings
Its of cutaneous chest wall emphysema. Occasio nally. a large
chest pneumomediastinum may lead to impaired systemic See Chapter 8. p.21O.
:heo- venous retu rn and respiratory compromise.
inurn
276 11 Diseases of the Mediastinum
Non-Neoplastic Mediastinal Widening
Mediastinal widening is a common radiographic finding. levels may be seen within discrete collections (Arm-
Anteroposterior (AP) supine views taken in shallow in- strong 1995).
spiration or expiration lead to foreshortening of medi- Upper gastrointestinal contrast swallow using low
astinal structures and to appa rent w idening of the medi- osmolar water-soluble contrast medium will show leak-
astinum. Causes of pathologic mediastinal widening inage of contrast into the mediastinum from an
clude mediastinal hemorrhage and innammation, esophageal perforation.
esophagea l, aortic and vascular dilatation, and lym ph
node en large ment.
Chronic Mediastinitis
Acute Mediastinitis Chronic mediastinitis is a granulomatous innammatory
disorder which may progress to fibrosis. Known causes a
Acute mediastinitis is a serious though rare pathologic include tuberculosis and in the United States, hi stoplas-
process with a mortality rate approaching 50 %. Initial mosis. However, many cases are of unknown etio logy.
diffuse purulent innammation progresses to abscess for- Idiopathic mediastinal fibrosis may be of autoimmune
mation and these are frequently multiple. Med iastinitis etiology and there may be an association with retrope ri-
may be secondary to esophageal perforation or post- toneal fibrosis (Ormond disease).
operative infection. Less com monly it results from direct Patients may initially be asymptomatic. Symptoms
spread of infection from the retropharyngea l space, usually result from ste nosis or occlusion of the superior
lung, or from suppu rative mediastinal lymph nodes. vena cava or from extrinsic narrowing of the esophagus
These patients tend to be very ill w ith severe retro- and tracheobronchial tree.
sternal chest pain and pyrexia. When esophageal per-
foration is present. there is associated dysphagia and
deep cerv ical emphysema. • Radiologic Findings
The chest radiograph usually shows mediastinal

• Radiologic Findings w idening ± calcification in cases of histoplasmosis. c
Other findings are determined by the severity of the ob-
The chest radiograph shows media stina l widening with structive phenomena and include pulmonary oligemia if
obliteration of fat planes, an accompanying pneumome- a pulmonary arte ry is involved. Narrowing of the trachea
diastinum, and associated unilateral or bilateral pleural and major bronchi may also be seen.
effusions. Computed tomography will demon strate 50ft tissue
In diffuse mediastinitis, computed tomography (a ) infiltration of the mediastinum and there may be airway
shows diffuse soft tissue infiltration of the mediastinum and vascular encasement. Dilated collateral vessels also
with loss of the normal fat planes. When there is pro- may be present.
gression to abscess formation, gas bubbles and air-nuid
Diseases of the Thoracic Aorta
The thoracic aorta runs cran ially in the anterior medi - The aortic isthmus lies just distal to the origin of the left
astinum (ascend ing aorta) from its origin at the aortic subclavian artery at the leve l of the ligamentum arterio- e
valve, curves posteriorly over the left main bronchus to sum.
form the aortic arch, and passes caudally to the dia-
phragm (descending aorta ). The normal diameters based
on cr data are:
• Aortic root: 3.7 ± 0.3 em.
Aortic Anomalies Other
• Ascending aorta: 3.3 ± 0.6 cm. • Lei
• Descending aorta: 2.4 ± 0.3 em. Coarctation of the aorta has been discussed in Chapter or!
10, p.244. dy,
Non-Neoplastic Media stinal Widening 277
Fig.l1 .4a- f Aortic and great vessel

anomalies (modified from Schinz 1983).
a Normal left-sided aortic arch. b Double
aortic arch. C, d Left aortic arch with an
aberra nt right subclavian artery. , Right sub-
clavian artery crossing the mediastinum be-
tween the trachea and esophagus. d Right
subclavian artery crossing behind the
esophagus.
e Right aortic arch, anterior type. f Right
aortic arch, posterior type.
r
s
al
is.
b-
if
ea
ue
"ay
Iso
left
rio-
Other common anomalies include (Figs. 11.4-11.6): subclavian artery becomes ectatic. When aneurys-
• Left-sided aortic arch with aberrant right subclavian mal, the artery may present as a superior mediastinal
artery. This is usually asymptomatic but may cause mass .
.pter
dysphagia (dysphagia luso ria ) in the elderly when the
a
a c
Fig.l1.Sa- c Right aortic arch, posterior type. Note the d is-

placement of the trachea (b) and the indentation of the
esophagus (e). This patient had presented clinically with dyspha-
b gia lu soria.
d
• Right aortic arch with aberrant left subclavian artelY is

the most com mon right arch anoma ly and is usua lly
Aortic Ectasia
asymptomatic. A right paratracheal soft -tissue
Thorc
shadow is seen on the frontal rad iograph and the ab- loss of normal vesse l elasticity res ults in aortic dilata-
errant subclavian artery produces a retroeso phageal ti on and ectasia; associated changes may be found in the An an
impression on the barium-filled esophagus at con- aortic valve. This degenerative process is common in the aortic
trast swallow. elderly and eventually may result in aneurysmal dilata- due tl
• Mirror image branching of a right-sided aortic arch is tion (Higgins 1992. Fig. 11.7). systen
associated w ith congenital heart disease in ove r 90 % syphil
of cases. and c~
flamm
Non-Neoplastic Mediastinal Widen ing 279
Fig. '1.6a-e Persistent left superior vena cava. Note the

low density widening of the superior mediastinum on the
chest radiograph (a). CT defines the course of the per-
sistent left SVC through to the coronary sinus (b- e).
c
b
le dis-
of the
yspha-
d
e
(ending aorta wh ile atherosclerosis most co mmonly in-

Thoracic Aortic Aneurysm and Dissection
dilata- volves the descending aorta .
An aneurysm is a saccular or fus iform dilatation of the • True aneurysms are saccula r dilatations involving all
. in the
. in the aortic lum en to greater than 5 em in diam eter. It may be layers of the aortic wa ll.
due to atherosclerosis (especially in individua ls with • False aneurysms res ult from ex travasat ion of blood
dilata-
sys temic a rte rial hypertension ). aortitis in patie nts w ith through a defect in the med ia to beneath the
syphilis, some vasculi tides inclu di ng Takayasu's disease adventi tia (Figs. 11.8. 11 .9 ). This may occur post
and cystic medial necrosis in Marfan's syndrome. 10- trauma or be seconda ry to bacterial se psis (mycotic
nammatory aneurysm s have a predil ection for the as- aneurysm).
• Di~
se,
Classi
prom
Blood
an in!
false
more
2 wee
tion i
the v,
impOJ
desce
b the a~
a Fig. 11.7 a, b Elongated, ectatic thoracic aorta. (type
Inl
ant 0
au th o
tra ml
rima!
also (
and e
UI,
An ull
phya,
throrr:
degre.
They I
mator
Pel
cally i
in pat
sive al
and al
longit
b w hy t
appea
ris et,
Th,
type P
Blesi
surgel
toms,
cation
Fig. 11 .~
cificati(
vestiga
Fig.ll.8a- c Traumatic aortic injury with rupture giving hemo- some 2
thorax and mediastinal hemorrhage. c matie f
Non-Neoplastic Mediastinal Widening 281
• Dissecting aneurysms and aortic dissection: Aortic dis-

sections have been classified into three entities:
- Classic aortic dissection due to a primary intimal
tear.
- Intramural hematoma.
- Penetrating atherosclerotic ulcer (PAU) (Ledbetter
et al. 1999. Coady et a1.1999. Willens et al. 1999).
Classic aortic dissection is an emergency which requires

prompt diagnosis and treatment (Pretre et al. 1997).
Blood dissects between the intima and media through
an intimal tear; this separates the layers and creates a
false lumen that may reunite with the true lumen at a
more distal level. Aortic dissections may be acute (first
2 weeks) or chronic (Crawford 1990). Sites of predilec-
tion are the proximal ascending aorta just superior to
the valve ring and the region of the aortic isthmus. It is
important to determine if a dissection is limited to the
descending aorta (type B dissection ) or if it also involves a
b the ascending ao rta and the origins of the great vesse ls
(ty pe A dissection. Fig. 11.10).
Intramural hematoma may be an early stage or a va ri-
ant of aortic dissection (Yoshida et al. 2003 ). Many
authors distinguish between aortic dissection and in-
tramural hematoma by the presence or absence of an in-
timal flap (Ma raj et al. 2000). Intramural hematoma is
also classified as type A or B depending on its location
and extent.
Ulcer-like projection/penetrating atherosclerotic ulcer.
An ulcer-like projection is defined at IT and angiogra-
phy as a localized blood-filled pouch protruding into the
thrombosed wa ll of the aorta and showing the same
degree of contrast enhancement as the aortic lumen.
They may develop in both types A and B intramural he- b
matoma.
Penetrating atherosclerotic ulcers, by contrast, typi-
cally involve the descending thoracic or abdominal aorta
in patients with severely atherosclerotic vessels. Exten-
sive atherosclerotic plaque may lead to medial scarring
and atrophy and these changes may limit the extent of
longitudinal dissection (Robe rts 1981 ). This may explain
b why the rate of progression of PAU to overt dissection
appears to be lower than for ulcer-like projections (Har-
ris et al. 1994. Sueyoshi et al. 2002 ).
The treatment of type A dissection and probably also
type A intramural hematoma is surgical while most type
B lesions are initially managed conservatively with
surgery being reserved for those with persistent symp-
tOI11S, extending dissections, or severe ischemic compli-
cations.
Fig.l1.9a-c False aneurysm post trauma. Crescent-shaped cal-

cification in the region of the aortic isthmus prompted further in-
vestigation (a). This patient had a history of major chest trauma
some 20 years earlier. CT (b) and aortography (c) show posttrau-
c matic false aneurysm. c
Fig.11.10 Classification of thoracic aortic

dissection. Types I- III in the Oe8akey classifi-
cation are compared with types A and B in
the Stanford classification (Higgins 1992) .
• Radiologic Findings obliteration of the superior retrosternal space is seen

with ascending aortic aneurysms
Helical computed tomography is used most commonly a
Aortic Aneurysms
for 2nd line imaging evaluation. It accurately defines the
The chest radiograph may show saccular or fu siform aor- severity and extent of aneurys mal dilatation and its rela-
ti c dilatation. There is associated intimal calcification in tionship to maj or branch vesse ls. It also demon strate s
up to 75 %of cases. On the lateral view. partial soft -tiss ue the presence of intraluminal thrombu s and the diameter
of the residua l lumen (Figs. 11 .11. 11.12).
c
Fig. 11:
a b thoraci
new sc
lateral.
Intran
The c/
men t
inside
gestiv.
Leakin
wi den
the di
ao rtic
c d COT
Fig . 11. 11 a- d Aneurysm of t he ascending aorta with dissection; to involve the arch (at b). The aneurysmal segment contains sensiti
CT shows a large aneurysm of the ascen ding aorta (a-d) with a some peripheral intraluminal thrombus (d ) and there is SVC com- (Ega n
localized dissect ion of the more distal ascending aorta extend ing pression (c). have r
Non-Neoplastic Mediastinal Widening 283
lrtic
"Iassifi-
B in
l2).
s seen
a b
manly
les the
:s rela-
strates
Imeter
d
Fig.11. 12 Initial chest rad iograph (a) shows a dilated ectatic lesion. CT coronal reformat (c) and axial image (d) show diffuse
thoracic aorta. Chest study (b) acqui red 4 months later shows atheromatous change with dilatation of the thoracic aorta and
b
new soft tissue opacity in the aortopulmonary window with development of a saccular ~aneurysm" containing intraluminal
lateral displacement of intimal calcification suggesting a vascular thrombus. There was no history of interval trauma.
Intramural Hematoma and Aortic Dissection

aortic dissection and intramura l hematoma to be 100 %
The chest radiograph may occasionally show displace- (Yosh ida et al. 2003).
ment of atheroma tous ca lcification to more than 1 cm Precontrast cr images show intramural hyperdensity
inside the aortic contour (Earnest 1979). a feature sug- with central displacement of intimal calcification in in-
gestive of aortic dissection in the correct clinical setting. tramural hematoma.
Leaking aortic dissection will result in mediastinal The sign ificance of new "ulcer- like projections" on
widen ing due to hemorrhage and hemothorax. When serial cr assessment of patients with aortic intramural
the dissection has extended proximally to involve the hematoma has been evaluated. Sueyoshi et al. found the
aortic root, a pericardial effu sion may be present. location of intramural hematoma in the ascending aorta
d Computed tomography has been shown to be both to be the principal predictor of development of these le-
sensitive and specific for diagnosis of aortic dissection sions. Seventy percent of patients who developed these
(Egan 1980. Gross 1980). More recently. Yoshida et al. ulcer-like projections then progressed to aortic enlarge-
have reported the accuracy of helica l cr in detection of ment or overt dissection (Sueyoshi et al. 2002 ).
cr features of dissection include two lumina se pa-

rated by an intimal flap; this flap appears as a curvilinear
lucency within the opacified aorta (Figs. 11.11, 11.13).
Differential opacification of the fal se lumen also may be
visible and is helpful in diagnosis when the intimal flap
is not see n (A rm strong et ai. 1995).
Helical volumetric CT with refor matted images in
selected planes defines the extent of intramural hema-
toma/dissection and demonstrates involvement of
major branch vessels in dissection. The proximal exte nt
of the intramural hematoma/dissection may also be de-
fined and when it exte nds proximally to involve the aor-
tic root, its relationship to the coronary sinuses ± in-
volvement of the coronary arteries may be identified
(Fig. 11.14).
a
Aortitis
Syphilitic mesao rtiti s is today a relatively rare entity and

is chara cterized by aneurysmal dilatation of the ascend-
ing aorta with associated aortic regurgitation.
Takayasu arteritis is characterized by stenoses of the
aorta, its main branches, and the pulmonary arteries.
Less co mmonly, it causes sacc ular or fusiform a
aneurysms (Lui 1985 ) which when multiple may be Fig. 11.14
found anywhere in the aorta (Armstro ng et ai. 1995). through I
Axial CT i
b
Mediastinal Hematoma
Neop
Mediastinal hemorrhage may result from vascular injury
caused by blunt or iatrogenic trauma. Spontaneous
bleeding most commonly results from rupture of an aor-
tic aneurysm. Vessel wall eros ion by a maligna nt tumor Both be
very occasionally may lead to mediastinal hemorrhage. astinum
normal
graph, tl
someti n
sions ar
suggest'
angle Sl
11.17).
Fig.11.13a-c leaking aortic dissection. Intimal dissection flap
is seen within the contrast-opacified aorta and there is a right- The
c sided hemothorax which demonstrates a blood-fluid level. goiters
normal
mediast
• Rad
Thyrai!
Thyroid
cause a
astinurr
Neoplastic Mediastinal Widening 285
pa-
ear
13).
be
lap
in
na-
of
ent
de-
tar-
in-
tied
and
'nd-
·the
ries.
arm a b c
, be Fig. 11.14 a-c Type A aortic dissection. Coronal reformats valve the aortic root but with sparing of the orig in of the right
). through the aorta show a Stanford type A dissection (a and b). coronary artery (e). There were no ECG/EKG changes and this
Axial CT image shows dissection flap extend ing proximally to in- patient had a successful aortic root replacement.
Neoplastic Mediastinal Widening

jury
::'DUS
aar-
mar Both benign and malignant tumors involve the medi- frequently associated with curvilinear tracheal devia-
age. astinum (Fig. 11.15). When tumors exte nd outside the tion and narrowing. Computed tomography accurately
normal mediastinal shadow on the frontal chest radio- defines the size and degree of retrosternal exte nsion of
graph, the angle of interface w ith the mediastinum may the goiter and shows the degree of trachea l deviation
sometimes be helpful in their differentiation from le- and compression.
sions arising from the adjacent lung. An obtuse angle A thyroid goiter is frequently heterogeneous in at-
suggests a lesion of media stinal origin w hile an acute tenuation due to areas of cystic degeneration and necro-
angle suggests a primary pulmonary lesion (Figs. 11.16, sis and it may contain foci of calcification (Fig. 11.19). The
11.17). surrounding fat planes should remain intact and no sig-
1 flap
right-
The most common mediastinal lesions are thyroid nificant adjacent lymph node enla rgement should be
goiters and lymph node enlargement (Table 11.2 ). The evident. The presence of e ither of these features should
normal thymus gives physio logical age- related superior raise the possibility of a thyroid neoplasm.
mediastinal widening in you ng children. Radionuclide thyroid scintigraphy provides an assess-
ment of thyroid function and in particu lar, determines
the activity of discrete thyroid nodules. Nodules display-
• Radiologic Findings ing increased tracer uptake (so called hot nodules ) al-
most invariably are benign and while the majority of
Thyroid Goiter those showing no/decreased tracer uptake relative to
normal thyroid parenchyma (so called cold nodules ) are
Thyroid goiters showing retrosternal extension may also benign, a small proportion may be neoplastic and
cause a goblet-shaped widening of the superior medi- further investigation including fine needle aspiration
astinum on the chest rodiograph (Fig. 11.18). This is may be merited.
Table 11
Anterii
Vessel!
Dilated
Persist!
Aortic !
Ascend
Corona
Thyroi
Goiter
Adenol
Carcinc
Pulmonary mass Mediastinal mass Pa rath)
Thymu
H yper~
Fig.1 1.16 Criteria for distinguishing med iastinal from pulmo- Tu mor~
nary masses. A pulmonary mass may be poorly demarcated from Teratal
a
surrounding aerated lu ng and its borders may form an acute lymph
angle with the mediastinum. A mediastinal mass is sharply de- lymph
marcated from adjacent lung and its borders form an obtuse Mesen
angle with the med iastinum. Cherne
Sternu
Tumor
Osteon
Cardia,
Pericarl
Divertil
Effusiol
Fig.ll. 1Sa-c Classification of mediastinal masses from (T cri- Epicard
teria (from O. H. Wegener: Canzk6rper-Computertomogrophie.
Berlin: Blackwell; 1992) Morga
a Solid masses
1 Retrosternal thyroid goiter All compo
2 Thymoma lymph no
3 Teratoma, dysgerminoma • Mesenc
b 4 Lymphoma mixed I
5 Retrotracheal goiter
6 Neurogenic tumors
7 Esophageal tumors, fibrosarcoma
I Posterior mediastinum
II Mid dle mediastinum
III Anterior mediastinum
b Cystic masses
8 Thyroid cyst
9 Thymic cyst
10 Cystic teratoma
11 Mesothelioma (lymphangioma)
12 Bronchogenic cyst
13 Meningocele
i
14 Neurenteric cyst
15 lymphangioma
c Lipid-containing masses
16 Thymolipoma
17 Dermoid cyst
18 lipoma
c 19 liposarcoma
Fig. 11 .1:
mediasti
lesions i
clavicle (
Table 11.2 Mediastinal masses (classified by mediastinal compartmental location) (modified from Meschan, 1981)
Anterior mediastinum Middle mediastinum Posterior mediastinum
Vessels: Vessels: Vessels:

Dilated superior vena cava Aortic/Great vessel aneurysm Aneurysm descending aortic
Persistent left SVC Pulmonary artery di latation Azygos/ Hemiazygos dilatation
Aortic arch anomaly Azygos vein dilatation Thoracic duct cysts
Ascending aortic aneurysm
Coronary sinus aneurysm
Thyroid: lymph nodes: Neurogenic:
Goiter Lymphoma Neurofibroma
Adenoma Lymph node metastases Schwan noma
Carcinoma Infectious mononucleosis Neuroblastoma
Parathyroid tumor Sarcoidosis Pheochromocytoma
Thymus: Tuberculosis Glomus tumor
Hyperplasia Histoplasmosis Chemodectoma
lulmo- Tumors Silicosis Lateral meningocele
d from Teratoma/Germ cell tumors: Tumors:
acute lymphangioma (cystic hygroma) Vagus or phrenic nerve t umors
)Iy de- lymphoma Chemodectoma
Jbtuse Mesenchymal tumor· Mesenchymal tumors·
Chemodectoma
Sternum: Trachea and esophagus: Vertebral column:
Tumor Tumor. diverticulum, megaesophagus SpondylOSiS
Osteomyelitis Paravertebral abscess
Extraosseous extension of metastasesl
myeloma
Extramedullary hematopoiesis
Cardiac: Bronchogenic and esophageal Bochdalek hernia
Pericardial cyst duplication cysts. Hiatus hernia
Diverticul um
Effu sion
Gcri- Epicardial fat pad
rraphie.
Morgagni hernia
All compartments: mediastinitis ± abscess fo rmation, hematogenous metastases, mesenchymal tumors,

lymph node enlargement. lipomatosis, fibrosis .
• Mesenchymal tumors include lipoma, fibroma, myoma, hemangioma, lymphangioma, chondroma, xanthofibroma.
mixed lumors, and their malignant counterparts.
Fig.ll.17 The ~cerv i cothoracic" si gn. Lesions in the anterior

media stinum t erm inate at the level of t he clavicle (left) whereas
lesions in the posterior mediastinum ext end superior to the
clavicle (right).
Fig. 11.18 Thyroid goiter gives Mgoblet·shaped" superi or medi·
astinal widening with trachea l narrowing. A right-Sided calcified
thyroid nodule is also present.
The Thymus
Thymic Hyperplasia
In infants and young children. the thymus occupies

much of the anterior mediastinum and lies anterior to
the great vessels. During these early years, there is con-
siderable variation in the normal size of the gland.
Two distinct histologic types of thymic hyperplasia
are recogni zed; true thymic hyperplasia and lymphoid
hyperplasia. True thymic hyperplasia is defined as en-
a largement of the thymus which remains normally or-
ganized beyond the upper limit of normal for a given
patient age. This entity is seen in patients recove ring
from recent "stress" including chemotherapy, co rti -
costeroid therapy, irradiation and thermal burns (Shi-
mosato et al. 1997. Mendelson 2001).
Lymphoid hyperplasia refers to an increased number
of lymphoid follicles and this e ntity most commonly is
seen in patients with myasthenia gravi s. being present in
up to 65 %of cases (Mendelson 2001).
The chest radiograph shows superior mediastinal
widening with a smooth or scalloped contour Co,
(Fig. 11.21 ). The lateral view may show obliteration of the ao
the retrosternal space and slight posterior displacement In you
of the trachea. tenuat
There
Fig. 1l.19a, b Thyroid goiter with retrosternal and retrotracheal increa:
extension. In thyr
mal in
Thym'
Thymi.
carcin!
epithe
and bi
ber of
into n
thymo
scopic
mama
give p
deposi
COli
thymo
diastin
Jeong'
astinal
in inva
2004).
Mo.
signal
tissue
geneol
1992 ).
a b from tl
Fig. 11.20a. b Anterior mediastinal tumor. Histology was consistent with thymoma. the he
Fig. 11.21 Thymic hyperplasia with

distinctive "sail-shaped~ shadow in
the superior mediastinum.
Computed tomography: Axial images at the level of

the aortic arch are optimal for evaluation of the thymus.
In young children, the thymus is homogeneous w ith at-
tenuation values close to those of adjacent soft tissues.
There is a gradual decrease in attenuation values with
increasing age due to fat deposition (Armstrong 1992).
In thymic hyperplasia, the gland though enlarged is nor-
mal in shape.
Thymic Tumors
Thymic epithelial tumors include thymoma and thymic

carcinoma (Fig. 11.20), These arise from thymic
epithelium and demonstrate varying histologic features
and biological behavior (Han et al. 2003). While a num-
ber of classifications exist, thymoma may be classified
into noninvasive and invasive subtypes. Noninvasive
thymoma is encapsulated completely with no micro-
scop ic evidence of extracapsular growth. Invasive thy-
moma shows extracapsu lar spread and sometimes may
give pleural and occasionally more distant metastatic
deposits.
Computed tomography features suggestive of invasive
thymoma include invasion of mediastinal fat and/or me-
diastinal vessels and the presence of pleural seeding.
Fig.11.22 Radiographic appearances of thymic hyperplasia
Jeong et al. have reported a lobulated contour and medi- (shaded area) in children and adolescents (from Meschan 1981).
astinal fat and great vessel invasion to be more common
in invasive thymoma and thymic carcinoma (Jeong et al.
2004).
Magnetic resonance imaging (MRI): Thymoma shows Positron emission tomography (PET): Sasaki et al. have
signal intensity similar to muscle or normal thymic suggested that PET may be helpful in distinguishing
tissue on Tl-weighted sequences and has hetero- thymic carcinoma from both invasive and noninvasive
geneous T2 signa l intensity (Han et al. 2003, Sakai et al. thymoma. They report a sensitivity of 84.6%, specificity
1992). MRI may be useful in distinguishing thymoma of 92.3 %, and accuracy of 88.5 % in this differentiation
b from thymic cysts when this is not possible on cr due to using a cut-off for standardized uptake value (SUV) of 5
the hemorrhagic or proteinous contents of the cyst. (Sasaki et al. 1999).
Thymic carcinoid is a rare primary malignant tumorof

the thymus with a poor prognosis. One-third of these
tumors are functionally active causing syndromes in-
cluding Cushing's syndrome. cr and MRI characteristi-
cally show a large anterior mediastinal mass often w ith
local invasion and differentiation from aggressive
thymic epithelial tumors may not be possible at imaging
(A rm strong 2000),
Thymic lymphoma: Lymphoma may involve the thy-
mus as part of disseminated disease or in isolation and
the nodular sclerosing variant of Hodgkin's disease is the
most common histologic type. Imaging differentiation
from other thymic tumors may be difficult. Distinguish-
ing diffuse lymphomatous infiltration from thymic hy-
perplasia may also be problematic (Armstrong 2000,
Mendelson 2001 ).
Mediastinal Lymph Node

Enlargement
• Hodgkin's disease and non- Hodgkin lymphoma, lymph

node metastases from thoracic and extra thoracic malig-
nancies, and sarcoidosis are the most common causes of
mediastinal lymph node enlargement.
See:
• Bronchial Carcinoma: Chapter 6, p. 157
• Hodgkin's and Non-Hodgkin's Lymphoma: Chapter 6, b
p,98 Fig. 11.
• Sarcoidosis: Chapter 3. p.91 large ri
geneOi
calcific
Primary Mediastinal Tumors:

Benign Teratoma and Malignant
Germ Cell Tumors ing te
carcin
early
Benign teratoma and malignant germ ce ll tumors are adult
relative ly uncommon and are thought to arise from ab- show~
errant cell nests in the mediastinum. Imaging of these 11.24.
b tumors is initially with chest radiography, proceeding to either
Fig. '1.23a. b Benign teratoma. Axial CT images show well-de- cr and/o r MRI. areas
fined anterior mediastinal mass containing areas of fat density. Benign teratomas are frequently asymptomatic and gions
foci of calcification, and discrete areas of low density soft tissue. may grow to a considerable size before detection. They rhage
are found most commonly in young adults, with a slight be pr<
female predominance. The chest radiograph shows an
anterior mediastinal mass. Computed tomography usu-
Thymofipoma is a rare, benign tumor that is usually ally shows a thick-walled fluid-containing cyst; the at-
asymptomatic and manifests as a large anterior medi- tenuation of its contents may be that of fat, fluid, or soft Neu
astinal mass. Histologically. it is composed of mature fat tissue (Suzuki et al. 1983, Fig. 11.23 ),
and normal thymic tissue and at cr and MRI, it appears Malignantgerm cell tumors may be divided in to sem i- Neuro
as a fatty mass with fibrous septa (Armstrong 2000). noma and non se minomatous germ cell tumors includ- nal tu
Neo plastic Mediast ina l Wid ening 291
J.
• •
lh
g-
of
b ___
'6. b
Fig. 11.24 a, b Malig nant teratoma. Chest radiograph shows Fig . 11.25a. b Malignant teratoma. Chest radiograph shows
large right-sided a nterior mediastina l mass (a ). CT shows hetero- large left-sided anterior med iastinal soft tissue mass (a). CT
geneously enhancing soft tissue mass containing mu ltiple foci of shows large heterogeneous ly enhancing soft tissue mass with
ca lcification and evidence of mediast inal invasion (b). compression of the main and left pulmonary arteries and with air-
way displacement and compression (b).
ing te ratocarci noma, em bryonal carci noma, and chorio- nerve roots or intercosta l nerves (peripheral nerve!
carcin oma. These tumors grow rapidly and metastasize nerve sheath tumors, neurofibroma /schwa nnoma). Oc-
early and are most commonly encountered in young cas ionally. they arise from the sy mpathetic trun k (ga n-
are adul t males. The chest radiograph characteristically glio neuro ma) or from paragangli onic cells (pheochro-
ab- shows a lobula te d anteri or medi astinal mass (Figs. mocyto ma).
lese 11.24 • . 11.25. ). Computed tomography demonstrates Neurogenic tumors typica lly appear as sha rpl y cir-
g to either a homogeneous soft-tiss ue t umor or mul ti ple cum scribed' homogeneous, ro und, or oval mass les ions.
areas of contrast enhance ment in te rspersed w ith re- They are of intermedi ate signal in te nsity on Tl -
and gions of low attenuation re prese nting e ither hemor- weighted MRI seque nces. hete roge neous to hy peri n-
'hey rhage or nec rosis. Scattered foc i of calcification may a lso tense on T2-we ighted sequences. and they enhance
ight be prese nt (Figs. 11.24b. 1l.25b ). greatly postad min istratio n of int ravenous gadolin ium
5 an (Figs. 11.26. 11.27 ). Periphera l nerve/ nerve sheath
usu- tum ors are fre quently located in the parave rtebra l re-
~ at- gion and so metimes may have a "d umbbell" config ura-
soft Neurogenic Tumors ti on w ith extrad ural an d parave rte bral /posterior medi-
astinal com ponents. In these cases, there may be as-
em i- Neuroge nic tumors accou nt for 20-30% of all medi asti- sociated w ideni ng of the neura l fo ramen (Fig. 11.28).
:Iud- nal tumors. Th ey most co mm only ari se from the thoracic
12 I
Compu
specific
monar}
made fJ
In othe
(GGO).
agnos is
that th,
a
cases, r
possibl<
clinical
logic fir
The '
• Grou
Fig . 11.26 Neu rogenic tumor histologically confirmed . The • Mult
t umor ma ss extends superior to the clavicle indi cating its poste- • Pulrr
rior location. However, the aortic arch remains sharply defined
suggesting that this lesion lies much more posteriorly than the • Intra
aorta. patt,
• Oem
• Inhm
GroUi
Consl
b
Ground-,
alveoli, !
tial char
tion of (
creased
vascular
The 0
filt rated
than bet
creased
bronchu,
Thed
opacificc
processe
• Acute
Pneur
c ca lly,
Fig.11.28 Axial Tl-weighted MRI shows dumbbell-shaped pe- Fig. 11.27 a- c Chest radiograph shows well-defined opacity nitya
ripheral nerve sheath tumor with paravertebral and extradural lying posteriorly on the left side in the superior mediastinum (a). gressi
components and with expansion of the neural foramen. Axial Tl-weighted pre and gadolinium-enhanced coronal MR im- years.
ages show lesion of intermediate Tl signal intensity which shows
tribut
avid peripheral enhancement. location, signal intensity. and en-
hancement characteristics were consistent with a periphera l (Fig. 1
nerve/nerve sheath tumor. • Acute
hemo
293
12 High-Resolution/Thin-Section (T Patterns
in Pulmonary Disease
Co mputed tomography (CT) is more sensi tive and more

spec ifi c tha n the chest radiograph in eva luati on of pul-
monary disease. A specific di ag nosis ca n sometimes be
made from cr findings as in centrilobular emphysema.
In other cases, for exa mpl e ground-glass opacifi cation
(GGO ). cr findin gs are less s pecific and a differential di -
agnosis may only be poss ibl e. This may reflect the fact
that the lung's response to different insults is, in many
a cases, relatively iso morphic. It is, howeve r, frequ ently
possibl e to shorten the differential diagnosis when the
clinical history a nd the duration of symptom s and rad io-
logic findings are considered.
The following cr pattern s will be co nsidered: a
• Ground-glass opacification and consolidation
• Multifoca l peripheral co nso lidation
• Pulmonary nodules
• Intra- and interlobular se ptal thickening and reti cular
pattern
• Decreased lung attenuation and cystic lung change
• Inhomogeneo us- mosaic lung attenua tio n
Ground-Glass Opacification-
Consolidation
b
Ground-glass opacification re flects partial filling of the b
alveoli, sometimes with a degree of associated intersti- Fig. 12.1 a, b Pneumocystis pneumonia. High-resolution CT
image shows bilatera l ground-glass opacification with evidence
tial change. th e latter generally bein g below the resolu - fl
of th e Mblack bronchus sign and with sparing of the subpleural
tion of computed tomography. Lung attenuation is in- lung.
creased but this increase is not suffici ent to obscure
vascular markings in contradistinction to consolidation.
The difference in attenuation values between the in- processes including Wegener's Granulomatosis and
filtrated lung parenchyma and air-filled bronchi is large r Anti-Glomerular Basement Membrane disease. It also
than between normal lung and air-filled bro nchi; this in- may be seen in hematolog ic di sorders and particu-
creased contrast leads to increased co ns picuity of the larly in the acute leuke mias w here it may be a
bronchus. the so ca lled "black bron chus" sign. manifestation of disease-i nduced bone marrow
The differential diagnos is of pulmonary ground -glass failure or a com plication of chemotherapy-induced
opacification includes acute and nonacute di sease thrombocytope nia.
processes: • Pulmonary Edema: Grou nd-glass opacification prob-
• Acute infection including Pneumocystis JirovecijCa rinii ably reflects a co mbination of inte rstitial and early
Pneumonia (PJP; PCP): This infection is characteristi- alveolar ede ma. It characteristically has a depend ent
c ca lly see n in patients with diminished ce llular immu- di stribution and may involve the posterior portions
acity ni ty and has been co nsid ered an index case for pro- of the uppe r lobes in patients confi ned to bed.
n (a). gress ion to AIDS in HIV-pos itive patients fo r many "Smooth" interlobular se ptal thi cke ning is also
Rim- years. GGO may be uniform or inhom ogeneou s in dis- frequently present and probably refl ects predomi -
haws tribution and may progress to fra nk consolidatio n nantly associated interstitial edema (Fig. 12.2).
d en-
_heraI
(Fig. 12.1; see also Chapter 3. p.87 ). • Hypersensitivity Pneumonitis/Extrinsic Allergic Alve-
• Acute Pulmonary Hem orrhage: Acute pulmonary olitis: Ground-glass opacification in a patchy or ho-
hemorrhage may be see n in a number of di sease moge neous distribution is a frequ e nt findin g in hy-
294 12 High-ResolutionfThin-Section CT Patterns in Pulmonary Disease
ing the entire secondary pulmonary lobule are Puh

manifestations ofRBILD-DI P with a tendency towards
more extensive and uniform change within the lobule
in DIP (see also Idiopathic Interstitial Pneumonias, The d
Chapter 3, p.95 ). tion/t
• Lymphocytic Interstitial Pneumonia (LIP) : LIP in adu lt tion i
HIV-negative patients is frequently found in patients type.
with Sjiigren syndrome. Ground-glass opacification, Ce,
areas of consolidation, and pulmonary cysts are statio
frequent CT findings (see also Sjiigren syndrome, whitt
Chapter 3, p. 102). 1-3m
• Alveolar Proteinosis: The etiology of this rare disease Disea~
is unknown but it may relate to a hereditary defect of Lal

su rfactant production wh ich decompensates to a somel
pathologic state when additional infectious or toxic dicate
insults are imposed (e. g.. the inhalation of tobacco persel
smoke, silicates. aluminum, kaolin, or sawdust). tis-int
Fig.12.2 Pulmonary edema with bilateral pleural effusions.
Pathologically, the alveoli are filled with copious pro- No
tein- and phospholipid-rich material. cr features are teristi
CGO in association with septal thickening leading to dicate
the characte ristic "crazy paving" appearance (Fig. chova~
12.3a, b). the di

• Peripheral Adenocarcinoma: Focal areas of persisting (Fig. I:
GGO may reflect slow growing adenocarcinomas NOI
with a lepidic pattern of growth (see a lso Solitary Pul- anator

monary Nodule, Chapter 6, p. 149 and Noguchi Classi- Pulmo
fication, Chapter 6, p. 161). thougl
mayd
Multifocal Peribronchial
Consolidation
• Multifoeal Bronchioloalveolar Carcinoma: Bronchi-

oloalveolar carcinoma showing a lepidic growth pat-
tern cha racteristically shows pulmonary consolida-
tion in a peribronchial distribution.
• Pulmonary Lymphoma: Pulmonary lymphoma is
characterized by nodular and linear areas of in-
creased attenuation and consolidation. These
changes tend to have their epicenter on the airway
wh ich may appear dilated and they correlate histo-
logically with lymphomatous infiltration in a peri-
bronchovascular distribution.
• Organizing Pneumonia: Organizing pneuIllonia or
cryptogenic organizing pneumonia represents an or-
ganizing pneumonia and a "proliferative" bronchioli-
tis. High-resolution CT (HRCT) shows areas of con-
Fig. 12.3a. b Alveolar proteinosis. CT images show marked sep- so lid ation and ground-glass opacification in a periph-
tal thickening superimposed on ground-glass opacification and
giving the Mcrazy paving" pattern.
eral subpleu ral distribution (see Fig. 4.26a, b).
• Chronic Eosinophilic Pneumonia: a manifes tations of "
Fig. 12.6
chronic eosinophilic pneumonia include peri - some de
bronchial consolidation that may have a peripheral
persensitivity pneumonitis (see also Hypersensitivity subpleu ral distribution in up to 50% of cases.
Pneumonitis, Chapter 5, p.145 ).
• Respiratory Bronchiolitis-Interstitial Lung Disease
(RBILO ) and Desquamative Interstitial Pneumonia
(DIP): Centrilobular nodules of GGO and GGO involv-
12 High-Resolution /Thin-Section CT Patterns in Pulmonary Disease 295
re Pulmonary Nodules
ds
lie
The distribution of pulmonary nodules on thin collima-
lS,
tion/hi gh- resolution CT images allows their classifica-
tion into centrilobular, perilymphatic. and random in
lit
Its type.
m,
Centrifobufar nodules are characteristica lly a manife-
Jre
station of sma ll airways disease-cellular bronchiolitis, in
le,
w hich case they tend to be well defined and average
1-3 mm in di ameter (Fig. 12.4; see also Small Airways
.se Disease. Chapter 4. p. 122 ).
of Larger less well-defined centrilobular nodules which
sometimes may be of ground-glass opacification may in- Fig.12.4 Cellular bronchiolitis. High-resolution CT image shows
a extensive bilateral well-defined centrilobular nodules and branch-
dicate peribronchiolar consolidation and are seen in hy-
de ing structures consistent with a cellular bronchiolitis.
:(0
persenSitiv ity pneumonitis and respiratory bronchioli-
;t). tis-interstitial lung disease (Figs. 12.5, 12.6).
~o
Nodules in a perilymphatic distribution are charac-
ue teristically seen in sarcoidosis. Perilymphatic change in-
to dicates a combination of centrilobular, peribron-
'ig. chovascular. and perifissural nodul es in keeping with
the distribution of the pulmonary lymphatic channels
ng (Fig. 12.7 ).
las Nodules with a random distribution show no specific
ul- anatomic distribution within the lung (Figs. 12.8. 12.9).
isi- Pulmonary metastases may show a random distribution
though on some occasions hematogenous metastases
may demonstrate a degree of angiocentricity.
Fig.12.5 Centrilobular nodules.
:hi-
·at-
da-
is
in-
ese
yay
;to-
eri-
or
or-
oli-
'on-
ph-
sof
Fig.12.6 Poorly-defined centrilobular nodules consistent with Fig. 12.7 Sarcoidosis. CT shows pulmonary nodules in a perilym-
eri- some degree of peri bronchiolar consolidation. phatic distribution. There are centrilobular and subpleural
eral nodules and there is ubeading" of the fissures and bronchovascu-
lar bundles.
296 12 High-Resolution{Thin-Section a Patterns in Pulmonary Disease
Fig.12.8 Pulmonary nodules in pneumoconiosis. Fig.12.9 Pulmonary metastases: (T shows bilateral profuse
nodularity in no specific anatomic distribution. Histology ac- Fig. 1
quired from trans bronchial biopsy was adenocarcinoma.
s
b
• I<
P
I,
n
ti
tr
eJ
fe
n,
in
m
• A~
ta
Fig.12.10 Pulmonary lymphangitis carcinomatosa with inter- Fig.12.11 Pulmonary lymphangitis carcinomatosa.
ca
lobular septal thickening in the right upper lobe.
Tl
dl
fn
pa
Intra- and Interlobular Septal Thick- degree of organization with development of a fine re- (F
ticular pattern within areas of hemorrhage 5-10 days
ening and Reticular Pattern post the acute event. Layering of blood along the
• Dr
tis
septa might also account in part for this appearance. tia
Thickening of the pulmonary interstitium may be due This combination of alveolar and interstitial change tic
to edema, inflammatory cells, neoplastic infiltration or may also give a crazy-paving appearance. • Ca
fibrosis. The distribution of change, the relative pro- • Pulmonary Lymphangitis Carcinomatosa: Pulmonary m,
portions of inter- to intralobular septal thickening, the lymphangitis carcinomatosa refers to neoplastic infil-
presence of accompanying features such as ground- tration of the pulmonary lymphatic channels. Septal
glass opacification and traction bronchiectasis together thickening may be "nodular" in contradistinction to
with the clinical setting will narrow the differential di- the smooth thickening of pulmonary edema. As-
Dec
agnosis. sociated centrilobular thickening is seen but ground- Cysl
• Interstitial Edema: Smaoth interlabular septal thick- glass opacification occurs only in a minority of cases.
ening tends to predominate in acute interstitial There may be associated pulmonary nodular
Emph
edema and is characteristically most marked in the metastases and pleural effusions are also common in dia
dependent portions of the lung. There is frequently (Figs. 12.10,12.11).
C€I
associated ground-glass opacification and the combi- • Alveolar Proteinosis: The original description of crazy
nantl)
nation may give a crazy-paving pattern. paving in which septal thickening is superimposed
• Subacute Pulmonary Hemorrhage: The presence of on ground-glass opacification was in alveolar protei-
blood within the lung parenchyma induces some nosis. It is now recognized that this appearance is not
12 High-Resolution/Thin-Section CT Patterns in Pulmonary Disease 297
e
Fig.1 2.12 Asbestosis with subpleural interstitial change.
.....--------------_. . .
specific to alveolar proteinosis and occurs in a num-
ber of other entities (see Fig. 12.16).
• Idiopathic Interstitial Pneumonias: Usual interstitial
pneumonia is characteri zed by septal and particu-
larly intra lobular septa l thickening giving rise to "fine
networks," a varying degree of architectural distor-
tion, traction bronchiectasis, and honeycombing. Dis-
tribution is characteristically subp leura l and periph-
era l and the differential diagnosis includes other
forms of idiopathic interstitial pneumonia including
nonspecific interstitial pneumonia (NSIP). asbestos-
induced in terstiti al fibro sis. and drug-induced pneu-
monitis (see Fig. 3.58).
b
• Asbestosis: Interstitial changes and fibrosis in asbes-
Fig. 12.13a. b Asbestos-induced pleural plaques with sub-
tos-induced interstitial lung disease characteristi-
pleural lung change. Chest radiograph (a) shows bilateral ca l-
cally have a lower zone and peripheral distribution. cified pleu ral plaques. CT (b) shows pleural plaque formation with
The frequent presence of associated asbestos-in- M
subpleural septal thickening giving a Ysubpleuralline and reticu-
duced benign pleural change helps in differentiation lar change in the lower lobes.
from the idiopathic interstitial pneumonias and in
particular, from usual interstitial pneumonia
'e- (Figs. 12.12.12.13).
.ys • Drug-induced pneumonitis: Drug-induced pneumoni- by rounded area s of decrea sed lung attenuation w hich
he tis is included in the differential diagnosis of intersti- surround the centrilobular bronchovascular bundle. The
ceo tial pneumonia particularly in a lower zone distribu- extent of involvement of the secondary pulmonary
Ige tion. lobule becomes more marked as disease progresses and
• Connective Tissue Disease-associated Interstitial Pneu- uniform decreased lung attenuation with Iittle-to- no re-
Ify monias: See Chapter 3. p.l00. sidua l intervening normal lung may be see n in severe
fiJ- advanced emphysema (Fi g. 12.14a. b ).
_tal Panfobufaremphysema is characteristically seen in in-
to
As-
Decreased Lung Attenuation and dividu als with alpha-l anti trypsin deficiency, tend s to
involve the lower lobes and in co ntradi stinction to cen-
1d- Cystic Lung Change trilobular emphysema, involves the entire secondary
ies. pulmonary lobul e. Uniform decreased lung attenuation
liar Emphysema: CT has been shown to have high se nsitivity is seen in the lower zones. This appearance may some-
10n in diagnosis of emphysema. times be difficult to distingui sh from the diffuse air trap-
Centri/obu/ar emphysema which affects predomi- ping which is so metimes seen in bronchiolitis oblite ran s
azy nantly the upper-to-mid zones is initially characterized (co nstrictive bronchiolitis).
sed
tei-
not
298 12 High-Resolution/Thin-Section CT Patterns in Pulmonary Disease
. ....._- b
Fig . .
Fig. 12.14a. b Centrilobular emphysema. Emphysematous lung surrounds the centrilobular bundle with sparing of the peripheral
lobule.
• Air trapping and constrictive bronchiolitis: see Inho-

mogeneous Mosaic/Lung Attenuation (p. 299).
• Honeycombing: This refers to the presence of multiple
cystic cavities that range from a few to several milli-
meters in diameter and which are surrounded by a
thick fibrous wall. Honeycombing cha racter istically
has a subpleural distribution and is frequently exten-
sive in end-stage fibrosis, particularly in end-stage
usual in te rstitial pneumonia (UJP) (Figs. 12.15,1 2.16).
• • Cavitating Lesions: Pyogenic lung abscess, tuber-
culous infection, septic pulmonary emboli, squamous
Fig. 1
cell neoplasia both primary and metastatic are thick
among pulmonary lesions wh ich may cavitate
(Fig. 12.17).
• Tuberous Sclerosis: Tuberous sclerosis is character-
ized by the triad of ep il epsy, cafe-au-lait s pots, and P'
hamartomatous lesions. We ll-defined discrete cystic al
Fig.12.15 Honeycombing consistent with advanced pulmonary Vi
fibrosis in rheumatoid lung disease. lesions may be seen scattered throughout the lungs
(Fig. 12.18). til
• Pulmonary Langerhans Cell Histiocytosis (PLCH): CT
changes in PLCH range from peribronchial and peri-
bronchiolar nodularity in early-stage disease through Inh,
cavitatory nodules and thick-walled cysts to thin-
wa ll ed and confluent cysts with fibrosis in advanced
lun
disease. Changes are most marked in the upper-to-
mid zones with relative spa ring of the basal lung lnhol
(Fig. 12.19). or a (
• Lymphangiomyomatosis (IJ\M): LAM is characteristi- • Gr
cally seen in premenopausal females. Cystic lung po
changes are similar to those seen in PLCH but tend to 1.
have a more diffuse di stribution (Fig. 12.20). There
may be an associated chylothorax.
• Lymphocytic Interstitia l Pneumonia: Discrete air-filled 2.
cysts scatte red through the lungs is a described find -
ing in LIP (see Fig. 3.72).
Fig.12. 16 Characteristic subpleural distribution of honey- • Cystic Lung Disease in Acquired Immunodeficiency
combing in idiopathic pulmonary fibrosis. Syndrome: Cystic lung disease tends to occur in
12 High-Reso luti on/Thin-Section CT Patterns in Pulmonary Disease 299
Fig. 12.17 Cavitating septic pulmonary emboli. Fig.12.18 Tuberous sclerosis: CT shows bilateral scattered air-
b fill ed cysts in a patient with known tuberous sclerosis.
a
y
1-
;e
).
r-
IS Fig.12.19 Pulmonary langerhans cell histiocytosis with many Fig.12.20 Lymphangiomyomatosis: CT shows cysts of varying
re thick-walled cysts. size and shape in the lung bilatera lly.
te
r-
ld
patients who have had recurrent episodes of PJP-PCP
and appearances may be indistinguishable from ad -
:ic
gs vanced PLCH (see Fig. 3.46). Cystic disease in thi s set-
ting predisposes to development of pneumothorax.
::T
ri-
gh Inhomogeneous-Mosaic
in-
Lung Attenuation
'ed
to-
ng Inhomoge neou s lung attenuation is usually due to one
or a comb ination of the following;
iti- • Ground-glass opacification in an inhomogeneous
109 patchy distribution (Fig. 12.21 ).
I to 1. Infiltrated secondary pulmonary lobu les are inter-
ere spe rsed w ith areas of normal lung giving inhomo-
geneous lung attenuation. Fig. 12. 21 Hypersensitivity pneumon itis with inhomogeneous
lung attenuation due to patchy distribution of ground-glass
,led 2. Pulmonary vessel density and vesse l caliber tend opacification.
nd- to remain uniform throughout both infiltrated and
no rma l lung.
'ncy
. in
300 12 High-Resolution/Thin-Section CT Patterns in Pulmonary Disease
2. Vessel caliber and vesse l density are decreased

w ithin areas of decreased lung perfusion. 13
3. Differences in atte nuation do not become more
pronounced in expiration.
• Constrictive bronchiolitis and air trapping (Fig. 12.23 a,
b).
1. Areas of air trapping are interspersed with areas of
normal lung. This gives inhomogeneous lung at-
tenuation on images acquired in inspiration. 1. n
2. Vessel caliber and vessel density both may be
decrea sed withi n the areas of air trapping due to
reflex vasoconstriction.
3. Differences in attenuation become more pro- . Dia
nounced on images acquired in expiration with
the normal increase in attenuation in areas of nor- Campi,
Fig.12. 22 True mosaic perfusion in chronic thromboembolic mal lung while areas of air trapping remain of cates tt
pulmonary hypertension. decreased attenuation. diagno!
• Inna
When areas of ground-glass opacification are seen in as- filtr;
sociation with air trapping. sarcoidosis and hypersensi- • Unil.
• True mosaic perfusion in chronic thromboembolic pul- tivity pneumonitis should be considered (see Fig. S.26a, • Pnel
monary arterial hypertension (CfEPH; Fig. 12.22). b ). • Pleu
1. Pulmonary vasc ular stenoses and occlusions lead larg'
to nonuniform pulmonary perfusion and an inho-
mogeneou s pattern of lung attenuation. The che
associa1
may su
phy (Cf
tions fo
Com
to that
siderinE
• An ir
nize!
widE
the t
indie
b
Fig. 12.23 a, b Air trapping: CT image shows inhomogeneous lung attenuation in inspiration (a) and this becomes more pronounced
on images acquired in expiration (b).
Fig. 13.1
301
13 Radiographic Signs and Differential Diagnosis
1. The Opaque Hemithorax (Tab le 13.1)
• Diagnostic Approach Ta ble 13.1 The opaque hemithorax
Pleural effu sion

Complete opac ifi cation of a hemithora x frequently indi-
Pleural thickening and fibrothorax
cates the presence of s ignificant di sease. The differential
Pleural mesothelioma and me tastatic pleural carcinomatosis
diagnosis includes:
Pneumonia
• Inflammatory or neoplastic unil ateral pulmonary in-
Atelectasis
filtration
Tuberculosis
• Unilate ral pulmonary atelectasis or agenesis
Pulmonary aplasia, agenesis. and pneumonectomy
• Pneumonectomy
Diaphragmatic hernia
• Pleural disease and most common ly the prese nce of a
Thoracic scoliosis and chest wall deformity
large pleural effusion
The chest radiograph shows the opaque hemithora x. any

associated mediastinal di splacement. and occasionally
may suggest the correct diagnosis. Computed tomogra- intrathoracic ma ss. While a pl eural effu sion may lead
phy (a) ± bronchoscopy are standard 2nd line investiga- to complete opacification of th e hemithorax in the
tion s for further assess ment. supine position, some aerated lung is usually visible
Co mpari son of the volume of the opaque hemith orax at the apices on upright views.
to that of the unaffected side is important when co n- • Ultrasound will show the presence of an effusion and
sidering the differential diagnosi s (Fig. 13.1 ): al low image-guided diagnostic as piration. Computed
• An inc rease in the volume of the hemith orax is recog- tomography. howeve r. is the imaging modality of
ni zed by contra lateral mediastinal di splaceme nt. choice for assessment of underlyi ng pulm onary and
wide ning of the intercostal spaces. and depression of mediastinal abnormality.
the hemidiaphragm. A large opaque hemithorax may • A decrease in the volume of the hemithorax is
indi cate either a massive pl eura l effusio n or a large manifest by ipsi lateral mediastinal di splacement.
Pneumonia Effusion Atelectasis

b
- No mediastinal shift - Contralateral mediastinal shift - Ipsilateral mediastinal shift

- Symmetrical intercostal spaces - Widened intercostal spaces - Narrow intercostal spaces
- Delayed blunting of the - Early. dense opaCification of t he - Elevation of the hemidiaphragm
costophrenic angle costophrenic angle
- Pulmonary vascular markings
are often visible
Fig. 13.1 The opaque hemithorax.

•
302 13 Radiographic Signs and Differential Diagnosis
Fig .13.2 Right lu ng atelectasis sec-

ondary to central bronchial carci-
noma. There is occlusion of the right
main bronchus and ipsilateral medi-
astinal displacement.
narrowing of the in te rcostal spaces, and elevati on of Pleural Mesothelioma and Metastatic Pleural
the hemidiaphragm. A small opaque hemithorax may Carcinomatosis
indicate a restricti ve pleura l process, pulmonary
atelectasis, pulmonary hypop lasia, or past pneu- An opaque hemithorax in pleural neoplasia may be due
monectomy. A fibrothorax may show a rind of calcifi- to the presence of an effusion and /or pleu ral tumor.
cation at its pulmonary interface. Co mplete lung Marked encasement of the underlying lung with result- b
atelecta sis is most commonly seconda ry to central ing atelectasis may lead to a decrea se in the size of the
bronchial carcinoma. Pulmonary hypop lasia is as- hemithorax.
sociated with marked ipsilateral mediastinal di s-
placement (see Chapter 2, p. 57), Atelectasis Tube
• An o paque hemithorax of normal volume may indi-
cate extensive unilateral pulmonary consolidatio n or Com plete pulmonary atelectasis results from occl usi on Tubel
it may be seen when a pleura l effu sion is as sociated of a main bronchus by carcinoma or less com mon ly by the e
with underlying pulmonary atelectasis. an aspirated foreign body, mucus plug, stricture, or such.
bronchial tear. The vo lume of the hemitho rax is reduced tures
and there is ipsilateral mediastinal displacement
• Differential Diagnosis (Fig, 13.2), A concomitant pleural effus ion, however, may Pulml
restore thoracic sy mmetry (Fig. 13.3 ). mone
Pleural Effusion
Pneumonia Thein
On upright views. the opacification is particularly media,
marked in the laterobasal hemithorax w ith bl unting of It is rare for pneumonic infiltration to involve the entire 13.4),
the cosrop hrenic angles. The effusion may be mobile lung. A we ll -penetrated chest radiogra ph may show
w ith changes in patient position. small res idual areas of normal lung and air-filled bronchi Thora.
traversing the co nso lida tion (air bronchogram), The di-
Pleural Thickening and Fibrothorax agnosis is su pported by clin ical findings of cough, Extrem
sputum production, pyrex ia, and leukocytosis, and by nence <
Empyema, tuberculous effusion, and hemothorax may iden tify ing the causative organism in sputum samples or opaqUE
reso lve leaving marked fibrou s pleural thickening. Thi s from blood cu ltures. views . .
may lead to seve re pulmonary encase ment with re sul t- ondary
ing venti latory impairment. pansior
The Opaque Hemithorax 303
sec-
;-
right
ledi-
• c
Fig. 13.3 a - c Opaque right hem ithorax. Chest radiograph (a )

shows opaque right hemithorax. CT images (b and c) show the
, due large effusion with extensive abnorma l soft tissue infiltrating the
mediastinum and right hilum and with right lung atelectasis. Di-
mor. agnosis was bronchial carcinoma and left midzone pulmonary
sult- b metastasis is noted.
f the
Tuberculosis (TB)
lsion Tu be rcul ous pneumonia very occasionally may involve

Iy by the entire lung in children. Computed tomography in
e, or such cases will usually reveal areas of cavitation ± fea-
uced tures of endobronchial spread.
ment
. may Pulmonary Aplasia. Agenesis. and Pneu-
monectomy
The involved hemithorax is small and there is ips il ate ral

mediastinal displacement (see Chapter 2. p.58) (Fig.
~ ntire 13.4).
show
onchi Thoracic Scoliosis and Chest Wall Deformity
le di-
ough. Extreme scoliosis with posterior unilateral rib promi-
ld by nence and thoracic deformi ty can occasionally mimic an
lesor opaque hemithorax, particularly on underexposed
views. This appearance may be accentuated by the sec- Fig. 13.4 left pneumonectomy: Chest radiograph shows
ondary ve nti latory restriction and pulmonary underex- opaque left hemithorax with ipsilateral mediastinal displace-
pansion seen in some of these cases. ment.
2. lobar and Segmental Opacification
• Diagnostic Approach Table 13.2 Lobar and segmental opacification
Lobar and segmental consolidation

The lung is subdivided into functional anatomic units • Bacterial pneumonia
and some pathologic processes tend not to transgress • Tuberculous pneumonia
lobar and/or segmental boundaries. Lobar/segmental • Bronchioloalveolar carcinoma
• Pulmonary infarction
opacification may be patchy or confluent depending on
the volume of re sidually aerated lung. Atelectasis:
Opacification may be due to consolidation or atelec- Absorption atelectasis
• Bronchial carcinoma
tasis. Occasionally. overlying pleural or chest wa ll le- • Endobronchial metastasis
sions may mimic segmental opacification. • Benign bronchial tumors
The commonest cause of lobar/segmental opacifica- • Bronchial mucus plug
tion is acute pneumonia. This can usually be diagnosed • Postoperative atelectasis
• Bronchial rupture and hematoma
from the clinical history and characteristic radiographic
• Inflammatory bronchial stricture and extrinsic compres-
appearances: these tend to resolve within days of co m- sion
mencing appropriate antibiotic therapy.
Relaxation atelectasis
DiagnOSis becomes more difficult and merits further • Pneumothorax
evaluation when radiographic abnormality persists. Fig. 13.5
• Pleural effusion
• Pleural tumor consolid.
Bronchial carcinoma is a frequent cause of pe rsistent
atelectasis and/or consolidation, particularly in older in- • Scoliosis
dividuals from ·'at risk" categories (see Chapter 6, p. 157). Pseudosegmental opacities
Bronchial obstruction by mucus plugs, foreign bod ies, • Interlobar effusion
• loculated pleural effusion
and benign tumors are less common causes of persistent
lobar/segmental opacification. Pulmonary infarction
may also lead to segmental opacification which is slow
to reso lve (see Chapter 7, p. 189).
Acute lobar and Segmental Pneumonia
(Figs. 13.5-13.10)
• Differential Diagnosis (Table 13.2) Classic lobar pneumonia caused by pneumococci or
Klebsiella pneumoniae has become a rarity. Because
Pseudosegmental Opacities bacterial pneu monia spreads from alveo lus to alveolus
through the pores of Kohn, lobar and segmental boun-
Loculated pleural effusions. interlobar effusions. chest daries create a reasonably effective barrier. Because of
wall tumors, and large pulmonary angiomata and this, the opacity exhibits at least one sharp border, even
tumors occasionally mimic segmental opacities in their if the consolidation does not involve the e ntire segment
shape and location but they never have an air broncho- (peripheral co nso lidation ).
gram or alveologram.
Tuberculous Pneumonia
Lobar and Segmental Consolidation Tuberculous pneumonia has a pred ilection for the upper
lobes and the apical segments of the lower lobes. Often
An inflammatory or neoplastic process may spread there are accompanying features of past tubercu losis
within the alveolar spaces of a segment until it reaches such as apica l pleural thickening and fibrocirrhotic
the segmental or lobar boundary. Aerated lung is re- changes in the apical parenchyma. Any upper lobar
placed by fluid and cellular infiltrate. Residually aerated segme ntal opacity persisting for weeks sho uld raise sus-
alveoli may appear as small "foamy" lucencies (pos itive picion of tuberculous pneumonia. particularly in at-risk a
air alveologram) and residual air within the bronchi gro up s of individ ual s. Fig. n. 7a
forms a pattern of branching radiolucent channels (posi-
tive air bronchogram) within the consolidation. Usually Bronchioloalveolar Carcinoma
the anatomic shape of the segments remain s unchanged So me bronchial carcinomas, es pecially those of bronchi- Pulmona
although a slight volume increase can occur in entiti es o loalveola r type, spread within the alveo li of a lung lobe Pulmona
such as Klebsiella pneumonia producing a convex border or segment and may be indistingui shable from pneu- which oc
w ith the adjacent normal lung. monic consolidation. lower 10
requisite
pulmona
2. Lobar and Segmental Opacification 305
lpres-
Fig. 13.S (T coronal reformat shows partial rig ht lower lobe Fig. 13.6 Right upper lobe consol idation with a minor degree of
consolidation with loss of definition of the right hemidiaphragm. associated atelectasis leading to slight superior displacement of
the right minor fissure.
cocci or
Because
alveolus
al boun-
cause of
jer, even
segment
he upper
es. Often
ercu losis
Icirrhotic
ler lobar
'aise sus-
In at-risk a b
Fig. 13.7 a, b Pneumonic consolidation involving the anterobasalleft lower lobe.
bronchi- Pulmonary Infarction Lobar and Segmental Atelectasis

lung lobe Pu lmonary infarcts appear as subtl e segmental opacities
m pneu- w hi ch occur predominantly in the subple ural lung of the • Absorption atelectasis (obstructive atelectasis) in
lower lobes. Left vent ricu lar failure usua lly is a pre- which there is in itial occlusion of the bronchial
requisite for the development of infarction following lumen followed by absorption of air in the distal lung:
pu lm onary embo lism. Airway obstru ction may be caused by tumor, mucus
plugs, foreign bod ies, inflammatory bronchial nar-
• Fig. 13.8 a, b Right middle lobe pneumonia. The right heart border is not visualized.
b
•
Fig. 13:
Fig.13 .9 Pneumonic consolidation involv- row

ing the anterior segment of the right upper by I
lobe lies adjacent to the minor fissure. syn(
laps
late:
• Rela
this
pnel
ing
may
the I
Volume
graphic
• Righ
trian
peric
• Righi
erati.
• Righi
tionl
13.15
shape
bralll
• Left l
tion I
Fig.G.
• Lingu
loss c
Atypical
of isolatf
fibrous a
2. Lobar and Segmental Opacification 307
b a b
Fig. 13. 10a, b Right middle lobe pneumonia.
rowing or occlusion, or extrinsic compression (e. g.,

er by lymph node enlargement in "right middle lobe"
syndrome). In most cases there is incomplete col-
la pse of the involved segment or lobe because of col-
lateral air drift thro ugh the pores of Kahn.
• Relaxation atelectasis (compression atelectasis): In
this case lung expansion is prevented by a
pneumothorax or large pleural effusion with result-
ing pu lmonary atelectasis. Thi s form of atelectasis
may persist for a short time following aspiration of
the effusion or pneumothorax.
Volume loss in a lobe tends to Ilave a specific radio-

graphic appea rance (Fig. 13.12 ):
• Right upper lobe atelectasis is manifest as a wedge!
Fig. 13. 11 Evolution of round atelectasis (from Hanke and
triangular-s haped opacity lying adjacent to the su-
Kretschmar 1983).
perior mediasti num (Fig. 13.14).
• Right middle lobe ate lectasis is associated with oblit-
eration!" loss" of the right card iac border.
• Right and left lower lobe ate lectasis lead to oblitera- Complete atelectasis appea rs radiographi cally as a
tion!" loss" of the respective hemid iap hragm (Fig. homogeneous shadow but initially some portions of the
13.15a, b) and in left lower lobe ate lectasis, a wedge- segment may still be ae rated. The following rad io-
shaped opacity may be visible in the left paraverte- graphic features characterize atelectasis:
bral/retroca rdiac region. • The shape and location of the opacification (see
• Left upper lobe atelectasis leads to "hazy" opacifica- Fig. 1.33).
tion of the left hemithorax (Figs. 13.16a, b, see also • Concavity of the segmental margin. This is clearly ap-
Fig.6.24a-c). preciated only at sites where the segment borders on
• Lingular segment atelectasis leads to obliterationJ the lobar boundary or interlobar fissure.
loss of the left card iac border. • Hyperexpansion of adjacent lung characterized by
decreased vascu lar markings and local hypertran-
Atypical appearances may be due to collateral aeration sradiancy.
of isolated boundary zones or may occur in cases where • Displacement of interlobar fissures and vascu lar
fibrous adhesions prevent uniform vol ume loss. shadows.
Right upper lobe atelectasis Left upper lobe atelectasis
Fig. 13
mu(u~
Right middle lobe atelectasis left lower lobe atelectasis Right lower lobe atelectasis
Fig. 13.12 lobar atelectasis.
a b
Fig . 13. 13 a, b Right upper lobe consolidat ion and at electasis due to endobronchial tumor. There is superior djsplacem~nt of the right
minor fissure and the major fissure is displaced anteriorly.
b
2. Lobar and Segmenta l Opacification 309
Fig. 13.14 Right upper lobe atelectasis due to an endobronchial

mucus plug.
a
b
Fig. 13 .1Sa. b Right lower lobe atelectasis . There is opacifica-
tion of the right cardiophrenic angle with ~loss" of t he rig ht
hemidiaphragm.
b
f the right
<l Fig. 13.16a, b l eft upper lobe atelectasis secondary to centra l

b bronchial carcinoma .
• Ipsil ateral shift of the medi astinum, elevation of th e d ram a, w hich occas iona lly shows fl occul ent ca lcifica- I
hem idiaphragm, na rrow ing of the in te rcostal spaces, tion, hamartomas, and amyloid tumo rs are compa ra- I
and transmedi as tinal herni ati on of th e opposi te lung. tive ly rare. r
These changes are see n w ith lobar or compl ete pul - II
monary atelectas is. Endobronchial Mucus Plugging t
This is ch aracte ri stically see n in severe asthma and in P
Central Bronchial Carcinoma pat ients w it h superimposed Allergic Bro nchopulmon ary n
Lobar or segmental atelectasis may be associated with Aspergill osis (A BPA).
ipsilatera l hila r enlarge ment ± medi astinal ly mph node T
enl arge ment. Bronchial Rupture and Hematoma ~
Severe thoracic inj uri es may ruptu re a main or lobar a
Endobronchial Metastases bronchu s w ith submucosal hematoma and di stal atelec- a
Breast carci noma and oth er tu mors occas ionally tas is. (I
metastasize to the wa ll of a lobar or segmenta l bron chu s

(see Fi g. 6.34 a, b ). Inflammatory Bronchial Strictures and Extrinsic F.
Benign Endobronchial Tumors

Compression
.,F.
Bro nchi al carc inoid is the most commo n benign tumor Infl ammatory bran chi al strictures may be seen in e nti - dl
to di splay end obron chial growth and lead to dista l ties such as tubercul ous infection and Wegene r's m
atelectas is. A small number of cases w ill deve lop bron - granul omatosis.
ch oceles di sta l to th e obstru cting tumor and branching The right middl e lobe bron chus is particula rly sus- P.
opaciti es may then be the predominan t radi ograph ic ceptible to co mpression by adjace nt tube rc ulou s lymph Ei
finding. Other end obronchial tumors incl ud ing chon- nodes resul ting in d ista l atelectasis. Pi
Tt
st:
se
Pu
3. Opacification which does not Conform to Anatomic Boundaries Pa
ail
tiz
to
Inhomogeneous and Regionally Table 13.3 Pulmonary opacification not conforming to lobar
and seg menta l bou ndaries Pu
Confluent Air Space Opacification Di l
Inflammatory
• Bronchopneumonia de
• As pi ration pneumonia mE
• Diagnostic Approach • Tuberculous pneumonia Gr;
• Fun gal pneu mon ia (sem i-invasive pulmonary asperg illosis)
• (hronic eosinophilic pneumonia
ibr
These are poorly-defined nonsegmental areas of con-
• Organizing pneu monia (OP) COl
solidation w hich may contain air bronch o- and air alve-
• Hypersensitivity pneumonitis
olog rams. The comm onest cause of nonsegmental con - • (hurg- Strauss allergic gra nulomatosis Ch,
solidation is bronchopneumonia, w hich is readily di ag-
Edema and hemorrhage Ch,
nosed w hen cl assi c prese nta tion is com bined w ith
• Pulmona ry edema mo
radi ographi c findin gs of patchy o r conflu ent air space • Pul monary hemorrhage in Wegener's granulomatosis and eff!
co nsolidation. antiglomeru lar base ment membrane disease
vas
Neoplastic
• Bronchioloalveolar carcinoma
Pul l
• Differential Diagnosis (Ta ble 13.3) • Primary pulm onary lym phoma and lun g involvement in
systemic lym phoma Bot
pho
Acute Bronchopneumonia Miscellaneous
• Ra diation pneumonitis spa l
This di sease is characterized by patchy ai r space
• Silicos is
shadowing characteri stica lly invo lving the mid-to- Iowe r
Bilateral symmetric opacification Rad
lung zones. Acute bron chopneumonia is usually d ue to
• Pulmonary edema and hemorrhage Air
bac teri al infection (Fig. 13.17).
• Infection includ ing pneu mocystis pneumonia the
• Hya line membrane disease in the newborn tis. I
• ARDS deg.
• Alveolar proteinosis
3. Opacification which does not Conform to Anatomic Boundaries 311
ca- Aspiration Pneumonia

.ra- Aspiration pneumonia characteristically involves the de -
pendent portions of the lung. most commonly the lower
lobes. Right lung involvement is more freque nt due to
the more vertical course of the bronchus intermedius.
I in Aspiration pn eumonia may be complicated by pulmo-
ary nary abscess formation.
Tuberculous Pneumonia
Multifocai areas ofbronchocentric consolidation may be
.bar a manifestation of endobronchial spread of tuberculosis
lec- and there may be associated micronodular shadowing
I consistent with a cellular bronchiolitis
Fungal Pneumonia
Fungal pneumonias and particularly semi-invasive
aspergillosis (Fig. 13.18) in older individuals with a mild
~nti degree of immunocompromise due to co- morbidities
a
lef's may manifest as patchy air space consolidation.
sus- Pulmonary Edema

mph Early-stage alveolar edema may have an inhomogeneous
patchy distribution in the mid-to-Iower lung zones.
There are characteristically features of associated inter-
stitial edema with peribronchial cuffing and interlobular
septal thicke ning.
Pulmonary Contusion
Patchy, confluent opacities representing sites of intra-
alveolar edema and hemorrhage are seen in the trauma-
tized lung. Pulmonary contusions typically resolve in 3
to 6 days except when infection supervenes.
lobar b
Pulmonary Hemorrhage Fig. 13.17 a, b Multifocal airspace consolidation not conforming
Diffuse pulmonary hemorrhage is associated with un - to segmental or lobar boundari es .
derlying di sease entities including Antiglomerular Base-
ment Membrane Disease (AGBMD ) and Wegener's
Granulomatosis. Initial multifocal opacification in a per-
105i5) ibronchovascular distribution may progress to areas of
confluent consolidation.
Churg-Strauss Allergic Granulomatosis

Chest radiographs may show transient. recurrent pneu-
monic infiltrates in addition to pericardial and pleural
5 and effusion in patients with this systemic necrotizing
vasculiti s.
Pulmonary Neoplasia
tin
Both bronchioloalveolar carcinoma and pulmonary lym-
phoma may be manifest radiographically as patchy air
space consolidation in a peribronchial distribution.
Radiation Pneumonitis and Fibrosis

Air space consolidation characteristically conforms to
the radiation portal in radiotherapy-induced pneumoni-
tis. Consolidation over time may organize leaving some
degree of interstitial fibrosis (Fig. 13.19). Fig. 13.18 Asperg ill oma: Mycetoma with air crescent is see n
within rig ht upper lobe cavity.
a
Fig.13. 19a- c Radiotherapy-induced pulmonary fibrosis. Chest a
radiograph (a) shows right-sided pulmonary opacification not
conforming to lobar or segmental boundaries. Patchy sclerosis in
the proximal diaphysis of the right humerus is characteristic of
old bone infarct. Axial CT image displayed at lung windows (b)
shows pulmonary change consistent with fibros is in the right
upper zone. CT displayed at bony windows (c) shows bone infarct
(
in rig ht proximal humerus.
Sarcoidosis (Fig. 13.20)

See Chapter 3, p. 91.
Adult Respiratory Distress Syndrome

See Chapte r 8, p. 208.
Bilateral Symmetric
Hazy Opacification
• Differential Diagnosis
• Bilateral posterior pleural effusio ns in a supine
a patie nt (Fig. 13.21., b ).
• Hyaline membrane disease-Acute respiratory
di stress sy ndrome in the newborn (Fig. 13.22),
• Adu lt respiratory distress syndrome- Diffuse alveo lar
damage (Fig. 13.23).
• Pulmonary infection, ede ma, hemorrhage
(Fig. 13.24),
• Alveo lar proteinosis (Fig. 13.25 ),
Fig. 13.20a. b Sarcoidosis. The chest radiograph (a ) shows bi·

lateral hilar and med iastinal lymph node enlargement with areas
of pulmonary consolidation. CT shows bilatera l hilar and medi-
astinal lymph node enlargem ent with areas of consol idation con-
b sistent with the "alveolar variant of sarcoidosis.
ft
3. Opacificat ion w hich does not Conform to Anatomic Boundaries 313
b
b
Fig. 13.21 a, b Pleural effusions in supine patient: Hazy opacifi-

cation of both hemithoraces on AP supine projection (a) is due t o
bilateral pleural effusions and underlying pulmonary atelectasis
a (b).
Fig. 13.22 Hyal ine membrane disea se with

bilateral Mground-glass opacification~ in a
preterm infant. Air bronchograms are vis-
c ible.
~olar
NS bi-
areas
medi- Fig.13.23 Adult respiratory distress syndrome in acute pan-
1 can· creatitis. Initial chest radiograph shows diffuse. bilateral pulmo-
nary opacification.
Fig. 13.24 Noncardiogenic pu lmonary edema

in a patient with renal impairment.
4.
. 1
Opa
nai l
naIl
for t
mor
med
thy r
Fig. 13.25 Alveolar proteinosis. Chest radio-

gra ph shows "hazy~ opacification of both lungs
with associated interstitial th ickenin g in patient
with alveolar proteinosis.
Pu
tut
wi1
Azy
can.
atel.
Va
4. Opacification involving the Upper Zone and/or Apicomediastinal Angle 315
a
4. Opacification involving the Upper Zone and/or
Apicomediastinal Angle
• Diagnostic Approach • Differential Diagnosis (Fig. 13.26. Table 13.4)
Opacification of the lung apex and upper paramediasti- Vascular and Mediastinal Lesions
nallung may be due to pulmonary. pleural. or mediasti-
nal disease. Pulmonary diseases showing a predilection Vascular Ectasia
for the upper lobe include tuberculosis, ABPA, and pul - Ectasia of superior mediastinal vessels leads to medi-
monary Langerhans cell histiocytosis (PLCH). Superi or astinal widening with a curved, sharply defined lateral
mediastinal widening may be due to vascular ectasia, border. Dilatation and elongation are particularly com-
thyroid goiter, or mediastinal lymph node enlargement. mon in elderly patients and may involve the left brachio-
cephalic vein, subclavian vein, superior vena cava, and
innominate artery. Computed tomography will confirm
the vascular ectasia when there is diagnostic uncer-
tainty.
g5
!nt Fig. 13.26 Upper zone
opacification .
Fibrocirrhotic
Pulmonary Tuberculoma tuberculosis. Aspergilloma Apical emphysema
tuberculosis apical pleural
with cavitation thickening
Azygos lobe Superi mposed Upper lobe atelectasis Pancoast tumor

consolidation! transverse process
atelectasis and costotransverse
articulation
Vascular ectasia and dilatation Thyroid gOiter Mediastinal mass lesions

(lymph node enlargement,
teratoma, thymic tumor, etc.)
Table 13.4 Upper zone and apicomediastinal angle opacifica- Aortic/Great Vessel Aneurysm
tion Aneurysmal dilatation of the aortic arch may produce a
Mediastinal large mediastinal density, genera lly with a convex
Vascular lateral border on the posteroanterior (PA ) chest rad io-
• Arterial and venous ectasia/ dilatation gra ph (see also Chapter 11. p.283 ). Aneurysma l dilata-
• Aortic aneurysm tion of a subclavian/anomalous right subclavian artery
Nonvoscular may lead to unilateral superior mediastinal wide ning.
• ThyrOid goiter and thyroid carcinoma
• Thymic hyperplasia and thymic tumors Retrosternal Goiter and other Mediastinal Soft Tissue
• Lymph node enlargement
• Benign cystic teratoma and germ cell tumors
lesions
• Peripheral nerve sheath tumors There is widen ing of the superior mediastinum and the
• Bronchogenic cyst trachea may be narrowed or displaced. Thyroid nodul es
• Lymphangioma (cystic hygroma) may show flocculent calcifi cation. See also Chap te r 11,
Pulmonary and Pleural p.285.
• Upper lobe pneumonia and atelect asis
• Upper lobe tuberculosis
• Bronchial carcinoma including Pancoast tumor Pulmonary and Pleural
• Aspergilloma
• Allergic bronchopulmonary aspergillosis Upper lobe Pneumonia
• Pulmonary Langerhans cell histiocytosis Pneumonia involving the apical segment of the right
• Sil icosis
• Apical fibrosiS in ankylosing spondylit is upper lobe or the apicoposterior segment of the left
• Apical pleural thickening upper lobe appears as a triangu lar paramediastinal
Miscellaneous opacity. Consolidatio n in the ante rio r segment of the
Fig. 13.l
• Azygos vein within fissure (Fig. 13.30) right upper lobe abuts the minor fi ssu re. upper Ie
Upper lobe Tuberculosis (Fig. 13.27)

Tuberculous infection sho uld be excluded in all cases of
persisting upper lobe consolidation (see a lso Chapter 3. Bronch
p. 72). Bronch
of the
Fig. 13.27 Right upper lobe tuberculo-
chest r
sis. cent ril
from a
distal
13.28 ).
SiliC05i~
Silicoti.
upper I
cating ~
lobes.
Pulmor
EarlY-51
upper-I
bases (:
Mucoid
Conge n
the ap i(
lobe. n
w ith n
branch!
All ergic
mucus
coianizi
4. Opacification involving the Upper Zo ne and/or Apicomed iasti nal Ang le 317
'e a
vex
lio-
Ita-
ery
g.
the
Jles
11 .
.ght
left
inal
the Fig.13.28 Radiation pneumonitis posttreatment of left hilarl Fig.13.29 Apical pleural thickening.
upper lobe bronchial carcinoma.
Bronchial Carcinoma
Bronchial carcinomas may occur in the superior su lcus
of th e lung and infiltrate locally (Pancoast tumor ). The
chest radiogra ph may demon strate destruction of adja-
D'
ce nt ribs. More commonly. bronchial carcinoma arising
from and occl uding the upper lobe bronchus leads to
distal upper lobe consolidation and atelectasis (Fig.
13.28).
Silicosis
Silicotic nodules sometimes may be concentrated in the
upper lobes. Progressive massive fibrosis (PM F) compli-
cating silicosis has a marked predilection for the upper
lobes.
Pulmonary langerhans Cell Histiocytosis

Early-stage nodular PLCH cha racteri sti cally involves the
upper-to-mid zones with relative sparing of the lung
bases (see also Chapter 6. p. 154 ).
Fig. 13.30 Pleural line associated with an azygos lobe.
Mucoid Impaction (Bronchocele Formation)
Congenital bronchial atresia occurs most commonly in
the apicoposterior segmental bronchu s of the left upper Apical Pleural Thickening
lobe. The ai rway di stal to the atresia is dilated and filled An apical pleura l peel may extend to involve the medi-
with mucus and appears as an elongated. partia lly astinal pleura and reach a thickness of several millime-
branched opacity in the left upper lobe (bronchocele). ters (Fig. 13.29).
Allergic bronchopulmonary aspergillosis also leads to
mucus plugging of bronchi and characteristica lly Azygos lobe and Fissure (Fig. 13.30)
colonizes dilated upper lobe bronchi. See Chapter 1. p. 14.
318 13 Radiographic Signs and Diffe re ntial Dia gnosis
5. lower lung and Cardiophrenic Angle Opacification Pne umc

Branch(
lung an
w ith ty
Lower lung and cardi oph renic angle opacification may Table 13.5 Lower zone and cardiophrenic angle opacification
solidati.
right m
res ul t fro m a variety of pulmonary, pleu ral, d iaphrag-
matic, and mediastina l processes.
Pulmonary man ia. I
• Vascular crowding cardiac
• Plate atelectasis
• Lower lobe consolidation and atelectasis
Lower II
• Differential Diagnosis (Fig. 13.31 , Tab le 13.5 ) • Right middle lobe consolidation and atelectasis ipsilate l
• Basal lung edema
• Bronchopulmonary sequestration Pulmon,
Crowding of Basal Vessels
During ex piratio n and in cases w here inspiratio n is re- Pleural-diaphragmatic Pulma n.
• Pleural effusion the gre;
stricted due to obesity or ascites. compression of the • Pleural thickening
basal pulmona ry vessels occurs, causing a bil ateral in- charact€
• Pleural tumor
crease in basal vascu lar markings. • Transdiaphragmatic hernias
se ptal II
• Tumors of the diaphragm progres~
Plate Atelectasis (Fig. 13.32) Me diastinal

• Epicardia l fat Brancho
These linear opacities, w hich may be up to 3 m m in
w idth and 10 em in length, are usua lly seen coursing • Pericardial cyst Brancho
• Mediastinal tumors located
ho rizo nta lly in the lower zones. There may be associated • Paravertebral abscess and osteophyte formation they ma
elevatio n of the ipsilateral hem idiaphragm.
may rea
graph cc
ter 2, p. ~
Plate atelectasis Right middle lobe Lower lobe Effusion or ple ural thickening
atelectasis atelectasis in the lateral costophrenic angle
Pericardial cyst
- Left ventricular - Esophagea l dilatation - Aortic ectasia
aneurysm - Partial eventration of - Scimitar syndrome
- Epicardial fa t pad the hemidiaphragm - Bronchopulmonary seq uest ration
- Hiatus hernia
Fig. 13.31 Basal and cardiomediastinal opacification.

5. lower lung and Cardiophrenic Angle Opacification 319
Pneumonic Consolidation
Bronchopneumonia commonly develops in dependent
lung and is characterized by patchy basal opacification
with typical acinar shadows of peri bronchiolar con-
solidation. Classic lobar pneumonia may also involve the
right middle and lower lobes as may aspiration pneu-
monia. Right middle lobe change appears as a right para-
cardiac opacity that obscures the right cardiac border.
Lower lobe consolidation leads to loss of visibility of the
ipsilateral hemidiaphragm.
Pulmonary Edema
Pulmonary edema is often basal in distribution due to
the greater hydrostatic pressure in these regions. It is
characterized by loss of vessel definition, interlobular
septal thickening. and peribronchial cuffing and it may
progress to air space shadowing (alveolar edema).
Fig. 13.32 Basal plate atelectas is in a postoperative patient.
Bronchopulmonary Sequestration
Bronchopulmonary sequestrations are most commonly
located in the vertebrophrenic angle. Radiographically, Basal Pleural Effusion (Fig. 13.33 )
they may be manifest as homogeneous opacities that In the upright position, the effusion gravitates toward s
may reach up to 10 em in diameter. The lateral radio- the lower zones with loss of both the posterior and
graph confirms their posterior location (see also Chap- lateral costophrenic angles. The effusion slopes super-
ter 2, p. 50). iorly towards the lateral chest wall and has a co ncave in-
terface with the lung.
Fig. 13.33 left basal pleural effu-

sion.
Basal Pleural Thickening

Basal pleural thickening may lead to blunting of the co-
stophrenic angles. There may be associated tenting of
the he midiaphragm towards the lung. Ultrasound will
differentiate pleural thickening from an effusion.
Diaphragmatic Hernias
Bochdalek and Morgagni herniae. particularly when
they co ntain only peritoneal fat, may be manifest radio-
graphically as soft tissue opacities in the lowe r zo nes.
Epicardial Fat Pad

The ca rdiophre ni c angle may be obliterated by fat. espe-
cially in obese individuals. cr demonstrates negative at-
tenuation va lues cha racteristic of lipid.
Pericardial Cyst
Pericardial cysts are well-defin ed relative ly low density
opacities that are a frequent radiograp hic finding and
• which fill the ca rdiophreni c angle. CT shows well-de-
fined les ions of fluid attenuation.
Paravertebral Abscess and Osteophyte Formation

A paravertebral abscess may be secondary to septic or
tubercu lous (cold abscess) di scitis and vertebral osteo-
myelitis. Lateral paravertebral osteophytes are as-
sociated with degenerative intervertebral disk change in
the lower thoracic spine (Fig. 13.34).
Fig. 13.34 a, b Round opacity in the right cardiophrenic angle is

b due to a large bridging osteophyte in the lower thoracic spine .
6. Pulmonary Nodules
Fig. 13.3E
• Diagnostic Approach actually frequently results from the summation of von Reck
many foci intercepted by the x-ray beam (Heitz-
The solitary pulmonary nodule is discussed in Chapter 6. man 1993 ).
p.149.
Fig. 13.3i
Superimposed extra pulmonary lesions including skin rotated v
Multiple pulmonary nodules tumors. su bcutaneous abnormalities. pleural plaques.
Pulmonary nodules are round opacities most commonly and bony enostoses may mimic the presence of lung
of soft tissue density that frequently have well-defined nodules on the chest radiograph (Figs. 13.35-13.37.
margins. Individual nodules range from < 1 to several 13.45. 13.46). Computed tomography is occasionally
millim ete rs in size. necessary in these cases to make the differentiation. fine d
They may be subclass ifi ed according to size: The pathological correlate of nodular opacification is ing n
• Macronodular opacities: 3-25 mm in diameter. variable: • Inter.
• Micronodular (m iliary ) opacities: less than 3 mm in • Alveolar-based nodules (Tab le 13.6): Focal opacities nod,
diameter (L. milium: millet seed). A miliary opac- may result from airspace filling with fluid. exudate. divid
ity on the radiograph may not correspond to a blood. or neoplastic tissue. These infiltrates must be gene
s ingle pulmonary focu s even when foci of similar 5-7 mm in diameter before they are vis ible on the cent
size can be seen hi stologica lly. A miliary pattern chest radiograph. These nodules may be poorly de-
6. Pulmo nary Nodules 321
Fig. 13.35 Rou nded opacity on

:0- the frontal chest radiograph. The
lateral view demonstrates the loca-
of tion and shape of the opacity (skin
vii i tumor, ri b enostosis. pulmonary
nodule. interlobar effusion,
segmental infiltrate, pleural tumor)
(from RObe).
,e n
io-
3.
)e-
at-
,ity
md
je-
or
~o-
e is
,e.
Fig. 13.36 Multiple nodular lesions projected onto the lu ng in

of von Reckli nghausen's (type 1) neurofibromatosis.
itz-
Fig . 13.37 a, b Bone island/enostosis in the right clavicle. The

kin rotated view confirms the location of the lesion. b
les,
109
.37,
lily
fin ed due to the ir irregular interface with surround- Table 13.6 Radiographic features of alveolar shadowing (from
:1 is ing normall y ae rated alveo li. Felson)
• Interstitial-based nodules: Gra nul omata and tumor 1. III-defined foca l opacification
:ies nodul es may be interstiti al in location. Th e size of in- 2. Confluent opacification
!te, div idual nodu les is very va riab le but these les ions are 3. Segmental or lobar distribution
be ge ne rally sharply demarcated w ith res pect to adja - 4. Butterfl y pattern in the perihilar lung
cent ae rated alveo li. 5. Air bronchogram and ai r alveologram
the
6. Peribronchiolar (acinar) nodu lar opacification
de-
Table 13.7 Pulmonary nodules • Differential Diagnosis (Tab le 13.7) In!

Extrapulmonary opacities
• Skin lesions: nipple, neurofibromas Neoplasia Ml
• Bony enostoses Py'
• Pleural plaques fin,
Metastases
• Interlobar effusion
These well-defined lesions show cons iderable variat ion thr
Pulmonary nodules in both individual size an d number (Fig. 13.38).
Neop/ostic Metastases from thyroid ca rcinoma may produce a fine ACI
• Pulmonary metastases miliary pattern of nodularity w hile re nal ce ll carcinoma Set
• Kaposi's sarcoma
• Malignant leiomyomatosis
is characte ri stically associated with large so ca lled "can-
nonball" metastases. Metastases from osteosarcoma or Mil
Infection He
chondrosa rcoma will show ossification or calcification,
• Miliary tuberculosis
• Endobronchial spread in 2° tuberculosis re spectively, w hile metastases from sq uamous cell pri- finl
• Histoplasmosis, blastomycosis, candidiasis. coccidioidomy- mary tumors have a tendency to cavitate.
cosis Se,
• Acute invasive aspergillosis Co.
Kaposi Sarcoma
Connective Tissue Disorders and Vasculitides See Chapter 3. p.98. brc
• Rheumatoid nodules od.
• Wegener granulomatosis
Malignant leiomyomatosis (Fig. 13.39) cas
Pneumoconioses This is a rare hamartomatous lung di sease arising from pat
• Silicosis bra
• Coal worker's pneumoconiosis
the vascular smooth-muscle cells of bronchi and alve-
olar septae. The di sease can lead to respiratory failure wit
Vascular ing
and death within a few years. Pleural involvement is
• Multiple pulmonary arteriovenous malformations
• Hemosiderosis frequent. resulting in a chylous effu sion. The chest radio- Ope
graph shows multiple confluent opacities 5-9 mm in di-
Hypersensitivity and Idiopathic
amete r with an acco mpanying honeycomb pattern. His!
• Pulmonary Langerhans cell histiocytosis
• Sarcoidosis See
• Hypersensitivity pneumonitis
Pm
Coa
Fig. 13.38 Multiple pulmonary See
metastases from known colon car-
cinoma.
SUic
The
wei
bin{
sem
Con
Rhe
The
and
cuta
We!
Typ.
freq
coni
The
phil
Vast
Mull
See I
6. Pulmonary Nodules 323
Infection
Multiple Pulmonary Abscesses and Septic Emboli

Pyogeni c abscesses present as single o r mul tiple. ill-de-
fined focal opacities up to 2 em in diameter scattered
throughout the lung (see Figs. 13.55 a. b. 13.56).
Acute Invasive Aspergillosis

See Chapter 3. p.81.
Miliary Tuberculosis
Hematoge nous spread of tuberculosis leads to diffuse
fine nod ul ar shadowing (mi li ary pattern ) (see Fig. 13.40).
Secondary Pulmonary Tuberculosis

Coarse. confluent acinar shadows are see n in endo-
bronchial spread of tuberculosis, w ith multi ple aci non -
odular opacities 3-6 mm in diameter coalesci ng to form
caseous foci of tuberculous pneumonia. A finer nodular
patte rn in seco ndary tuberculosis also indicates endo-
Fig . 13.39 Malignant leiomyomatosis confirmed at autopsy.
bronchial spread ofTB but with cha nges predominating
w ithin the bronchioles (cellular bronchiolitis). CT find-
ings are of centrilobular nodules and branching linear
opacities.
Histoplasmosis
See Chapter 3. p.84.
Pneumoconiosis
Coal Worker's Pneumoconiosis

See Chapter 5. p. 140.
Silicosis
The nodular form of silicos is is characterized by multiple
well-defined nodul es 1- 10 mm in diameter. often com-
bined with pulmonary fib rosis and cicatricial emphy-
se ma.
Connective Tissue Disorders and Vasculitides
Rheumatoid Nodules
These appear as subpleural nodules 3-7 mm in diamete r Fig. 13.40 Chest radiograph shows bilateral fin e nodular
and their size and numbe r wax and wane with the sub- shadowing.
cutaneous nodul es and with systemic disease activity.
Wegener Granulomatosis Hypersensitivity and Idiopathic

Typica lly. there are multiple nodul es or ma sses th at
frequently cavitate. The patients usually are qui te ill and Hypersensitivity Pneumonitis
co ncomitant sinusitis and hema turia may be presen t. Diffuse nodular shadow ing may be seen in the subacute
The diagnosi s is based on positive ANCA (a nti- neutro- stage of hyperse nsitivity pneumonitis.
philic cytoplasmic antibody ) titers.
Sarcoidosis (Fig. 13.41 )
Vascular The miliary stage of sarcoidosis is occasiona lly manifest
as diffuse nodul ar opacification w hich is most marked in
Multiple Arteriovenous Malformations the peri hilar lung. Hilar and mediastinal lymph nod e e n-
See Chapter 2, p. 61. large me nt is a frequent associated finding.
Pulmonary Langerhans Cell Histiocytosis

Radiographs in the granul omatous stage of this disease
show multiple. bilaterally sym metric pulmonary nodu-
les 1-10 mm in diameter, w hich are most numerous in
the upper zo nes and w ith re lative spa ring of the lung
bases.
-.6
Fig . 13.41 Sarcoidosis with bilateral hilar lymph node enlarge-
ment and fine nodular shadowing in the perihilar lung bilaterally. Fig. 13
1 Pr
2 Al
3 In
4 Br
5 PI
6 K(
7. linear Shadowing (Tables 13.8.13.9)
Table 13. 8 Vascular shadows in the lung Pulmonary arterial and ve nous line shadows give the Chest
pulmonary ma rkings wh ich are see n on the normal
• Normal pulmonary vascular markings
• Pulmonary congestion
chest radiogra ph. Vesse ls w hic h normally are below the Media
• Pulmonary plethora threshold of radiographic resolution become visible This Ii
• Atelectasis with "crowding" of pulmonary vessels when dilated leadi ng to an increase in linear markings. half o·
Thi s is observed in cardiogenic pulmonary edema and in orly t<
pulmonary plethora.
Table 13.9 Linear opacification Vascular markings may appea r increased when they Manul
Chest wall are crowded due to pulmonary ate lectasis. This "crowd- The c(
• Medial border of scapu la ing" of vesse ls is see n at the lung bases on normal ex- vertic;
• Manubrium sternum piratory views and in elevation of the hemidiaphragm. of the
• Rib companion shadows Large em physemato us bullae may also compress the poros i
• Clavicular companion shadow adjacent lung parenchyma and lead to vascul ar crowd-
• Extrapleural fat deposition
• Skin folds ing. Clavid
Line slladows are homoge neous linea r or band-like The UI
Pleura opacities that are sharply del inea ted with respect to ad- band-I
• Pleural reflections jacent aerated lung. They have sharper margins than repres
• Interlobar f issure, azygos fissure
• Linear pleural fibrosis/scarring
vascular shadows and are frequently so litary. beam.
• Pneumothorax Line shadows may be due to (Figs. 13.42. 13.43 ):
• Pneumoperitoneum • Chest wa ll stru ctures projected onto the lung Rib Co
• Accessory diaphragm • In terlobar fissures viewed tangentially Acorn
• Pulmonary scarring/fibrosis ri or be
Pulmonary
• Atelectasis • Disco id ate lectasis subela·
• Parenchymal bands • Thickened interlobular septa (Kerley A and B lines) the rib
• Bronchiectasis • Thi cke ned bronchial walls med i a~
• Kerley A lines guish i
• Kerley B lines
• Carcinomatous lymphangitis
wavy (
lung p.
7. Linear Shadowing 325
ase 7
ju-
; in
109
5_-
Hge-
rally. Fig.13.42 linear opacification (from Teschendorf). Fig.13.43 Other causes of linear opacification (from Teschen-
1 Pneumothorax 7 Apical pleural thickening dor!).
2 Atelectasis 8 Apicohilar strands of fibrous tissue , Axill ary fold 7 Anterior junction line
3 Interlobar fjssure 9 Kerley A lines 2 Skin fold 8 Azygoesophageal stripe
4 Bronchi ectasis 10 Pleural reflection at the major 3 Sternocleidomastoid muscle 9 Paravertebral stripe
5 Plate atelectasis fissure 4 Rib companion shadow 10 Para-aortic stripe
6 Kerley B lines l' Pulmonary parenchymal bands! 5 Clavicular com panion 11 Medial border of
scarring shadow scapula
6 Posterior superior junction '2 Extra pleu ral fat
line deposition
! the Chest Wall Structures Projected onto the Lung

rmal
v the Medial Border of the Scapula (Fig. 13.44 )
.sible This line shadow projects symmetrically onto the lateral
:ings. half of the upper-to- mid zones, It may be traced inferi-
ndin orly to the angle of the scapu la.
they Manubrium Sternum

owd- The cortex of the manubrium sternum is projected as a
11 ex- vertical stripe ove r the upper mediastinu m on both sides
agm. of the trachea. This stripe may be prominent in osteo-
;s the porosis.
'owd-
Clavicle Companion Shadow
d-Iike The upper border of the clavicle is associated with a
to ad- band- like shadow approximately 4 cm in width and this
than represents the overlying skin seen tange ntial to the
beam.
):
Rib Companion Shadow
A companion shadow is usually seen at the poste roinfe- Fig. 13.44 Vertical line shadow produced by the medial border
of the scapula.
riar border of the left 2nd rib; this correspo nd s to the
subcl avian artery. This shadow is not strictly parallel to
ines) the rib but is continuous medi ally with th e supra-aortic
mediastinal shadow. Its smooth margins serve to di stin-
guish it from an apica l pleural cap, which generally has a
wavy contour and shows tent- like exten sions into the
lung parenchyma.
Extrapleural Fat Deposition Platl

Fat deposition superficial to the parietal pleura may ap- Plat,
pear as a chest wall companion shadow. This is most ity 1
conspicuous along the lateral chest wall. ally
upw
Skin Folds curs
Skin folds are seen most frequently in cachectic patients and
who are imaged in the supine position. They appear as ateh
vertical, sharply defined linear densities. The lines often thOl
transcend the lung boundaries and this feature helps to It IT
distinguish them from pleural lines. (Fig.
adja
linear Opacities of Pleural Origin
Line.
Interlobar Fissures Dise
Interlobar pleural lines are visible in 15 to 20% of chest saw
radiographs. They are seen only when a significant part rion
ofthe fissure (i. e., several centimeters in length) is tan- pare
gential to the roentgen beam. These shadows are most whit
conspicuous when they are thickened as a result of fi-
brosis or subpleural edema (Figs. 13.45, 13.46). The
major and minor fissures are most commonly seen; in-
tersegmental fissures are occasionally visible (see Figs.
1.21, 1.25).
linear Pleural Scarring and Fibrosis

Areas of fibrosis secondary to pleural inflammation may
be drawn into strands by the motion of the pleural lay-
ers. These usually appear radiographically as vertical or
Fig.13.45 Typical oval shape of an interlobar effusion.
oblique lines.
Pneumothorax
The visceral pleura appears as a hairline shadow which
runs parallel to the chest wall in the presence of a
pneumothorax.
Pneumoperitoneum
In the presence of subdiaphragmatic free air, the hemidi-
aphragm appears as a thin, horizontal. superiorly convex
linear density.
Accessory Diaphragm
This is a very rare anomaly in which the accessory dia-
phragm appears as a sail-shaped opacity traversing the
right lower lobe. The radiographic appearance may be
mistaken for thickening of the interlobar fissure but may
be distinguished by its atypical course.
linear Opacities of Pulmonary Origin
Segmental Atelectasis
Segmental atelectasis may give a linear shadow that is
Fig.13.46 Interlobar effusion. Chest radiograph shows locu-
lated left basal hydropneumothorax and interlobar effusion. sharply defined where it borders on the interlobar fis-
sure. Segments 53, 52, and 58 most commonly give this
appearance.
7. Linear Shadowing 327
Plate Atelectasis, Fleischner Lines apicohilar linear markings are frequently seen in asso-
ap- Plate-like or discoid atelectas is appears as a linea r opac- ciation with upper lobe tuberculosis. There may be ar-
ost ity 1-3 mm in w idth and 4-10 mm in length, w hich usu - chi tectural di sto rtion w ith vascul ar and fissural dis-
ally run s horizontally in the lowe r zones and obliquely placement and cicatricial emphysema is a common as-
upward and laterally in the midzones (Fig. 13.47). It oc- sociated finding.
curs in association w ith elevation of the he midiaphragm
-nts and hypoventilation (e.g .. postoperative). Plate-like Pulmonary Encasement
i as atelectasis is a very common rad iographi c findin g. al- Pl eural neopla sia and particularly mesothelioma may
"ten though the exact mechanism of its occu rrence is unclear. infiltrate the in terlobar fi ss ures and encase the lung
s to It may relate to an infold ing of the visce ral pleura (Fig. 13.49 ).
(Fig. 13.48) or a band-like area of ate lectas is occurring
adjacent to connective tissue se pta. Bronchiectasis
Th e chest radiogra ph in bronchiecta sis occasionally
linear Pulmonary Scarring and Parenchymal Bands shows parallel linea r densiti es. w hi ch represe nt the par-
Disease processes including pneumonia, tuberculosis. all el bronchial wa ll s separated by an expa nded lumen.
lest sa rcoidosis, the pneumoconioses, and pleural inflamma- Known as "tramlines," these features are most co nspicu-
Jart t ion may lead to contractile sca rring of the lung ous in the paracardiac lung and are frequently associated
:an- parenchyma. These "scars" appear as linea r shadows w ith accentuated baso hilar markings.
lost which often radiate towards the hilum. Accentuated
f fi -
The
in-
' igs.
Fig . 13.47 Plate ate lecta sis due to hy-
poventilation.
may
lay-
II or
hich
of a
nidi-
nvex
. dia-
5 the
'y be
: may Fig. 13.48 The pleural hypothesis of plate
.1,. . .- Visceral pleura . - - Visceral pleura
atelectasis. Subsegmentallung contraction
due to bronchial obstruction leads to in-
drawing and folding of the visceral pleura,
Plate Obstructed which forms a band-like opacity on the
atelectasis bronchus chest radiograph (from Muller and Fraser
2001).
l1at is
Ir fis-
e this
328 13 Radiographic Signs and Diffe rential Diagnos is
, Kerley lin es
Kerley li nes re present thickened interlobu lar septa. Ke r-
ley B lines are most common, are up to 1 em in length,
and are seen most frequently in t he lateral costop hrenic
a ngles.
The less common Kerley A lines are th in lines up to
5 em in length which radiate from the hilum into the
• The
patt
mOl
Only a
be dial
fi ndi ng
lung especia lly into the uppe r zones. They are th inner Pasl
t han vasc ular shadows and are not b ranched. They rep- duratic
resent thicke ned interlobul a r septa in the a nterior por- proces!
tio ns of the upper lobe. A reticular patte rn is occasion- agnosi!
ally referred to as "Kerl ey C lines." iog ca r
• lymp h
The
the dia;
ha latio
Fig. 13.49 Lung encasement with linear shad owing in a patient onset,
with malignant pleural mesothelioma. sympto
• Dif
8. Reticular Shadowing
Intersti'
(Ca rdia
Vascula
• Diagnostic Approach se nsitive tha n the ches t radiograph to t he prese nce of in- bronchi
terstitial change. li nes al
Many pa thologic processes involve the in te rstitial con- The radi ogra phic features th at characte rize in tersti- lung. T
nective tiss ue of the lung. Inte rsti tial thi cke ning may be tia l lung d isease incl ude (Felso n 1966, Tab le 13. 10): tu res 0
due to ede ma, inflammato ry or neoplasti c in filtrat ion, or • The reticular patt ern refers to a fine network of mark- genic e(
fibros is. Inte rstitial fibros is is cha racterized by increased ings that may be d iffuse ly or regio nally distributed dialysis
coll agen deposit ion a nd re presents th e e nd stage of a through t he lungs. It is due to superim position of Longsta
number of d iseases. th icke ned intralobula r and inte rlobu lar septa. This edema!
The interstitium of the hea lthy lung generally forms a pattern has occasiona lly been referred to as Kerley C fib rosis
three-d im e nsiona l network that compl etely pe rmeates fin es.
the lu ng pare nchy ma. Thi s incl udes the perivenous co n- • Kerley B fi nes a re horizonta l li nes up to 1 mm in thick- Viral/M'
nective t issue, the co nnective tiss ue surrou ndi ng the ness and a pp roximately 10 mm in length, w hi ch are Reticule
bronchoarte ri al bundles, the inte rlob ular con nective seen most commonly in the lateral costophrenic an- perih ila
tissue septa, the base me nt mem bra ne of the alveoli , and gles. They represent thickened interlobula r septa in
the subp leu ral connective tissue. The perivascul a r con- t he lung periphery. Anatomic stu dies have shown Suba cul
nective tissue dimin ishes towards the periphe ry of the that interlobular septa are most numerous in the Areas 0
lung. anterior and late ral regions of the lower zones and fine reti
Interstitia l lung di sease in ma ny cases is we ll ad- the ante ri or aspect of th e uppe r lones.
va nced be fore cha nges a re visible radiographi ca lly. Thu s, • Kerley A lin es a re thin lin es up to 5 COl in le ngth t hat Pulman
it is not unco mm on to find normal chest radi ograp hs in rad iate fro m th e hilum in to the uppe r zo nes. They Pulmon
pat ie nts w ho have signifi can t cl ini ca l and spi rometri c re prese nt the thi cke ned in terlobu la r septa of t he in terstit
evide nce of rest rictive ve ntil a to ry impairment. Th in a nterior porti on of the upper lobe. They are seen septa l t,
co ll imation/high-resolution CT (HRCT) is much more m uch less freque ntly tha n Kerley B lines. the per
• The reticu lonodula r pattern refe rs to a reticu lar pat- pleural I
tern combined w it h miliary nodulation. The m ili -
Table 13. 10 Radiographic features of interstitial shadowing tary opacities are us ually due to small nodu les in Idiopath
(from Felson)
the inte rstiti um but sometimes they may represent The ch'
• Kerley A, B, and Clines a summation effect caused by intersecting line charact€
• Miliary nodules shadows. tributiol
• late radiographic signs, often appearing years after onset • Interlobar/subpleura l th ickening: Infiltration or fibro- nonspec,
of clinical symptoms
sis of the subpleural connective tissue leads to accen- is chara
• Honeycombing
• Thickened bronchovascular bundles tuation of t he interlobar fissures and accessory (Figs. 13
pleu ral li nes. Pneumo
8. Reticular Shadowing 329
• The honeyco mb pattern refers to a coarse reticula r Table 13.11 Interstitial and reticular shadowing
1. Ker- pattern that so metim es characterizes end-stage pul-
• Interstitial edema
' ngth, monary fibros is. • Acute interstitial pneumonia
l renic • Su bacute parenchymal hemorrhage
Only a small percentage of interstitial lung di sease s ca n • Pulmonary lymphangiti s carcinomatosis
up to be diagnosed on the basis of clinical and radiographic • Idiopat hic interstitial pneumonias
to the • Sarcoidosis
findings.
• Chronic hypersensitivity pneumonitis
linner Past rad iographs, if ava il able, will help determine the • Drug-ind uced pneumonitis
y rep- duration and progression of change. Determining if a • Connective-tissue associated interstitial lung disease
r por- process is acute or chronic may lim it the differential di- • Asbestosis
3.sion- agnos is. Othe r associated radiogra phic findings includ- • Hemosiderosis
• Chronic bronchitis (dirty lung)
ing ca rdiomegaly, pulmonary vascular dil atation , and • Bronchiectasis
lymph node enlargement may suggest th e diagnosis.
The history and clinical findings may also ad va nce
the diagnosis by disclosing factors such as toxic fum e in-
hal ation, dust ex posu re. a sudd en or insidi ous di sease
Jatient onset. fever. cough, hemoptysis. and extrapulmonary
sym ptoms and signs including join t and skin changes .
• Differential Diagnosis (Tab le 13.11 )
Interstitial Pulmonary Edema

(Cardiogenic and Noncardiogeni c, Fig, 13.50., b)
Vascul ar shadows have ill-defined bord ers, there is peri-
of in- bronchial cuffing, and reticu lar markings and Kerley B
li nes are most di stinct in the dependent posterobasal
tersti- lun g. There may be associated ca rdiomega ly and fea-
): tures of pulmonary ve nous hyperte nsio n. Noncardio-
mark- ge nic edema is most com monly seen in patients on re nal
buted dialys is w hen it is a manifestatio n of fluid overload. •
on of Longsta nding untreated/treatment- resi sta nt pulmonary
, This edema may eventually lead to some degree of interstitial
r/ey C fibrosis (see below),
thick- Viral/Mycoplasma Interstitial Pneumonia

:h are Reticular and linear shadowing is most marked in the
ic an- perihilar lung (see also Chapter 3, p. 65).
pta in
how n Subacute Pulmonary Hemorrhage
n the Areas of resolvi ng pulmona ry hemorrhage may give a
sand fin e reticular pattern (see also Fig, 3,77 ).
h that Pulmonary Lymphangitis Carcinomatosa

They Pulmonary lymphangiti s carci nomatosa is manifest as
)f the inte rstitial thicke ning wi th in particular inte rl obular
seen septal thicken ing w hich frequen tly is most marked in b
the perihilar regio ns and lower zones. An associated Fig. 13 .50a. b Interlobular septa l thickening: Chest rad iograph
r pat- pleural effusion is frequent (see also Chapter 6, p. 174). (a) shows marked bilateral septal thickening. CT (b) t hrough t he
mili- upper lung zones shows marked interlobular septal and cen-
les in Idiopathic Interstitial Pneumonias trilobu lar thickening .
°ese nt The chest radiograp h may show a reticular pattern
; line cha racteristica lly with a lower zo ne and su bpleural dis-
tribution in both usual interstitial pneumonia (UIP ) and
fibro- nonspecific interstitial pneum on ia (NS IP ). End-stage UIP
.ccen- is characteri zed by honeycombing in this distribution
:ssory (Figs. 13.51., b, 13.52; see also Idi opathic Interstitial
Pneumo ni as, Chapte r 3, p. 95).
ChrOl
Chro.
fibro,
most
grapt
Drug-
Drug!
daron
subpl
fibros
Radial
Radio
b time
chang
Fig. 13. 51 a, b Interstitial-reticu lar pattern. Chest rad iograph (a) portal
shows bilateral interstitial thickening. CT (b) shows su bpleural re- astina
• ticular change and some honeycombing. rior 2
Chron
Chron
tive ti:
graph,
mid-a
si lhoul
opacit.
zones
Fig. 13.52 a, b Pulmonary fibrosis with cicatricial emphysema

• and honeycombing .
Connective Tissue-Associated Interstitial Pneumonias Chronic Hypersensitivity Pneumonitis/Extrinsic Allergic

See Chapter 3, p. 100. Alveolitis (EAA)
Reticular change deve lops with progression to pu lm o-
Sarcoidosis nary fibrosis in individuals chronically exposed to the al-
Radiograp hs in stage II di sease show mi liary nodule s lergen.
and a reticular pattern that is most pro nou nced in t he
perihilar lung (Fig. 13.53). Associated bilateral hilar Asbestosis
lymph node enlargement is freq uently present. Asbestos- induced interstitial fibros is characteristica lly
Stage III disease is characterized by pulmonary fibro- has a lower zone distribution. Reticular shadow ing may
sis with a honeycom b pattern, which again tends to be be accompanied by asbestos-induced benign pl eural b
most marked in the perih ilar midzones (Fig. 13.54). disease, thus helping in differentiation from UIP.
8. Reticul ar Shadowing 331
Chronic Bronchitis
Chron ic recu rrent bronchitis may lead to peribronch ial
fibrosis with a radi ographic interstitial pattern that is
most marked in the lower zones. There may be radio-
graphic features of associated em physema.
Drug-Induced Interstitial Pneumonitis and Fibrosis

Drugs including bleo mycin. methotrexate, and amio-
darone may give an interstitial pneumonia in a basa l and
subpl eural distribution. This may progress to interstitial
fibrosis (see also Chapter 3, p. 108).
Radiation-Induced Pulmonary Fibrosis

Radiotherapy may indu ce a pneu moniti s w hich over
b time progresses to an interstitial fibrosis. Reticular
change is cha ra cteri stically co nfined to the radi ation
,h (a) portal with involvem ent of the med ial lung postmedi-
al re- astinal radiotherapy and with involvement of the ante-
rior 2 ems of the lung in breast rad iotherapy.
Fig. 13.53 Sarcoidosis: chest rad iograph shows bilateral reticu-
Chronic Pulmonary Edema and Hemosiderosis lar change in sarcoidosis.
Chronic, recurring pulmonary edema induces connec-
tive ti ssue pro liferation in the interstitium. Chest radio-
graphs show a relatively coarse reticular patte rn in the
mid- and lower zones, usually accompa ni ed by a cardiac
silhouette co nsiste nt with mitral stenosis. Micro nodular
opacities are occas ionally prese nt in the mid- and lowe r
zo nes and indicate hemosiderosis.
Fig.13.54a-c Pulmonary fibrosis in end-stage sarcoidosis.
, b
serna
!rgic
Imo-
1e al-
.cally
may
eura l b c
- _ __ . r( l!_
9. Cavitating Lung Lesions
• Diagnostic Approach Table 13.12 Cavitating lung lesions
Cavit ies are fo rmed whe n pus from an inflammatory • Pyogenic lung abscess and septic pulmonary emboli
• Pulmonary tuberculosis
process or liquefied nec rotic material fro m a neop lasm
• Mycotic abscess (invasive pulmonary aspergillosis)
erodes into a bronchu s and then is expecto ra ted. If all of • Echinococcal cyst
the fluid is not expectorated, rad iog raphs will demon- • Amebic abscess
strate an air-fluid level within the cavity (Table 13.12). • Wegener granulomatosis
• Rheumatoid nodules
• Progressive massive fibrosis
• Bronchial carcinoma
• Differential Diagnosis • Pulmonary metastases from extrapulmonary squamous
cell primary
• Lu ng abscess and se ptic pulm ona ry embo li: Figures
13.55, 13.56.
• Pulmonary tubercu losis: Figures 13.57,13.58.
• Echinococcal cyst: (Fig. 13.59) Ech inococcosis (hy-
datid disease) is ende mi c in Mediterranean reg ions,
Fig . .
Aus tralia, and Africa. Chest radiogra phs show iso-
lated, o r rarely, multiple homoge neous round masses
l - lO cm in diameter in the ce ntral lung. The pericyst • Angioinvasive pulmonary aspergillos is.
may e rode into a bronchi al lu men, causing a crescent • Wegener gran ul omatosis.
of air to form around the endocyst (meniscus sign). • Bronchial carcinoma: Fig. 13.60.
With rupture of the endocyst, th e coll apsed chitin • Pulmonary metastasi s fro m extra pulmo nary sq ua-
membrane may float on the fluid contents (water lily mous cell primary.
sign),
Fig. 13 .
• Rhf
teri
low
casi
• Silic
and
a b
Fig. 13.55 a, b Cavitation: septic pulmonary emboli.
9. Cavitating Lung Lesions 333
Fig. 13.56 Lung abscess secondary to aspiration pneumonia. Fig. 13.57 Cavitation: tuberculosis. Cavitating lesion is seen at
the left lung apex with adjacent poorly-defined nodular opacifica-
tion.
:Qua-
~
4
o
Fig. 13.59 Echinococcus with collapsed endocyst.
Fig.13. 58 Tubercu lous cavity.
• Rheumatic nodules: Rheumato id nodules are charac- may lead to the formation of large, confluent fibrotic
teristically found in a subpleural distribution in the masses or plaques in the upper lobes. In this setting.
lower zones. Central necrosi s and cav itation is oc- cavitation usually signifies tuberculous reactivation
casionally seen. but is occasionally due to idiopath ic liquefactive
• Si licosis and coal worker's pneumoco niosi s: Si licosis necrosis of the lesion.
and coal worker's pneumoconiosis (a nthracosi licosis)
b
---------------------------------=-----
a Fig . 13.60a, b Necrotizing large cell carcinom a.

B
~
10. Ring Shadows and Cystic Lung Disease (Ta ble 13.13)
• Diagnostic Approach
Air-fil led spaces ranging from a few millimeters to
• Emphysematous bullae: These thin-walled air-con-
several ce ntimeters in size may deve lop within the lung
tain ing lesio ns are found in all forms of emphysema.
parenchyma in a number of disease processes
When subpleural in distribution, they may rupture
(Fig. 13.61 ). These spaces appear as ring shadows when
into the pleural space to give a pneumothorax.
surrounded by aerated lung but they appear as radiol u-
• Cystic bronchiectasis: Foci of cystic bronchiectasis
cencies when they lie within consolidated lung.
may give ring shad ows of va riable wa ll thickness.
• Pulmonary Langerhans cell histiocytosis: Figure E
13.62. c
• Lymphocytic inte rstitial pneu mo ni a.
• Lymphangiomyomatosis (Figs. 13.63, 13.64 ).
Table 13.13 MCystic" lesions of the lung • Tuberous sclerosis.
• Traumatic lung cysts (Fig. 13.65): These les ions result
• Em physematous bullae
from pulmonary lacerations and most common ly in-
• Cystic bronchiectasis
• Honeycombing volve the subpleural parenchyma. They begin as
• Lymphangiomyomatosis (LAM) hemorrhagic areas appearing as patchy opacities and
• Tuberous sclerosis progress to elliptical air-filled cavities.
• Pulmonary Langerhans cell histiocytosis (PlCH) • Pneumatoceles: A check-valve mechani sm may give
• Lymphocytic interstitial pneumonia
• AIDS-related cystic lung change rise to giant cysts that occu py more than one-thi rd of
• Pneumatocele the lung and cause vascu la r and mediastinal dis-
• Congenital lung cysts placement. Pneumatoceles most often develop in
children and adolescents with staphylococcal pneu-
mo nia. but they also may form seconda ry to an in-
fected lung cyst or abscess.
Fig. 13.61
• Congenital lung cysts: Figure 13.66.
granulom
• AIDS-rela ted cystic lung cha nge.
I
I
10. Ring Shadows and Cysti c Lung Disease 335
Pseudocyst s
Parahilar Herniated lung
pseudocyst Rib contours
Bronchus seen end-on
Bifid rib
Hydropneumo-
t horax
Diaphragmatic Tuberculosis
hernia
Cavity
Cavitating
Q tuberculous
cartilage Healed
Hiatus hernia cavity o pneumonia
Congenital cystic lesions of the lung
Cystic
adenomatoid
malformation Bronchogenic cyst
(mediastinal)
Bronchogenic o
cyst (pulmonary)
Bronchopulmonary
sequestration
Bronchial ca rci noma ---~

--'1.---- Bronchial carcinoma
Fungus ball - - l4aJ

Fungal
cavity
Abscess
i-con-
serna.
Ipture
'ctasis
~ss.
?igure Echinococcal - --/-iaJ "'"\ -_ Wegener

cyst granulomatosis
Amebic
abscess
result
liy in-
/~~~:-_ _ Apical
~in as f1. bullous emphysema
:'s and Emphysematous - --1-'-
bulla
y give
lird of
,I dis- Cystic
bronchiectasis cyst
op in
pneu-
an in-
Fig. 13.61 Ring shadows on the chest rad iograph. Oahnert proposed the mnemonic CAVITY = carcinoma, autoimmune (Wegener
granulomatosis. rheumatoid disease, etc.). vascular (septic emboli). infection, trauma, young (= congenital).
a b
Fig. 13.62a. b Langerha ns ce ll histiocytosis with marked bilateral reticular cha nge.
Fig. 1
Fig. 1
11.
a
.
Puln
[
tram
m a r~
Fig. 13 .63 Lymphangioleiomyomatosis. Chest radiograph shows regie
lungs of increased volume with extensive bilateral cystic change.
1. A
n;
2. PI
d,
The'
limitl
si nce
b tent
Fig. 13.64a, b Lympha ngioleiomyomatosis. chest
11. Pulmonary Hypertransradiancy 337
\
I
Fig. 13.65 Posttraumatic lung cyst.
Fig. 13.66 Multiple congenital lung cysts.
11. Pulmonary Hypertransradiancy (Table 13.14)
•
Table 13.14 Pulmonary hypertransradiancy
• Diagnostic Approach
Extrapulmonary factors
Pu lmonary vascular shadows chiefly determine the • Overexposure
transradiancy of the lung an d the density of its linear • Grid cutoff
markings. Hypertransradi ancy, whether gene ralized or • Thoracic asymmetry (scoliosis. mastectomy. congenital
pectoral aplasia, unilat eral 50ft tissue compression)
regional may be due to: • Pneumothorax
1. A decrease in the calibe r and number of intrapulmo-
nary vessels Pulmonary factors
2. Pulmonary hyperinfla tion wh ich leads to decreased Emphysema
• In COPD and alpha- 1 antitrypsin deficiency
de nsity of vesse ls • localized emphysema (cicatricial emphysema, apical
bullous emphysema, progressive pulmonary dystrophy)
The "dark ness" of the lung on the chest radiograph has • Compensatory emphysema (atelectasis, lobectomy)
limi ted value in assess ing pulmo nary transrad iancy Air Trapping
since radiographic density is determined to a large ex- • Aspirated foreign body, endobronchial tumors, inflam-
matory strictures
tent by exposure factors and beam attenuation by the • Bronchiolitis obliterans
b
chest wall. Pulmonary vasoconstriction
• Acute and chronic thromboembolism
• Pulmonary artery hypoplasia
Fig. 13.67 Left pneumonectomy

with air-filled left hemithorax in
early postoperative period .
• Pulmonary hype rinfl ation leads to hypertransradi-

aney.
• Pulmonary oligemia. Stenosis or occlusion of central
pulmona ry arteries leads to distal vasoconstriction.
Diffuse Bilateral Hypertransradiancy
• Ove rexposure: On an overexposed rad iograph. both

lungs appear abnormally hypertransradiant as do the
soft tiss ues of the chest wa ll and mediasti num.
• Generalized emphyse ma: Th e chest radiograp h
shows signs of hype rexpans ion includ ing ba rrel
chest, depressed diaphragmatic leaflets, expa nsion of
the retrosternal space, and wide ning of the inter-
costal spaces (Fig. 13.68 ).
• Bronchiolitis obliterans-co nstri ctive bronchiolitis.
• Pulmona ry oligemia in pulmona ry arte ry hyperten-
sio n.
Fig. 13.68 ~Vanishing" lung.
Unilateral Hypertransradiancy
Vesse l caliber and the number of vascu lar shadows Thoracic Asymmetry
per square centimeter may be more re li able indicators of Severe scoliosis, mastectomy (Fig. 13.69 ), or congen ital
pulmonary transradiancy. absence of pectoral major may cause appa rent va riations
Typ ical causes of t horacic/pulmonary hypertran- in radiograph ic lung density.
srad iancy are listed below.
• Extrapulmonary causes. These include exposure fac- Swyer-James Syndrome (Fig. 13.70)
to rs, overlying soft tiss ues, recent pneumecto my, and An entire lung may appear hypertransradiant and signif-
pneumothorax (Fig. 13.67 ). icant air trapping is noted on expiratory views. The syn-
11. Pulmonary Hypertransradiancy 339
Fig. 13.69 Hypertransradiant

ny hemithorax following a right mas-
n tectomy.
radi- Fig.13 .70 Swyer-James synd rom e

with markedly decreased vascular
ntraJ markings in th e left hemithorax.
ion.
both
o the
:raph
larrel
on of
nter-
tis.
rten-
~ nital
Itions
ignif-
~syn-
I
Fig. 13.71 Pneu mothorax. Th"

Mos
ma li
Wes
12.
See 1
. 0
Detec
large(
pathc
mal I
shade
AI
• Th.
• Thl
161
Hil ar t
• Pu\
• PUll
• Hile
• Bro.
drome ha s been inte rpreted as a sequel to constrictive localized Emphysema
bronchiolitis in childhood. While initial radiographic de- Emphysematous lung change shows regional variation
scriptions of this entity suggested unilateral change. in many cases and in addition, associated bullous change • Oil
HRCT in most cases shows bilateral air trapping. may give regional hypertransradiancy. Special forms of Pulmor
"localized emphysema" include progressive pulmonary
The ag'
Pulmonary Artery Hypoplasia dystrophy and congenital lobar emp hysema. monar)
This congenital anomaly is usually characterized by a general
unilateral hypertransradiant lung and a small hemi- Compensatory Emphysema comma
thorax. Perfusion scintigraphy documents a marked per- Normal lung tis sue expands to fill the void produced by vessel 11
fusion deficit. The expiratory view does not show the air atelectasis or lobectomy and may show decreased
trapping which is seen in Swyer-James sy ndrom e. CT vascu lar markings and increased transradiancy. Pulmon,
angiography and conventional arteriography show There is
decreased vascularity and occasional vascular occlu- Poststenotic Hypertransradiancy arteries
sions. In the latte r case. the lung parenchyma derives its Bronchial stenosis is associated with impairment of with pn
blood supply from the bronchial arteries. aeration as well as a reflex decrease in vascularity. The There al
stenosis also may function as a check-valve leading to air right he.
Regional Hypertransradiancy trapping in the di stal lung.
Pulmona
Pneumothorax (Fig. 13.71) Pneumatocele Failure
Lateral to the thin line of the visceral pleura is a hyperlu- A large air-containing cyst may occupy the entire The cent
cent area devoid of pulmonary vascular markings. With hemithorax. It can develop as a result of staphylococcal sym merr
a large pne umothorax or tension pneumothorax, the pneumonia, especially in children. The volume of the le- poorly dl
collapsed lung appears dense. the hemithorax is hyper- sion changes within a few days. Tomography or cr can
transradiant, and there is contralateral mediastinal shift. define the wall of the pneumatocele.
12. Hil ar Enl argement 341
Thromboembolism based on t he cl ini ca l presentation (thrombosis in the

Most thromboemboli do not ca use ra di ographic abnor- lower ext remities, acute chest pain ), CT ev idence of
malit ies. although ci rcum sc ribed hypovascul arity (the th romboe mboli in major vessels, and perfusion scin tig-
Westermark sign) may be prese nt. The diagnosis is raphy. w hich shows wedge-shaped perfusion defects.
12. Hilar Enlargement
See Tabl e 13.15. Table 13. 15 Hilar Enlargement
Vascular
• Vascular ectasia
• Diagnostic Approach • Pulmonary venous hypertension
• Pulmonary artery hypertension
Detec tion of hilar abnormality is importa nt as an en- • Asymmetric pulmonary perfusion
larged hilum is frequently an indicator of sign ifi cant • Pulmonary artery aneurysm
pathology. However, variability in hilar shape is a nor- lymph node enlargement

mal phenome non since the hil um is a summation • lymphoma
shadow formed by bot h pulmonary arteries and vei ns. • Hilar lymph node metastases
A normal hilum is characte rized by the follow ing: • Tu berculous lymphaden itis
• Fungal infections (histoplasmosis, coccidioidomycosis,
• The lateral border is co ncave. blastomycosis)
• The di amete r of the right inte rlobar artery is less than • Castleman disease
16mm. • Sarcoidosis
• Silicosis
Hilar en largement m ay be due to:
Primary Neoplasia
• Pu lmonary artery dil atation • Central bronchial carcinoma
• Pul mona ry venou s dil atation • Carcinoid
• Hilar lym ph node en largement
• Bro nchial ca rcin oma
• Differential Diagnosis Asymmetrical Pulmonary Perfusion

Unilatera l decreased pulmonary pe rfus ion is associated
Pulmonary Artery Ectasia in the Elderly w ith a co mpensato ry increase in contra late ral lu ng per-
The age-related va riant of an ectatic o r e longated pul- fu sion with assoc iated u nilateral hil ar e nlargement. This
monary artery may produ ce a unila tera l hila r bulge or discrepa ncy may resu lt from unil ate ral vasc ular occl u-
genera l enla rgeme nt of the hilu m. Ectasia is particul arly sion in pulmonary thromboem bolic d isease or unil ate ral
comm on in e ld erly patie nts due to age-re lated loss of hypoventil ation with re fl ex vasoconstrictio n such as oc-
y vesse l wall e lasticity. curs in ca rci noma-associated bro nchi al stenosis.
d
Pulmonary Artery Hypertension Pulmonary Artery Aneurysm
There is d il atation of the main and central pu lmona ry Co nge ni ta l aneurysms of the pul mona ry artery are ex-
arteries w ith bilatera l symmetri c hil ar en large ment and tre mely ra re. Tu rbulence caused by pul monary artery
If with preservation of latera l hil ar co ncav ity (Fig. 13.72 ). stenosis may occasiona lly lead to postste notic d ilatati on
Ie There also may be radiograp hic featu res co nsiste nt w it h (Fig. 13.73 ).
ir right heart dilatation (see Cha pter 7, p. 184).
Lymphoma (Fig. 13.74 a, b)
Pulmonary Venous Hypertension ± Cong estive Heart There may be un i-or bilateral h il ar lymp h node en large-
Failure me nt ofte n in association w ith mediasti nal lymph node
re Th e central pu lmon ary veins are d il ated giv ing bilateral enl arge ment.
al symmetri c hil ar enl argement. In add ition, they may be
e- poo rly defin ed d ue to pe rivascul ar ede ma. Sarco idosis (Fig. 13.75)
,n Hila r lym ph node enlargem ent in sa rcoid osis is usually
bi lateral and symmetric. In contrast to lymphoma and
-- ------ . ( ( ~~
Fig. 13.na, b Pulmonary hypertension: Chest radiograph (a)

shows dilated main pulmonary artery and bilateral hilar en large-
ment. CT (b) confirms that changes are due to central pulmonary
artery dilatation. a
Fig. 1
hilum may be present and signifies lymph atic involve-

ment.
Hilar lymph Node Metastases

Asymmetric lymp h node enlargement is usually present.
The most common primary tum ors are bronchial and
breast carcinoma.
Bacterial and Viral Infection

Pulmonary infections may be associated w ith ips il ateral
hilar lymph node enla rgement although parenchymal
opacificatio n is usually the domi nant radiographi c find -
ing.
Tuberculous Infection
Unilateral hilar lymph nod e en largement may signify
tubercul ous lymphadenitis particularly in children and
these en larged nodes may compress the right middle
lobe bronchus lead ing to atelectasis.
Mycotic Infection
Fig.13.73 Pulmonary artery aneurysm: Chest radiograph shows Histoplasmosis, coccidi omycosis, an d spo rotrichosis
central pulmonary artery dilatation with marked right hilar en-
may give uni- o r bilateral hilar lymph node e nl argement.
largement in patient with longstanding Eisenmenge r's reaction.
Right hilar enlargement was due to a pulmonary artery The diagnosis is confirmed by identification of fungi in
aneurysm. biopsy specimens and by elevated t ite rs of precipitating Fig. 13
antibody. sis.
carcin oma, aerated lung is occasionally present between Silicosis

the hilar nodes and mediastinum. Symmetrical enlargement of bronchopulmonary and
hilar lym ph nodes is common in silicosis and is usually
Central Bronchial Carcinoma associated w ith nodular parenchymal disease. The
This may manifest as unilateral hilar e nl arge ment lymph nodes may show an eggs hell pattern of calcifica-
(Fig. 13.76). ·'Spiculate" shadow ing radiating from the tion (see Fig. S. lS ).
12. Hilar Enlargement 343
a b
IiIIIb
Fig. 13.74a, b Bilateral hi lar and mediastinal lymph node enlargement in Hodgkin's lymphoma.
?nt.
tnd
: ral
mal
nd-
nify
and
jdle
losis
lent.
gi in
Iting Fig.13.75 Bi lateral hilar lymph node enlargement in sarcoido- Fig. 13.76 l eft hilar enlargement due to bronchial carcinoma.
sis.
and
ually
The
ifica-
13. Intrathoracic Calcifications
Calcifications are a common finding on chest radio- Intrathoracic calcifications may be classified as dys-
graphs (Felson 1969). With its high atomic number, ca l- trophic, which gene rally signify an inactive or degenera-
cium is a stronger absorber of roentgen rays than a soft- tive process, and metastatic which are much less com-
tissue lesion of si milar size. Most intrathoracic calcifica- Illon and are found in disorders of calcium metabolism.
tions are recognized by their flocculent. granular, or
punctate appearance (Figs. 13.77, 13.79).
•
a
•
•
- Chon focus - Disseminated calcific tuberculosis Broncholit h Histoplasmosis
Pu/
- Primary complex - Varicella pneumonia
- Calcified apical tuberculosis
. [
• Pulm
o O.
3·
g'
...
'.-:-. "
<) o
in
m
Tt
di
- Silicosis - Hemosiderosis - Tuberculoma - Carcinoma ge
- Baritosis - Tuberous sclerosis - Cyst - Hamartoma o Ca
- Stannosis
eil
fib
in~
• Di~
rei
cal
Histo~
This (
Radio:
- Involuted breast fibroadeno ma foci ir
- Pleural thickening - Pleural plaques - Pul monary art ery calcification
- Thyroid nodu le - Diaphragmatic - Aortic calcification - Calcified t rachea l cartilage calcifil
- Dermoidl pleural plaques - Calcific pericarditis - Calcified rib cartilage
benign teratoma -left ventricular aneurysm - Rib osteochondroma
Past V
- Calcified valves
Heale<
- Coronary artery calcification
- Left atrial calcification pear;
- Calcified ductus arteriosus throu~
Fig.13.77 Intrathoracic calcifications.

, 3. Intratho racic Calcifications 345
ys-
-ra-
'm-
;m.
Fig.13.78a, b Intrapulmonary foreign body emboli. Patient

with a history of psychiatric disease inserted paper dips into the
... ._--- antecubital vein. They embolized to the pulmonary arteries

through the right heart but produced no symptoms .
Pulmonary Calcifications
Pulmonary Tuberculosis
• Old Ghon Focus. This round opacity measuring
3-10 mm in diameter showing flocculent or homo-
geneous calcification is usually located peripherally
in the mid zone. It represe nts the ca lcified, healed pri-
mary focu s of tuberculosis.
• Tuberculoma (Fig. 13.79). These nodu les may reach a
diameter of 4-5 em and show patchy or homo-
geneous calc ification.
• Calcified Apical Tuberculosis. Speck led and focal ca l-
cificat ions at both apices are usually associated wi th
fibrocirrhotic t uberculosis and apica l pleural thicken-
ing.
• Disseminated Ca lci fic Tubercu los is (Fig. 13.80). Thi s
reflects healed miliary tuberculosis in w hich multipl e
ca lcific nodules are scattered throughout the lungs.
Histoplasmosis
This disease is common in the u.s. and rare in Europe.
Radiogra phs in the healed stage show multiple calcific
Fig.13.79 Calcified left upper lobe tuberculoma.
foci in the lung parenchyma, often in association with
ca lcified hil ar lymph nodes.
Past Varicella Pneumonia (Fig. 13.81)

Hea led gran ulomas foll ow ing va ri cella pneumonia ap-
pear as nodular calcifications distributed uniformly
throughout both lungs.
346 13 Radiograp hic Signs and Differential Diagnosis
Fig. 13.80 Calcified granulomata He

in old tuberculosis. Oi
so
wi
sis
He
Ch
as!
m,
cal
fla
rhe
Pn,
Int
th,
Iyn
soc
hig
Me
Me
his1
olis
hy>
ho,
on
mal
Sci,
The
Fig. 13.81 Varicella pneumonia. the
Chest radiograph shows multiple cau:
bilateral calcified nodules con~
sistent with past varicella pneu-
monia. Alv(
Thi~
ably
(Pra
pho:
Patil
fu ne
gem
myr
catet
stan
upta
strat
intel
as a
cifiec
son'
Idiop
This
predr
sho'¥\
13. Intrathoracic Calcifications 347
Healed Parasitic Infestation

Disseminated miliary to pea-sized calcifica tions are
sometimes seen in persons who have lived in regions
where cysticercosis, schistosomiasis, and paragonimia-
sis (Fig. 13.82) are endemic.
Hemosiderosis
Chronic pulmonary edema particularly when found in
association with mitral stenosis may lead to develop-
ment of small. calcified hemosiderin granulomas. Lo-
cated mainly in the lower zones, they may reflect an in-
flammatory response to small parenchymal hemor-
rhages.
Pneumoconioses (see Fig. 13.83)

Intrapulmonary silicotic nodules may ca lcify, and often
there is concomitant eggshell calcification of the hi lar
lymp h nodes. Baritosis and stannosis may also be as-
sociated with multiple granular ca lcium deposits of very
high density scattered throughout the lung parenchyma.
Fig.13.82 Paragonimiasis with some lesions having a ~targetH
Metabolic Calcification pattern of calcification.
Metabolic calcifica tion in the lung often can be detected
histologically in patients with abnorma l ca lcium metab-
oli sm (i. e., primary or secondary hyperpa rathyroidism,
hypervitaminosis D, sarcoidosis). Thi s calcification,
however. tends to be so diffuse that it is seldom visible Tracheobronchial Calcifications
on radiographs except when it is precipitated in pneu-
monic exudates or sarcoid granulomas.
Scleroderma
Th e occurrence of Thibi erge-Weissenbach syndrome in Calcified Tracheobronchial Cartilage
the setting of scleroderma is a possible but infrequent The ca rtilage rings may be heavily calcified in elderly
e cause of miliary pulmonary ca lcification. patients. Plain radiographs in these cases may define the
tracheobronchial system peripherally to the level of the
Alveolar Microlithiasis subsegmental bronchi.
This is a familial disease of unknown etiology that prob-
ably has an autosomal recessive mode of inheritance Tracheopathia osteochondroplastica
(Prakash 1983 ). Amyloid bodies containing calcium This condition is characterized by the presence of very
phosphate are found in a large number of alveoli. slow-growing, osteocartilaginous nodules in the submu-
Patients present clinically with exertional dyspnea and cosa of the trachea and proximal bronchi. The calcified
function tests show abnormal diffusion. The disease nodules arise from the cartilage rings and usually do not
ge nerally has a good prognosis. Chest radiographs show cause significant respiratory impairment until after age
myriad micronodular opacities of calcific density lo- 50.
cated predominantly in the mid-to-Iower zones (sand-
storm lung ). Radionuclide scin tigraphy shows increased Broncholiths
uptake of bone-avid radiotracer in the lung. CT demon- These are concretions up to 5 mm in diameter that are
strates intra-acinar microliths accompanied by reactive formed by inspissated and ca lcified bronchial secretions.
interstitial fibrosis. Occasio nally, the pleura may appear They are commonly as sociated with bronchiectasis (Vix
as a lucent stripe wh ich contrasts sharply with the cal- 1978). Calcified peribronchial lym ph nodes (histoplas-
cified lung (black pleural stripe sign as described by Fel- mosis. TB. fungi ) may ga in access to the bronchial lumen
son 1973 b). through inflammatory fistulae and give rise to bron-
choliths. A radiologic diagnosis is possible only if the cal-
Idiopathic Pulmonary Ossification culi migrate, are expectorated (lithoptysis). or if CT ca n
This ra re disorder also termed ossifying pneumonitis define clearly their endobro nchial location (Conces et al.
predominantly affects elde rly men. Chest radi ographs 1991).
show reticular calcium deposits (Sc hmitt et al. 1978).
R,
n(
fa
or
•
•
a b
Fig. 13.83 a, b Eggshell calcification of hilar lymph nodes and calcified pulmonary nodules in silicosis. Bi
•
Die
car
for
ast
me
gui
ane
sou
•
• I
• I
b
· (
(
Fig. 13.84 a, b Pleural calcification secondary to hemothorax (a)
a and asbestos-induced pleural disease (b).
• 5
Lymph Node Calcification Pleural Calcifications n

r.
• Differential Diagnosis • Differential Diagnosis
• Tuberculous lymph node calcification. • Calcified fibrothorax (Fig. 13.84a ). See al so p. 224. • 1
• Eggshell calcification in sarcoidosis and silicosis • Calcified asbestos-induced pleural plaques: Pleural The
(Fig. 13.83). plaques may undergo hyaline degeneration (Fig. neec
13.84 b) and subsequently may calcify. strw
349
14 Thoracic Intervention
Radiologic interventions are minimally invasive diag- • Foreign body retrieval/extraction

nostic and therapeutic procedures which may be per- • Bronchial artery embolization
formed under ultrasound, computed tomography (CT), • Coi l embolization of pulmonary arteriovenous mal-
or fluoros copic gu idan ce. formation s (PAVM )
The fo ll ow ing interventions will be di scussed: • Embolization/occlusion of pu lmonary artery false
• Biopsy aneurysms
• Drainage
b
Biopsy
• Clinical Features and Indications When ultra so und guidance and a transcostal ap-
proach are used, the needle is introduced at the superior
Diagnostic fine needle aspiration (FNA) and core biopsy rib margin to protect the intercostal arteries.
ca n provid e cytologic, hi stologic, and microbiologic in- For biopsy of pu lm onary and mediastinal les ions, CT
formation on pulmonary, pleural, chest wa ll, and medi - is employed to accurately loca li ze the target lesion and
astinal lesions. FNA and core biopsy of pulmonary and the biopsy needle can be advanced under CT/CT-fluoro-
mediastinal lesions are usually performed und er cr scopic guidance avoiding surrounding vessels and other
guidance whereas more 5uperficiallesions of the pleura critical structures (Fig, 14,1 ),
and chest wall sometimes may be biops ied under ultra- It is eas iest for the patient to keep sti ll w hen imaging
so und guidance. is performed at functional resid ual capacity or in slight
inspiration.
Hi stolog ic and cytolog ic spec ime ns are acquired from
• Contraindications sol id lesions. Spring- loaded 18-gauge cutting needles
(TruCut type) are most co mmonly used (Fig. 14.2).
• Un cooperative patient (may require general anesthe-
sia ).
• Lung biopsy in a patient w ith severe respiratory im-
pai.ment (i. e., FEV1 of less than 1 li ter ), This group
w ill tolerate a pneumothorax poorly due to lack of
res piratory reserve.
b
• (oagu lopathy (minimum requiremen ts: platelet
count > 50 OOO/~L, Quick PT > 50 %, P1T > 50 s or INR
lrax (a) < 1.3- 1.4).
• Suspected mesothelioma is co nsid ered a co ntraindica-
tion in some centers. This is due to the ris k of seeding
tumor ce lls along the needle track. Howeve r, this ri sk
may be minimized by subsequent therapeutic ir-
radiation of the biopsy track.
• Technique
~24.
?leural Th e imaging procedure mu st defin e clearly the biopsy
1 (Fig.
needle path, the target lesion, and surrounding critical Fig. 14.1 CT-guided biopsy of area of subpleura l opacification
stru ctures. using 18G TruCut needle.
350 14 Thoracic Intervention
Fine needle diagnostic or therapeutic aspirates may

be taken from fluid coli ections. The needle gauge de - •
pends on the viscosity of the fluid contents. r Pie
vis
tra
• Complications pel
qu
A small pneumothorax is commonly seen after percu-
po
taneous lung biopsy w ith a reported incidence of 25-
tio
30 :t. Most of these. however. reso lve spontaneously and
be
needle aspiration and/or percutaneous tube drainage
are required in just a small number of cases.
Biopsy-related pulmonary hemorrhage and hemop-
tysis may also occur.
Fig.14.2 CT-guided biopsy of left upper lobe lesion with patient

in prone position and using l8G TruCut needle. The inner needle
•
with specimen notch has been advanced into the lesion. The F(
outer cutting sheath has not yet been deployed. al
h.
f,
g
a
Drainage e
s
t.
r
• Clinical Features and Indications aspiration may be sufficient or a catheter may be in- c
se rted using a "direct" or Seldinger technique and thi s t
Percutaneous needle aspiration and cathete r drainage is may be left in-situ for a few days until adequate drainage
employed for treatment of pleural effusion, empyema, has occurred (Fig. 14.3a. b).
and pneumothorax. It is usually performed under local
anesthes ia.
Prerequisites include a clear anatomical drainage • Contraindications
path and a discrete well-defined coliection which has
not become significantly locul ated. Simple needle • Coagulopathy (see above )
• Absence of a safe drainage pathway
Fig. 14.3 a, b CT-guided drainage of pleural empyema using Seldinger techniq ue. Fig. (a) shows guidewire which has been advanced
through the introducer needle into the collection. Fig. (b) shows correct placement of 12F pigtail catheter. a
Foreign Body Retri eval-Extraction 351
nay
• Technique These procedures are usually performed under local
de- anesthesia.
Pleural effusions and empyemas in many cases may be
\ visual ized sufficiently well w ith ultrasound to allow ul-
trasound -guided drainage. CT-guided drain age may be • Complications
performed if the co llection cannot be visua lized ade-
quately with ultrasound due to its small size, anatomic Potential complications include hemorrhage and infec-
rcu- position. or due to large patient body habitus. Collec- rion.
25- tions containing significant amounts of gas may also be
and bette r visualized with computed tomography.
,age
l Op-
Foreign Body Retrieval-Extraction
• Clinical Indications • Contraindications

rtient
?edle
. The Foreign bodies in the major systemic veins, right heart, The potential for compl ications from the foreign body
and pulmonary arteries may reflect fragments w hich should be weighed aga inst the risk of its retrieva l.
have become detached from venous catheters. Other
foreign bodies include fragments of puncture sets,
guidewi res, pacemaker leads, and embolization materi- • Technique
als from treatment of arteriovenous shunts. These for-
eign bodies tend to beco me lodged in the right atrium. The standard technique invo lves femoral venous access
superior vena cava, and left pulmonary artery. For percu- a nd use of a large- bore sheath. If the foreign body has
taneo us retrieval to be feasible the foreign body must be been present for some time, diagnostic angiography
radiographica lly visible and it must be possible to "me- should be performed to excl ud e secondary thrombus.
e in- chanically" grasp the object under fluoroscopic visualiza- Otherwise the retrieval may be preceded by lytic ther-
. this ti on. The object should not have been prese nt long apy. The preferred instrument is a gooseneck snare,
nage enough to allow endotheliali zation and vascular adhe- which is maneuvered over one end of the foreign body
sion to occur. under fluoroscopic gu idance and tightened so that it
forms a U-shaped loop when withdrawn. The retrieval
catheter and snared foreign body are withdrawn into the
sheath and extracted with it (Fig. 14.4 • . b). The alterna-
Fig. 14.4a, b
Catheter fragment
retrieval. (a) Frag-
ment of a ven-
tricu loatrial CSF
catheter which has
been "snared"
within the superior
vena cava. (b)
Catheter fragment
has been pulled in-
feriorly into the in-
ferior vena cava .
vanced
• b
rive use of a forceps catheter carries a higher ri sk of ves- • Results

se l wall injury and does not grasp the object as securely
as the snare. Success rates of approximately 90 % are reported in the
literature with some rate variation related to the clinical
indication.
• Complications
Complications are rare but include vascuJarinjury includ-
ing damage to the femoral vein and cardiac arrhythmias.
Bronchial Artery Embolization
1
t
• Clinical Features and Indications include systemic-pulmonary arterial shunts, which very
often originate from the bronchial arteries, regardless of a
Hemoptysis is alarming for the patient and when severe, the precipitating cause. If angiography detects this type
constitutes a life-threatening e mergency. Primary man- of cross-connection or shunt. it will be necessary to
agement may include oxygen administration, broncho- eithe r modify the embolization technique or terminate
scopic suction ± coagulation of the bleeding lesion and the procedure.
bronchial tamponade. Most severe hemoptyses result The pulmonary arteries to the region must be patent
from chronic inflammatory processes in the setting of as the residual systemic bronchial supply postemboliza-
bronchiectasis. tuberculosis. aspergilloma, or pneumo- tio n may be insufficient to prevent pulmonary ischemia.
co niosis. Neoplastic lesions and vascular anomalies in Interve ntion is contraindicated during active bleeding
the form of systemic-pulmonary arterial shunts (SPAS) and s hould be performed only after the patient has been
less commonly cause severe hemoptysis. If hemoptysis stabilized hemodynamically.
persists, interventional radiology in the form of
bron chial artery em bolization is indicated. The systemic
nutrient bronchial arteries are by far the most common • Technique
source of hemorrhage and hemostas is is achieved by
Fi,
identification and occlusion of the bleeding vessel.
The procedure is technically demanding and to date
The procedure co mm ences with an angiographic survey
of the thoracic aorta and the sup ra-aortic branches. In a r.
tc
there have been no study-based reports offering defini- cooperative patient. this makes it poss ible to identify ab- S,
tive criteria for patient se lection. We (5. Lange and col- normal bronchial arteries and other systemic arteries bl
leagues ) can recommend the following criteria based on supplying the lung: these are highly variable in their 51
our own experience of more than 150 procedures: origin and number.
bl
• Recurrent bleed ing episodes over a period of at least This is followed by se lective visualization of the iden-
rr
several months (bleeds within a one-month period tified bleeding sites and a systematic search for typical
are considered one episode). sources of bleeding.
• A singl e life-threatening bleed ing episode. If it is likely that the bronchoscopically- and angio-
• No real prospect of effective treatment of the primary graphically-identified bleed ing sites correspond (a C
disease. search is made for vascular pathology rather than tl
• Good correlation between the bron choscopica lly acutely bleeding vessels). it is appropriate to proceed s
identified bleeding si te and the bleeding so urce indi- with vessel embolization. n
cated by angiography. If multiple bron ch ial arteries in both lungs are iden- a
tified as potential causes of the hemoptysis. it may be L
preferable to occlude just one artery in a Sitting due to a
• Contraindications and Potential Risks the risk of bronchial ischemia. r
The interventional phase of the procedure immedi- s
The sys temic blood supply is part of a comprehensive ately follows the diagnostic phase (Fig. 14.5a-<). With t
arterial network that supplies all thoracic organs. We are the se lective catheter placed in the orifice of the
limited in our ability to fully defin e the cross-co nn ec- bron chial artery. a smaller-caliber tube is passed
tions within this network due to flow dynamics and this through it into the bronchial artery and advanced
ca n lead to unintended embolization and ischemia of the toward the target site. This coaxial technique prevents
trachea, esophagus, coronary orreries, or even the spinal embolization material from backing up into the aorta or
cord with an associated risk of paraplegia. Other issues accessing extrapuImonary organs through periaortic
Bronchial Artery Embolizatio n 353
I
b
f
~
•
)
.t
.-
J.
g
n
/
'y Fig.14.5a-c G3-year-old male with known bronchiectasi s and
recurrent episodes of bleeding from left lower lobe. (a) Initial aor-
a togram shows dilated bronchial arteries bilaterally (arrows). (b)
J-
Selective angiography shows elongation and dilatation of the left
"ir bronchial artery. Peripheral pulmonary vessels are opacified via

systemic-pu lmonary arterial shunts. (c) Angiogram post emboli-
zation shows stasis of contrast medium within the proximal
bronchial artery. Arrows indicate the Eth ibloc-occluded seg-
]-
ments. c
al
0-
(a collaterals. When the catheter has been securely posi- • Complications
m tioned and diagnostic angiograms show no sign ificant
,d systemic-pulmonary arterial sh unts. the e mboli zation In add ition to ischemic complications as described above.
material may be injected. Our favorite emboli zation there is an approximately 20 % incidence of retrostemai
n- agent is Ethibloc, a corn protein that solidifies in blood. pain and fever following embolization. This usually re-
be Lipiodol is added to the agent to improve visualization solves within a few days.
to and prolong the liquid phase so that the em bolization
mate ri al may be deposited along a significant arte rial
li- segme nt. Any misdirection of the material ca n be de- • Results
.th tected with reaso nabl e ce rtainty so that the injection
he ca n be stopped. Coils produce a very localized occlusion Sixty percent of our patients are free of recurrent
ed w hi ch is rapidly bypassed by direct or collateral revascu- hemoptysis for periods of up to 10 years. but our results
ed lari zatio n and particles may be difficult to co nfine to the vary co nsiderably depending on the ca usative disease
1tS target site. . and the degree of angiograph ic change. We know of no
or The procedure concludes with a di agnostic angio- comparative studies in treated and un treated patients.
tic graphic evaluation of the treated vessel.
t
calizi
Coil Embolization of Pulmonary Arteriovenous Malformations AVM
ble tc
• Clinical Features and Indications producing a right-to-Ieft shun t. Large untreated malfor-
mations carry a long-term risk of biventricular decom- . T
Soli tary pulmonary arteriovenous malformations (AVM ) pensation.
occur sporadically but these lesions are most commonly Pulmonary AVMs also comp romi se the ca pillary fil- Prepi
seen in hereditary hemorrhagic telangiectasia (HHT, tration function of the lung allowing venous emboli to phyc
Osler disease) where they develop in approximately 20 % enter th e syste mic arterial ci rculati on (paradoxica l em- and ,
of patients. They tend to enlarge and beco me more com- boli ) w ith co mpli cations including ce rebra l infarction. T
plex over time and a simple AVM co mposed of one affer- This risk of systemic em boli co nstitu tes the main indica- for I
ent artery and one effere nt ve in may progress to a com- tion for treatment of AVMs. strai
plex lesion invo lvi ng mul tiple afferent and efferent ves- Treatment of pulmona ry AVMs w ith a diameter of pul n
sels. The efferent ve ins lying adj ace nt to the shunt dil ate ~ 3 mill is recommended but small er lesions that are ta ne
and thi s ve nou s ectasia may mimic tumor "spi cu lations" easily accessible to angiography may also be treated. su[ri
on radiographs. Surgical treatment of AVMs has been largely abandoned F
Pulmonary AVMs allow direct flow of deoxygenated as these lesions generally can be occluded more selec- nary
blood from pulmonary arte ri es to the pulm onary ve nou s tive ly and at less risk with an interventiona l technique. imm
system thus bypassing the ca pillary bed and effectively The only exceptions to this rule are cases in w hich a 10- mol'
at Pi
they
F
sele.
posi
narT
Yen!
are ;
leas'
is nl
the
I
c
Co
•
b
.'
Tra!
coti
nar:
are
(1::
in i
The
1001
by c
fals
Fig. 14.6 a- c Embolization of pulmonary arteriovenous malfor- is v

mation. (a) Selective left pulmonary angiogram shows pulmo- anc'
nary arteriovenous malformation (PAVM). Arrows indicate early pat
opacification of draining vein. (b) PAVM selectively visualized in per
the LAO projection prior to embolization. There is rapid venous
rat(
filling. (c) Pulmonary angiogram immediately post coil emboliza-
tion shows some residual flow in the AVM which will cease when
thrombosis occurs. Arrows indicate venous ectasia. wit
Coil Embolization of Pulmonary Artery False Aneurysms 355
calized area of lung contains a hi gh concentration of treated using the sa me technique. In our experience, it
AVMs. Surgical resectio n in these cases may be prefera- takes approximately 60 min for coil embolization of
ble to numerous radiologic interventions. each AVM. Patients w ith resp iratory impairment may be
treated on a number of successive occasions.
for-
om- • Technique
• Complications
, fil- Preprocecture helical IT studies ± diagnostic angiogra-
Ii to phy define th e morphology and di str ibu tion of the AVMs In a tota l of 80 procedures, we have seen two instances
em- and allow planning of the interve nti on. of coil displacement. Both cases were managed easily by
rion. The femoral approach is preferred to the cubital ro ute retrieval from the systemic arteries. There is virtually no
hca- for pulmonary artery inte rventi ons as it provides a risk of late displacement owing to second ary thrombosis
straighter route thus facilitating catheter control in the in the occluded segme nt. Ra rely, the occlusion may in-
" of pulmonary arteries. This route also increases the dis- cite an inflammatory rea ction in the adjacent pleura. Oc-
: are tance between the operator and the image intensifier re- casionally, it may be necessary for technical reaso ns to
ated. sulting in lower occupati onal radiation ex posure. include sma ller, healthy pulmonary arteries in the oc-
nned Fiber co ils are preferred for emboli zatio n of pulmo- cl usion and this may give a circumscribed pulmonary in-
elec- nary AVMs. Detachable balloons offer the advantage of farction. Both of these complications have a reported in-
ique. immediate and total AVM occl usion but they are much cidence of less tha n 10 % and neither is assoc iated w ith
a 10- more difficul t to deploy and are ex tremely difficult to use signi ficant seque lae.
at peripheral sites. They are also difficult to retrieve if
they enter the systemic circ ul ation during the procedure.
For the embolization procedure, the feeding artery is • Results
selectively catheteri zed and the cathete r is stab ilized in
position. An inn er coaxial catheter is th en placed at the Thi s technique wi ll provide definitive closure of the AVM
narrowest point between the feedin g arte ry and the if the coi ls are placed in a close-packed arrangement. We
venous ectasia. It is used to introduce the coils, wh ich have had to reocclude seve ral AVMs fro m earli er pro-
are applied in a close-packed arrangement to occlude at cedures due to residua l patency. We have seen no in-
least a 1.5-cm segment of the arte ry. Definitive occlusion sta nces of late displacement. Patients with HHT require
is not produced by the coils but by the thrombosis that ongo ing follow- up for the early detection of new AVMs.
the co il s induce (Fig. 14.6a- c). Additional sh unts are
Coil Embolization of Pulmonary Artery False Aneurysms
b
• Clinical Features and Indications shows a well-circumsc ri bed pulmonary nodule. Helical
cr m ay show the vascular origin of the lesion and sur-
Traumatic false aneurys ms have largely replaced my- rounding gro und-glass opacifi catio n co ns istent w ith
cotic aneurysms as the most common form of pulmo- hemorrhage (Fig. 14.7 a-d ).
na ry artery false aneurysm. Traumatic false aneurys ms
are an iatrogen ic com pl icatio n w hich occur rarely
(1 :3000 ) as a complication of Swa n-Ga ntz ca theter use • Technique
in assessment of pulmonary capillary wedge pressure.
The pulmonary arterial wall may be damaged due to bal- The procedure may be performed under ge ne ral an-
loon overinflation or there may be vasc ula r perforation esthes ia in uncooperative patients.
by the catheter leadi ng to seco ndary deve lopment of a A femoral approach is again favored and in itial pul-
fal se aneurysm. monary angiogra phy with subsequent selective cathe-
The primary mortality rate of false aneurysm ru pture terization defi nes the m orph ology of the aneurysm and
is ve ry high and in the ra nge of 45-65 %. with asphyxia pare nt artery. Because the fal se aneu rysm and surrou nd -
and blood loss as th e immediate call ses of death. Among ing lung parenchyma offer very little mechanical re-
patients w ho surv ive this com plication, 30-40 % ex- sistance, the aim ofthe procedure is not to oblite rate the
perience recurrent bleeding w ith subsequent mortality aneurysma l sac but to occlude the parent arte ry just pro-
rates of 40-70 %. xima l to the site of injury. This procedure therefore is
Clini cal presentation of rupture is most com monly feasible only if this vascu lar segm ent is present. Once
with hemoptysis. The chest radiograph characte ristically aga in a coaxial system is employed as in the treatment of
Ab,
a
n
Ab,
I;
(
Ab l
e
l'
Act
a b a
e
1 p
Age
~
u
\
t
"
Ahl
fi
Aki
n
r
Ak~
II
2
Aid
l I,
Air,
R
b
All,
v
AI-:
n
c d d
Fig. 14.7 a-d Embolization of pulmonary artery false aneurysm. pulmonary artery and rim of surrounding parenchymal hemor- 11
(a) Chest radiograph shows new pulmonary nodule following re- rhage. (c) Selective angiography demonstrates the aneurysm \ Am
cent placement of a Swan-Ga ntz catheter: appearance highly arising from a midd le lobe vessel. (d ) Postprocedure ang iogram
I<
suggestive of development of fa lse aneurysm. (b) Contrast-en- shows satisfactory occlusion of the injured art ery and exclusion of
1:
hanced CT demonstrates rig ht middle lobe lesion with afferent the ~false aneurysm from the pulmonary circul ation.
M
Ao~
II
Ari'
n
11
pulmonary AVMs and th is provides access for precise lead to Signifi ca nt occlusion. A sign ificant pulmonary Aril
placement of close- packed fibe r co il s that exclude the artery occlus ion may cause isc hem ic pulmonary infarc- d
affected pulmonary artery and fa lse aneurysm from the ti on similar to that associated w ith pulm ona ry em- n
circulation. boli sm. c
II
Ani
e
• Complications • Results L
Arr
Coil displacemen t into the vessel distal to the si te offalse There appea rs to be no risk of recurre nce in cases where e
aneurysm formation is of no co nsequence. Iso lated coils the procedure is techni ca lly feas ible. L
migrating into other pulmonary arteries usually do not

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Radiology

Geraldine Walsh, MRCP, FRCR, FRANZCR

With a contribution by Michael Montag

Third edition, fully revised and updated

BIBLIOTECA U.M.F . IASI

~I 1111111 ~I~ 11111

1 Examination Technique and Normal Findings

Radiographic Examination. . . . . . . . . . . . . . . . . . . . . . . 2 Vascular System . .... . ...... . ... .... . . . .... . . 20

Bronchopulmonary Sequestrations . . . . . . . . . . . . . .. 50 Congenital Bronchial Atresia. . . . . . . . . . . . . . . . . . . . . 60

3 Infection and Inflammatory Disorders 64

Pneumonia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 64 Echinococciasis .. .. . .......... . .... ..... . .... 89

8 Thoracic Trauma 200

10 Radiology of Cardiac Disease 240

11 Diseases of the Mediastinum 274 1 I

Biopsy ......................................... 349 Coil Embolization of Pulmonary Arteriovenous

Reference list 357

274 1 Examination Technique and Normal Findings

The patient wea rs a short lead apro n. The upper

Characterist ics of a technically acceptabl e fro ntal chest

The technical parameters recommended for chest rad io-

Technical specifications Grid technique,

Automatic exposure control:

lateral Chest Radiograph

The patient, wea ring a lead apron. stand s sideways

contact with the cassette. The depth of inspiration, film Fluoroscopy

Grids are used to reduce scatter radiation, which de- • I

grid moves during the exposure, grid lines do not appear

The Normal Chest Radiograph

are identified, analyzed, and described. To reinforce thi s Ribs

Fig. 1.8 PA chest radiograph. Fig. 1.

Fig. 1.9 l atera l chest radiograph.

Clavicles Breast Shadow Juguli

. -i~~~~~~~!P!~~- , r - -- - - Companion shadow

n, part of Th e anterior and posterior axillary fold s have caudally

Ste rno cleidomasto id Muscle

The diaphragm form s the inferior boundary of the

Apposition of th e pleural leaves is made possible by

The apical pleura appears in profil e as a stripe. 2 mm in

Basal Pleural Reflection

A line may be seen passing medially and horizontally

The right lung extends in front of the vertebral column

The posterior parts of the lungs are contiguous to the

Two layers of visceral pleura separate the pulmonary

Major (Oblique) Fissures

Very occasionally. a tenting of the diaphragmatic pleura

Minor (Horizontal) Fissure

Azygos Lobe Fissure

The azygos vein normally runs medial to the right lung.

In 10% of the population, the mediobasal segment of the

Four pleural layers

ween the Azygos vein ------fIJ

Embryonic state Normal development Development of anomalous azygos lobe

The frontal chest radiograph di splays the lungs as they

• Right middle lobe factant. This phospholipid reduces surface tension A pr

Fig. 1.30 Branching pattern of the

o Site of o Site of centri- 0 Site of panlobular

Fig. 1.32a. b Pulm onary hemor-

Th e second ary lobule is th e smallest structural unit of

Upper lobe Lower lobe

chi are rei n-

ucosal lining Middle lobe

:~ contour. The Fig.1.33 Pulmona ry segments.

• Anatomy and Physiology

. -i~~~~~!P!- , r - -- - - Companion shadow