Chest review

Abscess
Risk factors
Smoking (70-80%)
Immunodeficiency
Bronchiectasis
Malignancy (lung cancer in 12%)
COPD
Steroids
Aspiration
Decreased level of consciousness
Seizures
Alcohol abuse
Swallowing disorders
Mechanical ventilationImaging
Thick, irregular wall
Thickness > 15 mm suggests neoplasm
Spherical
Small contact with chest wall
Bronchovascular markings extend to margin
Air-fluid levels (indicates bronchial communication)
Same AP and lateral dimensions

Acute interstitial pneumonia (AIP)
Hammon-Rich disease
Rapidly progressive organizing form of diffuse alveolar damage with intersitial pulmonary fibrosisClinical
Often history of prior illness suggestive of viral URI
Worsening dyspnea, hypoxemia, respiratory failure
Deterioratoin over days to weeks
Mortality: 50-100%
Mean age: 50 years

Histology
Diffuse alveolar damage
Exudative phase: injury to alveolar lining and endothelial cells results in pulmonary edema, inflammation, and hyaline membrane formation
Organizing phase: loose fibrosis and type II pneumocyte hyperplasia
Survivors may have significant residual parenchymal abnormalities

Etiology
Always idiopathic
Diagnosis of exclusion (rule out infection, toxin, drug exposure)
May represent idiopathic form of ARDS

Radiograph
Resembles ARDS
Most patients are intubated
Diffuse airspace opacification
Spares costophrenic angles

CT
Early exudative phase
Patchy bilateral ground glass opacities
Consolidation in dependent zones
Focal areas of sparing
Late organizing phase
Consolidation replaced by ground glass opacities
Traction bronchiectasis and architectural distortion: indicates fibrosis with poor prognosis

Adenocarcinoma
40% of lung cancer (most common NSCLC)
Increased risk with smoking but may not be related to smoking
Peripheral origin; alveolar surface epithelium of bronchial mucosal glands
May arise in scar tissue: scar carcinoma (rare)
Slow growth, early metastasesImaging
Peripheral (75%)
Solitary mass or nodule
More common in upper lobes and on the right
Spiculated or lobulated
Obstructive pneumonitis (25%)
Most have air bronchograms

Adenoid cystic carcinoma

Synonym: cylindroma

Epidemiology
2nd most common tracheal malignancy (after SCC)
20-35% of tracheal tumors

Demographics
Average age 40-50
M=F

Clinical
Cough, wheezing, dyspnea, hemoptysis

Pathology
Endotracheal, endobronchial mass
Sessile, polypoid, or annular growth
Proximal to distal spread
Surrounds and invades nerves
Encases vessels

Imaging
Mass within trachea or main bronchi
10-15% in lung periphery

Alpha-1-antitrypsin deficiency
Pathology
Alpha-1-antitrypsin inactivates neutrophil elastase
Production controlled by two genes
Deficiency leads to lung destruction
Smoking accelerates destructionImaging
Panacinar emphysema
Bronchiectasis
Airway thickening

Alveolar microlithiasis
Pathology
Diffuse intra-alveolar laminated calcium deposits
Autosomal recessive in 50%Clinical
Often asymptomatic (70%) despite gross radiographic abnormalities
Cough, dyspnea

Demographics
Age 30-50 (mean 35 years)
F > M in familial; M > F in sporadic

Natural history and prognosis
Slow progression may result in respiratory and cardiac failure

Location
Bilateral, symmetric
Peripheral, basal portions of lower lobes
Anterolateral portions of RML, lingula
Anterior portion of upper lobes

Imaging
Ground glass opacities in early disease
Micronodular discrete calcifications
Polygonal shaped densities from calcificied interlobular septal thickening
Calcifications along septa, bronchovascular bundles
Small cysts from emphysema
Black pleural line: extrapleural fat, subpleural cysts

Alveolar proteinosis
Pathology
Proteinaceous, lipid-rich surfactant from type II pneumocytes accumulates in alveoli
Unknown etiologyAssociations
Silicosis
Myeloproliferative disorders
Lymphoma
Immunodeficiency states

Clinical
Extensive sputum production (liters/day)
May be asymptomatic

Demographics
Adults 20-50 years
M > F (2:1)

Complications
Nocardiosis
Aspergillosis
Cryptococcosis
Lymphoma
Findings
Multifocal consolidation (looks worse than clinical symptoms)
Central “bat-wing” distribution similar to pulmonary edema
Crazy paving on CT: multifocal, panlobular ground glass and airspace opacities with septal thickenig
Sharp demarcation between normal and abnormal lung
Findings of superimposed opportunistic infection

Treatment
Whole lung lavage: 25-50L saline (therapy of choice)
Aerosollized proteolytic agents

Prognosis
After lavage, 70% remain symptom-free at 7 years

Amyloidosis
Tracheobronchial
Focal or diffuse tracheal thickening
Mural nodules
Submucosal calcifications
StricturesNodular parenchymal
Multiple sharply-marginated peripheral nodules
Rare cavitation
Calcification (20%)

Alveolar septal
Perilymphatic nodules
Subpleural
Septal
Peribronchovascular
Patchy distributuion
Resembles sarcoidosis
Nodules often calcified
Consolidation
Interlobular septal thickening, reticulation
Honeycombing

Pleural
Irregular pleural thickening, calcifications

Adenopathy
Multiple lymph node groups
Stippled, diffuse, or eggshell calcifications

Cardiac
Cardiomegaly

Ankylosing spondylitis
Lungs
Upper lobe fibrosis with traction bronchiectasis
Cystic air spaces, cavities
Mycetoma within cysts, cavitiesPleura
Pleural thickening and effusion
Pneumothorax

Aorta
Aortic regurgitation and aortic dilatation

Heart
Cardiomyopathy

Skeletal
Ankylosis
Squared vertebral bodies, shiny corners, syndesmophytes
Calcification, ossification of paraspinal ligaments

Apical cap (5)
Pancoast tumor
Lymphoma extending from neck or mediastinum
Hematoma
Abscess within neck
Radiation fibrosis
Asbestos
Mineralogy
Naturally occurring mineral fibers
Flexible and strong
Resistant to heat, corrossives, and electricityFiber types
Serpentine
Example: chrysotile
95% of commercially used fibers
Curly and pliable
Fragments easily
Dissolves easily (chemically unstable)
Less pathogenic
Amphiboles
Examples: amosite, crocidolite, anthophilite, tremolite, and actinolite
5% of commercially used fibers
Strong, broad fiber (often coated)
Does not fragment easily
Long (> 20 um)
Higher carcinogenic potential
Epidemiology
Risk professions: construction and demolition workers, insulation workers, pipe-fitters, shipbuilders, asbestos miners
Urban dwellers

Asbestos-body
Indicates exposure
Long fiber which is larger than macrophages
Coated with iron and protein (ferruginous body)
Beaded or clubbed appearance
Cannot be removed to regional lymph nodes
Remains in posterior lower lungs
Asbestos in lung found in two forms: uncoated fibers or asbestos bodies

Asbestos-related malignancy
Malignant mesothelioma
7000x increased risk
10% lifetime risk
Latency > 30 yearsBronchogenic carcinoma
5-7x increased risk
50-100x if smoke

Laryngeal carcinoma

GI malignancies
3x increased risk

Asbestos-related pleural disease
Pleural effusion
Most common abnormality
Early manifestation (first 20 years)
Usually sterile, serosanguinous exudate
Diagnosis of exclusion: rule out malignant mesothelioma, bronchogenic carcinoma, TBPleural plaque
Latency at least 20 years
Hyalinized collagen in submesothelial layer of parietal pleura
Uncoated asbestos fibers (asbestos bodies absent)
Focal interrupted areas of pleural thickening
No functional significance
Bilateral, posterolateral parietal pleura and central diaphragm
Spares apices and costophrenic angles
May calcify extensively
Only 15% visible by CXR
CT most sensitive and specific

Diffuse pleural thickening
Less frequent than focal plaques
May cause respiratory symptoms
Diffuse smooth pleural density
Criteria
>25% length of chest wall
3 mm thickness
8 cm width
5 cm craniocaudal extent
Spares mediastinal pleura (mediastinal involvement suggests mesothelioma)

Rounded atelectasis
Preceded by pleural effusion
Fibrotic tethering of lung to parietal pleura prevents focal reexpansion of lung after resolution of pleural effusion
Layers of invaginated pleura bound by fibrous adhesions
Surrounding atelectatic and fibrotic lung
Volume loss
Associated pleural plaques and pleural thickening
Broad area of pleural contact
Swirling vessels (“comet tail” sign)

Asbestosis
Clinical
Latency period inversely proportional to exposure level (at least 20 years)
Synergistic effect of cigarette smoke
Restrictive pulmonary function testingPathology
Associated with asbestos bodies
Fibrosis of respiratory bronchioles
Progressive involvement of terminal bronchioles, alveolar ducts, and alveolar septa

Imaging
Lower lobe and posterior predominance
Reticulonodular opacities
Parenchymal bands
Curvilinear subpleural lines
Honeycombing
Associated pleural disease
Need to image prone

Askin tumor
Large tumor of chest wall
Primitive neuroectodermal tumor (PNET)Demographics
Age 20-30 years
F > M (1.3 : 1)
9x more common in Caucasians

Natural history and prognosis
Overall poor survival (38% at 2 years, 14% at 6 years)
Metastatic disease (<25% survival) Imaging Heterogeneous enhancing chest wall mass with necrosis, hemorrhage Calcification rare Pleural effusion (>90%)
Metastases to lymph nodes, lung, and bone (10%)
Extensive necrosis after chemotherapy (pseudo-cystic appearance)

Treatment
Surgical excision
Radiation, chemotherapy

Aspergilloma
Pathology
Mycetoma, fungus ball
Composed of fungus, mucus, inflammatory cells
Saprophytic infection
Preexisting cavity or bulla
TB
Enstage sarcoid
EmphysemaTreatment
Surgical resection
Intracavitary administration of amphotericin

Findings
Focal intracavitary mass (3-6 cm), typically in upper lobes
Small area of consolidation around cavity
Monod sign
Air surrounding aspergilloma
Mimics crescent sign seen with invasive aspergillosis
Adjacent pleural thickening common
Fungus ball moves with changing position

Aspergillosis, allergic bronchopulomonary (ABPA)
Pathology
Complex hypersensitivity reaction (type 1)
Almost exclusively in patients with asthma, occasionally cystic fibrosis
Initial bronchospasm followed by bronchial wall edema (IgE mediated)
Ultimate bronchial wall damage, bronchiectasis, pulmonary fibrosisClinical
Elevated Aspergillus-specific IgE
Elevated precipitating IgG against Aspergillus
Peripheral eosinophilia
Positive skin test

Findings
Bifurcating opacities (finger in glove) from mucus plugging
Hyperdensity from manganese component
Lobulated masses
Fleeting pulmonary alveolar opacities (common)
Central, upper lobe saccular bronchiectasis (hallmark)
Bronchial wall thickening
Tree-in-bud opacities
May progess to pulmonary fibrosis predominating in upper lobe (endstage)
Cavitation (10%)

Treatment
Prednisone

Aspergillosis, invasive
Pathology
Severely immunocompromised patients (bone marrow transplants, leukemia)
Starts with endobronchial fungal proliferation
Leads to vascular invasion with thrombosis and infarction (angioinvasive infection)Additional sites of infection (30%)
Brain
Liver
Kidney
GI tract

Prognosis
High mortality (70-90%)

Findings
Multiple pulmonary nodules (40%)
Characteristic halo of ground glass opacity (represents pulmonary hemorrhage)
Cavitation within 2 weeks (50%)
Air crescent sign indicates recovery phase (increased granulocytic response)
Peribronchial opacities
Focal areas of consolidation

Treatment
Amphotericin

Aspergillosis, semi-invasive
Mildly immunocompromised
Similary pathophysiology as invasive aspergillosis
Progresses more chronically over monthsRisk factors
Diabetes
Alcoholism
Pneumoconioses
Malnutrition
COPD
Connective tissue disease
AIDS
Findings
Upper lobe consolidation progressing to cavitation over months
Pleural thickening
Nodules
Complex internal architecture within cavity
Contents of cavity often hyperdense

Treatment: amphotericin
Mortality 30%

Atypical adenomatous hyperplasia (AAH)
Atypical cuboidal epithelium lining alveoli and bronchioles
Probable precursor to BAC and adenocarcinoma
Patchy ground glass opacity
Usually < 5 mm
Atypical mycobacteria, airways disease
Clinical
Almost exclusively in elderly white women
Lady Windermere syndrome
No underlying lung disease
Chronic, minimally productive coughImaging
Bronchiectasis, distributed mainly in RML and lingula
Bilateral multifocal bronchiolitis: centrilobular and tree-in-bud nodules
Mosaic attenuation
Scarring, volume loss, architectural distortion
No cavitation, pleural effusion, extensive adenopathy

Atypical mycobacteria, fibrocavitary disease
Clinical
Elderly white men
Underlying lung disease (COPD, fibrosis)
Malaise, fever, weight loss, hemoptysis
Chronic, minimally productive cough
Imaging
Consolidation, masses, nodules
Upper lobe predominance
Cavitation
Feeding bronchus
Bronchogenic spread of infection with centrilobular and tree-in-bud nodules
Progressive fibrosis and atelectasis of affected areas
Bronchiectasis, bronchial wall thickening
No lymphadenopathy or pleural effusion
Atypical mycobacteria, hypersensitivity
Clinical
Hot tub use
Aerosolized water in showersImaging
Diffuse centrilobular nodules
Ground glass opacities

Atypical mycobacteria, immunocompromised
Clinical
CD4 < 50
Fever, sweats, weight loss, fatigue, diarrhea, dyspneaImaging
Normal or subtle pulmonary findings
Scattered alveolar opacities and centrilobular nodules (most common pattern)
Consolidation
Miliary disease
Lymphadenopathy with low-density necrotic centers
Pleural effusions

Atypical mycobacteria, infection
Organisms
M. avium-intracellulare
M. kansasii
M. xenopi
M. chelonei
M. gordoniae
M. fortuitumRoute of infection
Direct infection from soil or water
Not acquired by human-human transmission

No pattern of primary disease or reactivation
Infection is primary and may become chronic

Patterns of disease
Fibrocavitary disease
Airways disease
Pneumonia in immunocompromised
Hypersensitivity pneumonia

Berylliosis
Exposure
Used as copper alloy in manufacture of airplane landing gear, electronics, undersea communication cables, and household appliances (air conditioners, fluorescent strip lighting, and electric ranges)Forms of disease
Acute toxic chemical pneumonitis
Brief exposure of high levels of airborne beryllium
Chronic granulomatous disease
Cell-mediated hypersensitivity reaction to beryllium bound to tissue proteins
Noncaseating granulomas: indistinguishable from sarcoidosis
Involves lungs, liver, spleen, lymph nodes, and bone marrow
Usually presents 10-20 years after last exposure
Clinical: exertional dyspnea and restrictive PFTs
Treated with steroids

Radiography
Diffuse reticulonodular opacities

CT
Diffuse nodules
Occasional conglomerate masses
Bronchovascular thickening
Fibrosis, traction bronchiectasis in upper lungs
Pleural thickening
Lymphadenopathy

Distinctions between berylliosis and sarcoidosis
History of beryllium exposure
Positive beryllium transformation test
Increased concentration of beryllium in lung or lymph nodes
Negative Kveim test

Blastomycosis
Consolidation
Similar to postprimary TB
Upper lobe predominance
Usually central, paramediastinal
Rounded and ill-defined
May be mass-like
Air bronchograms
CavitationNodules
Satellite lesions around consolidation
May be remote from consolidation

Miliary disease
Hematogenous dissemination
More common than histoplasmosis

Associated findings
Adenopathy, pleural effusions, calcifications very uncommon
Bone lesions (25%)
Skin lesions are common

Bridging bronchus
Ectopic bronchus arising from left mainstem bronchus
Crosses mediastinum to supply RLL
Bronchial atresia
Pathology
Congenital atresia of segmental bronchus with normal distal architecture
Aeration of distal lung through collateral air driftAssociated abnormalities
Bronchogenic cyst
Sequestration
CCAM
CLE
PAPVR
Aplastic or hypoplastic lung
Pericardial defect

Demographics
Average age at presentation: 22 years
M > F (2:1)

Clinical
Often asymptomatic
Recurrent infections
Decreased breath sounds, wheeze over affected segment

Imaging
Bronchocele
Central nodule or mass representing mucoid impaction distal to atretic bronchus
Points towards hilum
May have air-fluid level
Hyperlucent and hypoperfused segment
Paucity of vessels
Bronchiectasis

Bronchiectasis, causes
Congenital
Cystic fibrosis
Williams-Campbell syndrome
Mounier-Kuhn syndrome
Kartagener’s syndrome
Pulmonary sequestration
Yellow nail syndromeInfection
Childhood infection
Chronic granulomatous infection
ABPA
Measles
Pertussis
Recurrent aspiration
TB
MAI

Inflammation
Sarcoidosis
Constrictive bronchiolitis
Diffuse panbronchiolitis

Bronchial obstruction
Neoplasm
Enlarged lymph nodes
Broncholith
Foreign body
Bronchial atresia

Immune deficiency

Radiation

Traction
Fibrosis
Pneumoconiosis

Bronchiectasis, classification
Cylindrical
Terminal divisions: 20 (normal tracheobronchial tree has 23-24 divisions)
Not end-stage
Fusiform dilatation
Tramlines
Signet ringsVaricose
Terminal divisions: 18
Destroys lung
Tortuous dilatation
Rare

Cystic
Terminal divisions: 4
Destroys lung
Saccular dilatation
String of cysts
Air-fluid levels common

Bronchiectasis, imaging
Radiography
Tramline: horizontal, parallel lines corresponding to thickened, dilated bronchi
Bronchial wall thickening (best seen end-on)
Indistinctness of central vessels due to peribronchovascular inflammation
AtelectasisCT
Increased bronchial conspicuity: bronchi seen in outer third of lung
Bronchi appear larger than accompanying vessels
Bronchial wall thickening
Signet ring sign: focally thickened bronchial wall adjacent to pulmonary arterial branch
CT has low positive predictive value for mild forms of bronchiectasis: bronchography may be indicated if clinical suspicion is high and CT is negative

Bronchioloalveolar carcinoma
Pathology
Subtype of adenocarcinoma
Slow lepidic growth pattern
Alveolar wall intact: spreads through airways
No stromal, vascular, or pleural invasion
Architecture preservedTypes
Mucinous
Alveolar spaces distended with mucin
May present with bronchorrhea
Non-mucinous
Alveolar fibrosis
Alveoli lined by type II cells

Patterns

Solitary nodule or mass (40%)

Focal or diffuse consolidation, ground glass opacity (30%)
Air bronchograms
Cavitation may be seen

Diffuse ill-defined nodules (30%)
May be centrilobular due to endobronchial spread
May be random mimicking hematogenous metastases

Bronchogenic cyst
Abormality of budding and differentiation of primitive foregut
Ventral defect containing respiratory epithelium
Asymptomatic unless mass effect (usually incidental finding)Location
Subcarinal (50%)
Paratracheal (20%)
Hilar, paracardiac (30%)

Imaging
Round mass with fluid density and intensity
Hyperdensity (40%) may be due to debris, hemorrhage, or infection
Imperceptible cyst wall
May contain calcification
Associated rib anomalies
Nonenhancing

Bronchogenic granulomatosis
Clinical
Dyspnea, cough, fever, malaise, and hemoptysis
Peripheral and tissue eosinophiliaPathlogy
Mucosal inflammation with histiocytes, eosinophils (asthmatics), and neutrophils (non-asthmatics)
Granulomatous destruction of bronchial walls
Secondary involvement of adjacent arteries
May be associated with fungal infection, TB, RA, and Wegener’s granulomatosis

Imaging
Nodules and consolidation
Upper lobe predominance
Usually unilateral (75%)
Associated findings of ABPA: bronchiectasis, mucoid impaction

Treatment and prognosis
Asthmatics respond to steroids
Some cases remit without treatment
Must rule out treatable infection and Wegener’s granulomatosis

Bronchus associated lymphoid tissue (BALT)
Basis for pulmonary lymphoid disorders
Lymphoid collections along bronchioles, interlobular septa, and pleura
Absent at birth and in normal adults
Common in young children (regresses by age 12)
Reappears with antigenic stimulation
Cigarette smoke
Connective tissue disease
AIDS
Calcifications (6 – broad)`
Metastases
Thyroid carcinoma
Mucinous adenocarcinoma
Osteogenic tumorsInfection
Varicella
Fungal
Tuberculosis
Parasitic (schistosomiasis)

Pneumoconiosis
Silicosis

Alveolar microlithiasis

Metastatic calcifications (renal failure)

Mitral stenosis

Carcinoid tumor

Typical carcinoid (80-90%)

Low-grade tumor

Demographics
Age 30-60
F > M

Natural history and prognosis
Lymph node metastases in 5%
5-year survival 90-95% (without lymph node metastases), 76-88% (with lymph node metastases)

Location
Main, lobar, or segmental bronchi (85%)
15% peripheral location
Tracheal location very rare

Imaging
Well-defined hilar, perihilar mass
May see endobronchial lesion
Post-obstructive atelectasis, pneumonia
Hyperinflation occasionally seen
Calcification in 30%
Avid enhancement

Atypical carcinoid (10-20%)

Intermediate grade tumor

Demographics
Older (age 40-70)
F > M

Natural history and prognosis
Lymph node metastases in 50-60%
5-year survival 40-70%
Liver metastases are very rare (carcinoid syndrome rarely develops)

Location
Most develop in lung periphery

Imaging
Well-defined nodule or mass in lung periphery
Calcification rare
Variable enhancement
Associated lymphadenopathy

Carcinosarcoma
Pathology
Epithelial component
SCC
Adenocarcinoma
Undifferentiated carcinoma
Mesenchymal component (usually dominant)
Spindle cell
Chondrosarcoma
Osteosarcoma
RhabdomyosarcomaDemographics
Middle-aged, elderly
M > F

Location
Peripheral
Large mass (average 6 cm)
Frequent necrosis, hemorrhage
Central
Endobronchial growth resembling mucus plugs
May extend into adjacent parenchyma, pleura, chest wall, mediastinum
Atelectasis, pneumonia

Cardiac bronchus
Distinct airway originating from medial wall of right mainstem bronchus or bronchus intermedius
Cephalic to origin of RML bronchus
Located in azygo-esophageal recess
Cardiac lobulus demarcated from RLL by anomalous fissure
Associated with consolidation
Castleman’s disease
Angiofollicular hyperplasia
Benign lymphoproliferative hyperplasia of lymph nodesEtiology
Unknown
Possible etiologies include chronic inflammation, autoimmune reaction, immunodeficiency, or hamartomatous hyperplasia

Histology
Hyaline vascular (90%)
Plasma cell (10%): more extensive; less enhancing; possible lymphomatous degeneration

Demographics
Age 20-50 years
F > M (F:1)

Distribution
Localized
Multicentric

Location
Thorax (70%)
Neck (10-15%)
Abdomen, retroperitoneum, pelvis (10-15%)

Imaging
Avidly enhancing enlarged mediastinal lymph nodes (especially in hyaline vascular type)
Prominent feeding vessels may be seen
Nonenhancing areas may reflect necrosis, fibrosis, degeneration
Nodal calcification may be presen

Cavities (4 – broad)
Infection
Pyogenic abscess
Septic emboli
Fungal infection
TuberculosisInflammation
Sarcoidosis
Wegener’s granulomatosis
Rheumatoid arthritis

Tumor
Squamous cell carcinoma
Lymphoma
Sarcoma
Transitional cell carcinoma

Trauma
Hematoma
Hydrocarbon aspiration

Cavities, benign vs. malignant
Maximal wall thickness
Benign: < 4 mm Indeterminate: 5-15 mm Malignant: > 16 mmMorphology
Eccentric cavity: suggests malignancy
Shaggy internal margins: suggests malignancy

Air-fluid level
Uncommon in cancer, TB
More common in Wegener’s, grossly infected lesions

Number and location
Solitary nodule more likely bronchogenic carcinoma

Chondroma
Benign cartilaginous tumor
Parenchymal or endobronchial
Young femalesCarney’s triad
Gastric epithelioid leiomyosarcoma
Functioning extra-adrenal paraganglioma
Pulmonary chondroma

Churg-Strauss syndrome
Pathology
Allergic angiitis and granulomatosis
Similar to polyarteritis nodosa
Affects skin, kidneys, lung, heart, CNS
Perinuclear-ANCA (p-ANCA) positive)Associations
Late-onset asthma (100%)
Allergic rhinitis and sinusitis (70%)
Eosinophilia

Demographics
Age: 10-40 years (mean age 28 years)
M=F

Clinical
Progressive asthma, sinus pain, myocardial involvement
Abdominal pain, diarrhea
Myalgias and neuritis

Imaging
Consolidation: predominantly peripheral (59%)
Nodules (12%)
Bronchiectasis and bronchial thickening
Interlobular septal thickening
Pleural effusions

Treatment
Prognosis relates to early diagnosis and therapy
High dose steroids usually effective
Cyclophosphamide in resistant cases
Therapy stopped after 6-12 months of remission

Chylothorax
Tumor (especially lymphoma)
Trauma
Iatrogenic
Penetrating or blunt trauma
Idiopathic
Lymphangioleiomyomatosis
Filariasis
Coal-worker’s pneumoconiosis (CWP), background
Epidemiology
Common in underground miners (9-27%)
Disease depends on type of inhaled coal: anthracite (50%) > bituminous > lignite (10%)Simple CWP
Clinical
Usually asymptomatic
Pathology
Coal macule: aggregation of dust around dilated respiratory bronchiole
Minimal fibrosis
Imaging
Small nodules in upper lobes (indistinguishable from silicosis)
Perilymphatic, centrilobular distribution
More symmetric and evenly distributed than sarcoidosis
Pseudoplaques: confluent subpleural nodules
Centrilobular emphysema
Lymphadenopathy with eggshell calcifications

Complicated CWP
Clinical
Respiratory impairment, disability, premature death
Pathology
Progressive massive fibrosis
Imaging
Progressive massive fibrosis: masses (> 1 cm) formed by coalescent nodules
Upper lobes (apical, posterior)
Lenticular shape with lateral margin paralleling chest wall
Usually bilateral
Migrates centrally with time
Emphysematous lung distal to PMF (risk for pneumothorax)
Superior hilar retraction

Coccidiomycosis, acute
Clinical
Incubation period 10-16 days
60% symptomatic
Pneumonia symptoms: fever, cough, pleuritic chest pain
Valley fever: allergic form with erythema nodosum or multiformeImaging
Consolidation (70%): usually unilateral, hilar, or basal
Multifocal nodular or patchy opacities
Peribronchiolar thickening
Lymphadenopathy (20%): mediastinal lymphadenopathy may herald dissemination
Pleural effusion (20%)

Coccidiomycosis, chronic
Clinical
5% of patients
Persistent symptoms may be present without dissemination
May be mildly immunocompromisedImaging
Progressive consolidation
Biapical fibronodular lesions
Cavitation: walls may be thick or thin (grape-skin)
Hilar retraction
Lymphadenopathy
Pneumothorax
Empyema

Coccidiomycosis, disseminated
Clinical
Immunocompromised
Non-Caucasian (Filipino, African American, Hispanic)
Mortality rate 50% even with early treatmentImaging
Miliary or reticulonodular pattern
Lymphadenopathy
Pericardial effusion
Involvement of skin, bone, meninges, GU tract

Consolidation, acute (12)
Pneumonia
Edema
Hemorrhage
Aspiration
Atelectasis
Infarction
Neoplasm
BAC
Lymphoma
Sarcoidosis
COP
Chronic eosinophilic pneumonia
Hypersensitivity pneumonitis
Lipoid pneumonia
Consolidation, chronic (10)
Bronchioloalveolar carcinoma
Cryptogenic organizing pneumonia (BOOP)
Alveolar proteinosis
Lymphoma
Pseudolymphoma
Lipoid pneumonia
Sarcoidosis
Eosinophilic pneumonia
Hypersensitivity pneumonitis
Post-obstructive pneumonia
Consolidation, peripheral (5)
Cryptogenic organizing pneumonia (COP)
Eosinophilic pneumonia
Infarct
Septic emboli
Contusion
Constrictive bronchiolitis
Bronchiolitis obliterans
Concentric peribronchiolar fibrosis with narrowing, obliteration of bronchiolar lumenCauses
Postinfectious (bacterial, mycoplasmal, or viral)
Toxic inhalation
Drugs (penicillamine, gold)
Post-transplant (lung, bone marrow)
Aspiration (gastric acid)
Collagen vascular disease
Inflammatory bowel disease
Idiopathic

CXR
May be normal
Hyperinflation
Subtle attenuation of peripheral vascular markings
Central airway dilatation

HRCT
Mosaic attenuation
Air trapping
Oligemia (reflex vasoconstriction in areas of poor ventilation)
Expiratory accentuation of mosaic attenuation
Bronchiectasis
Centrilobular nodules

Crazy paving (9)

Alveolar proteinosis

Hemorrhage

Edema
ARDS
CHF

Pneumonia
PCP
Viral

Eosinophilic pneumonia

Lipoid pneumonia

Bronchioloalveolar carcinoma

Sarcoidosis

NSIP

CREST syndrome
Calcinosis
Raynaud’s
Esophageal dysmotility
Sclerodactyly
Telangiectasia
Cryptococcosis
Cryptococcus neoformans
Worldwide distribution
Ubiquitous in soil, pigeon excreta
Inhalation of contaminated dustPopulation
Lymphoma
Steroid therapy
Diabetes
AIDS

Findings
Pulmonary mass
Multiple nodules
Segmental or lobar consolidation
Cavitation, adenopathy, effusions rare
Disseminated form: CNS and other organs

Cryptogenic organizing pneumonia (COP)
Previously known as BOOP (bronchiolitis obliterans organizing pneumonia)
Always idiopathicClinical
Cough, dyspnea, fever, chills, sweats, myalgias, weight loss
Short illness duration < 3 months
Elevated ESR, CRP, WBC
Bronchoalveolar lavage: increased number and proportion of lymphocytes
Most have 2-3 courses of antibiotics

Histology
Early phase
Fibroblastic plugs in alveoli
Fibrosis in alveolar walls
Late phase
Intraluminal branching fibrosis in respiratory bronchioles and alveolar ducts
Interstitial fibrosis

Demographics
Mean age: 55 years

Imaging
Consolidation (90%)
Unilateral or bilateral
Peripheral, peribronchial, and basal distribution
Ground glass opacities (75%)
Centrilobular nodules
Bronchial thickening and dilatation
Seen in regions of consolidation
Reverse halo
Central portion clears before rim
Relatively specific for COP

Treatment and prognosis
Most patients recover completely after oral steroids
Relapse may occur

Cystic fibrosis, imaging
Distribution
Upper lobes
Superior segments of lower lobesImaging
Bronchiectasis
Peribronchial wall thickening
Mucus plugging
Mosaic attenuation
Fibrotic changes
Recurrent pneumonia
Hilar adenopathy
Pulmonary arterial hypertension

Complications
Early
Lobar atelectasis (especially RUL)
Pneumonia
Late
Respiratory insufficiency
Hypertrophic pulmonary osteoarthropathy
Cor pulmonale and pulmonary arterial hypertension
Hemoptysis
Aspergillus superinfection

Cystic fibrosis, pathology
Pathology
Autosomal recessive
Abnormality in cystic fibrosis transmembrane conductance regulator protein
Regulates passage of ions through membranes of mucus-producing cells
Dysfunction of exocrine glands causing thick, tenacious mucus that accumulates and causes bronchitis and pneumonia
Reduced mucociliary transport: airway obstruction with massive mucous plulggingSpectrum of disease
Pulmonary (100%)
Chronic cough
Recurrent pulmonary infections: colonization of plugged airways by Staphylococcus and Pseudomonas
Progressive respiratory failure
Finger clubbing: hypertrophic osteoarthropathy from hypoxemia
GI tract
Pancreatic insufficiency (85%): steatorrhea, malabsorption
Cirrhosis
Rectal prolapse
Neonates: meconeum ileus, meconium peritonitis, intussusception
Sinusitis
Hypoplastic frontal sinus
Opacification of other sinuses
Infertility in males

Cysts
Pneumatocele
Post-traumatic
Post-infectious
PCP
Staphylococcus
Coccidiomycosis
Septic emboli
Hydrocarbon aspirationEmphysema
Bullae (located within lung parenchyma)
Blebs (located within layers of visceral pleura)

Cystic bronchiectasis

Langerhans cell histiocytosis

Lymphangioleiomyomatosis and tuberous sclerosis

Honeycombing in end-stage interstitial disease

Lymphoid interstitial pneumonia
Collagen vascular disease (Sjogren’s, RA, SLE)
Bone marrow transplantation
Immunodeficiency (common in pediatric HIV but rare in adult HIV)

Hydatid cyst

Congenital cysts
Intrapulmonary bronchogenic cysts (rib and vertebral anomalies common)
Cystic adenomatoid malformation
Sequestration

Hypersensitivity pneumonitis

Papillomatosis

Desquamative interstitial pneumonia (DIP)
Smoking-related interstitial lung disease
May represent end-stage RB-ILDDemographics
Age: 30-54 years
Males > females (2:1)

Clinical
Insidious onset of symptoms
Dyspnea
Cough
Restrictive PFTs with decreased DLCO

Pathology
Macrophage-laden bronchioles and alveolar spaces
Plasma cell and eosinophil interstitial infiltrate
Fibrosis

Imaging
Ground glass opacities
Diffuse
Symmetric
Peripheral and basal predominance
Reticulation
Interlobular septal thickening
Mild honeycombing
Cysts
Alveolar ducts
Bronchioles
Emphysematous spaces

DDX
Hypersensitivity pneumonitis
RB, RB-ILD (has centrilobular nodules; upper lobe predominant)
PCP
Sarcoidosis

Prognosis
Worse prognosis than RB-ILD
70% survival at 10 years
Improves with smoking cessation

Diaphragmatic paralysis
Phrenic nerve paralysis
Bronchogenic carcinoma
CNS injury, stroke
Spinal cord injury, myelitis
Peripheral nerve injury, inflammation
Erb’s palsyMuscular disorders
Myasthenia gravis
Polymyositis, dermatomyositis
SLE
Muscular dystrophy

Idiopathic

Diffuse panbronchiolitis
Pathology
Peribronchiolar inflammation with lymphocytes and plasma cells
Peribronchiolar fibrosis
Associated with HLA BW54Demographics
Most common in Japan
M > F (2:1)

Radiography
Diffuse nodules
Hyperinflation
Cysts and bullae in late disease

CT
Centrilobular and small airways nodules (tree-in-bud)
Mosaic attenuation
Cystic bronchiectasis in late disease

Doubling time
Time to double volume
1.25x increase in diameter correlates with doubled volume
Indicator of malignancy (ask for old films!)
Malignant range: 30-450 days
Inflammatory lesions more likely short (< 30 days)
Drug toxicity
Interstitial opacities
Bleomycin
Methotrexate
Carmustine
Cyclophosphamide
GoldConsolidation
Amiodarone
Cytosine arabinoside
IL-2
OKT3
Tricyclic antidepressants
Salicylates
Penicillamine
Anticoagulants

Nodules
Cyclosporine

Pleural effusion
Procainamide (SLE-like reaction)
Hydralazine (SLE-like reaction)
Bromocryptine
Methysergide
Ergotamine tartrate

Adenopathy
Phenytoin
Cyclosporine
Methotrexate

Eggshell nodal calcifications (6)
Silicosis
Coal worker’s pneumoconiosis
Sarcoidosis
Histoplasmosis
Tuberculosis
Treated lymphoma
Elevated diaphragm
Diaphragmatic paralysis
Phrenic nerve injury
Bronchogenic carcinoma
CNS, spinal cord lesionsImmobility due to pain
Rib fractures
Pleuritis
Pneumonia
PE

Mass lesions
Subpulmonic effusion
Subphrenic collection, abscess
Abdominal mass
Diaphragmatic hernia
Pleural tumor

Emphysema, centrilobular
Common
Associations
Smoking
Chronic bronchitis
Pathology
Areas of emphysema surrounding centrilobular bronchiole and artery
Imaging
Centrilobular or spotty lucencies
Walls usually not visible
Upper lobe predominance
Emphysema, panlobular
Uncommon
Associations
Alpha-1-antitrypsin deficiency
Smoking
IV methylphenidate (Ritalin) abuse
Pathology
Uniform destruction of secondary lobule
Imaging
Large lung volumes
Low attenuation
Small pulmonary vessels
Focal lucencies usually absent
Diffuse or lower lobe predominance
Emphysema, paraseptal
Common
Associations
Smoking
Centrilobular emphysema
Pathology
Destruction of subpleural lobules
Imaging
Subpleural lucencies
Marginated by interlobular septa
Bullae (>1 cm)
Pneumothorax
Upper lobe predominance
Empyema
Pus in pleural space
Exudate that contains organism on Gram stain
Polymicrobial anaerobe (35%)
Mixed aerobe/anaerobe (40%)Three stages
Exudative
Fibrinopurulent
Organizing

Other laboratory findings
Leukocytosis
Low pH
Low glucose

Causes
Postinfection (parapneumonic), 60%
Postsurgical, 20%
Post-trauma, 20%

Findings
Pleural fluid
Thickened enhancing pleura
Lenticular shape
Nondependent location
Disparate length of air-fluid level on AP and lateral views
Split pleura sign
Edema, thickening of extrapleural fat
Gas in pleural space
Thoracentesis
Brochpleural fistula
Gas-forming organism

Empyema necessitans
Spontaneous discharge of emypema through parietal pleura
Most commonly into chest wall to form subcutaneous abscessEtiology
Tuberculosis (73%)
Other infection (bacterial, fungal)
Malignancy

Endobronchial mass
Primary malignant tumors
Squamous cell carcinoma
Adenoid cystic carcinoma
Mucoepidermoid carcinoma
Small cell carcinoma
CarcinoidPrimary benign tumors
Hamartoma
Chondroma
Papilloma
Hemangioma

Metastases
Renal cell carcinoma
Melanoma
Colorectal carcinoma
Breast carcinoma
Thyroid carcinoma
Pancreatic carcinoma

Tuberculosis

Mechanical
Mucous plug
Foreign body
Broncholith

Amyloidosis

Eosinophilic pneumonia
Pathology
Acute: diffuse alveolar damage associated with large number of interstitial and alveolar eosinophils
Chronic: filling of alveoli with eosinophilic inflammatory infiltrate
Speculated to represent hypersensitivity reaction to unknown antigenClinical
Fever, dyspnea, chest pain
Hypoxemia
Acute more common in smokers
Chronic more common in asthmatics (90% nonsmokers)

Demographics
Acute: any age, M=F
Chronic: peak age 30s, F>M

Treatment
Rapid response to steroids

Acute imaging findings
Bilateral lower-lobe predominance
Ground glass opacities
Occasional localized areas of consolidation or small nodules
Band-like opacities paralleling chest wall
Interlobular septal thickening and thickening of bronchovascular bundles (crazy paving)
Small pleural effusions

Chronic imaging findings
Bilateral upper-lobe predominance
Peripheral consolidation and ground glass opacities
Recurrent in same location
Pleural effusions rare
Band-like opacities paralleling chest wall as consolidation clears from periphery

Extramedullary hematopoiesis
Paravertebral mass
Bone marrow extruded through cortical defects of vertebral bodiesCauses
Severe anemias (thalassemia)
Bone marrow replacement (myelofibrosis, osteopetrosis)

Findings
Multiple bilateral posterior mediastinal masses
Typically T7-T12
Coarse trabeculation, rib expansion
Marked enhancement

Fibrosing mediastinitis
Etiology
Infection
Histoplasmosis
Tuberculosis
Idiopathic
Often associated with other autoimmune diseases: retroperitoneal fibrosis, orbital pseudotumor, SLE, RA, Riedel thyroiditis
Drugs
Methysergide (used for migraine headaches)
Hemorrhage
Radiation therapyClinical
SVC syndrome
Hemoptysis
Dyspnea, cough

Demographics
Adults of any age
Most between 21 and 40

Imaging
Focal disease
Calcified matted nodes
Diffuse disease
Fibrous tissue replacing mediastinal fat
Usually not calcificed
Obstruction
SVC obstruction with abundant collaterals
Airway obstruction, narrowing with postobstructive atelectasis, pneumonitis
Pulmonary venous obstruction with pulmonary venous hypertension and interstitial edema
Pulmonary artery occlusion
Pericarditis

Fibrothorax

Fibrous obliteration of normal pleural space

Etiology
Tuberculosis
Bacterial empyema
Hemothorax
Asbestos-related pleural disease
Rheumatoid arthritis

Imaging
Volume loss
Smooth, uninterrupted pleural thickening
>25% of chest wall
>8 cm craniocaudal
>3 mm thickness
Mediastinal pleura spared
May be calcified

Fibrous tumor of pleura
Pathology
Large lobulated mass
Pedicle (50%)
Cysts, hemorrhage, necrosis with larger tumors
No relationship to asbestos exposure or smoking
Originate from visceral (80%) or parietal (20%) pleuraClassification
Benign with pedicle: lowest rate of recurrence
Benign with broad-based attachment
Malignant with pedicle
Malignant with broad-based attachment: highest rate of recurrence

Clinical
Cough, dyspnea, chest pain
Hypertrophic osteoarthropathy (17-30%): more common with tumors > 10 cm
Hypoglycemia (5%)

Demographics
Mean age 50 years
F > M

Imaging
Well-defined, solitary pleural-based mass
T1- and T2-hypointense
Pedunculated lesions may move
Displacement of structures, not invasion
Calcification (5% in benign, 20% in malignant)
Enhancement homogeneous in tumors < 6 cm; heterogeneous in larger lesions and malignant lesions (necrosis, hemorrhage)
No chest wall involvement
Pleural effusion (20%, more common with malignant tumors)

Treatment and prognosis
Surgical excision
Recurrence rate as high as 15% (requires long term surveillance)
Recurrence higher in malignant tumors with broad-based attachment
Malignancy has poor prognosis due to extensive intrathoracic metastatic disease (survival < 2 years)

Follicular bronchitis

Follicular hyperplasia of bronchus-associated lymphoid tissue (BALT)

Pathology
Antigenic stimulation of BALT
Hyperplastic lymphoid follicles with reactive germinal centers distributed along bronchioles and bronchi
Minimal alveolar extension

Demographics
Mean age 44 years

Associations
AIDS
Collagen vascular disease (RA, Sjogren’s)
Hypersensitivity

Clinical
Cough, dyspnea
Fever, weight loss

Radiography
Diffuse reticulonodular opacities

CT
Centrilobular nodules
Ground glass opacities
Air-trapping

DDX
Respiratory bronchiolitis
Hypersensitivity pneumonitis
Diffuse panbronchiolitis
Cystic fibrosis
Primary ciliary dyskinesia

Goodpasture’s syndrome
Features
Pulmonary hemorrhage
Iron deficiency anemia
GlomerulonephritisPathology
Binding of circulating antibodies to glomerular and alveolar basement membranes

Clinical
Hemoptysis
Renal failure

Imaging
Pulmonary hemorrhage
Consolidation and ground glass opacities with air bronchograms
Characteristic sparing of costophrenic angles
Clearing in 1-2 weeks
Repeated hemorrhage
Leads to hemosiderosis and pulmonary fibrosis
Interstitial reticular pattern

Ground glass opacity (acute x 4, chronic x 6)

Acute

Pulmonary edema
CHF
ARDS
AIP

Pulmonary hemorrhage

Pneumonia
Viral
Mycoplasma
PCP

Acute eosinophilic pneumonia

Chronic

Hypersensitivity pneumonitis

Chronic eosinophilic pneumonia

Alveolar proteinosis

Idiopathic interstitial pneumonia
UIP
NSIP
DIP
COP
RB, RB-ILD

Bronchioloalveolar carcinoma

Sarcoidosis

Halo sign (5 – broad)
Fungal
Invasive aspergillosis
Candidiasis
NocardiaBacterial
Legionella
Tuberculosis

Viral
CMV
HSV

Inflammatory
Wegener’s granulomatosis

Neoplastic
Lung cancer
Metastases
Angiosarcoma
Kaposi’s sarcoma

Hamartoma
Epidemiology
Most common benign tumor of lung (77%)
8% of solitary pulmonary nodules
3% of all lung tumorsDemographics
Age range: 30-70 years
F > M (F=M for endobronchial hamartomas)

Clinical
Asymptomatic (90%)
May cause hemoptysis, post-obstructive pneumonitis

Pathology
Composed of cartilage, connective tissue, muscle, fat, and bone
Cleft-like invaginations of entrapped respiratory epithelium
Easily shelled-out

Location
Usually peripheral (90%)
No lobar predilection

Imaging
Sharply defined, lobulated peripheral nodule
Calcification
Speckled or popcorn (chondroid)
10% of lesions < 2 cm 75% of lesions > 5 cm
Fat attenuation is pathognomonic (54%)

Hemangioma
Pathology
Lobular, well-marginated unencapsulated mass
Infiltrative
Classified as capillary, cavernous, or venousDemographics
Children and young adults
Most common subglottic mass in infant
M=F

Location
Most often anterior and superior mediastinum
May involve any region of thorax

Imaging
Lobular heterogenous mass
Phleboliths (30%)
Heterogeneous enhancement

Histoplasmosis, acute
Clinical
Flulike syndrome: fever, chills, cough
Retrosternal pain from mediastinal LN involvement
Erythema nodosum in women
ArthralgiaImaging
Poorly defined areas of consolidation
Multiple nodules (evolve to punctate calcifications)
Lymphadenopathy

Histoplasmosis, chronic
Clinical
Usually represents hypersensitivity reaction in patients with emphysema
Usually resolves in few weeksImaging
Upper lobe predominance
Similar findings to TB
Thick-walled bullae filled with fluid
Fibrosis, volume loss
Cavitation

Histoplasmosis, complications
Histoplasmoma
Residua of prior area of pneumonitis
Solitary nodule (<3 cm)
Sharply defined
Smaller satellite lesions
Central or diffuse calcification (diagnostic of benign lesion if less than 3 cm)
May increase in size
Hilar calcification common on ipsilateral sideBroncholithiasis
Calcified regional lymph node with erosion into airway
May obstruct bronchus

Mediastinal granuloma
Result of direct infection of mediastinal lymph nodes
Subcarinal or paratracheal mass
Enhancing capsule with low attenuation center in acute stage

Fibrosing mediastinitis
Proliferation of collagen and fibrous tissue within mediastinum
Most cases are secondary to histoplasmosis (calcified, focal paratracheal and subcarinal involvement)
Idiopathic form less common (noncalcified, diffusely infiltrating, unrelated to histoplasmosis)
SVC obstruction
Obstruction of pulmonary arteries and veins
Central airway narrowing
Esophageal narrowing

Histoplasmosis, disseminated
Clinical
30% infants < 2 years
20% immunocompromised
50% apparently normalImaging
Miliary nodules
AIDS-associated disease commonly extrathoracic (50%)

Hodgkin’s disease, classification
Rye classification
Lymphocyte predominant
2-10%
Excellent prognosis
Nodular sclerosis
40-80%
Very good prognosis
Mixed cellularity
20-40%
Good prognosis
Lymphocyte depleted
2-15%
Poor prognosisAnn Arbor staging
Single LN region or extralymphatic site
Two or more LN regions on same side of diaphragm; may include localized involvement of extralymphatic site
LN regions or extralymphatic sites on both sides of diaphragm
Disseminated involvement of one or more extralymphatic organs with or without LN involvement
Suffix specifying extralymphatic site
Suffix specifying splenic involvement

Honeycombing (8)
IPF (60%)
Collagen vascular disease
Scleroderma
RA
Asbestosis
Chronic hypersensitivity pneumonitis
Sarcoidosis
Silicosis
Langerhans cell histiocytosis
Drug toxicity
Bleomycin
Methotrexate
Busulfan
Vincristine
Adriamycin
Carmustine
Hydrocarbon pneumonitis

Aspiration of volatile hydrocarbons such as kerosine, gasoline, or turpentine

Demographics
“Fire-eater’s pneumonia”
Fire-eaters, petrochemical workers, painters, hazardous waste workers
40-50% in children < 6 years

Findings
Consolidation (may be fat density)
Well-defined cavitary nodules
Pneumatoceles

Natural history and prognosis
Most have resolution of acute lung injury with supportive care

Complications
Abscess
Effusion
Bronchopleural fistula
Bacterial superinfection

Hyperlucent lung (6 – broad)
Technical
Grid cutoff, malposition
Anode heel effect
RotationChest wall
Mastectomy
Poland syndrome (congenital absence of pectoralis muscle

Pleura
Pneumothorax

Lung
Hyperexpansion after resection or lobar collapse

Airway obstruction
Emphysema, bullae
Asthma
Mucous plug
Foreign body
Tumor
Swyer-James syndrome
Congenital lobar emphysema

Vascular (oligemia)
PE
Tumor invasion of pulmonary artery
Fibrosing mediastinitis
Pulmonary artery hypoplasia or aplasia
Scimitar syndrome (hypogenetic lung syndrome)

Hypersensitivity pneumonitis, imaging
Distribution
Middle lung predominance or even distribution throughout upper, mid, and lower lung zones
Costophrenic angles spared or less severely involved
Radiography
Acute
CXR abnormal in 10%
Fine nodular or reticulonodular pattern
Airspace consolidation
Subacute
CXR abnormal in 90%
Poorly defined small nodules
Diffuse opacities in middle and lower lungs
Chronic
Fibrosis with architectural distortion and volume lossCT
Acute
Small ill-defined centrilobular nodules
Bilateral airspace consolidation
Subacute
Patchy ground glass opacities
Ill-defined centrilobular nodules
Mosaic attenuation: “head-cheese” sign
Cysts
Chronic
Fibrosis with honeycombing, traction bronchiectasis, and architectural distortion
Superimposed subacute findings (centrilobular nodules and ground glass opacities)
Pulmonary hypertension

Hypersensitivity pneumonitis, pathology

Extrinsic allergic alveolitis

Pathology
Granulomatous inflammation of bronchioles and alveoli
Caused by immunologic response to inhaled organic material
Type III (Ag-Ab complex mediated) and type IV (cell-mediated) hypersensitivity reactions
Antigens often fungal spores or avian-related

Treatment
Antigen avoidance and removal from environment
Steroids

Diseases
Farmer’s lung: moldy hay (Micropolyspora faeni)
Bird fancier’s lung: avian excreta (pigeons, parakeets)
Humidifier lung: contaminated air conditioners (thermophilic actinomyces)
Bagassosis: moldy bagasse dust (Thermoactinomyces sacchari)
Malt worker’s lung: moldy malt (Aspergillus clavatus)
Maple bark stripper’s lung: moldy maple bark (Crystostroma corticale)
Mushroom worker’s lung: spores from mushrooms (thermophilic actinomyces)

Idiopathic pulmonary fibrosis, background
Progressive inflammation, fibrosis, and destruction of lung (end-stage lung)
Synonyms: usual interstitial pneumonia (UIP), cryptogenic fibrosing alveolitis (CFA, British)Demographics
Age: 40-70 years
Males > females

Clinical
Insidious onset dyspnea for more than 6 months
Restrictive ventilation
Rales and clubbing

Associations
Smoking
Dusty environments
Gastroesophageal reflux
Autoantibodies (ANA, RA)

Histology
Dense fibroblastic foci
Predominantly subpleural collagenous scarring
Diagnosis
Imaging (PPV 96%)
CT always abnormal in patients with IPF
Clinical (PPV 87%)
Histology
Agreement regarding presence or absence of IPF only 85%
Agreement in patients without IPF only 48%

DDX
Asbestosis
Collagen vascular disease (e.g. scleroderma, RA)
Drug-toxicity (e.g. amiodarone)
Chronic hypersensitivity pneumonitis (upper-mid lung zone)

Treatment
Steroids (useful in 50%)
Cytotoxic agents

Prognosis
Median survival: 2.5-3.5 years
68% mortality at 6 years

Idiopathic pulmonary fibrosis, imaging
Radiograph
Abnormal in 95%
Volume loss
Reticulonodular opacities
Lower lobe predominance
HoneycombingCT
Abnormal in 100%
Peripheral and lower lobe predominance
Irregular interlobular septal thickening
Intralobular septal thickening (lace-like or spider web appearance)
Subpleural reticulation
Stacked cystic spaces (honeycombing)
Parenchymal bands
Traction bronchiectasis
Architectural distortion
Ground glass opacities
Reflects active potentially-treatable disease
May be seen in areas of traction bronchiectasis (more irreversible disease)
Irregular fissures
Pulmonary hypertension, cardiomegaly

Pulmonary Infarct
10-60% of patients with PE
Multiple
Lower lobe distribution
Initially ill-defined; becomes well-defined over days
Triangular, subpleural opacities (Hampton’s hump)
Cavitation
Upper lobe infarcts
Large infarcts (>4 cm)
Superinfected infarcts
Shrinks from outside in (melts like an ice cube)
Residua: none or linear scar
Inflammatory pseudotumor
Synonyms
Plasma cell granuloma
Histiocytoma
Fibroxanthoma, xanthoma
Myofibroblastic tumor
Mast cell granulomaPathology
May begin as organizing pneumonia
Usually solitary tumefactive lesion
Destroys underlying lung architecture
May have aggressive features: vascular invasion, vertebral destruction, recurrence

Demographics
Wide age range (average 30 years)
Most common primary lung mass in children
M=F

Clinical
Most are asymptomatic
Many have history of respiratory infection

Imaging
Well-defined lobulated nodule or mass
May manifest as consolidation
Endobronchial lesions may occur
Variable enhancement, calcification

Treatment, prognosis
Surgical excision
Excellent prognosis
5% recurrence

Interstitial lung disease, basilar (mn x 7)

“BAD RASH”

Bronchiectasis
Asbestosis
Drug reaction
Rheumatoid arthritis
Aspiration
Scleroderma
Hamann-Rich syndrome (IPF)

Interstitial lung disease, patterns
Radiography
Small nodules
Reticular opacities
Interlobular septal thickening
Subpleural edema
Peribronchiolar opacities
HoneycombingCT
Stacked cystic spaces, honeycombing
Subpleural reticulation
Parenchymal bands
Ground glass opacities
Nodules
Interlobular septal thickening

DDX
Idiopathic interstitial pneumonias
Infection
TB
Viruses
Edema
Inflammation
Sarcoidosis
Hypersensitivity pneumonitis
Tumor

Interstitial lung disease, preserved lung volumes (5)
Lymphangioleiomyomatosis
Langerhans cell histiocytosis
Sarcoidosis
Cystic fibrosis
Amyloidosis
Kaposi’s sarcoma
AIDS-related multicentric neoplasm
Propensity to involve skin, lymph nodes, GI tract, and lungs
15-20% of AIDS patients
Pulmonary involvement in 20%Demographics
Homosexual or bisexual males with AIDS

Clinical
Dyspnea, cough, hemoptysis

Imaging
Lymphangitic carcinomatosis
Perilymphatic poorly-defined nodules (flame-shaped) (85%)
Peribronchovascular interstitial thickening and nodules (80%)
Interlobular septal thickening (40%)
Progresses to coalescent flame-shaped perihilar consolidation
Pleural effusions (40%)
Serosanguinous
Lymphadenopathy (50%)
Marked enhancement

Kartagener’s syndrome
Immotile cilia syndrome
Autosomal recessive
Deficiency of dynein arms of cilia causing immotility of respiratory, auditory, sperm ciliaClinical
Recurrent sinusitis, ear infections, pneumonia
Male infertility

Findings
Complete thoracic and abdominal situs inversus (50%)
Bronchiectasis, bronchial wall thickening
Centrilobular and tree-in-bud nodules from bronchiolitis
Mosaic attenuation
Sinus hypoplasia and mucosal thickening

Langerhans cell histiocytosis
Demographics
Almost exclusively in smokers
Slight male predominanceClinical
Cough and dyspnea most common
May be asymptomatic
Occasional bone lesion
Hemoptysis

Pathology
Nodules within and around airways
Cystic spaces represent dilated airways
Large histiocytes with eosinophilic cytoplasm
Birbeck granules (shaped like tennis rackets)

Imaging
Upper lobe predominance
Nodules which eventually become cystic
Numerous irregular, bizarre-shaped cysts
Fused and cloverleaf appearances
Thick or thin walls
Intervening normal lung
Pneumothorax (30%)
May progress to fibrosis and honeycombing

Large cell carcinoma
5% of lung cancer
Least common NSCLC
Poorly differentiated tumor
Neuroendocrine features
Usually peripheral
Large, bulky mass with areas of necrosis (70% > 4 cm at presentation)
Fast growth, early metastases
Lipoid pneumonia
Etiology
Exogenous accumulation of fat in lung
Most often secondary to mineral oil: older people who are constipated; may have swallowing dysfunction
Infants with feeding difficulties
In the past, from oily nose dropsPathophysiology
Animal fatty acids produce hemorrhagic bronchopneumonia
Mineral oil produces giant cell foreign body reaction
Interstitial septal thickening
Macrophages, enlarged lymphatics
Fibrosing reaction

Clinical
Usually asymptomatic
Best method of diagnosis is direct biopsy

Findings
Lower lobe predominance (predilection for right)
Alveolar consolidation (may be well-circumscribed)
May present as peripheral mass or nodule (simulates bronchogenic carcinoma)
Fat density may be seen
Crazy paving

Lobe collapse
Primary signs
Opacified lobe
Dispaced interlobar fissuresSecondary signs
Elevated hemidiaphragm
Mediastinal shift
Hilar displacement
Compensatory hyperinflation
Crowded vessels

Causes
Tumor
Endobronchial
Extrinsic (e.g. bronchogenic carcinoma)
Mucus plugging
Foreign body
Broncholith
RML syndrome
Compressive atelectasis

Lobe collapse, combined RML and RLL
Obstruction of bronchus intermedius
Major and minor fissures displaced downward
Obscuration of hemidiaphragm
Lobe collapse, combined RUL and RML
Bronchi are remote from each other
Single endobronchial lesion not sufficient to explain findings
May result from extrinsic mass or mucus plugging
Findings similar to LUL collapse
Lobe collapse, LLL
Left retrocardiac triangular opacity
Posterior displacement of left major fissure
Inferior displacement of left hilum
Lobe collapse, LUL
Hazy density on PA view
Obscuration of left heart border
Luftsichel
Para-aortic crescentic lucency from upward migration of superior segment of LLL
Anterior displacement of major fissure on lateral view
Juxtaphrenic peak
Traction on basal pleura by inferior pulmonary ligament
Lobe collapse, RLL
Triangular opacity in right retrocardiac region on PA film with obliteration of diaphragm
Posterior displacement of major fissure
Gatling gun sign
Air bronchograms clustered in RLL seen end-on below right hilus
Lobe collapse, RML
Obscuration of right heart border
Wedge-shaped opacity on lateral view
Downward displacement of minor fissure
Upward displacement of major fissure
RML syndrome
Recurrent atelectasis despite patent airway
Absent collateral ventilation
May have coexistent bronchiectasis
May have surrounding lymphadenopathy
Lobe collapse, RUL
Wedge-shaped opacity in right upper hemithorax
Elevation of minor fissure
Anterior displacement of major fissure
Reverse S sign of Golden
Rightward tracheal shift
Elevation of right hilum
Luftsichel
Hyperexpansion of superior segment of RLL or RML
Lucency between mediastinum and RUL opacity on PA view
More common in LUL collapse
Juxtaphrenic peak
More common in LUL collapse
Traction on basal pleura by inferior pulmonary ligament
Lung biopsy
True positive rate: 90-95%
False negatives usually due to poor needle placement, necrotic tissueContraindications (usually relative)
Severe COPD
Pulmonary HTN
Coagulopathy
Contralateral pneumonectomy
Suspected echinococcal cysts

Technique
Fluoroscopic or CT localization of nodule
Pass needle over superior border of rib to avoid intercostal vessels
Avoid passing through fissures
Coaxial needle system: 20-G outer needle, 22-G inner needle
Cytopathologist should be present in room to determine if sample is adequate and diagnostic
Chest film after procedure to determine presence of PTX

Pneumothorax (5-30%)
Risk factors
COPD,
Biopsies at lung apices
Deep lesions
Transgression of multiple pleural surfaces (fissures)
Most do not require chest tube
Indications for chest tube (5-10%)
PTX > 25%
Symptomatic

Hemoptysis (up to 20%)
Usually benign and self-limited
Severe hemoptysis requiring intervention is unusual

Tumor seeding extremely uncommon (1:20,000)

Lung cancer, staging
Stage 0
TIS – N0 – M0Stage 1A
T1 – N0 – M0
5-year survival 65%

Stage 1B
T2 – N0 – M0
5-year survival 40%

Stage 2A
T1 – N1 – M0
5-year survival 35%

Stage 2B
T2 – N1 – M0
T3 – N0 – M0
5-year survival 25%

Stage 3A
T3 – N1 – M0
T1-3 – N2 – M0
5-year survival 10%

Stage 3B
Any T – N3 – M0
T4 – Any N – M0
5-year survival 5%
Unresectable

Stage 4
Any T – Any N – M1
5-year survival 1%

Lung cancer, TNM
Primary tumor (T)
TX
Malignant cells with no visible tumor
T0
No evidence of tumor
TIS
Carcinoma in situ
T1
Mass < 3 cm T2 Mass > 3 cm
Invasion of visceral pleura
Involves major bronchus > 2 cm from carina
Lobar atelectasis
T3
Any tumor extending into chest wall, diaphragm, mediastinal fat, or pericardium
Whole lung atelectasis
Involves major bronchus < 2 cm from carina
T4
Any tumor invading heart, great vessels, trachea, esophagus, vertebral body, or carina
Malignant pleural effusion
Satellite nodule in ipsilateral lobeNodal involvement (N)
N0
No involvement
N1
Ipsilateral hilar nodes
N2
Ipsilateral mediastinal nodes
Subcarinal and midline nodes
N3
Contralateral mediastinal nodes
Any scalene, supraclavicular nodes

Distant metastatic involvement (M)
M0
None
M1
Present

Lung contusion
Endothelial damage: extravasation of blood into interstitium and alveoli
Occurs mainly in lung adjacent to solid structures: ribs, vertebra, heart, liver
Clinical: hemoptysis (50%)
Mortality rate: 15-40%Findings
Pulmonary opacities due to hemorrhage and edema
Air bronchograms commonly seen on CT; not always present if there is associated bronchial obstruction

Evolution
Appears 6-24 hours after injury
Resolves by 7-10 days

Nonresolving contusions (after 7-10 days)
Post-laceration hematoma
Aspiration
Hospital-acquired pneumonia
Atelectasis
ARDS

Lung laceration

Disrupted alveoli leading to radial retraction of parenchyma

Mechanisms of injury
Penetrating trauma (rib fracture)
Deceleration, shearing
Blunt trauma

Complications
Infection
Bronchopleural fistula (requires prolonged chest tube drainage)

Imaging
Air-fluid level within complex cystic space
Surrounding hemorrhage
Spherical and complex if resulting from blunt trauma
Conforms to path of penetrating object in penetrating trauma
Changing appearance with time
Evolution to pneumatocele, scar
Hemopneumothorax

Lymphadenopathy, calcified (5)
Tuberculosis
Fungal infection
Sarcoidosis
Silicosis
Treated lymphoma
Lymphadenopathy, hypervascular (2)
Castleman’s disease
Vascular metastases
Renal cell carcinoma
Thyroid carcinoma
Small cell lung cancer
Melanoma
Lymphadenopathy, low attenuation (5)
Tuberculosis
MAC
Fungal infection
Necrotic metastases
Squamous cell carcinoma
Thyroid carcinoma
Adenocarcinoma
Lymphoma
Lymphangioleiomyomatosis (LAM)
Demographics
Exclusively in women unless associated with tuberous sclerosis
Reproductive yearsClinical
Spontaneous pneumothorax
Chylothorax
Hemoptysis
Slowly progressive dyspnea

Pathology
Proliferation of smooth muscle cells along bronchioles, alveolar septa, arteries, veins, and lymphatics
Associated with tuberous sclerosis
Small air-filled cysts from air trapping throughout lungs
Enlarged thoracic duct
Enlarged lymph nodes

Natural history and prognosis
Slowly progressive course
Cor pulmonale, respiratory failure
5-year survival: 50-80%
Average survival: 10 years

Radiographic features
Basilar reticulonodular opacities
Normal or increased lung volume
Chylous pleural effusion (60-75%)
Pneumothorax (40%)
Honeycombing in late disease

CT
Numerous thin-walled cysts
Bilateral, diffuse throughout lungs
Lymphadenopathy
Chylous pleural effusion
Recurrent PTX
Honeycombing in late disease

Lymphangiography
Obstruction of lymphatic flow at multiple levels
Dilated lymphatics
Increased number of lymphatics

Treatment
Oophorectomy
Progesterone
Lung transplant

Lymphangioma
Pathology
Benign mesenchymal tumor
Proliferation of lymphatic vessels without communication with lymphatic tree
Lobular, well-marginated unencapsulated mass
InfiltrativeClassification
Simple
Capillary-sized lymphatic channels
More common in skin
Cavernous
Dilated lymphatic channels
Affects thorax, abdomen, bone
Cystic
Large lymphatic channels
Most common in neck

Demographics
Children and young adults
M > F

Location
Usually extend from neck into mediastinum (75%)
15% arise exclusively in mediastinum
Usually anterior and superior mediastinum

Imaging
Lobular, circumscribed infiltrative mass
Usually cystic with variable sized cysts
May appear solid secondary to high density contents (protein and hemorrhage)
No enhancement

Lymphangitic carcinomatosis

“Certain Cancers Spread Purely By Plugging The Lung Lymphatics”

Cervix
Colon
Stomach
Prostate
Breast
Pancreas
Thyroid
Lung
Laryngeal

Lymphoid disorders
Hyperplasias of bronchus-associated lymphoid tissue (BALT)
Follicular bronchitis (follicular hyperplasia)
Pseudolymphoma (nodular hyperplasia)
Lymphoid interstitial pneumonia (LIP, diffuse hyperplasia)NHL
Low grade B-cell lymphoma
Lymphomatoid granulomatosis

Immune impairment
Post-transplant lymphoproliferative disorder (PTLD)
AIDS

Lymphoid interstitial pneumonia (LIP)
Pathology
Diffuse hyperplasia of bronchus-associated lymphoid tissue (BALT)
Infiltration of alveolar septa with T-lymphocytes
Peribronchial germinal centers with B-lymphocytesDemographics
Age: 40-49 years
Females > males

Clinical
Insidious onset of cough and dyspnea
Fever, weight loss, arthralgia
BAL: lymphocytes with no clonality

Associations
Collagen vascular disease (Sjogren’s, RA, SLE)
Bone marrow transplantation
Immunodeficiency (common in pediatric HIV but rare in adult HIV)

Radiography
Lower lung reticulonodular opacities

CT
Diffuse ground glass opacities
Poorly defined centrilobular nodules
Perilymphatic nodules
Diffuse cystic airspaces
Complete or partial airway obstruction by lymphoid tissue
Thickened bronchovascular bundles
Adenopathy

Treatment: steroids

Lymphomatoid granulomatosis
Pathology
B-cell lymphoma
Associated with EBV
Angiocentric infiltration with vascular invasion and destructionDemographics
Mean age 48 years
M > F (2:1)

Clinical
Cough, dyspnea (100%)
Nodules, ulcers, rash
Malaise, weight loss
Altered mental status, ataxia, hemiparesis, seizures, neuropathy
Renal impairment

Imaging
Multiple bilateral nodules
Predominantly in mid and lower lobes
Cavitation (20%)
Vessel-associated
Larger masses corresponding to infarcts
Diffuse reticulonodular opacities
Hilar adenopathy (25%)

Treatment and prognosis
Mortality: 53-90%
Long term remissions possible with cyclophosphamide and steroids

Malignant mesothelioma
Risk much higher in asbestos workers
Latent period: 30-45 yearsHistologic variants
Epithelial (50%)
Best prognosis
Similar to adenocarcinoma
Mesenchymal (20%)
Mixed (30%)

Clinical
Chest pain, dyspnea, fever, weight loss
History of occupational exposure to asbestos in 80%

Demographics
Pead age 60-70 years
M > F (4:1)

Diagnosis
Need to differentiate from metastatic adenocarcinoma
Mesothelioma looks like adenocarcinoma on FNA (need core biopsy)

Imaging
Lobulated pleural thickening
Pleural effusion
Encasement of lobes and growth along fissures
Contraction of hemithorax (expansion with large pleural effusion)
Contralateral pleural plaques (20%)
May extend along needle or chest tube drainage tracts
Mediastinal, chest wall, and diaphragmatic invasion
Enhancement

Treatment and prognosis
Extrapleural pneumonectomy for resectable disease (5-year survival 25%)
Prophylactic irradiation of needle tracts
Palliative radiation therapy, chemotherapy
Dismal prognosis for unresectable disease, median survival 12 months

Mediastinal lipomatosis

Exuberant deposition of unencapsulated adipose tissue in mediastinum

Etiology
Obesity
Exogenous steroids
Cushing’s syndrome
Paraneoplastic production of ACTH
Multiple symmetric lipomatosis (Madelung disease, Launois-Bensaude disease)
Genetic
Prader-Willi syndrome
Angelman syndrome
Familial multiple lipomatosis

Associations
Lipomatous tissue in other anatomic regions
Insulin resistance
Hypertension
Stigmata of Cushing’s syndrome

Clinical
Usually asymptomatic
Obstructive sleep apnea

Natural history and prognosis
Benign indolent course
Regression with correction of underlying disorder

Imaging
Homogenous fat within mediastinum
No mass effect or invasion of adjacent structures
No soft tissue components

Mediastinal mass, anterior (5 broad)
Thymic mass
Thymic cyst
Thymoma
Thymolipoma
Thymic carcinoma
Thymic carcinoid
Thymic lymphoma
Thymic hyperplasiaGerm cell tumor
Mature teratoma
Immature teratoma
Seminoma
Non-seminomatous germ cell tumor
Embryonal carcinoma
Yolk sac tumor
Choriocarcinoma
Mixed germ cell tumor

Thyroid goiter

Lymphadenopathy
Tuberculosis
Fungal infection
Sarcoidosis
Lymphoma
Castleman’s disease

Vascular
Hemangioma
Lymphangioma

Mediastinal mass, anterior (cystic) (6)
Thymic cyst
Thymoma
Teratoma
Bronchogenic cyst
Pericardial cyst
Lymphangioma
Mediastinal mass, any compartment (6)
Hematoma
Abscess
Lymphadenopathy
Mesenchymal tumor
Lymphangioma
Hemangioma
Mediastinal mass, intense enhancement (6)
Thyroid goiter
Hemangioma
Castleman disease
Vascular metastases
RCC
Thyroid
Melanoma
Small cell carcinoma
Kaposi’s
Paraganglioma
Aneurysm, varices
Mediastinal mass, middle (7)
Adenopathy
Benign: sarcoid, TB, fungal, berylliosis
Malignant: metastases, lymphoma, leukemiaAirways, lungs
Bronchogenic cysts
Tracheal malignancy
Bronchogenic tumor

Esophageal
Hiatal hernia (common)
Esophageal duplication cysts
Neoplasm
Diverticula
Megaesophagus: achalasia, hiatal hernia, colonic interposition, Chaga’s, scleroderma
Varices

Thyroid goiter

Vascular, aneurysm
Aorta, branches
Sinus of Valsalva aneurysm
Pulmonary artery
Aberrant right subclavian artery with associated diverticulum

Heart
Pericardial cyst

Mediastinal soft tissues
Hemangioma
Lymphangioma
Mediastinal lipomatosis
Mediastinal hemorrhage
Pancreatic pseudocyst
Neurinoma from recurrent laryngeal nerve
Mesenchymal tumor
Abscess

Mediastinal mass, posterior
Neurogenic
Schwannoma
Neurofibroma
Neuroblastoma
Ganglioneuroblastoma
Ganglioneuroma
Paraganglioma
Lateral meningoceleSpinal
Neoplasm
Hematoma
Extramedullary hematopoiesis
Pyogenic spondylodiskitis

Vascular
Aneurysm
Azygos continuation of IVC

Mediastinal mass, superior (6)
Thyroid mass
Lymphadenopathy
Lymphoma
Lymphangioma
Small cell lung cancer
Aneurysm, vascular abnormality
Metastases, calcified (5)
Osteosarcoma
Chondrosarcoma
Synovial sarcoma
Papillary thyroid carcinoma
Mucinous adenocarcinoma (e.g. ovarian)
Metastases, cannonball (8)
Colorectal carcinoma
Renal cell carcinoma
Sarcoma
Melanoma
Head and neck tumors
Testicular tumors
Ovarian tumors
Breast carcinoma
Metastases, endobronchial (6)
Breast
Colorectal
Thyroid
Renal
Melanoma
Pancreas
Metastases, fast-growing (3)
Sarcomas
Melanoma
Germ cell neoplasms
Metastases, micronodular (3)
Papillary thyroid carcinoma
Melanoma
Choriocarcinoma
Metastases, pleural (8)
Thymoma
Lymphoma
Breast
Lung
Prostate
Thyroid
Renal
Gastric
Metastases, slow-growing
Benign metastasizing leiomyoma
Thyroid carcinoma
Metastatic calcifications
Secondary to hypercalcemia in patients with abnormal calcium and phosphate metabolism
Most common in patients with chronic renal failure and secondary hyperparathyroidismLocation
Interstitial: alveolar septa, bronchioles, arteries
May be associated with fibrosis
Predominates in upper lobes (most alkaline region)

Imaging
Fluffy, poorly-defined nodules and ground glass opacities (3-10 mm diameter)
Consolidation
Lobular and centrilobular distribution
Calcification may not be visible unless lung collapse present
Chest wall vascular calcifications
Uptake on bone scan

Microscopic polyangiitis
Pathology
Pulmonary analog of polyarteritis nodosa
Most common cause of pulmonary-renal syndrome
Affects lungs, kidneys, musculoskeletal, GI, and skin
Defect in capillary walls results in capillaritis and hemorrhage
May be related to immune complexesDemographics
Age: 40s
M > F

Laboratory
Anemia
Renal failure
Hemosiderin-laden macrophages in BAL fluid
p-ANCA positive (Wegener’s is c-ANCA positive)

Imaging
Diffuse pulmonary hemorrhage
Multifocal ground glass opacities, consolidation
Septal thickening
Centrilobular nodules in subacute phase

Mosaic attenuation
Small vessel disease
Chronic pulmonary embolismsSmall airways disease (reactive vasoconstriction)
Constrictive bronchiolitis
Asthma
Hypersensitivity pneumonitis
Infection
Bronchopneumonia
MAC
TB
Cystic fibrosis

Mounier-Kuhn syndrome

Tracheobronchomegaly

Pathology
Associated with Ehlers-Danlos (adults) and cutis laxis (children)
Thin atrophied muscular and elastic tissue in trachea and main bronchi
Increased collapsibility during forced expiration and cough

Demographics
Usually diagnosed age 30-50 years
M >> F (19:1)
Predisposition in blacks

Clinical
Recurrent pneumonia
Occasional hemoptysis, pneumothorax

Size
Trachea > 2.5 cm
Bronchus > 2.0 cm

Imaging
Marked dilatation of trachea and central bronchi
Corrugated effect due to redundant mucosa prolapsing through tracheal rings
Dilated airways on inspiration, collapse on expiration
Bronchiectasis
Hyperinflation, emphysema
Recurrent pneumonia
Fibrosis

Mucoepidermoid carcinoma
Pathology
Submucosal, smooth endobronchial mass
High grade tumors may have ragged, invasive appearanceDemographics
Wide age range
M=F

Clinical
Cough, hemoptysis, fever
Pneumonia

Location
Most in main or lobar bronchi
Few in trachea

Imaging
Solitary endobronchial nodule or mass
Distal atelectasis, consolidation

Necrotizing sarcoid granulomatosis

Probable vascular manifestation of disseminated or localized sarcoidosis

Demographics
Age: 20s-60s (mean age 49 years)
F > M (2.2:1)

Pathology
Noncaseating granulomas
Vasculitis
Pulmonary arteries, pulmonary veins
Found in areas away from parenchymal granulomas
Widespread coagulative necrosis (distinguishes from other types of sarcoidosis)

Clinical
Cough, dyspnea, fever, chest pain
Weight loss and fatigue
Asymptomatic in 15-40%
Rare extrapulmonary involvement (13%)

Imaging
Hilar adenopathy (up to 79%)
Subpleural and perivascular nodules (may be cavitary)
Parenchymal consolidation

Therapy and prognosis
May require no therapy
Prompt response to steroids

Neurofibromatosis
Progressive pulmonary fibrosis
Bullae in upper lobes
Chest wall and mediastinal neurofibromas
Intrathoracic meningoceles
Ribbon rib deformities
Nodule, calcifications
Benign
Diffuse
Central
Popcorn
LamellatedPotentially malignant
Stippled
Eccentric

Nodule, enhancement
Protocol
Nodule must be relatively spherical in shape and homogeneous without necrosis, calcification, or fat
Patient must be able to perform reproducible breath holds
Serial CT acquisitions before and at four 1-minute intervals after contrastCriteria
Enhancement < 15 HU highly predictive of benign process (NPV 96%) Enhancement > 15 HU concerning for malignancy, but only moderately specific (Sp 58%)

Nodule, solitary
Malignant tumor (50%)
Primary cancer (40%)
Metastasis (10%)Benign tumor (14%)
Hamartoma
Chondroma
Papilloma

Infection
TB
Fungal
Round pneumonia

Vascular
AVM
Varix

Inflammatory
Sarcoidosis
Wegener’s granulomatosis
RA
Inflammatory pseudotumor

Congenital
Sequestration

Lymphadenopathy

Fissural pseudotumor

Nodules, algorithm
Nodule types
SAD: small airways disease
CEN: centrilobular
PL: perilymphatic
RD: randomDo nodules abut pleural surface?
None: CEN, SAD
Few (<10%): indeterminate Many (>10%): PL, RD

PL, RD nodules
Distribution
Patchy: PL
Diffuse: nondiagnostic
Interstitium
Thickened: PL
Normal: RD

SAD, CEN nodules
Distribution
Patchy: SAD
Diffuse: nondiagnostic
Bronchiolar impaction
Present: SAD
Absent: CEN

Indeterminate nodules
Distribution
Patchy: PL or SAD
Diffuse: nondiagnostic
Interstitium
Thickened: PL
Bronchiolar impaction
Present: SAD
Nodule morphology
Uniform ground glass: CEN
Dense, mixed: CEN or RD

Nodules, centrilobular (11)
Features
Related to centrilobular bronchiole or artery
Centered 5-10 mm from pleura
Evenly spaced
Diffuse or patchyDDX
Bronchiolitis
Infectious
Constrictive
RB, RB-ILD
Follicular
Bronchopneumonia
Endobronchial spread of infection
TB
MAC
Endobronchial spread of tumor
BAC
Hypersensitivity pneumonitis
Cryptogenic organizing pneumonia
Pneumoconiosis
Silicosis
Asbestosis
Langerhans cell histiocytosis
Edema
Vasculitis
Talcosis

Nodules, perilymphatic (6)
Features
Subpleural nodules
Peribronchovascular nodules
Septal nodules
Patchy distributionDDX
Sarcoidosis
Lymphangitic spread of tumor
Silicosis
Coal worker’s pneumoconiosis
Amyloidosis
Lymphoid interstitial pneumonia

Nodules, random (4)
Features
Random distribution relative to lung structures
Subpleural nodules
Diffuse, uniform distributionDDX
Miliary tuberculosis
Miliary fungal infection
Hematogenous metastases
Sarcoidosis (diffuse)

Nodules, tree-in-bud (8)
Features
Dilatation, impaction of centrilobular airways
Clusters, rosettes
Centered 5-10 mm from pleura
More conspicuous than normal branching vessels
Often associated with centrilobular nodulesDDX
Endobronchial spread of TB, MAC
Bronchopneumonia
Bronchiectasis, bronchitis
Cystic fibrosis
Panbronchiolitis
Aspiration
ABPA
BAC

Nodules, vessel-associated

Metastatic disease

Infection
Fungal
TB
Bacteria
Septic emboli

Infarcts

Langerhans cell histiocytosis

Rheumatoid nodules

Granulomatosis and granulomatosis
Wegener’s granulomatosis
Churg-Strauss granulomatosis
Necrotizing sarcoidosis
Bronchocentric granulomatosis
Lymphomatoid granulomatosis

Non-Hodgkin’s lymphoma, pathology
Pathology
60% originate in lymph nodes; 40% in extranodal sites
85% arise from B cells; 15% arise from T cellsDemographics
All age groups: mean age 50 years
Increased incidence in patients with altered immune status
Transplant patients
AIDS
Congenital immunodeficiency
Collagen vascular diseases (RA, SLE)

Richter syndrome
Development of NHL as complication of CLL (may develop while CLL in remission)
High-grade
B-cell origin
Abrupt onset of constitutional symptoms with rapidly progressive lymphadenopathy and clinical deterioration
Poor prognosis
Resistant to current therapies

Non-seminomatous germ cell tumor, pathology
Pathology
Large, unencapsulated tumor
Hemorrhage, necrosis, ill-defined cystsTypes
Embryonal carcinoma
Yolk sac (endodermal sinus) tumor
Choriocarcinoma
Mixed germ cell neoplasm

Demographics
Age 30-40 years
Almost exclusively in males

Associations
Hematologic malignancy
Klinefelter syndrome (20%)

Clinical
Chest pain, dyspnea, cough

Imaging
Large, irregular anterior mediastinal mass
Heterogeneous with central necrosis and hemorrhage
Peripheral enhancing soft tissue nodules
Local invasion
Lymphadenopathy
Pleural and pericardial effusions

Treatment and prognosis
Chemotherapy and surgery
Poor prognosis, especially with elevated tumor markers

Nonspecific interstitial pneumonia (NSIP)
Group of interstitial lung disorders with more favorable prognosis than IPF
Mean age range: 40-50 years
Gradual onset with duration of symptoms 6 months to 3 years
Cellular, fibrotic, or mixed histologic patternsClinical
Dyspnea
Cough
Fatigue
BAL: increased percentage of lymphocytes

Distribution
Peribronchovascular
Lower lobe predominance
Subpleural clearing (distinguishes from IPF)

Imaging
Ground glass opacities
Consolidation
Reticulation
Traction bronchiectasis
Honeycombing infrequent

Prognosis
Variable but better than IPF
May completely recover, stabilize, or relapse

Pancoast tumor
Superior sulcus tumor
Tumor at lung apex extending into adjacent chest wallPathology
SCC (50%)
Adenocarcinoma (25%)

Clinical
Horner’s syndrome (ptosis, miosis, anhidrosis)
Pain radiating to arm (invasion of pleura, bone, brachial plexus, or subclavian vessels)
Hand muscle atrophy

Findings
Apical mass
Chest wall invasion
Involvement of subclavian vessels and brachial plexus
Bone involvement: rib, vertebral body

Papillomatosis, laryngotracheal
Pathology
HPV infection (types 6 and 11 most common)
Tropism for keratinizing epithelium
Usually self-limited infection
95% cases involve larynx
Entire respiratory tract vulnerableAirway dissemination (<1%)
Usually apparent in children and young adults
Peripartum transmission from infected mother
Surgical manipulation of laryngeal papillomas increases risk of dissemination

Clinical
Wheezing, stridor, dyspnea, hemoptysis
Postobstructive pneumonia

Demographics
Bimodal age distribution
Age < 10 years (juvenile papillomatosis) Age 21-50 years M=F in children, M>F in adults

Natural history and prognosis
Usually self-limited disease in young
Slow growth of lung nodules
Degeneration to SCC in 2%

Imaging
Airway papillomas
Multiple solid and cavitated nodules
May have postobstructive atelectasis, hyperinflation, or pneumonia
Rapid growth suspicious for SCC
Air-fluid level suspicious for superinfection

Paraneoplastic syndromes
Metabolic
Cushing’s syndrome (ACTH)
Inappropriate antidiuresis (SIADH)
Carcinoid syndrome (serotonin, other vasoactive substances)
Hypercalcemia (PTH, bone mets)
Hypoglycemia (insulin-like factor)Musculoskeletal
Neuromyopathies
Clubbing of fingers (HPO)
Periosteal reaction (HPO)

Acanthosis nigricans

Thrombophlebitis

Anemia

Pleural calcification (5)
Tuberculosis
Asbestos-related pleural disease
Empyema
Hemothorax
Talc
Pleural effusion

Transudate

Ultrainfiltrate of plasma

Devoid of inflammatory cells
Low protein
Protein < 3 g/dL
Protein (plasma/fluid) < 0.5
Low LDH
LDH < 200 IU
< 70% of serum level Common causes CHF Renal failure Cirrhosis Exudate Increased capillary permeability Inflammatory cells present High protein Protein > 3 g/dL
Protein (plasma/fluid) > 0.5
High LDH
LDH > 200 IU
> 70% serum level
Common causes
Infection
Tumor
Embolism

Pleural effusion, causes (7 broad)
Tumor
Bronchogenic carcinoma
Pleural metastases
Malignant mesothelioma
LymphomaInfection
Pneumonia
Tuberculosis
Empyema

Inflammation
Collagen vascular disease
Esophageal rupture
Pancreatitis
Subphrenic abscess
Meig’s syndrome (benign ovarian fibroma)

Cardiovascular
CHF
PE
Renal failure

Congenital
Hydrops (neonate)

Metabolic
Hypoproteinemia

Trauma

Pleural mass (5 broad)
Primary tumor
Mesothelioma
Fibrous tumor of pleura
Neurofibroma
LipomaMetastases
Thymoma
Lymphoma
Multiple myeloma
Lung
Breast
Prostate
Renal
Thyroid
Gastric
Ovarian

Infection
Tuberculosis
Actinomycosis

Asbestos-related pleural disease
Plaque
Diffuse pleural thickening

Trauma
Hematoma
Splenosis

Pneumoconiosis, classification

International Labor Classification (ILO)

Small opacities
Rounded (nodules)
p (<1.5 mm)
q (1.5 – 3 mm)
r (3-10 mm)
Linear (reticular)
s (fine)
t (medium)
u (coarse)
Reticulonodular
x (fine)
y (medium)
z (coarse)
Location (zone)
RU, RM, RL
LU, LM, LL
Profusion (concentration)
0 (normal)
1 (few nodules)
2 (lung markings still visible)
3 (lung markings obsured)

Large opacities
Size
A (<5 cm)
B (half of upper lung zone)
C (greater than half of upper lung zone)

Other features
Pleural thickening, plaques
Pleural calcifications

Benign pneumoconiosis (asymptomatic or minimal symptoms)
Stannosis (tin)
Baritosis (barium)
Siderosis (iron)

Fibrogenic pneumoconiosis (symptomatic)
Silicosis
Asbestosis
Coal worker’s pneumoconiosis

Pneumocystis carinii (jiroveci)

Opportunistic fungal infection

Associated with immunodeficiency
AIDS patients, especially CD4<200
Long-term corticosteroid therapy
Transplant patients
Chemotherapy
Congenital immunodeficiency
Malnutrition

Clinical
Non-productive cough, fever, dyspnea
Hypoxia on room air
Elevated LDH (90%)

Radiography
Perihilar or diffuse hazy opacities
Evolution to consolidation
Slight upper lobe distribution in patients on aerosolized pentamidine prophylaxis
Upper lobe cysts

CT
Patchy bilateral ground glass opacities
Upper lobe, parahilar predominance
Progression to consolidation
Pneumatocele: upper lobe bizarre-shaped cysts, usually in periphery of lung (AIDS patient)
Pneumothorax
Bronchopleural fistula
Crazy-paving from superimposed interlobular septal thickening
No pleural effusions or lymphadenopathy

Atypical patterns (5-10%)
Unilateral disease
Focal lesions
Cavitary nodules

Treatment
Trimethoprim-sulfamethoxazole, pentamidine, adjunctive steroids
Prophylaxis with trimethoprim-sulfamethoxazole or dapsone

Pneumomediastinum (6)
Pulmonary
Asthma
Barotrauma
Childbirth
PneumothoraxAirway
Tracheobronchial laceration

Esophagus
Esophageal perforation
Boerhaave’s syndrome

Head and neck
Facial fractures
Dental or retropharyngeal infection

Abdomen
Intraperitoneal or retroperitoneal bowel perforation
Retroperitoneal surgery

Post-surgical

Pneumonia, aspiration
Predisposing conditions
Anesthesia
Alcoholism
Seizure
Esophageal dysmotility
Neuromuscular diseases
Head and neck surgery
Altered mental statusOrganisms
Anaerobes
Gram-negative bacteria
Staphylococcus
Actinomycosis

Imaging
Bilateral disease common
Dependent distribution
Posterior segments of upper and lower lobes
Superior segments of lower lobes
Bronchiectasis in chronic aspiration

Pneumonia, clinical profiles
Community acquired
Pneumococcus
Mycoplasma
Viruses
Staphylococcus
Legionella
KlebsiellaHospital acquired
Staphylococcus
Anaerobes
Gram-negative organisms

Splenectomy
Pneumococcus

Cystic fibrosis
Pseudomonas

COPD
Haemophilus influenza
Branhamella catarrhalis

Sickle cell
Pneumococcus

Aspiration
Anaerboic organisms
Gram-negative bacteria
Staphylococcus
Actinomycosis

Pneumonia, Klebsiella
Friedlander’s pneumonia
Gram-negative organism
Often debilitated patients, alcoholicsImaging
Consolidation similar to S. pneumonia
Lobar expansion
Cavitation in 30-50%, typically multiple
Massive necrosis (pulmonary gangrene)
Pleural effusion uncommon

Pneumonia, patterns
Lobar consolidation
Suspicious for postobstructive pneumonia
Organisms
Pneumococcus
Staphylococcus
Klebsiella (especially with lobar expansion)
Legionella
Anaerobic or gram-negative organismsDiffuse interstitial pattern
Unusual
Organisms
Mycoplasma
Viral pneumonia
Staphylococcus

Parapneumonic effusion
Early
Staphylococcus
Pneumococcus
Late
Anaerobic or gram-negative infections

Hilar adenopathy
Rare
Organisms
TB
Mycoplasma
Fungi
EBV
Measles
Tularemia
Plague
Anthrax
Pertussis

Pneumatoceles
Late, may persist for months
Usually resolve
Organisms
Staphylococcus
Pneumocystis jiroveci

Cavitation
More common in upper lobes
Organisms
Staphylococcus
Anaerobes, gram-negative bacteria

Pneumonia, recurrent (6)
Bronchogenic carcinoma
Bronchiectasis
COPD
Alveolar proteinosis
Sequestration
Esophageal diverticulum
Pneumonia, resolution

Faster in nonsmokers and outpatients (within 2-3 weeks)

Timetable
2 weeks (50% resolution)
4 weeks (66% resolution)
6 weeks (75% resolution)
8 weeks (90% resolution)
Delayed with advancing age, involvement of multiple lobes, or complications (abscess, empyema)
Recommend follow-up in 6 weeks (unless symptoms worsen)

Nonclearance
Antibiotic resistance
Consider other pathogen (e.g. TB)
Recurrent infection
Obstruction pneumonitis due to tumor

Pneumonia, Staphylococcus
Microbiology
Gram-positive cocci in clusters
Commonly colonizes nasal passagesEpidemiology
Vast majority are hospital acquired
Common cause of death during outbreaks of influenza
Increased morbidity and mortality in elderly
MRSA increasingly common

Imaging
Patchy or lobar consolidation
Widespread rapid, severe lung destruction
Bilateral (>60%)
Abscess cavities (25-75%)
Pneumatocele formation with abscess healing (50%); may last for years
Parapneumonic effusion, empyema (66%)

Pneumonia, varicella
15% of infected patients have pneumonia
90% older than 20 yearsPredisposing factors
Lymphoma
Leukemia
Immunodeficiency
Pregnancy

Clinical
Present 2-3 days after appearance of skin eruption
Cough, dyspnea, tachypnea, pleuritic chest pain

Findings
Acute phase: multiple acinar opacities
Coalescence of acinar opacities to diffuse patchy airspace disease
1-2 mm calcifications throughout lungs after healing

Pneumothorax
Iatrogenic
Percutaneous biopsy
Barotrauma, ventilationTrauma
Lung laceration
Tracheobronchial rupture

Cystic lung disease
Bleb, bulla
COPD
Asthma
PCP
LAM
Langerhans cell histiocytosis
Honeycombing

Parenchymal necrosis
Infectious
Abscess
Cavitary pneumonia
Septic emboli
TB
Fungal
Cavitary neoplasm
Radiation

Catamenial
Pleural endometriosis

Post-pneumonectomy syndrome
Pathology
Airway obstruction after pulmonary resections
Due to extreme shift of mediastinum or rotation of hilar structures
Occurs most commonly after right pneumonectomy (or after left pneumonectomy and right arch present)Imaging
Air trapping, hyperinflated lung
Recurrent pneumonia, bronchiectasis
Narrowing of bronchi, trachea
Bronchomalacia
Marked mediastinal shift

Treatment
Surgical repositioning of mediastinal structures
Reexpansion of postpneumonectomy space (e.g. silicone implant)

Post-transplant lymphoproliferative disorder (PTLD)
Pathology
Driven by EBV infection
Diffuse polyclonal expansion with reduced T-cell control
Malignant transformation to NHLImaging
Multiple indistinct nodules along bronchovascular bundles
May cavitate
Ground glass opacities and consolidation
Septal thickening
Pleural effusion

Treatment
May respond to antiviral therapy and reduction in immunosuppression
Chemotherapy should be avoided

Progressive massive fibrosis (6)
Silicosis
Coal-worker’s pneumoconiosis
Berylliosis
Talcosis
Sarcoidosis
Tuberculosis
Pseudolymphoma

Nodular lymphoid hyperplasia

Pathology
Solitary subpleural mass
Lymphoid proliferation of polyclonal B-cells and T-cells
Numerous reactive germinal centers

Clinical
Usually asymptomatic

Associations
Sjogren’s syndrome
SLE
Transverse myelitis

Demographics
Middle age

Radiography
Solitary nodule
Focal consolidation

CT
Subpleural consolidation with indistinct margins
Air bronchograms (100%)
Usually solitary
Adenopathy, effusion suggests lymphoma

Pulmonary arterial hypertension, etiology (5)
Chronic lung disease
COPD
Pulmonary fibrosis
Anything that causes chronic hypoxiaCardiac disease
Left-to-right shunt, Eisenmenger syndrome
ASD
VSD
PDA
PAPVR
Mitral stenosis
LV failure
Atrial tumor

Chronic pulmonary embolism

Schistosomiasis

Primary pulmonary hypertension
Young women
Diagnosis of exclusion

Pulmonary arterial hypertension, findings
Enlarged central PAs
MPA > 30 mm
RPA > 20 mm
PA:Ao > 1
Rapid tapering of PAs towards periphery
Calcification of PAs (chronic)
Mosaic pattern of lung attenuation
Cardiomegaly
RVH
Straightening, bowing of interventricular septum towards LV
RV predominates at apex
Cor pulmonale
Pulmonary arterial hypertension, pressures
Normal
Psys = 20 mm Hg
Pdias = 10 mm Hg
Pmean = 14 mm Hg
Capillary wedge pressure = 5 mm HgDefinition of pulmonary arterial hypertension
Psys > 30 mm Hg
Pmean > 18 mm Hg

Pulmonary arteriovenous malformation (AVM)
Multiple in 35%, bilateral in 8%
Most in lower lobes (70%)
F > M (2:1)
Age: 20s-30sClinical
Dyspnea, cyanosis, clubbing
Pansystolic murmur
Stroke
Cerebral abscess

Imaging
Lung mass with feeding artery and draining vein
Change in size with Valsalva

Treatment
Coil embolization

Etiologies
Hereditary hemorrhagic telangiectasia (70%)
Osler-Weber-Rendu syndrome
15-20% have pulmonary AVMs
Other causes
Trauma
Infection
Hepatopulmonary syndrome (hepatogenic angiodysplasia)
Iatrogenic

Pulmonary artery aneurysm (10)

Pulmonary hypertension

Pulmonary valve stenosis

Vasculitis
Behcet’s disease
Giant cell arteritis
Takayasu’s arteritis
Hughes-Stovin syndrome

Mycotic
TB (Rasmussen aneurysm)
Endocarditis
Septic emboli
Necrotizing pneumonia

Iatrogenic
Pulmonary arterial catheters

Congenital

Idiopathic

Connective tissue disease
Marfan
Ehlers-Danlos

IV drug use

Trauma
Deceleration
Penetration

Pulmonary artery enlargement (3)
Pulmonary arterial hypertension
Pulmonary stenosis
Pulmonary artery aneurysm
Pulmonary artery neoplasms
Primary tumor
Angiosarcoma
Leiomyosarcoma
Rhabdomyosarcoma
Fibrosarcoma
Osteosarcoma
Chondrosarcoma
Undifferentiated sarcomaSecondary tumor
Lymphoma
Bronchogenic carcinoma
Breast cancer

Pulmonary blastoma
Pathology
Mixture of epithelial and mesenchymal elements
Both components are immature
Morphologic mimic of embryonic lungDemographics
Biphasic age distribution: 1st and 7th decades
M > F

Clinical
Cough, hemoptysis, dyspnea, chest pain

Imaging
Large, well-circumscribed peripheral mass
May invade pleura
Metastases

Pulmonary complications of transplantation
Early
Pulmonary edema
Fungal infection
CMV pneumonia
Pneumocystis jiroveci
GVHD
Diffuse alveolar hemorrhage
Idiopathic pulmonary syndromeLate
GVHD
Bronchiolitis obliterans
Cryptogenic organizing pneumonia
VZV
Late bacterial infections
PTLD
NHL

Pulmonary edema, etiology
Cardiogenic
Adults: CHF, MI, mitral regurgitation, ruptured chordae
Neonate: hypoplastic left heart, cor triatriatumRenal
Renal failure
Volume overload

Lung injury
Septic shock, neurogenic shock
Fat embolism
Inhalation injury: SO2, O2, Cl2, NO2
Aspiration, drowning

Pulmonary edema, grading
Grade 1
Vascular redistribution (10-17 mm Hg)
Cephalization of vessels
Pulmonary veins in 1st intercostal space > 3 mmGrade 2
Interstitial edema (18-25 mm Hg)
Peribronchovascular cuffing
Perihilar haziness
Kerley lines
Unsharp central pulmonary vessels (perivascular edema)
Pleural effusion

Grade 3
Alveolar edema (> 25 mm Hg)
Airspace disease: patchy consolidation, air bronchograms

Pulmonary edema, neurogenic
Upper lobe distribution
Enhanced sympathetic activity causes vasoconstriction of basal vessels
Redirects blood flow to upper lobes
Pulmonary embolism, CXR
PIOPED: CXR usually abnormal (84%), but also abnormal in patients without PE (66%)
Atelectasis
Westermark’s sign
Localized pulmonary oligemia (rare)
Hampton’s hump
Triangular peripheral cone of infarct
Blood in secondary pulmonary lobules
Fleishner sign
Increased diameter of pulmonary artery (> 16 mm)
Seen in acute PE
Disappears within few days
Cor pulmonale
Sudden increase in size of RV, RA
Pulmonary edema
Pleural effusion (50%)
Pulmonary gangrene (6)
Pneumococcus
Klebsiella
Anaerobes
Tuberculosis
Aspergillus
Mucormycosis
Pulmonary hemorrhage, diffuse (8)
Microscopic polyangiitis
Wegener’s granulomatosis
Churg-Strauss syndrome
Collagen vascular disease
Goodpasture’s syndrome
Behcet’s syndrome
IgA nephropathy
Idiopathic pulmonary hemorrhage
Pulmonary mass (7 broad)
Tumor
Bronchogenic carcinoma
Lymphoma
Metastasis
HamartomaInfection
Fungal
Parasitic
Abscess

Congenital
CCAM
Sequestration
Bronchogenic cyst

Inflammatory
Sarcoidosis
Wegener’s granulomatosis
RA
Inflammatory pseudotumor

Pneumoconiosis
Progressive massive fibrosis

Amyloidosis

Pleural and chest wall masses

Pulmonary stenosis, etiology
Valvular (most common)
Diaphragm with central hole
Bicuspid valve
Dysplastic valve with thickened immobile cusps (Noonan syndrome)
Carcinoid
Rheumatic heart diseaseSubvalvular
Hypoplastic crista supraventricularis in TOF
Discrete membrane
Double-chambered RV (anomalous muscle bar)
RV hypertrophy
Tumor

Supravalvular
Williams syndrome
Tetralogy of Fallot
Rubella
Tumor
Carcinoid
Thrombus
Surgical banding
Takayasu’s arteritis
Behcet’s disease

Pulmonic stenosis, findings
Post-stenotic dilatation of MPA and LPA
RPA normal in sizeRight ventricular hypertrophy
Hyperkinetic systolic narrowing of infundibulum
Hour-glass appearance of infundibulum beneath pulmonary valve
Infundibular stenosis may increase after repair of pulmonary valve stenosis (decreased afterload): fatal RV failure may occur

Systolic jet into pulmonary artery

Leaflet doming during systole

Pulmonary varix
Enlarged vein
Usually due to mitral stenosis
Usually near left atrium
Pulmonary venoocclusive disease (PVOD)
Occlusion of small pulmonary veins
Etiology unknown
Pathology: intimal fibrosisTriad
Pulmonary arterial hypertension
Pulmonary edema
Normal wedge pressure

Associations
Viral infection
Environmental toxins
Chemotherapy
Radiation
Oral contraceptives
Intracardiac shunts

CXR
Edema without cephalization
Pleural effusion
Cardiomegaly

CT
Secondary pulmonary arterial hypertension
Markedly small central pulmonary veins
Central and gravity-dependent ground glass opacities
Smoothly thickened interlobular septa
Normal-sized left atrium
Centrilobular nodules
Pleural effusion

Treatment
Lung transplantation

Relapsing polychondritis
Pathology
Collagen vascular disease
Inflammation, progressive destruction of cartilage throughout bodyLocation
Ear (90%)
Joints (80%)
Nose (70%)
Eye (65%)
Respiratory tract (55%)
Inner ear (45%)
Cardiovascular (25%)
Skin (15%)

Diagnostic criteria (> 3 needed)
Recurrent chondritis of auricles (painful ear)
Inflammation of ocular structures (conjunctivitis, scleritis, keratitis
Chondritis (painful) of laryngeal, tracheal cartilage
Cochlear, vestibular damage

Findings
Tracheal and bronchial wall thickening, narrowing, and progressive calcification
Spares posterior tracheal membrane
Focal or diffuse
Dynamic airway collapse with expiration
Atelectasis, pneumonia in lung distal to stenosis
Bronchiectasis from recurrent infection or destruction of cartilage
Aortic aneurysm
Cardiomegaly from aortic or mitral valve regurgitation

Respiratory bronchiolitis (RB, RB-ILD)
Definitions
Respiratory bronchiolitis (RB)
Asymptomatic
Respiratory bronchiolitis-interstitial lung disease (RB-ILD)
Dyspnea
Restrictive or mixed PFTsSmoking-related interstitial lung disease
Usually > 30 pack years
Good prognosis (reversible with smoking cessation)

Pathology
Peribronchiolar pigmented macrophages
Peribronchiolar fibrosis
Upper lobe predominance

Imaging
Centrilobular nodules
Poorly defined
2-3 mm
Upper lobe predominance
Ground glass opacities
Patchy
Bronchial wall thickening
Air trapping

DDX
Hypersensitivity pneumonitis
Nonspecific interstitial pneumonia (NSIP)
Desquamative interstitial pneumonia (DIP)
Langerhans cell histiocytosis

Rheumatoid arthritis
Pleural disease
Pleural thickening (20%)
Pleural effusion
PneumothoraxPulmonary disease
Rheumatoid lung nodules (20%)
Caplan’s syndrome
Fibrosis
Ground glass opacities and consolidation

Airway disease
Constrictive bronchiolitis
Follicular bronchitis
Bronchogenic granulomatosis

Lymphoid disease
Lymphoid interstitial pneumonia (LIP)

Arterial disease
Arteritis
Pulmonary hypertension

Rhinoscleroma
Pathology
Chronic granulomatous infection of airways
Klebsiella rhinoscleromatis: gram-negative bacteria
Primarily affects nasal cavity (95%) and nasopharynx (50%)
Paranasal sinuses spared unless ostiomeatal units obstructed
Laryngotracheal involvement in 15-40%%Demographics
Age: 10-30 years
F > M

Clinical
Nasal obstruction
Stridor
Epistaxis, rhinorrhea

Imaging
Irregular subglottic mucosal thickening
Diffuse symmetric narrowing
Crypt-like spaces nearly diagnostic

Right middle lobe syndrome

Recurrent or fixed atelectasis or consolidation of right middle lobe (or lingula)

Etiology
Central obstruction (30%)
Lymphadenopathy
Bronchostenosis
Endobronchial tumor
Peripheral obstruction (70%)
Lack of collateral ventilation due to complete fissures
Ineffective cough

Clinical
Chronic cough and nonspecific chest pain

Demographics
Middle-aged
F > M

Imaging
RML collapse with silhouetting of right heart border and wedge-shaped opacity on lateral view
Extrinsic compression from lymph nodes, mass, broncholith
Endobronchial tumor, foreign body
Varying degrees of consolidation and atelectasis
Bronchiectasis

Ritalin abuse
Precocious emphysema in patients who inject ritalin intravenously
Resembles alpha-1-antitrypsin deficiencyImaging
Large lung volumes
Panlobular emphysema
May see diffuse micronodular pattern with subsequent development of upper lobe conglomerate masses

Rounded atelectasis
Features
Volume loss
Ipsilateral pleural disease
Pleural plaques
Pleural effusion
Broad area of pleural contact
Swirling vessels (“comet tail” sign)
Associated with asbestos exposure
Need follow-up CT to exclude cancer
3 mo, 3 mo, 6 mo, 12 mo for total of 2 years
Sarcoidosis, imaging
Lymphadenoapathy (80%)
Symmetric hilar and paratracheal lymphadenopathy (Garland’s triad)
Other mediastinal lymph nodes
Calcifications common (may be eggshell)Pulmonary involvement (20%)
Upper lobe predominance
Perilymphatic nodules in subpleural, peribronchovascular, and septal distribution
Reticulonodular opacities on CXR
Ground-glass opacities
Fibrosis with honeycombing, architectural distortion, and traction bronchiectasis (central and upper lobe predominant)
Progressive massive fibrosis
Cysts, bullae
Secondary mycetomas
Alveolar sarcoidosis: nodular and mass-like areas of consolidation with air bronchograms
Cavitary vessel-associated nodules with necrotizing sarcoid granulomatosis

Pleural involvement
Pleural effusion (10%)
Pneumothorax from ruptured cysts, bullae

Airway involvement
Bronchiectasis
Airway wall thickening and stenoses

Atypical findings
Asymmetric lymphadenopathy
Mediastinal without hilar lymphadenopathy
Cavitation
Multiple masses
Solitary pulmonary nodule

Sarcoidosis, staging
Silzbach classification (plain film)
Stage 0: Initial normal film (10%)
Stage 1: Adenopathy (50%)
Stage 2: Adenopathy with pulmonary opacities (30%)
Stage 3: Pulmonary opacities without hilar adenopathy (10%)
Stage 4: Pulmonary fibrosis with or without adenopathyNatural history and prognosis
Stage 1
More benign course
75% regress to normal within 3 years
10% remain enlarged
15% progress to stages 2 and 3
Stage 2 and 3
20% develop progressive pulmonary fibrosis
Mortality 1-5%
Respiratory failure
Myocardial involvement
Cor pulmonale
Hemorrhage (e.g. mycetoma)

Scleroderma
Type of progressive systemic sclerosis (which also encompasses CREST)
After esophagus, lung is 2nd most common site
75% have evidence of lung disease at autopsy
25% have radiographic evidence of lung disease
1% present with pulmonary symptomsImaging
Interstitial fibrosis (most common)
Honeycombing (60%)
Septal thickening (45%)
Basal, posterior, peripheral predominance
Ground glass opacities may be present
Diffuse pleural thickening (30%)
Pulmonary vasculitis and pulmonary hypertension
Esophageal dilatation (40-80%)

Seminoma
Epidemiology
10-20% of mediastinal germ cell tumors
Most common malignant mediastinal germ cell tumorPathology
Large unencapsulated tumor
Homogeneous soft tissue mass

Demographics
Age 30-40 years
Almost exclusively male

Clinical
Chest pain, dyspnea, cough

Imaging
Large, bulky, well-defined anterior mediastinal mass
Homogeneous density and enhancement
Rare necrosis, cystic change (8%)
Calcification rare

Treatment and prognosis
Radiation therapy
Cisplatin-based chemotherapy
5-year survival nearly 100%

Septal thickening
Smooth
Lymphangitic spread of carcinoma or lymphoma
Pulmonary edema
Alveolar proteinosis
InfectionNodular
Lymphangitic spread of carcinoma or lymphoma
Sarcoidosis
Silicosis
Coal worker’s pneumoconiosis
Amyloidosis
Lymphoid interstitial pneumonia

Irregular
Interstitial fibrosis

Silicosis, imaging
Well-circumscribed nodules
Simple silicosis
1-10 mm
Upper-lobe and posterior predominance due to decreased lymphatic drainage
Perilymphatic, centrilobular and subpleural distribution
More symmetric and evenly distributed than sarcoidosis
Calcific nodulesProgressive massive fibrosis (PMF)
Complicated silicosis
Masses (> 1 cm) formed by coalescent nodules
Upper lobes (apical, posterior)
Lenticular shape with lateral margin paralleling chest wall
Usually bilateral
Migrates centrally with time
Emphysematous lung distal to PMF (risk for pneumothorax)
Superior hilar retraction
Cavitation due to ischemia or superinfection with TB

Pleural lesions
Candle-wax or pseudoplaques
Nodules concentrated along pleural surfaces within lymphatic loops

Lymphadenopathy
Calcifications in 10-20% (may be eggshell)

Silicoproteinosis
Seen with acute silicosis (exposure over few weeks)
Central butterfly alveolar pattern with air bronchograms
Crazy paving

Silicotuberculosis
Cavitation of conglomerate masses
Apical pleural reaction

Caplan syndrome
Manifestation of rheumatoid lung disease
Rhematoid nodules (necrobiotic nodules) on background of simple silicosis
More common with coal worker’s pneumoconiosis

Silicosis, pathology
Mineralogy
Silcon: element
Silicon dioxide (SiO2, silica) in quartz, cristobalite, tridy-mite
Silicone: synthetic polymerEpidemiology
Occupational exposure
Mining (gold, tin, copper, mica), quarrying (quartz), sandblasting, stonecutting, engraving, and foundry work
M > F

Pathology
Particles > 5 um removed by upper airways
Retained particles < 5 um Silica phagocytosed by pulmonary macrophages but not able to be dissolved Cytotoxic reaction causes formation of noncaseating granuloma Granulomas progress to form silicotic nodules (2-3 mm) Pulmonary fibrosis as nodules coalesce Nodules Central dense fibrosis Middle zone of concentric collagen Peripheral zone of dust-laden macrophages Natural history and prognosis Severity of disease related to total amount of inhaled dust Only 5% of patients with > 20 years exposure will develop pneumonconiosis
May be complicated by lung cancer

Treatment
Cease exposure; may progress despite removal from exposure (unlike coal worker’s pneumoconiosis)
Isoniazid (INH) prophylaxis

Small cell lung cancer, imaging
CT
Bulky mediastinal mass
Extensive necrosis, hemorrhage
Bronchial encasement, compression, obstruction
Post-obstructive pneumonitis, collapse
Pulmonary nodules
Pleural effusion
Vascular encasement, SVC syndromePET
Upstages limited disease to extensive disease in 15%

Small cell lung cancer, pathology
Neuroendocrine tumor
20% of primary lung cancerStaging
Limited disease (25%)
Mediastinum, hila, supraclavicular fossa
Feasible port for radiation therapy
Median survival 14-16 months
2-year survival 10%
Treatment: chemotherapy, radiation therapy
Prophylactic cranial irradiation
Extensive disease (75%)
Extra-thoracic disease
Thoracic disease without feasible port (pulmonary metastases, pleural effusion, axillary lymphadenopathy)
Median survival 8-11 months
2-year survival 2%
Treatment: chemotherapy; palliative radiation therapy

Etiology
Strong relationship to tobacco use
Radiation exposure
Exposure to bis-chloromethyl ether

Paraneoplastic syndromes
Limbic encephalitis
Cerebellar degeneration
Dermatomyositis, polymyositis
Eaton-Lambert syndrome
SIADH
Cushing syndrome (ectopic ACTH)
Hypercalcemic hyperparathyroidism

Demographics
Age 40s-60s
M > F

Small lung
Scimitar syndrome
Agenesis of pulmonary artery
Chronic atelectasis
Swyer-James syndrome
Squamous cell carcinoma
30% of lung cancer
Strongly associated with smoking
Arises from proximal segmental bronchi
Fast growth, late metastases
Most favorable prognosisParaneoplastic syndrome
Hyperparathyroidism from PTH-like substance

Findings
Cavitating lung mass (30%)
Wall thickness > 1 cm suggests malignant cavitary lesion
Usually central
Atelectasis, lobar collapse
Chest wall invasion
Pancoast tumor

Sternal dehiscence
Complication of median sternotomy (1-2% of cases)
Most cases ~ 9 days after surgery
Associated with mediastinitis in ~ 50%Predisposing factors
COPD
Obesity
Diabetes
Prolonged bypass time during surgery
Internal mammary artery grafting
Repeat surgery for mediastinal bleeding
Prolonged post-operative ventilation
Paramedian sternotomy (off-center)

Imaging
Midsternal stripe sign: midline vertical lucency over sternum > 3 mm usually abnormal
Progressive widening of midsternal stripe
Displaced (wandering) sternal wires: highly specific for dehiscence (85%)
Rotation (50%) or disruption (20%) of sternal wires
Wire abnormalities may precede clinical detection of dehiscence by mean of 3 days in 70%

Swyer-James syndrome
Unilateral lung hyperlucency
Secondary to virally-induced necrotizing and obliterative bronchiolitis
Hyperlucent, enlarged lung with static lung volume
Attenuation of pulmonary vessels
Systemic lupus erythematosus (SLE)
Pleural disease
Pleural effusion
Pleural thickeningPulmonary disease
Acute lupus pneumonitis
Fibrosing alveolitis

Diaphragmatic disease
Elevation
Basilar atelectasis

Talcosis
Pathology
Intravenous injection of oral medications containing magnesium silicate
When injected, small talc particles lodge in pulmonary vessels leading to foreign body reactionAgents
Ritalin
Cocaine
Heroin
Methadone
Acetaminophen
Meperidine
Diazepam

Imaging
Numerous small nodules
Ground glass opacities from confluent nodules
Upper lobe conglomerate masses
Possible high attenuation
May develop into progressive massive fibrosis

Teratoma
Epidemiology
60-75% of mediastinal germ cell neoplasmsDemographics
Children, young adults (< 30 years) M=F Pathology Large encapsulated tumor Cystic and solid components Elements of multiple germ cell layers Oily, sebaceous material Hair, teeth, bone Types Mature: well-differentiated Immature: >10% immature elements; low potential for malignancy

Clinical
Often asymptomatic
May have symptoms from compression, rupture

Imaging
Multiloculated cystic mass
Internal fat (75%)
May have fat-fluid levels
Soft tssue elements
Calcification

Treatment
Complete excision is curative
5-year survival 100%

Thymic carcinoid
Pathology
Aggressive neuroendocrine tumor
20% have metastases on presentation
50% are functionally active
Does not produce carcinoid syndrome
Associated with Wermer’s syndrome (MEN I) in 19-25%Demographics
Wide age range (average 43 years)
Men > women (3:1)

Clinical
Most present with symptoms related to mass effect or invasion of mediastinal structures
Cushing’s syndrome (ectopic ACTH) in 33-40%

CT
Hypervascular, enhancing solid anterior mediastinal mass
Localized or invasive
Calcifications and small areas of necrosis may be seen
Lymphadenopathy
Metastases to lung, pleura, brain
Osteoblastic bone metastases

Octreotide scan
Accumulation is nonspecific (also seen in other thymic tumors and lymphoma)

Treatment and prognosis
Complete excision may be curative, but local recurrences and metastases develop in 70%
Adjuvant radiation and chemotherapy often used
Poor prognosis: 5-year survival = 30%

Thymic carcinoma
Pathology
Aggressive epithelial carcinomaDemographics
Wide age range (mean 40s)
M > F

Clinical
Chest pain
Weight loss, fatigue
Night sweats

Imaging
Large lobulated, irregular anterior mediastinal mass
Heterogeneous enhancement with areas of necrosis
Calcification (10-40%)
Mediastinal invasion
Lymphadenopathy

Natural history and prognosis
Very poor prognosis
Progressive local growth and distant metastatic disease
5-year survival 30%

Thymic cyst
Pathology
Unilocular or multilocular with septations
Likely remnant of fetal thymopharyngeal ductClinical
Usually asymptomatic
Rare symptoms from mass effect

Imaging
Anterior mediastinal mass with single dominant or multiple thin-walled cysts
Fluid density, intensity
Occasional hemorrhage, calcification
No enhancement

Thymic hyperplasia
Pathology
Lymphoid hyperplasia (autoimmune thymitis)
Myasthenia gravis
Collagen vascular diseases (SLE, scleroderma, RA)
Hyperthyroidism
Addison’s disease
True hyperplasia (rebound thymic hyperplasia)
Follows chemotherapy (2 weeks to 14 months), steroids, or severe insultNormal thymus
< 20 years: < 18 mm > 20 years: < 13 mm > 30 years: convex margins abnormal

Findings
Enlarged thymus without focal mass
Fat interspersed in parenchyma
No increase in size over time

Thymic mass
Thymoma
Thymic carcinoma
Thymic carcinoid
Thymolipoma
Thymic hyperplasia
Thymic cyst
Thymolipoma
Pathology
Benign, encapsulated tumor
Contains both thymic and adipose tissue
Large size (75% > 500g)Demographics
Most common in children and young adults

Associations
Myasthenia gravis: 3% have thymolipomas
Aplastic anemia
Graves’ disease
Hypogammaglobulinemia
Lipomas in thyroid, pharynx

Clinical
Little or no symptoms

Imaging
Anterior, inferior mediastinal mass
Fatty and soft tissue elements
Usually large, conforms to shape of adjacent structures
Positional change in shape
Connection to thymus often seen (pedicle)

Thymoma, imaging
Oval, lobulated mass within anterior mediastinum
Usually asymmetric, projecting to one side
Homogeneous when small; heterogeneous when large
Calcification (1/3)
Capsular thin and linear calcifications
Scattered punctate calcifications less common
Cystic components, necrosis (1/3)Enhancement
No lymphadenopathy
Presence of lymphadenopathy excludes thymoma
Findings compatible with invasion
Indistinctness and obliteration of fat planes
Pericardial thickening, encasement of vessels
Pleural and transdiaphragmatic metastases

Thymoma, parathymic syndromes
Myasthenia gravis (35%)
15% of myastenia patients have thymomaHypogammaglobulinemia (10%)
5% of hypogammaglobulinemia patients have thymoma

Red cell aplasia (5%)
50% of aplastic anemia patients have thymoma

Thymoma, pathology

Most common anterior mediastinal tumor in adult

Demographics
Age > 40 years
M=F

Pathology
Encapsulated and invasive thymoma are histologically identical
Diagnosis of invasive thymoma (30%) depends on visualizing gross or microscopic extension beyond capsule
“Malignant thymoma” not appropriate terminology

Staging
Stage I
Intact capsule
93% 5-year survivial
Stage II
Microscopic capsular invasion
80% 5-year survival
Stage III
Invasion of local structures
70% 5-year survival
Stage IV
Pleural metastases (IVa)
Distant metastases (IVb)
50% 5-year survival

Treatment
Resection
Radiation, chemotherapy

Tracheal bronchus
“Pig bronchus”
Right upper lobe or segmental right upper lobe bronchus originating from trachea
Types
Supernumerary: coexists with normal RUL bronchus
Displaced: replaces RUL or segmental RUL bronchus
No clinical significance
Endotracheal intubation may obstruct bronchus
Tracheal diverticulum

Mucosal herniation through tracheal wall from increased intraluminal pressure

Etiology
Congenital
Supernumerary lung bud containing all layers of tracheal wall
Acquired
Chronic increased intraluminal pressure (coughing, emphysema)
Larger and wider mouth than congenital diverticula
Respiratory epithelium only

Imaging
Small rounded air-filled cyst
Right posterolateral tracheal wall at thoracic inlet
Tracheal communication rarely identified on imaging (multiplanar reformations may be useful)
Enlarges with expiration, shrinks on inspiration
Associated emphysema

Tracheal enlargement (3)
Mounier-Kuhn syndrome
Tracheomalacia
Fibrotic lung disease
Tracheal narrowing (8)

Saber-sheath trachea

Tracheopathia osteochondroplastica

Tracheomalacia

Inflammation
Relapsing polychondritis
Sarcoidosis
Wegener’s granulomatosis

Infection
Tuberculosis
Fungal infection
Rhinoscleroma

Post-intubation

Post-traumatic

Amyloidosis

Tracheal tumors (5 – broad)
Primary malignant tumors
Squamous cell carcinoma
Adenoid cystic carcinoma
Mucoepidermoid carcinoma
CarcinoidPrimary benign tumors
Papilloma
Hamartoma
Hemangioma
Chondroma
Lipoma

Local invasion
Esophageal carcinoma
Thyroid carcinoma
Lung carcinoma

Hematogenous metastases
Melanoma
Breast carcinoma

Tracheobronchial tear
Trachea, left mainstem bronchus
Air leak usually confined to mediastinum and subcutaneous tissuesRight mainstem bronchus, left distal bronchus
Pneumothorax not relieved by chest tube placement

Tracheobronchomalacia

Increased compliance and excessive collapsibility of trachea and bronchi

Etiology
Primary
Congenital weakness
Secondary
COPD
Intubation
Prior surgery
Radiation therapy
Long-standing extrinsic compression (e.g. thyroid mass, vascular ring, aneurysm)
Chronic inflammation (e.g. relapsing polychondritis)
Tracheoesophageal fistula
Trauma
Recurrent infection

Clinical
Intractable cough, dyspnea, wheezing, recurrent respiratory infections
Congenital: expiratory stridor, cough, difficulty feeding

Imaging
“Frown sign”: crescentic narrowing of tracheal lumen during expiration
Trachea may be normal or enlarged during inspiration
>50% reduction in airway lumen at expiration is diagnostic
May be focal or diffuse

Tracheopathia osteochondroplastica
Multiple submucosal osteocartilaginous nodules in tracheobronchial tree
Benign, rare condition
Most cases discovered incidentally at biopsySymptoms
Dyspnea, hoarseness, expiratory wheeze/stridor (airway obstruction)
Hemoptysis (mucosal ulceration)
Cough and sputum production
Pneumonia (rarely)

Demographics
Usually > 50 years
M > F

Findings
Calcified nodularity and thickening of tracheobronchial tree
Spares posterior membranous wall
Narrowed lumen
Distal 3/4 of trachea and proximal bronchi most commonly involved

Tuberculosis, complications (6 – broad)

End-stage lung disease

Hemoptysis
Bronchial artery enlargement and erosion in chronic cavities
Rasmussen aneurysms of pulmonary arteries

Empyema
Bronchopleural fistula
Empyema necessitans: spontaneous discharge of emypema through parietal pleura, most commonly into chest wall to form subcutaneous abscess

Mycetoma
Colonization of cavity

Pericardial involvement
Usually related to adjacent adenopathy
Constrictive pericarditis

Chest wall involvement
Hematogenous or direct spread

Tuberculosis, post-primary
Consolidation (50-70%)
Apical, posterior segments of upper lobes (85%)
Superior segments of lower lobes (14%)
Heterogeneous, nodular, linear
Focal areas of sparingCavitation (40-45%)
Thin or thick walls
Air-fluid levels (20%)
Cavitation, necrosis enable spread via airway, bloodstream, pleura

Nodules
Tuberculoma
Endobronchial TB: centrilobular and tree-in-bud nodules
Miliary TB: random nodules

Airways involvement
Bronchiectasis
Airway narrowing

Tuberculosis, primary
Lymphadenopathy
Hallmark of primary TB
Children (95%), young adults (43%), elderly (10%)
Right paratracheal, hilar
Ranke complex
Peripheral enhancement, central low-attenuationAtelectasis, overinflation
Children
Anterior segments of upper lobes
Medial segment of middle lobe, lingula

Consolidation
Mid and lower lung zones
Ghon focus
Unifocal (75%) > multifocal
May be segmental or lobar
Homogeneous, patchy, linear, nodular

Pleural effusion
Adults (38%), children (11%)
May be primary manifestation of disease
Unilateral pleural effusion in adult is suspicious for TB
Smear, culture usually negative
Pleural biopsy negative in 50%
Low glucose

Vacuthorax
Abnormally stiff lung (fibrosis)
Lung not able to reexpand to fill pleural space
Unlikely to benefit from thoracentesis
Vanishing lung syndrome
Idiopathic giant bullous emphysema
Often seen in young men
Progressive bullae
Asymmetric upper lobe involvement
Paraseptal and centrilobular emphysema
Most are smokers, but occasionally affects nonsmokers
Wegener’s granulomatosis
Upper respiratory tract
Progressive destruction of nasal cartilage and bone
Sinusitis
Eustachian tube obstruction, otitis media
Subglottic stricture
Ulcerative tracheobronchitis
Tracheal or bronchial stenosisPulmonary
Multiple nodules and masses with cavitation
Feeding vessels (88%)
Halo sign
Subpleural predominance
Basilar reticulonodular opacities
Airspace consolidation, hemorrhage
Pleural effusion (25%)
Adenopathy (rare)

GU
Focal glomerulonephritis
Erythrocyte casts and proteniuria
Vasculitis

Skin (50%)
Symmetric papulonecrotic lesions

Eye and orbit (30%)
Scleritis, conjunctivitis
Optic nerve and retro-orbital masses

CNS (30%)
Mononeuritis multiplex

Musculoskeletal
Migratory polyarthropathy

Williams-Campbell syndrome
Congenital bronchial cartilage deficiency
Cystic bronchiectasis
Ballooning of central bronchi on inspiration with collapse on expiration
Distal air trapping
Zonal predominance, Upper (8)
Upper lobes (PB CASSET)
Pneumocystis carinii
Berylliosis
Cystic fibrosis
Ankylosing spondylitis
Silicosis
Sarcoidosis
Eosinophilic granuloma (Langerhans cell histiocytosis)
Tuberculosis
Zonal predominance, Lower (6)
Lower lobes (BADDAS)
Bronchiectasis
Aspiration
Drugs
DIP
Asbestosis
Scleroderma, other collagen vascular diseases

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