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Elsevier - PMC COVID-19 Collection logoLink to Elsevier - PMC COVID-19 Collection
. 2020 Jun 22:1–71. doi: 10.1016/B978-0-323-06538-2.00001-9

Chest Imaging

Editors: Ralph Weissleder1, Jack Wittenberg2, Mukesh G Harisinghani3, John W Chen4
PMCID: PMC7315340

Imaging Anatomy

Gross lung anatomy

Segmental anatomy (Figs. 1-1 and 1-2)

Figure 1-1.

Figure 1-1

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Figure 1-2.

Figure 1-2

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Right Lung
Upper lobe Apical B1
Anterior B2
Posterior B3
Middle lobe Lateral B4
Medial B5
Lower lobe Superior B6
Medial basal B7
Anterior basal B8
Lateral basal B9
Posterior basal B10
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Left Lung
Upper lobe
 Upper Apicoposterior B1, 3
Anterior B2
 Lingula Superior B4
Inferior B5
Lower lobe Superior B6
Medial basal B7
Anterior basal B8
Lateral basal B9
Posterior basal B10
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Segmental CT anatomy (Fig. 1-3)

Figure 1-3.

Figure 1-3

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Bronchial CT anatomy (Fig. 1-4)

Figure 1-4.

Figure 1-4

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Plain film anatomic landmarks (Figure 1-5, Figure 1-6, Figure 1-7, Figure 1-8, Figure 1-9)

Figure 1-5.

Figure 1-5

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Figure 1-6.

Figure 1-6

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Figure 1-7.

Figure 1-7

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Figure 1-8.

Figure 1-8

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Figure 1-9.

Figure 1-9

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Lines
  • •

    Anterior junction line: 2-mm linear line that projects over the trachea. Represents the anterior right and left pleura.

  • •

    Posterior junction line: extends above clavicles

  • •

    Azygoesophageal line: interface between RLL air and mediastinum

  • •

    Left paraspinal line: extends from aortic arch to diaphragm

  • •

    Right paraspinal line

Paratracheal Stripe
  • •

    Abnormal if >4 mm

  • •

    Never extends below right bronchus

Fissures
    • •
      Minor (horizontal) fissure
    • •
      Major (oblique) fissure
    • •
      Azygos fissure
    • •
      Other fissures
      • Superior accessory lobe
      • Inferior accessory lobe
Upper Lobe Bronchi (Figs. 1-10 and 1-11)
Figure 1-10.

Figure 1-10

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Figure 1-11.

Figure 1-11

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    • •
      RUL bronchus always higher than LUL on lateral view
    • •
      Posterior wall of bronchus intermedius (right) normally <2 mm
    • •
      Tracheal bronchus (bronchus suis): 0.1% of population, arises from right wall of trachea (left much less common), supplies apical segment or occasionally entire right upper lobe
    • •
      Accessory cardiac bronchus: 0.1% of population, extends inferomedially from medial wall of bronchus intermedius or RLL bronchus toward mediastinum; may be blind ending

Parenchymal anatomy

Acinus

    • •
      Includes all structures distal to one terminal bronchiole. The terminal bronchiole is the last purely air-conducting structure.
    • •
      Acinus measures 7 mm
    • •
      Acinus contains about 400 alveoli

Secondary pulmonary lobule

    • •
      Polygonal structure, 1.5 to 2 cm in diameter
    • •
      Three to five acini per secondary lobule
    • •
      Supplied by several terminal bronchioles

Epithelium

  • The alveolar epithelium is made up of two cell types:
    • •
      Type 1 pneumocytes
    • •
      Type 2 pneumocytes: produce surfactant, have phagocytic ability, and regenerate

High-resolution computed tomography (HRCT) (Fig. 1-12)

Figure 1-12.

Figure 1-12

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Technique
    • •
      1- to 1.5-mm thin collimation
    • •
      High spatial frequency reconstruction
    • •
      Optional
      • Increase in kVp or mA (140 kVp, 170 mA)
      • Targeted image reconstruction (one lung rather than both to improve spatial resolution)
HRCT Anatomy
  • The basic pulmonary unit visible by HRCT represents the secondary pulmonary lobule:
    • •
      Polyhedral 1.5-cm structure surrounded by connective tissue (interlobular septa)
    • •
      Central artery and bronchiole
    • •
      Peripheral pulmonary veins and lymphatics in septum

Pulmonary function (Fig. 1-13)

Figure 1-13.

Figure 1-13

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Lung volumes, capacities, and flow rates

    • •
      Tidal volume (TV): normal respiratory cycle
    • •
      Vital capacity (VC): amount of air that can be expired with force after maximal inspiration
    • •
      Functional residual capacity (FRC): volume remaining in lung after quiet expiration
    • •
      Total lung capacity (TLC): volume contained in lung at maximum inspiration
    • •
      Forced expiratory volume (FEV): amount of air expired during 1 second (FEV1)

Mediastinum (Fig. 1-14)

Figure 1-14.

Figure 1-14

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    • •
      Superior mediastinum: plane above aortic arch; thoracic inlet structures
    • •
      Anterior mediastinum: contains thymus, lymph nodes, mesenchymal tissue; some classifications include the heart
    • •
      Middle mediastinum: contains heart, major vessels, bronchi, lymph nodes, and phrenic nerve
    • •
      Posterior mediastinum: starts at anterior margin of vertebral bodies; contains descending aorta, esophagus, thoracic duct, lymph nodes, nerves, and paravertebral areas

Imaging protocols

Standard chest ct protocol

Supine position. Scan in suspended inspiration at total lung capacity. Scan setup:

    • •
      5- × 5-mm sections from apex of the lungs to the adrenals
    • •
      Six 1.25-mm high-resolution cuts throughout lung at 2.5-cm intervals
    • •
      1-mm reconstructions through pulmonary nodules
    • •
      Number of different combinations of pitch and section thickness

In interstitial lung disease, the six cuts are repeated in prone position. Reconstruction is done with high-resolution bone algorithm.

  • Use of IV contrast:
    • •
      Evaluation of vascular structures, AVM, aortic dissection
    • •
      Evaluation of mediastinal tumors, enlarged lymph nodes
    • •
      Hilar masses
    • •
      Neck masses

Pulmonary embolism CT protocol

    • •
      Patient in supine position
    • •
      Scan range: adrenals to lung apex
    • •
      Injection of 140 mL of nonionic iodinated contrast at 3 mL/sec, with delay of 25 to 30 seconds. Scanning is performed with suspended respiration.
    • •
      Scans are retrospectively reconstructed from the dome of the diaphragm as 2.5-mm thick slices with 1-mm spacing.

Diagnostic radiology report (ACR)

An authenticated written interpretation should be performed on all radiologic procedures. The report should include the following items:

    • 1.
      Name of patient and other identifier (e.g., birth date, Social Security number, or hospital or office identification number)
    • 2.
      Name of the referring physician to provide more accurate routing of the report to one or more locations specified by the referring physician (e.g., hospital, office, clinic)
    • 3.
      History
    • 4.
      Name or type of examination
    • 5.
      Dates of the examination and transcription
    • 6.
      Time of the examination (for ICU/CCU patients) to identify multiple examinations (e.g., chest) that may be performed on a single day
    • 7.
      Body of the report:
      • •
        Procedures and materials
        • Include in the report a description of the procedures performed and any contrast media (agent, concentration, volume and reaction, if any), medications, catheters, and devices.
      • •
        Findings
        • Use precise anatomic and radiologic terminology to describe the findings accurately.
      • •
        Limitations
        • Where appropriate, identify factors that can limit the sensitivity and specificity of the examination. Such factors might include technical factors, patient anatomy, limitations of the technique, incomplete bowel preparation, and wrist examination for carpal scaphoid.
      • •
        Clinical issues
        • The report should address or answer any pertinent clinical issues raised in the request for the imaging examination. For example, to rule out pneumothorax state “There is no evidence of pneumothorax”; or to rule out fracture, “There is no evidence of fracture.” It is not advisable to use such universal disclaimers as “The mammography examination does not exclude the possibility of cancer.”
      • •
        Comparative data
        • Comparisons with previous examinations and reports when possible are a part of the radiologic consultation and report and optionally may be part of the “impression” section.
    • 8.
      Impression (conclusion or diagnosis)
      • •
        Each examination should contain an “impression” section.
      • •
        Give a precise diagnosis whenever possible.
      • •
        Give a differential diagnosis when appropriate.
      • •
        Recommend, only when appropriate, follow-up and additional diagnostic radiologic studies to clarify or confirm the impression.

Infection

General

Pathogens

    • Bacterial pneumonia
      • •
        Streptococcus pneumoniae (pneumococcus)
      • •
        Staphylococcus
      • •
        Pseudomonas
      • •
        Klebsiella
      • •
        Nocardia
      • •
        Chlamydia
      • •
        Neisseria meningitides
      • •
        Haemophilus influenzae
      • •
        Anaerobes
      • •
        Legionella
      • •
        Mycoplasma pneumoniae
      • •
        Actinomyces israelii
      • •
        Mycobacterium tuberculosis
    • Viral pneumonia (25% of community-acquired pneumonias)
      • •
        Influenza
      • •
        Varicella, herpes zoster
      • •
        Rubeola
      • •
        Cytomegalovirus (CMV)
      • •
        Coxsackievirus, parainfluenza virus, adenovirus, respiratory syncytial virus (RSV)
    • Fungal pneumonia
      • •
        Histoplasmosis
      • •
        Coccidioidomycosis
      • •
        Blastomycosis
      • •
        Aspergillosis
      • •
        Cryptococcosis
      • •
        Candidiasis
      • •
        Zygomycoses
    • Parasitic pneumonias
      • •
        Pneumocystis jiroveci Frenkel 1999 (formerly Pneumocystis carinii)
      • •
        Toxoplasma gondii

Acquisition of pneumonia

    • Community-acquired pneumonia
      • •
        S. pneumoniae, Haemophilus
      • •
        Mycoplasma
    • Hospital-acquired pneumonia (incidence 1%, mortality 35%): nosocomial infection
      • •
        Gram negatives: Pseudomonas, Proteus, Escherichia coli, Enterobacter, Klebsiella
      • •
        Methicillin-resistant Staphylococcus aureus (MRSA)
      • •
        Vancomycin-resistant enterococcus (VRE)
    • Pneumonia in immunosuppressed patients
      • •
        Bacterial pneumonia (gram negative) still most common
      • •
        Tuberculosis
      • •
        Fungal
      • •
        Pneumocystis pneumonia (PCP)
    • Endemic pneumonias
      • •
        Fungal: histoplasmosis, coccidioidomycosis, blastomycosis
      • •
        Viral
    • Aspiration-associated pneumonia (important)

Risk factors

The radiographic appearance of pulmonary infections is variable depending on pathogen, underlying lung disease, risk factors, and prior or partial treatment.

Community-Acquired Infections

Risk Factor Common Pathogens
Alcoholism Gram negatives, Streptococcus pneumoniae, M. tuberculosis, aspiration (mouth flora)
Old age S. pneumoniae, Staphylococcus aureus, aspiration
Aspiration Mouth flora (anaerobes)
Cystic fibrosis Pseudomonas, S. aureus, Aspergillus
Chronic bronchitis S. pneumoniae, H. influenzae
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    • Other risk factors for developing pneumonia:
      • •
        Bronchiectasis
      • •
        Coma, anesthesia, seizures (aspiration)
      • •
        Tracheotomy
      • •
        Antibiotic treatment
      • •
        Immunosuppression (renal failure, diabetes, cancer, steroids, AIDS)
      • •
        Chronic furunculosis (Staphylococcus)

Radiographic spectrum of pulmonary infections

Summary

Type Pathogen Imaging
Lobar Pneumonia
Infection primarily involves alveoli
Spread through pores of Kohn and canals of Lambert throughout a segment and ultimately an entire lobe
Bronchi are not primarily affected and remain air-filled; therefore:
  Air bronchograms
  No volume loss because airways are open
Nowadays uncommon due to early treatment
Round pneumonia (children): S. pneumoniae 		S. pneumoniae
K. pneumoniae
Others
 S. aureus
 H. influenzae
  Fungal		 Inline graphic
Inline graphic
Type Pathogen Imaging
Bronchopneumonia
Primarily affects the bronchi and adjacent alveoli
Volume loss may be present as bronchi fill with exudate
Bronchial spread results in multifocal patchy opacities		 S. aureus
Gram negatives
Others
  H. influenzae Mycoplasma 		graphic file with name u01-02-9780323065382.gif
Nodules
Variable in size
Indistinct margins		 Fungal
  Histoplasma
  Aspergillus
  Cryptococcus
  Coccidioides
Bacterial
  Legionella
  Nocardia
Septic emboli
  S. aureus 		graphic file with name u01-03-9780323065382.gif
Cavitary Lesions
Abscess: necrosis of lung parenchyma ± bronchial communication
Fungus ball (air crescent sign)
Pneumatoceles due to air leak into pulmonary interstitium (S. aureus) 		Anaerobes
Fungal
TB		 graphic file with name u01-04-9780323065382.gif
Diffuse Opacities
Reticulonodular pattern: interstitial peribronchial areas of inflammation (viral)
Alveolar location (PCP)
Miliary pattern: hematogenous spread (TB)		 Viral
Mycoplasma
PCP		 graphic file with name u01-05-9780323065382.gif
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Complications of Pneumonia
    • •
      Parapneumonic effusion
      • Stage 1: exudation: free flowing
      • Stage 2: fibropurulent: loculated
      • Stage 3: organization, erosion into lung or chest wall
    • •
      Empyema
    • •
      Bronchopleural fistula (fistula between bronchus and pleural space) with eroding pleural-based fluid collections
    • •
      Bronchiectasis
    • •
      Pulmonary fibrosis, especially after necrotizing pneumonia or acute respiratory distress syndrome (ARDS)
    • •
      Adenopathy

Resolution of pneumonia

    • •
      80%-90% resolve within 4 weeks
    • •
      5%-10% resolve within 4 to 8 weeks (usually in older or diabetic patients). Subsequent films should always show interval improvement compared with the prior films.
    • •
      Nonclearance
      • Antibiotic resistance
      • Consider other pathogen (e.g., M. tuberculosis)
      • Recurrent infection
      • Obstruction pneumonitis due to tumor

Bacterial infections

General

Common Pathogens
    • •
      S. pneumoniae, 50% (40 to 60 years)
    • •
      Mycoplasma, 30%
    • •
      Anaerobes, 10%
    • •
      Gram negatives, 5%
    • •
      Staphylococcus, 5%
    • •
      Haemophilus, 3% (especially in infants and patients with COPD)
Clinical Findings
    • Pneumonic syndrome
      • •
        Fever
      • •
        Cough
      • •
        Pleuritic pain
      • •
        Sputum
    • Ancillary findings
      • •
        Headache, arthralgia, myalgia
      • •
        Diarrhea
      • •
        Hemoptysis

Streptococcal pneumonia

Radiographic Features
    • •
      Lobar or segmental pneumonia pattern
    • •
      Bronchopneumonia pattern
    • •
      Round pneumonia (in children)

Staphylococcal pneumonia (Fig. 1-15)

Figure 1-15.

Figure 1-15

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Radiographic Features
    • •
      Bronchopneumonia pattern
    • •
      Bilateral, >60%
    • •
      Abscess cavities, 25%-75%
    • •
      Pleural effusion, empyema, 50%
    • •
      Pneumatoceles, 50% (check valve obstruction), particularly in children
    • •
      Central lines
    • •
      Signs of endocarditis

Pseudomonas pneumonia

Typical Clinical Setting
    • •
      Hospital-acquired infection
    • •
      Ventilated patient
    • •
      Reduced host resistance
    • •
      Patients with cystic fibrosis
Radiographic Features
  • Three presentations:
    • •
      Extensive bilateral parenchymal consolidation (predilection for both lower lobes)
    • •
      Abscess formation
    • •
      Diffuse nodular disease (bacteremia with hematogenous spread; rare)

Legionnaires' disease

Severe pulmonary infection caused by Legionella pneumophila; 35% require ventilation, 20% mortality. Most infections are community acquired. Patients have hyponatremia. Seroconversion for diagnosis takes 2 weeks.

Radiographic Features
    • Common features
      • •
        Initial presentation of peripheral patchy consolidation
      • •
        Bilateral severe disease
      • •
        Rapidly progressive
      • •
        Pleural effusions, <50%
      • •
        Lower lobe predilection
    • Uncommon features
      • •
        Abscess formation
      • •
        Lymph node enlargement

Haemophilus pneumonia

Caused by Haemophilus influenzae. Occurs most commonly in children, immunocompromised adults, or patients with COPD. Often there is concomitant meningitis, epiglottitis, and bronchitis.

Radiographic Features
    • •
      Bronchopneumonia pattern
    • •
      Lower lobe predilection, often diffuse
    • •
      Empyema

Mycoplasma pneumonia

Most common nonbacterial pneumonia (atypical pneumonia). Mild course. Age 5 to 20 years. Positive cold agglutinins, 60%.

Radiographic Features
    • •
      Reticular pattern
    • •
      Lower lobe predominance, often diffuse
    • •
      Consolidation, 50%
Complications
    • •
      Autoimmune hemolytic anemia
    • •
      Erythema nodosum, erythema multiforme
    • •
      Stevens-Johnson syndrome
    • •
      Meningoencephalitis

Klebsiella (friedländer) pneumonia

Gram-negative organism. Often in debilitated patients and/or alcoholics.

Radiographic Features
    • •
      Consolidation appears similar to that of infection with S. pneumoniae
    • •
      Lobar expansion
    • •
      Cavitation, 30%-50%, typically multiple
    • •
      Massive necrosis (pulmonary gangrene)
    • •
      Pleural effusion uncommon

Tuberculosis (TB) (Fig. 1-16)

Figure 1-16.

Figure 1-16

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Transmitted by inhalation of infected droplets of Mycobacterium tuberculosis or M. bovis. TB usually requires constant or repeated contact with sputum-positive patients because the tubercle does not easily grow in the immunocompetent human host. Target population includes:

    • •
      Patients of low socioeconomic scale (homeless)
    • •
      Alcoholics
    • •
      Immigrants: Mexico, Philippines, Indochina, Haiti
    • •
      Elderly patients
    • •
      AIDS patients
    • •
      Prisoners
Primary Infection (Fig. 1-17)
Figure 1-17.

Figure 1-17

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  • Usually heals without complications. Sequence of events includes:
    • •
      Pulmonary consolidation (1 to 7 cm); cavitation is rare; lower lobe (60%) > upper lobes
    • •
      Caseous necrosis 2 to 10 weeks after infection
    • •
      Lymphadenopathy (hilar and paratracheal), 95%
    • •
      Pleural effusion, 10%
    • •
      Spread of a primary focus occurs primarily in children or immunosuppressed patients
Secondary Infection (Fig. 1-18)
Figure 1-18.

Figure 1-18

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Active disease in adults most commonly represents reactivation of a primary focus. However, primary disease is now also common in adults in developed countries because there is no exposure in childhood. Distribution is as follows:

    • •
      Typically limited to apical and posterior segments of upper lobes or superior segments of lower lobes (because high Po2?)
    • •
      Rarely in anterior segments of upper lobes (in contradistinction to histoplasmosis)
Radiographic Features
    • •
      Exudative tuberculosis
      • Patchy or confluent airspace disease
      • Adenopathy uncommon
    • •
      Fibrocalcific tuberculosis
      • Sharply circumscribed linear densities radiating to hilum
    • •
      Cavitation, 40%
Complications (Fig. 1-19)
Figure 1-19.

Figure 1-19

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    • •
      Miliary TB may occur after primary or secondary hematogenous spread.
    • •
      Bronchogenic spread occurs after communication of the necrotic area with a bronchus; it produces an acinar pattern (irregular nodules approximately 5 mm in diameter).
    • •
      Tuberculoma (1 to 7 cm): nodule during primary or secondary TB; may contain calcification
    • •
      Effusions are often loculated.
    • •
      Bronchopleural fistula
    • •
      Pneumothorax

Comparison

Primary TB Reinfection TB
Location Usually bases Upper lobes, superior segment
LL
Appearance Focal Patchy
Cavitation No Frequent
Adenopathy as only finding Common No
Effusion Common Uncommon
Miliary pattern Yes Yes
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Nontuberculous mycobacterial (NTMB) infections

The two most common NTMB pathogens are M. avium-intracellulare and M. kansasii (less common: M. xenopi, M. chelonei, M. gordonae, M. fortuitum = “fast grower”). Unlike TB, NTMB infections are not acquired by human-human transmission but are a direct infection from soil or water. There is also no pattern of primary disease or reactivation: the infection is primary, although some may become chronic. The infection often occurs in elderly patients with COPD, older women in good health, and AIDS patients.

Radiographic Features
    • •
      NTMB infections may be indistinguishable from classic TB.
    • •
      Atypical features such as bronchiectasis and bronchial wall thickening are common.
    • •
      Nodules are common in older women.

CT Findings

Findings TB (%) MAI %
Nodules <1 cm 80 95
Nodules 1-3 cm 40 30
Mass >3 cm 10 10
Consolidation 50 50
Cavity 30 30
Bronchiectasis 30 95
Bronchial wall thickening 40 95
Septal thickening 50 15
Emphysema 20 20
Calcified granuloma 15 5
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Nocardia pneumonia

Caused by Nocardia asteroides, worldwide distribution. Common opportunistic invader in:

    • •
      Lymphoma
    • •
      Steroid therapy; especially transplant patients
    • •
      Pulmonary alveolar proteinosis (common)
Radiographic Features
    • •
      Focal consolidation (more common)
    • •
      Cavitation
    • •
      Irregular nodules

Actinomycosis

Actinomycosis is caused by Actinomyces israelii, a gram-positive normal saprophyte in oral cavity. Pulmonary disease develops from aspiration of organism (poor dentition) or from direct penetration into the thorax.

Radiographic Features
    • •
      Focal consolidation > cavitating mass
    • •
      Lymphadenopathy uncommon
    • •
      Extension into the chest wall and pleural thickening is less common today but still occurs and represents an important differential feature.

Pulmonary abscess

The spectrum of anaerobic pulmonary infections includes:

    • •
      Abscess: single or multiple cavities >2 cm, usually with air-fluid level
    • •
      Necrotizing pneumonia: analogous to abscess but more diffuse and cavities <2 cm
    • •
      Empyema: suppurative infection of the pleural space, most commonly as a result of pneumonia
Predisposing Conditions
    • •
      Aspiration (e.g., alcoholism, neurologic disease, coma)
    • •
      Intubation
    • •
      Bronchiectasis, bronchial obstruction
Treatment
    • •
      Antibiotics, postural drainage
    • •
      Percutaneous drainage of empyema
    • •
      Drainage/resection of lung abscess only if medical therapy fails

Sickle cell anemia

    • •
      Patients with sickle cell disease are at increased risk of pneumonia and infarction. These entities are difficult to differentiate, hence called acute chest syndrome.
    • •
      Pneumonias were originally due to pneumococci but now are due to viruses or Mycoplasma. Differential diagnosis includes atelectasis and infarct.
    • •
      Infarcts more frequent in adults than in children. Rare in children under 12 years of age.
    • •
      Consolidation is seen on chest films; resolves more slowly than in the general population, and tends to recur.

Viral pneumonia

General

Classification
    • DNA viruses
      • Unenveloped
        • •
          Parvoviruses
        • •
          Papovaviruses
        • •
          Adenoviruses
        • •
          Hepatitis viruses (hepatitis B)
      • Enveloped
        • •
          Herpesviruses (herpes simplex, Epstein-Barr, varicella zoster, CMV)
        • •
          Poxviruses (variola, molluscum contagiosum)
    • RNA viruses
      • Unenveloped
        • •
          Picornaviruses (hepatitis A, coxsackievirus)
        • •
          Caliciviruses
        • •
          Reoviruses
      • Enveloped
        • •
          Retroviruses (HIV)
        • •
          Arenaviruses
        • •
          Coronaviruses
        • •
          Togaviruses
        • •
          Bunyaviruses
        • •
          Orthomyxoviruses (influenza)
        • •
          Paramyxoviruses (mumps, measles, RSV, parainfluenza)
Occurrence
        • Immunocompetent hosts
          • Influenza
          • Hantavirus
          • Epstein-Barr
          • Adenovirus
        • Immunocompromised hosts
          • Herpes simplex
          • Varicella-zoster
          • Cytomegalovirus
          • Adenovirus
Spectrum of Disease
    • •
      Acute interstitial pneumonia: diffuse or patchy interstitial pattern, thickening of bronchi, thickened interlobar septa
    • •
      Lobular inflammatory reaction: multiple nodular opacities 5 to 6 mm (varicella; late calcification)
    • •
      Hemorrhagic pulmonary edema: mimics bacterial lobar pneumonia
    • •
      Pleural effusion: usually absent or small
    • •
      Chronic interstitial fibrosis (bronchiolitis obliterans)
Virus Centrilobular Nodules Lobar Ground-glass Diffuse Ground-glass Thickened Interlobular Septa Consolidation
Influenza +++ +++ + +
Epstein-Barr + + + +
CMV ++ ++ ++ + +
Varicella-zoster +++ + +
Herpes simplex + +++ + +++
Measles ++ + + +
Hantavirus +++ + ++
Adenovirus ++ + +++
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Influenza pneumonia

Influenza is very contagious and thus occurs in epidemics. Pneumonia, however, is uncommon.

Radiographic Features
    • •
      Acute phase: multiple acinar densities
    • •
      Coalescence of acinar densities to diffuse patchy airspace disease (bronchopneumonia type)

Varicella zoster pneumonia

Fifteen percent of infected patients have pneumonias; 90% are older than 20 years.

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

CMV pneumonia

Occurs most commonly in neonates or immunosuppressed patients.

Radiographic Features
    • •
      Predominantly interstitial infection, multiple small nodules (common)
    • •
      Adenopathy may be present

Swine-origin influenza a (H1N1) virus (S-OIV) infection

Epidemiologic data to date suggest that the newly emerged H1N1 virus, although transmissible from person to person, is of relatively low virulence. Chest radiographs are normal in more than half of patients. However, the disease can progress to bilateral extensive airspace disease in severely ill patients. These patients are also at a high risk for PE, which should be sought carefully on contrast enhanced CT scans.

Fungal infections

General

  • Two broad categories:
    • Endemic human mycoses (prevalent only in certain geographic areas):
      • •
        Histoplasmosis (Ohio, Mississippi, St. Lawrence River valleys)
      • •
        Coccidioidomycosis (San Joaquin Valley)
      • •
        Blastomycosis
    • Opportunistic mycoses (worldwide in distribution) occur primarily in immunocompromised patients (aspergillosis and cryptococcosis may also occur in immunocompetent hosts).
      • •
        Aspergillosis
      • •
        Candidiasis
      • •
        Cryptococcosis
      • •
        Mucormycosis
Radiographic Features
    • •
      Acute phase: pneumonic type of opacity (may be segmental, nonsegmental, or patchy); miliary (hematogenous) distribution in immunosuppressed patients
    • •
      Reparative phase: nodular lesions with or without cavitations and crescent sign
    • •
      Chronic phase: calcified lymph nodes or pulmonary focus with fungus (e.g., histoplasmosis)
    • •
      Disseminated disease (spread to other organs) occurs primarily in immunocompromised patients

Histoplasmosis (Fig. 1-20)

Figure 1-20.

Figure 1-20

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Histoplasma capsulatum is particularly prevalent in the Ohio, Mississippi, and St. Lawrence River valleys, although the agent is worldwide in distribution. The organism is most prevalent in soil that contains excrement of bats and birds (bat caves, chicken houses, old attics, or buildings).

Clinical Findings

Most patients are asymptomatic or have nonspecific respiratory symptoms, increased complement fixation titer, and positive H. capsulatum antigen.

Radiographic Features
    • Consolidation (primary histoplasmosis)
      • •
        Parenchymal consolidation
      • •
        Adenopathy is very common and may calcify heavily later on.
    • Nodular form (chronic histoplasmosis, reinfection)
      • •
        Histoplasmoma: usually solitary, sharply circumscribed nodule, most commonly in lower lobes
      • •
        Fibrocavitary disease in upper lobes indistinguishable from postprimary TB
      • •
        Cavitary nodules
    • Disseminated form (immunocompromised patients)
      • •
        Miliary nodules
      • •
        Calcifications in liver and spleen
Mediastinal Histoplasmosis

Mediastinal histoplasmosis may follow pulmonary histoplasmosis. Two distinct entities (which may not always be separable from each other):

    • Mediastinal granuloma
      • •
        Results from spread of H. capsulatum to lymph nodes
      • •
        Granulomas usually calcified
    • Mediastinal fibrosis (fibrosing mediastinitis)
      • •
        May cause superior vena cava syndrome, airway compression, PA occlusion, pericarditis
      • •
        Diffuse infiltration of mediastinum
      • •
        Multiple densely calcified nodes

Coccidioidomycosis (Fig. 1-21)

Figure 1-21.

Figure 1-21

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Coccidioides immitis is endemic in the southwest United States (San Joaquin Valley, “valley fever”) and in Central and South America. Infection occurs due to inhalation of spores in soil. Human-to-human infection does not occur.

Clinical Findings

Cutaneous manifestations common; 70% are asymptomatic.

Radiographic Features
    • Consolidation (primary form)
      • •
        “Fleeting” parenchymal consolidation, most commonly lower lobes
      • •
        Adenopathy in 20%
    • Nodular form (chronic form, 5%)
      • •
        15% cavitate
        • 50% have thin-walled cavity (suggestive of diagnosis)
        • 50% have thick-walled cavity (i.e., nonspecific)
        • May present with pneumothorax
      • •
        Nodules rarely calcify.
      • •
        Hilar or paratracheal adenopathy
    • Disseminated form (immunocompromised patients; rare: 0.5% of all forms)
      • •
        Miliary nodules
      • •
        Extrapulmonary spread

North american blastomycosis (Fig. 1-22)

Figure 1-22.

Figure 1-22

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    • •
      Caused by Blastomyces dermatitidis; uncommon infection. Most infections are self-limited.
    • •
      CXR is nonspecific: airspace disease > nodule (15% cavitate) or solitary mass > miliary spread.
    • •
      Focal blastomycosis typically occurs in paramediastinal location and has an air bronchogram, findings that may suggest the diagnosis.
    • •
      Satellite nodules around primary focus are common.
    • •
      Adenopathy, pleural effusions, and calcifications are very uncommon.
    • •
      Bone lesions, 25%
    • •
      Skin lesions are common.

Aspergillosis (Fig. 1-23)

Figure 1-23.

Figure 1-23

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Aspergillus is a ubiquitous fungus that, when inhaled, leads to significant lung damage. The fungus grows in soil, water, decaying vegetation, and hospital air vents. Infection with A. fumigatus > A. flavus, A. niger, or A. glaucus. There are four unique forms of pulmonary aspergillosis, each associated with a specific immune status.

Types of Aspergillosis

Type Lung Structure Immune Status Pathology
Allergic (ABPA) Normal Hypersensitivity Hypersensitivity → bronchiectasis, mucus plugging
Aspergilloma Preexisting cavity Normal Saprophytic growth in preexisting cavity
Invasive Normal Severely impaired Vascular invasion, parenchymal necrosis
Semi-invasive Normal Normal or impaired Chronic local growth, local cavity formation
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Allergic bronchopulmonary aspergillosis (ABPA)

ABPA represents a complex hypersensitivity reaction (type 1) to Aspergillus, occurring almost exclusively in patients with asthma and occasionally cystic fibrosis. The hypersensitivity initially causes bronchospasm and bronchial wall edema (IgE mediated); ultimately there is bronchial wall damage, bronchiectasis, and pulmonary fibrosis.

Clinical Findings

Elevated Aspergillus-specific IgE, elevated precipitating IgG against Aspergillus, peripheral eosinophilia, positive skin test. Treatment is with oral prednisone.

Radiographic Features
    • •
      Fleeting pulmonary alveolar opacities (common manifestation)
    • •
      Central, upper lobe saccular bronchiectasis (hallmark) (Fig. 1-24A )
    • •
      Mucus plugging (“finger-in-glove” appearance) (Fig. 1-24B) and bronchial wall thickening (common)
    • •
      Chronic disease may progress to pulmonary fibrosis predominantly in upper lobe (end stage).
    • •
      Cavitation, 10%
Figure 1-24.

Figure 1-24

Figure 1-24

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Aspergilloma (mycetoma, fungus ball)

Represents a saprophytic infection in preexisting structural lung disease (cavitary or bulla from TB, end-stage sarcoid, emphysema). Commonly in upper lobes, solitary lesions. The fungus grows in the cavity, creating a “fungus ball” consisting of fungus, mucus, and inflammatory cells. Treatment is with surgical resection and intracavitary administration of amphotericin.

Radiographic Features
    • •
      Focal intracavitary mass (3 to 6 cm), typically in upper lobes
    • •
      Air may surround the aspergilloma (Monod sign), mimicking the appearance of cavitation seen with invasive aspergillosis.
    • •
      Small area of consolidation around cavity is typical.
    • •
      Adjacent pleural thickening common
    • •
      Fungus ball moves with changing position

Invasive aspergillosis

Invasive aspergillosis has a high mortality (70%-90%) and occurs mainly in severely immunocompromised patients (bone marrow transplants, leukemia). The infection starts with endobronchial fungal proliferation and then leads to vascular invasion with thrombosis and infarction of lung (“angioinvasive infection”). Additional sites of infection (in 30%) are brain, liver, kidney, GI tract. Treatment is with systemic and/or intracavitary administration of amphotericin.

Radiographic Features (Fig. 1-25)
Figure 1-25.

Figure 1-25

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    • •
      Multiple pulmonary nodules, 40%
    • •
      Nodules have a characteristic halo of ground-glass appearance (represents pulmonary hemorrhage)
    • •
      Within 2 weeks, 50% of nodules undergo cavitation, which results in the air crescent sign. The appearance of the air crescent sign indicates the recovery phase (increased granulocytic response). Note that the air crescent sign may also be seen in TB, actinomycosis, mucormycosis, septic emboli, and tumors. Do not confuse the air crescent sign with the Monod sign (clinical history helps to differentiate).
    • •
      Other manifestations:
      • Peribronchial opacities
      • Focal areas of consolidation

Semi-invasive aspergillosis

This form of aspergillosis occurs in mildly immunocompromised patients and has a pathophysiology similar to that of invasive aspergillosis except that the disease progresses more chronically over months (mortality: 30%). Risk factors include diabetes, alcoholism, pneumoconiosis, malnutrition, and COPD. Treatment is with systemic and/or intracavitary administration of amphotericin.

Radiographic Features
    • •
      Appearance similar to that of invasive aspergillosis
    • •
      Cavitation occurs at 6 months after infection

Cryptococcosis

Caused by Cryptococcus neoformans, which is worldwide in distribution and ubiquitous in soil and pigeon excreta. Infection occurs through inhalation of contaminated dust.

Clinical Findings

Common in patients with lymphoma, steroid therapy, diabetes, and AIDS.

Radiographic Features
    • •
      Most common findings in lung are pulmonary mass, multiple nodules, or segmental or lobar consolidation.
    • •
      Cavitation, adenopathy, and effusions are rare.
    • •
      Disseminated form: CNS, other organs

Candidiasis

Caused by Candida albicans > other Candida species.

Clinical Findings

Typically in patients with lymphoreticular malignancy; suspect pulmonary disease if associated with oral disease. Often there is disseminated fungemia.

Radiographic Features
    • •
      Plain film is nonspecific: opacities (lower lobe) > nodules
    • •
      Nodular disease in disseminated form
    • •
      Pleural effusion, 25%
    • •
      Cavitation and adenopathy are rare.

Zygomycoses

    • Group of severe opportunistic mycoses caused by fungi of the Zygomycetes class:
      • •
        Mucormycosis (Mucor)
      • •
        Rhizopus
      • •
        Absidia
    • Zygomycoses usually have two major clinical manifestations:
      • •
        Pulmonary mucormycosis
      • •
        Rhinocerebral mucormycosis

Zygomycoses are uncommon infections and occur primarily in immunocompromised patients (leukemia, AIDS, chronic steroid use, diabetes).

Radiographic Features
    • •
      Radiographic features similar to those of invasive aspergillosis because of angioinvasive behavior of fungi

Aids

General

Acquired immunodeficiency syndrome is caused by HTLV type III (human T-cell lymphotrophic virus = HIV [human immunodeficiency virus]). HIV-1 and HIV-2 viruses are single-stranded RNA viruses that bind to CD4 present on T lymphocytes (other cells: glial cells, lung monocytes, dendritic cells in lymph nodes). The viral RNA genome is copied into DNA with the help of reverse transcriptase and integrated into the host cellular DNA.

Epidemiology

The U.S. Centers for Disease Control and Prevention (CDC) estimates that at the end of 2008, there were 682,668 people living with a diagnosis of HIV infection in the 50 states and five U.S.–dependent areas. However, the total number of people living with an HIV infection in the U.S. is thought to be more than 1 million. Groups at highest risk include:

    • •
      Homosexual males, bisexual males, 60%
    • •
      IV drug abusers (IVDAs), 25%
    • •
      Recipients of blood products, 3%
    • •
      Congenital from AIDS-positive mothers
    • •
      Heterosexual females: most rapidly growing group due to partners who are IVDAs
  • Known routes of HIV transmission:
    • •
      Blood and blood products
    • •
      Sexual activity
    • •
      In utero transmission
    • •
      During delivery

Clinical findings

    • •
      Lymphadenopathy
    • •
      Opportunistic infections
    • •
      Tumors: lymphoma, Kaposi sarcoma
    • •
      Other manifestations:
      • Lymphocytic interstitial pneumonia (LIP)
      • Spontaneous pneumothorax (development of cystic spaces, interstitial fibrosis related to PCP)
      • Septic emboli
    • •
      Clinical findings supportive of AIDS: (Fig. 1-26 )
      • CD4 count <200/mm3; the dysfunction of the immune system is inversely related to the CD4 count; PCP: CD4 <200 cells/mm3, MAI: CD4 <50 cells/mm3
      • >1 case of bacterial pneumonia per year
Figure 1-26.

Figure 1-26

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Opportunistic Infections
    • •
      Pneumocystis jiroveci Frenkel 1999, 70%
    • •
      Mycobacterial infection, 20%; CD4 counts often <50 cells/mm3
    • •
      Bacterial infection, 10% (S. pneumoniae, Haemophilus)
    • •
      Fungal infection (<5% of AIDS patients)
    • •
      Nocardia, <5%: cavitating pneumonia
    • •
      CMV pneumonia (common at autopsy)

Chest

General

    • •
      50% of all AIDS patients have pulmonary manifestations of infection or tumor.
    • •
      A normal CXR does not exclude the diagnosis of PCP.
    • •
      CMV is common at autopsy but does not cause significant morbidity or mortality; CMV antibody titers are present in virtually all patients with AIDS.
    • •
      Use of chest CT in AIDS patients:
      • Symptomatic patient with normal CXR; however, patients will commonly first undergo induced sputum or bronchoscopy or be put on empirical treatment for PCP.
      • To clarify confusing CXR
      • Workup of focal opacities, adenopathy, nodules

Spectrum of chest manifestations (Fig. 1-27)

Figure 1-27.

Figure 1-27

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    • Nodules
      • •
        Kaposi sarcoma (usually associated with skin lesions)
      • •
        Septic infarcts (rapid size increase)
      • •
        Fungal: Cryptococcus, Aspergillus
    • Large opacity: consolidation, mass
      • •
        Hemorrhage
      • •
        NHL
      • •
        Pneumonia
      • •
        Linear or interstitial opacities
      • •
        PCP
      • •
        Atypical mycobacteria
      • •
        Kaposi sarcoma
    • Lymphadenopathy
      • •
        Mycobacterial infections
      • •
        Kaposi sarcoma
      • •
        Lymphoma
      • •
        Reactive hyperplasia, rare in thorax
    • Pleural effusion
      • •
        Kaposi sarcoma
      • •
        Mycobacterial, fungal infection
      • •
        Pyogenic empyema
PCP infection (Figure 1-28, Figure 1-29, Figure 1-30)
Figure 1-28.

Figure 1-28

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Figure 1-29.

Figure 1-29

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Figure 1-30.

Figure 1-30

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Radiographic Features
    • •
      Interstitial pattern, 80%
      • CXR: bilateral perihilar or diffuse
      • HRCT: ground-glass appearance, predominantly in upper lobe with cysts
    • •
      Progression to diffuse consolidation within days
    • •
      Normal CXR in the presence of pulmonary PCP infection, 10%
    • •
      Multiple upper lobe air-filled cysts or pneumatoceles (10%) causing:
      • Pneumothorax
      • Bronchopleural fistulas
    • •
      Upper lobe PCP involvement is common, because aerosolized pentamidine may not get to upper lobes; upper lobe disease may mimic TB but the latter may have pleural effusions or lymphadenopathy, both of which are uncommon in PCP.
    • •
      Atypical patterns, 5%
      • Unilateral disease
      • Focal lesions, cavitary nodules
    • •
      PCP as a presenting manifestation of AIDS is decreasing because of effective prophylaxis.

Mycobacterial infection

M. tuberculosis > M. avium-intracellulare (this pathogen usually causes extrathoracic disease). CD4 cell count usually <50 cells/mm3.

Radiographic Features
    • •
      Hilar and mediastinal adenopathy common
      • Necrotic lymph nodes (TB) have a low attenuation center and only rim enhance with contrast.
      • MTB is more commonly associated with necrosis from MAI.
      • Adenopathy in Kaposi sarcoma or lymphoma enhances uniformly.
    • •
      Pleural effusion
    • •
      Other findings are similar to non-AIDS TB (upper lobe consolidations, cavitations)

Fungal infections

  • Fungal infections in AIDS are uncommon (<5% of patients).
    • •
      Cryptococcosis (most common); 90% have CNS involvement.
    • •
      Histoplasmosis: nodular or miliary pattern most common; 35% have normal CXR.
    • •
      Coccidioidomycosis: diffuse interstitial pattern, thin-walled cavities

Kaposi sarcoma (Fig. 1-31)

Figure 1-31.

Figure 1-31

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    • The most common tumors in AIDS are:
      • •
        Kaposi sarcoma (15% of patients); incidence declining; M:F = 50:1.
      • •
        Lymphoma (<5% of patients)
  • Pulmonary manifestations of Kaposi sarcoma (almost always preceded by cutaneous/visceral involvement):
    • •
      Nodules
      • 1 to 3 cm
      • Single or multiple
      • Virtually always associated with skin lesions
    • •
      Coarse linear opacities emanating from hilum
    • •
      Pleural effusions (serosanguineous), 40%
    • •
      Adenopathy
    • •
      Lymphangitic tumor spread

Aids-related lymphoma

  • Non-Hodgkin lymphoma (usually aggressive B-cell type) > Hodgkin lymphoma.

  • Poor prognosis. Spectrum includes:
    • •
      Solitary or multiple pulmonary masses ± air bronchogram, 25%
    • •
      AIDS-related lymphoma is typically an extranodal disease (CNS, GI tract, liver, bone marrow): adenopathy not very prominent.
    • •
      Pleural effusions are common.

Neoplasm

General

Location

  • Chest neoplasms are best categorized by their primary location:
    • •
      Lung tumors
    • •
      Pleural tumors
    • •
      Mediastinal tumors
    • •
      Tumors of the airway
    • •
      Chest wall tumors

Classification of pulmonary neoplasm

    • Malignant tumors
      • •
        Bronchogenic carcinoma
      • •
        Lymphoma
      • •
        Metastases
      • •
        Sarcomas, rare
    • Low-grade malignancies (previously bronchial adenoma)
      • •
        Carcinoid, 90%
      • •
        Adenoid cystic carcinoma (previously cylindroma, resembles salivary gland tumor), 6%
      • •
        Mucoepidermoid carcinoma, 3%
      • •
        Pleomorphic carcinoma, 1%
    • Benign tumors, rare
      • •
        Hamartoma
      • •
        Papilloma
      • •
        Leiomyoma
      • •
        Hemangioma
      • •
        Chemodectoma
      • •
        Pulmonary blastoma
      • •
        Chondroma
      • •
        Multiple pulmonary fibroleiomyomas
      • •
        Pseudolymphoma

Percutaneovus biopsy

  • The true positive rate of percutaneous lung biopsy is 90%-95%. False-negative results are usually due to poor needle placement, necrotic tissue, and so on. Tumor seeding is extremely uncommon (1:20,000).

  • Contraindications to biopsy are usually relative and include:
    • •
      Severe COPD
    • •
      Pulmonary hypertension
    • •
      Coagulopathy
    • •
      Contralateral pneumonectomy
    • •
      Suspected echinococcal cysts
Technique
    • 1.
      Fluoroscopic or CT localization of nodule
    • 2.
      Pass needle over superior border of rib to avoid intercostal vessels
    • 3.
      Avoid passing through fissures
    • 4.
      Coaxial needle system
      • •
        20-gauge outer needle
      • •
        22-gauge inner needle
    • 5.
      Cytopathologist should be present to determine if sample is adequate and diagnostic.
    • 6.
      Chest film after procedure to determine presence of pneumothorax
Complications
    • •
      Pneumothorax, 25%; 5%-10% require a chest tube (i.e., pneumothorax >25% or if patient is symptomatic)
    • •
      Hemoptysis, 3%

Bronchogenic carcinoma

Bronchogenic carcinoma refers broadly to any carcinoma of the bronchus. However, the use of the term is usually restricted to the following entities:

Classification

    • Adenocarcinoma (most common), 40%
      • •
        Bronchoalveolar carcinoma (often PET negative)
      • •
        Papillary adenocarcinoma
      • •
        Acinar adenocarcinoma
      • •
        Solid adenocarcinoma with mucus formation
    • Squamous cell carcinoma, 30%
      • •
        Spindle cell carcinoma
    • Small cell carcinoma, 15%
      • •
        Oat cell
      • •
        Intermediate cell type
      • •
        Combined oat cell carcinoma
    • Large cell carcinoma, 1%
      • •
        Giant cell carcinoma
      • •
        Clear cell carcinoma
    • Adenosquamous tumor

Risk factors for bronchogenic carcinoma

    • •
      Smoking: 98% of male patients and 87% of female patients with lung cancer smoke; 10% of heavy smokers will develop lung cancer. The strongest relationship between smoking and cancer has been established for SCC, followed by adenocarcinoma; the least common association is for bronchoalveolar carcinoma.
    • •
      Radiation, uranium miners
    • •
      Asbestos exposure
    • •
      Genetic predisposition (HLA-Bw44 associated?)

Radiographic spectrum

Primary Signs of Malignancy (Fig. 1-32)
Figure 1-32.

Figure 1-32

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    • •
      Mass (>6 cm) or nodule (<6 cm) with spiculated, irregular borders
    • •
      Unilateral enlargement of hilum: mediastinal widening, hilar prominence
    • •
      Cavitation
      • Most common in upper lobes or superior segments of lower lobes
      • Wall thickness is indicative of malignancy.
      • <4 mm: 95% of cavitated lesions are benign.
      • >15 mm: 85% of cavitated lesions are malignant.
      • Cavitation is most common in SCC.
    • •
      Certain tumors may present as chronic airspace disease: bronchoalveolar carcinoma, lymphoma.
    • •
      Some air bronchograms are commonly seen by HRCT in adenocarcinoma.
Secondary Signs of Malignancy (Fig. 1-33)
Figure 1-33.

Figure 1-33

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    • •
      Atelectasis (Golden inverted “S” sign in RUL, LUL collapse)
    • •
      Obstructive pneumonia
    • •
      Pleural effusion
    • •
      Interstitial patterns: lymphangitic tumor spread
    • •
      Hilar and mediastinal adenopathy
    • •
      Metastases to ipsilateral, contralateral lung

Locations of Tumors

Tumor Frequency Location Comments
Adenocarcinoma 40% Peripheral Scar carcinoma
Squamous cell carcinoma 30% Central, peripheral* Cavitation
Small cell carcinoma 15% Central, peripheral* Endocrine activity
Large cell carcinoma 1% Central, peripheral Large mass
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*

Rarely present as a resectable T1 lesion.

Paraneoplastic syndromes of lung cancer

  • Incidence: 2% of bronchogenic carcinoma
    • Metabolic
      • •
        Cushing syndrome (ACTH)
      • •
        Inappropriate antidiuresis (ADH)
      • •
        Carcinoid syndrome (serotonin, other vasoactive substances)
      • •
        Hypercalcemia (PTH, bone metastases)
      • •
        Hypoglycemia (insulin-like factor)
    • Musculoskeletal
      • •
        Neuromyopathies
      • •
        Clubbing of fingers (HPO)
    • Other
      • •
        Acanthosis nigricans
      • •
        Thrombophlebitis
      • •
        Anemia

Radiation pneumonitis

Radiation pneumonitis represents the acute phase of radiation damage and usually appears 3 weeks after treatment. Minimum radiation to induce pneumonitis is 30 Gy. The acute phase is typically asymptomatic but may be associated with fever and cough. Fibrosis usually occurs after 6 to 12 months.

Radiographic Features
    • •
      Diffuse opacities in radiation port
    • •
      HRCT allows better assessment of extent than plain film.

Tumor staging (Fig. 1-34)

Figure 1-34.

Figure 1-34

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TNM staging system, 7th edition (non–small cell lung cancer)

    • Primary tumor (T)
      • T0 No evidence of a primary tumor
      • T1 <3 cm, limited to lung, not more proximal than lobar bronchus
      • T1a ≤ 2 cm
      • T1b >2 and ≤ 3 cm
      • T2 >3 cm but ≤ 7 cm;
        • •
          or invades parietal pleura
        • •
          or involves main bronchus ≥ 2 cm distal to carina
        • •
          or atelectasis/obstructive pneumonia extending to hilum but not involving entire lung
      • T2a >3 but ≤ 5 cm
      • T2b >5 but ≤ 7 cm
      • T3 >7 cm;
        • •
          or directly invades chest wall, diaphragm, phrenic nerve, mediastinal pleura, parietal pericardium
        • •
          or mainstem bronchus <2 cm distal to carina
        • •
          or atelectasis/obstructive pneumonia involving entire lung
        • •
          or separate tumor nodules in a different ipsilateral lobe
      • T4 Heart, great vessels, trachea, recurrent laryngeal nerve, esophagus, vertebral body, or carina; or separate tumor nodules in a different ipsilateral lobe
    • Nodes (N)
      • N0 No lymph node involvement
      • N1 Ipsilateral hilar nodes
      • N2 Ipsilateral mediastinal or subcarinal nodes
      • N3 Contralateral hilar or mediastinal nodes; supraclavicular nodes
    • Metastases (M)
      • M0 No metastases
      • M1 Metastases
      • M1a Separate tumor nodules in contralateral lobe; or pleural nodules or malignant pleural dissemination
      • M1b Distant metastases
Unresectable Stages
    • •
      Tumors are unresectable if T4, N3, or M1 (stage 3b or 4)
    • •
      Stage 3b: N3, M0, any T; T4, M0, any N
    • •
      Stage 4: M1, any T, any N

5-Year survival

  • Overall 5-year survival rate is 14%.
    • Stage 1: 57%-67%
    • Stage 2: 39%-55%
    • Stage 3a (limited disease): 23%
    • Stage 3b (T4): 7%
    • Stage 3b (N3): 3%
    • Stage 4: 1%

Small cell cancer staging

Although the TNM system can also be used for small cell cancer, it is often not used because of the presence of metastasis at the time of diagnosis. Instead, a two-stage system is used: “limited” and “extensive.” Limited stage means the cancer is confined to one lung with ipsilateral lymph node metastasis (can be encompassed by a single radiation port) and has better prognosis. Extensive stage means metastasis to contralateral lung and nodes or to distant organs (including the pleura). About two thirds of patients with small cell cancer are at the extensive stage at first diagnosis.

Lymph node imaging

Anatomy (Fig. 1-35)
Figure 1-35.

Figure 1-35

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    • Anterior mediastinal nodes
      • •
        Parietal node group
        • Internal mammary nodes
        • Superior diaphragmatic nodes
      • •
        Prevascular node group (anterior to the great vessels)
    • Middle mediastinal nodes
      • •
        Paratracheal* ; the lowest node is the azygos node
      • •
        Subcarinal*: below bifurcation; drainage to right paratracheal nodes
      • •
        Subaortic; AP window node
      • •
        Tracheobronchial (pulmonary root, hilar)
    • Posterior mediastinal nodes
      • •
        Paraaortic
      • •
        Prevertebral
      • •
        Paraspinous: lateral to vertebral body
American Thoracic Society Classification (Fig. 1-36)
Figure 1-36.

Figure 1-36

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  • This classification system assigns numbers to regional lymph nodes:
    • •
      2R, 2L: paratracheal
    • •
      4R, 4L: superior tracheobronchial
    • •
      5, 6: anterior mediastinal
    • •
      7: subcarinal
    • •
      8, 9: posterior mediastinal
    • •
      10R, 10L: bronchopulmonary
    • •
      11R, 11L: pulmonary
    • •
      14: diaphragmatic
CT Criterion for Abnormal Nodes

Short-axis lymph node diameter >1 cm (60%-70% accuracy for differentiating between malignant and benign adenopathy)

Chest wall invasion

Accuracy for detection of chest wall invasion by CT is 40%-60%.

Radiographic Features (Fig. 1-37)
Figure 1-37.

Figure 1-37

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    • Reliable signs
      • •
        Soft tissue mass in chest wall
      • •
        Bone destruction
    • Unreliable signs
      • •
        Obtuse angles at contact between tumor and pleura
      • •
        >3 cm of contact between tumor and pleura
      • •
        Pleural thickening
      • •
        Increased density of extrapleural fat

Mediastinal invasion

Contiguous invasion of mediastinal organs, heart, great vessels, aerodigestive tract, and vertebra indicates nonresectability.

Radiographic Features
    • •
      Diaphragmatic paralysis (phrenic nerve involvement)
    • •
      Mediastinal mass with encasement of mediastinal structures
    • •
      MRI may be useful to detect vascular invasion.

Malignant pleural effusion

  • Development of pleural effusions usually indicates a poor prognosis. Presence of a documented malignant pleural effusion makes a tumor unresectable (M1). Incidence of pleural effusion:
    • •
      Bronchogenic carcinoma, 50%
    • •
      Metastases, 50%
    • •
      Lymphoma, 15%
Pathogenesis of Malignant Effusions
    • •
      Pleural invasion increases capillary permeability.
    • •
      Lymphatic or venous obstruction decreases clearance of pleural fluid.
    • •
      Bronchial obstruction → atelectasis → decrease in intrapleural pressure.

Central bronchial involvement

Tumors that involve a central bronchus usually cause lung collapse or consolidation. These tumors are considered unresectable (T4 tumors) only if they involve the carina.

Metastases to other organs

  • Lung tumors most frequently metastasize to:
    • Liver (common)
    • Adrenal glands (common)
      • •
        30% of adrenal masses in patients with adenocarcinoma are adenomas.
      • •
        Most adrenal masses in patients with small cell carcinomas are metastases.
      • •
        Tumor may be present in a morphologically normal-appearing gland.
    • Other sites (especially small and large cell tumors)
      • •
        Brain (common)
      • •
        Bones
      • •
        Kidney

Specific lung tumors

Adenocarcinoma

Now the most frequent primary lung cancer. Typically presents as a multilobulated, peripheral mass. May arise in scar tissue: scar carcinoma.

Bronchioloalveolar carcinoma

  • Subtype of adenocarcinoma; slow growth. The characteristic radiographic presentations are:
    • •
      Morphologic type
      • Small peripheral nodule (solitary form), 25% (most common)
      • Multiple nodules
      • Chronic airspace disease
    • •
      Air bronchogram
    • •
      Absent adenopathy
    • •
      Cavitation may be seen by HRCT (Cheerio sign)

Squamous cell carcinoma (SCC)

  • SCC is most directly linked with smoking. SCC carries the most favorable prognosis. The most characteristic radiographic appearances are:
    • •
      Cavitating lung mass, 30%
    • •
      Peripheral nodule, 30%
    • •
      Central obstructing lesion causing lobar collapse
    • •
      Chest wall invasion

Pancoast tumor (superior sulcus tumor)

Tumor located in the lung apex that has extended into the adjacent chest wall. Histologically, Pancoast tumors are often SCC.

Clinical Findings
    • •
      Horner syndrome
    • •
      Pain radiating into arm (invasion of pleura, bone, brachial plexus, or subclavian vessels)
Radiographic Features (Fig. 1-38)
Figure 1-38.

Figure 1-38

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    • •
      Apical mass
    • •
      Chest wall invasion
    • •
      Involvement of subclavian vessels
    • •
      Brachial plexus involvement
    • •
      Bone involvement: rib, vertebral body

Small cell carcinoma (neuroendocrine tumor, type 3)

  • Most aggressive lung tumor with poor prognosis. At diagnosis, two thirds of patients already have extrathoracic spread:
    • •
      Typical initial presentation: massive bilateral lymphadenopathy
    • •
      With or without lobar collapse
    • •
      Brain metastases

Large cell carcinoma

Usually presents as large (>70% are >4 cm at initial diagnosis) peripheral mass lesions. Overall uncommon tumor.

Carcinoid (neuroendocrine tumor, types 1 and 2)

Represent 90% of low-grade malignancy tumors of the lung. The 10-year survival with surgical treatment is 85%.

Types
    • •
      Typical carcinoid: local tumor (type 1)
    • •
      Atypical carcinoid (10%-20%): metastasizes to regional lymph nodes (type 2); liver metastases are very rare.
Radiographic Features
    • PET negative
    • Centrally located carcinoid, 80%
      • •
        Segmental or lobar collapse (most common finding)
      • •
        Periodic exacerbation of atelectasis
      • •
        Endobronchial mass
    • Peripherally located carcinoid, 20%
      • •
        Pulmonary nodule
      • •
        May enhance with contrast

Comparison of Clinical, Pathologic, and Imaging Findings in Neuroendocrine Tumors of the Lung

Findings Typical Carcinoid Atypical Carcinoid LCNEC SCLC
Demographic Features
Mean patient age (yr) 40-49 50-59 60-69 70-79
Association with smoking No Yes Yes Yes
M:F ratio 1:1 2:1 >2.5:1 >2.5:1
Histopathologic Features
Mitoses per 10 HPFs <2 2-10 >10 >50
Necrosis No Yes Yes Yes
Imaging Findings
Central to peripheral ratio 3:1 3:1 1:4 10-20:1
Calcification or ossification 30% 30% 9% Up to 23%
Extrathoracic metastases 15% 15% 35% 60%-70%
Enhancement High; central or rim High; central or rim High High with necrosis
FDG uptake at PET Low Low High High
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FDG, Fluorodeoxyglucose; HPF, High-Power Field; LCNEC, Large Cell Neuroendocrine Carcinoma; SCLC, Small Cell Lung Cancer.

Hamartoma (Fig. 1-39)

Figure 1-39.

Figure 1-39

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Hamartomas are the most common benign tumors of the lung composed of cartilage (predominant component), connective tissue, muscle, fat, and bone. 90% are peripheral, 10% are endobronchial.

Radiographic Features
    • •
      Well-circumscribed solitary nodules
    • •
      Chondroid “popcorn” calcification is diagnostic but uncommon (<20%).
    • •
      Fat attenuation within a lesion by HRCT is pathognomonic.

Carney triad

Predominant in Young Women
    • •
      Gastric smooth muscle tumors (epithelioid leiomyosarcoma)
    • •
      Functioning extraadrenal paraganglioma
    • •
      Pulmonary chondroma

Tracheobronchial papillomatosis

Radiographic Features
    • •
      Multiple, well demarcated nodules that can grow
    • •
      Cavitate with 2 to 3 mm thick walls
    • •
      Air fluid levels may develop
    • •
      Risk of squamous cell carcinoma 15 years after diagnosis

Pulmonary blastoma

Predominant in Males, Poor Prognosis
Radiographic Features
    • •
      Large peripheral mass that is well circumscribed
    • •
      May show pleural invasion and may metastasize

Lung metastases from other primary lesions

General

    • Pathways of metastatic spread from a primary extrathoracic site to lungs (in order of frequency):
      • •
        Spread via pulmonary arteries
      • •
        Lymphatic spread (celiac nodes → posterior mediastinal nodes + paraesophageal nodes) and in lung parenchyma
      • •
        Direct extension
      • •
        Endobronchial spread
    • Neoplasms with rich vascular supply draining into systemic venous system:
      • •
        Renal cell carcinoma
      • •
        Sarcomas
      • •
        Trophoblastic tumors
      • •
        Testis
      • •
        Thyroid
    • Neoplasms with lymphatic dissemination:
      • •
        Breast (usually unilateral)
      • •
        Stomach (usually bilateral)
      • •
        Pancreas
      • •
        Larynx
      • •
        Cervix
    • Other neoplasms with high propensity to localize in lung:
      • •
        Colon
      • •
        Melanoma
      • •
        Sarcoma
Radiographic Features
    • •
      Multiple lesions, 95% > solitary lesion, 5%
    • •
      Lung bases > apices (related to blood flow)
    • •
      Peripheral, 90% > central, 10%
    • •
      Metastases typically have sharp margins.
    • •
      Fuzzy margins can result from peritumoral hemorrhage (choriocarcinoma, chemotherapy).
    • •
      Cavitations are common in SCCs from head and neck primary lesions.

Calcified metastases

  • Calcifications in lung metastases are observed in:
    • Bone tumor metastases
      • •
        Osteosarcoma
      • •
        Chondrosarcoma
    • Mucinous tumors
      • •
        Ovarian
      • •
        Thyroid
      • •
        Pancreas
      • •
        Colon
      • •
        Stomach
    • Metastases after chemotherapy

Giant metastases (“cannon ball” metastases) in asymptomatic patient

    • •
      Head and neck cancer
    • •
      Testicular and ovarian cancer
    • •
      Soft tissue cancer
    • •
      Breast cancer
    • •
      Renal cancer
    • •
      Colon cancer

Sterile metastases

This term refers to pulmonary metastases under treatment that contain no viable tumor. Nodules typically consist of necrotic and/or fibrous tissue.

Chronic Lung Disease

Idiopathic diseases

Overview of Idiopathic Interstitial Pneumonias

Diagnosis Clinical Findings HRCT Features Differential Diagnosis
UIP/IPF 40-70 years, M>F; >6 month dyspnea, cough, crackles, clubbing; poor response to steroids Peripheral, basal, subpleural reticulation and honeycombing ± ground-glass opacity Collagen vascular disease, asbestosis, CHP, scleroderma, drugs (bleomycin, methotrexate)
NSIP 40-50 years, M = F; dyspnea, cough, fatigue, crackles; may respond to steroids Bilateral, patchy, subpleural ground-glass opacity, ± reticulation Collagen vascular disease, CHP, DIP
RB-ILD 30-50 years, M > F; dyspnea, cough Ground-glass, centrilobular nodules, ± centrilobular emphysema Hypersensitivity pneumonitis
AIP/diffuse alveolar damage Any age, M = F; acute-onset dyspnea, diffuse crackles and consolidation Ground-glass consolidation, traction bronchiectasis and architectural distortion ARDS, infection, edema, hemorrhage
COP Mean 55 years, M = F; <3 month history of cough, dyspnea, fever; may respond to steroids Subpleural and peribronchial consolidation ± nodules in lower zones; atoll sign (ring-shaped opacity) Collagen vascular disease, infection, vasculitis, sarcoidosis, lymphoma, alveolar carcinoma
DIP 30-54 years, M > F; insidious onset weeks to months of dyspnea, cough Ground-glass opacity, lower zone, peripheral Hypersensitivity pneumonitis, NSIP
LIP Any age, F > M Ground-glass opacity, ± poorly defined centrilobular nodules, thin-walled cysts and air trapping DIP, NSIP, hypersensitivity pneumonitis
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AIP, Acute Interstitial Pneumonia; CHP, Chronic Hypersensitivity Pneumonitis; COP, Cryptogenic Organizing Pneumonia; DIP, Desquamative Interstitial Pneumonitis; IPF, Idiopathic Pulmonary Fibrosis; LIP, Lymphoid Interstitial Pneumonia; NSIP, Nonspecific Interstitial Pneumonia; RB-ILD, Respiratory Bronchiolitis-Associated Interstitial Lung Disease; UIP, Usual Interstitial Pneumonia.

Usual interstitial pneumonia (UIP)

Multiple etiologies exist, which may produce a histologic pattern of UIP. Idiopathic pulmonary fibrosis (IPF) is the term used when no cause is identified; synonyms: cryptogenic fibrosing alveolitis (CFA, British term). Prognosis: mean survival 4 years (range 0.4 to 20 years). Lung biopsy is necessary for diagnosis. Treatment with steroids is useful in 50%, also cytotoxic agents.

Clinical Findings
    • •
      Clubbing, 60%
    • •
      Nonproductive cough, 50%
    • •
      Dyspnea
    • •
      Weight loss, 40%
Pathology
    • Pathologic changes are nonspecific and also occur in a variety of secondary disorders such as collagen vascular disease, drug reactions, pneumoconiosis, chronic hypersensitivity pneumonitis. Histology demonstrates alveolar fibrosis characterized by spatial and temporal heterogeneity, with architectural distortion.
Radiographic Features (Figs. 1-40 and 1-41)
Figure 1-40.

Figure 1-40

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Figure 1-41.

Figure 1-41

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    • Distribution
      • •
        IPF: Primarily in lower lung zones
      • •
        Peripheral subpleural involvement
    • HRCT pattern
      • •
        Early: ground-glass appearance
      • •
        Later: reticular pattern predominantly in lower lobes
      • •
        End stage: honeycombing
      • •
        Traction bronchiectasis indicates fibrosis.
    • Other
      • •
        Low lung volumes (fibrosis)
      • •
        Pulmonary hypertension with cardiomegaly (fibrosis), 30%
      • •
        Uncommon findings
        • Pleural thickening, 5%
        • Pneumothorax, 5%
        • Effusion, 5%

Sarcoid

The term sarcoid (sarcoma-like) was first coined by Caesar Boeck in 1899 to describe one of the skin lesions of sarcoidosis because of its histologic resemblance to a sarcoma. Systemic granulomatous disease of unknown etiology (lung, 90% > skin, 25% > eye, 20% > hepatosplenomegaly, 15% > CNS, 5% > salivary glands > joints > heart). Treatment is with steroids.

Clinical Findings

Ten to 20 times more common in blacks than in whites, 30% are asymptomatic.

Prognosis
    • Adenopathy only: more benign course
      • •
        75% regress to normal within 3 years
      • •
        10% remain enlarged
      • •
        15% progress to stages 2 and 3
    • Parenchymal abnormalities: 20% develop progressive pulmonary fibrosis
Associations
    • •
      Löfgren syndrome: acute febrile illness with bilateral hilar adenopathy and erythema nodosum in a patient with sarcoid. May also have uveitis or parotitis and arthralgias of large joints. These findings are associated with a favorable prognosis.
    • •
      Heerfordt syndrome: parotid gland enlargement, fever, uveitis, and cranial nerve palsies. The condition is usually self-limited and most commonly affects patients in the 2nd to 4th decades of life.
    • •
      Lupus pernio: violaceous (blue-purple) raised skin lesions on the cheeks and nose in a patient with sarcoid. Prognosis is poor.
    • •
      In HIV: A number of cases of new-onset sarcoid have been described in HIV patients after initiation of antiretroviral therapy with rise in CD4 count. This may be related to immune restoration. The radiologic features are similar to those of sarcoid in non-HIV patients.
Diagnosis
    • Biopsy
      • •
        Bronchial and transbronchial biopsy (sensitivity 90%)
      • •
        Open lung biopsy (sensitivity 100%)
      • •
        Lymph node, parotid gland, or nasal mucosa biopsy (sensitivity 95%)
      • •
        Mediastinoscopy (sensitivity 95%)
    • Kveim test (sensitivity 70%-90%). Problems:
      • •
        Unavailability of validated tissue suspension (made from splenic tissue of infected patients)
      • •
        Lack of reactivity late in the disease
      • •
        Delay of 4 to 6 weeks before reactivity occurs
Radiographic Features (Figs. 1-42 and 1-43)
Figure 1-42.

Figure 1-42

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Figure 1-43.

Figure 1-43

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    • Stages (Siltzbach classification, plain film):
      • Stage 0: initial normal film, 10%
      • Stage 1: adenopathy, 50%
        • •
          Symmetrical hilar adenopathy
        • •
          Paratracheal, tracheobronchial, and azygos adenopathy are commonly associated with hilar adenopathy (Garland triad).
        • •
          Calcification, 5%
      • Stage 2: adenopathy with pulmonary opacities, 30%
        • •
          Reticulonodular pattern
        • •
          Acinar pattern may coalesce to consolidation.
        • •
          Large nodules >1 cm (2%)
      • Stage 3: pulmonary opacities without hilar adenopathy, 10%
      • Stage 4: pulmonary fibrosis, upper lobes with bullae
      • Other less common plain film findings:
        • •
          Pleural effusion, 10%
        • •
          Unilateral hilar adenopathy, 1%-3%
      • •
        Eggshell calcification of lymph nodes
      • •
        Complications:
        • Pneumothorax (blebs, bullae)
        • Aspergillus with fungus ball: A complication of stage 4 disease. Pleural thickening may be the earliest indication of Aspergillus superinfection, occurring 2 to 3 years before appearance of an intracavitary fungus ball. The pleural thickening may achieve a thickness of 2 cm or more.
        • Cardiac arrhythmias: Early initiation of steroid therapy can help to prevent these arrhythmias.
        • Bronchostenosis with lobar/segmental collapse
CT Features
    • Lung parenchyma
      • •
        Nodules (90%), along lymphatic distribution (i.e., central or axial and subpleural)
      • •
        Linear pattern, 50%
      • •
        Ground-glass opacity, 25%
      • •
        Subpleural thickening, 25%
      • •
        Pseudoalveolar consolidation, 15%
    • Lymph nodes
      • •
        Adenopathy, 80%
    • Bronchi
      • •
        Wall abnormalities, 65%
      • •
        Luminal abnormalities, 25%
      • •
        Bronchiectasis, 10%
    • End stage
      • •
        Upper lobe fibrosis
      • •
        Bullae
      • •
        Traction bronchiectasis
67Ga Scintigraphic Findings

Accumulation of 67Ga is a sensitive but nonspecific indicator of active inflammation in patients with sarcoidosis. Gallium avidity cannot be used alone to establish a diagnosis of sarcoidosis. However, 67Ga imaging is useful in identifying extrathoracic sites of involvement, detecting active alveolitis, and assessing response to treatment.

Gallium uptake in thoracic lymph nodes, lungs, and salivary and lacrimal glands is particularly suggestive of sarcoidosis. How well the extent of gallium uptake in the lung correlates with the degree of alveolitis is controversial. However, 67Ga scans may be useful as a baseline study at the time of diagnosis. If results of 67Ga scintigraphy are initially positive, negative findings from a subsequent 67Ga scan obtained during the course of treatment suggest that alveolitis has resolved. In such a patient, gallium may be a useful marker for disease activity and response to therapy.

Nonspecific interstitial pneumonia (NSIP)

Important to distinguish from UIP given a better response to steroids. Patients are typically younger than those with UIP and symptoms are milder. Associated with drug exposure hypersensitivity pneumonitis and collagen vascular disease.

Pathology
    • Histologically characterized by spatial and temporal homogeneity of interstitial inflammation with varying degrees of fibrosis. Limited fibrosis identifies the cellular NSIP subtype; however, the fibrotic NSIP subtype is more common.
HRCT Features
    • •
      Patchy ground-glass opacities, reticular opacities, micronodules
    • •
      Subpleural, symmetric, without the basilar predominance seen in UIP
    • •
      Honeycombing occasionally seen in fibrotic subtype

Respiratory bronchiolitis-associated interstitial pneumonia (RB-ILD)

Smoking-related interstitial lung disease, representing a symptomatic form of the often incidentally detected respiratory bronchiolitis. Smoking cessation is key to treatment, although steroids may be helpful.

Pathology
    • Histologically characterized by respiratory bronchioles that are filled with macrophages.
HRCT Features
    • •
      Diffuse centrilobular nodules and ground-glass opacities
    • •
      Bronchial wall thickening
    • •
      Coexisting centrilobular emphysema may be noted

Desquamative interstitial pneumonia (DIP)

Represents the most severe form of the continuum of smoking-related interstitial lung disease (RB, RB-ILD, DIP).

Pathology
    • Histologically characterized by alveolar spaces that are filled with macrophages.
HRCT Features
    • •
      Diffuse ground-glass opacities (versus centrilobular distribution in RB-ILD)
    • •
      Peripheral and basilar predominance
    • •
      Septal thickening
    • •
      Occasional small cystic spaces

Cryptogenic organizing pneumonia (COP)

Formerly termed bronchiolitis obliterans organizing pneumonia (BOOP). Histologic pattern may also be seen in collagen vascular disease, drug exposure, and infection. Patients present with cough, mild dyspnea, and fever over several months; there may be an antecedent history of respiratory infection.

Pathology
    • Intraalveolar proliferation of granulation tissue is seen, with temporal uniformity.
HRCT Features
    • •
      Patchy consolidation or ground-glass opacities
    • •
      Subpleural, peribronchial, lower > upper lung distribution
    • •
      May also see small centrilobular nodules or large irregularly shaped masses
    • •
      Atoll sign: crescent-shaped opacity

Lymphoid interstitial pneumonia (LIP)

Women > men, associated with Sjögren syndrome, SLE, HIV infection; rarely idiopathic. Common in pediatric AIDS patients. Variable response to steroids. May progress to lymphoma in <20%. A localized form of LIP has been called “pseudolymphoma” because of histologic resemblance to lymphoma.

Pathology
    • Diffuse interstitial infiltrate composed of lymphocytes, plasma cells, and histiocytes.
HRCT Features
    • •
      Ground-glass opacities ± poorly defined centrilobular nodules
    • •
      Basilar distribution or diffuse
    • •
      Perivascular cysts
    • •
      Late honeycombing

Acute interstitial pneumonia (AIP)

Present with severe dyspnea requiring mechanical ventilation, usually several weeks after viral URI. Mortality, 50%. Men = women, supportive therapy although steroids may help. Formerly known as Hamman-Rich syndrome.

Pathology
    • Diffuse alveolar damage. Exudative phase demonstrates hyaline membranes and alveolar infiltration by lymphocytes. Progresses to organizing phase after 1 week, with alveolar wall thickening due to fibrosis.
HRCT Features
    • •
      Similar to ARDS, but often with a symmetric, posterior lower lobe distribution
    • •
      Exudative phase: ground-glass opacities, consolidation
    • •
      Organizing phase: architectural distortion, traction bronchiectasis, honeycombing

Lymphoproliferative disorders

Spectrum of lymphoid abnormalities in the chest characterized by accumulation of lymphocytes and plasma cells in the pulmonary interstitium or mediastinal/hilar lymph nodes. Believed to be due to stimulation of bronchus-associated lymphoid tissue by antigens.

Types

    • Nodal disorders
      • •
        Castleman disease (see Middle Mediastinal Tumors)
      • •
        Infectious mononucleosis
      • •
        Angioimmunoblastic lymphadenopathy: drug hypersensitivity
  • Pulmonary parenchymal disorders
    • •
      Plasma cell granuloma (inflammatory pseudotumor, histiocytoma)
    • •
      Pseudolymphoma
    • •
      Lymphocytic interstitial pneumonia (LIP)
    • •
      Lymphomatoid granulomatosis

Overview of Lymphoproliferative Diseases

Diagnosis Lung Nodes Effusion Malignancy
Nodes
Castleman disease Unaffected Yes No No
Infectious mononucleosis Mediastinal adenopathy Yes No No
Angioimmunoblastic lymphadenopathy Interstitial and alveolar opacity Yes 10% 30%
Parenchymal
Plasma cell granuloma Solitary pulmonary mass No No No
Pseudolymphoma Single or multiple parenchymal masses, air bronchograms No No 20%
LIP Bilateral interstitial disease No No <20%
Lymphomatoid granulomatosis Multiple pulmonary nodules, frequent cavitation Rare 35% 30%
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Differentiation of Lymphoma and Lymphoproliferative Disease

Parameter Lymphoproliferative Disorder Lymphoma
Location Parenchyma or lymph nodes but not both Parenchyma and lymph nodes
Lymphoid population Polyclonal Monoclonal
Onset Young patients (<30 years) Old patients (>50 years)
Prognosis Usually benign or low-grade malignancy Malignant
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Plasma cell granuloma

Local cellular proliferation of spindle cells, plasma cells, lymphocytes, and histiocytes in lung. Most common tumor-like pulmonary abnormality in children <15 years. Treatment is resection.

Radiographic Features (Fig. 1-44)
Figure 1-44.

Figure 1-44

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    • •
      Solitary lung mass 1 to 12 cm
    • •
      No or very slow growth
    • •
      Cavitation and calcification uncommon

Lymphangioleiomyomatosis (LAM)

Proliferation of smooth muscle cells along lymphatics in lung, thorax, and abdomen. Unknown etiology. Rare.

Clinical Findings

Young women presenting with spontaneous pneumothorax, chylothorax, hemoptysis, slowly progressive dyspnea. Ten-year survival 75%. Similar lesions may be seen in tuberous sclerosis (LAM has been dubbed a forme fruste of tuberous sclerosis).

Extrapulmonary LAM is rare.

Radiographic Features
    • Plain film/HRCT (Fig. 1-45 )
      • •
        Numerous cystic spaces, 90%
        • Size of cysts usually <5 to 10 mm
        • Thin walled
        • Surrounded by normal lung
      • •
        Recurrent pneumothorax, 70%
      • •
        Chylous pleural effusions, 25%
      • •
        Plain film: overinflation, irregular opacities, cysts
      • •
        Occasionally multiple nodules: multifocal micronodular pneumocyte hyperplasia
    • Lymphangiography
      • •
        Obstruction of lymphatic flow at multiple levels
      • •
        Dilated lymphatics
      • •
        Increased number of lymphatics
      • •
        Renal angiomyolipomas, which are often small and asymptomatic
      • •
        Chylous ascites (in up to one third of patients), uterine leiomyomas, and lymphaticoureteral and lymphaticovenous communications
      • •
        Abdominal and pelvic lymph angioleiomyomas
      • •
        Abdominal lymph nodes
Figure 1-45.

Figure 1-45

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Tuberous sclerosis

Identical lesions as in LAM

Collagen vascular diseases

Collagen vascular diseases have a common pathogenesis in the lung: immune response → inflammation (interstitial pattern, granuloma) → vasculitis → obstruction (e.g., respiratory insufficiency, PA hypertension).

Pearls

    • •
      Lower lungs are more frequently affected (higher blood flow).
    • •
      Vasculitides of large arteries (e.g., periarteritis nodosa) cause pulmonary hypertension.
    • •
      Most common complication is infection (secondary to immunosuppressive medications).

Rheumatoid arthritis (RA)

  • There are seven forms of pleuropulmonary disease associated with RA:
    • Rheumatoid lung nodules, 20% (necrobiotic)
      • •
        Usually multiple
      • •
        Nodules may change in size rapidly or disappear completely.
      • •
        Association between cutaneous and pulmonary nodules
    • Pleural effusion and pleuritis
      • •
        Clinically, pleuritis is the most common pulmonary feature of RA.
      • •
        Effusions are bilateral in the majority of patients.
      • •
        Proportionately more common in men
      • •
        Fluid has low pH and low glucose.
      • •
        Effusions are usually unilateral.
    • Caplan syndrome
      • •
        Nodular rheumatoid lung disease associated with pneumoconiosis fibrosing alveolitis
    • Constrictive bronchiolitis
    • Lymphoid hyperplasia
    • Pulmonary hypertension
Radiographic Features
    • •
      Bibasilar patchy alveolar opacities are early findings.
    • •
      Dense reticulonodular pattern is most frequent
    • •
      Pleural involvement, 20%
    • •
      End stage: honeycombing, PAH

Ankylosing spondylitis (AS)

    • •
      Pulmonary fibrocystic changes in 1%-10%
    • •
      Upper lobe fibrotic scarring, infiltration, cystic airspaces
    • •
      Ancillary findings:
      • Ossification of spinal ligaments, sacroiliitis
      • Cardiomyopathy

Systemic lupus erythematosus (SLE)

  • Pleural abnormalities are the most common findings.
    • •
      Pleural thickening
    • •
      Recurrent pleural effusions
    • •
      Pleuritis is thought to be pathogenetically similar to polyserositis affecting joints.
    • •
      Glucose level of pleural effusion is normal (decreased in RA).
  • Pulmonary disease: wide spectrum of findings, but the usual presentation is as acute lupus pneumonitis:
    • •
      Acute lupus pneumonitis: vasculitis and hemorrhage resulting in focal opacities at the lung bases
    • •
      Alveolar opacities, which may progress to ARDS
    • •
      Fibrosing alveolitis, rare
    • •
      Elevating diaphragm, atelectasis at bases (shown to be due to diaphragmatic dysfunction)
    • •
      Lupus-like disease can also be seen with drugs such as hydralazine and procainamide.

Other collagen vascular diseases with pulmonary manifestations

    • •
      Progressive systemic sclerosis (PSS) exists in two forms:
      • PSS with scleroderma
        • After esophagus, lung is the second most common site.
        • Interstitial fibrosis is the most common pulmonary manifestation.
        • Pulmonary vascular and pleural changes are less common.
      • PSS with CREST (calcinosis, Raynaud, esophageal dysmotility, sclerodactyly, telangiectasia)
        • Usually in older women
        • Long history of PSS with swollen fingers
        • Mild disease, slowly progressive, greater life expectancy
    • •
      Polymyositis, dermatomyositis
    • •
      Mixed connective tissue disease (MCTD)

Vasculitis and granulomatoses

Clinicoradiologic features suggestive of vasculitis

    • •
      Deforming of ulcerating upper airway lesions
    • •
      Palpable purpura
    • •
      Peripheral neuropathy
    • •
      Rapidly progressive glomerulonephritis
    • •
      Pulmonary renal syndrome
    • •
      Chest imaging showing nodular or cavitary disease
    • •
      Diffuse alveolar hemorrhage

Wegener granulomatosis

Systemic granulomatous process with destructive angiitis involving lung, upper respiratory tract, and kidney (necrotizing glomerulonephritis); type IV immune mechanism. The upper respiratory tract is affected in almost all patients, with lungs and kidneys involved in 90% and 80% of patients, respectively.

Radiographic Features (Fig. 1-46)
Figure 1-46.

Figure 1-46

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    • •
      Multiple nodules with cavitation (common)
    • •
      Interstitial, reticulonodular opacities at lung bases (earliest finding)
    • •
      Diffuse opacities (common) are due to:
      • Atelectasis: bronchoconstriction
      • Confluent nodules and masses
      • Pulmonary hemorrhage
      • Superimposed infection
    • •
      Other findings:
      • Pleural effusions, 25%
      • Adenopathy (rare)

Lymphomatoid granulomatosis

Now considered a B-cell lymphoma. Men > women. The multiple nodules are smaller than those in Wegener. Nodules are not numerous and tend to cavitate.

Churg-strauss—allergic angiitis and granulomatosis

Similar to polyarteritis nodosa, but patients have pulmonary diseases and asthma. Affects skin, kidneys, lung, heart, and CNS; eosinophilia.

Radiographic Features
    • •
      Patchy peripheral areas of consolidation
    • •
      Fleeting opacities
    • •
      Multiple nodules

Behçet disease

  • Chronic multisystem vasculitis, characterized by:
    • •
      Recurrent oral and genital ulcerations
    • •
      Uveitis
    • •
      Additional clinical manifestations in multiple organ systems
Radiographic Features
    • •
      Pulmonary arterial aneurysm: fusiform to saccular, commonly multiple and bilateral, located in the lower lobe or main pulmonary arteries
    • •
      Thickening of the aorta and SVC (vasculitis)
    • •
      Subpleural alveolar infiltrates, and wedge-shaped or rounded areas of increased density, which represent focal vasculitis and thrombosis resulting in infarction, hemorrhage, and focal atelectasis

Other chronic disorders

Langerhans cell histiocytosis (eosinophilic granuloma)

Langerhans cell histiocytosis consists of three clinical syndromes:

    • Letterer-Siwe: acute disseminated form
    • Hand-Schüller-Christian: chronic disseminated form
    • Eosinophilic granuloma:
      • •
        Solitary bone lesion
      • •
        Small cystic spaces in lung parenchyma
      • •
        3- to 10-mm pulmonary nodules
      • •
        Apical reticulonodular pattern
      • •
        Pneumothorax, 30%

Idiopathic pulmonary hemorrhage (IPH)

Recurrent pulmonary hemorrhage, which may result in interstitial fibrosis. Age usually <10 years.

Radiographic Features
    • •
      Diffuse airspace pattern (radiographic appearance similar to Goodpasture syndrome)
    • •
      Hilar adenopathy

Amyloid

Extracellular deposition of protein derived from light chains of monoclonal Ig.

Classification
    • •
      Primary amyloid: heart, lung (70%), skin, tongue, nerves
    • •
      Amyloid associated with multiple myeloma (carpal tunnel syndrome, common)
    • •
      Secondary amyloid (liver, spleen, kidney) in:
      • Chronic infections
      • Chronic inflammations
      • Neoplasm
    • •
      Heredofamilial amyloidosis (familial Mediterranean fever; other syndromes)
    • •
      Local amyloidosis in isolated organs
    • •
      Amyloid associated with aging
Radiographic Features
    • •
      Adenopathy and calcifications are common.
    • •
      Plain film findings are nonspecific, with multiple nodules or diffuse linear patterns.
    • •
      Pulmonary involvement can be either diffuse or focal.
    • •
      Diagnosis requires biopsy.

Neurofibromatosis

  • Twenty percent of patients with neurofibromatosis have pulmonary involvement:
    • •
      Progressive pulmonary fibrosis
    • •
      Bullae in upper lobes and chest wall
    • •
      Chest wall and mediastinal neurofibromas
    • •
      Intrathoracic meningoceles
    • •
      Ribbon deformities of the ribs

Pulmonary alveolar microlithiasis

Tiny calculi within alveoli. Unknown cause (hereditary). Rare.

Radiographic Features
    • •
      Sandlike microcalcifications of lung (black pleura sign)
    • •
      Bilateral, symmetrical involvement
    • •
      Pulmonary activity on bone scan

Alveolar proteinosis

Proteinaceous, lipid-rich surfactant from type II pneumocytes accumulates in alveoli. Unknown etiology (may be associated with lymphoma or acute silicosis). Extensive sputum production (liters/day). Diagnosed with biopsy, sputum electron microscopy for alveolar phospholipids. Prognosis: Some people with pulmonary alveolar proteinosis suffer from shortness of breath for their entire lifetime. However, this lung disorder is rarely fatal as long as patients undergo regular lung washings. Complications include nocardiosis, aspergillosis, cryptococcosis, and lymphoma. Treatment is with aerosolized proteolytic agents and bronchoscopic lung lavage with 10 to 20 L saline (therapy of choice).

Radiographic Features
    • •
      Bilateral, symmetrical airspace disease (butterfly, batwing pattern)
    • •
      Acinar pattern may become confluent (consolidation)
    • •
      CT: multifocal, panlobular, ground-glass, and airspace opacities with septal thickening (“crazy paving”)
    • •
      Other findings from superimposed opportunistic infection

Drug-induced lung disease

A large number of therapeutic drugs can cause lung toxicity. Because the findings are often nonspecific, a high index of suspicion is required. The most common abnormalities are:

    • Diffuse interstitial opacities
      • •
        Cytotoxic agents: bleomycin, methotrexate, carmustine, cyclophosphamide
      • •
        Gold salts
    • Pulmonary nodules (uncommon)
      • •
        Cyclosporine
      • •
        Oil aspiration
    • Focal ASD
      • •
        Amiodarone accumulates in lysosomes of phagocytes; high iodine content results in increased CT density of affected lung and liver
    • Diffuse ASD (pulmonary edema, hemorrhage)
      • •
        Cytotoxic agents: cytarabine, IL-2, OKT3
      • •
        Tricyclic antidepressants
      • •
        Salicylates
      • •
        Penicillamine
      • •
        Anticoagulants
    • Adenopathy
      • •
        Phenytoin (Dilantin)
      • •
        Cytotoxic agents: cyclosporine, methotrexate
    • Pleural effusions
      • •
        Drug-induced SLE
      • •
        Bromocriptine
      • •
        Methysergide, ergotamine tartrate

Inhalational Lung Disease

Pneumoconiosis

Pneumoconioses are caused by inhalation of inorganic dust particles that overwhelm the normal clearance mechanism of the respiratory tract.

Types

    • Benign pneumoconiosis: radiographic abnormalities are present while there are no symptoms or only minimal symptoms (not fibrogenic):
      • •
        Tin = stannosis
      • •
        Barium = baritosis
      • •
        Iron = siderosis
    • Fibrogenic pneumoconiosis (symptomatic)
      • •
        Silica = silicosis
      • •
        Asbestos = asbestosis
      • •
        Coal workers' pneumoconiosis (CWP)

International labor organization (ILO) classification (Fig. 1-47)

Figure 1-47.

Figure 1-47

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  • The ILO classification can be used to classify or follow pneumoconioses. All pneumoconioses have similar radiographic features that range from few tiny nodules to end-stage lung disease.
    • Small opacities
      • Size:
        • •
          Nodules: p = <1.5 mm, q = <3 mm, r = >3 to 10 mm
        • •
          Reticular: s = fine, t = medium, u = coarse
        • •
          Reticulonodular: x = fine, y = medium, z = coarse (this is not part of ILO classification)
      • Location (“zone”): upper middle and lower zone of each lung field
      • How many (profusion = concentration): category 1 = few nodules, category 2 = lung markings still visible, category 3 = lung markings obscured
    • Large opacities
      • Size: A = <5 cm, B = half of upper lung zone affected, C = > half of upper lung zone affected
    • Other features
      • Pleural thickening, plaques
      • Pleural calcification, diffuse

Silicosis

  • Causative agent is silicone dioxide (SiO2) in quartz, cristobalite, and tridymite. The severity of disease is related to the total amount of inhaled dust. Inhaled particles need to be <5 μm in diameter because larger particles are removed by upper airways. Treatment is to stop exposure; however, in contrast to CWP, silicosis may be progressive despite removal from a dust environment. Isoniazid (INH) chemoprophylaxis is advised. Occupations most at risk (only 5% of patients with >20 years' exposure will develop a complicated form of pneumoconiosis) are:
    • •
      Mining (gold, tin, copper, mica)
    • •
      Quarrying (quartz)
    • •
      Sandblasting
Pathology
    • •
      Silica is phagocytosed by pulmonary macrophages.
    • •
      Cytotoxic reaction causes formation of noncaseating granuloma.
    • •
      Granulomas develop into silicotic nodules (2 to 3 mm in diameter).
    • •
      Pulmonary fibrosis develops as nodules coalesce.
Clinical Findings (Fig. 1-48)
Figure 1-48.

Figure 1-48

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    • Chronic silicosis
      • •
        20 to 40 years of exposure
      • •
        Predominantly affects upper lobes
      • •
        Rarely develops into massive fibrosis
    • Accelerated silicosis
      • •
        5 to 15 years of heavy exposure
      • •
        Middle and lower lobes are also affected.
      • •
        Radiographic appearance is similar to that of alveolar proteinosis.
      • •
        Concomitant diseases:
        • TB, 25% (silicotuberculosis)
        • Collagen vascular disease, 10% (scleroderma, RA, SLE, Caplan syndrome)
  • Acute silicosis (silicoproteinosis)
    • •
      <3 years of exposure
    • •
      Fulminant course: diffuse multifocal ground-glass or airspace consolidations
    • •
      TB, 25%
  • Caplan syndrome
    • •
      RA
    • •
      Lung disease:
      • Silicosis (less common) or CWP (more common)
      • Rheumatoid nodules
Radiographic Features
    • Nodular pattern (common)
      • •
        Nodules: 1 to 10 mm
      • •
        Calcific nodules, 20%
      • •
        Upper lobe > lower lobe
      • •
        Coalescent nodules cause areas of conglomerate opacities.
    • Reticular pattern (may precede or be associated with the nodular pattern)
    • Hilar adenopathy
      • •
        Common
      • •
        Eggshell calcification, 5%
    • Progressive massive fibrosis (PMF)
      • •
        Masses (>1 cm) formed by coalescent nodules
      • •
        Usually in posterior segment of upper lobes
      • •
        Vertical orientation
      • •
        Cavitation due to ischemia or superinfection from TB
      • •
        Often bilateral
      • •
        Retracts hila superiorly
      • •
        Main differential diagnosis: neoplasm, TB, fungus
    • Concomitant TB

Coal workers' pneumoconiosis (CWP)

Development of pneumoconiosis depends on the kind of inhaled coal: anthracite (50% incidence of pneumoconiosis) > bituminous > lignite (10% incidence).

Pathology: coal macule around respiratory bronchioli with associated focal dust (centrilobular emphysema).

Radiographic Features
  • Radiographically indistinguishable from silicosis
    • •
      Simple (reticulonodular) pneumoconiosis
      • Upper and middle lobe predominance
      • Nodules: 1 to 5 mm
      • Centriacinar emphysema surrounds nodules.
    • •
      Complicated pneumoconiosis with progressive massive fibrosis
      • Usually evolves from simple CWP
      • Mass lesions >1 cm in diameter

Asbestos

  • Asbestos exposure causes a variety of manifestations:
    • Pleura
      • •
        Pleural plaques (hyalinized collagen)
      • •
        Diffuse thickening
      • •
        Benign pleural effusion (most common manifestation)
      • •
        Pleural calcification
    • Lung
      • •
        Interstitial fibrosis (asbestosis)
      • •
        Rounded atelectasis with comet tail sign of vessel leading to atelectatic lung
      • •
        Fibrous masses
    • Malignancy
      • •
        Malignant mesothelioma
      • •
        Bronchogenic carcinoma
      • •
        Carcinoma of the larynx
      • •
        GI malignancies
  • Pathogenicity of fibers: crocidolite (South Africa) > amosite > chrysotile (Canada).
    • High-risk professions:
      • •
        Construction, demolition
      • •
        Insulation
      • •
        Pipefitting and shipbuilding
      • •
        Asbestos mining

Asbestos-related pleural disease

Focal Pleural Plaques

Hyalinized collagen in submesothelial layer of parietal pleura. Focal interrupted areas of pleural thickening.

    • •
      Pleural plaques have no functional significance.
    • •
      Most common manifestation of asbestos exposure
    • •
      Preferred location: bilateral, posterolateral mid and lower chest
    • •
      Only 15% of pleural plaques are visible by CXR.
Diffuse Pleural Thickening
    • •
      Less frequent than focal plaques
    • •
      Unlike focal plaques, diffuse thickening may cause respiratory symptoms (abnormal pulmonary function test results)
    • •
      Thickening of interlobar fissures
    • •
      May be associated with round atelectasis
Pleural Calcifications

Pleural calcification in the absence of other histories (hemothorax, empyema, TB, previous surgery) is pathognomonic of asbestos exposure.

    • •
      Calcium may form in center of plaques.
    • •
      Contains uncoated asbestos fibers but no asbestos bodies
    • •
      Usually requires >20 years to develop
Benign Pleural Effusions

Early sign of asbestos-related disease. Usually sterile, serous exudate. The diagnosis is one of exclusion: rule out other causes of pleural effusion:

    • •
      Malignant mesothelioma
    • •
      Bronchogenic carcinoma
    • •
      TB
Round Atelectasis

Round-appearing peripheral atelectasis associated with pleural thickening. Although not unique to asbestos exposure, round atelectasis is common in patients with asbestos exposure and pleural thickening. Most commonly in posterior part of lower lobe.

Radiographic Features (Fig. 1-49)
Figure 1-49.

Figure 1-49

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    • •
      Round mass in lung periphery
    • •
      Thickened pleura (due to asbestos-related disease)
    • •
      Mass is most dense at its periphery.
    • •
      Mass is never completely surrounded by lung.
    • •
      Atelectasis forms an acute angle with pleura.
    • •
      Comet sign: bronchi and vessels curve toward the mass.
    • •
      Signs of volume loss: displaced fissure

Asbestosis

Refers exclusively to asbestos-related interstitial pulmonary fibrosis.

Radiographic Features
    • •
      Reticular, linear patterns
    • •
      Initial subpleural location
    • •
      Progression from bases to apices
    • •
      Honeycombing occurring later in the disease
    • •
      No hilar adenopathy

Malignancy in asbestos-related disease

    • •
      7000-fold increase of mesothelioma (10% risk during lifetime; latency >30 years after exposure)
    • •
      7-fold increase of bronchogenic carcinoma
    • •
      3-fold increase of GI neoplasm

Antigen-antibody–mediated lung disease

  • Allergic reactions in lung can cause one of four patterns of disease:
    • •
      Granulomatous alveolitis
      • Hypersensitivity alveolitis
      • Chronic beryllium disease
    • •
      Pulmonary eosinophilia (pulmonary infiltrations with eosinophilia [PIE])
    • •
      Asthma
    • •
      Goodpasture syndrome

Hypersensitivity pneumonitis (extrinsic allergic alveolitis)

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 are often fungal spores or avian-related antigens.

Hypersensitivity Alveolitis

Disease Antigen Source Antigen
Farmer's lung Moldy hay Micropolyspora faeni
Bird fancier's lung (pigeons, parakeets) Avian excreta Avian serum proteins
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 Cryptostroma corticale
Mushroom worker's lung Spores from mushrooms Thermophilic Actinomyces
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Radiographic Features
  • Acute, reversible changes
    • •
      Diffuse ground-glass pattern
    • •
      Reticulonodular interstitial pattern
    • •
      Patchy areas of consolidation (rare)
  • Chronic, irreversible changes
    • •
      Progressive interstitial fibrosis (often upper lobe predominance) with honeycombing
    • •
      Pulmonary hypertension

Chronic beryllium disease

T-cell–dependent granulomatous response to inhaled beryllium (beryllium copper alloy, fluorescent strip lighting). Now a rare disease.

Radiographic Features
    • Many similarities to sarcoidosis:
      • •
        Reticulonodular pattern → fibrosis
      • •
        Bilateral hilar lymph node enlargement
    • Distinction between berylliosis and sarcoidosis:
      • •
        History of exposure to beryllium
      • •
        Positive beryllium transformation test
      • •
        Increased concentration of beryllium in lung or lymph nodes
      • •
        Negative Kveim test

Pulmonary infiltrates with eosinophilia (PIE)

Group of diseases characterized by transient pulmonary opacities and eosinophilia (>500/mm3).

Types
    • Löffler syndrome (Simple pulmonary eosinophilia, SPE)
      • •
        Idiopathic origin
      • •
        Benign transient pulmonary opacities
      • •
        Minimally symptomatic, self-limited
      • •
        Rare
    • Acute eosinophilic pneumonia
      • •
        Acute febrile illness <5 days
      • •
        Hypoxemia
      • •
        Diffuse alveolar or mixed alveolar-interstitial opacities
      • •
        Response to steroids with no relapse after discontinuation of steroids
      • •
        >25% in BAL fluid
    • Chronic eosinophilic pneumonia (idiopathic origin)
      • •
        Severe, chronic pneumonia
      • •
        Predominantly nonsegmental peripheral opacities
    • Pneumonias of known origin:
      • •
        Allergic bronchopulmonary mycoses (type 1 + 2 hypersensitivity)
        • Aspergillus (ABPA is the most important one)
        • Rare: Candida, Curvularia lunata, Drechslera hawaiiensis, Helminthosporium, Stemphylium lanuginosum
      • •
        Helminth infection (nodular opacities, very high eosinophilia count, high IgE):
        • Ascaris
        • Schistosomiasis; 50% with pulmonary involvement
        • Toxocara canis
        • Microfiliariasis
      • •
        Drugs
        • Penicillin, tetracycline, sulfonamides
        • Salicylates
        • Chlorpropamide, imipramine
        • Nitrofurantoin (causes chronic interstitial eosinophilic alveolitis with progression to fibrosis)

Goodpasture syndrome

Three main features: pulmonary hemorrhage, iron-deficiency anemia, and glomerulonephritis. Binding of circulating antibodies to glomerular and alveolar basement membranes. Symptoms include hemoptysis and renal failure. Diagnosis is made by antiglomerular basement membrane antibody, immunofluorescence of antibody, and renal biopsy.

Radiographic Features
    • •
      Pulmonary hemorrhage: consolidation with air bronchogram
    • •
      Clearing of pulmonary hemorrhage in 1 to 2 weeks
    • •
      Repeated hemorrhage leads to hemosiderosis and pulmonary fibrosis → interstitial reticular pattern
    • •
      Renal findings

Toxin-induced interstitial pneumonitis/fibrosis

Drug-induced pulmonary toxicity

    • Chemotherapeutic drugs
      • •
        Bleomycin
      • •
        BCNU
      • •
        Cyclophosphamide
      • •
        Methotrexate
      • •
        Procarbazine
    • Other drugs
      • •
        Amiodarone
      • •
        Nitrofurantoin
      • •
        Gold
      • •
        Carbamazepine

Silo filler disease

    • •
      Due to NO2 production (yellow gas) in silos
    • •
      NO2 forms nitric acid (HNO3) in lungs, causing pulmonary edema and later COP.
    • •
      Silo filler disease only occurs in September and October, when silos are being filled.
    • •
      Safe NO2 levels below 5 ppm

Airway Disease

Trachea

Malignant tracheal neoplasm

Ninety percent of all tracheobronchial tumors are malignant.

Types
    • Primary malignancies
      • •
        SCC (most common)
      • •
        Adenoid cystic carcinoma (second most common)
      • •
        Mucoepidermoid (less common)
      • •
        Carcinoid (less common; strong contrast enhancement, octreotide uptake)
    • Metastases
      • •
        Local extension (common)
        • Thyroid cancer
        • Esophageal cancer
        • Lung cancer
      • •
        Hematogenous metastases (rare)
        • Melanoma
        • Breast cancer

Benign neoplasm

Only 10% of tracheobronchial tumors are benign. Benign tumors are typically <2 cm.

Types
    • Papilloma
      • •
        Common laryngeal tumors in children, rare in adults, often multiple
      • •
        May cause lung nodules
      • •
        Malignant potential-SCC. (These lesions are caused by the human papillomavirus and are benign but may degenerate into malignancies.)
    • Hamartoma
      • •
        Fat density is diagnostic.
      • •
        Often calcified (popcorn pattern)
    • Adenoma
      • •
        Rare

Saber-sheath trachea

Reduced coronal diameter (<⅔ of sagittal diameter). Only affects the intrathoracic trachea; the extrathoracic trachea appears normal.

    • •
      95% of patients have COPD
    • •
      More common in male patients
    • •
      Tracheal ring calcification is common.

Tracheopathia osteoplastica (TPO)

Foci of cartilage and bone develop in the submucosa of the tracheobronchial tree. Benign, rare condition. Most cases are discovered incidentally at autopsy.

Clinical Findings
    • •
      Dyspnea, hoarseness, expiratory wheeze/stridor (airway obstruction)
    • •
      Hemoptysis (mucosal ulceration)
    • •
      Cough and sputum production
    • •
      Rarely: atelectasis, pneumonia
Radiographic Features
    • •
      Calcified tracheobronchial tree, nodules, osteocartilaginous growth
    • •
      Thickening of tracheal cartilage
    • •
      Sparing of the posterior membranous portion
    • •
      Narrowed lumen
    • •
      Distal three fourths of the trachea and the proximal bronchi are most commonly involved.

Relapsing polychondritis

Collagen vascular disease characterized by inflammation and progressive destruction of cartilage throughout the body (ribs, trachea, earlobes, nose, joints). Rare.

Diagnostic Criteria (>3 needed)
    • •
      Recurrent chondritis of auricles (painful ear)
    • •
      Inflammation of ocular structures (e.g., conjunctivitis, scleritis, keratitis)
    • •
      Chondritis (painful) of laryngeal/tracheal cartilage
    • •
      Cochlear or vestibular damage
Radiographic Features
    • Trachea
      • •
        Diffuse narrowing (slitlike lumen)
      • •
        Thickening of tracheal wall
    • Location
      • •
        Ear, 90%
      • •
        Joints, 80%
      • •
        Nose, 70%
      • •
        Eye, 65%
      • •
        Respiratory tract, 55%
      • •
        Inner ear, 45%
      • •
        Other: cardiovascular, 25%; skin, 15%

Tracheobronchomalacia

  • Refers to weakening of tracheal and bronchial walls.
    • Primary (uncommon)
      • •
        Occurs in children
      • •
        May be associated with laryngomalacia
    • Secondary (more common)
      • •
        Intubation
      • •
        COPD
      • •
        Less common causes: recurrent infections, trauma, relapsing polychondritis
      • •
        Compression of trachea by vessels or mediastinal mass
Radiographic Features
    • •
      Collapsed walls of trachea and bronchi
    • •
      Recurrent pneumonia

Tracheobronchomegaly (mounier-kühn disease)

Atrophy and dysplasia of trachea and proximal bronchi. Associated with Ehlers-Danlos syndrome. The trachea measures >3 cm, and/or bronchi measure >2.4 cm. Tracheal diverticula.

Congenital bronchial atresia

Narrowing or obliteration of a subsegmental, segmental, or lobar bronchus.

    • •
      LUL > RUL > RML > RLL, LLL
    • •
      Mucus plugging of dilated distal bronchus
    • •
      Collateral ventilation distal to obstruction with air trapping → distal lung is hyperlucent

Chronic bronchial disease

Group of diseases characterized by increased airway resistance and reduction in expiratory flow. Entities include chronic bronchitis, emphysema, asthma, bronchiectasis, and cystic fibrosis. The most common combination is chronic bronchitis and emphysema, often referred to as chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD)

  • COPD is characterized by progressive obstruction to airflow. Two components:
    • •
      Chronic bronchitis is a clinical diagnosis: excessive mucus formation and cough for >3 months during 2 consecutive years; all other causes of expectoration have to be ruled out. The diagnosis of chronic bronchitis is based on clinical history; chest films add little information except to exclude other underlying abnormalities.
    • •
      Emphysema is a pathologic diagnosis: abnormal enlargement of airspace distal to the terminal nonrespiratory bronchiole.
    • The exact etiology of COPD is unknown:
      • •
        Tobacco smoke
      • •
        Industrial air pollution
      • •
        α1-Antitrypsin deficiency (autodigestion)
Clinical Syndromes
    • Blue bloaters
      • •
        Bronchitis, tussive type of COPD
      • •
        Episodic dyspnea due to exacerbation of bronchitis
      • •
        Young patients
    • Pink puffers
      • •
        Emphysematous type of COPD
      • •
        Progressive exertional dyspnea due to the emphysema
      • •
        Elderly patients
Radiographic Features
  • Features are nonspecific:
    • Tubular shadows (thickened bronchial walls)
      • •
        Parallel shadows if bronchiole is imaged in longitudinal section
      • •
        Thickening of bronchi imaged in axial section.
      • •
        Increased lung markings (“dirty chest”)
      • •
        Accentuation of linear opacities throughout the lung
      • •
        Very subjective finding

Emphysema

Abnormal enlargement of distal airspaces with destruction of alveolar walls with or without fibrosis. Underlying cause: imbalance of proteases and antiproteases.

Clinical Findings
    • •
      Chronic airflow obstruction
    • •
      Decreased FEV1

Types of Emphysema*

Panacinar Centroacinar Paraseptal
Predominant location Lower lobes Upper lobes Along septal lines (periphery of lung and branch points of vessels)
Distribution Homogeneous Patchy Peripheral
Associations α1-Antitrypsin deficiency, smoking Chronic bronchitis, smoking Smoking
Involvement All components of acinus homogeneously involved Center of pulmonary acinus involved Usually entire secondary pulmonary lobule
Imaging Inline graphicInline graphicInline graphic
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*

The designations “lobular” and “acinai” refer to the number of acini affected (a few acini make up a lobule).

Radiographic Features (Fig. 1-50)
Figure 1-50.

Figure 1-50

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    • Overinflation
    • •
      Flattening of hemidiaphragms (reliable sign): highest level of the dome is <1.5 cm above a straight line drawn between the costophrenic and the vertebrophrenic junctions.
    • •
      Tenting of diaphragm (invagination of thickened visceral pleura attached to septa between basal bullae)
    • •
      Saber-sheath trachea
    • •
      Other, less reliable signs:
      • Increase of retrosternal airspace >3 cm measured at level 3 cm below the sternomanubrial junction
      • Craniocaudal diameter of lung >27 cm
      • Anterior bowing of sternum
      • Accentuated kyphosis
      • Widely spaced ribs
    • Vascular abnormalities
      • •
        Decreased number of vessels in areas of abnormal lung
      • •
        Absence of peripheral pulmonary vessels
      • •
        Fewer arterial branches
      • •
        Central pulmonary artery increased in size
    • Emphysema
      • •
        Decreased attenuation of abnormal lung
      • •
        An air-fluid level indicates infection of a bulla.
    • HRCT
      • •
        Centriacinar (centrilobular): the central portion of the pulmonary lobule is involved.
      • •
        Panacinar (panlobular): the whole acinus is involved, and central arteries and bronchioles can be seen (usually at apices).
      • •
        Paraseptal: emphysematous changes adjacent to septal lines in periphery and along fissures
    • Pearls
      • •
        As emphysema becomes more severe with time, the CT differentiation of the three types of emphysema becomes more difficult.
      • •
        Different types of emphysema may coexist.
      • •
        Moderate to severe emphysema can be detected on CXR; for the detection of mild forms HRCT is usually required.
      • •
        HRCT is currently the most sensitive method to detect emphysema; however, normal HRCT does not rule out the diagnosis of emphysema.
      • •
        Always look at CXR before interpreting HRCT; occasionally, CXR changes of emphysema are more evident than HRCT changes (e.g., hyperinflation).
      • •
        20% of patients with emphysema have normal HRCT.
      • •
        40% of patients with abnormal HRCT have normal pulmonary function tests.
      • •
        Bullous lung disease is a severe form of emphysema that is highly localized and >1 cm in size.

Asthma

Hyperirritability of airways causes reversible airway obstruction (bronchial smooth muscle contraction, mucosal edema, hypersecretion of bronchial secretory cells: bronchospasm). The etiology is unknown (IgE participation).

Types
    • Extrinsic, allergic form
      • •
        Childhood asthma
      • •
        Immunologically mediated hypersensitivity to inhaled antigens
    • Intrinsic asthma
      • •
        Adults
      • •
        No immediate hypersensitivity
Radiographic Features
    • Normal CXR in majority of patients
    • Severe or chronic asthma:
      • •
        Air trapping, hyperinflation: flattened diaphragm, increased retrosternal airspace
      • •
        Limited diaphragmatic excursion
    • Bronchial wall thickening (tramlines), a nonspecific finding, is also seen in chronic bronchitis, cystic fibrosis, bronchiectasis, and pulmonary edema.
Complications
    • •
      Acute pulmonary infection
    • •
      Mucus plugs
    • •
      Allergic bronchopulmonary aspergillosis (ABPA)
    • •
      Tracheal or bronchial obstruction
    • •
      Pneumomediastinum/pneumothorax

Bronchiectasis

Irreversible dilatation of bronchi (reversible bronchial dilatation may be seen in viral and bacterial pneumonia). Recurrent pneumonias and/or hemoptysis

Morphologic Classification of Bronchiectasis

Cylindrical Varicose Cystic
Terminal divisions* 20 18 4
Pathology Not end stage Destroyed lung Destroyed lung
CXR, HRCT Fusiform dilatation, tramlines, signet signs Inline graphic Tortuous dilatation rare Inline graphic Saccular dilatation, “string of cysts,” AFL common Inline graphic
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*

Normal tracheobronchial tree has 23 to 24 divisions.

occur. HRCT is now the method of choice for workup of bronchiectasis.

Types
    • Congenital (rare)
      • •
        Abnormal secretions: cystic fibrosis
      • •
        Bronchial cartilage deficiency: Williams-Campbell syndrome
      • •
        Abnormal mucociliary transport: Kartagener syndrome
      • •
        Pulmonary sequestration
    • Postinfectious (common)
      • •
        Childhood infection
      • •
        Chronic granulomatous infection
      • •
        ABPA
      • •
        Measles
    • Bronchial obstruction
      • •
        Neoplasm
      • •
        Inflammatory nodes
      • •
        Foreign body
      • •
        Aspiration
Radiographic Features
    • Plain film
      • •
        Tramline: horizontal, parallel lines corresponding to thickened, dilated bronchi
      • •
        Bronchial wall thickening (best seen end-on)
      • •
        Indistinctness of central vessels due to peribronchovascular inflammation
      • •
        Atelectasis
    • HRCT (Fig. 1-51 )
      • •
        Conspicuous bronchi
      • Bronchi can be seen in outer third of lung.
        • Bronchi appear larger than accompanying vessels.
    • •
      Bronchial walls
        • Thickened walls
        • Signet ring sign: focally thickened bronchial wall adjacent to pulmonary artery branch
Figure 1-51.

Figure 1-51

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Pearls
    • •
      Bronchography may be indicated if clinical suspicion of bronchiectasis is high and CT is negative; CT has a low positive predictive value for mild forms of bronchiectasis. Bronchography is rarely performed alone.
    • •
      Differentiation of cystic bronchiectasis and cystic spaces in IPF (honeycombing) is difficult; bronchiectasis usually involves lower lobes; honeycombing is not associated with air-fluid levels.
    • •
      To distinguish emphysema from bronchiectasis, expiratory scans will show air trapping in bullae; cystic bronchiectasis will collapse.

Cystic fibrosis

Caused by an abnormality in the cystic fibrosis transmembrane conductance regulator protein, which regulates the passage of ions through membranes of mucus-producing cells. Autosomal recessive disease (incidence 1:2000).

Pathophysiology
    • •
      Dysfunction of exocrine glands causing thick, tenacious mucus that accumulates and causes bronchitis and pneumonia
    • •
      Reduced mucociliary transport: airway obstruction with massive mucus plugging
  • Spectrum 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
      • •
        Liver cirrhosis
      • •
        Rectal prolapse
      • •
        Neonates: meconium ileus, meconium peritonitis, intussusception
    • Other
      • •
        Sinusitis: hypoplastic frontal sinus, opacification of other sinuses
      • •
        Infertility in males
Radiographic Features
    • Severity of bronchiectasis
      • •
        Mild: lumen equal to adjacent blood vessels
      • •
        Moderate: lumen 2 to 3 times the size of adjacent blood vessels
      • •
        Severe: lumen >3 times the size of adjacent blood vessels
    • Peribronchial thickening
      • •
        Wall thickness ≥ the diameter of adjacent blood vessels
    • Mucus plugging
      • •
        Determine number of pulmonary segments involved
      • •
        Air trapping → increased lung volumes
      • •
        Collapse, consolidation
      • •
        Bullae
    • Location: predominantly upper lobes and superior segments of lower lobes
    • Other
      • •
        Reticular, cystic pattern of lung fibrosis
      • •
        Prominent hila:
        • Adenopathy
        • Large pulmonary arteries (PAH)
      • •
        Recurrent pneumonias
Complications
    • Early
      • •
        Lobar atelectasis (especially RUL)
      • •
        Pneumonia
    • Late
      • •
        Respiratory insufficiency, hypertrophic osteoarthropathy
      • •
        Recurrent pneumothorax (rupture of bullae or blebs)
      • •
        Cor pulmonale and pulmonary arterial hypertension
      • •
        Hemoptysis
      • •
        Aspergillus superinfection

Bronchiolitis obliterans

Bronchiolitis obliterans (Swyer-James syndrome, unilateral emphysema) refers to unilateral air trapping caused by obstruction of distal bronchioles.

Etiology of Adult Bronchiolitis
    • Obliterative
      • •
        Exposure to toxic fumes
      • •
        Bone marrow transplant
      • •
        Viral infections
      • •
        Drugs
    • Proliferative
      • •
        Acute infectious
      • •
        Respiratory bronchiolitis
      • •
        COP
      • •
        COPD
        • Asthma
        • Chronic bronchitis
CT Features
    • •
      Nodules with branching opacities: tree-in-bud appearance
    • •
      Ground-glass attenuation and consolidation
    • •
      Mosaic pattern
      • Seen with obliterative bronchiolitis
      • Mosaic pattern due to hypoxic vasoconstriction in areas of bronchiolar obstruction with redistribution to normal areas
      • Decreased size and number of vessels in affected lung with air trapping on inspiration/expiration CT; thus the apparent ground-glass-appearing lung is normal.
    • •
      Other nonspecific findings
      • Bronchiectasis
      • Bronchial wall thickening

Lung Injury

Trauma

    • Four major mechanisms of injury:
      • 1.
        Direct impact
      • 2.
        Sudden deceleration (motor vehicle accident): sudden torsion at interfaces of fixed (e.g., paraspinal) and mobile (e.g., lung) components
      • 3.
        Spallation: broad kinetic shock wave, which is partially reflected at a liquid-gas interface, leading to local disruption of alveoli and supporting structures
      • 4.
        Implosion: low-pressure afterwave that causes rebound overexpansion of gas bubbles
    • Other mechanisms of chest trauma include:
      • •
        Posttraumatic aspiration
      • •
        Inhalation injury
      • •
        Increased capillary permeability: fat emboli, oligemic shock, neurogenic pulmonary edema
Pearls
    • •
      Radiographic and clinical evidence of lung trauma is often absent in the first 2 to 3 hours after trauma.
    • •
      There is no consistent relationship between external chest wall injury and underlying lung injury, especially in children.
    • •
      Radiographic studies usually underestimate the true extent of pulmonary trauma.

Pneumothorax (Fig. 1-52)

Figure 1-52.

Figure 1-52

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  • Common causes:
    • Iatrogenic
      • •
        Percutaneous biopsy, 20%
      • •
        Barotrauma, ventilator, 20%
    • Trauma
      • •
        Lung laceration
      • •
        Tracheobronchial rupture
    • Cystic lung disease
      • •
        Bulla, bleb: often in healthy young men; 30% recurrence
      • •
        Emphysema, asthma
      • •
        PCP
      • •
        Honeycombing: end-stage interstitial lung disease
      • •
        Lymphangioleiomyomatosis (pneumothorax in 75% of cases)
      • •
        Eosinophilic granuloma (pneumothorax in 20% of cases)
    • Parenchymal necrosis
      • •
        Lung abscess, necrotic pneumonia, septic emboli, fungal disease, TB
      • •
        Cavitating neoplasm, osteogenic sarcoma
      • •
        Radiation necrosis
    • Other
      • •
        Catamenial: recurrent spontaneous pneumothorax during menstruation, associated with endometriosis of pleura

Radiographic features (Figs. 1-53 and 1-54)

Figure 1-53.

Figure 1-53

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Figure 1-54.

Figure 1-54

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    • Appearance
      • •
        Upright position
        • Air in pleural space is radiolucent.
        • White line of the visceral pleura is distinctly visible.
        • Volume loss of underlying lung
        • Supine position
        • Deep sulcus sign: anterior costophrenic angle sharply delineated
    • Detection
      • •
        Lateral decubitus (suspected side should be up, whereas it should be down for fluid); 5 mL of air detectable
      • •
        Upright expiration film
      • •
        CT most sensitive
    • Size of pneumothorax can be estimated but is rarely of practical use
      • •
        Average distance (AD in cm) = (A + B + C)/3
      • •
        % Pneumothorax ≈ AD (in cm) x 10, e.g.:
        • AD of 1 cm corresponds to a 10% pneumothorax
        • AD of 4 cm corresponds to a 40% pneumothorax

Tension pneumothorax (Fig. 1-55)

Figure 1-55.

Figure 1-55

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Valve effect during inspiration/expiration leads to progressive air accumulation in thoracic cavity. The increased pressure causes shift of mediastinum and ultimately vascular compromise. Treatment is with emergency chest tube placement.

Radiographic Features
    • •
      Overexpanded lung
    • •
      Depressed diaphragm
    • •
      Shift of mediastinum and heart to contralateral side

Percutaneous chest tube placement for pneumothorax

Indication
    • •
      All symptomatic pneumothoraces
Technique for Heimlich Valve Placement (for Biopsy-Induced Pneumothorax)
    • 1.
      Entry: midclavicular line, 2nd to 4th anterior intercostal space
    • 2.
      Aspirate air with 50-mL syringe.
    • 3.
      Use small drainage kit that includes a Heimlich valve (one-way airflow system). During expiration, positive intrapleural pressure causes air to escape through the valve.
Technique for Chest Tube Placement (Any Pneumothorax)
    • 1.
      Entry: posterior or lateral or region of largest pneumothorax as defined by CT
    • 2.
      Local anesthesia
    • 3.
      Place 12- to 16-Fr drainage catheter using trocar technique.
    • 4.
      Put catheter to wall suction.
    • 5.
      Catheter can be removed if there is no pneumothorax 24 hours after clamping of the catheter.

Contusion

Endothelial damage causes extravasation of blood into interstitium and alveoli.

Occurs mainly in lung adjacent to solid structures (e.g., ribs, vertebrae, heart, liver).

Appears 6 to 24 hours after injury. Hemoptysis is present in 50%. Mortality rate of 15%-40%.

Radiographic Features
    • •
      Pulmonary opacities are due to hemorrhage and edema.
    • •
      Air bronchograms are commonly seen by CT but are not always present if there is associated bronchial obstruction.
    • •
      Contusions usually appear 6 to 24 hours after trauma and resolve by 7 to 10 days.
    • •
      Opacities that do not resolve by 7 to 10 days may represent:
      • Postlaceration hematoma
      • Aspiration
      • Hospital-acquired pneumonia
      • Atelectasis
      • ARDS

Lung laceration (Fig. 1-56)

Figure 1-56.

Figure 1-56

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Produced by sharp trauma (rib fractures), deceleration, shearing, or implosion. Pathogenetically, there is a linear tear (may be radiographically visible) that becomes round or ovoid (pneumatocele) with time. Usually accompanied by hemoptysis and pleural and parenchymal hemorrhage. Bronchopleural fistulas are a common complication. Detection of a laceration is clinically important as lacerations can become secondarily infected and also lead to bronchopleural fistula, requiring prolonged chest tube drainage.

Types of Pulmonary Lacerations

Type Location Pneumothorax Mechanism
1 Midlung Variable Shear between parenchyma and tracheobronchial tree
2 Paraspinal Uncommon Shear due to sudden herniation of lower lobe parenchyma in front of vertebral column
3 Subpleural Usual Puncture by displaced rib fracture
4 Subpleural Usual Shear at site of transpleural adhesion
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Fat embolism

Lipid emboli from bone marrow enter pulmonary and systemic circulation. When complicated by ARDS, fat embolism has high mortality. Frequently CNS is also affected.

Radiographic Features
    • •
      Subject in patients with initially clear lungs, sudden onset of dyspnea, and multiple fractures.
    • •
      Interstitial and alveolar hemorrhagic edema produces a varied radiographic appearance.
    • •
      Radiographic opacities induced by fat embolism become evident only 48 hours after the incident (“delayed onset”).
    • •
      Opacities clear in 3 to 7 days.

Tracheobronchial tear

High mortality (30%). Requires early bronchoscopy for early detection to avoid later bronchostenosis. Two presentations:

    • •
      Tear of right mainstem and distal left bronchus: pneumothorax not relieved by chest tube placement. Most common locations are main bronchi (R > L); 75% occur within 2 cm of tracheal carina.
    • •
      Tear of trachea and left mainstem bronchus: air leaks are usually confined to mediastinum and subcutaneous tissues.

Diaphragmatic tear

Ninety percent of tears occur on the left side, 90% of clinically significant hemidiaphragm ruptures are overlooked initially, and 90% of strangulated diaphragmatic hernias are of traumatic etiology.

Radiographic Features (Fig. 1-57)
Figure 1-57.

Figure 1-57

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    • •
      Air-fluid levels or abnormal air collection above diaphragm
    • •
      Abnormal elevation of left hemidiaphragm with or without herniated gastric fundus or colon
    • •
      Contralateral tension displacement of mediastinum
    • •
      Abnormal location of NG tube
    • •
      Confirmation of tear by coronal MRI

Esophageal tear

    • •
      Esophageal tear (thoracic inlet, gastroesophageal junction)
    • •
      Blunt injuries usually seen in phrenic ampulla and cervical esophagus, whereas penetrating injuries can occur anywhere.
    • •
      Chest radiographs are nonspecific and usually show wide mediastinum, left pleural effusion, or hydropneumothorax.
    • •
      Pneumomediastinum is common but is a nonspecific finding.
    • •
      Pleural effusion has low pH and high amylase levels.

Other injuries

    • •
      Aortic injury
    • •
      Hemothorax
    • •
      Chylothorax
    • •
      Cardiac injury
    • •
      Fractures: rib, spine

Postoperative chest

Complications of surgical procedures

Mediastinoscopy
  • Complication rate, <2%:
    • •
      Mediastinal bleeding
    • •
      Pneumothorax
    • •
      Vocal cord paralysis (recurrent nerve injury)
Bronchoscopy
    • •
      Injury to teeth, aspiration
    • •
      Transient pulmonary opacities, 5%
    • •
      Fever, 15%
    • •
      Transbronchial biopsy:
      • Pneumothorax, 15%
      • Hemorrhage (>50 mL), 1%
Wedge Resection
    • •
      Air leaks (common)
    • •
      Contusion
    • •
      Recurrence of tumor
Median Sternotomy Complications
  • Complication rate, 1%-5%:
    • •
      Mediastinal hemorrhage
    • •
      Mediastinitis (focal fluid collection)
    • •
      Sternal dehiscence
    • •
      False aneurysm
    • •
      Phrenic nerve paralysis
    • •
      Osteomyelitis of sternum
Chest Tube Placement
    • •
      Horner syndrome (pressure on sympathetic ganglion)
    • •
      False aortic aneurysm

Pneumonectomy (Fig. 1-58)

Figure 1-58.

Figure 1-58

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Radiographic Features
    • •
      Two thirds of the hemithorax fills with fluid in 4 to 7 days; it is important that successive films demonstrate gradual fill-in and that the residual air bubble does not get bigger; an air bubble increasing in size is suggestive of a bronchopleural fistula.
    • •
      Gradual shift of the mediastinum and heart toward the pneumonectomy side
    • •
      Contralateral lung may normally be herniated toward the pneumonectomy side at the apex and mimic the presence of a residual lung.
Lobectomy
    • •
      Remaining lobes expand to fill the void; splaying of vessels
    • •
      Slight shift of mediastinum, elevation of hemidiaphragm
(Sub)segmental Resection
    • •
      Little or no parenchymal rearrangement
    • •
      Postoperative opacities (hemorrhage, contusion, edema) common

Postpneumonectomy syndrome

This rare syndrome refers to airway obstruction that occurs after pulmonary resections and is due to an extreme shift of the mediastinum or rotation of hilar structures. Occurs most often after right pneumonectomy or after left pneumonectomy when a right arch is present.

Radiographic Features (Fig. 1-59)
Figure 1-59.

Figure 1-59

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    • Airway obstruction
      • •
        Air trapping: hyperinflated lung
      • •
        Recurrent pneumonia, bronchiectasis
    • Narrowing of bronchi or trachea, bronchomalacia
    • Postsurgical changes
      • •
        Hyperinflation of contralateral lung
      • •
        Marked shift of mediastinum

Bronchopleural fistula (BPF)

A fistula between bronchus and pleural space develops in 2%-4% of pneumonectomy patients; with large fistulas, the fluid in the pneumonectomy cavity may drown the opposite healthy lung. Factors that predispose to BPF include:

    • •
      Active inflammation (TB), necrotizing infection
    • •
      Tumor in bronchial margin
    • •
      Devascularized bronchial stump, poor vascular supply
    • •
      Preoperative irradiation
    • •
      Contamination of the pleural space
Radiographic Features
    • Plain film
      • •
        Persistent or progressive pneumothorax
      • •
        Sudden shift of mediastinum to the normal side
    • Nuclear medicine
      • •
        Xenon leak
    • Sinography with nonionic contrast material
      • •
        Examination of choice to define the size of a pleural cavity and bronchial communication
      • •
        Alternatively, thin section CT may show communication.

Torsion

Lobar Torsion

A prerequisite for torsion is the presence of complete fissures. Predisposing factors include masses, pleural effusion, pneumothorax, pneumonia, and surgical resection of inferior pulmonary ligament. Rare.

    • •
      Most commonly the right middle lobe (RML) rotates on its bronchovascular pedicle.
    • •
      Obstruction of venous flow, ischemia, and necrosis result.
    • •
      Plain film: mobile opacity at different locations on different views
Cardiac Herniation

Rare. 50%-100% mortality. Most often occurs after a right pneumonectomy requiring intrapericardial dissection.

Radiographic Features (Fig. 1-60)
Figure 1-60.

Figure 1-60

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    • •
      Heart is rotated to the right
    • •
      Cardiac herniation through pericardial sac results in intrapericardial air, which originates from the postpneumonectomy space
    • •
      Presence of a notch
    • •
      Intracardiac catheters are kinked
    • •
      “Snow cone” appearance of heart border

Lung transplantation

Transplantation of the left lung is technically easier because of the longer left bronchus.

Radiographic Features
    • Reimplantation response
      • •
        Diffuse alveolar pattern of noncardiogenic pulmonary edema develops within 4 to 5 days in the transplanted lung owing to capillary leak. It never develops later.
      • •
        The alveolar pattern lasts 1 to several weeks.
    • Rejection
      • •
        Acute rejection is most commonly detected by biopsy when there are no associated radiographic findings; when radiographic findings are present, they include:
        • Diffuse interstitial pattern in peribronchovascular distribution
        • Septal thickening
        • Pleural effusion
        • Alveolar edema
      • •
        Chronic rejection
        • Bronchiolitis obliterans (air trapping on expiratory scans)
        • Bronchiectasis
    • Infections, 50% of patients
      • •
        Infections usually involve the transplanted lung, not the native lung, because of poor mucociliary clearance and/or lymphatic interruption.
      • •
        Pathogens: Pseudomonas, Staphylococcus > other bacterial, viral, fungal infections
    • Airways
      • •
        Leaks at bronchial anastomosis site are the most common abnormality and usually present as pneumomediastinum and/or pneumothorax in the perioperative period.
      • •
        Operations to prevent leaks
        • Omental flap around anastomosis
        • Telescope-type anastomosis
      • •
        Bronchial strictures may require stenting
    • Lymphoproliferative disorder
      • •
        Multiple or solitary pulmonary nodules or lymphadenopathy

Pulmonary Vasculature

Pulmonary artery hypertension

General

PAH is defined as Psys >30 mm Hg or Pmean >25 mm Hg. Normal pulmonary arterial pressures in adult:

    • •
      Psys: 20 mm Hg
    • •
      Pdias: 10 mm Hg
    • •
      Pmean: 14 mm Hg
    • •
      Capillary wedge pressure: 5 mm Hg
Causes of PAH
    • Primary PAH (females 10 to 40 years; rare)
    • Secondary PAH (more common)
      • •
        Eisenmenger syndrome
      • •
        Chronic PE
      • •
        Emphysema, pulmonary fibrosis
      • •
        Schistosomiasis (most common cause worldwide)
Classification
    • Precapillary hypertension
    • Vascular
      • •
        Increased flow: L-R shunts
      • •
        Chronic PE
      • •
        Vasculitis
      • •
        Drugs
      • •
        Idiopathic
    • Pulmonary
      • •
        Emphysema
      • •
        Interstitial fibrosis
      • •
        Fibrothorax, chest wall deformities
      • •
        Alveolar hypoventilation
    • Postcapillary hypertension
      • Cardiac
        • •
          LV failure
        • •
          Mitral stenosis
        • •
          Atrial tumor
      • Pulmonary venous
        • •
          Idiopathic venoocclusive disease
        • •
          Thrombosis
Radiographic Features
    • •
      Enlarged main PA (diameter correlates with pressure): >29 mm is indicative of PAH.
    • •
      Rapid tapering of PA toward the periphery
    • •
      Decreased velocity of pulmonary flow by MRA
    • •
      Calcification of the pulmonary arteries is pathognomonic but occurs late in the disease.
    • •
      Cardiomegaly (cor pulmonale)
    • •
      If the ratio of pulmonary artery diameter to aortic diameter is greater than 1 (rPA >1) by CT, there is a strong correlation with elevated mean PA pressure, particularly in patients <50 years of age.
      Types of Pulmonary EDEMA
      Signs Cardiac Renal Lung Injury
      Heart size Enlarged Normal Normal
      Blood flow Inverted Balanced Normal
      Kerley lines Common Common Absent
      Edema Basilar Central: butterfly Diffuse
      Air bronchograms Not common Not common Very common
      Pleural effusions Very common Common Not common
      graphic file with name u01-12-9780323065382.gif
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    • •
      By HRCT scans, both primary and secondary forms of pulmonary hypertension may produce a mosaic pattern of lung attenuation, a finding suggestive of regional variations in parenchymal perfusion. A vascular cause for the mosaic pattern is suggested when areas of high attenuation contain larger-caliber vessels and areas of low attenuation contain vessels of diminished size.

Pulmonary edema

Causes of Pulmonary Edema

    • Cardiogenic
      • Adults
        • •
          Left ventricular (LV) failure from CAD (most common)
        • •
          Mitral regurgitation (common)
        • •
          Ruptured chordae
        • •
          Endocarditis
      • Neonates
        • •
          TAPVC below diaphragm
        • •
          Hypoplastic left side of heart
        • •
          Cor triatriatum
    • Renal
      • •
        Renal failure
      • •
        Volume overload
    • Lung injury (increased permeability: capillary leak)
      • •
        Septic shock, neurogenic shock
      • •
        Fat embolism
      • •
        Inhalation: SO2, O2, Cl2, NO2
      • •
        Aspiration, drowning

Grading of cardiogenic pulmonary edema (Figure 1-61, Figure 1-62, Figure 1-63)

Figure 1-61.

Figure 1-61

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Figure 1-62.

Figure 1-62

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Figure 1-63.

Figure 1-63

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Fluid accumulation in the lung due to cardiogenic causes (CHF; pulmonary venous hypertension) follows a defined pattern:

    • Grade 1: vascular redistribution (10 to 17 mm Hg)
      • •
        Diameter of upper lobe vessels equal to or increased over diameter of lower lobe vessels at comparable distance from hilum
      • •
        Pulmonary veins in first intercostal space >3 mm in diameter
    • Grade 2: interstitial edema (18 to 25 mm Hg)
      • •
        Peribronchovascular cuffing, perihilar haziness
      • •
        Kerley lines (differential diagnosis: chronic fibrosis from edema, hemosiderin, tumor, etc.)
      • •
        Unsharp central pulmonary vessels (perivascular edema)
      • •
        Pleural effusion
    • Grade 3: alveolar edema (>25 mm Hg)
      • •
        Airspace disease: patchy consolidation, air bronchograms

Asymmetrical pulmonary edema

    • •
      Gravitational (most common)
    • •
      Underlying COPD (common)
    • •
      Unilateral obstruction of pulmonary artery: PE
    • •
      Unilateral obstruction of lobar pulmonary vein: tumor

Pulmonary embolism

Acute pulmonary embolism (PE) is associated with significant morbidity and mortality, causing 120,000 deaths/year in the United States.

Types
    • •
      Incomplete infarct: hemorrhagic pulmonary edema without tissue necrosis; resolution within days
    • •
      Complete infarct: tissue necrosis; healing by scar formation
Risk Factors
    • •
      Immobilization >72 hours (55% of patients with proved PE have this risk factor)
    • •
      Recent hip surgery, 40%
    • •
      Cardiac disease, 30%
    • •
      Malignancy, 20%
    • •
      Estrogen use (prostate cancer, contraceptives), 6%
    • •
      Prior deep vein thrombosis (DVT), 20%; risk factors:
      • Myocardial infarction
      • Thoracoabdominal surgery
      • Permanent pacemaker
      • Venous catheters
Clinical Findings
    • •
      Chest pain, 90%
    • •
      Tachypnea (>16 breaths/min), 90%
    • •
      Dyspnea, 85%
    • •
      Rales, 60%
    • •
      Cough, 55%
    • •
      Tachycardia, 40%
    • •
      Hemoptysis, 30%
    • •
      Fever, 45%
    • •
      Diaphoresis, 25%
    • •
      Cardiac gallop, 30%
    • •
      Syncope, 15%
    • •
      Phlebitis, 35%
Radiographic Features

Radiographic signs are nonspecific and are present only if a significant infarction occurs

Imaging Algorithm
    • •
      CT pulmonary angiography with axial CT of the inferior vena cava and the iliac, femoral, and popliteal veins is the mainstay of PE evaluation. If the findings are equivocal and clinical suspicion remains high, additional imaging is required (V./Q. scan, pulmonary angiography).
    • •
      V./Q. scan is preferred if iodinated contrast is contraindicated in the context of renal insufficiency or history of severe allergic reaction.
    • •
      Patients who have symptoms of deep vein thrombosis but not of pulmonary embolism initially undergo US, which is a less expensive alternative. If the findings are negative, imaging is usually discontinued; if they are positive, the patient is evaluated for pulmonary embolism at the discretion of the referring physician.
    • •
      In pregnant patients, CTA may be performed if there is high suspicion for PE and sonography fails to demonstrate lower extremity DVT. Axial CT of the IVC and the iliac, femoral, and popliteal veins is omitted.
Plain Film
    • •
      Westermark sign: localized pulmonary oligemia (rare)
    • •
      Hampton hump: triangular peripheral cone of infarct = blood in secondary pulmonary lobules (rare); does not grow → should reduce in size on successive radiographs
    • •
      Fleischner sign: increased diameter of pulmonary artery (>16 mm) seen in acute PE. It usually disappears within a few days.
    • •
      Cor pulmonale: sudden increase in size of RV, RA
    • •
      Pulmonary edema, atelectasis, pleural effusion, 50%
CT Findings in PE
    • •
      Adequately performed CT studies are essentially >90% sensitive and specific for large central emboli.
    • •
      Intraluminal filling defect surrounded by contrast
    • •
      Expanded unopacified vessel
    • •
      Eccentric filling defect
    • •
      Peripheral wedge-shaped consolidation
    • •
      Pleural effusion
    • •
      Allows evaluation of the inferior vena cava and the lower extremity veins to the knee
    • •
      Anatomic pitfalls in CT diagnosis of acute PE: lymph nodes, impacted bronchi, pulmonary veins, pulmonary arterial catheters, and pulmonary artery sarcomas.
    • •
      Technical pitfalls: respiratory or cardiac motion, poor bolus timing, quantum mottle, and edge-enhancing reconstruction algorithms
Scintigraphy
    • •
      Ventilation-perfusion mismatch
Angiography
    • •
      Constant intraluminal filling defects in PA
    • •
      Complete cut-off of PA or its branches
    • •
      Prolongation of the arterial phase; delayed filling and emptying of venous phase

Vasculitis

Overview of Pulmonary Vasculitides

Syndrome Pathology Other Affected Vessels
Polyarteritis nodosa Necrotizing vasculitis Renal, hepatic, and visceral aneurysm
Allergic granulomatous angiitis (Churg-Strauss syndrome) Granulomatous vasculitis Allergic history, eosinophilia
Hypersensitivity vasculitis Leukocytoclastic vasculitis Skin (common)
Henoch-Schönlein purpura vasculitis Leukocytoclastic Skin, GI, renal involvement usual
Takayasu arteritis Giant cell arteritis Aortic arch
Temporal arteritis Giant cell arteritis Carotid branches
Wegener granulomatosis Necrotizing granulomatous vasculitis Upper and lower respiratory tracts, glomerulonephritis
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Venous abnormalities

Pulmonary arteriovenous malformation (AVM)

Abnormal communication between pulmonary artery and veins. A communication between systemic arteries and pulmonary veins is much less common (<5%).

Types
    • Congenital, 60%
      • •
        Osler-Weber-Rendu disease (hereditary hemorrhagic telangiectasia)
    • Acquired, 40%
      • •
        Iatrogenic
      • •
        Infection
      • •
        Tumor
Radiographic Features
    • •
      Location: lower lobes, 70% > middle lobe > upper lobes
    • •
      Feeding artery, draining veins
    • •
      Sharply defined mass
    • •
      Strong enhancement
    • •
      Change in size with Valsalva/Mueller procedure
Complications
    • •
      Stroke, 20%
    • •
      Abscess, 10% (AVM acts as a systemic shunt)
    • •
      Rupture: hemothorax, hemoptysis, 10%

Pulmonary varices

Uncommon lesions that are typically asymptomatic and do not require treatment. Usually discovered incidentally.

Radiographic Features
    • •
      Dilated vein
    • •
      Usually near left atrium
Aortic Nipple

Normal variant (10% of population) caused by the left superior intercostal vein seen adjacent to the aortic arch. Maximum diameter of vein: 4 mm

Pulmonary venoocclusive disease (PVOD)

In the typical form there is occlusion of small pulmonary veins. The proposed initial insult in PVOD is venous thrombosis, possibly initiated by infection, toxic exposure, or immune complex deposition.

Radiographic Features
    • •
      Edema without cephalization
    • •
      Pleural effusions
    • •
      Cardiomegaly
    • •
      CT findings
      • Secondary pulmonary arterial hypertension
      • Markedly small central pulmonary veins
      • Central and gravity-dependent ground-glass lung attenuation
      • Smoothly thickened interlobular septa
      • Normal-sized left atrium
      • Centrilobular nodules

Pleura

General

Normal pleural anatomy

    • •
      Visceral pleura: covers lung
    • •
      Parietal pleura: covers rib (costal pleura), diaphragm (diaphragmatic pleura), mediastinum (mediastinal pleura)

  • Visceral and parietal pleura are continued at the pulmonary hilum and continue inferiorly as the inferior pulmonary ligament. Normal pleura (0.2 to 0.4 mm) is not visible by CT. Pleural thickening is present when a stripe of soft tissue is seen internal to a rib.

Diagnostic thoracentesis

Success rate 97%. Pneumothorax 1%-3% (<with blind thoracentesis).

Indication
    • •
      Suspected malignancy
    • •
      Suspected infection
Technique
    • 1.
      Use US to determine skin entry site.
    • 2.
      Anesthetize skin and subcutaneous and deep tissues.
    • 3.
      Advance 18- to 22-gauge spinal needle into collection, going over the superior border of the rib to avoid the neurovascular bundle.
    • 4.
      Aspirate 20 to 100 mL.

Therapeutic thoracentesis

Success rate, 95%. Pneumothorax 7%.

Indication
    • •
      Respiratory compromise from large pleural effusions
Technique
    • 1.
      Perform diagnostic thoracentesis
    • 2.
      Skin nick
    • 3.
      Place 7- to 10-Fr catheters for therapeutic thoracentesis. Remove catheter.
    • 4.
      Obtain CXR to check for pneumothorax.
Expansion Pulmonary Edema

Pulmonary edema may occur as a result of rapid evacuation of large amounts of pleural effusion. We routinely evacuate 2 to 3 L without complications. Do not aspirate both lungs in the same sitting because of the risk of expansion pulmonary edema and/or bilateral pneumothoraces.

Vacuthorax

If the lung parenchyma is abnormally stiff (fibrosis), it cannot reexpand and fill the pleural space, resulting in a “vacuthorax.” The patient is unlikely to benefit from thoracentesis in this circumstance.

Pneumothorax management

Success rate, >90%.

Indication for Intervention
    • •
      Symptomatic pneumothorax
    • •
      Pneumothorax, >20%
    • •
      Enlarging pneumothorax on subsequent CXR
    • •
      Tension pneumothorax
    • •
      Poor lung function of contralateral lung disease
Technique
    • 1.
      Two approaches
      • •
        2nd to 4th anterior intercostal space, midclavicular line
      • •
        6th to 8th intercostal space, midaxillary line or posterior
    • 2.
      Local anesthesia, skin nick
    • 3.
      Place 8- to 12-Fr catheters using a trocar technique. For the anterior approach, small Heimlich valve sets may be used.
    • 4.
      After the lung is fully reexpanded for 24 hours, the catheter is placed on water seal for 6 hours and then removed if there is no pneumothorax.
Persistent Pneumothorax in Patient with Chest Catheter
    • •
      Persistent leak from airways (bronchial injury, lung laceration)
    • •
      Loculated pneumothorax
    • •
      Anterior pneumothorax
    • •
      Obstructed catheter

Empyema drainage

Success rate, 80%. Complications (hemorrhage, lung injury), 2%.

Indication
    • •
      Pus on diagnostic thoracentesis
    • •
      Positive Gram stain
    • •
      Positive culture
Technique
    • 1.
      Choose entry site adjacent to largest collection using US or CT.
    • 2.
      Local anesthesia
    • 3.
      Diagnostic tap with 18-gauge needle. Send specimen for bacteriologic testing.
    • 4.
      Choice of drainage catheters
      • •
        10- to 16-Fr pigtail catheter for liquid effusions (usually placed by trocar technique)
      • •
        24-Fr catheter for thick collections (usually placed by Seldinger technique); dilators: 8, 10, 12, 14, 16, 20, etc.
    • 5.
      Put catheter to suction.
    • 6.
      Intrapleural tPA may be necessary for loculated effusions. tPA, 4-6 mg, is administered in up to 50 mL saline twice daily. Each administration consists of a clamping the tube and a dwell time of 30 minutes, after which the tube is placed back on suction.
Complications
    • •
      Technical catheter problems (clogging: change for larger catheter)
    • •
      Nonclearance of collection: surgical removal

Fluid collections

Pleural effusions

  • Excess fluid in the pleural space. There are two generic types: transudates and exudates:
    • •
      Transudate: ultrafiltrate of plasma; highly fluid, low in protein, devoid of inflammatory cells
    • •
      Exudate: increased permeability of microcirculation; rich in protein, cells, and debris

Differentiation Between Transudate and Exudate

Transudate Exudate
Protein <3 g/dL >3 g/dL
Protein (plasma/fluid) <0.5 >0.5
LDH <200 IU <70% of serum level >200 IU >70% of serum level
Common causes CHF, renal failure cirrhosis Infection (parapneumonic), tumor, embolism
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Causes
    • Tumor
      • •
        Bronchogenic carcinoma
      • •
        Pleural metastases
      • •
        Malignant mesothelioma
      • •
        Lymphoma
    • Inflammation
      • •
        Pneumonia, TB, empyema
      • •
        Collagen vascular disease
      • •
        Abdominal disease
        • Pancreatitis
        • Subphrenic abscess
        • Boerhaave syndrome
        • Meigs syndrome (benign ovarian fibroma)
    • Cardiovascular
      • •
        Congestive heart failure
      • •
        Pulmonary embolism
      • •
        Renal failure
    • Congenital
      • •
        Hydrops (neonate)
    • Metabolic
      • •
        Hypoproteinemia
    • Trauma
Radiographic Features (Fig. 1-64)
Figure 1-64.

Figure 1-64

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    • Lateral decubitus films
      • •
        Most sensitive: may detect as little as 25 mL
    • PA, lateral films: blunting of costophrenic angles
      • •
        Posterior costophrenic angle (>75 mL required)
      • •
        Lateral costophrenic angles (>175 mL required)
    • Large effusions
      • •
        All cardiophrenic angles obliterated
      • •
        Mediastinal shift
      • •
        Elevated diaphragm
    • Split pleura sign (CT, MRI): loculated fluid between visceral and parietal pleura with thickening of pleura. Thickened pleura may enhance with IV contrast.

Empyema

Empyema refers to either pus in the pleural space or an exudate that contains organism on a Gram stain (polymicrobial anaerobe, 35%; mixed aerobe/anaerobe, 40%; culture negative, 20%). There are three stages in the development of an empyema.

Overview

Parameter Stage 1 Stage 2 Stage 3
Pathology Exudative Fibrinopurulent Fibrinous
WBC count Normal >15,000/cm3 >15,000/cm3
pH Normal <7 <7
Glucose Normal <40 mg/dL <40 mg/dL
LDH >200 IU/L >200 IU/L >200 IU/L
Protein >3 g/L >3 g/L >3 g/L
Treatment Antibiotics Percutaneous drainage Surgery
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Causes
    • •
      Postinfection (parapneumonic), 60%
    • •
      Postsurgical, 20%
    • •
      Posttraumatic, 20%
Radiographic Features
    • •
      Pleural fluid collection
    • •
      Thick pleura
    • •
      Pleural enhancement
    • •
      Gas in empyema collection may be due to:
      • BPF (common)
      • Gas-forming organism (rare)
    • •
      Empyema necessitans: spontaneous extension of empyema into chest wall, forming a subcutaneous abscess that may eventually open to skin and form a fistula. Causes: TB (70%), Actinomyces, Nocardia

Differentiation Between Empyema and Abscess

Abscess Empyema
Cause Necrotizing pneumonia (anaerobes, fungus) Abscess extends to pleura; trauma, surgery
Shape Round Elliptical along chest wall
Air-fluid level A=B A ≠ B
Margins Sharp or irregular Sharp
Wall Thick Thin
Lung Normal position Displaced
Pleura Not seen Split
Vessel/
bronchi		 Within Displaced
Treatment Antibiotics, postural drainage, percutaneous drainage in nonresponders Percutaneous drainage
Inline graphicInline graphic
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Chylothorax

Chylothorax is caused by disruption of the thoracic duct. Daily chyle production of 1.5 to 2.5 L. Chyle contains chylomicrons from intestinal lymphatics and appears milky.

Causes
    • Tumor, 55% (especially lymphoma)
    • Trauma, 25%
      • •
        Iatrogenic duct laceration
      • •
        Sharp, blunt trauma
    • Idiopathic, 15%
    • Rare causes
      • •
        Lymphangioleiomyomatosis
      • •
        Filariasis

Pleural tumors

Fibrous tumor of the pleura

Unifocal tumor of the pleura. No relation to asbestos exposure. Fibrous tumors originate from visceral (70%) or parietal (30%) pleura, usually on a pedicle.

Clinical Findings
    • •
      Respiratory symptoms
    • •
      HPO, 15%
    • •
      Hypoglycemia, 5%
Types
    • •
      Benign, 80% (previously classified as benign mesothelioma)
    • •
      Invasive, 20% (unlike malignant mesothelioma, this tumor grows only locally)
Radiographic Features
    • •
      Well-delineated, solitary pleural-based mass; often lobulated
    • •
      Pedunculated, 30%; mass may flop into different locations from film to film.
    • •
      Chest wall invasion may be seen in the invasive form, absent in benign form.
    • •
      Tumor may grow in fissure and simulate the appearance of a solitary pulmonary nodule.
    • •
      Recurrence rate after surgical resection, 10%
    • •
      May have associated pleural effusion, necrosis

Malignant mesothelioma

Incidence is 500 new cases/year in the United States. Risk is 300 times larger in asbestos workers than in general population. Highest rates are in Seattle (shipyard industry) and St. Louis. Twenty to 40 years between asbestos exposure and tumor development. Three histologic variants (diagnosis usually requires an open pleural biopsy):

    • •
      Epithelial: difficult to differentiate from adenocarcinoma
    • •
      Mesenchymal
    • •
      Mixed
Radiographic Features (Figs. 1-65 and 1-66)
Figure 1-65.

Figure 1-65

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Figure 1-66.

Figure 1-66

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    • •
      Pleural thickening together with effusion, 60%
      • Isolated pleural thickening, 25%
      • Isolated pleural effusion, 15%
    • •
      Hemithoracic contraction, 25%
    • •
      Pleural calcification, 5%
    • •
      CT best shows full extent of disease:
      • Contralateral involvement
      • Chest wall and mediastinal involvement, 10%; diaphragm and abdominal extension
      • Pericardial involvement
      • Pulmonary metastases
    • •
      MRI useful to show chest wall or diaphragmatic extent

Other

Diaphragmatic paralysis

Paralysis of the diaphragm can be unilateral or bilateral.

Clinical Findings (Fig. 1-67)
Figure 1-67.

Figure 1-67

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    • •
      Unilateral paralysis is usually asymptomatic.
    • •
      Bilateral paralysis results in respiratory symptoms.
Causes
    • Phrenic nerve paralysis
      • •
        Bronchogenic carcinoma
      • •
        Neuropathies, postinfectious, nutritional
      • •
        Spinal cord injury, myelitis
      • •
        CNS injury: stroke
      • •
        Cardiac surgery
      • •
        Erb palsy (birth trauma)
    • Muscular disorders
      • •
        Myasthenia
      • •
        Polymyositis
      • •
        Muscular dystrophy
    • Idiopathic, 70%
Radiographic Features
    • •
      Elevated hemidiaphragm
    • •
      No motion of hemidiaphragm by fluoroscopy
    • •
      Paradoxical motion of hemidiaphragm using “sniff test”
    • •
      Reduced lung volume

Mediastinum

General

Approach to mediastinal masses

    • •
      Location
      • Anterior mediastinum
      • Superior mediastinum
      • Middle mediastinum
      • Posterior mediastinum
    • •
      Invasive or noninvasive mass
    • •
      Content: fat, cystic, solid, enhancement

Differentiation Between Mediastinal and Pulmonary Masses

Mediastinal Mass Pulmonary Mass
Epicenter in mediastinum Epicenter in lung
Obtuse angles with the lung Acute angles
No air bronchograms Air bronchograms possible
Smooth and sharp margins Irregular margins
Movement with swallowing Movement with respiration
Bilateral Unilateral
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Normal variants causing a wide mediastinum

    • •
      Anteroposterior (AP) projection instead of posteroanterior (PA) projection
    • •
      Mediastinal fat: obesity, steroid therapy
    • •
      Vascular tortuosity: elderly patients
    • •
      Low inspiratory supine position

Anterior mediastinal tumors

Thymoma

Thymoma is the most common anterior mediastinal tumor in the adult (very rare in children). Thirty percent are invasive (malignant thymoma). Parathymic syndromes are present in 40% of patients:

    • •
      35% of thymoma patients have myasthenia gravis (15% of myasthenia gravis patients have thymoma).
    • •
      Aplastic anemia (50% have thymoma)
    • •
      Hypogammaglobulinemia (15% have thymoma)
    • •
      Red cell aplasia
Pathology
    • Benign thymoma, 75%
      • •
        Common in patients with myasthenia
    • Malignant thymoma, 25%
      • •
        Local spread into pleura but no hematogenous metastases
      • •
        More common in patients without myasthenia
Radiographic Features (Fig. 1-68)
Figure 1-68.

Figure 1-68

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    • •
      Anterior mediastinal soft tissue mass
      • Asymmetrical location on one side
      • Homogeneous density and signal intensity
      • Some have cystic components
      • Contrast medium enhancement
    • •
      Invasive thymomas show growth through capsule into adjacent tissue. Drop metastases into pleural space are common.
    • •
      Calcifications, 20%

Thymolipoma

Thymolipomas are benign, encapsulated mediastinal tumors that contain both thymic and adipose tissue. The tumor occurs most frequently in children and young adults. Tumors usually grow to large sizes (75% are >500 g) with few or no symptoms.

Associations
    • •
      Myasthenia gravis (in 3% of thymolipomas)
    • •
      Aplastic anemia
    • •
      Graves disease
    • •
      Hypogammaglobulinemia
    • •
      Lipomas in thyroid, pharynx
Radiographic Features
    • •
      Anterior mediastinal mass contains fatty and soft tissue elements.
    • •
      The mass is usually large and displaces mediastinal structures and/or lungs.
    • •
      Small tumors may be difficult to detect.
    • •
      Large tumors mimic liposarcoma.

Benign thymic hyperplasia

Causes
    • •
      Myasthenia
    • •
      Thyrotoxicosis, Graves disease, Hashimoto thyroiditis
    • •
      Collagen vascular diseases:
      • SLE
      • Scleroderma
      • Rheumatoid arthritis
      • Behçet disease
    • •
      Rebound thymic hyperplasia:
      • Chemotherapy (hyperplasia is often a good prognostic indicator)
      • Addison disease
      • Acromegaly
Radiographic Features
    • •
      Enlarged thymus without focal masses; fat interspersed in parenchyma
    • •
      Size and morphology of normal thymus:
      • >20 years of age: <13 mm
      • >30 years of age: convex margins are abnormal
    • •
      No increase in size over time
    • •
      If clinical suspicion for malignancy is high, a biopsy should be performed.

Thyroid masses

Thyroid masses that extend into the mediastinum: goiter > adenoma, carcinoma, lymphoma. Location of goiters within mediastinum:

    • •
      Anterior to brachiocephalic vessels, 80%
    • •
      Posterior to brachiocephalic vessels, 20%
Radiographic Features
    • Goiters
      • •
        Thoracic inlet masses (thymomas are lower in the anterior mediastinum)
      • •
        Mass is contiguous with cervical thyroid and is well defined.
      • •
        Heterogeneous density by CT: calcium, iodine (70 to 120 HU), colloid cysts
      • •
        Tracheal displacement is the most common finding by CXR.
      • •
        CT: marked and prolonged contrast enhancement
      • •
        Nuclear scan with either 99mTc or 123I confirms the diagnosis (see Chapter 12).
    • Other
      • •
        Thyroid carcinoma has irregular borders.
      • •
        Thyroid lymphomas generally show little enhancement.

Germ cell tumors

  • Tumors arise from rests of primitive cells and are of variable malignant potential. Mnemonic: “SECTE”:
    • •
      Seminoma
    • •
      Embryonal cell carcinoma
    • •
      Choriocarcinoma
    • •
      Teratoma (70% of germ cell tumors), teratocarcinoma
    • •
      Endodermal sinus tumors (yolk sac tumors)
Teratoma (Fig. 1-69)
Figure 1-69.

Figure 1-69

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    • •
      20% are malignant; therefore all mediastinal teratomas should be surgically removed.
    • •
      Teratomas typically present as large mass lesions.
    • •
      Variable tissue contents:
      • Calcification, 30%
      • Fat, fat-fluid levels
      • Cystic areas
      • Soft tissue
Seminoma
    • •
      Rarely infiltrative
    • •
      Large, unencapsulated lesions
    • •
      Occasionally associated with testicular atrophy
Embryonal Cell Carcinoma
    • •
      Mediastinal invasion is the rule: poor prognosis (mean survival time <10 months).
    • •
      Elevated AFP and human chorionic gonadotropin (HCG)

Hodgkin lymphoma

The pathologic diagnosis is based on the presence of Reed-Sternberg cells. The cell of origin is the antigen-presenting interdigitating cells in the paracortical regions of the lymph node (not B or T cells). Ninety percent originate in the lymph nodes; 10% originate in extranodal lymphoid tissues of parenchymal organs (lung, GI tract, skin). Incidence is 1:50,000. Bimodal age distribution with peaks at 30 and 70 years.

Types of Hodgkin Lymphoma

Type Frequency Prognosis
Lymphocyte predominant (LP) <5% (young patients) Most favorable
Nodular sclerosing (NS) 70% Less favorable than LP
Mixed cellularity (MC) 25% (old patients) Less favorable than NS
Lymphocyte depleted (LD) <5% Worst prognosis
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Staging (ANN ARBOR)

Stage* Involvement
I Single node group or region
IE Single extranodal site
II Two or more nodes on same side of diaphragm
IIE Localized disease in an organ and node on same side of diaphragm
III Node groups on both sides of diaphragm
IIIE Above diaphragm + localized extralymphatic
IIIS Above diaphragm + spleen
IV Extension beyond above limit
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*

Constitutional symptoms (classification B) are present in 25%: fever, night sweats, weight loss.

Radiographic Features (Fig. 1-70)
Figure 1-70.

Figure 1-70

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    • •
      Superior mediastinal nodal (prevascular, paratracheal) involvement, 95%
    • •
      Contiguous progression from one lymph node group to the next
    • •
      Lung involvement, 15%
      • Pulmonary mass lesion, air bronchograms
      • Direct extension into lung from involved nodes (most common)
    • •
      Pleural effusions, 15%
    • •
      Posttherapeutic mediastinal changes common
      • Thymic cysts
      • Thymic hyperplasia
      • Persistent mediastinal masses may be present without representing active disease: 67Ga, PET scanning may be helpful for differentiation.
Pearls
    • •
      Recurrence of lymphoma
      • Radiation treatment: recurrence usually occurs outside the treatment field (commonly paracardiac region).
      • No radiation: recurrence usually in sites of previous involvement
    • •
      5% of treated Hodgkin patients will develop aggressive leukemias
    • •
      Radiation pneumonitis occurs 6 to 8 weeks after completion of the radiation and evolves to mature fibrosis by 1 year.

Non-hodgkin lymphoma (NHL)

Sixty percent of cases originate in lymph nodes and 40% in extranodal sites. Eighty-five percent arise from B cells and 15% from T cells. Occurs in 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
      Classifications of Non-Hodgkin Lymphoma*
      Working Formulation Rappaport Comment
      Low Grade
      Small, lymphocytic Lymphocytic, well differentiated Uncommon
      Follicular, small cleaved Nodular, poorly differentiated Most frequent type
      Follicular, mixed cells Nodular, mixed
      Intermediate Grade
      Follicular, large cells Nodular, histiocytic
      Diffuse, small cleaved Diffuse, lymphocytic
      Diffuse, mixed cell Diffuse, mixed
      Diffuse, large cell Diffuse, histiocytic GI involvement, 25%
      High Grade
      Immunoblastic Diffuse, histiocytic GI involvement, 25%
      Lymphoblastic Lymphoblastic Mediastinal mass, young patient
      Small, noncleaved Diffuse undifferentiated (Burkitt and non-Burkitt) Abdominal form (North America), craniofacial (Africa)
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      *
      Constitutional symptoms are more common than in Hodgkin disease.
Radiographic Features
    • Mediastinal and hilar adenopathy
      • •
        Often generalized at presentation
      • •
        Adenopathy may be noncontiguous.
    • Lung involvement
      • •
        May occur without adenopathy
      • •
        Patterns: mass, chronic ASD
    • Extrathoracic spread
      • •
        Nasooropharynx
      • •
        GI tract
      • •
        Spread to unusual sites common

Middle mediastinal tumors

Bronchopulmonary foregut malformations (Fig. 1-71)

Figure 1-71.

Figure 1-71

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  • Abnormalities in budding and differentiation of the primitive foregut. Depending on type, duplication cysts are also classified as posterior mediastinal masses. The lining of the cyst wall determines the cyst type:
    • •
      Bronchogenic cysts: ventral defects containing respiratory epithelium
    • •
      Enteric cysts: posterior defects containing gastrointestinal epithelium (gastric mucosa > esophageal mucosa > small bowel mucosa > pancreatic tissue)
      Differentiation Between Bronchogenic and Enteric Cysts
      Bronchogenic Cyst Enteric Cyst
      Location Ventral Dorsal
      Level Subcarinal Supracarinal
      Cyst wall Imperceptible Thick wall
      Symptoms Asymptomatic unless there is mass effect; usually as an incidental finding Symptomatic: peptic ulceration, distention
      Other imaging findings May contain calcification Vertebral body anomalies
      Associated rib anomalies Hemivertebra
      CT: no contrast enhancement Scoliosis
      T2 hypointense Spina bifida
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Radiographic Features (Fig. 1-72)
Figure 1-72.

Figure 1-72

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    • •
      Round mass of water/protein density
    • •
      Location
      • Bronchogenic cysts are mediastinal (75%) or pulmonary (25%). Mediastinal locations: subcarinal, 50%; paratracheal, 20%; hilar, paracardiac, 30%. Esophageal duplication cysts are located along the course of the esophagus.
    • •
      High CT density (40%) may be due to debris, hemorrhage, infection
    • •
      Calcifications in wall (rare finding)

Castleman disease (giant benign lymph node hyperplasia)

Large, benign mediastinal lymph node masses. Rare. Etiology is unknown (nodal hyperplasia vs. benign tumor). Two histologic types: hyaline vascular, 90%; plasma cell, 10% (associated with general symptoms: night sweats, fever, etc.). Age <30 years, 70%. Treatment is surgical excision. Includes hyaline vascular and plasma cell types.

Radiographic Features
    • •
      Bulky mediastinal mass lesion (3 to 12 cm): anterior > middle > posterior mediastinum
    • •
      Dense homogeneous contrast enhancement is the key feature (“vascular lesions”)
    • •
      Nodal calcification may be present.
    • •
      Involvement of lymph nodes in neck, axillae, and pelvis is rare.
    • •
      Slow growth

Fibrosing mediastinitis

Cause is mediastinal histoplasmosis; may be idiopathic. May result in obstruction of pulmonary artery, veins, bronchi. Calcified lymph nodes.

Posterior mediastinal tumors

Neural tumors

  • Posterior mediastinal neural tumors arise from:
    • Peripheral nerves, 45% benign
      • •
        Schwannoma (arise from nerve sheath)
      • •
        Neurofibroma (contain all elements of nerve)
    • Sympathetic ganglia (varying malignant potential)
      • •
        Ganglioneuroma (benign)
      • •
        Ganglioneuroblastoma
      • •
        Neuroblastoma (malignant)
    • Paraganglion cells, 2%
      • •
        Paraganglioma (chemodectoma, histologically similar to pheochromocytoma): functional tumors, may secrete catecholamines. Intense contrast enhancement. Found in AP window.
Radiographic Features (Fig. 1-73)
Figure 1-73.

Figure 1-73

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    • Schwannoma, neurofibroma
      • •
        Arise posteriorly, frequently in neural foramina
      • •
        May cause widening and erosion of neural foramina
      • •
        Usually round or oval and <2 vertebral bodies long
      • •
        Enhancement with contrast
      • •
        T2-weighted (T2W) very hyperintense
    • Sympathetic ganglia tumors
      • •
        Arise anterolaterally (more conspicuous on plain film)
    • •
      Usually elongated and fusiform (resembling sympathetic chain) and >2 vertebral bodies long

Extramedullary hematopoiesis

  • Paravertebral masses represent bone marrow extruded through cortical defects of vertebral bodies. Seen in congenital anemias (e.g., thalassemia). Suspect diagnosis if:
    • •
      Multiple bilateral posterior mediastinal masses
    • •
      Cortical bone changes by CT
    • •
      Clinical history of anemia
    • •
      Marked contrast enhancement

Other mediastinal disorders

Pneumomediastinum

  • Sources of mediastinal air:
    • Intrathoracic
      • •
        Trachea and major bronchi
      • •
        Esophagus
      • •
        Lung
      • •
        Pleural space
    • Extrathoracic
      • •
        Head and neck
      • •
        Intraperitoneum and retroperitoneum
Radiographic Features
    • •
      Subcutaneous emphysema
    • •
      Elevated thymus: thymic sail sign
    • •
      Air anterior to pericardium: pneumopericardium
    • •
      Air around pulmonary artery and main branches: ring around artery sign
    • •
      Air outlining major aortic branches: tubular artery sign
    • •
      Air outlining bronchial wall: double bronchial wall sign
    • •
      Continuous diaphragm sign: due to air trapped posterior to pericardium
    • •
      Air between parietal pleura and diaphragm: extrapleural sign
    • •
      Air in pulmonary ligament

Differential Diagnosis

General

Approach to CXR (Fig. 1-74)

Figure 1-74.

Figure 1-74

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    • 1.
      Lungs
      • •
        Focal or diffuse abnormalities
      • •
        Lung volumes
        • Increased or decreased
        • Right/left difference in density
      • •
        Hypolucent areas
    • 2.
      Trachea and bronchi
    • 3.
      Mediastinal lines
      • •
        Paratracheal stripe
      • •
        AP window
      • •
        Azygoesophageal recess
      • •
        Paraspinal lines
      • •
        Other lines
        • Anterior and posterior junction line
        • Posterior wall of intermediate bronchus
    • 4.
      Hila and cardiac contour
    • 5.
      Pleura, fissures
    • 6.
      Bones
      • •
        Focal metastases
      • •
        Rib notching
      • •
        Clavicles

Approach to ICU films

    • 1.
      Lines (check position)
    • 2.
      Pneumothorax, pneumomediastinum
    • 3.
      Focal parenchymal opacities
      • •
        Atelectasis
      • •
        Pneumonia
      • •
        Aspiration
      • •
        Hemorrhage
      • •
        Contusion
    • 4.
      Diffuse parenchymal opacities
      • •
        ARDS
      • •
        Pneumonia
      • •
        Edema
      • •
        Less common:
        • Aspiration
        • Hemorrhage

Directed search in apparently normal chest films

    • Lungs
      • •
        Hidden nodules
      • •
        Subtle interstitial disease
      • •
        Differences in lung density
      • •
        Retrocardiac disease
      • •
        Bronchiectasis
      • •
        Pulmonary embolism
    • Mediastinum
      • •
        Posterior mediastinal mass
      • •
        Tracheal lesions, deviation
      • •
        Subtle hilar mass lesions
    • Bones
      • •
        Lytic, sclerotic lesions
      • •
        Rib notching

Generic approaches to film interpretation

The “4 Ds”
    • •
      Detection
    • •
      Description
    • •
      Differential diagnosis
    • •
      Decision about management
Lesion Description
    • •
      Location
    • •
      Extent
    • •
      Characteristics
      • Signal intensity, density, echogenicity, etc.
      • Behavior after administration of contrast material
    • •
      Differential diagnosis

Universal differential diagnosis

  • Mnemonic: “TIC MTV:”
    • •
      Tumor
    • •
      Inflammation
      • Infectious
      • Noninfectious causes
    • •
      Congenital
    • •
      Metabolic
    • •
      Trauma, iatrogenic
    • •
      Vascular

Atelectasis

Lobar, segmental atelectasis (Fig. 1-75)

Figure 1-75.

Figure 1-75

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    • Endobronchial lesion
    • Extrinsic bronchial compression
      • •
        Tumor
      • •
        Lymphadenopathy
        • Malignant
        • Benign adenopathy (i.e., sarcoid rarely causes lobar collapse])

  • Rare causes

  • Bronchial torsion

Signs of lobar atelectasis

    • Direct signs
      • •
        Displacement of interlobar fissures (lobar collapse)
      • •
        Increase in opacity of the involved segment or lobe
    • Indirect signs
      • •
        Displacement of hila
      • •
        Mediastinal displacement
      • •
        Elevation of hemidiaphragm
      • •
        Overinflation of remaining normal lung
      • •
        Approximation of ribs
RUL Collapse (Figure 1-76, Figure 1-77)
Figure 1-76.

Figure 1-76

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Figure 1-77.

Figure 1-77

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    • •
      Elevation of minor fissure
    • •
      Shift of trachea to right
    • •
      Elevation of hilum
    • •
      Thickening of right paratracheal in complete collapse
RML Collapse
    • •
      Best seen on lordotic views
    • •
      RML syndrome: recurrent atelectasis despite an open orifice:
      • Absent collateral ventilation
      • Bronchus is surrounded by enlarged lymph nodes (TB)
      • May have coexistent bronchiectasis
RLL Collapse (Fig. 1-78)
Figure 1-78.

Figure 1-78

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    • •
      Triangular opacity in right retrocardiac region on PA film with obliteration of diaphragm
    • •
      Posterior displacement of right margin
    • •
      Opacity over the spine
LUL Collapse (Fig. 1-79)
Figure 1-79.

Figure 1-79

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    • •
      May be difficult to see: hazy density can be easily confused with loculated pleural effusion on PA film
    • •
      “Luftsichel”: radiolucency in upper lung zone that results from upward migration of superior segment of the left lower lobe (LLL)
    • •
      Anterior displacement of major fissure on lateral view
LLL Collapse (Fig. 1-80)
Figure 1-80.

Figure 1-80

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    • •
      Left retrocardiac triangular opacity on PA film
    • •
      Posterior displacement of left major fissure on lateral film
CT Findings of Lobar Collapse (Figs. 1-81)
Figure 1-81.

Figure 1-81

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    • •
      Increased density of collapsed lobe
    • •
      See figure for patterns.

Types of peripheral atelectasis

    • Relaxation
      • •
        Pleural effusion
      • •
        Pneumothorax
      • •
        Bullous disease
    • Atelectasis associated with fibrosis
      • •
        Granulomatous infections
      • •
        Pneumoconiosis
      • •
        Sarcoid
    • Resorptive atelectasis secondary to obstruction
      • •
        Platelike, discoid atelectasis
    • Depletion of surfactant (adhesive atelectasis; airways patent)
      • •
        ARDS of the newborn
      • •
        Radiation injury
    • Rounded atelectasis
      • •
        Due to pleural disease

Consolidation

Radiographic Features (Figs. 1-82 and 1-83)

Figure 1-82.

Figure 1-82

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Figure 1-83.

Figure 1-83

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    • Acinar shadow
      • •
        Air in acini (7 mm in diameter) is replaced by fluid or tissue
      • •
        May be confluence to form patchy densities
    • Air bronchogram
      • •
        Represents aerated airways in consolidated lung
      • •
        Air bronchogram may also be seen in some forms of collapse.
    • Absence of volume loss
      • •
        No displaced fissures
      • •
        No elevation of diaphragm
    • Nonsegmental distribution
      • •
        Intersegmental spread is common because channels of interalveolar communication (channels of collateral drift) allow passage of air and fluid
      • •
        Channels of collateral drift include:
        • Pores of Kohn (interalveolar openings)
        • Channels of Lambert (bronchioalveolar communications)
        • Direct airway anastomosis, 120 μm in diameter

Causes of consolidation

Fluid in Acini
    • Water (edema)
      • •
        Cardiac pulmonary edema
      • •
        Renal pulmonary edema
      • •
        Lung injury, pulmonary edema
    • Blood
      • •
        Trauma (most common)
      • •
        Bleeding disorder: anticoagulation, etc.
      • •
        Type II antigen-antibody reaction
      • •
        Goodpasture syndrome
      • •
        Henoch-Schönlein purpura
      • •
        Pulmonary infarct (Hampton hump)
      • •
        Vasculitis
    • Proteinaceous fluid
      • •
        Alveolar proteinosis
Inflammatory Exudate in Acini
    • Infection
      • •
        Bacterial infections (pus)
      • •
        Nocardia, actinomycosis, TB
    • Noninfectious
      • •
        Allergic hypersensitivity alveolitis
      • •
        Chronic eosinophilic pneumonia
      • •
        COP
      • •
        Pulmonary infiltration with eosinophilia
        • Loeffler syndrome
        • Chronic eosinophilic pneumonia
        • Pneumonitis
        • ABPA
        • Drugs: penicillin
      • •
        Aspiration of lipid material
      • •
        Sarcoid (resides only in interstitial space but encroaches on airspace to produce a pattern that mimics ASD)
Tumor in Acini
    • Bronchioalveolar carcinoma
    • Lymphoma

Pulmonary renal syndromes

These syndromes are characterized by pulmonary hemorrhage and nephritis.

Pulmonary findings usually present as consolidation on CXR.

    • •
      Goodpasture syndrome (anti-GBM positive)
    • •
      Wegener disease (ANCA positive; nodules are more common than ASD)
    • •
      SLE
    • •
      Henoch-Schönlein purpura
    • •
      Polyarteritis nodosa
    • •
      Penicillamine hypersensitivity

Acute respiratory distress syndrome (ARDS)

  • Clinical syndrome characterized by sudden onset of triad:
    • •
      Respiratory distress
    • •
      Hypoxemia
    • •
      Opaque, stiff lungs

After an incipient catastrophic event, mediators of injury are activated → inflammatory response → endothelial damage → injury, pulmonary edema (ARDS): ARDS runs independent course from initiating disease.

Radiographic Features
    • •
      Diffuse alveolar consolidation, commonly indistinguishable from pneumonia or pulmonary edema
    • •
      End stage
    • •
      Interstitial fibrosis and scarring
Causes
    • •
      Massive pneumonia
    • •
      Trauma
    • •
      Shock
    • •
      Sepsis
    • •
      Pancreatitis
    • •
      Drug overdose
    • •
      Near-drowning
    • •
      Aspiration

Chronic airspace disease

    • Tumors
      • •
        Bronchioalveolar carcinoma
      • •
        Lymphoma
    • Inflammation
      • •
        Tuberculosis, fungus
      • •
        Eosinophilic pneumonia
      • •
        Pneumonitis, BOOP/COP
      • •
        Alveolar sarcoid (mimics ASD)
    • Other causes
      • •
        Alveolar proteinosis
      • •
        Pulmonary hemorrhage
      • •
        Lipoid pneumonia, chronic aspiration

Pulmonary masses

Approach to solitary pulmonary nodule (Fig. 1-84)

Figure 1-84.

Figure 1-84

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Differentiation Between Benign and Malignant Nodules

Benign Malignant
Shape Round Irregular
Size <3 cm >3 cm
Spiculations No Yes
Edge Well defined Ill defined
Satellite lesions Yes No
Cavitation No Yes
Doubling time (in volume) <1 month or >2 years >1 month or <2 years
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  • The above-listed criteria do not allow reliable differentiation of a solitary pulmonary nodule. There are only three criteria by which a solitary pulmonary nodule can be judged benign:
    • •
      Fat density
    • •
      Specific types of benign calcifications (diffuse, central, popcorn, concentric):
      • >10% of a nodule consists of calcium with HU >200
      • Large or homogeneous calcification throughout nodule (exceptions: multiple metastases from osteosarcoma, thyroid carcinoma, etc.)
    • •
      Old films show no interval growth within a 2-year period
CT Workup
    • <4 mm: 99% benign if no known primary tumor
      • •
        Follow-up CT in 12 and 24 months; if no growth after 24 months, nodule is assumed benign.
      • •
        Follow-up CT in 3, 6, 12, and 24 months if clinical suspicion.
    • <4 to 8 mm: 94% benign if no known primary
      • •
        Follow-up at 3, 6, 12, and 24 months
      • •
        Consider PET or biopsy if high clinical suspicion
    • >8 mm: 50% malignant
      • •
        Percutaneous biopsy
      • •
        Other options: PET and surgical removal (VATS)
Pearls
    • •
      Always get a second imaging modality (CT > MR > angiogram) before sampling a solitary pulmonary nodule to exclude AV malformations. However, remember that 97% of all solitary nodules are either granulomas or primary carcinomas.
    • •
      Extrapulmonary densities may mimic pulmonary lesions.
      • Artifact (nipple, skin, electrodes)
      • Pseudotumor (fluid in fissure)
      • Pleural mass or plaque
      • Rib fracture
    • •
      Solitary pulmonary metastases seen on CXR will be truly solitary in only 50% of the cases.
    • •
      Any solitary pulmonary nodule in cancer patients requires further workup:
      • Comparison with old films
      • Percutaneous biopsy if large enough
      • Close follow-up (usually 3-month intervals)
    • •
      HRCT for nodule densitometry
      • Perform only in nodules <3.0 cm in diameter.
      • Densities of >200 HU indicate presence of calcification.

Hidden zones (Fig. 1-85)

Figure 1-85.

Figure 1-85

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  • Subtle pulmonary nodules are often missed if <3 cm and located in:
    • •
      Upper lobes (apices)
    • •
      Central, paramediastinal
    • •
      Superimposed onto ribs and clavicle

An effort should be made to perform a directed search in these regions to detect subtle lung cancer. This zone has also been called the lawyer zone. The threshold of lesion detection by plain film is approximately 9 mm.

Solitary nodule

Criteria: <6 cm. May be smooth, lobulated, discrete, circumscribed, calcified, cavitated, or have satellite lesions.

    • Tumor (45%)
      • •
        Primary carcinoma, 70%
      • •
        Hamartoma, 15%
      • •
        Solitary metastasis, 10%
    • Inflammation (53%); regional variations
      • •
        Histoplasmoma
      • •
        Tuberculoma
      • •
        Coccidioidomycosis
    • Other (2%)
      • •
        Vascular, 15%
        • AV fistula
        • Pulmonary varix (dilated pulmonary vein)
        • Infarct, embolism
      • •
        Congenital, 30%
        • Sequestration
        • Bronchial cyst
      • •
        Miscellaneous, 45%
        • Round pneumonia
        • Loculated effusion in fissure
        • Mucus plug
        • Enlarged subpleural lymph node
        • Silicosis (usually multiple nodules)

Multiple nodules

Multiplicity of pulmonary nodules often indicates hematogenous dissemination.

Causes
    • Metastases
    • Abscess
      • •
        Pyogenic: Staphylococcus > Klebsiella > Streptococcus
      • •
        Immunocompromised patient: Nocardia, Legionella
    • Granulomatous lung diseases
      • •
        Infectious
        • TB
        • Fungus: Aspergillus, Histoplasma
      • •
        Noninfectious
        • Sarcoid
        • Rheumatoid nodules
        • Silicosis
        • Wegener disease
        • Necrotizing granulomatous vasculitis
        • Histiocytosis
    • Unilateral pulmonary embolism

Miliary pattern (Fig. 1-86)

Figure 1-86.

Figure 1-86

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Special pattern of multiple pulmonary nodules characterized by small size and diffuse bilateral distribution (too numerous to count). If the nodules are small enough, also consider the differential diagnosis for nodular interstitial disease.

Causes
    • •
      Hematogenous infection: TB, histoplasmosis
    • •
      Hematogenous tumor seeding:
      • Metastases: thyroid, melanoma, breast, choriocarcinoma
      • Eosinophilic granuloma
      • Bronchioalveolar cancer
    • •
      Silicosis
    • •
      Sarcoid

Calcified lung nodules

    • Larger (>1 mm)
      • •
        Tumor
        • Metastases from medullary thyroid cancer
        • Mucinous or osteogenic metastases
      • •
        Infection
        • Previous varicella pneumonia
        • Histoplasmosis, coccidioidomycosis, TB
        • Parasites: schistosomiasis
      • •
        Other
        • Silicosis, CWP
    • Very small (0.1 to 1 mm; sandlike)
      • •
        Alveolar microlithiasis
      • •
        Chronic pulmonary venous hypertension
      • •
        “Metastatic” calcification from severe renal disease

Large (>6 CM) thoracic mass

    • Pulmonary
      • •
        Tumor
        • Bronchogenic carcinoma
        • Metastases (SCC from head and neck)
      • •
        Abscess
      • •
        Round atelectasis
      • •
        Intrapulmonary sequestration
      • •
        Hydatid disease
    • Extrapulmonary
      • •
        Fibrous tumor of the pleura
      • •
        Loculated pleural effusion
      • •
        Torsed pulmonary lobe
      • •
        Chest wall tumors (Askin tumor)
      • •
        AAA
      • •
        Mediastinal masses

Upper lung zone opacities with calcified adenopathy

    • •
      Silicosis
    • •
      Sarcoidosis
    • •
      Berylliosis
    • •
      CWP
    • •
      TB

Infection that can cause chest wall invasion

    • •
      Actinomyces
    • •
      Nocardia
    • •
      TB
    • •
      Blastomyces
    • •
      Aspergillus
    • •
      Mucor

Infection with lymphadenopathy

    • •
      TB
    • •
      Histoplasmosis (fungal)
    • •
      EBV (viral)

Cystic and cavitary lesions (Fig. 1-87)

Figure 1-87.

Figure 1-87

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Approach

  • The wall thickness and morphology are helpful (but not definitive) to determine if a cavitary lesion is benign or malignant.
    • Thickness (not always reliable)
      • •
        <2 mm, benign in 95%
      • •
        2 to 15 mm, malignant in 50%
      • •
        >15 mm, malignant in >95%
    • Morphology (not reliable)
    • Eccentric cavity: suggests malignancy
      • •
        Shaggy internal margins: suggests malignancy

Cysts (Figs. 1-88 and 1-89)

Figure 1-88.

Figure 1-88

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Figure 1-89.

Figure 1-89

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  • Parenchyma-lined space, filled with air or fluid
    • •
      Pneumatocele (posttraumatic, postinfectious): common
    • •
      Bulla (located within lung parenchyma), bleb (located within the nine histologic layers of the visceral pleura)
    • •
      Cystic bronchiectasis
    • •
      Langerhans cell histiocytosis
    • •
      Lymphocytic interstitial pneumonia
    • •
      Lymphangioleiomyomatosis
    • •
      Metastases
    • •
      Neurofibromatosis type 1
    • •
      Tracheobronchial papillomatosis
    • •
      Pneumocystis jiroveci pneumonia
    • •
      Congenital cysts
      • Intrapulmonary bronchogenic cysts (rib and vertebral body anomalies common)
      • Cystic adenomatoid malformation (multiple lesions)
      • Sequestration
    • •
      Hydatid cyst (onion skin appearance)

Cavity

  • Parenchymal necrosis due to inflammation (benign) or tumor (malignant)
    • Abscess
      • •
        Pyogenic: Staphylococcus > Klebsiella > Streptococcus
      • •
        Immunocompromised patient: Nocardia, Legionella
    • Cavitated tumor
      • •
        SCC (primary SCC > head and neck SCC > sarcoma metastases)
      • •
        Sarcoma
      • •
        Lymphoma
      • •
        TCC of the bladder
    • Cavitated granulomatous mass (often multiple)
      • •
        Fungus: Aspergillus, coccidioidomycosis (thin wall)
      • •
        TB
      • •
        Sarcoid, Wegener disease, rheumatoid nodules
      • •
        Necrotizing granulomatous vasculitis
    • Cavitated posttraumatic hematoma

Air crescent sign in cavity

This sign was originally described in aspergillosis and is most commonly seen there.

More recently, the sign has also been described with other entities:

    • •
      Mucormycosis
    • •
      Actinomycosis
    • •
      Septic emboli
    • •
      Klebsiella pneumoniae infection
    • •
      TB
    • •
      Tumors

Small cystic disease (Fig. 1-90)

Figure 1-90.

Figure 1-90

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    • True cyst wall
      • •
        Eosinophilic granuloma
      • •
        Lymphangioleiomyomatosis
      • •
        Cystic form of PCP
      • •
        Honeycombing in any end-stage interstitial disease
      • •
        LIP
    • No cyst wall
      • •
        Emphysema

Interstitial lung disease

Radiographic patterns of interstitial disease

Types of Densities
    • •
      Linear or reticular densities: thickened interlobular septa, fibrosis
    • •
      Reticulonodular densities: inflammation in peribronchovascular interstitium
    • •
      Nodular densities: granulomas
    • •
      Ground-glass opacity: usually represents acute interstitial disease (occasionally seen with chronic fibrosis)
      • Hazy increase in lung density
      • Vessels can be clearly seen through haze
    • •
      Honeycombing: ring shadows 2 to 10 mm; end-stage lung disease
Kerley Lines (Linear Densities) (Fig. 1-91)
Figure 1-91.

Figure 1-91

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    • Kerley B lines, peripherally located in interlobular septa:
      • •
        <2 cm long
      • •
        Peripheral
      • •
        Perpendicular to pleura
    • Kerley A lines:
      • •
        2 to 6 cm long
      • •
        Central
      • •
        No relationship to bronchioarterial bundles
    • Kerley C lines
      • •
        Fine network caused by superimposition of Kerley B lines

Approach

  • Define the following parameters:
    • •
      Type of pattern
    • •
      Distribution
    • •
      Lung volumes
    • •
      Evolution
    • •
      Pleural disease
    • •
      Lymph nodes
Generic Approach

Interstitial disease is due to thickening of interlobular septa (lymphatics, veins, or infiltration by cells), alveolar walls, and interstitium. Causes of thickening include

    • Fluid
      • •
        Water
        • Pulmonary edema
        • Venous obstruction (thrombosis)
      • •
        Proteinaceous material
        • Congenital pulmonary lymphangiectasia (very rare)
    • Inflammation
      • •
        Infectious (interstitial pneumonias)
        • Viral
        • Granulomatous (TB, fungal)
        • PCP
      • •
        Idiopathic
        • IPF
        • Sarcoid
      • •
        Collagen vascular disease
        • RA
        • Scleroderma
        • Ankylosing spondylitis
      • •
        Extrinsic agents
        • Pneumoconiosis (asbestos, silicosis, CWP)
        • Drugs
    • Tumor
      • •
        Interstitial tumors
        • Eosinophilic granuloma
      • •
        Lymphangitic tumor spread
      • •
        Desmoplastic reaction to tumor
        Mnemonic Approach to Differential Diagnosis
        Examples of Common Entities
        Distribution
        Upper lobes (“CASSET P”) Cystic fibrosis (not an interstitial disease)
        Ankylosing spondylitis
        Silicosis
        Sarcoid
        Eosinophilic granuloma (sparing of costophrenic angles)
        Tuberculosis
        Pneumocystis carinii
        Lower lobes (“BADAS”) Bronchiectasis (not an interstitial disease)
        Aspiration
        Drugs, DIP
        Asbestosis
        Scleroderma, other collagen vascular diseases
        Evolution
        Acute (“HELP”) Hypersensitivity (allergic alveolitis)
        Edema
        Lymphoproliferative
        Pneumonitis, viral
        Chronic (“LIFE”) Lymphangitic spread
        Inflammation, infection
        Fibrosis
        Edema
        Lung Volumes
        Increased Cystic fibrosis (associated with this pattern but not an interstitial disease)
        Eosinophilic granuloma (pneumothorax, 20%)
        Lymphangioleiomyomatosis (pneumothorax)
        Decreased Idiopathic pulmonary fibrosis
        Scleroderma
        Pleural Disease
        Pleural plaques Asbestosis
        Pleural effusion CHF
        Lymphangitic carcinomatosis
        Rheumatoid disease
        Lymph Nodes
        Enlarged Malignant adenopathy
        TB, fungus
        Sarcoid
        Calcified Silicosis
        Open in a new tab
        HRCT Patterns of Interstitial Lung Disease
        Imaging Causes
        Ground-Glass Opacity
        • Increased haze
        • All acute interstitial diseases
        		 graphic file with name u01-15-9780323065382.gif
        • Allergic hypersensitivity
        • All acute interstitial disease
          • DIP
          • Active IPF
          • Viral
        • PCP
        • BOOP/COP
        • Eosinophilic pneumonia
        • Pulmonary edema
        Reticulonodular Opacities
        • Peribronchovascular thickening (peribronchial cuffing on CXR)
        • Thickening of interlobular septa (Kerley lines)
        		 graphic file with name u01-16-9780323065382.gif
        • Pulmonary edema
        • Viral, mycoplasmal pneumonia, and PCP
        • Lymphangitic tumor spread
        • Pulmonary fibrosis
          • IPF
          • Secondary fibrosis
            • Drugs
            • Radiation
            • Collagen vascular disease
            • Hemosiderosis
        • Asbestosis
        Nodular Opacities
        1- to 2-mm interstitial nodules graphic file with name u01-17-9780323065382.gif Hematogenous infection
        Often associated with reticular opacities Hematogenous metastases
        Sarcoid
        Pneumoconiosis
        Silicosis
        CWP
        Histiocytosis (EG, also cysts)
        Cystic Spaces
        With or without walls graphic file with name u01-18-9780323065382.gif LymphangioleiomyomatosisCystic PCP
        Histiocytosis
        Honeycombing
        IPF
        LIP
        Any end-stage interstitial disease
        Open in a new tab

Crazy-paving appearance on HRCT

  • Ground-glass opacity with overlying geometric structures formed by thickened interlobular septa and intraseptal lines
    • •
      Pulmonary alveolar proteinosis
    • •
      ARDS
    • •
      PCP
    • •
      Lipoid pneumonia
    • •
      Hemorrhage
    • •
      Bronchoalveolar carcinoma (BAC)
    • •
      Pulmonary edema

Pulmonary hemorrhage

    • Focal
      • •
        PE
      • •
        Trauma (contusion)
      • •
        AVM
      • •
        Cancer (BAC)
    • Diffuse
      • •
        Wegener
      • •
        Goodpasture (resolves in days to weeks, can result in fibrosis)
      • •
        Idiopathic (children)
      • •
        Bone marrow transplant

Halo pattern of ground-glass opacity

    • •
      Early invasive aspergillosis in a leukemic patient: ground glass around a nodule of consolidation
    • •
      Hemorrhage around a neoplasm
    • •
      Postbiopsy pseudonodule

Peripheral ground-glass opacity and consolidation

    • •
      COP
    • •
      Infarcts
    • •
      Septic emboli
    • •
      Collagen vascular disease
    • •
      Contusion
    • •
      DIP
    • •
      Drug toxicity
    • •
      Eosinophilic pneumonia
    • •
      Fibrosis
    • •
      Sarcoidosis

Honeycombing pattern on HRCT

    • •
      UIP (idiopathic pulmonary fibrosis)
    • •
      Scleroderma/RA
    • •
      Asbestosis
    • •
      Chronic hypersensitivity pneumonitis
    • •
      Sarcoidosis
    • •
      Silicosis
    • •
      EG
    • •
      Drug toxicity: bleomycin

Diseases spreading along bronchovascular bundle

    • •
      Sarcoidosis
    • •
      Lymphoma
    • •
      Lymphangitic spread of tumor
    • •
      TB
    • •
      Kaposi sarcoma

Tree-in-bud appearance

    • Infection
      • •
        TB
      • •
        Bronchopneumonia
      • •
        Fungal
      • •
        Asian panbronchiolitis
      • •
        Viral pneumonias
    • Bronchial disease
      • •
        Bronchiolitis
    • Congenital disorders
      • •
        Cystic fibrosis
      • •
        Dyskinetic cilia syndrome
    • Other
      • •
        Allergic bronchopulmonary aspergillosis
      • •
        Lymphangitic carcinomatosis
      • •
        EG

Abnormal density

Hyperlucent lung

Hyperlucency may be lobar, segmental, subsegmental, or generalized. Hyperlucency may or may not be associated with overexpansion of lungs.

Causes
    • Airways
      • •
        Obstruction of airways (air trapping); inspiratory/expiratory films may be of use to accentuate the hyperlucency
        • Emphysema, bullae
        • Large airway obstruction: asthma, mucus plug
        • Small airway obstruction (bronchioli): Swyer-James syndrome (bronchiolitis obliterans)
        • Compensatory hyperexpansion of residual lung after: surgical lobectomy, chronic lobar collapse
      • •
        Cysts
      • •
        Congenital
        • Hypogenetic lung syndrome
        • Congenital lobar emphysema
    • Vascular (hyperlucency caused by oligemia)
      • •
        PE
      • •
        Pulmonary artery stenosis
    • Chest wall abnormalities
      • •
        Mastectomy
      • •
        Poland syndrome (congenital absence of pectoralis muscle)
    • Pleural
      • •
        Pneumothorax

Small lung (Fig. 1-92)

Figure 1-92.

Figure 1-92

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  • May be associated with either decreased or increased density
    • •
      Hypogenetic lung syndrome
    • •
      Agenesis of pulmonary artery
    • •
      Chronic atelectasis
    • •
      Bronchiolitis obliterans (Swyer-James syndrome)

Tracheobronchial lesions

Endobronchial lesions

Focal bronchial abnormality

Causes
    • Tumors, 80%
      • •
        Malignancy, 70%:
        • SCC (most common)
        • Low-grade malignancies
        • Adenocystic carcinoma
        • Mucoepidermoid carcinoma
        • Small cell carcinoma
        • Carcinoid
      • •
        Metastases, 5%: RCC, melanoma, colon, breast, thyroid
      • •
        Other: hamartoma, mucoepidermoid carcinoma, hemangioma
    • Inflammatory disease, 20%
      • •
        TB
    • Other
      • •
        Mucus plug
      • •
        Foreign body (fishbone, dental)
      • •
        Trauma
      • •
        Broncholith

Diffuse tracheal luminal abnormalities

    • Increased diameter
      • •
        Tracheobronchomegaly (Mounier-Kuhn syndrome)
      • •
        Pulmonary fibrosis
      • •
        Tracheomalacia
    • Decreased diameter
      • •
        Saber-sheath trachea (most common cause)
      • •
        Tracheopathia osteochondroplastica
      • •
        Tracheomalacia (decreased diameter on expiration)
      • •
        Relapsing polychondritis
      • •
        Amyloidosis
      • •
        Sarcoidosis
      • •
        Wegener disease
      • •
        Tuberculous and fungal stenosis

Bronchiectasis

    • Postinfectious (most common)
      • •
        Any childhood infection
      • •
        Recurrent aspiration
      • •
        ABPA: central bronchiectasis
      • •
        Chronic granulomatous infection
      • •
        Pertussis
    • Bronchial obstruction
      • •
        Neoplasm
      • •
        Foreign body
    • Congenital
      • •
        Cystic fibrosis (abnormal secretions)
      • •
        Bronchial cartilage deficiency: Williams-Campbell syndrome
      • •
        Abnormal mucociliary transport: Kartagener syndrome

Upper lobe bronchiectasis (Fig. 1-93)

Figure 1-93.

Figure 1-93

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    • •
      Cystic fibrosis
    • •
      TB
    • •
      Radiation
    • •
      ABPA (most commonly central)
    • •
      Mounier-Kuhn syndrome
    • •
      Agammaglobulinemia
    • •
      Kartagener syndrome

Mucoid (bronchial) impaction

Criteria: bronchus filled with soft tissue density (inspissated mucus); bronchi may be enlarged (bronchocele) or of normal size. No contrast enhancement.

Causes
    • •
      Asthma
    • •
      Cystic fibrosis
    • •
      ABPA
    • •
      Congenital bronchial atresia

Pleural disease

Pleural-based mass (Fig. 1-94)

Figure 1-94.

Figure 1-94

Open in a new tab
  • Soft tissue mass along the chest wall; obtuse angles with chest wall.
    • Tumor
      • •
        Mesothelioma (malignant): multifocal, diffuse
      • •
        Fibrous tumor of the pleura (benign); unifocal may be locally invasive
      • •
        Malignant thymoma and lymphoma often have appearance similar to that of mesothelioma
      • •
        Metastases: breast, lung, prostate, thyroid, renal
      • •
        Lipoma (most common benign tumor)
      • •
        Extrapleural tumors
        • Rib tumors
        • Children: EG, ABC, Ewing sarcoma, neuroblastoma
        • Adults: metastases > multiple myeloma > Paget disease, fibrous dysplasia
        • Plexiform neurofibromas in neurofibromatosis (bilateral)
    • Inflammatory
      • •
        Infectious: TB
      • •
        Asbestos related
      • •
        Actinomycosis (rib destruction)
    • Trauma, surgery, chest tubes

Calcified pleural plaques

  • The most common causes of calcified pleural plaques (mnemonic: “TAFT”) are:
    • •
      Tuberculosis (usually diffuse plaques)
    • •
      Asbestos-related plaques (usually focal plaques)
    • •
      Fluid (empyema, hematoma)
    • •
      Talc

Elevated hemidiaphragm (Fig. 1-95)

Figure 1-95.

Figure 1-95

Open in a new tab
    • Phrenic nerve paralysis
      • •
        Tumor
      • •
        Surgery
      • •
        Birth defect: Erb paralysis
    • Immobility because of pain
      • •
        Rib fractures
      • •
        Pleuritis, pneumonia
      • •
        PE
      • •
        Mass lesions
      • •
        Abdominal masses, subphrenic collection, abscess
      • •
        Diaphragmatic hernia
      • •
        Pleural tumors
      • •
        Subpulmonic effusion (apparent elevation of hemidiaphragm)

Mediastinum

Anterior mediastinal masses (Fig. 1-96)

Figure 1-96.

Figure 1-96

Open in a new tab
    • Thymic masses
      • •
        Thymic cyst
      • •
        Thymolipoma
      • •
        Thymoma
        • Cystic
        • Benign (noninvasive) thymoma
        • Malignant (invasive) thymoma
      • •
        Thymic carcinoma
      • •
        Thymic carcinoid
      • •
        Thymic lymphoma
    • Germ cell tumors (male > female)
      • •
        Seminoma
      • •
        Embryonal cell carcinoma
      • •
        Choriocarcinoma
      • •
        Teratoma
        • Lymphadenopathy: lymphoma, sarcoid, TB, etc.
        • Aneurysm and vascular abnormalities (involve both the anterior and superior mediastinal compartments)
  • Mnemonic for anterior mediastinal masses: the “4 Ts”:
    • •
      Thymoma (most common anterior mediastinal mass) + other thymic lesions
    • •
      Thyroid lesions
    • •
      T-cell lymphoma (Hodgkin disease and NHL)
    • •
      Teratoma and other germ cell tumors (seminoma, choriocarcinoma), 10%
Cystic Anterior Mediastinal Mass
    • •
      Thymic cyst (3rd pharyngeal pouch remnant)
    • •
      Cystic thymoma (contains solid components besides cysts)
    • •
      Teratoma
    • •
      Bronchogenic cysts (usually located in middle mediastinum)
    • •
      Pericardial cyst

Superior mediastinal mass

    • Descending through thoracic inlet
      • •
        Thyroid masses
      • •
        Adenopathy (primary head and neck tumors)
      • •
        Lymphatic cysts, cystic hygroma
    • Ascending through thoracic inlet
      • •
        Small cell carcinoma of the lung
    • Lymphoma
    • Aneurysm and vascular anomalies may involve both the anterior and superior mediastinal compartments.

Middle mediastinal mass

    • Adenopathy (often bilateral)
      • •
        Benign: sarcoid, TB, fungal infection, chronic beryllium exposure
      • •
        Malignant: metastases, lymphoma, leukemia
    • Congenital cysts
      • •
        Bronchogenic cysts (subcarinal, anterior trachea)
      • •
        Pericardial cysts
    • Aneurysm
      • •
        Aorta, aortic branches
      • •
        Pulmonary artery
    • Esophagus
      • •
        Hiatal hernia (common)
      • •
        Neoplasm
      • •
        Diverticula
      • •
        Megaesophagus: achalasia, hiatal hernia, colonic interposition
    • Other
      • •
        Mediastinal hemorrhage
      • •
        Mediastinal lipomatosis
      • •
        Bronchogenic cancer arising adjacent to mediastinum
      • •
        Aberrant RSA with diverticulum
      • •
        Varices
      • •
        Neurinoma from recurrent laryngeal nerve
      • •
        Malignancy of trachea
      • •
        Pancreatic pseudocyst

Adenopathy

    • Low-attenuation lymph nodes
      • •
        TB and fungal infections in AIDS (ring enhancement)
      • •
        Necrotic metastases (aggressive neoplasm)
      • •
        Lymphoma (occasionally)
    • Vascularized lymph nodes
      • •
        Castleman disease (giant benign nodal hyperplasia)
      • •
        Vascular metastases: renal cell, thyroid, small cell, melanoma
    • Calcified lymph nodes
      • •
        TB
      • •
        Histoplasmosis, other fungus
      • •
        Sarcoidosis
      • •
        Silicosis
      • •
        Radiation therapy

Posterior mediastinal mass (Fig. 1-97)

Figure 1-97.

Figure 1-97

Open in a new tab
    • Neurogenic, 90%
      • •
        Peripheral nerves (20 to 40 years; <2 vertebral bodies long): schwannoma and neurofibroma, 45%
      • •
        Sympathetic ganglia (<20 years; >2 vertebral bodies long): ganglioneuroma, neuroblastoma, sympathicoblastoma
      • •
        Paraganglionic cells: pheochromocytoma, paraganglioma (least common)
      • •
        Lateral meningomyelocele
    • Thoracic spine
      • •
        Neoplasm
      • •
        Hematoma
      • •
        Extramedullary hematopoiesis (bilateral)
      • •
        Diskitis
    • Vascular
      • •
        Aneurysm
      • •
        Azygos continuation (congenital absence of IVC with dilated azygos and hemiazygos veins)

Cardiophrenic angle mass

    • •
      Fat pad (most common cause)
    • •
      Diaphragmatic hernia (second most common)
      • Morgagni (anterior; 90% on right side)
      • Bochdalek (posterior; more common on left; not a true cardiophrenic mass)
    • •
      Pericardial cyst
    • •
      Cardiophrenic angle nodes (lymphoma usually recurrent, status postradiation)
    • •
      Aneurysm
    • •
      Dilated right atrium
    • •
      Anterior mediastinal mass
    • •
      Primary lung or pleural mass

Fatty mediastinal lesions

    • Purely fatty lesions
      • •
        Mediastinal lipomatosis
      • •
        Morgagni hernia (omentum)
      • •
        Bochdalek hernia (omentum)
      • •
        Periesophageal fat herniation
    • Tumors with fatty components
      • •
        Lipoma
      • •
        Liposarcoma
      • •
        Thymolipoma (children and young adults, lesions are usually very large)
      • •
        Germ cell tumors (also contain calcifications and cystic and solid regions)

High-density mediastinal lesions (noncontrast CT)

    • Calcified lymph nodes
    • Calcified primary mass
      • •
        Tumor
      • •
        Goiter
      • •
        Aneurysm
    • Hemorrhage

Densely enhancing mediastinal mass

    • Vascular
      • •
        Aneurysm
      • •
        Vascular abnormalities
      • •
        Esophageal varices
    • Hypervascular tumors: paraganglioma, metastasis from thyroid cancer, RCC
    • Goiter
    • Castleman disease

Retrocrural adenopathy

    • Inflammation
      • •
        Sarcoidosis
      • •
        LAM
      • •
        Amyloidosis
    • Infection
      • •
        AIDS
      • •
        TB
      • •
        M. avium
    • Lymphoma
    • Mets

Prominent hila (Fig. 1-98)

Figure 1-98.

Figure 1-98

Open in a new tab
    • Tumors
      • •
        Central bronchogenic carcinoma
      • •
        Lymphoma
    • Adenopathy
      • •
        Infectious: TB, fungi, histoplasmosis
      • •
        Inflammatory: sarcoid, silicosis
      • •
        Tumor: commonly oat cell, lymphoma, metastases
    • Pulmonary artery enlargement

Eggshell calcification in hilar nodes

    • •
      Silicosis, CWP
    • •
      Treated lymphoma
    • •
      Granulomatous disease such as histoplasmosis rarely contains eggshell calcification; diffuse calcifications are more common.
    • •
      Sarcoid (rare and late in disease)

Pneumomediastinum

  • Pulmonary
    • •
      Asthma (common)
    • •
      Barotrauma (intubation, diver)
    • •
      Childbirth
    • •
      Pneumothorax
  • Mediastinum
    • •
      Tracheobronchial laceration
    • •
      Esophageal perforation
    • •
      Mediastinal surgery
    • •
      Boerhaave syndrome
  • Abdomen
    • •
      Intraperitoneal or retroperitoneal bowel perforation
    • •
      Retroperitoneal surgery
  • Head and neck
    • •
      Esophageal rupture
    • •
      Facial fractures
    • •
      Dental or retropharyngeal infection, mediastinitis

Footnotes

*

These nodes are best assessed by mediastinoscopy; the remainder of nodes are best assessed by CT.

Suggested Readings

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Articles from Primer of Diagnostic Imaging are provided here courtesy of Elsevier

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