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Systematic Approach to Abnormal Chest Films

David S. Feigin, M.D.

I. DEFINITIONS

  1. Pattern: abnormalities of the lungs as seen on images
  2. Disease: causes of patterns as seen on specimens
  3. Diffuse pulmonary disease: nonspecific term for pulmonary disease involving all or most of the lungs and producing any pattern of abnormalities on chest films and CT.
  4. Infiltrative lung disease: nonspecific term for any restrictive pulmonary disease which infiltrates rather than destroys lung parenchyma.
  5. Nodule: often used to mean “small mass” – therefore, same causes as Mass (if number is countable)
  6. Interstitial lung disease: pathology term for thickening or destruction of pulmonary interstitium, which includes alveolar walls, septa and connective tissue surrounding bronchi and vessels (peribronchial and perivascular spaces). Correlates with functional term “restrictive lung disease” and with interstitial pattern on chest films.
  7. Consolidative Pattern: preferred over ‘alveolar pattern’ to describe the radiological pattern of filled air spaces
  8. Consolidative Pattern: “Large airways” (Bronchi) have visible walls on plain films when they are abnormally thickened. “Small airways” (mostly Bronchioles) have walls too small to be visible, even when thickened.

 

II. SYSTEMATIC APPROACH

A. PATTERN

  1. Mechanisms
  2. Features – texture, distribution

B. DIFFERENTIAL DIAGNOSIS, GENERAL – “DDG”

C. DIFFERENTIAL DIAGNOSIS, SPECIFIC – “DDS”

Based on:

  1. DDG
  2. Associated findings on image(s)
  3. All clinical information


III. ASSOCIATED FINDINGS

A. Complete search of image(s)

  1. Central airways
  2. Periphery of lungs – ptx, effusion
  3. Mediastinal contours

B. Hilum

  1. Enlarged pulmonary arteries – usually PAH
  2. Mass – same DDG as lung mass
  3. Lymphadenopathy – same DDG as lung mass

C. Compression (Compressive Atelectasis)

  1. NOT a true Pattern of disease, but may mimic consolidation and obstructive atelectasis
  2. Judge if vessels squeezed together by hypoventilation, effusion, emphysema or other causes


IV. PATTERNS

A. Mass

B. Consolidative

C. Interstitial

  1. linear
  2. nodular

D. Vascular

E. Airway

  1. bronchial
  2. bronchiolar (small airway)


V. MASS

A. Mechanism: local destruction, or possible destruction, of lung parenchyma

B. Features: any localized opacity not completely bordered by fissures or pleura – not shaped like an anatomic part of the lung (e.g. lobe or segment) – Distribution random, not lobar. May be large or small (“nodule”),solid or cavitated, smooth or lobulated, SOLITARY OR MULTIPLE (but countable)

C. DIFFERENTIAL DIAGNOSIS, GENERAL

  1. Malignancy – Primary, metastatic, lymphomatous
  2. Granulomatous disease - infectious or noninfectious, active or inactive.
  3. Other (non-granulomatous) inflammation, including pneumonia and abscess
  4. Benign neoplasm
  5. Congenital abnormality
  6. Crucial appearance characteristics for inactivity
  7. Calcification - Central, lamellar
  8. Evolution - 2 year stability or regression

E. Clinical variables

  1. Age
  2. Symptoms and signs
  3. Risk factors: smoking, occupation, exposure, previous carcinoma, concurrent diseases

F. HRCT Features – calcification, fat


VI. CONSOLIDATIVE (ALVEOLAR) PATTERN

A. Mechanism: produced in pure form only by alveolar filling, but may mimicked by alveolar collapse, airway obstruction, or rarely confluent interstitial thickening, or a combination of these.

B. Features

  1. Fluffy, cloud-like, coalescent opacities
  2. Complete air bronchograms – patent airways
  3. If sharp edges visible, they are in position of normal fissures -
  4. Distribution lobar

C. DIFFERENTIAL DIAGNOSIS, GENERAL

  1. Hemorrhage - Blood - Embolism, trauma
  2. Exudate - Pus - Pneumonia, pneumonitis
  3. Transudate - Water - Congestion, ARDS
  4. Secretions - Protein - Mucous plugging, alveolar proteinosis
  5. Malignancy - Cells - Alveolar cell carcinoma, lymphoma

D. HRCT features: may be same density as blood or may be ground-glass

  • GROUND-GLASS density favors ACTIVE process over chronic and MILD over severe

Mechanisms:

  1. Consolidative pattern with diffuse aerated alveoli
  2. Severe interstitial pattern
  3. Fatty material in consolidated alveoli
  4. Obstructive pneumonitis or alveolar proteinosis
  5. Vascular plethora – often mosaic – vessel or airway causes

 

VII. INTERSTITIAL PATTERNS

A. Mechanisms

  1. Diffuse or irregular thickening of lung interstices
  2. Architectural destruction of interstitium (honeycomb or “end stage” lung).

B. Features

  1. Linear form: reticulations (lines in all directions) and Septal lines (“Kerley lines”).
  2. Nodular form: rounded opacities that are: small, sharp, very numerous, evenly distributed and uniform in shape
  3. Destructive form: distinctive feature is cyst formation: peripheral, irregular

C. DIFFERENTIAL DIAGNOSIS, GENERAL

1. Linear form – “LIFE lines”

  • Lymphangitic spread of malignancy
  • Inflammation
  • Fibrosis
  • Edema

2. Nodular form

  • Granulomas
  • Hematogenous spread of malignancy
  • Pneumonoconiosis

3. Destructive form

  • Fibrosis – usually Fibrosing Alveolitis

D. HRCT Features: individual components of interstitium visible

  • Peribronchial thickening
  • Perivascular thickening
  • Alveolar wall thickening
  • Subpleural thickening
  • Thick-walled cystic spaces (honeycomb)

HRCT distribution of linear interstitial patterns:

  • L central
  • I diffuse or lower lungs
  • F peripheral
  • E central, with dilated vessels

E. Destructive form

  1. Permanent fibrotic lung destruction with architectural distortion of the parenchyma
  2. Early appearance is nonspecific, usually identical with linear form
  3. Late findings include peripheral cystic spaces (“Honeycomb” or “End Stage Lung”) and irregular reticulations with volume loss and deformity of lungs


VIII. VASCULAR PATTERNS

A. Mechanism: caused by increased or decreased perfusion pressure

B. Features: changes in diameter and shape of specific vessels

C. DIFFERENTIAL DIAGNOSIS, GENERAL

  1. Venous hypertension (PVH) - engorged veins, especially upper lungs
  2. Emphysema – all vessels compressed
  3. Arterial hypertension (PAH) - large central arteries with peripheral tapering
  4. Shunt vascularity – all vessels engorged

D. HRCT Features

  1. Individual vessels visible
  2. Mosaic ground-glass
  3. Lucent areas


IX. AIRWAY PATTERNS

A. Mechanisms

  1. Compete obstruction – obstructive atelectasis, collapse
  2. Partial obstruction – air trapping
  3. Thickening of bronchial walls
  4. Small airway disease – mixed obstruction

B. Features

  1. Complete obstruction - produces opacity and decreased volume of lung distal to the site of obstruction. May resemble localized consolidation, but without air bronchograms
  2. Partial obstruction - produces lucency and increased volume
  3. Bronchial wall thickening - tram tracks, central circles or cysts
  4. Bronchiolar (small airway) obstruction:
  • airway (“alveolar”) nodules: irregular in size, shape and distribution
  • small, irregular lucencies

C. DIFFERENTIAL DIAGNOSIS, GENERAL

  1. Complete obstruction - mucous plugs, foreign bodies and the DDG of Masses
  2. Partial obstruction - COPD, pneumatoceles
  3. Bronchial wall thickening – acute or chronic bronchitis, bronchiectasis
  4. Bronchiolar (small airway) obstruction – bronchiolitis

D. HRCT Features

  1. Complete bronchial obstruction – endobronchial or compressive cause
  2. Partial bronchial obstruction - localized air trapping - expiratory HRCT
  3. Bronchial wall thickening - thick-walled bronchi, tram tracks, “signet rings”
  4. Bronchiolar (small airway) obstruction – patchy ground-glass, tree-in-bud

E. Destructive Airway Disease - Bronchiectasis

  1. Characterized by central (perihilar) cystic spaces, increased lung volumes and thickened airway walls (circles and tram tracks)
  2. Distinct from destructive interstitial disease (see VI, E. ), although some patients also have secondary interstitial changes, especially localized fibrosis.


TABLE I. MASS - DIFFERENTIAL DIAGNOSIS, GENERAL (DDG)

  • Malignancy – Primary, metastatic, lymphomatous
  • Granulomatous disease - infectious or noninfectious, active or inactive.
  • Other (non-granulomatous) inflammation, including pneumonia and abscess
  • Benign neoplasm
  • Congenital abnormality


TABLE II. CONSOLIDATIVE PATTERN - DIFFERENTIAL DIAGNOSIS, GENERAL (DDG)

  • Hemorrhage - Blood - Embolism, trauma
  • Exudate - Pus - Pneumonia, pneumonitis
  • Transudate - Water - Congestion, ARDS
  • Secretions - Protein - Mucous plugging, alveolar proteinosis
  • Malignancy - Cells - Alveolar cell carcinoma, lymphoma


TABLE III. INTERSTITIAL PATTERNS - DIFFERENTIAL DIAGNOSIS, GENERAL (DDG)

  • Linear form — “LIFE lines”
  • Lymphangitic spread of malignancy
  • Inflammation
  • Fibrosis
  • Edema
  • Nodular form
  • Granulomas
  • Hematogenous spread of malignancy
  • Pneumoconiosis
  • Destructive form — Honeycomb (“end stage”) lung


TABLE IV. LINEAR INTERSTITIAL PATTERN - DIFFERENTIAL DIAGNOSIS, SPECIFIC (DDS)

  • Lymphangitic Spread
  • Metastatic malignancy
  • Primary malignancy (usually adenocarcinoma)
  • Langerhans Histiocytosis (Granulomatosis)
  • Lymphoma
  • Sjögrens Syndrome - LIP
  • Lymphangioleiomyomatosis (rare)

*NOTE: Sarcoid resembles lymphangitic spread, usually plus nodules

  • Inflammation
  • Infections: Viral, Mycoplasmal, Bacterial (usually early or mild), Pneumocystis carinii
  • Collagen Vascular Disease
  • Rheumatoid arthritis
  • SLE
  • Polymyositis and dermatomyositis
  • Scleroderma (progressive systemic sclerosis)
  • Hypersensitivity Pneumonitis – allergic alveolitis
  • Drug reactions
  • Waldenström macroglobulinemia
  • Amyloidosis
  • Idiopathic – usually Fibrosing Alveolitis (UIP)
  • Also: DIP, NSIP, ?COP
  • Fibrosis
  • Following inflammation (see above)
  • Including IPF
  • Asbestosis
  • Radiation pneumonitis
  • ? Talcosis
  • Neurofibromatosis
  • Edema
  • Cardiac
  • Renal
  • Fluid overload
  • Anemia


Table V. NODULAR INTERSTITIAL PATTERN - DIFFERENTIAL DIAGNOSIS, SPECIFIC (DDS)

Granulomatous Diseases

Infectious:

  • Tuberculosis
  • Atypical mycobacterial diseases - especially MAI
  • Fungal diseases, especially:
  • Histoplasmosis
  • Coccidioidomycosis
  • Blastomycosis (N. A. and S. A.)
  • Cryptococcosis
  • Sporotrichosis
  • Bacterial diseases, especially:
  • Nocardiosis
  • Actinomycosis

Non-infectious:

  • Sarcoidosis
  • Hypersensitivity Pneumonitis (HP)
  • Vasculitis-granulomatosis diseases
  • Wegener’s
  • Lymphocytic
  • Bronchocentric
  • Allergic (Churg-Strauss)
  • Langerhans Granulomatosis (eosinophilic granuloma, histiocytosis) (LCG)
  • Hematogenous Metastases
  • Pneumoconioses
  • Granulomatous
  • Silicosis
  • Berylliosis
  • “Benign”
  • Coal Worker’s Pneumoconiosis
  • Siderosis
  • Stannosis


Table VI. VASCULAR PATTERN - DIFFERENTIAL DIAGNOSIS, GENERAL (DDG)

  • Venous hypertension (PVH) - engorged veins, especially upper lungs
  • Emphysema – all vessels compressed
  • Arterial hypertension (PAH) - large central arteries with peripheral tapering
  • Shunt vascularity – all vessels engorged
  • Table VII. AIRWAY PATTERNS - DIFFERENTIAL DIAGNOSIS, GENERAL (DDG)
  • Complete obstruction - mucous plugs, foreign bodies and the
  • DDG of Masses
  • Partial obstruction - COPD, pneumatoceles
  • Bronchial wall thickening – acute or chronic bronchitis, bronchiectasis
  • Bronchiolar (small airway) obstruction – bronchiolitis
  • Table IX. BRONCHIOLAR OBSTRUCTION (SMALL AIRWAY DISEASE) - DIFFERENTIAL DIAGNOSIS, SPECIFIC (DDS)
  • Infectious – especially: viral, mycoplasmal, fungal
  • Allergic – hypersensitivity (HP)
  • Toxic – especially: chlorine, phosgene, oxides of nitrogen
  • Post-transplant
  • Idiopathic


David S. Feigin, M.D. - Professor of Radiology, Johns Hopkins University

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