Study Syllabus for Classification of Radiographs of Pneumoconioses

Clinical Overview

Major Occupational Lung Diseases

Granulomatous Diseases

Hypersensitivity Pneumonitis

Hypersensitivity pneumonitis (HP), also called extrinsic allergic alveolitis, is caused by inhalation of antigens that trigger a diffuse mononuclear cell inflammation of the small airways and lung parenchyma. The three broad categories of causal antigens are: (1) fungal and microbial agents, (2) animal proteins, and (3) low molecular weight chemicals.

The clinical presentation of HP has been classified as acute, subacute or chronic. The flu-like respiratory illness of acute HP occurs within 4 to 12 hours of exposure, with fever, cough, dyspnea, chills, malaise, chest tightness and myalgias. Physical examination may show fever, tachypnea, tachycardia, and rales. With subacute and chronic HP, patients report insidious onset of dyspnea on exertion, dry or minimally productive cough, fatigue, malaise, anorexia and weight loss. Bibasilar crackles may be detectable on lung auscultation; right heart failure and digital clubbing may be present in advanced cases of fibrosis. Pulmonary function testing shows restriction, obstruction or mixed abnormalities, often with decreased DLCO and/or exercise-induced gas exchange abnormalities.

The chest radiograph (CXR) is often normal in patients with HP, with an estimated sensitivity of only 10% [Hodgson et al. 1989]. In acute HP (Fig. 12), the CXR may show diffuse ground glass or airspace consolidation. Patients with subacute HP may have a combination of nodular or reticulonodular opacities with ground glass. Chronic fibrotic HP usually has a CXR appearance of reticular opacities with honeycombing. Though the HRCT pattern is variable depending on the stage of HP, characteristic findings include centrilobular ground-glass nodular opacities, diffuse ground-glass abnormality, and mosaic attenuation with expiratory air-trapping (Fig. 12, hypersensitivity pneumonitis showing features of ground glass opacity, traction bronchiectasis, and mosaic attenuation, and Fig. 13 showing air trapping at arrows). Such findings may be seen in patients with acute, subacute or chronic disease. The distribution of findings in acute or subacute HP is often diffuse, while the findings of chronic HP may show upper, middle or lower lung predominance [Silva et al. 2008]. Some patients with chronic HP develop lung fibrosis, characterized by reticular abnormality, traction bronchiectasis, and sometimes honeycombing, often in association with centrilobular nodularity, ground glass, or mosaic attenuation. Emphysema (Fig. 14, two different patients) and cystic change (Fig. 15) may also occur in chronic HP, even in never smokers.

Histologic findings vary depending upon the stage of disease. The classic HP triad of histopathologic features is lymphocytic alveolitis; small, loose non-necrotizing granulomas; and cellular bronchiolitis. In chronic HP, variable stages of interstitial fibrosis may be found including a nonspecific interstitial pneumonitis (NSIP) pattern, centrilobular and peribronchiolar fibrosis, bridging fibrosis, and a usual interstitial pneumonia (UIP)-like pattern. Findings of lymphocytic infiltration, giant cells, poorly formed granulomas, and bridging fibrosis can help differentiate HP from other fibrotic lung diseases.