Diffuse alveolar damage (DAD) is a common manifestation of drug-induced lung injury that results from necrosis of type II pneumocytes and alveolar endothelial cells.
Affected patients present with dyspnoea, cough, and occasionally fever. Diffusing capacity of the lung for carbon monoxide (DLCO) is characteristically decreased.
Drugs that most commonly cause DAD are bleomycin, busulfan, carmustine (BCNU), cyclophosphamide, melphalan, mitomycin, and gold salts.
Histopathologically, DAD is divided into an acute exudative phase and a late reparative or proliferative phase.
- the exudative phase, which is characterized by alveolar and interstitial oedema and hyaline membranes, is most prominent in the 1st week after lung injury.
- the reparative phase, which is characterized by proliferation of type II pneumocytes and interstitial fibrosis, typically occurs after 1 or 2 weeks.
Depending on the severity of the injury, fibrosis can improve significantly, remain stable, or progress to honeycomb lung.
Chest radiographs show bilateral heterogeneous or homogeneous opacities, often in a mid and lower lung distribution.
Progression to diffuse opacification is common.
High-resolution computed tomography in early DAD typically shows scattered or diffuse areas of ground-glass opacity.
Fibrosis typically develops within 1 week but initially may not be evident on chest radiographs. With progressive fibrosis, however, marked architectural distortion and honeycomb lung can occur.
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