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.
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Clinical presentation
Affected patients present with dyspnea, cough, and occasionally fever. The diffusion capacity of the lung for carbon monoxide is characteristically decreased.
Pathology
Etiology
Diffuse alveolar damage is the histological hallmark of acute respiratory distress syndrome (ARDS) and acute interstitial pneumonitis (AIP).
Drugs that most commonly cause diffuse alveolar damage are bleomycin, busulfan, carmustine (BCNU), cyclophosphamide, melphalan, mitomycin, and gold salts.
Microscopic appearance
Histopathologically, diffuse alveolar damage is divided into an acute exudative phase and a late reparative (proliferative) phase.
the exudative phase, which is characterized by alveolar and interstitial edema 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.
Radiographic features
Plain radiograph
Chest radiographs show bilateral heterogeneous or homogeneous opacities, often in a mid and lower lung distribution.
Progression to diffuse opacification is common.
CT
High-resolution computed tomography in early diffuse alveolar damage 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. However, with progressive fibrosis, marked architectural distortion and honeycomb lung can occur.
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