Pulmonary drug toxicity: Radiologic and pathologic manifestations

Pulmonary drug toxicity is increasingly being diagnosed as a cause of acute and chronic lung disease. Numerous agents including cytotoxic and noncytot oxic drugs have the potential to cause pulmonary toxicity. The clinical and radiologic manifestations of these drugs generally reflect the underlying histopathologic processes and include diffuse alveolar damage (DAD), nonspe cific interstitial pneumonia (NSIP), bronchiolitis obliterans organizing pn eumonia (BOOP), eosinophilic obliterative bronchiolitis, pulmonary hemorrha ge, edema, pneumonia, hypertension, or veno-occlusive disease. DAD is a com mon manifestation of pulmonary drug toxicity and is frequently caused by cy totoxic drugs, especially cyclophosphamide, bleomycin, and carmustine. It m anifests radiographically as bilateral hetero- or homogeneous opacities usu ally in the mid and lower lungs and on high-resolution computed tomographic (CT) scans as scattered or diffuse areas of ground-glass opacity. NSIP occ urs most commonly as a manifestation of carmustine toxicity or of toxicity from noncytotoxic drugs such as amidarone. At radiography, it appears as di ffuse areas of heterogeneous opacity, whereas early CT scans show diffuse g round-glass opacity and late CT scans show fibrosis in a basal distribution . BOOP, which is commonly caused by bleomycin and cyclophosphamide (as well as gold salts and methotrexate), appears on radiographs as hetero- and hom ogeneous peripheral opacities in both upper and lower lobes and on CT scans as poorly defined nodular consolidation, centrilobular nodules, and bronch ial dilatation. Knowledge of these manifestations and of the drugs most fre quently involved can facilitate diagnosis and institution of appropriate tr eatment.