Abstract Introduction Acute eosinophilic pneumonia (AEP) is a rare interstitial lung disease characterized by eosinophilic infiltration of the lung parenchyma, often triggered by environmental exposures or medications. Carbamazepine is a widely used antiepileptic drug, but reports of carbamazepine-induced AEP are rare. Recognition of this association is important for appropriate management of AEP. Case Description A man in his sixties with ischemic cardiomyopathy and epilepsy presented with progressive dyspnea, fever, and hypoxemia one month after starting carbamazepine therapy. Initial computed tomography (CT) revealed bilateral diffuse infiltrates and small pleural effusions (Fig.1-2). Laboratory evaluation showed leukocytosis without peripheral eosinophilia. Despite empiric treatment for community-acquired pneumonia, his condition deteriorated, requiring intubation. Later, bronchoscopy with bronchoalveolar lavage showed 28% eosinophils with a negative infectious workup, consistent with acute eosinophilic pneumonia. Carbamazepine was discontinued and systemic corticosteroids were initiated, resulting in rapid clinical and radiographic improvement with subsequent extubation (Fig. 3-4). Unfortunately, the patient later developed an unrelated ST-elevation myocardial infarction and transitioned to comfort care. Discussion Our case shows the importance of considering drug-induced AEP in patients with unexplained hypoxemic respiratory failure and pulmonary infiltrates, especially when infectious causes are excluded. Carbamazepine should be recognized as a potential trigger. Early recognition, discontinuation of the offending drug, and prompt initiation of corticosteroids are critical to improving outcomes and preventing rapid respiratory deterioration. This abstract is funded by: None
Salem et al. (Fri,) studied this question.