SESSION TITLE: Tuesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Diffuse alveolar hemorrhage (DAH) occurs as a result of endothelial alveolar-capillary cell injury. Although there are many etiologies for DAH, up to 10% of cases are due to drug toxicity. To our knowledge, we describe a rare case of flecainide-associated DAH likely with underlying diffuse alveolar damage (DAD). Dyspnea and hypoxia improved after cessation of flecainide and initiation of glucocorticoids. CASE PRESENTATION: A 59-year-old female with atrial fibrillation on chronic flecainide presented with a history of dyspnea and dry cough. Vital signs on admission showed hypoxemia with oxygen saturation of 89% on room air. Exam revealed diffuse expiratory wheezing. Chest radiograph showed diffuse interstitial disease with bibasilar lung opacification. She was managed as a case of community acquired multifocal pneumonia, however, remained hypoxemic requiring high flow nasal cannula refractory to antibiotics. Chest computed tomography (CT) demonstrated multifocal areas of ground glass opacities with superimposed interlobular septal thickening in a “crazy paving” pattern (Image 1). During hospitalization, patient developed worsening hypoxemia requiring BiPAP and was transferred to the ICU. Infectious, rheumatologic, and cardiac workup were negative. She was started on intravenous methylprednisolone while in the ICU for presumed ILD. Bronchoscopy was done and bronchoalveolar lavage (BAL) revealed progressively more bloody return in different aliquots consistent with DAH. A literature search showed flecainide linked to DAH and this was discontinued. Steroids were tapered down during a lengthy hospital course with progressive improvement in hypoxemia. Repeat CT of the chest showed significant improvement of ground glass opacities (Image 2). Patient was seen in outpatient clinic after she had a third CT chest performed. This showed further improvement in the ground glass opacities with bibasilar distribution of subpleural reticulation suggestive of underlying DAD with resultant fibrosis (Image 3). PFT’s further confirmed this with a significantly reduced diffusing capacity of 26%. DISCUSSION: There are numerous reports of drug-induced lung injuries and DAH. There have been a few case reports of lung toxicity associated with flecainide, which is felt to be secondary to a cell-mediated immunologic reaction, and is a diagnosis of exclusion. In our case, the patient presented with hypoxemic respiratory failure while on flecainide. Improvement was achieved after withdrawal of flecainide and initiation of steroids, supporting a drug-induced etiology over others. CONCLUSIONS: Our case highlights a rare but potentially lethal manifestation of flecainide-induced pulmonary toxicity. Early recognition of this may prevent irreversible damage leading to pulmonary fibrosis. Reference #1: Hanston P, Evrard P, Mahieu P, Wallemacq P, Friob M, Hassoun A: Flecainide-associated interstitial pneumonitis. Lancet 1991;337:371–372. DISCLOSURES: No relevant relationships by Tracy Ashby, source=Web Response No relevant relationships by Nimeh Najjar, source=Web Response No relevant relationships by Tiara Ong, source=Web Response No relevant relationships by Vandana Seeram, source=Web Response