Abstract 4364158: A Ticking Time Bomb, Acute Amiodarone-Induced Pulmonary Toxicity Leading to ARDS in a Nonagenarian: A Case Report

Amiodarone is an iodine-containing antiarrhythmic agent commonly used to manage ventricular and supraventricular arrhythmias. Despite its clinical efficacy, amiodarone has a well-documented side effect profile due to its lipophilic nature and tendency to accumulate in various organs. Amiodarone-induced pulmonary toxicity (APT) occurs in approximately 1–5% of patients, with acute presentations being rare (<1%). Acute APT typically presents as respiratory failure and, if not recognized promptly, can progress rapidly to acute respiratory distress syndrome (ARDS), which carries a mortality rate of nearly 50%, in contrast to a 10% mortality rate in subacute or chronic forms. We present the case of a 91-year-old woman with a history of persistent atrial fibrillation, HFpEF, hypertension, and peripheral vascular disease who presented with acute hypoxic respiratory failure while in atrial fibrillation. Within the same month, she was started on amiodarone 200 mg daily and subsequently underwent TEE-guided cardioversion. High-resolution chest CT on admission revealed new, extensive bilateral pulmonary infiltrates. She was admitted to the ICU, amiodarone was discontinued, and treated with diltiazem, digoxin, steroids, and empiric antibiotics under an ARDS protocol. DNAR/DNI status led to non-invasive ventilatory support. Bronchoscopy with BAL was negative for infection or malignancy; cytology revealed foamy macrophages. PFT showed a restrictive pattern and reduced DLCO. Her condition worsened, and she transitioned to comfort care, passing within 48 hours. Key mechanisms of APT include cytotoxic effects of iodine-rich metabolites, immune-mediated alveolar injury, oxidative stress, and phospholipid accumulation in alveolar macrophages. Risk is elevated in patients receiving high doses (>400 mg/day), IV administration, recent cardiothoracic surgery, and mechanical ventilation. Clinical features can mimic pneumonia, heart failure, or PE. Diagnosis is clinical and exclusionary. Immediate drug discontinuation and corticosteroids (methylprednisolone 500–1000 mg/day IV for ARDS) are essential, though mortality remains high. Residual fibrosis develops in 5–7% of survivors. Acute APT is a rare but serious adverse effect, especially in elderly patients with comorbidities. Early recognition is crucial. This case underscores the importance of vigilance, early recognition, and consideration of APT in the differential diagnosis of new respiratory symptoms in patients on amiodarone.