Amiodarone initiation for atrial fibrillation resulted in fatal acute pulmonary toxicity within 6 days in an 81-year-old man, despite discontinuation and corticosteroid therapy.
Case Report (n=1)
Acute amiodarone pulmonary toxicity can present as a fulminant, life-threatening complication within days of initiation, necessitating early recognition and discontinuation, particularly in elderly patients with underlying lung disease.
Abstract Background Amiodarone is a potent Class III antiarrhythmic agent, widely used for rhythm control after cardioversion in atrial fibrillation. Although effective, it carries a risk of pulmonary toxicity, with an overall incidence of 1–5% among users. Most cases occur with chronic use, but acute amiodarone pulmonary toxicity (APT) is a rare, potentially life-threatening complication that can develop within days to weeks of initiation. APT typically presents with dyspnea, nonproductive cough, hypoxemia, and new pulmonary infiltrates, often mimicking infection or heart failure. Case Presentation An 81-year-old man with COPD and paroxysmal atrial fibrillation post cardioversion and initiated on amiodarone 6 days prior presented to the hospital for evaluation of progressive dyspnea, hypoxemia, and hemoptysis. On arrival, he was hypoxic, tachypneic, and mildly hypertensive. Initial workup suggested HFpEF exacerbation with an elevated proBNP of 7,000 and CXR remarkable for diffuse pulmonary airspace opacities in the setting of oral diuresis recently held. IV diuresis led to transient improvement. However, worsening hypoxia prompted a chest CT, which revealed bilateral patchy ground-glass opacities. Amiodarone was discontinued, and prednisone 60 mg daily was initiated. Despite initial steroid therapy, the patient deteriorated, requiring critical care transfer for monitoring and pulse-dose steroids. Extensive infectious workup was negative. Rheumatology work-up was unremarkable. Despite transient improvement, the patient’s course was complicated by worsening hypoxia, work of breathing, and encephalopathy, requiring intubation. Family discussion confirmed a status of DNR and trial of intubation. Bronchoscopy showed atypical bronchial and squamous cells with severe acute inflammation, with no comment of lipid-laden macrophages. BAL was negative for pathogens, including PJP. Following failed attempts at weaning, comfort-focused care was pursued with family discussion. The patient expired four weeks post-cardioversion. Discussion Acute APT is a rare but fulminant cause of non-infectious pneumonitis and ARDS, occurring within one week of drug initiation. Though the BAL was negative for lipid-laden macrophage, its presence only confirms exposure and not toxicity. The clinical timeline, radiographic findings, negative infectious and autoimmune workup, and partial steroid responsiveness supported the diagnosis. Mortality from APT has been reported to exceed 50% in severe cases, particularly when complicated by ARDS. Early identification, discontinuation of amiodarone, and timely corticosteroid therapy are essential, but outcomes may remain poor despite best practices. Clinicians should maintain a high index of suspicion for acute APT in patients presenting with new pulmonary infiltrates and hypoxemia within weeks of drug initiation—particularly in elderly patients with underlying lung disease. This abstract is funded by: None
Mitchell et al. (Fri,) conducted a case report in Acute amiodarone pulmonary toxicity (n=1). Amiodarone was evaluated. Amiodarone initiation for atrial fibrillation resulted in fatal acute pulmonary toxicity within 6 days in an 81-year-old man, despite discontinuation and corticosteroid therapy.