Hepatic Dysfunction and Neurotoxicity in a Patient Receiving Long-Term Low-Dose Amiodarone Therapy

• Published in: The Journal of emergency medicine 2010-04, Vol.38 (3), p.337-339
• Main Authors: Arkun, Alp, MD, Van Deusen, Shawn K., MD, Grau, Timothy, MD, Birkhahn, Robert H., MD
• Format: Article
• Language: English
• Subjects: Aged, 80 and over; amiodarone; Amiodarone - adverse effects; Ammonia - blood; Anti-Arrhythmia Agents - adverse effects; Atrial Fibrillation - drug therapy; Chemical and Drug Induced Liver Injury - blood; Chemical and Drug Induced Liver Injury - etiology; Emergency; hepatotoxicity; Humans; Male; neurotoxicity; Neurotoxicity Syndromes - etiology
• ISSN: 0736-4679; 2352-5029
• DOI: 10.1016/j.jemermed.2008.01.006

Abstract Background: Amiodarone is commonly used in the treatment of refractory paroxysmal atrial fibrillation. Much of the literature focuses on the toxic effects of this medication in the setting of rapid loading or long-term therapy with high maintenance doses. However, patients have been known to develop multi-organ toxicities with long-term low-dose therapy. Case Report: We present a 90-year-old man with paroxysmal atrial fibrillation undergoing low-dose amiodarone therapy for a period of 18 months without medical follow-up who developed signs and symptoms consistent with neurotoxicity and hepatotoxicity in association with hyperammonemia. Upon discontinuation of the medication and treatment of the hyperammonemia, the patient had a rapid decline in symptoms and a return to his baseline status. Conclusion: Identifying toxicity early and correcting it rapidly may prevent life-threatening sequelae associated with amiodarone toxicity.