The Poison Review

Hepatic Dysfunction and Neurotoxicity in a Patient Receiving Long-Term Low-Dose Amiodarone Therapy.   Arkun A et al. J Emerg Med 2010;38:337-339.

Abstract

This instructive case report describes a 90-year-old male who developed neurotoxicity 18 months after starting amiodarone 200 mg daily for paroxysmal atrial fibrillation.  Neurologic manifestations included confusion, dizziness, proximal lower extremity weakness, and ataxia.  Work-up revealed mild hepatic dysfunction and increased serum ammonia levels, but no other specific cause of the neurologic findings.

The authors note that there are a number of adverse reactions associated with amiodarone.  Severe hepatic toxicity — including fulminant hepatitis and cirrhosis — have been reported following large IV loading doses or prolonged high oral doses of the drug.  Neurotoxicity occurs less frequently and can present with fatigue, proximal muscle weakness, ataxia, peripheral sensorimotor neuropathy, and tremor.  Interestingly, in contrast to many other drugs such as phenytoin that cause ataxia, nystagmus does not seem to occur in these cases. It is important periodically to monitor patients on chronic amiodarone therapy, and considering lowering the dose or discontinuing the drug if neurological impairment or evidence of hepatic dysfunction develop.

A recent case report described amiodarone-induced parksinonism with pathological specimens demonstrating accumulation of the drug in brain tissue.