Abstract

Amiodarone is a potent antiarrhythmic agent used for ventricular and atrial arrhythmias. Despite its efficacy, it has a wide range of adverse effects. We present a case of amiodarone toxicity manifesting with pulmonary and thyroid involvement, and review the key clinical features, diagnostic approach, and management strategies.

Keywords: amiodarone, toxicity, pulmonary toxicity, thyroid dysfunction, hepatitis, case report

Introduction

Amiodarone is a class III antiarrhythmic drug commonly used for life-threatening ventricular arrhythmias and atrial fibrillation. Its use is limited by a broad spectrum of toxicities affecting the lungs, thyroid, liver, skin, eyes, and nervous system. Chronic therapy, high cumulative doses, and individual susceptibility all contribute to toxicity. Early recognition is critical to prevent irreversible organ damage.

Case Presentation

A 68-year-old man with a history of persistent atrial fibrillation was treated with amiodarone 200 mg daily for the past two years. He presented with progressive dyspnea, dry cough, fatigue, and unintentional weight loss over three months. He denied fever or chest pain. His vital signs were normal except for a heart rate of 55 beats per minute. Physical examination revealed fine crackles in both lung bases and mild diffuse goiter.

Laboratory evaluation showed an elevated thyroid-stimulating hormone level of 12 mIU/L (reference 0.4–4.0) and a free thyroxine level at the lower limit of normal. Liver function tests were mildly elevated. Pulmonary function testing revealed a reduced diffusing capacity of the lungs for carbon monoxide. High-resolution computed tomography of the chest demonstrated bilateral interstitial infiltrates and ground-glass opacities. Bronchoalveolar lavage was performed and showed lymphocytic predominance, with no evidence of infection or malignancy.

Clinical Manifestations

Amiodarone toxicity can affect multiple organ systems. Pulmonary toxicity is the most serious and may present as interstitial pneumonitis, organizing pneumonia, or acute respiratory distress syndrome. Thyroid dysfunction is common, presenting as either hypothyroidism or hyperthyroidism. Hepatotoxicity ranges from mild transaminase elevation to cirrhosis. Other effects include corneal microdeposits, photosensitivity, peripheral neuropathy, and bradycardia.

Diagnosis

Diagnosis is largely clinical and requires a high index of suspicion in any patient on amiodarone with new respiratory, thyroid, or hepatic symptoms. Chest imaging, pulmonary function tests, and thyroid function panels are essential. For pulmonary toxicity, exclusion of infection and alternative causes is important; bronchoalveolar lavage may show lipid-laden macrophages or lymphocytosis. Liver biopsy may be needed in uncertain cases.

Management

The cornerstone of management is discontinuation of amiodarone, often in consultation with a cardiologist. For pulmonary toxicity, corticosteroids are commonly used, although evidence is limited. Thyroid dysfunction is managed according to the type: levothyroxine for hypothyroidism, and thionamides or perchlorate for hyperthyroidism. Hepatic toxicity typically resolves after drug withdrawal, but severe cases may require transplantation. Alternative antiarrhythmic agents should be considered for rhythm control.

Conclusion

Amiodarone toxicity is a complex clinical entity that can mimic other diseases. Routine monitoring of thyroid, liver, and pulmonary function is recommended during therapy. Prompt recognition and drug discontinuation are key to improving outcomes. Clinicians should maintain a low threshold for investigating symptoms suggestive of organ toxicity in patients on amiodarone.