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Amiodarone is a class III antiarrhythmic drug commonly used for treatment and prevention of cardiac arrhythmias. It is associated with a number of side effects including thyroid dysfunction due to its high iodine content and direct toxic effects. In the United States, 3 to 5 percent of patients treated with amiodarone develop hyperthyroidism. 1 Amiodarone-induced thyrotoxicosis (AIT) is divided into 2 types. Type 1 is associated with increased synthesis of thyroid hormone, whereas type 2 is associated with excessive release of thyroxine (T4) and triiodothyronine (T3) from a destructive process. The diagnosis of thyroid storm is based upon clinical findings which are exaggerations of typical hyperthyroidism involving the central nervous, gastrointestinal, and cardiovascular systems. The most accepted criteria to diagnose thyroid storm was created by Burch and Wartofsky who introduced a scoring system in 1993. 2 It provided a criterion to grade severity of thermoregulatory, cardiovascular, and central nervous system dysfunctions with scores greater than 45 being highly suggestive of thyroid storm. Medical therapy for thyroid storm is centered on thionamides, glucocorticoids, and beta-blockers. Plasma exchange and thyroidectomy have been used in patients whose hyperthyroidism is refractory to aggressive medical therapy. In our case, thyroid artery ablation also was utilized when too ill to undergo surgical thyroidectomy.

Amiodarone-Induced Thyroid Storm Treated with Plasmapheresis and Thyroid Artery Ablation