SUN-417 - A Balancing Act in Stormy Seas : A Case of Toxic Nodular Goiter Complicated by Amiodarone Induced Thyrotoxicosis

Amiodarone is commonly used to manage atrial arrhythmias with rapid ventricular response (RVR) but in 6 – 10% of patients can cause amiodarone induced thyrotoxicosis (AIT). Type 1 AIT, caused by iodine-induced hyperthyroidism in the setting of pre-existing thyroid disease, is less common than type 2 AIT, caused by destructive thyroiditis. In thyrotoxic patients with life threatening arrhythmias, the risks of AIT with amiodarone should be balanced against the benefits of rhythm control. Here we present a case of a toxic nodular goiter complicated by AIT.

A 62 year old male with no known past medical history presented with bilateral lower extremity edema and progressive dyspnea. He was hypertensive and tachycardic, and found to have a large unilateral goiter on physical exam. Labs on admission showed thyroid stimulating hormone (TSH) < 0.01 mcU/ml, elevated free thyroxine (FT4) of 5.5 ng/dL, and free triiodothyronine (FT3) of 4.0 pg/ml. His EKG showed atrial fibrillation with RVR and echocardiogram confirmed heart failure with reduced ejection fraction, which progressed to cardiogenic shock requiring intubation and inotropic support. Thyroid ultrasound and CT of the neck confirmed a 7.3 cm left sided thyroid nodule with mass effect on the trachea. He was initially started on amiodarone for the atrial fibrillation which was held due to risk of inducing AIT once his thyroid function labs resulted and instead ablation was performed. He was started on methimazole, IV glucocorticoids, Lugol’s solution and cholestyramine to manage the thyrotoxicosis.

Initially, his FT4 and FT3 improved to 1.3 and 2.2, respectively. However, on day 8, the patient developed atrial fibrillation with RVR, for which amiodarone was restarted as other agents were contraindicated due to hypotension and acute kidney injury. Subsequently, his FT4 increased to 5.4, consistent with AIT. Cholestyramine was resumed and hydrocortisone and methimazole were uptitrated. After a multidisciplinary discussion, amiodarone was continued. Once the patient improved and was converted back to sinus rhythm, amiodarone was weaned off and he was discharged with methimazole. Radioactive iodine uptake was limited as he was exposed to CT contrast and amiodarone. However, thyroid stimulating immunoglobulin was negative, which supports the diagnosis of toxic nodular goiter for initial thyrotoxicosis.

This patient experienced thyrotoxicosis twice during this admission- the first from a toxic nodule, then AIT. Since the half-life of amiodarone is approximately 100 days, there is no benefit from stopping it immediately. Furthermore, since amiodarone inhibits T4 to T3 conversion, beta-adrenergic receptors, and possibly T3 receptors, discontinuing it might worsen the acute thyrotoxicosis. This case highlights the complexity of managing thyroid storm with life threatening arrhythmias and considers whether to continue amiodarone in AIT.

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