ODP461 Amiodarone Induced Thyrotoxicosis With Severe Cardiac Disease Refractory to Medical Therapy and Plasmapheresis
Authors: Ravin Andrew , Figueroa Jonathan , Cheng Jennifer , Elmedani Sarah 
Published: November 2022

Introduction

Management of amiodarone induced thyrotoxicosis (AIT) presents the clinical challenge of differentiating between the two subtypes: Type I AIT, characterized by increased hormonal biosynthesis, and Type II AIT, a destructive thyroiditis since the treatment differs. We present a case of a patient with severe cardiac disease on long-term amiodarone who presented with thyrotoxicosis who was minimally clinically symptomatic despite significant biochemical thyroid function abnormalities and refractory to all medical interventions, including plasmapheresis, ultimately requiring total thyroidectomy.

Case Description

An 82 year-old-male with severe cardiac disease including coronary artery disease with prior CABG, EF of 25-30% with ICD, and atrial fibrillation on amiodarone, presented to the hospital due to palpitations and multiple shocks delivered by patient's ICD. EKG revealed atrial fibrillation and the ICD demonstrated episodes of sustained ventricular tachycardia. The Burch-Wartofsky score was 25. He had palpitations, tremors, and atrial fibrillation but no thyromegaly, thyroid bruits or thyroid eye disease. Thyroid function testing was TSH &lt;0. 01 ulU/mL (Normal 0.3 - 4.5 ulU/mL), FT4 5.29 ng/dL (Normal 0.5- 1.26 ng/dL). Thyroid ultrasound showed multiple sub-centimeter nodules without increased vascularity. Since patient had characteristics of both AIT subtypes, patient was started on treatments for both including hydrocortisone 100 mg TID, Lugol's Iodine 10 drops TID, methimazole 20 mg QID, propranolol 20 mg QID, cholestyramine 4g BID, and lithium 300 mg TID. Despite extensive medical management, the patient's thyroid levels remained grossly elevated with FT4 nadir of 4.37 ng/dL. Plasmapheresis was initiated every 1-2 days for a total of 6 treatments and the patient's FT4 improved to 3.52 ng/dL before increasing again. During this treatment period, the patient remained relatively asymptomatic but had severe cardiac disease which further complicated the urgency for thyroidectomy. Ultimately, he underwent a total thyroidectomy that caused the resolution of the thyrotoxicosis. He was started on levothyroxine and subsequent pathology revealed multi-nodular goiter with lymphocytic thyroiditis.

Discussion

This challenging case of amiodarone induced thyrotoxicosis in a patient with severe cardiac disease, refractory to extensive medical therapy including plasmapheresis and requiring total thyroidectomy, highlights the difficulty in management of AIT. Management of refractory AIT involves differentiating between the two clinical subtypes with the goal of expediently achieving a euthyroid state to avoid severe cardiac complications and mortality. This case was particularly challenging since our patient had relatively stable clinical status despite chemical thyrotoxicosis with characteristics of both subtypes of AIT. It was challenging to optimize a patient's thyroid levels prior to thyroidectomy, due to severe cardiac disease and persistent thyrotoxicosis. Ultimately, our patient was refractory to medical treatments for both AIT subtypes and plasmapheresis. The resolution of thyrotoxicosis was not achieved until he underwent total thyroidectomy

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