SUN-556 A Case of Fatal Amiodarone Induced Thyrotoxicosis

Abstract

BACKGROUND: Amiodarone is a class III anti-arrhythmic, which due to structural resemblance at the molecular level to thyroxine and high iodine content, is commonly associated with thyroid dysfunction. Amiodarone induced thyrotoxicosis (AIT) is classified into type 1 and type 2 differentiating between which is diagnostic challenge with delay in initiation of appropriate therapy leading to poor outcome. CASE: A 85-year old male is admitted with shortness of breath and palpitations. His past medical history was significant for paroxysmal atrial fibrillation, rhythm controlled on Amiodarone. On admission, vitals were normal with the exception of heart rate 120/min. Physical examination was significant for irregularly irregular pulse and a normal thyroid. EKG showed atrial fibrillation with rapid ventricular rate. Lab were consistent with thyrotoxicosis with TSH <0.010 (0.27 - 4.20 uIU/mL), Free T3 9.29 ng/dl (2.52 - 4.34 pg/mL), Free T4 5.86 (0.55-1.60 ng/dl), TSI 96% (<=122 %). Thyroid Doppler-sonography showed increased vascular flow to the left thyroid gland and Ultrasound imaging was consistent mild thyroid heterogeneity. A diagnosis of new-onset Amiodarone induced thyrotoxicosis (AIT) of indefinite/mixed type was established and Amiodarone was discontinued. Methimazole and Dexamethasone were started to treat mixed presentation of type 1 and type 2. In addition, Propranolol, Diltiazem and Esmolol infusion was added and titrated to maximal doses but he remained in persistent atrial fibrillation with rapid ventricular rate. When medical therapy failed, elective cardio-version was planned. However, the day prior to cardioversion, patient went into cardiac arrest. CPR was performed per ACLS protocol without return of spontaneous circulation. CONCLUSION: AIT can be divided in two type I/II. A mixed/indefinite form has been described in literature. It is imperative to differentiate between the subtypes of AIT to prevent potential delay in treatment. Ultrasound imaging is useful in determining the presence of Goiter as an underlying cause of AIT. It is hypothesized that in type 1 AIT there is an increased blood flow typical of hyperthyroidism. Radioactive iodine uptake is not utilized with recent amiodarone use, given the iodine content. Thionamides (Methimazole and propylthiouracil) are the drug of choice for type 1 AIT. A higher dose and longer duration of treatment is required, as iodine rich gland may not respond. Steroids (higher doses) are the mainstay of treatment for type 2 AIT. Thionamides have no role in the treatment of type 2 AIT. A mixed or indefinite often requires a complex approach to therapy with combination of steroids and thionamides. Total thyroidectomy may be considered as a therapeutic option in patients with resistant rhythm abnormalities secondary to amiodarone induced thyrotoxicosis.