MON-343 - Unmasking Severe Thyrotoxicosis Following Amiodarone Exposure: Refractory Atrial Fibrillation and Deep Venous Thrombosis Despite Anticoagulation.

Background:

Amiodarone is a common antiarrhythmic medication used for atrial fibrillation. It can affect thyroid functions with underlying iodine content or through direct toxicity. But how much is too much? We present a case of worsening thyrotoxicosis following exposure to amiodarone with refractory atrial fibrillation and deep venous thrombosis complications despite being on anticoagulants [1].

Methods:

Clinical data were obtained through retrospective review of electronic medical records, laboratory studies, and imaging findings. AI-assisted tools were used for grammatical editing; all content was reviewed and verified by the authors.

Clinical

Case:

66-year-old male with AFib on anticoagulant, cardiomyopathy, type 2 DM, and hypertension. Presented with shortness of breath and palpitations. He was found to be in atrial fibrillation with RVR and acute decompensated heart failure. Labs showed TSH with < 0.007 mIU/L (Ref: 0.45-4.5) with elevated free T4 3.7 ng/dL (Ref: 0.8-1.8), which suggests thyrotoxicosis.

Medical records revealed the patient was loaded with amiodarone for cardioversion despite having a suppressed TSH 0.004 uIU/ml ( Ref 0.47-5.00) and elevated freeT4 2.18 ( Ref 0.70-1.48). During hospitalization, thyroid functions further declined. Imaging showed a 4 mm TR4 isthmic nodule, with no evidence of Graves' disease.

The hospital course was complicated by upper extremity DVT despite therapeutic anticoagulants. He was started on methimazole and a beta-blocker with gradual improvement of symptoms and was transitioned to a different type of anticoagulant with a negative thrombophilia workup. After stabilization, he was discharged for continued medical management and close outpatient monitoring with reassessment following amiodarone discontinuation.

Discussion:

Amiodarone-induced thyrotoxicosis is divided into two forms: Type 1, due to iodine-induced hormone synthesis in an abnormal thyroid gland, and Type 2, due to destructive thyroiditis in a previously normal gland. Differentiating these is vital as management differs [2].

This case highlights the complexity of iodine excess with underlying thyroid disorders. Amiodarone may not have started the thyrotoxicosis, but it did exacerbate unrecognized hyperthyroidism [2]. Failure to review to recognize the cause will lead to anchoring diagnoses, which misdirect management[3,4].

Conclusion:
A baseline thyroid function test is essential prior to starting amiodarone. Failure to recognize pre-existing hyperthyroidism prior to amiodarone therapy may delay appropriate endocrine management and contribute to worsening thyrotoxicosis.

References :
1. Ross DS, et al. Thyroid. 2016;26(10):1343-1421.
2. Macchia PE, et al. Endotext. 2020.
3. Reddy V, et al. J Atr Fibrillation. 2017;10(1):1646.
4. Wu PY, et al. JCEM Case Rep. 2022.

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