SUN-351 - Euthyroxinemic Myxedema Coma on Amiodarone

Introduction/

Objective:
Myxedema Coma is a life-threatening manifestation of severe hypothyroidism that typically presents with an elevated thyroid stimulating hormone (TSH) and low Free thyroxine (Free T4). We present a rare case of clinically diagnosed myxedema coma despite a normal Free T4 and discordant thyroid function tests, demonstrating diagnostic challenges with amiodarone therapy and end stage renal disease (ESRD).

Case Presentation:
This is a 70-year-old female who presented to the emergency department with new-onset generalized weakness and altered mental status. Her past medical history was significant for subclinical hypothyroidism, ESRD on hemodialysis, and atrial fibrillation treated with amiodarone. Vitals showed hypothermia (93.4 F), bradycardia (49 bpm), normal blood pressure (117/72 mmHg). Blood glucose on arrival was in the 40s. Given these findings, a serum thyroid panel was obtained which revealed a TSH 142.367 uIU/L, Free T4 0.95ng/dL (0.89-1.76), and Free T3 64ng/dL (60-181). A validated scoring system (Popoveniuc) was applied and was highly suggestive of myxedema coma.

The patient was admitted to the intensive care unit for close monitoring. Despite a normal Free T4 level and given the known consequences of myxedema coma if left untreated, she was empirically treated with intravenous levothyroxine, oral liothyronine, intravenous steroids, and dextrose. Repeat thyroid studies the following day demonstrated improvement (TSH 33.954 uIU/mL and Free T4 1.48ng/dL) along with normalization of body temperature and heart rate. She eventually transitioned to oral levothyroxine prior to discharge and amiodarone was discontinued.

Discussion:
Myxedema coma remains a clinical diagnosis and may occur without classic laboratory findings. In this particular case, the co-presentation of markedly elevated TSH and a normal T4 may be explained by the known effect of amiodarone to suppress type 1 5’-deiodinase, leading to impaired peripheral conversion of T4 to T3. Additionally, ESRD may alter protein binding and affect thyroid hormone metabolism. These combined effects may cause functional hypothyroidism where serum thyroid hormone levels may not always reflect activity at the tissue level.

Conclusion:
This case highlights that myxedema coma can occur despite normal Free T4 levels in patients with ESRD and medications which can impair thyroid hormone metabolism. Additionally, laboratory values may underestimate clinical severity, as thyroid function tests may not reflect tissue-level thyroid hormone activity. For these reasons, the importance of early recognition and empiric treatment based on clinical suspicion remains critical to reducing morbidity and mortality.

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