ESA-SRB-AOTA 2019

Myxedema coma in a patient with subclinical hypothyroidism (#800)

Shui-Boon Soh 1 , Tunn-Lin Tay 1
  1. Changi General Hospital, Singapore

Myxedema coma (MC) is a rare manifestation of decompensated hypothyroidism, usually occurring in severe biochemical hypothyroidism. We describe an unusual case of myxedema coma in a patient with subclinical hypothyroidism.

A 55-year-old man with medical history of diabetes mellitus, hyperlipidemia, hypertension, chronic kidney disease and previous stroke was admitted for acute stroke. After 9 days of hospitalization, he was noted to have worsening drowsiness (Glasgow Coma Scale E4V1M4) as well as profound hypothermia (32.10C) and bradycardia (41 beats/minute). New or worsening stroke was ruled out on brain imaging. He was not on new rate-control cardiac medication. There were no clinical evidence of sepsis, pericardial/pleural effusions and intestinal obstruction. His free triiodothyronine (fT3) was 2.6pmol/L (2.6 – 5.7), free thyroxine (fT4) 10.75pmol/L (10-20), and thyroid stimulating hormone (TSH) 8.18mIU/L (0.4-4.0). Thyroid peroxidase and thyroglobulin antibodies were both negative. Electrolytes were normal, apart from mild hyperphosphatemia of 1.85mmol/L (0.65-1.65) which was in keeping with his chronic kidney disease. Inflammatory markers were not elevated. Synacthen test showed peak cortisol response of 557nmol/L. MC was diagnosed based on clinical ground. He was commenced on intravenous thyroxine (IV T4) 200mcg, with intravenous glucocorticoid and continuous cardiac monitoring. IV T4 was continued at 300mcg the next day. There was significant clinical improvement to IV T4 therapy – drowsiness improved and body temperature and pulse rate increased to 36.0-37.40C and 71-79 beats/minute respectively. IV T4 was subsequently converted to oral Levothyroxine 100mcg daily, and he was discharged to community hospital.                                                                       

It is unusual for MC to occur in subclinical hypothyroidism. This case illustrates the importance of looking beyond thyroid function test in the evaluation for MC which remains a clinical diagnosis. Though not clearly understood, this may be explained by the inability of circulating thyroid hormones to accurately reflect the true tissue bioavailability in some patients.

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