Endocrine Abstracts

A 58-year old previously independent man with background of poorly-controlled hypothyroidism, T2DM, hypertension, ischaemic cardiomyopathy, and CKD presented to hospital feeling generally unwell, with a dry cough. His regular medications included anti-hypertensives, L-thyroxine 50 μg daily, linagliptin, insulin, aspirin, atorvastatin, and thiamine. On admission, the TSH was 83 mIU/l, free T4 6.5 pmol/l and free T3 was 1.9 pmol/l; four months earlier, the TSH was 58 mIU/l. He was noted to have staphylococcal septicaemia and acute kidney injury; bacterial endocarditis was excluded. He developed a pruritic, maculopapular rash that was thought due to dry skin. There was a history of non-compliance with L-thyroxine. Despite increasing the dose to 150 μg od, the TSH continued to rise to >100; the free T4 rose to 14.7, but the fee T3 was 2.0. Over the next two weeks, he became more confused, hypothermic, had a respiratory arrest and was admitted to ITU. Infective and paraneoplastic causes of encephalopathy were excluded. A diagnosis of myxoedema coma was made: L-thyroxine 200 μg was administered daily via a nasogastric tube along with IV liothyronine 10 μg 8-hourly; the total daily dose of hormone was based on weight. IV hydrocortisone was commenced until normal adrenal function was confirmed. TSH was monitored every 48 hours until reduction was noted (it halved every 48 h), then weekly. Improved thyroid function was allied to improvement in consciousness, body temperature, blood pressure and renal function. He was moved to a general ward where he able to make a good recovery, including resolution of his dermopathy. Thyroid hormone replacement was then maintained on L-thyroxine 175 μg od alone. This case illustrates how myxoedema coma may occur following a non-thyroidal illness on a background of hypothyroidism. We believe this was due to reduced conversion of T4 to T3 due to sepsis, leading to myxoedema with reduced absorption of L-thyroxine, setting up a cycle that led to myxoedema coma. This case also illustrates the protean manifestations of severe hypothyroidism. Patients with encephalopathy should be screened for hypothyroidism and thyroid function closely monitored if conscious level deteriorates in patients with pre-existing hypothyroidism.