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Endocrine Abstracts (2023) 90 EP1045 | DOI: 10.1530/endoabs.90.EP1045

ECE2023 Eposter Presentations Thyroid (128 abstracts)

Myxoedema Coma, Life Threatening with Multiple Exacerbating Factors, Presenting with Bradycardia and Hypoglycaemia, Rare Interesting Experience with Bizarre Hormonal Imbalances

Mohammed Alfahal 1 , Maria Omer 2 , Omer Abdalla 3 , Gideon Mlawa 4 & Mustafa Taha 5


1London North West University Healthcare NHS Trust, London, United Kingdom, 2Royal Liverpool University Hospital, United Kingdom, 3National Ribat University, Internal Medicine, Khartoum, Sudan, 4Queen’s Hospital, Acute Medicine, Endocrinology, Romford, United Kingdom, 5University of Khartoum, Khartoum, Sudan


A 91-year-old lady presented with bradycardia ‘HR ~36, she was alert and conscious initially. Soon after the initial assessment, she was found unresponsive; with blood glucose of 0.8 mmol/l; bradyapnoec; BP 151/59; GCS 5/15; temp ‘32.8°C’. She was aroused after resuscitation with intravenous Dextrose, GCS 15/15 with an element of confusion, the temperature did not exceed 34.9°C despite active warming. The patient looked in a low mood, barely audible, with bilateral reactive constricted pupils and hyporeflexia. The face was velvety and dry. She has hypothyroidism, AF on amiodarone, osteoporosis and multiple joint replacements. ECG showed atrial fibrillation with a slow ventricular response, low amplitude waves and QTc (469ms).

Initial investigation: Normal T4 and elevated TSH. INR 1.4 (on warfarin). Elevated creatinine. K+6.3; Na+ 123 mmol/l. Diagnosis of myxoedema coma was based on refractory hypothermia, AF with slow ventricular response, wide pulse pressure, hyporeflexia and hypoglycaemia with partial response to IV glucose. Liothyronine (T3) 80 mg-IV administered one hour after hydrocortisone 200 mg IV. Six hours after T3 administration, the core temperature increased to 36.6°C, the heart rate went up to 80 before settling at 60 bpm, QTc shortened to a normal range (410ms) and the patient regained consciousness and was communicating clearly.

Discussion: Myxedema coma reported in patients with undiagnosed hypothyroidism (1) and patients on levothyroxine as in amiodarone-induced myxedema coma (2) In this case it was multifactorial with amiodarone being a chief trigger. Omeprazole could be a contributory factor (3). Amiodaron inhibit conversion of T4 to T3 (5). With short half-life of the T3 in comparison to T4 and the very long half-life of amiodarone, serum-free T3 levels expected to decline soon with a single dose of Liothyronine - even after stopping the amiodarone. Causes of hyponatremia other than severe hypothyroidism was considered (4). Hyponatraemia, hyperkalaemia and hypoglyceamia indicate possible hypo-adrenal state

Conclusion: The threshold to suspect myxoedema coma should be lower in patients with a background of hypothyroidism; on amiodarone or with the following (bradycardia/bradypnea/hypothermia/hypoglycaemia) Heart rate, core body temperature, level of consciousness and respiratory rate are good parameters of response to thyroxine. When Amiodarone triggers myxoedema coma, continued T3 therapy with low doses may give better results than T4 therapy as the amiodarone effect on T4 conversion continues for a long time after discontinuation of therapy. Many factors should be considered to determine the correct dose of IV Liothyronine including age, weight, cardiovascular risk factors and metabolic demands.

Volume 90

25th European Congress of Endocrinology

Istanbul, Turkey
13 May 2023 - 16 May 2023

European Society of Endocrinology 

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