Endocrine Abstracts

Section 1: Case History: We present the case of a 52-year-old found female found collapsed at home with a three-week history of polyuria, polydipsia and lassitude on a background of primary hypothyroidism and non-insulin-dependent diabetes. On examination, she was hypothermic at 32°C, hypotensive (blood pressure 90/60 mmHg), newly oliguric, and had a Glasgow coma scale (GCS) of 9/15. A diagnosis of severe diabetic ketoacidosis (DKA) was made on admission.

Section 2: Investigations: Initial ABG demonstrated a pH <6.8 (7.35–7.45), ketones 6.0 mmol/l (<0.1), an undetectable bicarbonate level <5 mmol/l (22–26 mmol/L) and glucose 38 mmol/l. Admission thyroid function showed TSH 9.04 (0.27–4.2 mIU/l) and T4 16.3 (12–22 pmol/l). Initial estimated glomerular filtration rate (eGFR) was calculated at <15 ml/min (90–120 ml/min/1.73m²) which subsequently normalised. An autoimmune diabetes screen was sent given her ketosis. Computed tomography (CT) Brain was normal. CT thorax abdomen and pelvis ruled out acute pancreatitis and showed bibasal consolidation.

Section 3: Results and treatment: She was admitted to ICU, whereby she was intubated and ventilated for 5 days, treated with broad-spectrum antimicrobials, converted to subcutaneous insulin, and weaned off CVVHD. However, despite the resolution of her DKA, her GCS did not improve post-weaning of sedation. Repeat TFTs, five days off sedation, in the euglycemic state, showed a TSH 87 mIU/l, T4 6.1p mol/l and T3 <2.0 pmol/l (3.1–6.8 pmol/l). Alternative causes of metabolic encephalopathy were excluded. 20 micrograms(mcg) of intravenous triiodothyronine (T3) was given twice daily and titrated to a mid-normal T3 level. This resulted in improved GCS from 9 to 12/15 after three doses and complete resolution to 15/15 after eight doses. Anti-glutamic acid decarboxylase (anti-GAD) antibodies were positive at >2000 units/ml, confirming a diagnosis of latent autoimmune diabetes in adults (LADA). She was discharged home on oral L-thyroxine and a basal-bolus insulin regime.

Section 4: Conclusions and points for discussion: DKA precipitating a myxoedema coma is a rare phenomenon. It can present atypically compared to a classical myxoedema coma, without bradycardia or longstanding history of untreated hypothyroidism. Other expected features can be absent such as hyponatraemia which usually results from excess antidiuretic hormone and inadequate aquaresis. However, in this case, the corrected sodium was only mildly deranged, we suspect, due to her osmotic diuresis and severe kidney injury. Furthermore, hyperglycaemia is known to inhibit TSH secretion, which can mask the diagnosis. This case highlights the challenging diagnosis of myxoedema coma and how DKA can conceal clinical and laboratory features.