Endocrine Abstracts

67 year old lady presented to emergency department with general decline, osmotic symptoms and weight loss of 10 kg in the past 6 weeks, worsening over the past 10 days. She had been reviewed in weight loss clinic 6 months prior, however no aetiology was identified (normal glucose level at the time). No other systemic complaints. Past medical history was unremarkable except for a fracture of right ankle. She was hyperglycaemic with a mixed picture of Diabetic Ketoacidosis and Hyperglycaemic Hyperosmolar state. (pH 7.156, Bicarbonate 11.1, Ketones 6.4 mmol/l, Glucose 43.1 mmol/l, Calculated Serum osmolality- 371 mmol/l). Her initial sodium was 155 mmol/l. She was started on fixed rate intravenous insulin and fluids as per DKA/HHS protocols. She was noted to be polyuric (urine output >50 ml/kg /24 hours, with pale urine color) and hypernatremic which was attributed to severe hyperglycemia. DKA resolved by 12 hours of treatment and she was switched to variable rate insulin with fluids. She remained persistently hypernatremic despite normal range glucose levels and aggressive fluid resuscitation (and kept in positive fluid balance) and was managed in ITU. Her sodium rose progressively from 155 on admission to 178 mmol/l over 24 hours. She was reviewed by Endocrinology team at this point. Further investigations requested (paired osmolalities): Serum osmolality 345 mosm/kg, Urine osmolality 370 mosm/kg, Urine sodium 56 mmol/l, Serum sodium 171 mmol/l, Urea 4.1 mmol/l, Creatinine 53 micromol/l). Random cortisol (15:30-539 nmol/l), TSH 0.86 mIU/l, FT4 15.5 pmol/l, Prolactin 241 mIU/l, Estradiol 92 pmol/l, LH 6.5 IU/l, FSH 7.9 IU/l, C peptide 12 pmol/l (174-960). CT Head reported partial empty sella (MRI pituitary awaited). CT Pancreas ruled out pancreatic malignancy. Endocrinology team diagnosed possible vasopressin insufficiency based on hypernatremia with raised serum osmolality, inappropriate low urine osmolality with ongoing polyuria. A trial dose of Desmopressin 2 mg IV was administered following which the urine output dropped to almost nil, and sodium gradually improved from 155 mmol/l from 171 mmol/l. No further desmopressin doses were administered, polyuria/hypernatremia resolved. She was confirmed to have T1DM (low C-peptide levels, positive GAD and IA-2 Antibody). MRI pituitary showed thickened pituitary stalk and absence of bright spot. Aim of discussion is possible mechanism of this temporary vasopressin insufficiency following diabetic emergency management, as well discussion of MRI findings and persistent secondary hypogonadism.