Endocrine Abstracts

This case describes a 23-year-old male with known epilepsy, who was admitted to hospital with generalised tonic-clonic (GTC) seizures and acute severe hyponatraemia. He had been feeling generally unwell for two days, but had not doubled his steroids. He has panhypopituitarism due to Langerhans’ histiocytosis, including arginine vasopressin deficiency (AVP-D). His medication included antiepileptics, hydrocortisone, (nasal) desmopressin (DDAVP), levothyroxine and topical testosterone. He was intubated and transferred to the intensive care unit (ICU) upon having further GTC seizures and Type 2 Respiratory Failure with consequent acidosis. Serum sodium was 113 mmol/l, urine osmolality 691 mOsm/kg and urinary sodium 70 mmol/l; renal profile and serum glucose were normal. Cerebral oedema was evident on CT. Hypertonic (2.7%) saline, 150 ml, was given as an intravenous bolus, causing a rise of only 3 mmol/l. Therefore, a further 150 ml bolus of hypertonic saline was given. DDAVP was delayed to avoid further reduction in serum sodium, but the urine output rose rapidly (>300 ml/h) and was followed by a rise in serum sodium to 129 mmol/l. The reinstitution of DDAVP 1 mg SC led to a fall in serum sodium to 124; the rise in serum sodium was more than 8 mmol/l in 24 hours, a cause for concern. This complex case illustrates the challenges with managing acute hyponatraemia in AVP-D. The presence of cerebral oedema with seizures may suggest rapid occurrence of hyponatraemia. The major threat to health was worsening of this oedema with risk of coning and therefore the aim of treatment should be about this. Traditional concern about rapid correction leading to osmotic demyelination syndrome (ODS) has been questioned by a recent retrospective study, which showed more rapid correction to be associated with lower mortality compared to slower change and poor correlation with ODS (1). The urine osmolality showed that DDAVP was still therapeutically present, but the urine sodium suggested inadequate amount of steroid for physiological stress; the hyponatraemia was probably due to continued use of DDAVP without appropriate increase in steroid replacement. Nevertheless, restarting DDAVP should not be delayed beyond 24 hours from the last dose and should be restarted as soon as urine out output exceeds 100 ml/h. Close monitoring of urine output as well as other physiological parameters behove management in a critical care setting (2).