Endocrine Abstracts

Hyponatraemia is the commonest electrolyte abnormality observed in clinical practise. It is a potential cause of substantial morbidity and mortality. Drug history, fluid volume status in addition to serum and urine biochemistry is essential for optimal management.

We report a case of a 50-year-old female with known psychosis admitted to the Mental Health Unit and treated with Citalopram, Mirtazepine, Risperidone, Clonazepam and Procyclidine. Admission plasma sodium was 125 mmol/l.

During admission she was noted to be drinking large amounts of fluids. Eight days later she had a respiratory arrest. Respiratory rate was 6 breath per minute and GCS 3/15. She was intubated, infused 1.5 l 0.9% saline i.v. and a CT brain scan performed. The latter demonstrated extensive cerebral oedema. Sodium on arterial blood was 99 mmol/l.

On admission to ITU plasma sodium was 103 mmol/l, urine osmolality 76 mOsmol/kg, plasma osmolality 223 mOsmol/kg and urine sodium 13 mmol/l. Renal, thyroid and adrenal function were normal.

After 5 h on fluid restriction in ITU, her sodium rose from 103 to 115 mmol/l. She was started on 5% dextrose 500 ml/h. Retrospectively, fluid balance charts showed urine output of 1 l/h and an 11 l deficit over 17 h. Her plasma sodium was 135 mmol/l at that stage.

Throughout ITU admission her GCS remained 3/15 and pupils were fixed and dilated. Brainstem death was confirmed 48 h post admission to ITU.

The most likely cause of hyponatraemia in this case is a combination of psychogenic polydypsia with anti-psychotic-induced SIADH. Cerebral oedema is the likely cause of the respiratory arrest. Pontine demeylination due to rapid correction of plasma sodium is a likely cause of brainstem death.

This case highlights the challenges in management of acute severe multi-factorial hyponatraemia. It also emphasizes importance of regular sodium and fluid balance evaluation on patients receiving multiple agent therapy for mental health disorders.