Endocrine Abstracts

Introduction: Hyponatraemia is a common cause of morbidity and mortality affecting 15–28% of inpatients. Tolvaptan is a competitive vasopressin 2 antagonist licensed to treat hyponatraemia secondary to the syndrome of inappropriate anti-diuretic hormone secretion (SIADH). There has been concern that tolvaptan treatment may lead to rapid overcorrection of sodium in a minority of patients, thus potentially leading to osmotic demyelination syndrome.

Methods: We conducted a retrospective case note audit of tolvapatan use from May 2010 to September 2014.

Results: Seventeen patients were identified as having been prescribed tolvaptan; eight were males, nine were females (mean age 78.6 years±8.5 S.D.). One male patient had a diagnosis of heart failure; the remaining 16 patients had a diagnosis of SIADH. The starting dose of tolvaptan was 15 mg in 16 patients; however, one patient was admitted on 60 mg. The mean sodium prior to starting treatment was 118.7 mmol/l. The mean sodium 48 h post prescription was 125.8 mmol/l. 12 out of 17 patients (71%) had appropriate investigations (cortisol, TSH, osmolalities, and urinary sodium) prior to prescription. Two out of 17 patients (12%) had adequate serum sodium monitoring at recommended 6 h intervals, per BNF guidance, between 0 and 48 h after starting tolvaptan. Three out of 17 patients (17%) exceeded the recommended limits of sodium change. There was however no neurological sequelae to suggest osmotic demyelination.

Conclusions: Tolvaptan is efficacious for the treatment of hyponatraemia. There were no documented episodes of harm from rapid sodium overcorrection in our sample size. The potential for over correction can be minimised by vigilant monitoring and anticipatory corrective action. A model for optimisation of serum sodium monitoring on an in-patient basis is suggested involving careful coordination between pharmacy, laboratory medicine, and medical teams.