Endocrine Abstracts

Hyponatraemia is the commonest electrolyte abnormality in hospitalised patients and every published series has demonstrated that hyponatraemia is associated with increased mortality and substantial morbidity, including longer duration of hospital stay. The debate between the contribution between hyponatraemia and the causative condition to the increased mortality remains to be resolved, but increasing evidence points to an independent association with hyponatraemia. It is not clear whether all causes of hyponatraemia increase mortality; in particular, it is not certain whether the prognosis is better or worse in hyponatraemia due to SIADH or non-SIADH causes. The diagnosis of SIADH requires the distinction from hypovolaemic or hypervolaemic hyponatraemia, and the exclusion of glucocorticoid deficiency, and is helped by clinical alogorithms. Many patients with SIADH will see rapid resolution of hyponatraemia with treatment of the underlying cause – for instance SIADH due to pneumonia. However, chronic symptomatic hyponatraemia may need specific therapy. First line therapy recommended by most guidelines is fluid restriction, despite the absence of a firm evidence base, the difficulty in adherence, and well known predictors of clinical failure, such as UOsm >600 mOsm/kg. Second line treatments include demeclocycline, frusemide plus oral salt, urea and vasopressin receptor antagonists, of which only tolvaptan is licensed in Europe. All, with the exception of tolvaptan, lack prospective randomised trial evidence, and urea has no license or available preparation for clinical use. Tolvaptan is effective and has well documented guidelines to prevent overcorrection, but widespread use is limited by the high unit cost of the drug. Acute hyponatraemia (<48 h), particularly when associated with neurological irritation, carries a high mortality, and is associated with permanent neurological damage in survivors. Emergency elevation of plasma sodium is needed, and current recommendations are for the use of bolus hypertonic saline to ensure an elevation in pNa of 4–6 mmol/l in 4 h, with gradual elevation over the first 24 h of 8–12 mmol/l. Higher rates of rise should be corrected with IV dextrose, and/or dDAVP, to prevent osmotic demyelination.