Hyponatremia in acute intracranial disorders: cerebral salt wasting

Hyponatraemia is a frequent finding in the course of an acute intracranial disease, especially after a subarachnoid haemorrhage. The fall in plasma sodium concentration is usually mild and not below 124 mmol/l but may reach dangerously low levels with serious neurological complications. In the early 1950s the cause of the hyponatraemia was believed to be primarily excessive natriuresis and therefore named 'cerebral salt wasting'. After the description of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) this was favoured as the most likely explanation. Only in recent years has it become evident that many hyponatraemic patients with acute brain disease are actually hypovolaemic. This is compatible with the original diagnosis of cerebral salt wasting. The increased plasma concentrations of natriuretic peptides are likely to mediate the increased natriuresis. Cerebral salt wasting can be treated with a simple regimen of water and salt suppletion. If needed a mineralocorticoid like fludrocortisone can be given to increase renal tubular sodium reabsorption.