Cerebral aneurysm: Electrolytes

Aneurysmal subarachnoid hemorrhage occurs in approximately 1 per 10,000 persons in the United States every year, accounting for 5–15% of all strokes. The overall case fatality of all‐cause SAH is as high as 50%. Aneurysmal SAH carries a 30-day mortality rate of 45%. Of those who survive, nearly 1/3 suffers significant and permanent neurological disability.

Cerebral vasospasm remains a major cause of death and disability in patients who experience subarachnoid hemorrhage (SAH) from a ruptured cerebral aneurysm. Despite nearly 50 years of research, there remains a paucity of effective therapies to prevent or reverse this condition. Other major complications include: re-bleeding, hydrocephalus, cardiopulmonary dysfunction, and electrolyte disturbances; of note, non-neurological complications of SAH develop in more than half of patients.

Electrolyte disturbances

SAH is frequently accompanied by hyponatremia, hypokalemia, hypocalcamia, and hypomagnesemia. Hyponatremia develops in approximately 30% of cases as a result of either the cerebral salt wasting (CSW) syndrome or the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The cerebral salt wasting syndrome is thought to be caused by the secretion of brain and atrial natriuretic hormone, which leads to a negative sodium balance, hyponatraemia, and intravascular volume depletion.

Apart from infusions of normal saline (or rarely hypertonic saline) to maintain euvolemia, therapeutic options for the cerebral salt wasting syndrome are limited. Some studies have shown that the administration of fludrocortisone and hydrocortisone can prevent or reduce intravascular volume depletion and decreased the incidence of negative sodium balance.

SIADH is accompanied by retention of excess free water. Stringent fluid restriction would appear to be the treatment of choice; however, salt-containing infusions are usually used during SAH to ensure a normal to high intravascular volume.