Effect of fludrocortisone in the management of hyponatremia after aneurysmal subarachnoid hemorrhage.

Abstract

Aneurysmal subarachnoid hemorrhage (aSAH) is associated with significant morbidity, particularly related to delayed cerebral ischemia (DCI). Hyponatremia, defined as a serum sodium level < 135 mmol/l, is a common complication of aSAH and is associated with the development of DCI. Fludrocortisone is used to decrease natriuresis and improve hyponatremia, but has failed to demonstrate a reduction in the frequency of cerebral vasospasm or DCI. Using the ProReSHA database, we retrospectively analyzed the impact of fludrocortisone on the development of DCI in patients hospitalized in neurocritical care unit after aSAH and presenting hyponatremia. Two hundred sixteen patients were included, 88 in the fludrocortisone group and 128 in the control group. DCI occurred in 35 (39.8%) patients in the fludrocortisone group and 34 (26.6%) in the control group (p = 0.058). Hyponatremia was significantly deeper in the fludrocortisone group than in the control group (median [interquartile range]: 130 [128-131] vs. 132 [131-133] mmol/l; p < 0.001), and lasted longer (6.0 [4.0-8.3] vs. 3.0 [2.0-5.0] days; p < 0.001). An ancillary analysis stratified according to the etiology of hyponatremia (cerebral salt wasting syndrome or syndrome of inappropriate secretion of antidiuretic hormone) also found no significant difference regarding DCI occurrence (33.3% vs. 44.6%; p = 0.238) but a significantly lower natriuresis in the cerebral salt wasting syndrome group (225 [187-308] vs. 293 [253-359] mmol/d; p = 0.01). Fludrocortisone did not prevent the development of DCI in patients admitted to a neurocritical care unit for an aneurysmal subarachnoid hemorrhage and presenting with hyponatremia. Effect of fludrocortisone in the management of hyponatremia after aneurysmal subarachnoid hemorrhage.