Prophylactic management of excessive natriuresis with hydrocortisone for efficient hypervolemic therapy after subarachnoid hemorrhage

Abstract

Background and purpose: Hyponatremia caused by excessive natriuresis is common in patients with aneurysmal subarachnoid hemorrhage (SAH). Natriuresis decreases the total blood volume through osmotic diuresis and increases the risk of symptomatic cerebral vasospasm. In such patients, hypervolemic therapy is difficult to achieve without causing hyponatremia because sodium replacement provokes further natriuresis and osmotic diuresis. We examined the effects of hydrocortisone, which promotes sodium retention, in patients with SAH.

Methods: Twenty-eight SAH patients were randomized into 2 groups after direct surgery: group 1 patients without hydrocortisone treatment (n=14) and group 2 patients with hydrocortisone treatment (1200 mg/d for 10 days; n=14). Both groups underwent hypervolemic therapy by aggressive sodium and water replacement. The goal of the hypervolemic therapy was to maintain the serum sodium level >140 mEq/L and the central venous pressure (CVP) within 8 to 12 cm H2O.

Results: Group 2 demonstrated a lower sodium excretion (P<0.05) and higher serum sodium level (P<0.05) compared with group 1. Hyponatremia developed in 6 patients (43%) in group 1 and 0 patients in group 2 (P<0.05). Group 2 also demonstrated a lower urine volume, lower infusion volume (P<0.05) required for hypervolemic therapy, and higher CVP (P<0.05). Failure to maintain CVP was observed in 12 patients (86%) in group 1 and 3 patients (21%) in group 2 (P<0.05). Hydrocortisone caused no serious side effects.

Conclusions: Hydrocortisone clearly attenuates excessive natriuresis. Prophylactic hydrocortisone administration appears to have a therapeutic value in inducing hypervolemia efficiently after SAH.