On the basis of the concept of central salt wasting syndrome, hypotonic dehydration due to sodium-diuresis is considered to be a cause of cerebral vasospasms. To treat hyponatremia found in the acute stage of ruptured cerebral aneurysm, when sodium is solely supplemented, a large volume of infusion is required because of acceleration of sodium excretion. This makes treatment difficult in many cases. Hence, paying attention to the sodium balance in the acute stage of subarachnoid hemorrhage, we examined the effect of fludrocortisone acetate, a mineralocorticoid which accelerates resorption of sodium in the renal tubules on the sodium balance.
The subjects were 25 patients with ruptured cerebral aneurysm who underwent radical operation within 2 days after onset. They were allocated into fludrocortisone acetate (0.3mg/day) administration group (N=10) and no administration group (N=15) and at random. During the course of administration, infusion was performed actively using water balance and CVP as indexes. Sodium in serum and urine was continuously monitored, and a sodium balance sheet was made.
In the no administration group, the sodium balance tended to be negative from the third day after onset, accompanied by urine volume increase. In the fludrocortisone acetate administration group, decreased sodium excretion in urine was observed and the water balance was easily corrected. In addition, the prevalence of symptomatic cerebral vasospasms tended to be low.
In the acute stage of subarachnoid hemorrhage, the water and sodium balances tend to be negative from the third day after onset, and patients become dehydrated. When this state lasts a long time without correction, hyponatremia and symptomatic cerebral vasospasms occur easily. To avoid this state, administration of fludrocortisone acetate appeared to be effective.
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