Abstract
Hyponatremia after subarachnoid hemorrhage (SAH) is considered to correlate with salt wasting syndrome. The exact mechanism is still not understood, but brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) have been suspected as main factors. In the past few years, fludrocortisone has been advocated to inhibit natiruretics after SAH.
We examined BNP and ANP level at 2 different time periods (3 to 7 days, and 9 to 15 days) in 14 patients with spontaneous SAH. Patients were divided into 2 groups: controls (6 patients) and patients treated with fludrocortisone (8 patients). Without fludrocortisone all patients tended to develop hyponatremia, but with fludrocortisone most patients had normonatremia. In the former group, BNP were increased, but in the latter group both BNP and ANP level were decreased during the sub-acute stage except for hyponatremic cases. Fludrocortisone was effective to control salt loss, and may suppress BNP.
BNP is thought to be responsible for natriuresis. Therapeutic overhydration might cause an increase of both BNP and ANP.
