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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
