Hyponatremia in Patients with Subarachnoid Hemorrhage (A Study of Blood Volume).
- Author:
Seong Ho PARK
1
;
Ho Jin MYUNG
Author Information
1. Department of Neurology, College of Medicine, Seoul National University.
- Publication Type:Original Article
- MeSH:
Blood Volume;
Brain;
Central Nervous System;
Diagnosis;
Diuretics;
Humans;
Hyponatremia*;
Inappropriate ADH Syndrome;
Mannitol;
Natriuresis;
Plasma;
Seoul;
Serum Albumin;
Sodium;
Subarachnoid Hemorrhage*;
Tomography, X-Ray Computed;
Water
- From:Journal of the Korean Neurological Association
1986;4(1):78-85
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
This study was performed to account for the hyponatremic phenomenon in patients with subarachnoid hemorrhage (SAH) and to discuss the concept of SIADH which has been disputed as a responsible mechanism. The diagnosis of SAH was made by brain CT scans and the patients were managed under the protocol now being used in Seoul National University Hospital. Blood voulmes were measured in six hyponatremic (Na+<135mEq/L) patients with SAH, by using radioiodinated-human serum albumin (125-RIHSA) and claculating with Dilution Method. The same measurements were made in two control groups also. Group-I was composed of six subjects without SAH, who were given no diuretics and were neither fluid-restricted nor bed-ridden. Group-II comprised six eunatremic patients with SAH or ICH, who were managed under the same protocol as in the hyponatremic group. Mean blood volumes (ml/kg) of the hyponatremic group (RCV, 19.5+2.1; PV, 34.2+4.1; TBV, 53.7+4.2) were significantly contracted in comparison with both control groups. As for mean plasma and total blood volume, two control groups showed no significant difference statistically. Therefore the effect of mannitol on natriuresis and water excretion seemed negligible, if normal saline had been replaced as in the protocol. Considering the above findings, the remarkable contraction of blood volumes in the presence of hyponatremia in the patients with SAH could not be explained in the view of SIADH which is usually associated with increased blood volume. In conclusion the suggested mechanism of hyponatremia in SAH in this study seems the primary natriuresis with a resultant contraction of blood volume, which is probably caused by the damaged central nervous system. So, in the aspect of management of hyponatremia in the patients with SAH, both supplement of sodium and expansion of blood volume should be considered.
