Serum Sodium Concentration Changes Causes Delayed Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage.
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Hyponatremia following subarachnoid hemorrhage is associated with hypovolemia and is a cause of delayed cerebral vasospasm. The purpose of this study was to investigate whether a sufficient volume of infusion would decrease sodium disorders and delayed cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Twenty-six patients with aneurysmal subarachnoid hemorrhage were operated on within 24 hours after the onset, and positive water balance was maintained using crystalloid and/or colloid solutions for 2 weeks postoperatively. The patients were divided into the spasm group (8 cases) or no-spasm group (18 cases) depending on their cerebral blood velocity, clinical symptoms, and radiological findings. Although the maximal and minimal serum sodium concentrations of the no-spasm group (146±2.4mEq/l, 137±5.3mEq/l, respectively) remained within normal ranges, those of the spasm group (150±8.7mEq/l, 132±10.3mEq/l, respectively) fluctuated widely. The increase in the serum sodium concentration in the spasm group was frequently associated with excretion of hypotonic urine and loss of free water. Furthermore, the onset of vasospasm followed the decrease in serum sodium concentration in the spasm group. The perfusion volumes assessed by central venous pressure and the concentrations of serum total protein were comparable between the groups. We concluded that the delayed cerebral vasospasm could not be prevented in those patients whose serum sodium concentrations widely fluctuated even though hypovolemia was avoided. Since the cause of the increase in the serum sodium concentration is the excretion of the hypotonic urine in the early phase of subarachnoid hemorrhage, control of the urine osmolarity and the serum sodium concentration is important in preventing delayed cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
- 一般社団法人 日本救急医学会の論文
一般社団法人 日本救急医学会 | 論文
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