Abstract
Clinical significance and pathogenesis of neurogenic hypernatremia were investigated in 38 patients with angiographically proven internal carotid artery (ICA) occulsion. Patients were classified into two groups : group A (died within 2 weeks) and group B (survived more than 2 weeks), and the changes of their sodium metabolism were studied. The number of cases indicating hypernatremia (serum Naγ150 mEq/l) in group A : 16/18 (89%) exceed group B : 1/20 (5%) (p<0.01). There was no significant difference between group A and B in the mean amount of the sodium administered, infusion volume, BUN, Ht and creatinine. In 16 cases of hypernatremia in group A, an increase in the K/Na ratio in urine and a decrease in sodium out-put/intake ratio to below 1 were observed from two days before the onset of hypernatremia. The hypothesis here is that an excessive reabsorption of sodium has led these results. However, no significant changes were observed in already-known hormons including aldosterone. And the CT findings show that low density area at the anterior portion of the IIIrd ventricle exists in all cases of group A (100%) while it exists in 4 to 20 cases of group B (20%).
The above results allow us to consider that neurogenic hypernatremia accompanied with acute phase of ICA occlusion brings about poor prognosis. As for the pathogenesis, the over-reabsorption of sodium related with the damage at the anterior portion of the IIIrd ventricle and with some unknown substance such as aldosterone were suggested.
