Prevention of delated ischemic neurological deficits (DIND) following subarachnoid hemorrhage (SAH) has been tried by the surgical removal of subarachnoid hematoma as much as possible during the operation and continuous drainage of the cerebral ventricle and cistern postoperatively. Concomitant pharmacotherapies with administration of mannitol, glyceol, steroid, nizophenon, low-molecular dextran, barbital, Ca++ antagonists, or antithrombocyte agents as well as management of Hypervolemia and

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... rtension have been used and the clinical outcome is generally improving. In spite of the above treatments, however, prognosis is still infavorable in some cases. Delayed vasospasm is thought to be caused by an angiospastic substance produced in the course of decomposition of the shed blood. We administered urinastatin and gebaxate medilate, polyvalent anti-enzymatic agents, immediately after SAH and our clinical observation has led to the impression that the treatment could prevent DIND in the patients. Methods and results: This study involved 36 patients who were admitted to our hospital without delay after the onset of SAH during the period of April 1986 to October 1987. 200,000 U/day of Urinastatin 1,000 mg/day of gabexate mesilate were administered by intravenous drip infusion for 10 days to three weeks starting immediately after SAH. As a result, none of the 36 cases developed DIND postoperatively. It has been considered that direct operation is indicated for cases of Grade I-III at anytime, but not for Grade IV in the period of five to 10 post-SAH days because of the occurrence of postoperative vasospasm. We ignored these limitation on direct operation in all case and experienced no occurrence of DIND. Therefore, the preventive administration of urinastatin and gabexate mesilate seemed to be very effective. This therapy was, however, ineffective in patients who had had apparent DIND prior to the treatment. There were no side effects of the administration of urinastatin and gabexate mesilate. Discussion: The elucidation of how such preventive administration of polyvalent anti-proteinases prevents the occurrence of DIND must wait for further investigations. Nevertheless, the mechanism seems to involve the effects on stabilizing the membrane, protecting the tissue from disintegration, inhibiting free radical reaction, and preventing micro-thrombopoiesis.