Ades P E, Fabre M, Aesch B, Rieant J F, Buchet S, Lamotte C, Jan M
Agressologie. 1989 Jun;30(7):431-6.
Morbidity after aneurysmal subarachnoid hemorrhages is proceeding from many factors; ischemic etiology is underestimated and frequently thought to be vasospasm related only. Other undoubted mechanisms are in the setting of ischemic disorders after ruptured aneurysms. The management of these disorders is relevant of new calcium blockers. Early administration of prophylactically oral nimodipine, with temporary intravenous administration of the therapy after surgery or in the setting of delayed ischemic deterioration, were assigned to 36 patients with aneurysm surgery. Efficacy was judged on prevention and outcome of ischemic disorders at discharge and three months later using the Glasgow Outcome Scale. On all, twenty-nine patients were disabled from any etiology; twenty made full or improved recoveries at discharge; twenty-eight get independent conditions of life at 3 months. Fourteen patients have return to their pre-rupture activity. Twenty-two surgical patients (61%) set an undoubtly ischemic disability during any time of their hospitalization, but many etiologies were identified in majority of cases. Spasm is the main factor of stroke in only 6 patients, and one of the ischemic factors in 15 cases. Among these ischemic deteriorations, twenty improved or made full recovery at discharge and get independent life at 3 months. No death with spasm. These data support the assumption that vasodilatating is not the only mode of nimodipine action. Hypervolemia must be adjunct with nimodipine to prevent regional hypoperfusion.