In the scope of a late intervention policy on ruptured intracranial aneurysms, on D.+12 on an average, we first used tranexamic acid, at moderate doses: 3 g orally or 1.5 g intravenously per day. We, subsequently, added nimodipine, usually 240 mg orally per day or 2 mg intravenously per hour. The medical treatment consisted of amply sufficient hydration, and in systematic and regular administration of analgesics and sedatives. Hypotension was absolutely avoided; if necessary, an antihypertensive treatment was prescribed very cautiously. Phenytoin was regularly given. In the present study, we try to answer the following questions: (1) Can we confirm that the preventive action of tranexamic acid remains as effective, when doses, markedly lower than usually recommended, are used? (2) Does nimodipine prevent the increase of pre-operative ischaemic complications, which should be expected when tranexamic acid is administered? Amongst 101 patients with SAH of proven aneurysmal origin, 84 were treated with tranexamic acid and nimodipine. In 25 patients, an aneurysm was not visualised; 21 received this treatment. For several reasons, only a retrospective study was possible, to evaluate the results of our antifibrinolytic and calcium-blocking therapies, on rebleeding and pre-operative delayed ischaemia. We compared, therefore, similar cases from the literature, with our own cases, taking into consideration the clinical grades, the days of admission and of intervention, the moment of rebleeding and of delayed pre-operative ischaemia, etc. The following impressions emerge: (1) same effectiveness of moderate doses of tranexamic acid; (2) no increase of pre-operative delayed ischaemic complications, in comparison with patients not receiving antifibrinolytics but nimodipine; (3) important role of a devastating initial bleed and of operative complications; (4) difficulty of avoiding rebleeding at D.0, whatever the therapeutic measures, medical and/or surgical.
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