Magnesium als profylaxe voor vasospasmen en ‘delayed cerebral ischemia’ bij subarachnoïdale bloedingen

Background: About 1 in 4 patiënts with subarachnoid hemorrhage (SAH) suffer from ‘delayed cerebral ischemia’ (DCI) between days 2-14 after onset. DCI is a major cause of morbidity and mortality, it is thought to be responsible for up to half of death and disability among SAH-patients. Cerebral vasospasm is a substantial contributor to it’s occurence. Treatment with magnesium in addition to the usual treatment with nimodipine has shown promising results on the incidence of vasospasm and DCI in a number of studies. Therefore, as of May 2005, all SAH-patients in the Isala klinieken in Zwolle have been treated with a combination of magnesiumsulfate and nimidopine. The goal of this study is to examine whether this combined treatment has resulted in a decrease in cerebral vasospasm and DCI as compared to treatment with nimodipine alone. Methods: A total of 91 patiënts with non-traumatic, aneurysmal SAH, who underwent surgery and were subsequently admitted to the intensive care unit in the Isala klinieken were included. 45 patients received nimodipine only, 46 received treatment with both magnesiumsulfate and nimodipine. Transcranial dopplers ultrasonography was performed as a daily routine for the monitoring of vasospasm, defined as mean cerebral bloodflow velocities exceding 120 cm/s. DCI was defined as a decrease in EMV-score of two points or more, or the development of focal neurological deficits during admission. Occurence of these study endpoints in both groups was compared using a chi-square test. Logistic regression models were used to adjust for other patiëntcharacteristics. Time of onset of vasospasm in both groups was compared with Kaplan-Meier analysis. Results: Vasospasm during admission occurred in 25 (54%) patients who received magnesiumsulfate and nimodipine and in 24 (52%) patients who were treated with nimodipine alone. (p=0.75). A two point decrease in EMV occured in 16% vs. 17% (p=0.94) and focal neurological deficits in 30% vs. 20% (p=0.34), respectively. In regression analyses magnesium suppletion did not play a significant role in the occurence of either vasospasm or DCI. Finally, in a Kaplan-Meier analysis, the moment of occurence of vasopasm in both studygroups also did not differ significantly. Conclusion: In this study, supplementing patients with magnesium did not influence the development of vasospasm or DCI. Thus, there seems to be no place for magnesium in the treatment of patients with a SAH.