Collignon Frederic P, Friedman Jonathan A, Piepgras David G, Pichelmann Mark A, McIver Jon I, Toussaint L Gerard, McClelland Robyn L
Department of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota, USA.
Neurocrit Care. 2004;1(4):441-8. doi: 10.1385/NCC:1:4:441.
Recent evidence suggests that magnesium may be neuroprotective in the setting of cerebral ischemia, and therapeutic magnesium infusion has been proposed for prophylaxis and treatment of delayed ischemic neurological deficit (DIND) resulting from vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH). We studied the association between serum magnesium levels, the development of DIND, and the outcomes of patients with SAH.
We studied 128 consecutive patients with aneurysmal SAH treated at our institution between 1990 and 1997 who had a serum magnesium level measured at least once during the acute phase of their hospitalization. Delayed ischemic neurological deficit was defined as severe (major focal deficit or coma), moderate (incomplete focal deficit or decreased sensorium without coma), or none.
There was no significant difference in mean, minimum, or maximum serum magnesium levels between patients with and without DIND (1.93, 1.83, 2.02 versus 1.91, 1.84, 1.97 mg/dL, respectively). Similarly, no difference was found in mean serum magnesium levels among patients with severe (1.94 mg/dL), moderate (1.92 mg/dL), or no DIND (1.91 mg/dL). Analyses of serum magnesium levels before (0-4 days following SAH), during (4-14 days following SAH), and after (greater than 14 days following SAH) the period of highest risk for vasospasm revealed no association with the development or severity of DIND. Permanent deficit or death resulting from vasospasm and Glasgow Outcome Scale score at longest follow-up were similarly unaffected by serum magnesium levels overall or during any time interval. Forty (31.5%) patients were hypomagnesemic (less than 1.7 mg/dL) during hospitalization, but no difference in outcome (p = 0.185) or development of DIND (p = 0.785) was found when compared to patients with normal (1.7-2.1 mg/dL) or high (greater than 2.1 mg/dL) magnesium serum levels.
We identified no relationship between serum magnesium levels and the development of DIND or outcome following aneurysmal SAH. Based on these data, magnesium supplementation to normal or high-normal physiological ranges seems unlikely to be beneficial for DIND resulting from vasospasm. However, no inference can be made regarding the value of therapeutic infusion of magnesium to supraphysiological levels.
最近的证据表明,镁在脑缺血情况下可能具有神经保护作用,有人提出静脉输注镁剂用于预防和治疗动脉瘤性蛛网膜下腔出血(SAH)患者因血管痉挛导致的迟发性缺血性神经功能障碍(DIND)。我们研究了血清镁水平、DIND的发生与SAH患者预后之间的关系。
我们研究了1990年至1997年在我院接受治疗的128例连续的动脉瘤性SAH患者,这些患者在住院急性期至少测量过一次血清镁水平。迟发性缺血性神经功能障碍被定义为严重(严重局灶性缺损或昏迷)、中度(不完全局灶性缺损或无昏迷的意识减退)或无。
发生DIND和未发生DIND的患者之间,血清镁的平均、最低或最高水平无显著差异(分别为1.93、1.83、2.02mg/dL与1.91、1.84、1.97mg/dL)。同样,严重DIND(1.94mg/dL)、中度DIND(1.92mg/dL)或无DIND(1.91mg/dL)的患者之间,血清镁平均水平也无差异。对血管痉挛风险最高时期之前(SAH后0 - 4天)、期间(SAH后4 - 14天)和之后(SAH后大于14天)的血清镁水平分析显示,其与DIND的发生或严重程度无关。血管痉挛导致的永久性缺损或死亡以及最长随访时的格拉斯哥预后评分同样不受总体血清镁水平或任何时间段血清镁水平的影响。40例(31.5%)患者在住院期间存在低镁血症(低于1.7mg/dL),但与血清镁水平正常(1.7 - 2.1mg/dL)或高(大于2.1mg/dL)的患者相比,其预后(p = 0.185)或DIND的发生(p = 0.785)无差异。
我们发现血清镁水平与动脉瘤性SAH后DIND的发生或预后之间无相关性。基于这些数据,将镁补充至正常或高正常生理范围似乎不太可能对血管痉挛导致的DIND有益。然而,对于静脉输注镁至超生理水平的价值无法得出结论。