Zhongguo cuzhong zazhi (Aug 2022)
血糖波动对动脉瘤性蛛网膜下腔出血后迟发性脑缺血及30天死亡的影响 The Impact of Blood Glucose Fluctuation on Delayed Cerebral Ischemia and 30-day Mortality in Aneurysm Subarachnoid Hemorrhage
Abstract
目的 探讨血糖波动与动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,aSAH)患者发生迟发性脑缺血(delayed cerebral ischemic,DCI)及30 d死亡的关系。 方法 回顾性收集并分析aSAH患者的临床资料。连续收集患者14 d空腹血糖水平并按其特征分为4组:稳定组(第1天<7 mmol/L,2~14 d均<10mmol/L)、不稳定组(第1天<7 mmol/L,2~14 d至少1次≥10 mmol/L)、控制良好组(第1天≥7 mmol/L,2~14 d均<10 mmol/L)和控制不良组(第1天≥7 mmol/L,2~14 d至少1次≥10 mmol/L),采用单因素和多因素分析探索血糖波动对患者发生DCI和30 d全因死亡的影响。 结果 研究共纳入341例患者,其中血糖稳定组212例,不稳定组23例,控制良好组62例,控制不良组44例。单因素分析显示,4组的DCI发生率差异有统计学意义(P=0.043),其中不稳定组DCI发生率最高(39.13%),其次是控制不良组(29.55%)、稳定组(17.92%)和控制良好组(17.74%);30 d全因死亡率差异也有统计学意义(P<0.001),其中控制不良组死亡率最高(15.91%),其次是不稳定组(13.04%)、控制良好组(6.45%)和稳定组(1.42%)。多因素logistic回归分析显示,血糖控制不稳定(OR 6.032,95%CI 1.941~18.747,P=0.002)和控制不良(OR 2.889,95%CI 1.247~6.691,P=0.013)是aSAH患者发生DCI的危险因素,同时,血糖控制不稳定(OR 14.033,95%CI 1.971~99.921,P=0.008)和控制不良(OR 19.723,95%CI 3.597~108.143,P=0.001)也是aSAH患者30 d全因死亡的危险因素。 结论 aSAH患者血糖控制不稳定或控制不良与DCI和30 d死亡相关。 Abstract: Objective To clarify the relationship of blood glucose fluctuation and delayed cerebral ischemia and 30-day mortality in aneurysmal subarachnoid hemorrhage (aSAH) patients. Methods The data of aSAH patients were collected and retrospectively analyzed. Continuous 14-day fasting blood glucose level was collected and patients were divided into four groups: stable (Day 1, <7 mmol/L; Day 2-14, all <10 mmol/L), unstable (Day 1, <7 mmol/L; Day 2-14, at least once ≥10 mmol/L), well-controlled (Day 1, ≥7 mmol/L; Day 2-14, all <10 mmol/L) and bad-controlled (Day 1, ≥7 mmol/L; Day 2-14, at least once ≥10 mmol/L). Univariate and multivariate analysis were used to analyze the impact of glucose fluctuation on delayed cerebral ischemia and 30-day all-cause mortality. Results A total of 341 patients were included, with 212 cases in stable group, 23 in unstable group, 62 in well-controlled group and 44 in bad-controlled group. The incidence of delayed cerebral ischemia among the four groups as follows: the highest incidence was 39.13% in unstable group, then 29.55% in bad-controlled group, 17.92% in stable group and the lowest was 17.74% in well-controlled group, with statistical difference (P=0.043). 30-day all-cause mortality as follows: the highest mortality was 15.91% in bad-controlled group, then 13.04% in unstable group, 6.45% was in well-controlled group, and the lowest was 1.42% in stable group, with statistical difference (P<0.001). Logistic regression analysis showed that unstable and bad-controlled blood glucose were risk factors of delayed cerebral ischemia occurrence (OR 6.032, 95%CI 1.941-18.747, P=0.002; OR 2.889, 95%CI 1.247-6.691, P=0.013) and 30-day all-cause mortality (OR 14.033, 95%CI 1.971-99.921, P=0.008; OR 19.723, 95%CI 3.597-108.143, P=0.001) in aSAH patients. Conclusions The unstable and bad-controlled blood glucose levels in aSAH patients were associated with delayed cerebral ischemia and 30-day mortality.
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