Mowery Nathan T, Gunter Oliver L, Guillamondegui Oscar, Dossett Lesly A, Dortch Marcus J, Morris John A, May Addison K
Department of Surgery, Wake Forest University, Winston-Salem, North Carolina 27157, USA.
J Trauma. 2009 Jan;66(1):145-51; discussion 151-3. doi: 10.1097/TA.0b013e3181938c5e.
Both hyper- and hypoglycemia have been associated with poor outcome in traumatic brain injury (TBI). Neither the risks nor benefit of tight glucose control (goal range, 80-110 mg/dL) have been documented in the TBI population.
To analyze whether densely collected blood glucose data, using a computerized algorithm, to maintain tight glycemic control will reveal significant differences in blood glucose control between survivors and nonsurvivors in patients with TBI.
From October 2005 to April 2006, all ventilated, critically ill surgical patients with TBI Abbreviated Injury Scale score of >or=3 were placed on an automated, euglycemia protocol with every 2-hour blood glucose sampling. Mortalities within 24 hours were excluded. The protocol calculates the insulin rate using a linear equation (rate = blood glucose - 60[M]). M is an adapting multiplier and used here as a marker for insulin resistance (IR).
Of 1,636 trauma intensive care unit admissions 160 patients, (median Injury Severity Score 34, mortality 13.1%) had 10,071 samples collected. Median glucose 115.6 mg/dL, with 41% of values between 80 and 110 mg/dL, 81% between 80 and 150 mg/dL, and 0.3% <40 mg/dL. The median blood glucose was statistically different but not clinically different among the patients who lived and died (114; interquartile range, 109-132 vs. 118; 111-136, p = 0.01). The median insulin dose was a unit per hour higher among the patient who died (4.2; 2.7-5.9 vs. 3.2; 2.4-5.0, p = 0.006). A logistic regression model demonstrated insulin rate (odds ratio 0.736, 95% confidence interval, 0.549-0.985, p = 0.039) to be the only independent predictor of mortality among the measures of blood glucose control.
Nonsurvivors with TBI have significantly higher markers of IR (insulin rate and multiplier). Markers of glucose control (median glucose, hypoglycemic episodes, and the percentage of values in range) did not differ clinically among groups. Despite this stress IR, tight glycemic control appears possible and safe with low levels of hypoglycemic episodes in the TBI population.
高血糖和低血糖均与创伤性脑损伤（TBI）的不良预后相关。在TBI患者中，严格血糖控制（目标范围为80 - 110mg/dL）的风险和益处均未得到证实。
分析使用计算机算法密集收集血糖数据以维持严格血糖控制是否会揭示TBI患者幸存者和非幸存者之间血糖控制的显著差异。
2005年10月至2006年4月，所有创伤严重程度评分（AIS）≥3分的接受机械通气的重症外科TBI患者均采用自动血糖正常化方案，每2小时进行一次血糖采样。排除24小时内死亡的患者。该方案使用线性方程（速率 = 血糖 - 60[M]）计算胰岛素输注速率。M是一个适应性乘数，在此用作胰岛素抵抗（IR）的指标。
在1636例入住创伤重症监护病房的患者中，160例患者（损伤严重程度评分中位数为34，死亡率为13.1%）共采集了10071份样本。血糖中位数为115.6mg/dL，41%的值在80至110mg/dL之间，81%在80至150mg/dL之间，0.3%<40mg/dL。存活和死亡患者的血糖中位数在统计学上有差异，但在临床上无差异（114；四分位间距，109 - 132 vs. 118；111 - 136，p = 0.01）。死亡患者的胰岛素剂量中位数每小时高1个单位（4.2；2.7 - 5.9 vs. 3.2；2.4 - 5.0，p = 0.006）。逻辑回归模型显示，在血糖控制指标中，胰岛素输注速率（比值比0.736，95%置信区间，0.549 - 0.985，p = 0.039）是死亡率的唯一独立预测因素。
TBI非幸存者的IR指标（胰岛素输注速率和乘数）显著更高。血糖控制指标（血糖中位数、低血糖发作次数及达标值百分比）在各组间临床上无差异。尽管存在这种应激性IR，但在TBI患者中进行严格血糖控制似乎是可行且安全的，低血糖发作水平较低。
