N. Mowery, O. Gunter, Oscar D. Guillamondegui, Lesly A. Dossett, Marcus J. Dortch, John A. Morris, A. May
{"title":"应激性胰岛素抵抗是外伤性脑损伤死亡率的一个标志。","authors":"N. Mowery, O. Gunter, Oscar D. Guillamondegui, Lesly A. Dossett, Marcus J. Dortch, John A. Morris, A. May","doi":"10.1097/TA.0b013e3181938c5e","DOIUrl":null,"url":null,"abstract":"BACKGROUND 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. OBJECTIVE 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. METHODS 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). RESULTS 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. CONCLUSION 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.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"5 1","pages":"145-51; discussion 151-3"},"PeriodicalIF":0.0000,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"47","resultStr":"{\"title\":\"Stress insulin resistance is a marker for mortality in traumatic brain injury.\",\"authors\":\"N. Mowery, O. Gunter, Oscar D. Guillamondegui, Lesly A. Dossett, Marcus J. Dortch, John A. Morris, A. May\",\"doi\":\"10.1097/TA.0b013e3181938c5e\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"BACKGROUND 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. OBJECTIVE 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. METHODS 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). RESULTS 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. CONCLUSION 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.\",\"PeriodicalId\":92962,\"journal\":{\"name\":\"The journal of cardiothoracic trauma\",\"volume\":\"5 1\",\"pages\":\"145-51; discussion 151-3\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2009-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"47\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The journal of cardiothoracic trauma\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1097/TA.0b013e3181938c5e\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The journal of cardiothoracic trauma","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/TA.0b013e3181938c5e","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 47
摘要
背景:高血糖和低血糖都与创伤性脑损伤(TBI)的不良预后相关。严格控制血糖(目标范围80-110 mg/dL)的风险和益处在TBI人群中都没有记录。目的:分析采用计算机化算法密集收集血糖数据以维持严格的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着差异。方法2005年10月至2006年4月,所有TBI简易损伤量表评分>或=3分的通气危重外科患者均采用自动血糖测定方案,每2小时采集一次血糖。不包括24小时内的死亡率。该方案使用线性方程计算胰岛素率(率=血糖- 60[M])。M是一种自适应乘数,在这里用作胰岛素抵抗(IR)的标记。结果在1636例外伤重症监护病房入院的160例患者中(损伤严重程度评分中位数为34,死亡率为13.1%)采集了10071份样本。葡萄糖中位数为115.6 mg/dL,其中41%在80 - 110 mg/dL之间,81%在80 - 150 mg/dL之间,0.3% <40 mg/dL。生存和死亡患者的中位血糖有统计学差异,但无临床差异(114;四分位数范围,109-132 vs. 118;111 ~ 136, p = 0.01)。死亡患者的中位胰岛素剂量每小时高1个单位(4.2;2.7-5.9 vs. 3.2;2.4 ~ 5.0, p = 0.006)。logistic回归模型显示胰岛素率(优势比0.736,95%可信区间0.549-0.985,p = 0.039)是血糖控制指标中唯一的独立预测因子。结论创伤性脑损伤非幸存者的IR指标(胰岛素率和乘数)明显升高。血糖控制指标(中位数血糖、低血糖发作和范围内值的百分比)在组间没有临床差异。尽管有这种应激性IR,但在TBI人群中,严格的血糖控制对于低血糖发作的低水平来说是可能和安全的。
Stress insulin resistance is a marker for mortality in traumatic brain injury.
BACKGROUND 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. OBJECTIVE 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. METHODS 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). RESULTS 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. CONCLUSION 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.