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Window of Opportunity to Mitigate Trauma-induced Coagulopathy Fibrinolysis Shutdown not Prevalent Until 1 Hour Post-injury

机译:减轻创伤诱导的凝血病纤维蛋白溶解的机会窗口损伤术后1小时才普遍存在

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Objective: The aim of this study was to delineate the kinetics of coagulation dysregulation after injury in children. Summary Background Data: Trauma-induced coagulopathy is common and portends poor outcomes in severely-injured children. Transfer to pediatric trauma centers is common; time from injury to laboratory testing is therefore highly variable. Methods: Records of severely injured children age = 3), fibrinolysis shutdown (SD; LY30 = 3 defined severe traumatic brain injury (TBI). Variables of interest included demographics, injury mechanism, medications, mortality, and functional disability. Wilcoxon rank-sum and Kruskal-Wallis testing were utilized for skewed continuous data, and Chi-square or Fisher exact test was used for categorical data. To determine independent predictors of SD, multivariable logistic regression modeling was performed using the time from injury variable as well as variables determined a priori to be clinically relevant contributors to the development of SD (TBI, injury mechanism, and age). Results: A total of 285 patients were included: median (interquartile range) age = 11 (6-15), injury severity score = 17 (10-25), 75% blunt mechanism, 32% severe TBI, 11% mortality, 28% functional disability. None received antifibrinolytics or blood products before TEG testing. Physiologic phenotype was predominant within 1 hour of injury (51%); beyond 1 hour, fibrinolysis SD was the predominant phenotype (1-3 hours = 46%, >3 hours = 59%). Patients with TBI had significant increase in incidence of fibrinolysis SD beyond 1 hour after injury as compared to non-TBI patients. Physiologic fibrinolysis was associated with survival at all timepoints (P = 0.005). Conclusions: Fibrinolysis SD is a reactive, compensatory mechanism that is evident soon after injury. There appears to be an early and brief window of opportunity for intervention to mitigate the progression to TIC. Further studies should focus on understanding the dynamic events occurring immediately after injury to identify specific targets for intervention.
机译:目的:本研究的目的是描绘儿童损伤后凝血失调的动力学。发明内容背景数据:创伤诱发的凝血病是常见的,并且在严重受伤的儿童中移植差的结果。转移到儿科创伤中心是常见的;因此,从实验室测试受伤的时间是高度变化的。方法:严重受伤的儿童年龄= 3),纤维蛋白溶解关闭(SD; LY30 = 3定义严重创伤性脑损伤(TBI)。兴趣的变量包括人口统计,伤害机制,药物,死亡率和功能性残疾。威尔克森排名 - 总和和Kruskal-Wallis测试用于偏斜连续数据,并且Chi-Square或Fisher精确测试用于分类数据。为了确定SD的独立预测因子,使用来自伤害变量的时间以及确定的变量进行多变量的逻辑回归建模先验是在临床上有关贡献的贡献者,以发展SD(TBI,伤害机制和年龄)。结果:共用285名患者:中位数(四分位数)龄= 11(6-15),伤害严重程度得分= 17(10-25),钝机175%,TBI严重32%,死亡率为11%,功能性残疾28%。没有接受TEG检测前的抗纤维蛋白溶胶或血液产品。生理表型是主要的机智HIN 1小时伤害(51%);超过1小时,纤维蛋白溶解SD是主要的表型(1-3小时= 46%,> 3小时= 59%)。与非TBI患者相比,TBI患者在损伤后1小时超过1小时的纤维蛋白溶解率显着增加。生理纤维蛋白溶解与所有时间点的存活相关(p = 0.005)。结论:纤维蛋白溶解SD是一种反应性的补偿机制,损伤后很快就明。似乎是一个早期和简短的干预机会窗口,以减轻TIC的进展。进一步的研究应专注于理解伤害后立即发生的动态事件,以确定干预的特定目标。

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