White Nathan J, Newton Jason C, Martin Erika J, Mohammed Bassem M, Contaifer Daniel, Bostic Jessica L, Brophy Gretchen M, Spiess Bruce D, Pusateri Anthony E, Ward Kevin R, Brophy Donald F
*Division of Emergency Medicine, University of Washington, and Puget Sound Blood Center Research Institute, Seattle, WA; †Coagulation Advancement Laboratory, Department of Pharmacotherapy & Outcomes Science, Virginia Commonwealth University, Richmond, VA; ‡Department of Clinical Pharmacy, Faculty of Pharmacy, Cairo University, Cairo, Egypt; §Pharmacotherapy & Outcomes Science and Department of Neurosurgery, Virginia Commonwealth University, Richmond, VA; ‖Department of Anesthesiology, Virginia Commonwealth University, Richmond, VA; ¶US Army Medical Research and Materiel Command, Fort Detrick, MD; #Michigan Center for Integrative Research in Critical Care, University of Michigan, Ann Arbor, Michigan.
Shock. 2015 Aug;44 Suppl 1(0 1):39-44. doi: 10.1097/SHK.0000000000000342.
Anticoagulation, fibrinogen consumption, fibrinolytic activation, and platelet dysfunction all interact to produce different clot formation responses after trauma. However, the relative contributions of these coagulation components to overall clot formation remain poorly defined. We examined for sources of heterogeneity in clot formation responses after trauma.
Blood was sampled in the emergency department from patients meeting trauma team activation criteria at an urban trauma center. Plasma prothrombin time of 18 s or longer was used to define traumatic coagulopathy. Mean kaolin-activated thrombelastography (TEG) parameters were calculated and tested for heterogeneity using analysis of means. Discriminant analysis and forward stepwise variable selection with linear regression were used to determine if prothrombin time, fibrinogen, platelet contractile force (PCF), and D-dimer concentration, representing key mechanistic components of coagulopathy, each contribute to heterogeneous TEG responses after trauma.
Of 95 subjects, 16% met criteria for coagulopathy. Coagulopathic subjects were more severely injured with greater shock and received more blood products in the first 8 h compared with noncoagulopathic subjects. Mean (SD) TEG maximal amplitude (MA) was significantly decreased in the coagulopathic group (57.5 [SD, 4.7] mm vs. 62.7 [SD, 4.7], t test P < 0.001). The MA also exceeded the ANOM predicted upper decision limit for the noncoagulopathic group and the lower decision limit for the coagulopathic group at α = 0.05, suggesting significant heterogeneity from the overall cohort mean. Fibrinogen and PCF best discriminated TEG MA using discriminant analysis. Fibrinogen, PCF, and D-dimer were primary covariates for TEG MA using regression analysis.
Heterogeneity in TEG-based clot formation in emergency department trauma patients was linked to changes in MA. Individual parameters representing fibrin polymerization, PCFs, and fibrinolysis were primarily associated with TEG MA after trauma and should be the focus of early hemostatic therapies.
抗凝、纤维蛋白原消耗、纤溶激活和血小板功能障碍相互作用,导致创伤后出现不同的凝血反应。然而,这些凝血成分对整体凝血形成的相对贡献仍不明确。我们研究了创伤后凝血反应异质性的来源。
在城市创伤中心,对符合创伤团队启动标准的患者在急诊科采集血液。血浆凝血酶原时间为18秒或更长被用于定义创伤性凝血病。计算平均高岭土激活血栓弹力图(TEG)参数,并使用均值分析测试其异质性。采用判别分析和线性回归的向前逐步变量选择来确定凝血酶原时间、纤维蛋白原、血小板收缩力(PCF)和D-二聚体浓度(代表凝血病的关键机制成分)是否各自导致创伤后TEG反应的异质性。
95名受试者中,16%符合凝血病标准。与非凝血病受试者相比,凝血病受试者受伤更严重,休克更严重,且在最初8小时内接受了更多血液制品。凝血病组的平均(标准差)TEG最大振幅(MA)显著降低(57.5 [标准差,4.7] 毫米对62.7 [标准差,4.7],t检验P < 0.001)。在α = 0.05时,MA也超过了非凝血病组的ANOM预测上限决策限和凝血病组的下限决策限,表明与总体队列均值存在显著异质性。使用判别分析时,纤维蛋白原和PCF对TEG MA的区分最佳。使用回归分析时,纤维蛋白原、PCF和D-二聚体是TEG MA的主要协变量。
急诊科创伤患者基于TEG的凝血形成异质性与MA变化有关。代表纤维蛋白聚合、PCF和纤溶的个体参数主要与创伤后TEG MA相关,应成为早期止血治疗的重点。