损伤后血栓表型的变化：MA-R 比值和脆弱血栓。
Variations in clot phenotype following injury: The MA-R ratio and fragile clots.
机构信息
From the Department of Surgery, University of Wisconsin School of Medicine and Public Health (J.H., B.L.Z., S.A.S), Madison, Wisconsin; Department of Surgery, University of Texas Health Science Center at Houston (E.E.F., C.E.W.), Houston, Texas; and Department of Surgery, University of Alabama at Birmingham (J.B.H.), Birmingham, Alabama.
出版信息
J Trauma Acute Care Surg. 2022 Mar 1;92(3):504-510. doi: 10.1097/TA.0000000000003442.
INTRODUCTION
Trauma-induced coagulopathy is a continuum ranging from hypercoagulable to hypercoagulable phenotypes. In single-center studies, the maximum amplitude (MA) to r-time (R) (MA-R) ratio has identified a phenotype of injured patients with high mortality risk. The purpose of this study was to determine the relationship between MA-R and mortality using multicenter data and to investigate fibrinogen consumption in the development of this specific coagulopathy phenotype.
METHODS
Using the Pragmatic Randomized Optimal Platelet and Plasma Ratios data set, patients were divided into blunt and penetrating injury cohorts. MA was divided by R time from admission thromboelastogram to calculate MA-R. MA-R was used to assess odds of early and late mortality using multivariable models. Multivariable models were used to assess thrombogram values in both cohorts. Refinement of the MA-R cut point was performed with Youden index. Repeat multivariable analysis was performed with a binary CRITICAL and NORMAL MA-R.
RESULTS
In initial analysis, MA-R quartiles were not associated with mortality in the penetrating cohort. In the blunt cohort, there was an association between low MA-R and early and late mortality. A refined cut point of 11 was identified (CRITICAL: MA-R, ≤11; NORMAL: MA-R, >11). CRITICAL MA-R was associated with mortality in both penetrating and blunt subgroups. In further injury subgroup analysis, CRITICAL patients had significantly decreased fibrinogen levels in the blunt subgroup only. In both blunt and penetrating injury, there was no difference in time to initiation of thrombin burst (lagtime). However, both endogenous thrombin potential and peak thrombin levels were significantly lower in CRITICAL patients.
CONCLUSIONS
MA-R identifies a trauma-induced coagulopathy phenotype characterized in blunt injury by impaired thrombin generation that is associated with early and late mortality. The endotheliopathy and tissue factor release likely plays a role in the cascade of impaired thrombin burst, possible early fibrinogen consumption and the weaker clot identified by MA-R.
LEVEL OF EVIDENCE
Therapeutic/care management, level II.
简介
创伤诱导的凝血障碍是一个连续的过程，范围从高凝状态到高凝表型。在单中心研究中，最大振幅（MA）与 r 时间（R）的比值（MA-R）已经确定了一种高死亡率风险的损伤患者表型。本研究的目的是使用多中心数据确定 MA-R 与死亡率之间的关系，并研究纤维蛋白原消耗在这种特定凝血障碍表型发展中的作用。
方法
使用实用随机优化血小板和血浆比例数据集，将患者分为钝性和穿透性损伤队列。从入院血栓弹性图的 r 时间中除以 MA 时间来计算 MA-R。使用多变量模型评估 MA-R 比值对早期和晚期死亡率的影响。使用多变量模型评估两个队列中的血栓图值。使用 Youden 指数对 MA-R 切点进行细化。使用二进制 CRITICAL 和 NORMAL MA-R 进行重复多变量分析。
结果
在初始分析中，穿透性损伤队列中 MA-R 四分位数与死亡率无关。在钝性损伤队列中，低 MA-R 与早期和晚期死亡率之间存在关联。确定了 11 的细化切点（CRITICAL：MA-R，≤11；NORMAL：MA-R，>11）。CRITICAL MA-R 与穿透性和钝性损伤亚组的死亡率均相关。在进一步的损伤亚组分析中，只有在钝性损伤亚组中，CRITICAL 患者的纤维蛋白原水平显著降低。在钝性和穿透性损伤中，CRITICAL 患者的凝血酶爆发起始时间（lagtime）没有差异。然而，CRITICAL 患者的内源性凝血酶潜能和峰值凝血酶水平明显较低。
结论
MA-R 确定了一种创伤诱导的凝血障碍表型，其特征是钝性损伤中凝血酶生成受损，与早期和晚期死亡率相关。内皮病变和组织因子释放可能在凝血酶爆发受损的级联反应中发挥作用，可能导致早期纤维蛋白原消耗和 MA-R 识别的较弱血栓。
证据水平
治疗/护理管理，II 级。
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