Division of Acute Care Surgery, Department of Surgery, The University of Texas Health Science Center and the McGovern School of Medicine, Houston, Texas.
Center for Translational Injury Research, Houston, Texas.
Shock. 2019 Mar;51(3):273-283. doi: 10.1097/SHK.0000000000001160.
Thrombelastography (TEG) fibrinolysis shutdown after trauma is associated with increased mortality due to hypercoagulability-associated organ failure. However, a lack of mechanistic data has precluded the development of novel interventions to treat shutdown.
To define the pathophysiology of TEG shutdown in severely injured, bleeding patients through secondary analysis of the PROPPR trial.
Fibrinolysis was characterized in PROPPR subjects using admission TEG lysis at 30 min (LY30) or plasmin-antiplasmin (PAP) levels. LY30 categories were low (<0.9%), moderate (0.9-2.9%), or high (≥ 3%). PAP was classified as low (<1,500 μg/L), moderate (1,500-20,000 μg/L), or high (>20,000 μg/L). Demographics, outcomes, admission TEG values, platelet count and function, standard coagulation tests, and coagulation proteins were compared.
Five hundred forty-seven patients had TEG data and 549 patients had PAP data available. Low LY30 was associated with reduced platelet count and aggregation, poorer TEG clot formation, prolonged clotting times, and reduced fibrinogen and alpha2 antiplasmin. Compared to moderate PAP, low PAP subjects had similar platelet parameters, TEG values, fibrinogen, and alpha2 antiplasmin, but reduced tPA, and elevated PAI-1. D-Dimer values increased as PAP increased, however patients with low LY30 had elevated D-Dimer compared with moderate LY30 patients. Most low LY30 deaths were due to TBI (45%) and hemorrhage (42%) versus one of each cause (TBI, hemorrhage, MOF) in low PAP patients.
Low TEG LY30 does not reflect shutdown of enzymatic fibrinolysis with hypercoagulability, but rather a coagulopathic state of moderate fibrinolysis with fibrinogen consumption and platelet dysfunction that is associated with poor outcomes.
创伤后血栓弹力图(TEG)纤维蛋白溶解关闭与高凝相关的器官衰竭导致死亡率增加有关。然而,由于缺乏机制数据,因此无法开发治疗关闭的新干预措施。
通过对 PROPPR 试验的二次分析,定义严重创伤和出血患者 TEG 关闭的病理生理学。
使用 PROPPR 受试者入院 TEG 溶解的 30 分钟 LY30 或纤溶酶-抗纤溶酶(PAP)水平来描述纤维蛋白溶解。LY30 类别为低(<0.9%)、中(0.9-2.9%)或高(≥3%)。PAP 分为低(<1500μg/L)、中(1500-20000μg/L)或高(>20000μg/L)。比较了人口统计学数据、结局、入院 TEG 值、血小板计数和功能、标准凝血试验和凝血蛋白。
547 例患者有 TEG 数据,549 例患者有 PAP 数据。低 LY30 与血小板计数和聚集减少、TEG 凝块形成较差、凝血时间延长以及纤维蛋白原和α2 抗纤溶酶减少有关。与中 PAP 相比,低 PAP 患者的血小板参数、TEG 值、纤维蛋白原和α2 抗纤溶酶相似,但 tPA 减少,PAI-1 升高。随着 PAP 的增加,D-二聚体值增加,然而,与中 LY30 患者相比,低 LY30 患者的 D-二聚体升高。大多数低 LY30 死亡是由于 TBI(45%)和出血(42%),而低 PAP 患者则是每种原因(TBI、出血、MOF)各一例。
低 TEG LY30 并不反映高凝状态下的酶性纤维蛋白溶解关闭,而是反映出伴有纤维蛋白原消耗和血小板功能障碍的中等纤维蛋白溶解的凝血病状态,与不良结局相关。