Brohi Karim, Cohen Mitchell J, Ganter Michael T, Schultz Marcus J, Levi Marcel, Mackersie Robert C, Pittet Jean-François
Department of Surgery, The Royal London Hospital, London, United Kingdom.
J Trauma. 2008 May;64(5):1211-7; discussion 1217. doi: 10.1097/TA.0b013e318169cd3c.
Coagulopathy is present at admission in 25% of trauma patients, is associated with shock and a 5-fold increase in mortality. The coagulopathy has recently been associated with systemic activation of the protein C pathway. This study was designed to characterize the thrombotic, coagulant and fibrinolytic derangements of trauma-induced shock.
This was a prospective cohort study of major trauma patients admitted to a single trauma center. Blood was drawn within 10 minutes of arrival for analysis of partial thromboplastin and prothrombin times, prothrombin fragments 1 + 2 (PF1 + 2), fibrinogen, factor VII, thrombomodulin, protein C, plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (tPA), and D-dimers. Base deficit was used as a measure of tissue hypoperfusion.
Two hundred eight patients were studied. Systemic hypoperfusion was associated with anticoagulation and hyperfibrinolysis. Coagulation was activated and thrombin generation was related to injury severity, but acidosis did not affect Factor VII or PF1 + 2 levels. Hypoperfusion-induced increase in soluble thrombomodulin levels was associated with reduced fibrinogen utilization, reduction in protein C and an increase in TAFI. Hypoperfusion also resulted in hyperfibrinolysis, with raised tPA and D-Dimers, associated with the observed reduction in PAI-1 and not alterations in TAFI.
Acute coagulopathy of trauma is associated with systemic hypoperfusion and is characterized by anticoagulation and hyperfibrinolysis. There was no evidence of coagulation factor loss or dysfunction at this time point. Soluble thrombomodulin levels correlate with thrombomodulin activity. Thrombin binding to thrombomodulin contributes to hyperfibrinolysis via activated protein C consumption of PAI-1.
25%的创伤患者入院时存在凝血病，其与休克相关，死亡率增加5倍。近期研究表明，凝血病与蛋白C途径的全身激活有关。本研究旨在描述创伤性休克引起的血栓形成、凝血和纤溶紊乱。
这是一项对入住单一创伤中心的严重创伤患者进行的前瞻性队列研究。患者到达后10分钟内采集血液，分析部分凝血活酶时间、凝血酶原时间、凝血酶原片段1+2（PF1+2）、纤维蛋白原、因子VII、血栓调节蛋白、蛋白C、纤溶酶原激活物抑制剂-1（PAI-1）、凝血酶激活的纤溶抑制物（TAFI）、组织纤溶酶原激活物（tPA）和D-二聚体。碱缺失用作组织灌注不足的指标。
共研究了208例患者。全身灌注不足与抗凝和高纤溶状态相关。凝血被激活，凝血酶生成与损伤严重程度相关，但酸中毒不影响因子VII或PF1+2水平。灌注不足导致可溶性血栓调节蛋白水平升高，与纤维蛋白原利用率降低、蛋白C减少和TAFI增加相关。灌注不足还导致高纤溶状态，tPA和D-二聚体升高，与观察到的PAI-1减少相关，而TAFI无变化。
创伤性急性凝血病与全身灌注不足相关，其特征为抗凝和高纤溶状态。在这个时间点没有凝血因子丢失或功能障碍的证据。可溶性血栓调节蛋白水平与血栓调节蛋白活性相关。凝血酶与血栓调节蛋白结合通过消耗PAI-1的活化蛋白C导致高纤溶状态。
