Acute coagulopathy of trauma: Hypoperfusion induces systemic anticoagulation and hyperfibrinolysis
Acute coagulopathy of trauma: Hypoperfusion induces systemic anticoagulation and hyperfibrinolysis
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DOI：
10.1097/ta.0b013e318169cd3c
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发表时间：
2008-05-01
影响因子：
--
通讯作者：
Pittet, Jean-Francois
中科院分区：
文献类型：
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作者：
Brohi, Karim;Cohen, Mitchell J.;Pittet, Jean-Francois
背景：25%的创伤患者入院时存在凝血功能障碍，这与休克相关，且死亡率增加5倍。近期发现这种凝血功能障碍与蛋白C通路的系统性激活有关。本研究旨在描述创伤性休克的血栓形成、凝血和纤溶紊乱情况。
方法：这是一项针对入住单一创伤中心的严重创伤患者的前瞻性队列研究。患者到达后10分钟内采集血液，用于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）、组织型纤溶酶原激活物（tPA）和D - 二聚体。碱缺失被用作组织低灌注的衡量指标。
结果：对208名患者进行了研究。全身性低灌注与抗凝和纤溶亢进相关。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。低灌注导致可溶性血栓调节蛋白水平升高，这与纤维蛋白原利用减少、蛋白C降低以及TAFI增加相关。低灌注还导致纤溶亢进，表现为tPA和D - 二聚体升高，这与观察到的PAI - 1降低相关，而与TAFI的改变无关。
结论：创伤性急性凝血功能障碍与全身性低灌注相关，其特征为抗凝和纤溶亢进。在该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激活的蛋白C消耗PAI - 1导致纤溶亢进。
Background: 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.Methods: 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 pqothrombin 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 Ddiniers. Base deficit was used as a measure of tissue hypoperfusion.Results: . 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.Conclusions: . 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-I.