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急性创伤性凝血病的发病机制 被引量:9

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摘要 急性创伤性凝血病(acute traumatic coagulopathy,ATC)是由组织损伤和休克驱动的机体早期内源性凝血功能障碍过程,与多发伤患者的病死率增加和不良预后相关。损伤控制性复苏诊疗策略主要是针对创伤性出血患者相对较长的院前诊断治疗阶段。ATC的主要机制是严重创伤后内皮细胞活化产物蛋白C引起的快速抗凝和纤维蛋白溶解。持续失血、低体温、酸中毒和血液稀释可加重 ATC,并导致全身止血系统的紊乱。虽然目前血小板活化、纤溶酶原应用、内皮功能紊乱等与神经-激素路径之间的相互作用在 ATC发病机制中所起的作用仍不确切,但上述的相互作用的研究有可能为 ATC的治疗提供新的靶点。传统凝血试验(standard coagulation tests, SCT)检测在严重创伤性出血的早期诊疗中意义不大。血栓弹力图分析仪(thrombelastography,TEG)、旋转式血栓弹力测定法(rotational thrombelastometry/-graphy,ROTEM)等,可以快速地评估全血中凝血动力学,在创伤性出血的诊疗中比 SCT更具有价值。
出处 《重庆医学》 CAS CSCD 北大核心 2014年第18期2374-2377,共4页 Chongqing medicine
关键词 创伤 凝血病 机制
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参考文献26

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同被引文献98

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