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Trauma-induced coagulopathy
Nature Reviews Disease Primers ( IF 76.9 ) Pub Date : 2021-04-29 , DOI: 10.1038/s41572-021-00264-3
Ernest E Moore 1, 2 , Hunter B Moore 2 , Lucy Z Kornblith 3 , Matthew D Neal 4 , Maureane Hoffman 5 , Nicola J Mutch 6 , Herbert Schöchl 7 , Beverley J Hunt 8 , Angela Sauaia 2, 9
Affiliation  

Uncontrolled haemorrhage is a major preventable cause of death in patients with traumatic injury. Trauma-induced coagulopathy (TIC) describes abnormal coagulation processes that are attributable to trauma. In the early hours of TIC development, hypocoagulability is typically present, resulting in bleeding, whereas later TIC is characterized by a hypercoagulable state associated with venous thromboembolism and multiple organ failure. Several pathophysiological mechanisms underlie TIC; tissue injury and shock synergistically provoke endothelial, immune system, platelet and clotting activation, which are accentuated by the ‘lethal triad’ (coagulopathy, hypothermia and acidosis). Traumatic brain injury also has a distinct role in TIC. Haemostatic abnormalities include fibrinogen depletion, inadequate thrombin generation, impaired platelet function and dysregulated fibrinolysis. Laboratory diagnosis is based on coagulation abnormalities detected by conventional or viscoelastic haemostatic assays; however, it does not always match the clinical condition. Management priorities are stopping blood loss and reversing shock by restoring circulating blood volume, to prevent or reduce the risk of worsening TIC. Various blood products can be used in resuscitation; however, there is no international agreement on the optimal composition of transfusion components. Tranexamic acid is used in pre-hospital settings selectively in the USA and more widely in Europe and other locations. Survivors of TIC experience high rates of morbidity, which affects short-term and long-term quality of life and functional outcome.



中文翻译:

创伤引起的凝血病

失控的出血是外伤患者死亡的一个可预防的主要原因。创伤性凝血病 (TIC) 描述了由创伤引起的异常凝血过程。在 TIC 发展的早期,通常会出现低凝状态,导致出血,而后期 TIC 的特点是与静脉血栓栓塞和多器官衰竭相关的高凝状态。TIC 背后有多种病理生理机制;组织损伤和休克协同激发内皮、免疫系统、血小板和凝血激活,而“致命三联征”(凝血障碍、体温过低和酸中毒)会加剧这种激活。创伤性脑损伤在 TIC 中也起着独特的作用。止血异常包括纤维蛋白原耗竭、凝血酶生成不足、血小板功能受损和纤溶失调。实验室诊断基于通过常规或粘弹性止血测定检测到的凝血异常;然而,它并不总是符合临床状况。管理重点是通过恢复循环血量来停止失血和逆转休克,以预防或降低 TIC 恶化的风险。复苏时可使用各种血液制品;然而,对于输血成分的最佳组成尚无国际共识。在美国,氨甲环酸选择性地用于院前急救,而在欧洲和其他地区则更广泛地使用。TIC 幸存者的发病率很高,影响短期和长期的生活质量和功能结果。

更新日期:2021-04-29
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