Meledeo Michael A, Herzig Maryanne C, Bynum James A, Wu Xiaowu, Ramasubramanian Anand K, Darlington Daniel N, Reddoch Kristin M, Cap Andrew P
From the Coagulation and Blood Research Group(M.A.M., M.C.H., J.A.B., X.W., D.N.D, K.M.R., A.P.C.), US Army Institute of Surgical Research, Joint Base San Antonio-Fort Sam Houston, Texas; and Department of Biomedical, Chemical and Materials Engineering (A.K.R.), San Jose State University, San Jose, California.
J Trauma Acute Care Surg. 2017 Jun;82(6S Suppl 1):S33-S40. doi: 10.1097/TA.0000000000001431.
Acute traumatic coagulopathy (ATC) is the failure of coagulation homeostasis that can rapidly arise following traumatic injury, hemorrhage, and shock; it is associated with higher injury severity, coagulation abnormalities, and increased blood transfusions. Acute traumatic coagulopathy has historically been defined by a prolonged prothrombin time, although newer, more informative measurements of hemostatic function have been used to improve diagnosis and support clinical decision making. The underlying biochemical mechanisms of and best practice therapeutics for ATC remain under active investigation because of its significant correlation to poor outcomes. The wide range of hypothesized mechanisms for ATC results from the large number of symptoms, phenotypes, and altered states in these patients as observed by multiple research groups. Much like the ancient fable of blind men describing an elephant from their limited perspectives, the limited nature of clinical and laboratory tools used to diagnose coagulopathy or evaluate hemostatic function has made finding causation difficult. The prolonged prothrombin time, degree of fibrinolysis, depletion of coagulation factors and inhibitors, and general failure of the blood have all been identified as being primary indicators for ATC. Therapeutic interventions including recombinant coagulation factors, antifibrinolytics, and blood products have been used with varying degrees of success as they are used to address specific symptoms. To truly understand the causes of ATC, research efforts must recognize the complexity of the hemostatic system and get to the heart of the matter by answering the question: "Is ATC a pathological condition that develops from the observed deficiencies in coagulation, fibrinolysis, and autoregulation, or is ATC an adaptive response generated as the body attempts to restore perfusion and avoid massive organ failure?" Because patient management must proceed without definitive answers regarding the entire causative chain, the current therapeutic focus should be on using what knowledge has been gained to the patient's advantage: control hemorrhage, maintain appropriate homeostatic balances of coagulation proteins, and restore oxygen perfusion.
急性创伤性凝血病（ATC）是指在创伤、出血和休克后迅速出现的凝血稳态失衡；它与更高的损伤严重程度、凝血异常及输血增加有关。急性创伤性凝血病在历史上一直通过凝血酶原时间延长来定义，尽管目前已采用更新的、更具信息量的止血功能检测方法来改善诊断并支持临床决策。由于ATC与不良预后显著相关，其潜在的生化机制和最佳治疗方法仍在积极研究中。多个研究小组观察到，这些患者存在大量症状、表型和状态改变，这导致了ATC的多种假设机制。就像古代盲人摸象的寓言故事一样，用于诊断凝血病或评估止血功能的临床和实验室工具的局限性使得确定病因变得困难。凝血酶原时间延长、纤维蛋白溶解程度、凝血因子和抑制剂的消耗以及血液的整体功能障碍均已被确定为ATC的主要指标。包括重组凝血因子、抗纤维蛋白溶解剂和血液制品在内的治疗干预措施在用于解决特定症状时取得了不同程度的成功。为了真正理解ATC的病因，研究工作必须认识到止血系统的复杂性，并通过回答以下问题抓住问题的核心：“ATC是一种因观察到的凝血、纤维蛋白溶解和自动调节缺陷而发展的病理状态，还是身体为恢复灌注并避免大规模器官衰竭而产生的一种适应性反应？”由于在没有关于整个因果链的确切答案的情况下仍需对患者进行管理，当前的治疗重点应是利用已获得的知识为患者谋福利：控制出血、维持凝血蛋白的适当稳态平衡并恢复氧灌注。
