Madurska M J, Sachse K A, Jansen J O, Rasmussen T E, Morrison J J
Department of Vascular Surgery, Queen Elizabeth University Hospital, 1345 Govan Road, Glasgow, G51 4TF, UK.
Department of Anesthesia, University of Texas Health Science Center at San Antonio, Texas, USA.
Eur J Trauma Emerg Surg. 2018 Feb;44(1):35-44. doi: 10.1007/s00068-017-0833-3. Epub 2017 Sep 16.
Fibrinolytic dysregulation is an important mechanism in traumatic coagulopathy. It is an incompletely understood process that consists of a spectrum ranging from excessive breakdown (hyperfibrinolysis) and the shutdown of fibrinolysis. Both hyperfibrinolysis and shutdown are associated with excess mortality and post-traumatic organ failure. The pathophysiology appears to relate to endothelial injury and hypoperfusion, with several molecular markers identified in playing a role. Although there are no universally accepted diagnostic tests, viscoelastic studies appear to offer the greatest potential for timely identification of patients presenting with fibrinolytic dysregulation. Treatment is multimodal, involving prompt hemorrhage control and resuscitation, with controversy surrounding the use of antifibrinolytic drug therapy. This review presents the current evidence on the pathophysiology, diagnostic challenges, as well as the management of this hemostatic dysfunction.
Level III.
纤维蛋白溶解失调是创伤性凝血病的重要机制。这是一个尚未完全理解的过程，包括从过度分解（高纤维蛋白溶解）到纤维蛋白溶解停止的一系列情况。高纤维蛋白溶解和停止都与过高的死亡率和创伤后器官衰竭有关。病理生理学似乎与内皮损伤和灌注不足有关，已确定有几种分子标志物起作用。虽然没有普遍接受的诊断测试，但粘弹性研究似乎为及时识别出现纤维蛋白溶解失调的患者提供了最大潜力。治疗是多模式的，包括迅速控制出血和复苏，抗纤维蛋白溶解药物治疗的使用存在争议。本综述介绍了关于这种止血功能障碍的病理生理学、诊断挑战以及管理的当前证据。
三级。
