Department of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Strasbourg University (UNISTRA); Strasbourg University Hospital, Medical Intensive Care Unit - NHC; INSERM (French National Institute of Health and Medical Research), Strasbourg, France.
J Thromb Haemost. 2023 Dec;21(12):3360-3370. doi: 10.1016/j.jtha.2023.05.028. Epub 2023 Sep 16.
Disseminated intravascular coagulation can occur due to different causes but commonly following sepsis. Trauma-induced coagulopathy (TIC) occurs on hospital arrival in approximately 25% of seriously injured patients who initially presents with impaired hemostasis and a bleeding phenotype that can later progress to a prothrombotic phase. Following traumatic injury, ineffective hemostasis is driven by massive blood loss, tissue damage, and hyperfibrinolysis. This initial impaired hemostasis continues until surgical or other management strategies not only to stop the causes of hemorrhage but also progresses to a prothrombotic and hypofibrinolytic state, also termed fibrinolytic shutdown. Prothrombotic progression is also promoted by inflammatory mediator release, endothelial injury, and platelet dysregulation, which is commonly seen in sepsis with increased mortality. Unlike TIC, the early phase of sepsis is frequently complicated by multiorgan dysfunction described as sepsis-induced coagulopathy (SIC) that lacks a hemorrhagic phase. The phenotypes of SIC and TIC are different, especially in their initial presentations; however, patients who survive TIC may also develop subsequent infections and potentially sepsis and SIC. Although the pathophysiology of SIC and TIC are different, endothelial injury, dysregulated fibrinolysis, and coagulation abnormalities are common. Management includes treatment of the underlying cause, tissue injury vs infection is critical, and supportive therapies, such as hemostatic resuscitation and circulatory support are essential, and adjunct therapies are recommended in guidelines. Based on clinical studies and certain guidelines, additional therapies include tranexamic acid in the limited timing of initial traumatic injury and anticoagulants, such as antithrombin and recombinant thrombomodulin in disseminated intravascular coagulation.
弥散性血管内凝血可能由不同的原因引起，但通常是在脓毒症之后。创伤诱导的凝血障碍（TIC）在大约 25%的严重创伤患者中在入院时发生，这些患者最初表现为止血功能受损和出血表型，随后可能进展为血栓形成期。创伤后，大量失血、组织损伤和纤维蛋白溶解亢进导致无效止血。这种最初的止血功能障碍持续到手术或其他管理策略不仅可以止血，还可以进展为血栓形成和低纤维蛋白溶解状态，也称为纤维蛋白溶解关闭。促血栓形成的进展还受到炎症介质释放、内皮损伤和血小板失调的促进，这些在脓毒症中很常见，死亡率增加。与 TIC 不同，脓毒症的早期阶段常伴有多器官功能障碍，称为脓毒症诱导的凝血障碍（SIC），缺乏出血阶段。SIC 和 TIC 的表型不同，尤其是在其初始表现中；然而，TIC 幸存的患者也可能随后发生感染，并可能发生脓毒症和 SIC。尽管 SIC 和 TIC 的病理生理学不同，但内皮损伤、纤维蛋白溶解失调和凝血异常是常见的。治疗包括治疗潜在病因，组织损伤与感染的区别至关重要，支持性治疗，如止血复苏和循环支持是必不可少的，指南推荐辅助治疗。基于临床研究和某些指南，其他治疗方法包括创伤初始有限时间内使用氨甲环酸和抗凝剂，如抗凝血酶和重组血栓调节素在弥散性血管内凝血中。
