Department of Acute and Critical Care Medicine, Sapporo Higashi Tokushukai Hospital, Sapporo, Japan.
Division of Acute and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
J Thromb Haemost. 2020 Sep;18(9):2232-2244. doi: 10.1111/jth.14931.
Trauma-induced coagulopathy (TIC) may progress to disseminated intravascular coagulation (DIC) due to dysregulated inflammatory and coagulofibrinolytic responses to trauma.
We explored how DIC and TIC elicit the same coagulofibrinolytic changes which lead to massive transfusion.
Severely injured trauma patients with an injury severity score ≥ 16 were prospectively included. Platelet counts, global markers of coagulation and fibrinolysis and specific markers of thrombin and plasmin generation, anticoagulation, endothelial injury, and inhibition of fibrinolysis were measured at presentation to the emergency department (0 hour) and 3 hour after arrival. The patients were subdivided into those with and without DIC and those with and without TIC using the 0-hour data. Time courses of specific markers and the frequency of massive transfusion were evaluated. The association of various variables with DIC development was also confirmed.
Two hundred and seventy-six patients were eligible for the analyses. The severity of injury (odds ratio; 1.038, P = .022) and thrombin generation (odds ratio; 1.014, P = .024) were associated with the development of DIC. Both DIC and TIC patients showed increased thrombin generation, insufficient anticoagulation controls, endothelial injury and increased fibrinolysis followed by elevated plasminogen activator inhibitor-1 levels at 0 and 3 hours. The frequency of massive transfusion was higher in both DIC (33.6% vs 7.9%, P < .001) and TIC (50.0% vs 13.3%, P < .001) patients than in those without DIC or TIC, respectively.
Disseminated intravascular coagulation and TIC evoked the same coagulofibrinolytic responses in severely injured trauma patients immediately after trauma and needed massive transfusion.
创伤诱导的凝血障碍（TIC）可能由于对创伤的炎症和凝血纤溶反应失调而进展为弥漫性血管内凝血（DIC）。
我们探讨了 DIC 和 TIC 如何引起相同的凝血纤溶变化，从而导致大量输血。
前瞻性纳入严重创伤患者，损伤严重程度评分≥16。在急诊科就诊时（0 小时）和到达后 3 小时测量血小板计数、凝血和纤溶的全局标志物以及凝血酶和纤溶酶生成、抗凝、内皮损伤和纤溶抑制的特异性标志物。根据 0 小时的数据将患者分为有和无 DIC 组以及有和无 TIC 组。评估特定标志物的时间过程和大量输血的频率。还证实了各种变量与 DIC 发展的关联。
276 名患者符合分析条件。损伤严重程度（比值比；1.038，P=.022）和凝血酶生成（比值比；1.014，P=.024）与 DIC 发展相关。DIC 和 TIC 患者均表现出凝血酶生成增加、抗凝控制不足、内皮损伤和纤溶增加，随后在 0 小时和 3 小时时纤溶酶原激活物抑制剂-1 水平升高。DIC（33.6%比 7.9%，P<.001）和 TIC（50.0%比 13.3%，P<.001）患者的大量输血频率均高于无 DIC 或 TIC 患者。
严重创伤患者创伤后立即发生弥散性血管内凝血和 TIC，引起相同的凝血纤溶反应，需要大量输血。
