Abstract
BackgroundWe conducted a prospective observational study for investigating coagulofibrinolytic changes and mechanisms of antithrombin (AT) alternations in trauma.MethodsTrauma patients hospitalized for more than seven days were analyzed for coagulofibrinolytic biomarkers. The patients were stratified into two groups according to AT activity level on admission (day 0), comprising normal AT and low AT patients.ResultsThirty-nine patients (median Injury Severity Score 20) exhibited initial coagulatory activation and triphasic fibrinolytic changes. AT activity did not show a negative linear correlation with levels of thrombin-antithrombin complex (TAT), a marker of coagulation activity and AT consumption, but was strongly correlated with levels of albumin (Alb), an index of vascular permeability, on day 0 (r = 0.702, p < 0.001). Furthermore, Alb was one of the independent predictors for AT on day 0. IL-6 on day 0 and thrombomodulin (TM) levels during the study period, reflecting systemic inflammation and endothelial cell injury, respectively, were significantly higher in the lower AT group (n = 10) than in the normal group (n = 29) (IL-6, p = 0.004; TM, p = 0.017). On days 2 and 4, TAT levels in the lower AT group were significantly higher than in the normal group.ConclusionsTrauma caused clear triphasic coagulofibrinolytic changes. Decreased AT in the later phase might lead to a prolonged hypercoagulation. AT reduction in the initial phase of trauma is strongly associated with extravascular leakage as suggested by the association of Alb depletion with IL-6 and TM elevation, but not with AT consumption.
Highlights
We conducted a prospective observational study for investigating coagulofibrinolytic changes and mechanisms of antithrombin (AT) alternations in trauma
acute traumatic coagulopathy (ATC) is a state of activation of the anticoagulant protein C (PC) pathway caused by shock and tissue hypoperfusion, leading to hypocoagulation and subsequent fibrinolysis
The parameters reflecting systemic immune response and coagulofibrinolytic activation were notably elevated on day 0 (IL-6, 108.5 [40.8–250.3] pg/mL; thrombin-antithrombin complex (TAT), 88.0 [30.1–200.0] μg/L; plasmin inhibitor complex (PIC), 9.1 [2.8–17. 8] μg/mL)
Summary
We conducted a prospective observational study for investigating coagulofibrinolytic changes and mechanisms of antithrombin (AT) alternations in trauma. Coagulofibrinolytic disorder has been termed trauma-induced coagulopathy (TIC) The mechanisms of this disorder are still controversial, though they may include disseminated intravascular coagulation (DIC) with a fibrinolytic phenotype or acute traumatic coagulopathy (ATC) [3,4,5]. In the first hours after trauma, plasminogen activator inhibitor-1 (PAI-1) activity has not increased sufficiently to counteract this, and hyperfibrinolysis consumes α2-plasmin inhibitor (α2PI), which accelerates further fibrinolysis. This pattern of hypercoagulation and hyperfibrinolysis causes consumption of platelets and coagulation factors, resulting in DIC with a fibrinolytic phenotype characterized by bleeding tendency when hemostasis becomes dysregulated [3]. Activated PC pathway abrogates PAI-1 and increases t-PA, resulting in further hyperfibrinolysis [4, 5]
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