Abstract
BackgroundImpaired haemostasis following shock and tissue trauma is frequently detected in the trauma setting. These changes occur early, and are associated with increased mortality. The mechanism behind trauma-induced coagulopathy (TIC) is not clear. Several studies highlight the crucial role of fibrinogen in posttraumatic haemorrhage. This study explores the coagulation changes in a swine model of early TIC, with emphasis on fibrinogen levels and utilization of fibrinogen.MethodsA total of 18 landrace pigs were anaesthetized and divided into four groups. The Trauma-Shock group (TS) were inflicted bilateral blast femoral fractures with concomitant soft tissue injury by a high-energy rifle shot to both hind legs, followed by controlled exsanguination. The Shock group (S) was exposed to shock by exsanguination, whereas a third group was exposed to trauma only (T). A fourth group (C) served as control. Physiological data, haematological measurements, blood gas analyses and conventional coagulation assays were recorded at baseline and repeatedly over 60 minutes. Thrombelastometry were performed by means of the tissue factor activated ExTEM assay and the platelet inhibiting FibTEM assay. Data were statistically analysed by repeated measurements analyses method.ResultsA significant reduction of fibrinogen concentration was observed in both the TS and S groups. INR increased significantly in the S group and differed significantly from the TS group. Maximum clot firmness (MCF) of the ExTEM assay was significantly reduced over time in both TS and S groups. In the FibTEM assay a significant shortening of the clotting time and an increase in MCF was observed in the TS group compared to the S group.ConclusionDespite a reduction in clotting capability measured by ExTEM MCF and a reduced fibrinogen concentration, extensive tissue trauma may induce an increased fibrin based clotting activity that attenuates the hypocoagulable tendency in exsanguinated animals.
Highlights
Impaired haemostasis following shock and tissue trauma is frequently detected in the trauma setting
In this study we aim to develop a large animal model to characterize the immediate changes in coagulation, focusing on fibrinogen availability and utilization following the combination of massive tissue injury and severe hypoperfusion
Measurements of blood loss and shock Of the 18 animals included in the experimental groups, 16 completed the protocol
Summary
Impaired haemostasis following shock and tissue trauma is frequently detected in the trauma setting These changes occur early, and are associated with increased mortality. Some studies suggest that an abnormal expression of thrombomodulin on the endothelial surface activates excessive amounts of protein C, which in turn diverts haemostasis in the direction of hypocoagulability and hyperfibrinolysis [7,8]. Opponents of this theory argue that coagulopathy in trauma is merely a fibrinolytic phenotype of disseminated intravascular coagulopathy, as can be seen in any type of patients with serious hypoperfusion [9]. Others focus on endothelial cell and glycocalyx damage as critical components of TIC [10]
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