Coagulopathy and traumatic shock: Characterizing hemostatic function during the critical period prior to fluid resuscitation

Abstract

Aims Identifying early changes in hemostatic clot function as a result of tissue injury and hypoperfusion may provide important information regarding the mechanisms of traumatic coagulopathy. A combat-relevant swine model was used to investigate the development of coagulopathy during trauma by monitoring hemostatic function during increasing severity of shock. Methods Swine were injured (soft tissue + femur fracture) and hemorrhaged while continuously monitoring Oxygen Debt (OD) by indirect calorimetry at the airway. Hemostatic function was assessed by Thrombelastography (TEG), Prothrombin Time (PT), Partial Thromboplastin Time (PTT), and fibrinogen concentration and compared before hemorrhage (D0) and during shock when OD = 40 and 80 ml/kg. An instrumented sham group was used for comparison. Results N = 23 swine ( N = 18 hemorrhage, N = 5 sham) weighing 45 ± 6 kg were studied after removing an average of 34 ± 14% of blood volume during hemorrhage. Hgb, Hct, platelet counts, PT and PTT did not change with increasing OD ( p < 0.05). Fibrinogen was reduced significantly by OD = 40 ml/kg (mean diff. = −59.9 mg/dl, 95% CI diff. [−95.1, −24.6]). TEG parameters representing clot initiation ( R) and polymerization ( K and Alpha Angle) did not change with increasing OD during shock ( p > 0.053). Clot strength (MA) was reduced in the hemorrhage group by OD = 80 ml/kg (mean diff. = −4.1 mm, 95% CI diff. [−7.4, −0.8]). Conclusion In this swine model of traumatic shock, fibrinogen was significantly reduced and an isolated reduction in clot strength (MA) was found with increasing OD. Fibrinogen consumption and altered platelet function may account for the earliest changes in hemostatic function during traumatic shock.