Impaired clot formation and hemostasis in experimental traumatic hemorrhage model

Uncontrolled hemorrhage with hemostatic derangement still represents a major preventable cause of death following severe traumatic injury. The purpose of this experimental study was to further investigate the overall hemostasis potential and clot formation after severe traumatic hemorrhage.

Male New Zealand white rabbits ( n  = 12) were subjected to traumatic injury with 40% hemorrhage of their estimated blood volume. The rate of thrombin generation was measured by calibrated automated thrombogram assay, overall hemostatic potential (OHP) by fibrin-aggregation on spectrophotometer, and microvesicles using flow cytometry. The clot structure was analyzed using scanning electron microscopy (SEM).

After traumatic hemorrhage, standard laboratory coagulation parameters showed decreased platelet count and fibrinogen, and increased INR and lactate. The OHP and overall coagulation potential (OCP) declined by 59% ( P  < 0.001) and 51% ( P  < 0,001), respectively. Overall fibrinolytic potential increased from 82% to 86% ( P  = 0.008). Platelet derived CD9 positive microvesicles decreased by 84% ( P  = 0.002). Endogenous thrombin potential decreased from 483 RFU/min to 383 RFU/min ( P  = 0.005). SEM analysis of the fibrin clot structure showed a more porous clot with a decrease in fiber diameter from 72 μm to 56 μm ( P  = 0.002).

This experimental study provides important aspects on coagulopathy and clot structure after traumatic hemorrhage including reduced thrombin generation and hyperfibrinolysis resulting in a more porous fibrin clot with lower density and thinner fibers. The methods used may be applied in the clinical research setting to gain further insights about hemostasis and clot formation for targeted therapy after traumatic hemorrhage.