PB0522 - Characterization of Coagulopathy in a Swine Muscle Injury Model

Background: Previous studies have exhibited the procoagulant activity of skeletal muscle and tissue injury. However, injuries from varying mechanisms lead to the heterogeneity of trauma-induced coagulopathy, which entails difficulties in translational clinical research. Development and validation of a real-life model of trauma-induced coagulopathy following muscle injury are required to study its underlying mechanisms.

Aims: To translate a pig model of muscle injury and describe coagulopathy associated with it.

Methods: 16 female Yorkshire swine (40-50 kg) sustained isolated muscle injury by captive bolt gunshots over bilateral hind legs. Blood samples were collected at baseline and 24 hours after injury to measure clotting times, thromboelastography, and muscle injury parameters, including creatinine kinase and myoglobin. Fibrin generation turbidity was analyzed using a spectrophotometer, and platelet function was evaluated by flow cytometry. Data were analyzed by paired Wilcoxon Rank Sign tests.

Results: Creatine kinase and myoglobin levels were significantly elevated after muscle injury. This model exhibited phenotype associated with hypercoagulability, including higher final clot turbidity in fibrin generation, shorter R time and higher maximum amplitude on thromboelastography, along with more platelet granule secretion in resting condition. On the other hand, signatures of hypocoagulability including prolonged recalcified clotting time and prothrombin time were measured.

Conclusion(s): This pig muscle injury model possesses components of both hyper- and hypocoagulability, likely reflecting the heterogeneity of trauma in patients where mixed phenotypes of coagulopathy are present, as well as the potential of further translation to trauma scenarios.