The role of factor V in trauma-induced coagulopathy: an observational and experimental study

In bleeding patients with trauma-induced coagulopathy (TIC), factor (F)V becomes depleted, which may not be corrected with existing treatment strategies. It is currently unknown whether supplementing FV or FVa improves TIC.

To explore the relationship between FV activity and mortality in trauma patients, and to investigate the effect of FV(a) supplementation in addition to other treatment strategies in an in vitro model of TIC.

The association between FV activity and mortality was studied using an international prospective cohort study of trauma patients. In an in vitro whole blood and plasma model of TIC, the effect of FV(a) on rotational thromboelastometry and fibrin formation was studied. Effects of FV(a) were evaluated either as a standalone therapy or as adjunctive therapy in combination with tranexamic acid, fibrinogen concentrate, and/or prothrombin complex concentrate.

A total of 1285 patients were included, with a median injury severity score of 16 (interquartile range: 8-26). Decreased FV activity was associated with increased mortality. In the whole blood TIC model, FVa increased maximum clot firmness and reduced fibrinolysis, both as a single and combination therapy. In the plasma TIC model, with lower tissue factor concentrations than in the whole blood model, FV(a) prolonged clotting times, both as a single treatment and in combination with other treatments.

FV depletion after trauma is associated with increased mortality. In an in vitro model of TIC, FV(a) results in procoagulant, antifibrinolytic, and anticoagulant effects. Further research is highly warranted.