• R Wiegner, S Denk, M Kalbitz, M Weiss, F Gebhard, and M Huber-Lang.
• Department of Orthopedic Trauma, Hand, Plastic and Reconstructive Surgery, University Hospital Ulm, Germany.
• Shock. 2015 Oct 1;44 Suppl 2:23.

IntroductionSevere tissue trauma leads to an early excessive activation of the complement and the coagulation system which is associated with a poor outcome. Besides extensive interactions between the two cascades on a fluid-phase level, studies suggest that key molecules in coagulation are expressed on leukocytes. Therefore, we examined the potential crosstalk between complement and coagulation on the leukocyte surface, and aimed to identify the involved molecular mechanisms especially after polytrauma.MethodsA prospective clinical study was conducted in patients after severe trauma (ISS≥32) and healthy volunteers. The study was approved by the Independent Local Ethics Committee of the University of Ulm. Blood was obtained upon admission to the ER and 4 h, 12 h, 24 h, 48 h, 120 h and 240 h after trauma. Key players of complement and coagulation on the leukocyte cell surface were analyzed by flow cytometry in comparison to expression profiles in healthy volunteers.ResultsAll leukocytes showed significantly increased expression of PAI-1 during later time points after trauma, possibly accounting for decreased fibrinolysis and enhanced risk of thrombosis. TCC was significantly incorporated in monocyte membranes at increased amounts early after trauma, returning to base line levels on days 5 and 10. A similar expression pattern was observed for thrombomodulin, an essential regulator of protein C activation. TCC levels on monocytes positively correlated with thrombomodulin expression and negatively with platelet counts.ConclusionThe data are indicative of so far unknown interactions between complement and coagulation on a cellular level and the potential role of leukocyte surface molecules in the development of coagulopathy after trauma.

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