Platelet dysfunction is a suggested driver of trauma-induced coagulopathy. However, there is still a paucity of data regarding the impact of injury pattern on platelet function and the association of platelet dysfunction on transfusion requirements and mortality. In this retrospective cohort study, patients were grouped into those with isolated severe traumatic brain injury (TBI group), those with major trauma without TBI (MT group), and a combination of both major trauma and traumatic brain injury (MT + TBI group). Platelet function was assessed by whole blood impedance aggregometry (Multiplate®, MP). Three different platelet activators were used: adenosine-diphosphate (ADP test), arachidonic acid (ASPI test), and thrombin activated peptide-6 (TRAP test). Blood transfusion requirements within 6 h and 24 h and the association of platelet dysfunction on mortality was investigated. A total of 328 predominantly male patients (75.3%) with a median age of 53 (37–68) years and a median ISS of 29 (22–38) were included. No significant difference between the TBI group, the MT group, and the MT + TBI group was detected for any of the investigated platelet function tests. Unadjusted and adjusted for platelet count, the investigated MP assays revealed no significant group differences upon ER admission and were not able to sufficiently predict massive transfusion, neither within the first 6 h nor for the first 24 h after hospital admission. No association between platelet dysfunction measured by MP upon ER admission and mortality was observed. Conclusion: Injury pattern did not specifically impact platelet function measurable by MP. Platelet dysfunction upon ER admission measurable by MP was not associated with transfusion requirements and mortality. The clinical relevance of platelet function testing by MP in trauma patients not on platelet inhibitors is questionable.

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Management of bleeding in patients on nonvitamin-K antagonist oral anticoagulants (NOAC) is challenging because therapeutic options are few and their effectiveness is unpredictable [1,2]. Idarucizumab is an antibody fragment which binds both free and thrombin-bound dabigatran, and the idarucizumab-dabigatran complex is then cleared by the kidneys. Idarucizumab was developed by the manufacturer of dabigatran to reverse the anticoagulant effects of the NOAC dabigatran. The substance was tested in healthy male volunteers and showed immediate, complete and sustained reversal of dabigatran-induced anticoagulation, and was well tolerated [3].

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