부산대학교 도서관

Introduction: Platelets contribute to hemostasis by rapidly sticking, aggregating, and contracting at wounds to stabilize blood clots. There is evidence that severe trauma with blood loss can render platelets dysfunctional, which is associated with increased mortality. However, this platelet dysfunction has not been well described.Hypothesis: We hypothesize that there is significant platelet dysfunction present in those trauma patients requiring urgent platelet transfusion for treatment of bleeding.Methods: We conducted a prospective observational trial of trauma patients presenting to a U.S. Level I trauma center. Subjects were enrolled and blood samples collected for blood chemistries, cell counts, coagulation, clot formation by rotational thromboelastometry (ROTEM), platelet aggregation after activation by thrombin, ADP, arachidonic acid, collagen, and ristocetin, and platelet contractile force by mechanical shear activation. Subject demographics, blood products transfused, and mortality were abstracted from the medical record. Subjects were grouped according to the need for any platelet transfusion within 24 hours of arrival and data were compared using T test with significance at alpha < 0.05.Results: Of 110 total subjects, 17 (15%) received any blood product transfusion within 24 hours of ED arrival. Of those receiving transfusions, 9/17 (53%) received an average of 3.1 (2.3) apheresis platelet units over 24 hours while 1.7(1.0) of these units were transfused within the first 4 hours of care. There were no differences in standard plasma coagulation tests (all p>0.06), and ROTEM parameters (all p>0.10). Platelet count was not different (164.7 vs. 230.4 x10^6/ml, p=0.1), but total platelet aggregation area under the curve to ADP (26.1 vs. 53.7, p=0.007) and arachidonic acid were decreased (20.9 vs. 41.7, p=0.03) in the transfused group. Platelet shear-initiated contraction force was also decreased (77.0 vs. 113.8 nN, p=0.04) in the platelet transfusion group.Conclusion: Platelets from Emergency Department trauma patients requiring urgent platelet transfusions remained reactive to thrombin, but were dysfunctional in their ability to aggregate in response to ADP, arachidonic acid, and shear stimulation.