Low level of procoagulant platelet microparticles is associated with impaired coagulation and transfusion requirements in trauma patients

BACKGROUND: Following activation, platelets release small vesicles called platelet-derived microparticles (PMPs). PMPs accelerate thrombin generation and thus clot formation at sites of injury by exposing the procoagulant membrane phospholipid phosphatidylserine (PS). The role of PMPs in coagulopathy and hemorrhage following trauma remains elusive. We hypothesized that low levels of PS-positive PMPs (PS + PMPs) would be associated with impaired clot formation. METHODS: This is a prospective observational study of 210 trauma patients admitted directly to a Level 1 trauma center. Plasma levels of PS + PMPs were determined by flow cytometry. Coagulation status was assessed by rotational thrombelastometry, and impaired clot formation was defined by an alpha angle less than 63 degrees using the tissue factor-based EXTEM reagent. Transfusion requirement was assessed by number of units of red blood cells (RBCs) transfused within 24 hours of admission; platelet aggregation capacity was evaluated by the Multiplate assay; and injury severity was determined by the Injury Severity Score (ISS). RESULTS: The median ISS was 17, and blood samples were obtained after a median of 65 minutes following injury. Significantly lower levels of PS + PMPs were found in patients with impaired clot formation (p < 0.001). A low level of PS + PMPs was associated with a higher number of RBCs transfused during the initial 24 hours after admission (p < 0.03) when corrected for risk factors, for example, platelet count, hemoglobin level, and ISS. Platelet aggregation and PS + PMPs did not correlate significantly. CONCLUSION: Low levels of PMPs were associated with impaired clot formation in trauma patients at admission and also with the number of RBC transfusions. This suggests that PMPs may play an important and not previously investigated role in trauma-induced coagulopathy. Copyright (C) 2014 by Lippincott Williams & Wilkins