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A prospective study of platelet function in trauma patients

2016; Lippincott Williams & Wilkins; Volume: 80; Issue: 5 Linguagem: Inglês

10.1097/ta.0000000000001017

2163-0763

Matthew T. Ramsey, Timothy C. Fabian, Charles P. Shahan, John P. Sharpe, Scott E. Mabry, Jordan A. Weinberg, Martin A. Croce, Lisa K. Jennings,

Venous Thromboembolism Diagnosis and Management

BACKGROUND Exsanguination associated with acute traumatic coagulopathy is a leading cause of death following injury. While platelets occupy a pivotal role in clot formation, clinical research has been scant because of complexities resulting from the need for rapid handling and complex testing of platelet functions. While the thrombin pathway has been proposed as a mediator of platelet dysfunction in trauma, it has not been systematically investigated. The purpose of this study was to evaluate the thrombin pathway in platelet dysfunction. METHODS Forty trauma patients and 20 noninjured controls were enrolled in the study at a Level I trauma center. Platelet aggregation was tested by light transmission aggregometry with two agonists, adenosine diphosphate (ADP) and thrombin receptor agonist peptide (TRAP). Mean fluorescence intensity and percent positivity of CD62 on ADP-activated platelets were evaluated using flow cytometry. Enzyme-linked immunosorbent assays were performed to evaluate the concentrations of D-dimer, thrombin-antithrombin complex (TAT), and prothrombin fragment 1 + 2 (PF 1 + 2) in each sample. RESULTS Compared with healthy controls, trauma patients had significantly decreased ADP- and TRAP-mediated platelet aggregation and ADP-mediated CD62 expression. In trauma patients, TRAP-mediated aggregation was inversely proportional to head Abbreviated Injury Scale (AIS) score. Glasgow Coma Scale (GCS) score was directly proportional to TRAP- and ADP-mediated aggregation. When compared with controls, significant differences of D-dimer, TAT, and PF 1 + 2 were found. Measures of shock, including admission blood pressure, pulse, base deficit, and lactate level, did not correlate with platelet dysfunction. CONCLUSION Trauma patients have significantly lower levels of platelet activation and aggregation compared with healthy controls. Severity of head injury was significantly correlated with platelet dysfunction in a stepwise fashion. Trauma patients also have significantly increased levels of D-dimer, TAT, and PF 1 + 2 when compared with healthy controls. Our data suggest that the thrombin receptor pathway plays an important role in platelet dysfunction in trauma. LEVEL OF EVIDENCE Prognostic and epidemiologic study, level III.