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Updated: Mar 23, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Inhibition of platelet function is common following even minor injury
Sarah Sirajuddin1, Carrie Valdez, Louis DePalma
1From the Center for Trauma and Critical Care (S.S., C.V., P.M., R.S., M.S., B.S.), Department of Surgery, and Department of Pathology (L.D.), The George Washington University, Washington, District of Columbia.
Background:
Hemorrhage remains the leading cause of preventable death following injury. Whereas significant attention has been paid to the coagulation cascade, there are fewer studies evaluating platelet dysfunction following injury. Thrombelastogram platelet mapping (TEG-PM) allows for the measurement of maximal potential clot strength and clot strength selectively caused by arachidonic acid and adenosine disphosphate receptors on the platelet. The purpose of this study was to determine the incidence and magnitude of receptor-specific platelet dysfunction following injury in patients who are not otherwise pharmacologically anticoagulated.
Methods:
A retrospective study of adult trauma patients evaluated at a Level I trauma center from August 2013 to September 2014 was conducted. Platelet function was assessed using TEG-PM. Patients on any anticoagulant or antiplatelet medication were excluded. Patients were divided into those with and without radiographically evident traumatic brain injury (TBI). Demographic variables, Injury Severity Score (ISS), injury pattern, laboratory test results, and mortality were abstracted. Statistical comparisons were made using the Student's t test or Mann-Whitney U-test.
Results:
The study includes 459 patients, 92% following blunt injury. Median ISS was 5. Patients with TBI (n = 102) were significantly older (median age, 54 years vs. 35 years), were more severely injured (median ISS, 10 vs. 4), had a longer stay and higher mortality (9% vs. 0.3%). Maximal potential clot strength was normal in all cohorts, but the arachidonic acid and adenosine diphosphate pathways were significantly inhibited (30% ± 26% and 58% ± 27%, respectively). There was no correlation between TEG-PM values and ISS, length of stay, or mortality. There was no difference in the TBI cohort. There were no significant differences in TEG-PM parameters in those with an ISS greater than 14. There was no significant change in TEG-PM following platelet transfusion.
Conclusion:
Marked platelet inhibition is common following minor injury. Whereas the clinical significance of this finding remains unknown, the results of this study should be factored in the overall resuscitative strategy.
Level Of Evidence:
Prognostic/epidemiogic study, level III.
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