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Platelet Dysfunction Persists After Trauma Despite Balanced Blood Product Resuscitation
*Taylor E Wallen1, *Matthew Baucom1, *Dennis Hanseman1, *Charles E Wade2, *John B Holcomb3, Timothy A Pritts1, Michael D Goodman1
1University of Cincinnati, Cincinnati, OH;2University of Texas Health Science Center at Houston, Houston, TX;3University of Alabama Birmingham, Birmingham, AL

Objective(s): Platelet activation and aggregation are critical to the initiation of hemostasis following trauma with hemorrhage. Platelet dysfunction has been recognized as a contributing factor to acute traumatic coagulopathy. The goal of this study was to evaluate the timing and severity platelet dysfunction in massively transfused traumatically injured patients during the first 72 hours after injury.
Methods: A retrospective secondary analysis of platelet count and function was performed using samples from the PROPPR study collaborative. Assessments of platelet characteristics were measured at 8 timepoints during the first 72 hours of hospitalization and compared between 30-day survivors and non-survivors. Platelet function was analyzed with the use of serial thrombelastography and impedance aggregometry with agonists including: arachidonic acid (AA), adenosine diphosphate (ADP), collagen (COL), and thrombin receptor activating peptide (TRAP). Platelet counts were assessed via flow cytometry for CD41 and CD61 positive cells.
Results: The quantity and functionality of platelets from 680 patients were analyzed. Platelet counts were significantly reduced from baseline to 72 hours after hospital admission with further reductions noted in non-survivor compared to survivor cohorts (Figure 1A). Platelet aggregation via ADP, AA, COL, and TRAP was significantly reduced in non-survivor patients at all time points compared to survivor patients (Figure 1B). The nadir of platelet aggregation was at 4-6 hours after admission with notable improvements in viscoelastic maximum clot formation and agonist-induced aggregation by 12 hours without concomitant improvement in platelet count (Figure 1B). There were no significant differences in platelet aggregation or quantity between patients randomized to the 1:1:1 and 1:1:2 resuscitation cohorts.
Conclusion: Persistence and severity of platelet dysfunction following traumatic injury is associated with post-injury mortality despite balanced blood product resuscitation. Platelet
aggregability starts to recover 12 hours after injury independent of worsening thrombocytopenia. Failure of this recovery process portends a poor prognosis.
Figure 1: A. Platelet Counts and B. Aggregation via Adenosine Diphosphate agonism from hospital admission to 72 hours ** p<0.001 between survivor and non-survivor groupsADP-adenosine diphosphate


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