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Accession Number:
AD1004385
Title:
Defining Platelet Function During Polytrauma
Descriptive Note:
Technical Report,10 Jan 2011,09 Jan 2014
Corporate Author:
Virginia Commonwealth University Richmond United States
Report Date:
2014-04-01
Pagination or Media Count:
772.0
Abstract:
This is the final report of W81XWH-11-2-0089 which was focused on defining platelet function during polytrauma. The goals of the study were to 1 collect real time blood and plasma samples in severe trauma patients and 2 define the relationships between platelet function and injury patternsseverity, shock, transfusion and other clinical outcomes. A total of 148 severely injured patients were screened and 99 were enrolled into this trial. Blood sampling occurred in the Emergency Department before any intervention, and then at 8, 12, 24, 48 and 72 hours. The primary results showed that based on two-way ANOVA of the effects of injury severity score ISS and shock category on clot formation parameters, only PT met criteria for being significantly co-dependent on both ISS and shock state. PTT was only affected by shock state, and fibrinogen was independently affected by both ISS and shock with a very strong trend towards co-dependence. Notably, there was no effect ofISS or shock on whole blood clot onset times TEG-R, FOT, fibrin polymerization time TEG-K time, lysis TEG-LY30, or clotelastic modulus. TEG alpha angle and platelet contractile force were affected only by shock, while there were independent effects of both ISS category and shock category on TEG-MA and G. There were no significant interactions present between ISS and shock category for any whole-blood clot formation parameters all interaction p values 0.05. We conclude that plasmatic, rather than whole-blood clot formation parameters require both severe injury and shock to be present in order to become abnormal after trauma. Our data suggests that profound injury or shock, and more likely shock, are independently associated with abnormal clot formation in whole blood. These changes are perhaps mediated by changes in fibrinogen concentration and platelet dysfunction.
Distribution Statement:
APPROVED FOR PUBLIC RELEASE
