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An Objective View of the Effectiveness of Platelet Transfusion in Trauma Utilizing Thromboelastography
*Mathew Edavettal, *Brian W Gross, *James Alzate, *Frederick B Rogers
Lancaster General Hospital, Lancaster, PA
Objective: Platelet dysfunction (PD) may contribute to more severe bleeding in traumatic brain injury (TBI). One approach to treat this is to administer platelets. We sought to determine the efficacy of platelet administration on correcting PD utilizing objective platelet mapping outcomes as measured by thromboelastography (TEG).
Design: Retrospective chart review, May 2014 - February 2015.
Setting: Level II community trauma center.
Patients: TBI patients who received one thromboelastogram with platelet mapping showing PD who subsequently received a secondary thromboelastogram. Patients were divided into two groups: Group 1 received platelets between thromboelastograms and Group 2 did not receive platelets between thromboelastograms.
Intervention(s): Administration of platelets to TBI patients with PD at physician discretion, or no administration of platelets.
Main Outcome Measure(s): Adenosine diphosphate (ADP) and arachidonic acid (AA) pathway percent inhibition (PI) and maximum amplitude (MA). ADP and AA are factors that activate platelets so that platelet aggregation is augmented. TEG is able to measure the ability of platelets to respond to these factors by measuring the MA of the clot formed when these factors are administered in vitro.
Results: 423 TBI patients underwent thromboelastography from May 2014 - February 2015, of which 38 received two thromboelastograms with the first showing PD. Of this subset, 25 patients had platelets transfused. In the platelet group, change in AA MA significantly decreased compared to those in the non-platelet group (p=0.017). No significant change in ADP MA (p=0.593), or ADP PI (p=0.627) was observed. However a trend toward significance was observed in AA PI (p=0.075).
Conclusions: Platelet administration to patients with PD as measured by TEG resulted in improved AA pathway dysfunction, but not ADP pathway dysfunction.
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