Early platelet dysfunction: an unrecognized role in the acute coagulopathy of trauma

Abstract

Background: Our aim was to determine the prevalence of platelet dysfunction using an end point of assembly into a stable thrombus after severe injury. Although the current debate on acute traumatic coagulopathy has focused on the consumption or inhibition of coagulation factors, the question of early platelet dysfunction in this setting remains unclear.

Study design: Prospective platelet function in assembly and stability of the thrombus was determined within 30 minutes of injury using whole blood samples from trauma patients at the point of care using thrombelastography-based platelet functional analysis.

Results: There were 51 patients in the study. There were significant differences in the platelet response between trauma patients and healthy volunteers, such that there was impaired aggregation to these agonists. In trauma patients, the median ADP inhibition of platelet function was 86.1% (interquartile range [IQR] 38.6% to 97.7%) compared with 4.2 % (IQR 0 to 18.2%) in healthy volunteers. After trauma, the impairment of platelet function in response to arachidonic acid was 44.9% (IQR 26.6% to 59.3%) compared with 0.5% (IQR 0 to 3.02%) in volunteers (Wilcoxon nonparametric test, p < 0.0001 for both tests).

Conclusions: In this study, we show that platelet dysfunction is manifest after major trauma and before substantial fluid or blood administration. These data suggest a potential role for early platelet transfusion in severely injured patients at risk for postinjury coagulopathy.

Copyright © 2012 American College of Surgeons. Published by Elsevier Inc. All rights reserved.

Figures

Figure 1. Overview of TEG platelet mapping

The clot strength, depicted on the y-axis, in response to platelet agonists MAADP or MAAA is compared to the maximum hemostatic activity (MAThrombin). The percent platelet inhibition in response to either the ADP or AA agonist is calculated using the following equation: (100 − [(MAADP(AA) − MAFibrin)/(MAThrombin − MAFibrin)× 100]. Normal tracing (1a) shows that the ADP or AA stimulated thrombus formation is similar to the maximum hemostatic activity (MAADP or AA equals MAThrombin). A representative tracing from a trauma patient on arrival to the ED (1b) shows that the ADP or AA stimulated thrombus is profoundly impaired, with the contribution of MAADP and MAAA to clot formation both less than 3% of total clot strength.

Figure 2

Median % ADP Receptor Inhibition in trauma patients compared to healthy volunteers, including stratification according to shock (Base Deficit), blood transfusion (RBCs), and tissue injury (ISS).

Figure 3

Median % AA (TXA2) Receptor Inhibition in trauma patients compared to healthy volunteers, including stratification according to shock (Base Deficit), blood transfusion (RBCs), and tissue injury (ISS).

Figure 4

A 37 year old female presented to the MHSB trauma center with a grade V liver laceration, multiple rib fracture, and a grade I splenic injury following a snowboarding crash. She was coagulopathic in the ED with a systolic blood pressure of 70 mmHg. Her initial coagulation profile and platelet mapping tracings are depicted (4a). She received 4 units PRBC, 2 units plasma, and 2 apheresis units of platelets in the first 1.5 hours following arrival. Resuscitation was goal directed, using TEG platelet function analysis to monitor blood component resuscitation; initial ADP inhibition of 90% improved substantially following administration of blood products (Figure 4b). After reversing her coagulopathy, the patient was successfully managed non-operatively with selective hepatic artery angioembolization.