As the population ages, it is more common to encounter patients with traumatic brain injury (TBI) who are on antithrombotic therapy for preexisting illnesses. Premorbid use of antithrombotic medications such as warfarin, aspirin, and clopidogrel may increase the risk and severity of traumatic intracranial hemorrhage and may predispose patients to enlargement of these posttraumatic lesions.1,2 Standard laboratory analyses are used in patients with TBI to evaluate the degree of anticoagulation due to vitamin K antagonists (ie, warfarin) as well as guide goal-directed reversal of the anticoagulatory effects of these medications to acceptable subtherapeutic levels.3–7 Unfortunately, these routine coagulation tests are insufficient to evaluate platelet activity and guide hemostatic therapy in TBI patients on antiplatelet therapy.
Recently, point-of-care aspirin response unit (ARU) and P2Y12 response unit (PRU) assays for evaluating aspirin- and thienopyridine-induced platelet inhibition have become widely available and have undergone extensive external validation in the cardiac literature.8–15 The assays enable platelet function testing for patients taking aspirin, P2Y12 inhibitors (clopidogrel, ticlopidine, or prasugrel), and IIb/IIIa inhibitors (abciximab or eptifibatide)8–12 and has demonstrated nearly 100% sensitivity and 96% specificity for the detection of antiplatelet function.16 However, there are currently insufficient data demonstrating the utility of the ARU and PRU assays in assessing platelet function in patients with TBI. In the current study, we evaluated the ARU and PRU assays for the detection of platelet inhibition in TBI patients on premorbid antiplatelet agents.
From Utility of the Aspirin and P2Y12 Response Assays to Determine the Effect of Antiplatelet Agents on Platelet Reactivity in Traumatic Brain Injury by Phillip V. Parry, MD; Phillip A. Choi, BS; Joshua S. Bauer, MS; David M. Panczykowski, MD; Ava M. Puccio, RN, PhD; David O. Okonkwo, MD, PhD