Be Aware of Potential for Significant Platelet Dysfunction in TBI Patients Platelet Dysfunction and Platelet Transfusion in Traumatic Brain Injury

Background: Platelet function, which is important for initial coagulation after traumatic brain injury (TBI), may be negatively altered by medication or the injury itself. Platelet transfusion is associated with increased risk of complications and/or death. Objective: To determine if platelet transfusion would improve aspirin-induced, but not trauma-induced platelet dysfunction. Design: Single-institution, prospective, case cohort study. Methods: Patients with intracranial hemorrhage (subdural, epidural, subarachnoid, and/or intraparenchymal) after TBI were assessed with platelet count and hematocrit initially after admission and at the next clinical blood draw after admission. Platelet function was assessed by a Multiplate multiple electrode aggregometer (but clinicians were blinded to results). Patients on anticoagulation therapy other than aspirin or clopidogrel, a history of thrombocytopenia or other coagulopathy, or non-head, neck, or face Abbreviated Injury Scale score >3 were excluded. All patients on pre-injury aspirin therapy were transfused 1 unit of apheresis platelets <4 hours after admission. Patients taking aspirin and given transfusion were compared to those not taking aspirin. Results: Of the 17 patients prospectively enrolled (median admit Glasgow Coma Scale score of 15), 12 were taking aspirin (including 3 also on clopidogrel). Ten were taking aspirin 81 mg and 2 were taking aspirin 325 mg. All 12 received platelet transfusions; none of the 5 non-aspirin patients received transfusions. Aspirin patients were older (median age, 79.5 years) than non-aspirin patients (67 years). All aspirin patients had abnormal arachidonic acid (median, 19 U) and collagen platelet activation (median, 25.5 U), whereas nonaspirin patients had normal arachidonic activation (median, 46 U) but abnormal collagen activation (median, 37.0 U). Platelet count did not vary over time for non-aspirin patients. After platelet transfusion in aspirin patients, arachidonic activation improved (median, 26 U), but collagen activation was unchanged (median, 24 U). Platelet count did not vary over time in aspirin and transfusion patients. Conclusions: Patients with TBI have abnormal platelet function in response to collagen that is not improved with transfusion of 1 unit of apheresis platelets. Patients taking platelets had their abnormal response to arachidonic acid improve with platelet transfusion Reviewer's Comments: This small study demonstrates that aspirin, as well as brain injury itself, negatively impacts platelet function, and that transfusion of platelets can correct some of these changes. The clinical relevance of these changes is not defined by the study, as subsequent neurological status and CT scans were beyond its scope. Many unanswered questions are left hanging, including impact of severity of brain injury (clinical and radiographic), timing of assessment, optimal amount of platelet transfusion, impact of platelet count, etc. Neurosurgeons should be aware of the potential for significant platelet dysfunction in patients with TBI. (Reviewer-N. Scott Litofsky, MD, FACS).