Rethinking Platelet Dysfunction in Traumatic Brain Injury: From Platelet Count to Hemostatic Phenotype

Coagulopathy after traumatic brain injury (TBI) is multifactorial and dynamic, with major implications for hemorrhagic progression and outcome. Platelet dysfunction is an underrecognized component that may occur despite preserved platelet count. For the purpose of this point of view, platelet dysfunction refers to any measurable impairment in agonist-induced aggregation, receptor-pathway responsiveness [adenosine diphosphate (ADP)/P2Y12 and arachidonic acid (AA)/ cyclooxygenase-1 (COX-1) axes], or platelet contribution to whole-blood-clot strength, occurring disproportionate to or in the absence of thrombocytopenia. Functional impairment can appear early and has been associated with TBI severity, intracranial hemorrhage progression, transfusion requirements, and mortality. Conventional coagulation tests and platelet count are insufficient to identify this phenotype. Platelet function assays, including thromboelastography (TEG) with platelet mapping, may help characterize selected high-risk patients. However, the evidence remains largely observational, thresholds are heterogeneous, interassay concordance is poor, and platelet transfusion or desmopressin should not be regarded as routine interventions. This point of view reframes platelet dysfunction after TBI as a dynamic hemostatic phenotype and argues for prospective phenotype-guided trials.