Hemostatic disturbances in traumatic brain injury: from mechanism to management

Abstract

Coagulopathy following traumatic brain injury (TBI) is increasingly being recognized as a determinant of hematoma expansion and outcome. Unlike systemic trauma, where coagulopathy is often driven by hemorrhagic shock, TBI appears to induce a unique brain-derived hemostatic response. In this review, we discuss the mechanisms underlying TBI-induced coagulopathy, its diagnostic challenges, and association with hematoma expansion. We further evaluate evidence from randomized trials targeting coagulopathy in TBI, including interventions such as tranexamic acid, plasma, recombinant Factor VIIa, and fibrinogen. While several studies show proof of concept, clinical benefit remains inconsistent, likely due to issues of timing, heterogeneity, and underpowered study design. Moving forward, ultra-early and individualized approaches guided by real-time hemostatic monitoring may offer the most promising path. A better understanding of the temporal and mechanistic dynamics of coagulopathy will be essential for improving treatment strategies and patient outcomes.