Traumatic brain injury-induced coagulopathy

Abstract

Coagulopathy after traumatic brain injury is frequent and predicts poor clinical outcomes for the patients. Despite their similar clinical manifestations, traumatic brain injury-induced coagulation is mechanistically distinct from coagulopathy arising from trauma to the body and limbs and associated hemorrhagic shock. The former is often consumptive in nature and evolves rapidly from an injury-induced hypercoagulable state, whereas the latter is commonly deficient and dilutional due to substantial blood loss, tissue hypoperfusion and ischemia, and fluid resuscitation. Despite extensive reports of its high prevalence, severe clinical presentations and association with poor outcomes, traumatic brain injury-induced coagulopathy remains poorly understood mechanistically. Recent studies have suggested that extracellular vesicles released from injured brains play a key role in causing and disseminating systemic traumatic brain injury-induced coagulopathy. These extracellular vesicles contain membrane fragments and intracellular granules such as mitochondria. They promote coagulopathy by disrupting the endothelial integrity, activating platelets and endothelial cells, and propagating oxidative stress. In this chapter, we provide a comprehensive review of the pathogenesis of traumatic brain injury-induced coagulopathy and its underlying mechanisms. We discuss its clinical epidemiology, risk factors, clinical presentations, laboratory diagnoses, and outcome assessments, and we also identify key knowledge gaps in understanding, diagnosing, and managing this severe complication of traumatic brain injury.