Traumatic brain injury: pathophysiology and emergency management

Traumatic brain injury (TBI) is the most common cause of deaths and disabilities in young adults in the developed world. The World Health Organization (WHO) estimates the worldwide incidence at roughly 600/100,000 inhabitants/year. The American Centers for Disease Control and Prevention (CDC) estimate that up to 5.3 million US-citizens suffer from TBI-induced neurocognitive or functional impairment. The primary damage is mediated by a mechanic lesion of neuronal and glial structures. The amount or localisation of tissue damage explains a mild, medium or severe clinical presentation. Persistent deficits and the high mortality rate can also be attributed to secondary brain damage, which is caused by neurovascular phenomena, microthrombosis, release of neurotransmitters, excitotoxicity, and most notably, neuroinflammatory processes. The consecutive breakdown of cellular energy metabolism leads to cell depolarisations, which can be monitored by electroence-phalography as waves of cortical spreading depressions (CSDs). The presence of CSDs is an indicator for unfavourable outcome. Hence, medical treatment pre-dominantly aims at avoiding or at least reducing secondary brain damage. This requires best possible treatment in the preclinical and emergency room setting. Main goals are maintenance of oxygenation and perfusion. The current guidelines are discussed highlighting the emergency treatment of TBI patients.