Abstract
In blunt head trauma, primary brain injury takes the form of surface contusions and fractures, diffuse axonal injury and intracranial hemorrhage. Secondary damage may result from delayed pathological events including cerebral ischemia, brain edema and increased intracranial pressure (ICP). These events reinforce one another and may lead to a fatal disturbance of the balance between oxygen delivery and oxygen demand. Improvement or maintenance of this balance is a main issue in the treatment of severe head-injured patients. In this respect reduction of ICP is a key tool as it may improve brain perfusion and attenuate the pathologic cascade. Therapeutic interventions that adequately reduce ICP do not necessarily improve and may even impair tissue oxygenation (Unterberg et al., 1997a). This addresses the need for adequate monitoring of brain oxygenation during and after treatment.
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