13 Closed Head Injury

Closed head injury is the leading cause of death in young patients in industrialized countries. Patients who survive the initial injury are susceptible to sustaining secondary cerebral insults which are initiated by the release of endogenous neurotoxic inflammatory mediators. The presence of hypoxia and hypotension in the early resuscitative period represents the ‘‘key’’ parameter for induction of secondary brain injury and adverse outcome. The neuroinflammatory response in the injured brain contributes to cerebral edema, increased intracranial pressure (ICP), and decreased cerebral perfusion pressure (CPP). ICP monitoring and CPP therapy are recommended as a standard for patients with severe closed head injury. The ICP should be kept below 15 mmHg and the CPP above 70 mmHg in order to avoid secondary insults due to cerebral hypoperfusion. If a CPP 70 mmHg cannot be achieved by lowering the ICP, the mean arterial pressure (MAP) should be artificially raised by the use of catecholamines (CPP = MAP – ICP). Arterial ‘‘demand’’ hypertension in head-injured patients should not be lowered therapeutically since this physiological response is aimed at maintaining an adequate CPP once the cerebrovascular autoregulation has failed.