Craniocerebral trauma--new pathophysiological and therapeutic viewpoints

Abstract

The prognosis has markedly improved during the last years after mild and moderate head injuries. After severe head trauma, this evolution could not be observed so far. This requires a better understanding of pathophysiological interaction, especially in the subacute and late phase of trauma. Review article. Causes for the development of secondary brain damage are the intracranial space demand after traumatic injury and edema formation which max result in ischemia, as well as inflammatory processes. Both isolated severe head trauma and polytrauma with or without brain damage may result in a systemic inflammatory response syndrome due to the synthesis of cytokines and other inflammatory mediators which may cause a single or multiple organ failure. The hypermetabolism after severe head trauma is often regarded as an interaction between the central nervous system and the whole organism by the activation of the neuroendocrine axis. Moreover, coagulation, metabolism and fracture healing are influenced by the onset of SIRS as well. Our knowledge about the bidirectional inflammatory interaction between brain and whole organism is still limited. It is generally accepted that extracranial complications are highly influential in determining the outcome from severe head injury.