[Traumatic brain injury: impact on timing and modality of fracture care]

Traumatic brain injury (TBI) represents the major "killing factor" after trauma in young individuals. Those patients who survive the initial injury are highly susceptible to secondary insults to the injured brain which are mainly caused by hypotension and/or hypoxia in the early resuscitative period. Furthermore, a potent inflammatory cascade is initiated within the injured brain which leads to the development of brain edema and delayed neuronal cell death. This profound endogenous neuroinflammatory response after TBI, which is phylogenetically aimed at repairing lesioned tissue and defending the brain from invading pathogens, is in large part responsible for the extent of secondary brain damage and adverse outcome. Thus, the optimal management of the multiply injured patient, based on a thorough understanding of the pathophysiological alterations after TBI, should avoid an iatrogenic "second hit" which may be devastating to the injured brain. The standard approach of "early total care" for isolated fractures should be strictly avoided in brain-injured patients in favor of an "orthopedic damage control" concept with temporary external fixation of long bone fractures and priority given to early transfer to intensive care. The present review provides an up-to-date overview on the neuroinflammatory pathophysiology of brain injury and its implications for an optimized concept of fracture care in TBI patients.