Is there a role for hyperoxia in the management of severe traumatic brain injury?

The pathophysiological features of neurotrauma, including traumatic brain injury (TBI) and spinal cord injury, involve a primary mechanical injury that reflects the complex interplay of contusion, compression, and shear and rotational forces as well as a series of vascular, metabolic, molecular, and inflammatory processes that synergistically culminate in a process termed secondary injury. 2,5,8,9 Although improved outcomes after TBI have occurred due to the use of restraint systems in automobiles, protocol-driven critical care management, and judicious use of decompressive surgery, no significant attenuation of secondary injury mechanisms has yet occurred in the clinical setting, despite promising data from animal models. There are persuasive data implicating mitochondrial dysfunction and delayed apoptosis or programmed cell death in the pathobiological mechanisms of neuronal cell death after TBI. Based on some animal models and preliminary clinical data, it has been postulated that impairments in oxygen delivery and extraction could be involved in the mechanism of posttraumatic mitochondrial dysfunction in neurons. 1,7