Blast-induced brain injury and posttraumatic hypotension and hypoxemia.

Explosive munitions account for more than 50% of all wounds sustained in military combat, and the proportion of civilian casualties due to explosives is increasing as well. But there has been only limited research on the pathophysiology of blast-induced brain injury, and the contributions of alterations in cerebral blood flow (CBF) or cerebral vascular reactivity to blast-induced brain injury have not been investigated. Although secondary hypotension and hypoxemia are associated with increased mortality and morbidity after closed head injury, the effects of secondary insults on outcome after blast injury are unknown. Hemorrhage accounted for approximately 50% of combat deaths, and the lungs are one of the primary organs damaged by blast overpressure. Thus, it is likely that blast-induced lung injury and/or hemorrhage leads to hypotensive and hypoxemic secondary injury in a significant number of combatants exposed to blast overpressure injury. Although the effects of blast injury on CBF and cerebral vascular reactivity are unknown, blast injury may be associated with impaired cerebral vascular function. Reactive oxygen species (ROS) such as the superoxide anion radical and other ROS, likely major contributors to traumatic cerebral vascular injury, are produced by traumatic brain injury (TBI). Superoxide radicals combine with nitric oxide (NO), another ROS produced by blast injury as well as other types of TBI, to form peroxynitrite, a powerful oxidant that impairs cerebral vascular responses to reduced intravascular pressure and other cerebral vascular responses. While current research suggests that blast injury impairs cerebral vascular compensatory responses, thereby leaving the brain vulnerable to secondary insults, the effects of blast injury on the cerebral vascular reactivity have not been investigated. It is clear that further research is necessary to address these critical concerns.