Brain hypoxia is exacerbated in hypobaria during aeromedical evacuation in swine with TBI.

Background: There is inadequate information on the physiological effects of aeromedical evacuation on wounded warfighters with traumatic brain injury (TBI). At altitudes of 8,000 ft., the inspired oxygen is lower than standard sea level values. In troops suffering TBI, this reduced oxygen may worsen or cause secondary brain injury. We tested the hypothesis that the effects of prolonged aeromedical evacuation on critical neurophysiological parameters (i.e., brain oxygenation [PbtO2]) of swine with a fluid percussion injury (FPI) -TBI would be detrimental compared to ground (normobaric) transport. Methods: Yorkshire swine underwent FPI-TBI with pre-transport stabilization before being randomized to a 4 h aeromedical transport at simulated flight altitude of 8,000 ft. (HYPO, N = 8) or normobaric ground transport (NORMO, N = 8). Physiological measurements (i.e., PbtO2, cerebral perfusion pressure [CPP], intracranial pressure [ICP], regional cerebral blood flow [rCBF], mean arterial blood pressure [MAP], and oxygen transport variables) were analyzed. Results: Survival was equivalent between groups. Measurements were similar in both groups at all phases up to and including onset of flight. During the flight, PbtO2, CPP and MAP were significantly lower in HYPO vs. NORMO groups, respectively. At the end of flight, rCBF was lower in HYPO vs. NORMO groups. Other parameters such as ICP, cardiac output and mean pulmonary artery pressure were not significantly different between the two groups. Conclusion: A 4 h aeromedical evacuation at simulated flight altitude of 8,000 ft. caused a notable reduction in neurophysiological parameters compared to normobaric conditions in this TBI swine model. Results suggest hypobaric conditions exacerbate cerebral hypoxia and may worsen TBI in casualties already in critical condition. Evidence Level II, Animal Research (C) 2016 Lippincott Williams & Wilkins, Inc.

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