Hypobaric Conditions in Cabin Altitude Restricted Aeromedical Evacuation Induce Systemic Inflammation Following Porcine Traumatic Brain Injury.

INTRODUCTION

Secondary injury following traumatic brain injury (TBI) commonly results from hypoxia. Cabin Altitude Restriction (CAR) is used in postinjury aeromedical evacuation (AE) to reduce the hypobaric effects of flight on wounded warriors. Previous work has shown increased inflammation after high altitude exposure following TBI. The aim of this study is to determine the level of systemic inflammation induced by the hypobaric conditions of CAR after TBI.

METHODS

Forty-eight female pigs were utilized to test TBI vs. sham, CAR hypobaria and standard cabin (SC) hypobaria vs. ground conditions; as well as relative hypoxia. Traumatic brain injury was induced by controlled cortical injury. Hypobaric conditions were established in an altitude chamber at levels of 5000 ft (CAR) or 8000 ft (SC) for 90 min with or without relative hypoxia (95% SpO2 for 5000 ft or 90% SpO2 for 8000 ft) while at altitude. Serum cytokines were analyzed via enzyme linked immunosorbent assay at the 90-min and 6-h post-injury timepoints.

RESULTS

Serum interleukin (IL)-1b, IL-6, and tumor necrosis factor-alpha were significantly elevated following TBI with exposure to altitude-induced hypobaria/hypoxia at CAR and SC altitude pressure compared to ground level, normoxic conditions. This increase in cytokine release was present immediately post-flight and following 4 h of post-flight observation.

CONCLUSIONS

The CAR-prescribed cabin altitude of 5000 ft may not be sufficient in ameliorating altitude-induced inflammatory cytokine release following TBI. This altitude effect was not rescued with supplemental oxygen to promote SpO2 of 100%, demonstrating a hypobaric effect independent of altitude-related hypoxia. Further study may focus on delayed AE after injury rather than CAR for early post-injury flight.