Defining the Systemic Response to Flight After Polytrauma in a Murine Model.

Abstract

INTRODUCTION: Aeromedical evacuation continues to grow and push altitude boundaries as unmanned aerial vehicle feasibility is explored. The inherent hypobaric, hypoxic environment that comes with aeromedical evacuation is known to be deleterious in various injury models, but no studies have investigated the effects of post-injury flight after polytrauma. This study hypothesized that hypobaric hypoxia inherent to the aeromedical evacuation environment potentiates the proinflammatory milieu of murine polytrauma, worsens systemic and organ-level endotheliopathy, and modulates coagulability. MATERIALS AND METHODS: Mice underwent a polytrauma model consisting of midline laparotomy, rectus muscle crush, splenectomy, and hemorrhagic shock, followed by simulated flight for one hour at 12,000 feet. Cohorts included untouched, flight alone, polytrauma, and polytrauma with flight. Whole blood and lungs were collected. Serum inflammatory markers, serum endotheliopathy markers, lung immunohistochemistry, and coagulation profiles were analyzed. RESULTS: Flight combined with polytrauma was found to elevate systemic proinflammatory cytokines, including IL-1&#x3b2;, MCP-1, MIP-1&#x3b1;, and TNF&#x3b1;, from control levels (P&#x2009;<&#x2009;.05). Notably, IL-1&#x3b1; was uniquely increased from polytrauma to polytrauma with flight (P&#x2009;<&#x2009;.05). The endotheliopathy biomarker, syndecan, was increased by polytrauma and polytrauma with flight compared to controls, but without a difference between polytrauma and polytrauma with flight. Lung histological markers of endothelial disruption and rotational thromboelastometry parameters were unchanged by flight after polytrauma. CONCLUSIONS: In this murine model of polytrauma and post-injury flight, early altitude exposure after polytrauma had an additive effect on the proinflammatory state, with the potential to differentiate flight exposure utilizing IL-1&#x3b1;. Early altitude exposure did not, however, exacerbate trauma-induced coagulopathy or endotheliopathy. Future studies should continue to address the physiologic basis of worsened clinical outcomes after early post-injury aeromedical evacuation.