HYPOBARIA DURING LONG RANGE FLIGHT RESULTED IN SIGNIFICANTLY INCREASED HISTOPATHOLOGICAL EVIDENCE OF LUNG AND BRAIN DAMAGE IN A SWINE MODEL

Background Aeromedical evacuation to definitive care is standard in current military conflicts. However, there is minimal knowledge on the effects of hypobaria on either the flight crew or patients. The effects of hypobaria was investigated using healthy swine. Methods Anesthetized Yorkshire swine underwent a simulated 4 h “transport” to an altitude of 2,441 m (8,000 ft.; HYPO, N = 6) or at normobaric conditions (NORMO, N = 6). Physiological and biochemical data were collected. Organ damage was assessed for hemorrhage, inflammation, edema, necrosis and, for lungs only, microatelectasis. Results All parameters were similar prior to and after “transport” with no significant effects of hypobaria on hemodynamic, neurologic, or oxygen transport parameters, nor on blood gas, chemistry, or complete blood count data. However, the overall Lung Injury Score was significantly worse in the HYPO than the NORMO group (10.78 ±1.22 vs. 2.31 ± 0.71, respectively) with more edema/fibrin/hemorrhage in the subpleural, interlobular and alveolar space, more congestion in alveolar septa, and evidence of microatelectasis (vs. no microatelectasis in the NORMO group). There was also increased severity of pulmonary neutrophilic (1.69 ±0.20 vs. 0.19 ±0.13) and histiocytic inflammation (1.83 ±0.23 vs. 0.47 ±0.17) for HYPO vs. NORMO, respectively. On the other hand, there was increased renal inflammation in NORMO compared to HYPO (1.00 ±0.13 vs. 0.33 ±0.17, respectively). There were no histopathological differences in brain (whole or individual regions), liver, pancreas or adrenals. Conclusion Hypobaria, itself, may have an adverse effect on the respiratory system, even in healthy individuals and this may be superimposed on combat casualties where there may be pre-existing lung injury. The additional effects of anesthesia and controlled ventilation on these results are unknown and further studies are indicated using awake models to better characterize the mechanisms for this pathology and the factors that influence its severity. Level of Evidence Level II, Therapeutic/Care Management Corresponding author: Anke H. Scultetus, M.D. NeuroTrauma Department, Naval Medical Research Center, 503 Robert Grant Avenue, Silver Spring, MD 20910, Phone: 301-319-9526, Fax: 301-319-7486, E-mail: anke.h.scultetus2.civ@mail.mil Conflict of interest statement: For all authors, no conflicts are declared. Source of Funding: This work was funded by CDMRP award W81XWH-13-2-0022. Meetings: This manuscript was presented (D. Malone) as an oral quick shot at the 31st Annual Scientific Assembly for the Eastern Association for the Surgery of Trauma (EAST) held in Lake Buena Vista, FL from January 9-13, 2018. © 2018 Lippincott Williams & Wilkins, Inc.

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