Effect of hypobaria and hyperoxia during sepsis on survival and energy metabolism

Choi, Myeongjin; Tamrakar, Pratistha; Schuck, Patrícia Fernanda; Proctor, Julie L.; Moore, Ashley; Asbury, Katrina; Fiskum, Gary; Coksaygan, Turhan; Cross, Alan S.

doi:10.1097/ta.0000000000001909

Cited by 3 publications

(1 citation statement)

References 25 publications

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“…The adverse effects of air transport-relevant hypobaria exposure following TBI in rats led to experiments testing the consequences of hypobaria in other injury paradigms. Using a rat model of polymicrobial sepsis, there were no significant changes in serum cytokine levels or mortality when rats were exposed to 8,000 ft hypobaria for 6 h, starting at 24 h postinjury (6). A similar exposure to hypobaria also had no significant effect in a mouse model of hemorrhagic shock (7).…”

Section: Introductionmentioning

confidence: 94%

Air-Evacuation-Relevant Hypobaria Following Traumatic Brain Injury Plus Hemorrhagic Shock in Rats Increases Mortality and Injury to the Gut, Lungs, and Kidneys

Proctor

Medina

Rangghran

et al. 2021

Shock

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Rats exposed to hypobaria equivalent to what occurs during aeromedical evacuation within a few days after isolated traumatic brain injury exhibit greater neurologic injury than those remaining at sea level. Moreover, administration of excessive supplemental O 2 during hypobaria further exacerbates brain injury. This study tested the hypothesis that exposure of rats to hypobaria following controlled cortical impact (CCI)-induced brain injury plus mild hemorrhagic shock worsens multiple organ inflammation and associated mortality. In this study, at 24 h after CCI plus hemorrhagic shock, rats were exposed to either normobaria (sea level) or hypobaria (¼8,000 ft altitude) for 6 h under normoxic or hyperoxic conditions. Injured rats exhibited mortality ranging from 30% for those maintained under normobaria and normoxia to 60% for those exposed to 6 h under hypobaric and hyperoxia. Lung histopathology and neutrophil infiltration at 2 days postinjury were exacerbated by hypobaria and hyperoxia. Gut and kidney inflammation at 30 days postinjury were also worsened by hypobaric hyperoxia. In conclusion, exposure of rats after brain injury and hemorrhagic shock to hypobaria or hyperoxia results in increased mortality. Based on gut, lung, and kidney histopathology at 2 to 30 days postinjury, increased mortality is consistent with multi-organ inflammation. These findings support epidemiological studies indicating that increasing aircraft cabin pressures to 4,000 ft altitude (compared with standard 8,000 ft) and limiting excessive oxygen administration will decrease critical complications during and following aeromedical transport.

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Section: Introductionmentioning

confidence: 94%

Air-Evacuation-Relevant Hypobaria Following Traumatic Brain Injury Plus Hemorrhagic Shock in Rats Increases Mortality and Injury to the Gut, Lungs, and Kidneys

Proctor

Medina

Rangghran

et al. 2021

Shock

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Influence of Time to Transport to a Higher Level Facility on the Clinical Outcomes of US Combat Casualties with TBI: A Multicenter 7-Year Study

et al. 2019

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IntroductionTraumatic brain injury (TBI) is a leading cause of death and disability worldwide and is associated with mortality rates as high as 30%. Patients with TBI are at high risk for secondary injury and need to be transported to definitive care expeditiously. However, the physiologic effects of aeromedical evacuation are not well understood and may compound these risks. Combat TBI patients may benefit from delayed aeromedical evacuation. The goal of this study was to evaluate the impact of transport timing out of theater via Critical Care Air Transport Teams (CCATT) to a higher level facility on the clinical outcomes of combat casualties with TBI.Materials and MethodsWe performed a retrospective review of patients with TBI who were evacuated out of theater by CCATT from January 2007 to May 2014. Data abstractors collected flight information, vital signs, procedures, in-flight assessments, and outcomes. Time to transport was defined as the time from injury to CCATT evacuation out of combat theater. We calculated descriptive statistics and constructed regression models to determine the association between time to transport and clinical outcomes. This study was approved by the U.S. Air Force 59th Medical Wing Institutional Review Board.ResultsWe analyzed the records of 438 patients evacuated out of theater via CCATT and categorized them into three groups: patients who were transported in one day or less (n = 165), two days (n = 163), and three or more days (n = 110). We used logistic regression models to compare outcomes among patients who were evacuated in two days or three or more days to those who were transported within one day while adjusting for demographics, injury severity, and injury type. Patients who were evacuated in two days or three or more days had 50% lower odds of being discharged on a ventilator and were twice as likely to return to duty or be discharged home than those who were evacuated within one day. Additionally, patients transported in three or more days were 70% less likely to be ventilated at discharge with a GCS of 8 or lower and had 30% lower odds of mortality than those transported within one day.ConclusionsIn patients with moderate to severe TBI, a delay in aeromedical evacuation out of the combat theater was associated with improved mortality rates and a higher likelihood of discharge to home and return to duty dispositions. This study is correlational in nature and focused on CCATT transports from Role III to Role IV facilities; as such, care must be taken in interpreting our findings and future studies are needed to establish a causal link between delayed evacuation and improved discharge disposition. Our study suggests that delaying aeromedical evacuation of TBI patients when feasible may confer benefit.

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A two-hit model of sepsis plus hyperoxia causes lung permeability and inflammation

Bastarache

Smith

Jesse

et al. 2022

American Journal of Physiology-Lung Cellular and Molecular Phys

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Mouse models of acute lung injury (ALI) have been instrumental for studies of the biologic underpinnings of lung inflammation and permeability, but murine models of sepsis generate minimal lung injury. Our goal was to create a murine sepsis model of ALI that reflects the inflammation, lung edema, histologic abnormalities and physiologic dysfunction that characterize ALI. Using a cecal slurry (CS) model of polymicrobial abdominal sepsis and exposure to hyperoxia (95%), we systematically varied timing and dose of the CS injection, fluids and antibiotics and dose of hyperoxia. We found that CS alone had a high mortality rate that was improved with the addition of antibiotics and fluids. Despite this, we did not see evidence of ALI as measured by bronchoalveolar lavage (BAL) cell count, total protein, CXCL-1 or by lung wet:dry weight ratio. Addition of hyperoxia (95% FiO2) to CS immediately after CS injection increased BAL cell counts and CXCL-1 and lung wet:dry weight ratio but was associated with 40% mortality. Splitting the hyperoxia treatment into two 12 hour exposures (0-12 hours24-36 hours) after CS injection increased survival to 75% and caused significant lung injury compared to CS alone as measured by increased BAL total cell count (92500 vs 240000, p=0.0004), BAL protein (71 vs 103 ug/ml, p=0.0030, and lung wet:dry weight ratio (4.5 vs 5.5 p=0.0005), and compared to sham as measured by increased BAL CXCL-1 (20 vs 2372 pg/ml, p<0.0001), and histologic lung injury score (1.9 vs 4.2, p=0.0077). Additionally, our final model showed evidence of lung epithelial (increased BAL and plasma RAGE) and endothelial (increased Syndecan-1 and sulfated glycosaminoglycans) injury. In conclusion, we have developed a clinically relevant mouse model of sepsis-induced ALI using IP injection of CS, antibiotics and fluids, and hyperoxia. This clinically relevant model can be used for future studies of sepsis-induced ALI.

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Effect of hypobaria and hyperoxia during sepsis on survival and energy metabolism

Abstract: We conclude that neither "in-flight" hyperoxia nor hypobaria exacerbate sepsis or neurologic injury.

Cited by 3 publications

References 25 publications

Air-Evacuation-Relevant Hypobaria Following Traumatic Brain Injury Plus Hemorrhagic Shock in Rats Increases Mortality and Injury to the Gut, Lungs, and Kidneys

Air-Evacuation-Relevant Hypobaria Following Traumatic Brain Injury Plus Hemorrhagic Shock in Rats Increases Mortality and Injury to the Gut, Lungs, and Kidneys

Influence of Time to Transport to a Higher Level Facility on the Clinical Outcomes of US Combat Casualties with TBI: A Multicenter 7-Year Study

A two-hit model of sepsis plus hyperoxia causes lung permeability and inflammation

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