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Background: The effects of resuscitative endovascular balloon occlusion of the aorta (REBOA) on progression of traumatic brain injury (TBI) are unclear. Two hypotheses prevail: increased mean arterial pressure may improve cerebral perfusion, or cause cerebral edema due to elevated intracranial pressure. This study compares outcomes in hypotensive, blunt trauma patients with TBI treated with and without REBOA. Methods: A retrospective analysis compared hypotensive (systolic blood pressure [SBP] >90) blunt trauma patients with TBI treated with REBOA to those treated without. Patients with spontaneous circulation at admission and at initiation of aortic occlusion were included. Patients requiring cardiopulmonary resuscitation in the emergency department (ED) were excluded. Radius matching used age, injury severity score (ISS), abbreviated injury score (AIS)head, and Glasgow coma score (GCS) and SBP at ED arrival. Results: Of 232 patients, 135 were treated with REBOA and 97 without. REBOA patients were older and had higher ISS, AIS-head, AIS-chest and AIS- extremity. There was no difference in TBI severity, and mortality. In the matched analysis (n = 76 REBOA, n = 54 non-REBOA), there was no difference in ISS, AIS-head, pre-hospital, ED, or discharge GCS, ED SBP, or mortality. Despite longer hospital stays for REBOA patients, there was no difference in intensive care unit length of stay, rate of discharge home, or discharge GCS. Conclusions: REBOA was used in more severely injured patients, but was not associated with higher mortality rate. REBOA should be considered for use in patients with non-compressible torso hemorrhage and concomitant TBI, as it did not increase mortality, and outcomes were similar to non-REBOA patients.

The endothelial glycocalyx (EGX) contributes to the permeability barrier of vessels and regulates the coagulation cascade. EGX damage, which occurs in numerous disease states, including sepsis and trauma, results in endotheliopathy. While influenza and other viral infections are known to cause endothelial dysfunction, their effect on the EGX has not been described. We hypothesized that the H1N1 influenza virus would cause EGX degradation. Human umbilical vein endothelial cells (HUVECs) were exposed to varying multiplicities of infection (MOI) of the H1N1 strain of influenza virus for 24 hours. A dose-dependent effect was examined by using an MOI of 5 (n = 541), 15 (n = 714), 30 (n = 596), and 60 (n = 653) and compared to a control (n = 607). Cells were fixed and stained with FITC-labelled wheat germ agglutinin to quantify EGX. There was no difference in EGX intensity after exposure to H1N1 at an MOI of 5 compared to control (6.20 vs. 6.56 Arbitrary Units (AU), p = 0.50). EGX intensity was decreased at an MOI of 15 compared to control (5.36 vs. 6.56 AU, p

The endothelial glycocalyx (EGX) contributes to the permeability barrier of vessels and regulates the coagulation cascade. EGX damage, which occurs in numerous disease states, including sepsis and trauma, results in endotheliopathy. While influenza and other viral infections are known to cause endothelial dysfunction, their effect on the EGX has not been described. We hypothesized that the H1N1 influenza virus would cause EGX degradation. Human umbilical vein endothelial cells (HUVECs) were exposed to varying multiplicities of infection (MOI) of the H1N1 strain of influenza virus for 24 hours. A dose-dependent effect was examined by using an MOI of 5 (n = 541), 15 (n = 714), 30 (n = 596), and 60 (n = 653) and compared to a control (n = 607). Cells were fixed and stained with FITC-labelled wheat germ agglutinin to quantify EGX. There was no difference in EGX intensity after exposure to H1N1 at an MOI of 5 compared to control (6.20 vs. 6.56 Arbitrary Units (AU), p = 0.50). EGX intensity was decreased at an MOI of 15 compared to control (5.36 vs. 6.56 AU, p

BackgroundThe goal of this study was to determine if IL-22:Fc would Acute Respiratory Distress Syndrome (ARDS).Summary background dataNo therapies exist for ARDS and treatment is purely supportive. Interleukin-22 (IL-22) plays an integral component in recovery of the lung from infection. IL-22:Fc is a recombinant protein with a human FC immunoglobulin that increases the half-life of IL-22.Study designARDS was induced in C57BL/6 mice with intra-tracheal lipopolysaccharide (LPS) at a dose of 33.3 or 100 ug. In the low-dose LPS group (LDG), IL-22:FC was administered via tail vein injection at 30 minutes (n = 9) and compared to sham (n = 9). In the high-dose LPS group (HDG), IL-22:FC was administered (n = 11) then compared to sham (n = 8). Euthanasia occurred after bronchioalveolar lavage (BAL) on post-injury day 4.ResultsIn the LDG, IL-22:FC resulted in decreased protein leak (0.15 vs. 0.25 ug/uL, p = 0.02). BAL protein in animals receiving IL-22:Fc in the HDG was not different. For the HDG, animals receiving IL-22:Fc had lower BAL cell counts (539,636 vs 3,147,556 cells/uL, p = 0.02). For the HDG, IL-6 (110.6 vs. 527.1 pg/mL, p = 0.04), TNF-α (5.87 vs. 25.41 pg/mL, p = 0.04), and G-CSF (95.14 vs. 659.6, p = 0.01) levels were lower in the BAL fluid of IL-22:Fc treated animals compared to sham.ConclusionsIL-22:Fc decreases lung inflammation and lung capillary leak in ARDS. IL-22:Fc may be a novel therapy for ARDS.