ABSTRACT
Background: In 2017, the Bony Facial Trauma Score (BFTS) was developed to quantify and describe bony trauma of the face. Objective: To compare BFTSs for the need of hospital admission, intensive care unit (ICU) admission, surgery, tracheostomy tube placement, cervical spine (c-spine) injury, and mortality. Methods: A retrospective review of patients sustaining bony facial trauma from January 1, 2017 to November 30, 2019 was done. Logistic regression modeling measured the association between BFTS and admission status, need for operative repair, tracheostomy, mortality, ICU admission, and c-spine injury. Results: Three hundred six patients were included for this analysis. Median BFTS was 3.5 (interquartile range, 5), while the average age was 45.0 years (standard deviation, 22.3). The most common mechanisms of injury were motor vehicle accident (44.8%) and ground-level fall (32.5%). BFTS was found to correlate with the following (p < 0.05): admission (odds ratio [OR] 1.06, 95% confidence interval [CI] 1.01-1.13), mortality (OR 1.05, 1.00-1.10), tracheostomy (OR 1.11, 1.07-1.17), operative management (OR 1.16, 1.11-1.22), ICU (OR 1.07, 1.03-1.11), and c-spine injury (OR 1.05, 95% CI 1.03-1.11). Conclusion: A significant correlation was found between BFTS and all the outcomes investigated.
Subject(s)
Facial Injuries , Humans , Middle Aged , Facial Injuries/surgery , Tracheostomy , Retrospective Studies , Logistic ModelsABSTRACT
Clostridium perfringens epsilon toxin (ETX) is responsible for causing the economically devastating disease, enterotoxaemia, in livestock. It is well accepted that ETX causes blood brain barrier (BBB) permeability, however the mechanisms involved in this process are not well understood. Using in vivo and in vitro methods, we determined that ETX causes BBB permeability in mice by increasing caveolae-dependent transcytosis in brain endothelial cells. When mice are intravenously injected with ETX, robust ETX binding is observed in the microvasculature of the central nervous system (CNS) with limited to no binding observed in the vasculature of peripheral organs, indicating that ETX specifically targets CNS endothelial cells. ETX binding to CNS microvasculature is dependent on MAL expression, as ETX binding to CNS microvasculature of MAL-deficient mice was not detected. ETX treatment also induces extravasation of molecular tracers including 376Da fluorescein salt, 60kDA serum albumin, 70kDa dextran, and 155kDA IgG. Importantly, ETX-induced BBB permeability requires expression of both MAL and caveolin-1, as mice deficient in MAL or caveolin-1 did not exhibit ETX-induced BBB permeability. Examination of primary murine brain endothelial cells revealed an increase in caveolae in ETX-treated cells, resulting in dynamin and lipid raft-dependent vacuolation without cell death. ETX-treatment also results in a rapid loss of EEA1 positive early endosomes and accumulation of large, RAB7-positive late endosomes and multivesicular bodies. Based on these results, we hypothesize that ETX binds to MAL on the apical surface of brain endothelial cells, causing recruitment of caveolin-1, triggering caveolae formation and internalization. Internalized caveolae fuse with early endosomes which traffic to late endosomes and multivesicular bodies. We believe that these multivesicular bodies fuse basally, releasing their contents into the brain parenchyma.
