This comparative-effectiveness study provides evidence for major practice variation in surgical management of severe TBI. Although ages differed between the 2 cohorts, the results suggest that a more aggressive approach, including earlier surgery, larger craniotomy, and removal of bone flap, may reduce ICP, prevent cortical spreading depolarizations, and improve outcomes. In particular, patients requiring evacuation of subdural hematomas and contusions may benefit from decompressive craniectomy in conjunction with lesion evacuation, even when elevated ICP is not a factor in the decision to perform surgery.

Introduction: SARS-CoV-2 has been identified as the pathogen causing the outbreak of Coronavirus Disease 2019 that started in Wuhan, China, in December 2019. SARS-CoV-2 has human-to-human transmission ability and universally contagious to all populations. The main transmission patterns are respiratory droplets transmission and contact transmission. The purpose of this study is to propose a protocol that may be used as a guide to reduce the incidence of COVID-19 infections among otolaryngology care teams. Methods: A prospective cohort study was conducted to show the efficacy of our protocol to prevent transmission to health-care providers from March 11, 2020 through April 14, 2020. The protocol consisted of a series of protective measures that we applied to all health-care providers, then testing of our providers for COVID-19 using reverse transcription polymerase chain reaction along with immunoglobulin M (IgM) and immunoglobulin G (IgG) testing at the end of the study period to ensure effectiveness. Results: Our protocol resulted in zero transmissions to our health-care providers during the duration of the initial study. We were involved in greater than 150 sinonasal, skull base, open airway, and endoscopy procedures during this study. At the conclusion of the initial 5 weeks, we had no health-care providers test positive for SARS-CoV-2. Conclusion: According to our proposed protocol, we were able to provide care for all patients in clinic, hospital, emergent, intensive, and surgical settings with no transmission of SARS-CoV-2 by symptomatology and post evaluation testing.

Spinal cord injury (SCI) often results in irreversible and permanent neurological deficits and long-term disability. Vasospasm, hemorrhage, and loss of microvessels create an ischemic environment at the site of contusive or compressive SCI and initiate the secondary injury cascades leading to progressive tissue damage and severely decreased functional outcome. Although the initial mechanical destructive events cannot be reversed, secondary injury damage occurs over several hours to weeks, a time frame during which therapeutic intervention could be achieved. One essential component of secondary injury cascade is the reduction in spinal cord blood flow with resultant decrease in oxygen delivery. Our group has recently shown that administration of fluorocarbon (Oxycyte) significantly increased parenchymal tissue oxygen levels during the usual postinjury hypoxic phase, and fluorocarbon has been shown to be effective in stroke and head injury. In the current study, we assessed the beneficial effects of Oxycyte after a moderate-to-severe contusion SCI was simulated in adult Long-Evans hooded rats. Histopathology and immunohistochemical analysis showed that the administration of 5 mL/kg of Oxycyte perfluorocarbon (60% emulsion) after SCI dramatically reduced destruction of spinal cord anatomy and resulted in a marked decrease of lesion area, less cell death, and greater white matter sparing at 7 and 42 days postinjury. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining showed a significant reduced number of apoptotic cells in Oxycyte-treated animals, compared to the saline group. Collectively, these results demonstrate the potential neuroprotective effect of Oxycyte treatment after SCI, and its beneficial effects may be, in part, a result of reducing apoptotic cell death and tissue sparing. Further studies to determine the most efficacious Oxycyte dose and its mechanisms of protection are warranted.