Novel Technology Deployed for Remote Ventilator Management by Respiratory Therapists During the COVID-19 Pandemic: Lessons Learned.

A novel remote ventilator management (control) technology (Omnitool) was implemented for use with ICU patients during the COVID-19 pandemic to mitigate in-person respiratory therapist interactions and preserve personal protective equipment. In the latter half of 2020, eight mechanical ventilators were purchased and enabled for Omnitool deployment through the application of a vendor software option. Subsequently, these ventilators were outfitted with commercially available informatics hardware that permitted remote communication and management via the existing hospital network. In total, 17 patients with COVID-19 respiratory failure were placed on Omnitool enabled ventilators between January 1, 2021-April 30, 2021. The median Omnitool use days was 10. Deployment of a novel remote ventilator management technology is feasible; however, further study is needed to simplify the set up and utilization of the system. Future demands for remote ventilator management are predictable, whether in rural areas, military scenarios without adequate RT staffing, or in circumstances with new and easily transmissible toxic infections, and will continue to encourage the development of relatively easy to apply informatics-based solutions. Herein we share five lessons learned from our Omnitool deployment.

Inflammatory Leptomeningeal Cytokines Mediate COVID-19 Neurologic Symptoms in Cancer Patients.

SARS-CoV-2 infection induces a wide spectrum of neurologic dysfunction that emerges weeks after the acute respiratory infection. To better understand this pathology, we prospectively analyzed of a cohort of cancer patients with neurologic manifestations of COVID-19, including a targeted proteomics analysis of the cerebrospinal fluid. We find that cancer patients with neurologic sequelae of COVID-19 harbor leptomeningeal inflammatory cytokines in the absence of viral neuroinvasion. The majority of these inflammatory mediators are driven by type II interferon and are known to induce neuronal injury in other disease states. In these patients, levels of matrix metalloproteinase-10 within the spinal fluid correlate with the degree of neurologic dysfunction. Furthermore, this neuroinflammatory process persists weeks after convalescence from acute respiratory infection. These prolonged neurologic sequelae following systemic cytokine release syndrome lead to long-term neurocognitive dysfunction. Our findings suggest a role for anti-inflammatory treatment(s) in the management of neurologic complications of COVID-19 infection.

Inflammatory leptomeningeal cytokines mediate delayed COVID-19 encephalopathy.

SARS-CoV-2 infection induces a wide spectrum of neurologic dysfunction. Here we show that a particularly vulnerable population with neurologic manifestations of COVID-19 harbor an influx of inflammatory cytokines within the cerebrospinal fluid in the absence of viral neuro-invasion. The majority of these inflammatory mediators are driven by type 2 interferon and are known to induce neuronal injury in other disease models. Levels of matrix metalloproteinase-10 within the spinal fluid correlate with the degree of neurologic dysfunction. Furthermore, this neuroinflammatory process persists weeks following convalescence from the acute respiratory infection. These prolonged neurologic sequelae following a systemic cytokine release syndrome lead to long-term neurocognitive dysfunction with a wide range of phenotypes.