Development of a Sterile Personal Protective Equipment Donning and Doffing Procedure to Protect Surgical Teams from SARS-CoV-2 Exposure during the COVID-19 Pandemic.

Background: The coronavirus disease 2019 (COVID-19) pandemic has become an increasingly challenging problem throughout the world. Because of the numerous potential modes of transmission, surgeons and all procedural staff represent a unique population that requires standardized procedures to protect themselves and their patients. Although several protocols have been implemented during other infectious disease outbreaks, such as Ebola virus, no standardized protocol has been published in regard to the COVID-19 pandemic. Methods: A multidisciplinary team of two surgeons, an anesthesiologist, and an infection preventionist was assembled to create a process with sterile attire adapted from the National Emerging Special Pathogen Training and Education Center (NETEC) donning and doffing process. After editing, a donning procedure and doffing procedure was created and made into checklists. The procedures were simulated in an empty operating room (OR) with simulation of all personnel roles. A "dofficer" role was established to ensure real-time adherence to the procedures. Results: The donning and doffing procedures were printed as one-page documents for easy posting in ORs and procedural areas. Pictures from the simulation were also obtained and made into flow chart-style diagrams that were also posted in the ORs. Conclusions: Coronavirus disease 2019 (COVID-19) is a quickly evolving pandemic that has spread all over the globe. With the rapid increase of infections and the increasing number of severely ill individuals, healthcare providers need easy-to-follow guidelines to keep themselves and patients as safe as possible. The processes for donning and doffing personal protective equipment (PPE) presented here provide an added measure of safety to surgeons and support staff to provide quality surgical care to positive and suspected COVID-19-positive patients.

Hypoxic/Ischemic models in newborn piglet: comparison of constant FiO2 versus variable FiO2 delivery.

A comparison of a constant (continuous delivery of 4% FiO2) and a variable (initial 5% FiO2 with adjustments to induce low amplitude EEG (LAEEG) and hypotension) hypoxic/ischemic insult was performed to determine which insult was more effective in producing a consistent degree of survivable neuropathological damage in a newborn piglet model of perinatal asphyxia. We also examined which physiological responses contributed to this outcome. Thirty-nine 1-day-old piglets were subjected to either a constant hypoxic/ischemic insult of 30- to 37-min duration or a variable hypoxic/ischemic insult of 30-min low peak amplitude EEG (LAEEG <5 microV) including 10 min of low mean arterial blood pressure (MABP <70% of baseline). Control animals (n = 6) received 21% FiO2 for the duration of the experiment. At 72 h, the piglets were euthanased, their brains removed and fixed in 4% paraformaldehyde and assessed for hypoxic/ischemic injury by histological analysis. Based on neuropathology scores, piglets were grouped as undamaged or damaged; piglets that did not survive to 72 h were grouped separately as dead. The variable insult resulted in a greater number of piglets with neuropathological damage (undamaged = 12.5%, damaged = 68.75%, dead = 18.75%) while the constant insult resulted in a large proportion of undamaged piglets (undamaged = 50%, damaged = 22.2%, dead = 27.8%). A hypoxic insult varied to maintain peak amplitude EEG <5 microV results in a greater number of survivors with a consistent degree of neuropathological damage than a constant hypoxic insult. Physiological variables MABP, LAEEG, pH and arterial base excess were found to be significantly associated with neuropathological outcome.

Loss of glial glutamate transporters and induction of neuronal expression of GLT-1B in the hypoxic neonatal pig brain.

The homeostasis of glutamate is critical to normal brain function; deficiencies in the regulation of extracellular glutamate are thought to be a major determinant of damage in hypoxic brains. Extracellular levels of glutamate are regulated mainly by plasmalemmal glutamate transporters. We have evaluated the distribution of the glutamate transporter GLAST and two splice variants of GLT-1 in the hypoxic neonatal pig brain using this as model of neonatal humans. In response to severe hypoxic insults, we observe a rapid loss of two glial glutamate transporters from specific brain regions, such as the CA1 region of the hippocampus, but not the dentate gyrus. The spatial distribution of loss accords with patterns of damage in these brains. Conversely, we demonstrate that hypoxia evokes the expression of a splice variant of GLT-1 in neurons. We suggest that this expression may be induced in response to elevated extracellular glutamate around these neurons, and that this splice variant may represent a useful marker for direct quantification of the extent of likely neuronal damage in hypoxic brains.