Infection Prevention Precautions for Routine Anesthesia Care During the SARS-CoV-2 Pandemic.

Many health care systems around the world continue to struggle with large numbers of SARS-CoV-2-infected patients, while others have diminishing numbers of cases following an initial surge. There will most likely be significant oscillations in numbers of cases for the foreseeable future, based on the regional epidemiology of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Less affected hospitals and facilities will attempt to progressively resume elective procedures and surgery. Ramping up elective care in hospitals that deliberately curtailed elective care to focus on SARS-CoV-2-infected patients will present unique and serious challenges. Among the challenges will be protecting patients and providers from recurrent outbreaks of disease while increasing procedure throughput. Anesthesia providers will inevitably be exposed to SARS-CoV-2 by patients who have not been diagnosed with infection. This is particularly concerning in consideration that aerosols produced during airway management may be infective. In this article, we recommend an approach to routine anesthesia care in the setting of persistent but variable prevalence of SARS-CoV-2 infection. We make specific recommendations for personal protective equipment and for the conduct of anesthesia procedures and workflow based on evidence and expert opinion. We propose practical, relatively inexpensive precautions that can be applied to all patients undergoing anesthesia. Because the SARS-CoV-2 virus is spread primarily by respiratory droplets and aerosols, effective masking of anesthesia providers is of paramount importance. Hospitals should follow the recommendations of the Centers for Disease Control and Prevention for universal masking of all providers and patients within their facilities. Anesthesia providers should perform anesthetic care in respirator masks (such as N-95 and FFP-2) whenever possible, even when the SARS-CoV-2 test status of patients is negative. Attempting to screen patients for infection with SARS-CoV-2, while valuable, is not a substitute for respiratory protection of providers, as false-negative tests are possible and infected persons can be asymptomatic or presymptomatic. Provision of adequate supplies of respirator masks and other respiratory protection equipment such as powered air purifying respirators (PAPRs) should be a high priority for health care facilities and for government agencies. Eye protection is also necessary because of the possibility of infection from virus coming into contact with the conjunctiva. Because SARS-CoV-2 persists on surfaces and may cause infection by contact with fomites, hand hygiene and surface cleaning are also of paramount importance.

Abbreviated right-sided heart echocardiogram and the STOP-Bang questionnaire-a useful relationship for preoperative patient evaluation?

STUDY OBJECTIVE: The aims of this study were to (1) explore the incidence of right-sided heart dysfunction (RHD) and STOP-Bang questionnaire responses consistent with obstructive sleep apnea (OSA) and (2) assess the relationship between patients with STOP-Bang questionnaire responses consistent with OSA and echocardiographic findings suggestive of RHD. DESIGN: Observational study. SETTING: Tertiary academic center preoperative clinic. PATIENTS: Two hundred patients presenting for elective surgery to the University of Utah preoperative clinic. INTERVENTION: Abbreviated transthoracic right-sided echocardiogram and STOP-Bang questionnaire. MEASUREMENTS: Tricuspid annular plane systolic excursion, tissue Doppler-derived tricuspid lateral annular systolic velocity (S'), and the tricuspid inflow E wave to tricuspid annular tissue Doppler e' wave ratio (E/e') for the presence of RHD, as well as responses to STOP-Bang questionnaire. MAIN RESULTS: A total of 140 echocardiograms were analyzed after exclusion of participants with incomplete STOP-Bang questionnaires and inadequate images. Thirty-five patients (25%) reported 5 or more positive responses to the STOP-Bang questionnaire. Forty-six patients (35%) had abnormal right-sided heart measurements. Of the 35 patients with STOP-Bang scores 5 or greater, 11 (31%) had evidence of RHD. No correlation was observed between STOP-Bang scores and the echocardiography metrics of RHD. CONCLUSIONS: This preliminary study suggests that there are numerous sources of RHD, among one of which is sleep apnea, and/or the STOP-Bang questionnaire is not a sensitive tool for predicting RHD. We conclude that although the STOP-Bang questionnaire is easy to implement in a preoperative clinical setting, it is not useful in identifying patients at risk for RHD.

Ethanol decreases agrin-induced acetylcholine receptor clustering in C2C12 myotube culture.

We investigated the effect of ethanol on skeletal muscle development using C2C12 cell culture. The ethanol concentrations of 10mM, 25mM, and 100mM, were tested because plasma samples of alcohol-dependent individuals fall within this range. We assessed two specific events in skeletal muscle development, the fusion of myoblasts to form myotubes and the acetylcholine receptor (AChR) clustering associated with neuromuscular synapse formation. We report that ethanol does not effect myotube formation or the viability of myoblasts or myotubes in C2C12 cell culture. However, ethanol does effect AChR clustering on C2C12 myotubes. As motor neurons approach skeletal muscle during development, agrin is released by motor neurons and induces AChR clustering on muscle fibers. In our experiments, agrin was applied to cell cultures during the period when myoblasts fuse to form myotubes. In cell cultures exposed to ethanol during myotube formation, agrin-induced AChR clustering was decreased compared to untreated cultures. In cell cultures exposed to ethanol during myoblast proliferation, with ethanol removed during myotube formation, agrin-induced AChR clustering was unaffected. We conclude that exposure to a physiologically relevant concentration of ethanol during the specific period of myotube formation decreases agrin-induced AChR clustering.