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Background: Auditory brainstem response (ABR) testing is considered to be relatively resistant to effects of volatile anesthetics. The impact of newer anesthetics on interpretability of ABR testing is unknown. This study compared sevoflurane versus propofol anesthesia on qualitative interpretability of ABR click-testing in children., Methods: This prospective double-blind crossover study enrolled children (≤18 years old) receiving general anesthesia for elective ABR testing. All subjects received both sevoflurane and propofol anesthesias in the same ABR testing session. Deidentified ABR data were reviewed by 5 audiologists (blinded to anesthetic and patient) to determine threshold levels for hearing loss. The primary outcome was qualitative interpretability (false positive) of ABR click-testing., Results: Each patient was tested at 4 different intensities in each ear: generating 624 records under each anesthetic, for a total of 1248 records. A few patients were tested at 5 different intensities in a single ear accounting for the additional 11 records, yielding 1259 records. Under sevoflurane anesthesia, 21 of the same patients (37 ears) were identified with abnormal ABR levels consistent with hearing loss (one or both ears). The probability of a patient being diagnosed with hearing "loss" in one or both ears was significantly less with propofol versus sevoflurane anesthesia (mid P =.0312). If patients with bilateral loss are compared, the mid P value is 0.0098. The effect size based on patients was medium to large, with a minimum value of Cohen w = 0.320., Conclusions: Sevoflurane produced more false positives for hearing loss and suggested more severe hearing loss than propofol. False-positive ABR tests, produced by certain anesthetic agents, can have significant life-long impact and negative psychosocial and developmental implications. Use of the intravenous anesthetic propofol is superior to sevoflurane for ABR testing in children., Competing Interests: Conflicts of Interest: See Disclosures at the end of the article., (Copyright © 2021 International Anesthesia Research Society.)

Many algorithms, checklists, and escalation pathways have been created to encourage perioperative teams to share a mental model and approach patient care as a team. Respecting and empowering the many voices involved in patient care is crucial to avoid errors and improve patient safety. None of the concepts described herein are novel; however, sustained improvements in operating room culture remain elusive in many organizations. The implementation of practices directed toward driving change in operating room culture has led to improvements in Occupational Safety and Health Administration (OSHA) recordables, perioperative communication, and patient care practices. In this paper, we will review the importance of culture, mutual accountability, and communication in improving patient care, and share several of the processes that have been created at our pediatric tertiary care center.

Directing intraoperative neurophysiologic monitoring (IONM) is a patient care activity for which no formal training programs exist, even though the need for well-trained practitioners is readily evident while caring for patients with diseases of the brain, spinal cord, spinal column, or nervous system. Here, we present the theoretical basis and institutional experience for a successful model of learning a new and complex set of skills: the medical direction of IONM. In a major academic institution, a clinical community of practice absorbed new members with professional backgrounds ranging from a recent neuroanesthesia fellowship to several decades of neuroanesthesia practice and trained them in a collaborative cognitive apprenticeship model to medically direct IONM. Our community of practice comprises experienced technicians, a diplomate of the American Board of Neurophysiologic Monitoring (DABNM), and six neuroanesthesiologists. This group forms the base of the scaffolding or structure where the apprenticeship and learning take place. The clinical community of practice has trained eight new members in the medical direction of IONM. The group has also trained four outside anesthesiologists-one of whom went on to become certified as a DABNM-who went on to develop the IONM program at a major children's hospital. This collaborative cognitive apprenticeship in anesthesiology to learn the medical direction of IONM is quite innovative as it integrates new members and expands the range of existing ones. In our model, the entire community is elevated by the reciprocal interactions of master clinicians, novice apprentices, and the community of practice.

The article Is the new ASNM intraoperative neuromonitoring supervision "guideline" a trustworthy guideline? A commentary, written by Stanley A. Skinner, Elif Ilgaz Aydinlar, Lawrence F. Borges, Bob S. Carter, Bradford L. Currier, Vedran Deletis, Charles Dong, John Paul Dormans, Gea Drost, Isabel Fernandez‑Conejero, E. Matthew Hoffman, Robert N. Holdefer, Paulo Andre Teixeira Kimaid, Antoun Koht, Karl F. Kothbauer, David B. MacDonald, John J. McAuliffe III, David E. Morledge, Susan H. Morris, Jonathan Norton, Klaus Novak, Kyung Seok Park, Joseph H. Perra, Julian Prell, David M. Rippe, Francesco Sala, Daniel M. Schwartz, Martín J. Segura, Kathleen Seidel, Christoph Seubert, Mirela V. Simon, Francisco Soto, Jeffrey A. Strommen, Andrea Szelenyi, Armando Tello, Sedat Ulkatan, Javier Urriza and Marshall Wilkinson, was originally published electronically on the publisher's internet portal (currently SpringerLink) on 05 January 2019 without open access. With the author(s)' decision to opt for Open Choice the copyright of the article changed on 30 January 2019 to © The Author(s) 2019 and the article is forthwith distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license and indicate if changes were made. The original article has been corrected.

Background: Volatile anesthetics, such as isoflurane, are widely used in infants and neonates. Neurodegeneration and neurocognitive impairment after exposure to isoflurane, midazolam, and nitrous oxide in neonatal rats have raised concerns regarding the safety of pediatric anesthesia. In neonatal mice, prolonged isoflurane exposure triggers hypoglycemia, which could be responsible for the neurocognitive impairment. We examined the effects of neonatal isoflurane exposure and blood glucose on brain cell viability, spontaneous locomotor activity, as well as spatial learning and memory in mice., Methods: Seven-day-old mice were randomly assigned to 6 h of 1.5% isoflurane with or without injections of dextrose or normal saline, or to 6 h of room air without injections (no anesthesia). Arterial blood gases and glucose were measured. After 2 h, 18 h, or 11 wk postexposure, cellular viability was assessed in brain sections stained with Fluoro-Jade B, caspase 3, or NeuN. Nine weeks postexposure, spontaneous locomotor activity was assessed, and spatial learning and memory were evaluated in the Morris water maze using hidden and reduced platform trials., Results: Apoptotic cellular degeneration increased in several brain regions early after isoflurane exposure, compared with no anesthesia. Despite neonatal cell loss, however, adult neuronal density was unaltered in two brain regions significantly affected by the neonatal degeneration. In adulthood, spontaneous locomotor activity and spatial learning and memory performance were similar in all groups, regardless of neonatal isoflurane exposure. Neonatal isoflurane exposure led to an 18% mortality, and transiently increased Paco(2), lactate, and base deficit, and decreased blood glucose levels. However, hypoglycemia did not seem responsible for the neurodegeneration, as dextrose supplementation failed to prevent neuronal loss., Conclusions: Prolonged isoflurane exposure in neonatal mice led to increased immediate brain cell degeneration, however, no significant reductions in adult neuronal density or deficits in spontaneous locomotion, spatial learning, or memory function were observed.