For decades, the question of neonatal anesthetic toxicity has variably met with passionate concern, perplexity, or indifference among the anesthesia practitioner and investigator communities. What began as a laboratory observation and academic curiosity of unknown clinical relevance, leading to clinical research and clinical concern, was elevated to a real clinical predicament by an unexpected 2016 U.S. Food and Drug Administration (FDA) Safety Announcement declaring that “repeated or lengthy use of general anesthetic and sedation drugs during surgeries or procedures in children younger than 3 years or in pregnant women during their third trimester may affect the development of children’s brains,” with admonitions to healthcare professionals, parents, pregnant women, and caregivers. This was followed in 2017 by FDA–approved formalized changes to several drug labels to memorialize this warning. The aftermath has seen heightened consternation and confusion, with variable response among parents, practitioners, regulators, anesthesiology societies, healthcare institutions, and their risk managers, as well as changes (or not) in informed consent, and several position statements and commentaries. Having allowed this initial flurry to subside, Anesthesiology this month features two comprehensive review articles and accompanying editorials on anesthetic developmental neurotoxicity in animals and in humans.
- Overexpression of lncRNA Gm15621 alleviates apoptosis and inflammation response resulting from sevoflurane treatment through inhibiting miR-133a/Sox4.
- Role of autophagy in sevoflurane-induced neurotoxicity in neonatal rat hippocampal cells.
- The positive allosteric modulation of GABAA receptors mRNA in immature hippocampal rat neurons by midazolam affects receptor expression and induces apoptosis.
- Euxanthone Ameliorates Sevoflurane-Induced Neurotoxicity in Neonatal Mice.
- Toxicity mechanism of sevoflurane in neural stem cells of rats through DNA methylation.