British journal of anaesthesia
-
Anaesthetic gases account for ∼3% of the carbon footprint of the entire healthcare sector and up to 63% of the emissions originating from surgical care. Transitioning to predominant use of total intravenous anaesthesia (TIVA) has been proven a safe and effective strategy to reduce this footprint, yet its adoption has been slow in most countries. Interventions at the national level have been limited to regulatory action (e.g. banning of desflurane) and publication of nonbinding recommendations and best practices. ⋯ Meeting the two main concerns among anaesthetists, patient safety and professional autonomy, the guideline requires all Dutch anaesthetic practices to adopt a local protocol whose main message is 'TIVA when possible, inhalation anaesthesia when necessary'. Central to the approach was the integration within the national quinquennial quality control audits. Adoption and implementation will be monitored and evaluated in an ongoing research project.
-
Malignant hyperthermia (MH) susceptibility is associated with variants in RYR1, the gene encoding the skeletal muscle ryanodine receptor-1 (RyR1), in 70-75% of patients. Functional characterisation demonstrating an increased sensitivity to RyR1 agonists is necessary among other criteria for inclusion in the European Malignant Hyperthermia Group list of MH susceptibility diagnostic variants. ⋯ The variants p.Glu342Lys, p.Leu2288Ser p.Phe2340Leu, and p.Arg2676Trp are pathogenic or likely pathogenic for MH and can be used for presymptomatic testing for MH susceptibility. As current knowledge on the p.Val3324Ala, p.Phe4076Leu, and p.Trp5020Cys variants remains insufficient, they are still classified as variants of uncertain significance.
-
Anaesthesia-induced burst suppression signifies profound cerebral inactivation. Although considerable efforts have been directed towards elucidating the electroencephalographic manifestation of burst suppression, the neuronal underpinnings that give rise to isoflurane-induced burst suppression are unclear. ⋯ Isoflurane-induced burst suppression might be primarily driven by the synchronous activities of excitatory pyramidal neurones in the cortex, which could be bidirectionally regulated by manipulating the activity of inhibitory PV interneurones. Our findings provide new insights into the neuronal mechanisms underlying burst suppression.