Endotracheal tube cuff rupture during anesthesia in 2 dogs.

A 15-year-old intact male dachshund dog weighing 4.3 kg and a 5-year-old intact male mixed-breed dog weighing 13.6 kg were referred for examination because of paraparesis and facial paralysis, respectively. Magnetic resonance imaging (MRI) of the thoracolumbar region and brain was performed. The dogs were premedicated with IV butorphanol, 0.2 mg/kg body weight (BW) and midazolam, 0.2 mg/kg BW. Anesthesia was induced with IV propofol, 4 to 5 mg/kg BW and maintained with sevoflurane in oxygen. The dachshund was orotracheally intubated with a 5.0-millimeter internal diameter endotracheal (ET) tube. During positioning in the MRI room, intermittent positive pressure ventilation (IPPV) was applied. The mixed-breed dog was orotracheally intubated with a 6.0-millimeter internal diameter ET tube. After inflation of the ET tube cuff, a leaking test was done by applying positive pressure ventilation. In both dogs, a distinct "popping" sound was heard when positive pressure was applied, after which air leakage from the cuff was evident. Failure to inflate the pilot balloon led to suspicion of a ruptured cuff. Reintubation was completed, both dogs remained stable during anesthesia, and no postanesthetic complications were observed. Rupture of both cuffs, which was visually confirmed, was thought to be caused by overinflation of the cuff, repeated sterilization of the ET tubes, and positive pressure ventilation. Repeated sterilization of ET tubes with ethylene oxide can alter the physical integrity of cuffs. Care should be taken not to overinflate ET tube cuffs, especially when they have been repeatedly sterilized, as cuff rupture may result in failure to provide adequate IPPV. Key clinical message: This report describes 2 cases in which ET tube cuff rupture was noted during anesthesia for MRI.

Rupture du ballonnet du tube endotrachéal pendant l'anesthésie chez 2 chiens. Un chien teckel mâle intact de 15 ans pesant 4,3 kg et un chien croisé mâle intact de 5 ans pesant 13,6 kg ont été référés pour examen en raison de paraparésie et de paralysie faciale, respectivement. Une imagerie par résonance magnétique (IRM) de la région thoraco-lombaire et du cerveau a été réalisée. Les chiens ont reçu une prémédication avec du butorphanol IV, 0,2 mg/kg de poids corporel (PC), et du midazolam, 0,2 mg/kg PC. L'anesthésie a été induite avec du propofol IV, 4 à 5 mg/kg de PC et maintenue avec du sévoflurane dans de l'oxygène. Le teckel a été intubé par voie orotrachéale avec un tube endotrachéal (TE) de diamètre interne de 5,0 millimètres. Lors du positionnement dans la salle d'IRM, une ventilation intermittente à pression positive (VIPP) a été appliquée. Le chien de race mixte a été intubé par voie orotrachéale avec un TE de 6,0 millimètres de diamètre interne. Après le gonflage du ballonnet du TE, un test d'étanchéité a été effectué en appliquant une ventilation à pression positive. Chez les deux chiens, un son distinct de « claquement ¼ a été entendu lorsqu'une pression positive a été appliquée, après quoi une fuite d'air du ballonnet est devenue évidente. Le fait de ne pas gonfler le ballon pilote a fait soupçonner une rupture du ballonnet. Une ré-intubation a été effectuée, les deux chiens sont restés stables pendant l'anesthésie et aucune complication post-anesthésique n'a été observée. La rupture des deux ballonnets, confirmée visuellement, aurait été causée par un surgonflage du ballonnet, une stérilisation répétée des TE et une ventilation à pression positive. La stérilisation répétée des TE avec de l'oxyde d'éthylène peut altérer l'intégrité physique des ballonnets. Il convient de veiller à ne pas surgonfler les ballonnets des TE, en particulier lorsqu'ils ont été stérilisés à plusieurs reprises, car la rupture du ballonnet peut entraîner l'incapacité de fournir une VIPP adéquate.Message clinique clé:Ce rapport décrit 2 cas dans lesquels une rupture du ballonnet du TE a été constatée lors d'une anesthésie pour IRM.(Traduit par Dr Serge Messier).

Influencing Factors of Delirium during Recovery in Urological Postoperative Patients Undergoing Sevoflurane Anaesthesia.

OBJECTIVE: To analyse the incidence and influencing factors of delirium during recovery in urological postoperative patients undergoing sevoflurane anaesthesia. METHODS: The clinical data of patients undergoing sevoflurane anaesthesia in the urology surgery department in our hospital from January 2022 to December 2022 were retrospectively analysed. The incidence of delirium during the recovery period was recorded by using the Chinese version of the Confusion Assessment Method (CAM) for Severity of Delirium after surgery, and the patients were divided into occurrence and non-occurrence groups. Whether delirium occurred during recovery was determined through univariate analysis. In binary logistic regression analysis, the occurrence of emergence delirium was the dependent variable, and the variables with statistical differences in the univariate analysis were the independent variables. The influencing factors of emergence delirium in post-urological surgery patients who underwent sevoflurane anaesthesia were determined. RESULTS: Delirium during recovery occurred in 10 of 100 patients (10.00%). Odds ratio (OR) of age (OR = 1.445, p = 0.022), history of diabetes (OR = 1.798, p = 0.010), operation time (OR = 1.670, p = 0.008), American Society of Anesthesiologists (ASA) classification (OR = 1.740, p = 0.006) and sevoflurane inhalation concentration (OR = 1.890, p = 0.001) are the influencing factors of postoperative delirium in urologic patients undergoing sevoflurane anaesthesia. CONCLUSIONS: Age, history of diabetes, operation time, ASA classification and sevoflurane inhalation concentration are the influencing factors.

Sirtuin 3 (SIRT3) improves sevoflurane-induced postoperative cognitive impairment by regulating mitochondrial oxidative stress.

One of the most prevalent co-operative disorders is postoperative cognitive dysfunction (POCD), however, its pathogenesis remains unclear. Thus, the aim of this work was to evaluate SIRT3's impact on cognitive decline in aged mice under anesthesia. Adeno-associated virus SIRT3 vector (AAV-SIRT3) or empty vector (AAV-VEH) was injected into the hippocampal region of aged mice after sevoflurane induction in order to upregulate the expression of SIRT3. The expression levels of SIRT3, pro-inflammatory cytokines, and apoptotic factors in hippocampus tissues were identified by PCR, Western blotting, TUNEL staining, and enzyme-linked immunosorbent assay (ELISA), and the cognitive function of mice was assessed. The SIRT3 expression was down-regulated in the hippocampal tissue of anesthetized mice. SIRT3 overexpression can improve the learning and memory ability, reduce the escape latency, and increase the residence time in the platform and platform crossing ability of mice. The overexpression of SIRT3 in hippocampus can reduce the oxidative stress response and inflammatory response induced by anesthesia in mice, increase the superoxide dismutase (SOD) expression level, and decrease the expression level of MDA and inflammatory factors in hippocampus. In addition, SIRT3 overexpression can also reduce anesthetic-induced hippocampal cell apoptosis. By reducing the hippocampus mitochondrial oxidative stress response, SIRT3 plays a significant role in the pathophysiology of POCD in mice and is a potential target for POCD treatment and diagnosis.

Efficacy of Sevoflurane and Propofol Anesthesia on Perioperative Adverse Cardiovascular Events and Hemodynamics in Elderly Patients With Diabetes.

PURPOSE: This study was undertaken to compare the effects of sevoflurane and propofol anesthesia on perioperative hemodynamics and perioperative adverse cardiovascular events (PACE) in elderly patients with diabetes undergoing general anesthesia for noncardiac surgery. METHODS: According to the random number table (n = 40), 80 patients with diabetes undergoing noncardiac general anesthesia were divided into a control group and an observation group. In the control group, the patients were given propofol 4 to 6 mg/(kg·h), continuously pumped to maintain anesthesia. In the observation group, the patients were given maintained concentration of sevoflurane for 1 to 1.5 minimum alveolar concentration (MAC) for continuous inhalation, while remifentanil with volume fraction of 0.05 to 1 µg/(kg·min) was given for continuous pumping in both groups. The heart rate (HR) and mean arterial pressure (MAP) of the patients were recorded, and the serum creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) contents before anesthesia (T0), immediately after surgery (T3), and 24 hours later (T4) as well as the blood glucose levels at T0 and T3 were compared between the two groups. The occurrence of PACE in the two groups was compared during the perioperative period. FINDINGS: The HR and MAP 5 minutes after intubation (T1), 1 hour after skin incision (T2), and at T3 in the two groups were significantly lower than those of T0 (P < 0.05), whereas the MAP and HR of T1, T2, and T3 in the observation group were significantly higher than those of the control group (P < 0.05). The T3 blood glucose levels were significantly higher in the two groups than that in T0 (P < 0.05), and the T3 blood glucose levels in the observation group were significantly lower than that in the control group (P < 0.05). CK-MB and cTnI in the two groups were significantly higher at T3 and T4 than T0 (P < 0.05), whereas CK-MB and cTnI in the observation group were significantly lower than in the control group at T3 and T4 (P < 0.05). The incidence of hypotension and PACE was significantly lower in the observation group than in the control group (P < 0.05). IMPLICATIONS: Compared with propofol IV general anesthesia, sevoflurane inhalation anesthesia can improve perioperative hemodynamics stability and reduce the incidence of PACE in elderly patients with diabetes undergoing noncardiac surgery.

Dysregulation of iron homeostasis and ferroptosis in sevoflurane and isoflurane associated perioperative neurocognitive disorders.

In recent years, sevoflurane and isoflurane are the most popular anesthetics in general anesthesia for their safe, rapid onset, and well tolerant. Nevertheless, many studies reported their neurotoxicity among pediatric and aged populations. This effect is usually manifested as cognitive impairment such as perioperative neurocognitive disorders. The wide application of sevoflurane and isoflurane during general anesthesia makes their safety a major health concern. Evidence indicates that iron dyshomeostasis and ferroptosis may establish a role in neurotoxicity of sevoflurane and isoflurane. However, the mechanisms of sevoflurane- and isoflurane-induced neuronal injury were not fully understood, which poses a barrier to the treatment of its neurotoxicity. We, therefore, reviewed the current knowledge on mechanisms of iron dyshomeostasis and ferroptosis and aimed to promote a better understanding of their roles in sevoflurane- and isoflurane-induced neurotoxicity.

Effect of propofol and sevoflurane on postoperative fatigue after laparoscopic hysterectomy.

BACKGROUND: Postoperative fatigue syndrome (POFS) is an important factor in postoperative recovery. However, the effect of anesthetic drugs on postoperative fatigue in female patients has been rarely studied. This study compared the effects of maintaining general anesthesia with propofol or sevoflurane on the incidence of POFS in patients undergoing laparoscopic hysterectomy. METHODS: This prospective, single-blind, randomized controlled trial enrolled patients scheduled for laparoscopic hysterectomy. Eligible patients were randomized into the propofol and sevoflurane groups. The primary outcome was the incidence of POFS within 30 Days, defined by a simplified identity consequence fatigue scale (ICFS-10) scores≥24 or Visual Analogue Scale (VAS) scores of fatigues>6. Secondary outcomes were perioperative grip strength, early ambulation and anal exhaust after surgery, and inpatient days. RESULTS: 32 participants were assigned to the propofol group (P) and 33 to the sevoflurane group (S). Incidence of POFS on postoperative D1 was P (8/32) vs. S (10/33) (p = 0.66, 95% confidence interval [CI]: 16.4-27.00); D3 P (2/32) vs. S (5/33) (p = 0.45,95% CI:5.96-23.76). POFS were not found on postoperative D5 and D30. There were no differences in perioperative grip strength, early ambulation and anal exhaust after surgery, and inpatient days between the two groups. CONCLUSIONS: POFS after scheduled laparoscopic hysterectomy was unaffected by anesthesia with propofol vs. sevoflurane. The incidence of POFS was highest on the first postoperative day, at 27.7%, and declined progressively over the postoperative 30 days. Trial registration Chinese Clinical Trial Registry (No. ChiCTR 2,000,033,861), registered on 14/06/2020).

Liraglutide improves sevoflurane-induced postoperative cognitive dysfunction via activating autophagy and inhibiting apoptosis.

BACKGROUND: Postoperative cognitive dysfunction (POCD) is a common postoperative complication in elderly patients. Liraglutide (LRG) has high homology (97%) with natural glucagon like peptide-1, and it has been proved to be effective in some nervous system diseases. Whether LRG could regulate POCD has not been reported. METHODS: Sevoflurane (Sev) was used to simulate postoperative cognitive dysfunction (POCD) model. Morris water maze test was performed to evaluate the memory ability and neurological function of rats. Escape latency, swim distance, crossing platform times, average velocity, and targeting quadrant time were analyzed. The cell apoptosis, mRNA and protein expression were measured through flow cytometry, PCR, and western blotting, respectively. RESULTS: LRG significantly improved the memory ability and neurological function of Sev-treated rats, but 3-MA reversed the effects of LRG. LRG remarkably inhibited apoptosis but up-regulated autophagy related proteins both in vivo and in vitro levels. However, knocking down AMPK could markedly reverse the influence of LRG on apoptosis, autophagy, and cell apoptosis. CONCLUSIONS: LRG induced autophagy activation can maintain cell homeostasis and promote cell survival by blocking the apoptotic pathway. LRG could improve Sev-induced POCD via activating autophagy, inhibiting apoptosis, and regulating AMPK/mTOR signaling pathway. This study provides a novel therapeutic strategy for the prevention and treatment of POCD.

Cerebellar Purkinje cell firing promotes conscious recovery from anesthesia state through coordinating neuronal communications with motor cortex.

Background: The neurobiological basis of gaining consciousness from unconscious state induced by anesthetics remains unknown. This study was designed to investigate the involvement of the cerebello-thalamus-motor cortical loop mediating consciousness transitions from the loss of consciousness (LOC) induced by an inhalational anesthetic sevoflurane in mice. Methods: The neural tracing and fMRI together with opto-chemogenetic manipulation were used to investigate the potential link among cerebello-thalamus-motor cortical brain regions. The fiber photometry of calcium and neurotransmitters, including glutamate (Glu), γ-aminobutyric acid (GABA) and norepinephrine (NE), were monitored from the motor cortex (M1) and the 5th lobule of the cerebellar vermis (5Cb) during unconsciousness induced by sevoflurane and gaining consciousness after sevoflurane exposure. Cerebellar Purkinje cells were optogenetically manipulated to investigate their influence on consciousness transitions during and after sevoflurane exposure. Results: Activation of 5Cb Purkinje cells increased the Ca2+ flux in the M1 CaMKIIα+ neurons, but this increment was significantly reduced by inactivation of posterior and parafascicular thalamic nucleus. The 5Cb and M1 exhibited concerted calcium flux, and glutamate and GABA release during transitions from wakefulness, loss of consciousness, burst suppression to conscious recovery. Ca2+ flux and Glu release in the M1, but not in the 5Cb, showed a strong synchronization with the EEG burst suppression, particularly, in the gamma-band range. In contrast, the Glu, GABA and NE release and Ca2+ oscillations were coherent with the EEG gamma band activity only in the 5Cb during the pre-recovery of consciousness period. The optogenetic activation of Purkinje cells during burst suppression significantly facilitated emergence from anesthesia while the optogenetic inhibition prolonged the time to gaining consciousness. Conclusions: Our data indicate that cerebellar neuronal communication integrated with motor cortex through thalamus promotes consciousness recovery from anesthesia which may likely serve as arousal regulation.

Liproxstatin-1 alleviates ferroptosis in sevoflurane anesthesia-induced cognitive deficits of aged mice: The role oxidative stress.

In this study, we aimed to validate the hypothesis that the interplay between sevoflurane, oxidative stress and ferroptosis is crucial for the pathogenesis of sevoflurane-induced cognitive impairment in aged individuals. The mice with sevoflurane-induced cognitive impairment were used to explore the effects of sevoflurane on oxidative stress, iron homeostasis, and cognitive function in aged mice. Iron content and oxidative stress markers were analyzed in hippocampal tissue homogenates using specific assays. Additionally, the levels of iron death-related markers (Fth1 and Gpx4) were assessed by real-time PCR and Western blotting. Morris Water Maze and novel object recognition (NOR) tests were conducted to evaluate cognitive function. Sevoflurane exposure in aged mice resulted in a significant increase in iron overloading in the hippocampus, followed by a subsequent stabilization. Oxidative stress levels were elevated in the hippocampal tissue of sevoflurane-exposed mice, and a significant correlation was observed between iron death and oxidative stress. Liproxstatin-1, a ferroptosis inhibitor, effectively ameliorated the decline in memory and learning abilities induced by sevoflurane anesthesia. Liproxstatin-1 treatment reduced iron overload and oxidative stress in the hippocampal tissue of aged mice. The expression of Fth1 and Gpx4, iron death-related markers, was downregulated following Liproxstatin-1 intervention. Our findings suggest that sevoflurane anesthesia disrupts iron homeostasis, leading to increased oxidative stress and cognitive impairment in aged mice. These results highlight the potential of targeting iron-mediated processes to mitigate sevoflurane-induced cognitive impairment in the aging population.

Siglec-E Ligand Downregulation on Hippocampus Neurons Induced Inflammation in Sevoflurane-Associated Perioperative Neurocognitive Disorders in Aged Mice.

Activated microglia-induced inflammation in the hippocampus plays an important role in perioperative neurocognitive disorders. Previous studies have shown that sialic acid-binding immunoglobulin-like lectin 3 (hSiglec-3, ortholog of mouse Siglec-E) engagement in microglia and its glycan ligands on neurons contributes to inflammatory homeostasis through an endogenous negative regulation pathway. This study aimed to explore whether the glycan ligand alteration on neurons plays a role in sevoflurane-induced perioperative neurocognitive disorders. This study's data has shown that a slight Siglec-E ligands' expression decrease does not induce inflammation homeostasis disruption. We also demonstrated that the ligand level on neurons was decreased with age, and the reduced Siglec-E ligand expression on neurons caused via sevoflurane was induced by neuraminidase 1. Furthermore, this study has shown that the Siglec-E ligand expression decline caused by age and sevoflurane treatment could decrease the ligands' level, thus leading to inflammatory homeostasis disruption. This research provided a novel mechanism for perioperative neurocognitive disorder susceptibility in the elderly.

Differential effects of sevoflurane and desflurane on frontal intraoperative electroencephalogram dynamics associated with postoperative delirium.

STUDY OBJECTIVE: Intraoperative electroencephalogram (EEG) patterns associated with postoperative delirium (POD) development have been studied, but the differences in EEG recordings between sevoflurane- and desflurane-induced anesthesia have not been clarified. We aimed to distinguish the EEG characteristics of sevoflurane and desflurane in relation to POD development. DESIGN AND PATIENTS: We collected frontal four-channel EEG data during the maintenance of anesthesia from 148 elderly patients who received sevoflurane (n = 77) or desflurane (n = 71); 30 patients were diagnosed with delirium postoperatively. The patients were divided into four subgroups based on anesthetics and delirium status: sevoflurane delirium (n = 17), sevoflurane non-delirium (n = 60), desflurane delirium (n = 13), and desflurane non-delirium (n = 58). We compared spectral power, coherence, and pairwise phase consistency (PPC) between sevoflurane and desflurane, and between non-delirium and delirium groups for each anesthetic. MAIN RESULTS: In patients without POD, the sevoflurane non-delirium group exhibited higher EEG spectral power across 8.5-35 Hz (99.5% CI bootstrap analysis) and higher PPC from alpha to gamma bands (p < 0.005) compared to the desflurane non-delirium group. Conversely, in patients with POD, no significant EEG differences were observed between the sevoflurane and desflurane delirium groups. For the sevoflurane-induced patients, the sevoflurane delirium group had significantly lower power within 7.5-31.5 Hz (99.5% CI bootstrap analysis), reduced coherence over 8.9-23.8 Hz (99.5% CI bootstrap analysis), and lower PPC values in the alpha band (p < 0.005) compared with the sevoflurane non-delirium group. For the desflurane-induced patients, there were no significant differences in the EEG patterns between delirium and non-delirium groups. CONCLUSIONS: In normal patients without POD, sevoflurane demonstrates a higher power spectrum and prefrontal connectivity than desflurane. Furthermore, reduced frontal alpha power, coherence, and connectivity of intraoperative EEG could be associated with an increased risk of POD. These intraoperative EEG characteristics associated with POD are more noticeable in sevoflurane-induced anesthesia than in desflurane-induced anesthesia.

Diffuse alveolar hemorrhage following inhaled sevoflurane: A rare complication of inhalational anesthesia.

Sevoflurane is a commonly used inhalational anesthetic agent for inducing and maintaining general anesthesia. However, it has been associated with a rare but serious pulmonary condition known as diffuse alveolar hemorrhage (DAH). DAH is characterized by decreased hemoglobin levels, diffuse pulmonary infiltration, and respiratory failure with hypoxemia. We present a case of DAH in a healthy young adult who experienced this condition following general anesthesia with inhaled sevoflurane during an uncomplicated orthopedic procedure. Notably, there were no other risk factors or known causes that could account for the development of DAH in this patient.

Phoenixin-20 ameliorates Sevoflurane inhalation-induced post-operative cognitive dysfunction in rats via activation of the PKA/CREB signaling.

Post-operative cognitive dysfunction (POCD) is a common complication after surgery due to the usage of anesthetics, such as Sevoflurane, which severely impacts the life quality of patients. Currently, the pathogenesis of Sevoflurane-induced POCD has not been fully elucidated but is reportedly involved with oxidative stress (OS) injury and aggravated inflammation. Phoenixin-20 (PNX-20) is a PNX peptide consisting of 20 amino acids with promising inhibitory effects on OS and inflammation. Herein, we proposed to explore the potential protective function of PNX-20 on Sevoflurane inhalation-induced POCD in rats. Sprague-Dawley (SD) rats were treated with 100 ng/g PNX-20 for 7 days with or without pre-inhalation with 2.2% Sevoflurane. Markedly increased escape latency and decreased time in the target quadrant in the Morris water maze (MWM) test, and aggravated pathological changes and apoptosis in the hippocampus tissue were observed in Sevoflurane-treated rats, which were markedly attenuated by PNX-20. Furthermore, the aggravated inflammation and OS in the hippocampus observed in Sevoflurane-treated rats were notably abolished by PNX-20. Moreover, the brain-derived neurotrophic factor (BDNF), protein kinase A (PKA), and phospho-cAMP response element binding protein/cAMP response element binding protein (p-CREB/CREB) levels were markedly decreased in Sevoflurane-treated rats, which were memorably increased by PNX-20. Our results indicated that PNX-20 ameliorated Sevoflurane inhalation-induced POCD in rats via the activation of PKA/CREB signaling, which might supply a new treatment approach for POCD.

Protocol for a randomized controlled trial to reduce pediatric anesthesia emergence delirium by titration of sevoflurane anesthesia using brain function monitoring.

BACKGROUND: Emergence agitation or emergence delirium is a common complication of unknown etiology in pediatric anesthesia. Pediatric anesthesia emergence delirium (PAED) has been reported most commonly in younger children and may occur in about 30% of children up to 5-6 years old. Exposure to anesthetic agents may contribute to PAED, and we hypothesized that a management strategy to minimize exposure to volatile anesthetics may reduce PAED. Electroencephalography (EEG) signatures captured and displayed by brain function monitors during anesthesia change with concentration of sevoflurane and level of unconsciousness, and these EEG signatures may be used to inform titration of anesthetics. METHODS: A single-center, parallel-group, two-arm, superiority trial with a 1:1 allocation ratio will be performed to compare the incidence of PAED following standard sevoflurane anesthesia (maintained at 1.0MAC) and EEG-guided anesthesia (minimum concentration to sustain surgical anesthesia as determined by monitoring of EEG signatures). Participants between 1 and 6 years of age undergoing surgical procedures involving minimal postoperative pain will be randomly assigned to receive standard (n = 90) or EEG-guided (n = 90) anesthesia. PAED score will be assessed by a blinded observer in the PACU on arrival and after 5, 10, 15, and 30 min. DISCUSSION: Anesthesia management with proactive use of brain function monitoring is expected to reduce exposure to sevoflurane without compromising surgical anesthesia. We expect this reduced exposure should help prevent PAED. Routinely administering what may be considered standard levels of anesthetic such as 1.0 MAC sevoflurane may be excessive and potentially associated with unfavorable sequelae such as PAED. TRIAL REGISTRATION: Japan Registry of Clinical Trials (jRCT) jRCTs032210248. Prospectively registered on 17 August 2021.

Sucking lollipop after awakening from sevoflurane anesthesia reduces the degree of emergence agitation in children undergoing ambulatory surgery: A prospective randomized controlled trial.

BACKGROUND: Emergence agitation (EA) is a common complication in pediatric anesthesia, especially in preschool children maintained by sevoflurane, with incidence ranging up to 80%. The purpose of the study was to determine whether sucking lollipop after awakening from sevoflurane anesthesia reduced the degree of EA in children undergoing ambulatory surgery. METHODS: In this prospective study, 40 children aged 2 to 6 years scheduled for ambulatory surgery with sevoflurane were enrolled. They were randomly allocated to 1 of 2 groups after evaluating baseline EA levels using the pediatric anesthesia emergence delirium (PAED) scale immediately after awakening from general anesthesia: group L (sucking lollipop) or group C (control group, without sucking lollipop). The primary outcome was the overall PAED score after intervention. Pain score, parental satisfaction, the incidence of propofol rescue and negative postoperative behavioral changes (NPOBCs) were assessed. RESULTS: The overall PAED score after intervention was significantly lower in Group L compared with Group C, with an estimated difference of -1.857 (95% CI, -2.884 to -0.831; P < .001) using generalized estimating equations. However, no significant intergroup differences were observed in the pain score, parental satisfaction, the incidence of propofol rescue and NPOBCs. CONCLUSIONS: Sucking lollipop after awakening from sevoflurane anesthesia reduced the degree EA in children undergoing ambulatory surgery.

Fgf2 and Ptpn11 play a role in cerebral injury caused by sevoflurane anesthesia.

Sevoflurane is a new inhaled anesthetic, which has better physical properties than the existing inhalational anesthetics, rapid induction, less tissue uptake, and faster recovery. Sevoflurane can directly dilators cerebral blood vessels and increase cerebral blood flow, but it also reduces cerebral oxygen metabolism rate, thereby reducing cerebral blood flow. However, the role of Fgf2 and Ptpn11 in cerebral injury caused by sevoflurane anesthesia remains unclear. The sevoflurane anesthesia brain tissue datasets GSE139220 and GSE141242 were downloaded from gene expression omnibus (GEO). Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis (WGCNA) was performed. Construction and analysis of protein-protein interaction (PPI) Network. Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG), comparative toxicogenomics database (CTD) were performed. A heat map of gene expression was drawn. TargetScan was used to screen miRNAs regulating DEGs. 500 DEGs were identified. According to GO, in Biological Process analysis, they were mainly enriched in response to hypoxia, blood vessel development, inner ear development, neural tube closure, and aging. In Cellular Component (CC), they were mainly enriched in plasma membrane, integral component of membrane, and basal lamina. In Molecular Function (MF), they were mainly associated with protein binding, Wnt-activated receptor activity, and organic anion transmembrane transporter activity. In the KEGG analysis, they were mainly enriched in proteoglycans in cancer, pathways in cancer, transcriptional misregulation in cancer, basal cell carcinoma, thyroid hormone signaling pathway. In the Metascape enrichment analysis, the GO enrichment items revealed upregulated regulation of vascular endothelial cell proliferation, platelet-derived growth factor receptor signaling pathway, inner ear development, and response to hypoxia. A total of 20 modules were generated. Gene Expression Heatmap showed that the core genes (Fgf2, Pdgfra, Ptpn11, Slc2a1) were highly expressed in sevoflurane anesthesia brain tissue samples. CTD Analysis showed that the 4 core genes (Fgf2, Pdgfra, Ptpn11, Slc2a1) were associated with neurodegenerative diseases, brain injuries, memory disorders, cognitive disorders, neurotoxicity, drug-induced abnormalities, neurological disorders, developmental disorders, and intellectual disabilities. Fgf2 and Ptpn11 are highly expressed in brain tissue after sevoflurane anesthesia, higher the expression level of Fgf2 and Ptpn11, worse the prognosis.

Sevoflurane-induced hypotension causes cognitive dysfunction and hippocampal inflammation in mice.

Sevoflurane commonly adopted for anesthetic in clinical practice, however, its influences on cerebral blood flow and cognitive function remain controversial. Herein, the sevoflurane-induced hypotension on arterial blood pressure, cerebral blood flow, cognitive function, and hippocampal inflammation was investigated in mice. A significant decrease in arterial blood pressure and cerebral blood flow was indicated by the sevoflurane anesthesia treatment. Moreover, sevoflurane-induced hypotension was associated with the impaired cognitive function and the increased levels of NLRP3 inflammasome activation and oxidative stress in hippocampus. These findings suggest that sevoflurane-induced hypotension may lead to the cognitive dysfunction and hippocampal inflammation.

Predictors of Low Risk for Delirium during Anesthesia Emergence.

BACKGROUND: Processed electroencephalography (EEG) is used to monitor the level of anesthesia, and it has shown the potential to predict the occurrence of delirium. While emergence trajectories of relative EEG band power identified post hoc show promising results in predicting a risk for a delirium, they are not easily transferable into an online predictive application. This article describes a low-resource and easily applicable method to differentiate between patients at high risk and low risk for delirium, with patients at low risk expected to show decreasing EEG power during emergence. METHODS: This study includes data from 169 patients (median age, 61 yr [49, 73]) who underwent surgery with general anesthesia maintained with propofol, sevoflurane, or desflurane. The data were derived from a previously published study. The investigators chose a single frontal channel, calculated the total and spectral band power from the EEG and calculated a linear regression model to observe the parameters' change during anesthesia emergence, described as slope. The slope of total power and single band power was correlated with the occurrence of delirium. RESULTS: Of 169 patients, 32 (19%) showed delirium. Patients whose total EEG power diminished the most during emergence were less likely to screen positive for delirium in the postanesthesia care unit. A positive slope in total power and band power evaluated by using a regression model was associated with a higher risk ratio (total, 2.83 [95% CI, 1.46 to 5.51]; alpha/beta band, 7.79 [95% CI, 2.24 to 27.09]) for delirium. Furthermore, a negative slope in multiple bands during emergence was specific for patients without delirium and allowed definition of a test for patients at low risk. CONCLUSIONS: This study developed an easily applicable exploratory method to analyze a single frontal EEG channel and to identify patterns specific for patients at low risk for delirium.

The m6A Reader YTHDF1 Improves Sevoflurane-Induced Neuronal Pyroptosis and Cognitive Dysfunction Through Augmenting CREB-BDNF Signaling.

Sevoflurane is one of the most widely used anesthetics in surgery which is the main cause of postoperative cognitive dysfunction (POCD). Previous reports confirmed that YTHDF1 is differently expressed in sevoflurane-induced POCD, while the roles and mechanistic details remain unclear. The molecular expressions were assessed using qRT-PCR, western blot, immunofluorescence and immunohistochemistry. Pathological change in the hippocampus tissues was analyzed using HE staining. Cognitive ability in rats was measured using MWM test. Hippocampal neuronal viability and apoptosis were measured by MTT assay and flow cytometry, respectively. The levels of pro-inflammatory cytokines were assessed using ELISA. The interaction between YTHDF1 and CREB was analyzed by RNA immunoprecipitation assay. YTHDF1 was significantly decreased in hippocampus tissues by sevoflurane exposure, and its overexpression could improve sevoflurane-induced neuron damage and cognitive dysfunction. Meanwhile, YTHDF1 upregulation repressed sevoflurane-induced activation of NLRP3 inflammation and pyroptosis in hippocampus tissues. Subsequently, YTHDF1 directly interacted to CREB mRNA to augment its stability and translation via a m6A-dependent manner, thus activating CREB/BDNF pathway. In addition, the inactivation of CREB/BDNF pathway could reverse the protective effects of YTHDF1 overexpression on sevoflurane-mediated neuronal damage and pyroptosis. These findings revealed that YTHDF1 improved sevoflurane-induced neuronal pyroptosis and cognitive dysfunction through activating CREB-BDNF signaling.