Sevoflurane Anesthesia Research Articles

244 A Systematic Review of Epileptiform Changes During Sevoflurane Anesthesia In Infants and Children

OBJECTIVES/GOALS: Early clinical case reports have described incidental epileptiform changes during electrophysiological monitoring. The objective of this study was to perform a systematic review of all existing investigations of epileptiform activity during sevoflurane use in pediatric anesthesia. The heterogenous EEG data will be analyzed in a meta analysis METHODS/STUDY POPULATION: A targeted, PICO-based clinical question was crafted and registered a priori on PROSPERO on 3/19/21. Under the guidance of a librarian from the Albert Einstein College of Medicine, a boolean search string was generated to search articles and gray literature for terms such as pediatric, sevoflurane and electroencephalogram in PubMed, OVID, Cochrane, Google Scholar, etc. We utilized the software platform tool COVIDENCE to manage our review. 495 references were imported for initial screening. 56 English-language, full-text studies were included for further review. The final 13 references were included in data extraction and Newcastle-Ottawa bias assessment. The characteristics of the studies and their primary outcomes were collected in tabular form. Strategies for data synthesis were discussed weekly. RESULTS/ANTICIPATED RESULTS: Epileptiform changes reported in the literature during pediatric sevoflurane anesthesia ranged from 0 - 95%. EEG data were acquired using a variety of recording systems with variable number of leads and heterogeneous outcomes reported. The periods of anesthesia monitoring were also heterogeneous. Characteristics of the studies are presented in Table 1. 495 references were imported for screening with 13 final references for data extraction. EEG abnormalities were reported in 204/649 (31.4%) subjects ranging in age from neonate to 18 years; the majority of studies utilized less than 16 channels of (10/13, 76.9%) (Table 1). There was variability in sevoflurane dosing, premedication (e.g., midzolam, hydroxyzine), and periods of anesthesia monitored. DISCUSSION/SIGNIFICANCE: There was heterogeneity noted across reviewed literature including study design, phases of anesthesia, ventilation methods, number of EEG leads recorded and adjuvant anesthetics administered. Nevertheless, this review rigorously classified epileptiform activity during Sevoflurane thereby influencing modern anesthesia.

Janus Kinase Mediates Faster Recovery From Sevoflurane Anesthesia Than Isoflurane Anesthesia in the Migratory Locusts.

Inhalation anesthetics isoflurane and sevoflurane have been widely used in clinical practice for anesthesia. However, the molecular mechanisms underlying the faster recovery from sevoflurane anesthesia than isoflurane anesthesia remain largely undetermined. Herein, we use RNA-seq, RNA interference, quantitative real-time PCR and western blotting to explore the mechanisms of recovery from isoflurane and sevoflurane anesthesia in the migratory locusts. Although the migratory locusts show similar anesthetic responses to these two chemicals in corresponding half-maximal effective concentrations (EC50s), the recovery from sevoflurane anesthesia is significantly faster than that for isoflurane anesthesia after 30 min of anesthetic exposure. Transcriptome analysis shows that those transcripts involved in cytoskeletal components, Janus kinase (JAK) pathway and cuticle protein are differentially expressed in locust brains in response to isoflurane and sevoflurane. RNAi knockdown confirms that Actin, Myosin-like protein 84B (Mlp84B), JAK and cuticle protein NCP56 do not affect anesthetic response of the locusts to these two chemical anesthetics. Moreover, actin, Mlp84B and NCP56 do not affect differential recovery from isoflurane and sevoflurane anesthesia, whereas RNAi knockdown of JAK and its partner STAT5B does not affect anesthetic recovery from isoflurane but elongates recovery duration from sevoflurane anesthesia. Thus, JAK may mediate faster recovery from sevoflurane anesthesia than from isoflurane anesthesia in the migratory locust. This finding provides novel insights into the molecular mechanism underlying faster recovery from sevoflurane anesthesia than isoflurane anesthesia.

The influence of TIVA or inhalation anesthesia with or without intravenous lidocaine on postoperative outcome in colorectal cancer surgery: a study protocol for a prospective clinical study

BackgroundAnesthetic agents are mandatory in colorectal cancer patients undergoing surgery. Studies published so far have shown that anesthetic drugs and intervention may have different impacts on patient’s outcome. Among these drugs, propofol and, more recently, local anesthetics have been mostly targeted.Methods/designThis study will be a prospective randomized control trial aiming to include 400 patients scheduled for curative colorectal surgery. Patients will be randomized to have general anesthesia with propofol or with sevoflurane. Each study group will be further divided into 2 subgroups of patients, of which one will receive intravenous lidocaine perioperatively. The primary outcome is to compare the incidence of cancer recurrence and survival after propofol versus sevoflurane anesthesia added or not intravenous lidocaine. Secondary outcomes will include the severity of postoperative pain, resumption of bowel function, morphine consumption, length of hospital stay, postoperative chronic pain, and rate of postoperative complications.DiscussionTo our knowledge, this is the first randomized control trial registered on ClinicalTrials.gov designed to compare the effects of two different anesthetic techniques added perioperative intravenous lidocaine infusion on long-term outcomes exclusively in colorectal cancer patients undergoing surgery. The study will bring more accurate data on the effect of propofol-TIVA and perioperative iv lidocaine on the incidence of recurrences after intended curative colorectal surgery.Trial registrationClinical Trial Registration NCT02786329. Registered on 1 June 2016

Inhibition of unfolded protein response prevents post-anesthesia neuronal hyperactivity and synapse loss in aged mice.

Delirium is the most common postoperative complication in older patients after prolonged anesthesia and surgery and is associated with accelerated cognitive decline and dementia. The neuronal pathogenesis of postoperative delirium is largely unknown. The unfolded protein response (UPR) is an adaptive reaction of cells to perturbations in endoplasmic reticulum function. Dysregulation of UPR has been implicated in a variety of diseases including Alzheimer's disease and related dementias. However, whether UPR plays a role in anesthesia‐induced cognitive impairment remains unexplored. By performing in vivo calcium imaging in the mouse frontal cortex, we showed that exposure of aged mice to the inhalational anesthetic sevoflurane for 2 hours resulted in a marked elevation of neuronal activity during recovery, which lasted for at least 24 hours after the end of exposure. Concomitantly, sevoflurane anesthesia caused a prolonged increase in phosphorylation of PERK and eIF2α, the markers of UPR activation. Genetic deletion or pharmacological inhibition of PERK prevented neuronal hyperactivity and memory impairment induced by sevoflurane. Moreover, we showed that PERK suppression also reversed various molecular and synaptic changes induced by sevoflurane anesthesia, including alterations of synaptic NMDA receptors, tau protein phosphorylation, and dendritic spine loss. Together, these findings suggest that sevoflurane anesthesia causes abnormal UPR in the aged brain, which contributes to neuronal hyperactivity, synapse loss and cognitive decline in aged mice.

Spectral Entropy Monitoring Accelerates the Emergence from Sevoflurane Anesthesia in Thoracic Surgery: A Randomized Controlled Trial.

The clinical efficacy of spectral entropy monitoring in improving postoperative recovery remains unclear. This trial aimed to investigate the impact of M-Entropy (GE Healthcare, Helsinki, Finland) guidance on emergence from anesthesia and postoperative delirium in thoracic surgery. Adult patients undergoing video-assisted thoracoscopic surgery for lung resection at a medical center were randomly allocated into the M-Entropy guidance group (n = 39) and the control group (n = 37). In the M-Entropy guidance group, sevoflurane anesthesia was titrated to maintain response and state entropy values between 40 and 60 intraoperatively. In the control group, the dosing of sevoflurane was adjusted based on clinical judgment and vital signs. The primary outcome was time to spontaneous eye opening. M-Entropy guidance significantly reduced the time proportion of deep anesthesia (entropy value <40) during surgery, mean difference: −21.5% (95% confidence interval (CI): −32.7 to −10.3) for response entropy and −24.2% (−36.3 to −12.2) for state entropy. M-Entropy guidance significantly shortened time to spontaneous eye opening compared to clinical signs, mean difference: −154 s (95% CI: −259 to −49). In addition, patients of the M-Entropy group had a lower rate of emergence agitation (absolute risk reduction: 0.166, 95% CI: 0.005–0.328) and delirium (0.245, 0.093–0.396) at the postanesthesia care unit. M-Entropy-guided anesthesia hastened awakening and potentially prevented emergence agitation and delirium after thoracic surgery. These results may provide an implication for facilitating postoperative recovery and reducing the complications associated with delayed emergence and delirium.

Botulinum Toxin Injection in Horizontal Rectus Muscles Without Electromyography Using an Open Sky Versus a Closed Sky Technique.

To ascertain whether electromyographic control when injecting botulinum toxin in the horizontal rectus muscles is necessary, and to compare the open sky and closed sky injection techniques that are used without electromyographic control. The records of 135 patients with horizontal strabismus who received botulinum toxin injections were reviewed retrospectively. Sevoflurane or propofol anesthesia was used in children, and topical benoxinate hydrochloride was used in adults. Patients received a bilateral injection of 2.5 to 15 IU of botulinum toxin, without electromyographic control, into the medial or lateral rectus muscles to correct esotropia or exotropia, respectively. An open sky technique was used in 31 patients, and a closed sky technique was used in 104 patients. Postoperative alignment within 10 prism diopters (PD) of orthotropia was considered a successful outcome. A successful outcome at 6 months of follow-up was achieved in 47% of all patients: 59% of patients in the open sky group and 44% of patients in the closed sky group (P = .151). Botulinum toxin injection corrected a mean of 14 ± 9.705 PD in patients in the open sky group and 31 ± 20.589 PD in patients in the closed sky group to obtain mean residual angles of 21 ± 16.692 and 13 ± 11.901 PD, respectively. The results obtained without electromyographic assistance were not remarkably different from the studies using electromyographic control. Moreover, because the results of the open sky technique were not significantly superior to the closed sky technique, the latter was favored to shorten the operative time and postoperative convalescence, and to reduce the risk of postoperative adhesions and scarring, which made re-operations difficult. [J Pediatr Ophthalmol Strabismus. 2022;59(6):388-395.].

Renal function during sevoflurane or total intravenous propofol anaesthesia: a single-centre parallel randomised controlled study

BackgroundThe choice of anaesthetic may influence regulation of renal perfusion and function. We investigated renal function in patients anaesthetised with propofol or sevoflurane before surgery and postoperatively. MethodsPatients with ASA physical status 1–2 planned for spinal surgery were randomised to propofol or sevoflurane anaesthesia. Blood and urine were collected before anaesthesia, during anaesthesia (before surgery), during postoperative care, and the day after surgery. ResultsTwenty-seven patients completed the study protocol (average age, 51 yr; average BMI, 28 kg m−2) and 11 were women. Urine output and sodium excretion were lower during sevoflurane anaesthesia (n=14) than during propofol anaesthesia (n=13) (0.3 vs 1.1 ml kg−1 h−1 [P=0.01] and 2.6 vs 6.0 mmol h−1 [P=0.04], respectively). Urinary potassium excretion was lower during anaesthesia than after, without intergroup difference (2.3 vs 5.7 mmol h−1, P<0.001). Sevoflurane anaesthesia increased plasma renin compared with baseline (138 vs 23 mIU L−1, P<0.001) and propofol anaesthesia (138 vs 27 mIU L−1, P=0.008). Plasma arginine–vasopressin did not change significantly during anaesthesia, but was elevated postoperatively compared with baseline irrespective of anaesthetic (21 vs 12 ng L−1, P=0.02). Sevoflurane caused higher postoperative plasma creatinine than propofol (83 vs 66 mmol L−1, P=0.01). Kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin did not change significantly in either group. ConclusionsSevoflurane anaesthesia reduced urine output and sodium excretion and increased plasma renin compared with propofol anaesthesia. The impact of this on acute kidney injury and fluid resuscitation during surgery warrants further investigation. Clinical trial registrationEudraCT: 2017-001646-10; Clinicaltrials.gov: NCT0333680.

A Neural Circuit from the Paraventricular Thalamus to the Bed Nucleus of the Stria Terminalis for the Regulation of States of Consciousness during Sevoflurane Anesthesia in Mice.

The neural circuitry underlying sevoflurane-induced modulation of consciousness is poorly understood. This study hypothesized that the paraventricular thalamus bed nucleus of the stria terminalis pathway plays an important role in regulating states of consciousness during sevoflurane anesthesia. Rabies virus-based transsynaptic tracing techniques were employed to reveal the neural pathway from the paraventricular thalamus to the bed nucleus of the stria terminalis. This study investigated the role of this pathway in sevoflurane anesthesia induction, maintenance, and emergence using chemogenetic and optogenetic methods combined with cortical electroencephalogram recordings. Both male and female mice were used in this study. Both γ-aminobutyric acid-mediated and glutamatergic neurons in the bed nucleus of the stria terminalis receive paraventricular thalamus glutamatergic projections. Chemogenetic inhibition of paraventricular thalamus glutamatergic neurons prolonged the sevoflurane anesthesia emergence time (mean ± SD, hM4D-clozapine N-oxide vs. mCherry-clozapine N-oxide, 281 ± 88 vs. 172 ± 48 s, P < 0.001, n = 24) and decreased the induction time (101 ± 32 vs. 136 ± 34 s, P = 0.002, n = 24), as well as the EC5 0 for the loss or recovery of the righting reflex under sevoflurane anesthesia (mean [95% CI] for the concentration at which 50% of the mice lost their righting reflex, 1.16 [1.12 to 1.20] vs. 1.49 [1.46 to 1.53] vol%, P < 0.001, n = 20; and for the concentration at which 50% of the mice recovered their righting reflex, 0.95 [0.86 to 1.03] vs. 1.34 [1.29 to 1.40] vol%, P < 0.001, n = 20). Similar results were observed during suppression of the paraventricular thalamus bed nucleus-stria terminalis pathway. Optogenetic activation of this pathway produced the opposite effects. Additionally, transient stimulation of this pathway efficiently induced behavioral arousal during continuous steady-state general anesthesia with sevoflurane and reduced the depth of anesthesia during sevoflurane-induced burst suppression. In mice, axonal projections from the paraventricular thalamic neurons to the bed nucleus of the stria terminalis contribute to regulating states of consciousness during sevoflurane anesthesia.

Sevoflurane diminishes neurogenesis and promotes ferroptosis in embryonic prefrontal cortex via inhibiting nuclear factor-erythroid 2-related factor 2 expression.

Prenatal sevoflurane exposure may pose neurotoxicity to embryonic brain development and lead to cognitive dysfunction in offspring, but the underlying mechanism is still unclear. We aimed to investigate whether sevoflurane could cause neurogenesis abnormality and ferroptosis in embryonic prefrontal cortex (PFC) and to identify the role of nuclear factor-erythroid 2-related factor 2 (Nrf2) in the sevoflurane-related neurotoxicity. We used the rodents and primary neural stem cells to examine whether sevoflurane impacted proliferation, differentiation, ferroptosis and apoptosis in the neural stem cells of embryonic PFC. In addition, the expression of Nrf2 and the intensity of reactive oxygen species (ROS) were also assessed to explore the underlying molecular mechanism. Our results showed that sevoflurane exposure in third trimester could lead to neurogenesis inhibition and ferroptosis in-vivo embryonic PFC, with little influence on apoptosis. Moreover, a significant decrease in the expression of Nrf2 as well as an increase in ROS accumulation were also found in neural stem cells after sevoflurane anesthesia. We conclude that Nrf2-related neurogenesis inhibition and ferroptosis are a central mechanism contributing to sevoflurane-induced neurotoxicity in embryonic brain. The results of the present study are the first to demonstrate that ferroptosis and the expression of Nrf2 are involved in sevoflurane-related neurotoxicity in embryonic brain, which provides new vision for consideration in anesthesia-associated neurological abnormalities.

Neurodevelopmetal effects of maternal blood pressure management with noradrenaline during general anaesthesia for nonobstetric surgery in the pregnant rabbit model.

In pregnant women, anaesthesia-induced hypotension is commonly treated using phenylephrine or noradrenaline, the rationale being to maintain uterine perfusion pressure and thereby uterine blood flow. Evidence for this strategy during general anaesthesia for nonobstetric surgery is absent. To analyse the effects of treating anaesthesia-induced hypotension with noradrenaline on brain development of rabbit foetuses of mothers subjected to general anaesthesia for nonobstetric surgery. We hypothesised that treatment of maternal hypotension would improve foetal outcomes. Randomised controlled laboratory study using 21 pregnant rabbits (does) at 28 days of gestation. Two hours of sevoflurane anaesthesia for a laparotomy without treatment of anaesthesia-induced hypotension (hypotension group) or with maintaining maternal mean arterial pressure above 80% of the awake value using noradrenaline (noradrenaline group). In the control group, does remained untouched. At term, all pups were delivered by caesarean section. One day later, the neurobehaviour of the pups was assessed and brains were harvested. Neuron density in the frontal cortex for the comparison of noradrenaline groups versus hypotension groups was the primary outcome; the neurobehavioural scores and other histological outcomes were secondary outcomes. In the noradrenaline groups and hypotension groups, neuron density in the frontal cortex was similar (1181 ± 162 versus 1189 ± 200 neurons mm-2, P = 0.870). However, significantly less foetal survival, lower sensory scores in neurobehavioural assessment and less proliferation were observed in the noradrenaline group when compared with the hypotension group. Neuron densities in other regions, total cell densities, biometrics and synaptogenesis were not affected. There were no differences between the control group and hypotension group. During general anaesthesia for nonobstetric surgery in rabbits, treatment of anaesthesia-induced hypotension using noradrenaline did not affect neuron densities but was associated with impaired foetal outcomes according to several secondary outcome parameters. Further studies are needed to investigate any clinical relevance and to determine the target blood pressure in pregnant women during general anaesthesia.KEY POINTSIn pregnant women, anaesthesia-induced hypotension is commonly treated using phenylephrine or noradrenaline, with the rationale to maintain uterine perfusion pressure and thereby uterine blood flow.Evidence for this strategy during general anaesthesia for nonobstetric surgery is absent.We investigated the effects of treating anaesthesia-induced hypotension with noradrenaline on the brain development of rabbit foetuses, of mothers subjected to general anaesthesia for nonobstetric surgery.We hypothesised that treatment of maternal hypotension would improve foetal outcomes.Neuron densities were similar but significantly less foetal survival, impaired neurobehaviour and less proliferation were observed after treatment of anaesthesia-induced hypotension with noradrenaline, compared with untreated hypotension.

Electro-Acupuncture Pretreatment Ameliorates Anesthesia and Surgery-Induced Cognitive Dysfunction Via Inhibiting Mitochondrial Injury and nEuroapoptosis in Aged Rats.

Postoperative cognitive dysfunction (POCD) remains one of the most common complications following anesthesia and surgery (AS) in the elderly population. Calcium-mediated mitochondrial injury has been proved to induce cognitive impairment in a variety of neurologic diseases. In the current study we determined whether electro-acupuncture (EA) pretreatment ameliorated AS-induced POCD in aged rats, as well as the underlying mechanism. Eighty SD rats (18months, male) were randomly assigned into four groups (n = 20): C, C + EA, POCD and EA + POCD. Rats in Group POCD and EA + POCD were subjected to exploratory laparotomy under sevoflurane anesthesia. Rats of Group C + EA and EA + POCD received a 5-day EA stimulation at Hegu, Neiguan and Zusanli acupoints before AS. At 3rd day after AS, open field test along with Morris water maze test were employed to examine the cognitive function of aged rats. Then hippocampal tissues were stripped and hippocampal neuronal amount, expression level of cleaved caspase-9 level, cytochrome c (Cyt C), cleaved caspase-3 level, Bcl-2, Bax, ROS expression level, apoptosis rate, mitochondrial membrane potential (MMP), cytosolic calcium concentration ([Ca2+]c), opening level of mitochondrial permeability transition pore (mPTP) and ultrastructure of hippocampal neurons were detected separately. EA pretreatment inhibited AS-induced cognitive dysfunction. Furthermore, EA pretreatment decreased level of [Ca2+]c, MMP, mPTP, ROS and hippocampal mitochondrial disruption and enhanced neuronal amount. In addition, EA pretreatment notably reduced the AS-induced increased level of cleaved caspase-9, cleaved caspase-3 and expression of Cyt c, Bax/Bcl-2 ratio, as well as neuronal apoptosis rate in aged rats. EA pretreatment ameliorates AS-induced POCD in aged rats, the potential mechanism may be associated with inhibiting calcium overload and ameliorating mitochondrial injury and neuroapoptosis in hippocampal neurons.

Science, Medicine, and the Anesthesiologist

Science, Medicine, and the Anesthesiologist

Effect of Flumazenil on Emergence Agitation after Orthognathic Surgery: A Randomized Controlled Trial.

Flumazenil, a gamma-aminobutyric acid receptor antagonist, can promote arousal even under general anesthesia without the use of benzodiazepines. We hypothesized that flumazenil could promote arousal and reduce emergence agitation in patients undergoing orthognathic surgery with sevoflurane anesthesia. One hundred and two patients were randomly allocated to the control or flumazenil group. Saline or flumazenil was administered at the end of the surgery. The incidence of emergence agitation was measured by using Aono’s four-point scale, with scores of 3 and 4 indicating emergence agitation. The primary outcome was the incidence of emergence agitation. Secondary outcomes included duration of emergence agitation and time intervals between the discontinuation of anesthetics, first response, extubation, and post-anesthesia care-unit discharge readiness. The incidence of emergence agitation was 58.3% and 38.9% in the control and flumazenil groups, respectively, but it was not statistically significant. However, the duration of emergence agitation was shorter in the flumazenil group (p = 0.012). There were no significant differences in the time intervals between the discontinuation of anesthetics, first response, and extubation. Although flumazenil did not reduce the incidence of emergence agitation in patients undergoing orthognathic surgery with sevoflurane anesthesia, it can be considered as an option for awakening patients in terms of improving emergence profiles.

Inhibition of Adult Hippocampal Neurogenesis Plays a Role in Sevoflurane-Induced Cognitive Impairment in Aged Mice Through Brain-Derived Neurotrophic Factor/Tyrosine Receptor Kinase B and Neurotrophin-3/Tropomyosin Receptor Kinase C Pathways.

Sevoflurane anesthesia induces cognitive impairment, which may lead to perioperative neurocognitive disorders (PND). However, the factors and molecular mechanism underlying this impairment remains unclear. Adult hippocampal neurogenesis (AHN) in the subgranular zone of the hippocampus has been implicated in cognitive processes. Nonetheless, the direct role of AHN in sevoflurane-induced cognitive impairment has never been demonstrated. In this study, we explored the age and the concentration factors and the role of AHN inhibition in sevoflurane-induced cognitive impairment in sevoflurane inhalation model mice. We found that 3% sevoflurane exposure induced significant cognitive impairment and inhibition of AHN in aged mice but not adult mice. Expression of BDNF/TrkB and NT-3/TrkC was also decreased by 3% sevoflurane exposure in aged mice. Hippocampal brain-derived neurotrophic factor (BDNF) or Neurotrophin-3 (NT-3) microinjection could partially improve the sevoflurane-induced cognitive impairment and AHN inhibition, respectively. These results demonstrate that the cognitive impairment caused by sevoflurane inhalation is related to patient age and sevoflurane concentration. In conclusion, the molecular mechanism of cognitive impairment in the elderly is related to the inhibition of AHN through the BDNF/TrkB and NT-3/TrkC pathways. Thus, sevoflurane inhalation anesthesia may be safe for adult patients, but caution should be exercised when administering it to the elderly.

Effect of dexmedetomidine on emergence delirium and recovery parameters with sevoflurane and desflurane anaesthesia in children : a double randomized study

Background: Emergence delirium in pediatric patients is a significant cause of increased anxiety among parents. The incidence of emergence delirium in children varies mainly according to the anesthetic agents used. Methods: In this prospective, double-blind, randomized trial, 152 children of age group 1-6 years were randomized into two groups after induction of anesthesia: Group S received Sevoflurane, and Group D received Desflurane. Children in the S group were further randomized into subgroup S- Dex (receiving dexmedetomidine 0.3 mcg/kg in 5 ml saline) and subgroup S-Saline (receiving saline 5 ml). Similarly, Group D was also randomized into two subgroups; D-Dex and D-Saline. We compared perioperative hemodynamic variables, postoperative emergence delirium, recovery profile, pain scoring, the requirement of rescue analgesics, and time to discharge. Results: At 5, 15, and 30 minutes, the incidence of emergence delirium was significantly higher in S-Saline and D-Saline groups than S-Dex and D-Dex groups. Both PAED and FLACC scores were significantly higher in the S-Saline group than the S-Dex group and the D-Saline group compared to the D-Dex group (P&lt;0.05). Significantly more patients required analgesia in the S-Saline group than in the S-Dex group (P&lt;0.05). No significant difference for analgesia was present between D-Saline and D-Dex groups. (p = 0.153). Discharge time was significantly longer in S-Dex and D-Dex groups as compared to S-Saline and D-saline groups. Conclusions: Dexmedetomidine effectively reduced the incidence of emergence delirium and postoperative pain in pediatric patients undergoing surgery using Sevoflurane and Desflurane anesthesia.

Abstract No.: ABS3115: Effect of sevoflurane vs desflurane on blood glucose level in patients undergoing intracranial neurosurgery: A randomised control study

Background & Aims:Patients undergoing neurosurgery are prone to neurological damage due to the anaerobic metabolism of blood glucose. In this study we aimed to to compare the effect of sevoflurane and desflurane on blood glucose levels in patients undergoing intracranial surgery.Methods:All consenting patients of either gender 18-65 years belonging to American Society of Anesthesiologists (ASA) physical status I & II scheduled for intracranial surgery under sevoflurane or desflurane maintenance anaesthesia were included. Patients suffering from diabetes, thyroid dysfunction, renal or hepatic disease, on steroids, beta-adrenergic blocking agents, insulin or oral hypoglycaemic agents, pregnant or lactating patients, chronic alcoholic patients, and non-consenting patients were excluded from the study. The enrolled patients were randomised in the sevoflurane and desflurane groups. The periodic glucose level was measured hourly after induction until completion of surgery using the glucose oxidase peroxidase method.Results:A total of 70 patients was included in the study. Both sevoflurane and desflurane when used as maintenance anaesthetics cause changes in blood sugar levels. Sevoflurane causes a gradual increase in blood sugar intraoperatively whereas desflurane causes an initial rise in blood sugar followed by a decline in blood sugar level in euglycemic patients. There was a significant difference in the trend of blood sugar (mg/dL) over time between the two groups (p =<0.001).Conclusion:The changes in blood sugar level by both agents were statistically significant but clinically insignificant as the values remained within clinically normal range and there were no episodes of hypo or hyperglycaemia.

The effect of low flow anesthesia with sevoflurane on oxidative status: A prospective, randomized study.

Objectives:To assess the impact of low-flow, mid-flow, and high-flow sevoflurane anesthesia on the oxidative state by measuring thiol/disulfide levels in patients undergoing surgery.Methods:The study included 99 patients randomly assigned to 3 groups. In the low-flow anesthesia group, the fresh gas flow was diminished to 1 L.min-1 for anesthesia maintenance after 6 L.min-1 was administered for the first 10 minutes. In the mid-flow anesthesia group, fresh gas flow was applied as 2 L.min-1. In the high-flow anesthesia group, the fresh gas flow was administered as 4 L.min-1 throughout the operation. Blood samples were obtained before induction, at the 60th minute after induction, and at 2 hours postoperatively. Native thiol, total thiol, disulfide analyzed and disulfide/native thiol percentage, disulfide/total thiol percentage, and native thiol/total thiol percentage were calculated.Results:Disulfide values in mid-flow and low-flow anesthesia were significantly lower at the 60th minute after induction compared to the high-flow anesthesia group. In the group evaluations, intraoperative native thiol levels in the high-flow group were found to be substantialy lower than preoperative values.Conclusion:It was sighted that low-flow anesthesia with sevoflurane prohibited oxidative damage. It was concluded that low flow anesthesia can be utilized safely in this respect.

Increase of Cardioprotective Effectiveness of Remote Ischemic Preconditioning during Cardiac Surgery

The objective. To increase the effectiveness of cardioprotection during coronary artery bypass grafting (CABG) by using a modified technique of remote ischemic preconditioning (RIPC).Subjects and Methods. A prospective randomized study included 119 patients (aged 18 to 75 years) undergoing on-pump CABG. Patients were divided in 5 groups: Group 1 ‒ Sevoflurane control (ContrSevo), RIPC was not used, sevoflurane anesthesia (n = 24); Group 2 ‒ RIPC1 sevoflurane (RIP1Sevo), RIPC with ischemia-reperfusion of one lower limb, sevoflurane anesthesia (n = 26); Group 3 ‒ RIPC2 sevoflurane (RIP2Sevo), RIPC with ischemia-reperfusion of two lower limbs, anesthesia sevoflurane (n = 23); Group 4 ‒ Propofol control (ContrProp), RIPC was not used, propofol anesthesia (n = 22); Group 5 ‒ RIPC2 propofol (RIP2Prop), RIPC with ischemia-reperfusion of two lower limbs, propofol anesthesia (n = 24). The serum troponin I concentration (cTnI) (baseline, and 30 minutes, 12, 24, 36 and 48 hours after СPB weaning). Hemodynamic parameters and indicators of the clinical postoperative course also were evaluated. The impact ischemic-reperfused tissue mass of RIPC on the cardioprotection was assessed by comparing the groups of ContrSevo, RIPC1Sevo, and RIPC2Sevo. To assess the impact of propofol on the RIPC-induced cardioprotection, the groups of ContrProp and RIPC2Prop were compared.Results. Statistically significant differences in cTnI were found between the ContrSevo and the RIPC2Sevo at points of 12, 24 and 36 hours: ContrSevo 1.83 (1.3; 2.24) ng/ml, RIP2Sevo 1.28 (0.75; 1.63) ng/ml after 12 hours (p = 0.02), ContrSevo 1.44 (0.98; 2.26) ng/ml, RIPC2Sevo 1.17 (0.55; 1.66) ng/ml after 24 hours (p = 0.046), ContrSevo 1.26 (0.86; 1.72) ng/ml, and RIPC2Sevo 0.81 (0.47; 1.24) ng/ml after 36 hours (p = 0.035). No differences in the cTnI were found between the groups of ContrSevo and RIPC1Sevo, RIPC1Sevo and RIPC2Sevo at any stage of the study. There were no statistically significant differences between the groups when comparing hemodynamic parameters. In the RIPC2Sevo Group, arrhythmias requiring cardioversion or drug therapy were significantly less frequent compared to ContrSevo (1 vs. 6) (p = 0.047). There were no other significant differences in the postoperative clinical course. When comparing the groups of ContrProp and RIP2Prop, no significant differences were found in cTnI and hemodynamic parameters as well as in the postoperative clinical course.Conclusions. A greater mass of ischemic-reperfused peripheral tissue is accompanied by greater RIPC-induced cardioprotection. A modified protocol for RIPC with ischemia-reperfusion of two lower limbs with sevoflurane anesthesia enhances cardioprotection during on-pump CABG. The modified RIPC protocol with ischemia-reperfusion of two lower limbs with sevoflurane anesthesia reduces the risk of arrhythmias requiring cardioversion or drug therapy. Propofol inhibits the RIPC-induced cardioprotection with ischemia-reperfusion of two lower limbs.

Correlation between bispectral index and patient state index in children under sevoflurane anesthesia.

Because the unanticipated arousal or hemodynamic instability during anesthesia may adversely affect the physical and emotional welfare of children, adequate management of the anesthesia depth is required. We aimed to compare Bispectral Index (BIS) and Patient State Index (PSI) in children during sevoflurane anesthesia and evaluate PSI as depth of anesthesia monitor in children aged 6months-12years. In this prospective observational study, children aged 6months-12years old scheduled for elective surgery under sevoflurane anesthesia were enrolled from November 2018 to June 2019. We monitored BIS and PSI at different sevoflurane concentrations. The primary outcome was the correlation between BIS and PSI. The correlation between BIS and PSI at different sevoflurane concentrations (at 1, 1.5, and 2 MACs) and at different age groups (6months-2years, 2-7years, and 8-12years) was also investigated. Bispectral index and PSI showed a fair correlation (r=.430; 95% confidence interval [CI], 0.297-0.546; p<.001). Two values were fairly correlated at 1, 1.5, and 2 MAC (r=.544; 95% CI, 0.314-0.716; p<.001, r=.509; 95% CI, 0.283-0.699; p<.001, and r=.315; 95% CI, 0.047-0.522; p=0.007). BIS and PSI values showed a fair correlation in 6months - 2year and 8-12year groups (r=.696; 95% CI, 0.519-0.813; p<.001 and r=.297; 95% CI, -0.017 to 0.543; p<.021), but there was not significant correlation in 2-7years group (r=.190; 95% CI, -0.015 to 0.374; p=.052). There was a fair correlation between BIS and PSI in children under sevoflurane anesthesia. The use of BIS and PSI as an indicator for anesthesia depth by sevoflurane is not reliable in pediatric patients.

Current status of sevoflurane anesthesia in association with microglia inflammation and neurodegenerative diseases.

Sevoflurane is one of the most commonly used volatile anesthetics in clinical practice and is often used in pediatric anesthesia and intraoperative maintenance. Microglia exist in the central nervous system and are innate immune cells in the central nervous system. Under external stimulation, microglia are divided into two phenotypes: proinflammatory (M1 type) and anti-inflammatory (M2 type), maintaining the stability of the central nervous system through induction, housekeeping, and defense functions. Sevoflurane can activate microglia, increase the expression of inflammatory factors through various inflammatory signaling pathways, release inflammatory mediators to cause oxidative stress, damage nerve tissues, and eventually develop into neurodegenerative diseases. In this article, the relationship between sevoflurane anesthesia and microglia inflammation expression and the occurrence of neurodegenerative diseases is reviewed as follows.