Etomidate Administration Research Articles

Pretreatment with Esketamine Reduces Etomidate-Induced Myoclonus During the Induction of Anesthesia: A Randomized Controlled Trial.

Myoclonus is a common problem during induction of anesthesia with etomidate. A variety of agents, including opioids and lidocaine, reduced the incidence of myoclonus. However, there is no reported literature evaluating the effect of esketamine pretreatment on etomidate-induced myoclonus. We investigated the influence of pretreatment with esketamine on the incidence of etomidate-induced myoclonus. This is a prospective, double-blind, and randomized controlled trial. One hundred patients aged 18-65 scheduled for elective surgery under general anesthesia (including urology surgery, gynaecology surgery, general surgery, and thoracic surgery) were randomly allocated into two groups, each consisting of 50 patients. Esketamine was pretreated with 0.1 mg/kg 60 s before the initiation of etomidate in Group ESK, while normal saline was administered as the placebo (Group C). During the first 1 minute after etomidate administration, myoclonus incidence and severity were assessed. In addition, we measured the hemodynamic changes and side effects of esketamine before administering etomidate. In group ESK, 14 patients (28%) had myoclonus (degrees of myoclonus: mild 2, moderate 7, severe 5), and 32 patients (64%) in group C (mild 6, moderate 5, severe 21) (P< 0.001). In group ESK, myoclonus incidence and severity were significantly lower than in group C (P< 0.001). Esketamine 0.1mg/kg IV pretreatment significantly reduce the incidence and the severity of severe myoclonus of etomidate-induced myoclonus without significant adverse effects.

Comparative study between dexmedetomidine and midazolam as pre-medication for the prevention of etomidate-induced myoclonus and attenuation of stress response at endotracheal intubation in laparoscopic cholecystectomies

Background: Myoclonus is a common issue in etomidate anesthesia induction, and various drugs have been used to reduce its incidence, highlighting the ongoing search for better alternatives in anesthesiology. Aims and Objectives: The study analyzed the impact of dexmedetomidine (DEX) and midazolam pre-treatment on etomidate-induced myoclonus incidence, stress response at laryngoscopy, and intubation during etomidate induction. Materials and Methods: A prospective randomized controlled intervention study (superiority trial) was done involving 42 patients of age 20–60 years, randomly allocated in two equal groups (Group D: Inj. DEX was given as infusion (0.5 μg/kg) in 10 mL 0.9% normal saline over 10 min and 5 min before induction. Group M: Inj. Midazolam was given 0.02 mg/kg, prepared in 10 mL 0.9% normal saline, to be infused over 10 min and 5 min before induction). Myoclonus was graded after intravenous administration of etomidate (0.3 mg/kg) and hemodynamic response to laryngoscopy and intubation were observed at various time intervals. Statistical analysis was done using SPSS version 27.0. Independent t-test/Mann–Whitney test (for non-parametric data) and Chi-square test/Fisher’s exact test were used to compare variables. A P&lt;0.05 was considered statistically significant. Results: The study found that DEX effectively suppressed stress response due to intubation compared to midazolam, with mean myoclonus gradation (Mean±SD) in Group-D and Group-M being 0.6190±0.7400 and 1.6667±0.8563, respectively, indicating a significant distribution with group. Conclusion: DEX was found to be more effective than midazolam in preventing etomidate-induced myoclonus and attenuating stress response compared to midazolam.

Etomidate Depresses Spontaneous Complex Spikes Activity of Cerebellar Purkinje Cells via Cannabinoid 1 Receptor in vivo in Mice

Introduction: Complex spikes (CSs) activity of cerebellar Purkinje cells plays critical roles in motor coordination and motor learning by transferring information to cerebellar cortex, which is an accessible and useful model for neurophysiological investigation. Etomidate is an ultrashort-acting nonbarbiturate intravenous anesthetic, which inhibits the spontaneous activity of cerebellar Purkinje cells through activation of GABA_A and glycine receptors in vivo in mice. However, the effect of etomidate on the spontaneous CSs activity of cerebellar Purkinje cells in living mouse is not clear. Methods: We here investigated the effects of etomidate on spontaneous CSs activity of cerebellar Purkinje cell in urethane-anesthetized mice by electrophysiology recording technique and pharmacological methods. Results: Our results showed that cerebellar surface perfusion of etomidate significantly depressed the activity of spontaneous CSs, which exhibited decreases in the number of spikelets and the area under curve (AUC) of the CSs. The etomidate-produced inhibition of CSs activity was persisted in the presence of GABA_A and glycine receptors antagonists. However, application of cannabinoid 1 (CB1) receptor antagonist, AM-251, completely blocked the etomidate-induced inhibition of CSs. Furthermore, application of the CB1 receptor agonist, WIN55212-2, induced a decrease of CSs. Moreover, in the presence of a specific protein kinase A (PKA) inhibitor, KT5720, etomidate failed to produce decreases in the spikelets number and the AUC of the spontaneous CSs. Conclusion: These results indicate that cerebellar surface application of etomidate facilitates CB1 receptor activity resulting in a depression of spontaneous CSs activity of Purkinje cells via PKA signaling pathway in mouse cerebellar cortex. Our present results suggest that the etomidate administration may impair the function of cerebellar cortical neuronal circuitry by inhibition of the climbing fiber – Purkinje cells synaptic transmission through activation of CB1 receptors in vivo in mice.

Effect of vitamin C on adrenal suppression following etomidate for rapid sequence induction in trauma patients: a randomized clinical trial

BackgroundEtomidate is an imidazole derivative that is widely used in the emergency department for Rapid Sequence Intubation (RSI). Although it has a safe hemodynamic profile, there are some concerns about its suppressant effects on the adreno-cortical axis. Vitamin C, as an antioxidant, can play a protective role in this issue.MethodIn a controlled clinical trial, we studied adult traumatic patients who needed RSI with etomidate. In one group underwent RSI with etomidate and cortisol levels were measured three hours later. In the other group, we administered one gram of vitamin C before etomidate administration, and the cortisol level was measured three hours later.ResultsFifty-one patients have been studied. The serum cortisol level was significantly lower after RSI with etomidate in both groups. In the Vitamin C group, there was a significantly higher cortisol level after RSI in comparison to the control group.ConclusionEtomidate can suppress the cortisol level in trauma patients who undergo RSI. Vitamin C can reduce this suppressant effect of etomidate.Trial registrationIRCT registration number: IRCT20090923002496N11, URL of trial registry record: https://en.irct.ir/trial/34586, Date of trial registration: 19/04/2019. Full date of the first registration: 30/05/2019.

Polymorphisms of pharmacogenetic candidate genes affect etomidate anesthesia susceptibility.

Purpose: Etomidate is widely used in general anesthesia and sedation, and significant individual differences are observed during anesthesia induction. This study aimed to explore the molecular mechanisms of different etomidate susceptibility at the genetic level. Methods: 128 patients were enrolled in the study. The bispectral index (BIS), mean arterial pressure (MAP) and heart rate (HR) were recorded when the patients entered the operating room for 5 min, before the administration of etomidate, 30 s, 60 s, 90 s, 120 s and 150 s after the administration of etomidate, and the corresponding single nucleotide polymorphisms (SNPs) were analyzed. Results: Significant individual differences were observed in etomidate anesthesia. The results of two-way ANOVA showed that CYP2C9 rs1559, GABRB2 rs2561, GABRA2 rs279858, GABRA2 rs279863 were associated with the BIS value during etomidate anesthesia; UGT1A9 rs11692021 was associated with the Extended Observer’s Assessment of Alertness and Sedation (EOAA/S) score during etomidate anesthesia; GABRB2 rs2561 was associated with MAP. Multiple linear stepwise regression model results showed that CYP2C9 rs1559, GABRA2 rs279858 and GABRB2 rs2561 were associated with the BIS value and UGT1A9 rs11692021 was associated with the EOAA/S score; GABRB2 rs2561 was associated with MAP. Conclusion: GABRA2 rs279858, GABRB2 rs2561, CYP2C9 rs1559 and UGT1A9 rs11692021 are the SNPs with individual differences during etomidate anesthesia. This is the first to study the SNPs of etomidate, which can provide certain evidence for the future use of etomidate anesthesia and theoretical basis for precision anesthesia.

Hemodynamics in Helicopter Emergency Medical Services (HEMS) Patients Undergoing Rapid Sequence Intubation With Etomidate or Ketamine.

Rapid sequence intubation (RSI) is performed by helicopter emergency medical services (HEMS) providers to establish airway control. Common induction agents are etomidate and ketamine, both touted to have relatively stable hemodynamic profiles. Limited data comparing these medications in the air medical setting exist. Compare administration of ketamine and etomidate on peri-intubation hemodynamics. A retrospective chart review of intubations performed by a HEMS program over 69 months was completed. Heart rate (HR) change, systolic blood pressure (SBP) change, and hypotension with etomidate or ketamine use were measured. There were 258 patients induced with etomidate and 48 with ketamine. Etomidate patients showed a +1.161% change in HR (SD ± 22.7) and -0.49% change in SBP (SD ± 25.0). Ketamine patients showed a -4.7% change in HR (SD ± 16.7) and 17.2% change in SBP (SD ± 43.4). The p-values for percentage change in HR and SBP between etomidate and ketamine were 0.0830 and 0.0018, respectively. Twenty-five episodes of postadministration hypotension occurred with etomidate, and two with ketamine (p=0.028). Both ketamine and etomidate are appropriate for intubation of HEMS patients. Ketamine was preferentially selected for hypotensive patients with statistically significant improvement in SBP. Although statistically significant, both ketamine and etomidate had relative low incidences of hypotension.

Hemodynamic Effects of Ketamine Versus Etomidate for Prehospital Rapid Sequence Intubation

ObjectiveRapid sequence intubation (RSI) is often required in managing critically ill patients in the prehospital setting. Although etomidate is a commonly used induction agent for RSI, ketamine has gained new interest in prehospital management with reported neutral hemodynamic effects. Limited data exist to support ketamine as an alternative to etomidate, particularly in the prehospital setting. The purpose of this study was to evaluate hemodynamic changes after the administration of ketamine versus etomidate in prehospital RSI. MethodsThis retrospective study evaluated adult patients undergoing prehospital RSI over 13 months within a regional emergency transport medicine service. Hypotension was defined as a 20% decrease in systolic blood pressure (SBP) within 15 minutes of receiving ketamine or etomidate. Hemodynamic data were collected 15 minutes before and 15 minutes after administration or until additional sedative medications were given. Data were analyzed using SPSS software (Version 21; IBM Corp, Armonk, NY), with P < .05 considered significant. ResultsOne hundred thirteen patients met the inclusion criteria (ketamine, n = 33; etomidate, n = 80), with the primary reasons for intubation being respiratory failure and trauma. There was no difference between the incidence of patients who experienced a 20% decrease in SBP (16% etomidate vs. 18% ketamine, P = .79). There were no significant differences in SBP pre- to postadministration between ketamine and etomidate. ConclusionNo hemodynamic differences occurred between patients who received ketamine versus etomidate for prehospital RSI. Neither drug was associated with an increased need for additional sedatives, and neither drug was associated with an increased first-pass intubation success rate. Larger, prospective, powered studies are required to identify patients who may benefit from either ketamine or etomidate.

A Comparative Study of Valsalva Maneuver, Lidocaine, and Valsalva Maneuvers with Administration of Lidocaine to Reduce the Pain Associated with Administration of Etomidate During General Anesthesia.

ObjectivesThe purpose of this study is a comparison of Valsalva, lidocaine, and Valsalva with administration of lidocaine to reduce the pain associated with administration of etomidate.MethodsThe present study is a clinical trial study. The number of samples in each group was 30 and a total of 90 people were selected. This study was a clinical trial and the subjects were randomly divided into three groups: Group 1: Valsalva, 2: Lidocaine, 3: Valsalva and Lidocaine. Pain due to etomidate was rated on a VAS from 1 (painless) to 3 (worst imaginable pain) and their information was recorded. The collected information was entered into SPSS 22 and analyzed with appropriate statistical tests.ResultsA total of 90 subjects participated in the present study and were divided into 3 groups: Valsalva, lidocaine, and Valsalva with lidocaine. No significant difference was observed between demographic variables in the study groups. There was a significant relationship between severity of pain in the three groups. According to the results, the highest pain intensity was in the Valsalva group and the lowest pain intensity was in the Valsalva with lidocaine group.ConclusionsValsalva with lidocaine reduces the severity of pain caused by etomidate to a greater extent than other groups.

Propofol, Ketamine, and Etomidate as Induction Agents for Intubation and Outcomes in Critically Ill Patients: A Retrospective Cohort Study.

To evaluate the association between the administration of propofol, ketamine, and etomidate and ICU, hospital mortality, and length of stay. Retrospective single-center cohort study. ICUs in a tertiary medical center, between January 01, 2012, and December 31, 2017. Critically ill adult patients given a single IV anesthetic for intubation. Primary outcomes were ICU and hospital mortality. Secondary outcomes were ICU- and hospital-free days through 28 days. An inverse probability of treatment weighed approach was used. The propensity score was estimated using a generalized logit model as a function of patient characteristics, admission source, ICU type, readmission status, length of ICU stays prior to intubation, and acute physiology score. Mortality outcomes were assessed with weighted logistic regression and -free days assessed by weighted linear regression with Bonferroni correction for pairwise comparisons. Of 2,673 patients, 36% received propofol, 30% ketamine and 34% etomidate. Overall ICU and hospital mortality were 19% and 29%, respectively. Patients given ketamine had higher odds of ICU mortality (1.45; [95% CI, 1.07-1.94]; p = 0.015) and patients given etomidate had higher odds of ICU mortality (1.87; 1.40-2.49; p < 0.001), hospital mortality (1.43; 1.09-1.86; p = 0.009), and less ICU-free days (-2.10; -3.21 to -1.00; p < 0.001) than those given propofol. Patients given ketamine and etomidate had similar odds of hospital mortality (1.06; 0.80-1.42; p = 0.761) and similar hospital-free days (0.30; -0.81 to 1.40; p = 0.600). Compared with ketamine and etomidate, propofol was associated with better outcome in critically ill patients undergoing anesthesia for intubation. Even after adjusting for severity of illness prior to intubation, residual confounders cannot be excluded.

Pretreatment with dexmedetomidine and magnesium sulphate in prevention of etomidate induced myoclonus - A double blinded randomised controlled trial.

Pretreatment with dexmedetomidine and magnesium sulphate in prevention of etomidate induced myoclonus - A double blinded randomised controlled trial.

The effect of midazolam or lidocaine administration prior to etomidate induction of anesthesia on heart rate, arterial pressure, intraocular pressure and serum cortisol concentration in healthy dogs

ObjectiveTo evaluate selected effects of midazolam or lidocaine administered prior to etomidate for co-induction of anesthesia in healthy dogs. Study designProspective crossover experimental study. AnimalsA group of 12 healthy adult female Beagle dogs. MethodsDogs were premedicated with intravenous (IV) butorphanol (0.3 mg kg–1), and anesthesia was induced with etomidate following midazolam (0.3 mg kg–1), lidocaine (2 mg kg–1) or physiologic saline (1 mL) IV. Heart rate (HR), arterial blood pressure, respiratory rate (fR) and intraocular pressure (IOP) were recorded following butorphanol, after co-induction administration, after etomidate administration and immediately following intubation. Baseline IOP values were also obtained prior to sedation. Etomidate dose requirements and the presence of myoclonus, as well as coughing or gagging during intubation were recorded. Serum cortisol concentrations were measured prior to premedication and 6 hours following etomidate administration. ResultsBlood pressure, fR and IOP were similar among treatments. Blood pressure decreased in all treatments following etomidate administration and generally returned to sedated values following intubation. HR increased following intubation with midazolam and lidocaine but remained stable in the saline treatment. The dose of etomidate (median, interquartile range, range) required for intubation was lower following midazolam (2.2, 2.1–2.6, 1.7–4.1 mg kg−1) compared with lidocaine (2.7, 2.4–3.6, 2.2–5.1 mg kg−1, p = 0.012) or saline (3.0, 2.8–3.8, 1.9–5.1 mg kg−1, p = 0.015). Coughing or gagging was less frequent with midazolam compared with saline. Myoclonus was not observed. Changes in serum cortisol concentrations were not different among treatments. Conclusions and clinical relevanceMidazolam administration reduced etomidate dose requirements and improved intubation conditions compared with lidocaine or saline treatments. Neither co-induction agent caused clinically relevant differences in measured cardiopulmonary function, IOP or cortisol concentrations compared with saline in healthy dogs. Apnea was noted in all treatments following the induction of anesthesia and preoxygenation is recommended.

Hippocampal astrocyte dysfunction contributes to etomidate-induced long-lasting synaptic inhibition

Cognitive impairments following the use of general anesthetics are well documented but the underlying mechanisms are unclear. Here, long-lasting cognitive deficits were observed in aged mice following administration of etomidate at a clinically relevant concentration (20 mg/kg); these deficits were closely related to hippocampal synaptic inhibition and astrocyte dysfunction. Using microdialysis and magnetic-activated cell-sorting techniques, we found that astrocyte secretion of glutamate, d-serine, and ATP, as well as astrocyte function, were depressed in the hippocampus following treatment with etomidate. Interestingly, hippocampal astrocyte inhibition (designer receptors exclusively activated by designer drugs; DREADDs) had no effect on the initial synaptic inhibition, but reversed synaptic and cognitive depression in the long term. Furthermore, continual activation of hippocampal astrocytes following administration of a sedative dose (8 mg/kg) of etomidate induced synaptic inhibition and cognitive dysfunction. Our results indicate that general anesthetic-induced hippocampal astrocyte dysfunction plays a role in maintaining synaptic inhibition, which eventually induces long-lasting cognitive deficits.

Phospholipase C-related inactive protein type-1 deficiency affects anesthetic electroencephalogram activity induced by propofol and etomidate in mice.

The general anesthetics propofol and etomidate mainly exert their anesthetic actions via GABA A receptor (GABAA-R). The GABAA-R activity is influenced by phospholipase C-related inactive protein type-1 (PRIP-1), which is related to trafficking and subcellular localization of GABAA-R. PRIP-1 deficiency attenuates the behavioral reactions to propofol but not etomidate. However, the effect of these anesthetics and of PRIP-1 deficiency on brain activity of CNS are still unclear. In this study, we examined the effects of propofol and etomidate on the electroencephalogram (EEG). The cortical EEG activity was recorded in wild-type (WT) and PRIP-1 knockout (PRIP-1 KO) mice. All recorded EEG data were offline analyzed, and the power spectral density and 95% spectral edge frequency of EEG signals were compared between genotypes before and after injections of anesthetics. PRIP-1 deficiency induced increases in EEG absolute powers, but did not markedly change the relative spectral powers during waking and sleep states in the absence of anesthesia. Propofol administration induced increases in low-frequency relative EEG activity and decreases in SEF95 values in WT but not in PRIP-1 KO mice. Following etomidate injection, low-frequency EEG power was increased in both genotype groups. At high frequency, the relative power in PRIP-1 KO mice was smaller than that in WT mice. The lack of PRIP-1 disrupted the EEG power distribution, but did not affect the depth of anesthesia after etomidate administration. Our analyses suggest that PRIP-1 is differentially involved in anesthetic EEG activity with the regulation of GABAA-R activity.

Critical Illness-Related Corticosteroid Insufficiency in Cardiogenic Shock Patients: Prevalence and Prognostic Role.

Cardiogenic shock shares with septic shock common hemodynamic features, inflammatory patterns, and most likely similar complications such as critical illness-related corticosteroid insufficiency. The aim of this study was to evaluate the prevalence of critical illness-related corticosteroid insufficiency in cardiogenic shock patients and to secondarily assess its prognostic value on 90-day mortality. A single-center prospective observational study conducted over a 3-year period and including all patients with cardiogenic shock. Main exclusion criteria were patients with prior cardiac arrest, sepsis, ongoing corticosteroid therapy, and etomidate administration. A short corticotropin test was performed in the first 24 h following admission. Serum cortisol levels were measured before (T0) and 60 min (T60) after administration of 250 μg of cosyntropin. Critical illness-related corticosteroid insufficiency was defined according to the 2017 consensus definition (basal total cortisol<10 μg·dL or a delta cortisol T60-T0<9 μg·dL) as well as the thresholds published in 2016 in cardiogenic shock patients associated with worst prognosis (basal total cortisol>29 μg·dL and delta cortisol T60-T0<17 μg·dL). Seventy-nine consecutive patients hospitalized in intensive care for cardiogenic shock met the inclusion criteria. Overall mortality was 43% at day 90. Forty-two percent had critical illness-related corticosteroid insufficiency using the 2017 consensus definition and 32% using the 2016 cardiogenic shock thresholds. Presence of critical illness-related corticosteroid insufficiency was not an independent factor associated with 90-day mortality irrespective of the thresholds used. Critical illness-related corticosteroid insufficiency is a frequent occurrence in medical cardiogenic shock. However, in this study, such insufficiency was not associated with prognosis.

Oxycodone for prevention of etomidate-induced myoclonus: a randomized double-blind controlled trial.

ObjectiveThis study was performed compare the effectiveness of oxycodone and fentanyl in reducing the incidence and severity of etomidate-induced myoclonus.MethodsIn total, 162 patients with an American Society of Anesthesiologists physical status of I or II were assigned at random to three groups. Patients assigned to Group O received 0.1 mg/kg of oxycodone (n = 54), those assigned to Group F were given 1 µg/kg of fentanyl (n = 54), and those assigned to Group S were given an equal volume of saline intravenously 2 minutes prior to administration of 0.3 mg/kg of etomidate (n = 54). The incidence and severity of myoclonus was evaluated 2 minutes after etomidate administration. The patients’ vital signs, coughing, nausea, dizziness, and other related adverse reactions were also recorded.ResultsThe incidence of myoclonus was significantly lower in Group O (0.0%) than in Group F (31.5%) and Group S (72.2%); the intensity was also lowest in Group O. All patients in each group had stable cardiovascular profiles.ConclusionsIntravenous injection of 0.1 mg/kg of oxycodone 2 minutes prior to etomidate is more effective in preventing etomidate-induced myoclonus during general anesthesia than is 1 µg/kg of fentanyl.

Anesthetic Drug Discovery and Development: A Case Study of Novel Etomidate Analogs.

All currently available general anesthetic agents possess potentially lethal side effects requiring their administration by highly trained clinicians. Among these agents is etomidate, a highly potent imidazole-based intravenous sedative-hypnotic that deleteriously suppresses the synthesis of adrenocortical steroids in a manner that is both potent and persistent. We developed two distinct strategies to design etomidate analogs that retain etomidate's potent hypnotic activity, but produce less adrenocortical suppression than etomidate. One strategy seeks to reduce binding to 11β-hydroxylase, a critical enzyme in the steroid biosynthetic pathway, which is potently inhibited by etomidate. The other strategy seeks to reduce the duration of adrenocortical suppression after etomidate administration by modifying the drug's structure to render it susceptible to rapid metabolism by esterases. In this chapter, we describe the methods used to evaluate the hypnotic and adrenocortical inhibitory potencies of two lead compounds designed using the aforementioned strategies. Our purpose is to provide a case study for the development of novel analogs of existing drugs with reduced side effects.

Comparison of pretreatment with dexmedetomidine with midazolam for prevention of etomidate-induced myoclonus and attenuation of stress response at intubation: A randomized controlled study.

Background and Aims:Myoclonus is a common problem during induction of anesthesia with etomidate. A variety of drugs have been used to decrease the incidence of myoclonus. In this study we compared the effects of dexmedetomidine and midazolam pretreatment on the incidence of etomidate induced myoclonus. We also studied the effects of these drugs on attenuation of stress response at laryngoscopy and intubation on induction with etomidate.Material and Methods:Eighty adult patients (18 to 60 years age) of either sex, American Society of Anestheiologists physical status I and II undergoing elective general surgeries under general anesthesia were randomly allocated into two groups. Group D patients received Inj. Dexmedetomidine (0.5 μg/Kg) and Group M received Inj. Midazolam (0.015 mg/Kg) in 10 ml saline over ten minutes. Myoclonus was graded after intravenous administration of etomidate (0.3mg/Kg) and hemodynamic response to laryngoscopy and intubation were observed at various time intervals. Analysis of statistical data was done using Statistical Package for Social Sciences (SPSS) version 21.0. Quantitative variables were compared using Independent T Test/Mann Whitney test (for non-parametric data). Qualitative variables were compared using Chi-Square test/Fisher's Exact Test. A P value of < 0.05 was considered statistically significant.Results:In Group D, 22 out of 40 (55%) patients did not have any myoclonus during induction with etomidate, and none of the patients had grade 3 (severe) myoclonus. In Group M, 19 out of 40 patients (47.5%) had grade 2 (moderate) and 6 patients (15%) had grade 3 myoclonus. Stress response due to intubation was more effectively suppressed by dexmedetomidine as compared to midazolam.Conclusion:Incidence of myoclonus among patients who underwent pre-treatment with dexmedetomidine was significantly lesser than those who underwent pre-treatment with midazolam. Greater degree of attenuation of stress response in the dexmedetomidine group was observed as compared to midazolam group.

Pretreatment with Oxycodone Simultaneously Reduces Etomidate-Induced Myoclonus and Rocuronium-Induced Withdrawal Movements During Rapid-Sequence Induction.

BackgroundEtomidate and rocuronium are often paired in rapid-sequence anesthesia induction. However, the effect of pretreatment with oxycodone on myoclonic and withdrawal movements has not been previously investigated.The aim of this study was to evaluate the effects of oxycodone on the incidence and severity of etomidate-induced myoclonus and rocuronium-induced nociceptive withdrawal movements during rapidsequence anesthesia induction.Material/MethodsWe randomly divided 120 patients into the saline group (group S) and the oxycodone group (group O) (n=60 in each group). Patients received 0.05 mg/kg oxycodone or saline intravenously 2 min before administration of 0.3 mg/kg etomidate. The occurrence and severity of myoclonus were assessed after administration of etomidate, then rocuronium was injected, followed by evaluation of withdrawal movements.ResultsThe total frequency of involuntary movements following sequential administration of etomidate and rocuronium was significantly lower in Group O than in Group S (28.3% vs. 90%, p<0.001). The total frequency and grade 3 severity of myoclonus following etomidate injection in Group O was significantly lower than in Group S (25.0% vs. 63.3% for total frequency; 0 vs. 10 for grade 3 severity, P<0.001). The total frequency and grade 3 intensity of withdrawal movements were significantly less in Group O than in Group S (6.7% vs. 73.3% for total frequency; 0 vs. 11 for grade 3 intensity, P<0.001).ConclusionsOxycodone is effective for simultaneously preventing etomidate-induced myoclonus and rocuronium-induced withdrawal movements during general anesthesia induction.

ET-26 hydrochloride (ET-26 HCl) has similar hemodynamic stability to that of etomidate in normal and uncontrolled hemorrhagic shock (UHS) rats.

ObjectiveET-26 HCl is a promising sedative–hypnotic anesthetic with virtually no effect on adrenocortical steroid synthesis. However, whether or not ET-26 HCl also has a sufficiently wide safety margin and hemodynamic stability similar to that of etomidate and related compounds remains unknown. In this study, the effects of ET-26 HCl, etomidate and propofol on therapeutic index, heart rate (HR), mean arterial pressure (MAP), maximal rate for left ventricular pressure rise (Dmax/t), and maximal rate for left ventricular pressure decline (Dmin/t) were investigated in healthy rats and a rat model of uncontrolled hemorrhagic shock (UHS).Methods50% effective dose (ED50) and 50% lethal dose (LD50) were determined after single bolus doses of propofol, etomidate, or ET-26 HCl using the Bliss method and the up and down method, respectively. All rats were divided into either the normal group and received either etomidate, ET-26 HCl or propofol, (n = 6 per group) or the UHS group and received either etomidate, ET-26 HCl or propofol, (n = 6 per group). In the normal group, after preparation for hemodynamic and heart-function monitoring, rats were administered a dose of one of the test agents twofold-higher than the established ED50, followed by hemodynamic and heart-function monitoring. Rats in the UHS group underwent experimentally induced UHS with a target arterial pressure of 40 mmHg for 1 hour, followed by administration of an ED50 dose of one of the experimental agents. Blood-gas analysis was conducted on samples obtained during equilibration with the experimental setup and at the end of the experiment.ResultsIn the normal group, no significant differences in HR, MAP, Dmax/t and Dmin/t (all P > 0.05) were observed at any time point between the etomidate and ET-26 HCl groups, whereas HR, MAP and Dmax/t decreased briefly and Dmin/t increased following propofol administration. In the UHS group, no significant differences in HR, MAP, Dmax/t and Dmin/t were observed before and after administration of etomidate or ET-26 HCl at ED50 doses (all P > 0.05). Administration of propofol resulted in brief, statistically significant reductions in HR and Dmax/t, with a brief increase in Dmin/t (P ˂ 0.05), while no significant differences in MAP were observed among the three groups. The blood-lactate concentrations of rats in the ET-26 HCl group were significantly lower than those in etomidate and propofol groups (P ˂ 0.05).ConclusionsET-26 HCl provides a similar level of hemodynamic stability to that obtained with etomidate in both healthy rats, and rat models of UHS. ET-26 HCl has the potential to be a novel induction anesthetic for use in critically ill patients.

Parecoxib sodium pretreatment reduces myoclonus after etomidate: A prospective, double-blind, randomized clinical trial .

Myoclonus induced by etomidate during induction of general anesthesia is a common phenomenon. This prospective, randomized, saline-controlled clinical study was performed to evaluate the effect of parecoxib sodium pretreatment on the incidence and severity of etomidate-induced myoclonus. 60patients, American Society of Anesthesiologists (ASA) physical status I or II, aged 20 to 60 years, who were scheduled to undergo elective laparoscopic cholecystectomy under general anesthesia, were allocated randomly into one of two groups to receive parecoxib sodium 40mg intravenous (group P, n=30) or the same volume of saline (group S, n=30) 30minutes before administration of etomidate (0.3mg/kg). Myoclonus was assessed on a scale of 0-3. Postoperative side effects were recorded. The two groups were comparable with regard to baseline characteristics. The incidence of myoclonus was significantly lower in the parecoxib sodium group (11/30; 37%) than in the saline group (21/30; 70%) (p<0.05). The severity of myoclonic movements was also significantly reduced by parecoxib sodium (p<0.05). There were no significant differences between the two groups with respect to postoperative side effects. Pretreatment with intravenous injection of parecoxib sodium 40mg significantly reduced the incidence and severity of etomidate-induced myoclonus without significant side effects. .