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PubMed2004

Improving the success rate of laryngeal mask airway insertion during etomidate induction by using fentanyl or succinylcholine.

BACKGROUND: Smooth and successful insertion of a laryngeal mask airway (LMA) during etomidate induction requires a proper mouth opening and efforts to minimize airway reflexes such as gagging, coughing, or laryngospasm. We hypothesized that the concurrent use of fentanyl or succinylcholine with etomidate, the induction agent, could reduce the occurrence of airway reflexes and increase the success rate of LMA. METHODS: Sixty adult patients, ASA class I-II, scheduled for surgery under general anesthesia, were randomly allocated into three groups: group I in which patients were given etomidate 0.3 mg/kg alone; group 2 in which patients were given fentanyl 2 microg/kg and etomidate 0.3 mg/kg; groups 3 in which patients were give etomidate 0.3 mg/kg and succinylcholine 1 mg/kg. All patients were premedicated with atropine 0.01 mg/kg. When induction of anesthesia began we recorded the time from administering the designated regiminal agent or agents to the time of relaxation of jaw (the ease of mouth opening) and checked the patient for any excitatory movement after administering the induction agents. After inserting the LMA, we checked for signs of airway reflexes. Student's t test, Chi-square and Fisher's exact test were used to analyze the data. A value of P < 0.05 was considered significant. RESULTS: There were no significant differences in demographic data among the the three groups. The concurrent use of fentanyl or succinylcholine with etomidate during induction could significantly reduce the occurrence of excitatory movements and airway reflexes after LMA insertion, and increase the success rate of LMA insertion in comparison with using etomidate alone. Comparing the two adjutant agents, the concurrent use of succinylcholine could provide a significantly better jaw relaxation, shorten the time to insert the LMA and increase the success rate of LMA insertion. CONCLUSIONS: As an induction agent to facilitate insertion of LMA, etomidate alone was far from perfect. The concurrent use of 2 microg/kg of fentanyl with etomidate might significantly reduce the occurrence of airway reflexes in response to LMA insertion and increase the success rate of insertion. However, concurrent use of 1 mg/kg succinylcholine with etomidate might provide better results in terms of shortened time for the LMA insertion, jaw relaxation, and the success rate of LMA insertion than that of fentanyl.

Adult↗
PubMed1990

Visual evoked potentials during etomidate administration in humans.

The effects of etomidate on visual evoked potentials (VEP) were studied in 22 patients undergoing gynaecological procedures. They were divided into two groups: the etomidate group (12 patients) and the fentanyl-N2O-etomidate group (ten patients). In the etomidate group, etomidate 0.3 mg.kg-1 was given as a bolus injection during induction of anaesthesia which was followed by an infusion of etomidate 0.05 mg.kg-1.min-1. No significant changes were observed in the amplitudes of P100 or N70. Latencies of the P60, N70, and P100 were slightly increased. In the fentanyl-N2O-etomidate group, a bolus injection of 0.3 mg.kg-1 of etomidate was given during anaesthesia with 3-4 micrograms.kg-1 of fentanyl and 60 per cent nitrous oxide. The amplitude of the P100 was significantly decreased and the latencies of the P60 and N70 were significantly increased. In conclusion, interpretation of the VEP during etomidate administration alone was not hard to perform but, when given together with fentanyl-nitrous oxide anaesthesia, the VEP was affected significantly making its interpretation difficult.

Adult↗
PubMed2005

Etomidate attenuates phenylephrine-induced contraction in isolated rat aorta.

PURPOSE: A previous study has shown that etomidate inhibits the angiotensin II-induced calcium influx in rat aortic smooth muscle cells. The goals of our current in vitro study were to investigate the effect of etomidate on phenylephrine-induced contraction in rat aorta, and to elucidate the associated signalling pathway. METHODS: Endothelium-denuded aortic rings were suspended for isometric tension recording. Concentration-response curves for phenylephrine (10(-9) to 10(-6) M), 5-hydroxytryptamine (10(-7) to 10(-4) M) and potassium chloride (10 to 60 mM) were generated in the presence and absence of etomidate (5 x 10(-6), 3 x 10(-5), 5 x 10(-5) M). For the rings pretreated with verapamil (10(-5) M), the phenylephrine concentration-response curves were generated in the presence and absence of etomidate (5 x 10(-5) M). In the rings exposed to calcium-free isotonic depolarizing solution, the contractile response induced by the addition of calcium was assessed in the presence and absence of etomidate (5 x 10(-5) M). RESULTS: Etomidate (5 x 10(-5) M) produced a significant rightward shift in the concentration-response curves for phenylephrine, 5-hydroxytryptamine and potassium chloride. Etomidate (5 x 10(-5) M) did not alter phenylephrine-induced contraction in the rings pretreated with verapamil. Etomidate (5 x 10(-5) M) significantly attenuated the contractile response induced by the addition of calcium in the calcium-free isotonic depolarizing solution. CONCLUSION: The results suggest that etomidate, which exceeds the clinically relevant concentration, attenuates the phenylephrine-induced contraction by having an inhibitory effect on the calcium influx by blocking the L-type calcium channels in the rat aortic vascular smooth muscle.

Anesthetics, Intravenous↗
PubMed1988

Hormonal effects of an induction dose of etomidate for patients undergoing urgent myocardial revascularization.

The use of etomidate for induction of anesthesia in patients requiring urgent coronary artery surgery provides good cardiovascular stability. However, long-term etomidate infusions may cause transient signs of adrenocortical suppression. The purpose of this study was to determine whether an induction bolus dose of etomidate would cause clinically relevant endocrine dysfunction in urgent coronary artery bypass patients. With institutional review board approval, 11 patients were prospectively randomized to a diazepam (control) or etomidate rapid sequence induction. The diazepam group (n=6; mean, 69 years) received 0.4 mg/kg of diazepam. The etomidate group (n=5; mean, 54 years) received 0.3 mg/kg of etomidate. Maintenance anesthesia included nitrous oxide, oxygen, pancuronium, and fentanyl in increments up to 32 microg/kg. Hemodynamics, cortisol, epinephrine, and norepinephrine were measured both intraoperatively and postoperatively. The only significant difference between the two groups in hemodynamic parameters was a higher heart rate in the etomidate group. Both agents adequately controlled the stress response to intubation as judged from the levels of epinephrine, norepinephrine. and cortisol. However, in both groups epinephrine and norepinephrine increased between intubation and removal of the aortic cross-clamp. Cortisol also increased from the time of cross-clamp removal to 12 and 24 hours post-bypass. During anesthesia and surgery in the pre-bypass period, there was a decrease in cortisol over time in the etomidate group, and there was an increase with diazepam. Thus, etomidate provided stable hemodynamics, possible mild intraoperative adrenocortical suppression, a depressed hormonal stress response to intubation, and a normal hormonal reaction to the later part of surgery and the postoperative period.

Aged↗
PubMed2006

Neuroprotective effect of etomidate on functional recovery in experimental spinal cord injury.

OBJECTIVE: Primary impact to the spinal cord causes rapid oxidative stress after injury. To protect neural tissue, it is important to prevent secondary pathophysiological mechanisms. Etomidate, a strong antiexcitotoxic agent, stimulates the gamma aminobutyric acid (GABA) receptors. The purpose of this study was to investigate neurobehavioral and histological recovery and to evaluate the biochemical responses to treatment of experimental spinal cord injury (SCI) in rats with etomidate or methylprednisolone (MP) or both etomidate and MP. MATERIAL AND METHODS: Seventy-two rats were randomly allocated into six groups: a control group (laminectomy alone), a trauma group (laminectomy+trauma), a methylprednisolone group (30 mg/kg MP), an etomidate group (2 mg/kg), a methylprednisolone and etomidate combined treatment group (30 mg/kg MP and 2 mg/kg etomidate) and a vehicle group. Six rats from each group were killed at the 24th hour after the injury. Malondialdehyde, glutathione, nitric oxide and xanthine oxidase levels were measured. Neurological functions of the remaining rats were recorded weekly. Six weeks after injury, all of those rats were killed for histopathological assessment. RESULTS: Etomidate treatment revealed similar neurobehavioral and histopathological recovery to MP treatment 6 weeks after injury. Combined treatment did not provide additional neuroprotection. CONCLUSION: Etomidate treatment immediately after spinal cord injury has similar neuroprotection to MP. In spite of different neuroprotection mechanisms, combined treatment with MP and etomidate does not provide extra protection.

Animals↗
PubMed2001

[Epileptic seizures from etomidate? The human Kv1.1 potassium channel in humans].

OBJECTIVE: It is a matter of dispute whether etomidate exhibits an epileptogenic action. It is also disputed whether frequently observed myocloni induced by etomidate are related to seizure-like activity in the EEG. The clinical effects of anaesthetic agents reflect their molecular action. A possible epileptogenic action of etomidate should, therefore, result from action on a molecular target that has yet to be identified. Suppression of Kv1.1 channels may be associated with epilepsy in men. Inhibition of Kv1.1 channels by etomidate at clinically relevant concentrations would, thus, argue in favour of an epileptogenic action of etomidate. METHODS: Patch-clamp recordings of the pharmacological action of etomidate on cloned and functionally expressed human Kv1.1 channels. RESULTS: Etomidate inhibits human Kv1.1 channels in a concentration-dependent and reversible manner. The IC50-value is 400 microM, the Hill-coefficient is 2. The ratio of free clinical plasma concentrations and the IC50-value is 0.006. At plasma concentrations determined in a clinical setting Kv1.1 channels would be suppressed by less than 0.01%. CONCLUSION: The small effect of etomidate on human Kv1.1 channels at these concentrations questions an epileptogenic action of etomidate caused by inhibition of Kv1.1 channels.

Cells, Cultured↗
PubMed1984

Inhibition of adrenal steroidogenesis by the anesthetic etomidate.

The use of the intravenous anesthetic etomidate for prolonged sedation has been associated with low levels of plasma cortisol and increased mortality. We measured the cortisol and aldosterone responses to ACTH stimulation in five patients receiving etomidate, and we also studied the direct effects of etomidate on enzymes in the rat steroidogenic pathway. One patient who was receiving a 20-hour infusion of etomidate (1.3 to 1.5 mg per kilogram of body weight per hour) had marked adrenocortical suppression that was still evident four days after etomidate was discontinued. Four surgical patients receiving etomidate during their operations were all found to have adrenal suppression four hours after the operation; mean (+/- S.D.) increases in cortisol and aldosterone after ACTH stimulation were only 1.8 +/- 0.5 micrograms per deciliter and 0.5 +/- 1.1 ng per deciliter, respectively. In rat adrenal cells, etomidate produced a concentration-dependent blockade of the two mitochondrial cytochrome P-450-dependent enzymes, cholesterol-side-chain cleavage enzyme, and 11 beta-hydroxylase, without evident inhibition of the microsomal enzymes in the glucocorticoid pathway. Physicians should be aware that etomidate inhibits adrenal steroidogenesis, and they should consider treating selected patients with corticosteroids if etomidate is used.

Adrenal Cortex↗
PubMed1985

Cerebral functional, metabolic, and hemodynamic effects of etomidate in dogs.

The effects of a continuous infusion of etomidate on cerebral function, metabolism, and hemodynamics and on the systemic circulation were examined in six dogs. The infusion rate of etomidate was progressively increased at 20-min intervals from 0.02 to 0.4 mg X kg-1 X min-1 for 2 h. Cerebral oxygen consumption (CMRO2) decreased until there was cessation of neuronal function as reflected by the onset of an isoelectric EEG. This occurred during an infusion of 0.3 mg X kg-1 X min-1 etomidate when the animals had received a total of 10.7 mg X kg-1 over 91 min. At this time the CMRO2 was 2.6 ml X min-1 X 100 g-1, 48% of control. Thereafter, despite continued administration of etomidate to a total dose of 21.4 mg X kg-1, CMRO2 did not decrease further. Cerebral blood flow (CBF) decreased in association with a marked increase in cerebrovascular resistance but was independent of changes in CMRO2. CBF decreased precipitously from 145 +/- 23 to 72 +/- 6 ml X min-1 X 100 g-1 during the lowest infusion rate of 0.02 mg X kg-1 X min-1 etomidate and stabilized at 34-36 ml X min-1 X 100 g-1 during an infusion rate of 0.1 mg X kg-1 X min-1. CBF remained at this level despite the continued administration of etomidate and a further decrease in CMRO2. Etomidate produced physiologically minor but statistically significant changes in the systemic hemodynamic variables. Assays of cerebral metabolites taken at the end of the infusion revealed a normal energy state and a very mild but significant increase in cerebral lactate to 1.49 mumol X g-1. We conclude that etomidate is a potent, direct cerebral vasoconstrictor that appears to be independent of its effect on CMRO2 and that the cerebral metabolic effects of etomidate are secondary to its effect on neuronal function, with little if any direct or toxic effects on metabolic pathways.

Anesthesia, Intravenous↗
PubMed1992

Prostaglandin-related microvascular dilation in pentobarbital- and etomidate-anesthetized rats.

Etomidate is characterized by minimal systemic cardiovascular effects, but its effect on the microvasculature has not been assessed. We compared the microvasculature of etomidate-anesthetized animals to that of animals anesthetized with pentobarbital, since its effects on the microvasculature are known. Male Sprague-Dawley rats were anesthetized with etomidate or pentobarbital. The cremaster muscle was prepared for microscopic viewing, leaving the neural and vascular supply intact. Small arterioles were near their maximal diameters in etomidate-anesthetized rats, whereas the pentobarbital group had a large dilator capacity (maximal diameter-basal diameter/basal diameter). The effect on resting arteriolar diameters of endothelium-derived relaxing factor (EDRF) and prostaglandin synthesis inhibitors was tested. Dilator capacity was not affected by the EDRF inhibitor nitro-L-arginine, but it was significantly increased by mefenamic acid and ibuprofen in etomidate-anesthetized animals. To test whether dilator and constrictor mechanisms were normal, serotonin concentration-response curves were obtained in pentobarbital and etomidate-anesthetized animals with and without mefenamate or ibuprofen present. The dilation of small arterioles to serotonin in the etomidate groups with mefenamate or ibuprofen was not significantly different from that of the pentobarbital groups. Serotonin produced a comparable constriction of large arterioles in both anesthetic groups. The topical application of etomidate to the cremaster muscle did not affect arteriolar diameters. Thus, etomidate appears to trigger the release of dilator prostaglandins in striated muscle through a central or indirect mechanism.

Anesthesia, Intravenous↗
PubMed2001

Intravenous etomidate for procedural sedation in emergency department patients.

OBJECTIVE: To determine the safety and effectiveness of intravenous (IV) etomidate for the sedation of patients undergoing painful procedures in the emergency department (ED). METHODS: A two-part feasibility study for ED patients receiving IV etomidate for painful ED procedures was undertaken. In the initial phase, a retrospective series of patients receiving etomidate for ED procedural sedation was considered. This phase served as the basis for a descriptive, prospective feasibility study of consecutive ED patients. During the second phase, patients were evaluated for complications related to IV etomidate sedation or the procedure performed. Immediately following the procedure, the physician was asked to complete a data collection sheet documenting the patient's etomidate dose, the number of doses required to complete the procedure, the analgesic used, the complications of the procedure, and the patient's procedural recall. RESULTS: Intravenous etomidate was administered to nine patients during the initial study phase and 51 during the prospective, descriptive phase. Indications for sedation included dislocation reduction (25), cardioversion (7), fracture reduction (20), abscess incision and drainage (4), foreign body removal (3), and chest thoracostomy (1). Physicians used 0.1-mg/kg IV bolus etomidate. A mean of 1.6 doses of etomidate was used to complete procedures (range 1-3 doses). Of the 60 patients in both study groups, 59 (98%) achieved adequate sedation by physician's assessment. Procedural success was documented for 56 patients (93%). There were 12 complications reported: oxygen desaturation below 90% (5), myoclonus (4), vomiting (1), pain with injection (1), and a brief bradycardic episode (1). No patient required assistance with ventilation or endotracheal intubation. CONCLUSIONS: Intravenous etomidate can be administered safely and effectively to provide appropriate conscious sedation for short, painful ED procedures.

Adult↗
PubMed2003

Etomidate for rapid-sequence intubation in young children: hemodynamic effects and adverse events.

OBJECTIVES: Physicians commonly use etomidate for adult rapid-sequence intubation (RSI), but the manufacturer does not recommend its use for children under 10 years of age due to a lack of data. The authors present their experience with etomidate for pediatric RSI in order to further develop its risk-benefit profile in this age group. METHODS: Trained abstractors reviewed the medical records for all children under 10 years old who received etomidate for RSI between July 1996 and April 2001. RESULTS: 105 children, with an average age of 3 (+/-2.9) years, received a median dose of 0.32 (+/-0.12) mg/kg of etomidate. The systolic blood pressure increased an average of 4 mm Hg (95% CI = -3.3 to 9.2); the diastolic blood pressure increased 7 mm Hg (95% CI = -3.1 to 11) within 10 minutes of receiving etomidate. The heart rate increased an average of 10 beats/min (95% CI = 4.0 to 17.4). Complications included three patients who vomited within 10 minutes of etomidate administration. There were no cases of documented myoclonus, status epilepticus, or new-onset seizures. Thirty-eight patients received corticosteroids during the hospital course, none for suspected adrenal insufficiency. Three patients died, all from severe brain injury. CONCLUSIONS: In children less than 10 years old, etomidate seems to produce minimal hemodynamic changes, and appears to have a low risk of clinically important adrenal insufficiency, myoclonus, and status epilepticus. The association between etomidate and emesis (observed in less than 3% of enrolled patients) remains unclear. For clinical situations in which minimal blood pressure changes during RSI are critical, etomidate appears to have a favorable risk-benefit profile for children under 10 years old.

Child, Preschool↗
PubMed2004

Etomidate elevates intracellular calcium levels and promotes catecholamine secretion in bovine chromaffin cells.

Etomidate, an intravenous imidazole general anaesthetic, is thought to produce anaesthesia by modulating or activating ionotropic Cl(-)-permeable GABA(A) receptors. Chromaffin cells are known to express functional GABA(A) receptors with properties similar to their neuronal counterparts. We have shown that activation of the GABA(A) receptors, with specific GABA(A) agonists, leads to cellular excitation. Our goal was to determine whether etomidate mimicked this response and to explore the functional consequences of this activation. Imaging experiments with the Ca(2+)-indicator dye fura-2 were used to assay [Ca(2+)](i). Bovine adrenal chromaffin cells were superfused with a variety of GABA(A)-selective drugs to determine their effects on [Ca(2+)](i). Amperometric measurements were used to assay catecholamine release in real-time. We show that bovine adrenal chromaffin cells were excited by etomidate at clinically relevant concentrations. Etomidate directly activated GABA(A) receptors found in chromaffin cells thereby elevating [Ca(2+)](i). The effects of etomidate were mimicked by the specific GABA(A) agonist muscimol and blocked by the specific antagonist bicuculline. Our data show that low concentrations of etomidate modulated GABA(A) receptor activation by muscimol. Blockade of voltage-dependent Ca(2+) channels prevented the elevation of [Ca(2+)](i) by GABA. Application of etomidate directly to the chromaffin cells elicited robust catecholamine secretion from these cells. The data indicate that clinically relevant concentrations of etomidate can directly activate GABA(A) receptors, which, due to the positive anion equilibrium potential, depolarizes chromaffin cells. This depolarization activates voltage-dependent Ca(2+) channels thereby stimulating catecholamine release. Our data suggest that circulating catecholamine levels may be elevated after etomidate application.

Animals↗
PubMed2004

Etomidate for procedural sedation in the emergency department.

OBJECTIVE: To review the current efficacy and safety evidence for the use of etomidate for procedural sedation in the emergency department (ED). DATA SOURCES: MEDLINE (1966-December 2003), EMBASE (1980-December 2003), PubMED (1966-December 2003), and Cochrane Database of Systemic Reviews (up to December 2003) were searched for full-text reports published in English on the use of etomidate in humans. Search terms included etomidate, procedural sedation, conscious sedation, relocation, dislocation, abscess incision, abscess drainage, and cardioversion. STUDY SELECTION AND DATA EXTRACTION: Prospective and retrospective studies evaluating efficacy or safety endpoints using etomidate for procedural sedation in the ED were included. All studies were evaluated independently by both authors. For clinical outcomes (efficacy, safety), the definitions specified by each study were used. DATA SYNTHESIS: Three observational studies and 5 prospective, randomized controlled trials were included in this review. Onset of action and time to recovery following etomidate were rapid and found to be comparable to that of propofol and thiopental but significantly faster than that of midazolam. The dose of etomidate for procedural sedation ranged from 0.15 to 0.22 mg/kg. No significant hemodynamic effects were observed; however, respiratory depression resulting in oxygen desaturation to <90% or apnea appears to occur in approximately 10% of patients undergoing procedural sedation with etomidate with or without analgesia. The most prominent adverse effect reported with etomidate was myoclonus, occurring in 20-45% of patients. CONCLUSIONS: Etomidate is an appropriate and valuable agent for performing procedural sedation in the ED. The rapid onset and recovery time and relative lack of significant hemodynamic and respiratory effects may facilitate optimal and safe conditions for procedural sedation in the ED.

Emergency Service, Hospital↗
PubMed1985

[Experiences with "etomidate pro infusione" in heart surgery interventions with extracorporeal circulation].

The results of experimental studies with etomidate demonstrating positive hemodynamic effects as well as a decrease in intracranial pressure induced a study using etomidate during cardiac surgery. This randomized study including 506 patients should prove the influence of etomidate on the rate of psychic disturbances after cardiac surgery. Patients treated with etomidate received a loading dose of 1 mg/kg b.w. etomidate within 15 minutes followed by a continuous infusion of 1 mg/kg b.w./h until the end of ECC. Patients without etomidate were the control group. Psychic disturbances were observed in 25% of the control group and in 30% of the etomidate group. In both groups of patients there was a fair number of patients with perioperative cardiopulmonary problems (artificial ventilation longer than 24 hours; catecholamine therapy: epinephrine greater than 5 micrograms/min longer than 3 hours): 8% in the control group and 20% in the etomidate group. These results indicate that etomidate does not beneficially influence the rate of psychic disturbances after open-heart surgery; it may induce, however, cardiopulmonary side effects after cardiac surgery. The results of recent studies indicating drug induced adrenal insufficiency are discussed.

Adolescent↗
PubMed1992

A Comparison Between Etomidate and Methohexital for Anesthesia in ECT.

Twenty patients were enrolled in a prospective, randomized, open vial, within-patient, crossover design study of methohexital and etomidate anesthesia for electroconvulsive therapy (ECT). Methohexital (1.0 mg/kg) and etomidate (0.3 mg/kg) were each given for two ECTs. While there were no differences in hemodynamics between the etomidate and methohexital groups, etomidate had a 24% longer mean wakeup time than methohexital. There was no difference between etomidate and methohexital in recovery room stay, induction time, or seizure duration. There was no difference in cardiac rhythms. More patients had pain on injection with etomidate than with methohexital. Increased incidence of pain on injection and a longer initial wakeup time are drawbacks to etomidate, but etomidate compared favorably to methohexital in hemodynamics. Etomidate is an acceptable alternative to methohexital, especially when barbiturates may be contraindicated.

Journal Article↗
PubMed2003

Mapping quantitative trait loci mediating sensitivity to etomidate.

Long- and Short-Sleep (LS and SS) mice were selectively bred for differences in ethanol-induced loss of the righting reflex (LORR) and have been found to differ in LORR induced by various anesthetic agents. We used a two-stage mapping strategy to identify quantitative trait loci (QTLs) affecting duration of LORR caused by the general anesthetic etomidate and brain levels of etomidate (BEL) following regain of the righting reflex. Analysis of recombinant-inbred strains derived from a cross between LS and SS mice (LSXSS) yielded a heritability estimate of 0.23 for etomidate-induced LORR and identified one marker that showed suggestive linkage for a QTL, on mouse Chromosome (chr) 12. Mapping in an F(2) population derived from a cross between inbred LS and SS (ILS and ISS) revealed a significant QTL for etomidate-induced LORR on Chr 12, and two significant QTLs mediating BEL on Chrs 6 and 12. Several QTLs showing suggestive linkage for etomidate-induced LORR and BEL were also identified in the F(2) population. Brain levels of etomidate in the RI and F(2) mice suggested that differences in LORR were due to differential central nervous system sensitivity, rather than differential etomidate metabolism. Interestingly, the region on Chr 7 has also been identified as a region influencing ethanol-induced LORR, suggesting the possibility of a common genetic mechanism mediating etomidate and ethanol sensitivity. These QTL regions need to be further narrowed before the testing of candidate genes is feasible.

Analysis of Variance↗
PubMed1996

Mechanisms of etomidate potentiation of GABAA receptor-gated currents in cultured postnatal hippocampal neurons.

The effect of etomidate, an imidazole general anesthetic, on GABAA receptor function was studied in cultured hippocampal neurons. At a clinically relevant concentration of 4.1 microM, etomidate shifts the GABA dose response to the left (ED50 shift from 10.2 to 5.2 microM), with no change in the maximum current evoked by saturating concentrations of GABA. At a higher concentration of 82 microM, etomidate directly induces current in the absence of GABA. Etomidate selectively increases the amplitude and prolongs the duration of miniature inhibitory postsynaptic currents without significant effects on miniature inhibitory postsynaptic currents. The combined effects of etomidate on miniature inhibitory postsynaptic current amplitude and duration enhance the total charge transfer by 280% during a spontaneous synaptic event. Analysis of single channels opened by GABA indicates that 8.2 microM etomidate increases the probability of channels being open 13-fold and increases the effective channel open time two-fold. Given the present understanding of central inhibitory synapses, the effect of etomidate on channel kinetics is most likely to be the predominant mechanism which influences the synaptic function. In addition, etomidate, through its modulation of both channel kinetics and open probability, is likely to have a large impact on extrasynaptic GABAA receptor function.

Anesthetics, General↗
PubMed2006

Etomidate versus midazolam for procedural sedation in pediatric outpatients: a randomized controlled trial.

STUDY OBJECTIVE: Midazolam is widely used for procedural sedation and analgesia. Etomidate has been studied mostly in adults. Our objective is to compare the efficacy of etomidate and midazolam for achieving procedural sedation and analgesia in children. METHODS: A randomized, double-blind, emergency department and orthopedic clinic-based trial was carried out among patients aged 2 to 18 years with displaced extremity fractures. Patients were administered 1 microg/kg of fentanyl and either 0.2 mg/kg of etomidate or 0.1 mg/kg of midazolam. Adequate sedation was defined, for the purpose of this study, as a score of 4 or more on the Ramsay Sedation Scale. The primary outcome was induction and recovery time. The rates of adverse events, success of fracture reduction, and parent and physician satisfaction were also compared. RESULTS: From April to August 2004, 100 of 128 eligible patients were enrolled (age 8.7+/-3.7 years; 50% male patients). A higher proportion of patients attained adequate sedation among those who received etomidate: 46 of 50 (92%) versus 18 of 50 (36%) (delta 56%; 95% confidence interval [CI] 38% to 69%). Time taken for induction (hazard ratio 4.9; 95% CI 2.2 to 10.9) and time taken for recovery (hazard ratio 2.8; 95% CI 1.5 to 5.1) were lower among patients who received etomidate. The rates of adverse events were similar in both groups, except for myoclonus and pain at the injection site, which was more frequent in the etomidate group. CONCLUSION: Induction and recovery times are shorter with etomidate compared with midazolam. At the dosages used for procedural sedation and analgesia among children with displaced extremity fracture, etomidate has higher efficacy in comparison with midazolam.

Adolescent↗