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PubMed2006

Etomidate-Lipuro is associated with considerably less injection pain in children compared with propofol with added lidocaine.

BACKGROUND: Propofol is associated with a high incidence of injection pain in children, even if given together with lidocaine. A new lipid formulation of etomidate (Etomidate-Lipuro) has been found in adults to cause very little discomfort during i.v. injection. The aim of the present prospective, double-blind, randomized trial was to compare the incidence of injection pain during i.v. induction of anaesthesia between propofol with added lidocaine (previous standard) and this new etomidate formulation in paediatric patients. METHODS: A total of 110 paediatric patients, aged 2-16 years, scheduled for outpatient surgery were planned to be included in the study. The primary end point of the study was the incidence of injection pain during induction of anaesthesia as assessed by a four-point scale as described previously. The occurrence of myoclonic muscular activity was registered as a secondary end point (four-point scale). An interim analysis after 80 patients was requested by the Ethics' Committee. RESULTS: The study was stopped after the inclusion of 80 patients. A significantly lower incidence of injection pain was found in the Etomidate-Lipuro group as compared with the propofol-lidocaine group (5.0% vs 47.5%, P<0.001). The use of etomidate was associated with a significantly higher incidence of myoclonic activity compared with propofol-lidocaine (85.0% vs 15%, P<0.001). CONCLUSIONS: The use of a new lipid formulation of etomidate is associated with significantly less injection pain than propofol with added lidocaine in children. This finding may warrant a change in clinical practice in order to avoid unnecessary pain in children.

Adolescent↗
PubMed1986

Regional brain glucose utilization in rats during etomidate anesthesia.

The influence of etomidate on regional cerebral function as reflected by regional cerebral glucose utilization (rCMRGlc) was studied. Three experiments were performed. In the first, rats had both left femoral vessels cannulated and were placed in restraining cages. Etomidate was infused intravenously (12 mg/kg) at a rate of 6 mg X kg-1 X min-1. This large dose had a modest effect on blood pressure and heart rate, which could be explained by the elimination of stress in restrained rats, and no effect on body temperature, Pao2, PaCo2, or pH. A second group of rats were used to determine the effect of etomidate on the ratio of brain glucose to plasma glucose, which is necessary for calculating rCMRGlc. In the third experiment rCMRGlc was measured in unstressed rats. The rats were anesthetized with an intravenous dose of 1, 2, 6, or 12 mg/kg etomidate infused at a rate of 6 mg X kg-1 X min-1. Etomidate had a marked effect on glucose consumption in many, but not all, cerebral structures. The forebrain (telencephalon and diencephalon) was most affected (-25% to -35%) while the hindbrain was minimally affected. There was no demonstrable dose dependency; 1 mg/kg depressed rCMRGlc as much as 12 mg/kg. The pattern of rCMRGlc depression is in accord with the minimal effects observed on physiologic variables and similar to that caused by the steroid anesthetic Althesin, although the depression seen was not as severe. The pattern of metabolic depression produced by etomidate differs markedly from that produced by barbiturates, which affect all brain regions to a similar degree.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1998

Comparison of the effect of etomidate and desflurane on brain tissue gases and pH during prolonged middle cerebral artery occlusion.

BACKGROUND: The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in patients who had middle cerebral artery occlusion for > 15 min. METHODS: After a craniotomy, a probe that measures PO2, PCO2, and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. RESULTS: During baseline conditions, tissue PO2, PCO2, and pH were similar between the two groups (PO2 = 15 mmHg, PCO2 = 60 mmHg, pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue PO2 decreased in five of six patients without a change in PCO2 or pH. During administration of 9% desflurane, tissue PO2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15). CONCLUSION: These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue PO2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.

Adult↗
PubMed2004

Gamma-aminobutyric acid type A receptor beta 2 subunit mediates the hypothermic effect of etomidate in mice.

BACKGROUND: The authors have previously described that the gamma-aminobutyric acid type A (GABAA) receptor beta 2N265S mutation results in a knock-in mouse with reduced sensitivity to etomidate. After recovery from etomidate anesthesia, these mice have improved motor performance and less slow wave sleep. Because most clinically used anesthetics produce hypothermia, the effect of this mutation on core body temperature was investigated. METHODS: The effect of etomidate and propofol on core body temperature were measured using radiotelemetry in freely moving GABAA receptor beta 2N265S mutant mice and wild-type controls. RESULTS: beta 2N265S mutant mice have a reduced hypothermic response to anesthetic doses of etomidate compared with wild-type controls and after a transient loss of righting reflex regain normothermia more rapidly compared with wild-type controls. Subanesthetic doses of etomidate produce hypothermia, which was not observed in the mutant mice. Vehicle administration resulted in a stress-induced hyperthermic response in both genotypes. Propofol produced a hypothermic response that was similar in both genotypes. CONCLUSIONS: The GABAA receptor beta 2 subunit mediates a significant proportion of the hypothermic effects of etomidate. As the beta 2 subunit mediates postrecovery ataxia and sedation, anesthetic agents that do not have in vivo potency at beta 2 subunit-containing receptors offer the potential for surgical anesthesia with improved recovery characteristics.

Animals↗
PubMed2005

Opposing actions of etomidate on cortical theta oscillations are mediated by different gamma-aminobutyric acid type A receptor subtypes.

BACKGROUND: Cortical networks generate diverse patterns of rhythmic activity. Theta oscillations (4-12 Hz) are commonly observed during spatial learning and working memory tasks. The authors ask how etomidate, acting predominantly via gamma-aminobutyric acid type A (GABAA) receptors containing beta2 or beta3 subunits, affects theta activity in vitro. METHODS: To characterize the effects of etomidate, the authors recorded action potential firing together with local field potentials in slice cultures prepared from the neocortex of the beta3(N265M) knock-in mutant and wild type mice. Actions of etomidate were studied at 0.2 microm, which is approximately 15% of the concentration causing immobility ( approximately 1.5 microm). RESULTS: In preparations derived from wild type and beta3(N265M) mutant mice, episodes of ongoing activity spontaneously occurred at a frequency of approximately 0.1 Hz and persisted for several seconds. Towards the end of these periods, synchronized oscillations in the theta band developed. These oscillations were significantly depressed in slices from beta3(N265M) mutant mice (P < 0.05). In this preparation etomidate acts almost exclusively via beta2 subunit containing GABAA receptors. In contrast, no depression was observed in slices from wild type mice, where etomidate potentiates both beta2- and beta3-containing GABAA receptors. CONCLUSIONS: At concentrations assumed to cause sedation and amnesia, etomidate depresses theta oscillations via beta2-containing GABAA receptors but enhances these oscillations by acting on beta3 subunit containing receptors. This indicates that the overall effect of the anesthetic reflects a balance between enhancement and inhibition produced by different GABAA receptor subtypes.

Action Potentials↗
PubMed1997

The use of ketamine or etomidate to supplement sufentanil/N2O anesthesia does not disrupt monitoring of myogenic transcranial motor evoked responses.

Intraoperative monitoring of myogenic transcranial motor evoked responses (tc-MERs) requires an anesthetic technique that minimally depresses response amplitudes. Acceptable results have been obtained during opioid/N2O anesthesia, provided that the concentration of N2O does not exceed 50%. However, this technique may necessitate supplementation with additional agents to achieve adequate depth of anesthesia. Etomidate and ketamine have been reported anecdotally or in nonsurgical situations to produce little tc-MER depression. We investigated the effects on tc-MER amplitude and latency of supplementation of a sufentanil/N2O anesthetic with etomidate or ketamine in patients undergoing spinal instrumentation. Anesthesia was induced with etomidate 0.3 mg/kg and sufentanil 1.5 mg/kg and maintained with sufentanil 0.5 mg/kg/h and N2O 50%. Muscle relaxation was kept at 25% of control. Paired transcranial electrical stimulation was performed. Each patient randomly received either ketamine (0.5 mg/kg) or etomidate (0.1 mg/kg) as a single bolus intravenously, during stable surgical conditions. Triplicate tc-MERs were recorded from the tibialis anterior muscles before and 2, 5, 10, and 15 min after drug administration. Administration of ketamine did not significantly change tc-MER amplitudes, whereas etomidate resulted in a transient amplitude depression to 72% of control (p < 0.05) at 2 min after injection. Latency remained unchanged with both drugs. In conclusion, the data suggest that both ketamine (0.5 mg/kg) and etomidate (0.1 mg/kg) can be used to supplement sufentanil/N2O anesthetic without disrupting tc-MER monitoring.

Adolescent↗
PubMed2005

Customized anesthetic preservation of ictal threshold in electroconvulsive therapy: role of adjunctive remifentanil with etomidate.

We present a case of anesthesia for electroconvulsive (ECT) therapy that was complicated by emetic sensitivity to etomidate, fragile ictal threshold, and mild pseudocholinesterase deficiency. The anesthetic was designed in this patient taking all his issues in consideration. The mild pseudocholinesterase deficiency necessitated a (50-75%) reduction in succinylcholine dosage, careful monitoring of the train of four, and postictal amnestic coverage to prevent paralysis upon waking. The significant emetic response to etomidate prompted substitution to propofol and preemptive ondansetron. Propofol significantly raised the ictal threshold but significantly reduced the postprocedural emesis. Eventually, this clinical challenge was resolved with adjunctive use of low-dose etomidate and remifentanil. This combination preserved the ictal parameters, providing patient comfort, good clinical response, and therapeutic efficacy. Although seizure duration and quality often are restored with hyperventilation and caffeine, this case necessitated a return to etomidate for the restoration of satisfactory ictal parameters. Although this effect of remifentanil has been described with methohexital, and etomidate with alfentanil, to the best of our knowledge, this is the first reported case of adjunctive remifentanil with etomidate for preserving ictal threshold. The outpatient course of ECT was thus completed with all psychiatric and anesthetic goals satisfied: adequate seizure quality and duration, no paralysis upon waking, no post-ECT nausea and vomiting, and patient satisfaction. Anesthesiologists should be aware of factors influencing the seizure duration and, keeping in mind the coexisting medical conditions of the patient, adjustments should be made to get the best possible outcome.

Adult↗
PubMed1982

Outpatient sedation for oral surgery. A new technique using etomidate.

In an attempt to exploit the benefits and to reduce the incidence of side-effects of etomidate during intravenous sedation for nervous patients undergoing oral surgery under local analgesia, a series of four clinical trials were undertaken: a pilot study in which etomidate was preceded by a combination of pentazocine and diazepam; a double-blind study in which saline was randomly substituted for the etomidate, and two further studies in which the administration of etomidate was preceded by that of either pentazocine or diazepam alone. The combination of a small dose of diazepam (0.1 mg/kg) with an initial dose of etomidate (0.1 mg/kg) followed by increments of the latter as necessary proved to be most successful in reducing the severity of unwanted reactions while retaining the unique advantages of etomidate.

Adult↗
PubMed1989

The effects of speed of injection on induction with propofol. A comparison with etomidate.

One hundred and eighty female patients received either propofol 2.5 mg/kg or etomidate 0.3 mg/kg injected over 20, 40 or 80 seconds for induction of anaesthesia after premedication with temazepam 20 mg. The mean induction times for both etomidate and propofol were significantly reduced with increasing speed of injection. The mean induction times for etomidate were significantly less than propofol at the slower rates of injection. At each speed of injection, the decrease in systolic, mean and diastolic arterial blood pressures with etomidate were less than with propofol. The decrease in systolic blood pressure was not significantly affected by injection speed for either drug. Apnoea occurred significantly more frequently with propofol than with etomidate at each speed of injection and the incidence of apnoea greater than 60 seconds with propofol was significantly higher when injected over 20 seconds than 80 seconds. The incidence of pain on injection was unaffected by injection speed for either drug. The incidence of myoclonus and (or) hypertonus was significantly higher following etomidate.

Adult↗
PubMed1985

Effect of a single bolus of etomidate upon eight major corticosteroid hormones and plasma ACTH.

In a prospective controlled trial we investigated the effect of an induction dose of etomidate (0.26 mg/kg i.v.) on plasma ACTH, progesterone, 17 alpha OH-progesterone, 11-deoxycortisol, cortisol, cortisone, corticosterone, 11-deoxycorticosterone, and aldosterone in seven males undergoing general anaesthesia. Seven other male patients receiving thiopentone at induction (5.0 mg/kg i.v.) served as controls. Plasma ACTH concentrations rose higher in the etomidate group (346 +/- 124 vs. 117 +/- 74 pg/ml, mean +/- SEM), but the difference was not significant. After etomidate we found a clear suppression of plasma cortisol (P less than 0.01), cortisone (P less than 0.01), corticosterone (P less than 0.01), and aldosterone (P less than 0.05) compared to corticosteroid levels after induction with thiopentone. Plasma 11-deoxycortisol and 11-deoxycorticosterone concentrations were grossly elevated 210 min after etomidate (91 +/- 28 nmol/l and 7.04 +/- 0.47 nmol/l, respectively, P less than 0.01) demonstrating inhibition of 11 beta-hydroxylation of both glucocorticoid and mineralocorticoid intermediates. In contrast, no significant difference in plasma progesterone and 17 alpha-OH-progesterone levels was found between the two groups indicating that the cholesterol-side-chain cleavage enzyme is less sensitive to etomidate than 11 beta-hydroxylase. Our results suggest that after induction of anaesthesia with a single bolus of etomidate, inhibition of other enzymes in the corticosteroid-synthetic pathway (e.g. cholesterol-side-chain cleavage enzyme) is of little clinical relevance.

17-alpha-Hydroxyprogesterone↗
PubMed1987

Comparison of the effects of etomidate and its fluoro analogue, R 8110, on plasma cortisol, 11 beta-deoxycortisol, 17 alpha-hydroxyprogesterone and testosterone concentrations in dogs.

R 8110, an imidazole derivative, was shown to be clinically superior to etomidate for induction and maintenance of anaesthesia in dogs. The present study compared the effects of intravenous (i.v.) R 8110, etomidate and Ringer solution on cortisol biosynthesis by the adrenal gland in seven male labradors. A tetracosactide challenge was carried out 30 min after the i.v. injection of 3 mg/kg of both drugs and after i.v. Ringer solution (1 ml/kg). Etomidate and R 8110 both suppressed the cortisol response to tetracosactide almost completely and increased the plasma 11 beta-deoxycortisol levels more than 20 fold. Maximal 11 beta-deoxycortisol values were reached 120 min after R 8110, and not less than 300 min after etomidate. Plasma 17 alpha-hydroxyprogesterone and testosterone concentrations did not differ between placebo and R 8110 treatment, but they decreased after etomidate. These results indicate that the effects of R 8110 on steroid biosynthesis in dogs are less pronounced than those of etomidate and are largely limited to a temporary inhibition of the 11 beta-hydroxylase in the adrenal gland.

17-Hydroxycorticosteroids↗
PubMed1988

Comparative effects of etomidate and its fluoro analogue, R 8110 on testicular, adrenal and ovarian steroid biosynthesis.

The effects, of etomidate and of its fluoro analogue, R 8110, on adrenal, testicular and ovarian steroid biosynthesis were compared using cultures of guinea-pig adrenal, rat adrenal capsular, rat testicular and rat ovarian granulosa cells. At a concentration of 100 nM, etomidate inhibited the adrenal 11-hydroxylation of glucocorticoid and mineralocorticoid biosyntheses, producing a decrease in cortisol and corticosterone and an accumulation of 11-deoxycortisol and 11-deoxycorticosterone in guinea-pig adrenal and rat capsular adrenal cell suspensions, respectively. At higher concentrations (greater than 10(-6) M), etomidate also inhibited ovarian oestradiol production, testicular androgen formation and ovarian progesterone synthesis. The latter action suggests an effect on ovarian aromatase, on testicular 17 alpha/17,20-lyase activities and finally on cholesterol side-chain cleavage. The fluoro analogue of etomidate, R 8110, was ten times less potent as an inhibitor of 11-hydroxylation and affected progesterone formation only slightly in adrenal cell suspensions. Testosterone production was less affected by R 8110 than by etomidate. The increase of progestins suggests that the 17 alpha/17,20-lyase activities are the most sensitive testicular enzymatic reactions to R 8110. For inhibition of ovarian oestradiol production, R 8110 was twenty times more potent than etomidate.

Adrenal Cortex Hormones↗
PubMed1987

Electrophysiological studies of the effects of the general anaesthetic etomidate on frog myelinated nerve fibre.

The effects of the general anaesthetic etomidate (0.1 to 1 mM) upon the node of Ranvier of frog isolated nerve fibres were investigated under current and voltage clamp conditions. When added to the external solution, etomidate reversibly decreased the amplitude of the action potential. The action potential block, induced by the drug, was reversed by increasing the membrane potential. Etomidate rapidly and reversibly blocked the Na current with an apparent dissociation constant of 0.6 mM. In the presence of the drug, the steady-state inactivation-voltage curve of the Na current was shifted towards negative voltages. The block of Na current by etomidate was partially removed by repetitive depolarization preceded by a 50 ms period of hyperpolarization. In contrast, the block was enhanced when the repetitive depolarization was not preceded by hyperpolarization. This suggests that Na channels were preferentially blocked by the drug in the inactivated state. The K current was reversibly blocked by etomidate with an apparent dissociation constant of 0.2 mM. In the presence of the drug, the K current showed an apparent fast inactivation suggesting that K channels were blocked in the open state. We conclude that at higher concentrations than those attainable in the mammalian brain following single anaesthetic doses the general anaesthetic etomidate has a "local anaesthetic-like' action on the peripheral nervous system.

Action Potentials↗
PubMed2004

Midazolam is more likely to cause hypotension than etomidate in emergency department rapid sequence intubation.

OBJECTIVE: To compare the haemodynamic effect of low dose midazolam and etomidate as induction agent in emergency department rapid sequence intubation. METHODS: A prospective observational study in two phases. In phase one, midazolam 2-4 mg was used as induction agent and in phase two, etomidate 0.2-0.3 mg/kg was used. The haemodynamic data were recorded before and after intubation for comparison. Changes in mean systolic blood pressure were analysed with SPSS software. RESULTS: A 10% decrease in mean systolic blood pressure was observed in the midazolam group (p = 0.001) while there was no significant change in the etomidate group. Some 19.5% of patients had hypotension after being given midazolam while only 3.6% with etomidate (p = 0.002). Patients older than 70 tended to have more hypotension episodes but the difference was not statistically significant. CONCLUSIONS: Midazolam, even in low dose, was more likely than etomidate to cause significant hypotension when used as an induction agent for rapid sequence intubation. Etomidate is a better alternative.

Age Factors↗
PubMed2003

Midazolam pretreatment reduces etomidate-induced myoclonic movements.

During induction of anaesthesia with etomidate, myoclonic muscle movements are frequent. In this study, pretreatment with a small dosage of etomidate or midazolam was compared with placebo for the prevention of myoclonic muscle movements. Sixty patients, premedicated with oral midazolam, were pretreated in a randomized double-blinded fashion with etomidate 0.05 mg/kg i.v., midazolam 0.015 mg/kg i.v. or normal saline i.v. (placebo) in three groups of 20 patients each. The pretreatment was followed after 90 seconds by etomidate 0.3 mg/kg i.v. One minute after onset of hypnosis, induction of anaesthesia was completed with sufentanil and rocuronium. From the time of pretreatment to completion of anaesthesia, patients were observed for myoclonic muscle movements by a single physician, blinded to group allocation. Myoclonic movements were graded on a scale of 0 to 3. The incidence of myoclonic movements was significantly lower in patients pretreated with midazolam (4 of 20) compared with placebo (18/20) (P < 0.01). Midazolam 0.015 mg/kg i.v., administered 90 seconds before induction of anaesthesia with etomidate, is effective in reducing etomidate-induced myoclonic muscle movements.

Anesthetics, Intravenous↗
PubMed2004

Effect of etomidate on endothelium-dependent relaxation induced by acetylcholine in rat aorta.

The goals of this in vitro study were to investigate effects of etomidate on endothelium-dependent relaxation induced by acetylcholine in rat aorta, and to elucidate the associated cellular mechanism. In endothelium-intact rings precontracted with phenylephrine 10(-6) M, dose-response curves for acetylcholine (10(-9) to 10(-5) M) and calcium ionophore (10(-9) to 10(-6) M) were generated in the presence and absence of etomidate (5 x10(-6) 10(-5) M). In endothelium-intact or -denuded rings precontracted with phenylephrine 10(-6) M, sodium nitroprusside (10(-9) to 10(-6) M) dose-response curves were generated in the presence and absence of etomidate (10(-5)M). Etomidate (5 x10(-6), 10(-5)M) produced a significant rightward shift in the dose-response curves induced by acetylcholine (receptor-mediated endothelium-dependent agonist) and calcium ionophore A23187 (non receptor-mediated endothelium-dependent agonist). Etomidate (10(-5)M) had no effect on sodium nitroprusside (endothelium-independent nitric oxide donor)-induced vasorelaxant response in both endothelium-intact and -denuded rings. These results indicate that etomidate at clinically relevant concentrations attenuates endothelium-dependent relaxation induced by acetylcholine by an acting at a site distal to the endothelial muscarinic receptor, but proximal to guanylate cyclase activation of vascular smooth muscle in rat aorta.

Acetylcholine↗
PubMed1978

Effects of etomidate given in repeated doses.

Fifty fit, female patients were given four consecutive intravenous doses of etomidate 10 mg, so as to maintain sleep, after establishment of epidural block for postpartum sterilization. A matched group was given four doses of thiopentone 125 mg. Cumulative hypnotic effect, as judged by increasing sleep duration with second and subsequent doses, was much less with etomidate than with thiopentone. Etomidate did not depress blood pressure, whereas it fell progressively with successive doses of thiopentone. Injection pain was reported in 68% of patients receiving etomidate, and this tended to increase with successive doses; 12% also showed local inflammation at the injection site. Tremor, due to etomidate, was common, but did not increase with successive doses. Feelings of sleepiness, lasting several hours after waking, were more common after thiopentone than after etomidate.

Anesthesia, Epidural↗
PubMed2006

Use of etomidate as an induction agent for rapid sequence intubation in a pediatric emergency department.

OBJECTIVES: Although etomidate is widely used for rapid sequence intubation (RSI), there is no consensus on the optimal induction agent and no prospective pediatric emergency department (ED) study exists. The objective of this study was to assess the effectiveness and safety of etomidate as an induction agent for RSI in the pediatric ED. METHODS: Data on RSI conditions and complications were collected prospectively on patients undergoing RSI in a tertiary pediatric ED from January 2003 to December 2003. ED hemodynamic data and inpatient data were collected retrospectively via chart review. RESULTS: Seventy-seven of 101 patients requiring intubation underwent RSI with etomidate. The mean (+/- SD) age was 8.2 (+/- 6.2) years. All 77 patients were successfully intubated. Intubation condition data were available for 69 of 77 patients (89.6%). Conditions were good in 68 of 69 (99%; 95% confidence interval = 92.2% to 99.9%). The mean (+/- SD) maximal percent decrease in systolic blood pressure was 10% (+/- 13.6%). A greater than 20% maximal percent decrease in systolic blood pressure occurred in 12 of 69 patients (17.4%; 95% confidence interval = 9.3% to 28.4%). There was no relationship between seizures after etomidate administration and prior seizure history (p = 0.25). Corticosteroids were given to 29 of 77 patients post-RSI for varying diagnoses. All eight patients given corticosteroids for shock were in shock at the time of intubation. CONCLUSIONS: In the pediatric ED setting, etomidate as an induction agent provided successful RSI conditions and resulted in varied hemodynamic changes that were especially favorable in those patients presenting in decompensated shock. Hypotension and seizures were uncommon and occurred in patients with confounding diagnoses. Until the significance of a single dose of etomidate on adrenal dysfunction is further clarified, caution should be used in those patients at risk for adrenal insufficiency.

Adolescent↗