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PubMed2006

Etomidate, pharmacological adrenalectomy and the critically ill: a matter of vital importance.

Etomidate is a potent suppressant of adrenal steroidogenesis,effectively inducing reversible pharmacological adrenalectomy. Recent evidence suggests that for every five patients with septic shock given etomidate without corticosteroid supplementation, one patient will die as a consequence. Other critically ill patients are also at possible risk, and this risk requires further exploration. Etomidate will also confound investigations into the effects of disease states on adrenal function, and should therefore be avoided. A moratorium on the use of etomidate in critically ill patients outside clinical trials may be prudent until its safety is established.

Adrenal Cortex Function Tests↗

PubMed2005

Adrenal insufficiency in meningococcal sepsis: bioavailable cortisol levels and impact of interleukin-6 levels and intubation with etomidate on adrenal function and mortality.

CONTEXT: Adequate adrenal function is pivotal to survive meningococcal sepsis. OBJECTIVES: The objective of the study was to evaluate adrenocortical function in meningococcal disease. DESIGN: This was an observational cohort study. SETTING: The study was conducted at a university-affiliated pediatric intensive care unit. PATIENTS: Sixty children with meningococcal sepsis or septic shock participated in the study. MAIN OUTCOME MEASURES: The differences in adrenal function between nonsurvivors (n = 8), shock survivors (n = 43), and sepsis survivors (n = 9) on pediatric intensive care unit admission were measured. RESULTS: Nonsurvivors had significantly lower median cortisol to ACTH ratio than shock survivors and sepsis survivors. Because cortisol binding globulin and albumin levels did not significantly differ among the groups, bioavailable cortisol levels were also significantly lower in nonsurvivors than sepsis survivors. Nonsurvivors had significantly lower cortisol to 11-deoxycortisol ratios but not lower 11-deoxycortisol to 17-hydroxyprogesterone ratios than survivors. Using multiple regression analysis, decreased cortisol to ACTH ratio was significantly related to higher IL-6 levels and intubation with etomidate (one single bolus), whereas decreased cortisol to 11-deoxycortisol ratio was significantly related only to intubation with etomidate. Aldosterone levels tended to be higher in nonsurvivors than shock survivors, whereas plasma renin activity did not significantly differ. CONCLUSIONS: Our study shows that the most severely ill children with septic shock had signs of adrenal insufficiency. Bioavailable cortisol levels were not more informative on adrenal function than total cortisol levels. Besides disease severity, one single bolus of etomidate during intubation was related to decreased adrenal function and 11beta-hydroxylase activity. Decreased adrenal function was not related to decreased 21-hydroxylase activity. Based on our results, it seems of vital importance to take considerable caution using etomidate and consider combining its administration with glucocorticoids during intubation of children with septic shock.

17-alpha-Hydroxyprogesterone↗

PubMed1993

Excitatory effects and electroencephalographic correlation of etomidate, thiopental, methohexital, and propofol.

Excitatory movements have been observed during induction of anesthesia with etomidate, thiopental, methohexital, and propofol. We studied the frequency of these excitatory effects and correlated movements with electroencephalographic (EEG) findings in 67 unpremedicated patients (mean age 66.1 yr, range 45-82 yr). Excitatory effects, including myoclonus, tremor, and dystonic posturing, occurred in 86.6% of patients receiving etomidate; 69.2% of the patient responses were myoclonic. Multiple spikes appeared on the EEG in 22.2% of the etomidate patients. The frequency of excitatory effects was 16.6% after thiopental, 12.5% after methohexital, and 5.5% after propofol. None of the patients receiving thiopental, methohexital, or propofol developed myoclonic or seizure activity. In most patients, the excitatory movements were coincident with the early slow phase of the EEG which corresponds to the beginning of deep anesthesia. We conclude that perhaps caution should be exercised when administering etomidate to patients with a history of seizures as the myoclonic activity is associated with seizure activity. The incidence of excitatory movements after administration of propofol is very low.

Aged↗

PubMed1994

Quantifying the interaction of rocuronium (Org 9426) with etomidate, fentanyl, midazolam, propofol, thiopental, and isoflurane using closed-loop feedback control of rocuronium infusion.

The present study was designed to evaluate the interactions of rocuronium with etomidate, fentanyl, midazolam, propofol, thiopental, and isoflurane using closed-loop feedback control of infusion of rocuronium. Sixty patients were randomly assigned to one of six sequences where anesthesia was maintained with etomidate, fentanyl, midazolam, propofol, or thiopental and nitrous oxide, or with isoflurane and nitrous oxide. The possible interaction of rocuronium with the anesthetics was quantified by determining the asymptotic steady-state rate of infusion (Iss) of rocuronium necessary to produce a constant 90% neuromuscular block. This was accomplished by applying nonlinear curve fitting to data on the cumulative dose requirement during the initial 90-min period after bolus administration of rocuronium. Patient characteristics and controller performance, i.e., the ability of the controller to maintain the neuromuscular block constant at the set-point, did not differ significantly between the groups. Iss values calculated per lean body mass were 0.64 +/- 0.22, 0.60 +/- 0.15, 0.61 +/- 0.21, 0.67 +/- 0.31, 0.63 +/- 0.15, and 0.39 +/- 0.17 mg.kg-1.h-1 in the etomidate, fentanyl, midazolam, propofol, thiopental, and isoflurane groups, respectively. The isoflurane group had a lower steady-state rate of infusion of rocuronium than the other five groups (P < 0.05). Compared to intravenous anesthetics, etomidate, fentanyl, midazolam, propofol, or thiopental, isoflurane reduced the infusion requirement of rocuronium by 35%-40%.

Adult↗

PubMed2001

Anesthetic induction agents, sympathetic nerve activity and baroreflex sensitivity: a study in rabbits comparing thiopental, propofol and etomidate.

The mechanisms of arterial hypotension following intravenous anesthetic induction agents are multifactorial. The purpose of this study was to evaluate and compare the effects of thiopental, propofol and etomidate on hemodynamics, sympathetic outflow and arterial baroreflex sensitivity using not only neuraxis-intact but also totally baro-denervated rabbits. A total of 60 rabbits was anesthetized with urethane, tracheotomized, and mechanically ventilated with oxygen in nitrogen (FiO2 0.5). The left renal sympathetic nerve was isolated and placed on a bipolar electrode to record renal sympathetic nerve activity (RSNA). Thirty animals underwent a surgical preparation of total baroreceptor denervation. Bolus injections of an anesthesia induction dose of thiopental 4 mg/kg and twice the induction dose of propofol 4 mg/kg significantly decreased RSNA to the same extent (19.4+/-6.7 and 19.7+/-5.2% reduction, mean +/- SEM) and mean arterial pressure (MAP) also to the same extent (19.5+/-4.6 and 22.1+/-3.1% reduction) in the neuraxis-intact animals. RSNA was increased (34.5+/-6%) without reduction of MAP by an induction dose of etomidate, 0.3 mg/kg. Sympathetic barosensitivity was attenuated even 10 min after thiopental at 4 mg/kg or propofol at 4 mg/kg (68% and 54% of control, respectively). Propofol at 2 mg/kg (induction dose) and etomidate at 0.6 mg/kg decreased RSNA and MAP only in the baro-denervated animals. It was found from the barosensitivity study that patients can be hemodynamically unstable even though blood pressure has returned to normal after thiopental and propofol administration. Data suggest that etomidate can even stimulate the sympathetic nervous system and increase sympathetic outflow. It was also clearly found from the baro-denervated animal study that thiopental was stronger than propofol in directly suppressing sympathetic outflow at the induction dose.

Anesthetics, Intravenous↗

PubMed1976

Clinical use of etomidate, influence on blood pressure and heart rate. Comparison with thiopentone and methohexital.

This study deals with blood pressure and heart rate measurements during the use of etomidate after premedication; the injection of etomidate is always preceded by 0.10 mg of fentanyl. Etomidate is compared with thiopentone and methohexitone. There appears to be no gross difference between the drugs as far as the blood pressure is concerned: it is decreased by 15-20%. The influence on the heart rate is typical for each drug: whereas thiopentone causes a rise of 23%, and methohexitone of nearly 40%, the rate remains constant in the etomidate series.

Adolescent↗

PubMed2000

[Effect of propofol and etomidate for anesthesia induction on plasma total cortisol concentration].

OBJECTIVE: To investigate the effect of propofol and etomidate for anesthesia induction on adrenocortical function. METHODS: The plasma total cortisol concentration was determined in 20 patients who were treated with propofol or etomidate. RESULTS: After propofol induction, the plasma total cortisol level decreased from (308.7 +/- 27.4) nmol/L to (267.7 +/- 31.2) nmol/L at post-medication 2 hours, increased to (400.2 +/- 26.9) nmol/L at postmedication 5 hours and restored to premedication level at postmedication 24 hours [(306.4 +/- 35.4) nmol/L]. After etomidate induction, the plasma total cortisol level decreased from (309.1 +/- 36.6) nmol/L to (115.9 +/- 29.7) nmol/L at postmedication 2 hours, maintained (171.1 +/- 34.7) nmol/L at postmedication 5 hours and restored to premedication level at postmedication 24 hours [(311.8 +/- 46.2) nmol/L]. CONCLUSIONS: Propofol induction has little effect on adrenocortical function whereas etomidate induction inhibits adrenocortical function.

Adrenal Cortex↗

PubMed1990

[The modification of injection pain and the incidence of thrombophlebitis following etomidate].

A prospective study with 161 patients was performed to investigate the effects of intravenous local anaesthetics on the pain of injection following etomidate injection. After placebo injection 56.6% of the patients reported on pain after etomidate, but only 29% after 20 mg lidocaine i.v. Lidocaine combined with venous congestives significantly reduced the incidence of pain to 3.35%. A dilution of etomidate with water (ratio 1:1) had a lower effect (17.6% incidence of pain). The rate of postoperative thrombophlebitis was lowest in the group with combined lidocaine with venous congestives at 7.4%, in opposition to a rate of 18% in the remaining groups. In comparison to a second contralateral venous cannula without applied etomidate the venous sequelae did not increase significantly.

Adult↗

PubMedDate not supplied

[Anesthesia for cardioversion. A comparison of propofol and etomidate].

Anaesthesia for elective direct current cardioversion (DCC) was induced with propofol (Diprivan) 1.2 mg/kg in 28 patients and with 0.2 mg/kg etomidate (Hypnomidate) in 20 patients. These mostly high risk patients (NYHA class II to III) were successfully treated with defibrillation. Blood pressure and heart rate were recorded before and after induction and at 2 minutes intervals up to 20 minutes after DCC. Both anaesthetic agents caused mild hypotension. Heart rate did not change significantly after induction but fell significantly after DCC from the mean value of 124 +/- 26 bpm and 122 +/- 37 bpm to 94 +/- 19 bpm and to 91 +/- 19 bpm in propofol and etomidate treated patients respectively. Four patients became apnoeic necessitating assisted ventilation for approximately four minutes. All propofol treated patients had rapid recovery times and opened eyes on command within 5.6 +/- 1.9 minutes after induction, and were fully orientated about 4 minutes later also. Complete amnesia was observed in all patients in this group. In contrast etomidate induced anaesthesia did not cause respiratory depression, but the recovery time was longer. Four patients of this group complained of recall of DCC. In 7 patients due to involuntary movements or myoclonus, after induction with etomidate reliable EKG monitoring appeared to be difficult.

Adult↗

PubMedDate not supplied

[Etomidate perfusion in neurosurgery].

In this prospective study, 20 patients undergoing mean duration (2-3 h) neurosurgical operations on fossa cranii posterior, and cervical and dorsolumbar rachis, were induced with 0.3 mg/kg etomidate bolus dose. To maintain anesthesia, etomidate perfusions at 10 micrograms/kg/min (group I) and 20 microg/kg/min (group II) were administered. Fentanyl at fractionated doses was used as analgesic without association to nitrous oxide and relaxation was achieved with pancuronium bromide. Quality of hypnosis, changes in serum concentration of cortisol as well as hemodynamic and electrolyte changes were evaluated. Serum concentrations of cortisol, glucose, sodium and potassium were measured in basal state, and during perioperative and postoperative period. Hemodynamic status was monitored and side effects were recorded. Patients of group I presented signs of deficient hypnosis consisting of marked sympathetic response. When etomidate perfusion ceased, both groups presented serum concentrations of cortisol under the lower normal limit. Six hours after operation, mean serum concentration of cortisol in group 2 patients was significantly lower than in group I patients; in their samples, a dose-dependent recovery was detected. Serum glucose concentration increased during anesthesia and operation and serum electrolyte concentration remained within normal range during perioperative and postoperative periods. Our results demonstrate that a 20 micrograms/kg/min etomidate infusion is adequate to achieve neuroanesthesia when nitrous oxide administration is contraindicated.

Adult↗

PubMed1989

[Hemodynamic effects of etomidate in the child: a study of the dose-effect relation].

In order to determine haemodynamic effects of increasing etomidate dosage, 18 healthy anaesthetized children aged 3 to 8 years were randomly given etomidate as a bolus: 0.125 mg/kg (group I; n = 6), 0.25 mg/kg (group II; n = 6) or 0.5 mg/kg (group III; n = 6). Heart rate (HR), mean arterial pressure (MAP). Doppler aortic flow (DAF) and equivalents for systolic index (SI) and systemic vascular resistances (SVR) variations after etomidate administration were compared. Spearman's rank correlation test shows a significant relationship between increasing etomidate dosage and both decreased SI and increased SVR. This suggests to decrease dosage when reducing SI is unlikely.

Anesthesia, Inhalation↗

PubMed1987

[Changes in expression of lymphocyte surface markers following administration of etomidate, midazolam or methohexital].

Stress alters cellular immunity, affecting lymphocyte function, total lymphocyte count, and the frequency distribution of the lymphocyte subpopulations. Cortisol may mediate these stress-related changes, and drugs affecting cortisol levels might therefore alter lymphocyte patterns. Etomidate and midazolam both prevent the normal perioperative cortisol increase in minor surgery, but the mechanisms by which they do this are not identical: etomidate inhibits steroid synthesis in the adrenal cortex, leading to low cortisol and high ACTH levels, whereas midazolam primarily prevents ACTH increases. Methohexital has little or no influence on cortisol levels. By comparing the effects of these three drugs on the expression of lymphocyte surface markers and the interleukin-2 (Il-2) receptor, we hoped to gain further information on the effects of perioperative cortisol changes on cellular immunity. METHODS. Healthy, young male patients scheduled for routine body surface operations were premedicated with 2 mg flunitrazepam the evening before surgery and 50 mg promethazine and 15 mg piritramide i.m. 1 h before arrival in the operating room. Anaesthesia was induced with 0.2-0.3 mg fentanyl, 2 mg pancuronium, and either etomidate (0.3 mg/kg body wt.), midazolam (0.2 mg/kg body wt.), or methohexital (1.5 mg/kg body wt.). The induction bolus was followed by an infusion at the rate of 0.36 mg/kg/h for etomidate, 0.09 mg/kg/h for midazolam, and no infusion for methohexital. Intubation was facilitated with 100 mg succinylcholine. The patients were ventilated to normocapnia with 66% nitrous oxide in oxygen. Fentanyl was given as 0.1 mg bolus injections whenever necessary.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1985

Serum levels of cortisol in man during etomidate, fentanyl and air anesthesia, compared with neurolept anesthesia.

The effects of etomidate and fentanyl given as a mixture in continuous infusion and of a classical neuroleptanalgesia, with droperidol and fentanyl, on the serum cortisol levels were compared during and after anesthesia in sixteen patients who were to undergo major abdominal surgery. The results showed that the postoperative increase of serum cortisol levels which occurred in the neurolept group was absent in the group receiving etomidate and fentanyl infusion. During etomidate-fentanyl anesthesia there was a more significant decrease of serum cortisol and no rise in serum cortisol levels in response to synthetic ACTH injection. Etomidate and fentanyl, given as a continuous infusion during major abdominal surgery, block the adrenal mechanism to secrete endogenous cortisol in response to stress or after the administration of adreno-corticotrope hormone.

Adrenocorticotropic Hormone↗

PubMed1985

Modulation of a GABA-ergic inhibitory circuit in the in vitro hippocampus by etomidate isomers.

A pulse-paired stimulation technique was used to examine the in vitro effects of the isomers of etomidate on synaptic transmission between Schaffer collaterals and CA1 pyramidal cells in the guinea pig hippocampus. Etomidate produced a dose-related, stereospecific, reversible increase in paired-pulse inhibition. Replacement of Cl- by isethionate reversed the inhibition induced by (+)-etomidate. Together with earlier biochemical evidence, these results show that in the mammalian CNS (+)-etomidate enhances central inhibition by increasing the effectiveness of gamma-aminobutyric acid (GABA) in a chloride-dependent fashion.

Animals↗

PubMed1985

Inhibition of corticosteroidogenesis by etomidate.

The effects of the intravenous anesthetic etomidate have been investigated on ACTH-induced steroidogenesis in vitro, using purified isolated rat adrenal cells. It was found that etomidate almost completely blocked corticosterone production induced by physiological concentrations of ACTH at doses of 200 ng or greater. The mean inhibitory etomidate concentration resulting in 50% inhibition approximated 1.5 X 10(-7)M which is in the range of concentrations measured after clinical doses of etomidate.

Adrenal Cortex↗

PubMed1988

Sedating ventilated asthmatics: etomidate reconsidered.

The use of etomidate and fentanyl infusions to sedate four asthmatics who required artificial ventilation and were receiving high dose steroids is described. The non-asthmatic patients who had not received steroids were also given etomidate combined with either fentanyl or alfentanil by infusion. Use of this sedative technique was suspended in June 1983, following reports of excess mortality associated with the long-term administration of etomidate. Retrospective measurements of plasma cortisols were subnormal in 5 of the 10 patients who did not receive steroids and remained low 12 hours after discontinuation of the infusion in two cases. All the asthmatics survived, but two of the non-asthmatic patients died. Despite its adverse effects, we still feel there may be a place for etomidate infusion in selected asthmatic patients, provided that steroid replacement is given.

Adolescent↗

PubMed1988

Dual effect of etomidate on mineralocorticoid biosynthesis.

The effects of the intravenous anesthetic agent etomidate on adrenal steroidogenesis were studied in 14 pre-menopausal women undergoing abdominal hysterectomy. Anesthesia was induced with either thiopentone (group A) or etomidate (groups B and C) and maintained with nitrous oxide-oxygen 0.5% halothane (groups A and B) or an infusion of etomidate to supplement nitrous oxide-oxygen (group C). Serum concentrations of cortisol, aldosterone and 11-deoxycorticosterone (DOC) were measured pre-induction, at the end of surgery, and at 4, 10 and 24 hours after induction. In group A, concentrations of all three hormones were significantly elevated in response to surgery. In group B, the increases in cortisol and aldosterone were obtunded, but there was a greater increase in DOC at 4 hours after induction. In group C, there were no increases in cortisol or aldosterone up to 4 hours after induction, and the increase in DOC was significantly lower than in group B. These results suggest that etomidate inhibits adrenal steroidogenesis at two separate sites. With low doses of the drug, as used for induction, 11 beta-hydroxylase is inhibited lowering both cortisol and aldosterone secretion. The reduction in aldosterone is, however, offset by a rise in DOC. With higher doses, there is an additional early pathway effect so that the compensatory rise in DOC is reduced.

Adult↗

PubMed1985

Quantitation of the EEG and pharmacodynamic modelling of hypnotic drugs: etomidate as an example.

Six volunteers were subjected to an infusion of etomidate designed to generate linearly increasing plasma concentrations with a slope of 0.05 microgram ml-1 min-1. Cessation of infusion was determined by the occurrence of burst suppression patterns on the EEG. Infusion was restarted when the volunteers recovered personal and temporal orientation. This cycle was repeated twice. The drug input function, the pharmacokinetic parameters of etomidate as derived from a 'least squares' fit, and the median EEG frequency were used to establish a pharmacological model of etomidate. Two modelling procedures, the pharmacokinetic-pharmacodynamic, and the input-output modelling procedure, are compared. These procedures yield different results with respect to the kinetic data. As one possible explanation, a different pharmacokinetic behaviour of etomidate in the venous blood and at the site of drug action is discussed.

Adult↗