|Systematic (IUPAC) name|
|Biological half-life||75 min|
|Excretion||Renal (85%) and biliary (15%)|
|ATC code||N01AX07 (WHO)|
|Molar mass||244.289 g/mol[[Script error: No such module "String".]]|
|Boiling point||392 °C (738 °F)|
Etomidate is a short acting intravenous anaesthetic agent used for the induction of general anaesthesia and for sedation for short procedures such as reduction of dislocated joints and cardioversion. It was discovered at Janssen Pharmaceutica in 1964.
Etomidate is commonly used in the emergency setting as part of a rapid sequence induction to induce anesthesia or for conscious sedation. It is often used in this setting since it has a rapid onset of action and a low cardiovascular risk profile, and therefore is less likely to cause a significant drop in blood pressure than other induction agents.
At the typical dose, anesthesia is induced for about 5–10 minutes even though the half-life of drug metabolism is approximately 75 minutes. This is because etomidate is redistributed from the plasma to other tissues.
The anaesthetic induction dose for adult humans is 0.3 mg/kg intravenously, with a typical dose ranging from 20-40 mg. In common with all induction agents, etomidate causes loss of consciousness after one arm-brain circulation time. In very brief procedures such as cardioversion, a 10 mg dose may be used which may be repeated for effect.
DOSING: ADULTS — Anesthesia: I.V.: Initial: 0.2-0.6 mg/kg over 30-60 seconds for induction of anesthesia; maintenance: 5-20 mcg/kg/minute
Etomidate is highly protein bound in blood plasma and is metabolised by hepatic and plasma esterases to inactive products. It exhibits a bi-exponential decline, with a redistribution half-life of 2–5 minutes and an elimination half-life of 68–75 minutes.
The use of etomidate infusions for sedation of critically ill patients in intensive care units has been associated with increased mortality, which is due to suppression of steroid synthesis (both glucocorticoids and mineralocorticoids) in the adrenal cortex, which sometimes leads to death due to an adrenal crisis; Thus, etomidate contributes to critical illness–related corticosteroid insufficiency. This effect has been demonstrated after a single dose, and lasts about 24 hours. In addition, concurrent use of etomidate with opioids and/or benzodiazepines , which independently and characteristically lower cortisol levels, significantly exacerbates this side effect.  This is especially significant because many patients who are given etomidate are already on some form of narcotic pain reliever. Also, benzodiazepines like diazepam and lorazepam are used extensively - both in emergency medicine and in the treatment of psychiatric illnesses and seizure disorders. There is no evidence that a single induction dose of etomidate has any effect on morbidity or mortality. However, some sources advise giving a prophylactic dose of steroids (e.g. hydrocortisone) if etomidate is used.
Seizure-like activity is occasionally seen with anesthetic induction. In the absence of concurrent EEG monitoring, it is difficult to ascribe this to cortical activity. Myoclonic movement originating at the spinal cord level is often a likely mechanism. Excitatory phenomena, and epileptiform movements and EEG activity may be observed during induction. Etomidate consistently increases the amplitude of somatosensory evoked potentials (in contrast to most anaesthetic agents).
Etomidate in the propylene glycol formulation may produce pain on injection, a side effect which is less likely with the lipid formulation.
Post operative vomiting is more common than with other induction agents.
Etomidate is usually presented as a clear colourless solution for injection containing 2 mg/ml of etomidate in an aqueous solution of 35% propylene glycol, although a lipid emulsion preparation (of equivalent strength) has also been introduced. Etomidate is presented as a racemic mixture, but only the D-isomer has pharmacological activity.
- Onset of action: 30-60 seconds
- Peak effect: 1 minute
- Duration: 3-5 minutes; terminated by redistribution
- Distribution: Vd: 2-4.5 L/kg
- Protein binding: 76%
- Metabolism: Hepatic and plasma esterases
- Half-life elimination: Terminal: 2.6 hours
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Cotton, B. A., O. D. Guillamondegui, S. B. Fleming, R. O. Carpenter, S. H. Patel, J. A. Morris, Jr. and P. G. Arbogast (2008). "Increased risk of adrenal insufficiency following etomidate exposure in critically injured patients." Arch Surg 143(1): 62-7; discussion 67.
den Brinker, M., A. C. Hokken-Koelega, J. A. Hazelzet, F. H. de Jong, W. C. Hop and K. F. Joosten (2008). "One single dose of etomidate negatively influences adrenocortical performance for at least 24h in children with meningococcal sepsis." Intensive Care Med 34(1): 163-8.
Hildreth, A. N., V. A. Mejia, R. A. Maxwell, P. W. Smith, B. W. Dart and D. E. Barker (2008). "Adrenal suppression following a single dose of etomidate for rapid sequence induction: a prospective randomized study." J Trauma 65(3): 573-9.
Marik, P. E., S. M. Pastores, D. Annane, G. U. Meduri, C. L. Sprung, W. Arlt, D. Keh, J. Briegel, A. Beishuizen, I. Dimopoulou, S. Tsagarakis, M. Singer, G. P. Chrousos, G. Zaloga, F. Bokhari and M. Vogeser (2008). "Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: consensus statements from an international task force by the American College of Critical Care Medicine." Crit Care Med 36(6): 1937-49.
Mullins, M. E. and D. L. Theodoro (2008). "Lack of evidence for adrenal insufficiency after single-dose etomidate." Arch Surg 143(8): 808-9; author reply 809.
Sacchetti, A. (2008). "Etomidate: not worth the risk in septic patients." Ann Emerg Med 52(1): 14-6.
Sprung, C. L., D. Annane, D. Keh, R. Moreno, M. Singer, K. Freivogel, Y. G. Weiss, J. Benbenishty, A. Kalenka, H. Forst, P. F. Laterre, K. Reinhart, B. H. Cuthbertson, D. Payen and J. Briegel (2008). "Hydrocortisone therapy for patients with septic shock." N Engl J Med 358(2): 111-24.
Tekwani, K., H. Watts, C. Chan, K. Rzechula, S. Nanini and E. Kulstad (2008). "The effect of single-bolus etomidate on septic patient mortality: a retrospective review." West J of Emerg Med 9(4): 195-200.
Tekwani, K. L., H. F. Watts, K. H. Rzechula, R. T. Sweis and E. B. Kulstad (2009). "A prospective observational study of the effect of etomidate on septic patient mortality and length of stay." Acad Emerg Med 16(1): 11-4.
Vinclair, M., C. Broux, P. Faure, J. Brun, C. Genty, C. Jacquot, O. Chabre and J. F. Payen (2008). "Duration of adrenal inhibition following a single dose of etomidate in critically ill patients." Intensive Care Med 34(4): 714-9.
Walls, R. M. and M. F. Murphy (2008). "Clinical controversies: etomidate as an induction agent for endotracheal intubation in patients with sepsis: continue to use etomidate for intubation of patients with septic shock." Ann Emerg Med 52(1): 13-4.de:Etomidat ru:Этомидат
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- Vanlersberghe C, Camu F. Etomidate and other non-barbiturates. Handbook of Experimental Pharmacology. 2008;(182):267-82. PMID 18175096
- Drexler B, Jurd R, Rudolph U, Antkowiak B. Distinct actions of etomidate and propofol at beta3-containing gamma-aminobutyric acid type A receptors. Neuropharmacology. 2009 Sep;57(4):446-55. PMID 19555700
- "Opioid and benzodiazepine contributions to etomidate-associated adrenal insufficiency". Springer Berlin / Heidelberg, Intensive Care Medicine Volume 34, Number 11 / November, 2008, p. 2117-8. Retrieved December 28, 2009.