ETOMIDATE  can be used routinely in all patients as an induction agent                   ( Con - Debate )
Dr Nandita Mehta
Professor   & Head
ASCOMS& Hospital
Jammu – J&K

Etomidate is an intravenous anaesthetic agent commonly used in emergency departments and ICUs for intubation of critically ill patients. First described in 1965, it was originally developed as an imidazole anti-fungal agent . During animal testing, it was noticed to produce sedation and was introduced as a hypnotic into clinical practice in 1972. The pharmacodynamics of etomidate is well understood and studied. Unrelated to its hypnotic effect, etomidate strongly stimulates central α2 adrenergic receptors with characteristic lack of vasodilatation or myocardial depression, leading to little change in the heart rate or blood pressure after an induction dose of etomidate.
Though etomidate has many attractive characteristics and has been used for nearly 40 years in clinical practice, and significantly in the critically ill. It has a very high therapeutic index of safety as a hypnotic agent, the lethal dose being up to 12 times the hypnotic dose, providing a good safety profile among all the other available induction agents. Etomidate has very few cardiovascular effects and it has a favourable kinetic profile, producing rapid onset loss of consciousness within one arm brain circulation of injection with a rapid offset due to both redistribution and metabolism.
Despite being a wonderful agent , etomidate is still not popular, neither as an induction agent nor for prolonged  sedation in critically ill ICU patients.The drug is still not recommended for routine use for  various reasons given below

• Etomidate is not available around the world and is generally not the first line induction agent for elective surgical cases; this reduces exposure and familiarity with the drug amongst junior and senior doctors.
• Etomidate is a hydrophobic compound associated with pain on injection. Reported incidence of pain is 1.2% to 42%, which is worse with etomidate in aqueous solutions in comparison to the formulation in 35% propylene glycol. Formulation into medium chain-length lipids or cyclodextrins appears to further decrease the incidence of injection pain.
• Some reports suggest that propylene glycol, carrier for etomidate, can be associated with a small degree of hemolysis. Additionally, high-dose prolonged infusion has been reported to result in propylene glycol toxicity (a hyperosmolar state).
• The main concern, however, has been the inhibition of steroid synthesis produced by etomidate.  Etomidate is a very potent inhibitor of steroid synthesis, acting on the adrenal gland as an inhibitor of 11beta-hydroxylase, a mitochondrial enzyme that converts 11-deoxycortisol to cortisol and 11-deoxycorticosterone to corticosterone. The dosage of etomidate for intravenous induction is 0.2 to 0.3 mg/kg, and whilst the etomidate blood concentration required for hypnosis is 200 ng/ml, a blood concentration of only 10 ng/ml can significantly reduce plasma concentrations of cortisol, cortisone and aldosterone. Indeed, low dose infusion of etomidate has been used in the treatment of Cushing's disease to suppress steroid genesis. Although this effect is reversible, the duration of adrenal suppression after a bolus dose of etomidate remains for several hours after the hypnotic effect has worn off and much longer after prolonged infusion and in the critically ill.  Concerns are shown, whether a single bolus dose of etomidate is associated with adrenal suppression and can cause harm in critically ill patients , particularly patients with sepsis, where there is much controversy surrounding the need for an adequate steroid response. Enzyme inhibition lasts 4 to 8 hours after an intravenous induction dose of etomidate. Conceivably, patients experiencing sepsis or hemorrhage, and who might require an intact cortisol response, would be at a disadvantage should etomidate be administered.
• Etomidate has been associated with grand mal seizures and produces increased EEG activity in epileptogenic foci. This feature has proved useful for intraoperative mapping of seizure foci before surgical ablation.
• Etomidate is associated with a frequent incidence of myoclonic movement and trismus. Myoclonus is not thought to be associated with seizure-like EEG activity. The myoclonic movement is believed to result from activity either in the brainstem or in deep cerebral structures.                                                                                
• Etomidate does not inhibit sympathetic tone or myocardial function, and at typical anaesthetic induction doses produces minimal blood pressure and heart rate changes in patients, including those with valvular or ischemic heart disease. For the same reason, etomidate does not block sympathetic responses to laryngoscopy and intubation, and these are often blunted by premedication with opioids.
• Post-operative nausea and vomiting incidence after induction with etomidate is around 40%, comparable to that following barbiturate, and higher than that following propofol. More recently, the incidence of nausea after induction with etomidate in lipid emulsion was reported to be similar to that associated with propofol, while the incidence of vomiting was higher with etomidate.
• Etomidate enhances the neuromuscular blockade of nondepolarizing neuromuscular blockers.

• High cost: in a 50 kg patient induction dose of etomidate costs Rs350/-, whereas in same patient propofol induction will cost between Rs120-150/-  (different brands).

• Hiccups or coughing may accompany etomidate induction.