Etomidate metabolism is rapidly metabolized by hydrolysis of the ethyl ester side chain to its carboxylic acid ester, resulting in a water-soluble, pharmacologically inactive compound.
Hepatic microsomal enzymes and plasma esterases are responsible for this hydrolysis. Hydrolysis is nearly complete, as evidenced by recovery of < 3% of an administered dose of etomidate metabolism as unchanged drug in urine. Seventy six per cent is bound to plasma protein mainly albumin.
The following is an extract from Miller’s Anesthesia 7th edition about etomidate metabolism –
Etomidate metabolism occurs in the liver primarily by ester hydrolysis to the corresponding carboxylic acid of etomidate (major metabolite) or by N-dealkylation. The main metabolite is inactive. Only 2% of the drug is excreted unchanged, the rest being excreted as metabolites by the kidney (85%) and bile (13%).
Etomidate has been used for induction and maintenance of anesthesia . The induction dose of etomidate is 0.2 to 0.6 mg/kg, and it is reduced by premedication with an opiate, a benzodiazepine, or a barbiturate.
Onset of anesthesia after a routine induction dose of 0.3 mg/kg of etomidate is rapid (one arm–brain circulation) and is equivalent to anesthesia obtained with an induction dose of thiopental or methohexital.
The duration of anesthesia after a single induction dose is linearly related to the dose—each 0.1 mg/kg administered provides about 100 seconds of loss of consciousness. Repeat doses of etomidate by bolus or infusion prolong the duration of hypnosis.
Recovery after multiple doses or an infusion of etomidate is still usually rapid. The addition of small doses of fentanyl with etomidate for short surgical procedures reduces the required dose of etomidate and allows earlier awakening.
In children, induction by rectal administration of etomidate has been obtained with 6.5 mg/kg. Hypnosis occurs in 4 minutes. At this dose, hemodynamics are unaltered, and recovery is still rapid.