Etomidate

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• Even a SINGLE induction dose of etomidate inhibits adrenal 11-beta-hydroxylase and the cholesterol side-chain cleavage enzyme, suppressing cortisol and aldosterone synthesis for 8 to 24 hours. In septic shock this adrenal suppression is clinically significant and may increase mortality — this is the central controversy. If etomidate is used for a septic patient, consider a stress-dose corticosteroid, and prefer ketamine where the adrenal axis is already compromised.
• Myoclonus on induction is common and can be violent — involuntary movements that can fracture a tooth, dislodge a line, or be mistaken for seizures. Reduce it with opioid or benzodiazepine pretreatment, or by giving the dose slowly. It is NOT a seizure, but in the epilepsy-monitoring setting it must be distinguished from the target epileptiform activity.
• Pain on injection and venous irritation are caused by the propylene glycol vehicle (35 percent), not the drug itself. In a small dorsal hand vein the pain can be severe and precipitate withdrawal. Use a large antecubital vein, give an opioid or lidocaine pretreatment, or use the lipid emulsion formulation (Etomidate-Lipuro), which largely abolishes the pain.
• Etomidate produces epileptiform EEG activity and can ACTIVATE a seizure focus — useful for epilepsy surgery (mapping the focus) but a hazard in the patient with a known seizure disorder who is NOT being operated on for that focus. Distinguish this from myoclonus, which is subcortical and not a seizure.
• Nausea and vomiting are more frequent than with propofol — give an antiemetic, particularly in the day-surgery or PONV-prone patient.
• Although haemodynamically neutral in the majority, etomidate can still cause apnoea and airway loss after an induction dose, especially with an opioid. Equipment for airway control and ventilation must always be immediately available; haemodynamic stability is not a licence for an unprepared airway.