Etomidate

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• Etomidate potently inhibits adrenal 11-beta-hydroxylase, suppressing cortisol and aldosterone while raising 11-deoxycorticosterone (single-case LC-MS/MS exact; duration specifics standard teaching). In septic shock this is the central controversy — mortality similar to ketamine in pooled RCTs, with less collapse but more adrenal suppression. If etomidate is used for a septic patient, follow local protocol on stress-dose corticosteroid, and prefer ketamine where the adrenal axis is already compromised.
• Myoclonus on induction is common — in one gastroscopy trial 58 percent saline versus 28/16 percent with oliceridine pretreatment. It can dislodge a line or be mistaken for seizure activity; distinguish clinically and reduce with opioid pretreatment per protocol.
• Pain on injection and venous irritation are caused by the vehicle, not the drug itself, worse in a small dorsal hand vein. Use a large vein or the lipid emulsion formulation (Etomidate-Lipuro) per formulary; percentage specifics standard teaching.
• EEG burst suppression occurred in 29.34 percent with etomidate versus none with remimazolam in one retrospective induction comparison (limited by ASA imbalance); seizure-focus mapping specifics are not quantified there — distinguish myoclonus from epileptic activity clinically.
• Nausea and vomiting are more frequent than with propofol — give an antiemetic per protocol, particularly in the day-surgery or PONV-prone patient.
• Although haemodynamically neutral in trials, 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.