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Etomidate-associated adrenal insufficiency — SCE Acute Medicine MCQ

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EasyAcute Renal and Metabolic EmergenciesEtomidate-associated adrenal insufficiencySCE Acute Medicine

A 29-year-old woman presents with vomiting, weakness, confusion or collapse. Relevant history includes diabetes, kidney disease, endocrine disease or a treatment trigger. On assessment, volume status and bedside physiology are abnormal. Investigations show refractory shock with low cortisol after etomidate exposure. What is the most likely underlying cause/mechanism?

Educational content. Not a substitute for clinical judgement or local policy.

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Correct answer: A — Adrenal steroid synthesis inhibition

The key discriminator is that refractory shock with low cortisol after etomidate exposure, which makes Adrenal steroid synthesis inhibition the single best answer. Defective neuromuscular transmission is less appropriate because it does not address the dominant acute risk in the vignette; Immune-mediated small-vessel vasculitis would fit a different presentation or later stage of care. Impaired free-water excretion from ADH activity and Sodium-channel blockade are suboptimal because they would either delay time-critical treatment or follow the wrong acute pathway. Teaching point: SCE-style acute medicine questions usually test prioritisation using physiology, timing and a guideline-defined threshold, rather than isolated factual recall.

Reference: Society for Endocrinology adrenal guidance; BNF