PharmacologyTier 1Medical Sciences concept

Stress-dose corticosteroid adjustment in adrenal insufficiency

Core concept

Patients on chronic glucocorticoid therapy or with established adrenal insufficiency cannot mount a normal cortisol stress response -- physiological/surgical/infective stress requires exogenous dose escalation to prevent adrenal (Addisonian) crisis
Normal physiology: cortisol rises several-fold during illness/surgery via HPA axis activation -- suppressed/absent in adrenal insufficiency or HPA suppression from exogenous steroids
Applies to primary AI (Addison's), secondary/tertiary AI (pituitary/hypothalamic disease or steroid-induced HPA suppression)

Dose adjustment scales with stress severity: minor illness (e.g. mild infection, dental work) -> double usual oral dose; moderate (e.g. moderate surgery, significant infection with fever) -> higher dose +/- IV hydrocortisone; major (major surgery, critical illness, trauma) -> IV hydrocortisone (e.g. 50-100mg) then continuous infusion or divided dosing, tapering back to maintenance as stress resolves
HPA suppression from exogenous steroids can persist for up to a year after stopping long-term/high-dose therapy -- risk continues even after the steroid itself has been withdrawn
Any dose/duration threshold for "significant suppression risk" is a rule of thumb, not absolute -- individual risk assessment (dose, duration, timing of last dose) matters more than a fixed cut-off

Trap: assuming a patient who stopped long-term steroids "a few months ago" no longer needs stress dosing -- HPA recovery is unpredictable and can take up to 12 months
Missed stress dosing -> Addisonian crisis: hypotension refractory to fluids, hyponatraemia, hyperkalaemia (primary AI only), hypoglycaemia, abdominal pain, collapse -- treat empirically with IV hydrocortisone if suspected, do not wait for confirmatory cortisol
Perioperative teams must be alerted to any history of chronic steroid use (even inhaled/topical at high doses can occasionally suppress the axis) before elective surgery

Same HPA suppression principle underlies why abrupt steroid withdrawal (rather than tapering) after prolonged therapy risks adrenal crisis independent of acute stress
Distinguishes primary AI (mineralocorticoid deficiency too -> hyperkalaemia, hyponatraemia, hypotension) from secondary/steroid-induced AI (mineralocorticoid axis intact via RAAS, so hyperkalaemia typically absent)
Relates to synACTHen (short Synacthen) testing used to assess HPA axis recovery before considering steroid weaning off stress-dose cover

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