Diagnosis
Addisonian crisis (acute adrenal insufficiency)
Key clinical clues
- Chronic fatigue and weight loss with skin hyperpigmentation
- Hyponatremia, hyperkalemia, and hypoglycemia together
- Hypotension refractory to IV fluids alone
- Markedly low cortisol with elevated ACTH confirming primary adrenal insufficiency
- Hydrocortisone should not be delayed for confirmatory labs when crisis is suspected
First-line treatment
IV hydrocortisone and fluids
The hyperpigmentation is the clue that localises the lesion to the adrenal gland itself. ACTH is cleaved from the same precursor as melanocyte-stimulating hormone, so when a failing adrenal removes cortisol's negative feedback, ACTH climbs and the skin darkens with it. That cannot happen when the pituitary is the problem, which is how primary adrenal insufficiency separates itself from secondary at the bedside. The electrolytes then show both hormones are missing rather than one: hyponatraemia with hyperkalaemia is mineralocorticoid failure, since aldosterone normally trades potassium for sodium, while the hypoglycaemia is glucocorticoid failure. The finding that makes this a crisis is hypotension that does not respond to fluid alone. Cortisol is permissive for catecholamines, so without it the vessels cannot answer either her own adrenaline or anything given through a drip, and volume by itself will not fix a vasculature that has stopped listening. Treatment is intravenous hydrocortisone, 100 mg as a bolus and repeated, alongside saline and dextrose for the glucose. The rule worth carrying is one of sequence: draw the cortisol and ACTH, then treat immediately, because waiting for confirmation is how these patients die. At stress dose hydrocortisone has enough mineralocorticoid activity of its own that fludrocortisone is unnecessary acutely, and whatever illness precipitated the crisis is treated alongside.