15 Sept 2026 · Case #010
Addisonian crisis (acute adrenal insufficiency)
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Diagnosis
Addisonian crisis (acute adrenal insufficiency)
First-line treatment
IV hydrocortisone and fluids
How the diagnosis is reached
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.
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
The case in full
Presenting complaint
Patient history
A 34-year-old man arrives with three days of nausea, vomiting and abdominal pain, and today became confused and profoundly weak. His wife says he has been tired and losing weight for months, and that his skin looks oddly tanned despite little sun.
Physical examination
Physical examination
He is hypotensive and tachycardic, and appears acutely unwell. Skin examination reveals diffuse hyperpigmentation, most pronounced over the knuckles, elbows, and gum line.
| Parameter | Value | Reference |
|---|---|---|
| Blood pressure | 78/50 mmHg | – |
| Heart rate | 122 bpmRef 60–100 | 60–100 |
| Temperature | 38.1 °CRef 36.1–37.5 | 36.1–37.5 |
Basic metabolic panel
Laboratory results
Electrolytes and glucose are checked.
| Parameter | Value | Reference |
|---|---|---|
| Sodium | 126 mEq/LRef 135–145 | 135–145 |
| Potassium | 6.1 mEq/LRef 3.5–5.0 | 3.5–5.0 |
| Glucose | 58 mg/dLRef 70–100 | 70–100 |
Response to fluids
Clinical course
Two litres of intravenous normal saline are given. Mean arterial pressure is recorded every 15 minutes throughout.
Hormone studies
Laboratory results
A random cortisol level and ACTH are drawn.
| Parameter | Value | Reference |
|---|---|---|
| Random cortisol | Markedly lowRef Elevated expected under stress | Elevated expected under stress |
| ACTH | Markedly elevatedRef 7.2–63 pg/mL | 7.2–63 pg/mL |
Clinical course
Clinical course
No infectious source is identified on initial workup, though the acute illness likely served as the precipitant for decompensation in someone with previously undiagnosed chronic adrenal insufficiency.