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Endocrine

Addison’s Disease & Adrenal Crisis

Verified · Sep 2026

Addison’s disease is acquired primary adrenal insufficiency: destruction of the bilateral adrenal cortex — most often autoimmune — causing loss of cortisol, aldosterone, and adrenal androgens, with adrenal crisis as its life-threatening acute presentation.

The disorder behind bronze skin, salt craving, the low-sodium-high-potassium pattern, sick-day dosing, the emergency hydrocortisone injection — and the shock that does not answer to fluids or pressors until a steroid is given.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 Three levels of failure — and only one loses aldosterone

Adrenal insufficiency is named for where the axis breaks, and the level decides the entire clinical picture. Primary insufficiency is adrenal-cortex pathology itself, producing "glucocorticoid and mineralocorticoid deficiency" — this is Addison’s disease, in which autoimmune destruction of the bilateral cortex costs the patient cortisol, aldosterone, and adrenal androgens together. Secondary insufficiency is reduced pituitary ACTH, and tertiary is reduced hypothalamic CRH — most commonly from chronic exogenous steroid. Both of these typically have "preserved mineralocorticoid function," because "Mineralocorticoid levels are regulated by the renin-angiotensin system that is independent of hypothalamic or pituitary signals."

That one sentence generates the highest-yield rule on the page: only primary adrenal insufficiency causes mineralocorticoid/aldosterone loss. So patients with secondary insufficiency "are more likely to have hypoglycemia but will not have dehydration, hyperkalemia, or skin hyperpigmentation." Hyperkalemia and hyperpigmentation are the two findings that tell you the lesion is in the adrenal gland itself — and, just as importantly, their absence does not rule out adrenal insufficiency in a patient who has been taking steroids.

Addison’s disease is uncommon — incidence about 0.6 per 100,000 annually, prevalence 4 to 11 per 100,000 — presenting between ages 30 and 50 and more often in women. The danger is not its rarity but its tempo: it "usually manifests as an insidious and gradual onset of nonspecific symptoms, often resulting in a delayed diagnosis," with declining health over weeks or months. The consequence is stark. About 50% of patients with Addison’s disease are first diagnosed during an acute crisis — the disease announces itself by nearly killing the patient.

The three levels of adrenal insufficiency. Only primary disease destroys the cortex itself and therefore loses aldosterone — which is why hyperkalemia and hyperpigmentation localize the lesion to the adrenal gland.

02 What cortisol loss does — and what aldosterone loss does

The two hormones fail in different directions, and knowing which does what is how a nurse reads the labs. Aldosterone deficiency causes sodium wasting and potassium retention. Sodium leaves in the urine and drags water with it, so intravascular volume falls, producing hyponatremia, hyperkalemia, metabolic acidosis, orthostatic hypotension and salt craving. Volume depletion also raises ADH activity, which deepens the hyponatremia further.

Cortisol deficiency is more insidious and, in the acute setting, more lethal. Cortisol normally permits catecholamines to work: "without glucocorticoids, catecholamines cannot exert their full impact" on adrenergic receptors. That is the single most important sentence in adrenal crisis — it explains profound shock that does not respond to fluids or vasopressors until glucocorticoid is given. Pushing more norepinephrine into a patient with no cortisol is pushing on a disconnected lever. Cortisol also restrains cytokine release; without it, uncontrolled inflammation brings vasodilation and capillary leak, adding a distributive component to the hypovolemia. And cortisol drives gluconeogenesis and glycogenolysis, so its absence produces hypoglycemia — "more prevalent in children," where it may be the presenting sign.

One further mechanism explains the anorexia that runs through every account of this disease: with cortisol feedback gone, uninhibited CRH release suppresses appetite. Put the whole picture together and the chronic patient is a slowly dehydrating, salt-hungry, weight-losing, exhausted person whose blood pressure falls when they stand — and the acute patient is in shock that the usual resuscitation does not fix.

The two deficiencies converge on shock by different routes — and the reason a pressor alone fails is that catecholamines cannot act on adrenergic receptors without cortisol.

03 Why the skin darkens — and why sometimes it does not

In autoimmune Addison’s disease, antibodies form against the adrenal steroidogenic enzyme 21-hydroxylase in approximately 90% of patients, and cell-mediated mechanisms contribute alongside them; the HLA haplotypes DR3-DQ2 and DR4-DQ8 confer risk. The cortex is destroyed progressively — cortisol falls first, aldosterone later — which is part of why the presentation creeps.

The hyperpigmentation follows directly from that destruction. Losing cortisol removes the negative feedback on the pituitary, producing "elevation of adrenocorticotropic (ACTH) and melanocyte-stimulating hormone (MSH) hormones due to the loss of negative feedback inhibition." ACTH and MSH rise together and bind melanocyte receptors, darkening skin and mucosa. It is "generalized and most prominent in sun-exposed and pressure areas," and the specific sites are worth memorizing because they are where a nurse can actually see it: palmar creases, gingival mucosa, lips (particularly the vermilion border), elbows, knuckles, posterior neck, breast areolae, nipples, and nail beds. It occurs in almost all patients with Addison’s disease.

Now the mirror image, and the trap that the scenario on this page is built around. In secondary and tertiary insufficiency, ACTH is low — so there is no hyperpigmentation at all. The patient who develops adrenal insufficiency by stopping chronic prednisone has the opposite appearance: they may still look Cushingoid, with facial fullness, a dorsocervical fat pad, and truncal obesity. A nurse waiting for bronze skin before taking adrenal insufficiency seriously will miss the most common version of this disease.

04 Adrenal crisis — the emergency that will not wait for a lab result

Adrenal crisis is "a severe, life-threatening endocrine emergency resulting from acute adrenal insufficiency," and it has a definition a nurse can apply at the bedside: either absolute hypotension (systolic BP below 100 mm Hg) or relative hypotension (a drop of 20 mm Hg or more from the patient’s baseline), with improvement within 1 to 2 hours of parenteral glucocorticoid. Note what that means practically — the response to treatment is part of the definition, so treatment is also the diagnostic manoeuvre.

The trajectory is fast and the early signs are worthless in isolation. The prodrome is "weakness, fatigue, nausea, vomiting, fever, lower chest or abdominal pain, anorexia, back pain, dizziness, somnolence, and confusion," with salt cravings among the less frequent presentations — and the abdominal presentation can be convincing enough to be described as "an acute abdomen resembling a surgical emergency". Untreated, it advances to hypotension, altered mental status and obtundation, then fever that can reach 40.5 °C (105 °F) or higher, then circulatory collapse, cyanosis, shock, coma, and death. And the blood pressure gives less warning than anyone expects: as many as half of patients develop shock with no preceding hypotension, so a normal reading an hour ago is not reassurance.

That tempo produces the rule that governs everything else. "The treatment of adrenal crises should never be delayed to obtain blood work to determine the underlying etiology. Prompt administration of hydrocortisone is of the utmost importance." ACTH stimulation testing is not done acutely — only after stabilization. Draw the cortisol and ACTH as you treat, not before. Where the diagnosis is genuinely unestablished, dexamethasone 4 mg IV is the test-friendly choice because it does not interfere with cortisol assays — but the priority is never in doubt: in an Addisonian crisis, delayed treatment can be fatal.

The crisis pathway. Because up to half of patients develop shock with no preceding hypotension, and because response to glucocorticoid is part of the definition, treatment precedes confirmation. Doses are from the 2016 Endocrine Society guideline and the 2024 ESE/Endocrine Society joint guideline.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Autoimmune adrenalitis — the most common cause; antibodies against the adrenal cortex, particularly 21-hydroxylase (present in about 90%) Infection — tuberculosis (adrenal enlargement with caseating granulomas), HIV, cytomegalovirus, sepsis, disseminated fungal infection, syphilis Adrenal hemorrhage — DIC, trauma, anticoagulation, bleeding disorders, and meningococcemia (Waterhouse-Friderichsen syndrome) Infiltration — hemochromatosis, amyloidosis, metastases, sarcoidosis, lymphoma Abrupt withdrawal of chronic exogenous glucocorticoid — causes tertiary insufficiency and is an explicitly listed cause of adrenal crisis; the version encountered most often in practice modifiable Nonadherence to glucocorticoid replacement therapy modifiable Drugs that block adrenal steroidogenesis — ketoconazole, etomidate (11β-hydroxylase), fluconazole, metyrapone, mitotane modifiable Immune checkpoint inhibitors and tyrosine-kinase inhibitors modifiable Drugs that accelerate cortisol clearance — phenytoin and rifampin; rifampin specifically requires a higher replacement dose modifiable Starting levothyroxine in undiagnosed adrenal insufficiency — thyroid hormone raises cortisol clearance and can precipitate crisis modifiable Secondary causes — pituitary hemorrhage or infarction, including Sheehan syndrome Autoimmune polyglandular syndromes — type 1 (hypoparathyroidism, Addison’s, mucocutaneous candidiasis) and type 2 (autoimmune thyroiditis, type 1 diabetes, pernicious anemia, vitiligo) Age 30–50 at presentation, more common in women; up to 50% develop a second autoimmune condition

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Fatigue, generalized weakness, weight loss and reduced appetite early Expected
Why: Cortisol deficiency, compounded by uninhibited CRH suppressing appetite. These are the earliest and least specific findings, present for weeks to months — which is precisely why the diagnosis is missed until a crisis forces it.
Hyperpigmentation — the hallmark, and only in primary disease Expected
Why: Loss of cortisol feedback raises ACTH and MSH together, and they bind melanocyte receptors. Generalized but most prominent in sun-exposed and pressure areas: palmar creases, gingival mucosa, lips and vermilion border, elbows, knuckles, posterior neck, breast areolae, nipples, nail beds. Present in almost all patients with Addison’s disease — and absent in secondary and tertiary disease.
Salt craving Expected
Why: Aldosterone deficiency wastes sodium in the urine, and the craving is the body asking for it back. A classic and highly suggestive history item that patients rarely volunteer unless asked directly.
Orthostatic hypotension and dizziness on standing Hold & notify
Why: Sodium wasting drags water with it, depleting intravascular volume. This is both a fall risk now and a warning of impending crisis — the blood pressure is already operating without its mineralocorticoid support.
Nausea, vomiting, abdominal pain, chronic diarrhea and anorexia Hold & notify
Why: Cortisol deficiency and volume depletion; in crisis the abdominal findings can produce an acute abdomen appearance. Vomiting is doubly dangerous — it signals impending crisis and simultaneously blocks absorption of the oral steroid that would prevent it.
Hypoglycemia Hold & notify
Why: Without cortisol there is no gluconeogenesis or glycogenolysis to defend the glucose. It is more prevalent in children, where unexplained hypoglycemia and seizures may be the presenting sign.
Poor skin turgor with increased pigmentation Expected
Why: The visible sign of a chronic, ongoing volume deficit from sodium wasting — the dehydration is not an acute event but a baseline state.
Decreased axillary and pubic hair in women; vitiligo Expected
Why: The adrenal cortex also makes androgens, and in women adrenal androgens are the main source — so their loss thins axillary and pubic hair. Vitiligo reflects the associated autoimmunity rather than the hormone loss.
Amenorrhea and loss of libido in women Expected
Why: Adrenal androgen deficiency plus the systemic effects of chronic cortisol deficiency. Premature ovarian failure also occurs in up to 10% of women with Addison’s disease.
Crisis prodrome — weakness, nausea, vomiting, fever, abdominal, chest or back pain, dizziness, somnolence, confusion, salt craving Hold & notify
Why: The acute decompensation announcing itself in entirely nonspecific language. Recognizing this stage is the whole game — everything downstream is harder and more dangerous to treat.
Hypotension, altered mental status and obtundation — the cardinal crisis progression late Report immediately
Why: Cortisol deficiency prevents catecholamines from acting on adrenergic receptors while volume depletion and capillary leak strip the circulation. Untreated it advances to fever reaching 40.5 °C (105 °F) or higher, then circulatory collapse, cyanosis, shock, coma and death.
Shock arriving with no preceding hypotension late Report immediately
Why: As many as half of patients develop shock with no preceding hypotension — a previously normal blood pressure is not reassurance and must never be used to downgrade concern in a patient with a compatible story.
Peaked T waves on the ECG Report immediately
Why: Hyperkalemia from aldosterone deficiency — so this finding appears in primary disease. The progression by level: peaked T waves at 5.5–6.5 mEq/L, flattening or loss of P waves at 6.5–7.5, QRS widening at 7–8, severe arrhythmias and a sine-wave pattern at 8–10. Generalized muscle weakness and flaccid paralysis typically appear above 6.0 mEq/L.
A Cushingoid appearance instead of hyperpigmentation — facial fullness, dorsocervical fat pad, truncal obesity
Why: The anti-cue. A patient in crisis from chronic steroid use has low ACTH, so no bronzing, and may still carry the appearance the steroid produced. Waiting for bronze skin before suspecting adrenal insufficiency will miss the most common presentation of all.

Diagnostics

Test In this disorder Normal
Standard-dose cosyntropin (ACTH) stimulation test Dose is 250 µg IV. Cutoffs are assay dependent. Not performed acutely — only after stabilization, because treatment cannot wait for it The confirmatory test: peak cortisol below 500 nmol/L (18 µg/dL) at 30 or 60 minutes indicates adrenal insufficiency Endocrine Society 2016 guideline (rec 2.1) Peak cortisol above 18 µg/dL is a normal response
Early-morning serum cortisol A value of 18 µg/dL or above effectively excludes it; intermediate values are equivocal and require the stimulation test. In crisis this is drawn as treatment is given, not before it The screening test: a low early-morning cortisol together with a high ACTH is suggestive of adrenal insufficiency Addison Disease — StatPearls —
Plasma ACTH In central (secondary or tertiary) disease the ACTH is inappropriately normal or low. This single value is what separates Addison’s disease from steroid-withdrawal insufficiency, and it is the same physiology that explains the hyperpigmentation Markedly elevated in primary adrenal insufficiency — the adrenal is failing and the pituitary is shouting at it Addison Disease — StatPearls —
Plasma renin and aldosterone (measured simultaneously) Measured specifically to determine whether mineralocorticoid deficiency is present, which decides whether the patient needs fludrocortisone in addition to glucocorticoid. Plasma renin is also the marker used to titrate that dose long-term In Addison’s disease: low aldosterone with elevated plasma renin activity — the mineralocorticoid axis is calling for a hormone the cortex cannot make Endocrine Society 2016 guideline (rec 2.5) —
Electrolytes, glucose and renal function The hyperkalemia does not occur in secondary disease, so its presence points to a primary cause. Hyponatremia grading for context: mild 130–135, moderate 125–130, severe below 125 mEq/L, at which somnolence, confusion, seizures and cardiorespiratory collapse appear. Hyperkalemia is generally above 5.0–5.5 mEq/L The pattern to recognize: hyponatremia + hyperkalemia + hypoglycemia; hypercalcemia may occur, and creatinine may be raised from prerenal failure —
Complete blood count An unexplained eosinophilia in a chronically unwell, weight-losing patient is a quiet pointer toward adrenal insufficiency. TSH may also be slightly elevated — but treat the adrenal insufficiency first, because starting levothyroxine raises cortisol clearance and can precipitate crisis Neutropenia, lymphocytosis and eosinophilia; normocytic normochromic anemia is also described —
Etiology work-up Additional studies as indicated: PPD for tuberculosis; adrenal CT or MRI for hemorrhage, calcification, infiltration, or the small glands of autoimmune disease; chest radiograph; and pituitary MRI if ACTH is inappropriately low Validated 21-hydroxylase antibody assay for autoimmune disease; very-long-chain fatty acids when adrenoleukodystrophy is suspected Endocrine Society 2016 guideline (rec 2.6, ungraded) —

Complications

Warning: Adrenal crisis — the complication that defines the disease Report immediately
Systolic BP below 100 mm Hg or a fall of 20 mm Hg or more from baseline, progressing to altered mental status, obtundation, high fever, circulatory collapse, coma and death. Untreated, it is fatal.
Crises occur in 6–8% of patients with adrenal insufficiency annually (4–6 per 100 patient-years), with a mortality of 0.5 per 100 patient-years — and a 6% mortality rate even among well-educated patients, which is the honest reason teaching reduces but does not eliminate the risk. The heralding cue is the nonspecific prodrome, especially vomiting or diarrhea that stops oral steroid absorption, plus any drop in blood pressure. Recovery is not clean either: survivors report depression, chronic fatigue, inability to work and poor quality of life.
Warning: Electrolyte emergencies — hyperkalemic arrhythmia and severe hyponatremia Report immediately
Uncorrected electrolyte abnormalities cause seizures, arrhythmias and coma. Any hyperkalemic ECG change, or a sodium below 125 mEq/L, is an emergency in its own right.
Hyperkalemia progresses on the ECG from peaked T waves (5.5–6.5 mEq/L) through loss of P waves (6.5–7.5) and QRS widening (7–8) to a sine-wave pattern (8–10). The sequence when ECG change is present is calcium gluconate first for membrane stabilization, then insulin with dextrose to shift potassium intracellularly, a β₂-agonist, bicarbonate if acidotic, then binders or dialysis. Chronic hyponatremia must not be corrected faster than 10 mEq/L in the first 24 hours, because rapid correction risks osmotic demyelination syndrome — though in crisis the sodium usually rises on its own as volume and cortisol are restored.
Caution: Over-replacement — the other side of the dosing problem
Too much glucocorticoid produces obesity, diabetes, osteoporosis and frank Cushing’s syndrome; too much mineralocorticoid produces hypertension. In children, excess glucocorticoid suppresses growth.
This is why replacement is titrated to "the lowest possible dose that controls symptoms" and why fludrocortisone is adjusted to keep plasma renin in the reference range rather than by feel. Mineralocorticoid replacement is monitored through "supine and standing blood pressure as well as pulse, edema, serum potassium, and plasma renin activity" — so new edema or a rising blood pressure is a reason for a dose review, not something to keep going through.
Caution: A second autoimmune disease
Up to 50% of patients with Addison’s disease develop another autoimmune condition, so continued clinical monitoring is recommended indefinitely.
The associated conditions are the polyglandular ones: autoimmune thyroiditis, type 1 diabetes, pernicious anemia, Graves disease, hypoparathyroidism, myasthenia gravis and vitiligo. One has a specific trap attached — starting levothyroxine for newly found hypothyroidism in an undiagnosed or under-replaced patient accelerates cortisol clearance and can precipitate crisis, so the adrenal replacement comes first.
Caution: Excess mortality from ordinary events
Mortality in this population is driven by respiratory infections, adverse cardiovascular events and stroke — illnesses that are survivable in other patients but that stress an axis which cannot respond.
Poorer outcomes track with altered mental status at presentation, advanced comorbidities, and multiple endocrine disorders. Set against that, the prognosis with adequate replacement is genuinely good — most patients live an active life, and the difference between those two outcomes is largely made up of sick-day dosing, adherence, and whether an emergency injection was available when it was needed.

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Corticosteroids First-line
Endocrine · prednisone

Here the class is the treatment, not the cause — the exact mirror of Cushing’s syndrome, and replacement is lifelong. The 2016 Endocrine Society guideline recommends hydrocortisone 15–25 mg in two or three divided oral doses daily, with the largest dose on waking so the schedule mimics the normal diurnal cortisol curve; prednisone 3–5 mg/day is an alternative. Dexamethasone is recommended against for maintenance because dose titration is difficult and Cushingoid side effects follow. In primary disease only, the mineralocorticoid half is added — fludrocortisone, usually 0.05–0.2 mg daily, titrated to keep plasma renin in range, with the explicit instruction that patients must not restrict salt. The two rules that save lives are dose rules: sick-day dosing (double the glucocorticoid above 38 °C, triple it above 39 °C, for the 2–3 days of illness, while leaving the mineralocorticoid dose unchanged) and the crisis dose — 100 mg hydrocortisone IV or IM immediately, then 200 mg over 24 hours.
Electrolyte & Fluid Replacement First-line High-alert
Renal

The other half of crisis treatment, given alongside the steroid rather than after it: 1000 mL of isotonic saline immediately, or 5% glucose in isotonic saline where hypoglycemia is present so volume and glucose are corrected together — up to 2–3 litres as urgently as possible, and in children a 20 mL/kg bolus repeatable to 60 mL/kg within an hour for shock. The electrolytes largely correct themselves once cortisol and volume are restored, but must be monitored, and hyperkalemia with ECG change still needs its own treatment sequence. In the subacute phase saline continues at a slower rate for 24–48 hours, and fludrocortisone is started only once the saline stops — while it is running, the salt load is covering the mineralocorticoid need. Long-term the same class becomes dietary: liberal salt intake, adequate sodium in the diet, and increased electrolyte-containing fluids during illness.

Beyond medications

  • Level of care. Every adrenal-crisis patient needs consultation with intensivists and admission to an intensive care unit, with close monitoring and treatment of the precipitating infection with antibiotics. Hydrocortisone may be given IV or IM, and continuous infusion is described as a superior delivery method compared with intermittent boluses.
  • If hydrocortisone is unavailable, substitutes exist in a clear order: prednisolone 25 mg bolus then two further 25 mg doses in the first 24 hours; methylprednisolone 40 mg every 24 hours; and dexamethasone 4 mg every 24 hours — the least preferred option, though it is the one that does not interfere with cortisol assays when the diagnosis is still unestablished.
  • The emergency home kit is not optional. Patients "should always carry an emergency medicine shot after consulting with their clinicians," and clinicians should "ensure the availability of intramuscular hydrocortisone at home." Contents: injectable 100 mg hydrocortisone sodium succinate or 4 mg dexamethasone, 0.9% sterile normal saline vials, and syringes; prefilled dexamethasone syringes are an alternative. The parenteral emergency dose when oral medication cannot be taken is 100 mg IM for adults (the crisis dose), and 50 mg/m² for children.
  • Medical alert identification and a steroid card. Guideline best practice: all patients should carry a steroid emergency card and medical alert identification to inform health personnel of the need for increased glucocorticoid doses and for immediate parenteral steroid in an emergency — with crisis dosing information written on it, because the patient may be confused or unconscious when it is needed.
  • Stress dosing by procedure size. Major surgery, trauma or critical illness: hydrocortisone 100 mg IV followed by a continuous infusion of 200 mg/24 h. By procedure size, a bedside scheme runs 25 mg IV on the day for minor procedures, 50–75 mg on the day and postoperative day 1 for moderate, and 100–150 mg in divided doses on the day and days 1–2 for major.
  • The route rule (2024 ESE/Endocrine Society joint guideline): oral glucocorticoid for minor stress with no hemodynamic instability and no prolonged vomiting or diarrhea; parenteral glucocorticoid for moderate-to-major stress, procedures under general or regional anesthesia, procedures requiring prolonged inability to take oral intake, hemodynamic instability, or prolonged vomiting or diarrhea. And crucially — adrenal crisis should be considered irrespective of the glucocorticoid type, route and dose, so an inhaled or topical steroid user is not exempt.
  • Follow-up and dose adjustments. Annual endocrinology follow-up for adults and every 3–6 months for children, with continued surveillance for a second autoimmune disease. Three situations require a higher glucocorticoid dose: pregnancy, concurrent rifampin, and starting thyroid hormone. DHEA may be considered in women for psychological well-being, and only after glucocorticoid and mineralocorticoid replacement is already optimal.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Monitor vital signs including orthostatic blood pressures, heart rate, temperature, level of consciousness, glucose, intake and output, hemodynamic status and daily weight — and treat a systolic BP below 100 mm Hg or a fall of 20 mm Hg from this patient’s own baseline as crisis until proven otherwise.
Why: Those two numbers are the actual definition of adrenal crisis, and the relative one matters because a hypertensive patient can be in crisis at a pressure that looks unremarkable on the chart.
Do not use a normal blood pressure recorded earlier in the shift to downgrade concern.
Why: As many as half of patients develop shock with no preceding hypotension. The trend is not protective, so the decision rests on the whole picture — prodrome, trigger, and trajectory — rather than on the last set of vitals.
Read the electrolytes as a pattern rather than as separate results: hyponatremia plus hyperkalemia plus hypoglycemia, with a possibly raised creatinine from prerenal failure.
Why: The three move together because one hormone failure drives each — aldosterone loss for the sodium and potassium, cortisol loss for the glucose — and the hyperkalemia specifically localizes the lesion to the adrenal gland, since it does not occur in secondary disease.
Obtain an ECG when the potassium is elevated and escalate on any hyperkalemic change.
Why: The progression runs from peaked T waves at 5.5–6.5 mEq/L through loss of P waves and QRS widening to a sine-wave pattern at 8–10 — and muscle weakness or flaccid paralysis typically appears above 6.0. Each step is closer to an arrhythmia, so the ECG change is the action trigger, not the number alone.
Assess pigmentation deliberately at the sites where it shows: palmar creases, gingival mucosa, lips and vermilion border, elbows, knuckles, posterior neck, areolae, nipples and nail beds — and document its absence as meaningfully as its presence.
Why: Hyperpigmentation occurs in almost all patients with Addison’s disease and in none with secondary or tertiary disease, so it sorts the diagnosis. A patient on chronic steroids may instead look Cushingoid, which is the opposite of what a nurse is watching for.
Ask directly about salt craving, dizziness on standing, and any vomiting or diarrhea — and recheck blood pressure and edema at follow-up.
Why: Salt craving is highly suggestive and rarely volunteered; orthostasis signals the volume deficit; vomiting signals both impending crisis and an inability to absorb the oral dose. New edema and a rising blood pressure point the other way, to mineralocorticoid over-replacement.
Interventions & safety
Treat first, test second. When crisis is suspected, establish IV access with large-gauge needles, draw electrolytes, glucose, plasma cortisol and ACTH, and give hydrocortisone and isotonic saline without waiting for any result.
Why: Guideline wording is unambiguous: treatment "should never be delayed to obtain blood work to determine the underlying etiology," and delayed treatment can be fatal. The labs are drawn during the treatment, not before it.
Anticipate hydrocortisone 100 mg IV or IM immediately, then 200 mg over 24 hours by continuous infusion or 6-hourly injection, alongside 1000 mL of isotonic saline immediately — as 5% glucose in saline if the patient is hypoglycemic.
Why: The two arms treat different mechanisms: the steroid restores the permissive effect that lets catecholamines work, and the saline replaces the volume that sodium wasting removed. Response within 1–2 hours is part of the definition of crisis.
When shock persists, expect more glucocorticoid — not more vasopressor — to be the answer, and say so when escalating.
Why: "Without glucocorticoids, catecholamines cannot exert their full impact" on adrenergic receptors, so a pressor titrated upward in an untreated crisis is acting on a disconnected mechanism. This is the single most misread situation in the disorder.
Switch the patient to the parenteral route for moderate-to-major stress, anesthesia, prolonged inability to take oral intake, hemodynamic instability, or prolonged vomiting or diarrhea — and consider crisis irrespective of the steroid type, route or dose the patient was on.
Why: The oral route fails exactly when it is needed most, because the illness that raises the requirement is usually the illness that causes the vomiting. And an inhaled or topical steroid user is not exempt from axis suppression.
In the subacute phase, continue IV isotonic saline at a slower rate for 24–48 hours, treat the precipitating infection, taper the parenteral glucocorticoid over 1–3 days to the oral maintenance dose, and start fludrocortisone only after the saline is stopped.
Why: While saline is running, the salt load is already covering the mineralocorticoid requirement — adding fludrocortisone on top risks over-replacement, and the sequence matters more than the timing feels like it should.
Correct chronic hyponatremia no faster than 10 mEq/L in the first 24 hours, and treat hyperkalemia with ECG change in sequence: calcium gluconate first, then insulin with dextrose, a β₂-agonist, bicarbonate if acidotic, then binders or dialysis.
Why: Rapid sodium correction risks osmotic demyelination syndrome; calcium gluconate comes first in hyperkalemia because it stabilizes the myocardium immediately while the shifting agents take time to work.
Patient teaching
Teach the sick-day rules until the patient can recite them: double the glucocorticoid dose above 38 °C (100.4 °F), triple it above 39 °C (102.2 °F), for the usual 2–3 days of illness, with increased electrolyte-containing fluids — and do not change the mineralocorticoid dose.
Why: Illness raises the cortisol requirement that the patient cannot generate, and gastrointestinal or flu-like illness is the single most common trigger of adrenal crisis. The mineralocorticoid stays fixed because the deficiency it corrects does not change with fever.
Teach self- or lay-administration of the emergency injection, keep the kit stocked, and include at least one family member or caregiver in the teaching — and that a severe infection or diarrhea, or vomiting that stops the tablets staying down, needs immediate medical attention, in an emergency room if necessary.
Why: Crisis presents with confusion, somnolence and vomiting — states in which the patient can neither swallow a tablet nor reliably draw up an injection. The guideline makes the kit and the education an explicit requirement, not an optional extra.
Teach that doses must never be skipped and never abruptly stopped.
Why: Nonadherence and abrupt cessation are both listed triggers of adrenal crisis, and both are entirely preventable. This is the same rule the Cushing’s page teaches from the opposite direction — one disorder is caused by the steroid, the other by its absence.
Have the patient carry a steroid emergency card and medical alert identification with crisis dosing information on it.
Why: It tells clinicians who have never met the patient that this person needs increased glucocorticoid and immediate parenteral steroid — precisely at the moment the patient is too confused or collapsed to say it.
Teach the symptoms to name and report: nausea, vomiting, abdominal pain, weight loss, dizziness, confusion, hypoglycemia, fever, diminished well-being — and, separately, new swelling (edema).
Why: The first list is the crisis prodrome, and naming it converts a vague feeling of illness into a specific action. The second list is over-replacement pointing the opposite way, which needs a dose review rather than a dose increase.
Teach liberal salt intake — patients should not restrict salt — with adequate dietary sodium and monitoring of weight and blood pressure, plus more electrolyte-containing fluid during illness.
Why: Aldosterone deficiency wastes sodium continuously, so the salt craving is physiologically appropriate and should be respected rather than corrected. Note the contrast with the low-sodium advice most cardiac and renal patients receive — this population is the exception.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The cues that matter: hypotension that has not responded to 2 litres of crystalloid or to two upward titrations of norepinephrine, a relative fall of far more than 20 mm Hg from his own baseline of 138/84, tachycardia, fever, confusion, hypoglycemia at 52 mg/dL, hyponatremia at 129, and a creatinine that has nearly doubled. The history is the diagnosis hiding in plain sight: two years of prednisone, stopped four days ago, with no stress dose given for surgery. And two findings are cues precisely because they are missing — there is no hyperpigmentation and the potassium is a perfectly normal 4.2.

  2. 2
    Analyze cues

    Two years of prednisone suppressed CRH and ACTH and produced functional adrenal atrophy — this is tertiary adrenal insufficiency, and surgery is a listed crisis trigger on top of a four-day withdrawal. Now explain the absent findings rather than being reassured by them. Aldosterone is regulated by the renin-angiotensin system, not by ACTH, so secondary and tertiary insufficiency preserve mineralocorticoid function — which is exactly why his potassium is normal and why he is not bronzed. A nurse who requires hyperkalemia and bronze skin before considering adrenal insufficiency will rule out the correct diagnosis on the strength of two findings that were never going to be there. Meanwhile his Cushingoid appearance is not evidence against the diagnosis — it is evidence for it, because it is the fingerprint of the steroid that suppressed the axis. The refractory shock has its own explanation: without glucocorticoid, catecholamines cannot exert their full impact on adrenergic receptors, so the norepinephrine is acting on a disconnected lever.

  3. 3
    Prioritize

    This is adrenal crisis by definition — systolic 74 against a baseline systolic of 138 is far past the 20 mm Hg relative threshold — and untreated it progresses to circulatory collapse, coma and death. Priority one is parenteral hydrocortisone, ahead of any further pressor titration and ahead of any confirmatory test, because "treatment of adrenal crises should never be delayed to obtain blood work." Priority two is volume plus glucose together. Priority three is the hypoglycemia at 52 in its own right. The hyponatremia will largely correct itself as cortisol and volume are restored, and the fever needs a source investigated — but neither competes with the steroid.

  4. 4
    Generate solutions

    Draw plasma cortisol and ACTH as you treat, not before — and note that if the team wanted to preserve the diagnostic window entirely, dexamethasone 4 mg IV does not interfere with cortisol assays, though hydrocortisone is the preferred agent here because the mechanism, not the assay, is the problem. Give hydrocortisone 100 mg IV immediately, then 200 mg over the next 24 hours by continuous infusion or 6-hourly injection. Run 1000 mL of isotonic saline immediately, as 5% glucose in isotonic saline so the volume and the glucose of 52 are corrected in one line. Expect improvement within 1 to 2 hours — that response is part of the definition. Escalate for ICU admission, and investigate the fever. Note the specific thing not to do: keep climbing the norepinephrine and conclude this is septic shock.

  5. 5
    Take action

    Act and call simultaneously. The SBAR: "58-year-old, one hour post-cholecystectomy, on prednisone 15 mg daily for two years and stopped four days ago with no stress-dose cover. BP 74/42 against a baseline of 138/84, unresponsive to 2 litres of crystalloid and two norepinephrine titrations. Confused, febrile at 38.4, glucose 52, sodium 129, potassium normal at 4.2, no hyperpigmentation — consistent with tertiary adrenal crisis. Requesting hydrocortisone 100 mg IV now then 200 mg over 24 hours, 1000 mL of 5% glucose in isotonic saline now, cortisol and ACTH drawn during treatment, and ICU admission." The traps to name out loud: do not chase the pressure with more pressor, do not dismiss adrenal insufficiency because the potassium is normal and the skin is not bronzed, and do not wait for a cortisol result before giving the steroid.

  6. 6
    Evaluate

    Success within 1 to 2 hours: blood pressure rising and the norepinephrine weaning down, mentation clearing, glucose corrected, urine output returning as the prerenal creatinine falls. Over the next days: saline continues at a slower rate for 24–48 hours, the parenteral steroid tapers over 1–3 days to his oral maintenance dose, and the fever source is treated. He does not need fludrocortisone — his aldosterone was never lost. Before discharge the real prevention work happens: a steroid emergency card and medical alert identification, an emergency injection kit with teaching for him and his wife, the sick-day rules, and a corrected understanding that "hold your medicines before surgery" never included his prednisone. The re-escalation triggers he leaves with: vomiting he cannot keep down, dizziness on standing, confusion, or fever — inject and seek emergency care, do not wait.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Post-anesthesia care unit · 1115, one hour after an elective laparoscopic cholecystectomy

A 58-year-old man with polymyalgia rheumatica who has taken prednisone 15 mg daily for the past two years. At his pre-operative visit he was told to "hold your regular medicines the morning of surgery," so he stopped the prednisone four days ago to be safe and did not mention it. He is now hypotensive despite fluids, and a norepinephrine infusion has been started and titrated up twice.

1115 vitals — BP 74/42 (baseline 138/84) · HR 122 · RR 24 · T 38.4 °C · SpO₂ 97% on 2 L
Assessment — drowsy, rousable but confused · rounded face, dorsocervical fat pad, truncal obesity · no hyperpigmentation of palmar creases, gums or knuckles · skin warm, capillary refill 4 seconds
Fluids/pressors — 2 L lactated Ringer’s given · norepinephrine started 20 minutes ago and increased twice, with no BP response
Labs — Na⁺ 129 mEq/L · K⁺ 4.2 mEq/L · glucose 52 mg/dL · creatinine 1.6 mg/dL (baseline 0.9)
Chart — prednisone 15 mg daily listed on the home medication list · last dose four days ago per the patient’s wife · no stress-dose steroid ordered pre-operatively
Q1 Select all that apply
Which findings support adrenal crisis in this patient? Select all that apply.
  1. A. Hypotension unresponsive to 2 L of crystalloid and to norepinephrine titration
  2. B. Systolic BP 74 against a documented baseline of 138
  3. C. Glucose 52 mg/dL
  4. D. Potassium 4.2 mEq/L
  5. E. Absence of hyperpigmentation
Reveal answer & rationale
Answer: A, B, C
Shock that does not answer fluids or vasopressors is the signature of cortisol deficiency, because catecholamines cannot exert their full impact on adrenergic receptors without glucocorticoid (A). A fall of far more than 20 mm Hg from the patient’s own baseline meets the relative-hypotension definition of crisis (B). Hypoglycemia follows from the loss of cortisol-driven gluconeogenesis and glycogenolysis (C). The normal potassium (D) and the absent hyperpigmentation (E) are neither supporting nor refuting — both are aldosterone- and ACTH-dependent findings that occur only in primary disease, and this patient has tertiary insufficiency from steroid withdrawal. Treating their absence as evidence against the diagnosis is the central trap of this case.
Q2 Multiple choice
The patient remains hypotensive. Which action should the nurse anticipate first?
  1. A. Increase the norepinephrine infusion rate again
  2. B. Administer hydrocortisone 100 mg IV now, drawing cortisol and ACTH during treatment
  3. C. Send a cosyntropin stimulation test and hold treatment until the result returns
  4. D. Give a fludrocortisone 0.1 mg tablet to replace the missing mineralocorticoid
Reveal answer & rationale
Answer: B
Parenteral hydrocortisone is the first action, and the labs are drawn as it is given — "the treatment of adrenal crises should never be delayed to obtain blood work" (B). Escalating the pressor (A) is the intuitive move and the wrong one: without cortisol, the catecholamine cannot act fully on its receptors, so more drug acts on a disconnected mechanism. Waiting for a cosyntropin test (C) inverts the rule — stimulation testing is not performed acutely, only after stabilization. Fludrocortisone (D) fails on three counts: this is tertiary disease with preserved aldosterone, it is an oral tablet in a patient who is confused and shocked, and even in primary disease the mineralocorticoid is not what reverses a crisis.
Q3 Put in order
Put the nurse’s first four actions in priority order:
  1. A. Draw plasma cortisol, ACTH, electrolytes and glucose
  2. B. Administer hydrocortisone 100 mg IV
  3. C. Start 1000 mL of 5% glucose in isotonic saline
  4. D. Document the medication history and notify the surgical team of the missed stress dose
Reveal answer & rationale
Correct order: B → C → A → D
The steroid comes first because it is the only intervention that addresses the mechanism causing the refractory shock (B). Volume with glucose follows immediately, correcting the depletion and the hypoglycemia of 52 in one line (C). The blood work is drawn during treatment rather than before it — it guides later management but must never delay the first two steps (A). Documentation and team notification matter enormously for preventing the next crisis, but they never precede reversing this one (D). Any order that places A before B reproduces exactly the delay the guideline warns can be fatal.
Q4 Multiple choice
Before discharge, which statement by the patient indicates that sick-day teaching has been effective?
  1. A. "If I get a fever over 38 degrees I will double my prednisone, and I will also double my fludrocortisone."
  2. B. "If I get a fever over 38 degrees I will double my steroid dose, and if I cannot keep it down I will use the injection and get help."
  3. C. "If I feel unwell I will stop the steroid for a day so my body can recover on its own."
  4. D. "If I get a fever I will wait 48 hours to see whether it settles before changing anything."
Reveal answer & rationale
Answer: B
The sick-day rule is to double the glucocorticoid above 38 °C and triple it above 39 °C for the 2–3 days of illness, and to switch to the injection when vomiting prevents absorption — which is the situation that makes gastrointestinal illness the most common crisis trigger (B). Option A adds a real error: the mineralocorticoid dose does not change on sick days. Option C describes the precise action that precipitates crisis. Option D delays during the window when the requirement is rising and the patient is least able to meet it. Note this patient is on prednisone for another condition and does not take fludrocortisone at all — his aldosterone was never lost.
Q5 Multiple choice
A colleague asks why hyperpigmentation was absent in this patient when the textbook calls bronze skin the hallmark of adrenal insufficiency. The best explanation is:
  1. A. Hyperpigmentation takes years to develop and his disease was too acute
  2. B. Hyperpigmentation requires high ACTH, which occurs only in primary disease — his ACTH is low because the steroid suppressed it
  3. C. His Cushingoid features masked the underlying pigmentation changes
  4. D. Hyperpigmentation appears only in patients with autoimmune polyglandular syndrome
Reveal answer & rationale
Answer: B
Losing cortisol feedback in primary disease raises ACTH and MSH together, and they bind melanocyte receptors to darken skin and mucosa. In secondary and tertiary disease the ACTH is low or inappropriately normal, so there is no hyperpigmentation at all (B). Option A misstates the mechanism as a matter of time rather than of ACTH level. Option C is invented — Cushingoid fat redistribution does not conceal palmar-crease or gingival pigmentation. Option D is wrong: hyperpigmentation occurs in almost all patients with Addison’s disease regardless of whether a polyglandular syndrome is present.

Common questions

What causes addison’s disease & adrenal crisis?
Common causes and risk factors include autoimmune adrenalitis — the most common cause; antibodies against the adrenal cortex, particularly 21-hydroxylase (present in about 90%), infection — tuberculosis (adrenal enlargement with caseating granulomas), hiv, cytomegalovirus, sepsis, disseminated fungal infection, syphilis, adrenal hemorrhage — dic, trauma, anticoagulation, bleeding disorders, and meningococcemia (waterhouse-friderichsen syndrome), infiltration — hemochromatosis, amyloidosis, metastases, sarcoidosis, lymphoma, abrupt withdrawal of chronic exogenous glucocorticoid — causes tertiary insufficiency and is an explicitly listed cause of adrenal crisis; the version encountered most often in practice, and others.
What are the early signs of addison’s disease & adrenal crisis?
Early findings include Fatigue, generalized weakness, weight loss and reduced appetite.
Which findings should a nurse report immediately in addison’s disease & adrenal crisis?
Report immediately: Hypotension, altered mental status and obtundation — the cardinal crisis progression, Shock arriving with no preceding hypotension, Peaked T waves on the ECG, Adrenal crisis — the complication that defines the disease, Electrolyte emergencies — hyperkalemic arrhythmia and severe hyponatremia. These signal deterioration that needs rapid intervention.
Why do some patients with adrenal insufficiency have high potassium and bronze skin while others have neither?
Because it depends on where the axis is broken. Primary disease (Addison’s) destroys the adrenal cortex itself, so both cortisol and aldosterone are lost — aldosterone loss wastes sodium and retains potassium, producing hyperkalemia — and the missing cortisol feedback lets ACTH and MSH rise together, darkening skin and mucosa. Secondary and tertiary disease act at the pituitary or hypothalamus; aldosterone is driven by the renin-angiotensin system rather than by ACTH, so it is preserved, and ACTH is low rather than high. Those patients have hypoglycemia but no hyperkalemia and no hyperpigmentation — and, if their cause was chronic steroid therapy, they may look Cushingoid instead.
Why does the blood pressure in adrenal crisis not respond to fluids or vasopressors?
Because cortisol is what lets catecholamines work: "without glucocorticoids, catecholamines cannot exert their full impact" on adrenergic receptors. Giving more norepinephrine to a patient with no cortisol is pressing a disconnected lever. The answer is parenteral glucocorticoid — 100 mg hydrocortisone IV or IM, then 200 mg over 24 hours — alongside 1000 mL of isotonic saline given immediately. Improvement within 1 to 2 hours of the steroid is actually part of how adrenal crisis is defined.
What exactly are the sick-day rules?
Double the glucocorticoid dose for a fever above 38 °C (100.4 °F) and triple it above 39 °C (102.2 °F), continuing until recovery — usually 2 to 3 days — with increased electrolyte-containing fluids. Do not change the mineralocorticoid (fludrocortisone) dose. Switch to the emergency injection for moderate-to-major stress, anesthesia, hemodynamic instability, or prolonged vomiting or diarrhea, because the oral route fails exactly when the requirement is highest. Gastrointestinal and flu-like illness is the most common trigger of adrenal crisis, which is why this teaching carries more weight than any other on the page.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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