Adrenal (Addisonian) Crisis
Endocrinology
Illness script · Endocrinology
Adrenal (Addisonian) Crisis
Life-threatening acute glucocorticoid (± mineralocorticoid) deficiency causing hemodynamic collapse, typically precipitated by physiologic stress.
This illness script for Adrenal (Addisonian) Crisis covers predisposing factors, classic presentation, mechanism, workup, management, and the clinical pivots that separate it from look-alikes—written for USMLE Step 1 and clerkship reasoning.
01
Predisposing factors
- Known primary adrenal insufficiency (Addison's disease) + missed steroids
- Abrupt withdrawal of chronic exogenous glucocorticoids
- Bilateral adrenal hemorrhage (Waterhouse-Friderichsen: meningococcemia)
- Pituitary apoplexy causing acute secondary adrenal insufficiency
- Critical illness without steroid dose escalation ('sick-day rules' not followed)
- Adrenal metastases (lung, breast, melanoma)
02
Presentation
- Profound hypotension/shock unresponsive to IV fluids and vasopressors
- Nausea, vomiting, diffuse abdominal pain (can mimic acute abdomen)
- Profound fatigue, altered mental status, fever
- Hyponatremia + hyperkalemia (primary AI) or isolated hyponatremia (secondary AI)
- Hypoglycemia, especially in children
- Chronic stigmata if known Addison's: hyperpigmentation of creases, buccal mucosa
03
Pathophysiology
- Cortisol deficiency → loss of vascular tone, impaired catecholamine response → refractory hypotension
- Primary disease: concurrent aldosterone deficiency → urinary sodium wasting, hyperkalemia, volume depletion
- ACTH excess (primary) → MSH cross-reactivity → hyperpigmentation (chronic, not acute feature)
- Hypoglycemia from loss of gluconeogenic cortisol effect
04
Diagnostics
- Random serum cortisol <18 mcg/dL highly suggestive; <3 mcg/dL diagnostic
- ACTH stimulation test: cortisol fails to rise >18 mcg/dL post-250 mcg cosyntropin (confirm after crisis stabilized)
- Plasma ACTH: elevated in primary AI, low/normal in secondary AI
- Labs: hyponatremia, hyperkalemia, hypoglycemia, eosinophilia, lymphocytosis
- Do NOT delay treatment to complete workup — draw cortisol + ACTH, then treat immediately
05
Management
- Immediate: IV hydrocortisone 100 mg bolus, then 50–100 mg q6–8h (covers both gluco- and mineralocorticoid)
- Aggressive IV normal saline ± dextrose (D5NS) for volume repletion and hypoglycemia
- Identify and treat precipitating cause (infection, surgery, trauma)
- Dexamethasone alternative if ACTH stim test still pending (does not cross-assay)
- Fludrocortisone added once oral intake resumes for primary AI; taper steroids to maintenance gradually
- Avoid: stopping steroids abruptly; using etomidate in at-risk patients (blocks 11β-hydroxylase)
06
Clinical pivots
How to separate this script from the look-alikes that show up on exams and on the wards.
Septic shock
Addisonian crisis refractory to fluids + vasopressors with hyponatremia/hyperkalemia/eosinophilia; cortisol confirms
Acute abdomen (surgical)
Adrenal crisis mimics abdomen but resolves dramatically with IV hydrocortisone — avoid unnecessary laparotomy
Hypovolemic shock (other cause)
Hyperkalemia + hyponatremia + hyperpigmentation + known steroid use strongly favors adrenal crisis
Secondary adrenal insufficiency (pituitary)
Secondary AI has low ACTH, no hyperkalemia (aldosterone intact), no hyperpigmentation — cortisol still low
Keep reading
Full library- AdenomyosisEctopic endometrial glands/stroma within the myometrium, causing a diffusely enlarged, boggy, tender uterus.
- Alcohol WithdrawalCNS hyperexcitability syndrome following abrupt cessation or reduction of chronic heavy alcohol use, ranging from tremor to life-threatening seizures and delirium.
Educational use only. This illness script is a study framework, not medical advice. Confirm decisions with current guidelines and your clinical supervisors.