Adrenal Crisis - A Guide for EMT Students

1. DEFINITION

• Tintinalli's Emergency Medicine, p. 1499
• Sabiston Textbook of Surgery, p. 1563

2. CAUSES

Underlying Conditions (Who is at risk?)

• Autoimmune adrenalitis (most common cause in developed countries)
• Tuberculosis or fungal infection destroying the glands
• Bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome - classically from meningococcal sepsis)
• HIV/AIDS-related adrenal destruction
• Adrenal metastases

• Pituitary tumors, apoplexy (sudden hemorrhage), or surgical removal
• Traumatic brain injury / severe head trauma
• Autoimmune hypophysitis
• Radiation to the pituitary

• Abrupt withdrawal or missed doses of chronic corticosteroid therapy - this is by far the most common trigger EMTs will see. Any patient on long-term prednisone, dexamethasone, or similar drugs is at risk.

Crisis Precipitants (Triggers - what pushes a vulnerable patient into crisis?)

• Infection - the most common trigger, especially gastrointestinal infections
• Severe physical illness, trauma, or burns
• Major surgery
• Extreme physical exertion
• Acute cardiovascular event (MI, stroke)
• Missed or vomited steroid doses
• Certain medications (checkpoint inhibitors, etomidate, ketoconazole)

EMT Pearl: Always ask patients who look "sick but you can't explain why" if they take steroids or have a steroid emergency card/bracelet.

• Tintinalli's Emergency Medicine, p. 1499
• Harrison's Principles of Internal Medicine 22E (2025), p. 1285

3. SIGNS & SYMPTOMS

Cardinal Signs of Acute Crisis

Differentiating Primary vs. Secondary (helpful in-hospital, less critical in the field)

The "Great Mimic" Warning

• Septic shock
• Acute abdomen / surgical emergency
• Neurological emergency (confusion, coma)

If a patient has unexplained shock that does not respond to fluids and you cannot find another cause - think adrenal crisis. - Tintinalli's Emergency Medicine, p. 1500

4. CLINICAL ASSESSMENT (Prehospital Focus for EMTs)

Scene Size-Up & Dispatch Clues

• Patient found unresponsive, hypotensive, with vomiting/abdominal pain
• History of Addison's disease, pituitary disease, or chronic steroid use
• Steroid alert card, medic-alert bracelet, or home emergency injection kit

Primary Survey (ABCDE)

• Hypotension (often systolic < 90 mmHg) - the hallmark finding
• Tachycardia
• Poor perfusion: pale/mottled skin, delayed capillary refill, weak rapid pulse
• Look for signs of dehydration

• GCS - assess level of consciousness
• Blood glucose (capillary/fingerstick) - hypoglycemia is common and immediately treatable
• Pupils

• Look for medic-alert bracelets/necklaces, wallet cards, steroid emergency card
• Look for hyperpigmentation (bronze skin, dark mucous membranes)
• Look for evidence of steroid use (cushingoid appearance, steroid inhalers/tablets at scene)

Key History Questions (SAMPLE - from patient, bystanders, or medical alert)

• Known Addison's disease or adrenal insufficiency?
• Currently taking corticosteroids (prednisone, hydrocortisone, dexamethasone, etc.)?
• Missed any doses recently? Vomited their morning medication?
• Recent illness, infection, injury, or surgery?
• Do they carry an emergency hydrocortisone injection kit?

Red Flags Pointing to Adrenal Crisis

• Unexplained hypotension not responding to IV fluids
• Hypoglycemia in a non-diabetic
• History of chronic steroid use + acute illness
• Altered mental status with no other clear cause
• Abdominal pain + hypotension without obvious surgical cause

5. MANAGEMENT

The EMT Priorities: ABCs + Early Recognition + Rapid Transport

The Golden Rule: Do not delay treatment waiting for lab confirmation. Treat based on clinical suspicion.

• Tintinalli's Emergency Medicine, p. 1501; ISMP Canada Safety Bulletin, 2025

Step-by-Step Prehospital Management

• Ensure patent airway; consider positioning
• Apply supplemental oxygen (SpO2 target ≥ 94%)
• Be prepared to support ventilation in obtunded patients

• Establish large-bore IV access (2 lines if possible)
• Normal saline (0.9% NaCl) is the fluid of choice - aggressive resuscitation
• If hypoglycemic: administer dextrose-containing saline (D5NS) or dextrose bolus per protocol
• Target: begin correcting hypotension
• Typical hospital protocol: 2-3 liters NS in the first 6 hours

• Obtain capillary blood glucose immediately
• Hypoglycemia is common and rapidly correctable in the field
• Give IV dextrose (D50W 25g in adults, or D10W in pediatrics) per protocol if glucose is low

EMT Note: Basic EMTs typically cannot administer hydrocortisone. Your role is to recognize the crisis, treat hypoglycemia, administer IV fluids, and transport rapidly. Some patients carry their own hydrocortisone auto-injector (like Solu-Cortef) and may self-administer or need assistance.

• Only used AFTER steroid therapy has been given
• Norepinephrine, dopamine, or phenylephrine if shock persists despite fluids + steroids
• Vasopressors are relatively ineffective without adequate cortisol replacement because cortisol is required for catecholamine sensitivity

• Continuous cardiac monitoring (ECG changes from hyperkalemia)
• Repeat vital signs every 5 minutes in unstable patients
• Blood glucose monitoring

• If infection suspected: alert receiving hospital for antibiotics
• Identify and communicate any known triggers to receiving team

• All confirmed or suspected adrenal crisis patients require ICU admission
• Pre-notify the receiving facility - this is a time-critical emergency

If Patient Has a Home Emergency Injection Kit

6. SUMMARY - ADRENAL CRISIS AT A GLANCE

SUSPECT IT when:
  → Unexplained hypotension/shock
  → Known steroid user + acutely ill
  → Steroid medic-alert card or bracelet
  → Hypoglycemia without clear cause

ASSESS:
  → ABCDE + fingerstick glucose
  → Scene clues (medications, alert cards)
  → Hyperpigmentation? (primary AI)

TREAT (prehospital):
  1. Airway + O2
  2. IV Normal Saline (aggressive)
  3. Dextrose if hypoglycemic
  4. Hydrocortisone 100 mg IV/IM (if in scope)
  5. Rapid transport → ICU
  6. Pre-notify hospital

DO NOT:
  → Wait for labs before treating
  → Give vasopressors before steroids
  → Forget to look for the precipitating cause

Key References

• Tintinalli's Emergency Medicine: A Comprehensive Study Guide, Table 230-4, pp. 1499-1501
• Sabiston Textbook of Surgery, pp. 1563-1564
• Bailey and Love's Short Practice of Surgery (28th Ed.), p. 1330
• Harrison's Principles of Internal Medicine 22E (2025), p. 1285
• ISMP Canada Safety Bulletin: Adrenal Crisis Management, Oct 2025
• EMCrit IBCC: Adrenal Crisis & Steroid Pharmacology, Sept 2025

Note for EMT Scope of Practice: Corticosteroid administration is typically within the Paramedic or AEMT scope. Basic EMTs should focus on recognition, airway management, IV fluid therapy, dextrose for hypoglycemia, and rapid transport with early notification. Always follow your local medical director's protocols and standing orders.

Pathophysiology of Adrenal Crisis

Step 1 - Normal HPA Axis: The Foundation

STRESS / STRESSOR
       ↓
Hypothalamus → releases Corticotropin-Releasing Hormone (CRH)
       ↓
Anterior Pituitary → releases ACTH (adrenocorticotropic hormone)
       ↓
Adrenal Cortex → produces CORTISOL + ALDOSTERONE
       ↓
Negative feedback back to hypothalamus & pituitary (keeps levels in check)

Step 2 - What Cortisol Normally Does (Why Its Absence is Lethal)

A. Glucose Homeostasis

• Stimulates gluconeogenesis (making new glucose in the liver from amino acids and glycerol)
• Promotes glycogenolysis (breaking down liver glycogen into glucose)
• Inhibits peripheral glucose uptake, inducing mild insulin resistance
• Net result: keeps blood glucose elevated during stress

"In hypocortisolism, there is hypoglycemia." - Costanzo Physiology, 7th Ed., p. 438

B. Vascular Tone & Blood Pressure ("Permissive Effect")

• Cortisol up-regulates alpha-1 adrenergic receptors on vascular smooth muscle
• This makes blood vessels sensitive to catecholamines (norepinephrine, epinephrine)
• Without this permissive effect, even high circulating catecholamines cannot maintain vasoconstriction

"Glucocorticoids exert a permissive and enhancing effect on catecholamine signaling by sensitizing arterial smooth muscle cells to beta-adrenergic stimulation... Cardiac contractility and peripheral vascular tone are thus maintained, explaining why the hemodynamic collapse that accompanies acute adrenal insufficiency can be remedied by glucocorticoid administration." - Sabiston Textbook of Surgery, p. 1560

C. ADH (Anti-Diuretic Hormone) Regulation

• Cortisol normally suppresses ADH release
• Low cortisol → ADH rises → kidneys retain free water → dilutes sodium in blood

D. Immune & Inflammatory Modulation

• Cortisol suppresses excessive inflammatory cascades
• Without cortisol, the inflammatory response goes unchecked
• This contributes to fever, vasodilation, and organ dysfunction

Step 3 - What Aldosterone Normally Does

• Promotes Na+ reabsorption from urine back into blood
• In exchange, secretes K+ and H+ into urine
• Net effect: retains sodium and water → maintains intravascular volume and blood pressure

"Aldosterone deficiency results in salt losses and clinical hypovolemia. The hypovolemia may further stimulate ADH release. Finally, the aldosterone deficiency may also cause hyperkalemia." - Symptom to Diagnosis, 4th Ed., p. 7286-7287

Step 4 - The Pathophysiological Cascade of Adrenal Crisis

TRIGGER (infection, missed steroids, trauma, surgery...)
              ↓
  Demand for cortisol EXCEEDS supply
              ↓
    ┌─────────────────────────────────────────┐
    │         CORTISOL DEFICIENCY             │
    └─────────────────────────────────────────┘
          ↓               ↓               ↓
  Gluconeogenesis     Catecholamine    ADH suppression
     FAILS            sensitization      LOST
          ↓           LOST                ↓
    HYPOGLYCEMIA    Arterioles don't   Free water retained
                    vasoconstrict          ↓
                          ↓           HYPONATREMIA
                   Vasodilatation
                          ↓
    ┌─────────────────────────────────────────┐
    │      ALDOSTERONE DEFICIENCY             │
    │       (primary AI only)                 │
    └─────────────────────────────────────────┘
          ↓               ↓               ↓
    Na+ wasted        K+ retained     H+ retained
    in urine              ↓               ↓
          ↓          HYPERKALEMIA   METABOLIC
    HYPOVOLEMIA       (can cause      ACIDOSIS
          ↓           arrhythmia)
    More hypotension
          ↓
    ──────────────────────────────────────
    COMPOUND SHOCK:
    Distributive (no vascular tone) +
    Hypovolemic (no volume) +
    Cardiogenic (poor cardiac output)
    → REFRACTORY to IV fluids alone
    → REFRACTORY to vasopressors alone
    ──────────────────────────────────────

Step 5 - Why Crisis Becomes Lethal Without Treatment

1. Cardiovascular collapse - vasodilation + hypovolemia combine into profound shock that does not respond to IV fluids or vasopressors because cortisol is absent
2. Hypoglycemia - brain glucose supply fails → seizures, coma, death
3. Electrolyte catastrophe - severe hyponatremia causes cerebral edema; severe hyperkalemia causes fatal arrhythmias
4. Metabolic acidosis - from tissue hypoxia (shock) + H+ retention (aldosterone loss)
5. Renal shutdown - from severe hypovolemia/shock → acute kidney injury + azotemia (rising creatinine/BUN)

Step 6 - Primary vs. Secondary: Pathophysiology Differences

"Adrenal crisis is usually seen in patients with Addison disease because of mineralocorticoid deficiency but can also present in patients with secondary or tertiary adrenal insufficiency who undergo severe physiologic stress." - Rosen's Emergency Medicine, p. 2577

Step 7 - Why Vasopressors Alone Don't Work (Critical EMT Concept)

• The catecholamine receptors on blood vessels are down-regulated without cortisol's "permissive" effect
• You can push as much vasopressor as you want, but the vessel walls won't respond adequately
• Only after hydrocortisone is given do vasopressors begin to work

Summary Diagram: What Each Hormone Loss Causes

References

• Costanzo Physiology, 7th Ed., pp. 437-438 - Actions of glucocorticoids
• Sabiston Textbook of Surgery, p. 1560 - Cortisol permissive effect on catecholamines
• Rosen's Emergency Medicine, pp. 2576-2578 - HPA axis diagram and pathophysiology
• Symptom to Diagnosis, 4th Ed., pp. 7265-7286 - Aldosterone deficiency mechanism
• StatPearls - Adrenal Crisis (Updated Feb 2025) - Glucocorticoid effects on glucose homeostasis
• Medscape - Adrenal Crisis Pathophysiology - Cortisol, aldosterone, and vascular tone

Adrenal Crisis - Simplified Pathophysiology

The Big Picture (One Sentence)

Think of It Like This - A Simple Analogy

• The engine (your heart and blood vessels) can still run without oil for a short time
• But under stress (infection, injury, missed medication), the engine seizes up completely
• No matter how hard you press the accelerator (vasopressors), the engine won't respond
• The only fix is to add the oil back (give hydrocortisone)

The Two Hormones That Fail

The Pathophysiology - Step by Step

1. The Trigger Hits

2. Blood Pressure Collapses (The Most Dangerous Part)

Normal: Adrenaline → arteries tighten → Blood pressure maintained ✓

Crisis:  Adrenaline → arteries DO NOT respond → vasodilation → BP crashes ✗

3. Blood Sugar Drops (Hypoglycemia)

• Telling the liver to make new glucose (gluconeogenesis)
• Breaking down glycogen stores

4. Salt and Water Are Lost (Volume Depletion)

5. The Compound Crash

      Cortisol deficiency          Aldosterone deficiency
             │                              │
    ┌────────┴────────┐            ┌────────┴────────┐
    │                 │            │                 │
 No vascular     No glucose     Salt lost        K+ builds up
 tone            made           in urine              │
    │                 │            │            Arrhythmia
 Vasodilation    HYPOGLYCEMIA  HYPOVOLEMIA      risk
    │                              │
    └──────────────┬───────────────┘
                   │
          REFRACTORY SHOCK
          (blood pressure crashes
           and won't come back up
           with fluids alone)
                   │
           If untreated → DEATH

Why Treatment Works

The key point: giving hydrocortisone is not just replacing a hormone - it is literally restoring the ability of blood vessels to maintain blood pressure. That is why steroids must come before or alongside vasopressors, not after.

One-Line Summary Per Mechanism

• No cortisol + stress = vessels go limp → shock
• No cortisol = liver stops making glucose → hypoglycemia
• No aldosterone = kidneys dump salt → dehydration + low BP + high potassium
• All three at once = life-threatening emergency