In a 42-year-old male with chronic fatigue, unintentional weight loss, bronze hyperpigmentation, orthostatic hypotension, tachycardia, hyponatremia, hyperkalemia, hypoglycemia, low cortisol and elevated ACTH, what is the most likely diagnosis?

Primary Adrenal Insufficiency (Addison's Disease)

This patient has primary adrenal insufficiency (Addison's disease), confirmed by the combination of low cortisol with elevated ACTH, along with classic clinical features including bronze hyperpigmentation, orthostatic hypotension, hyponatremia, hyperkalemia, and hypoglycemia. 1

---

CJMM Phase 1: Recognize Cues

Four Abnormal Assessment Findings:

• Bronze hyperpigmentation of skin, elbows, and gums—pathognomonic for primary adrenal insufficiency due to elevated ACTH stimulating melanocytes 1, 2
• Orthostatic hypotension (BP 88/54 mm Hg with further drop when standing)—reflects mineralocorticoid deficiency 1, 3
• Unintentional weight loss of 15 lb in 3 months with decreased appetite 4, 3
• Generalized weakness and fatigue with muscle weakness 4, 3

Two Abnormal Laboratory Values:

• Hyponatremia (128 mEq/L)—present in 90% of newly diagnosed adrenal insufficiency cases 1, 5
• Hyperkalemia (5.8 mEq/L)—occurs in approximately 50% of primary adrenal insufficiency cases due to aldosterone deficiency 1, 5

---

CJMM Phase 2: Analyze Cues

How Laboratory Findings Relate to Symptoms:

The low cortisol with elevated ACTH confirms primary adrenal insufficiency, where the adrenal glands themselves are destroyed and cannot produce cortisol despite maximal ACTH stimulation from the pituitary 1, 5. The elevated ACTH directly causes the bronze hyperpigmentation by stimulating melanocytes 2, 4.

Hyponatremia results from two mechanisms: cortisol deficiency impairs free water excretion (similar to SIADH), and aldosterone deficiency causes renal sodium wasting 1. Hyperkalemia occurs from aldosterone deficiency, which normally promotes potassium excretion 1, 5. However, hyperkalemia is only present in ~50% of cases, so its absence never rules out the diagnosis 1, 6.

How Cortisol Deficiency Affects Blood Pressure and Glucose:

Cortisol deficiency causes hypotension through multiple mechanisms: impaired vascular tone, reduced cardiac output, and decreased responsiveness to catecholamines 1. Aldosterone deficiency worsens hypotension by causing volume depletion from sodium and water loss 1, 3.

Hypoglycemia occurs because cortisol is essential for gluconeogenesis—without adequate cortisol, the liver cannot maintain blood glucose during fasting states 1, 7. The patient's glucose of 62 mg/dL reflects this impaired glucose production 1.

---

CJMM Phase 3: Prioritize Hypotheses

Most Likely Health Problem:

Primary adrenal insufficiency (Addison's disease) 1, 5

The diagnosis is essentially confirmed by:

• Cortisol <250 nmol/L with elevated ACTH in acute illness is diagnostic of primary adrenal insufficiency 1, 5
• Classic triad: hyperpigmentation, hypotension, and electrolyte abnormalities 5, 4

One Life-Threatening Complication:

Adrenal crisis with cardiovascular collapse 1, 6

This patient is already showing early signs with BP 88/54 mm Hg and orthostatic changes. Without immediate treatment, progression to shock, severe hypotension requiring vasopressors, altered mental status, and death can occur within hours 1, 6.

Priority Concern at This Time:

Hypotension (88/54 mm Hg) with orthostatic changes and tachycardia (102 bpm) 1, 6

This represents impending adrenal crisis requiring immediate intervention. The combination of hypotension, tachycardia, and orthostatic changes indicates significant volume depletion and inadequate cardiovascular compensation 1, 3.

---

CJMM Phase 4: Generate Solutions

Two Priority Nursing Interventions:

1. Establish large-bore IV access immediately and begin 0.9% normal saline infusion at 1 L/hour (at least 2L total) 1, 6

   • Volume resuscitation is critical as these patients have severe sodium and water depletion 1
   • Monitor vital signs every 15 minutes initially 1

2. Draw blood for morning cortisol and ACTH levels BEFORE administering any steroids 1, 6

   • These baseline values are essential for confirming the diagnosis 1, 5
   • However, never delay treatment for diagnostic testing if the patient is unstable 1, 6

Anticipated Medications:

Immediate treatment (within minutes):

• Hydrocortisone 100 mg IV bolus immediately 1, 6
• Continue with hydrocortisone 50 mg IV every 6 hours or 200 mg/24 hours continuous infusion 1

Once stabilized (typically 24-48 hours):

• Hydrocortisone 15-25 mg daily in divided doses (typically 10 mg at 7 AM, 5 mg at 12 PM, 2.5-5 mg at 4 PM) 1, 2
• Fludrocortisone 0.05-0.1 mg daily for mineralocorticoid replacement in primary adrenal insufficiency 1, 2

---

CJMM Phase 5: Take Action

Immediate Nursing Actions if Patient's Condition Worsens:

If hypotension worsens or patient becomes altered:

• Administer hydrocortisone 100 mg IV push immediately—do not wait for physician order in life-threatening situation 1, 6
• Increase IV fluid rate to maximum (1-2 L/hour of 0.9% saline) 1, 6
• Call rapid response team 1
• Prepare for possible ICU transfer 1
• Monitor glucose every 30-60 minutes and treat hypoglycemia with D50W if <70 mg/dL 1
• Continuous cardiac monitoring for arrhythmias from hyperkalemia 1

Critical pitfall to avoid: Never delay treatment of suspected adrenal crisis for diagnostic procedures—mortality is high if untreated 1, 6.

Patient Education That Should Begin Today:

Once patient is stable enough to comprehend:

1. Lifelong medication requirement: This is a permanent condition requiring daily hydrocortisone and fludrocortisone for life—never stop these medications 1, 4

2. Stress dosing protocol: Double or triple usual dose during illness, fever, or physical stress 1, 4

   • Teach specific scenarios: fever >100°F, vomiting/diarrhea, dental procedures, minor injuries 1

3. Emergency injectable hydrocortisone kit: Patient must carry hydrocortisone 100 mg IM injection kit at all times with self-injection training 1, 4

4. Medical alert identification: Must wear medical alert bracelet or necklace stating "Adrenal Insufficiency" to trigger emergency treatment 1, 4

5. Warning signs of adrenal crisis: Severe weakness, confusion, severe vomiting/diarrhea, severe abdominal pain—these require immediate ER visit 1, 6

---

CJMM Phase 6: Evaluate Outcomes

Findings That Indicate Improvement:

• Blood pressure normalizes (systolic >100 mm Hg without orthostatic changes) 1
• Heart rate decreases to 60-100 bpm 1
• Sodium normalizes to 135-145 mEq/L 1
• Potassium normalizes to 3.5-5.0 mEq/L 1
• Glucose stabilizes >70 mg/dL 1
• Patient reports improved energy, decreased nausea, improved appetite 1, 2
• Hyperpigmentation begins to fade (takes weeks to months) 2

Findings That Require Urgent Reevaluation:

• Persistent or worsening hypotension despite IV fluids and hydrocortisone—may indicate inadequate dosing or concurrent sepsis 1
• Altered mental status, confusion, or decreased consciousness—indicates progression to adrenal crisis 1, 6
• Persistent hyponatremia <130 mEq/L after 24 hours—may indicate inadequate glucocorticoid replacement 1
• Worsening hyperkalemia >6.0 mEq/L—requires cardiac monitoring and possible treatment with calcium gluconate, insulin/glucose, or kayexalate 1
• Development of peripheral edema or hypertension—indicates excessive fludrocortisone dosing requiring reduction 1, 2
• Persistent nausea/vomiting preventing oral intake—requires continued IV hydrocortisone 1

Follow-up testing required within 1-2 weeks:

• Cosyntropin stimulation test to confirm diagnosis if not done acutely (peak cortisol <500 nmol/L diagnostic) 1, 5
• 21-hydroxylase autoantibodies to identify autoimmune etiology (positive in ~85% of cases) 1, 5
• If autoantibodies negative, adrenal CT to evaluate for hemorrhage, tuberculosis, or other structural causes 1, 5
• Screen for other autoimmune conditions: thyroid function, diabetes, vitamin B12, celiac disease 1, 4