Hypernatremia - Medicine Viva

Q: Define hypernatremia.

Key point for viva: Hypernatremia is strictly a hyperosmolar condition. It NEVER occurs with normal or low osmolality.

Q: What is the normal defense against hypernatremia?

1. Thirst - even a 1% rise in serum osmolality triggers thirst, prompting water intake
2. ADH (vasopressin) - released from the posterior pituitary in response to hyperosmolality; promotes water reabsorption in the collecting duct

Q: How do you classify the causes of hypernatremia?

1. Hypovolemic Hypernatremia

• Urine Na+ <10 mmol/L (extrarenal) or >20 mmol/L (renal)
• Urine osmolality >800 mOsm/kg with extrarenal loss (kidneys conserving appropriately)

2. Euvolemic (Normovolemic) Hypernatremia

• Head trauma, pituitary surgery/tumor, granulomatous disease (sarcoidosis, histiocytosis), hypoxia, inherited

• Drugs: lithium (most common), demeclocycline, amphotericin B, vaptans, foscarnet
• Electrolyte disorders: hypercalcemia, hypokalemia
• Sickle cell disease, Sjögren syndrome, amyloidosis
• Mutant vasopressin receptors (rare)

3. Hypervolemic Hypernatremia

• Hypertonic saline infusion
• Sodium bicarbonate infusion (e.g., resuscitation)
• Hyperaldosteronism, Cushing syndrome
• Salt poisoning (accidental or deliberate ingestion of concentrated NaCl)

Q: What are the clinical features?

• Mild: Thirst, irritability, restlessness, tremors, ataxia
• Moderate: Confusion, lethargy, muscle cramps, hyperreflexia, fever, nausea/vomiting
• Severe: Seizures, focal neurological deficits, decreasing consciousness, coma, intracranial hemorrhage (due to tearing of bridging veins as brain shrinks)

Important viva point: Severity of symptoms correlates with rapidity of onset, not just the absolute sodium level. In chronic hypernatremia (slow rise), brain cells generate "idiogenic osmoles" (organic solutes like myoinositol, glutamine) to restore intracellular volume - so symptoms may be absent even at Na >175 mmol/L. In acute hypernatremia, symptoms can appear at Na >160 mmol/L.

Q: What investigations would you order?

1. Serum sodium (confirm >145) + serum osmolality (always elevated)
2. Urine osmolality - key discriminator:
   • <100-200 mOsm/kg → DI (central or nephrogenic)
   • >800 mOsm/kg → extrarenal water loss or hypertonic sodium gain
   • 300-800 mOsm/kg → osmotic diuresis or partial DI
3. Urine sodium (<10 mmol/L extrarenal; >20 mmol/L renal)
4. 24-hour urine solute excretion:
   • <600 mOsm/day + polyuria → DI
   • >800-1000 mOsm/day → osmotic diuresis
5. Blood glucose (rule out HHNS/DKA)
6. Serum calcium, potassium (nephrogenic DI causes)

• Water deprivation test followed by desmopressin (DDAVP) administration
• Central DI: urine concentrates with DDAVP
• Nephrogenic DI: no response to DDAVP

Q: How do you treat hypernatremia?

Step 1: Address hemodynamic instability

Step 2: Calculate and replace the free water deficit

Free Water Deficit = 0.4 × premorbid weight (kg) × [(Na/140) - 1]

Step 3: Rate of correction

• Acute hypernatremia (<24-48 hrs): can correct more rapidly
• Chronic/unknown duration: reduce sodium by no more than 0.5-1.0 mmol/L/hour, and no more than 10-12 mmol/L in 24 hours
• Rationale: Rapid correction in chronic hypernatremia risks cerebral edema - because brain cells have accumulated idiogenic osmoles; when free water floods in suddenly, brain cells swell excessively

Step 4: Fluid choice

• Oral tap water (if patient can drink) - best option
• D5W (5% dextrose in water) - provides free water IV
• Half-normal saline (0.45% NaCl) - provides hypotonic solution
• Account for ongoing losses (insensible ~1 L/day + urine losses)

Step 5: Specific causes

• Central DI: Intranasal or IV desmopressin (DDAVP)
• Nephrogenic DI: Remove offending drug; low-sodium diet + thiazide diuretics (paradoxically reduce urine volume); NSAIDs (adjunct)
• Osmotic diuresis/DKA: Insulin + fluid therapy
• Hypervolemic hypernatremia: Hypotonic fluids + loop diuretics; dialysis if severe

Monitoring

• Check serum sodium every 4 hours during correction
• Monitor volume status closely to avoid hypervolemia

Q: What is the prognosis?

Diagnostic Algorithm

High-Yield Viva Points Summary

Hypernatremia - Simple Viva Answer

"What is hypernatremia?"

"What causes it?" - Remember 3 types by volume

HYPOVOLEMIC          EUVOLEMIC           HYPERVOLEMIC
(dehydrated)         (normal volume)     (overloaded)

Water lost >         Pure water loss      Too much salt
sodium lost                               given/taken

Examples:            Examples:            Examples:
- Diarrhea           - Diabetes           - Hypertonic saline
- Vomiting             Insipidus (DI)     - Soy sauce ingestion
- Burns              - Fever/sweating     - Hyperaldosteronism
- Sweating           - Not drinking
- Loop diuretics       enough water

Diabetes Insipidus (DI) is the most important cause to know well.

• Central DI = brain not making ADH (head injury, tumor)
• Nephrogenic DI = kidney not responding to ADH (lithium, hypercalcemia)

"Why does the patient get symptoms?"

Exam trick: Acute onset = symptoms at Na ~160. Chronic = symptoms only at Na >175 (because brain makes "idiogenic osmoles" to protect itself over time).

"How do you investigate?"

• <200 → Diabetes Insipidus
• >800 → Extrarenal loss (diarrhea, burns) or sodium overload
• 300-800 → Osmotic diuresis (diabetes, mannitol)

"How do you treat it?"

Step 1 - Shocked patient? Give normal saline first (save life first)

Step 2 - Calculate water deficit:

Water deficit = 0.4 × weight (kg) × [(Na/140) - 1]

Step 3 - Replace SLOWLY

Do NOT drop Na faster than 10-12 mEq/L per day If you correct too fast → cerebral edema → patient gets worse

Step 4 - Fluid choice:

• Drinking water orally (best)
• D5W (5% dextrose) IV
• Half normal saline (0.45% NaCl)

Step 5 - Treat the cause:

• Central DI → Desmopressin (DDAVP)
• Nephrogenic DI → Stop lithium, thiazide diuretics, low-salt diet
• DKA → Insulin + fluids

One-line memory tricks

Diagnostic Algorithm