Sodium Disorders

Sodium Disorders: Hyponatremia & Hypernatremia

(Fluid and Electrolyte Balance — Clinical Medicine)

I. Hyponatremia (Na⁺ < 135 mEq/L)

Pathophysiology

• Dilutional disorder: excess water relative to sodium.

• Most commonly due to increased ADH (vasopressin) → water retention → ↓ plasma osmolality.

Mechanism Summary

1. ↓ Blood volume or ↓ BP → JG cells release renin → ↑ angiotensin II.

2. Angiotensin II:

   • Vasoconstricts arterioles (↑ BP)

   • Stimulates aldosterone (Na⁺ reabsorption in distal nephron)

   • Stimulates ADH release from posterior pituitary

3. ADH → binds V₂ receptors in collecting duct → inserts aquaporin-2 channels → water reabsorbed → dilutional ↓Na⁺.

Clinical Classification

Type	Volume Status	Common Causes	Comments
Hypovolemic Hyponatremia	↓ ECF	Diuretics, vomiting, diarrhea	Loss of Na⁺ + water; ADH ↑ to conserve water
Euvolemic Hyponatremia	Normal ECF	SIADH, hypothyroidism, adrenal insufficiency	Water retained, Na⁺ constant
Hypervolemic Hyponatremia	↑ ECF	CHF, cirrhosis, nephrotic syndrome	Na⁺ and water ↑, but water ↑ more

Symptoms

• Mild (125–135 mEq/L): Headache, nausea, lethargy

• Moderate (115–125 mEq/L): Confusion, vomiting

• Severe (<115 mEq/L): Seizures, coma, respiratory arrest (cerebral edema)

II. Hypernatremia (Na⁺ > 145 mEq/L)

Pathophysiology

• Water deficit relative to sodium.

• Less common because thirst and ADH usually protect against it.

Major Causes

Category	Example	Mechanism
Water Loss (most common)	Dehydration, fever, burns	Free water loss > Na⁺ loss
ADH Deficiency	Central Diabetes Insipidus	↓ ADH release → water loss
ADH Resistance	Nephrogenic DI (lithium, kidney disease)	Tubules unresponsive to ADH
Excess Sodium	Hypertonic saline, Cushing’s	Na⁺ gain exceeds water gain

Symptoms

• Thirst, dry mucous membranes

• Neurologic: irritability → seizures → coma (due to brain shrinkage)

III. Compensation & Hormonal Links

Hormone	Action	Clinical Note
ADH	Water retention	↑ in SIADH → hyponatremia
Aldosterone	Na⁺ retention, K⁺ excretion	↓ in Addison’s → hyponatremia
ANP/BNP	Na⁺ and water loss	Counteracts RAAS

IV. Diagnostic Pearls

• Always check serum osmolality:

  • ↓ Osmolality → true hyponatremia

  • Normal Osmolality → pseudohyponatremia (hyperlipidemia, hyperproteinemia)

• Urine Na⁺ and urine osmolality help identify cause:

  • Urine Na⁺ < 20 mEq/L → extrarenal loss (vomiting, diarrhea)

  • Urine Na⁺ > 20 mEq/L → renal loss (diuretics, SIADH)

V. Quick Clinical Interpretation

Disorder	Core Problem	Brain Effect	Treatment Focus
Hyponatremia	Too much water	Swelling (cerebral edema)	Slow Na⁺ correction (hypertonic saline if severe)
Hypernatremia	Too little water	Shrinkage	Free water replacement (D5W, oral fluids)

Takeaways

• Sodium disorders are water balance problems, not just sodium problems.

• ADH and RAAS are the main regulators.

• Always assess volume status first.

• Rapid correction (especially of chronic hyponatremia) can cause osmotic demyelination, go slow.