Epidemiology


Etiology


Pathophysiology

  • ↑ ADH secretion → receptor-mediated signaling cascade in the distal convoluted tubules and the collecting ducts of the kidneys → build-up of additional water canals (aquaporin-2) in the luminal cell membrane
  • Water is drawn out of the urine and into the hyperosmolar kidney tissue → concentration of urine and ↑ Urine osmolality (becomes higher than serum osmolality)
  • Water retention → ↓ serum osmolality with transient volume expansion → ↑ ANP, ↑ BNP, and ↓ aldosterone → ↑ urinary sodium and water excretion → normal extracellular fluid volume and low plasma osmolality (euvolemic hyponatremia)
  • Osmotic fluid shifts → cerebral edema and ↑ intracranial pressure (may occur in patients with extremely low Na+ levels)

Clinical features

Symptoms of hyponatremia

  • Mild
    • Anorexia
    • Nausea, vomiting
    • Headache
    • Muscle cramps
  • Moderate
    • Muscle weakness
    • Lethargy
    • Confusion
  • Severe

Tip

Both SIADH and Primary hyperaldosteronism have no edema. A hyponatremic patient with edema should raise suspicion for other conditions (e.g. congestive heart failure).


Diagnostics


Treatment

  • Always treat the underlying cause.
  • Asymptomatic/Mild HyponatremiaFluid restriction (<800 mL/day) is first-line. Salt tablets can be added.
  • Moderate/Severe Hyponatremia: ADH antagonists (e.g., TolvaptanConivaptan). Demeclocycline is a second-line option.
  • Severe, Symptomatic (seizures, coma): Hypertonic saline (3% NaCl). Administer slowly.
  • Complication of Treatment: Rapid correction of chronic hyponatremia (>8-10 mEq/L in 24h) can cause Osmotic Demyelination Syndrome (ODS), previously known as Central Pontine Myelinolysis. Remember: “From low to high, your pons will die.”