Introduction

• Definition: serum sodium concentration >158 mEq/L.
  
  Normal ranges and abnormal values are dependent on equipment used and reference ranges established for that equipment.
• Sodium is the major cation of extracellular fluid (ECF).
• It does not freely move into the intracellular space (ICF) of most cells but is dependent on the action of the Na/K ATPase pump and it is therefore the major determinant of plasma osmolality.
• Water moves freely between the ECF and ICF following an osmotic gradient.
• Measured serum sodium concentration does not reflect total body sodium content but indicates the amount of sodium relative to the amount of ECF water.
• Hypernatremia always implies hyperosmolality.

Pathogenesis

Etiology

• Free water loss.
• Increased sodium intake.

Predisposing factors

General

• None.

Pathophysiology

• Serum sodium concentration is a reflection of the amount of sodium relative to the volume of total body water.
• Hypernatremic patients may have decreased, increased or normal total body sodium content.
• Hypernatremia must be assessed with volume status.
• Hypernatremia may be acute of chronic:  
  • In acute hypernatremia the brain does not have time to adjust to the increased extracellular osmolality and an equally rapid decrease in sodium concentration should prevent brain intracellular dehydration and shrinkage. 
  • In chronic hypernatremia where the hypernatremia has developed slowly over days or weeks, the brain has had time to compensate and has responded to high sodium concentration with increased intracellular osmolarity. 
• Hypernatremia associated with hypervolemia (impermeant solute gain):
  • Salt poisoning.
  • Iatrogenic:
    • Administration of hypertonic saline (3% or 7.5% NaCl).
    • Administration of sodium bicarbonate Sodium bicarbonate.
    • Administration of total parenteral nutrition.
    • Hyperaldosteronism.
    • Hypercortisolism (rarely severe hypernatremia).
• Hypernatremia associated with normovolemia or mild hypovolemia (pure water loss).
  • Primary hypodipsia or adipsia.
  • Associated with:
    • Hypothalamic granulomatous meningo-encephalitis.
    • Hydrocephalus Hydrocephalus.
    • CNS lymphoma Lymphoma.
  • Inadequate access to water.
  • Diabetes insipidus Diabetes insipidus :
    • Central (inadequate release of ADH).
    • Nephrogenic (inadequate response to ADH).
  • Fever (high insensible water loss).
  • High environmental temperature leading to high insensible water loss (often associated with panting).
• Hypernatremia associated with hypovolemia (hypotonic fluid loss):
  • Gastrointestinal losses.
  • Vomiting Vomiting.
  • Diarrhea.
  • Sequestration (ie small intestinal obstruction Intestine: obstruction ).
• Third space losses:
  • Peritonitis Peritonitis.
  • Pancreatitis Pancreatitis: chronic.
• Burns.
• Renal losses:
  • Osmotic diuresis (diabetes mellitus Diabetes mellitus , mannitol administration Mannitol ).
  • Chronic renal failure Heart: congestive heart failure.
  • Non-oliguric acute renal failure Kidney: acute kidney injury (AKI).
  • Post-obstructive diuresis.

Timecourse

• Clinical signs more common with severe, acute hypernatremia.
• If hypernatremia chronic (over at least 2-3 days) it is possible that there will be no or minor clinical signs.

Diagnosis

Treatment