Hypernatremia

Hypernatremia is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • Hypernatremia is defined as a plasma [Na+] >145 mEq/L and represents a state of hyperosmolality (see Disorders of Sodium Concentration section).
  • Hypernatremia may be caused by a primary Na+ gain or a water deficit, the latter being much more common. Normally, this hyperosmolar state stimulates thirst and the excretion of a maximally concentrated urine. For hypernatremia to persist, one or both of these compensatory mechanisms must be impaired.
  • Impaired thirst response may occur in situations where access to water is limited, often due to physical restrictions (institutionalized, handicapped, postoperative, or intubated patients) or mental impairment (delirium, dementia).
  • Hypernatremia due to water loss. The loss of water must occur in excess of electrolyte losses to raise [Na+].
    • Nonrenal water loss may be due to evaporation from the skin and respiratory tract (insensible losses) or loss from the GI tract. Diarrhea is the most common GI cause of hypernatremia. Osmotic diarrhea (induced by lactulose, sorbitol, or malabsorption of carbohydrate) and viral gastroenteritis, in particular, result in disproportional water loss.
    • Renal water loss results from either osmotic diuresis or diabetes insipidus (DI).
      • Osmotic diuresis is frequently associated with glycosuria and high osmolar feeds. In addition, increased urea generation from accelerated catabolism, high-protein feeds, and stress-dose steroids can also result in an osmotic diuresis.
      • Hypernatremia secondary to nonosmotic urinary water loss is usually caused by impaired vasopressin secretion (central diabetes insipidus [CDI]) or resistance to the actions of vasopressin (nephrogenic diabetes insipidus [NDI]). Partial defects occur more commonly than complete defects in both types.
      • The most common cause of CDI is destruction of the neurohypophysis from trauma, neurosurgery, granulomatous disease, neoplasms, vascular accidents, or infection. In many cases, CDI is idiopathic.
      • NDI may either be inherited or acquired. Acquired NDI often results from a disruption to the renal concentrating mechanism due to drugs (lithium, demeclocycline, amphotericin), electrolyte disorders (hypercalcemia, hypokalemia), medullary washout (loop diuretics), and intrinsic renal diseases.
  • Hypernatremia due to primary Na+ gain occurs infrequently because of the kidney’s capacity to excrete the retained Na+. However, it can rarely occur after repetitive hypertonic saline administration or chronic mineralocorticoid excess.
  • Transcellular water shift from ECF to ICF can occur in circumstances of transient intracellular hyperosmolality, as in seizures or rhabdomyolysis.

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