Hyponatremia represents a relative excess of water in relation to sodium. It can be induced by a marked increase in water intake (primary polydipsia) or, in the great majority of cases, by impaired water excretion resulting from advanced renal failure or from persistent release of antidiuretic hormone (ADH) induced by reduced effective arterial blood volume, the syndrome of inappropriate ADH secretion (SIADH), thiazide diuretics, adrenal insufficiency, or hypothyroidism. (See "Causes of hyponatremia".)
Most patients with hyponatremia have chronic (ie, gradual onset) hyponatremia, a serum sodium concentration above 120 meq/L, and appear asymptomatic, although subtle neurologic abnormalities may be present when the serum sodium is between 120 and 130 meq/L. (See 'Necessity for therapy' below.)
Initial treatment in such patients typically consists of slow correction of the hyponatremia via fluid restriction or, if volume depletion is present, the administration of isotonic saline (or oral salt tablets) [1-3]. Vasopressin receptor antagonists also may be helpful. Among patients with SIADH, isotonic saline may worsen the hyponatremia. (See 'SIADH' below.)
More aggressive therapy is indicated in patients who have symptomatic or severe hyponatremia (serum sodium concentration below 120 meq/L). In this setting, initial therapy usually consists of hypertonic saline with or without vasopressin receptor antagonists.
The following issues are reviewed in this topic: