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The underlying cause should be treated where possible.

Patients with a plasma sodium concentration greater than 125 mmol/l rarely need specific therapy for hyponatraemia.

Seek secondary care advice if plasma sodium <= 125 mmol/l.

Management will vary with respect to whether the patient is hypovolaemic, normovolaemic or hypervolaemic.

  • hypovolaemic hyponatraemia
    • key step in the successful treatment of hypovolaemic hyponatraemia is to first establish that volume depletion is indeed present
    • treatment is via correction of the volume deficit - the relative water excess will correct itself
    • when ECF volume depletion is obvious and potentially life-threatening
      • resuscitation with isotonic fluid will likely have been initiated empirically - this would have occurred event before laboratory tests have been returned
      • volume expansion should be continued until blood pressure is restored and the patient has clinical euvolaemia
      • if the initial volume estimate is equivocal
        • then a fluid challenge with 0.5 to 1 L of isotonic (0.9%) saline can be both diagnostic and therapeutic
        • with the exception of cerebral salt wasting, and cases occurring soon after thiazides are started, hypovolaemic hyponatraemia is usually chronic rather than acute - thus use of hypertonic (3%) saline is seldom indicated in such cases
          • if hypertonic saline is used, a diuretic should not be added until the volume deficit is fully corrected
      • vasopressin receptor antagonists may have a role in management
  • normovolaemic (euvolaemic) hyponatraemia:
    • treatment of patients with euvolaemic hyponatraemia will vary greatly depending on their presentation
      • most important factor guiding initial therapy is the presence of neurologic symptoms
      • cases of acute hyponatraemia (arbitrarily defined as <48 hours' duration) are usually symptomatic if the hyponatraemia is severe (<=120 mmol/L)
        • patients at greatest risk from neurologic complications from the hyponatraemia
        • should be corrected to higher serum [Na+] levels promptly
      • patients with more chronic hyponatraemia (>=48 hours in duration) who have minimal neurologic symptomatology are at little risk from complications of hyponatraemia itself - however they can develop central pontine myelinolysis (osmotic demyelination) following rapid correction
        • no indication to correct these patients rapidly, and they should be treated using slower-acting therapies
      • note that the majority of patients with hyponatraemia present with hyponatraemia of indeterminate duration and with varying degrees of milder neurologic symptomatology
        • in this group the hyponatraemia will have been present sufficiently long to allow some degree of brain volume regulation, but not long enough to prevent some brain oedema and neurologic symptomatology
        • prompt treatment of such patients is generally recommended
      • usually fluid restriction is used as the initial therapy:
        • restriction of fluid intake to 500 ml per day to raise plasma sodium to 130 mM
        • frequent measurements of plasma osmolality and sodium
        • monitoring of body weight
        • demeclocycline hydrochloride - may be given in some circumstances if water restriction is poorly tolerated or ineffective
      • more detailed information about the management of SIADH is given in the linked item
  • hypervolaemic hyponatraemia
    • for all diseases associated with oedema formation, dietary sodium restriction and diuretic therapy are the mainstays of therapy
    • when hyponatraemia occurs, fluid restriction to amounts less than insensible losses plus urine output is necessary to cause a negative solute-free water balance, but is often difficult to achieve
    • not known whether hyponatraemia is just a marker for disease severity in CHF and cirrhosis or an actual contributor to poor outcome
      • CHF
        • no guidelines or published regimens addressing the best method of treating mild or moderate hyponatremia in the event treatment is desired
        • fluid restriction as the usual therapeutic intervention
      • cirrhosis
        • conventional therapies used for the treatment of ascites include sodium restriction, diuretic therapy, and large-volume paracentesis - most effective diuretic combination consists of a potassium-sparing, distal-acting diuretic such as spironolactone along with a loop diuretic
        • only definitive therapy for refractory ascites with cirrhosis is liver transplantation

Excessively rapid correction of hyponatraemia may cause central pontine myelinolysis.


  • (1) hyponatraemia Treatment Guidelines 2007: Expert Panel Recommendations The American Journal of Medicine 2007; 120 (11);S1:S1-S21.

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