Management of hyponatremia: Providing treatment and avoiding harm

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Patients with hyponatremia and cirrhosis

The focus of treatment remains water and salt restriction and judicious use of loop diuretics and aldosterone antagonists such as spironolactone (Aldactone).

Tolvaptan has been effective at raising the serum sodium level in patients with cirrhosis, 26 while conivaptan should be avoided at present because of vasodilation from V1a receptor antagonism and its potential effects on systemic hemodynamics and risk of variceal bleeding.30

As the severity of cirrhosis increases, the only effective treatment of hyponatremia is liver transplantation.

Patients with SIADH

In most cases, water restriction is the mainstay of therapy. Adequate nutritional intake should also be stressed so that enough solute is available for ongoing water excretion. Although fluid restriction is usually effective, many patients cannot adhere to the level of restriction required.

In cases in which fluid restriction is not effective on its own, demeclocyline can be used to antagonize ADH action and increase water excretion. Sodium tablets and loop diuretics can also be used, taking care to avoid hypovolemia from diuretic-induced sodium losses. The use of tolvaptan in patients with SIADH has resulted in short-term increases in serum sodium.26 A recent study has suggested that this effect can be sustained with longer-term treatment,28 but further studies are needed to show a complementary clinical benefit (eg, improved neurocognition) to guide the use of these costly agents in clinical practice.

Patients with diuretic-induced hyponatremia

Thiazide diuretics should be discontinued and hypovolemia and hypokalemia should be corrected with isotonic saline and potassium supplementation. As the hypokalemia is corrected and the diuretic effect and hypovolemic stimulus to ADH dissipates, water excretion can increase rapidly, resulting in a brisk change in serum sodium.

Serum sodium levels should be closely monitored during therapy to avoid overcorrection. For this reason, use of hypertonic saline should generally be avoided. Hypotonic fluid— eg, half-normal (0.45%) or quarter-normal (0.22%) saline or even desmopressin—may become necessary in the later stages of therapy to avoid overly rapid correction.

Patients with exercise-associated hyponatremia

Patients at highest risk of exercise-associated hyponatremia include those who drink too much fluid during a long-distance race, who have low body weight, who are female, who exercise longer than 4 hours, and who use nonsteroidal anti-inflammatory drugs.31 The cause of hyponatremia is likely multifactorial, with excessive water intake coupled with sodium losses and impaired renal excretion of water due to ADH action and impaired renal dilution. To prevent exercise-associated hyponatremia, fluid intake should be limited to 400 to 800 mL/hour, with the higher end recommended for larger athletes and hotter climates.

Consensus recommendations suggest that most patients with mild hyponatremia (serum sodium 130 to 135 mmol/L) should be treated with fluid restriction and clinical observation, as spontaneous water diuresis leads to improvement in the serum sodium level. Importantly, the reflex to provide isotonic saline infusions should be avoided unless clear signs of volume depletion are present. Intravenous saline has the potential to worsen hyponatremia in the presence of ADH. In addition, some athletes will have retained water in the gastrointestinal tract that may be mobilized after the race, resulting in worsening of hyponatremia.32

In athletes with severe hyponatremia (serum sodium < 120 mmol/L) or symptomatic exercise-associated hyponatremia (lethargy, respiratory depression, seizures), hypertonic saline is the treatment of choice. One protocol suggests giving 100 mL of 3% saline over 10 minutes in the field, followed by prompt transportation to hospital.33


  • Hyponatremia is a common electrolyte disorder that in its most severe form requires urgent therapy with hypertonic saline to correct cerebral edema.
  • In patients without serious signs or symptoms of cerebral edema, recent observations suggest there may be clinically important symptomatology relating to mild neurocognitive dysfunction and an association with risk of bone fracture.
  • Multiple treatment strategies are available according to the underlying extracellular fluid volume status and cause of hyponatremia. These include fluid and sodium restriction and augmentation of urinary water excretion with various nutritional and pharmacologic strategies. The most novel therapy includes antagonism of the vasopressin V2 receptor with a class of aquaretic agents known as vaptans.
  • There can be serious neurologic injury associated with overly rapid correction of chronic hyponatremia or undercorrection of acute symptomatic hyponatremia.
  • Clinicians must be familiar with the details of each of the treatments and have an appreciation of the importance of careful monitoring during treatment.

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