Management of hyponatremia: Providing treatment and avoiding harm

Author and Disclosure Information



Determine the duration of hyponatremia

One should try to ascertain when the hyponatremia started, as its duration is important in determining the proper pace of correction.

Figure 1.

The brain begins to adapt to hyponatremia within minutes, and the cerebral adaptation is maximal within 2 to 3 days (Figure 1).6

At the onset of hyponatremia, water moves from the extracellular fluid into cells, pulled in by osmosis. The brain can decrease the net amount of water entering into the neurons (and thus regulate its volume) by increasing the flow of water from the interstitium into the cerebrospinal fluid via increased interstitial hydraulic pressure.7

Over the next several days, inorganic solutes (eg, potassium and sodium salts) and various organic solutes are transported out of the cells. In patients in whom this process has had time to occur, treatment of hyponatremia with hypertonic fluids raises the plasma osmolality faster than the cells can recapture the previously transported osmoles. In this situation, overly rapid correction can cause excessive loss of intracellular water, resulting in cell shrinkage and osmotic demyelination syndrome. Osmotic demyelination usually presents during treatment of hyponatremia after an initial improvement in mental status, with worsening neurologic function and various neurologic signs, including paresis and ultimately even death.6

In patients with acute-onset hyponatremia (ie, with onset within the past 48 hours), in whom the above cerebral adaptations have not had time to occur completely, rapid correction is unlikely to result in osmotic demyelination.

In view of the serious risk of osmotic demyelination, if the timing of development of hyponatremia cannot be determined, one should assume it is chronic (> 48 hours) and avoid rapid overcorrection (see discussion below on the rate of correction).

On the other hand, patients who have severe neurologic signs or symptoms initially need their serum sodium increased urgently to safer levels, regardless of the timing of onset (see below for suggested approach). Subsequent treatment of hyponatremia—after the serum sodium level has been raised enough to reverse neurologic symptoms—will be influenced by the duration of the hyponatremia, with careful avoidance of overly rapid correction, especially in patients with chronic hyponatremia.

Assess the patient’s volume status to determine the proper initial treatment

In patients with hypo-osmolar hyponatremia who do not need urgent therapy with hypertonic saline, the initial treatment is based on clinical and laboratory assessment of extracellular fluid volume status, including spot urine sodium measurement (Table 3).3 This will be discussed further below.

Check urine osmolality to assess for hyponatremic states in which urinary dilution is intact

Measuring urine osmolality is useful in ascertaining whether hyponatremic patients are making appropriately dilute urine (< 100 mOsm/kg). If they are, the cause of the hyponatremia may be excessive water intake, a reset osmostat, or low solute intake. In addition, patients with hypovolemic hyponatremia may have appropriately dilute urine soon after treatment with isotonic intravenous fluids.

The serum sodium concentration often returns to normal if the underlying cause is eliminated (eg, if excessive fluid intake is stopped). If there are no serious signs or symptoms, this can usually be accomplished without additional therapy with intravenous fluids or medications, thereby avoiding the risk of overcorrection.

Search for causes of rapidly correctable hyponatremia

If hyponatremia is due to one of several important underlying causes, it may reverse rapidly once the underlying cause has been eliminated (Table 4). Examples: restricting water intake in patients with psychogenic polydipsia, discontinuing thiazide diuretics, replenishing depleted fluid volume, stopping desmopressin (DDAVP), and giving glucocorticoid replacement to those who are glucocorticoid-deficient.


Patients with hypo-osmolar hyponatremia and serious signs or symptoms of cerebral edema (lethargy, respiratory depression, seizures) need rapid initial correction of the serum sodium level, as this is a true medical emergency.

Certain patients are at greater risk of developing cerebral edema from hyponatremia (Table 2).

On the other hand, patients with chronic hyponatremia are very unlikely to present with signs or symptoms of cerebral edema. In fact, in a patient with chronic hyponatremia, care must be taken to avoid overcorrection beyond that needed to reverse severe signs and symptoms. In the rare case in which a patient with chronic hyponatremia presents with signs or symptoms of cerebral edema, the hypertonic saline infusion must be stopped as soon as the signs or symptoms have resolved. Further rapid changes in serum sodium must be avoided.

During correction of hyponatremia, some patients are at particularly high risk of osmotic demyelination syndrome secondary to underlying abnormalities in cerebral osmotic regulation. These include patients with alcoholism, malnutrition, hypokalemia, and burns, and elderly women on thiazide diuretics.8 These patients should be monitored vigilantly for overly rapid correction during treatment.


The goal of the initial, rapid phase of correction is to reverse cerebral edema.

Patients with serious signs or symptoms should receive hypertonic (3%) saline at a rate of about 1 mL/kg/hour for the first several hours.8 Those with concomitant hypervolemia (as in congestive heart failure) or underlying cardiovascular disease should also receive a loop diuretic to aid in free-water excretion and to prevent volume overload from the saline infusion. This regimen usually raises the serum sodium concentration enough (usually by about 1 mmol/L/hour) to decrease cerebral edema and improve symptoms.

In patients having active seizures or showing signs of brain herniation, 3% saline can be given initially at a higher rate of about 2 to 3 mL/kg/hour over the first few hours. An alternative approach is an initial 50-mL bolus of 3% saline and an additional 200 mL given over the subsequent 4 to 6 hours.9

No study has compared the efficacy and safety of these approaches, and clinicians should always monitor extracellular fluid volume status, neurologic status, and serum sodium levels closely in any patient treated with hypertonic saline.

After severe signs and symptoms have resolved, 3% saline is promptly discontinued and appropriate therapy is initiated based on the patient’s volume status and underlying cause of hyponatremia (see discussion below).

Next Article: