Updated: Jul 16, 2021
  • Author: Eric E Simon, MD; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Practice Essentials

Hyponatremia—defined as a serum sodium concentration of less than 135 mEq/L—is a common and important electrolyte imbalance that can be seen in isolation or, as most often is the case, as a complication of other medical illnesses (eg, heart failure, liver failure, kidney failure, pneumonia). [1, 2] The normal serum sodium concentration is 135-145 mEq/L. Joint European guidelines classify hyponatremia in adults according to serum sodium concentration, as follows [3] :

  • Mild: 130-134 mmol/L
  • Moderate: 125-129 mmol/L
  • Profound: < 125 mmol/L

Hyponatremia is also classified according to volume status, as follows:

  • Hypovolemic hyponatremia: decrease in total body water with greater decrease in total body sodium
  • Euvolemic hyponatremia: normal body sodium with increase in total body water
  • Hypervolemic hyponatremia: increase in total body sodium with greater increase in total body water

Hyponatremia can be further subclassified according to effective osmolality, as follows:

  • Hypotonic hyponatremia
  • Isotonic hyponatremia
  • Hypertonic hyponatremia

Corrrection of hyponatremia varies according to its source, its severity, and its duration. In patients whose hyponatremia has a known duration of > 48 hours, treatment must be calibrated to avoid osmotic demyelination syndrome (ODS), which may result from overly rapid correction.

Signs and symptoms

Symptoms range from nausea and malaise, with mild reduction in the serum sodium, to lethargy, decreased level of consciousness, headache, and (if severe) seizures and coma. Overt neurologic symptoms most often are due to very low serum sodium levels (usually < 115 mEq/L), resulting in intracerebral osmotic fluid shifts and brain edema.

See Presentation for more detail.


There are three essential laboratory tests in the evaluation of patients with hyponatremia that, together with the history and the physical examination, help to establish the primary underlying etiologic mechanism: urine osmolality, serum osmolality, and urinary sodium concentration.

Urine osmolality

Urine osmolality helps differentiate between conditions associated with impaired free-water excretion and primary polydipsia. A urine osmolality greater than 100 mOsm/kg indicates impaired ability of the kidneys to dilute the urine.

Serum osmolality

Serum osmolality readily differentiates between true hyponatremia and pseudohyponatremia. The latter may be secondary to hyperlipidemia or hyperproteinemia, or may be hypertonic hyponatremia associated with elevated glucose, mannitol, glycine (posturologic or postgynecologic procedure), sucrose, or maltose (contained in IgG formulations).

Urinary sodium concentration

Urinary sodium concentration helps differentiate between hyponatremia secondary to hypovolemia and syndrome of inappropriate antidiuretic hormone secretion (SIADH). With SIADH (and salt-wasting syndrome), the urine sodium is greater than 20-40 mEq/L. With hypovolemia, the urine sodium typically measures less than 25 mEq/L. However, if sodium intake in a patient with SIADH (or salt-wasting) happens to be low, then urine sodium may fall below 25 mEq/L.

See Workup for more detail.


Hypotonic hyponatremia accounts for most clinical cases of hyponatremia and can be treated with fluids. Acute hyponatremia (duration < 48 hours) can be safely corrected more quickly than chronic hyponatremia. The treatment of hypertonic and pseudohyponatremia is directed at the underlying disorder in the absence of symptoms.

Intravenous fluids and water restriction

Administer isotonic saline to patients who are hypovolemic to replace the contracted intravascular volume. Patients with hypovolemia secondary to diuretics may also need potassium repletion, which, like sodium, is osmotically active.

Treat patients who are hypervolemic with salt and fluid restriction, plus loop diuretics, and correction of the underlying condition. The use of a V2 receptor antagonist may be considered.

For euvolemic, asymptomatic hyponatremic patients, free water restriction (< 1 L/day) is generally the treatment of choice. There is no role for hypertonic saline in these patients.

When treating patients with overtly symptomatic hyponatremia (eg, seizures, severe neurologic deficits), hypertonic (3%) saline should be used.

Pharmacologic treatment

Two vasopressin receptor antagonists, conivaptan (Vaprisol) and tolvaptan (Samsca), are approved for treatment of euvolemic and hypervolemic hyponatremia. Both agents increase urinary free water excretion. Conivaptan is administered intravenously; tolvaptan is administered orally, With both agents, initiation and reinitiation of therapy must take place in hospital, where serum sodium levels can be monitored closely.

See Treatment and Medication for more detail.



Hypo-osmolality (serum osmolality < 280 mOsm/kg) always indicates excess total body water relative to body solutes or excess water relative to solute in the extracellular fluid (ECF), as water moves freely between the intracellular and the extracellular compartments. This imbalance can be due to solute depletion, solute dilution, or a combination of both.

Under normal conditions, renal handling of water is sufficient to excrete as much as 15-20 L of free water per day. Further, the body's response to a decreased osmolality is decreased thirst. Thus, hyponatremia can occur only when some condition impairs normal free water excretion. [4] Generally, hyponatremia is of clinical significance only when it reflects a drop in the serum osmolality (ie, hypotonic hyponatremia), which is measured directly via osmometry or is calculated as 2(Na) mEq/L + serum glucose (mg/dL)/18 + BUN (mg/dL)/2.8. Note that urea is not an effective osmole, so when the urea levels are very high, the measured osmolality should be corrected for the contribution of urea.

The recommendations for treatment of hyponatremia rely on the current understanding of CNS adaptation to an altered serum osmolality. In the setting of an acute drop in the serum osmolality, neuronal cell swelling occurs due to the water shift from the extracellular space to the intracellular space (ie, Starling forces). Swelling of the brain cells elicits the following two osmoregulatory responses:

  • It inhibits both arginine vasopressin secretion from neurons in the hypothalamus and hypothalamic thirst center. This leads to excess water elimination as dilute urine.

  • There is an immediate cellular adaptation with loss of electrolytes, and over the next few days, there is a more gradual loss of organic intracellular osmolytes. [5]

Therefore, correction of hyponatremia must take into account the chronicity of the condition. Acute hyponatremia (duration < 48 h) can be safely corrected more quickly than chronic hyponatremia. Correction of serum sodium that is too rapid can precipitate severe neurologic complications. Most individuals who present for diagnosis, versus individuals who develop it while in an inpatient setting, have had hyponatremia for some time, so the condition is chronic, and correction should proceed accordingly.



United States

The incidence of hyponatremia depends largely on the patient population and the criteria used to establish the diagnosis. Among hospitalized patients, 15-20% have a serum sodium level of < 135 mEq/L, while only 1-4% have a serum sodium level of less than 130 mEq/L. The prevalence of hyponatremia is lower in the ambulatory setting.

The US armed forces reported 1579 incident diagnoses of exertional hyponatremia among active \service members from 2003 through 2018, for a crude overall incidence rate of 7.2 cases per 100,000 person-years. Cases occurred both in training facilities and theaters of war. Diagnosis and treatment without hospitalization was accomplished in 86.3% of cases. [6]  


Severe hyponatremia (< 125 mEq/L) has a high mortality rate. In patients whose serum sodium level falls below 105 mEq/L, and especially in alcoholics, the mortality is over 50%. [7]

In patients with acute ST-elevation myocardial infarction, the presence of hyponatremia on admission or early development of hyponatremia is an independent predictor of 30-day mortality, and the prognosis worsens with the severity of hyponatremia. [8] Bae et al reported that in hospitalized survivors of acute myocardial infarction, the presence of hyponatremia at discharge was an independent predictor of 12-month mortality. The study involved 1290 patients. [9]

Similarly, cirrhotic patients with persistent ascites and a low serum sodium level awaiting transplant have a high mortality risk despite low severity (MELD) scores (see the MELD Score calculator). The independent predictors—ascites and hyponatremia—are findings indicative of hemodynamic decompensation. [10, 11]

A study by Huang et al indicated that in patients with chronic kidney disease, hyponatremia and hypernatremia are associated with an increased risk for all-cause mortality and for deaths unrelated to cardiovascular problems or malignancy. Hyponatremia was also found to be linked to an increased risk for cardiovascular- and malignancy-related mortality in these patients. The study included 45,333 patients with stage 3 or 4 chronic kidney disease, 9.2% of whom had dysnatremia. [12]

Race-, Sex-, and Age-related Demographics

Hyponatremia affects all races.

No sexual predilection exists for hyponatremia. However, symptoms are more likely to occur in young women than in men. Hyponatremia is more common in elderly persons, because they have a higher rate of comorbid conditions (eg, heart, liver, or kidney failure) that can lead to hyponatremia.