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  • Author: Eric E Simon, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
Updated: Jul 26, 2016

Practice Essentials

Hyponatremia is an important and common electrolyte abnormality 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, renal failure, pneumonia). The normal serum sodium level is 135-145 mEq/L. Hyponatremia is defined as a serum sodium level of less than 135 mEq/L. Joint European guidelines classify hyponatremia in adults according to serum sodium concentration, as follows[1, 2] :

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

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.

Hyponatremia is 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

See Clinical 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

Conivaptan, a V1A and V2 vasopressin receptor antagonist, is available only for intravenous use and is approved for use in the hospital setting for euvolemic and hypervolemic hyponatremia. It is contraindicated in hypovolemic patients. It induces both a water and sodium diuresis with improvement in plasma sodium levels.

See Treatment and Medication for more detail.



Hypoosmolality (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.[3] 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. [4]

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.


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%.[5]

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.[6] 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.[7]

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.[8, 9]

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.[10]

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 anhigher rate of comorbid conditions (eg, cardiac, hepatic, or renal failure) that can lead to hyponatremia.

Contributor Information and Disclosures

Eric E Simon, MD Professor of Medicine, Chief, Section of Nephrology and Hypertension, Tulane University School of Medicine; Director, Nephrology Training, Medical Director, Dialysis Clinic, Inc, Canal Street

Eric E Simon, MD is a member of the following medical societies: American Federation for Medical Research, American Heart Association, American Physiological Society, American Society of Nephrology, Central Society for Clinical and Translational Research, International Society of Nephrology, National Kidney Foundation, Phi Beta Kappa, American Society for Cell Biology, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.


Seyed Mehrdad Hamrahian, MD Assistant Professor of Medicine, Jefferson Medical College of Thomas Jefferson University

Seyed Mehrdad Hamrahian, MD is a member of the following medical societies: American Society of Nephrology, International Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

Federico J Teran, MD Instructor of Clinical Medicine, Section of Nephrology and Hypertension, Tulane University School of Medicine

Federico J Teran, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, Louisiana State Medical Society, National Kidney Foundation, Renal Physicians Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

James H Sondheimer, MD, FACP, FASN Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director of Hemodialysis, Harper University Hospital at Detroit Medical Center; Medical Director, DaVita Greenview Dialysis (Southfield)

James H Sondheimer, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology

Disclosure: Receive dialysis unit medical director fee (as independ ent contractor) for: DaVita .

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Central pontine myelinolysis, MRI FLAIR
Extrapontine myelinolysis T2
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