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A more recent article on sodium disorders is available.

This is a corrected version of the article that appeared in print.

Am Fam Physician. 2015;91(5):299-307

Author disclosure: No relevant financial affiliations.

Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders are associated with an increased risk of morbidity and mortality. Plasma osmolality plays a critical role in the pathophysiology and treatment of sodium disorders. Hyponatremia and hypernatremia are classified based on volume status (hypovolemia, euvolemia, and hypervolemia). Sodium disorders are diagnosed by findings from the history, physical examination, laboratory studies, and evaluation of volume status. Treatment is based on symptoms and underlying causes. In general, hyponatremia is treated with fluid restriction (in the setting of euvolemia), isotonic saline (in hypovolemia), and diuresis (in hypervolemia). A combination of these therapies may be needed based on the presentation. Hypertonic saline is used to treat severe symptomatic hyponatremia. Medications such as vaptans may have a role in the treatment of euvolemic and hypervolemic hyponatremia. The treatment of hypernatremia involves correcting the underlying cause and correcting the free water deficit.

Hyponatremia is a common electrolyte disorder defined as a serum sodium level of less than 135 mEq per L.13 A Dutch systematic review of 53 studies showed that the prevalence of mild hyponatremia was 22.2% in geriatric hospital wards, 6.0% in nongeriatric wards, and 17.2% in the intensive care unit.2 The prevalence of severe hyponatremia (serum sodium level less than 125 mEq per L) was 4.5%, 0.8%, and 10.3%, respectively. It is estimated that hyponatremia occurs in 4% to 7% of the ambulatory population, with rates of 18.8% in nursing homes.24

Clinical recommendationEvidence ratingReferencesComments
In patients with severe symptomatic hyponatremia, the rate of sodium correction should be 6 to 12 mEq per L in the first 24 hours and 18 mEq per L or less in 48 hours.C13, 14 Consensus guidelines based on systematic reviews
A bolus of 100 to 150 mL of hypertonic 3% saline can be given to correct severe hyponatremia.C13, 14 Consensus guidelines based on small studies
Vaptans appear to be safe for the treatment of severe hypervolemic and euvolemic hyponatremia but should not be used routinely.C14 Consensus guidelines based on observational studies
Chronic hypernatremia should be corrected at a rate of 0.5 mEq per L per hour, with a maximum change of 8 to 10 mEq per L in a 24-hour period.C33 Expert opinion

Hyponatremia is associated with increased morbidity and mortality.16 In patients with heart failure who undergo cardiac surgery, hyponatremia increases rates of postoperative complications, length of hospital stay, and mortality.5,6 Mild hyponatremia in the ambulatory setting is associated with increased mortality (hazard ratio = 1.94) compared with normal sodium levels.3 Patients who develop hyponatremia during hospitalization have increased mortality rates compared with those who have hyponatremia on admission.7,8 It is unclear if hyponatremia is a marker for poor prognostic outcomes or merely a reflection of disease severity. Its presence suggests a worse prognosis in patients with liver cirrhosis, pulmonary hypertension, myocardial infarction, chronic kidney disease, hip fractures, and pulmonary embolism.1,810

Etiology and Pathophysiology

The most common classification system for hyponatremia is based on volume status: hypovolemic (decreased total body water with greater decrease in sodium level), euvolemic (increased total body water with normal sodium level), and hypervolemic (increased total body water compared with sodium).11

Plasma osmolality has a role in the pathophysiology of hyponatremia. Osmolality refers to the total concentration of solutes in water. Effective osmolality is the osmotic gradient created by solutes that do not cross the cell membrane. Effective osmolality determines the osmotic pressure and the flow of water.11 Plasma osmolality is maintained by strict regulation of the arginine vasopressin (also called antidiuretic hormone [ADH]) system and thirst. If plasma osmolality increases, ADH is secreted and water is retained by the kidneys, thus decreasing serum osmolality. If plasma osmolality decreases, ADH also decreases, resulting in diuresis of free water and a return to homeostasis.12,13

Diagnostic Approach to Hyponatremia

Symptoms of hyponatremia depend on its severity and on the rate of sodium decline. Gradual decreases in sodium usually result in minimal symptoms, whereas rapid decreases can result in severe symptoms. Polydipsia, muscle cramps, headaches, falls, confusion, altered mental status, obtundation, coma, and status epilepticus may indicate the need for acute intervention. Most patients with hyponatremia are asymptomatic, and hyponatremia is noted incidentally. Volume status should be assessed to help determine the underlying cause11,13 (Figure 11116 [corrected]).

The diagnostic workup should include a history and physical examination with specific attention to cardiac, cancer, pulmonary, surgical, endocrine, gastrointestinal, neurologic, and renal histories (Table 1).1113 Diuretics, carbamazepine (Tegretol), and selective serotonin reuptake inhibitors can cause hypovolemia; therefore, medications should be reviewed. Alcohol and illicit drug use (especially beer and 3,4-methylenedioxymethamphetamine [“Ecstasy”]) can cause hyponatremia.1113 Athletes should be asked about training regimens because high endurance activities can lead to hyponatremia.

Hyperglycemia (e.g., in diabetic ketoacidosis)Elevated glucose levels (> 400 mg per dL [22.2 mmol per L]), elevated anion gapInsulin, intravenous fluids, isotonic saline
HyperlipidemiaElevated total and low-density lipoprotein cholesterol levelsStatin therapy
Hyperproteinemia (e.g., in multiple myeloma)Serum and urinary monoclonal protein, bone marrow biopsy, lytic bone lesions detected on radiographyChemotherapy
Laboratory errorsRepeat sodium levels
Hypovolemic hyponatremia
Cerebral salt wastingDiagnosis of exclusion (e.g., head injuries, intracranial hemorrhage); urinary sodium > 20 mEq per LIsotonic or hypertonic saline
Diuretic useClinical; urinary sodium > 20 mEq per LStop diuretic therapy
Gastrointestinal loss (e.g., diarrhea, vomiting)Clinical; urinary sodium < 20 mEq per LIntravenous fluids
Mineralocorticoid deficiency (e.g., Addison disease [primary], pituitary failure [secondary], hypothalamic failure [tertiary])Low aldosterone and morning cortisol levels, hyperkalemia, increased plasma renin level, low or increased adrenocorticotropic hormone level (cause-dependent), urinary sodium > 20 mEq per L, positive results on cosyntropin stimulation test, 21-hydroxylase autoantibodies (Addison disease), computed tomography of adrenal glands to rule out infarctionSteroid replacement therapy
Osmotic diuresisElevated glucose level, mannitol useCorrect glucose level, stop mannitol use
Renal tubular acidosisUrinary osmolar gap, increased urinary pH, urinary sodium > 25 mEq per L, fractional excretion of bicarbonate > 15% to 20%, hyperchloremic acidosis, decreased serum bicarbonate level, potassium abnormalities (type dependent)Correct acidosis, sodium bicarbonate
Salt-wasting nephropathiesUrinary sodium > 20 mEq per LCorrect underlying cause
Third spacing (e.g., bowel obstruction, burns)Clinical; computed tomographyIntravenous fluids, relieve obstruction
Euvolemic hyponatremia
3,4-methylenedioxymeth-amphetamine (“Ecstasy”) useUrine drug screen
Beer potomania syndromeExcessive alcohol consumption, low serum osmolalityTherapy to decrease alcohol use and nutritional counseling to increase protein intake
Exercise-associated hyponatremiaClinicalIsotonic or hypertonic saline, depending on symptoms
Glucocorticoid deficiencyLow aldosterone, morning cortisol, and adrenocorticotropic hormone levels, hyperkalemia, increased plasma renin levelSteroid replacement therapy
HypothyroidismElevated thyroid-stimulating hormone level, low free thyroxine levelThyroid replacement therapy
Low solute intakeClinicalIncrease sodium intake
Nephrogenic SIADHSame as SIADH, with low vasopressin levelsFluid restriction, loop diuretics
Psychogenic polydipsiaHistory of schizophrenia with excessive water intakePsychiatric therapy
Reset osmostatFree water challenge test, normal fractional excretion of uric acid (urate)Treat underlying disease
SIADHDecreased osmolality, urinary osmolality > 100 mOsm per kg, euvolemia, urinary sodium > 20 mEq per L, absence of thyroid disorders or hypocortisolism, normal renal function, no diuretic useFluid restriction, consider vaptans
SIADH secondary to medication use (e.g., barbiturates, carbamazepine [Tegretol], chlorpropamide, diuretics, opioids, selective serotonin reuptake inhibitors, tolbutamide, vincristine)SIADH with use of causative agentStop causative medication
Water intoxicationClinical; excessive water intakeDiuresis
Hypervolemic hyponatremia
Heart failureClinical (e.g., jugular venous distention, edema), elevated B-type natriuretic peptide level, echocardiography, urinary sodium < 20 mEq per LDiuretics, angiotensin-converting enzyme inhibitors, beta blockers
Hepatic failure/cirrhosisElevated liver function tests, ascites, elevated ammonia level, biopsy, urinary sodium < 20 mEq per LFurosemide (Lasix), spironolactone (Aldactone), transplant
Nephrotic syndromeUrinary protein, urinary sodium < 20 mEq per LTreat underlying cause
Renal failure (acute or chronic)Blood urea nitrogen–to-creatinine ratio, glomerular filtration rate, proteinuria, urinary sodium > 20 mEq per LCorrect underlying disease with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers

Laboratory tests include a complete metabolic panel and urinary sodium and creatinine levels.11,13 Serum osmolality and fractional excretion of sodium should be calculated (eTable A). Measurement of thyroid-stimulating hormone, urinary uric acid, adrenocorticotropic hormone, plasma cortisol, and brain natriuretic peptide may be considered in select patients to rule out other causes.13 The diagnosis of reset osmostat (a variation of syndrome of inappropriate antidiuretic hormone secretion [SIADH] in which ADH secretion occurs despite low plasma osmolality) may be aided using fractional excretion of urate (uric acid) in nonedematous patients who have hyponatremia that does not respond to usual treatment.17

Corrected sodiumMeasured sodium + 0.024 × (serum glucose − 100)*
Measured sodium + 0.016 × (serum glucose − 100)
Normal = 135 to 145 mEq per L
Online calculators available at and
Fractional excretion of sodium([Plasma creatinine × urinary sodium] / [plasma sodium × urinary creatinine]) × 100
Prerenal < 1%, intrinsic > 1%, and postrenal > 4%
Online calculators available at and
Infusion rate of sodiumOnline calculators for the rate of infusion and the concentration of sodium required are available at,, and
Serum sodium correction should generally not proceed faster than 0.5 mEq per L per hour for the first 24 to 48 hours; however, in severely symptomatic patients, the rate can be 1.0 to 2.0 mEq per L per hour; these situations typically require use of 3% saline
The goal is to raise the serum sodium level not to exceed 10 to 12 mEq per L in the first 24 hours and 18 mEq per L in the first 48 hours
Isotonic saline contains 154 mEq of sodium per L, and 3% saline contains 513 mEq of sodium per L
Serum osmolality(Sodium × 2) + (glucose / 18) + (blood urea nitrogen / 2.8)
Normal = 280 to 295 mOsm per kg
In patients with hyperglycemia, uncorrected sodium should be used to calculate the osmolality
Online calculators available at and
Sodium deficitTotal body water % × weight in kg × (desired sodium − actual sodium)
For total body water %, use 0.6 for men and 0.5 for women
Example: for a 70-kg man with a serum sodium level of 120 mEq per L and a desired serum sodium level of 140 mEq per L, the calculation is 0.6 × 70 (140 − 120) = 42 × 20 = 840 mEq
Online calculator available at
Water deficitVolume (L) = (total body water %) × weight in kg × [(sodium − 140) / 140]
For total body water %, use 0.45 for women older than 65 years, 0.5 for women 65 years and younger and for men older than 65 years, and 0.6 for men 65 years and younger and for children
Example: for a 70-kg man with a serum sodium level of 120 mEq per L, the calculation is 0.6 × 70 × ([120 − 140] / 140) = 42 × (−20 / 140) = 42 × (−1 / 7) = −6 L
Online calculators available at and


Pseudohyponatremia occurs when seemingly low sodium levels are actually normal. Causes include hyperglycemia, hyperproteinemia, mannitol use, or laboratory errors. Osmolality remains unchanged, and patients are usually euvolemic.12,13 A corrected sodium calculation is needed in the setting of hyperglycemia (eTable A).

Hypovolemic Hyponatremia

There are numerous causes of hypovolemic hyponatremia (Table 1).1113 Patients typically have signs and symptoms associated with volume depletion (e.g., vomiting, diarrhea, tachycardia, elevated blood urea nitrogen–to-creatinine ratio). Urinary sodium levels are typically less than 20 mEq per L unless the kidney is the site of sodium loss. Fractional excretion of sodium is often inaccurately elevated in patients receiving diuretics because of diuretic-induced natriuresis; fractional excretion of urea can be utilized in these patients instead. Fractional excretion of urea less than 35% is more sensitive and specific for diagnosing prerenal azotemia in this setting.18 Treatment generally consists of volume repletion with isotonic (0.9%) saline, occasional use of salt tablets, and treatment of the underlying condition.13,14 Monitoring of urine output is recommended because output of more than 100 mL per hour can be a warning sign of overcorrection.14

Euvolemic Hyponatremia

Euvolemic hyponatremia is most commonly caused by SIADH, but can also be caused by hypothyroidism and glucocorticoid deficiency. Euvolemia is diagnosed by findings from the history and physical examination, low serum uric acid levels, a normal blood urea nitrogen–to-creatinine ratio, and spot urinary sodium greater than 20 mEq per L. Diuretic therapy can artificially elevate urinary sodium, whereas a low-salt diet can artificially lower urinary sodium, thus clouding the diagnosis of hypovolemia vs. euvolemia. Treatment generally consists of fluid restriction and correcting the underlying cause. Fluid restriction should be limited to 500 mL less than the daily urinary volume.13 Salt and protein intake should not be restricted. Predictors of failure with fluid restriction include urinary osmolality greater than 500 mOsm per kg, 24-hour urinary volume less than 1.5 L, an increase in the serum sodium level of less than 2 mEq per L within 24 to 48 hours, and a serum sodium level less than the sum of the urinary sodium and potassium levels.13 Volume status can be difficult to determine; therefore, a trial of intravenous fluids may be warranted.11 Sodium levels in patients with SIADH will decrease further with intravenous fluid administration. The use of demeclocycline (Declomycin) and lithium is not recommended because of an increased risk of harm.14

Hypervolemic Hyponatremia

Hypervolemic hyponatremia occurs when the kidneys cannot excrete water efficiently. In volume overload states, the effective arterial blood volume is decreased compared with venous volume, resulting in excess ADH secretion. The most common causes of hypervolemic hyponatremia are heart failure, cirrhosis, and kidney injury. Treatment consists of correcting the underlying cause, sodium and fluid restriction, and diuretic therapy to increase excretion of solute-free water.13,14 A randomized controlled trial of 46 patients with heart failure showed that restricting fluid intake to 1 L per day improved quality of life 60 days after discharge.19

Severe Symptomatic Hyponatremia

Severe symptomatic hyponatremia occurs when sodium levels decrease over less than 24 hours. Severe symptoms (e.g., coma, seizures) typically occur when the sodium level falls below 120 mEq per L, but can occur at less than 125 mEq per L. Severe symptomatic hyponatremia must be corrected promptly because it can lead to cerebral edema, irreversible neurologic damage, respiratory arrest, brainstem herniation, and death. Treatment includes the use of hypertonic 3% saline infused at a rate of 0.5 to 2 mL per kg per hour until symptoms resolve. At this time, vaptans have no role in the treatment of symptomatic hyponatremia because of the potential for overcorrection of sodium and variable sodium fluctuations.13 Loop diuretics may be needed in patients with concurrent symptomatic hyponatremia and volume overload. The rate of sodium correction should be 6 to 12 mEq per L in the first 24 hours and 18 mEq per L or less in 48 hours.1214 An increase of 4 to 6 mEq per L is usually sufficient to reduce symptoms of acute hyponatremia.20 Rapid correction of sodium can result in osmotic demyelination (previously called central pontine myelinolysis). Overcorrection is common and is typically caused by rapid diuresis secondary to decreasing ADH levels. Every attempt should be made not to overcorrect sodium levels. One study of 25 patients with severe symptoms and sodium levels less than 120 mEq per L showed that concurrent treatment with a weight-based dose of 3% saline and 1 to 2 mcg of desmopressin every six to eight hours resulted in a rate of correction of 3 to 7 mEq per L per hour without causing overcorrection.21 Another study used a 100-mL bolus of 3% saline infused over 10 minutes in marathon runners; symptoms improved without over-correcting. This method increased sodium levels by 1.5 to 2.0 mEq per L per hour.13,22,23 Guidelines from the European Society of Endocrinology recommend infusing one dose of 150 mL of 3% saline over 20 minutes, with sodium monitoring every 20 minutes until symptoms resolve.14 This regimen may be repeated if the patient remains symptomatic or until the goal sodium target of 5 mEq per L is achieved (Figure 213,14,2023[ corrected]).


Vaptans (conivaptan [Vaprisol] and tolvaptan [Samsca]) are vasopressin-receptor antagonists approved for the treatment of hospitalized patients with severe hypervolemic and euvolemic hyponatremia (eTable B). However, their use in the management of hyponatremia is controversial. Several trials have demonstrated that vaptans increase sodium levels in patients with cirrhosis and heart failure.24 In the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan, patients with hyponatremia and heart failure who received tolvaptan had an associated reduction in cardiovascular morbidity and mortality, although there were several confounding variables, and further study is needed.25 The Study of Ascending Levels of Tolvaptan in Hyponatremia (SALT) trials demonstrated increased sodium levels with tolvaptan in patients with SIADH, cirrhosis, and heart failure.26 An extension of these studies, the SALTWATER trial, showed that long-term use of tolvaptan is safe and effective in increasing sodium levels, although this study did not specify subgroups.27,28 Regardless of their effectiveness in increasing sodium levels, vaptans—specifically tolvaptan—should not be used in patients with hepatic impairment because they may worsen liver function.29,30 The European Society of Endocrinology recommends against the routine use of vaptans, citing a lack of reduction in overall mortality rates and increased risk of rapid overcorrection.14 Further study is needed to clarifiy the role of vaptans.

DrugConivaptan (Vaprisol)Tolvaptan (Samsca)
IndicationsShort-term use for hospitalized patients with hypervolemic or euvolemic hyponatremia associated with heart failure or syndrome of inappropriate antidiuretic hormone secretion with sodium < 125 mEq per LApproved for use for up to 30 days for hypervolemic or euvolemic hyponatremia associated with heart failure or syndrome of inappropriate antidiuretic hormone secretion with sodium < 125 mEq per L
Dosing20 mg intravenously (in 100-mL dextrose 5% solution) infused over 30 minutes as a loading dose, followed by continuous infusion of 20 mg over 24 hours for two to four days; may increase to 40 mg over 24 hours; do not exceed four days15 mg orally once daily; after 24 hours may increase to 30 mg once daily, then titrate to desired sodium concentration (maximum of 60 mg per day)
Patients with moderate hepatic impairment: 10 mg infused over 30 minutes as a loading dose, followed by a continuous infusion of 10 mg over 24 hours (0.42 mg per hour) for two to four days; may increase to a maximum dose of 20 mg over 24 hours (0.83 mg per hour) if serum sodium is not increasing sufficiently; do not exceed four days
PharmacodynamicsMetabolized by CYP3A4Metabolized by CYP3A4
Half-life: five to eight hoursOnset: two to four hours
Excretion: feces (83%), urine (12%, primarily as metabolites)Peak: four to eight hours
Half-life: five to 12 hours
Excretion: feces
SafetyAdverse effects:Adverse effects:
More common: fever, hypokalemia, injury to intravenous site, orthostatic hypotensionMore common: nausea, pollakiuria, polyuria, thirst, xerostomia
Less common: anemia, atrial fibrillation, confusion, constipation, dehydration, diarrhea, dry mouth, electrocardiographic abnormalities, erythema, headache, hematuria, hyperglycemia, hypertension, hypoglycemia, hypomagnesia, hyponatremia, hypotension, insomnia, nausea, oral candidiasis, pain, peripheral edema, pharyngolaryngitis, phlebitis, pneumonia, polyuria, pruritus, thirst, urinary tract infection, vomitingLess common: anorexia, constipation, fever, gastrointestinal bleeding, hepatotoxicity, hyperglycemia, hypernatremia, weakness
Change intravenous site every 24 hours; avoid corn productsDo not use for more than 30 days or in patients with underlying liver disease because of risk of hepatotoxicity; avoid consumption of grapefruit juice
Contraindicated in patients with anuria or concurrent use of CYP3A inhibitorsLiver function should be monitored frequently
Not recommended for patients with creatinine clearance less than 30 mL per minute per 1.73 m2 (0.50 mL per second per m2)Contraindicated in patients with hypovolemic hyponatremia, anuria, or concurrent use of CYP3A inhibitors, or when there is an urgent need to increase sodium levels
Not recommended for patients with creatinine clearance less than 10 mL per minute per 1.732 (0.17 mL per second per m2)
Price*$687 for 100 mL of solution (20 mg of conivaptan)$3,440 for 10 15- or 30-mg tablets
ConsiderationsVaptans should be initiated in the inpatient setting to monitor sodium levels
No reports of osmotic demyelination; however, vaptans can rapidly overcorrect
Hypovolemic hyponatremia should be ruled out before initiating therapy
Should not be used in patients with severe symptomatic hyponatremia
Good safety profile for limited use in current studies; further study needed to evaluate long-term use, effects, cost-effectiveness, and effects on morbidity and mortality
Optimal regimens and dosages are unclear


Hypernatremia is defined as a serum sodium level greater than 145 mEq per L. It is associated with increased morbidity and mortality in the inpatient setting.31,32 Hypernatremia is caused by net water loss (increased loss or decreased intake) or, rarely, sodium gain. Patients at increased risk include those with an impaired thirst mechanism or restricted access to water (e.g., those with altered mental status, intubated patients, infants, older adults).

Symptoms of hypernatremia in infants can include tachypnea, muscle weakness, restlessness, a high-pitched cry, insomnia, lethargy, and coma. Seizures usually occur only in cases of inadvertent sodium loading or rapid rehydration. In adults, symptoms tend to be mild and may include anorexia, muscle weakness, restlessness, nausea, and vomiting. Severe symptoms are likely to occur with acute increases in plasma sodium levels or at concentrations greater than 160 mEq per L. Hypernatremia can cause brain shrinkage, resulting in vascular rupture and intracranial bleeding.33


The cause of hypernatremia is usually evident from the history and physical examination, and is typically water loss (e.g., gastrointestinal loss, restricted access to water) or sodium gain (Table 2).3,12,33,34 Patients are often asymptomatic but can present with irritability, nausea, weakness, altered mental status, or coma. Water loss can be pure water loss (e.g., in diabetes insipidus) or hypotonic fluid loss (e.g., renal, gastrointestinal, or cutaneous losses). Sodium gain is usually iatrogenic from the infusion of hypertonic solutions. Laboratory studies are not necessary if the cause is apparent from the history, but frequent electrolyte checks are recommended during correction. When the cause is not clear, laboratory studies should be guided by the history12 (Figure 335 ).

Hypovolemic hypernatremia
Body fluid loss (e.g., burns, sweating)ClinicalFree water replacement
Diuretic useClinicalStop diuretic
Gastrointestinal loss (e.g., vomiting, diarrhea, fistulas)ClinicalFree water replacement
Heat injuryElevated temperature, myoglobinuria, elevated creatinine levelIntravenous fluids, supportive care
Osmotic diuresis (e.g., hyperosmolar nonketotic coma, mannitol use, enteral feeding)Elevated glucose level; sodium level often elevated after correctionCorrect glucose level, stop causative agent
Post-obstructionClinicalSupportive care
Euvolemic hypernatremia
Central diabetes insipidusClinical history of central nervous system insult; urinary concentration after administration of desmopressinTreatment is rarely required unless thirst is impaired
FeverClinicalTreat underlying cause
Hyperventilation/mechanical ventilationClinicalAdjust ventilation
HypodipsiaClinicalIncrease free water consumption
Medications (e.g., amphotericin, aminoglycosides, lithium, phenytoin [Dilantin])Medication reviewStop causative medication
Nephrogenic diabetes insipidusHistory of nephrotoxic medication use (amphotericin, demeclocycline [Declomycin], foscarnet, lithium, methoxyflurane), failure to concentrate urine after administration of desmopressinStop causative medication
Sickle cell diseaseHemoglobin electrophoresisTreat underlying disease
Suprasellar and infrasellar tumorsMagnetic resonance imagingTreat underlying disease
Hypervolemic hypernatremia
Cushing syndrome24-hour urinary cortisol and adrenocorticotropic hormone levels, dexamethasone suppression testTreat underlying disease
HemodialysisClinical historyTreat underlying disease
HyperaldosteronismHistory of hypertension and hypokalemia, plasma aldosterone-to-renin ratio,3 history of hypertension and hypokalemiaTreatment usually not needed for hypernatremia
Iatrogenic (e.g., salt tablet or salt water ingestion, saline infusions, saline enemas, intravenous bicarbonate, enteral feedings)Recent administration of hypertonic saline, enteral feedings, sodium bicarbonate infusion, or hypertonic dialysisStop causative medication, rapid free water replacement

Diabetes insipidus is caused by a defect in ADH, either at the level of the central nervous system (central diabetes insipidus) or kidneys (nephrogenic diabetes insipidus). Inappropriately dilute urine (osmolality less than 300 mOsm per kg) in the setting of hypernatremia suggests diabetes insipidus. Hyperaldosteronism can cause mild hypernatremia but is rarely clinically relevant. Hyperglycemia can also cause hypernatremia, even after correction of glucose levels.36


The treatment of hypernatremia involves treating the underlying cause and correcting the water deficit. Determining volume status and calculating the total body water deficit are important(eTable A). When correcting the total body water deficit, oral or enteral free water should be used whenever possible. When intravenous fluids are required, hypotonic solutions should be used. Rapid over-correction can result in cerebral edema; therefore, the least amount of fluid possible should be used.33 eTable C lists the sodium content of various intravenous fluids.

In patients with rapid development of hypernatremia, sodium can be corrected quickly with isotonic saline or water without increasing the risk of cerebral edema. A correction rate of 1 mEq per L per hour is considered safe in these patients.12,36 In patients with hypernatremia that developed over a longer period, the sodium level should be corrected at a rate of 0.5 mEq per L per hour, with no more than an 8 to 10 mEq per L decrease over 24 hours.33,36,37 The target sodium level should be 145 mEq per L.33

FluidSodium concentration (mEq per L)
Dextrose 5%0
Dextrose 5% with sodium chloride 0.2%34
Sodium chloride 0.45%77
Lactated Ringer solution130
Sodium chloride 0.9%154

Data Sources: We searched the Cochrane database, Dynamed, PubMed, PEPID, Clinical Evidence, the National Guideline Clearinghouse, UpToDate, and OVID using the key terms hyponatremia, hypernatremia, vaptans, diagnosis, and treatment. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Search dates: November 15, 2013; March 1, 2014; and October 5, 2014.

The views expressed are those of the authors and do not reflect the official policy of the Department of the Army, the Department of Defense, or the U.S. government.

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