Dining Out Ask for nutrition information before you order, and select a lower sodium meal. Ask that no salt be added to your meal. Order vegetables with no salt added or fruit as a side item. Split a meal with a friend or family member. Keep takeout and fast food to an occasional treat.

Choose a Heart-Healthy Diet The Dietary Approaches to Stop Hypertension DASH eating plan is a simple, heart-healthy diet that can help prevent or lower high blood pressure.

Range of Sodium Content for Selected Foods. Page last reviewed: August 23, Content source: National Center for Chronic Disease Prevention and Health Promotion , Division for Heart Disease and Stroke Prevention. home Sodium Intake and Health. Get Email Updates. To receive email updates about this page, enter your email address: Email Address.

What's this? Division of Nutrition, Physical Activity, and Obesity. Stroke Heart Disease Cholesterol High Blood Pressure Million Hearts® WISEWOMAN. In most cases, hyponatremia results when the elimination of total body water decreases.

The pathophysiology of hyponatremia will be discussed later in this article. Most patients with hyponatremia are asymptomatic. Symptoms do not usually appear until the plasma sodium level drops below mEq per L mmol per L and usually are nonspecific e.

The development of clinical signs and symptoms also depends on the rapidity with which the plasma sodium level decreases. In the event of a rapid decrease, the patient can be symptomatic even with a plasma sodium level above mEq per L. Poor prognostic factors for severe hyponatremia in hospitalized patients include the presence of symptoms, sepsis, and respiratory failure.

Figure 1 13 shows an algorithm for the assessment of hyponatremia. The patient then should be classified into one of the following categories: hypervolemic edematous , hypovolemic volume depleted , or euvolemic.

Hyponatremia in the presence of edema indicates increased total body sodium and water. This increase in total body water is greater than the total body sodium level, resulting in edema.

The three main causes of hypervolemic hyponatremia are congestive heart failure, liver cirrhosis, and renal diseases such as renal failure and nephrotic syndrome.

These disorders usually are obvious from the clinical history and physical examination alone. Hyponatremia in a volume-depleted patient is caused by a deficit in total body sodium and total body water, with a disproportionately greater sodium loss, whereas in euvolemic hyponatremia, the total body sodium level is normal or near normal.

Differentiating between hypovolemia and euvolemia may be clinically difficult, especially if the classic features of volume depletion such as postural hypotension and tachycardia are absent. Laboratory markers of hypovolemia, such as a raised hematocrit level and blood urea nitrogen BUN -to-creatinine ratio of more than 20, may not be present.

In fact, results of one study 15 showed an increased BUN-to-creatinine ratio in only 68 percent of hypovolemic patients. Two useful aids for evaluating euvolemic or hypovolemic patients are measurement of plasma osmolality and urinary sodium concentration.

Plasma osmolality testing places the patient into one of three categories, normal, high, or low plasma osmolality, while urinary sodium concentration testing is used to refine the diagnosis in patients who have a low plasma osmolality.

The combination of hyponatremia and normal plasma osmolality to mOsm per kg [ to mmol per kg] of water can be caused by pseudohyponatremia or by the post-transurethral prostatic resection syndrome. The phenomenon of pseudohyponatremia is explained by the increased percentage of large molecular particles, such as proteins and fats in the serum, relative to sodium.

These large molecules do not contribute to plasma osmolality, resulting in a state in which the relative sodium concentration is decreased, but the overall osmolality remains unchanged. Severe hypertriglyceridemia and hyperproteinemia are two causes of this condition in patients with pseudohyponatremia.

These patients usually are euvolemic. The post-transurethral prostatic resection syndrome consists of hyponatremia with possible neurologic deficits and cardiorespiratory compromise. Although the syndrome has been attributed to the absorption of large volumes of hypotonic irrigation fluid intraoperatively, its pathophysiology and management remain controversial.

Increased plasma osmolality more than mOsm per kg of water in a patient with hyponatremia is caused by severe hyperglycemia, such as that occurring with diabetic ketoacidosis or a hyperglycemic hyperosmolar state. It is caused by the presence of glucose molecules that exert an osmotic force and draw water from the intracellular compartment into the plasma, with a diluting effect.

Osmotic diuresis from glucose then results in hypovolemia. Fortunately, hyperglycemia can be diagnosed easily by measuring the bedside capillary blood glucose level. Patients with low plasma osmolality less than mOsm per kg of water can be hypovolemic or euvolemic.

The level of urine sodium is used to further refine the differential diagnosis. Excess renal sodium loss can be confirmed by finding a high urinary sodium concentration more than 30 mmol per L.

In these patients, the main causes of hyponatremia are renal disorders, endocrine deficiencies, reset osmostat syndrome, syndrome of inappropriate antidiuretic hormone secretion SIADH , and drugs or medications.

Because of their prevalence and importance, SIADH and drugs deserve special mention, and the author will elaborate on these causes later in the article.

Renal disorders that cause hyponatremia include sodium-losing nephropathy from chronic renal disease e. Endocrine disorders are uncommon causes of hyponatremia.

Diagnosing hypothyroidism or mineralocorticoid deficiency i. In either case, the serum levels of thyroid-stimulating hormone TSH , cortisol, and adrenocorticotropic hormone ACTH should be measured, because hypothyroidism and hypoadrenalism can coexist as a polyendocrine deficiency disorder i.

The reset osmostat syndrome occurs when the threshold for antidiuretic hormone secretion is reset downward. Patients with this condition have normal water-load excretion and intact urine-diluting ability after an oral water-loading test.

The condition is chronic—but stable—hyponatremia. Patients with extra-renal sodium loss have a low urinary sodium concentration less than 30 mmol per L as the body attempts to conserve sodium.

Causes include severe burns and gastrointestinal losses from vomiting or diarrhea. Diuretic therapy, on the other hand, can cause either a low or a high urinary-sodium concentration, depending on the timing of the last diuretic dose administered, but the presence of concomitant hypokalemia is an important clue to the use of a diuretic.

Medications and drugs that cause hyponatremia are listed in Table 1. Diuretics cause a hypovolemic hyponatremia. Fortunately, in most cases, stopping the offending agent is sufficient to cause spontaneous resolution of the electrolyte imbalance.

Antidiuretic hormone causes water retention, so hyponatremia then occurs as a result of inappropriately increased water retention in the presence of sodium loss. The diagnostic criteria for SIADH are listed in Table 2.

SIADH is a diagnosis of exclusion and should be suspected when hyponatremia is accompanied by urine that is hyperosmolar compared with the plasma. This situation implies the presence of a low plasma osmolality with an inappropriately high urine osmolality, although the urine osmolality does not necessarily have to exceed the normal range.

Another suggestive feature is the presence of hypouricemia caused by increased fractional excretion of urate.

Any cerebral insult, from tumors to infections, can cause SIADH. Less common causes include acute intermittent porphyria, multiple sclerosis, and Guillain-Barré syndrome.

The treatment of hyponatremia can be divided into two steps. First, the physician must decide whether immediate treatment is required. This decision is based on the presence of symptoms, the degree of hyponatremia, whether the condition is acute arbitrarily defined as a duration of less than 48 hours or chronic, and the presence of any degree of hypotension.

The second step is to determine the most appropriate method of correcting the hyponatremia. Shock resulting from volume depletion should be treated with intravenous isotonic saline.

Acute severe hyponatremia i. In patients with chronic hyponatremia, overzealous and rapid correction should be avoided because it can lead to central pontine myelinolysis. In patients who have difficulty adhering to fluid restriction or who have persistent severe hyponatremia despite the above measures, demeclocycline Declomycin in a dosage of to 1, mg daily can be used to induce a negative free-water balance by causing nephrogenic diabetes insipidus.

Loop diuretics can be used in severe cases. Newer agents such as the arginine vasopressin receptor antagonists have shown promising results 39 and may be useful in patients with chronic hyponatremia.

In all patients with hyponatremia, the cause should be identified and treated. Some causes, such as congestive heart failure or use of diuretics, are obvious. Other causes, such as SIADH and endocrine deficiencies, usually require further evaluation before identification and appropriate treatment.

DeVita MV, Gardenswartz MH, Konecky A, Zabetakis PM. Incidence and etiology of hyponatremia in an intensive care unit. The more chronic the hyponatremia and the lower the serum sodium concentration, the greater the risk of complications from overaggressive therapy and the greater the need for monitoring to avoid overcorrection.

Determine the severity degree of hyponatremia — Although a variety of definitions have been used, we use the following:. Determine the severity of symptoms — Symptoms due to hyponatremia are typically classified as severe or mild to moderate; some patients are or appear to be asymptomatic:.

See "Manifestations of hyponatremia and hypernatremia in adults", section on 'Clinical manifestations of acute hyponatremia'.

Severe symptoms such as seizures are relatively common in patients with an acute and marked reduction in the serum sodium concentration. Without time for brain adaptation to occur, affected patients can develop severe neurologic manifestations, including coma, brainstem herniation, and death.

By contrast, seizures and other severe neurologic manifestations are relatively uncommon in patients with chronic hyponatremia even among those with severely decreased serum sodium concentrations. As an example, a single-center study identified seizures in 3 of patients 2.

However, in patients with chronic hyponatremia, the risk for convulsions may be higher in patients with an underlying seizure disorder and in patients who are withdrawing from alcohol.

In patients with severe, chronic hyponatremia, these findings are usually not associated with impending herniation. See "Manifestations of hyponatremia and hypernatremia in adults", section on 'Clinical manifestations of chronic hyponatremia'.

Thus, such patients are often offered chronic therapies to normalize the serum sodium concentration in an effort to treat these subtle manifestations [ 9 ] and to avoid the possibility that the serum sodium concentration will fall further and produce more serious symptoms.

Chronic therapies that are used include oral urea , salt tablets and furosemide , or vasopressin antagonists. However, there is no evidence proving that these therapies decrease the risk of falls and fractures.

Determine the need for hospitalization — Patients at high risk for complications from untreated hyponatremia and those at high risk for complications from overcorrection of hyponatremia should be treated in hospital settings that allow frequent assessments of the patient's neurologic condition, accurate measurements of urine output, and frequent measurements of the serum sodium concentration.

Such patients include:. By contrast, patients with mild hyponatremia and asymptomatic patients with moderate hyponatremia usually do not require hospitalization. Treatment of patients who do not require hospital admission varies according to the cause of hyponatremia.

Chronic treatment of these disorders is discussed separately:. GOALS OF THERAPY — The treatment of hyponatremia in hospitalized patients has four important goals: to prevent further declines in the serum sodium concentration, to decrease intracranial pressure in patients at risk for developing brain herniation, to relieve symptoms of hyponatremia, and to avoid excessive correction of hyponatremia in patients at risk for osmotic demyelination syndrome ODS [ 10 ].

Our approach to attaining these goals, both during initial therapy ie, the first six hours after recognition of the electrolyte disturbance and during subsequent therapy the first several days , is presented below. See 'Acute hyponatremia: Initial therapy first six hours ' below and 'Subsequent therapy first several days ' below.

Prevent a further decline in serum sodium — The risk of a further fall in the serum sodium concentration is especially high for the following groups:. In such patients, delayed absorption of ingested water from the gastrointestinal tract may produce a further decline in the serum sodium concentration.

Large volumes of isotonic fluid produce volume expansion and result in increased sodium excretion in the urine. If antidiuretic hormone ADH levels are high, the excretion of this sodium in a concentrated urine will cause the serum sodium to fall further, a phenomenon that has been called "desalination" [ 11 ].

Thus, administration of additional isotonic saline should be avoided in such patients. Prevent brain herniation — Fatal herniation is the most dreaded complication of hyponatremia. Herniation has been reported almost exclusively in the following settings:.

Concurrent hypoxemia, which may result from noncardiogenic pulmonary edema or hypoventilation, can exacerbate hyponatremia-induced cerebral edema and lead to a vicious cycle ending in death [ 6 ]. In contrast to the clinical settings listed above, other patients with hyponatremia have virtually no risk of herniation.

Although such patients who are hospitalized with hyponatremia have a high mortality rate, deaths associated with hyponatremia are primarily due to the underlying disease and are rarely caused by cerebral edema. Relieve symptoms of hyponatremia — It is important to determine whether or not hyponatremia may be producing symptoms and to relieve those symptoms by raising the serum sodium concentration.

See 'Determine the severity of symptoms' above and "Manifestations of hyponatremia and hypernatremia in adults", section on 'Hyponatremia'. The urgency and, therefore, the aggressiveness of treatment to raise the serum sodium varies depending upon the severity of symptoms, the acuity of hyponatremia, the level of the serum sodium concentration, and the patient's underlying condition.

Thus, if symptoms persist after an increase of this magnitude, there is no benefit and, in some cases, potential harm from correcting at a faster rate. Overly rapid correction of hyponatremia can result from efforts to raise the serum sodium, such as administration of hypertonic saline or vasopressin antagonists, or from elimination of the underlying cause of hyponatremia, such as the administration of saline to patients with true volume depletion, the administration of glucocorticoid therapy in adrenal insufficiency, or water restriction in patients with self-induced water intoxication.

See 'Diagnose and treat the underlying cause of hyponatremia' below. Some patients are at particularly high or low risk for ODS see "Osmotic demyelination syndrome ODS and overly rapid correction of hyponatremia", section on 'Risk factors for ODS' :.

These patients have not had time for the brain adaptations that reduce the severity of brain swelling but also increase the risk of harm from rapid correction of the hyponatremia. See "Manifestations of hyponatremia and hypernatremia in adults", section on 'Osmolytes and cerebral adaptation to hyponatremia'.

Complications of overly rapid correction of hyponatremia were once called "central pontine myelinolysis CPM ," but the term "osmotic demyelination syndrome ODS " was introduced to describe these complications for several reasons: because demyelination may be more diffuse and does not necessarily involve the pons, because not all patients with posttreatment neurologic symptoms have demonstrable anatomic lesions, and because not all patients with central pontine myelinolysis have experienced a rapid increase in serum sodium figure 1 [ 14 ].

See "Osmotic demyelination syndrome ODS and overly rapid correction of hyponatremia". In symptomatic patients with acute hyponatremia or in patients with severe symptoms, this goal should be achieved quickly, over six hours or less.

Thereafter, the serum sodium can be maintained at a constant level for the remainder of the hour period to avoid overly rapid correction.

In general, the same rate of rise can be continued on subsequent days until the sodium is normal or near normal. For this reason, the therapeutic goal should not be too close to rates that can result in patient harm. Thus, patients requiring emergency therapy can be corrected rapidly in the first several hours of the hour period.

Related Pathway s : Hyponatremia: Initial inpatient management in adults with moderate to severe hyponatremia. Because of osmotically driven water flow across the blood-brain barrier, an acute onset of hyponatremia can result in life-threatening cerebral edema.

Thus, even mild symptoms in acute hyponatremia present a medical emergency that requires prompt and aggressive treatment with hypertonic saline to prevent brain herniation.

Placement of a central venous catheter before administering hypertonic saline is not necessary , and attempts to do so can delay potentially life-saving therapy; 3 percent sodium chloride can be safely administered in a peripheral vein [ ].

However, we do not give hypertonic saline if the hyponatremia is already autocorrecting due to a water diuresis. Alternatively, autocorrection can be detected by remeasuring the serum sodium. However, the results of this remeasurement must be available expeditiously.

A point-of-care sodium analyzer if available provides helpful and rapid information about the trajectory of the serum sodium in such patients. We then monitor the patient for symptoms and remeasure the serum sodium concentration every one to two hours to determine the need for additional therapy.

Patients with self-induced water intoxication may have a further decline in serum sodium, even after presentation, due to delayed absorption of ingested water. In addition, patients who have ingested large volumes of water are volume expanded, which results in increased sodium excretion in the urine.

If antidiuretic hormone ADH levels are high due to a nonosmotic stimulus such as nausea, the excretion of sodium in a concentrated urine will cause the serum sodium to fall, a phenomenon that has been called "desalination" [ 11 ].

A table summarizing the emergency management of acute hyponatremia in adults is provided table 1. An alternative approach, recommended in by European organizations, is to treat with two mL bolus infusions of 3 percent saline , each given over 20 minutes, measuring the serum sodium between infusions [ 28 ].

Based upon broad clinical experience, the administration of hypertonic saline is the only rapid way to raise the serum sodium concentration and improve neurologic manifestations and outcomes in patients with severe, symptomatic hyponatremia [ 12,18,21, ].

Although mannitol has been used to treat cerebral edema, it is potentially nephrotoxic and can also lower the serum sodium concentration, making it more difficult to monitor the hyponatremia.

Vaptans have variable efficacy, and their onset of action is too slow to be recommended in patients with acute hyponatremia. However, such patients should undergo monitoring to detect a further decrease in serum sodium in which case hypertonic saline may become necessary.

See 'Monitoring' below. In all patients with acute hyponatremia, we employ additional measures to prevent the serum sodium from further decreasing, such as discontinuing medications that could contribute to hyponatremia and limiting the intake of hypotonic fluids.

See 'Additional measures in all patients' below. Rather, our initial approach includes general measures that are applicable to all hyponatremic patients ie, identify and discontinue drugs that could be contributing to hyponatremia; identify and, if possible, reverse the cause of hyponatremia; and limit further intake of water [eg, fluid restriction, discontinue hypotonic intravenous infusions].

Severe symptoms or known intracranial pathology — In all patients with severe symptoms of hyponatremia eg, seizures, obtundation, coma, respiratory arrest , we treat with a mL bolus of 3 percent saline followed, if symptoms persist, by up to two additional mL doses to a total dose of mL ; each bolus is infused over 10 minutes [ 40 ].

The presence of moderate to severe hyponatremia in a patient with intracranial pathology such as recent traumatic brain injury, recent intracranial surgery or hemorrhage, or an intracranial neoplasm or other space-occupying lesion should raise concern for increased intracranial pressure and possible risk for herniation.

Thus, we treat such patients with a mL bolus of 3 percent saline , followed, if symptoms persist, with up to two additional mL doses to a total dose of mL over the course of 30 minutes.

However, if such patients are hospitalized, we do not suggest hypertonic saline. In addition, the measures taken to prevent osmotic demyelination syndrome ODS in patients with severe hyponatremia described below are generally not necessary. Rather, our initial approach in such patients is to take general measures that are applicable to all hyponatremic patients ie, identify and discontinue drugs that could be contributing to hyponatremia; identify and, if possible, reverse the cause of hyponatremia; and limit further intake of water.

However, some patients with moderate hyponatremia have risk factors for ODS eg, alcohol use disorder, hypokalemia, malnutrition, advanced liver disease or have arginine vasopressin disorders formerly called diabetes insipidus and have desmopressin-induced hyponatremia.

These individuals, despite not having severe hyponatremia, can develop ODS, and more care should be taken to avoid overly rapid correction. Such measures are described below.

Some patients may also require desmopressin dDAVP to prevent overly rapid correction. See 'If cause of hyponatremia is rapidly reversible' below.

There is evidence that 3 percent saline can be safely infused in a peripheral vein [ 25,26,41 ], and there is no evidence that it causes vascular thrombosis or extravasation injury. Nevertheless, some hospitals have policies stating that 3 percent saline can only be infused in a central vein.

Such policies may cause some clinicians to choose isotonic saline instead of hypertonic saline for patients who are believed to be hypovolemic; however, isotonic saline should be avoided in patients with severe hyponatremia.

If 3 percent saline cannot be used because of hospital policy restrictions, options include infusion of 1. See 'Use of isotonic saline in symptomatic or severe hyponatremia' below.

There are limited data to inform the choice between slow, continuous infusion and intermittent boluses of 3 percent saline in patients with severe hyponatremia and mild to moderate symptoms. One unblinded trial compared continuous infusion 0.

The two groups had similar rates of symptom resolution and overcorrection. However, at these doses, therapeutic relowering with 5 percent dextrose in water was required in approximately one-half of the patients, and despite this intervention, overcorrection was frequent.

Because most of the patients were at very low risk of developing osmotic demyelination, the safety of these regimens could not be established. For those with rapidly reversible causes of hyponatremia as examples, patients with hypovolemia, thiazide-associated hyponatremia, or arginine vasopressin disorders who have desmopressin-induced hyponatremia who are likely to develop a water diuresis during the course of therapy, or in those who are at high risk of developing ODS, we simultaneously initiate or continue desmopressin to prevent overly rapid correction.

Patients with severe hyponatremia are at risk of worsening symptoms if the serum sodium falls further and, conversely, at risk of osmotic demyelination if the serum sodium rises too quickly. The lower the serum sodium concentration, the greater the risk. For reasons discussed below, we prefer 3 percent saline in such patients to treat hyponatremia, even among those who are thought to be hypovolemic.

Isotonic saline can be given concurrently with 3 percent saline , if needed, to correct symptomatic hypovolemia or prerenal azotemia. See 'Use of isotonic saline in symptomatic or severe hyponatremia' below and 'Isotonic saline in true volume depletion' below.

Patients with arginine vasopressin disorders formerly called diabetes insipidus who develop hyponatremia while taking desmopressin should be considered a high-risk group because they can become hypernatremic if desmopressin is discontinued.

Oral or intranasal outpatient dosing should be converted to the parenteral route to ensure an effective antidiuresis while hyponatremia is being corrected. A bolus of hypertonic saline can be given at the start of therapy to help relieve troublesome symptoms if these are present.

The rate of infusion of hypertonic saline is then adjusted to achieve the desired rate of correction. Desmopressin makes the rate of correction resulting from hypertonic saline more predictable because it prevents an unexpected water diuresis from occurring during the course of therapy.

With this approach, desmopressin is given to eliminate the potential for urinary water losses, in essence creating a state of iatrogenic SIADH that can be managed more predictably with hypertonic saline. The approach can be used to treat both hypovolemic hyponatremia and SIADH.

It is particularly attractive in patients who are at high risk of developing ODS from overly rapid correction of hyponatremia. We recommend against the less frequent desmopressin dosing that is typically used to treat arginine vasopressin disorders ie, every 12 or 24 hours.

These dosing schedules allow escape from the antidiuretic effect and emergence of a water diuresis, possibly resulting in overly rapid correction of hyponatremia. If desmopressin is used, it is important to restrict free water intake to avoid an unwanted decrease in the serum sodium concentration.

For this reason, we do not use desmopressin in patients who are at high risk for self-induced water intoxication eg, psychotic patients. Some experts prefer to withhold desmopressin initially, giving it only if a water diuresis develops during the course of therapy [ 19,43 ].

However, we find this strategy to be labor intensive and often unsuccessful, associated with an unacceptably high incidence of unintentional overcorrection. Once a water diuresis begins, washout of the renal medullary gradient may result in a delay in achieving the full antidiuretic effect of desmopressin.

Other clinicians may choose not to use desmopressin and instead partially replace urinary water losses with intravenous 5 percent dextrose in water to prevent overly rapid correction. However, in our experience, that strategy is less effective and more difficult to manage than using desmopressin.

Large doses of 5 percent dextrose will also exacerbate thiamine deficiency, hypokalemia, and hypophosphatemia if these are present. If the proactive strategy of hypertonic saline with desmopressin is chosen, there is less need for frequent measurements of the serum sodium concentration and urine output; once it has been established that a large urine output has been prevented and that hypertonic saline is increasing the serum sodium concentration at the desired rate, measurements of the serum sodium every six hours are usually sufficient.

If cause of hyponatremia is unlikely to be rapidly reversible — We do not use desmopressin in patients who are unlikely to develop a water diuresis during the course of therapy.

As examples:. In edematous patients, such as those with heart failure, coadministration of furosemide with hypertonic saline may be required to prevent worsening hypervolemia. Several groups have reported favorable outcomes treating heart failure patients in this manner [ ].

These include:. Discontinue those drugs unless there is no reasonable substitute and stopping the medication would cause serious harm. See "Diagnostic evaluation of adults with hyponatremia". There is no evidence to support this practice. Although the eventual goal is normalization of the serum sodium concentration, the therapeutic goal on any given day should not be a predefined serum sodium level, as this will often lead to overcorrection of hyponatremia when the serum sodium concentration is very low [ 4 ].

Monitoring — In patients with acute hyponatremia, we monitor the patient for symptoms and remeasure the serum sodium concentration hourly to determine the need for additional therapy.

Patients who are treated for chronic hyponatremia in the hospital should have their serum sodium measured often enough to ensure an appropriate rate of correction and to allow the clinician to react quickly to impending overly rapid correction eg, every four hours.

In addition, the urine output should be monitored, and, if increasing, the urine osmolality, urine sodium, and urine potassium should be measured. An increase in urine output and a decrease in the urine cation concentration can signify that the rate of correction is accelerating, and, in this setting, the serum sodium should be measured more frequently eg, every two hours.

Subsequent therapy of chronic hyponatremia. See 'Potassium replacement in hypokalemic patients' below. If the serum sodium begins to fall again, hypertonic saline can be resumed as needed to preserve the desired increase in serum sodium for the day.

Fluid restriction — Fluid restriction to below the level of urine output is indicated for the treatment of symptomatic or severe hyponatremia in edematous states such as heart failure and cirrhosis , syndrome of inappropriate antidiuretic hormone SIADH , and advanced kidney function impairment.

Restriction to 50 to 60 percent of daily fluid requirements may be required to achieve the goal of inducing negative water balance [ 31 ].

Fluid restriction is also warranted in hyponatremic patients with primary polydipsia in whom increased fluid intake is the primary problem.

See "Causes of hypotonic hyponatremia in adults", section on 'Primary polydipsia due to psychosis'. The effectiveness of fluid restriction alone can be predicted by the urine-to-serum cation ratio the concentration of the urine cations, sodium Na and potassium K , to the serum sodium concentration; ie, the concentrations of the urine [Na] plus the urine [K] divided by the serum [Na] [ 47 ].

A ratio less than 0. Similarly, if fluid must be given or the serum sodium concentration must be raised quickly because of symptomatic hyponatremia, the cation concentration of the administered fluid must exceed the cation concentration of the urine.

Other therapies for chronic hyponatremia. Loop diuretics in patients with a high urine cation concentration — Concurrent use of a loop diuretic may be beneficial in patients with SIADH who have a urine-to-serum cation ratio greater than 1.

By inhibiting sodium chloride reabsorption in the thick ascending limb of the loop of Henle, furosemide interferes with the countercurrent mechanism and induces a state of antidiuretic hormone ADH resistance, resulting in the excretion of a less-concentrated urine and increased water loss.

See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion SIADH and reset osmostat", section on 'Salt plus a loop diuretic'.

Given hourly, salt tablets can substitute for hypertonic saline in nonurgent situations [ 48 ]. Oral salt tablets may also be effective in hypovolemic patients who are treated as outpatients in combination with reversing the cause of hypovolemia. Calculating the dose of oral salt tablets uses the same principles as intravenous isotonic or hypertonic saline : 9 g of oral salt provides a similar quantity of sodium as 1 L of isotonic saline mEq but without any water; 1 g of oral salt is equivalent to 35 mL of 3 percent saline.

See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion SIADH and reset osmostat", section on 'Oral salt tablets'.

Oral salt tablets should not be given to edematous patients eg, those with heart failure, cirrhosis. See "Hyponatremia in patients with heart failure" and "Hyponatremia in patients with cirrhosis". Urea in patients with SIADH — Urea administered orally or enterally via a gastric tube will increase the serum sodium concentration by increasing the excretion of electrolyte-free water [ 49 ].

Urea is an alternative to the combination of loop diuretics and oral salt tablets [ 43 ]. Favorable short- and long-term outcomes with urea therapy for hyponatremia have been reported in patients with syndrome of inappropriate antidiuretic hormone SIADH [ ]. See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion SIADH and reset osmostat", section on 'Urea'.

Urea is available in the United States and Europe either as a palatable, flavored medical food dispensed in 15 g packets or as unflavored urea in bulk containers. Potassium replacement in hypokalemic patients — Potassium is as osmotically active as sodium. As a result, giving potassium usually for concurrent hypokalemia can raise the serum sodium concentration and osmolality in hyponatremic patients [ ].

Since most of the potassium that is retained in the body enters the cells, electroneutrality is maintained in one of three ways, each of which will raise the serum sodium concentration:.

These hydrogen ions are buffered by extracellular bicarbonate and, to a much lesser degree, plasma proteins.

This buffering converts the bicarbonate ions to carbon dioxide and water, and the bicarbonate is replaced by the chloride that was infused with potassium which, as noted, is exchanged for hydrogen ions.

The increased intracellular osmolality due to potassium leads to water movement into the cells. The net effect is that concurrent administration of potassium must be taken into account when estimating the sodium deficit and anticipating the rate of correction of the hyponatremia.

This relationship becomes clinically important in the patient with severe diuretic or vomiting-induced hyponatremia who is also hypokalemic. If the patient is a 70 kg man, the total body water TBW will be approximately 40 liters 60 percent of body weight. Thus, giving potassium chloride alone will correct both the hyponatremia and the hypokalemia [ 54,55 ].

Giving additional sodium may lead to an overly rapid elevation in the serum sodium concentration and potentially cause osmotic demyelination syndrome ODS [ 57 ]. See 'Avoid overcorrection' above. This solution will generally not increase the serum sodium. Oral preparations of potassium chloride will raise the serum sodium as they contain no or little water [ 42 ].