After the sodium has been corrected at the appropriate rate for 24 hours, desmopressin is stopped. Hypertonic saline can then be stopped, or, if required for continuing correction of hyponatremia, continued..
For patients with rapid-onset hyponatremia and neurologic symptoms, rapid correction is accomplished by giving mL of hypertonic saline IV over 15 minutes.
This dose can be repeated once if neurologic symptoms are still present. This amount in mEq OR mmol may be calculated using the sodium deficit formula as.
Adjustments may be needed based on serum sodium concentrations, which are monitored closely during the first few hours of treatment. Patients with seizures, coma, or altered mental status need supportive treatment, which may involve endotracheal intubation Tracheal Intubation Most patients requiring an artificial airway can be managed with tracheal intubation, which can be Orotracheal tube inserted through the mouth Nasotracheal tube inserted through the nose Patients meeting the criteria for cerebral salt wasting should not be fluid restricted because fluid restriction can cause brain vessel vasospasm.
Although isotonic saline should correct the cause of hyponatremia, use of hypertonic saline is recommended to prevent more severe hyponatremia if indeed SIADH is present. The selective vasopressin V2 receptor antagonists conivaptan IV and tolvaptan oral are treatment options for severe or resistant hyponatremia. These drugs are potentially dangerous because they may correct serum sodium concentration too rapidly; they are typically reserved for severe Conivaptan is indicated for treatment of hypervolemic and euvolemic hyponatremia.
It requires close monitoring of patient status, fluid balance, and serum electrolytes and so its use is restricted to hospitalized patients. A loading dose is given followed by a continuous infusion over a maximum of 4 days. It is not recommended in patients with advanced chronic kidney disease estimated glomerular filtration rate Tolvaptan is a once daily tablet indicated for hypervolemic and euvolemic hyponatremia.
Close monitoring is recommended especially during initiation and dosage changes. Tolvaptan use is limited to 30 days because of the risk of liver toxicity.
Tolvaptan is not recommended for patients with advanced chronic kidney disease or liver disease. Its effectiveness can be limited by increased thirst. Tolvaptan use is also limited by high cost. Both of these drugs are strong inhibitors of CYP3A cytochrome P, family 3, subfamily A and as such have multiple drug interactions.
Other strong CYP3A inhibitors eg, ketoconazole , itraconazole , clarithromycin , retroviral protease inhibitors should be avoided. Clinicians should review the other drugs the patient is taking for potentially dangerous interactions with V2 receptor antagonists before initiating a treatment trial. Fluid restriction alone is frequently not enough to prevent recurrence of hyponatremia.
Oral salt NaCl tablets can be used with dosage adjusted to treat mild to moderate chronic hyponatremia in these patients. Oral urea is a very effective treatment for hyponatremia, but it is tolerated poorly by patients due to its taste. A newer oral formulation of urea has been developed to enhance palatability.
Osmotic demyelination syndrome previously called central pontine myelinolysis may follow too-rapid correction of hyponatremia. Demyelination classically affects the pons, but other areas of the brain can also be affected. Malnutrition also includes overnutrition. Undernutrition can result from inadequate ingestion of nutrients, malabsorption, impaired metabolism, loss Flaccid paralysis, dysarthria, and dysphagia can evolve over a few days or weeks after a hyponatremic episode.
The classic pontine lesion may extend dorsally to involve sensory tracts and leave patients with a "locked-in" syndrome an awake and sentient state in which patients, because of generalized motor paralysis, cannot communicate, except by vertical eye movements controlled above the pons. Damage often is permanent. In such cases, inducing hyponatremia with hypotonic fluid may mitigate the development of permanent neurologic damage.
Hyponatremia is potentially life threatening. The degree, duration, and symptoms of hyponatremia are used to determine how quickly to correct the serum sodium. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Manual was first published in as a service to the community.
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Common Health Topics. Videos Figures Images Quizzes Symptoms. Symptoms and Signs. Exclusion of translocational hyponatremia and pseudohyponatremia Identification of the cause.
Mild to moderate hyponatremia Severe hyponatremia Rapid-onset hyponatremia Hypertonic saline solution Selective receptor antagonists Chronic hyponatremia Osmotic demyelination syndrome. Key Points. Electrolyte Disorders. Test your knowledge. Primary aldosteronism is caused by autonomous production of aldosterone by the adrenal cortex due to hyperplasia, adenoma, or carcinoma.
Which of the following is an uncommon symptom of this disorder? More Content. Hyponatremia By James L. Click here for Patient Education. Recently Added. Renal fluid losses resulting in hypovolemic hyponatremia may occur with mineralocorticoid deficiency Addison Disease Addison disease is an insidious, usually progressive hypofunctioning of the adrenal cortex.
Administration of drugs that impair renal water excretion. Serum and urine electrolytes and osmolality. Clinical Calculator. When hypovolemic, 0. Acute hyponatremia with known rapid onset ie, within. Acute psychogenic polydipsia. Rapid-onset hyponatremia is problematic because the cells of the central nervous system have not had time to remove some of the intracellular osmolar compounds used to balance intracellular and extracellular osmolality.
These drugs are potentially dangerous because they may correct serum sodium concentration too rapidly; they are typically reserved for severe. Conivaptan is indicated for treatment of hypervolemic and euvolemic hyponatremia. It is not recommended in patients with advanced chronic kidney disease estimated glomerular filtration rate. Tolvaptan is a once daily tablet indicated for hypervolemic and euvolemic hyponatremia.
Mild metabolic alkalosis and normal K- is seen in hypopituitarism because of higher plasma aldosterone levels. In case of doubt, one can initiate 0. Hypovolemic hyponatremia improves with 0. Etiology of hyponatremia. Acute hyponatemia is generally symptomatic.
The risk of brain herniation is high and rapid correction is needed. Acute hyponatremia is common in marathon runners, patients with primary polydipsia and users of ecstasy. These patients have not had time for the brain adaptations to occur. Chronic hyponatremia- It is generally asymptomatic or has mild symptoms.
However; it may present with seizures if hyponatremia is very severe. Patients with mild symptoms eg, dizziness, forgetfulness, gait disturbance should be treated with less aggressive therapy. Among patients with urine to serum electrolyte ratio greater than 1, in whom fluid restriction will not be sufficient to achieve the desired goal, additional therapy includes salt tablets and if necessary, a loop diuretic. An alternative approach is the initiation of a vasopressin antagonist without fluid restriction.
Rate of correction: In chronic hyponatremia the brain undergoes adaptation and hence the risk of cerebral herniation is very low unlike the risk in acute hyponatremia. Instead very rapid correction can lead to osmotic demyelination syndrome ODS. Hence, chronic hyponatremia generally needs gradual correction.
High risk of ODS is seen esp. Osmotic demyelination-It is a rare, but severe and sometimes irreversible disorder. It presents with locked in syndrome i.
This disorder was formerly called central pontine myelinolysis CPM , but the name was changed because demyelination is more diffuse and does not necessarily involve the pons and. Recently, it has been shown that ODS can be reversed by relowering sodium and giving desmopressin. Potassium added to the solution should be included in the formula i. However, these formulae have limitations and cannot be used to accurately predict the magnitude of change in serum sodium and frequent measurements are necessary.
In the current guidelines these formulae are not used. In addition water restriction, salt, urea, demeclocycline and vaptans are used according to the etiology. In cases of chronic hyponatremia or mild symptoms water restriction is the main cornerstone of treatment. Diurectics and vaptans are the other drugs used. The cation concentration of the administered fluid must exceed the cation concentration of the urine.
Careful monitoring of the serum sodium is essential to prevent very rapid correction. Fluid restriction: The effectiveness of fluid restriction can be predicted by the urine to serum electrolyte ratio as described above. All fluids, not only water, must be included in the restriction; several days of restriction are usually necessary before a significant increase in plasma osmolality occurs; and only fluid, not sodium, should be restricted.
Thirst, can be ameliorated by substituting hard candy or ice chips for drinking fluids. Thiazides should not be used. Demeclocycline: Causes a nephrogenic form of diabetes insipidus, thereby decreasing urine concentration even in the presence of high plasma AVP levels. Treatment must be continued for several days to achieve maximal diuretic effects; one should wait 3 to 4 days before deciding to increase the dose.
Demeclocycline can cause reversible azotemia and sometimes nephrotoxicity, especially in patients with cirrhosis and should be discontinued if increasing azotemia occurs. Fluid restriction is warranted in hyponatremic patients with primary polydipsia in whom increased fluid intake is the primary problem. Glucocorticoid deficiency should be excluded by proper tests. Treatment consists of Glucocorticoids for adrenal insufficiency suppress ADH. As risk of ODS is high general guidelines for chronic hyponatremia should be followed.
Low solute intake should be corrected. Risk of ODS is small. Presentation may be acute or chronic. Mostly it is chronic. Sodium chloride, usually as 0. K may be added if required. Gastrointestinal losses- may be acute or chronic. Urine Cl is a better marker for volume status in patients with vomiting instead of Urine Na. Both K and bicarbonate deficits should be corrected along with volume correction. CSW may present acutely.
Moslty 0. Thiazides induced hyponatremia is usually chronic and should be corrected slowly as risk of ODS is high. K should also be supplemented. Patients with thiazide-induced hyponatremia are at high risk for a recurrence and should not be rechallenged with a thiazide. Mineralocorticoid deficiency associated hyponatremia is chronic and responsds to 0.
Fludrocortisone may be need for long term treatment. Water restriction is the mainstay of therapy. Vaptans act on vasopressin receptors as antagonists. The V2 receptors cause antidiuresis, while V1a and V1b receptors cause vasoconstriction and adrenocorticotropic hormone ACTH release, respectively.
The vasopressin receptor antagonists produce a water loss aquaresis without affecting sodium and potassium excretion. Vaptans are the most appropriate physiological approach to treat hyponatremia as they do not deplete electrolytes and restriction of fluids is not needed.
They do not stimulate the neurohormonal system and cause no renal impairment. Treatable causes of Euvolemic Hyponatremia should be excluded e. Vaptans are useful for chronic hyponatremia. Vaptans are used in addition to fluid restriction and sodium chloride administration. Tolvaptan significantly increased serum sodium concentration. Even with modest sodium improvement there was significant increase in mental scores.
But the effect was not clinically significant and long-term efficacy was doubtful as the patients were followed up for only 30 days. Thus liver function tests should be performed initially and LFT should be repeated three to four months after initiating therapy and then again at six-month intervals.
If liver injury is suspected, tolvaptan should be discontinued. Recently FDA has recommended Tolvaptan use but not for greater than 4 wks. Fluid restriction should not be used during the active phase of correction, thereby allowing the patient's thirst to compensate for vigorous aquaresis. Appropriate caution should be exercised in patients treated with tolvaptan for hyponatremia for extended periods e.
Patients who are refractory to or unable to tolerate or obtain other therapies for hyponatremia and in whom the benefit of tolvaptan treatment outweighs the risks, remain candidates for long- term therapy with tolvaptan; but in such cases, liver function tests should be monitored carefully and serially i. Conivaptan is FDA approved for euvolemic hyponatremia in hospitalized patients. It is available only as an intravenous preparation and is given as a mg loading dose over 30 min, followed by a continuous infusion.
Generally, the mg continuous infusion is used for the first 24 h. Therapy is limited to a maximum duration of 4 days because of drug-interaction effects with other agents metabolized by the CYP3A4 hepatic isoenzyme.
Hyponatremia in CHF is chronic and should be corrected till serum Na is normal and symptoms improve. The level of serum Na should be normalized so that diuretic therapy for CHF can be optimised.
In some studies, hyponatremia was associated with increased mortality and increased rate of re-hospitalization in patients of acute heart failure.
Further studies of the Vaptans are necessary to determine whether serum sodium normalization will be translated into a better long-term prognosis in patients with CCF. However Tolvaptan has been found to be hepatotoxic and hence USFDA has limited their use only in those hyponatremic patients with end-stage liver disease who are awaiting imminent liver transplantation, who are at little risk of added hepatic injury and will benefit from correction of hyponatremia before surgery to decrease the risk of ODS postoperatively.
In earlier studies the patients with cirrhosis were found to have improved serum sodium levels with vaptans however therewas no clear difference between Vaptans and control groups regarding mortality, variceal bleeding, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome, or renal failure. Hence is contraindicated in cirrhosis. Satvaptan was found to maintain sodium levels long term in cirrhotics however it's use is also limited.
Contraindications to vaptans-Vasopressin receptor antagonists should not be used in hyponatremic patients who are volume depleted.
Vaptans should not be used to treat the type of euvolemic hyponatremia caused by emetic stimuli or secondary adrenal insufficiency and they are ineffective in the vasopressin-independent form of SIADH caused by an activating mutation of the V 2 receptor. They are ineffective where AVP levels are appropriate, for example, cerebral salt wasting and psychogenic polydipsia.
Tolvaptan has less potential for drug-drug interactions. Coadministration of conivaptan with potent inhibitors of CYP3A4 , such as ketoconazole, itraconazole, clarithromycin, ritonavir and indinavir is contraindicated. Weight, serum sodium, Blood pressure, liver functions should be monitored every 15 days for months then monthly. Serum potassium and kidney functions should be monitored regularly. Hyponatremia is a frequently encountered problem in clinical practice and is an important cause of morbidity and mortality.
Establishment of etiology and appropriate treatment improves outcome. A knowledge of recent guidelines of treatment and the appropriate use of vaptans is essential for all clinicians for proper diagnosis and management. Source of Support: Nil. Conflict of Interest: No. National Center for Biotechnology Information , U. Indian J Endocrinol Metab. Manisha Sahay and Rakesh Sahay. Author information Copyright and License information Disclaimer.
Corresponding Author: Dr. E-mail: moc. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3. This article has been cited by other articles in PMC. Abstract Hyponatremia is an important and common clinical problem.
Individuals with the condition may need to restrict fluid intake, take salt tablets, or use medications. The outlook for people with low sodium levels depends on the severity of the condition and the underlying cause. Acute hyponatremia, which develops quickly, is more severe than chronic cases, which have a longer onset time.
In severe cases, hyponatremia can be fatal. To improve their outlook, people should be aware of the symptoms of hyponatremia and seek prompt medical attention if they experience any of them. Those at risk of low sodium levels should be especially vigilant. Dark-colored urine and thirst are classic signs that someone is dehydrated.
The simple solution is to drink more. But when dehydration occurs in the…. Gatorade contains electrolytes that rehydrate people after exercise, but it also contains sugar and artificial colors.
Is Gatorade good or bad for…. High levels indicate hyperchloremia, while low levels…. Drinking too much water can lead to water intoxication, which can be fatal. However, this is rare. Learn about the symptoms, causes, and risk factors…. What are the symptoms of low sodium levels? Medically reviewed by Gerhard Whitworth, R. Share on Pinterest Hyponatremia can cause fatigue and headaches.
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