For patients with SIADH due to reversible factors e. nausea, medications , DDAVP may be beneficial because such patients may over-correct after the cause of SIADH is removed.

Overall, a proactive DDAVP strategy should work fine for any patient with SIADH. None of the patients had excessive correction. Overall the Adrogue-Madias equation appeared to predict changes in sodium reasonably well:.

Although this is an uncontrolled case series, it does support the efficacy and safety of this approach. The only noted adverse event was one patient who developed pulmonary edema requiring diuresis.

A recent systematic review of DDAVP use concluded that the proactive strategy was associated with the lowest incidence of over-correction. However, this evidence was mostly derived from the Sood study MacMillan This physiology illustrates the danger of vaptans e.

conivaptan, tolvaptan in hyponatremia. Vaptans inhibit the vasopressin receptor, causing renal excretion of free water:. Rapid water excretion may cause sodium over-correction. Vaptans may cause patients to transition from hyponatremia to hypernatremia with subsequent osmotic demyelination syndrome Malhotra The ability to inadvertently push patients into a hypernatremic state is uniquely dangerous compared to most mechanisms of sodium over-correction which stop once the sodium normalizes.

Thus, the European consensus guidelines recommend against using vaptans. An expert panel funded by the manufacturer of tolvaptan recommended that vaptans could be used in some situations. Surprisingly, a recent NEJM review article supported the use of vaptans, accepting this expert panel over the European consensus guidelines.

The review admits that there are no RCTs comparing vaptans to other therapies for hyponatremia. According to this review, to prevent over-correction the urine output must be replaced with intravenous D5W after the sodium has increased to the target level.

This is exactly the opposite of using DDAVP: vaptans induce uncontrolled renal water excretion, which must then be replaced. As discussed above, trying to keep up with renal free water excretion can be difficult. Perhaps the greatest challenge of managing severe hyponatremia is avoiding sodium over-correction, which may cause permanent neurologic disability.

Understanding the physiology of sodium over-correction allows us to anticipate this, but it is still unclear when it will occur. DDAVP appears to be the most effective approach to reversing, arresting, or preventing sodium over-correction.

Unfortunately there is little evidence regarding exactly how we should use this. For patients at the highest risk of osmotic demyelination syndrome, it may be safest to start DDAVP proactively in order to avoid over-correction entirely. Stay tuned: This is the second part of a three-part series on hyponatremia.

Next week we will proceed further down the rabbit hole to discuss extremely unconventional treatments for hyponatremia. Image credits. Author Recent Posts. Social Me. Josh Farkas. Josh is the creator of PulmCrit.

He is an associate professor of Pulmonary and Critical Care Medicine at the University of Vermont. Latest posts by Josh Farkas see all. PulmCrit wee: Polypharmacy in the ICU — when in doubt, deprescribe - January 30, PulmCrit hot take: VAP prophylaxis PROPHY-VAP trial - January 22, PulmCrit — Validation of my model for converting VBGs to ABGs - January 1, Share this: Facebook Twitter Reddit Pinterest Email Print.

Notify of. new follow-up comments new replies to my comments. We may delete without a full, true name. Your Job i. intensivist, CCRN, etc. oldest newest most voted. Inline Feedbacks.

Thanks a lot! I wish I had known this stuff when I was a fellow. anonymous newby. This approach is very innovative but limited to hypovolemic cases only. Ramy hanna.

I was wondering if you could apply the opposite reasoning for severe hypernatraemia. Reply to Derek Louey. Bryan Boone. Christoph Schwarz. What's Your Job?

Abdalla Kaware. nice review… Can we use vasopressin if DDAVP isnt available? thanks What's Your Job? Daniel Shepshelovich. Do … Read more » What's Your Job?

Patricia Gildroy. One of the biggest challenges … Read more » What's Your Job? Who We Are We are the EMCrit Project , a team of independent medical bloggers and podcasters joined together by our common love of cutting-edge care, iconoclastic ramblings, and FOAM.

Subscribe by Email. Generally speaking, there are two things to worry about with a patient with hyponatremia. First, hyponatremia may worsen, leading to severe complications e. Second, hyponatremia may overcorrect too rapidly, leading to osmotic demyelination. More information on the DDAVP clamp is located here.

The DDAVP clamp-bolus strategy is a slight modification of the DDAVP clamp section above. In the DDAVP clamp-bolus strategy, sodium is adjusted using discrete boluses of fluid, rather than a continuous infusion:.

This section describes treatment of SIADH with an ongoing cause which is difficult or impossible to remove e. malignancy, severe brain injury, or medications.

Always be sure to look for all potential reversible causes of SIADH e. There are two preferred treatment strategies for chronic SIADH: oral urea or loop diuretic plus sodium. In either case, a moderate amount of fluid restriction should also be employed.

Over-correction will occasionally happen. With proper management, this can be rapidly fixed and patients will do fine. This is completely backwards. Meanwhile, vaptans have a unique capacity to cause runaway water loss and overcorrection.

This isn't just my opinion — the European guidelines for hyponatremia recommend against vaptan use for treatment of hyponatremia. Want to Download the Episode?

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View Topic. Font Size Small Normal Large. Osmotic demyelination syndrome ODS and overly rapid correction of hyponatremia. Formulary drug information for this topic. No drug references linked in this topic.

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In fact, sodium stores are very tightly regulated. In cases though where sodium intake is too low for chronic periods, it can disrupt many physiologic and metabolic processes — having the most damaging effect on cardiovascular systems.

The takeaway? Are there easy ways to lower salt quickly? Hop in a sauna, or on a treadmill and get moving! The fastest way to lower total body salt content is too sweat. But remember, sodium content in the body is tightly controlled for optimal regulation and will change day to day based on your diet.

This system is tightly regulated to manage blood pressure and ensure the body maintains a very specific sodium balance. When blood volume or sodium concentration gets too high, the body gets triggered to excrete more sodium through the kidneys so yes, consuming more fluids to help you urinate would be helpful in this case.

In contrast, when blood volume is too low or sodium concentration becomes too low, the kidneys are triggered to reabsorb sodium. To recap, it seems that past recommendations may not hold true based on current literature.

Many people who have been told they consume too much sodium, might be consuming within optimal limits. However, every person is an individual case. Making these small changes can quickly lower your sodium intake and help you feel better all around!

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Nutrition Trending Simple Strategies for Managing Sodium Intake. All About Salt For starters, sodium is a major electrolyte that regulates fluid balance within the body. If you have high blood pressure you should most definitely cut back on sodium intake.

Sodium has a direct correlation with blood pressure in that it increases water retention in arterial vessels. Your urine is a very dark color. This will be more of an indication of hydration status. Isotonic saline will initially raise the serum sodium more slowly than hypertonic saline until near-euvolemia is attained and ADH secretion is suppressed.

In addition, some patients with hypovolemia may have coexistent syndrome of inappropriate ADH SIADH due to stress and will not respond well to isotonic saline. Thus, hypertonic saline will be predictably more effective in rapidly alleviating symptoms of severe hyponatremia.

After euvolemia is established, the slow correction in patients receiving isotonic saline may accelerate due to suppression of ADH, leading to a marked water diuresis. This rapid rise in serum sodium in patients who were, until that point, correcting slowly may produce an excessive hour increase in the serum sodium.

Initial therapy with a combination of hypertonic saline and desmopressin dDAVP can quickly improve symptoms of hyponatremia while preventing overly rapid correction. Do not use isotonic saline in edematous patients — Isotonic saline should not be used to treat hyponatremia associated with edematous disorders.

Unlike patients with true volume depletion, saline will not result in the excretion of dilute urine. Do not use isotonic saline in SIADH — In contrast to hypovolemia, the response to administered isotonic saline is different in a hyponatremic patient with syndrome of inappropriate antidiuretic hormone SIADH secretion.

Assuming the patient is euvolemic, the administered sodium is excreted in the urine because the response to aldosterone and atrial natriuretic peptide is normal. However, the water is retained because of the persistent action of ADH.

Thus, when 1 liter of isotonic saline is administered to a patient with SIADH, the sodium is excreted in the urine while some of the water is retained, worsening the hyponatremia.

A few simple calculations can illustrate this point. The retention of one-half of the administered water will lead to a further reduction in the serum sodium concentration even though the serum sodium concentration will temporarily increase because the isotonic saline is hypertonic to the patient.

With these assumptions:. Support for possible harm from isotonic saline was provided in a report of 22 women who underwent uncomplicated gynecologic surgery and had been treated with modest volumes of only isotonic saline or near-isotonic Ringer's lactate [ 11 ].

At 24 hours after induction of anesthesia, the serum sodium fell by a mean of 4. Fatalities from severe hyponatremia have been reported following the administration of large volumes of isotonic fluid after surgery [ 11 ].

Use of predictive formulas — Several formulas have been proposed to estimate the direct effect of a given fluid eg, normal saline or hypertonic saline on the serum sodium concentration.

However, these formulae do not consider the effect of treatment of volume and composition of the urine output. As example, in the absence of any urine output, the following calculations apply:. The TBW, rather than extracellular fluid volume, is used in these formulas since, although the administered sodium will stay in the extracellular space, water moves from the intracellular to extracellular space in response to the administered sodium to equalize the osmolality of the two fluid compartments.

Because TBW in liters is approximately 0. However, these formulas have a number of limitations and cannot be used to accurately predict the magnitude of change in serum sodium [ ]. When hypertonic saline is given, the increase in serum sodium is often greater than that predicted by the formula [ 72,73 ].

In addition, the maximum recommended rate of correction at 24 and 48 hours was exceeded in 11 and 10 percent, respectively [ 72 ].

Inadvertent overcorrection was due to a documented water diuresis in 40 percent of patients, which, as mentioned above, can occur when saline therapy corrects hypovolemia, thereby removing the hypovolemic stimulus to the release of ADH and permitting rapid excretion of the excess water.

By contrast, in patients with persistent SIADH secretion, the administered sodium will be excreted in the urine, and some of the water will be retained; as a result, the increase in serum sodium after 3 percent saline will be less than that predicted by formulas, and the serum sodium may actually fall after isotonic saline.

Thus, after the administration of hypertonic saline, there will be an initial large rise in the serum sodium concentration, followed by reduction toward baseline after the administered sodium has been excreted. At this time, the rise in the serum sodium due to the net loss of mL of water can be calculated.

Predictive formulas can, however, be valuable adjuncts to therapy. If the increase in serum sodium is more than predicted by the formula, one should suspect that an increase in water excretion has occurred because the original cause for water retention has ended eg, euvolemia has been restored in a patient with hypovolemic hyponatremia or desmopressin has worn off in a patient with desmopressin-induced hyponatremia.

Such a deviation of the actual increase in serum sodium from the predicted increase should prompt strict monitoring of urine output and, in many cases, replacement of water losses or treatment with desmopressin to stop them.

In addition, if serial measurements of urine chemistries urine sodium, potassium, and creatinine and urine volume are available, a predictive formula including these data can be useful:.

An online calculator is available to apply the formula, which is based on careful balance studies and serial measurements of body sodium, potassium, and water content, performed in the s [ 71 ]. However, rather than an actual measurement of TBW, the value is estimated from the patient's sex, weight, age, and height.

The calculator allows a comparison of the expected change in serum sodium with its actual change which should be measured frequently. As with other formulas, differences between observed and expected values suggest a change in urine output and composition, which should be reevaluated.

The severity of hyponatremia and the severity of symptoms are presented above. See 'Determine the severity degree of hyponatremia' above and 'Determine the severity of symptoms' above.

If hyponatremia persists at the time of discharge, patients who were treated in the hospital for severe hyponatremia or symptomatic moderate hyponatremia will require continued therapy as outpatients.

However, the following should be considered before discharging a patient who required inpatient treatment for hyponatremia:. Thus, this patient should be monitored as an inpatient for the next 24 hours after withdrawal of desmopressin, rather than being discharged, and water losses should be replaced, if necessary, to avoid excessive correction.

In addition, the appropriate dose of tolvaptan should be determined in the hospital while carefully monitoring the patient's urine output. If tolvaptan is ineffective, then other strategies should be used for outpatient management of the hyponatremia.

If tolvaptan successfully increases the patient's serum sodium, then discharge should be delayed until it is established that the patient is able to replace their water losses induced by the drug. Thereafter, the need for continued tolvaptan therapy should be reassessed every 30 days.

Outpatient management of patients who no longer require hospital admission varies according to the cause of hyponatremia.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. See "Society guideline links: Hyponatremia" and "Society guideline links: Fluid and electrolyte disorders in adults". These articles are best for patients who want a general overview and who prefer short, easy-to-read materials.

Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword s of interest. See 'Introduction' above.

Evaluation prior to therapy. See 'Determine the need for hospitalization' above. Initial treatment. See 'Goals of therapy' above and 'Goal rate of correction' above. We then monitor the patient for symptoms and remeasure the serum sodium concentration hourly to determine the need for additional therapy.

However, we do not give these patients hypertonic saline if the hyponatremia is already autocorrecting due to a water diuresis. See 'Asymptomatic' above. See 'Symptomatic even mild symptoms ' above.

See 'Severe symptoms or known intracranial pathology' above. In addition, among those with reversible causes of 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 desmopressin dDAVP to prevent overly rapid correction.

Subsequent treatment. See 'Monitoring' above. See 'Discontinuing hypertonic saline used as initial therapy' above. See 'Fluid restriction' above. See 'Other therapies for chronic hyponatremia' above.

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View Topic. Font Size Small Normal Large. Overview of the treatment of hyponatremia in adults. Formulary drug information for this topic. No drug references linked in this topic. Find in topic Formulary Print Share.

View in. Language Chinese English. Author: Richard H Sterns, MD Section Editor: Michael Emmett, MD Deputy Editor: John P Forman, MD, MSc Contributor Disclosures. All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan This topic last updated: Oct 25, Hyponatremia and risk of seizures: a retrospective cross-sectional study. Epilepsia ; Sterns RH. Severe symptomatic hyponatremia: treatment and outcome. A study of 64 cases. Ann Intern Med ; Chow KM, Kwan BC, Szeto CC.

Clinical studies of thiazide-induced hyponatremia. J Natl Med Assoc ; Sterns RH, Cappuccio JD, Silver SM, Cohen EP. Neurologic sequelae after treatment of severe hyponatremia: a multicenter perspective. J Am Soc Nephrol ; Soupart A, Penninckx R, Stenuit A, et al.

Treatment of chronic hyponatremia in rats by intravenous saline: comparison of rate versus magnitude of correction. Kidney Int ; Ayus JC, Varon J, Arieff AI. Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Renneboog B, Musch W, Vandemergel X, et al.

Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. Am J Med ; Gankam Kengne F, Andres C, Sattar L, et al.

Mild hyponatremia and risk of fracture in the ambulatory elderly. QJM ; Schrier RW, Gross P, Gheorghiade M, et al. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia.

N Engl J Med ; Treatment of Severe Hyponatremia. Clin J Am Soc Nephrol ; Steele A, Gowrishankar M, Abrahamson S, et al. Postoperative hyponatremia despite near-isotonic saline infusion: a phenomenon of desalination.

Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol ; Chawla A, Sterns RH, Nigwekar SU, Cappuccio JD. Mortality and serum sodium: do patients die from or with hyponatremia?

Ayus JC, Wheeler JM, Arieff AI. Postoperative hyponatremic encephalopathy in menstruant women. Karp BI, Laureno R.

Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine Baltimore ; Moritz ML, Ayus JC. The pathophysiology and treatment of hyponatraemic encephalopathy: an update. Nephrol Dial Transplant ; Berl T. Treating hyponatremia: damned if we do and damned if we don't.

Verbalis JG, Goldsmith SR, Greenberg A, et al. Hyponatremia treatment guidelines expert panel recommendations. Am J Med ; S1. Adrogué HJ, Madias NE. The challenge of hyponatremia. Sterns RH, Hix JK, Silver S.

Treatment of hyponatremia. Curr Opin Nephrol Hypertens ; Ayus JC, Caputo D, Bazerque F, et al. Am J Kidney Dis ; Rafat C, Schortgen F, Gaudry S, et al. Use of desmopressin acetate in severe hyponatremia in the intensive care unit.

Tormey WP, Carney M, Cuesta M, Sreenan S. Reference Change Values for Sodium Are Ignored by the American and European Treatment Guidelines for Hyponatremia. Clin Chem ; Mesghali E, Fitter S, Bahjri K, Moussavi K.

J Emerg Med ; Jones GM, Bode L, Riha H, Erdman MJ. Am J Crit Care ; Dillon RC, Merchan C, Altshuler D, Papadopoulos J. Incidence of Adverse Events During Peripheral Administration of Sodium Chloride 3. J Intensive Care Med ; Meng L, Nguyen CM, Patel S, et al. Association between continuous peripheral i.

Am J Health Syst Pharm ; Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol ; G1. Ayus JC, Arieff A, Moritz ML.

Hyponatremia in marathon runners. Hew-Butler T, Ayus JC, Kipps C, et al. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, Clin J Sport Med ; Sarnaik AP, Meert K, Hackbarth R, Fleischmann L. Management of hyponatremic seizures in children with hypertonic saline: a safe and effective strategy.

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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 ].

Thus, when calculating the impact of a particular regimen on the serum sodium concentration, one must consider the sodium plus potassium concentration of the solution, not simply the sodium concentration.

Similar considerations apply to calculating the impact of fluid losses induced by vomiting, diarrhea, or diuretic therapy.

Vasopressin receptor antagonists — An alternative or possible addition to fluid restriction and sodium chloride administration in patients with hyponatremia is the use of an ADH receptor antagonist [ 59 ]. There are multiple receptors for the ADH vasopressin: the V1a, V1b, and V2 receptors.

The V2 receptors primarily mediate the antidiuretic response, while V1a and V1b receptors principally cause vasoconstriction and mediate adrenocorticotropic hormone ACTH release, respectively [ 18,60 ].

The vasopressin receptor antagonists produce a selective water diuresis also called aquaresis without affecting sodium and potassium excretion. The ensuing loss of free water will tend to correct the hyponatremia. However, thirst increases significantly with these agents, which may limit the rise in serum sodium [ 9,60 ].

Some oral formulations, such as tolvaptan , mozavaptan, satavaptan, and lixivaptan, are selective for the V2 receptor, while an intravenous agent, conivaptan , blocks both the V2 and V1a receptors. Only tolvaptan and conivaptan are available in the United States. The US Food and Drug Administration FDA warns that tolvaptan should not be used in any patient for longer than 30 days and should not be given at all to patients with liver disease including cirrhosis.

We believe that a reasonable exception to this US FDA recommendation can be made for hyponatremic patients with end-stage liver disease who are awaiting liver transplantation. Correction of hyponatremia is desirable in such patients to avoid a rapid perioperative increase in the serum sodium concentration, and the clinical impact of a drug-related exacerbation of liver injury in this setting is likely to be negligible.

See "Hyponatremia in patients with cirrhosis". With respect to conivaptan , there are concerns that the concurrent V1a receptor blockade might lower the blood pressure and increase the risk of variceal bleeding in patients with cirrhosis since vasopressin is used to treat active bleeding in such patients a V1a effect.

There is also a concern that V1a receptor blockade might worsen kidney function in patients with cirrhosis since terlipressin , a V1a receptor agonist, has been used to treat hepatorenal syndrome. The studies that have evaluated the use of vasopressin receptor antagonists in the different settings in which hyponatremia occurs are presented elsewhere:.

However, the difference was usually not clinically significant, and long-term efficacy is uncertain since the duration of follow-up was only 30 days. In an open-label extension called SALTWATER , patients were treated with tolvaptan for a mean follow-up of almost two years [ 61 ].

The responses were similar in SIADH and heart failure and were more modest in cirrhosis. The main adverse effects were abnormally frequent urination, thirst, dry mouth, fatigue, polyuria, and polydipsia.

Adverse effects that were possibly or probably related to tolvaptan led to discontinuation of therapy in six patients 5. Vasopressin receptor antagonists should not be used in hyponatremic patients who are volume depleted in whom volume repletion with saline is the primary therapy.

See 'Isotonic saline in true volume depletion' below. A greater than 2. Based upon these data, the US FDA initially issued a safety warning regarding the use of tolvaptan [ 64 ], recommending that liver function tests be promptly performed among patients who report symptoms that suggest liver injury, including fatigue, anorexia, right-upper-quadrant discomfort, dark urine, or jaundice.

However, the US FDA subsequently determined that tolvaptan should not be used in any patient for longer than 30 days, or at all in patients with liver disease including cirrhosis , because it may potentially lead to liver failure or death [ 65 ].

See "Autosomal dominant polycystic kidney disease ADPKD : Treatment". In the SALT trials, 1. Because of frequent overcorrection after 15 mg of tolvaptan the only dose available in the United States , many countries now market a 7. Approach to impending overcorrection — In view of the often severe and permanent adverse consequences of ODS, prevention is essential.

Prevention and treatment of overly rapid correction and ODS are discussed in detail elsewhere. See "Osmotic demyelination syndrome ODS and overly rapid correction of hyponatremia", section on 'Prevention and treatment of ODS'.

The risk for overly rapid correction is higher if the cause of impaired water excretion is likely to be reversible eg, in hypovolemic patients , thereby resulting in a water diuresis that can produce an abrupt rise in the serum sodium. An increase in urine output and a decrease in the urine cation concentration can signify a water diuresis that will accelerate the rate of correction.

These patients tend to autocorrect since ADH is physiologically suppressed, permitting rapid excretion of large volumes of free water. However, the acute onset of hyponatremia in these disorders is associated with a low risk of ODS due to overly rapid correction.

Diagnose and treat the underlying cause of hyponatremia — In addition to the specific therapies that are aimed at correcting the hyponatremia, therapy should also be directed at the underlying disease. Determining the cause of hyponatremia is presented elsewhere algorithm 2.

There are several circumstances in which the underlying cause of hyponatremia can be corrected quickly; the risk of overly rapid correction is high in such settings see 'Avoid overcorrection' above :. In this setting, restoration of euvolemia will suppress the release of ADH which has a half-life of only 15 to 20 minutes , thereby allowing rapid excretion of the excess water.

See "Hyponatremia and hyperkalemia in adrenal insufficiency". This can occur when the cause of SIADH is self-limited disease eg, nausea, pain, surgery or with the cessation of certain drugs that cause SIADH eg, desmopressin [dDAVP], selective serotonin reuptake inhibitors such as fluoxetine or sertraline.

See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion SIADH ", section on 'Etiology'. Elimination of the diuretic restores the ability to excrete maximally dilute urine. There are a number of other causes of hyponatremia that can be corrected in which the serum sodium rises more slowly.

This is most often seen with thyroid hormone replacement in patients with hypothyroidism and by gradually reversing the cause of SIADH by, for example, the treatment of tuberculosis or meningitis or the cessation of long-acting drugs.

See "Causes of hypotonic hyponatremia in adults" and "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion SIADH ", section on 'Etiology'.

Isotonic saline is also indicated in patients who are overtly hypovolemic with hypotension, prerenal azotemia, or orthostatic symptoms. The degree to which isotonic saline will raise the serum sodium concentration in hyponatremic patients varies with the cause of the hyponatremia.

As illustrated by the following discussion, the response to isotonic saline differs with the cause of hyponatremia. Isotonic saline in true volume depletion — In states of true volume depletion eg, diarrhea, vomiting, diuretic therapy , the administered sodium and water will initially be retained.

In this setting, isotonic saline corrects the hyponatremia by two mechanisms:. At this time, the serum sodium concentration may return rapidly toward normal; in some patients, overly rapid correction of hyponatremia can lead to the severe neurologic disorder osmotic demyelination syndrome ODS [ 54,68 ].

The management of such patients is discussed separately. See "Osmotic demyelination syndrome ODS and overly rapid correction of hyponatremia", section on 'Patients who have exceeded correction limits rescue strategy '. Isotonic saline is indicated in patients who are overtly hypovolemic with hypotension, prerenal azotemia, or orthostatic symptoms.

Although isotonic saline will raise the serum sodium in hyponatremic patients with true hypovolemia, we concurrently give hypertonic saline if the hyponatremia is acute or severe and symptomatic. Isotonic saline will initially raise the serum sodium more slowly than hypertonic saline until near-euvolemia is attained and ADH secretion is suppressed.

In addition, some patients with hypovolemia may have coexistent syndrome of inappropriate ADH SIADH due to stress and will not respond well to isotonic saline. Thus, hypertonic saline will be predictably more effective in rapidly alleviating symptoms of severe hyponatremia.

Wrestling with normal kidneys is difficult. Usually at some point something exciting happens in the ICU, attention is diverted, and before you know it the sodium is too high. High rates of D5W may induce hyperglycemia.

Others have reported difficulty with this strategy Perianayagam ; Gharaibeh A more powerful approach to excessive water excretion is to provide desmopressin DDAVP, 2 micrograms IV q8hr; Sood DDAVP stimulates the V2-vasopressin receptors in the kidney, causing renal retention of water figure above.

This eliminates unpredictable excretion of water from the kidneys:. With blockade of renal water excretion, the Adrogue-Madias equation will be more accurate.

This allows control of the sodium based on fluid administration:. For example, if you wish to stop the rise of sodium, DDAVP may be given and fluid intake stopped. This will halt intake and output of free water, so the sodium should remain stable.

This approach is easier to achieve than titrating a D5W infusion: just order the DDAVP, stop fluid inputs, and you're done. If the patient is neglected for a few hours, the sodium will probably be fine. The risk of osmotic demyelination syndrome depends on the average change in sodium over time, so if the sodium over-corrects this can still be remedied by decreasing the sodium to its original target.

Combining DDAVP with carefully calculated doses of D5W may achieve this. This is obviously not the preferred strategy for managing sodium. However, it is important to recognize that sodium over-correction is not an unfixable problem. Even if the patient seems OK neurologically, it is probably safest to lower the sodium.

By the time symptoms of osmotic demyelination syndrome emerge, the optimal window for intervention has passed. Consider a patient admitted with chronic, asymptomatic hyponatremia due to hypovolemia. Nothing dramatic must be done initially. Fluid resuscitation may be undertaken with careful monitoring of the serum sodium concentration.

At some point, vasopressin levels will fall and the sodium will start really climbing. Once the sodium has increased a fair amount i. perhaps ~8 mM or urine output accelerates, DDAVP and fluid restriction may be initiated to stop the rise in sodium.

When the DDAVP has been stopped, the sodium will continue to rise:. The physiology underlying this strategy is supported by an observational study of this approach by Rafat They showed that DDAVP administration decreased the urine output and increased the urine tonicity, causing a halt in the rate of sodium correction over time:.

The weakness of this strategy is that it initially requires constant vigilance to detect overcorrection, with intervention at just the right moment. This is not foolproof. For example, in the Rafat series, about half of patients still over-corrected their sodium.

The proactive DDAVP strategy represents the most definitive approach to controlling sodium. This is performed as follows:. As shown below, a proactive DDAVP approach has two advantages in symptomatic hyponatremia compared to less aggressive management.

First, immediately increasing the sodium will rapidly bring the sodium to a safe level and relieve symptoms. Second, proactive DDAVP prevents endogenous over-correction.

Perhaps the most important contraindication to DDAVP is inability to control oral fluid intake e. due to psychogenic polydipsia. If DDAVP is given and the patient continues to have significant fluid intake, this will exacerbate the hyponatremia.

Patients with pure hypervolemic hyponatremia e. heart failure, cirrhosis will not benefit from this approach. These patients usually have mild hyponatremia and rarely over-correct their sodium, so there is little rationale for DDAVP.

Additionally, hypertonic saline therapy would worsen volume overload. However, for a patient with multifactorial hyponatremia e. a patient with profound hyponatremia due to mild heart failure, beer potomania, and thiazide diuretics , a proactive DDAVP strategy may still be considered along with furosemide diuresis.

For patients with SIADH due to a chronic stimulus e. malignancy , there is little benefit from administering DDAVP. However, DDAVP won't hurt either it will probably have no effect. For patients with SIADH due to reversible factors e. nausea, medications , DDAVP may be beneficial because such patients may over-correct after the cause of SIADH is removed.

Overall, a proactive DDAVP strategy should work fine for any patient with SIADH. None of the patients had excessive correction. Overall the Adrogue-Madias equation appeared to predict changes in sodium reasonably well:. Although this is an uncontrolled case series, it does support the efficacy and safety of this approach.

The only noted adverse event was one patient who developed pulmonary edema requiring diuresis. A recent systematic review of DDAVP use concluded that the proactive strategy was associated with the lowest incidence of over-correction.

However, this evidence was mostly derived from the Sood study MacMillan This physiology illustrates the danger of vaptans e. conivaptan, tolvaptan in hyponatremia. Vaptans inhibit the vasopressin receptor, causing renal excretion of free water:. Rapid water excretion may cause sodium over-correction.

Vaptans may cause patients to transition from hyponatremia to hypernatremia with subsequent osmotic demyelination syndrome Malhotra The ability to inadvertently push patients into a hypernatremic state is uniquely dangerous compared to most mechanisms of sodium over-correction which stop once the sodium normalizes.

Thus, the European consensus guidelines recommend against using vaptans. Chain restaurants with 20 or more locations must provide nutrition information, including sodium content, to customers upon request. Over time, your taste buds can adjust to less salt. Studies show that when people follow a lower-sodium diet, they start to prefer it, and that the foods they once enjoyed taste too salty.

Try it and see for yourself! There are several salt substitutes on the market that replace some or all of the sodium with potassium. Potassium salt tastes similar to sodium chloride, except when heated it can have a bitter aftertaste.

Talk with your health care professional about whether a salt substitute is right for you. Written by American Heart Association editorial staff and reviewed by science and medicine advisors. See our editorial policies and staff. Eat Smart. American Heart Association Cookbooks.

Nutrition Basics. Healthy For Good: Spanish Infographics. Home Healthy Living Healthy Eating Eat Smart Sodium How to Reduce Sodium in Your Diet. Most people should cut back on sodium to improve their health. When shopping for food: Choose packaged and prepared foods carefully.

Compare labels and choose the product with the lowest amount of sodium per serving you can find. Different brands of the same food can have lower or higher sodium levels.

Compare this with the same serving of prepared rotisserie chicken pre-seasoned with sodium, which can have mg of sodium a serving! Select condiments with care. For example, soy sauce, bottled salad dressings, dips, ketchup, jarred salsas, capers, mustard, pickles, olives and relish can be loaded with sodium.

Look for reduced-sodium or lower-sodium versions.