eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders

Hyponatremia: Treatment & Medication

Author: Eric E Simon, MD, Associate Professor, Department of Medicine, Tulane University School of Medicine; Co-Director of Nephrology Training, Medical Director, Dialysis Clinic, Inc
Coauthor(s): Seyed Mehrdad Hamrahian, MD, Staff Nephrologist, Ochsner Medical Center
Contributor Information and Disclosures

Updated: May 29, 2009

Treatment

Medical Care

The recommendations for treatment of hyponatremia rely on the current understanding of the central nervous system (CNS) adaptation to an alteration in serum osmolality. In the setting of an acute drop in the serum osmolality, neuronal cell swelling occurs due to the water shift from the extracellular space to the intracellular space (ie, Frank Starling forces). Therefore, correction of hyponatremia should take into account the limited capacity of this adaptation mechanism to respond to acute alteration in the serum tonicity, because the degree of brain edema and consequent neurologic symptoms depend as much on the rate and duration of hypotonicity as they do on its magnitude.

  • The treatment of hypertonic and pseudohyponatremia is directed at the underlying disorder in the absence of symptoms.
  • Hypotonic hyponatremia accounts for most clinical cases of hyponatremia. The first step in the approach and evaluation of hypotonic hyponatremia is to determine whether emergency therapy is warranted. Guide treatment by the 3 following factors:
    • Patient's volume status
    • Duration and magnitude of the hyponatremia
    • Degree and severity of clinical symptoms
  • Administer isotonic saline to patients who are hypovolemic to replace the contracted intravascular volume (thereby treating the cause of vasopressin release). Patients with hypovolemia secondary to diuretics may also need potassium repletion, which, like sodium, is osmotically active. Treat patients who are hypervolemic with salt and fluid restriction, plus diuretics, and correction of the underlying condition.
    • For normovolemic (euvolemic), asymptomatic, and mildly hyponatremic patients, free water restriction (<1 L/d) is generally the treatment of choice. Base the volume of restriction on the patient's renal diluting capacity. For instance, a fluid restriction to 1 L/d, enough to raise the serum sodium in some patients, may exceed the renal free water excretion capacity in others, necessitating more severe restriction. This approach is recommended for patients with asymptomatic SIADH.
    • Pharmacologic agents can be used in some cases of more refractory SIADH, allowing more liberal fluid intake. Demeclocycline is the drug of choice to increase the diluting capacity of the kidneys, by achieving vasopressin antagonism and a functional diabetes insipidus. This treatment requires 3-4 days for maximal effect. Demeclocycline is contraindicated in cirrhotic patients. Other agents, such as lithium, have been used with variable success. Lithium is also associated with several untoward effects, including thyroid dysfunction, interstitial kidney disease, and, in overdosage, CNS dysfunction, which make its use problematic.
    • The treatment of psychogenic polydipsia can be difficult and may require psychiatric and pharmacologic intervention.
  • Treating patients with overtly symptomatic hyponatremia in whom rapid correction of the hyponatremia is warranted is more challenging because it carries a significant risk of inducing neurologic damage and the guidelines for treatment are not uniformly agreed upon.
  • Acute hyponatremia (duration <48 h) can be safely corrected more quickly than chronic hyponatremia. A symptomatic patient with acute hyponatremia is more in danger from brain edema. This mandates rapid correction.
    • In contrast, a symptomatic patient with chronic hyponatremia is more at risk from rapid correction of hyponatremia. Correction of serum sodium that is too rapid can precipitate severe neurologic complications, such as central pontine myelinosis, which can produce spastic quadriparesis, swallowing dysfunction, pseudobulbar palsy, and mutism.
    • A symptomatic patient with unknown duration of hyponatremia is the most challenging, warranting a prompt but controlled and limited correction of hyponatremia, until symptoms resolve.
    • However, excessive therapy and fear of osmotic demyelination should not deter prompt and definitive treatment.
  • In chronic, severe symptomatic hyponatremia, the rate of correction should not exceed 0.5-1 mEq/L/h, with a total increase not to exceed 12 mEq/L/d. It is necessary to correct the hyponatremia to a safe range (usually to no greater than 120 mEq/L) rather than to a normal value. Spontaneous diuresis secondary to ADH suppression with intravascular volume repletion could lead to unnoticed overcorrection.
    • The following equation helps to estimate an expected change in serum Na in respect to characteristics of infusates used22 : Change in serum Na = [(infusate Na + infusate K) - serum Na] / [Total body water +1]
    • This correction is usually best achieved with hypertonic (3%) saline. Note that normal saline can exacerbate hyponatremia in patients with SIADH, who may excrete the sodium and retain the water. A liter of normal saline contains 154 mEq sodium chloride (NaCl) and 3% saline has 513 mEq NaCl. Management decisions should also factor in ongoing renal free water and solute losses. Alternately, the combination of intravenous normal saline and diuresis with a loop diuretic (eg, furosemide) also elevates the serum sodium concentration. This latter approach often is useful for patients with high urine osmolality, because the loop diuretic acts to reduce urine osmolality. Concomitant use of loop diuretics increases free water excretion and also decreases the risk of fluid overload.
    • During therapy, closely monitor serum electrolytes (ie, every 2-4 h) to avoid overcorrection.
    • With patients who are acutely symptomatic (duration <48 h, such as after surgery), the treatment goal is to increase the serum sodium level by approximately 1-2 mEq/L/h for 3-4 hours until the neurologic symptoms subside or until plasma Na is over 120 mEq/L.23 Others recommend an even more rapid correction.2
    • A new class of drugs, AVP receptor antagonists, designed specifically to promote aquaresis (ie, electrolyte-sparing excretion of free water), has been evaluated in clinical trials for the treatment of hyponatremia.24,25 Currently, there is a lack of clinical experience with the use of these drugs in hospitalized patients. Nevertheless, the so-called aquaretic agents may become a promising therapeutic option for the treatment of hypervolemic or euvolemic hyponatremia, especially in the setting of heart failure.26

Consultations

Consultation with either a nephrologist or a critical care specialist is often of considerable value in managing patients with symptomatic or refractory hyponatremia.

Diet

  • Free water restriction often is appropriate for patients with normovolemic hypotonic hyponatremia.
  • Individuals who are undernourished need to maintain an appropriate solute intake. In fact, in patients with SIADH, a high protein intake increases the solute load for excretion, thereby removing more free water. Although unpalatable, oral urea has been used to achieve the same effect.
  • Patients with hyperglycemia or hyperlipidemia should receive appropriate nutritional counseling.

Medication

The primary treatments used in the management of hyponatremic patients rely on the use of intravenous sodium-containing fluids (normal saline or hypertonic saline) and fluid restriction. Less commonly, loop diuretics (eg, furosemide) or demeclocycline are used. A new class of drugs, AVP receptor antagonists (eg, conivaptan), is now available.24,25

Diuretics

Loop diuretics occasionally are used in patients with hyponatremia to increase renal free water excretion.


Furosemide (Lasix)

High-ceiling diuretic with a prompt onset of action that acts upon ascending limb of loop of Henle to inhibit sodium/potassium/chloride cotransport system, thereby increasing solute delivery to distal renal tubules, which acts to increase free water excretion. This can lead to increased aldosterone production, resulting in increased sodium absorption. Absorbed readily from the GI tract and also available in parenteral preparations. Diuresis begins 30-60 min with oral vs 5 min with IV administration. Potassium excretion also is increased. Elderly patients may have greater sensitivity to effects of furosemide.

Adult

10-80 mg PO or IV 1-4 times/d; higher doses may be required for patients with renal insufficiency; 600 mg/d PO maximum; 4 mg/min IV maximum

Pediatric

1-2 mg/kg PO q6-12h

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, and BUN determinations during first few months of therapy and periodically thereafter; may cause hypokalemia

Antibiotics

Certain antibiotics may affect renal ADH action.


Demeclocycline (Declomycin)

Can cause insensitivity of distal renal tubules to the action of ADH and produce a nephrogenic diabetes insipidus. Effects are seen within 5 days and are reversed within 2-6 days following cessation of therapy.

Adult

300-600 mg PO bid; consult with nephrologist

Pediatric

<8 years: Not recommended
>8 years: 3-6 mg/lb (6-12 mg/kg) PO, depending upon severity of disease, divided bid/qid; use in children in consultation with pediatric nephrologist

Bioavailability may decrease with coadministration of antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; may increase hypoprothrombinemic effects of anticoagulants (monitor prothrombin activity); coadministration with oral contraceptives may decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; caution with preexisting hepatic (metabolism) and renal (primary excretion route) impairment resulting in increased half life; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

Arginine vasopressin antagonists

Treats hyponatremia through V2 antagonism of AVP in the renal collecting ducts. This effect results in aquaresis (excretion of free water).24,25


Conivaptan (Vaprisol)

Arginine vasopressin antagonist (V1A, V2) indicated for euvolemic (dilutional) and hypervolemic hyponatremia. Increases urine output of mostly free water, with little electrolyte loss. Over 80% of conivaptan excreted in feces and the rest in urine.

Adult

20 mg IV loading dose (infuse over 30 min), followed by 20 mg via continuous IV infusion over 24 h; continue treatment for additional 1-3 d as 20-mg/d continuous IV infusion, not to exceed 4 d

Pediatric

Not established

Sensitive CYP3A4 substrate and potent CYP3A4 inhibitor; coadministration with potent CYP3A4 inhibitors significantly increases Cmax and AUC; coadministration with CYP3A4 substrates (eg, midazolam, simvastatin, amlodipine) may increase substrate's toxicity; significantly decreases digoxin clearance

Documented hypersensitivity; hypovolemic hyponatremia; coadministration with potent CYP3A4 inhibitors (eg ketoconazole, itraconazole, clarithromycin, ritonavir, indinavir)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Rapid correction of serum sodium level may result in serious sequelae (eg, osmotic demyelination); may cause infusion site reactions (most common adverse effect, over 50%), hypokalemia, headache, thirst, and vomiting; caution with hepatic impairment; limited data available in CHF and hepatic or renal impairment


Tolvaptan (Samsca)

Selective vasopressin V2-receptor antagonist. Indicated for hypervolemic and euvolemic hyponatremia (ie, serum sodium level <125 mEq/L) or less-marked hyponatremia that is symptomatic and has resisted correction with fluid restriction. Used for hyponatremia associated with congestive heart failure, liver cirrhosis, and syndrome of inappropriate antidiuretic hormone secretion. Initiate or reinitiate in hospital environment only.

Adult

15 mg PO qd initially; may increase at 24-h intervals to 30 mg/d; not to exceed 60 mg/d

Pediatric

Not established

Acts as a CYP3A substrate, P-gp inhibitor, and weak CYP3A inhibitor; CYP3A inhibitors (see Contraindications) may lead to marked increase in serum concentrations; avoid coadministration with moderate CYP3A inhibitors (eg, erythromycin, fluconazole, aprepitant, diltiazem, verapamil); also avoid coadministration with CYP3A inducers (eg, rifampin, rifabutin, rifapentine, barbiturates, phenytoin, carbamazepine, St. John's wort), as these may decrease tolvaptan serum levels by up to 85% and thereby decrease effectiveness; coadministration with grapefruit juice results in a 1.8-fold increase of serum levels; dose reduction may be required when coadministered with P-gp inhibitors (eg, cyclosporine)
May increase risk for hyperkalemia when administered with drugs known to increase serum potassium levels (eg, ACE inhibitors, potassium-sparing diuretics); may increase serum levels of P-gp substrates (eg, digoxin)

Documented hypersensitivity; urgent correction of hypovolemia; individuals unable to sense or respond to thirst; hypovolemic hyponatremia; strong CYP3A inhibitors (eg, ketoconazole, clarithromycin, itraconazole, ritonavir, indinavir, nelfinavir, saquinavir, nefazodone, telithromycin); anuria

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Initiate only in hospital setting, since serum sodium levels and volume status require close monitoring; rapid rise in sodium levels may cause osmotic demyelination syndrome, resulting in serious neurologic sequelae, including dysarthria, mutism, dysphagia, lethargy, affective changes, spastic quadriparesis, seizures, coma, and death; use caution with cirrhosis, since may increase risk for GI bleeding; may cause hyperkalemia and other electrolyte concentration abnormalities; common adverse effects include thirst, xerostomia, asthenia, constipation, pollakiuria or polyuria, and hyperglycemia

More on Hyponatremia

Overview: Hyponatremia
Differential Diagnoses & Workup: Hyponatremia
Treatment & Medication: Hyponatremia
Follow-up: Hyponatremia
References
Further Reading
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References

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Keywords

hyponatremia, SIADH, electrolyte, electrolytes, electrolyte imbalance, sodium deficiency, furosemide, hypertonic hyponatremia, hyponatraemia, hyponatremia treatment, hyponatremia causes, hyponatremia correction, tolvaptan, conivaptan, cerebral salt wasting, normotonic hyponatremia, hypotonic hyponatremia, normovolemic hypotonic hyponatremia, euvolemic hypotonic hyponatremia, abnormal electrolyte level, abnormal electrolyte distribution, congestive heart failure, liver failure, renal failure, hyperlipidemia, paraproteinemia, pseudohyponatremia, liver cirrhosis, nephrotic syndrome, severe hypoproteinemia, syndrome of inappropriate ADH secretion, severe hypothyroidism, adrenal insufficiency

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Contributor Information and Disclosures

Author

Eric E Simon, MD, Associate Professor, Department of Medicine, Tulane University School of Medicine; Co-Director of Nephrology Training, Medical Director, Dialysis Clinic, Inc
Eric E Simon, MD is a member of the following medical societies: American Federation for Medical Research, American Heart Association, American Society for Cell Biology, American Society of Nephrology, Association for Psychological Science, Central Society for Clinical Research, International Society of Nephrology, National Kidney Foundation, Phi Beta Kappa, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Coauthor(s)

Seyed Mehrdad Hamrahian, MD, Staff Nephrologist, Ochsner Medical Center
Seyed Mehrdad Hamrahian, MD is a member of the following medical societies: American Society of Nephrology and National Kidney Foundation
Disclosure: Nothing to disclose.

Medical Editor

James H Sondheimer, MD, Director of Hemodialysis Unit, Harper Hospital; Associate Professor, Department of Internal Medicine, Division of Nephrology, Wayne State University School of Medicine
James H Sondheimer, MD is a member of the following medical societies: American College of Physicians and American Society of Nephrology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine, Director of Nephrology Training Program, Kidney Disease Program, University of Louisville School of Medicine; Director, Metabolic Stone Clinic
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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