Pediatric Hyponatremia Treatment & Management

  • Author: Muthukumar Vellaichamy, MD, FAAP; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Jul 27, 2011
 

Medical Care

  • Principles of treatment in hyponatremia
    • The most common and devastating effects of hyponatremia are of CNS origin. Therefore, identifying the risk factors that lead to hyponatremia and instituting prompt treatment while avoiding complications is crucial.
    • Although cerebral adaptation to low serum Na occurs slowly, it protects the brain from deleterious effects of hypo-osmolality. However, this protective mechanism leaves the brain susceptible to osmotic demyelination syndrome (ODS) during treatment, especially in persons with chronic hyponatremia, if the correction is rapid.
  • Equations used in managing hyponatremia
    • To estimate the effect of 1 L of any infusate on serum Na concentration: Change in Na concentration = (infusate Na level - serum Na level)/(total body water + 1)
    • To estimate the effect of 1 L of any infusate containing Na and potassium (K) on serum Na concentration: Change in serum Na level = [(infusate Na level + infusate K level) - serum Na level]/(total body water + 1)
  • Na concentrations of various fluids used in pediatric practice
    • 5% NaCl in water - 855 mEq/L
    • 3% NaCl in water - 513 mEq/L
    • 0.9% NaCl in water - 154 mEq/L
    • Ringer lactate solution - 130 mEq/L
    • 0.45% NaCl in water - 77 mEq/L
    • 0.2% NaCl in water - 34 mEq/L
    • 5% dextrose in water - 0 mEq/L
  • Management of hypovolemic hyponatremia
    • The immediate goal is to correct volume depletion with normal saline. As soon as the patient is hemodynamically stable, hyponatremia should be corrected as per the treatment principles described below. In patients with seizure, 3% NaCl should be given while volume depletion is being corrected.
    • No consensus has been reached about the optimal treatment of symptomatic hyponatremia. However, guidelines for hydration management have been established.[5] Physiologic considerations indicate that a relatively small increase in the serum Na concentration, on the order of 5%, should substantially reduce cerebral edema. Available evidence indicates that even a 9 mEq/L increase in serum Na concentration over 24 hours can result in demyelinating lesions. Given the risk of demyelinating lesions, the recommended rate of correction should not exceed 8 mEq/L/d. Even hyponatremia-induced seizures can be stopped with changes in serum Na concentration of only 3-7 mEq/L.
    • Treatment of normovolemic hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH) can include fluid restriction, along with the administration of normal saline; the use of 3% NaCl, and intravenous (IV) administration of furosemide may also be needed. Furosemide is given to offset the volume expansion created by the 3% Na infusion. As previously discussed, when confronted with neurologic symptoms the plan is to raise the serum Na concentration until symptoms resolve, this can be done by giving doses of 1-2 mL/Kg of 3% saline, symptoms typically resolve with a rise in sodium of 3-7 mEq/L; subsequently, closely monitor electrolyte levels so that the correction does not exceed 8 mEq/L/d. This appears to leave little room for elevation of serum sodium after immediately addressing symptoms; however, it appears that maintaining control of the absolute rise over 24 hours remains beneficial, even after the immediate emergent increase in serum sodium.
  • Management of hypervolemic hyponatremia: In patients with hypervolemic hyponatremia, restrict fluids, administer 3% NaCl to stop the symptoms, and treat the underlying cause.
  • Management of asymptomatic hyponatremia
    • In asymptomatic individuals with hypovolemic hyponatremia, one should not rush to correct hyponatremia. The main principle is to avoid hypotonic fluids and to slowly correct Na levels, especially when hyponatremia has been present for 48 hours or longer. When the duration of hyponatremia is unknown, as is encountered in outpatient settings, assume hyponatremia is chronic and treat accordingly. Closely monitor electrolyte values, and the rate of correction should not exceed 8 mEq/L/d.
    • In patients with normovolemic hyponatremia, restriction of fluids to two-thirds (or less) of the volume needed for maintenance is the mainstay of treatment. Diuretics can be administered with fluid restriction to remove excessive free water. Once again, the change in Na levels should not exceed 8 mEq/L/d.
    • In recalcitrant euvolemic hyponatremia, one can use demeclocycline to induce therapeutic nephrogenic diabetes insipidus, which might help eliminate excessive water. However, one must remember that total correction should not exceed the established goal.
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Consultations

  • Transfer patients with symptomatic hyponatremia to a pediatric ICU for appropriate treatment and close monitoring.
  • Consult an endocrinologist when patients have hypothyroidism or adrenal insufficiency.
  • Consult a nephrologist when patients have salt-losing nephropathy, renal failure, or recalcitrant hyponatremia.
  • Appropriate neurosurgical care is required when CNS conditions are the cause of SIADH.
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Diet

  • Patients with salt-wasting disorders (eg, salt-losing nephropathies) need Na supplementation throughout the period of continued loss of excessive Na.
  • Patients with SIADH and renal failure require fluid restriction.
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Contributor Information and Disclosures
Author

Muthukumar Vellaichamy, MD, FAAP  Clinical Assistant Professor, Department of Pediatrics, University of Kansas School of Medicine-Wichita, Wesley Medical Center

Muthukumar Vellaichamy, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

G Patricia Cantwell, MD, FCCM  Professor of Clinical Pediatrics, University of Miami, Leonard M Miller School of Medicine; Chief, Division of Pediatric Critical Care Medicine, Medical Manager, Urban Search & Rescue, South Florida TF-2, Medical Director, Holtz Children's Hospital Palliative Care Team, Medical Director, Tilli Kids – Pediatric Initiative of Hospice Care of SE Florida, Director, Pediatric Critical Care Transport, Holtz Children's Hospital/Jackson Memorial Hospital

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Barry J Evans, MD  Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Mary E Cataletto, MD  Director of Children's Sleep Services, Winthrop Sleep Disorders Center, Mineola, NY; Professor of Clinical Pediatrics, State University of New York at Stony Brook, Stony Brook, NY

Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians

Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Timothy E Corden, MD  Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

Acknowledgments

The author would like to acknowledge his partner at work, mentor, and great physician Lindall Smith, MD, for reading the manuscript and offering valuable advice.

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