Pediatric Hyponatremia Workup

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

Laboratory Studies

  • Verify the accuracy of laboratory results in patients with hyponatremia.
  • Exclude pseudohyponatremia.
    • Findings on flame emission spectrophotometry
      • If Na measurement is performed by using flame emission spectrophotometry, hyponatremia is falsely low in patients with hyperproteinemia and hypertriglyceridemia.
      • Raised proteins and lipid levels increase the nonaqueous portion of plasma, which normally forms 7% of the plasma.
      • However, new ion-specific Na electrodes measure Na from only the aqueous phase, enabling accurate estimation of serum Na concentrations.
    • Correction factors for raised proteins and lipids
      • Triglycerides (in milligrams per deciliter) X 0.002 = decrease in plasma Na level (in milliequivalents per liter)
      • (Plasma protein level [in grams per deciliter] - 8) X 0.25 = decrease in plasma Na (in milliequivalents per liter)
  • Exclude distributive hyponatremia.
    • Distributive hyponatremia occurs when the plasma glucose concentration exceeds 100 mg/dL.
    • Each 100-mg/dL increase in the glucose level above 100 mg/dL leads to a 1.6-mEq/L decrease in the Na concentration.
  • Obtain routine laboratory studies to assess the following:
    • Serum Na level
    • Serum osmolality
    • BUN and creatinine levels
    • Urine osmolality
    • Urine Na level
  • Urine Na level changes according to the type of hyponatremia.
    • Hypovolemic hyponatremia
      • Renal losses caused by diuretic excess, osmotic diuresis, salt-wasting nephropathy, adrenal insufficiency, proximal renal tubular acidosis, metabolic alkalosis, or pseudohypoaldosteronism result in a urine Na concentration of more than 20 mEq/L.
      • Extrarenal losses caused by vomiting, diarrhea, sweat, or third spacing result in a urine Na concentration of less than 20 mEq/L secondary to increased tubular reabsorption of Na.
    • Normovolemic hyponatremia: When hyponatremia is caused by syndrome of inappropriate antidiuretic hormone secretion (SIADH), reset osmostat, glucocorticoid deficiency, hypothyroidism, or water intoxication, the urine Na concentration is more than 20 mEq/L.
    • Hypervolemic hyponatremia
      • If hyponatremia is caused by an edema-forming states (eg, congestive heart failure, hepatic failure), the urine Na concentration is less than 20 mEq/L because effective arterial perfusion is low despite an increase in total body water. Use of diuretics affects urine Na concentration.
      • If hyponatremia is caused by acute or chronic renal failure, the urine Na concentration is more than 20 mEq/L.
    • SIADH: Urine sodium concentration is more than 40mEq/L with normal dietary salt intake.
    • Cerebral salt-wasting syndrome (CSWS): Urine loss is significantly higher and frequently exceeds 80 mEq/L.
  • Special laboratory studies include tests of the following:
    • Aldosterone level
    • Cortisol level
    • Free T4 and thyroid-stimulating hormone (TSH) levels
    • Adrenocorticotropic hormone (ACTH) level
    • Antidiuretic hormone (ADH) level
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Imaging Studies

  • Neuroimaging (only if clinically indicated, not routinely performed)
    • CT scanning is useful for evaluating causative intracranial pathologies, such as tumors, hydrocephalus, and hemorrhage. It is also useful for detecting cerebral edema and demyelinating lesions that occur during treatment. CT scanning is superior to MRI in delineating hemorrhage and calcifications.
    • MRI is sensitive for detecting tumors and demyelination.
  • Abdominal imaging (only if clinically indicated, not routinely performed)
    • Ultrasonography may be performed to detect abdominal masses, such as those due to bilateral adrenal hyperplasia, and adrenal tumors.
    • CT and MRI may help in further delineating the tumor.
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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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