Pediatric Hyponatremia Follow-up

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

Deterrence/Prevention

  • Carefully monitor patients receiving drugs that can cause hyponatremia.
  • Give careful consideration to the type of intravenous (IV) hydrating solution used in pediatric patients. The findings of one study conclude that the use of hypotonic maintenance fluids increases the incidence of hyponatremia because they decrease blood sodium levels in normonatremic patients. Isotonic maintenance fluids did not increase the incidence of dysnatremia and showed a reduced incidence of hyponatremia in the patients studied. The findings suggest that the administration of isotonic fluids should be considered the standard of care in critically ill children.[6]
  • Prudently monitor serum electrolytes in postoperative patients, patients on IV fluids, and in those with brain tumors, intracranial infections, pulmonary infections, or head trauma.
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Complications

  • Osmotic demyelination syndrome (ODS): Brain damage and cerebral demyelination can develop if the serum Na level raises rapidly in chronic hyponatremia.
    • Epidemiology: The exact incidence of ODS is unknown, and data are derived primarily from autopsy series. In 3548 consecutive autopsies in adults with ODS, the typical lesions were found in 9 (0.25%).[7] In another study, Sterns et al observed myelinolysis in as many as 25% of patients with hyponatremia who were treated with aggressive protocols.[8] The incidence is highest among high-risk groups.
    • Risk factors
      • Alcoholism (common)
      • Malnutrition (common)
      • After prolonged diuretic use (frequent)
      • Psychogenic polydipsia (rare if acute)
      • Burns (infrequent, and often in context of hypernatremia)
      • Liver transplantation (well recognized)[9]
      • Pituitary surgery (rare)
      • Urologic or gynecologic surgery, especially if it involved glycine infusions (rare)
      • Correcting serum Na into hypernatremic levels
      • Hypoxia
    • Subtypes
      • Central pontine myelinolysis (CPM): Lesions are confined to the pons.
      • Extrapontine myelinolysis (EPM): Lesions are confined to the basal ganglia, cerebrum, and cerebellum.
      • ODS: CPM and EPM lesion sites are both present.
    • Pathogenesis: The pathogenesis of ODS is unknown. Cells conditioned to hypo-osmotic hyponatremia may have a decreased adaptive capacity to osmotic stress. The predilection for myelinolysis in the pons is thought to be a result of the grid arrangement of the oligodendrocytes in the base of pons, which limits their mechanical flexibility and, therefore, their capacity to swell. During hyponatremia, these cells can adapt only by losing ions instead of swelling. This limitation makes them prone to damage when Na is replaced. The risk factors mentioned above make normal adaptation difficult.
  • Clinical manifestations of CPM:
    • Ataxia
    • Coma
    • Depressed or absent reflexes
    • Dysarthria
    • Dysphasia
    • Lethargy
    • Ophthalmoplegia
    • Quadriparesis
  • Clinical manifestations of EPM:
    • Akinesis
    • Ataxia
    • Catatonia
    • Choreoathetosis
    • Cogwheel rigidity
    • Disorientation
    • Dysarthria
    • Dystonia
    • Emotional lability
    • Extra pyramidal symptoms
    • Gait disturbance
    • Movement disorders
    • Mutism
    • Myoclonus
    • Myokymia
    • Parkinsonism
    • Rigidity
    • Tremor
  • Diagnosis of CPM: The diagnosis of CPM is based on clinical suspicion and confirmed with imaging studies. MRI is the primary method for diagnosis and is superior to CT. During the acute phase, symmetrical and hypointense lesions can be identified on a T1-weighted MRI. During the subacute phase, symmetrical and hypointense lesions are seen on T2-weighted images. Lesions on MRI may appear days to weeks after the onset of symptoms; in some cases, these may resolve, over months.
  • Management
    • At present, supportive treatment is all that can be recommended with certainty. Therefore, prevention becomes important because hyponatremia is preventable and causes neurologically significant morbidity and mortality.
    • To the authors' knowledge, no trials for the treatment of ODS have been conducted. Small case series or single case reports of treatments, including steroids, IV immunoglobulin, and thyrotrophin-releasing hormone, have all shown good outcomes. However, the results are difficult to interpret because of the lack of clinical trials.
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Prognosis

  • Older reports of ODS indicated almost a 100% mortality rate within 3 months after hospital admission.
  • More recent studies of ODS reveal a relatively mild clinical course without substantial neurologic deficits in survivors.
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Patient Education

  • Advise parents not to replace diarrheal fluid loss with hypotonic fluids such as tea or soda.
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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.

References

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