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Pediatric Hypernatremia Clinical Presentation

  • Author: Ewa Elenberg, MD, MEd; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Feb 13, 2014
 

History

Patients in certain situations or with certain conditions are at risk for hypernatremia, as follows:

  • Hospitalized patients who receive exclusive intravenous fluids
  • Patients with coma
  • Newborns
  • Toddlers
  • Patients with diabetes insipidus
  • Patients receiving alkali therapy
  • Patients with diarrhea
  • Patients with fever
  • Patients with renal disorders (eg, dysplasia, medullary cystic disease, polycystic kidney disease, tubulointerstitial disease)
  • Patients with obstructive uropathy
  • Patients with electrolyte disturbances (eg, hypokalemia, hypercalcemia)
  • Patients with heat stroke or excessive hypotonic fluid loss

Signs and symptoms of hypernatremia include the following:

  • Irritability
  • High-pitched cry or wail
  • Periods of lethargy interspersed with periods of irritability
  • Altered sensorium
  • Seizures
  • Increased muscle tone
  • Fever
  • Rhabdomyolysis[2, 3]
  • Oligoanuria
  • Excessive diuresis
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Physical

Skin turgor is a physical finding in patients with hypernatremia. Extracellular and plasma volumes tend to be maintained in hypernatremic dehydration until dehydration is severe (ie, when the patient loses >10% of body weight).

When dehydration is severe, skin turgor is reduced, and the skin develops a characteristic doughy appearance.

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Causes

Causes of hypovolemic hypernatremia include the following:

  • Diarrhea
  • Excessive perspiration
  • Renal dysplasia
  • Obstructive uropathy
  • Osmotic diuresis

Causes of euvolemic hypernatremia include the following:

  • Central diabetes insipidus causes
  • Idiopathic causes
  • Head trauma
  • Suprasellar or infrasellar tumors (eg, craniopharyngioma, pinealoma)
  • Histiocytosis
  • Sickle cell disease
  • Cerebral hemorrhage
  • Infection (meningitis, encephalitis)
  • Nephrogenic diabetes insipidus causes
  • Congenital (familial) conditions
  • Renal disease (obstructive uropathy, renal dysplasia, medullary cystic disease, reflux nephropathy, polycystic disease)
  • Systemic disease with renal involvement (sickle cell disease, sarcoidosis, amyloidosis)
  • Drugs (amphotericin, phenytoin, lithium, aminoglycosides, methoxyflurane)

Causes of hypervolemic hypernatremia include the following:

  • Improperly mixed formula
  • NaHCO3 administration
  • NaCl administration
  • Primary hyperaldosteronism
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Contributor Information and Disclosures
Author

Ewa Elenberg, MD, MEd Associate Professor of Pediatrics, Renal Section, Texas Children's Hospital, Baylor College of Medicine

Ewa Elenberg, MD, MEd is a member of the following medical societies: American Society of Nephrology, American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

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, Wilderness Medical Society

Disclosure: Nothing to disclose.

References
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Figure A: Normal cell. Figure B: Cell initially responds to extracellular hypertonicity through passive osmosis of water extracellularly, resulting in cell shrinkage. Figure C: Cell actively responds to extracellular hypertonicity and cell shrinkage in order to limit water loss through transport of organic osmolytes across the cell membrane, as well as through intracellular production of these osmolytes. Figure D: Rapid correction of extracellular hypertonicity results in passive movement of water molecules into the relatively hypertonic intracellular space, causing cellular swelling, damage, and ultimately death.
 
 
 
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