Pediatric Hypernatremia Clinical Presentation

  • Author: Ewa Elenberg, MD; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Jan 10, 2012
 

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

  • Hypovolemic hypernatremia
    • Diarrhea
    • Excessive perspiration
    • Renal dysplasia
    • Obstructive uropathy
    • Osmotic diuresis
  • Euvolemic hypernatremia
    • Central diabetes insipidus causes
    • Idiopathic causes
    • Head trauma
    • Suprasellar or infrasellar tumors (eg, craniopharyngioma, pinealoma)
    • Granulomatous disease (sarcoidosis, tuberculosis, Wegener granulomatosis)
    • Histiocytosis
    • Sickle cell disease
    • Cerebral hemorrhage
    • Infection (meningitis, encephalitis)
    • Associated cleft lip and palate
    • 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)
  • Hypervolemic hypernatremia
    • Improperly mixed formula
    • NaHCO3 administration
    • NaCl administration
    • Primary hyperaldosteronism
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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Coauthor(s)

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, Chief, Division of Pediatric Critical Care Medicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

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.

References

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  20. Peker E, Kirimi E, Tuncer O, Ceylan A. Severe hypernatremia in newborns due to salting. Eur J Pediatr. Jul 2010;169(7):829-32. [Medline].

  21. Roscelli JD, Yu CE, Southgate WM. Management of salt poisoning in an extremely low birth weight infant. Pediatr Nephrol. Apr 1994;8(2):172-4. [Medline].

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  24. Visser L, Devuyst O. Physiopathology of hypernatremia following relief of urinary tract obstruction. Acta Clin Belg. 1994;49(6):290-5. [Medline].

 
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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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