eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Hypernatremia

Author: Ewa Elenberg, MD, Assistant Professor, Department of Pediatrics, Renal Section, Texas Children's Hospital, Baylor College of Medicine
Coauthor(s): Muthukumar Vellaichamy, MD, FAAP, Clinical Assistant Professor, Department of Pediatrics, University of Kansas School of Medicine-Wichita, Wesley Medical Center
Contributor Information and Disclosures

Updated: Nov 2, 2009

Introduction

Background

Hypernatremia is defined as a serum sodium concentration of more than 145 mEq/L. It is characterized by a deficit of total body water (TBW) relative to total body sodium levels due to either loss of free water, or infrequently, the administration of hypertonic sodium solutions.1

In healthy subjects, the body's 2 main defense mechanisms against hypernatremia are thirst and the stimulation of vasopressin release.

Figure A: Normal cell. Figure B: Cell initially r...

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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Figure A: Normal cell. Figure B: Cell initially r...

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.


Pathophysiology

Hypernatremia represents a deficit of water in relation to the body's sodium stores, which can result from a net water loss or a hypertonic sodium gain. Net water loss accounts for most cases of hypernatremia. Hypertonic sodium gain usually results from clinical interventions or accidental sodium loading. As a result of increased extracellular sodium concentration, plasma tonicity increases. This increase in tonicity induces the movement of water across cell membranes, causing cellular dehydration.

The following 3 mechanisms may lead to hypernatremia, alone or in concert:

  • Pure water depletion (eg, diabetes insipidus)
  • Water depletion exceeding sodium depletion (eg, diarrhea)
  • Sodium excess (eg, salt poisoning)

Sustained hypernatremia can occur only when thirst or access to water is impaired. Therefore, the groups at highest risk are infants and intubated patients.

Because of certain physiologic characteristics, infants are predisposed to dehydration. They have a large surface area in relation to their height or weight compared with adults and have relatively large evaporative water losses. In infants, hypernatremia usually results from diarrhea and sometimes from improperly prepared infant formula or inadequate mother-infant interaction during breastfeeding.

Hypernatremia causes decreased cellular volume as a result of water efflux from the cells to maintain equal osmolality inside and outside the cell. Brain cells are especially vulnerable to complications resulting from cell contraction. Severe hypernatremic dehydration induces brain shrinkage, which can tear cerebral blood vessels, leading to cerebral hemorrhage, seizures, paralysis, and encephalopathy.

In patients with prolonged hypernatremia, rapid rehydration with hypotonic fluids may cause cerebral edema, which can lead to coma, convulsions, and death.

Frequency

United States

Hypernatremia is primarily a hospital-acquired condition occurring in children of all ages who have restricted access to fluids, mostly due to significant underlying medical problems such as a chronic disease, neurologic impairment, a critical illness, or prematurity. The incidence is estimated to be greater than 1% in hospitalized patients. Hospital-acquired hypernatremia accounts for 60% of hypernatremia cases in children. Gastroenteritis contributes to the hypernatremia in only 20% of cases. The group most affected is intubated, critically ill patients. Most cases result from a failure to freely administer water to patients. The incidence of breastfeeding-related hypernatremia is 1-2%.

International

In developing nations, the reported incidence is 1.5-20%.

Mortality/Morbidity

In children with acute hypernatremia, mortality rates are as high as 20%. Neurologic complications related to hypernatremia occur in 15% of patients. The neurologic sequelae consist of intellectual deficits, seizure disorders, and spastic plegias. In cases of chronic hypernatremia in children, the mortality rate is 10%.

Race

No predilection is documented.

Sex

No sex difference is known.

Age

In the pediatric population, hypernatremia usually affects newborns and toddlers who depend on caretakers for water, as well patients of any age who have significant underlying medical problems such as a chronic disease, neurologic impairment, a critical illness, or prematurity.

Clinical

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
    • Rhabdomyolysis2,3
    • Oligoanuria
    • Excessive diuresis

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.

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

More on Hypernatremia

Overview: Hypernatremia
Differential Diagnoses & Workup: Hypernatremia
Treatment & Medication: Hypernatremia
Follow-up: Hypernatremia
Multimedia: Hypernatremia
References
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References

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  2. Abramovici MI, Singhal PC, Trachtman H. Hypernatremia and rhabdomyolysis. J Med. 1992;23(1):17-28. [Medline].

  3. Yang TY, Chang JW, Tseng MH, Wang HH, Niu DM, Yang LY. Extreme hypernatremia combined with rhabdomyolysis and acute renal failure. J Chin Med Assoc. Oct 2009;72(10):555-8. [Medline].

  4. [Guideline] Mentes JC. Hydration management. Iowa City (IA): University of Iowa Gerontological Nursing Interventions Research Center, Research Dissemination Core; 2004 Feb. [Full Text].

  5. Konetzny G, Bucher HU, Arlettaz R. Prevention of hypernatraemic dehydration in breastfed newborn infants by daily weighing. Eur J Pediatr. Sep 26 2008;[Medline].

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  16. Moritz ML, Manole MD, Bogen DL, Ayus JC. Breastfeeding-associated hypernatremia: are we missing the diagnosis?. Pediatrics. Sep 2005;116(3):e343-7. [Medline].

  17. Palevsky PM. Hypernatremia. Semin Nephrol. Jan 1998;18(1):20-30. [Medline].

  18. Paneth N. Hypernatremic dehydration of infancy: an epidemiologic review. Am J Dis Child. Aug 1980;134(8):785-92. [Medline].

  19. 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].

  20. Trachtman H. Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II. Pediatr Nephrol. Jan 1992;6(1):104-12. [Medline].

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Further Reading

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Keywords

hypernatremia, high serum sodium, pure water depletion, sodium excess, water depletion exceeding sodium depletion, total body water, TBW, Na, salt poisoning, dehydration, thirst, sodium loading, diabetes insipidus, diarrhea, gastroenteritis, dysplasia, medullary cystic, polycystic, tubulointerstitial disease, obstructive uropathy, heat stroke, rhabdomyolysis, oligoanuria, craniopharyngioma, pinealoma, sarcoid, tuberculosis, Wegener granulomatosis, histiocytosis, sickle cell disease, meningitis, encephalitis, cleft lip and palate, amyloidosis

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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 Academy of Pediatrics, American Medical Association, and American Society of 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.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
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.

 
 
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