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 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.
Epidemiology
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.
Conley SB. Hypernatremia. Pediatr Clin North Am. Apr 1990;37(2):365-72. [Medline].
Abramovici MI, Singhal PC, Trachtman H. Hypernatremia and rhabdomyolysis. J Med. 1992;23(1):17-28. [Medline].
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].
[Guideline] Mentes JC. Hydration management. Iowa City (IA): University of Iowa Gerontological Nursing Interventions Research Center, Research Dissemination Core; 2004 Feb. [Full Text].
Konetzny G, Bucher HU, Arlettaz R. Prevention of hypernatraemic dehydration in breastfed newborn infants by daily weighing. Eur J Pediatr. Sep 26 2008;[Medline].
Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. May 18 2000;342(20):1493-9. [Medline].
Avner ED. Clinical disorders of water metabolism: hyponatremia and hypernatremia. Pediatr Ann. Jan 1995;24(1):23-30. [Medline].
Berl T. Disorders of water metabolism. In: Schrier RW, ed. Renal and Electrolyte Disorders. 5th ed. Lippincott-Raven; 1997.
Brown RG. Disorders of water and sodium balance. Postgrad Med. Mar 1993;93(4):227-8, 231-4, 239-40 passim. [Medline].
DeVita MV, Michelis MF. Perturbations in sodium balance. Hyponatremia and hypernatremia. Clin Lab Med. Mar 1993;13(1):135-48. [Medline].
Finberg L. Hypernatremic (hypertonic) dehydration in infants. N Engl J Med. Jul 26 1973;DA - 19730822(4):196-8. [Medline].
Ho L, Bradford BJ. Hypernatremic dehydration and rotavirus enteritis. Clin Pediatr (Phila). Aug 1995;34(8):440-1. [Medline].
Lin M, Liu SJ, Lim IT. Disorders of water imbalance. Emerg Med Clin North Am. Aug 2005;23(3):749-70, ix. [Medline].
Molteni KH. Initial management of hypernatremic dehydration in the breastfed infant. Clin Pediatr (Phila). Dec 1994;33(12):731-40. [Medline].
Moritz ML, Ayus JC. Preventing neurological complications from dysnatremias in children. Pediatr Nephrol. Dec 2005;20(12):1687-700. [Medline].
Moritz ML, Ayus JC. The changing pattern of hypernatremia in hospitalized children. Pediatrics. Sep 1999;104(3 Pt 1):435-9. [Medline].
Moritz ML, Manole MD, Bogen DL, Ayus JC. Breastfeeding-associated hypernatremia: are we missing the diagnosis?. Pediatrics. Sep 2005;116(3):e343-7. [Medline].
Palevsky PM. Hypernatremia. Semin Nephrol. Jan 1998;18(1):20-30. [Medline].
Paneth N. Hypernatremic dehydration of infancy: an epidemiologic review. Am J Dis Child. Aug 1980;134(8):785-92. [Medline].
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].
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].
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].
Unal S, Arhan E, Kara N, Uncu N, Aliefendioglu D. Breast-feeding-associated hypernatremia: retrospective analysis of 169 term newborns. Pediatr Int. Feb 2008;50(1):29-34. [Medline].
Visser L, Devuyst O. Physiopathology of hypernatremia following relief of urinary tract obstruction. Acta Clin Belg. 1994;49(6):290-5. [Medline].
Print
