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. 
In healthy subjects, the body's 2 main defense mechanisms against hypernatremia are thirst and the stimulation of vasopressin release.
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 three 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.
Patients usually recover from hypernatremia.
Patients with recurrent hypernatremic dehydration develop neurologic sequelae, especially infants with diabetes insipidus.
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%.
Although seizures can occur because of hypernatremia per se, this is rare. They usually occur during the treatment of hypernatremia because of a rapid decline in serum sodium levels. Therefore, slowly correcting hypernatremia is important.
Other complications include the following:
Cerebral edema, especially during treatment
No predilection is documented.
No sex difference is known.
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.
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%.
In developing nations, the reported incidence is 1.5-20%.
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