Overview Hypernatremia is the medical term used to describe having too much sodium in the blood. Sodium is an important nutrient for proper functioning of the body. Read on to learn more about the role of sodium and when high levels may result in a medical emergency. How are sodium levels controlled? Hypernatremia can occur when there is a too much water loss or too much sodium gain in the body. The result is too little body water for the amount of total body sodium.
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Corresponding author. Correspondence author: Soo Wan Kim, M. Tel: , Fax: , rk. Abstract Hypernatremia reflects a net water loss or a hypertonic sodium gain, with inevitable hyperosmolality. Importantly, the sensation of intense thirst that protects against severe hypernatremia in health may be absent or reduced in patients with altered mental status or with hypothalamic lesions affecting their sense of thirst and in infants and elderly people.
Non-specific symptoms such as anorexia, muscle weakness, restlessness, nausea, and vomiting tend to occur early. More serious signs follow, with altered mental status, lethargy, irritability, stupor, and coma.
Acute brain shrinkage can induce vascular rupture, with cerebral bleeding and subarachnoid hemorrhage. However, in the vast majority of cases, the onset of hypertonicity is low enough to allow the brain to adapt and thereby to minimize cerebral dehydration.
Organic osmolytes accumulated during the adaptation to hypernatremia are slow to leave the cell during rehydration. Therefore, if the hypernatremia is corrected too rapidly, cerebral edema results as the relatively more hypertonic ICF accumulates water. Keywords: Hypernatremia, Cell volume regulation, Diabetes insipidus Hypernatremia, defined as a rise in the serum sodium concentration to a value exceeding mmol per liter, is a common electrolyte disorder.
Because sodium is a functionally impermeable solute, it contributes to tonicity and induces the movement of water across cell membranes. Therefore, hypernatremia invariably denotes hypertonic hyperosmolality and always causes cellular dehydration, at least transiently. Although correction of transient increases in plasma osmolality is usually well tolerated, correction of chronic plasma hypertonicity with rehydration therapy may be accompanied by brain swelling, herniation, and death 1.
The clinical differences between acute and chronic osmolar disorders can be understood through a consideration of the different mechanisms by which cells in the brain regulate their volume in response to brief and sustained osmotic challenges 2.
Pathophysiology As in other types of cells, hypertonically stressed brain cells regulate their volume initially by the rapid uptake of electrolytes 3.
With a prolonged elevation of plasma osmolality, however, most excess electrolytes in the brain are replaced by organic solutes. These solutes have historically been termed "idiogenic osmoles" because they were unidentified and thought to be produced by the brain cells themselves 4. Studies in animals and cultured cells 5 have revealed that idiogenic osmoles are the same organic osmolytes used by all organisms for volume regulation.
The most important organic osmolytes in the mammalian brain include myo-inositol, taurine, glycerylphosphorylcholine, and betaine, which are accumulated primarily by uptake from extracellular fluids through the activation of sodium-dependent cotransporters 5. Beginning on the first day of the hypernatremia, brain volume is largely restored due noth to water movement from the cerebrospinal fluid into the brain thereby increasing the interstitial volume 5 and to the uptake of solutes by the cells thereby pulling water into the cells and restoring the cell volume 5 - 7.
The latter response involves an initial uptake of sodium and potassium salts, followed by the later accumulation of osmolytes, which in animals consists primarily of myo-inositol and the amino acids glutamine and glutamate 6 , 7.
Myo-inositol is taken up from the extracellular fluid via an increase in the number of sodium-myo-inositol cotransporters in the cell membrane 8 , whereas the source uptake from the extracellular fluid or production within the cells of glutamine and glutamate is at present unknown. The cerebral adaptation in hypernatremia has two important clinical consequences: Chronic hypernatremia is much less likely to induce neurologic symptoms. Assessment of symptoms attributable to hypernatremia is often difficult because most affected adults have underlying neurologic disease.
The latter is required to diminish the protective thirst mechanism that normally prevents the development of hypernatremia, even in patients with diabetes insipidus. Correction of chronic hypernatremia must occur slowly to prevent rapid fluid movement into the brain and cerebral edema, changes that can lead to seizures and coma 9. Although the brain cells can rapidly lose potassium and sodium in response to this cell swelling, the loss of accumulated osmolytes occurs more slowly, a phenomenon that acts to hold water within the cells 5.
The loss of myoinositol, for example, requires both a reduction in synthesis of new sodium-inositol cotransporters 8 and the activation of a specific inositol efflux mechanism in the cell membrane The delayed clearance of osmolytes from the cell can predispose to cerebral edema if the plasma sodium concentration is lowered too rapidly. Net water loss accounts for the majority of cases of hypernatremia 1.
It can occur in the absence of a sodium deficit pure water loss or in its presence hypotonic fluid loss. Hypertonic sodium gain usually results from clinical interventions or accidental sodium loading.
Because sustained hypernatremia can occur only when thirst or access to water is impaired, the groups at highest risk are patients with altered mental status, intubated patients, infants, and elderly persons Hypernatremia in infants usually results from diarrhea, whereas in elderly persons it is usually associated with infirmity or febrile illness 12 , Thirst impairment also occurs in elderly patients Often the cause is evident from the history.
Measurement of urine osmolality in relation to the plasma osmolality and the urine sodium concentration help if the cause is unclear Fig. Patients with diabetes insipidus present with polyuria and polydipsia and not hypernatremia unless thirst sensation is impaired. Central diabetes insipidus and nephrogenic diabetes insipidus may be differentiated by the response to water deprivation failure to concentrate urine followed by the V2-receptor agonist desmopressin, causing concentration of urine in patients with central diabetes insipidus.
Adult data sparse. Rapidly dropping the sodium concentration could theoretically cause cerebral edema and herniation. Retrospective studies actually correlate slower correction of sodium with worse outcomes. Patients with active neurologic disease and pre-existing cerebral edema. Bottom line? By far the most common problem is dropping the sodium too slowly.
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