Hyponatremia is a relatively common disorder occurring in up to 6% of hospitalized patients and can occur through any mechanism that produces a relative excess of body water to body sodium. Although most hyponatremia patients are asymptomatic, severe symptomatic hyponatremia is a medical emergency that may lead to cerebral edema, tentorial herniation and death. More aggressive therapy is indicated in these patients. However, in some patients, the treatment itself may result in central nervous system demyelination that may be associated with permanent neurologic sequelae. The therapeutic strategy that should guide optimal treatment of hyponatremia requires attention to the following four factors: the patient’s volume status, the presence or absence of symptoms, duration of hypo-osmolality, and the presence or absence of risk factors for the development of neurologic complication. An initial categorization according to the clinical ECF volume status of the patient will allow a determination of the appropriate initial therapy in the majority of cases. The importance of duration of hyponatremia and the presence or absence of symptoms relates to how well the brain has adapted to the hyponatremia. The severity of hyponatremia is also an important consideration because osmotic demyelination is rarely seen in patients with the initial serum sodium greater than 120 mEq/l. Clinical surveys have identified subgroups of patients at greatest risk for developing neurologic complication of hyponatremia. Optimal therapy of these patients must consider balancing the risks of hyponatremia against the risks of correction for each patient individually. Although individual variability in response to treatment is considerable, consensus guidelines for treating hyponatremic patients allow a rational and safe therapeutic approach to minimize the neurologic complications.

Keywords:
Hyponatremia, Hypo-osmolality, Acute cerebral edema, Central pontine myelinolysis
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2002
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