Abstract

Renal water conservation minimizes the progression of hypernatremia, but the ultimate defense against progressive hypernatremia is the stimulation of thirst by hypertonicity with a resultant increase in water ingestion. Defects in thirst may result from focal lesions involving the hypothalamic osmoreceptors, but more commonly are the result of lesions that impair higher cortical processes required for thirst perception and water ingestion. In response to hypernatremia, the brain undergoes adaptive responses to minimize osmotic shrinkage. Initially there is a rapid uptake of electrolytes, while a slower adaptive phase involves the accumulation of organic osmolytes. The rate at which these solutes can be extruded from the brain dictates the rate at which water replacement can be safely administered during treatment. The incidence of hypernatremia ranges from less than 1% to more than 3% in clinical series. While hypernatremia in nonhospitalized patients is predominantly a disease of the elderly, and is commonly a manifestation of infection or inadequate nursing care, hospital-acquired hypernatremia occurs in a patient population more closely resembling the general hospitalized population and results from inadequate water prescription to patients who are unable to self-regulate water intake. Mortality rates range from approximately 40% to more than than 60%.