|| Checking for direct PDF access through Ovid
We review literature from the past 18 months on the treatment of hyponatremia. Therapy must address both the consequences of the untreated electrolyte disturbance (including fatal cerebral edema due to acute water intoxication) and the complications of excessive therapy (the osmotic demyelination syndrome).Correction of hyponatremia by 4–6 mEq/l within 6 h, with bolus infusions of 3% saline if necessary, is sufficient to manage the most severe manifestations of hyponatremia. Planning therapy to achieve a 6 mEq/l daily increase in the serum sodium concentration can avoid iatrogenic brain damage by staying well clear of correction rates that are harmful. Conservative correction goals are wise because inadvertent overcorrection is common. Administration of desmopressin to halt a water diuresis can help prevent overcorrection; if overcorrection occurs, therapeutic relowering of the serum sodium concentration is supported by data in experimental animals and was found to be safe in a small observational clinical trial. Even mild and apparently asymptomatic hyponatremia may lead to falls because of impaired gait, and an increased likelihood of fracture because of hyponatremia-induced osteoporosis, a newly described entity. Recently approved vasopressin antagonists now make it possible to normalize the serum sodium concentration on a chronic basis, but practical considerations have limited their use.