Sodium and Water Disorders: Evaluation and Management

Abstract

Dysnatremias are among the most common electrolyte abnormalities encountered in hospitalized patients. Proper fluid management and early detection are important in the prevention and treatment of dysnatremias. Virtually all acutely ill patients are at risk for developing hyponatremia due to numerous hemodynamic and non-hemodynamic stimuli for arginine vasopressin (AVP) release. One of most common causes of hyponatremia in hospitalized patients is the syndrome of inappropriate antidiuresis (SIAD). An elevated fractional excretion of urate is helpful in establishing a diagnosis of SIAD. A major contributing factor to the development of hospital-acquired hyponatremia is the administration of hypotonic fluids. Recent clinical practice guidelines have recommended isotonic maintenance fluids for the prevention of hospital-acquired hyponatremia. Hyponatremic encephalopathy is the most serious complication of hyponatremia. Consensus guidelines have recommended intermittent bolus therapy with 3% sodium chloride for the treatment of hyponatremic encephalopathy. Excessive therapy of severe and chronic hyponatremia can also lead to neurologic injury due to cerebral demyelination. Hospital-acquired hypernatremia occurs in patients who have restricted access to fluids in combination with ongoing free water losses. A group at high-risk for developing hypernatremia in the outpatient setting is that of the breastfed infant due to insufficient lactation. Patients at risk for severe hospital-acquired hyponatremia are those with diabetes insipidus. A useful test for distinguishing central from nephrogenic diabetes insipidus is plasma copeptin testing. Copeptin can be used as a surrogate marker of AVP as it is easier and more reliable to measure.