Practical management of exercise-associated hyponatremic encephalopathy: the sodium paradox of non-osmotic vasopressin secretion.

Exercise-associated hyponatremia (EAH) is a potentially fatal fluid imbalance largely resulting from sustained fluid intake beyond the capacity for fluid excretion during endurance exercise. Common symptoms include vomiting, confusion, altered mental status, and seizures; however, these symptoms can also be seen with hypernatremic encephalopathy, making measurement of plasma sodium concentration imperative when athletes present with these symptoms. Recent evidence supports the inappropriate secretion of the antidiuretic hormone, arginine vasopressin (AVP), as the primary pathophysiological mechanism underlying the development of dilutional EAH. It appears that AVP is stimulated normally during prolonged endurance running by non-osmotic factors such as an exercise-induced plasma volume decrease; therefore, any excess fluid intake will likely be retained, and sodium will likely be excreted. The capacity for a small concentrated bolus of a hypertonic saline solution to rapidly reverse cerebral edema and remove any decreased plasma volume stimulus to AVP secretion is the most efficacious treatment for acute EAH encephalopathy to date. The prompt administration of an intravenous (IV) bolus of hypertonic saline in the field or hospital setting can be lifesaving once EAH is documented. Conversely, oral sodium supplementation will not prevent the development of EAH encephalopathy if exuberant fluid intake combined with non-osmotic secretion of AVP occurs during prolonged physical activity. As a result, the seemingly paradoxical use of sodium supplementation as the most effective practical management therapy (IV bolus) and ineffective preventive strategy can be reconciled through a more complete understanding of the pathophysiological mechanisms underlying EAH.