Cerebral salt wasting: truths, fallacies, theories, and challenges.

BACKGROUND The reported prevalence of cerebral salt wasting has increased in the past three decades. A cerebral lesion and a large natriuresis without a known stimulus to excrete so much sodium (Na ) constitute its essential two elements. OBJECTIVES To review the topic of cerebral salt wasting. There is a diagnostic problem because it is difficult to confirm that a stimulus for the renal excretion of Na is absent. DESIGN Review article. INTERVENTION None. MAIN RESULTS Three fallacies concerning cerebral salt wasting are stressed: first, cerebral salt wasting is a common disorder; second, hyponatremia should be one of its diagnostic features; and third, most patients have a negative balance for Na when the diagnosis of cerebral salt wasting is made. Three causes for the large natriuresis were considered: first, a severe degree of extracellular fluid volume expansion could down-regulate transporters involved in renal Na resorption; second, an adrenergic surge could cause a pressure natriuresis; and third, natriuretic agents might become more potent when the effective extracellular fluid volume is high. CONCLUSIONS Cerebral salt wasting is probably much less common than the literature suggests. With optimal treatment in the intensive care unit, hyponatremia should not develop.