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

Abstract

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.