Cerebral Salt Wasting: Pathophysiology, Diagnosis, and Treatment

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Historical aspects

Early studies of hyponatremia in patients with cerebral disease published in the 1950s described the presence of polyuria, elevated urinary sodium levels, and dehydration despite the presence of a low serum sodium concentration and adequate fluid intake. This syndrome was termed “cerebral salt wasting.” At the time, CSW was suspected to be the major cause of hyponatremia in patients with central nervous system (CNS) injury. Shortly after its original description, however, a syndrome of

Clinical relevance

Hyponatremia is frequently encountered in patients with neurologic disease. A recent analysis of 316 patients with aneurysmal SAH detected hyponatremia in 57% of patients.10 Although previous investigators have reported lower frequencies,11, 12, 13 it is still the most commonly encountered electrolyte disturbance in the neurologic intensive care unit. Adding to its importance are the occasional serious consequences of severe hyponatremia, which include seizures and worsening of cerebral edema.

Pathophysiology of CSW

Despite the clear association between the presence of CSW and severe neurologic disease, the mechanism underlying this association has not yet been clearly identified. Maintenance of body sodium and water homeostasis is a vital physiologic process. It is largely governed by intricate interactions between the autonomic nervous system and humoral factors that influence the kidney's handling of sodium and water. Disruption of the normal interactions between these systems can generate sodium and

Diagnosis of CSW

Differentiating CSW from most other common causes of hyponatremia (diuretic use, adrenal insufficiency, extrarenal-induced volume-deplete states, hypothyroidism, congestive heart failure)115 is typically not difficult. Obtaining a meticulous history and inventory of recent medications and laboratory studies often reveals the correct diagnosis. The challenge lies in the differentiation of CSW from SIADH, because both disorders cause similar serum and urine laboratory abnormalities and occur in

Treatment

The mainstay of therapy for CSW is replacement of the sodium and water that is lost as a result of pathologic natriuresis and diuresis. This is in direct contrast to the treatment of SIADH, the crux of which is free water restriction. Patients with CSW typically have significant extracellular volume depletion and a total-body sodium deficit of at least 2 mmol of sodium/kg body weight.66 In patients who are hypovolemic, a reasonable initial management strategy is administration of normal saline

Summary

CSW is a syndrome of hypovolemic hyponatremia caused by natriuresis and diuresis. Once thought of as a rare novelty, recent clinical and basic science research has shown that CSW exists, is not uncommon in patients with certain types of brain injury, and can have significant negative consequences if not properly diagnosed and treated. The mechanisms underlying this syndrome have yet to be precisely delineated, although existing evidence strongly implicates abnormal elevations in circulating

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