Cerebral Salt Wasting: Pathophysiology, Diagnosis, and Treatment

Cerebral salt wasting (CSW) is a syndrome of hypovolemic hyponatremia caused by natriuresis and diuresis. The mechanisms underlying CSW have not been precisely delineated, although existing evidence strongly implicates abnormal elevations in circulating natriuretic peptides. The key in diagnosis of CSW lies in distinguishing it from the more common syndrome of inappropriate secretion of antidiuretic hormone. Volume status, but not serum and urine electrolytes and osmolality, is crucial for making this distinction. Volume and sodium repletion are the goals of treatment of patients with CSW, and this can be performed using some combination of isotonic saline, hypertonic saline, and mineralocorticoids.

Hyponatremia can be a vexing problem for those who care for critically ill neurologic patients. Although seemingly simple at first glance, the accurate diagnosis and effective treatment of hyponatremia can be complex. The chief difficulty in this setting often lies in determining what is driving the fall in serum sodium concentration. Cerebral salt wasting (CSW) is a disorder of sodium and water handling that occurs as a result of cerebral disease in the setting of normal kidney function. It is characterized by hyponatremia in association with hypovolemia and, as the name implies, is caused by natriuresis. In routine clinical practice, distinguishing this condition from the more familiar syndrome of inappropriate secretion of antidiuretic hormone (SIADH) can be quite difficult. Nonetheless, this task is crucial because treatments for the two conditions are fundamentally different. Accordingly, it is important for physicians caring for critically ill neurologic patients to have a thorough understanding of this disorder. This article reviews the pathophysiology of CSW. Building on these basic concepts, a rational approach to its diagnosis and treatment is outlined.

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 euvolemic hyponatremia associated with normal urine output and inappropriately high levels of antidiuretic hormone (ADH) was described in a patient with bronchogenic carcinoma. This was later termed as the “syndrome of inappropriate antidiuretic hormone release.” Following this discovery and over the subsequent 30 years, hyponatremia that developed in patients with neurologic diseases, such as subarachnoid hemorrhage (SAH), was generally attributed to SIADH. Beginning in the 1980s, several key studies challenged this concept by demonstrating in patients with aneurysmal SAH a syndrome of low blood volume, natriuresis with a net negative sodium balance, and high urinary output, which was consistent with CSW and not SIADH. These publications led to the modern acceptance of CSW as an important cause of hyponatremia in patients with brain injury and to important research that followed investigating the pathophysiologic disturbances of salt and water homeostasis in patients with neurologic disease.

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