Cerebral salt wasting (CSW) syndrome is a condition characterized by hyponatremia and the excess loss of extracellular fluid that occurs in individuals with a central nervous system injury. It is difficult to distinguish from the syndrome of inappropriate antidiuretic hormone (SIADH), and there is debate regarding whether CSW is a distinct entity or whether it reflects complex physiologic adaptation. For those who endorse CSW, it is thought to be a condition in which renal salt wasting is triggered by a central nervous system injury such as a subarachnoid hemorrhage. CSW has also been described in central nervous system infections, malignancies, and infiltrative diseases. CSW is differentiated from SIADH in that it is accompanied by hypovolemia with secondary ADH release, while SIADH usually is not associated with hypovolemia.

The etiology and incidence of salt wasting due to central nervous system injury is not known. It is a rare cause of hyponatremia and has likely decreased in incidence due to early delivery of isotonic saline in patients with subarachnoid hemorrhage.

Clinically, patients develop hypotension, hemoconcentrated blood cell lines (elevated hemoglobin, platelets, and perhaps WBC count), and high urine output. Symptoms typically manifest within 10 days of cerebral injury. Hyponatremia is a serologic marker paramount to establishing the diagnosis.

If appropriately treated, CSW should resolve fully within a few weeks of diagnosis, and no long-term follow-up is warranted.