Hyponatremia is a common electrolyte disorder in the setting of central nervous system (CNS) disease. This is usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) [1-4].
Cerebral salt-wasting (CSW) is another potential cause of hyponatremia in those with CNS disease, particularly in patients with subarachnoid hemorrhage. CSW is characterized by hyponatremia and extracellular fluid depletion due to inappropriate sodium wasting in the urine . However, some authorities contend that CSW does not really exist and is only a misnomer for what is actually SIADH, with the putative salt wasting being due to unappreciated volume expansion [6,7].
Issues related to CSW, including the differentiation from SIADH, will be reviewed here. The causes and diagnosis of hyponatremia, causes and treatment of SIADH, and the general management of patients with subarachnoid hemorrhage are presented separately. (See "Causes of hyponatremia in adults" and "Evaluation of adults with hyponatremia" and "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)" and "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat" and "Treatment of aneurysmal subarachnoid hemorrhage".)
With respect to pathophysiology, two issues need to be addressed: the mechanism of salt-wasting; and the mechanism of hyponatremia.
The mechanism by which cerebral disease might lead to renal salt-wasting is poorly understood. Two putative mechanisms are disruption of neural input to the kidney and central elaboration of a circulating natriuretic factor [8,9]: