Cerebral salt-wasting syndrome (CSWS) is a medical entity that leads to hyponatremia and hypovolemia due to dehydration, as a result of an acute or chronic and persistent underlying CNS disorder, including trauma, tumors, and other pathologies.
Patients present with the clinical manifestations of hyponatremia and hypovolemia. In general, a case of very mild hyponatremia tends to produce no noticeable symptoms; however, it has been observed that even non-severe hyponatremia can lead to devastating clinical manifestations . A serum sodium concentration lower than 135 mEq/L, but over 115 mEq/L usually leads to nausea and malaise. Values less than 135 mEq/L lead to profound neurological symptomatology due to cerebral edema, including a diminished level of consciousness and lethargy, cephalalgia, epileptic phenomena and, eventually, even a comatose state . There is a positive correlation between the decrease in sodium levels and the aggravation of symptoms: as the concentration of sodium in the serum of the patient declines, symptoms are exacerbated.
Hypovolemia leads to symptoms that entail dried mucous membranes (oral or nasal cavity), dry skin that lacks elasticity, sunken anterior fontanelle, and tachycardia. Profound hypovolemia causes hypotension. A vital clinical characteristic of patients affected by cerebral salt-wasting syndrome is that the aforementioned manifestations tend to respond positively to volume and sodium replacement  . Massive polyuria that can be reversed with the simultaneous administration of vasopressin and cortisone acetate, hypotension, the absence of cardiac symptoms and hypovolemia, constitute a potential clinical picture of a patient with central diabetes insipidus and CSWS, according to a recent study .
CSWS is a syndrome difficult to diagnose, due to the lack of a specific set of tests to detect any pathognomonic result. The primary difficulty is its differentiation from the syndrome of inappropriate antidiuretic hormone secretion (SIADH), due to a significant similarity between these two distinct entities. The workup involved in the diagnostic procedure encompasses:
Serum sodium concentration
Reveals hyponatremia, namely a serum sodium concentration < 135 mEq/L.
CSWS is expected to lead to increased urine flow and dilute urine, whereas SIADH leads to a low urine flow and concentrated urine.
Urinary sodium concentration
CSWS leads to a high urinary sodium concentration, that exceeds 40 mEq/L, followed by a negative net sodium balance.
Fractional excretion of uric acid (FEUA) is increased in patients with the cerebral salt-wasting syndrome and hyperuricemia is detected. These findings tend to remain, despite the reversion or hyponatremia. On the contrary, the same findings that are observed in SIADH tend to regress after the correction of serum sodium  .
Cerebral salt-wasting syndrome leads to an increase in the fractional excretion of phosphate (FEP), in contradistinction to SIADH .