Cerebral salt wasting syndrome (CSW-cerebral salt wasting) was first described in 1950 by Peters.
Renal loss of sodium as a result of intracranial disease, producing hypo- natremia and a decrease in extracellular fluid volume.
Patients present with excessive natriuresis and hyponatremic dehydration.
This syndrome can occur in patients who have sustained damage to the central nervous system (e.g. patients with subarachnoid bleeding, bacterial meningitis or after neurosurgery).
Cerebral salt wasting (CSW) has been suggested to precede the development of symptomatic vasospasm.
Patients with aneurysmal SAH may have CSW with hyponatremia which mimics SIADH, however there is usually also hypovolemia in CSW. In this setting, fluid restriction may exacerbate vasospasm induced ischemia 2) 3) 4) 5).
The mechanism whereby the kidneys fail to conserve sodium in CSW is not known, and may be either a result of an as yet unidentified natriuretic factor or direct neural control mechanisms.
Criteria for CSW included hyponatremia <135 mEq/L, and urine output >4 L in 12 hours with urine sodium >40 mEq/L.
Laboratory tests (serum and urinary electrolytes and osmolalities) may be identical with SIADH and CSW 6).
Furthermore, hypovolemia in CSW may stimulate ADH release. To differentiate: CVP, PCWP, and plasma volume (a nuclear medicine study) are low in hypovolemia (i.e. CSW).
The two most important differences between CSW and SIADH being extracellular volume and salt balance. An elevated serum [K+] with hyponatremia is incompatible with the diagnosis of SIADH.
Differentiating this syndrome with the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which may occur in the same group of patients, is necessary in order to administer the correct treatment which consists of fluid restriction and sodium replacement in SIADH and fluid and sodium replacement as well as occasional mineralocorticoid therapy in CSW 7).
Positive salt balance.
Avoid excessively rapid correction of hyponatremia or overcorrection which may be associated with osmotic demyelination as with SIADH.
○ Hydrate patient with 0.9%NS at 100–125 ml/hr. For severe cases, 3% saline at 25–50 cc/hr is occasionally required. ○ Do not give furosemide.
○ Salt may also be simultaneously replaced orally.
○ Blood products may be needed if anemia is present.
○ Medications a) Fludrocortisone acetate acts directly on the renal tubule to increase sodium absorption. Ben- efits of giving 0.2 mg IV or PO q d in CSW have been reported, 9) but significant complications of pulmonary edema, hypokalemia and HTN may occur.
b) Urea: an alternative treatment using urea may be applicable to the hyponatremia of either SIADH or CSW, and therefore may be used before the cause has been ascertained: urea (Ureaphil®) 0.5 grams/kg (dissolve 40 gm in 100–150 ml NS) IV over 30–60 mins q 8 hrs 10)
Use NS + 20 mEq KCl/Lat 2 ml/kg/hr as the main IV until the hyponatremia is corrected (unlike mannitol, urea does not increase ADH secretion). They supplemented with colloids (viz. 250 ml of 5% albumin IV q 8–12 hrs x 72 hrs).