SIADH VS CSW

Hyponatremia may be associated with natriuresis due to an increase in the level of atrial natriuretic factor (ANF). This may explain the frequency with which cerebral salt wasting is seen in SAH patients. Also common is the occurrence of inappropriate secretion of antidiuretic hormone (SIADH) although it is less common than cerebral salt wasting. Differentiating between the two entities is important because fluid restriction can increase blood viscosity as well as the risk of cerebral ischemia associated with vasospasm. Laboratory values may be identical in the two conditions and for this reason determination of central venous pressure (CVP) and/or pulmonary capillary wedge pressure (PCWP) are critical as these measurements are low in cerebral salt wasting and normal or elevated in SIADH. A negative salt balance is apparent in cerebral salt wasting and measurements of urinary sodium concentrations may be helpful. An elevation of serum potassium with hyponatremia is incompatible with the diagnosis of SIADH.

Hyponatremia occurs frequently,likely secondary to elevated brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP). 

These peptides cause cerebral salt wasting (CSW), which is characterized by hyponatremia in the setting of hypovolemia. 

Urine osmolality can be normal or inappropriately high and urine sodium is invariably high. 

Serum electrolytes may be identical to patients with the syndrome of inappropriate antidiuretic hormone (SIADH).

- In CSW, treatment should include fluid and sodium replacement, which is contrary to treatment of SIADH.
- Specific treatments include normal saline or 2–3% saline fluid replacement and (optional) oral or nasogastric (NG) salt tablet administration.
- Correction should be slow, because of the possibility of central pontine myelinolysis (CPM). An initial correction of 10%, followed by correction of 10 mEq/L every 24 hours is recommended.

Neurocritical care, critical care in neurology