- Some patients develop the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after SAH and are appropriately managed with fluid restriction.
- SIADH, which is characterized by normovolemia or mild hypervolemia, is treated by volume restriction.
- However, hyponatremia after SAH is more likely to be the result of the cerebral salt-wasting syndrome, which probably occurs as a result of the release of a natriuretic peptide by the brain.
- Cerebral salt-wasting syndrome is characterized by the triad of hyponatremia, volume contraction, and high urine sodium concentrations (>50 mmol/L). The distinction between this syndrome and SIADH is important.
- Cerebral salt wasting is associated with a contracted intravascular volume. Fluid restriction and further volume contraction may be especially deleterious in a patient after SAH and should be avoided.
- Although the clinical distinction between these two causes of hyponatremia (SIADH and cerebral salt-wasting syndrome) may be difficult, management of both is simple: administration of isotonic fluids using intravascular normovolemia as the end point.