Cerebral salt wasting syndrome in a patient affected of spontaneous frontoparietal subdural haematoma

Abstract

Ever since cerebral salt wasting syndrome (CSW) was first described in 1950, there have been debates over its existence and whether it has an important place in the differential diagnosis of hyponatraemia. We report the case of a neurosurgical patient with sustained hyponatraemia and abnormally high sodium loss in the urine, with signs of fluid volume depletion. Hyponatraemia was not corrected after an intravenous infusion of saline solution. Stable concentrations of blood sodium above 130 mmol/l were achieved with the administration of 100 mg of hydrocortisone daily, with an ensuing reduction in sodium elimination through the urine.

Figure 1

Variations in sodium concentrations in the different phases of intensive treatment. Phase 1, immediate postoperative period after subdural haematoma evacuation. Phase 2, manifestation of hyponatraemia. Patient with haemodynamic stability, central venous pressure 6–11 mm Hg. Phase 3, treatment with supplementary parenteral sodium. Minimum level of serum sodium of 120 mmol/l with excessive sodium excretion (maximum of 714 mmol/24 h). Phase 4, response to corticoid treatment (intravenous hydrocortisone 100 mg/day) with fluctuations due to variations in the level of sodium supplementation. Phase 5, corticoid treatment progressively discontinued with sodium values of around 130 mmol/l. Phase 6, new decrease in serum sodium values causing re-establishment of corticoid treatment.