Cerebral salt wasting in children. The need for recognition and treatment.

OBJECTIVES

To describe a salt-wasting syndrome in children with central nervous system (CNS) insults and to differentiate it from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and diabetes insipidus so that it may be more readily diagnosed and treated.

DESIGN

Case reports.

SETTING

Community teaching hospital.

PATIENTS: Two inpatients with CNS insults (closed head trauma in one and seizure disorder, spastic diplegia, mental retardation, and hydrocephalus in the other).

SELECTION CRITERIA: Evidence of hyponatremia accompanied by elevated urine sodium concentration and excessive urine output.

INTERVENTIONS: Volume-for-volume urine replacement with 0.9% and/or 3% sodium chloride. Oral salt supplementation was required for brief periods to maintain normal plasma sodium concentration after discharge from the hospital.

MEASUREMENTS AND MAIN

RESULTS

Both patients had hyponatremia, high urine sodium concentrations, hypovolemia, and excessive urine output while receiving maintenance fluids. They also had elevated plasma atrial natriuretic hormone (ANH) concentrations, decreased aldosterone concentrations, and decreased [corrected] plasma renin activity for their degree of hyponatremia and negative fluid balance. Both patients maintained normal serum electrolyte concentrations with appropriate treatment.

CONCLUSIONS

These patients showed true salt wasting associated with acute or chronic CNS injury, with hormonal patterns consistent with "inappropriate" ANH secretion and distinct from the SIADH. It is important to distinguish cerebral salt wasting (CSW) from the two other major disturbances of water metabolism seen following CNS injury (ie, SIADH and diabetes insipidus), because incorrect diagnosis and treatment could greatly increase morbidity in CSW. The etiologic roles of ANH or brain natriuretic peptide in CSW need to be further elucidated.