RESUMO
BACKGROUND: 3% sodium chloride solution is the accepted treatment for hyponatremic encephalopathy, but evidence-based guidelines for its use are lacking. STUDY DESIGN: A case series. SETTING & PARTICIPANTS: Adult patients presenting to the emergency department of a university hospital with hyponatremic encephalopathy, defined as serum sodium level < 130 mEq/L with neurologic symptoms of increased intracranial pressure without other apparent cause, and treated with a continuous infusion of 500mL of 3% sodium chloride solution over 6 hours through a peripheral vein. PREDICTORS: Hyponatremic encephalopathy defined as serum sodium level < 130 mEq/L with neurologic symptoms of increased intracranial pressure without other apparent cause. OUTCOMES: Change in serum sodium level within 48 hours, improvement in neurologic symptoms, and clinical evidence of cerebral demyelination, permanent neurologic injury, or death within 6 months' posttreatment follow-up. RESULTS: There were 71 episodes of hyponatremic encephalopathy in 64 individuals. Comorbid conditions were present in 86% of individuals. Baseline mean serum sodium level was 114.1±0.8 (SEM) mEq/L and increased to 117.9±1.3, 121.2±1.2, 123.9±1.0, and 128.3±0.8 mEq/L at 3, 12, 24, and 48 hours following the initiation of 3% sodium chloride solution treatment, respectively. There was a marked improvement in central nervous system symptoms within hours of therapy in 69 of 71 (97%) episodes. There were 12 deaths, all of which occurred following the resolution of hyponatremic encephalopathy and were related to comorbid conditions, with 75% of deaths related to sepsis. No patient developed neurologic symptoms consistent with cerebral demyelination at any point during the 6-month follow-up period. LIMITATIONS: Lack of a comparison group and follow-up neuroimaging studies. Number of cases is too small to provide definitive assessment of the safety of this protocol. CONCLUSIONS: 3% sodium chloride solution was effective in reversing the symptoms of hyponatremic encephalopathy in the emergency department without producing neurologic injury related to cerebral demyelination on long-term follow-up in this case series.
