NEUROLOGIC SEQUELAE AFTER TREATMENT OF SEVERE HYPONATREMIA - A MULTICENTER PERSPECTIVE

Severe, symptomatic hyponatremia is often treated urgently to increase the serum sodium to 120 to 130 mmol/L. Recently, this approach has be en challenged by evidence linking ''rapid correction'' (>12 mmol/L per day) to demyelinating brain lesions. However, the relative risks of p ersistent, severe hyponatremia and iatrogenic injury have not been wel l quantified. Data were sought on patients with serum sodium levels le ss than or equal to 105 mmol/L from the membership of the American Soc iety of Nephrology. Respondents were given a report form asking specif ic questions regarding the cause of hyponatremia, presenting symptoms, rate of correction, and neurologic sequelae. Data on 56 patients were analyzed. Fourteen developed posttherapeutic complications (10 perman ent, 4 transient) after correction to a serum sodium >120 mmol/L. Elev en of these 14 patients (including 3 with documented central pontine m yelinolysis) had a biphasic course in which neurologic findings initia lly improved and then worsened on the second to sixth day. Posttherape utic complications were not explained by age, sex, alcoholism, present ing symptoms, or hypoxic episodes. Increased chronicity of hyponatremi a and a high rate of correction in the first 48 h of treatment were si gnificantly associated with complications. No neurologic complications were observed among patients corrected by <12 mmol/L per 24 h or by < 18 mmol/L per 48 h or in whom the average rate of correction to a seru m sodium of 120 mmol/L was less than or equal to 0.55 mmol/L per hour. It was concluded that patients with severe chronic hyponatremia are m ost likely to avoid neurologic complications when their electrolyte di sturbance is corrected slowly.