Background: Patients with self-induced water intoxication usually tolerate a large, rapid increase in plasma sodium without developing osmotically induced central pontine myelinolysis. However, we have previously reported a case of clinically suspected pontine myelinolysis in a patient with self-induced water intoxication. The purpose of our study was to investigate if a subgroup of these patients may also be vulnerable to neurologic complications of hyponatremia therapy.
Method: Over a 10-year period, we identified retrospectively 12 polydipsic patients having a total of 24 episodes of symptomatic hyponatremia with plasma sodium < or = 115 mmol/L. The mode of treatment, the kinetics of correction, and the neurologic outcome were recorded. The presence of alcoholism was noted.
Results: Seven patients recovered uneventfully from 19 episodes of symptomatic hyponatremia. Five patients had delayed neurologic complications. Late therapy and/or respiratory arrest might have been associated with the complications for 2 patients. The other 3 patients experienced clinical features of central pontine myelinolysis leading to death in 1. Patients with neurologic complications had a higher maximal 24-hour increase in plasma sodium concentration (21.8 +/- 3.9 vs. 15.5 +/- 5.1 mmol/L, p < .02), and a higher incidence of both overcorrection to hypernatremia and chronic alcoholism, often associated with poor nutrition. All 5 patients became water intoxicated at home, and 2 patients with pontine dysfunction had subacute rather than acute hyponatremia.
Conclusion: A large rapid increase in plasma sodium may also be detrimental in patients with self-induced water intoxication when they are alcoholic, malnourished, and have nonacute hyponatremia.