High incidence of neurologic complications following rapid correction of severe hyponatremia in polydipsic patients.

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.

Salt wastage, plasma volume contraction and hypokalemic paralysis in self-induced water intoxication.

Eleven episodes of severe hyponatremia secondary to hiccup-induced potomania were recorded in 3 years in a man who had essential hypertension, a low protein intake and a normal diluting ability. Paradoxical increase in hematocrit and plasma protein with acute extensive natriuresis was associated as well as urine potassium loss and hypokalemia producing paralysis in 1 episode. During a chronic water loading test, the defect in water excretion was related to a low urine solute delivery which was partially reverted by the natriuretic response to plasma volume expansion, promoting water diuresis.