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.

[Short loss of consciousness: etiology and diagnostic approach. Results of a prospective study].

Transient loss of consciousness is a frequent reason for hospitalization, but very few prospective studies have been devoted to this topic. Our study involved 150 patients who were admitted for sudden and total loss of consciousness (syncope) with spontaneous return to normality. All patients underwent thorough physical examination, standard laboratory tests, electrocardiography (ECG) and radiography of the chest.