Polyuria and refractory hypernatremia after cardiopulmonary arrest.

A patient exhibited brain damage, polyuria, and refractory hypernatremia after myocardial infarction and cardiopulmonary arrest. Serum vasopressin levels were relatively fixed and inappropriately low for the elevated serum osmolality. Hypernatremia persisted despite administration of vasopressin; after vasopressin was discontinued, serum sodium value was corrected with small doses of furosemide and replacement of free water. In her case, impairment of osmotic homeostasis could not be attributed to either simple resetting or complete destruction of osmoreceptors; metabolic normalization required an unusual therapeutic approach.