ACUTE HYPONATREMIC ENCEPHALOPATHY AFTER A CEREBROVASCULAR ACCIDENT

A 66-year-old hypertensive male with acute intracerebral hemorrhage de veloped acute hyponatremic coma 3 days after the addition of enalapril and a combination of amiloride and a thiazide diuretic td his hypoten sive regimen. The patient recovered consciousness and serum sodium nor malized 2 days after fluid restriction and withdrawal of both medicati ons. Three weeks later, upon inadvertent reinstitution of enalapril an d indapamide, severe hyponatremic encephalopathy promptly recurred; re covery was again rapid following fluid restriction and withdrawal of b oth medications. This temporal relationship establishes the thiazide d iuretic or the angiotensin converting enzyme inhibitor or both as the cause of the profound symptomatic hyponatremia in this patient. Result s of simultaneous serum and urine osmolality assays on several occasio ns were consistent with a decrease in free water clearance, a result o f either increased antidiuretic hormone (ADH) secretion or potentiatio n of its peripheral action, and thiazide-induced natriuresis. The use of a thiazide diuretic in the presence of either of these aberrations of ADH homeostasis most likely explains the profound and rapid develop ment of hyponatremia. Drug-induced disturbances in serum osmolality ar e a potentially reversible cause of deterioration of the mental state in a patient with an acute cerebrovascular accident.