Captopril-induced hyponatremia with irreversible neurologic damage.
A 61-year-old Chinese-American man with a history of congestive heart failure and hypertension was admitted to the San Francisco Veterans Administration Hospital with confusion, cortical blindness, and generalized flaccidity. Serum sodium level on admission was 114 meq/liter. Administration of captopril had been begun for afterload reduction two weeks before admission with a concomitant fall in serum sodium level from 137 meq/liter to 126 meq/liter in one week. A history of marked thirst with consumption of large volumes of water was reported for over one week prior to hospitalization. Despite correction of the hyponatremia within 24 hours at a rate of 0.9 meq/liter per hour, the patient remained semi-comatose and died four days later with a gastrointestinal bleed. It is suggested that the thirst phenomenon and hyponatremia were caused by the introduction of captopril. This lead to irreversible neurologic damage and death, despite the correction of the serum sodium level.
D002216:Captopril / Q000009:adverse effects* / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy; D006801:Humans; D007010:Hyponatremia / Q000139:chemically induced* / Q000150:complications; D008297:Male; D008875:Middle Aged; D009422:Nervous System Diseases / Q000209:etiology*; D012964:Sodium / Q000097:blood; D013894:Thirst / Q000187:drug effects
D002216:Captopril; D012964:Sodium