Al-Mufti H I, Arieff A I
Am J Med. 1985 Dec;79(6):769-71. doi: 10.1016/0002-9343(85)90530-3.
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.
一名61岁的华裔美国男性，有充血性心力衰竭和高血压病史，因意识模糊、皮质盲和全身弛缓无力入住旧金山退伍军人管理局医院。入院时血清钠水平为114毫当量/升。入院前两周开始使用卡托普利降低后负荷，同时血清钠水平在一周内从137毫当量/升降至126毫当量/升。据报告，在住院前一周多的时间里，患者有明显口渴并大量饮水的病史。尽管在24小时内以每小时0.9毫当量/升的速度纠正了低钠血症，但患者仍处于半昏迷状态，四天后因胃肠道出血死亡。提示口渴现象和低钠血症是由卡托普利的使用引起的。尽管纠正了血清钠水平，但这导致了不可逆的神经损伤和死亡。
