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Captopril-induced hyponatremia with irreversible neurologic damage
The American Journal of Medicine
|December 1, 1985
Summary
Captopril use in a patient with heart failure led to severe hyponatremia (low sodium) and confusion. Despite sodium correction, irreversible neurological damage and death occurred, suggesting a link between captopril and these adverse events.
Area of Science:
- Nephrology
- Cardiology
- Neurology
Background:
- A 61-year-old male with congestive heart failure and hypertension was admitted with confusion and cortical blindness.
- The patient presented with a critically low serum sodium level of 114 meq/liter.
Observation:
- Captopril was initiated two weeks prior for afterload reduction, coinciding with a drop in serum sodium from 137 to 126 meq/liter.
- The patient reported excessive thirst and high water intake for over a week before hospitalization.
Findings:
- Rapid correction of hyponatremia (0.9 meq/liter per hour) did not reverse the patient's semi-comatose state.
- The patient died four days after admission due to a gastrointestinal bleed.
Implications:
- This case suggests captopril may induce thirst and severe hyponatremia, potentially leading to irreversible neurological damage.
- The findings highlight the critical need to monitor electrolytes in patients initiating captopril therapy, especially those with pre-existing conditions.
- This case underscores the potential for severe adverse events, including death, despite therapeutic interventions for drug-induced hyponatremia.