Mrs. G., A fairly active 91-year old woman of thin build -- who was still driving until this episode -- went for routine blood work 3 weeks ago, and was noted to have an elevated serum potassium level of 7.4 mmol/L. She had a history of hypertension, mild aortic stenosis, chronic atrial fibrillation, as well as stage 4 chronic kidney disease (estimated glomerular filtration rate 20-25 mL/min) and chronic lymphocytic lymphoma. Her creatinine had been stable for > 2 years, at 160-180 µmol/L.
Mrs. G. was admitted to hospital and treated with sodium polystyrene, insulin and salbutamol. She normally takes rabeprazole, a proton pump inhibitor, 20 mg a day, enalapril 20 mg twice a day, aspirin once daily, furosemide 20 mg and spironolactone 25 mg a day. Once in hospital, both enalapril and spironolactone were stopped. She was discharged home a day later.
Since discharge, Mrs. G. has gained 7 kg and experienced swelling of both legs up to the mid-abdomen. With increasing shortness of breath, she goes back to emergency, where she's noted to be in overt heart failure. She's once again admitted. The dose of furosemide is increased and digoxin added to her regimen. After 24 hours, her breathing has improved, but she's now feeling sick to her stomach, though without vomiting, chest pain, tightness, palpitations or dizziness.
The examination reveals a blood pressure of 146/78 mm Hg with irregular rhythm, bilateral transmitted aortic stenosis murmur and decreased air entry in both lower lungs with dullness. Beyond the leg edema, there's some swelling of the anterior abdominal wall and sacrum. Laboratory results are: hemoglobin 116 g/L, creatinine 175 µmol/L and potassium 4.2 mmol/L. A chest x-ray shows a small amount of bilateral pleural effusion and an electrocardiogram reveals atrial fibrillation with a rate of 104 beats per minute.
Why are all these symptoms suddently happening to Mrs. G.?
Mrs. G. had iatrogenic digoxin toxicity.
When Mrs. G. presented in congestive heart failure with chronic atrial fibrillation, the dose of furosemide was increased, and the dyspnea improved. Then she got 1.25 mg of digoxin within 24 hours. It's likely that the nausea and other symptoms were due to toxicity to this medication.
Further doses were stopped and a trough digoxin level showed the concentration was markedly elevated -- 5.6 ng/mL. Even though she hadn't developed junctional rhythm, she was treated with digoxin-specific antibody Fab fragment (Digibind), and luckily her symptoms improved within a few hours.
The dose prescribed was higher than required, based on Mrs. G.'s renal function and age -- a reduction of at least 50% would have been warranted. This case highlights the importance of appropriate dosing of medications, especially with a narrow therapeutic index and drugs that are excreted by the kidneys. Older age should always be taken into consideration.
There's also another teaching point here, and that's the importance of non-pharmacologic therapy -- especially dietary education. The patient should have been informed about a low potassium diet, and this should have been reinforced at periodic visits to check for adherence. Instead, the medications that likely were helpful for her underlying heart failure, i.e. enalapril and spironolactone, were stopped and NOT resumed after correction of hyperkalemia, even though she was tolerating them well for over 3 years.
It's essential to resume cardiac medications that have been tolerated by the patient and that appear to be beneficial at keeping the individual stable. Of course, these should be restarted one at a time, with careful monitoring of electrolytes and renal function, all the while reinforcing dietary modifications to control the serum potassium. The discontinuation of these drugs and not resuming them later likely resulted in her present condition -- and that, by definition, is also iatrogenic in origin.
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