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Fatal hyperkalaemia in an elderly patient: case report A 91-year-old man developed fatal hyperkalaemia during treatment with digoxin, enalapril and spironolactone. The man, who had been receiving enalapril 5mg once daily and furosemide 40mg once daily for heart failure since 2001, underwent a gallbladder surgery in 2004. His renal function progressively worsened. Lowering his enalapril and furosemide doses caused dyspnoea and, hence, enalapril 5mg once daily and furosemide 40mg twice daily were continued. In April 2006, his potassium level was 5.7 mmol/L along with a creatinine level of 179 µmol/L, which increased to 212 µmol/L in June 2006. In August 2006, he was diagnosed with a very mild heart failure with atrial fibrillation and started receiving spironolactone 25mg once daily, digoxin 0.0625mg once daily and acenocoumarol; at this time, his potassium and creatinine levels were 4.3 mmol/L and 156 µmol/L, respectively. In September 2007, he briefly lost consciousness. The man’s furosemide dose was decreased but, the next day, he once again developed syncope. He was hospitalised. At this time, his BP was 75/55mm Hg and his potassium, urea and creatinine levels were 7.7 mmol/L, 67.3 mmol/L and 327 µmol/L, respectively. His medication was adjusted and he received an infusion, following which his laboratory values improved. However, he developed symptoms of heart failure along with pulmonary oedema. An ultrasound revealed worsened heart function. He subsequently died with symptoms of very severe heart failure. Author comment: The addition of spironolactone was risky in the context of his severe renal function disorder. RAAS inhibitors can cause potassium retention by lowering aldosterone concentration. Digoxin increases potassium levels in the blood, and renal failure leads to high digoxin levels. Derksen S, et al. A fatal case hypercalcemia in a 91-year-old patient: crucial laboratory control was neglected. Pharmaceutisch Weekblad 143: 14-15, No. 3, 801122790 2008 [Dutch; summarised from a translation] - Netherlands

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Reactions 20 Sep 2008 No. 1220