Role of medications in symptomatic hyperkalemia

Sir, In recent years, angiotensin-converting enzyme inhibitors (ACE-Is), angiotensin II receptor blockers (ARBs), spironolactone and beta-adrenergic antagonists have been used to treat heart failure as first-line therapy.1 However, these medications can cause hyperkalaemia as a side-effect.2 We evaluated the medications and clinical profiles of patients with symptomatic hyperkalaemia in recent years. We studied 40 consecutive patients with symptomatic hyperkalaemia, admitted between January 2001 and December 2006. Hyperkalaemia was defined as serum potassium >6.0 mmol/l. Medications and clinical profiles were evaluated; patients who underwent haemodialysis were excluded. Data are expressed as means ± SD. Paired and unpaired Student's t-tests were used; differences were considered significant at p < 0.05 There were 11 men and 29 women, with a mean age of 83 ± 8 years (Table 1). The chief complaints were fatigue or paralysis in 10 patients (25%), dyspnoea in 8 (20%) and disturbed consciousness in 7 (18%). Laboratory studies showed serum sodium 133.0 ± 6.2 mmol/l; potassium 7.3 ± 0.9 mmol/l; BUN 60 ± 24 mg/dl; creatinine 2.6 ± 0.9 mg/dl; pH 7.36 ± 0.12; and base excess −8.0 ± 5.7. Fourteen patients (35%) had hypotension (systolic blood pressure <100 mmHg), and 32 patients (80%) had bradycardia (pulse rate <60 bpm). Ten patients (25%) received ACE-Is; 11 (28%) received ARBs; 16 (40%) received spironolactone; and 9 (23%) received beta-adrenergic antagonists for heart failure or hypertension. Five patients (13%) received non-steroidal anti-inflammatory drugs (NSAIDs), 5 (13%) received digoxin, and one (3%) received intravenous nafamostat mesilate. Eleven patients (28%) had diabetes, and 19 (48%) had signs of dehydration on clinical examination. Patient characteristics Cr, creatinine; ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker; NSAID, non-steroidal anti-inflammatory drug; NM, not measured. Patient characteristics Cr, creatinine; ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker; NSAID, non-steroidal anti-inflammatory drug; NM, not measured. An electrocardiogram on admission showed sinus rhythm in 13 patients (33%), junctional rhythm with sinus arrest in 25 (62%) and atrial fibrillation in 2 (5%). Third-degree atrioventricular block was found in one patient (3%). There was no significant difference in serum sodium, potassium, BUN or creatinine between patients with sinus rhythm and those with junctional rhythm with sinus arrest. Eight patients (20%) had paroxysmal atrial fibrillation during hospitalization. Medications with hyperkalaemic potential were discontinued transiently or permanently. Emergency haemodialysis was performed in 5 patients (13%), and temporary ventricular pacing in 14 (35%). Intravenous infusion of glucose-insulin, calcium gluconate, furosemide and/or sodium bicarbonate decreased potassium to 4.5 ± 0.7 mmol/l (p < 0.01); BUN 42 ± 27 mg/dl (p < 0.01); and creatinine 2.0 ± 1.1 mg/dl (p = 0.01). Three patients (8%) died of worsening general condition, despite normalized serum potassium. These patients, admitted for symptomatic hyperkalemia, had often received medications with hyperkalaemic potential. Many also had conditions that might predispose to hyperkalaemia with such medications: older age, diabetes, chronic kidney disease. Schepkens et al. recently evaluated 25 hyperkalaemic patients treated with ACE inhibitors and spironolactone (57 ± 32 mg), and recommended that daily spironolactone dose should not exceed 25 mg.2 In our patients, mean daily dose of spironolactone (30 ± 10 mg) was lower, but our patient were also older. Thus, even low doses of spironolactone should be used with caution, especially in older patients, or with diabetes or chronic kidney disease. NSAIDs,3 digoxin4 and nafamostat mesilate5 are also known to have hyperkalaemic potential, and clinicians should carefully evaluate whether to give patients these medications.