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Optimisation of Digoxin Maintenance Dose in Toxicity
Author(s) -
Bhindi Arun K
Publication year - 2010
Publication title -
journal of pharmacy practice and research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.222
H-Index - 22
eISSN - 2055-2335
pISSN - 1445-937X
DOI - 10.1002/j.2055-2335.2010.tb00726.x
Subject(s) - digoxin , medicine , heart failure , atrial fibrillation , spironolactone , creatinine , renal function , cardiology
Background Digoxin pharmacokinetics can be altered by disease states, age‐related decline in renal function, decreased skeletal muscle mass and drug interactions. Aim To report a case of digoxin toxicity in a patient with advanced congestive heart failure in atrial fibrillation and worsening renal failure; and to describe the application of pharmacokinetic principles in the optimisation of digoxin dosing. Clinical details A 59‐year‐old Caucasian male presented with a week long history of abdominal pain, increased dyspnoea and lethargy. His medical history included heart failure, atrial fibrillation, hypertension, ischaemic heart disease, type 2 diabetes, acute on chronic renal failure, dyslipidaemia, anaemia and morbid obesity. His serum biochemistry revealed hyperkalaemia of 6.9 mmol/L, elevated creatinine of 407 μmol/L (prior baseline 247 μmol/L) and a trough serum digoxin concentration of 3.4 nmol/L at steady state on an oral maintenance digoxin dose of 125 microgram daily. His calcium and magnesium levels were in the normal range. Outcomes Hyperkalaemia was corrected and the potassium‐sparing medications, spironolactone and perindopril, were withheld. Digoxin was withheld until digoxin's serum concentration returned to the therapeutic range. A reduced maintenance dose of digoxin 62.5 microgram on alternate days was calculated and recommended by the clinical pharmacist. At discharge, the patient felt significantly better and was able to engage with activities of daily living. Perindopril and spironolactone were recommenced once the potassium had returned to normal levels. The patient was unaware of signs and symptoms of digoxin toxicity and the clinical pharmacist provided counselling prior to discharge. The patient's local doctor was requested to closely monitor his renal function and potassium levels and to check his trough serum digoxin concentration if toxicity was suspected. Conclusion Pharmacists and clinicians need to understand digoxin's pharmacokinetics in various clinical settings to be able to make appropriate dose adjustments.