Iranian Red Crescent Medical Journal LETTER TO THE EDITOR Good Outcome after Digoxin Toxicity Despite Very High Serum Potassium Level Dear Editor, Digoxin, as a cardiac glycoside extracted from the Digitalis lanata1 is widely used in the treatment of different heart diseases, such as atrial fibrillation, atrial flutter and heart failure.2 Its effect is to increase myocardial contractility while mildly prolonging the duration of contraction. The result is decreased heart rate, increased blood pressure and stroke volume, leading to increased tissue perfusion, improved myo- cardial function and hemodynamics.2 Digoxin inter- acts with verapamil, amiodarone, and erythromycin, leading to increase in its plasma level.3 Arrhythmo- genesis and atrio-ventricular conduction arrhythmias such as paroxysmal atrial tachycardia with A-V block are diagnostic for digoxin toxicity.4 Without the use of digoxin-specific Fab fragments, in a recent review, mortality after digoxin toxicity have been reported to be zero in patients with acute digoxin toxicity and po- tassium levels less than 5.0 meq/dl, 50% in potassium levels between 5.0 and 5.5, and 100 percent in those with potassium levels above 5.5 meq/dl.5 Serum potas- sium levels above 5.0 meq/dl in patients with acute cardiac digoxin toxicity has been proposed as an abso- lute indication for digoxin-specific Fab fragments.5 We present a case of acute digoxin toxicity with high po- tassium level and good outcome despite unavailability of digoxin-specific Fab fragments. The patient was a 75 year-old lady, who was ad- mitted in intensive care unit (ICU) for management of respiratory failure after pulmonary emboli and pul- monary arterial hypertension. She had tracheostomy tube due to prolonged mechanical ventilation and her Glascow Coma Score was 11. The patient was receiv- ing digoxin 0.25 mg daily via nasogastric tube for treatment of right sided heart failure. In ICU course due to feeding intolerance and decreased gastric mo- tility, intravenous erythromycin (500 mg every 6 hours) was started as a prokinetic agent. Two days later, probably as a complication of drug interaction (digoxin and erythromycin), she developed vomiting, diarrhea, bradycardia, atrial fibrillation in favor of digoxin toxicity (Figure 1). In her concomitant lab-data, serum potassium was reported 6.6 meq/l and repeated sample confirmed hyperkalemia (6.5 meq/lit); no hemolysis was report- ed and samples were taken from central venous line. So digoxin was hold and its serum level was checked with HPLC (High Performance Liquid Chromatog- raphy) method which was 3.2 ng/ml, in favor of di- goxin toxicity (serum more than 2 ng/ml is consid- ered as toxic range). After holding digoxin and supportive management (close EKG monitoring, holding maintenance intra- venous KCl, and administration of 50% dextrose- regular insulin intravenously to control hyperkalemia) but without the use of 'digoxin-specific Fab frag- ments' (unfortunately digifab was unavailable at that time), signs and symptoms of digoxin toxicity was relieved and the patient survived despite concomitant high serum potassium 6.6 meq/l. Digoxin effect is to increase intracellular amounts of Ca2+ ions and K+ conductance. Other effects of this drug are increase in the refractory period of sino- atrial and AV nodes, decreasing it in the atria and ven- Fig. 1: Atrial fibrillation. EKG of the Patient concomitant to “digoxin toxicity”. Iran Red Crescent Med J 2011; 13(9):680-681 ©Iranian Red Crescent Medical Journal