The volume of distribution is a population average and may vary among individuals. Dosage calculations are based on a steady state volume of distribution of approximately 5 L/kg for digoxin, which is used to convert serum digoxin concentrations to total body burden of digoxin in milligrams.14 Allergic reactions occur in about 1% of infusions.Adjust the dosage of DIGIFAB according to the amount of digoxin to be neutralized. Heart failure or atrial fibrillation with rapid ventricular response (presumed re-emergent due to removal of digoxin effect) occurs in up to 3% of patients. The concentration therefore rises many fold after digoxin-specific antibody fragments are given even in the absence of rebound toxicity. 14 Serum digoxin concentration is of no use in diagnosis, because it measures the digoxin in the complexes with antibody fragments as well as unbound digoxin. 21 It can develop 12–24 hours after treatment, but up to 10 days later in patients with renal failure. This occurs in about 2% of patients given a full neutralising dose. ‘Rebound’ toxicity 14 is the reappearance of toxicity after an initial response to digoxin-specific antibody fragments. 21 Serum potassium should be frequently monitored. 14 Hypokalaemia occurs as a result of treatment in about 4% of patients. Hypomagnesaemia and, more importantly, hypokalaemia (common with diuretic use) should be corrected before or during administration because digoxin-specific antibody fragments will further lower potassium. ‘Reverse tick’ T-wave inversion is not a sign of toxicity. 12 With severe toxicity, ventricular tachycardia (which may be bidirectional) and ventricular fibrillation can occur. However, sinus bradycardia, atrioventricular block and ventricular ectopy are more common. Characteristic arrhythmias are those in which a tachyarrhythmia occurs simultaneously with sinus or atrioventricular node suppression, such as atrial and junctional tachycardia with atrioventricular block. Almost any arrhythmia can occur, with the exception of atrial tachyarrhythmias with a rapid ventricular response, 8 because these usually require intact conduction in the atrioventricular node. 9Īrrhythmias can occur even if the patient has no symptoms. 8 Cardiac arrhythmias account for most deaths. 10 Visual effects (blurred vision, colour disturbances, haloes and scotomas) are rarer in contemporary practice. They commonly include lethargy, confusion and gastrointestinal symptoms (anorexia, nausea, vomiting, diarrhoea and abdominal pain). The clinical features of toxicity are often non-specific. 11 These conditions include hypokalaemia, hypomagnesaemia, hypercalcaemia, myocardial ischaemia, hypoxaemia and acid–base disturbances. They at least partly account for patients who develop toxicity when their serum digoxin concentration is within the therapeutic range. 10Īlthough the serum digoxin concentration does predict the likelihood of toxicity, 8, 11 several conditions increase sensitivity to digoxin. 8 Consequently, a higher serum digoxin concentration for a given dose occurs in patients with renal impairment, lower body weight and in those taking amiodarone, verapamil, macrolides, azole antifungals and cyclosporin, which inhibit P-glycoprotein transport. Transport by P-glycoprotein also contributes to elimination. The elimination of digoxin is mainly by renal clearance and is prolonged in patients with renal impairment. 9 This applies in both acute and chronic poisoning. Only a post-distribution measurement reflects the severity of intoxication and this is the measurement that can help when calculating the dose of digoxin-specific antibody. This means that the serum digoxin concentration is inaccurate unless taken at least six hours after the last dose. ![]() Digoxin also causes an increase in vagal activity, reducing activity in the sinus node and prolonging conduction in the atrioventricular node.Īfter a dose of digoxin, distribution to the tissues takes several hours. 8 Inhibition of this pump causes the hyperkalaemia commonly seen in toxicity. Increased intracellular calcium increases cardiac contractility, but also the risk of tachyarrhythmias. Digoxin increases intracellular calcium in myocardial cells indirectly, by inhibiting the sodium–potassium pump in the cell membrane.
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