The diagnosis of digoxin toxicity is based primarily on clinical suspicion and clinical features (including ECG changes) suggestive of digoxin intoxication, and can be confirmed by assessment of serum digoxin levels. Digoxin toxicity can occur as a result of acute, chronic or acute-on-chronic over-ingestion; most cases involve chronic toxicity in the setting of deteriorating renal function. Serum digoxin levels do not correlate consistently with toxicity; consequently, digoxin levels should be interpreted cautiously when considering the diagnosis of digoxin toxicity. Digoxin toxicity predominantly affects the elderly and risk factors include renal impairment, electrolyte imbalances (hypokalaemia, hypomagnesaemia, hypercalcaemia) and dehydration. Interactions between digoxin and other drugs (including calcium channel blockers, non-steroidal anti-inflammatory drugs, diuretics, macrolide antibiotics) are possible and may increase the risk of digoxin toxicity in particular patient groups. Symptoms of digoxin toxicity include gastrointestinal (loss of appetite, nausea, vomiting, diarrhoea), neurological (headache, confusion, lethargy), visual (blurring, halos and occasionally alterations in colour perception) and cardiac (arrhythmia, often associated with fatigue) disturbances. Cardiac toxicity is the leading cause for concern and can include a broad range of arrhythmias including bradycardia, all degrees of atrioventricular block, premature ventricular contractions and ventricular tachycardia, as well as hypotension and cardiogenic shock.
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For all patients with suspected digoxin toxicity, general and cardiac health status should be assessed as well as concomitant therapy and recent intercurrent illnesses. Distribution of ingested digoxin to tissues takes several hours and accurate measurement of serum digoxin levels requires at least 6 h to have passed from the last ingestion; therefore, management of acute toxicity should not be delayed while waiting for measurements of digoxin concentrations. In the absence of clinical signs, serum digoxin levels should be re-evaluated at an appropriate time-point after last ingestion for accurate assessment of potential toxicity. Renal function should be assessed and monitored in all patients presenting with suspected digoxin toxicity: digoxin is eliminated primarily by the kidneys. Serum electrolytes should be measured: hypokalaemia, hypercalcaemia and hypomagnesaemia can exacerbate the effects of digoxin toxicity. -
All patients should be monitored with serial electrocardiograms (ECGs).
Typical features of digoxin toxicity include arrhythmias, ST segment depression (‘scooped out’ appearance), T wave flattening and increased U wave amplitude. ECG changes may occur in individuals receiving digoxin but without digoxin toxicity.
Continuous cardiac monitoring should be offered, if available, especially if ECG disturbances are present.
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