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Home | Articles | Poisoning | Digoxin Poisoning

Digoxin Poisoning

Last updated 3rd December 2020

Last updated on 19th May 2014 by Calum Murray

Toxicity

  1. Absorption of digoxin is slow and peak effects can be delayed up to 6 – 12 hours. The half life of digoxin can be up to 30 – 50 hours.
  2. The therapeutic concentration is 1-2 microgram/L 6 hours post dose. Toxicity likely if serum digoxin >3micrograms/l and severe toxicity may be seen with serum digoxin >4 microgram/L
  3. The fatal dose is variable depending on whether patients are already taking digoxin therapeutically or are digoxin naive – acute overdoses in patients on regular therapy are likely to be more toxic than in naive patients dose-for-dose.
  4. The effects of digoxin may be potentiated by co-ingestion of a number of medications, including quinidine, erythromycin, verapamil, diltiazem and amiodarone 
  5. Patients with pre-existing acute or chronic renal failure are also at greater risk of toxicity.
  6. Death usually occurs from ventricular arrhythmias, conduction impairment or pump failure.

Clinical Features

  1. General – nausea, vomiting, diarrhoea early on, which may be followed by headache and confusion.
  2. Cardiac – there may be marked bradycardia with PR and QRS prolongation, sinus arrest, varying degrees of AV block with escape rhythms including paroxysmal atrial tachycardia with AV block, junctional tachycardia, frequent ventricular ectopics and bigeminy. Hypotension, ventricular tachycardia and ventricular fibrillation may be sseen in severe toxicity.
  3. Metabolic – hyperkalaemia is common in acute overdose.

General Management

  1. Always use the ABCDE approach
  2. The benefit of gastric decontamination is uncertain. Consider 50g activated charcoal if symptomatic or presents within 1 hour of ingestion of 20 micrograms/kg body weight or more.
  3. Consider repeated doses of oral activated charcoal to increase elimination, if not vomiting and the airway can be protected.
  4. Measure urea, electrolytes, magnesium and creatinine in all patients. Serum potassium correlates with cardiotoxicity.
  5. Ensure continuous record of HR, BP and ECG
  6. Measure the QRS duration and QT interval on 12 lead ECG. There are specific treatments for QRS prolongation (e.g. sodium bicarbonate) and QT prolongation (e.g. magnesium sulphate).
  7. Measure serum digoxin at least 6 hours post ingestion
  8. Treat bradycardia with atropine and hyperkalaemia with insulin/ dextrose and calcium, at least initially. Correct hypokalaemia and hypomagnesaemia if present

Digoxin Specific Antibodies

  1. The treatment of choice for severe bradyarrhythmias, for life-threatening ventricular arrhythmias and for severe hyperkalaemia in patients with digoxin poisoning. The antidote effect is usually seen within 15-30 minutes of administration.
  2. Serum digoxin does not reflect total body load and complete neutralisation is not necessary in digoxin-naïve patients. Give half the estimated dose required for full neutralisation initially then monitor for 6-12 hours. The remainder may be given if there is no clinical response within 2 hours 
  3. In acute-on-chronic Digoxin poisoning give full neutralisation dose if dose ingested known. If not a half neutralising dose based on
  4. plasma digoxin concentration should normally be used, followed by monitoring for 6-12hours. The remainder may be given if there is no clinical response within 2 hours
  5. The calculation for the number of vials of digoxin specific antibodies required may be found on the Toxbase website
  6. Note that following treatment with digoxin specific antibodies, current immunoassays will give falsely elevated digoxin concentrations as they measure both free digoxin and Fab-digoxin complexes.

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