Recommendations

Key Recommendations

The main goal of treatment is to correct cardiac toxicity. Treatment of cardiac toxicity usually leads to resolution of central nervous system and gastrointestinal (GI) symptoms.

Initial treatment includes:

  • General supportive care

  • Discontinuation of digoxin therapy and prevention of further exposure

  • Prevention of further GI absorption

  • Administration of digoxin-specific antibody fragments (digoxin immune Fab)

  • Treatment of specific complications: for example, dysrhythmias and electrolyte abnormalities

Treatment of chronic toxicity is based on the clinical signs and symptoms, not the serum digoxin concentration, which might be just above or within the therapeutic range. If a serum digoxin concentration cannot be obtained, patients are managed based on their presentation, ECG findings, and laboratory results. If toxicity is suspected and the patient is unstable, antidotal therapy is administered prior to confirmatory results. For patients with chronic digitalis poisoning, therapy may require only a few digoxin immune Fab vials. There is no change in therapy for patients with kidney failure other than to note that the elimination half-life of digoxin is prolonged.

Contact the Poison Center early for advice on management. American Poison Centers: poison help Opens in new window

If deliberate self-poisoning has taken place, request a specialist mental health assessment at the earliest opportunity.[26]​ See Suicide risk mitigation.

Supportive care

General supportive care includes initial and ongoing assessment of airway, breathing, and circulation, stabilizing as necessary. Supplemental oxygen is given and endotracheal intubation performed if needed.

Patients require continuous cardiac monitoring and pulse oximetry with consideration of end tidal CO2.[3]

Initial treatment of hypotension and volume depletion should be corrected with isotonic intravenous fluids, with caution for patients with congestive heart failure. Electrolyte abnormalities, particularly hypokalemia and hypomagnesemia, should be corrected.[3]

Digoxin binding therapy

Digoxin binding (with digoxin immune Fab) is used in patients with the following features:[3][7][30]

  • Severe toxicity or hemodynamic compromise

  • Symptomatic bradyarrhythmias

  • Ventricular dysrhythmias

  • Any patient with suspected digoxin toxicity and hyperkalemia (potassium concentrations >5.5 mEq/L to >6 mEq/L; indication for digoxin immune Fab varies depending on source, consult local guidance)[3][7]

  • Acute ingestion of >4 mg digoxin in a healthy child (or 0.1 mg/kg)

  • Acute ingestion of >10 mg digoxin in a healthy adult

  • Serum digoxin concentration of ≥10 nanograms/mL 4-6 hours after ingestion (steady state)

  • Serum digoxin concentration of >4 nanograms/mL at any time[7]​ 

If indicated, 15 vials of digoxin immune Fab is the quantity typically needed to treat one patient.[31] One study suggests 1-2 vials administered in a stepwise fashion based on clinical response.[32] Patients who receive digoxin immune Fab have a drop in the serum potassium as it moves intracellularly.[33][34][35]​ Some patients who have been treated for hyperkalemia and who have also received digoxin immune Fab develop profound hypokalemia. Therefore, serial potassium measurements are made when patients receive both digoxin immune Fab and other therapies to decrease potassium.[36]

After administration of digoxin immune Fab, serum digoxin concentrations are usually falsely elevated (10- to 30-fold). Serum digoxin concentration can be measured again 3-4 days after the dose is given,​ but has been reported to be elevated for up to 10 days, especially in patients with renal insufficiency.[37][38][39]​ In certain patients with chronic digoxin toxicity, supportive care is suggested to have similar outcomes to digoxin immune Fab.[40]

Management of electrolyte abnormalities

Digoxin immune Fab is indicated in patients with suspected digoxin toxicity and hyperkalemia (potassium concentrations >5.50 mEq/L to >6 mEq/L; indication for digoxin immune Fab varies depending on source, consult local guidance).[3][7]

In patients with chronic digoxin toxicity, hyperkalemia is only further corrected (e.g., with insulin/glucose) if it is considered life-threatening, because digoxin binding therapy is likely to cause a drop in serum potassium and therefore is a risk of producing hypokalemia.

Calcium has historically not been used to treat hyperkalemia in patients with suspected digoxin toxicity as there are concerns it may induce arrhythmia or cardiac arrest. The risk of harm from calcium in patients with digoxin toxicity has not been quantified; however, there is also no evidence of benefit.[41]

Patients with hypokalemia or hypomagnesemia require additional potassium or magnesium with careful monitoring to restore normal serum levels.

GI decontamination

There is a role for GI decontamination with activated charcoal in patients with an acute ingestion of digoxin.[7][42][43][44]​​[45]​​​ The primary goal of activated charcoal is to decrease GI absorption of the drug.[43][44]

Bradycardia management

If the patient does not respond to digoxin immune Fab or it is not immediately available, symptomatic bradycardia can be treated with atropine.[36] In adults, atropine can be given every 3-5 minutes until there is a response or the maximum dose is reached. Pediatric patients with symptomatic bradycardia require lower doses of atropine.

Alternatively, a temporary pacing wire can be inserted in patients with evidence of significant bradycardia or atrioventricular (AV) block and hemodynamic compromise if digoxin immune Fab is not adequate or not readily available.

Tachyarrhythmia management

Type IB anti-arrhythmics (e.g., phenytoin, lidocaine) can be used if digoxin immune Fab is unavailable or is being prepared and patients have rapid ventricular dysrhythmias unresponsive to supportive measures.

Transthoracic electrical cardioversion for atrial tachyarrhythmias is associated with the development of lethal ventricular dysrhythmias, so is not used.[46]

Overdrive suppression with a transvenous pacemaker is also avoided because of associated iatrogenic complications that have been seen in as many as 36% of patients.[47][48]

Patients with ventricular fibrillation or pulseless ventricular tachycardia require defibrillation along with immunotherapy.

Hemodynamic compromise management

In patients with signs of hemodynamic insufficiency and/or compromise (e.g., hypotension, altered consciousness), digoxin immune Fab is given as primary management. As a bridge to the administration of digoxin immune Fab, intravenous fluids and direct-acting vasopressors (e.g., phenylephrine, norepinephrine [noradrenaline]) are used. Cardiac contractility (inotropy) is typically preserved in patients with digoxin toxicity.

If hypotension persists after administration of digoxin immune Fab, consider the possibility of mixed overdose, effects of other underlying drugs, or another cause, such as sepsis or cardiogenic shock.

Alternatively, a temporary pacing wire can be inserted in patients with evidence of significant bradycardia or AV block and hemodynamic compromise if the patient does not respond to digoxin immune Fab, or it is not readily available.

Ongoing monitoring and change of treatment

Ideally, digoxin is discontinued and a different drug for rate control or a different inotrope prescribed (for atrial fibrillation, atrial flutter, or heart failure, respectively). If the patient has to remain on digoxin for some clinical reason, then the dose of digoxin is adjusted for the patient's drug profile. Glomerular filtration rate and serum digoxin concentration is monitored regularly.

Use of this content is subject to our disclaimer