Recommendations
Key Recommendations
Suspect digoxin toxicity if a patient who has been prescribed digoxin presents with typical symptoms, and particularly in a patient with renal insufficiency.
Chronic digoxin toxicity is a more common presentation than acute digoxin toxicity.
A patient with acute digoxin toxicity will likely be asymptomatic for minutes to hours after an exposure to digoxin, after which they will rapidly deteriorate.
Take a full medical history and, in particular, establish any cardiac conditions or renal impairment.
Order digoxin level, urea and electrolytes, and blood glucose in all patients who present with suspected digoxin toxicity or exposure.
Wait at least 6 hours after ingestion before taking serum digoxin measurements.[1] Take the samples more urgently if severe toxicity is suspected and treatment with digoxin-specific antibody (Fab) fragments is being considered.[1]
If deliberate self-poisoning has taken place, request a specialist mental health assessment at the earliest opportunity.[22] For further information, see Suicide risk mitigation.
Suspect digoxin toxicity if a patient who has been prescribed digoxin presents with typical symptoms, and particularly in a patient with renal insufficiency.
Chronic digoxin toxicity is a more common presentation than acute digoxin toxicity.
Practical tip
Patients with chronic toxicity tend to be more severely unwell than those with acute toxicity because patients who are prescribed digoxin for an existing condition will typically have risk factors for digoxin toxicity (e.g., age >55 years, renal failure, comorbidities).
Chronic toxicity has a more indolent course over days to weeks with a less obvious presentation compared with acute toxicity; chronic toxicity is more common in elderly patients.
Symptoms of toxicity from chronic therapy may be variable, but are often preceded by dehydration.[1]
Consider chronic toxicity if any of the following symptoms are present: nausea, anorexia, abdominal pain, weakness, fatigue, palpitations, syncope, dyspnoea, disturbances of colour vision with a tendency to yellow halos (xanthopsia), blurred vision, and diplopia. Patients most often present with gastrointestinal signs (anorexia and vomiting) and generalised non-specific symptoms (generalised weakness and malaise), but could also present with central nervous system depression.
Bear in mind that a patient with acute digoxin toxicity will likely be asymptomatic for minutes to hours after an exposure to digoxin, after which they will rapidly deteriorate. Life-threatening cardiac effects may take more than 12 hours to fully develop.[1]
Symptoms of acute toxicity usually include nausea, vomiting, anorexia, diarrhoea, and/or abdominal pain (less common), which may develop within 1-2 hours of acute overdose.[1]
Palpitations, syncope, and dyspnoea may also occur. Acute digoxin toxicity may cause virtually any dysrhythmia.
Take a thorough drug history, including any supplements, herbal remedies, non-prescription medications, and plant ingestions. Pay particular attention to the use of p-glycoprotein/cytochrome 3A4 inhibitors.
If you suspect acute digoxin toxicity, proceed sensitively to establish whether the overdose was accidental or intentional. If deliberate self-poisoning has taken place, request a specialist mental health assessment at the earliest opportunity.[22] For further information, see Suicide risk mitigation.
Ask the patient about the specific drug taken (if known) and the dose and time of ingestion. Use this information to establish whether a toxic dose has been taken (clinical and patient factors may affect what constitutes a toxic dose). Consult your approved clinical toxicology resource (e.g., TOXBASE in the UK) for toxic doses and/or seek advice from your national or regional poisons information service. National Poisons Information Service: TOXBASE Opens in new window
Take a full medical history and, in particular, establish any cardiac conditions or renal impairment.
Patients with renal impairment, hypokalaemia, hypomagnesaemia, hypercalcaemia, and hypothyroidism may be at higher risk of digoxin intoxication than others.[20]
Perform a 12-lead ECG in all patients with suspected digoxin toxicity.
Acute overdose usually causes a marked bradycardia with PR and QRS prolongation.[1]
Arrhythmias are common if there is pre-existing heart disease.
Patients may have dysrhythmias, which are associated with increased automaticity and decreased atrioventricular (AV) conduction (e.g., atrial flutter and atrial fibrillation with high-degree AV block, non-paroxysmal atrial tachycardia with block, accelerated junctional rhythms, and/or bi-directional ventricular tachycardia).[23]
Premature ventricular contractions are the most common dysrhythmia.
Bigeminy or trigeminy occur frequently.
Chronic digoxin toxicity is most often associated with bradyarrhythmias (ventricular tachyarrhythmias also occur).
The only rhythm disturbances that are not definitively associated with digoxin toxicity are supraventricular tachyarrhythmias with a rapid ventricular response (e.g., paroxysmal atrial tachycardia and sinus tachycardia).
Repeat ECGs if possible, especially in symptomatic patients or in those who have ingested other cardiotoxic medications.[1]
Be aware that ventricular tachycardia and ventricular fibrillation may occur in patients with severe toxicity.[1]
Check and monitor vital signs, including the patient’s pulse and blood pressure, and use telemetry. Pulse and blood pressure monitoring are critical.
Order digoxin level, urea and electrolytes, renal function tests, and blood glucose in all patients who present with suspected digoxin toxicity or exposure.
Consider arterial or venous blood gas. This may be required when managing metabolic acidosis.[1] See Management recommendations.
Serum digoxin level
Measure serum digoxin concentrations in patients with suspected digoxin toxicity or at high risk for developing digoxin toxicity.[20] Take the measurements at least 6 hours after ingestion.[1]
Serum digoxin concentrations are only truly reflective after distribution is complete (4-6 hours after the last dose).
Take samples more urgently if severe toxicity is suspected and treatment with digoxin-specific antibody (Fab) fragments is being considered.[1]
Interpret the serum digoxin concentration in the context of the wider clinical picture. Plasma concentrations do not correlate well with features of toxicity.[1]
Cardiac effects may take more than 12 hours to fully develop.[1]
Severe toxic effects may be seen with digoxin concentrations greater than 4.0 microgram/L (4.0 nanogram/mL; 5.2 nanomol/L).[1]
Young children tend to tolerate a higher peak plasma digoxin concentration than adolescents and adults.[1]
There is no exact serum digoxin concentration that is predictive of toxicity. There are a number of factors that can affect a patient's susceptibility to digoxin (e.g., hypokalaemia, volume status, comorbidities, age, and chronic disease).[24]
The elimination of digoxin is slow (half-life is 30-40 hours with normal renal function and up to 100 hours in patients with impaired renal function), therefore repeated samples may not be clinically helpful.[1] Bear in mind that elevated digoxin concentrations can occur after treatment with digoxin-specific antibodies.[25] Routinely used assays measure both free digoxin and Fab-digoxin complexes and therefore report apparently high digoxin levels following treatment with digoxin-specific antibodies.[1]
Electrolytes
Always check serum potassium concentrations; they are important as a marker for prognosis in acute digoxin toxicity.[1] A patient with acute digoxin toxicity may have hyperkalaemia (≥5.0 mmol/L [≥5.0 mEq/L]), which is a marker of severe toxicity. Severe hyperkalaemia (≥6.5 mmol/L [≥6.5 mEq/L]) that is resistant to conventional treatments is considered an indication for digoxin-specific antibody therapy.
Measure serum magnesium levels, as low levels exacerbate cardiac manifestations of digoxin toxicity.
Glucose
Check capillary blood glucose.[1] This may require monitoring as part of the management of hyperkalaemia.
Renal function tests
Assess renal function because this influences the rate of clearance of digoxin from the bloodstream.[1]
Use of this content is subject to our disclaimer