Digoxin toxicity

Digoxin toxicity may be acute, acute on chronic, or chronic. Overdose can occur either intentionally or accidentally.

Typically presents with components of gastrointestinal, constitutional, and/or cardiovascular symptoms.

Diagnosis is based on symptoms and laboratory data. At therapeutic digoxin concentrations (0.6 to 1.2 nanomol/L [0.5 to 0.9 nanograms/mL]), ECG may show PR-interval prolongation and a scooped ST segment. With toxicity, ECG may show signs of increased automaticity (premature ventricular contractions), atrioventricular nodal blockade, and slowed ventricular response.

Treatment includes supportive care to ensure that the patient is well hydrated, including treatment of any acute kidney injury and hyperkalaemia. If appropriate, treatment with digoxin-specific antibody (Fab) fragments may be required.

Digoxin is a cardiac glycoside indicated for the treatment of chronic heart failure and persistent atrial fibrillation.[1]National Poisons Information Service. TOXBASE: Digoxin. Dec 2019 [internet publication]. https://www.toxbase.org/poisons-index-a-z/d-products/digoxin----------------  In therapeutic doses, digoxin increases cardiac contractility and controls the heart rate.

Digoxin toxicity is a clinical diagnosis that relies in part on ECG findings such as signs of increased automaticity and atrioventricular node blockade (premature ventricular contractions, slowed ventricular response), but also on clinical features, history of digoxin intake, history of other illnesses, and elevated digoxin concentrations. Serum digoxin concentration is usually greater than the therapeutic range of 0.6 to 1.2 nanomol/L (0.5 to 0.9 nanograms/mL). In addition to pharmaceuticals, toxicity can also occur from exposure to a number of plants and animals that contain cardioactive corticosteroids, including dogbane, foxglove, lily of the valley, oleander, yellow oleander, red quill, and the Bufo species toad. This topic only covers toxicity from pharmaceutical digoxin.