Digoxin toxicity

Digoxin toxicity can be acute or chronic, intentional, or accidental. 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 doses (0.5 to 0.9 nanograms/mL), ECG typically shows PR-interval prolongation and a scooped ST segment. With toxicity, ECG also shows signs of increased automaticity (premature ventricular contractions), atrioventricular nodal blockade, and slowed ventricular response.

Treatment includes supportive care, discontinuation of digoxin therapy and prevention of further gastrointestinal absorption, administration of digoxin-specific antibody fragments (digoxin immune Fab) if indicated, and management of any arrhythmias or electrolyte abnormalities.

There are no long-term complications of poisoning in patients treated appropriately for chronic digoxin toxicity, as long as anoxic brain injury, myocardial infarction, or terminal dysrhythmias have not occurred prior to treatment.

Digoxin is the most commonly prescribed cardiac glycoside (also known as a cardioactive steroid). It is indicated for the treatment of atrial fibrillation and heart failure.[1]Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation: a report of the American College of Cardiology/American Heart Association joint committee on clinical practice guidelines. Circulation. 2024 Jan 2;149(1):e1-156. https://pmc.ncbi.nlm.nih.gov/articles/PMC11095842 http://www.ncbi.nlm.nih.gov/pubmed/38033089?tool=bestpractice.com [2]Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association joint committee on clinical practice guidelines. Circulation. 2022 May 3;145(18):e895-1032. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063 http://www.ncbi.nlm.nih.gov/pubmed/35363499?tool=bestpractice.com ​ 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). Serum digoxin concentration is usually greater than the therapeutic range, but may not be elevated; therapeutic range is 0.8 to 2 nanograms/mL, with narrower range (0.5 to 0.9 nanograms/mL) for heart failure.[3]Andrews P, Anseeuw K, Kotecha D, et al. Diagnosis and practical management of digoxin toxicity: a narrative review and consensus. Eur J Emerg Med. 2023 Dec 1;30(6):395-401. https://pmc.ncbi.nlm.nih.gov/articles/PMC10599802 http://www.ncbi.nlm.nih.gov/pubmed/37650725?tool=bestpractice.com ​ In addition to pharmaceuticals, toxicity can also occur from exposure to several plants and animals that contain cardiac glycosides, including dogbane, foxglove, lily of the valley, oleander, yellow oleander, red quill, and the Bufo species toad. Although these other toxins are clinically similar, this topic specifically discusses toxicity from pharmaceutical digoxin.