| Digoxin toxicity | |
|---|---|
| Other names | Digoxin poisoning, digoxin overdose |
 | |
| Drawings of Digitalis purpurea | |
| Specialty | Emergency medicine |
| Symptoms | vomiting, loss of appetite, confusion, blurred vision, changes in color perception, decreased energy[1] |
| Complications | Heart dysrhythmia[1] |
| Causes | Excessive digoxin, plants such as foxglove[1][2] |
| Risk factors | Low potassium, low magnesium, high calcium[1] |
| Differential diagnosis | Acute coronary syndrome, hyperkalemia, hypothyroidism, beta blocker toxicity[2] |
| Treatment | Supportive care, activated charcoal, atropine, digoxin-specific antibody fragments[2][1] |
| Frequency | ~2,500 cases per year (US)[2] |
Digoxin toxicity, also known as digoxin poisoning, is a type of poisoning that occurs in people who take too much of the medication digoxin or eat plants such as foxglove that contain a similar substance.[1][2] Symptoms are typically vague.[1] They may include vomiting, loss of appetite, confusion, blurred vision, changes in color perception, and decreased energy.[1] Potential complications include an irregular heartbeat, which can be either too fast or too slow.[1]
Toxicity may occur over a short period of time following an overdose or gradually during long-term treatment.[1] Risk factors include low potassium, low magnesium, and high calcium.[1] Digoxin is a medication used for heart failure or atrial fibrillation.[3] An electrocardiogram is a routine part of diagnosis.[2] Blood levels are only useful more than six hours following the last dose.[1]
Activated charcoal may be used if it can be given within two hours of the person taking the medication.[1] Atropine may be used if the heart rate is slow while magnesium sulfate may be used in those with premature ventricular contractions.[2] Treatment of severe toxicity is with digoxin-specific antibody fragments.[1] Its use is recommended in those who have a serious dysrhythmia, are in cardiac arrest, or have a potassium of greater than 5 mmol/L.[1] Low blood potassium or magnesium should also be corrected.[1] Toxicity may reoccur within a few days after treatment.[1]
In Australia in 2012 there were about 140 documented cases.[1] This is a decrease by half since 1994 as a result of decreased usage of digoxin.[1] In the United States 2500 cases were reported in 2011 which resulted in 27 deaths.[2] The condition was first described in 1785 by William Withering.[4]
- ^ a b c d e f g h i j k l m n o p q r s Pincus, M (February 2016). "Management of digoxin toxicity". Australian Prescriber. 39 (1): 18–20. doi:10.18773/austprescr.2016.006. PMC 4816869. PMID 27041802.
- ^ a b c d e f g h Palatnick, W; Jelic, T (February 2014). "Emergency department management of calcium-channel blocker, beta blocker, and digoxin toxicity". Emergency Medicine Practice. 16 (2): 1–19, quiz 19–20. PMID 24883458. Archived from the original on 2014-05-14.
- ^ Gheorghiade, M; van Veldhuisen, DJ; Colucci, WS (30 May 2006). "Contemporary use of digoxin in the management of cardiovascular disorders". Circulation. 113 (21): 2556–64. doi:10.1161/circulationaha.105.560110. PMID 16735690.
- ^ Feldman, Arthur M. (2008). Heart Failure: Pharmacologic Management. John Wiley & Sons. p. 26. ISBN 9781405172530. Archived from the original on 2017-09-10.