Digoxin toxicity
Digoxin toxicity | |
---|---|
Other names | Digoxin poisoning, digoxin overdose |
Frequency | ~2,500 cases per year (US)[2] |
Digoxin toxicity, also known as digoxin poisoning, is a type of
Toxicity may occur over a short period of time following an
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]
Signs and symptoms
Digoxin toxicity is often divided into acute or chronic toxicity. In both of these toxicity, cardiac effects are of the greatest concern. With an acute ingestion, symptoms such as nausea, vertigo, and vomiting are prominent. On the other hand, nonspecific symptoms are predominant in chronic toxicity. These symptoms include fatigue, malaise, and visual disturbances.[5]
The classic features of digoxin toxicity are nausea, vomiting, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance (blurred or
Diagnosis
In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.[7]
ECG
In digoxin toxicity, the finding of frequent premature ventricular beats (PVCs) is the most common and the earliest dysrhythmia.
Blood test
The level of digoxin for treatment is typically 0.5-2 ng/mL.[8] Since this is a narrow therapeutic index, digoxin overdose can happen. A serum digoxin concentration of 0.5-0.9 ng/mL among those with heart failure is associated with reduced heart failure deaths and hospitalizations.[9] It is therefore recommended that digoxin concentration be maintained in approximately this range if it is used in heart failure patients.
High amounts of the electrolyte potassium (K+) in the blood (hyperkalemia) is characteristic of digoxin toxicity.[6] Digoxin toxicity increases in individuals who have kidney impairment. This is most often seen in elderly or those with chronic kidney disease or end-stage kidney disease.[10]
Treatment
The primary treatment of digoxin toxicity is
Other treatment that may be used to treat life-threatening arrhythmias until Fab is acquired are magnesium, phenytoin, and lidocaine. Magnesium suppresses digoxin-induced ventricular arrhythmias while phenytoin and lidocaine suppresses digoxin-induced ventricular automaticity and delay afterdepolarizations without depressing AV conduction. In the case of an abnormally slow heart rate (bradyarrhythmias), Atropine, catecholamines (isoprenaline or salbutamol), and/or temporary cardiac pacing can be used.[8]
References
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- ^ from the original on 2014-05-14.
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- ISBN 9781405172530. Archivedfrom the original on 2017-09-10.
- ^ PMID 11207409.
- ^ PMID 12007081.
- ^ Dugdale, David. "Digitalis toxicity". MedlinePlus. Archived from the original on 1 November 2014. Retrieved 30 October 2014.
- ^ PMID 3529634.
- PMID 16339157.
- ^ S2CID 7538601.
- PMID 2188752.