digoxin toxicity
{{Infobox medical condition (new)
| name = Digoxin toxicity
| synonyms = Digoxin poisoning, digoxin overdose
| image = Digitalis purpurea Koehler drawing.jpg
| caption = Drawings of Digitalis purpurea
| field = Emergency medicine
| symptoms = vomiting, loss of appetite, confusion, blurred vision, changes in color perception, decreased energy
| complications = Heart dysrhythmia
| onset =
| duration =
| types =
| causes = Excessive digoxin, plants such as foxglove
| risks = Low potassium, low magnesium, high calcium
| diagnosis =
| differential = Acute coronary syndrome, hyperkalemia, hypothyroidism, beta blocker toxicity
| prevention =
| treatment = Supportive care, activated charcoal, atropine, digoxin-specific antibody fragments
| medication =
| prognosis =
| frequency = ~2,500 cases per year (US)
| deaths =
}}
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. Symptoms are typically vague. They may include vomiting, loss of appetite, confusion, blurred vision, changes in color perception, and decreased energy. Potential complications include an irregular heartbeat, which can be either too fast or too slow.
Toxicity may occur over a short period of time following an overdose or gradually during long-term treatment.{{cite journal|last1=Pincus|first1=M|title=Management of digoxin toxicity.|journal=Australian Prescriber|date=February 2016|volume=39|issue=1|pages=18–20|doi=10.18773/austprescr.2016.006|pmid=27041802|pmc=4816869}} Risk factors include low potassium, low magnesium, and high calcium. Digoxin is a medication used for heart failure or atrial fibrillation.{{cite journal|last1=Gheorghiade|first1=M|last2=van Veldhuisen|first2=DJ|last3=Colucci|first3=WS|title=Contemporary use of digoxin in the management of cardiovascular disorders.|journal=Circulation|date=30 May 2006|volume=113|issue=21|pages=2556–64|pmid=16735690|doi=10.1161/circulationaha.105.560110|doi-access=free}} An electrocardiogram is a routine part of diagnosis. Blood levels are only useful more than six hours following the last dose.
Activated charcoal may be used if it can be given within two hours of the person taking the medication. Atropine may be used if the heart rate is slow while magnesium sulfate may be used in those with premature ventricular contractions. Treatment of severe toxicity is with digoxin-specific antibody fragments. 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. Low blood potassium or magnesium should also be corrected. Toxicity may reoccur within a few days after treatment.
In Australia in 2012 there were about 140 documented cases. This is a decrease by half since 1994 as a result of decreased usage of digoxin. In the United States 2500 cases were reported in 2011 which resulted in 27 deaths.{{cite journal|last1=Palatnick|first1=W|last2=Jelic|first2=T|title=Emergency department management of calcium-channel blocker, beta blocker, and digoxin toxicity.|journal=Emergency Medicine Practice|date=February 2014|volume=16|issue=2|pages=1–19; quiz 19–20|pmid=24883458|url=http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=396|url-status=live|archive-url=https://web.archive.org/web/20140514075336/http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=396|archive-date=2014-05-14}} The condition was first described in 1785 by William Withering.{{cite book|last1=Feldman|first1=Arthur M.|title=Heart Failure: Pharmacologic Management|date=2008|publisher=John Wiley & Sons|isbn=9781405172530|page=26|url=https://books.google.com/books?id=6IfumyQQ35wC&pg=PA26|language=en|url-status=live|archive-url=https://web.archive.org/web/20170910174059/https://books.google.com/books?id=6IfumyQQ35wC&pg=PA26|archive-date=2017-09-10}}
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.{{cite journal|last1=Ma|first1=G|last2=Brady|first2=WJ|last3=Pollack|first3=M|last4=Chan|first4=TC|title=Electrocardiographic manifestations: digitalis toxicity.|journal= The Journal of Emergency Medicine |date=February 2001|volume=20|issue=2|pages=145–52|pmid=11207409|doi=10.1016/s0736-4679(00)00312-7}}
The classic features of digoxin toxicity are nausea, vomiting, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance (blurred or yellow vision). It is also associated with cardiac disturbances including irregular heartbeat, ventricular tachycardia, ventricular fibrillation, sinoatrial block and AV block.{{cite journal|last1=Eichhorn|first1=EJ|last2=Gheorghiade|first2=M|title=Digoxin.|journal=Progress in Cardiovascular Diseases|date=2002|volume=44|issue=4|pages=251–66|pmid=12007081|doi=10.1053/pcad.2002.31591}}
Diagnosis
In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.{{cite web|last1=Dugdale|first1=David|title=Digitalis toxicity|url=https://www.nlm.nih.gov/medlineplus/ency/article/000165.htm|website=MedlinePlus|access-date=30 October 2014|url-status=live|archive-url=https://web.archive.org/web/20141101042647/http://www.nlm.nih.gov/medlineplus/ency/article/000165.htm|archive-date=1 November 2014}}
=ECG=
In digoxin toxicity, the finding of frequent premature ventricular beats (PVCs) is the most common and the earliest dysrhythmia. Sinus bradycardia is also very common. In addition, depressed conduction is a predominant feature of digoxin toxicity. Other ECG changes that suggest digoxin toxicity include bigeminal and trigeminal rhythms, ventricular bigeminy, and bidirectional ventricular tachycardia.
=Blood test=
The level of digoxin for treatment is typically 0.5-2 ng/mL. 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.{{cite journal|last1=Ahmed|first1=A|last2=Rich|first2=MW|last3=Love|first3=TE|last4=Lloyd-Jones|first4=DM|last5=Aban|first5=IB|last6=Colucci|first6=WS|last7=Adams|first7=KF|last8=Gheorghiade|first8=M|title=Digoxin and reduction in mortality and hospitalization in heart failure: a comprehensive post hoc analysis of the DIG trial.|journal=European Heart Journal|date=January 2006|volume=27|issue=2|pages=178–86|pmid=16339157|doi=10.1093/eurheartj/ehi687|pmc=2685167}} 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. 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.{{cite journal|last1=Yang|first1=EH|last2=Shah|first2=S|last3=Criley|first3=JM|title=Digitalis toxicity: a fading but crucial complication to recognize.|journal=The American Journal of Medicine|date=April 2012|volume=125|issue=4|pages=337–43|pmid=22444097|doi=10.1016/j.amjmed.2011.09.019|s2cid=7538601 |url=http://www.escholarship.org/uc/item/2g74c8n4}}
Treatment
The primary treatment of digoxin toxicity is digoxin immune fab, which is an antibody made up of anti-digoxin immunoglobulin fragments. This antidote has been shown to be highly effective in treating life-threatening signs of digoxin toxicity such as hyperkalemia, hemodynamic instability, and arrhythmias.{{cite journal|last1=Antman|first1=EM|last2=Wenger|first2=TL|last3=Butler VP|first3=Jr|last4=Haber|first4=E|last5=Smith|first5=TW|title=Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments. Final report of a multicenter study.|journal=Circulation|date=June 1990|volume=81|issue=6|pages=1744–52|pmid=2188752|doi=10.1161/01.cir.81.6.1744|doi-access=free}} Fab dose can be determined by two different methods. First method is based on the amount of digoxin ingested whereas the second method is based on the serum digoxin concentration and the weight of the person.
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.{{cite journal|last1=Bhatia|first1=SJ|title=Digitalis toxicity--turning over a new leaf?|journal=The Western Journal of Medicine|date=July 1986|volume=145|issue=1|pages=74–82|pmid=3529634|pmc=1306817}}
References
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{{Medical resources
| DiseasesDB =
| ICD10 = {{ICD10|T|46|0|t|36}}
| ICD9 = {{ICD9|972.1}}
| ICDO =
| OMIM =
| MedlinePlus = 000165
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| eMedicineTopic =
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{{Poisoning and toxicity}}
Category:Poisoning by drugs, medicaments and biological substances
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