Difference between revisions of "Digoxin toxicity"

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| field          = [[Emergency medicine]]
 
| field          = [[Emergency medicine]]
 
| symptoms        = vomiting, loss of appetite, confusion, blurred vision, changes in color perception, decreased energy<ref name=AP2016/>
 
| symptoms        = vomiting, loss of appetite, confusion, blurred vision, changes in color perception, decreased energy<ref name=AP2016/>
| complications  = [[Heart dysrhythmia]]<ref name=AP2016/>
+
| complications  = [[Arrhythmia|Heart dysrhythmia]]<ref name=AP2016/>
 
| onset          =  
 
| onset          =  
 
| duration        =  
 
| duration        =  
Line 17: Line 17:
 
| treatment      = [[Supportive care]], [[activated charcoal]], [[atropine]], [[digoxin-specific antibody fragments]]<ref name=EB2014/><ref name=AP2016/>
 
| treatment      = [[Supportive care]], [[activated charcoal]], [[atropine]], [[digoxin-specific antibody fragments]]<ref name=EB2014/><ref name=AP2016/>
 
| medication      =  
 
| medication      =  
| prognosis      =  
+
| prognosis      = 1 to 5%<ref name=STAT2020/>
 
| frequency      = ~2,500 cases per year (US)<ref name=EB2014/>
 
| frequency      = ~2,500 cases per year (US)<ref name=EB2014/>
 
| deaths          =  
 
| deaths          =  
Line 25: Line 25:
  
 
<!-- Cause and diagnosis -->
 
<!-- Cause and diagnosis -->
Toxicity may occur over a short period of time following an [[overdose]] or gradually during long-term treatment.<ref name=AP2016>{{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}}</ref> Risk factors include [[hypokalaemia|low potassium]], [[hypomagnesaemia|low magnesium]], and [[hypercalcaemia|high calcium]].<ref name=AP2016/> Digoxin is a medication used for [[heart failure]] or [[atrial fibrillation]].<ref>{{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}}</ref> An [[electrocardiogram]] is a routine part of diagnosis.<ref name=EB2014/> Blood levels are only useful more than six hours following the last dose.<ref name=AP2016/>
+
Toxicity may occur over a short period of time following an [[overdose]] or gradually during long-term treatment.<ref name=AP2016>{{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}}</ref> Risk factors include [[hypokalaemia|low potassium]], [[hypomagnesaemia|low magnesium]], and [[hypercalcaemia|high calcium]].<ref name=AP2016/> Digoxin is a medication used for [[heart failure]] or [[atrial fibrillation]].<ref>{{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}}</ref> An [[electrocardiogram]] is a routine part of diagnosis.<ref name=EB2014/> Blood levels are only useful more than six hours following the last dose.<ref name=AP2016/>
  
 
<!-- Treatment -->
 
<!-- Treatment -->
[[Activated charcoal]] may be used if it can be given within two hours of the person taking the medication.<ref name=AP2016/> [[Atropine]] may be used if the heart rate is slow while [[magnesium sulfate]] may be used in those with [[premature ventricular contraction]]s.<ref name=EB2014/> Treatment of severe toxicity is with [[digoxin-specific antibody fragments]].<ref name=AP2016/> Its use is recommended in those who have a serious dysrhythmia, are in [[cardiac arrest]], or have a potassium of greater than 5&nbsp;mmol/L.<ref name=AP2016/> Low blood potassium or magnesium should also be corrected.<ref name=AP2016/> Toxicity may reoccur within a few days after treatment.<ref name=AP2016/>
+
[[Activated charcoal (medication)|Activated charcoal]] may be used if it can be given within two hours of the person taking the medication.<ref name=AP2016/> [[Atropine]] may be used if the heart rate is slow while [[magnesium sulfate]] may be used in those with [[premature ventricular contraction]]s.<ref name=EB2014/> Treatment of severe toxicity is with [[digoxin-specific antibody fragments]].<ref name=AP2016/> Its use is recommended in those who have a serious dysrhythmia, are in [[cardiac arrest]], or have a potassium of greater than 5&nbsp;mmol/L.<ref name=AP2016/> Low blood potassium or magnesium should also be corrected.<ref name=AP2016/> Toxicity may reoccur within a few days after treatment.<ref name=AP2016/>
  
<!-- Epidemiology -->
+
<!-- Epidemiology and prognosis -->
In Australia in 2012 there were about 140 documented cases.<ref name=AP2016/> This is a decrease by half since 1994 as a result of decreased usage of digoxin.<ref name=AP2016/> In the United States 2500 cases were reported in 2011 which resulted in 27 deaths.<ref name=EB2014>{{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|deadurl=no|archiveurl=https://web.archive.org/web/20140514075336/http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=396|archivedate=2014-05-14|df=}}</ref> The condition was first described in 1785 by [[William Withering]].<ref>{{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|deadurl=no|archiveurl=https://web.archive.org/web/20170910174059/https://books.google.com/books?id=6IfumyQQ35wC&pg=PA26|archivedate=2017-09-10|df=}}</ref>
+
In Australia in 2012 there were about 140 documented cases.<ref name=AP2016/> This is a decrease by half since 1994 as a result of decreased usage of digoxin.<ref name=AP2016/> In the United States 2500 cases were reported in 2011 which resulted in 27 deaths.<ref name=EB2014>{{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|archiveurl=https://web.archive.org/web/20140514075336/http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=396|archivedate=2014-05-14}}</ref> The risk of death is 1 to 5% and up to 15 to 30% with chronic digoxin toxicity.<ref name=LIT2020/><ref name=STAT2020>{{cite web |last1=Rehman |first1=Rameez |last2=Hai |first2=Ofek |title=Digitalis Toxicity |url=https://www.ncbi.nlm.nih.gov/books/NBK459165/ |website=StatPearls |publisher=StatPearls Publishing |accessdate=8 September 2020 |date=2020}}</ref> The condition was first described in 1785 by [[William Withering]].<ref>{{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|archiveurl=https://web.archive.org/web/20170910174059/https://books.google.com/books?id=6IfumyQQ35wC&pg=PA26|archivedate=2017-09-10}}</ref>
  
 
==Signs and symptoms==
 
==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.<ref name=Ma2001>{{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}}</ref>
 
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.<ref name=Ma2001>{{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}}</ref>
  
The classic features of digoxin toxicity are nausea, vomiting, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance (blurred or [[Xanthopsia|yellow vision]]). It is also associated with cardiac disturbances including [[Heart arrhythmia|irregular heartbeat]], [[ventricular tachycardia]], [[ventricular fibrillation]], sinoatrial block and [[Atrioventricular block|AV block]].<ref name=Eichhorn2002>{{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}}</ref>
+
The classic features of digoxin toxicity are nausea, vomiting, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance (blurred or [[Xanthopsia|yellow vision]]). It is also associated with heart disturbances including [[Arrhythmia|irregular heartbeat]], [[ventricular tachycardia]], [[ventricular fibrillation]], sinoatrial block and [[Atrioventricular block|AV block]].<ref name=Eichhorn2002>{{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}}</ref>
  
 
==Diagnosis==
 
==Diagnosis==
In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.<ref>{{cite web|last1=Dugdale|first1=David|title=Digitalis toxicity|url=https://www.nlm.nih.gov/medlineplus/ency/article/000165.htm|website=MedlinePlus|accessdate=30 October 2014|deadurl=no|archiveurl=https://web.archive.org/web/20141101042647/http://www.nlm.nih.gov/medlineplus/ency/article/000165.htm|archivedate=1 November 2014|df=}}</ref>
+
In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.<ref>{{cite web|last1=Dugdale|first1=David|title=Digitalis toxicity|url=https://www.nlm.nih.gov/medlineplus/ency/article/000165.htm|website=MedlinePlus|accessdate=30 October 2014|url-status=live|archiveurl=https://web.archive.org/web/20141101042647/http://www.nlm.nih.gov/medlineplus/ency/article/000165.htm|archivedate=1 November 2014}}</ref>
  
 
===ECG===
 
===ECG===
 
[[File:DigToxCrop.jpg|thumb|upright=1.3|An ECG showing digoxin toxicity with the classic "scooped out" ST segment]]
 
[[File:DigToxCrop.jpg|thumb|upright=1.3|An ECG showing digoxin toxicity with the classic "scooped out" ST segment]]
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.<ref name="Ma2001"/>
+
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 [[Electrocardiography|ECG]] changes that suggest digoxin toxicity include bigeminal and trigeminal rhythms, ventricular bigeminy, and bidirectional ventricular tachycardia.<ref name="Ma2001"/>
  
 
===Blood test===
 
===Blood test===
Line 53: Line 53:
 
[[File:Digibind.jpg|thumb|Digoxin immune Fab used to treat digoxin toxicity]]
 
[[File:Digibind.jpg|thumb|Digoxin immune Fab used to treat digoxin toxicity]]
  
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.<ref>{{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}}</ref> 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.<ref name= Yang2012/>
+
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.<ref>{{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}}</ref> 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.<ref name= Yang2012/>
  
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]], [[catecholamine]]s ([[isoprenaline]] or [[salbutamol]]), and/or temporary [[Transvenous pacing|cardiac pacing]] can be used.<ref name=Bhatia1986>{{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}}</ref>
+
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]], [[catecholamine]]s ([[isoprenaline]] or [[salbutamol]]), and temporary [[Transvenous pacing|cardiac pacing]] can be used.<ref name=Bhatia1986>{{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}}</ref>
 +
 
 +
High blood potassium can be treated with insulin and glucose as well as sodium bicarbonate.<ref name=LIT2020>{{cite web |title=Digoxin Toxicity • LITFL • CCC Toxicology |url=https://litfl.com/digoxin-toxicity-ccc/ |website=Life in the Fast Lane • LITFL • Medical Blog |accessdate=8 September 2020 |date=11 January 2019}}</ref> Other treatments include [[calcium gluconate]] and [[dialysis]].<ref name=LIT2020/> While there is a proposed risk from calcium gluconate this risk has not been substantiated.<ref name=LIT2020/>
 +
 
 +
==Prognosis==
 +
The risk of death is 1 to 5% and up to 15 to 30% with chronic digoxin toxicity.<ref name=LIT2020/><ref name=STAT2020/>
 +
{{-}}
  
 
==References==
 
==References==

Latest revision as of 12:47, 24 April 2021

Digoxin toxicity
Other names: Digoxin poisoning, digoxin overdose
Digitalis purpurea Koehler drawing.jpg
Drawings of Digitalis purpurea
SpecialtyEmergency medicine
Symptomsvomiting, loss of appetite, confusion, blurred vision, changes in color perception, decreased energy[1]
ComplicationsHeart dysrhythmia[1]
CausesExcessive digoxin, plants such as foxglove[1][2]
Risk factorsLow potassium, low magnesium, high calcium[1]
Differential diagnosisAcute coronary syndrome, hyperkalemia, hypothyroidism, beta blocker toxicity[2]
TreatmentSupportive care, activated charcoal, atropine, digoxin-specific antibody fragments[2][1]
Prognosis1 to 5%[3]
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.[4] 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 risk of death is 1 to 5% and up to 15 to 30% with chronic digoxin toxicity.[5][3] The condition was first described in 1785 by William Withering.[6]

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.[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 heart disturbances including irregular heartbeat, ventricular tachycardia, ventricular fibrillation, sinoatrial block and AV block.[8]

Diagnosis

In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.[9]

ECG

An ECG showing digoxin toxicity with the classic "scooped out" ST segment

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.[7]

Blood test

The level of digoxin for treatment is typically 0.5-2 ng/mL.[10] 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.[11] 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.[8] 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.[12]

Treatment

Digoxin immune Fab used to treat digoxin toxicity

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.[13] 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.[12]

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 temporary cardiac pacing can be used.[10]

High blood potassium can be treated with insulin and glucose as well as sodium bicarbonate.[5] Other treatments include calcium gluconate and dialysis.[5] While there is a proposed risk from calcium gluconate this risk has not been substantiated.[5]

Prognosis

The risk of death is 1 to 5% and up to 15 to 30% with chronic digoxin toxicity.[5][3]

References

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 Pincus, M (February 2016). "Management of digoxin toxicity". Australian Prescriber. 39 (1): 18–20. doi:10.18773/austprescr.2016.006. PMC 4816869. PMID 27041802.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 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.
  3. 3.0 3.1 3.2 Rehman, Rameez; Hai, Ofek (2020). "Digitalis Toxicity". StatPearls. StatPearls Publishing. Retrieved 8 September 2020.
  4. 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.
  5. 5.0 5.1 5.2 5.3 5.4 "Digoxin Toxicity • LITFL • CCC Toxicology". Life in the Fast Lane • LITFL • Medical Blog. 11 January 2019. Retrieved 8 September 2020.
  6. Feldman, Arthur M. (2008). Heart Failure: Pharmacologic Management. John Wiley & Sons. p. 26. ISBN 9781405172530. Archived from the original on 2017-09-10.
  7. 7.0 7.1 Ma, G; Brady, WJ; Pollack, M; Chan, TC (February 2001). "Electrocardiographic manifestations: digitalis toxicity". The Journal of Emergency Medicine. 20 (2): 145–52. doi:10.1016/s0736-4679(00)00312-7. PMID 11207409.
  8. 8.0 8.1 Eichhorn, EJ; Gheorghiade, M (2002). "Digoxin". Progress in Cardiovascular Diseases. 44 (4): 251–66. doi:10.1053/pcad.2002.31591. PMID 12007081.
  9. Dugdale, David. "Digitalis toxicity". MedlinePlus. Archived from the original on 1 November 2014. Retrieved 30 October 2014.
  10. 10.0 10.1 Bhatia, SJ (July 1986). "Digitalis toxicity--turning over a new leaf?". The Western Journal of Medicine. 145 (1): 74–82. PMC 1306817. PMID 3529634.
  11. Ahmed, A; Rich, MW; Love, TE; Lloyd-Jones, DM; Aban, IB; Colucci, WS; Adams, KF; Gheorghiade, M (January 2006). "Digoxin and reduction in mortality and hospitalization in heart failure: a comprehensive post hoc analysis of the DIG trial". European Heart Journal. 27 (2): 178–86. doi:10.1093/eurheartj/ehi687. PMC 2685167. PMID 16339157.
  12. 12.0 12.1 Yang, EH; Shah, S; Criley, JM (April 2012). "Digitalis toxicity: a fading but crucial complication to recognize". The American Journal of Medicine. 125 (4): 337–43. doi:10.1016/j.amjmed.2011.09.019. PMID 22444097.
  13. Antman, EM; Wenger, TL; Butler VP, Jr; Haber, E; Smith, TW (June 1990). "Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments. Final report of a multicenter study". Circulation. 81 (6): 1744–52. doi:10.1161/01.cir.81.6.1744. PMID 2188752.

External links

Classification
External resources