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]
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]
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]
In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.[7]
ECGEdit
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.[5]
Blood testEdit
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]
TreatmentEdit
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.[11] 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.[10]
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]
ReferencesEdit
^ abcdefghijklmnopqrsPincus, M (February 2016). "Management of digoxin toxicity". Australian Prescriber. 39 (1): 18–20. doi:10.18773/austprescr.2016.006. PMC4816869. PMID 27041802.
^ abcdefghPalatnick, 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. 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. ISBN9781405172530. from the original on 2017-09-10.
^ abMa, 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.
^ abEichhorn, EJ; Gheorghiade, M (2002). "Digoxin". Progress in Cardiovascular Diseases. 44 (4): 251–66. doi:10.1053/pcad.2002.31591. PMID 12007081.
^Dugdale, David. "Digitalis toxicity". MedlinePlus. from the original on 1 November 2014. Retrieved 30 October 2014.
^ abBhatia, SJ (July 1986). "Digitalis toxicity--turning over a new leaf?". The Western Journal of Medicine. 145 (1): 74–82. PMC1306817. PMID 3529634.
^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. PMC2685167. PMID 16339157.
^ abYang, 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.
^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 linksEdit
October 20, 2023
digoxin, toxicity, also, known, digoxin, poisoning, type, poisoning, that, occurs, people, take, much, medication, digoxin, plants, such, foxglove, that, contain, similar, substance, symptoms, typically, vague, they, include, vomiting, loss, appetite, confusio. 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 Digoxin toxicityOther namesDigoxin poisoning digoxin overdoseDrawings of Digitalis purpureaSpecialtyEmergency medicineSymptomsvomiting 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 Frequency 2 500 cases per year US 2 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 Contents 1 Signs and symptoms 2 Diagnosis 2 1 ECG 2 2 Blood test 3 Treatment 4 References 5 External linksSigns and symptoms EditDigoxin 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 yellow vision It is also associated with cardiac disturbances including irregular heartbeat ventricular tachycardia ventricular fibrillation sinoatrial block and AV block 6 Diagnosis EditIn individuals with suspected digoxin toxicity a serum digoxin concentration serum potassium concentration creatinine BUN and serial electrocardiograms is obtained 7 ECG Edit nbsp An ECG showing digoxin toxicity with the classic scooped out ST segmentIn 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 5 Blood test Edit 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 Edit nbsp Digoxin immune Fab used to treat digoxin toxicityThe 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 11 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 10 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 Edit 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 amp Sons p 26 ISBN 9781405172530 Archived from the original on 2017 09 10 a b 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 a b Eichhorn EJ Gheorghiade M 2002 Digoxin Progress in Cardiovascular Diseases 44 4 251 66 doi 10 1053 pcad 2002 31591 PMID 12007081 Dugdale David Digitalis toxicity MedlinePlus Archived from the original on 1 November 2014 Retrieved 30 October 2014 a b Bhatia SJ July 1986 Digitalis toxicity turning over a new leaf The Western Journal of Medicine 145 1 74 82 PMC 1306817 PMID 3529634 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 a b 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 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 Edit Retrieved from https en wikipedia org w index php title Digoxin toxicity amp oldid 1095129260, wikipedia, wiki, book, books, library,
