Digoxin Toxicity


Article Author:
Earl Cummings


Article Editor:
Henry Swoboda


Editors In Chief:
Wanda Wright
Cynthia Oster


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
6/4/2019 6:43:55 PM

Introduction

Derived from the foxglove plant (Digitalis spp.), digoxin is a cardiac glycoside that historically was used for "dropsy" (edema) and is currently used as an inotrope to improve systolic dysfunction in patients with congestive heart failure (CHF) and as an atrioventricular nodal blocking agent for managing atrial tachydysrhythmias. Digoxin may improve the quality of life in CHF patients, but it does not confer a mortality benefit, and its narrow therapeutic index limits its utility. Digoxin toxicity can present acutely, by an intentional or accidental overdose (i.e., therapeutic misadventure), or chronically, such as when patients on digoxin develop an acute kidney injury. Similar toxicity can occur after exposure to cardioactive steroids in plants such as oleander, red squill, or dogbane or from animals such as Bufo toads.[1][2][3][4]

Etiology

Digoxin exhibits its therapeutic and toxic effects by poisoning the sodium-potassium ATPase. The subsequent increase in intracellular sodium leads to increased intracellular calcium by decreasing calcium expulsion through the sodium-calcium, cation exchanger. Higher intracellular calcium increases inotropy which can be of symptomatic benefit in CHF. At toxic levels, automaticity can be increased as well. Digoxin also increases vagal tone by decreasing dromotropy at the AV node. This can be used to control atrial tachydysrhythmias.

Epidemiology

Approximately 1% of CHF patients treated with digoxin develop toxicity. Additionally, 1% of adverse drug effects in patients greater than age 40 are due to digoxin toxicity; the incidence rises to greater than 3% in patients over age 85. Plant ingestions account for 80% of pediatric exposure; the remaining 20% of pediatric ingestions arise from medications. In general, ventricular dysrhythmias are more common in the elderly whereas supraventricular dysrhythmias are more common in children.

Pathophysiology

Increased intracellular calcium from the poisoning of the Na-K transporter and AV nodal blockade from increased vagal tone are the primary causes of digoxin toxicity. The former leads to increased automaticity and inotropy; the latter leads to decreased dromotropy. Hyperkalemia can be a marker of severe toxicity in acute poisoning. The role of potassium is less clear in chronic toxicity, although it has been linked to higher mortality despite traditional teaching that hypokalemia worsens the dysfunction at the Na-K transporter.[5][6][7]

Toxicokinetics

Digoxin's therapeutic half-life is between 30 to 40 hours, but this may change in overdose. Digoxin excretion is primarily renal, and for this reason, patients with poor or worsening renal function, such as patients who are elderly or have CKD, are more likely to develop toxicity. Digoxin levels start to plateau at 6 hours, which is after tissue redistribution has occurred; earlier levels may thus be misleadingly high. Cardiovascular toxicity may have delayed manifestation of up to 8 to 12 hours post ingestion.

History and Physical

Gastrointestinal upset is the most common symptom of digoxin toxicity. Patients also may report visual symptoms, which classically present as a yellow-green discoloration, and cardiovascular symptoms, such as palpitations, dyspnea, and syncope. Elderly patients frequently will present with vague symptoms, such as dizziness and fatigue. The most important historical detail in evaluating a random digoxin level is the time of the last dose.

Evaluation

For patients with acute digoxin toxicity, it is critical to obtain an ECG, a basic metabolic panel, and digoxin levels on arrival. These tests should be repeated at 6 hours post ingestion. Digoxin effect on the ECG is characterized by diffuse scooping of the ST segments which can be seen with therapeutic levels and is not associated with toxicity. The most common ECG abnormality is frequent PVCs, although the "pathognomonic" ECG finding is bidirectional ventricular tachycardia. However, this has been reported in aconitine poisoning. [8][9][10]

In the setting of acute overdose, acetaminophen and aspirin levels can help screen for occult overdose. 

In chronic toxicity, the cause of toxicity should be sought. Common causes include infection, renal failure, and accidental overdose. Serum digoxin levels do not always correlate with toxicity given variable tissue levels and other factors affecting digoxin's toxicodynamic effects.

Treatment / Management

Digoxin-specific antibody antigen-binding fragments (DSFab), brand name Digibind or Digifab, are an effective antidote that directly binds digoxin.

DSFab is indicated for life-threatening toxicity including:

  • Ventricular arrhythmias
  • High-grade heart blocks
  • Hypotension
  • Symptomatic bradycardia
  • Potassium greater than five meq/L in acute overdose
  • Acute ingestions greater than 10 mg in an adult or greater than 4 mg in a child
  • Digoxin Concentration greater than 15 ng/mL measured at any time
  • Digoxin Concentration greater than 10 ng/mL measured 6 hours post ingestion.

Empiric dosing of DSFab can be given at a dose of ten to 20 vials for critically ill patients after acute overdose, three to six vials for chronic toxicity in adults, or one to two vials for chronic toxicity in children. 

DSFab also can be dosed as follows:

(0.8 times the ingested dose)/0.5 = Number of vials of DSFab for acute overdose

(Digoxin level (steady state) x Weight (kg))/100 = Number vials of DSFab for acute or chronic overdose

DSFab fragments also can be given for poisoning with natural toxins, but the dosing is unclear.

The typical DSFab infusion is over 30 minutes, but it may be given as a bolus for critical patients. The onset of effect is approximately 20 minutes, with complete effect usually seen within 90 minutes. 

Care should be taken to completely reverse digoxin in patients who are chronically taking digoxin, as reversal may exacerbate their underlying disease. These patients should be closely monitored afterward for the same reasons. 

If DSFab is not available, then treatments such multidose-activated charcoal, atropine, and antidysrhythmics such as phenytoin or lidocaine may be employed. Cardioversion and pacing may induce dysrhythmias and are typically not used, but they may be needed in patients without other therapeutic options.

Dialysis also may be indicated in the patient with acute renal failure or refractory hyperkalemia; however, it is not useful as a treatment for digoxin toxicity itself.

Disposition depends on the patient's symptoms and stability as well as their potassium and digoxin levels.

Differential Diagnosis

Bidirectional ventricular tachycardia, classically described as pathognomonic for digoxin toxicity, may also be seen in aconitine (wolfsbane, monkshood) poisoning, and in patients that have familial catecholaminergic polymorphic ventricular tachycardia (CPVT).[11]

Pearls and Other Issues

Many analyzers cannot measure free digoxin concentrations, and in this setting, digoxin levels should not be followed after administration of DSFab.

In patients with the end-stage renal disease, dissociation of the DSFab-digoxin complex may occur and cause recurrent toxicity.

Calcium is traditionally considered contraindicated in hyperkalemic patients with digoxin toxicity for fear of 'stone heart syndrome,' an irreversible state of global myocardial contraction.   This is based on animal evidence and case report, but more recent literature found no evidence of increased mortality with calcium administration. In general, hyperkalemia in the setting of digoxin toxicity should be treated primarily with DSFab fragments if available.

A classic but uncommon side effect of digoxin is the appearance of yellow halos around lights, called xanthopsia, and altered color vision, called chromatopsia. This may have influenced the work of Dutch impressionist painter Vincent Van Gogh in paintings such as "The Starry Night" as he reportedly used foxglove for the treatment of his 'dropsy' which is an old term for edema due to CHF.

Enhancing Healthcare Team Outcomes

Digoxin toxicity can present in many ways and is best managed by a multidisciplinary team that includes a cardiologist, emergency department physician, poison control, internist and a nephrologist. Because digoxin toxicity can result in life threatening arrhythmias, prompt monitoring and treatment are vital. The key is patient education about drug safety. Parents should store the drug in a locked cabinet away from the reach of children. in addition, any old pills should be returned back to the pharmacist. When treated promptly, the outcomes are good but any delay in treatment can lead to death.[12][13] (Level V)

 

 

 

 


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Digoxin Toxicity - Questions

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A patient on digoxin suddenly started to develop premature ventricular contractions after he was started on a diuretic. What is the most likely reason that this occurred?



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Which of the following would be part of the management of symptomatic digoxin toxicity in a hemodynamically stable patient with a potassium level of 2.7 mEq/L?



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Which of the following is not used to treat digoxin toxicity?



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An elderly patient presenting for an acute overdose of an unknown medication has nausea, vomiting, confusion, and palpitations. They also complain of blurry vision. ECG shows atrial fibrillation with a regular, slow ventricular response. Which medication is the most likely cause of these symptoms?



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Which of the following ECG findings is least likely to be found in digoxin toxicity?



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Which of the following is a common early sign of digoxin toxicity?



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A 65-year-old with atrial fibrillation presents to the clinic with complaints of fatigue, anorexia, vomiting, and a headache. He claims that he has not been feeling well for a few days, his vision is blurred, and he is seeing "green." This morning he has pain in his eyes in the presence of sunlight. He takes several medications but cannot remember the names. Physical findings include a slow heart rate that is irregular. He most likely is suffering from which condition?



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Which of the following electrolyte disturbances does not increase digoxin toxicity?



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Which of the following is not considered treatment for digoxin toxicity?



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Which of the following is most likely seen in a patient with digoxin toxicity?



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Which of the following is a classic symptom seen in digoxin toxicity?



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A 65-year-old man is started on digoxin. which of the following is a common complication of digoxin toxicity?



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Which of the following is a classic symptom of digoxin toxicity?



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Digoxin toxicity may present with which of the following symptoms?



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A patient is taking digoxin. He is started on furosemide for leg swelling and presents complaining of palpitations. Which electrolyte disturbance is most likely to be present?



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Which electrolyte abnormality can potentiate cardiac arrhythmias caused by digoxin toxicity?



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Which of the following is not a common or classic symptom of digoxin toxicity?



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Which of the following is not an appropriate management of digoxin toxicity?



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Which of the following factors does not commonly contribute to digitalis toxicity?



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Which of the following is a common cardiac presentation of digoxin intoxication?



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Which of the following electrolyte changes may exacerbate digoxin toxicity?



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Which of the following drugs can decrease serum digoxin levels?



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Which of the following electrolytes can be used in the management of digoxin-induced arrhythmias?



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A 5-year-old child has been on digoxin for nine months. He is brought to the emergency department with a decreased appetite, headache, visual changes, muscle weakness, and fatigue. What is the most appropriate next step in the management of this patient?



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A 63-year-old male with dilated cardiomyopathy on digoxin is brought to the emergency department with lightheadedness and palpitations. Vital signs show blood pressure of 100/60 mmHg, apical heart rate of 50 bpm, and respiratory rate of 18. Cardiac exam shows an irregularly irregular rhythm with a gallop and an apical systolic murmur. ECG shows an atrial rate with ventricular escape rhythm at 50 bpm. Which of the following interventions would not be appropriate?



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A 63-year-old male is directly admitted with flu-like symptoms. The patient has been on oral furosemide 20 mg daily and oral digoxin 0.125 mg daily for 2 years. The digoxin dose was increased to 0.25 mg daily 2 weeks ago. What lab tests would be appropriate?



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Which of the following is most suggestive of digoxin toxicity?



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A 68-year-old man is brought to your emergency department in extremis. The EMS crew reports that he lives alone and was found down by his neighbors. An empty, unmarked pill bottle was found at the scene. Respiratory rate is 34/min and labored, pulse 72 bpm, and pulse oximetry is 91% on a non-rebreather mask. Glasgow coma scale is 11. Rectal temperature is 96.6 F. Fingerstick glucose is 99 mg/dl. The 12-lead ECG shows atrial fibrillation with a regular ventricular escape rhythm of 40 bpm. What is the most likely cause of these ECG findings?



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Which of the following ECG manifestations of digoxin is associated with toxicity?



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Which drug in overdose would cause bradycardia?



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A patient is taking digoxin. Which of the following drugs is likely to increase the digoxin concentration?



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Which of the following is not a symptom seen in digoxin toxicity?



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A patient with atrial fibrillation presents to your pharmacy with a prescription for furosemide. Being an astute pharmacist, what potentially serious side effect might be a cause for concern?



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A 73-year-old African American female with past medical history of congestive heart failure, atrial fibrillation, hypertension, type 2 diabetes mellitus, and hyperlipidemia presents to the emergency department with dizziness and palpitations. The patient gives a history of being on digoxin. On physical examination, she has a regular heart rate of 50 bpm; blood pressure is 133/72 mmHg, respiratory rate of 18/minute, and temperature of 98.4 F. Her electrocardiogram shows junctional tachycardia with no specific ST-T wave changes. Her laboratory testing shows toxic levels of digoxin. What is the next step in the management of this patient?



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Digoxin Toxicity - References

References

Ershad M,Khalid MM, Cardioactive Steroid Toxicity 2018 Jan;     [PubMed]
Supervía Caparrós A,Salgado García E,Calpe Perarnau X,Galicia Paredes M,García Gibert L,Córdoba Ruiz F,Clemente Rodríguez C,Nogué Xarau S, Immediate and 30 days mortality in digoxin poisoning cases attended in the Hospital Emergency Services of Catalonia, Spain. Emergencias : revista de la Sociedad Espanola de Medicina de Emergencias. 2019 Ene;     [PubMed]
Chan BS,Isbister GK,Page CB,Isoardi KZ,Chiew AL,Kirby KA,Buckley NA, Clinical outcomes from early use of digoxin-specific antibodies versus observation in chronic digoxin poisoning (ATOM-4). Clinical toxicology (Philadelphia, Pa.). 2018 Dec 26;     [PubMed]
Botelho AFM,Pierezan F,Soto-Blanco B,Melo MM, A review of cardiac glycosides: Structure, toxicokinetics, clinical signs, diagnosis and antineoplastic potential. Toxicon : official journal of the International Society on Toxinology. 2019 Feb;     [PubMed]
Smolders EJ,Ter Horst PJG,Wolters S,Burger DM, Cardiovascular Risk Management and Hepatitis C: Combining Drugs. Clinical pharmacokinetics. 2018 Sep 27;     [PubMed]
Menezes RG,Usman MS,Hussain SA,Madadin M,Siddiqi TJ,Fatima H,Ram P,Pasha SB,Senthilkumaran S,Fatima TQ,Luis SA, Cerbera odollam toxicity: A review. Journal of forensic and legal medicine. 2018 Aug;     [PubMed]
Mladěnka P,Applová L,Patočka J,Costa VM,Remiao F,Pourová J,Mladěnka A,Karlíčková J,Jahodář L,Vopršalová M,Varner KJ,Štěrba M, Comprehensive review of cardiovascular toxicity of drugs and related agents. Medicinal research reviews. 2018 Jul;     [PubMed]
Cosmi F,Tarquini B,Mariottoni B,Cosmi D, [Digitalis, a drug to be scrapped?] Giornale italiano di cardiologia (2006). 2017 Feb;     [PubMed]
Takahashi N, [Therapeutic Drug Monitoring of Antiarrhythmic Drugs]. Rinsho byori. The Japanese journal of clinical pathology. 2016 Dec;     [PubMed]
Tatlisu MA,Ozcan KS,Gungor B,Zengin A,Karatas MB,Nurkalem Z, Inappropriate use of digoxin in patients presenting with digoxin toxicity. Journal of geriatric cardiology : JGC. 2015 Mar;     [PubMed]
Hu YH,Tai CT,Tsai CF,Huang MW, Improvement of Adequate Digoxin Dosage: An Application of Machine Learning Approach. Journal of healthcare engineering. 2018;     [PubMed]
Limon G,Ersoy G,Oray NC,Bayram B,Limon O, Retrospective evaluation of patients with elevated digoxin levels at an emergency department. Turkish journal of emergency medicine. 2016 Mar;     [PubMed]
Richter S,Brugada P, Bidirectional ventricular tachycardia. Journal of the American College of Cardiology. 2009 Sep 22     [PubMed]

Disclaimer

The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of CNS-Adult Health. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for CNS-Adult Health, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in CNS-Adult Health, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of CNS-Adult Health. When it is time for the CNS-Adult Health board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study CNS-Adult Health.