Know that digoxin has a narrow therapeutic window with several complications and toxicities

Know that digoxin has a narrow therapeutic window with several complications and toxicities: Excerpt from Avoiding Common Pediatric Errors

Author: Mindy Dickerman, MD

What to Do - Interpret the Data, Take Action

Obtaining digoxin levels in specific circumstances can be lifesaving.

Digoxin is the most widely used cardiac glycoside. These agents inhibit the sodium-potassium-adenosine triphosphate (Na+-K+ATPase) pump and, therefore, block active transport of Na+ and K+ across cell membranes. Increased intracellular Na+ reduces the transmembrane Na+ gradient and subsequently increases activity of the Na+-Ca+ exchanger, which causes intracellular calcium to rise. It is this increased intracellular Ca+ that augments myofibril activity in cardiac myocytes, causing a positive inotropic actionand therefore isusedfortreatmentofcongestiveheartfailure.Digoxin is also used to slow the ventricular rate in certain tachyarrhythmias.

Digoxin can cause toxicity by increasing vagal tone that may lead to direct atrioventricular depression and arrhythmias. Clinically, a patient may present with acute or chronic digoxin toxicity. There are several dysrhythmias that can result, most commonly frequent premature ventricular beats. Bidirectional ventricular tachycardia is specific for digoxin toxicity but is rarely seen. Noncardiac symptoms of toxicity may include anorexia, nausea, vomiting headache, fatigue, depression, dizziness, confusion, memory loss, delirium, and hallucinations. Visual disturbances, specifically xanthopsia, seeing yellow halos around objects, have been reported. Vague symptoms can lead to a misdiagnosis of viral syndrome, so a high degree of suspicion must be maintained. Chronic toxicity may lead to renal failure.

Digoxin toxicity can occur if a condition or medication changes the metabolism or excretion of the drug. This can happen if a patient is in renal failure. Some of the medications that can affect digoxin metabolism include quinidine, cyclosporine, verapamil, tetracycline, erythromycin, and rifampin.

If you suspect your patient has digoxin toxicity, immediately place the patient on a cardiac monitor. Bradycardia is the most common vital sign change. If stable, these patients should have an electrocardiogram performed and a chemistry and digoxin level drawn. Hyperkalemia will usually be seen in acute toxicity due to the inhibition of the Na+-K+-ATPase and a resultant rise in extracellular K+. Hyperkalemia may not be seen in chronic digoxin toxicity because the kidneys had time to compensate or the patient is on diuretics that promote potassium excretion.

Serum digoxin levels need to be interpreted with caution. High levels do not always indicate toxicity. In the case of an acute exposure, digoxin will slowly redistribute into the tissues after it is absorbed in the plasma. False-positive results may occur in the presence of digoxin, such as immunoreactive substances, which can be seen in neonates, pregnancy, and other disease states. Therapeutic levels in children are reported between 0.5 and 2.0 ng/mL. Levels >10 ng/mL may be associated with significant toxicity and treatment with digoxin-specific Fab should be considered.

Ifapatientwithdigoxintoxicityhascardiacdysrhythmiaswithhemodynamic instability, Fab fragments are first-line therapy Digoxin-specific Fab fragments are antibody fragments produced by enzymatic cleavage of sheep immunoglobulin G antibodies to digoxin. Several antiarrhythmics have been used to treat digoxin toxicity associated dysrhythmias. Antiarrhythmics that depress atrioventricular nodal conduction are contraindicated because they can worsen cardiac toxicity. If there has been an acute ingestion within 6 to 8 hours, charcoal can be administered for gastrointestinal decontamination. Intravenous potassium and magnesium may be beneficial in patients with chronic digoxin toxicity. Calcium and beta blockers should be avoided. Electrical cardioversion should be performed with extreme caution and as a last resort.

Suggested Readings

Antman EM, Wenger TL, Butler VP Jr, et al. Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments. Final report of a multicenter study. Circulation. 1990;81:1744–1752.
Morris SA, Hatcher HF, Reddy DK. Digoxin therapy for heart failure: an update. Am Fam Physician. 2006;74:613–618.

Book Source Details

• Book Title: Avoiding Common Pediatric Errors
• Author(s): Anthony D Slonim MD, DrPH; Lisa Marcucci MD
• Year of Publication: 2008
• Copyright Details: Avoiding Common Pediatric Errors, Copyright © 2008 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: Avoiding Common Pediatric Errors Authors: Anthony D Slonim MD, DrPH; Lisa Marcucci MD Publisher: Lippincott Williams & Wilkins Copyright: 2008 ISBN: 0-7817-7489-6

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