Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
DIGOXIN PEDIATRIC vs LANOXIN
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Inhibits sodium-potassium ATPase, increasing intracellular sodium, which promotes calcium influx via sodium-calcium exchanger, enhancing cardiac contractility. Also increases vagal tone, slowing AV conduction.
Inhibits Na+/K+ ATPase, increasing intracellular Ca2+ via Na+/Ca2+ exchange, enhancing cardiac contractility and reducing conduction through AV node.
Heart failure (FDA-approved for pediatric patients with heart failure),Atrial fibrillation (off-label for rate control in pediatric patients)
Heart failure (NYHA class II-IV) with reduced ejection fraction,Atrial fibrillation and atrial flutter for rate control (off-label: paroxysmal supraventricular tachycardia)
For pediatric patients, digoxin pediatric dosing is weight-based; no standard adult dose. Typical pediatric loading dose: 10-12 mcg/kg orally divided every 6-8 hours, with maintenance: 5-10 mcg/kg/day divided every 12 hours. For infants <1 month, loading: 10-15 mcg/kg, maintenance: 4-6 mcg/kg/day. For children 1-24 months, loading: 15-20 mcg/kg, maintenance: 5-8 mcg/kg/day. For children >2 years, loading: 10-15 mcg/kg, maintenance: 3-5 mcg/kg/day.
0.125-0.25 mg orally once daily; loading dose 0.5-0.75 mg orally divided over 24-48 hours if rapid digitalization required.
Terminal elimination half-life in neonates is 35-70 hours, infants 18-30 hours, children 12-30 hours, and adults 36-48 hours; prolonged in renal impairment and hypothyroidism.
Terminal elimination half-life is approximately 36-48 hours in patients with normal renal function; prolonged to 3.5-5 days in anuria.
Primarily renally excreted unchanged; minimal hepatic metabolism (mostly via reduction, hydrolysis, and conjugation in older children).
Primarily hepatic via CYP3A4 and renal excretion of unchanged drug; undergoes biliary excretion and enterohepatic recirculation.
Renal excretion accounts for 50-70% of elimination as unchanged drug; biliary/fecal excretion accounts for 30-40%, primarily as metabolites; enterohepatic recirculation occurs.
Renal excretion of unchanged drug (60-80%) and biliary/fecal elimination (20-40%).
25% bound to serum albumin; binding decreases in uremia and hyperbilirubinemia.
25-30% bound primarily to albumin.
Vd: 6-10 L/kg in infants and children, 5-7 L/kg in adults; large Vd indicates extensive tissue binding, particularly to cardiac muscle (Na+/K+-ATPase).
Vd approximately 6-7 L/kg; indicates extensive tissue binding, particularly to cardiac muscle.
Oral: 60-80% (elixir 70-85%, tablets 60-75%); IM: 70-85% (but erratic absorption and pain limit use); IV: 100%.
Oral: 60-80%; Intravenous: 100%.
Digoxin is primarily renally excreted. For pediatric patients, if GFR <30 m L/min/1.73m2, reduce maintenance dose by 50% and monitor serum levels. For GFR 30-60, reduce dose by 25-50%. In neonates with renal impairment, dose reduction proportional to creatinine clearance.
GFR >50 m L/min: no adjustment; GFR 10-50 m L/min: reduce dose by 50% or use 0.125 mg every 48 hours; GFR <10 m L/min: reduce dose by 75% or use 0.0625 mg daily; monitor digoxin levels.
Digoxin is minimally hepatically metabolized; no dose adjustment required for hepatic impairment. However, in Child-Pugh class C, monitor levels due to potential altered distribution.
No specific Child-Pugh based dose adjustment; use caution in severe hepatic impairment due to potential toxicity; monitor levels.
See standard_dosing. Weight-based dosing: total digitalizing dose (TDD) and maintenance as above. For premature infants, TDD 10-15 mcg/kg, maintenance 3-5 mcg/kg/day divided q12h. For full term neonates, TDD 15-20 mcg/kg, maintenance 5-7 mcg/kg/day. For infants 1-24 months, TDD 20-25 mcg/kg, maintenance 7-10 mcg/kg/day. For children 2-10 years, TDD 10-15 mcg/kg, maintenance 5-7 mcg/kg/day. For children >10 years, TDD 10-15 mcg/kg, maintenance 3-5 mcg/kg/day. Divide TDD into 3-4 doses every 6-8 hours. Maintenance started 12 hours after last loading dose.
Loading dose: 10-15 mcg/kg orally divided every 8 hours over 24 hours; maintenance: 5-10 mcg/kg/day orally in 2 divided doses; maximum 0.25 mg/day.
Not applicable for pediatric formulation. For elderly, use adult digoxin dosing with caution: reduced renal function may require lower maintenance doses. Typical adult maintenance: 0.0625-0.25 mg daily based on renal function and lean body mass.
Start with 0.0625-0.125 mg orally daily; adjust based on renal function and drug levels; due to decreased lean body mass and renal clearance.
Toxicity can be life-threatening. Use caution in renal impairment, electrolyte disturbances (hypokalemia, hypomagnesemia, hypercalcemia). Narrow therapeutic index requires monitoring.
None; however, toxicity is common and potentially fatal. Not a formal black box warning due to age of drug.
Monitor serum digoxin levels, renal function, electrolytes (potassium, magnesium, calcium). Risk of arrhythmias (including ventricular fibrillation, bradycardia, AV block). Use with caution in patients with thyroid disease, acute myocardial infarction, or myocarditis.
Toxicity risk: hypokalemia, hypomagnesemia, hypercalcemia increase sensitivity,Renal impairment requires dose adjustment,Digoxin immune Fab for life-threatening overdose,Pregnancy category C,Monitor serum levels and ECG
Ventricular fibrillation, hypersensitivity to digitalis preparations, hypokalemia (uncorrected), hypercalcemia (uncorrected), AV block (second or third degree) unless pacemaker present.
Hypersensitivity,Ventricular fibrillation,AV block (unless pacemaker present),Wolff-Parkinson-White syndrome with atrial fibrillation,Hypertrophic obstructive cardiomyopathy,Hypokalemia or hypercalcemia (relative)
High-fiber foods may decrease absorption; take digoxin 1 hour before or 2 hours after meals. Avoid natural licorice, which can cause hypokalemia and increase toxicity. Maintain consistent dietary potassium intake.
High-fiber foods (bran) may decrease absorption; take digoxin 2 hours before or after high-fiber meals. Potassium-rich foods (bananas, oranges, spinach) can affect toxicity risk; maintain consistent intake. Avoid excessive licorice (glycyrrhizin can cause hypokalemia). Grapefruit juice may increase digoxin absorption; avoid large amounts.
Digoxin crosses the placenta. First trimester: No increased risk of major malformations reported in human studies. Second/third trimester: Potential for fetal toxicity (e.g., bradycardia, cardiac arrhythmias) at maternal toxic doses. No known teratogenicity at therapeutic doses.
Digoxin crosses the placenta. First trimester: No increased risk of major malformations reported in human studies; animal studies show no teratogenicity at clinically relevant doses. Second/third trimester: Risk of fetal toxicity (bradycardia, arrhythmias) if maternal serum levels are supratherapeutic; therapeutic maternal levels are generally safe. Chronic use may be associated with reduced birth weight.
Digoxin is excreted into breast milk in low concentrations. M/P ratio approximately 0.6–0.9. Infant dose via milk is <1% of maternal weight-adjusted dose, unlikely to cause adverse effects in term infants. Caution in preterm or neonates with renal impairment.
Digoxin is excreted into breast milk in low concentrations. M/P ratio approximately 0.6–0.9. At typical maternal doses (0.125–0.5 mg/day), the estimated infant dose is less than 10% of the weight-adjusted neonatal maintenance dose, usually considered compatible with breastfeeding. Monitor infant for signs of digoxin toxicity (bradycardia, poor feeding, vomiting).
During pregnancy, increased volume of distribution and renal clearance may reduce serum digoxin levels. Dose adjustments may be required based on therapeutic drug monitoring; typical dose increase of 20–30% in third trimester. Postpartum, reduce dose to prepregnancy level to avoid toxicity.
Pregnancy increases glomerular filtration rate (GFR) and volume of distribution, which may lower serum digoxin concentrations; dose adjustments are often needed. Monitor serum levels and adjust dose to maintain therapeutic range (0.5–2.0 ng/m L). Consider increasing dose by 30-50% in later pregnancy if levels are low; postpartum dose may need reduction to prepregnancy levels.
Monitor serum digoxin levels (therapeutic range 0.5-2 ng/m L) and renal function, especially in neonates. Correct hypokalemia, hypomagnesemia, and hypercalcemia before administration to reduce toxicity risk. Use with caution in patients with WPW, hypertrophic cardiomyopathy, or incomplete heart block. Dosing in infants and children is based on weight and renal function.
Check serum digoxin level 6-8 hours after last dose; therapeutic range 0.5-2.0 ng/m L. Hypokalemia, hypomagnesemia, hypercalcemia increase toxicity risk. Use with caution in renal impairment (reduce dose). Monitor for bradycardia and arrhythmias. Avoid in patients with AV block (except pacemaker) or hypertrophic cardiomyopathy. Loading dose: 10-15 mcg/kg lean body weight. Maintenance: 0.125-0.25 mg daily. Consider drug interactions with amiodarone, verapamil, quinidine, and macrolides.
Take exactly as prescribed; do not double up doses.,Monitor for signs of toxicity: nausea, vomiting, vision changes (yellow-green halos), arrhythmias.,Keep medication out of reach of children; immediate medical attention if overdose suspected.,Do not stop abruptly without consulting healthcare provider.,Inform healthcare provider of all medications, including OTC and herbal supplements.
Take digoxin exactly as prescribed, usually once daily. Do not miss doses or double up.,Monitor pulse before each dose; hold and contact prescriber if heart rate <60 bpm.,Report symptoms of toxicity: nausea, vomiting, diarrhea, blurred vision, yellow-green halos, confusion, or irregular heartbeat.,Avoid over-the-counter antacids, laxatives, or kaolin-pectin; they reduce absorption. Take digoxin 2 hours apart from such products.,Maintain consistent intake of potassium-rich foods (bananas, oranges) unless otherwise instructed. Avoid excessive salt substitutes.,Keep all appointments for blood tests (digoxin levels, potassium, kidney function).,Store at room temperature away from light and moisture.
"Eflornithine, an ornithine decarboxylase inhibitor used in the treatment of African trypanosomiasis and hirsutism, may reduce the therapeutic efficacy of digoxin, a cardiotonic glycoside used for heart failure and atrial fibrillation. The proposed mechanism involves eflornithine-induced alterations in gastrointestinal motility or absorption, potentially decreasing digoxin bioavailability. This could lead to subtherapeutic digoxin levels, diminished inotropic and chronotropic effects, and increased risk of arrhythmias or worsening heart failure."
"Osimertinib, a tyrosine kinase inhibitor used in non-small cell lung cancer, can inhibit P-glycoprotein (P-gp) transport in the gastrointestinal tract and kidneys, leading to increased absorption and reduced renal clearance of digoxin. This elevation in serum digoxin concentration heightens the risk of digoxin toxicity, including cardiac arrhythmias (e.g., bradycardia, atrial tachycardia with block) and gastrointestinal symptoms such as nausea and vomiting. Clinical monitoring for digoxin toxicity is warranted, especially when initiating or adjusting osimertinib therapy."
"Lenvatinib, a tyrosine kinase inhibitor, may reduce the therapeutic efficacy of digoxin by interfering with its cardiotonic effects. This interaction could lead to decreased inotropic support in patients with heart failure, potentially worsening cardiac function and clinical outcomes. The clinical consequence is a possible loss of rate control in atrial fibrillation or diminished contractility in systolic dysfunction."
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about DIGOXIN PEDIATRIC vs LANOXIN, answered by our medical review team.
DIGOXIN PEDIATRIC is a Cardiac Glycoside that works by Inhibits sodium-potassium ATPase, increasing intracellular sodium, which promotes calcium influx via sodium-calcium exchanger, enhancing cardiac contractility. Also increases vagal tone, slowing AV conduction.. LANOXIN is a Cardiac Glycoside that works by Inhibits Na+/K+ ATPase, increasing intracellular Ca2+ via Na+/Ca2+ exchange, enhancing cardiac contractility and reducing conduction through AV node.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between DIGOXIN PEDIATRIC and LANOXIN depend on the specific clinical indication. These are both Cardiac Glycoside agents and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of DIGOXIN PEDIATRIC is: For pediatric patients, digoxin pediatric dosing is weight-based; no standard adult dose. Typical pediatric loading dose: 10-12 mcg/kg orally divided every 6-8 hours, with maintenance: 5-10 mcg/kg/day divided every 12 hours. For infants <1 month, loading: 10-15 mcg/kg, maintenance: 4-6 mcg/kg/day. For children 1-24 months, loading: 15-20 mcg/kg, maintenance: 5-8 mcg/kg/day. For children >2 years, loading: 10-15 mcg/kg, maintenance: 3-5 mcg/kg/day.. The standard adult dose of LANOXIN is: 0.125-0.25 mg orally once daily; loading dose 0.5-0.75 mg orally divided over 24-48 hours if rapid digitalization required.. Dosing should always be individualized based on indication, renal and hepatic function, age, and other patient factors.
No direct drug-drug interaction has been formally documented between DIGOXIN PEDIATRIC and LANOXIN in current clinical databases. However, individual patient risk factors including other medications, organ function, and comorbidities should always be evaluated by a qualified healthcare provider.
The maternal-fetal safety profiles differ. DIGOXIN PEDIATRIC is classified as Category A/B. Digoxin crosses the placenta. First trimester: No increased risk of major malformations reported in human studies. Second/third trimester: Potential for fetal toxicity (e.g., brady. LANOXIN is classified as Category C. Digoxin crosses the placenta. First trimester: No increased risk of major malformations reported in human studies; animal studies show no teratogenicity at clinically relevant dose. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.