Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
DIGOXIN PEDIATRIC vs CEDILANID-D
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.
Digitalis glycoside; inhibits Na+/K+-ATPase, increasing intracellular calcium and cardiac contractility.
Heart failure (FDA-approved for pediatric patients with heart failure),Atrial fibrillation (off-label for rate control in pediatric patients)
Heart failure,Atrial fibrillation,Atrial flutter
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.
0.05 to 0.2 mg intravenously or intramuscularly, administered slowly over 5 minutes; initial dose 0.15 to 0.2 mg, then 0.1 to 0.15 mg every 30 minutes up to a total of 0.4 mg. Oral: 0.05 to 0.2 mg daily for maintenance.
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 36-48 hours in patients with normal renal function; prolonged to >100 hours in severe renal impairment, requiring dose adjustment.
Primarily renally excreted unchanged; minimal hepatic metabolism (mostly via reduction, hydrolysis, and conjugation in older children).
Hepatic (minor); primarily renally excreted unchanged.
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 accounts for 60-70% of elimination; biliary/fecal excretion accounts for 30-40%, with enterohepatic circulation present.
25% bound to serum albumin; binding decreases in uremia and hyperbilirubinemia.
25-30% bound to plasma 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).
6-10 L/kg; large Vd indicates extensive tissue distribution and high cardiac tissue affinity.
Oral: 60-80% (elixir 70-85%, tablets 60-75%); IM: 70-85% (but erratic absorption and pain limit use); IV: 100%.
Oral: 70-80%; IV: 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: reduce dose by 50% or extend dosing interval to every 36-48 hours. GFR <10 m L/min: avoid use or reduce dose by 75%.
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.
Child-Pugh Class A: no adjustment. Child-Pugh Class B: reduce dose by 25-50%. Child-Pugh Class C: avoid use or reduce dose by 75%.
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.
Digitalizing dose: 0.01-0.02 mg/kg IV or IM, given in divided doses over 24 hours. Maintenance: 10-20% of digitalizing dose daily. Not recommended for neonates due to prolonged half-life.
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.
Reduce dose by 25-50% due to decreased renal function and increased sensitivity. Monitor serum levels and renal function closely.
Toxicity can be life-threatening. Use caution in renal impairment, electrolyte disturbances (hypokalemia, hypomagnesemia, hypercalcemia). Narrow therapeutic index requires monitoring.
Can cause potentially fatal arrhythmias; use only when clearly indicated and monitor serum levels.
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.
Narrow therapeutic index; toxicity risk increased with hypokalemia, hypomagnesemia, hypercalcemia, renal impairment; monitor ECG and drug levels.
Ventricular fibrillation, hypersensitivity to digitalis preparations, hypokalemia (uncorrected), hypercalcemia (uncorrected), AV block (second or third degree) unless pacemaker present.
Ventricular fibrillation, digitalis toxicity, hypersensitivity, AV block (unless pacemaker present), Wolff-Parkinson-White syndrome.
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.
Avoid licorice, which can cause hypokalemia. Maintain consistent intake of potassium-rich foods (bananas, oranges) to avoid fluctuations. No known significant food interactions beyond electrolyte effects.
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.
Pregnancy Category C. First trimester: No adequate human studies; animal studies show fetal risk. Second/third trimester: Risk of fetal bradycardia, cardiac glycoside toxicity; avoids if possible.
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.
Deslanoside is excreted in breast milk; estimated infant dose 0.1-0.5% of maternal weight-adjusted dose; M/P ratio not well defined. Monitor infant for bradycardia, feeding difficulties; benefit likely outweighs risk.
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.
Increased renal clearance in pregnancy may require higher doses; monitor serum drug levels and adjust accordingly. Reduced dosing in third trimester may be needed due to volume expansion.
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.
Cedilanid-D (deslanoside) is a rapidly acting parenteral digitalis glycoside. Use with extreme caution in renal impairment due to reduced clearance. Monitor serum potassium and magnesium; hypokalemia and hypomagnesemia potentiate toxicity. Administer slow IV push over 5 minutes to avoid arrhythmias. Therapeutic drug monitoring less common due to short half-life of 33 hours. Contraindicated in ventricular tachycardia and AV block (unless due to atrial fibrillation).
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 exactly as prescribed; do not double doses.,Report symptoms of toxicity: nausea, vomiting, visual disturbances (yellow-green halos), irregular heartbeat.,Avoid over-the-counter medications without consulting doctor.,Maintain consistent potassium intake; avoid high-potassium foods or supplements unless advised.,Monitor daily weight and report rapid weight gain or edema.
"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 CEDILANID-D, 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.. CEDILANID-D is a Cardiac Glycoside that works by Digitalis glycoside; inhibits Na+/K+-ATPase, increasing intracellular calcium and cardiac contractility.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between DIGOXIN PEDIATRIC and CEDILANID-D 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 CEDILANID-D is: 0.05 to 0.2 mg intravenously or intramuscularly, administered slowly over 5 minutes; initial dose 0.15 to 0.2 mg, then 0.1 to 0.15 mg every 30 minutes up to a total of 0.4 mg. Oral: 0.05 to 0.2 mg daily for maintenance.. 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 CEDILANID-D 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. CEDILANID-D is classified as Category C. Pregnancy Category C. First trimester: No adequate human studies; animal studies show fetal risk. Second/third trimester: Risk of fetal bradycardia, cardiac glycoside toxicity; avo. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.