CRYSTODIGIN
Clinical safety rating: caution
Comprehensive clinical and safety monograph for CRYSTODIGIN (CRYSTODIGIN).
Cardiac glycoside that inhibits the Na+/K+-ATPase pump, leading to increased intracellular sodium, which in turn promotes calcium influx via the Na+/Ca2+ exchanger, resulting in increased myocardial contractility (positive inotropy). It also has negative chronotropic and dromotropic effects via vagomimetic action.
| Metabolism | Primarily renal excretion; minimal hepatic metabolism. Not significantly metabolized by cytochrome P450 enzymes. |
| Excretion | Primarily renal excretion of unchanged drug; ~80-90% eliminated in urine, ~10-20% in feces via biliary excretion. |
| Half-life | Terminal elimination half-life approximately 1.6–1.9 days (38–45 hours) in patients with normal renal function; prolonged in renal impairment. |
| Protein binding | ~20–25% bound to plasma proteins, primarily albumin. |
| Volume of Distribution | Vd approximately 5–10 L/kg, indicating extensive tissue distribution; clinical significance: large Vd means low plasma concentration relative to total body load, necessitating loading doses. |
| Bioavailability | Oral: 60–80% (variable, depends on formulation and gastrointestinal factors); Intravenous: 100%. |
| Onset of Action | Intravenous: 5–30 minutes; Oral: 0.5–2 hours. |
| Duration of Action | Therapeutic effect persists for 3–4 days after cessation due to slow elimination; clinical monitoring of toxicity signs recommended. |
0.5 mg intravenously over 2-4 hours, then 0.25 mg every 6 hours as needed up to a total of 1.5 mg in 24 hours.
| Dosage form | INJECTABLE |
| Renal impairment | CrCl 10-50 mL/min: reduce dose by 25-50%; CrCl <10 mL/min: reduce dose by 50-75% or use alternative. |
| Liver impairment | Child-Pugh class B: reduce dose by 50%; Child-Pugh class C: avoid use. |
| Pediatric use | Loading dose: 10-20 mcg/kg intravenously over 2-4 hours; maintenance: 5-10 mcg/kg every 6 hours as needed. |
| Geriatric use | Start at lower end of dosing range (0.25 mg intravenously), adjust based on renal function and response, monitor for toxicity. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for CRYSTODIGIN (CRYSTODIGIN).
| Breastfeeding | Excreted in breast milk in low concentrations (M/P ratio approximately 0.75-1.0). Considered compatible with breastfeeding; monitor infant for signs of toxicity (bradycardia, vomiting). |
| Teratogenic Risk | Pregnancy Category C. First trimester: Association with fetal cardiac glycoside toxicity and malformations in animal studies; limited human data. Second trimester: Potential for fetal bradycardia and hypoxia due to placental transfer. Third trimester: Risk of neonatal digitalis toxicity, including arrhythmias and heart block. |
■ FDA Black Box Warning
None.
| Serious Effects |
["Ventricular fibrillation","Known hypersensitivity to digoxin or other digitalis glycosides","Hypercalcemia","Hypokalemia (uncorrected)","Atrioventricular block (second- or third-degree) unless a pacemaker is present","Hypertrophic obstructive cardiomyopathy (relative contraindication)"]
| Precautions | ["Narrow therapeutic index; toxicity can be life-threatening.","Hypokalemia, hypomagnesemia, and hypercalcemia increase risk of digoxin toxicity.","Electrolyte monitoring and dose adjustment in renal impairment.","Patients with acute myocardial infarction, myocarditis, or severe pulmonary disease may be at increased risk of arrhythmias."] |
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| Fetal Monitoring |
| Maternal: Serum digoxin levels, ECG, renal function, electrolytes (K+, Mg2+). Fetal: Heart rate monitoring, ultrasound for hydrops or arrhythmias. Neonatal: ECG and serum digoxin levels at birth. |
| Fertility Effects | No known direct effects on fertility in humans. Animal studies show no impairment at therapeutic doses. |