OXYTOCIN 10 USP UNITS IN DEXTROSE 5%
Clinical safety rating: caution
Comprehensive clinical and safety monograph for OXYTOCIN 10 USP UNITS IN DEXTROSE 5% (OXYTOCIN 10 USP UNITS IN DEXTROSE 5%).
Increases intracellular calcium in uterine myofibrils, stimulating contractions. Binds to oxytocin receptors in myometrium and mammary glands.
| Metabolism | Metabolized primarily by oxytocinase in the liver, kidney, and placenta. Also degraded by peptidases in the gastrointestinal tract when given orally (not clinically used). |
| Excretion | Renal: >99% as unchanged drug; <1% hepatic metabolism and biliary excretion. |
| Half-life | Terminal half-life: 1-6 minutes (IV); clinical effect ceases rapidly after infusion stops due to rapid clearance. |
| Protein binding | Low; approximately 30%, primarily bound to albumin. |
| Volume of Distribution | 0.2-0.3 L/kg; reflects distribution primarily in extracellular fluid. |
| Bioavailability | IV: 100%; IM: approximately 80-85%. |
| Onset of Action | IV: 1 minute; IM: 3-5 minutes. |
| Duration of Action | IV: 30-60 minutes (after infusion end); IM: 2-3 hours. |
IV infusion: 0.5-2 mU/min, increased by 1-2 mU/min every 30-60 min until desired uterine activity, then reduce; max 20 mU/min.
| Dosage form | INJECTABLE |
| Renal impairment | No specific GFR-based dose adjustment for oxytocin. Use with caution in severe renal impairment due to fluid overload risk from dextrose 5%. |
| Liver impairment | No specific Child-Pugh-based adjustment. Use with caution in severe hepatic impairment. |
| Pediatric use | Not indicated in pediatric patients. Use in adolescents for labor induction similar to adult dosing. |
| Geriatric use | Not typically used in geriatric population. If used, start at low end of dosing range and monitor for fluid overload and cardiovascular effects. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for OXYTOCIN 10 USP UNITS IN DEXTROSE 5% (OXYTOCIN 10 USP UNITS IN DEXTROSE 5%).
| Breastfeeding | Exogenous oxytocin is rapidly metabolized in maternal plasma and gastrointestinal tract; it is not orally bioavailable to the infant. Endogenous oxytocin is essential for milk ejection. No M/P ratio is established; however, systemic levels from exogenous administration are negligible in breast milk. Considered compatible with breastfeeding. |
| Teratogenic Risk | Oxytocin is not associated with structural teratogenicity. In the first trimester, no increased risk of congenital anomalies has been reported. In the second and third trimesters, exogenous oxytocin is used therapeutically for induction/augmentation of labor and may cause uterine hyperstimulation, leading to fetal distress, hypoxia, or preterm birth if not properly monitored. |
■ FDA Black Box Warning
Oxytocin should be administered only by intravenous infusion with careful monitoring. Severe adverse effects, including uterine rupture, water intoxication, and fetal distress, can occur. It is not intended for prolonged use.
| Serious Effects |
["Hypersensitivity to oxytocin","Cephalopelvic disproportion","Fetal distress where vaginal delivery is not imminent","Uterine scarring (e.g., prior cesarean section)","Placenta previa"]
| Precautions | May cause uterine hyperstimulation leading to fetal distress, uterine rupture, or maternal death. Risk of water intoxication with high doses or prolonged infusion. Monitor maternal vital signs, uterine activity, and fetal heart rate continuously. |
Loading safety data…
| Fetal Monitoring | Continuous fetal heart rate monitoring and maternal uterine activity monitoring are required. Assess maternal vital signs, fluid balance (risk of water intoxication), and signs of uterine hyperstimulation. Monitor for fetal bradycardia, late decelerations, or variable decelerations, and adjust infusion rate accordingly. |
| Fertility Effects | Oxytocin does not affect fertility. It is used therapeutically during labor and has no known impact on ovulation, implantation, or gamete transport. No endogenous hormonal disruption relevant to fertility. |