QLexNursing

Uterine rupture

🟣 Excessive uterine stimulation from oxytocin can overwhelm scarred or overstretched myometrium, predisposing to uterine rupture, especially with TOLAC/VBAC, grand multiparity, or uterine overdistension.

🟣 Clinical red flags include sudden, severe abdominal pain, loss of fetal station, abnormal fetal heart rate (FHR), and vaginal bleeding, sometimes with cessation or weakening of contractions.

🟣 Rupture compromises maternal hemodynamics and fetal oxygenation, making it a time-critical obstetric emergency.

🟣 Prevention centers on low-dose titration, strict adherence to institutional protocols, and continuous electronic fetal monitoring (EFM).

🟣 Immediate actions when suspected: stop oxytocin, call obstetrics/anesthesia, prepare for urgent laparotomy, and stabilize the mother with IV access and blood products as indicated.

Uterine tachysystole

🟣Oxytocin can cause uterine tachysystole, classically >5 contractions in 10 minutes averaged over 30 minutes, or prolonged contractions/hypertonus with inadequate relaxation.

🟣Tachysystole reduces uteroplacental perfusion, increasing risk of fetal hypoxemia and late decelerations, necessitating prompt intervention.

🟣Nursing priorities: stop or reduce oxytocin, reposition the patient (left lateral), IV fluid bolus, and apply oxygen if indicated to optimize fetal oxygen delivery.

🟣 If hyperstimulation persists, tocolysis (e.g., terbutaline per protocol) may be used to restore a safer contraction pattern.

🟣Close documentation of contraction frequency, duration, resting tone, and FHR responses is essential for maternal–fetal safety.

Placental abruption

🟣Oxytocin-induced hyperstimulation and increased intrauterine pressure can precipitate shearing forces at the uteroplacental interface, risking premature placental separation.

🟣Hallmarks include painful vaginal bleeding, uterine tenderness/rigidity (hypertonus), and nonreassuring FHR patterns, signaling compromised fetal oxygenation.

🟣Abruption threatens maternal hemorrhage and coagulopathy; rapid recognition and escalation of care are critical.

🟣Management focuses on discontinuing oxytocin, resuscitating the mother (fluids, blood products as needed), and expediting delivery when indicated.

🟣Prevention depends on careful dosing, avoiding tachysystole, and continuous EFM to identify fetal distress early.

Water intoxication (hyponatremia)

🟣Oxytocin has antidiuretic (vasopressin-like) properties; high doses or prolonged infusions with hypotonic fluids can cause water retention and dilutional hyponatremia.

🟣Early findings include headache, nausea, vomiting, lethargy, progressing to confusion, seizures, or coma with severe Na⁺ decline.

🟣Risk mitigation requires using isotonic carriers, limiting total free water, monitoring intake/output, and checking serum sodium during prolonged inductions.

🟣If suspected, stop oxytocin, assess electrolytes, implement fluid restriction, and treat significant hyponatremia per protocol (e.g., hypertonic saline under close monitoring).

🟣Education emphasizes that not “water loss” but water retention is the concern—hence vigilance for neurologic changes and strict fluid balance is vital.