Uterine hyperstimulation

Systematic review has found vaginal misoprostol in the dosages used to be associated with more uterine hyperstimulation with non-reassuring fetal heart rate changes than is PGE2. As misoprostol was also more potent as a uterine stimulant in these trials, it is difficult to be sure whether the difference is pharmacological or purely dose related.


Meconium-stained liquor is significantly more common with labour induction with misoprostol than with either vaginal or intracervical PGE2. We have previously postulated that certain myometrial stimulants may cross the placenta to stimulate fetal bowel smooth muscle and cause meconium passage. However, misoprostol and dinopros-tone have similar stimulatory effects on rat ileum relative to the myometrial effect [12]. An alternative explanation for the increased meconium passed during misoprostol induction of labour is that the resistance of misopros-tol to placental 15-hydroxyprostaglandin dehydrogenase enables more misoprostol to enter the fetal circulation than does PGE2.


Precipitate delivery (labour < 2 h) has been described as a complication of misoprostol. Most reviews and trials have not documented the occurrence of precipitate delivery. In fact 'mean time to delivery' is frequently given as a primary endpoint. Precipitate deliveries may contribute to apparently favourable mean induction to delivery times, without being identified as an unfavourable outcome. The importance of precipitate delivery is that it may be a marker for excessive uterine response to misoprostol and risk of uterine rupture.


There have been numerous reports of rupture of an unscarred uterus following misoprostol labour induction, including a maternal death within 7hof labour induction with one dose of misoprostol 50 ^g vaginally in a healthy woman with uneffaced cervix. Without a reliable basis of comparison, it is unclear whether the risk of uterine rupture following misoprostol induction is greater or less than with other methods of labour induction.


Several cases of rupture of uterine scars following misoprostol induction have been reported. A recent retrospective study found significantly more cases of uterine rupture or dehiscence following cervical ripening with misoprostol than when oxytocin or prostaglandin E2 were used. Misoprostol should not be used in women with uterine scars.


The relationship between misoprostol use and Caesarean section is a complex one. The trend in randomized trials has been an increase in Caesarean sections for fetal heart rate abnormality and a reduction for poor progress of labour, giving a reduction overall.


Despite increases in uterine hyperstimulation, most reviews and trials have shown no significant difference in perinatal outcome following misoprostol labour induction versus other methods.


Increased post-partum haemorrhage was noted in a retrospective study of misoprostol induction compared with the general obstetric population (58/1037 versus

394/11255) and in a randomized trial following labour induction with vaginal misoprostol 50 ^g versus 25 ^g 4-hourly (9.8 versus 2.2%).

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