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Out of 104 cases of induced labour, it was found that in 60% of the cases the fetal head presented itself in an occipito-posterior position. This unusually high percentage has not been explained.
A triad consisting of (a) prostaglandin F2 alpha infusion, (b) dilation of the uterine cervix by low frequency vibrations and (c) early low amniotomy was used to induce labor in ten women after intrauterine fetal death had occurred. Vaginal delivery was successful in all cases, with a mean induction-to-delivery interval of 5.4 +/- 0.8 hours. Vibratory dilation effectively prepares the cervix for the intense prostaglandin-induced uterine contractions and thereby reduces the risk of cervical laceration and fistula. The dilation of the cervical canal also makes an early low amniotomy possible and easy. This study demonstrates a highly effective, safe and relatively nontraumatic method for uterine evacuation after intrauterine fetal death.
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OBJECTIVES: Both the onset of labor and time to delivery during betamethasone-induced delivery are delayed by omega-3 polyunsaturated fatty acid (PUFA) administration to pregnant sheep. That fatty acid also inhibits the labor-related increase in maternal plasma estradiol and maternal and fetal prostaglandin E(2). To evaluate the mechanism of inhibition of prostaglandin production and delay of onset of labor and time of delivery in PUFA-treated sheep, we determined the effect of PUFA on myometrial prostaglandin H synthase (PGHS) 1 and 2 and oxytocin receptor mRNA levels in betamethasone-induced labor. METHODS: At 124 days' gestation, a 20% emulsion of either intralipid (IL, n = 6) or PUFA (n = 6) was infused continuously (3 mL/kg per day) intravenously (IV) to the ewe. At 125 days' gestation, betamethasone was administered IV (10 microg/h over 48 hours) to fetuses of both intralipid- and PUFA-treated ewes. Myometrium was collected at necropsy either during betamethasone-induced labor as evaluated by myometrial electromyography or within 5 days of the termination of betamethasone infusion, if delivery did not occur after fetal betamethasone infusion. Total myometrial RNA was analyzed by Northern blot for oxytocin receptor and PGHS1 and 2 mRNA normalized for 18s. RESULTS: Treatment with PUFA decreased myometrial PGHS2 mRNA but did not alter myometrial PGHS1 and oxytocin receptor mRNA after betamethasone administration. CONCLUSIONS: This finding provides a mechanism whereby PUFA delays betamethasone-induced delivery in sheep and suggests a potential role of PUFA as an effective tocolytic agent in human pregnancy.
The authors report on a series of 1 838 deliveries of which 358 (19.5%) were induced. The caesarean section rate when induction was undertaken for social convenience (delivery on pre-set dates) was 1.7%, but when induction had to be carried out the caesarean section rate was 10%. Fetal and maternal morbidity when induction was carried out on social grounds was the same as for the general population. The number of inductions that were performed was not sufficiently large to alter the work rate in the labour ward and the ways in which this could be evened out are discussed. We have considered the different techniques to ripen the cervix, particularly when premature induction by rupture of the membranes is required.
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Saliva specimens were collected approximately every 6 hours from day 280 to day 294 by 16 women who labored on day 294. There was a normal rise in the mean saliva estriol/progesterone ratio in the six who went into labor spontaneously but no change in the 10 whose labor was induced.
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Labor was induced for medical reasons at or near term in altogether 200 patients. All women had amniotomy and were then randomly assigned to either oral prostaglandin E2 (PGE2) or intravenous infusion of oxytocin (Oxy). In this study PGE2 and Oxy treatment were compared with respect to time to contractions. Other not randomized but prognostic variables compared here were, e.g. dilatation, parity and Bishop score. All comparisons were performed with the life table technique. Labor was established earlier in the Oxy group than in the PGE2 group of patients. In both treatment groups parity and dilatation were more strongly related to start of contractions than to Bishop score.
Oral prostaglandin E2 appears to play a dual role in human parturition. It induces normal uterine contractions and softens the cervix, thereby decreasing the resistance of the cervix to dilatation. Labor and delivery with oral PGE2 is achieved with less total uterine work when compared with spontaneous nonstimulated labor. This contention is supported by the fact that the rate of cervical dilatation in the active phase of labor is faster (2.73 cm/hr) than that reported by Hendricks et al. for ideal labor (2.12 cm/hour), yet uterine contractility is not increased. Analysis of the composite data of Friedman and Sachtleman in 1974 also shows a more rapid active phase dilatation in the PGE2-stimulated labors (3.3 cm/hour) as compared with spontaneous labor (2.98 cm/hour). Oral PGE2 offers a safe and efficacious alternative to oxytocin for the induction of labor in women. It appears to have a major advantage over oxytocin. The softening effect of PGE2 on the cervix would make this drug an ideal agent for use in patients with low Bishop scores who have medical indications for induction of labor. Regardless of route of administration, prostaglandin E2 is a potent uterine stimulant and must be used with the same precautions and safeguards as intravenous oxytocin.
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Amniotic fluid prostaglandin levels were measured serially in 15 patients who underwent successful induction of labor and compared with those of patients presenting in spontaneous labor. At comparable cervical dilation the induced group demonstrated significantly lower prostaglandin levels. Four of these patients delivered without any increment in prostaglandins while in the remaining patients increases in prostaglandins followed the attainment of efficient uterine contractions by several hours. These data support the hypothesis that oxytocin acts directly on myometrial cells and not primarily by prior generation of prostaglandin synthesis in the membranes.
Prostaglandin E2 (PGE2), but not oxytocin, treatment to induce parturition brought about an increase (p less than 0.001) in maternal serum levels of total estrogens (conjugated and nonconjugated estriol). There was no increase in nonconjugated estriol. To explore if the changes were related to an altered enterohepatic circulation, cholic acid assay in maternal serum was used. There were no changes in cholic acid which parallelled those in total estrogens. It is concluded that PGE2 does not appear to affect enterohepatic circulation of steroids, and it is suggested that the increase in total estrogens may be caused by changes in the kidney excretion of estriol.
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Intravenous ethanol infusion significantly reduced oxytocin-induced uterine activity in pregnant patients at term. The dose response to oxytocin was linear when plotted log2 x in all patients studied, and the line was shifted to the right by alcohol, but the slope remained essentially unchanged. These results suggest that alcohol directly inhibits the effect of oxytocin on the myometrium, although the possibility of some central inhibition of oxytocin release cannot be discounted.