Expert Commentary

Prostaglandin E2, oxytocin may raise risk of rupture after previous cesarean

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Context

When labor does not begin spontaneously and delivery is indicated, the question of risk with labor induction becomes a critical issue—especially for women with a previous lower-segment cesarean delivery, most of whom are candidates for a trial of labor with their next pregnancy.

Objective

To compare maternal and neonatal outcomes of spontaneous and induced labor following 1 previous cesarean delivery.

Method

A population-based study of 3,746 women (2,943 spontaneous and 803 induced labors) with 1 previous cesarean delivery who underwent a trial of labor between January 1992 and January 2000.

Outcome

Researchers noted a trend toward higher uterine rupture rates in women who had induced labor by any method compared to spontaneous labor (0.7% versus 0.3%, P = .128), as well as in women who underwent dinoprostone (prostaglandin E2 [PGE2]) versus other induction methods, (1.1% versus 0.6%, P = .62), though neither outcome was statistically significant.

The induced-labor group had more frequent:

  • early postpartum hemorrhage (7.3% versus 5%; odds ratio [OR] 1.66; 95% confidence interval [CI] 1.18, 2.32)
  • cesarean delivery (37.5% versus 24.2%; OR 1.84; 95% CI 1.51, 2.25)
  • neonatal intensive care unit admission (13.3% versus 9.4%; OR 1.69; 95% CI 1.25, 2.29)

Expert Commentary

The proportion of women undergoing a trial of labor after cesarean delivery has been decreasing since the mid-1990s, and optimal management of these women is controversial. What’s more, for over a decade we have been increasing labor induction rates for all women in all gestational age ranges.1

An association between PGE2 and rupture of a uterine scar was reported more than 20 years ago.2 Unfortunately, since that time, only a handful of studies with more than 100 patients have explored this association. Even fewer studies have evaluated the risk of induction with oxytocin for women undergoing a trial of labor after prior cesarean.

My colleagues and I were able to document a rate of uterine rupture of 2.3% for women undergoing induction with oxytocin, compared with 0.7% for those who had spontaneous labor.3 More recently, an increased rate of uterine rupture was reported in women induced without prostaglandins compared to women undergoing repeat cesarean, with a relative risk of 4.9 (95% CI 2.4, 9.7).4

Oxytocin, PGE2 were assessed, but not mechanical induction or artificial rupture. Delaney and Young endeavor to put these risks into perspective. They were able to specifically assess the effects of oxytocin and PGE2 among the 803 women who had labor induced.

Unfortunately, the number of women who experienced artificial rupture of membranes and mechanical methods of induction was inadequate to draw conclusions.

Did a statistical error occur? The difference in the rate of uterine rupture for women with spontaneous labor was not statistically significant compared to those receiving oxytocin (n = 600) or PGE2 (n = 179), yet the risk of uterine rupture in the oxytocin group more than doubled, and almost quadrupled among those receiving PGE2. Thus, the possibility of a type II statistical error must be strongly considered.

Rupture risk is almost 3 times greater for women receiving PGE2 but less than twofold higher for women given oxytocin compared to those in spontaneous labor.

Combined data suggest heightened risk of rupture. When this study is combined with previous studies,3,4,6 the rate of rupture is 1.7% with PGE2 and 0.62% with spontaneous labor (P <.0001 similarly using data from the same studies women whose labor was induced with oxytocin had a rupture rate of versus in spontaneous>P = .005).

(The rates of uterine rupture for those in spontaneous labor vary slightly due to the inclusion of different sets of studies evaluating these 2 questions in the review by Sanchez-Ramos et al.6)

Clinical difference. Although both differences are statistically significant, the clinical differences vary. Those receiving PGE2 have a risk of rupture almost 3 times greater than women in spontaneous labor, and those receiving oxytocin have less than a twofold increased risk.

All conclusions are based on studies that are not randomized, which limits the strength of any recommendations.

Other risks linked to induction: cesarean, neonatal intensive care unit admission, hemorrhage. Uterine rupture is not the only complication of labor induction in women with a prior cesarean. Delaney and Young also document an increased risk of cesarean delivery, admission to a neonatal intensive care unit, and early postpartum hemorrhage.

Their findings confirm those reported among gravidas undergoing labor induction without a prior cesarean.7,8 The presence of a uterine scar is associated with uterine rupture, and induction itself remains a significant risk factor for these other adverse outcomes.

Bottom line

The risk of rupture with PGE2 induction. This study, when combined with current literature, suggests a greater risk of uterine rupture when PGE2 is used to induce labor in women with a prior cesarean. This risk is likely higher than many women would find acceptable.

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