Discussion
We found that after a previous caesarean section women who had not previously given birth vaginally and those who had labour induced with prostaglandin were at increased risk of uterine rupture. The same two factors were associated with the risk of perinatal death due to uterine rupture. In contrast, delivering in a hospital with low throughput was not associated with uterine rupture overall but was associated with an increased risk of perinatal death due to uterine rupture. We found that uterine rupture was three times more likely to result in death of the infant if the delivery took place in a hospital with births a year. Confining trials of labour to larger obstetric units may therefore reduce the risk of perinatal death associated with uterine rupture during a trial of labour.
The finding that units with high throughput had lower rates of perinatal death due to uterine rupture is plausible. Hospitals with greater throughput are more likely to have resident obstetric, anaesthetic, and neonatal services as well as a dedicated obstetric operating theatre. These factors would allow a faster response to fetal distress due to uterine rupture, which in turn would allow more rapid delivery and resuscitation of the neonate. We did not have information on the structure of services at each unit over the period of study. However, the factors are likely to be highly correlated and interdependent. A unit with no resident obstetric or anaesthetic cover is unlikely to have a dedicated obstetric operating theatre or a resident experienced neonatologist. Therefore, even if these data were available, it would be extremely difficult to determine the independent contributions of each of these factors in reducing the risk of death. Therefore, the total number of births is a useful composite measure of the level of support and has the pragmatic advantage of being easy to define.
Study strengths and weaknesses
Previous large scale analyses of the factors determining uterine rupture could not reliably distinguish between asymptomatic dehiscence of the previous caesarean section scar and clinically significant, symptomatic uterine rupture.1 8 9 The failure to define the event may lead to ascertainment bias. As asymptomatic dehiscence of the scar will generally be identified during a subsequent caesarean section, there will be increased ascertainment of uterine rupture for any exposure that is associated with an increased risk of caesarean delivery. As we were able to study perinatal death due to uterine rupture, this allowed us to identify catastrophic rupture that would be ascertained irrespective of the mode of delivery. We conclude that the associations between uterine rupture and no previous vaginal birth and induction of labour with prostaglandin are unlikely to be explained by ascertainment bias. Previous studies have suggested that the protective effect of a previous vaginal birth is observed whether it preceded or followed the first caesarean delivery.10
Findings are comparable with previous studies
The estimates of absolute risk in the present analysis are comparable with those from previous studies. The overall rate of successful vaginal delivery of 74.2% is similar to the generally quoted overall figure of 75%.11 The overall rate of uterine rupture of 0.35% is consistent with that reported in a previous large scale Swiss study.9 The overall risk of perinatal death due to uterine rupture (one in 2100) is similar to the one in 2600 reported in a study from Washington State, USA.1 The risk among large obstetric units (one per 4700) is similar to a case series from a large obstetric centre in California (one per 4200).12 Although the total number of perinatal deaths in our study was relatively small (17), this is almost three times more than reported in a recent meta-analysis of all previous studies.13 Guise et al commented that the risk of death in Scotland, as cited from our previous report,2 was 10 times higher than reported in other studies.13 However, the figure they quoted was for perinatal death due to all causes related to delivery. The absolute risk of death due to uterine rupture in our previous study (4.5 per 10 000) was similar to the overall risk in our current analysis. Both fall within the 95% confidence intervals of the meta-analysis. We believe that the current data give the best estimate of the absolute risk of perinatal death among women attempting vaginal birth after caesarean.
A previous population based study had shown an association between induction of labour with prostaglandin and uterine rupture.1 This finding led the American College of Obstetricians and Gynecologists to recommend avoidance of prostaglandin in women with a previous caesarean section. However, the number of women was small (366) and this was less than 2% of the study population. In the present study, we had data on 4475 women who had labour induced with prostaglandin, which was 12.5% of our cohort. Our analyses confirmed that induction of labour with prostaglandin, but not other methods, was independently associated with an increased risk of uterine rupture, including catastrophic rupture leading to perinatal death. It remains to be determined whether this is due to a specific pharmacological effect or whether the use of prostaglandin is merely a marker for a woman with an unfavourable cervix.
We defined trial of labour as any woman who had a single previous caesarean birth who was delivered at term by a means other than planned caesarean section. The cohort studied probably includes some women who were due for planned repeat caesarean section but attended in early labour, had an emergency caesarean delivery, and did not truly attempt vaginal birth. However, women delivering at or after 40 weeks are unlikely to have requested planned repeat caesarean section. We found that the nature and strength of associations in the present study were similar when we confined analyses to births at or after 40 weeks' gestation, and misclassification of attempted vaginal birth is unlikely to have significantly affected our results.
Conclusion
In summary, we have shown that the risk of uterine rupture is increased among women who have not previously given birth vaginally and those undergoing induction of labour with prostaglandin. Our data show that the risk of consequent death of the infant is lower in obstetric units with higher throughput. Although other interpretations could be made, we believe the most plausible explanation for these findings is that the facilities generally available at larger obstetric units reduce the risk of perinatal death in the event of uterine rupture. The same is probably true of other obstetric emergencies. Perinatal deaths could, therefore, potentially be reduced by confining high risk births to large obstetric units or by providing additional facilities at smaller units.
Answers to all your Biology Questions
