BMJ  2004;329:375 (14 August), doi:10.1136/bmj.38160.634352.55 (published 19 July 2004)

Paper

Factors predisposing to perinatal death related to uterine rupture during attempted vaginal birth after caesarean section: retrospective cohort study

Gordon C S Smith, professor1, Jill P Pell, consultant2, Dharmintra Pasupathy, specialist registrar3, Richard Dobbie, senior statistician4

1 Department of Obstetrics and Gynaecology, Cambridge University, Cambridge CB2 2QQ, 2 Department of Public Health, Greater Glasgow NHS Board, Glasgow G3 8YU, 3 Departments of Obstetrics and Gynaecology, Addenbrooke's NHS Trust, Cambridge CB2 2SW, 4 Information and Statistics Division, Common Services Agency, Edinburgh EH5 3SE

Correspondence to: G C S Smith gcss2{at}cam.ac.uk

Abstract

Objective To determine the factors associated with an increased risk of perinatal death related to uterine rupture during attempted vaginal birth after caesarean section.

Design Population based retrospective cohort study.

Setting Data from the linked Scottish Morbidity Record and Stillbirth and Infant Death Survey of births in Scotland, 1985-98.

Participants All women with one previous caesarean delivery who gave birth to a singleton infant at term by a means other than planned repeat caesarean section (n = 35 854).

Main outcome measures All intrapartum uterine rupture and uterine rupture resulting in perinatal death (that is, death of the fetus or neonate).

Results The overall proportion of vaginal births was 74.2% and of uterine rupture was 0.35%. The risk of intrapartum uterine rupture was higher among women who had not previously given birth vaginally (adjusted odds ratio 2.5, 95% confidence interval 1.6 to 3.9, P < 0.001) and those whose labour was induced with prostaglandin (2.9, 2.0 to 4.3, P < 0.001). Both factors were also associated with an increased risk of perinatal death due to uterine rupture. Delivery in a hospital with < 3000 births a year did not increase the overall risk of uterine rupture (1.1, 0.8 to 1.5, P = 0.67). However, the risk of perinatal death due to uterine rupture was significantly higher in hospitals with < 3000 births a year (one per 1300 births) than in hospitals with ≥ 3000 births a year (one per 4700; 3.4, 1.0 to 14.3, P = 0.04).

Conclusion Women who have not previously given birth vaginally and those whose labour is induced with prostaglandin are at increased risk of uterine rupture when attempting vaginal birth after caesarean section. The risk of consequent death of the infant is higher in units with lower annual numbers of births.

Introduction

Uterine rupture during attempted vaginal birth after a previous caesarean section is a rare event that affects about one in 200 women,1 and consequent death of the infant is even rarer, affecting about one per 2000.2 Analysis of the factors determining perinatal death due to uterine rupture therefore requires data from large numbers of women. Most large scale databases of births lack detailed information on the cause of perinatal death and the obstetric characteristics of the population. Consequently, we know of no reports of the risk factors for perinatal death due to uterine rupture during attempted vaginal birth after previous caesarean section. We linked national registries of pregnancy discharge data and perinatal death to determine the factors associated with this event.

Methods

The inclusion criteria for the study were that a woman had previously had one caesarean section and was delivered in her current pregnancy by a means other than planned caesarean section. We excluded women with more than one previous caesarean, those with multiple gestations, those delivering before 37 weeks' gestation, and those delivering beyond 43 weeks' gestation. We also excluded cases in which the infant died from causes other than intrapartum uterine rupture.

Data sources—The Scottish Morbidity Record (SMR2) collects information on clinical and demographic characteristics and outcomes for all patients discharged from Scottish maternity hospitals. The register is subjected to regular quality assurance checks and has been > 99% complete since the late 1970s.3 The register collects both specific obstetric data and up to six ICD-9 (international classification of diseases, ninth revision) or ICD-10 (10th revision) diagnostic codes relating to the admission. SMR2 records were linked to records from the Scottish Stillbirth and Infant Death Survey. This national register routinely classifies all perinatal deaths in Scotland.4

Definitions—We defined trial of labour as a singleton delivery at term by a means other than planned caesarean section in a women with only one previous caesarean delivery. The definition of perinatal death due to uterine rupture was that the obstetric cause of death was coded as "mechanical" under the modified Wigglesworth classification5 and that the ICD-9 diagnostic code for intrapartum uterine rupture (665.1) was listed under the specific diagnoses. Intrapartum uterine ruptures that did not result in perinatal death were identified with ICD-9 and ICD-10 diagnostic codes 665.1 and O711, respectively. Hospital throughput was defined as the total number of births recorded in the SMR2 database for the given hospital over the given year. Hospital throughput was categorised into above or below the median (3000 births).

Statistical analyses—We summarised continuous variables with medians and interquartile ranges. We used the Fisher's exact test for univariate comparisons of dichotomous data. Multivariate analysis was performed with logistic regression analysis.

Results

There were 871 283 SMR2 birth records for Scotland for 1985-98. In total, 39 729 (4.6%) women had had one previous caesarean delivery and were delivered by a means other than planned caesarean section. We excluded 3875 (9.8%) records (see exclusion criteria above) leaving a study group of 35 854.

We looked for associations between maternal, fetal, and hospital characteristics recorded in SMR 2, and the risk of uterine rupture with or without perinatal death.

On univariate analysis, with the 35 854 women who attempted vaginal birth as the denominator, the risk of uterine rupture was higher in women who had not previously given birth vaginally and in women who had been induced with prostaglandin but not with other methods of induction (table 1). These associations remained highly significant in multivariate analysis and the point estimates were similar (table 2). Delivery in a hospital with < 3000 births a year was not associated with the risk of uterine rupture overall.


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Table 1 Univariate obstetric associations with uterine rupture and perinatal death due to uterine rupture. Figures are numbers (percentages) unless stated otherwise

 

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Table 2 Multivariate analysis (with odds ratios and 95% confidence intervals) of risk of uterine rupture and perinatal death due to uterine rupture

 

The risk of perinatal death due to uterine rupture was also higher in women who had not previously given birth vaginally and in women who had been induced with prostaglandins but not with other methods of induction (table 1). However, in addition, delivery in a hospital with < 3000 births a year was associated with a significantly increased risk of perinatal death due to uterine rupture. The risk of perinatal death was about one in 1300 in hospitals with < 3000 births a year and one in 4700 in hospitals with ≥ 3000 births a year.

Among the 124 cases of uterine rupture, there were 17 (13.7%) intrapartum stillbirths or neonatal deaths. There were 63 uterine ruptures in hospitals delivering < 3000 women per year and 13 (20.6%) resulted in perinatal death. In hospitals delivering ≥ 3000 women a year there were 61 uterine ruptures and four (6.6%) resulted in perinatal death (P=0.03). Among women with uterine rupture, the relative risk of perinatal death in a hospital with < 3000 births a year was about threefold (table 3).


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Table 3 Factors associated with perinatal death among women with documented uterine rupture. Figures are numbers (percentages) unless stated otherwise

 

Of the 12 633 women who had previously given birth vaginally, 1499 (11.8%) were induced with prostaglandin compared with 2976 of the 20 215 (12.8%) women who had not done so (P = 0.006). We used a logistic regression model to estimate the absolute risk of uterine rupture (including cases in which the infant survived and cases in which the infant died) in relation to different combinations of parity and induction of labour with prostaglandin in relation to 1998 rates. Among women who had not previously given birth vaginally, the risk of uterine rupture without induction of labour with prostaglandin was one in 210 and with induction of labour with prostaglandin was one in 71. Among women with a previous vaginal birth, the risk of uterine rupture without induction of labour with prostaglandin was one in 514 and with induction of labour with prostaglandin was one in 175.

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. 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 < 3000 births a year.

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.

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 6 7 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.8

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%.9 The overall rate of uterine rupture of 0.35% is consistent with that reported in a previous large scale Swiss study.7 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).10

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.


What is already known on this topic

Attempting vaginal birth after previous caesarean (VBAC) carries the risk of uterine rupture, which may result in perinatal death

No studies to date have examined the factors associated with perinatal death due to uterine rupture during attempted VBAC

No studies to date have examined the organisation of health care and the risk of perinatal death due to uterine rupture during attempted VBAC

What this study adds

For women attempting VBAC, no previous vaginal birth and induction of labour with prostaglandin were associated with uterine rupture resulting in perinatal death

The risk of perinatal death due to uterine rupture was greater in hospitals with lower annual numbers of deliveries


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.


Editorial by Guise

This is the abridged version of an article that was posted on bmj.com on 19 July 2004: http://bmj.com/cgi/doi/10.1136/bmj.38160.634352.55

Contributors: See bmj.com

Funding: None.

Competing interests: None declared.

Ethical approval: Not required.

References

  1. Lydon-Rochelle M, Holt VL, Easterling TR, Martin DP. Risk of uterine rupture during labor among women with a prior cesarean delivery. N Engl J Med 2001;345: 3-8.[Abstract/Free Full Text]
  2. Smith GCS, Pell JP, Cameron AD, Dobbie R. Risk of perinatal death associated with labor after previous cesarean delivery in uncomplicated term pregnancies. JAMA 2002;287: 2684-90.[Abstract/Free Full Text]
  3. Cole SK. Scottish maternity and neonatal records. In: Chalmers I, McIlwaine GM, eds. Perinatal audit and surveillance. London: Royal College of Obstetricians and Gynaecologists, 1980: 39-51.
  4. McIlwaine GM, Dunn FH, Howat RC, Smalls M, Wyllie MM, MacNaughton MC. A routine system for monitoring perinatal deaths in Scotland. Br J Obstet Gynaecol 1985;92: 9-13.[ISI][Medline]
  5. Hey EN, Lloyd DJ, Wigglesworth JS. Classifying perinatal death: fetal and neonatal factors. Br J Obstet Gynaecol 1986;93: 1213-23.[ISI][Medline]
  6. Gregory KD, Korst LM, Cane P, Platt LD, Kahn K. Vaginal birth after cesarean and uterine rupture rates in California. Obstet Gynecol 1999;94: 985-9.[Abstract/Free Full Text]
  7. Rageth JC, Juzi C, Grossenbacher H. Delivery after previous cesarean: a risk evaluation. Swiss Working Group of Obstetric and Gynecologic Institutions. Obstet Gynecol 1999;93: 332-7.[Abstract/Free Full Text]
  8. Zelop CM, Shipp TD, Repke JT, Cohen A, Lieberman E. Effect of previous vaginal delivery on the risk of uterine rupture during a subsequent trial of labor. Am J Obstet Gynecol 2000;183: 1184-6.[CrossRef][ISI][Medline]
  9. Flamm BL. Vaginal birth after caesarean (VBAC). Best Pract Res Clin Obstet Gynaecol 2001;15: 81-92.[CrossRef][Medline]
  10. Miller DA, Diaz FG, Paul RH. Vaginal birth after cesarean: a 10-year experience. Obstet Gynecol 1994;84: 255-8.[Abstract/Free Full Text]
(Accepted 3 June 2004)


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