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Obstetrics & Gynecology:
doi: 10.1097/01.AOG.0000102706.84063.C7
Original Research

The Association of Maternal Weight With Cesarean Risk, Labor Duration, and Cervical Dilation Rate During Labor Induction

Nuthalapaty, Francis S. MD; Rouse, Dwight J. MD, MSPH; Owen, John MD

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From the Center for Research in Women's Health, Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, Alabama.

Received June 20, 2003. Received in revised form September 19, 2003. Accepted September 26, 2003.

Address reprint requests to: Francis S. Nuthalapaty, MD, Department of Obstetrics and Gynecology, University of Alabama at Birmingham, 619 19th Street South, OHB 451, Birmingham, AL 35249–7333; e-mail: francis@nuthalapaty.net.

Dr. Rouse's effort was supported by NIH grant number 1 K24 HD01375-01, and Dr. Owen's effort was supported by NIH grant number 1 K24 HD043314-01.

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Abstract

OBJECTIVE: To assess the relationship among maternal weight and cesarean delivery, cervical dilation rate, and labor duration.

METHODS: We used a secondary analysis of 509 term women who were previously enrolled in a prospective observational study of a labor induction protocol in which standardized criteria were used for labor management. A variety of analyses were performed, both unadjusted and adjusted. P < .05 was considered significant.

RESULTS: The mean ± standard deviation weight of women who underwent a cesarean (97 ± 29 kg) was significantly higher than that of women who were delivered vaginally (87 ± 22 kg, P < .001). In a logistic regression model of nulliparas who comprised 71% of the study population, after adjustment for the confounding effects of infant birth weight, maternal age, initial cervical dilation, and diabetes, for each 10-kg increase in maternal weight, the odds ratio for cesarean delivery was significantly increased (odds ratio 1.17; 95% confidence interval 1.04, 1.28). In a linear regression model also limited to nulliparas and after adjusting for the same confounders, the rate of cervical dilation was inversely associated with maternal weight: for each 10-kg increment, the rate of dilation was decreased by 0.04 cm/h (P = .05). Similarly, labor duration was positively associated with maternal weight: for each 10-kg increment, an increase in the oxytocin to delivery interval of 0.3 hours was observed in nulliparas (P = .02). Neither lower rates of oxytocin administration to heavier women nor diminished uterine responsiveness (as reflected in measured Montevideo units) accounted for the slower labor progress.

CONCLUSION: In nulliparous women undergoing labor induction, maternal weight was associated with a higher cesarean risk and longer labor and was inversely proportional to the cervical dilation rate.

LEVEL OF EVIDENCE: II-2

Obese women are at increased risk for several adverse pregnancy outcomes.1–5 Chief among these outcomes is the association between obesity and cesarean birth.6–10 At least 2 plausible hypotheses have been advanced to explain this increased risk. Cnattingius et al6 in their 1998 analysis of 92,623 deliveries in Sweden postulated that the higher rate of cesarean births in overweight women was due to the higher associated incidence of pregnancy complications and subsequent labor inductions in overweight women. Others7,8 have postulated that soft tissue dystocia in the maternal pelvis may explain the higher cesarean rate.

In a previous investigation,11 we evaluated a standardized labor induction protocol that required that specific criteria be met before a cesarean was performed for nonprogressive labor (failed induction and active phase labor arrest). Data accumulated for that investigation were used to determine whether there was a relationship between maternal weight and cesarean risk in women whose labor induction was managed in a standardized fashion. In addition, we sought to characterize the relationship between maternal weight and both labor progress and duration.

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MATERIALS AND METHODS

Women in this secondary analysis were previously enrolled in an observational study of a standardized labor induction protocol that was conducted at the University of Alabama at Birmingham hospital between September 1997 and October 1999.11 Eligibility criteria included the following: vertex presentation, singleton gestation greater than or equal to 36 weeks, indicated induction (eg, ruptured membranes, hypertensive disease), and a cervix dilated no more than 2 cm. Clinical chorioamnionitis diagnosed before the initiation of oxytocin and a previous cesarean delivery were exclusion criteria. The majority of women with intact membranes and cervical dilatation less than 2 cm received extraamniotic saline infusion (for up to 12 hours) for cervical ripening concomitant with initiation of oxytocin.12 Other methods of cervical ripening were not used. All women received dilute intravenous oxytocin, initiated at 2 mU/min and increased by 2–5 mU/min every 15 minutes over 2 hours to 30 mU/min or until regular painful uterine contractions ensued or labor progressed. The protocol required amniotomy within 24 hours of starting oxytocin. After membrane rupture, the protocol specified placement of an intrauterine pressure catheter (and a fetal scalp electrode) and titration of the oxytocin to achieve at least 200 Montevideo units.

If the fetal heart rate pattern was reassuring, cesarean delivery before the active phase of labor (defined as cervical dilatation of at least 4 cm and 90% effacement or 5 cm of cervical dilatation, regardless of effacement) was not permitted for nonprogressive labor before oxytocin had been administered for at least 12 hours beyond the time of membrane rupture. Once in the active phase as defined above, cesarean was not performed for nonprogressive labor before at least 4 hours of oxytocin augmentation with a sustained uterine contraction pattern of greater than 200 Montevideo units. However, because it is not always possible to achieve a sustained uterine contraction pattern greater than 200 Montevideo units, cesarean delivery for active phase labor arrest was permitted after 6 hours of oxytocin augmentation regardless of the uterine contraction pattern.13,14 All cervical examinations were recorded, as were the duration and maximum rate of oxytocin administration.

Institutional review board approval was obtained to perform this secondary analysis. Continuous data were compared by using either the Wilcoxon rank sum test and expressed as the mean plus 1 standard deviation. Categorical data were compared by using χ2 or the Mantel–Haenszel test of trends where appropriate. We compared the last-recorded maternal weight between women who underwent cesarean and those who delivered vaginally in the entire population to determine whether there was a significant relationship. We then explored the relationship between maternal weight and cesarean risk using a logistic regression model. The relationships between maternal weight (and maternal weight quartile groups) and labor duration (defined as the interval from oxytocin to delivery), and the rate of cervical dilation were modeled using linear regression and analysis of variance with a Tukey multiple-range t test. For each regression model, we further included 3 recognized confounders: maternal age, infant birth weight, and initial cervical dilation in a multivariable analysis.6,15–19 We then performed univariate analyses for other potential confounders, such as race, preinduction cervical ripening, epidural use, and induction indications. Of these, only maternal diabetes was determined to have a significant association with both cesarean delivery and maternal weight and, thus, this was also included in the multivariable regression models. Because of the well-known and pronounced confounding effect of parity on labor progress and cesarean rate, we stratified the analyses by parity (nulliparous versus parous). Data were analyzed using SAS 8.0 (SAS Institute, Cary, NC), and P < .05 was considered to represent statistical significance.

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RESULTS

Maternal demographic and intrapartum characteristics are listed in Table 1. The overall cesarean delivery rate was 20%. The mean weight of women who underwent cesarean delivery was significantly higher than that of women who were delivered vaginally. Compared with nulliparous women in the lowest weight quartile, nulliparous women in the highest quartile had a 2.5 times higher cesarean delivery rate (Table 2). In a logistic regression model confined to nulliparas, the odds of cesarean delivery increased by 25% for each 10-kg increase in maternal weight. In parous women, although there was an association between increased maternal weight and cesarean delivery, it was not statistically significant (Table 3).

Table 1
Table 1
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Table 2
Table 2
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Table 3
Table 3
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Overall, nulliparous patients had a mean cervical dilation rate of 0.8 ± 0.8 cm/h compared with 1.4 ± 1.1 cm/h for parous women (P < .001). Nulliparous women in the highest weight quartile had a significantly lower mean cervical dilation rate than those in the lowest weight quartile (P = .01). In the multiple-range t test, the highest 3 quartiles were statistically similar and significantly different than the lower 3 quartiles, which were also statistically similar at the P = .05 level. In multiparous women, the cervical dilation rates were statistically similar across weight quartiles (P = .15, Table 2). In the unadjusted regression model (Table 3), there was a significant inverse relationship between cervical dilation rate and maternal weight, regardless of parity.

The mean duration from oxytocin initiation to delivery for nulliparous women was 13.8 ± 7.1 hours, and for parous women, it was 9.0 ± 5.5 hours (P < .001). Nulliparous women in the highest weight quartile had a mean duration of oxytocin initiation to delivery that was 5 hours greater than that of nulliparous women in the lowest quartile (P < .001). In the multiple-range t test, the highest weight quartile was significantly different from the lower 3 quartiles, which were statistically similar at the P = .05 level. Similarly, multiparous women in the highest weight quartile had a mean duration of oxytocin initiation to delivery that was 3.6 hours greater than that of multiparous women in the lowest quartile (P = .01, Table 2). In the multiple range t test, the highest 3 quartiles were statistically similar and significantly different than the lowest 3 quartiles, which were also statistically similar at the P = .05 level. In the unadjusted regression models (Table 3), there was a direct relationship between maternal weight and the induction to delivery interval for both nulliparous (P < .001) and parous (P = .003) women.

The results of the adjusted multivariable regression models are summarized in Table 3. Among nulliparas, the odds ratio for cesarean delivery remained significantly increased. Likewise, labor duration remained positively and significantly associated with maternal weight in nulliparas. After adjustment, although cervical dilation rate retained an inverse relationship with maternal weight, this association was no longer statistically significant (P = .05). In parous women, adjustment attenuated all of the relationships, and none were significant.

Neither lower rates of oxytocin administration to heavier women nor diminished uterine responsiveness (as reflected in measured Montevideo units) accounted for their higher rates of cesarean, slower labor progress, or increased duration of labor. In fact, nulliparous women in the lowest weight quartile received oxytocin at a mean maximum rate of 21 mU/min compared with a mean rate of 28 mU/min in the highest quartile (P = .001). Similarly, parous women in the lowest weight quartile received oxytocin at a mean maximum rate of 16 mU/min compared with a rate of 24 mU/min in the highest weight quartile (P = .02). Nulliparous women in the lowest weight quartile achieved an average maximum of 208 Montevideo units compared with those in the highest quartile, who achieved an average maximum of 227 Montevideo units (P = .08). Similarly, multiparous women in the lowest weight quartile achieved an average maximum of 217 Montevideo units compared with an average maximum of 237 Montevideo units in the highest quartile (P = .6).

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DISCUSSION

Similar to previous investigations,5–10 we found that in nulliparous women, as maternal weight increased, so did the risk for cesarean delivery. The important findings of this investigation are that, irrespective of parity, higher maternal weight is independently associated with a decreased rate of cervical dilation and an increased duration of labor. These associations persisted in nulliparous patients after controlling for known risk factors for cesarean delivery, such as maternal age, infant birth weight, initial cervical dilation, and maternal diabetes. Moreover, they were profound (ie, a 17% increase in the risk of cesarean for each 10-kg increase in maternal weight) and not explained by either oxytocin dose or measured uterine activity, both of which were found to increase with increasing maternal weight.

A particular strength of this study is that the labors of all women were uniformly managed. Importantly, criteria for cesarean in both the latent and active phases of labor were prespecified. This approach minimized the tendency for labor management to be predicated on individual patient characteristics or physician preference, thus minimizing the biases that may be introduced by such individualization.

A potential limitation of this study was its relatively small sample size, which may have limited our ability to detect weight-associated changes in labor duration and cervical dilation rates, especially among parous women. Also, we recognize that there are many potential confounders of labor progress. Our analyses considered those that have been previously recognized6,15–19 and, within our cohort, bore a significant relationship to both maternal outcome and weight.

Our data are consistent with the hypothesis put forward by Crane et al7 and Kaiser and Kirby8 that obesity results in a relative excess of soft tissue in the pelvis that can lead to dystocia. The soft tissues of the pelvis, such as muscle, connective tissue, and adipose, may each have variable effects on labor progress. However, in this observational study, we have no direct data to either confirm or refute this hypothesis.

In summary, among nulliparas undergoing labor induction, maternal weight is an important determinant of cesarean risk and is inversely associated with labor progress, independent of initial cervical status, maternal age, infant birth weight, and maternal diabetes.

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REFERENCES

1. Lu GC, Rouse DJ, DuBard M, Cliver S, Kimberlin D, Hauth JC. The effect of the increasing prevalence of maternal obesity on perinatal morbidity. Am J Obstet Gynecol 2001;185:845–9.

2. Baeten JM, Bukusi EA, Lambe M. Pregnancy complications and outcomes among overweight and obese nulliparous women. Am J Public Health 2001;91:436–40.

3. Cnattingius S, Bergstrom R, Lipworth L, Kramer MS. Prepregnancy weight and the risk of adverse pregnancy outcomes. N Engl J Med 1998;338:147–52.

4. Perlow JH, Morgan MA, Montgomery D, Towers CV, Porto M. Perinatal outcome in pregnancy complicated by massive obesity. Am J Obstet Gynecol 1992;167:958–62.

5. Johnson JW, Longmate JA, Frentzen B. Excessive maternal weight and pregnancy outcome. Am J Obstet Gynecol 1992;167:353–70.

6. Cnattingius R, Cnattingius S, Notzon FC. Obstacles to reducing cesarean rates in a low-cesarean setting: the effect of maternal age, height, and weight. Obstet Gynecol 1998;92:501–6.

7. Crane SS, Wojtowycz MA, Dye TD, Aubry RH, Artal R. Association between pre-pregnancy obesity and the risk of cesarean delivery. Obstet Gynecol 1997;89:213–6.

8. Kaiser PS, Kirby RS. Obesity as a risk factor for cesarean in a low-risk population. Obstet Gynecol 2001;97:39–43.

9. Witter FR, Caulfield LE, Stoltzfus RJ. Influence of maternal anthropometric status and birth weight on the risk of cesarean delivery. Obstet Gynecol 1995;85:947–51.

10. Brost BC, Goldenberg RL, Mercer BM, Iams JD, Meis PJ, Moawad AH, et al. The Preterm Prediction Study: association of cesarean delivery with increases in maternal weight and body mass index. Am J Obstet Gynecol 1997;177:333–7.

11. Rouse DJ, Owen J, Hauth JC. Criteria for failed labor induction: prospective evaluation of a standardized protocol. Obstet Gynecol 2000;96:671–7.

12. Guinn DA, Goepfert AR, Christine M, Owen J, Hauth JC. Extra-amniotic saline, laminaria, or prostaglandin E(2) gel for labor induction with unfavorable cervix: a randomized controlled trial. Obstet Gynecol 2000;96:106–12.

13. Rouse DJ, Owen J, Savage KG, Hauth JC. Active phase labor arrest: revisiting the 2-hour minimum. Obstet Gynecol 2001;98:550–554.

14. Rouse DJ, Owen J, Hauth JC. Active-phase labor arrest: oxytocin augmentation for at least 4 hours. Obstet Gynecol 1999;93:323–328.

15. Parrish KM, Holt VL, Easterling TR, Connell FA, LoGerfo JP. Effect of changes in maternal age, parity, and birth weight distribution on primary cesarean delivery rates. JAMA 1994;271:443–7.

16. Martel M, Wacholder S, Lippman A, Brohan J, Hamilton E. Maternal age and primary cesarean section rates: a multivariate analysis. Am J Obstet Gynecol 1987;156:305–8.

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18. Yeast J, Jones A, Poskin M. Induction of labor and the relationship to cesarean delivery: a review of 7001 consecutive inductions. Am J Obstet Gynecol 1999;180:628–33.

19. Bishop EH. Pelvic scoring for elective induction. Obstet Gynecol 1964;24:266–8.

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