Obstetrics & Gynecology:
Intrauterine Pressure During the Second Stage of Labor in Obese Women
Buhimschi, Catalin S. MD*; Buhimschi, Irina A. MD*; Malinow, Andrew M. MD†‡; Weiner, Carl P. MD†
From the *Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut; †Department of Obstetrics, Gynecology and Reproductive Sciences, and ‡Department of Anesthesiology, The University of Maryland School of Medicine, Baltimore, Maryland.
Received July 18, 2003. Received in revised form September 9, 2003. Accepted September 26, 2003.
Address reprint requests to: Dr. Catalin Buhimschi, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University, 333 Cedar Street, New Haven, CT 06510; e-mail: firstname.lastname@example.org.
We acknowledge Wayne State University for providing salary support to the principal investigator during his fellowship training at this institution.
OBJECTIVE: The perception that obese women have longer labors and a higher frequency of operative delivery because they are “poor pushers” persists despite the absence of objective study. We tested the hypothesis that obese women generate inadequate intrauterine pressure during the second stage of labor.
METHODS: Intrauterine pressure was prospectively measured in 71 women during the second stage of labor. Obesity was defined as a body mass index (BMI) greater than 29 (n = 17). A BMI below 25 was normal (n = 40). Women with a BMI between 26 and 29 (n = 14) were considered overweight. All women labored with epidural analgesia and were alert and responsive throughout the study. After recording the baseline contractility, a standardized Valsalva maneuver was performed during contractions. The area under the intrauterine pressure curve (integral) was used as an estimate of uterine contractility.
RESULTS: All women delivered vaginally. There were no significant differences in baseline uterine contractility among obese, overweight, and normal women either before (obese 1,787 mm Hg/s; 95% confidence interval [CI] 1,164, 2,742 versus normal 1,569 mm Hg/s; 95% CI 718, 2,371 versus overweight 1,770 mm Hg/s; 95% CI 1,305, 2,835; P = .223) or during Valsalva maneuver (obese 2,831 mm Hg/s; 95% CI 1,771, 4,599 versus normal 2,637 mm Hg/s; 95% CI 1,240, 4,390 versus overweight 2,813 mm Hg/s; 95% CI 1,209, 4,982; P = .742). A BMI greater than 25 was associated with a higher frequency of oxytocin augmentation (P = .037). Univariate analysis revealed a relationship between labor duration and BMI (r = 0.299, P = .018). Obese women labored longer during the active phase (one-way analysis of variance, P = .02), but second-stage duration was similar among groups (one-way analysis of variance P = .44). Obesity did not increase the incidence of perineal lacerations (P = .82) or frequency of operative delivery (relative risk obese versus nonobese = 0.212; 95% CI 0.04, 1.05).
CONCLUSION: Obese women produce second-stage intrauterine pressures equivalent to women with a normal BMI, although they may require oxytocin augmentation more often.
LEVEL OF EVIDENCE: II-2
Obesity is a major and expanding health problem worldwide1 because obese adults constitute the fastest-growing fraction of the population.2,3 The prevalence of overweight, reproductive-aged (25–44 years) women in the United States varies between 30% and 40%.4 An understanding of the impact of obesity on reproduction is of increasing importance as women choose to delay childbearing until later in life.5
Obesity has challenged obstetricians for decades. Obese people are at increased risk for serious medical complications, such as diabetes, hypertension, hepatic and gallbladder diseases, osteoarthritis, and cancer.6 Because pregnancy represents a complex adaptive challenge, it is not surprising that obesity-related comorbidity is associated with poor perinatal and neonatal outcome.7 Obese pregnant women have a higher prevalence of gestational diabetes, preeclampsia, fetal growth restriction, and thromboembolic accidents.8,9
Obesity complicates the management of labor by a proven association with macrosomia, shoulder dystocia, cephalopelvic disproportion, and high incidence of operative delivery.9–11 It is also associated with prolonged labor and increased surgical morbidity.11 Because uterine contractility is a major determinant of labor progression,12 the increased prevalence of prolonged labor, primary inertia, operative delivery, and more frequent need for oxytocin augmentation in obese women seems consistent with decreased uterine contractility.11
One explanation for these findings is that obese women have an inborn tendency to have weaker contractions, leading to labor arrest.11 Although this explanation may appeal to stereotypes, it remains untested. We tested the hypothesis that obese women have inadequate intrauterine pressures during the second stage of labor.
MATERIALS AND METHODS
Intrauterine pressure was measured electronically in 71 women who were monitored prospectively during the second stage of labor. All women labored with epidural analgesia and were alert and responsive throughout the study. After recording the baseline contractility, standardized Valsalva maneuver was performed during contractions. Obesity was defined as a body mass index (BMI = kg/m2) greater than 29 (n = 17).13 Women with a BMI less than 26 were considered normal (n = 40), and those with a BMI from 26 to 29 (n = 14) were considered overweight. The University of Maryland Medical System (n = 64) and Wayne State University (n = 8) Institutional Review Boards approved the study protocol, and all patients were enrolled after providing written, informed consent. Women in active labor (defined as a cervical dilatation more than 4 cm with regular uterine contractions) were identified in the Labor and Delivery suite based on the availability of one of the investigators. Ninety percent of the women who were approached agreed to participate. The study period lasted from 1999 to 2002.
Potential subjects were women with a singleton vertex experiencing normal cervical dilatation and descent during active labor. The onset of labor was identified and noted in the medical chart as the time of beginning of painful, regular uterine contractions. One investigator (C.S.B.) performed manual pelvimetry on all patients and concluded the bony pelvis was adequate before delivery. The same examiner performed the cervical examinations reported. The onset of the second stage of labor was defined as the time of full cervical dilatation and was identified by digital examination. Exclusion criteria included an abnormal pelvic cavity, suspected fetal macrosomia (more than 4,500 g by clinical and/or ultrasound evaluation), grand multiparity (para 5 and over),14 fetal heart rate abnormalities at enrollment (bradycardia, tachycardia, or prolonged variable decelerations), placentation abnormalities (low-lying placenta, abruptio placenta), uterine malformations, scarred uterus, or a history of previous shoulder dystocia.
All women labored at least 1 hour with requested epidural or combined spinal-epidural analgesia before initiation of intrauterine pressure monitoring (approximately 80% of women under our care request epidural analgesia).15 A modified Bromage score (0–3) was used prospectively by the attending anesthesiologists to assess the degree of lower motor block. The median score was 0 for both right and left legs. The 0–3 score evaluates lower extremity motor block: 0 = no block; 1 = block at the hips but not the knees or ankles; 2 = block at the hips and knees but not the ankles; and 3 = block at the hips, knees, and ankles.16 The median rostral dermatome of sensory anesthesia (to pinprick) reached T6-T7.
Intrauterine pressure was measured electronically with a sensor-tip catheter (Graphic Control, Buffalo, NY) inserted into the uterine cavity under sterile conditions. The intrauterine pressure catheter was connected to a data acquisition system (CB Sciences, Dover, NH) and the data analyzed by using Chart V 4.0 AD-Instruments software (2000, Castle Hill, Australia). Uterine activity was recorded during the second stage of labor before any study intervention to provide a baseline contractile period. Thus, each woman also acted as her own control.
Each woman began pushing after the cervix was fully dilated, and the fetal head had reached at least +1 station to minimize the negative effects of prolonged pushing, such as maternal exhaustion. Women were counseled and trained to perform the Valsalva maneuver in a standardized fashion with maximal effort. The laboring position and method used during pushing were similar for all women. To determine the maximum expulsive effort, three Valsalva maneuvers (each approximately 10 seconds in duration) were performed during a contraction.17 This is the technique routinely used in the Labor and Delivery Ward at both University of Maryland and Wayne State University. Oxytocin infusion was initiated during the active phase of labor for treatment of dysfunctional labor independent of our study if deemed clinically necessary by the attending obstetrician. Once adequate uterine contractility was achieved (more than 200 Montevideo units or cervical dilatation over 1 cm/h), the oxytocin dose was held constant throughout the first and second stages of labor.
The methodology was previously described in detail.18 A clinically uninvolved investigator blinded to outcome and BMI group assignment analyzed each intrauterine pressure recording. The following raw parameters for each contraction were calculated: integral (area under the curve displaced from baseline tone and expressed as mm Hg/s), maximum amplitude (in mm Hg), tone (minimum amplitude in mm Hg), and the duration of each analyzed period (in seconds), which included either the contraction or the periods in which the Valsalva maneuver was superimposed over the contraction. Uterine activity (in Montevideo units) was calculated as the product of amplitude (maximum − minimum) multiplied by the number of contractions per 10-minute epoch. The raw parameters were averaged for at least 3–4 events (spontaneous or enhanced contractions). Finally, the integral (area under the intrauterine pressure curve) was used to assess uterine contractility because it includes both the amplitude and duration of uterine contractions in contrast to the Montevideo calculation.
Based on our previous investigation,17 we calculated the number of patients needed to detect a significant difference in expulsive effort of 900 mm Hg/s (for intrauterine pressure integral) with a standard deviation of about 30–40% of the mean. Such values were previously observed, clinically relevant maneuvers, such as McRoberts with Valsalva during the second stage. Twelve women provided sufficient power to detect differences of 360 mm Hg/s among the study groups with a power of 0.8 and an alpha of 0.05.
All data sets were subjected to normality testing by using the Kolmogorov-Smirnov method. The data are reported as mean ± standard error of the mean (for normally distributed data) with 95% confidence intervals (CI) or as median and range (for skewed data). Statistical comparisons between groups were performed by using the one-way or two-way repeated analysis of variance (ANOVA) followed by Tukey's test, post hoc Student-Newman-Keuls tests, or Student t tests as appropriate. Proportions were compared with χ2 or Fisher exact tests. Data without a normal distribution were compared with Mann-Whitney rank sum test. A P < .05 was considered a statistically significant difference among groups. Uni- and multivariate analysis with linear regression modeling was applied to identify significant associations between maternal, fetal, or labor characteristics as independent variables and obesity as the dependent variable. A Pearson product moment correlation was used to measure colinearity between the selected independent variables as well as other relevant correlations between dependent and independent variables. The impact of labor duration was assessed by using a survival analysis model (GraphPad Prism 3.02 for Windows, GraphPad Software, San Diego, CA) with censoring of patients delivered operatively.
Maternal age, parity, and gestational age did not differ among groups (Table 1). All women delivered vaginally. Obese women delivered heavier babies than either the normal or overweight women (mean ± standard error of the mean 3,444 ± 105 g versus 3,145 ± 66 g versus 3,204 ± 97 g, P = .04, one-way ANOVA). Oxytocin augmentation was more common in women with a BMI greater than 25 (P = .04, Fisher exact test). The proportion of normal ponderal nulliparous women versus nulliparous women with a BMI more than 25 requiring oxytocin augmentation to achieve adequate contractility and cervical dilatation in the active phase was similar (55.5% versus 75%, Fisher exact test, P = .442).
There were no significant differences in baseline intrauterine pressure among obese, overweight, and normal women before (spontaneous: obese 1,787 mm Hg/s; 95% CI 1,164, 2,742 versus normal 1,569 mm Hg/s; 95% CI 718, 2,371 versus overweight 1770 mm Hg/s; 95% CI 1,305, 2,835; one-way ANOVA, P = .223) or during the Valsalva maneuver (enhanced: obese 2,831 mm Hg/s; 95% CI 1,771, 4,599 versus normal 2,637 mm Hg/s; 95% CI 1,240, 4,390 versus overweight 2,813 mm Hg/s; 95% CI 1,209, 4,982; one-way ANOVA, P = .742) (Table 2). There was no significant difference in baseline intrauterine pressure among obese, overweight, and normal women, either before (one-way ANOVA, P = .074) or during the Valsalva maneuver (one-way ANOVA, P = .121), with or without inclusion of patients requiring operative vaginal delivery. There was no significant difference in intrauterine pressure among the 3 groups after stratifying them by BMI (two-way repeated measures ANOVA, F = 0.666, P = .517). Within each group, there was a significant difference between basal intrauterine pressure and the intrauterine pressure accomplished during “pushing” (two-way repeated measures ANOVA, F = 112.25, P < .001). There was no significant interaction between BMI and state of pushing (two-way repeated measures ANOVA, F = 0.017, P = .982). Figure 1A displays the maximal expulsive force (enhanced) as a function of BMI in univariate model (univariate r = 0.162, P = .197). To account for a possible influence of parity on a patient's pushing ability, we performed a multivariate analysis with linear regression modeling that showed that neither BMI nor parity was a significant determinant of the patient's ability to elevate their intrauterine pressure while “pushing” (BMI: P = .495, parity: P = .770).
There was a significant relationship between labor duration and BMI (univariate r = 0.299, P = .018), confirmed by a survival analysis of labor duration censoring women who delivered operatively (log rank test, P = .048; Figure 1B). Obese women had longer labors secondary to a longer active phase (one-way ANOVA, F = 3.942, P = .025) but not second stage (one-way ANOVA, F = 0.188, P = .829), even after excluding women who delivered operatively (one-way ANOVA, F = 0.474, P = .757). Neither overweight nor obese women in this cohort had an increased rate of operative delivery (relative risk obese versus nonobese 0.212; 95% CI 0.04, 1.05). Operative deliveries consisted of vacuum extractions or forceps applications due to severe variable decelerations of the fetal heart rate or maternal exhaustion. Obese women did not suffer a higher frequency of perineal laceration.
The present study tested the hypothesis that obese women generate inadequate intrauterine pressure during the second stage of labor. We demonstrated that the contractility and pushing ability of obese women was similar to those of thinner women during the second stage, assuming appropriate oxytocin augmentation of active phase dysfunction. Thus, the working hypothesis was rejected.
Obese women are at increased risk of obstetric complications, including prolonged labor, perineal lacerations, fetal macrosomia, a high frequency of emergency caesarean delivery, increased total operative time, increased intraoperative bleeding, and prolonged hospitalization.9,19,20 Most of these previous studies examining labor morbidity in obese women focused solely on the frequency of labor and surgical complications.
The clinical findings herein are similar to those previously reported by other investigators.11 In a study population of 4,258 women, Jasen et al11 observed that obese women required more oxytocin augmentation, had an increased incidence of early amniotomy, and had an increased incidence of secondary inertia, but not of instrumental or cesarean delivery. Although the authors offer several possible explanations for their findings (first, narrow pelves with increased soft tissue deposition, and second, an inborn tendency for weaker contractions), little is known about the underling mechanisms for the morbid events associated with an increased BMI. We find that once obese women reach the second stage of labor, their ability to increase IP is similar to women with a normal BMI.
In the current study, linear regression analysis revealed a direct relationship between the overall duration of labor and BMI. We demonstrate that “poor progress” in obese patients is likely due to active-phase dysfunction rather than a longer second stage.11 We confirm previous reports that the longer labors of obese women are associated with an increased need for oxytocin stimulation.11 Although it is possible that hypocontractility is present earlier in labor before the initiation of oxytocin, it remains that “inadequate” uterine contractility during the second stages of labor is not the source of the increased incidence of labor complications associated with a high BMI. It is possible that modern electronic assessment of intrauterine pressure provides obstetricians with satisfactory information upon which they can initiate oxytocin in a timely fashion, eliminating differences in the second stage that might occur naturally. However, the increased incidence of intra- or postsurgical complications, such as longer operative time, blood loss, postoperative endometritis, and hospitalization time in obese women, may bias obstetricians toward “higher tolerance” for a protracted active phase to avoid a “difficult” caesarean or operative vaginal delivery.20,21 The interpretation of the present findings indicates that when macrosomia is excluded, the fetal head is engaged, and the cervix is fully dilated, labor complications are due to factors other than poor contractility or “pushing performance.” The a priori exclusion of macrosomia may explain some of our findings. Although a trial of labor in the context of fetal macrosomia (more than 5,000 g) is contraindicated by the American College of Obstetricians and Gynecologists,22 completion of a research protocol to confirm or refute the present results in a subgroup of obese women who should attempt “natural delivery” of a macrosomic fetus would be difficult and possibly unethical.
Previous studies link obstetrical emergencies like shoulder dystocia with predisposing factors, such as fetal macrosomia, vacuum extraction, forceps deliveries, and prolonged active and second stages of labor.23,24 The lack of an increased incidence of operative delivery in obese women should not be a surprise because obstetricians currently adopt a more “observational” approach to the labor curve of obese patients in the second stage, hoping that a normal descent of fetal head will lead to an uneventful vaginal delivery. It remains unclear in the literature whether the increased frequency of caesarean delivery in obese women reflects acute maternal or fetal emergencies (preeclampsia, abruption, prolapsed cord, variable decelerations) or more subtle diagnoses, such as cephalopelvic disproportion.8,10,19,20 The current study reveals that uterine contractility and inability to “push” do not constitute a risk factor per se for obese women.
Uterine contractility increases as the cervix dilates,25 but maximal force is achieved most probably once the cervix is fully dilated.18,26 Fetal expulsion is facilitated by voluntary maternal pushing effort that represents the concerted contraction of abdominal muscles occurring simultaneously with a forced expiratory effort against a closed glottis. Studies of pulmonary function in obese patients reveal that body habitus alone does not account for changes in individual pulmonary functions and that ventilatory defects do not occur more frequently in obese women.27 However, isokinetic trunk muscle strength studies suggest that obese women have stronger trunk flexion strength measurements compared with lean women.28 Our findings concur, demonstrating similar pushing abilities of obese and normal women.
We conclude that although obese women may require oxytocin augmentation more often to correct intrauterine pressure during active labor, their ability to push is equivalent to women with BMIs in the normal range. Thus, the increased incidence of labor complications reported in both overweight and obese patients cannot be explained by inadequate intrauterine pressure or maternal expulsive efforts in the second stage.
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