Obstetrics & Gynecology:
The Association of Maternal Obesity With Fetal pH and Base Deficit at Cesarean Delivery
Edwards, Rodney K. MD, MS; Cantu, Jessica MD; Cliver, Suzanne BA; Biggio, Joseph R. Jr MD; Owen, John MD, MSPH; Tita, Alan T. N. MD, PhD
Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Alabama Birmingham School of Medicine, Birmingham, Alabama.
Corresponding author: Rodney K. Edwards, MD, MS, 176F 10270J, 619 19th Street South, Birmingham, AL 35249-7333; e-mail: email@example.com.
Financial Disclosure The authors did not report any potential conflicts of interest.
The authors thank the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the Maternal-Fetal Medicine Units Network, and the Cesarean Section Registry Protocol Subcommittee for making the database available for the project. The contents of this report represent the views of the authors and do not represent the views of the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network or the National Institutes of Health.
Presented at the 33rd annual meeting of the Society for Maternal-Fetal Medicine, February 11–16, 2013, San Francisco, California.
OBJECTIVE: To evaluate the association between maternal body mass index (BMI) and umbilical cord acid-base status at the time of cesarean delivery.
METHODS: We conducted a retrospective multicenter cohort study using data from the Cesarean Section Registry of the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Women were included if they delivered a live, nonanomalous singleton at 37–41 weeks of gestation by prelabor cesarean under spinal anesthesia. We excluded women with diagnoses that might be associated with uteroplacental insufficiency. Body mass index at delivery was examined both as a continuous and categorical exposure, and acid-base status was based on cord arterial pH and base deficit.
RESULTS: There were 5,742 mother–neonate pairs who met criteria for analysis. Among possible confounders (including sociodemographic variables, number of previous uterine incisions, diabetes, hematocrit, neonatal gender, and birth weight), African American race, birth weight, parity, and smoking status were significantly associated with both BMI and acid-base parameters. Adjusted for those four factors, with increasing BMI category (less than 25, 25–29.9, 30–34.9, 35–39.9, and 40 or higher), mean pH decreased from 7.25 to 7.22 (P<.001), proportion with pH less than 7.1 increased from 3.5% to 7.7% (P=.011), mean base deficit increased from 4.01 mmol/L to 4.83 mmol/L (P=.030), and proportion with base deficit of 12 mmol/L or more increased from 0.6% to 4.7% (P=.003). When BMI was analyzed continuously and adjusted for these confounders, for every 10-unit increase in BMI, cord arterial pH decreased by 0.01 (P<.001) and base deficit increased by 0.26 mmol/L (P=.005).
CONCLUSION: For women undergoing nonemergent prelabor cesarean delivery under spinal anesthesia, fetal pH declines and base deficit rises as maternal BMI increases.
LEVEL OF EVIDENCE: II
Obesity is defined as a body mass index (BMI, calculated as weight (kg)/[height (m)]2) of 30 or higher.1 The prevalence of obesity in reproductive-aged women in the United States has increased dramatically; currently, 34% of women 20–39 years of age are obese.2 This problem affects all racial and ethnic groups, but non-Hispanic African American women are at greater risk (47%) than Hispanic women such as Mexican Americans (40%) or non-Hispanic white women (31%).2 Obesity is associated with an increased risk of many pregnancy complications, and the effect is dose-dependent; these complications include hypertension, gestational diabetes, venous thromboembolism, fetal death, preterm birth, postterm birth, birth defects, macrosomia, shoulder dystocia, and anesthesia complications.3–12 Additionally, obesity is associated with an increased likelihood of labor induction, failure to progress in labor (whether the labor is spontaneous or induced), cesarean delivery, and cesarean delivery complications such as increased operative time, wound infection or disruption, and hemorrhage.13–17 Using BMI, classes of obesity have been described: BMI values of 30–34.9, 35–39.9, and 40 or higher define individuals as having class I, II, or III obesity, respectively.18 As with the thresholds for overweight and obesity, the thresholds for various classes of obesity apply to nonpregnant individuals, and no pregnancy-specific thresholds have been established.
In the general obstetric population, data are mixed as to whether obesity is a risk factor for adverse fetal acid-base status at birth.19,20 Because labor abnormalities are more common in obese pregnant women, cesarean deliveries (both primary and repeat) are more common. The most common type of anesthesia for repeat (or other scheduled prelabor) cesarean deliveries is spinal anesthesia. In the general obstetric population, spinal anesthesia has been shown to be associated with lower cord pH values than epidural or general anesthesia.21,22 We hypothesize that obese women undergoing cesarean delivery are at increased risk for lower fetal pH and higher fetal base deficit in the umbilical artery, immediately before delivery, as a result of the weight of the abdominal wall causing impaired venous return and reduced placental perfusion. Spinal anesthesia, resulting in relative hypotension, may accentuate these effects. The principal objective of this study was to evaluate the association between maternal BMI and umbilical cord acid-base status at the time of prelabor cesarean delivery under spinal anesthesia.
MATERIALS AND METHODS
We conducted a retrospective multicenter cohort study using data from the Cesarean Section Registry of the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. The registry was developed from data collected prospectively from 1999 to 2002 at 19 academic medical centers. For the first 2 years of the study, all patients delivering by a vaginal birth after cesarean or by cesarean (primary or repeat) were enrolled. In the second 2 years of the study, only patients that delivered by vaginal birth after cesarean delivery or repeat cesarean delivery were included. Detailed methods for the registry have been described elsewhere.23 Briefly, medical records were reviewed by study nurses centrally trained by the data coordinating center of the Maternal-Fetal Medicine Units Network. The prospective nature of the study allowed treating physicians to be contacted to resolve questions. Periodic audits also were conducted throughout the collection of data. The institutional review board of the University of Alabama at Birmingham approved the current retrospective study.
From the registry database, we included women if they delivered a live, nonanomalous singleton neonate between 37 0/7 weeks and 41 6/7 weeks of gestation by prelabor cesarean under spinal anesthesia. Exclusion criteria were birth weight less than 2,500 g; asthma; chronic hypertension; preeclampsia or gestational hypertension; renal, heart, or connective tissue disease; pulmonary edema; placental abruption; or chorioamnionitis. Patients undergoing cesarean delivery after ruptured membranes or as a result of a nonreassuring fetal heart rate tracing also were excluded. The database contains up to one value for cord pH and base deficit that is coded as arterial, venous, or unknown. We included only arterial cord values.
All data management and analyses were performed using SAS 9.1. Categorical data were analyzed using the Mantel-Haenszel test for trend, and continuous variables were analyzed with analysis of covariance. All tests of statistical significance were two-tailed and used an α of 0.05. Because we were interested in evaluating the association of maternal BMI with fetal acid-base status at the time of delivery, we evaluated BMI at the time of delivery rather than BMI before the pregnancy or at the first prenatal visit. BMI was examined both as a continuous and categorical (BMI less than 25, 25–29.9, 30–34.9, 35–39.9, and 40 or higher) exposure, and fetal acid-base status was based on cord arterial pH (less than 7.1) and base deficit (12 mmol/L or greater). There is no uniformly agreed-on threshold for defining acidemia. Although an arterial cord pH of 7.10 is approximately two standard deviations below the mean and others have used this threshold,19 most neonates with values more extreme than even more restrictive thresholds (eg, arterial pH less than 7.00 or base deficit of more than 16 mmol/L) do not have complications associated with acidemia. Therefore, we refer to “adverse acid-base status” or “lower pH and higher base deficit” throughout the article rather than “acidemia.” We also analyzed pH and base deficit as continuous variables. Logistic regression was used to adjust the results for identified confounding variables.
Of 56,983 total women in the registry who were delivered by cesarean, 5,742 mother–neonate pairs met our criteria for analysis (Fig. 1). Some variables of interest were missing data for more than half of the cohort (eg, 29,645 women did not have data for cord pH and 31,463 did not have data for base deficit; most of those women also met other exclusion criteria). Demographic data, stratified by BMI categories of less than 25, 25–29.9, 30–34.9, 35–39.9, and 40 or higher, are presented in Table 1.
Among several possible confounders (including sociodemographic variables, number of previous uterine incisions, diabetes, hematocrit, neonatal gender, and birth weight), four—African American race, birth weight, parity, and smoking status—were significantly associated with both BMI and fetal acid-base parameters (umbilical arterial pH and base deficit). When analyzed continuously and adjusted for these four factors, umbilical arterial pH decreased (P<.001) and base deficit increased (P=.005) per unit increase in BMI. For every 10-unit increase in BMI, the pH decreased by 0.01 and the base deficit increased by 0.26 mmol/L. Umbilical arterial pH and base deficit results, analyzed by BMI category, are shown in Table 2. Of note, none of the neonates in this cohort were diagnosed with hypoxic–ischemic encephalopathy.
The type of abdominal incision was missing for 3,098 of the 5,742 women. Therefore, this variable was not included in the analyses reported. However, as a post hoc analysis, we repeated the logistic regression analyses for only those 2,644 women with known abdominal incision types. Ethnicity, birth weight, parity, and smoking status again were the confounders associated with both BMI and acid-base parameters (defined either by pH or base deficit). In the collective group, abdominal incision type was not a significant variable in these models (P=.795 for pH model; P=.295 for base deficit model). For women with a BMI of less than 35, Pfannenstiel incisions, compared with vertical incisions, were not associated with umbilical artery base deficit of 12 mmol/L or more (relative risk [RR] 0.64, 95% confidence interval [CI] 0.35–1.18) or pH less than 7.1 (RR 0.94, 95% CI 0.60–1.49). However, for women with a BMI of 35 or more, Pfannenstiel incisions, compared with vertical incisions, were associated with a higher proportion with umbilical artery base deficit of 12 mmol/L or more (RR 3.40, 95% CI 1.56–7.42). In the women with BMI of 35 or more, those with Pfannenstiel incisions, compared with vertical incisions, had a higher proportion with pH less than 7.1, but this difference did not quite reach statistical significance (RR 1.74, 95% CI 0.99–3.07) (Table 3).
The data from this study demonstrate that, for women undergoing nonemergent prelabor cesarean delivery under spinal anesthesia, obesity is an independent risk factor for lower fetal pH and higher fetal base deficit and that pH declines and base deficit rises as BMI increases. We chose to restrict our analysis to nonlaboring patients to avoid the difficulty in estimating the effect of labor of varying durations and intensity. Likewise, we excluded women who were delivered by cesarean as a result of a nonreassuring fetal heart rate tracing. Furthermore, we excluded women who had medical or obstetric complications that might be associated with uteroplacental insufficiency. Therefore, we demonstrated an association among obesity, spinal anesthesia, and fetal acid-base parameters in a selected population at low risk for acidemia; the effect could be more clinically relevant in higher risk groups. For the reasons described here, our enrollment criteria were quite restrictive. Consequently, most women in the database undergoing cesarean delivery were excluded from our analysis. Although excluding such a large proportion of the cohort could introduce unmeasured bias, this potential weakness was necessary to limit unmeasured bias introduced by labor, fetal heart rate tracing abnormalities, and medical or obstetric conditions that could be associated with uteroplacental insufficiency.
As with all such analyses, our study is limited by its retrospective nature and the fact that these data were collected with the purpose of conducting other analyses. Biases such as misclassification potentially affect our results. As an example, we cannot be certain that all cord gases classified as arterial are correctly classified. However, we think that it is very unlikely that such misclassification could have introduced a systematic bias related to BMI. The large proportion of women that were excluded from the analysis is a potential concern, but we anticipated that a large number of women would be excluded as a result of our restrictive enrollment criteria. The inability to evaluate type of abdominal incision as an exposure in the majority of women is a limitation. Likewise, cord gas data were not available for many women who otherwise would have met our enrollment criteria, because some of the centers in the network did not routinely assess cord gases. It would be anticipated that there would be center-related differences between those women who had cord gas data available for analysis and those for whom these data are missing (eg, demographic differences between centers that collect cord gases universally and those that do not). However, there is no variable in the data set to account for site of delivery, thus precluding assessment of that factor in the analysis. Ideally, time from skin incision to delivery of the neonate would be included as a separate variable. However, having already included the number of prior uterine incisions as a variable, time from skin incision to delivery of the neonate is in the causal pathway of obesity being associated with lower pH and higher base deficit in the umbilical artery. Therefore, it was not evaluated in the models. Finally, we do not have information related to the details of anesthesia management (eg, management of spinal anesthesia-related hypotension) at participating centers.
Among the strengths of our study, these data were carefully collected prospectively by trained research staff at centers experienced in clinical research. In addition, despite very strict enrollment criteria for the current analysis, we had a fairly robust sample size.
Others have reported on the association between obesity and fetal acid-base status. However, the findings have not been consistent. Galan and colleagues,19 in a retrospective cohort study, reported that women with class II or III obesity (BMI 35 or higher) were more likely to have an umbilical artery pH less than 7.10 than were normal-weight women (adjusted odds ratio 2.15, 95% CI 1.05–4.38). In contrast, Maisonneuve and colleagues,20 in a case–control study, reported that cases (umbilical artery pH less than 7.00) were more likely to be obese (BMI 30 or higher) than controls, but the difference did not remain statistically significant in multivariate analysis. Both of these studies included women from the general obstetric population, so factors such as labor varying fetal status might have had an effect on the results.
It is possible that the effect of BMI on fetal acid-base status is the result of impaired pulmonary function caused by obesity. However, we speculate that at least part of the cause of the association between obesity and fetal acid-base status that we found in our analysis is the weight of the abdominal wall causing impaired venous return and decreased placental perfusion. Furthermore, we postulate that retraction of the panniculus to create a Pfannenstiel abdominal incision in selected extremely obese pregnant women might exacerbate the effect. This idea seems to be supported by our finding that Pfannenstiel incisions were associated with lower pH and higher base deficit in the neonates of women with a BMI of 35 or higher but not those women with a BMI of less than 35.
Obesity is a topic that, for obstetrics, has increased greatly in relevance in the past few decades. In a study from our center over a 20-year period from 1980 to 1999, the obesity rate in the obstetric population (BMI 30 or higher before pregnancy) more than doubled from 16% to 36%.24 Since then, the obesity rate among reproductive-aged women in the United States has continued to increase. In 1999, the rate was 28%; it was 34% in 2008.3 The rate at our center currently exceeds 40%. Reversing this trend of an increasing prevalence of obesity would be ideal. Short of that goal, we should at least try to minimize the likelihood of complications in such patients. Whether the association between obesity and fetal acid-base status exists in other populations and whether obesity causes an increased propensity to spinal anesthesia-related hypotension should be evaluated. Likewise, because the rate of cesarean delivery has increased dramatically in recent years and because obesity is associated with an increased likelihood of cesarean delivery, the advantages and disadvantages of various approaches to cesarean delivery in obese women (eg, type of abdominal incision) should be investigated further. Such analyses should include fetal acid-base status among the outcomes evaluated.
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© 2013 by The American College of Obstetricians and Gynecologists.
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