Obesity is a complex and multifactorial metabolic heterogeneous disorder that chronically affects the individual. The World Health Organization (WHO) characterizes obesity as a pandemic health issue with a higher prevalence in females than males. In the United States, more than 33% of women are obese.¹ Obesity is the second leading cause of preventable deaths. While the complete pathogenesis of obesity is only partly understood, its effects on health are far reaching, with the aggregate cost of obesity in the United States ranging from 5% to 7% of annual medical expenditures.² Obesity is defined as 35% or greater total body fat in women.³

In 1832, Quetelet proposed an index to characterize human health status (Table 20-1).⁴ Keys reaffirmed the validity of this index in 1972 by introducing the concept of the body mass index (BMI) and recommending it as a proxy for measuring body fat.⁵ WHO and the National Institutes of Health (NIH) in the United States classify obesity utilizing BMI. This marker is defined as the individual’s body weight divided by the square of his or her height, or BMI = W/H², and is reported as kilograms per square meter (kg/m²) (Table 20-1). BMI values are age independent and are used for both sexes. Maternal ethnicity is under scrutiny to determine its association with BMI.

Obesity represents increasingly serious maternal and perinatal health concerns when associated with a woman’s pregnancy. In 1988, Thomson and Hanley stated that short maternal stature and increased BMI predisposed patients to difficult labor. WHO estimated that 60% of women between the ages of 20 and 40 years are overweight or obese, as classified by their BMI. In the United States, more than 50% of pregnant women are overweight or obese, and 8% of reproductive-age women are extremely obese, with a BMI greater than 50 kg/m², a group that is rapidly increasing,¹ as reaffirmed by the National Health and Nutrition Examination Survey (NHANES).

Women suffering from obesity are at an increased risk for delayed conception.⁶ In the preconception period, obstetricians have an opportunity to counsel obese women. Timing of these efforts is critical to pre-date the pregnancy and decrease, or eliminate, the fetal exposure to in utero triggers that will affect the fetuses’ life in the long term.

It has been demonstrated by a number of studies that 25%–35% of children from obese mothers are obese by 11 years of age. They have an increased risk of developing metabolic syndrome (MS), defined as the presence of obesity, hypertension, dyslipidemia, and glucose intolerance.⁷ Once pregnant, they have an increased risk for multiple morbidities. The Barker hypothesis⁸ clearly expresses the need to understand the origins of common complex adult-onset medical disorders, obesity among them. Parental obesity changes the molecular composition of the sperm and the oocyte, and it modifies the epigenetic reprogramming that occurs at the time of conception, both of which negatively affect embryonic and fetal development.⁹ In our study of 228 pregnant women with a BMI higher than 50 kg/m² (extreme obesity), we found a prevalence of 31.8% for carbohydrate intolerance (pregestational or gestational diabetes) and 46.3% for hypertensive diseases (chronic, gestational, or preeclampsia).

Early prenatal care is not frequent in this population because irregular menses or a false sense of inability to conceive makes early pregnancy detection an infrequent clinical event. The use of pelvic ultrasound is impaired by the maternal body habitus. The use of invasive transvaginal evaluation becomes necessary, as early pregnancy prior to 18 weeks may be compromised. Complete fetal surveys are frequently difficult, and repeated exams do not improve the exploration. Often, some fetal segments are suboptimally visualized during the entire pregnancy. The practice of bariatric obstetrics presents a number of challenges to the clinicians. As obese women approach the third trimester, they are at an increased risk for intrauterine fetal death and altered fetal growth.

The use of serial fetal ultrasound evaluations late in pregnancy in the obese is hindered by excessive acoustic shadowing, rendering the exams inaccurate and of little clinical use. Occasionally, the vaginal transducer is occasionally placed in the maternal navel, the area where the abdominal wall is thinner and allows for increasing ease in the examination. Changes in the maternal position on the examining table or combined transvaginal-transabdominal access may be necessary to complete the fetal evaluation. 4

During labor, obese women often experience abnormal labor patterns, complications with anesthesia management, or complicated and emergent cesarean deliveries. Their neonates are at risk for needing neonatal resuscitation and admission to the neonatal intensive care unit. The maternal complications extend to the postpartum period, with postpartum hemorrhage (PPH), surgical site infections (SSIs), and abnormal clotting events. These issues prolong the maternal recovery period and negatively affect her ability to care for her newborn infant. Further, obesity and its ongoing metabolic consequences, represented by a chronic inflammatory condition, may affect the proper function of the placenta, with possible dire consequences on fetal growth, development, and maturity. These effects, if not corrected early in the gestational period by appropriate interventions, will influence placental function and gene expression, and therefore negatively affect maternal and perinatal outcomes.¹⁰

It is beyond the scope of this chapter to provide a comprehensive review and bibliography associated with human parturition, human labor, and our understanding of its clinical evolution through the last decades. The definitions of normal and abnormal labor present a challenge to investigators and clinicians. Since the work of Samuel Reynolds,¹¹ arguably considered the “father of the uterus,” and others,¹² investigators have attempted to provide a plausible physiologic explanation for the onset of spontaneous term labor in the human,¹³ yet this has proven to be difficult to determine.

Labor is defined as the physiologic process that occurs from the onset of regular uterine contractions until the expulsion of the placenta. This tight definition implies that uterine contractions cause demonstrable and progressive cervical changes.¹⁴ At the myometrial site, the interaction between calcium and the calmodulin-myosin light-chain kinase sequence is critical for normal uterine contractions to occur. Clinicians use frequency of uterine contractions, maternal discomfort generated during these contractions, cervical effacement, and cervical dilation to mark the beginning of active labor.

Progress of labor was made objective in 1954 by Friedman¹⁵ when he described a characteristic pattern of cervical dilation, time, and the descent of the fetal presenting part. In 1972, Friedman defined protraction disorders of labor as either when the cervix stops dilating or when the fetus stops descending, per unit time (1 hour).¹⁶ This approach not only allowed obstetricians to make a diagnosis of abnormal labor but also allowed them to understand that several factors influence labor progression or lack thereof, and that at certain times active interventions may be required.

In the last decade, efforts have been made to reevaluate the original labor curve in view of evolving demographics and changes in obstetrical care. In 2004, half a century after Friedman’s original publication, Cesario conducted a multi-institutional international survey of maternity units providing labor care. This study included nulliparous and multiparous women aged 14 to 44 with a single, live, vertex fetus, in spontaneous labor without the use of synthetic oxytocin or labor analgesia. Over 400 patients were involved; 23% were nulliparous. The average length of labor was similar to that described by Friedman; however, a wider range of “normal” was found in the new study.¹⁷ This finding emphasizes the clinical importance of differentiating normal from abnormal labor beyond subjectivity. In 2002, Zhang et al. again challenged Friedman’s concepts, and while they uncovered differences from the original Friedman labor curve,¹⁸ maternal BMI was not included as a variable.

The beginning of normal labor is difficult to establish accurately, and the progress of normal labor is subject to considerable biologic variation. This clinical debate continues in association with the new consensus for the safe reduction of primary cesarean deliveries, released by the American College of Obstetricians and Gynecologists (ACOG) and the Society for Maternal Fetal Medicine.¹⁹ This consensus is based on the findings of newer research that focuses on patterns of spontaneous labor. Study methodologies and labor analysis techniques that have evolved over the past half-century were questioned,²⁰ and it was determined that, in the absence of obvious maternal-fetal complications, the treatment of labor abnormalities and dystocia secondary to “failure to progress” must extend beyond immediate performance of a cesarean delivery.²¹

Dystocia, defined as an abnormal uterine contractility pattern, a fetal structural or positional anomaly, a maternal pelvic anatomic anomaly, or some combination thereof, is the leading indication for cesarean operative delivery, accounting for approximately 50% of the cesareans performed in the United States. Clinical criteria needed to establish the diagnosis of dystocia are multiple. In 2009, cesarean delivery prevalence in the United States was 32.9%, with an average mean prevalence of 22.0% in women with no previous cesarean section.^22,23 In our study group of 228 extremely obese parturients, BMI of 50 kg/m² or greater, the cesarean delivery prevalence was 63% for nulliparous patients and 19.2% for multiparous patients, with a vaginal delivery occurring in only 22.4% of cases. This information demonstrates the difficulty of accurately reporting the prevalence of term, spontaneous labor and delivery in obese women and comparing this to the prevalence of labor in nonobese women with singleton, cephalic fetuses without other labor abnormalities.

For over a decade, it has been postulated that the course of labor in overweight and obese women differs from that in normal weight women, and that elevated maternal BMI is associated with dysfunctional labor. Maternal obesity may be an independent or a synergistic factor for uterine contraction dysfunction.^24,25 One area of research focuses on cholesterol and its effect on labor because increased BMI and hypercholesterolemia often coexist. Cholesterol, an essential component of the cell membrane in humans, has been reported to be an important factor in the control of smooth muscle contractility. In animal studies, increased cholesterol is associated with a decrease in myometrial activity; cholesterol may be related to uterine quiescence.²⁶

Efforts are ongoing to elucidate the basic physiologic causes of this myometrial dysfunction and its association with maternal obesity in humans. For example, investigators are exploring the role of caveolae.²⁵ Caveolae are the invaginations of the cell membrane of myometrial cells, and they are stabilized by the cholesterol-binding protein caveolin. This area of the myometrial cell membrane may be involved in the excitation-contraction phase of myometrial cells and may be influenced by hormone levels, specifically of estrogens. The increase in cholesterol and triglycerides in normal human pregnancies maintains the nutrient supply needed by the growing fetus and may be necessary to maintain uterine quiescence in the early weeks of pregnancy, yet high levels of cholesterol, often present in obese patients, may hinder normal uterine contractility during labor.²⁶ Changes in lipid metabolism during pregnancy may lead to abnormal labor in obese women. Evidence has also been offered linking stress and maternal obesity to labor dysfunction, wherein increased levels of leptin, a hormone secreted by adipose tissue and uterine tissue and believed to increase in times of stress, synergistically impair the contractile mechanisms of the myometrium and lead to abnormal labor and increased cesarean rate.²⁷

Adipose tissue in the visceral compartments has been considered an active endocrine organ that produces and releases biologically active elements, such as adipocytokines or adipokines. One of these elements is apelin, an adipocytokine expressed in several tissues, including the placenta, but primarily in adipose tissue. Apelin levels are increased in the obese population. In vitro studies have demonstrated a relaxing effect of apelin on smooth muscle, such as the myometrium, the mechanism of which has not been completely elucidated. The adipokine ghrelin has also been reported to have a potential role in metabolic modulation of uterine contractility in the obese parturient. In addition, the chronic low-grade inflammatory state characterized by obesity increases oxidative stress, and this effect is responsible for an irregular production of adipokines, which have adverse systemic effects.^27,28

One of these systemic effects may be a higher concentration of maternal serum lactic acid, secondary to increased acidosis.^29,30 In vitro studies have demonstrated that this metabolic change may affect the myometrium in the human, specifically by reducing contraction amplitude and decreasing response to oxytocin.³⁰

Evidence is also accumulating that demonstrates the independent influence of maternal obesity on the progress of labor. The myometrium of obese women in labor contracts with less power and less frequency and has less calcium transmembrane flux than that of the nonobese pregnant women.³¹

In the obese patient, the first stage of labor is often characterized by slow progress, unrelated to fetal size,³² resulting in dysfunctional patterns of dilation, the mechanism of which may be mediated by any of the factors discussed previously. A recent study revealed a 3-fold increase in the rate of arrest of dilation during the first stage of spontaneous labor in obese women when compared to nonobese women with otherwise-uncomplicated term pregnancies. Specifically, arrest of dilation was diagnosed in 5.5% of the lean women and in 18.8% of the obese women (p = .002). Intensity of contractions was not reported. The difference in neonatal weights in the two groups was not statistically significant and did not explain the dystocia diagnosed in the obese group. The diagnosis of arrest of labor was made by utilizing Friedman’s definitions and laborgram²² (Table 20-2). These definitions have been utilized in the training of obstetricians and clinically applied for the last 50 years. A revision of this classical approach, with the objective of safely preventing a primary cesarean to meet the goal of Healthy People 2020, has been published, yet the labor patterns specific to the obese parturient were not addressed by Friedman’s database, Zhang’s studies, or the consensus documents.

A recent large study conducted by the Swedish registry reviewed over 50,000 nulliparous women with singleton pregnancies and spontaneous labor onset and documented BMI.³³ Time in labor was reported. Oxytocin for augmentation was utilized in 45% of normal-weight women and in 55.1% of class III obese women (p < .001). The emergency cesarean rate, defined as a cesarean performed while in active labor, was 5.1% in normal-weight women and 15.6% in obese parturients (p < .001). There was a significant association between BMI and length of labor, with BMI less than 18.5 and BMI greater than 40, p < .001. In the obese population, prolonged labor was confined to the first stage of labor. While the predominant etiology of this dysfunction is unclear, an additional factor considered was increased maternal intrapelvic soft tissue.³⁴

Understanding the physiology of labor in the obese parturient is critical to improve the clinical management of labor in this population. Further supportive evidence was provided by Vahratian et al. in the observational study of 612 term nulliparous obese patients: Obese women were more likely to have an inadequate contraction pattern during the first stage of labor, requiring oxytocin for induction or augmentation. The authors showed a trend to slower progress from 4 to 6 cm of cervical dilation and a longer median duration from 4 to 10 cm of cervical dilation (7.0 vs. 5.4 hours, p < .001). It was again demonstrated that labor progression in obese women, when compared to normal-weight women, is significantly slower prior to 7 cm of cervical dilation (Figure 20-1). This is a consistent clinical finding in various obese patient populations, and it must be noted before interventions are performed (Figure 20-2).³⁵