INTRODUCTION — Pregnant people with obesity are at increased risk for an array of maternal and perinatal complications, and the risks are amplified with increasing severity of the condition [1-3]. It has been estimated that one-quarter of pregnancy complications (eg, gestational hypertension, preeclampsia, gestational diabetes, preterm birth, large for gestational age [LGA] infant) are attributable to maternal obesity or overweight . Patients with prepregnancy obesity followed by high gestational weight gain have the highest risks of pregnancy complications. Offspring of pregnant people with obesity are at increased risk of developing obesity in childhood and as adults [4,5].
Obstetric providers should be aware of these risks and modify patient care before pregnancy, during pregnancy, and postpartum to reduce the risk of these adverse outcomes. Although clinical practice guidelines for management of pregnant people and people planning pregnancy with obesity vary, they consistently recommend pregnancy risk counseling, a healthy diet, exercise, and dietician referral for managing weight loss and gestational weight gain [6,7].
This topic will discuss issues related to obesity and pregnancy. Obesity in the nonpregnant population is reviewed separately. (See "Obesity in adults: Prevalence, screening, and evaluation" and "Overweight and obesity in adults: Health consequences" and "Obesity in adults: Overview of management".)
PATHOBIOLOGY — Adipose tissue is an active endocrine organ. When present in excess, it can have dysregulatory effects on metabolic, vascular, and, particularly, inflammatory pathways in many organ systems during pregnancy, and thereby affect obstetric outcomes [8,9]. For example, obesity-related insulin resistance and abnormalities in inflammatory pathways can affect placental growth and function  and have been linked to development of preeclampsia [11,12]. The observation that some obesity-related pregnancy complications increase with increasing severity of obesity supports the role of obesity in the pathogenesis of these adverse outcomes .
Maternal obesity may affect long-term offspring outcomes as a result of epigenetic changes induced by fetal exposure to increased levels of glucose, insulin, lipids, and inflammatory cytokines during development. These in utero effects may cause permanent or transient changes in metabolic programming, leading to adverse health outcomes in adult life (fetal origins of adult disease theory [Barker hypothesis]) [14,15]. The potential programming effects of maternal overnutrition are difficult to study, however, because of the complex relationships between the maternal metabolic milieu and the developing fetus and the influence of postnatal factors, including lifestyle and environment .
DEFINITION AND CLASSIFICATION OF OBESITY — Obesity in the nonpregnant population is defined and classified as shown in the table (table 1). (See "Obesity in adults: Prevalence, screening, and evaluation", section on 'Body mass index'.)
This standard definition/classification for the nonpregnant population do not adapt well to the pregnant population since a pregnant person's weight increases over a relatively short interval of time, and much of the weight gain is related to accretion of mass (ie, fetus, placenta, amniotic fluid, blood) that will be lost at delivery. Since no standard pregnancy-specific definition of obesity exists, pregnant patients are often considered obese or nonobese based on their prepregnancy body mass index (BMI). (See "Gestational weight gain", section on 'Physiologic weight gain'.)
PREVALENCE OF OBESITY IN REPRODUCTIVE-AGE FEMALES — The prevalence of obesity in reproductive-age and pregnant females varies widely depending upon the definition used, study year, and characteristics of the study population, but has increased in concordance with the increased prevalence of obesity in the general population and is projected to continue to increase . For example:
In the United States, National Center for Health Statistics data for 2017 to 2018 indicated :
●Proportion of females ages 20 to 39 years with obesity (body mass index [BMI] ≥30 kg/m2): 39.7 percent
●Prevalence by race: non-Hispanic Black females (57 percent), Hispanic females (44 percent), non-Hispanic White females (40 percent), non-Hispanic Asian females (17.2 percent)
●Proportion of adults (female and male) ages 20 to 39 years with severe obesity (ie, class 3: BMI ≥40 kg/m2): 9 percent
In Finland, the incidence of severe obesity (BMI ≥40 kg/m2) among mothers of singletons was (1.91 percent) in 2018, which represented a 103 percent increase since 2004 .
POTENTIAL ISSUES IN PREGNANCY
Overall risk of severe morbidity or mortality — In a population-based study including over 740,000 pregnant people, the composite "severe maternal morbidity or mortality" rates by body mass index (BMI) were :
●Normal BMI – 143 per 10,000
●Overweight – 160 per 10,000
●Class 1 obesity – 168 per 10,000
●Class 2 obesity – 178 per 10,000
●Class 3 obesity – 203 per 10,000
Severe morbidity included hemorrhage requiring transfusion; serious cardiac, respiratory, cerebrovascular, or hematologic complications; venous thrombosis/embolism; sepsis; shock; hepatic or renal failure; anesthesia-related complications; and uterine rupture.
Compared with pregnant people with BMIs in the normal range, a small but statistically significant increase in the composite outcome was observed in overweight patients and those with class 1, 2, and 3 obesity: adjusted odds ratio (OR) 1.1, 1.1, 1.2, and 1.4, respectively.
Pregnant people with BMI ≥50 kg/m2 (super obesity) have a very high risk of adverse maternal and perinatal outcomes (adjusted OR 2.5 to 80) compared with those with BMI <50 kg/m2 . The rate of serious maternal morbidity, including renal failure, air and thrombotic embolism, heart failure, mechanical ventilation, and transfusion, was 556 per 10,000 births .
Early pregnancy loss — Obesity appears to modestly increase the risk of early pregnancy loss. Differences in patient characteristics and study designs, however, limit the validity of findings in systematic reviews.
●In a systematic review evaluating obesity and miscarriage, the frequency of ≥1 miscarriage after spontaneous conception by BMI classification was: obese (16.6 percent), overweight (11.8 percent), normal (10.7 percent) . When compared with the normal BMI group, the odds of having ≥1 miscarriage were increased in the obese BMI (OR 1.31, 95% CI 1.18-1.46) and overweight BMI (OR 1.11, 95% CI 1.00-1.24) groups.
●In a systematic review evaluating obesity and recurrent miscarriage, among patients with recurrent miscarriage, the presence of obesity nearly doubled the risk of future pregnancy loss compared with a normal BMI (OR 1.75, 95% CI 1.24-2.47) . Overweight nonobese patients may also be at increased risk compared with those with a normal BMI (OR 1.15, 95% CI 0.87-1.51).
The etiology of the increased risk for pregnancy loss is not clear. Euploid embryos accounted for the observed increased risk among the overweight and obese groups in one study , but not in another . One mechanism for early excess loss of euploid embryos may be an unfavorable hormonal environment related to excess weight and leading to poor endometrial receptivity . Another mechanism may be endometrial inflammation related to polycystic ovarian syndrome (PCOS); PCOS has been associated with a miscarriage rate that is 20 to 40 percent higher than the baseline rate in the general obstetric population . A prospective study suggested that pregnancy worsens the low-grade chronic inflammation commonly seen in PCOS patients and may account, at least in part, for the excess risk of adverse pregnancy outcomes, such as miscarriage .
●Occult type 2 diabetes – Obesity is a risk factor for development of type 2 diabetes. If screening has never been performed or not performed recently, patients will not be aware that they have diabetes. Screening in early pregnancy will detect these patients. (See 'First trimester' below.)
●Gestational diabetes – The prevalence of gestational diabetes mellitus (GDM) is significantly higher in individuals with obesity than in the general obstetric population [29,30]. The risk increases with increasing maternal weight and BMI (table 2) and increased by 0.92 percent for every 1 kg/m2 increase in BMI in one review [1,31,32]. The increased risk of GDM is related to an exaggerated increase in insulin resistance in the obese state .
Pregnancy-associated hypertension — Maternal BMI is consistently reported as an independent risk factor for both preeclampsia and gestational hypertension (table 2) [34-42]. In a systematic review of 13 cohort studies comprising nearly 1.4 million pregnant people, the risk of preeclampsia doubled with each 5 to 7 kg/m2 increase in prepregnancy BMI . This relationship persisted in studies that excluded individuals with chronic hypertension, diabetes mellitus, or multiple gestations, and after adjustment for other confounders. Studies of patients who underwent bariatric surgery suggest that weight loss significantly reduces the occurrence of preeclampsia. (See "Fertility and pregnancy after bariatric surgery", section on 'Preeclampsia and other hypertensive disorders of pregnancy'.)
The mechanism whereby obesity imparts an increased risk for preeclampsia is not well defined. The pathophysiologic changes associated with obesity-related cardiovascular risk, such as insulin resistance, hyperlipidemia, heightened state of systemic inflammation, and oxidative stress may also be responsible for the increased incidence of preeclampsia in pregnant people with obesity as these factors can also affect placental development and function [43-46]. In particular, adipose tissue is a rich source of proinflammatory cytokines, which can promote the expression of maternal antiangiogenic factors that have been implicated in the pathogenesis of preeclampsia. (See "Overweight and obesity in adults: Health consequences", section on 'Hypertension' and "Preeclampsia: Pathogenesis".)
Indicated and spontaneous preterm birth — Obesity increases the risk of medically indicated preterm birth, primarily due to obesity-related maternal disorders, such as hypertension, preeclampsia, and diabetes. In a systematic review, pregnant people who were overweight or obese had an increased risk of induced preterm birth compared with those of normal BMI (relative risk [RR] 1.30, 95% CI 1.23-1.37, five studies), and the risk increased with increasing weight .
Whether obesity increases the risk for spontaneous preterm birth is less clear. The systematic review found no difference in the rate of spontaneous preterm birth between groups; however, heterogeneity was high. A subsequent population-based cohort study from Sweden of over 1.5 million singleton deliveries confirmed that pregnant people who were overweight or obese were at increased risk of medically indicated preterm birth at all gestational ages . There was a significant relationship between severity of obesity and risk of spontaneous extremely preterm birth between 22 and 27 weeks, but not for very preterm (28 to 31 weeks) or moderately preterm (32 to 36 weeks) birth after adjustment of confounders. The authors hypothesized that obesity-related inflammatory up-regulation, as well as other factors (eg, subclinical genital tract infection), increased the risk of spontaneous extremely preterm birth.
Several studies have also demonstrated an independent association between PCOS and spontaneous preterm birth, including cervical insufficiency [49,50]. The precise mechanism by which PCOS modulates the risk for spontaneous preterm birth or cervical insufficiency, independent from, or as part of, the obesity effects, is unclear but may be related to changes in the hormonal milieu (eg, increased relaxin levels) that weaken the cervical collagen matrix.
Postterm pregnancy — The body of evidence supports an association between obesity and postterm pregnancy (eg, OR 1.2 to 1.7 in four population-based studies [29,31,51,52]) [29,31,51-55].
The mechanism by which obesity prolongs pregnancy has not been determined. One hypothesis is that gestational age calculated from last menstrual period (LMP) overestimates true fetal age because females with obesity tend to be oligo-ovulatory; this hypothesis is supported by studies of early ultrasound assessment of gestational age in this population that found the estimated date of delivery (EDD) by LMP was earlier than the EDD by ultrasound [56-58].
In addition, a multitude of prelabor changes in the placenta, cervix, amnion, and myometrium contribute to the onset of labor. Obesity-related hormonal changes may interfere with the hormonal pathways for the initiation of parturition and delay its onset, probably by affecting the propagation and synchronization of uterine contractions [59-63]. For example, obesity is associated with elevated circulating levels of tumor necrosis factor-alpha, and the combination of obesity and periodontal disease is associated with elevated serum interleukin-1 beta concentrations [64,65]. In turn, IL-1 beta downregulates decidual cell progesterone receptor  to promote functional progesterone withdrawal and both cytokines up-regulate third trimester decidual cell mediators of preterm birth, including Colony Stimulating Factor-2 (CSF2) and interleukin-8 that recruit and/or activate granulocytes, matrix metalloproteinases (MMPs) 1-3 that efficiently degrade fetal membrane and cervical extracellular matrices, and prostaglandin F2 that promotes myometrial contractions [61-63,66]. Other postulated hormonal and mechanistic changes include decreased placental corticotropin-releasing hormone and fetal cortisol release, decreased MMP function, decreased connexin-43 gap junction expression, increased leptin and cholesterol levels, increased reactive oxygen species, and increased free fatty acids . (See "Physiology of parturition at term".)
Multifetal pregnancy — An increased incidence of dizygotic but not monozygotic twin gestation has been observed among pregnant people with obesity [30,68,69]. In an analysis of nearly 52,000 pregnancies (561 twin pregnancies) in the Collaborative Perinatal Project, the incidence of dizygotic twins in pregnant people with BMI ≥30 kg/m2 versus <25 kg/m2 was 1.1 and 0.5 percent, respectively . These data were derived from patients in 12 hospitals in the United States from 1959 to 1966, before widespread use of agents for ovulation induction.
The association between increased maternal BMI and dizygotic twinning has been attributed to elevated follicle-stimulating hormone (FSH) levels in females with obesity, although a direct relationship between obesity and elevated FSH has not been proven.
Obstructive sleep apnea — The prevalence of obstructive sleep apnea (OSA) progressively increases as BMI increases. OSA may be precipitated or exacerbated during pregnancy and may increase the risk for preeclampsia and GDM.
Postpartum, patients with OSA may be more susceptible to respiratory depression associated with neuraxial analgesia with either continuous epidural lipophilic opioid solutions (eg, containing fentanyl), or single-injection hydrophilic long-acting neuraxial opioids (eg, morphine, hydromorphone). However, data on this issue are limited, and the incidence of respiratory depression is unknown. (See "Obstructive sleep apnea in pregnancy" and "Intraoperative management of adults with obstructive sleep apnea", section on 'Regional anesthesia/analgesia'.)
Carpal tunnel syndrome — Both obesity and pregnancy are associated with an increased risk of carpal tunnel syndrome. (See "Neurologic disorders complicating pregnancy", section on 'Carpal tunnel syndrome'.)
Detection of congenital anomalies — The incidence of congenital anomalies is increased in fetuses of pregnant people with obesity (see 'Congenital anomalies' below). However, anomalies are more difficult to detect with prenatal ultrasonography, resulting in fewer optimal examinations and prenatal diagnoses [70-78]. Maternal obesity reduces the detection of fetal anomalies by at least 20 percent compared with pregnant people with a normal BMI [74,77,79].
Progress of labor — Maternal obesity appears to have a modest impact on labor progression that is independent of fetal size [80-89] but related to maternal BMI. For example, in a large study, the median times for nulliparous patients to dilate from 4 to 10 cm at BMI <25, 30 to 34.9, 35 to 39.9, and ≥40 kg/m2 were 5.4, 6, 6.7, and 7.7 hours, respectively, after adjustment for confounders . A similar trend was observed in parous patients.
The duration of the second stage of labor does not appear to differ among patients whose prepregnancy BMI falls into normal, overweight, and obese categories [82,84,90].
Induction issues — Pregnant people with obesity are at increased risk for labor induction due to their increased risk for pregnancy complications requiring early delivery [51,55,91]. They are also at increased risk for longer inductions, induction failure, and cesarean birth for induction failure. The magnitude of risk is illustrated by the following representative studies:
●Labor duration – In one study, the duration of labor in induced nulliparous people increased by 0.3 hours for each 10 kg increment in weight (adjusted for maternal age, infant birth weight, initial cervical dilation, and diabetes); this relationship was not observed in parous people .
●Induction failure – In another study, pregnant people with obesity were twice as likely to experience a failed induction as those of normal weight, and the risk increased with increasing class of obesity (ORs for class 1, 2, and 3: 1.85, 2.30, and 2.89, respectively) .
●Cesarean birth – In a study of induction of pregnant people with class 3 obesity, the cesarean birth rate by BMI were :
•BMI 40 to 50 kg/m2: 46 percent
•BMI 50 to 60 kg/m2: 63 percent
•BMI >60 kg/m2: 69 percent
Cesarean birth — Obesity is a risk factor for both planned and intrapartum cesarean birth, and the risk increases with increasing maternal weight [93,94]. In the United States in 2020, the cesarean birth rate in patients of normal BMI, obesity class 1, obesity class 2, and obesity class 3 was approximately 25, 37, 43, and 52 percent, respectively .
Obesity-related pregnancy complications, higher infant birth weight, and increased frequency of preterm and postterm birth account for some of the excess risk of cesarean birth [95-101]. However, obesity also appears to be an independent risk factor, possibly because of the adverse effects on labor progress described above. (See 'Progress of labor' above.)
Cesarean birth of the pregnant patient with obesity is associated with numerous perioperative concerns, which are reviewed separately. (See "Cesarean birth: Overview of issues for patients with obesity" and 'Venous thromboembolism' below.)
Trial of labor after cesarean birth — Observational studies have generally reported that a trial of labor after a cesarean birth (TOLAC) is less likely to result in vaginal birth in pregnant people with obesity (eg, failed TOLAC with normal BMI: 15 percent; obese BMI: 30 percent in one large study ). For this reason, BMI is one of the variables included in calculators that estimate an individual's chances of having a vaginal birth after a previous cesarean birth. However, obesity is not a contraindication to TOLAC; the decision should made through the process of shared medical decision-making. (See "Choosing the route of delivery after cesarean birth", section on 'Patients with obesity'.)
Anesthesia considerations — Pregnant patients with obesity undergoing neuraxial anesthesia for labor or delivery have been reported to have higher rates of multiple attempts at placement , inadvertent dural puncture , failed analgesia requiring a repeat procedure , and hypotension . If general anesthesia is required, obesity is one of the factors predictive of a difficult airway [106,107]. (See "Anesthesia for the patient with obesity".)
Complications related to macrosomia — Macrosomia (defined as birth weight >4000 g) is more common in offspring of pregnant people with obesity (table 2) and an important risk factor for shoulder dystocia. (See "Shoulder dystocia: Risk factors and planning birth of high-risk pregnancies", section on 'High birth weight' and "Shoulder dystocia: Risk factors and planning birth of high-risk pregnancies", section on 'Maternal obesity and excessive gestational weight gain'.)
Other potential intrapartum complications of macrosomia include dysfunctional labor, and, in turn, operative intervention (forceps or vacuum assisted vaginal birth, cesarean birth), maternal genital tract laceration, and postpartum hemorrhage. (See "Fetal macrosomia", section on 'Risk factors'.)
Postpartum hemorrhage — One meta-analysis noted an increased risk of postpartum hemorrhage (PPH) in patients with obesity  whereas another did not . An association between obesity and PPH would not be surprising because obesity is associated with several complications (eg, macrosomia, induced labor, preeclampsia, cesarean birth) that are also risk factors for PPH. (See "Overview of postpartum hemorrhage", section on 'Risk factors for PPH'.)
Venous thromboembolism — Obesity, the pregnant/postpartum state, and cesarean birth are independent risk factors for venous thromboembolism (VTE), which is a major cause of maternal morbidity and mortality, particularly postpartum . In one review, the odds of postpartum VTE in patients with class 1, 2, and 3 obesity were OR 2.5, 2.9, and 4.6, respectively, compared with postpartum patients with a normal BMI . The absolute risk of VTE in patients with one or more risk factors for VTE depends on the individual risk factors. (See "Deep vein thrombosis in pregnancy: Epidemiology, pathogenesis, and diagnosis", section on 'Risk factors' and 'Postpartum care' below.)
Infection — Pregnant people with obesity are at higher risk for postpartum infection (eg, wound, endometritis), regardless of mode of delivery and despite use of prophylactic antibiotics [31,34,106,112-114]. Poor vascularity of subcutaneous adipose tissue and formation of seromas and hematomas account, at least in part, for the increased risk of wound infection. Some prophylactic antibiotic dosing regimens differ for obese versus nonobese patients. (See "Cesarean birth: Overview of issues for patients with obesity".)
Respiratory depression — Patients with OSA are at increased risk for respiratory depression when opioids are administered for postpartum pain control. (See 'Obstructive sleep apnea' above and "Obstructive sleep apnea in pregnancy", section on 'Postpartum management'.)
Postpartum depression — A meta-analysis of 62 studies of obesity and mental disorders during pregnancy and postpartum noted an increased risk for postpartum depression in people with obesity (OR 1.30, 95% CI 1.20-1.42) .
Congenital anomalies — As noted, pregnant people with obesity are at increased risk for having a fetus with congenital anomalies, including neural tube defects (NTDs), cardiac malformations, orofacial defects, and limb reduction abnormalities . The risk appears to increase with an increasing degree of maternal obesity. The mechanism for these associations is not well-defined but is likely related to an altered nutritional milieu during fetal development .
●In a systematic review (39 studies) and meta-analysis (18 studies), compared with offspring of pregnancies in females with a normal BMI, offspring of females with obesity were at increased risk of :
•NTDs(OR 1.87, 95% CI 1.62-2.15), spina bifida (OR 2.24, 95% CI 1.86-2.69), hydrocephaly (OR 1.68, 95% CI 1.19-2.36).
•Cardiovascular anomalies (OR 1.30, 95% CI 1.12-1.51), septal anomalies (OR 1.20, 95% CI 1.09-1.31).
•Cleft palate (OR 1.23, 95% CI 1.03-1.47), cleft lip and palate (OR 1.20, 95% CI 1.03-1.40).
•Anorectal atresia (OR 1.48, 95% CI 1.12-1.97).
•Limb reduction anomalies (OR 1.34, 95% CI 1.03-1.73).
By contrast, the risk of gastroschisis was significantly reduced (OR 0.17, 95% CI 0.10-0.30).
Other systematic reviews have demonstrated that as the severity of maternal obesity increased, the risk for NTD and congenital heart anomalies also increased [117,118]. The increasing risk for NTD associated with increasing maternal body weight appears to be an independent relationship, unrelated to folic acid supplementation or underlying maternal diabetes .
However, there are several limitations to these data. Although most studies attempted to adjust for confounders such as diabetes, adjustment factors varied among the studies. As diabetes is an established risk factor for fetal anomalies, incompletely accounting for diabetes or poor first-trimester glycemic control may explain some or all of the increased risks reported in the studies . In addition, criteria for obesity and ascertainment of obesity were not consistent across all studies.
Of note, one study noted that pregnant people with obesity did not experience the typical reduction in NTD risk associated with standard doses of folic acid supplementation, suggesting that folate deficiency may not be the underlying etiology of NTDs in these individuals . (See "Folic acid supplementation in pregnancy".)
A reduction in congenital anomalies after bariatric surgery has not been observed consistently, although this may be related to the relatively small numbers of patients and low absolute risk of a congenital abnormality, as well as the confounding impact of micronutrient deficiencies . (See "Fertility and pregnancy after bariatric surgery", section on 'Pregnancy outcomes'.)
Perinatal mortality — Risks for fetal, neonatal, and infant death are all increased in the setting of maternal obesity [122,123]. In a meta-analysis of cohort studies, even modest increases in maternal BMI increased the risk of death . The 44 publications included >10,000 fetal deaths, >16,000 stillbirths, >4000 perinatal deaths, >11,000 neonatal deaths, and nearly 5000 infant deaths. The major findings were:
●Per each five-unit increase in maternal BMI, the relative risk of death was:
•Fetal death (spontaneous fetal death during pregnancy or labor): RR 1.21, 95% CI 1.09-1.35
•Stillbirth (fetal death at week 20 to 28 or more completed weeks of gestation [definition varied between studies and different cutoff points were used]): RR 1.24, 95% CI 1.18-1.30
•Perinatal death (stillbirth and early neonatal death): RR 1.16, 95% CI 1.00-1.35
•Neonatal death (death following a live birth but before age 28 days): RR 1.15, 95% CI 1.07-1.23
•Infant death (death of a liveborn infant before age 1 year): RR 1.18, 95% CI 1.09-1.28
●The absolute risk of death per 10,000 pregnancies by BMI was:
•BMI 20 kg/m2 (normal weight reference group): Fetal death 76; stillbirth 40; perinatal death 66; neonatal death 20; infant death 33
•BMI 25 kg/m2 (overweight group): Fetal death 82; stillbirth 48; perinatal death 73; neonatal death 21; infant death 37
•BMI 30 kg/m2 (obese group): Fetal death 102; stillbirth 59; perinatal death 86; neonatal death 24; infant death 43
Thus, overweight and obese patients had an absolute increase in stillbirth of approximately 1 in 1000 and 2 in 1000, respectively, compared with the normal weight reference group.
Several hypotheses have been proposed to explain these observations. Pregnant people with obesity have higher rates of diabetes and hypertension than nonobese pregnant people; however, a proportion of the excess risk of death remains after adjustment for these factors . Other potential etiologies include metabolic changes associated with obesity (hyperlipidemia with reduced prostacyclin production) and nocturnal apnea with transient oxygen desaturation. It is also possible that confounding factors, such as maternal age, smoking, and congenital anomalies in offspring, account for the disparity. In addition, external fetal heart rate monitoring may not provide a clear tracing in pregnant people with severe obesity and thus the performance of emergency cesarean birth may be delayed while fetal status is being ascertained. Although most studies attempted to adjust for confounders, adjustment factors varied among the studies.
Other concerning observations regarding the increased risk for stillbirth in pregnant patients with obesity in large studies [125,126]:
●The risk of stillbirth increased with increasing obesity severity:
•Class 1 obesity adjusted hazard ratio (aHR): 1.3, 95% CI 1.2-1.4
•Class 2 obesity aHR 1.4, 95% CI 1.3-1.6
•Class 3 obesity aHR 1.9, 95% CI 1.3-1.6
●Black people with obesity experienced a higher risk of stillbirth compared with White people without obesity: aHR 1.9, 95% CI 1.7-2.1. White people with obesity also experienced a higher risk of stillbirth compared with White people without obesity: aHR 1.4, 95% CI 1.3-1.5, but the aHR was lower than that for Black people with obesity.
●The risk for stillbirth increased with advancing gestational age among pregnant people with BMI ≥40 kg/m2 and ≥50 kg/m2:
•At 30 to 33 weeks, aHR 1.41 and 1.69, respectively
•At 34 to 36 weeks, aHR 1.78 and 1.61, respectively
•At 37 to 39 weeks, 3.20 and 2.95, respectively
•At 40 to 42 weeks, 3.30 and 8.91, respectively
A reduction in perinatal mortality has not been reported consistently after bariatric surgery, although this may be related to the relatively small numbers of patients and very low absolute risk of perinatal death. (See "Fertility and pregnancy after bariatric surgery", section on 'Pregnancy outcomes'.)
Preterm birth — Offspring of pregnant people with obesity are more likely to be born preterm (see 'Indicated and spontaneous preterm birth' above), which exposes them to the short- and long-term sequelae of prematurity. (See "Preterm birth: Definitions of prematurity, epidemiology, and risk factors for infant mortality" and "Short-term complications of the preterm infant" and "Late preterm infants" and "Long-term neurodevelopmental impairment in infants born preterm: Epidemiology and risk factors".)
Large for gestational age — Both prepregnancy obesity and gestational weight gain play an important role in determining birth weight. Several studies have reported that increasing prepregnancy weight has a linear relationship with birth weight [53,127,128]; as a result, pregnant people with obesity are at increased risk of having a large for gestational age (LGA) newborn [29,30,38,51,53,98,106,112,113,129,130].
This relationship is independent of the increased prevalence of GDM in patients with obesity but may relate to maternal and fetal hyperinsulinemia [39,96,131]. Maternal genotype may also play a role . In a prospective longitudinal study, fetuses of pregnant people with obesity and without major chronic diseases had longer femur and humerus lengths and larger head circumferences than those of pregnant people without obesity in the second half of pregnancy . Beginning at 32 weeks of gestation, they also had larger abdominal circumferences than those of pregnant people without obesity. These relationships persisted after exclusion of patients with pregnancy complications that can impact fetal growth (eg, gestational diabetes, preeclampsia).
Two potential sequelae of being LGA are:
●Shoulder dystocia. (See "Shoulder dystocia: Risk factors and planning birth of high-risk pregnancies".)
●Predisposition to obesity later in life. (See "Large for gestational age newborn", section on 'Potential long-term effects'.)
Childhood obesity and cardiometabolic morbidity — Having one parent with obesity increases the risk of obesity by two- to threefold; two parents with obesity increases the risk up to 15-fold. In utero nutritional excess and development in an obesogenic environment may lead to permanent changes of fetal metabolic pathways. This increases the risk of childhood and adult diseases related to these pathways, such as hypertension, hyperglycemia and insulin resistance, hyperlipidemia, coronary artery disease, obesity/increased adiposity, and nonalcoholic fatty liver disease . However, shared genetic or familial lifestyle also plays a role in the development of these disorders. (See "Definition, epidemiology, and etiology of obesity in children and adolescents" and "Overview of the health consequences of obesity in children and adolescents".)
Neurodevelopment — Changes in the uterine environment related to maternal obesity may contribute to maladaptive programming of the fetal brain. An increasing body of evidence suggests that prenatal and lactational exposure to maternal obesity and high-fat diet are associated with neurodevelopmental and psychiatric disorders in offspring. These disorders include cognitive impairment, autism spectrum disorders, attention deficit hyperactivity disorder, anxiety and depression, schizophrenia, eating disorders, and propensity for reward-driven behavior [134-137]. Most studies have not controlled for antenatal maternal anxiety and depression, which can impact the frequency of psychopathologic disorders in offspring (see "Antenatal depression: Risks of cognitive impairment and psychopathology in the offspring"). Genetic, social, and environmental risk factors may also contribute to neurodevelopment in offspring . Adjustment for these and other factors attenuates reported associations between maternal obesity and childhood neuropsychological development (eg, OR 2.47 before adjustment versus 1.91 after adjustment in one study ).
An increased risk of cerebral palsy (CP) has been observed in offspring of overweight and obese pregnant people. In a meta-analysis of eight cohort and case-control studies including almost eight million participants, the relative risks of CP in offspring of overweight, obese, and class 3 obese mothers were RR 1.29, 1.45, and 2.25, respectively . The association was inconsistent when the results were stratified by study location, study design, and certain confounding variables. In one of the population-based cohort studies, part of the increased risk appeared to be mediated by asphyxia-related neonatal complications , which have been reported to be more prevalent in offspring of mothers who are overweight or obese . The same group reported a predisposition to childhood epilepsy that was attenuated but persisted after adjusting for multiple maternal and neonatal confounders .
Possible mechanisms for adverse neurodevelopmental effects in offspring include neuroinflammation; increased oxidative stress; and dysregulated insulin, glucose, leptin, serotonergic, and dopaminergic signaling.
Asthma — A meta-analysis of observational studies noted an association between maternal obesity in pregnancy and risk of current asthma/wheeze in offspring (OR 1.35, 95% CI 1.08-1.68); maternal asthma history did not account for the findings . The biologic mechanisms for this association have not been elucidated but may involve obesity-related changes in inflammatory pathways and dietary exposures.
Preconception counseling, evaluation, and care — Because of obesity-associated pregnancy risks, a nonjudgmental discussion about reproductive planning is ideally initiated well before conception. This discussion includes:
●Information about the adverse effects of obesity on fertility and long-term health. (See "Natural fertility and impact of lifestyle factors" and "Overweight and obesity in adults: Health consequences".)
●Information about the potential pregnancy complications associated with obesity and effects of maternal obesity on offspring, as described above. (See 'Potential issues in pregnancy' above.)
●Preconception evaluation for obesity-associated medical comorbidities (eg, diabetes, hypertension, sleep apnea) and appropriate intervention to optimize health status.
•(See "Obesity in adults: Prevalence, screening, and evaluation", section on 'Assessing obesity-related health risk'.)
•(See "Overweight and obesity in adults: Health consequences".)
•(See "Obesity in adults: Overview of management".)
●Counseling about the benefits of preconception weight loss. (See 'Prepregnancy weight loss' below.)
●Information about how to achieve weight loss. The United States Preventive Services Task Force (USPSTF) recommends offering adults with a body mass index (BMI) ≥30 kg/m2 referral to intensive multicomponent behavior interventions for weight loss and weight loss maintenance .
•(See "Obesity in adults: Role of physical activity and exercise".)
•(See "Obesity in adults: Overview of management".)
●Counseling about indications for therapy escalation. When lifestyle interventions do not result in significant weight loss, therapy escalation may include antiobesity medication or bariatric surgery.
•(See "Obesity in adults: Drug therapy".)
•(See "Fertility and pregnancy after bariatric surgery".)
•(See "Bariatric surgery for management of obesity: Indications and preoperative preparation".)
•(See "Outcomes of bariatric surgery".)
●Routine preconceptional care. (See "The preconception office visit".)
Prepregnancy weight loss — Before attempting to conceive, patients with obesity should be encouraged to undertake a weight reduction program (diet, exercise, behavior modification), and possibly adjunctive medical therapy or bariatric surgery, if indicated, because weight loss (even a small reduction in weight) appears to have beneficial effects on reproductive function, pregnancy outcome, and overall health [144-152].
Data from observational studies of females with prepregnancy weight loss support its benefits. For example:
●A population-based study estimated that a 10 percent reduction in prepregnancy BMI may reduce the risk of preeclampsia, gestational diabetes, indicated preterm birth, large for gestational age (LGA)/macrosomia, and stillbirth by 10 percent, while a 20 to 30 percent reduction may reduce risks of cesarean birth and shoulder dystocia .
●Other population-based retrospective cohort studies have observed that patients with obesity who reduced their BMI between pregnancies by one or two units or more substantially reduced their risk of having a LGA newborn, improved the likelihood of a vaginal birth after a cesarean birth (VBAC), and reduced risks of gestational diabetes mellitus (GDM) and stillbirth compared with those who maintained their weight [149-153]. In one study, interpregnancy weight loss ≥2 BMI units was associated with 40 percent reduction in risk of LGA .
●Among patients with obesity who undergo bariatric surgery, the risks for preeclampsia, GDM, and LGA/macrosomia are reduced compared with those who have not undergone a bariatric procedure. The risks for spontaneous preterm birth, cesarean birth, and congenital anomalies appear to be the same or lower than in those who have not undergone a bariatric procedure, but data are less consistent than for other outcomes. These data are reviewed separately. (See "Fertility and pregnancy after bariatric surgery", section on 'Pregnancy outcomes'.)
Role of pharmacotherapy — Most drugs prescribed for weight reduction have not been studied in pregnant patients or have adverse fetal effects. Therefore such drugs should not be used during pregnancy (see "Obesity in adults: Overview of management" and "Obesity in adults: Drug therapy"). Reproductive-age patients using these drugs prior to pregnancy should be counseled about contraceptive options, particularly long-acting reversible contraceptives . They should be counseled that weight loss medications should be discontinued prior to conception. If not discontinued prepregnancy, they should be stopped as soon as pregnancy occurs.
After discussion with their clinician, patients taking metformin for the purpose of weight loss may consider continuation after conception since pregnancy safety experience is available as a result of its role for treatment of gestational diabetes and pregestational type 2 diabetes (see "Gestational diabetes mellitus: Glucose management and maternal prognosis", section on 'Metformin' and "Pregestational (preexisting) diabetes mellitus: Antenatal glycemic control", section on 'Metformin'). However, efficacy has not been demonstrated. In a trial of patients who were overweight or obese randomly assigned to initiate metformin versus placebo at 10 to 20 weeks of gestation, pregnancy and birth outcomes (eg, macrosomia, gestational diabetes) did not differ significantly between groups . Total gestational weight gain trended lower in the metformin group, but the adjusted mean value was only 1.18 kg less (95% CI –2.37-0.01).
PREGNANCY MANAGEMENT — Given the associations between obesity and adverse pregnancy outcome described above, modifications to routine prenatal care (see "Prenatal care: Initial assessment") have been suggested for this population, as described below. Patients with class 2 or 3 obesity, obesity with comorbidities, or obesity with risk factors for adverse pregnancy outcome may benefit from care with a multidisciplinary care team that may include the primary obstetric provider, maternal-fetal medicine specialist, and registered dietician. As delivery approaches, the addition of an obstetric anesthesiologic may be helpful to coordinate anesthesia and delivery considerations.
Baseline assessments and referrals
●Weight and body mass index (BMI).
●Blood pressure using an appropriately sized cuff.
●Early ultrasound examination to establish gestational age accurately and determine whether there is a multifetal gestation.
●Medication review, particularly weight loss medication exposure, which should be discontinued, and use of noninsulin anti-hyperglycemic drugs, which are often discontinued in favor of insulin therapy. (See "Pregestational (preexisting) diabetes mellitus: Antenatal glycemic control", section on 'Patients on noninsulin antihyperglycemic agents prior to pregnancy'.)
•Diabetes screening, if not performed within the past 12 months (see "Gestational diabetes mellitus: Screening, diagnosis, and prevention", section on 'Screening for undiagnosed type 2 diabetes in early pregnancy'). Screening procedures may need to be modified in patients who have undergone bariatric surgery. (See "Fertility and pregnancy after bariatric surgery", section on 'Gestational diabetes'.)
•The cost-effectiveness of checking quantitative urine protein, serum creatinine concentration, platelet count, and liver biochemistries has not been established, but this baseline information can be useful for comparison with laboratory values later in pregnancy if needed. Obesity is a known risk factor for nonalcoholic fatty liver disease, which can be associated with elevated aspartate aminotransferase and alanine aminotransferase levels. (See "Epidemiology, clinical features, and diagnosis of nonalcoholic fatty liver disease in adults".)
●Patients with excessive daytime sleepiness, witnessed apneas, or unexplained hypoxia may benefit from evaluation for obstructive sleep apnea (OSA) by a sleep medicine specialist. OSA is common among obese pregnant patients and has been observed in 15.4 percent of pregnant patients with a BMI >30 kg/m2 . (See "Obstructive sleep apnea in pregnancy".)
●Patients with suspected underlying cardiopulmonary disease can benefit from referral to cardiology or pulmonary medicine for evaluation and management. Signs and symptoms can include: dyspnea, orthopnea, resting respiratory rate >16 breaths/minute, resting heart rate >90 beats/minute, palpitations, syncope, chest pain, hypertension, oxygen saturation ≤95 percent, heart murmur, wheezing or basilar rales. (See "Obesity in adults: Prevalence, screening, and evaluation", section on 'Assessing obesity-related health risk'.) .
●Referral to a registered dietician for ongoing consultation provides patients with dietary plans, goals, and guidance about healthy lifestyle choices. Working with a registered dietician throughout pregnancy and the puerperium can help patients plan meals to optimize gestational weight gain and minimize postpartum weight retention . However, randomized trials involving intensive intervention, such as a weekly weight management group combining expertise from a commercial weight loss program and clinical advice from midwives, generally have not been successful in limiting gestational weight gain and reducing BMIs by 12 months following birth, in part because of poor adherence .
●Patients who have undergone bariatric surgery should be evaluated for nutritional deficiencies that require treatment. (See "Fertility and pregnancy after bariatric surgery", section on 'Micronutrient supplementation'.)
Counseling — The patient should receive information regarding potential pregnancy risks associated with obesity (see 'Potential issues in pregnancy' above) and appropriate gestational diet, weight gain, and exercise. The patient's diet, change in weight, and physical activity should be reviewed at each prenatal and postpartum visit. (See "Nutrition in pregnancy: Dietary requirements and supplements" and "Nutrition in pregnancy: Assessment and counseling".)
Gestational weight gain — The National Academy of Medicine (NAM, formerly the Institute of Medicine [IOM]) recommendations for gestational weight gain are widely accepted (table 3) . For pregnant people with obesity, limiting gestational weight gain may reduce the risk of some adverse pregnancy outcomes, such as LGA/macrosomia. However, in one review, 46 percent of patients with obesity had gestational weight gain above the NAM guidelines, indicating widespread challenges in meeting these goals . Inadequate weight gain and gestational weight loss are associated with an increased risk of small for gestational age newborns and therefore not recommended .
Issues related to gestational weight gain and loss are discussed in detail separately. (See "Gestational weight gain", section on 'Overweight and obese pregnant people'.)
Exercise — Exercise has multiple health benefits. Pregnant people can continue most prepregnancy exercise programs or initiate an exercise program, which can help control gestational weight gain [162,163] and may improve some pregnancy outcomes (eg, reduced risk of gestational diabetes) . (See "Exercise during pregnancy and the postpartum period" and "Gestational diabetes mellitus: Screening, diagnosis, and prevention", section on 'Lifestyle interventions for risk reduction'.)
Fetal aneuploidy screening — Pregnant people with obesity are not at increased risk for fetal aneuploidy compared with those of normal BMI; however, obesity can reduce screening performance. Limitations and challenges of the various screening and diagnostic modalities should be recognized and patients counseled appropriately.
●Cell-free fetal DNA screening is more likely to result in test failure (no result) in pregnant people with obesity because they may have a lower fetal fraction of the cell-free DNA. In addition, the chance of a false-negative result is slightly higher compared with patients who are not obese. These risks and management of such patients (repeat cell-free DNA screening versus diagnostic testing) are discussed separately. (See "Prenatal screening for common aneuploidies using cell-free DNA", section on 'Maternal obesity'.)
●First- and second-trimester serum-based biomarker tests are adjusted for maternal weight; thus, obesity does not affect test performance. However, accurate nuchal translucency measurement may be more difficult to obtain, and in one study the failure rate increased with increasing maternal BMI category . While the authors did not attempt to delineate the potential benefits of transvaginal over transabdominal approach, theoretically, use of transvaginal sonography may offer improved ascertainment of nuchal translucency measurements irrespective of degree of obesity.
●Diagnostic procedures (eg, amniocentesis, chorionic villus sampling) are more challenging technically in patients with versus without obesity. Techniques to optimize visualization during ultrasound include avoiding transpannus imaging, repositioning the transducer for improved scanning angle, or placing a vaginal probe in the umbilicus. Use of a low-frequency transducer and a narrow sector width may also help to increase tissue penetration and improve imaging success during diagnostic procedures .
Low-dose aspirin — Pregnant people with obesity plus additional risk factors for development of preeclampsia may benefit from prophylaxis with low-dose aspirin. We follow the approach suggested by the United States Preventive Services Task Force (USPSTF)  and endorsed by the American College of Obstetricians and Gynecologists . Identification of patients with obesity and an appropriate combination of moderate risk factors to be considered high risk is subjective and determined case by case, as the data describing the magnitude of the association between moderate risk factors and development of preeclampsia vary widely and lack consistency. These data and use of low-dose aspirin for preeclampsia prophylaxis are discussed in more detail separately. (See "Preeclampsia: Prevention".)
Fetal ultrasound survey — A specialized (or detailed or comprehensive) fetal anatomic survey is performed at 18 to 20 weeks of gestation to screen for fetal anomalies. Because abdominal adiposity may make interpretation difficult, follow-up ultrasound assessment(s) may be needed to complete the anatomic survey . (See "Overview of ultrasound examination in obstetrics and gynecology", section on 'Detailed examination' and "Overview of ultrasound examination in obstetrics and gynecology", section on 'Patient preparation'.)
Ultrasound interpretation is limited as degrees of obesity increase, even when the anatomic survey is delayed until 22 to 24 weeks . Therefore, it is our practice to use maternal serum alpha-fetoprotein in addition to ultrasound to screen for neural tube defects and other relevant congenital anomalies in patients with obesity. (See "Neural tube defects: Overview of prenatal screening, evaluation, and pregnancy management", section on 'Screening tests'.)
The American Heart Association Scientific Statement on Diagnosis and Management of Fetal Cardiac Disease does not specifically cite maternal obesity as an indication for fetal echocardiography . In our opinion, however, unless all components of the fetal cardiac evaluation are adequately visualized during the obstetric ultrasound, the increased risk and lower detection rates for fetal cardiac malformations are sufficient to support the use of fetal echocardiography in these pregnancies. (See "Congenital heart disease: Prenatal screening, diagnosis, and management", section on 'Standard cardiac evaluation' and "Congenital heart disease: Prenatal screening, diagnosis, and management", section on 'Advanced fetal cardiac evaluation'.)
Screening for gestational diabetes — If diabetes has not been identified previously (eg, before pregnancy or early in pregnancy), then screening for gestational diabetes using a standard approach (one step or two step) is recommended at 24 to 28 weeks of gestation. (See "Gestational diabetes mellitus: Screening, diagnosis, and prevention", section on 'One- and two-step approaches'.)
Alternative methods of screening are recommended for patients with Roux-en-Y gastrojejunostomy or other malabsorptive bypass forms of bariatric surgery because a glucose load may incite maternal dumping syndrome. Such approaches may include checking fasting and post breakfast blood glucose levels or an intravenous glucose tolerance test (if available). (See "Fertility and pregnancy after bariatric surgery", section on 'Gestational diabetes'.)
Assessment of fetal growth — Clinical assessment of fetal size by abdominal palpation and accurate measurement of fundal height is more challenging in patients with obesity. After 28 weeks of gestation, we believe ultrasound assessment of fetal growth every four to six weeks is reasonable.
Assessment of fetal well-being — Although an obesity-associated increased risk for perinatal mortality that increases with gestational age has been reported (see 'Perinatal mortality' above), the mechanism is unclear and the value of antenatal fetal surveillance with nonstress tests or biophysical profile scoring in this setting has not been studied. Therefore, we initiate antepartum fetal assessment for standard indications, not for obesity alone. The American College of Obstetricians and Gynecologists has stated that weekly antenatal surveillance beginning at 37+0 weeks of gestation may be considered for patients with pregnancy BMI 35.0 to 39.9 kg/m2 and beginning at 34+0 weeks for those with prepregnancy BMI ≥40 kg/m2 .
External cephalic version — While study results have been mixed regarding the effect of obesity on the success of external cephalic version (ECV), obesity is not a contraindication to the procedure . A successful ECV is particularly beneficial in patients with obesity, given the significant surgical risks of cesarean birth in these patients. (See "External cephalic version", section on 'Potential contraindications'.)
Planning for postpartum contraception — Planning for postpartum contraception, either reversible or permanent, should be initiated before delivery. (See "Contraception: Counseling for females with obesity" and "Overview of female permanent contraception" and "Postpartum permanent contraception: Procedures".)
Labor and delivery
Equipment and instruments — The labor and delivery unit should have appropriate physical resources (eg, gowns, beds, stirrups, operating room tables, scales, transport vehicles and equipment, lifting equipment, floor-anchored toilet, surgical instruments) for caring for patients with severe obesity. (See "Hospital accreditation, accommodations, and staffing for care of the bariatric surgical patient" and "Cesarean birth: Overview of issues for patients with obesity".)
Fetal monitoring — Obtaining a continuous fetal heart rate tracing with an external Doppler ultrasound transducer can be difficult in patients with obesity . Placement of an internal fetal scalp electrode solves this problem if needed.
Anesthesia consultation — Evaluation by an anesthesiologist prior to labor or in early labor is recommended for all pregnant patients with obesity because of their higher risk of anesthetic challenges and complications. (See "Preanesthesia medical evaluation of the patient with obesity" and "Anesthesia for the patient with obesity".)
Patients should be counseled regarding the benefits and risks of neuroaxial anesthesia for vaginal or cesarean birth compared with unmedicated labor and other types of analgesia and anesthesia. Early placement of a catheter for neuraxial anesthesia may obviate the need for general anesthesia if an emergency cesarean birth is needed .
Timing and route of delivery
●Timing – Each institution should evaluate its approach and develop guidelines for the timing of delivery in patients with obesity as they approach or reach term. Because of the increased risk for stillbirth and other maternal and neonatal complications related to continued fetal growth, our approach is to deliver patients with obesity at 39+0 to 40+0 weeks of gestation. (See "Induction of labor with oxytocin", section on 'Medical and obstetric indications'.)
•In one protocol, pregnant people meeting any of the following criteria were delivered by their estimated date of delivery (EDD): (1) prepregnancy BMI ≥40 kg/m2, (2) prepregnancy BMI 35 to 39.9 kg/m2 plus gestational diabetes mellitus (GDM) or LGA fetus, or (3) prepregnancy BMI 30 to 34.9 kg/m2 plus GDM and LGA fetus .
Adoption of this protocol was associated with a 10.8 percent reduction in cesarean birth (from 42.4 to 31.6 percent) and a 3 percent reduction in macrosomia (from 6.6 to 3.6 percent). Stillbirth rates did not change, but the study had insufficient power to detect a clinically significant reduction.
•In a retrospective cohort study, compared with expectant management, "elective" labor induction of nulliparous or parous patients with obesity at 39 or 40 weeks was associated with an approximately 20 percent reduction in cesarean birth and a 40 to 70 percent reduction in macrosomia . A nonstatistically significant trend toward fewer infant deaths was noted with induction at 39 weeks.
●Route – The route of delivery should be based on standard obstetric indications. Planned cesarean birth is not clearly associated with less overall morbidity than planned vaginal birth, including among patients with extreme obesity.
In a meta-analysis of observational studies, pregnant patients with BMI ≥40 kg/m2 attempting vaginal birth were at a higher risk of postpartum hemorrhage (PPH) but lower risk of wound disruption when compared with those undergoing planned cesarean birth, with no difference in any other maternal or perinatal outcomes . These findings suggest that there is true clinical equipoise regarding the optimal mode of delivery in patients with BMI ≥40 kg/m2 and no prior cesarean birth. However, the higher PPH risk in those undergoing labor with anticipated vaginal birth should be interpreted with caution, given inconsistencies in definitions of PPH among studies and heterogeneity among study participants.
If cesarean birth is planned, preparation (counseling, specialized equipment, infection and venous thromboembolism prophylaxis, anesthesia) and modifications of the operative procedure in patients with obesity are reviewed separately. (See "Cesarean birth: Overview of issues for patients with obesity".)
●Reducing the risk of complications – If cesarean birth was performed, modify postcesarean monitoring and care to reduce the risk of obesity-associated postsurgical complications. This may include continuous pulse oximetry, respiratory physiotherapy, multimodal analgesia, and thromboprophylaxis (mechanical in all patients, pharmacologic in patients at highest risk). (See "Cesarean birth: Overview of issues for patients with obesity", section on 'Postoperative care'.)
●Breastfeeding – Encourage breastfeeding and provide additional support. Patients with obesity are less likely to initiate breastfeeding as compared with nonobese patients, and obesity has been identified as a risk factor for delayed lactogenesis . (See "Initiation of breastfeeding".)
●Contraception – Intrauterine contraception is safe and effective and may be safer and more effective in this population than estrogen-progestin contraceptives, although the latter are also an acceptable choice. (See "Contraception: Counseling for females with obesity".)
●Postpartum screening – Screen patients with gestational diabetes for glucose intolerance at 4 to 12 weeks after delivery. (See "Gestational diabetes mellitus: Glucose management and maternal prognosis", section on 'Follow-up'.)
●Postpartum weight loss – Support patients in their efforts to lose gestational and pregestational weight gain, avoid postpartum weight gain, and achieve a healthy BMI. Provide counseling and referrals for behavioral counseling interventions to improve diet and exercise, as appropriate. Achieving a healthy BMI has overall health benefits and can decrease the risk of obesity-related pregnancy complications in a subsequent pregnancy [149,179]. (See "Obesity in adults: Overview of management".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pregnancy in women with obesity" and "Society guideline links: Obesity in adults".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Beyond the Basics topics (see "Patient education: Losing weight (Beyond the Basics)" and "Patient education: Evaluation of infertility in couples (Beyond the Basics)" and "Patient education: Ovulation induction with clomiphene (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition/classification – Obesity in pregnancy is defined as prepregnancy body mass index (BMI) ≥30 kg/m2. Classification is described in the table (table 1). (See 'Definition and classification of obesity' above.)
●Pathobiology of adipose tissue – Adipose tissue is an active endocrine organ; when present in excess, it can have dysregulatory effects on metabolic, vascular, and inflammatory pathways in many organ systems, and thereby lead to a variety of reproductive and medical problems. (See 'Pathobiology' above.)
●Pregnancy outcomes – Compared with pregnant people with BMI <25 kg/m2, pregnancies among people with obesity are at increased risk for several adverse outcomes, including early pregnancy loss, congenital anomalies, stillbirth, pregnancy-associated hypertension, preterm and postterm birth, gestational diabetes mellitus (GDM), multifetal gestation, cesarean birth, and birth of a large for gestational age (LGA)/macrosomic infant. (See 'Potential issues in pregnancy' above.)
●Maternal comorbidities – Pregnant people with obesity are also at increased risk for some medical disorders, such as sleep-related breathing disorders, carpal tunnel syndrome, postpartum depression, and venous thromboembolism (VTE). (See 'Potential issues in pregnancy' above.)
●Planning and counseling – Ideally, health care providers should discuss reproductive planning with patients with obesity well before conception, including (see 'Prepregnancy management' above):
•The adverse effects of obesity on fertility.
•Potential pregnancy complications.
•Evaluation for obesity-associated medical comorbidities (eg, diabetes, hypertension) and appropriate intervention to optimize maternal health status.
•Counseling about the benefits of weight loss before attempting to conceive, which can reduce the risk of pregnancy complications. Some patients could benefit from referral for bariatric surgery. (See 'Prepregnancy weight loss' above.)
●Modifications to prenatal care – Given the associations between obesity and adverse pregnancy outcome, modifications to routine prenatal care include (see 'Pregnancy management' above):
•Diabetes screening – Screening for diabetes in early pregnancy. (See 'Baseline assessments and referrals' above.)
•Gestational weight gain – Limiting gestational weight gain (table 3) (see 'Gestational weight gain' above) by encouraging regular exercise and dietary modifications. (See "Exercise during pregnancy and the postpartum period".)
•Ultrasound examination – Routine ultrasound examination to establish an accurate gestational age and for fetal anatomic survey. (See 'Fetal ultrasound survey' above.)
-Fetal echocardiography – Fetal echocardiography, unless the standard obstetric ultrasound assessment of the four chambers and outflow tract is optimal and normal. (See 'Fetal ultrasound survey' above.)
•Aneuploidy screening – Discussing the additional challenges and limitations of fetal aneuploidy screening. Patients with obesity are not at increased risk for fetal aneuploidy; however, obesity can affect screening test performance. Cell-free DNA screening is more likely to result in test failure in patients with obesity because they have a lower fetal fraction of the cell-free DNA. (See 'Fetal aneuploidy screening' above.)
•Sleep disordered breathing – Asking about snoring, excessive daytime sleepiness, witnessed apneas, or unexplained hypoxia, which suggest the possibility of obstructive sleep apnea (OSA). These patients may benefit from a referral to a sleep medicine specialist for diagnosis and treatment. (See 'Obstructive sleep apnea' above and 'Baseline assessments and referrals' above.)
•Low-dose aspirin – Initiating low-dose aspirin at the end of the first trimester to reduce the risk of preeclampsia in patients with risk factors in addition to obesity. (See 'Low-dose aspirin' above.)
•Antenatal fetal surveillance – Although stillbirth risks are increased in the setting of maternal obesity, there is no evidence demonstrating improved pregnancy outcome with routine use of antenatal fetal surveillance with nonstress tests or biophysical profile scoring. Testing should be initiated for standard indications. (See 'Assessment of fetal well-being' above.)
●Labor and delivery
•Anesthesia consultation – Early evaluation by an anesthesiologist is desirable given the potential for intrapartum complications. (See 'Anesthesia consultation' above.)
•Delivery timing – Delivery timing and indications for labor induction are not altered solely based on maternal obesity; however, induction by the estimated date of delivery is reasonable and does not appear to increase cesarean birth rates. (See 'Timing and route of delivery' above.)
•Preparation – Appropriate equipment should be available for caring for patients with obesity. These patients have special issues with respect to preparation for cesarean birth (counseling, specialized equipment, infection and venous thromboembolism prophylaxis, anesthesia), modifications of the operative procedure, and postpartum care. (See 'Equipment and instruments' above and "Cesarean birth: Overview of issues for patients with obesity".)
•Labor – The median duration of labor from 4 to 10 cm dilation is longer for both overweight and obese patients compared with normal-weight patients, which should be considered when evaluating labor progress in the first stage. (See 'Progress of labor' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Francis S Nuthalapaty, MD, and Dwight J Rouse, MD, MSPH, who contributed to an earlier version of this topic review.
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170 : Delay of Fetal Anatomy Ultrasound Assessment Based on Maternal Body Mass Index Does Not Reduce the Rate of Inadequate Visualization.
171 : Diagnosis and treatment of fetal cardiac disease: a scientific statement from the American Heart Association.
174 : Influence of maternal body mass index on accuracy and reliability of external fetal monitoring techniques.
176 : Term Elective Induction of Labor and Pregnancy Outcomes Among Obese Women and Their Offspring.
177 : Birth outcomes in women with body mass index of 40 kg/m2 or greater stratified by planned and actual mode of birth: a systematic review and meta-analysis.
178 : Prepregnant overweight and obesity diminish the prolactin response to suckling in the first week postpartum.
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