Obesity has been associated with subfertility due to increased insulin resistance (see Table 43-2). In their review, Neill and Nelson-Piercy (2001) linked impaired fecundity in women with a BMI in excess of 30 kg/m². In the many overweight and obese women who achieve pregnancy, there are a number of increased and interrelated adverse perinatal outcomes. Marked obesity is unequivocally hazardous to the pregnant woman and her fetus.

PREVALENCE. Because the overall prevalence of obesity has increased over the past several decades, the prevalence of obesity complicating pregnancy has also increased. Before adoption of the BMI, investigators used a variety of definitions of obesity to assess risks during pregnancy. For example, in the study shown in Figure 43-4, four definitions were used. Regardless of how obesity was defined, all groups showed substantive increases in prevalence over the 20-year study. Ehrenberg and colleagues (2002) reported similar findings in a 15-year study in Cleveland.

WEIGHT LOSS DURING PREGNANCY. Because maternal catabolism is, intuitively, not good for fetal growth and development, the Institute of Medicine (1992) recommends that even women who are obese (BMI of 30 kg/m2 or higher) should not attempt weight loss during pregnancy. These women should, however, limit weight gain to less than 15 pounds.

MATERNAL MORBIDITY. Increased maternal morbidity results from obesity, defined variably as more than 150 percent of ideal body weight, BMI greater than 35 kg/m², BMI greater than 40 kg/m², and 150 pounds or more greater than ideal body weight (Bianco, 1998; Cedergren, 2004; Garbaciak, 1985; Isaacs, 1994; Kabiru and Raynor, 2004; Kumari, 2001, and all their colleagues). These investigators chronicled significantly increased incidences of a number of disorders including chronic hypertension, gestational diabetes, preeclampsia, fetal macrosomia, as well as higher rates of cesarean delivery and postpartum complications.

In a nurse-midwife practice, women whose BMI exceeded 29 kg/m² had a two- to fourfold increased cesarean delivery rate (Kaiser and Kirby, 2001). Similarly, in a physician private practice, the cesarean delivery rate for dystocia was increased sixfold in obese nulliparas (Young and Woodmansee, 2002). In another study, only 15 percent of obese women with a previous cesarean delivery succeeded in having a subsequent vaginal delivery (Chauhan and colleagues, 2001). These same investigators stratified women by BMI category and reported a successful trial of labor in 82 percent of women who weighed less than 200 lb, in 57 percent of those weighing 200 to 299 lb, and in only 13 percent of those weighing more than 300 lb (Carroll and collaborators, 2003). Although Edwards and co-workers (2003) reported a success rate of greater than 50 percent, they showed that costs for a planned trial of labor and elective cesarean delivery were equivalent.

Second-trimester dilatation and evacuation was reported to take longer and be more difficult in women whose BMI was 30 kg/m² or greater (Dark and co-workers, 2002).

In addition, there are reports of increased adverse pregnancy outcomes in overweight women with a BMI of 25 to 29.9 kg/m². Sebire and collaborators (2001) studied 287,213 singleton pregnancies delivered in the North West Thames Region of London. Their results are shown in Table 43-3 according to BMI category. Cunningham and associates (1986) reported that obesity (weight greater than 200 pounds) and hypertension were common co-factors in causing peripartum heart failure. Myles and co-workers (2002) found that obesity was an independent risk factor for postcesarean infection morbidity. Finally, obese women are less likely to breast feed (Li and colleagues, 2003).

Preeclampsia. Obesity is a consistent risk factor for preeclampsia (Cedergren, 2004; Jensen and associates, 2003; Sebire and colleagues, 2001). In a review of studies that included over 1.4 million women, O’Brien and collaborators (2003) found that the preeclampsia risk doubled with each 5 to 7 kg/m² increase in prepregnancy BMI. In obese, nonpregnant individuals, at least some of the long-term cardiovascular morbidity was thought to be due to obesity-mediated systemic inflammation and endothelial dysfunction (Brook and associates, 2001). According to Davi and colleagues (2002), this phenomenon was associated more with android obesity (apple shape) than gynoid obesity (pear shape) - one characteristic of the metabolic syndrome discussed on page 1009. It has become apparent that endothelial activation plays an integral role in preeclampsia. Obesity is associated with low-grade inflammation, and Wolf and co-workers (2001) linked these two conditions by providing intriguing evidence that inflammation may explain, at least partly, the association of obesity with preeclampsia. More recently, Ramsay and collaborators (2002) confirmed that obese pregnant women had significantly elevated levels of serum interleukin-6 and C-reactive protein as well as evidence of impaired endothelial function. Specifically, 23 pregnant women with a median BMI of 31 kg/m2 were compared with 24 with a median BMI of 22 kg/m². Obese women had significantly higher levels of triglycerides, very-low-density lipoprotein cholesterol, insulin, and leptin.

Long-Term Consequences. It is intuitive that excessive prepregnancy weight can be used to predict long-term obesity with its attendant morbidity and mortality. Rooney and Schauberger (2002), however, reported that excess weight gain during pregnancy - but not prepregnancy weight - is a predictor of long-term obesity. They followed 540 women postpartum for a mean duration of 8.5 years. During this period, the average weight gain was 6.3 kg. Women who had gained less than the recommended amount of weight during pregnancy were on average 4.1 kg heavier at the end of the follow-up period. Women who gained the recommended amount were 6.5 kg heavier. Finally, women who gained more than the recommended amount were 8.4 kg heavier.

Contraception. Oral contraceptive failure is more likely in overweight women. In reviewing studies on hormonal contraceptive efficacy, it is apparent that the typical study subject is not representative of the average American woman. As discussed earlier, at least 50 percent of American women have a BMI greater than 25 kg/m2 and thus are considered to be overweight (see Table 43-2). In contraceptive studies, however, the majority of subjects have a BMI between 18 and 28 kg/m² (Holt and co-workers, 2002; Zieman and collaborators, 2002). In one study, the mean serum medroxyprogesterone acetate concentration was lower in the women with a BMI greater than 28 kg/m² compared with that of those with a lower BMI (Rahimy and associates, 1999). Efficacy of the Ortho-Evra patch was studied by Zieman and colleagues (2002). In their analysis of the pooled data from three multicenter studies, they found a significant association between increasing body weight and contraceptive failure. Holt and colleagues (2002) studied 755 women with 2822 person-years of pill use and found that those in the highest weight quartile (70.5 kg or more) had a 1.6-fold increased risk of pregnancy. Importantly, women in this quartile who used very-low-dose oral contraceptives had a four- to fivefold increased pregnancy rate.

PERINATAL MORBIDITY AND MORTALITY. Both fetal and neonatal complications are increased in obese women. For example, obese women, variably defined, have a two- to threefold risk for a fetus with a neural-tube defect or other anomalies (Mikhail, 1996; Waller, 1994; Werler, 1996, and all their collaborators). In another study, Shaw and colleagues (1996, 2000) reported that women with a BMI of 30 kg/m² or more had a twofold increased incidence of neural-tube defects compared with that of control women. In a case-control study from the Atlantic Birth Defects Risk Factor Surveillance Study, Watkins and associates (2003) reported a 3.5-fold increase in neural-tube defects in obese women. They also found a two- to threefold increased incidence in omphalocele, heart defects, and multiple anomalies. The last two were also increased twofold in overweight women whose BMI was 25 to 29.9 kg/m².

Two important and interrelated co-factors that contribute to excessive perinatal morbidity and mortality are chronic hypertension and diabetes mellitus, both of which are associated with obesity (Stephansson and colleagues, 2001). Chronic hypertension is a well-known cause of fetal growth restriction. Pregestational diabetes increases the rate of birth defects. Gestational diabetes is complicated by excessive numbers of large-for-gestational age and macrosomic infants. Whatever the cause(s), the prevalence of macrosomic infants is increased in obese women (Bianco and co-workers, 1998; Cedergren, 2004; Isaacs and associates, 1994). There are also long-term sequelae for macrosomic infants born to these mothers. Low-birthweight infants have lower subsequent risks of type 2 diabetes, insulin resistance, and metabolic syndrome, whereas infants who weigh more than 4000 g have increased risks (Innes and colleagues, 2002). From preliminary observations, Armstrong and colleagues (2002) reported that breast feeding decreases the risk of childhood obesity in these large infants. Alternatively, Ruowei and co-workers (2003) reported that obese women were less likely to breast feed.

An increased incidence of otherwise inexplicable late-pregnancy stillbirths has been associated with obesity. Cnattingius and colleagues (1998) found a significant 1.6-fold increase in the stillbirth rate in women with a BMI of 25 to 29.9 kg/m². The rate was increased 2.6-fold for women with a BMI of 30 kg/m² or more. In addition, early neonatal death was nearly doubled in nulliparous women with a BMI of 30 kg/m2 or higher. Stephansson and associates (2001) used the same database for a case-control study of 649 nulliparas who had stillbirths. They confirmed an almost threefold late-stillbirth rate in women with a BMI of greater than 25 kg/m². They attributed the increase to socioeconomic deprivation and pregnancy complications, particularly preeclampsia and diabetes. Baydock and Chari (2002) found that a prepregnancy BMI of greater than 30 kg/m² was an independent risk factor for stillbirth.

MANAGEMENT. A program of weight reduction is probably unrealistic during pregnancy. If such a regimen is chosen, however, it is mandatory that the quality of the diet be monitored closely and that ketosis be avoided (Rizzo and associates, 1991). Close prenatal surveillance detects most early signs of diabetes or hypertension. Standard screening tests for fetal anomalies are sufficient. Accurate assessment of fetal growth usually requires serial sonography. Wolfe and colleagues (1990) have highlighted the technical difficulties with ultrasonic fetal visualization in women with a BMI above the 90th percentile. Antepartum and intrapartum fetal heart rate monitoring are likewise made more difficult, and sometimes these are even impossible.

Evaluation by anesthesia personnel is performed at a prenatal visit or on arrival at the labor unit (American College of Obstetricians and Gynecologists, 2002). Special attention to complications that might arise during labor and delivery is mandatory. For cesarean delivery, forethought is given to optimal placement and type of abdominal incision to access the fetus and to the intervening tissue thickness. Individual differences in maternal body habitus preclude any one approach as superior (Gilstrap and colleagues, 2002). Meticulous attention to achieving a structurally secure closure is mandatory.

PREGNANCY FOLLOWING SURGICAL PROCEDURES FOR OBESITY. A number of surgical procedures have been designed to treat morbid obesity by either decreasing gastric volume or bypassing gastrointestinal absorption (Brolin, 2002; Yanovski and Yanovski, 1999). Buchwald and associates (2004) in a meta-analysis found these procedures to improve or resolve diabetes, hyperlipidemia, hypertension, and obstruction sleep apnea. Although none are recommended during pregnancy, invariably more women will become pregnant subsequent to these procedures as their popularity grows (Sheiner and associates, 2004). According to the American Society for Bariatric Surgery (2003), there were 47,000 surgeries for obesity in 2001, 63,000 in 2002, and over 100,000 for 2003 (Mitka, 2003; Steinbrook, 2004).

Jejunoileal Bypass. This was one of the earliest surgical methods that was successful for weight loss. In this procedure, the duodenum is divided and anastomosed to the terminal jejunum very near the ileocecal junction. Thus, the vast majority of the small bowel is bypassed with resultant diminished food absorption. This procedure was followed by significant long-term morbidity and mortality, and it has been abandoned by most surgeons. Older reports chronicled shorter gestations, lower mean birthweight, and more small-for-gestational-age infants after weight reduction (Knudsen and Kallen, 1986).

Gastric Bypass. This older procedure excludes the lower 90 percent of the stomach by creating an upper gastrojejunostomy. Printen and Scott (1982) described 51 pregnancies in 45 morbidly obese women who had antenatal gastric bypass surgery. Complications were uncommon, and fetal growth restriction was not increased in the 46 infants delivered. Richards and colleagues (1987) reported similar experiences with 57 pregnancies at the University of Utah. These women weighed an average of 194 pounds before and 147 pounds after surgery. Compared with preprocedure pregnancies, mean birthweight decreased from 3600 to 3200 g, and the incidence of large-for-gestational-age infants decreased from 37 to 16 percent. Impressively, the incidence of pregnancy-associated hypertension fell from 46 to 9 percent.

Gastroplasty. There are several variations of surgical gastroplasty in which a narrow channel is created through the stomach by using stapling devices. The vertical-banded gastroplasty is the most popular bariatric procedure performed currently (Brunicardi and associates, 2001). Subsequent pregnancy outcomes have been chronicled. Bilenka and colleagues (1995) described 14 pregnancies in nine women who had undergone the procedure. The mean weight loss was 80 pounds, and the women had fewer complications compared with their preprocedure pregnancies. Martin and co-workers (2000) described 23 pregnancies in women after adjustable gastric banding. For three women with excessive nausea and vomiting, band adjustment to decrease obstruction was successful. Dixon and associates (2001) described 22 pregnancies in 20 women who were using the Lap-Band System. In this method, the gastric band is laparoscopically placed 2 cm below the gastroesophageal junction. An internal balloon reservoir is adjusted by saline instillation into percutaneously placed tubing. The mean weight loss before pregnancy was 30 kg. Weight gain during pregnancy averaged 8.3 kg, and there were few complications. Mean birthweights of infants were similar before and after maternal banding.

Roux-en-Y Bypass. This type of bypass is the most effective bariatric procedure currently in use (Brunicardi and associates, 2001). It most often is performed laparoscopically. The procedure is depicted in Figure 43-5. The proximal stomach is transected to leave a 30-mL pouch. A gastroenterotomy is made by connecting the proximal end of the distal jejunum which was divided 60 cm distal to the ligament of Treitz. The Roux-en-Y enteroenterostomy is completed 60 cm distal to the gastrojejunostomy. Brunicardi and colleagues (2001) summarized four series totaling almost 400 men and nonpregnant women. Mean weight loss at 1 year in the four series ranged from 21 to 43 kg. In the largest study, at 1 year, 300 patients had lost a mean of 80 percent of their excessive weight. At 5 years, 50 to 75 percent of the weight loss had been maintained, and at 14 years maintenance of lost weight still exceeded 50 percent (American Society of Bariatric Surgery, 2003). Current costs are $20,000 to $50,000 (Steinbrook, 2004).

Wittgrove and associates (1998) described 49 pregnancies in 36 women after a Roux-en-Y bypass. There were 17 who had delivered at least one child prior to surgery. When prior pregnancy outcomes were compared with those after bypass, there was a dramatic reduction in hypertension (40 versus 0 percent), diabetes (24 versus 0 percent), and infant weight greater than 4000 g (30 versus 5 percent). At least one maternal death from herniation and obstruction has been reported (Moore and colleagues, 2004).

References
_{Abate N: Obesity and cardiovascular disease: Pathogenetic role of the metabolic syndrome and therapeutic implications. J Diabetes Complications 14:154, 2000}

Allison DB, Fontaine KR, Manson JE, et al: Annual deaths attributable to obesity in the United States. JAMA 282:1530, 1999

Alpert MA: Obesity cardiomyopathy: Pathophysiology and evolution of the clinical syndrome. Am J Med Sci 321:225, 2001

American College of Obstetricians and Gynecologists: Weight Control: Assessment and management. Clinical updates in women’s health care. Vol II, No. 3, 2003

American College of Obstetricians and Gynecologists: Obstetric analgesia and anesthesia. Practice Bulletin No. 36, July 2002

American Society for Bariatric Surgery, 2003. http://www.asbs.org/html/rationale/rationale.html.

Armstrong J, Reilly JJ; Child Health Information Team: Breastfeeding and lowering the risk of childhood obesity. Lancet 359:2003, 2002

Baydock S, Chari R: Prepregnancy obesity as an independent risk factor for unexplained stillbirth. Obstet Gynecol 99:74S, 2002

Bianco AT, Smilen SW, Davis Y, et al: Pregnancy outcome and weight gain recommendations for the morbidly obese woman. Obstet Gynecol 91:97, 1998

Bilenka B, Ben-Shlomo I, Cozacov C, et al: Fertility, miscarriage and pregnancy after vertical banded gastroplasty operation for morbid obesity. Acta Obstet Gynecol Scand 74:42, 1995

Bray GA: Low-carbohydrate diets and realities of weight loss. JAMA 289:1853, 2003

Brolin RE: Bariatric surgery and long-term control of morbid obesity. JAMA 288:2793, 2002

Brook RD, Bard RL, Rubenfire M, et al: Usefulness of visceral obesity (waist/hip ratio) in predicting vascular endothelial function in healthy overweight adults. Am J Cardiol 88:264, 2001

Brunicardi FC, Reardon PR, Matthews BD: The surgical treatment of obesity. In Townsend CM, Beauchamp RD, Evers BM, et al (eds): Sabiston Textbook of Surgery, 16th ed. Philadelphia, WB Saunders, 2001, p 247

Buchwald H, Avidor Y, Braunwald E, et al: Bariatric surgery: A systematic review and meta-analysis. JAMA 292:1724, 2004

Calle EE, Rodriguez C, Walker-Thurmond K, et al: Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 348:1625, 2003

Calle EE, Thun MJ, Petrelli JM, et al: Body-mass index and mortality in a prospective cohort of US adults. N Engl J Med 341:1097, 1999

Carroll CS Sr, Magann EF, Chauham SP, et al: Vaginal birth after cesarean section versus elective repeat cesarean delivery: Weight-based outcomes. Am J Obstet Gynecol 188:1516, 2003

Cedergren MI: Maternal morbid obesity and the risk of adverse pregnancy outcome. Obstet Gynecol. 103:219, 2004

Chauhan SP, Magann EF, Carroll CS, et al: Mode of delivery for the morbidly obese with prior cesarean delivery: Vaginal versus repeat cesarean section. Am J Obstet Gynecol 185:349, 2001

Chen S, Noguchi Y, Izumida T, et al: A comparison of the hypotensive and hypoglycemic actions of an angiotensin converting enzyme inhibitor, an AT1a antagonist and troglitazone. J Hypertens 14:1325, 1996