Obesity during pregnancy can be associated with numerous maternal and perinatal risks. These risks may increase proportionately to the level of obesity.^1,2,3 Therefore, addressing and managing these potential risk factors pose a challenge to the obstetrician and the anesthesiologist.

Obesity is a multifactor, chronic disease involving social, cultural, physiologic, metabolic, endocrine, genetic, psychological, and behavioral components, resulting in excess adipose and tissue mass.⁴ The modern basis of therapy for demographic determination is the body mass index (BMI) or the Quetelet index. It is measured by body weight in kilograms divided by the height in square meters (kg/m²). The standard for ideal body weight (IBW), the sex-specific desired weight for persons with small-, middle-, and large-build frames, is published in Metropolitan Life Insurance tables.⁵

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  Anorexia is defined as a BMI of less than 17.5 in both men and women.

  
  
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  Ideal weight is defined as a BMI of 19.1–25.8 in women and 20.7–26.4 in men.

  
  
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  Overweight is defined as a BMI of 27.3–32.3 in women and 27.9–31.1 in men.

  
  
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  Obesity is defined as a BMI of 32.4–34.9 in women and 31.2–34.9 in men.

  
  
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  Morbid obesity is defined as a BMI greater than 40.

  
  
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  Superobesity is defined as BMI greater than 50.

Obesity in pregnancy is defined as prepregnancy BMI of 30 kg/m² or greater.⁶ The definition of obesity in pregnant women involves issues unique to this population because the pregnant woman’s weight increases over a relatively short interval of time, and much of this weight gain is related to accretion of matter that will be lost at delivery: the fetus, amniotic fluid, and blood.

The prevalence of obesity in reproductive-aged and pregnant women varies widely depending on the definition used, year, and characteristics of the study population but has increased in concordance with the increased prevalence of obesity in the general population.^7,8 In the 2009–2010 National Health and Nutrition Examination Survey (NHANES), 31.9% of women of reproductive age (20 to 39 years old) were obese (BMI ≥ 30 kg/m²); the prevalence was highest in non-Hispanic blacks (56.2%).⁹ By comparison, in 1980 (before routine calculation of BMI), only 7% of women weighed over 200 pounds at their first prenatal visit.⁸

Central Mechanisms

Regulation of appetite by the hypothalamus involves the collaboration or interaction of the satiety center in the ventromedial hypothalamic nucleus and the feeding center in the lateral hypothalamus.¹⁰ These areas involve numerous neurotransmitters and modulators that regulate appetite. Long-term signals communicating information about the energy stores and endocrine status of the body are mediated predominantly by humoral mechanisms. Short-term signals, mediated by gut hormones and neural signals from the brain and the gut, regulate meal initiation and termination¹⁰ (Figure 25-1). The hypothalamic arcuate nucleus integrates these signals. Energy expenditure, modulated by both long- and short-term signals, is mediated by the actions of the sympathetic nervous system on brown fat.

Neuropeptides expressed in the hypothalamus are classified into anabolic or catabolic peptides. Appetite stimulating, or orexigenic, peptides include neuropeptide Y (NPY), agouti-related peptide (AgRP), melanin-concentrating hormone (MCH), and orexin (ORX).¹⁰ Appetite-inhibiting, or anorexigenic, peptides such as corticotropin-releasing hormone (CRH), alpha-melanocyte-stimulating hormone (α-MSH), and cocaine and amphetamine–regulated transcript (CART) decrease food intake,¹⁰ and selective cannabinoid 1 (CB1) receptor blockade decreases food intake.¹¹

Peripheral Mechanisms

Numerous peripheral factors transmit afferent signals to the central nervous system to control the expression of orexigenic and anorexigenic neurotransmitters that regulate short-term and long-term food intake and expenditure. Short-term signals related to meals, like nutrients (glucose, amino acids, fatty acids) and gastrointestinal hormones (glucagon-like peptide 1 [GLP-1], peptide YY [PYY], cholecystokinin [CCK]), promote the feeling of satiety and limit the size of meals. Gastrointestinal mechanoreceptors and chemoreceptors sense the presence and type (caloric content) of food in the gastrointestinal tract and contribute to the feeling of satiety in the immediate postprandial period. These short-term signals do not produce sustained changes in energy balance and body adiposity.¹²

Long-term regulators of energy homeostasis include insulin, leptin, and possibly ghrelin (an appetite-stimulating gastric peptide). These hormones normally regulate food intake and energy expenditure to ensure that energy homeostasis is maintained so that body weight and adiposity remain relatively constant.¹²

The following are peptides that decrease appetite or increase energy expenditure:

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  leptin; CCK; insulin; GLP-1; gut hormone fragment PYY; gastrin-releasing polypeptide (GRP); enterostatin; pancreatic hormones (glucagon, amylin, and pancreatic polypeptide); vasopressin; calcitonin; apolipoprotein A-IV; the cyclized form of histidyl-proline, thyrotropin-releasing hormone.¹²

The following are peptides that increase appetite or decrease energy expenditure:

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  ghrelin, desacetyl melanocyte-stimulating hormone, growth hormone, prolactin.

Hence, it is not clear whether obesity is a direct cause of an adverse pregnancy outcome or whether the association between obesity and adverse pregnancy outcome is due to factors that are shared characteristics of both entities. Adverse outcomes are often attributed to the increased prevalence of diabetes in obese women. However, glucose-tolerant obese women are also at greater risk of adverse outcome; therefore, other pathways are likely to play a role.¹³ The pathogenesis of some adverse outcomes may be adipose tissue-related dysregulation of metabolic, vascular, and inflammatory pathways, which can affect many organ systems.¹⁴ The risk of some pregnancy complications rises with increasing obesity, which supports this hypothesis.¹⁵

In addition, epigenetic changes in response to increased fetal exposure to glucose, lipids, and inflammatory cytokines may result in permanent or transient changes in metabolic programming, leading to adverse health outcomes in adult life.¹⁶

Both obesity and pregnancy are associated with significant physiologic changes, and many of these changes have similar implications (Tables 25-1 and 25-2).^17,18 In early pregnancy, even before the uterus is large enough to affect respiratory function, women begin to have a sensation of dyspnea. This sensation likely occurs from the increased alveolar ventilation seen in pregnant patients, which is probably secondary to progesterone effects on the respiratory center in the brainstem. By the fifth month of pregnancy, the mechanical effects of the growing uterus begin to produce a progressive decrease in expiratory reserve volume (ERV), residual volume (RV), and functional residual capacity (FRC), which at term are about 15%–20% below those of the nonpregnant state.¹⁹

Several studies^19,20 have shown that obesity in nonpregnant subjects is associated with a decrease in ERV, RV, and FRC, most likely caused by the added weight and decreased compliance of the chest wall. However, obese pregnant women did not have an additional significant reduction in FRC, as is the case in normal-weight pregnant patients. It is possible that these findings can be partially explained by the fact that the study was performed with the patients in the sitting position.¹⁹ The supine, especially the Trendelenburg, position worsen lung volumes significantly. Another possible explanation is that the relaxing effect of progesterone on smooth muscle decreases airway resistance, thus reducing some of the negative effects of obesity on the respiratory system.^17,18 Arterial blood gas analysis demonstrates hypoxemia in the obese parturient much more frequently than in the nonobese, which suggests a greater degree of venoarterial shunting.¹⁹ This is especially true when the FRC is further reduced by the induction of general anesthesia or when the patient assumes the supine or the Trendelenburg position.²⁰ The FRC may fall below the closing capacity, leading to airway closure, especially in the dependent lung regions, thereby causing increased venoarterial shunting.²⁰

The work of breathing is increased in obese parturients due to chest wall weight, and they typically show a rapid and shallow breathing pattern.²¹ This in turn leads to a higher ventilatory requirement and oxygen cost of breathing.^20,22 Hence, excess body weight increases oxygen consumption and CO₂ production in a linear fashion.²¹ These physiologic changes make the obese parturient particularly prone to rapid desaturation, stressing the importance of adequate denitrogenation (“preoxygenation”) before induction of general anesthesia.

In nonobese pregnant women, physiologic changes during pregnancy are thought to protect against obstructive sleep apnea due to high circulating levels of progesterone, which is a ventilatory stimulant.²³ However, obesity increases the risk for obstructive sleep apnea significantly, and this is not uncommon in the obese pregnant woman. Obstructive sleep apnea has been associated with increased systemic, and possibly pulmonary, hypertension. In addition, these patients are at an increased risk for coronary artery disease, stroke, and cardiac arrhythmias.²⁴ Maternal oxygen desaturation, occurring as a result of apnea, may result in fetal hypoxia and poor fetal growth.²⁵