Morbid Obesity

J. Sudharma Ranasinghe

Donald H. Penning

Obesity is a metabolic disease in which abnormal or excessive accumulation of adipose tissue represents greater than normal proportion of body mass. Obesity is increasing in prevalence amongst pregnant women across the United States (1). The prevalence of obesity is growing at an alarming rate worldwide, and by 2015 it is expected that approximately 700 million people will be obese (2). The World Health Organization also projects that by 2025, more than 50% of the United States population will have a BMI >30 kg/m² (Fig. 35-1).

In the United States obesity rates has reached epidemic proportions with extreme obesity (BMI >40 kg/m²) showing the greatest increase, particularly among women (3). According to the latest data from the National Health and Nutrition Examination Survey (NHANES) in 2007 to 2008, the prevalence of obesity was 32.2% among adult men and 35.5% among adult women in the United States (4) and certain ethnic groups are affected more than others (5). The dramatically increasing rate of obesity in the general population also extends to women of reproductive age. Obesity increases the risk for cesarean delivery significantly and thus also the need for anesthesia. Anesthesiologists are thus increasingly faced with the care for morbidly obese parturients.

Overweight and obesity are major risk factors for a number of chronic diseases, including diabetes, ischemic heart disease, stroke, hypertension, hypercoagulability, osteoarthritis, gall bladder disease, and several types of cancer. There is evidence that risk of chronic disease increases progressively from a BMI of 21 kg/m². Obesity caused by poor diet and physical inactivity is now the second leading cause of death in the United States (3). In pregnant women, obesity is associated with serious consequences on birth outcome (6).

Definitions

Body mass index (BMI) is a simple, clinically relevant measure of overweight and obesity in adult population. It can be easily computed and well correlated with the risk of mortality. It is defined as the total body weight (TBW) in kilograms divided by the square of the height in meters (kg/m²). The World Health Organization (WHO) defines “overweight” as a BMI ≥25, obesity as a BMI ≥30. Obesity is further categorized by BMI into Class I (30 to 34.9); Class II (35 to 39.9) and Class III obesity (>40). Morbid obesity is BMI ≥40 kg/m² and super obesity is classified as a BMI ≥50 kg/m² (7).

Although there are no pregnancy-specific definitions of obesity, the American College of Obstetricians and Gynecologists (ACOG) recommends using height and weight measured at the first prenatal visit to calculate the BMI. Pregnant women are considered obese when the BMI is ≥30 kg/m², and morbidly obese when the BMI is ≥40 kg/m². The maternal body weight is expected to increase during pregnancy due to increase in blood volume, fetus, placenta, amniotic fluid, and deposition of new fat and protein. The normal mean maternal weight increase during pregnancy is 17% of the pre-pregnancy weight or about 12 kg (8). However, it is important to recognize that the allowable weight gain during pregnancy varies by pre-pregnancy BMI (8) (Table 35-1). Obesity is an increasing problem in women of child-bearing age. According to the data from the NHANES survey, at least 60% of women of child-bearing age are overweight or obese (3).

There are several subgroups of obese individuals.

Simple obesity
Obesity hypoventilation syndrome (OHS) also referred to as “Pickwickian syndrome” comprises 5% to 10% of obese individuals. Fortunately, patients with OHS are usually not seen in labor and delivery due to two reasons: (1) This syndrome usually develops later in life and (2) patients with OHS are unlikely to get pregnant.
Obesity-related metabolic syndrome: Increasing incidence of obesity worldwide has led to the recognition of this obesity-related metabolic syndrome also referred to as syndrome X, which is characterized by “truncal” obesity, insulin resistance or glucose intolerance (hyperglycemia), altered lipid levels, low HDL cholesterol, and high LDL cholesterol—that foster plaque buildup in arteries prothrombotic state, high fibrinogen or plasminogen activator inhibitor-1 in the blood; proinflammatory state (e.g., elevated serum C-reactive protein), and hypertension (9). Obesity-related metabolic syndrome carries a different risk profile than obesity alone. These patients are at a greater risk for coronary artery disease (CAD), obstructive sleep apnea (OSA), hypercoagulability with predisposition to deep vein thrombosis (DVT), and pulmonary dysfunction.

Physiologic Disturbances

Both obesity and pregnancy are associated with significant physiologic changes in multiple organ systems. Many of the physiologic effects of pregnancy and obesity are additive and can lead to considerable functional impairment and decreased physiologic reserves. Therefore, obstetric- and anesthetic-related complications are more frequent in obese parturients. A report of anesthesia-related maternal deaths in Michigan (1985 to 2003) confirms that obesity is an important risk factor for anesthesia-related maternal mortality (10). In the 2003–2005 Confidential Enquiries into Maternal and Child Health (CEMACH) report from the UK, there were six women who died from problems directly related to anesthesia, and obesity was a factor in four of them (11).

Figure 35-1 Projected prevalence of obesity in adults by 2025. The Global Challenge of Obesity and the International Obesity Task Force. http://www.iuns.org/

Respiratory Changes

Lung Volumes and Pulmonary Function Tests (PFTs)

Pregnancy is associated with significant anatomical and functional changes in the respiratory system. Similar to pregnancy, obesity reduces the expiratory reserve volume (ERV), residual volume (RV), and functional residual capacity (FRC). One would speculate that when an obese woman gets pregnant these changes in lung volumes will be markedly accentuated. However, according to a study by Eng et al. (12), such is not the case. They found that in obese women with reduced pre-pregnancy FRC, further reduction in pregnancy is limited. The reason for this finding is not clear. In some respects, pregnancy may reduce some of the negative effects of obesity on respiratory system. Progesterone is a direct respiratory stimulant and increases the sensitivity of brainstem to carbon dioxide. The relaxing effect of progesterone on smooth muscle decreases airway resistance. Oxygenation and ventilation of obese pregnant women in the upright position seem to be intermediate between normal-weight–term pregnant women and obese, nonpregnant women (13) (Table 35-2).

Table 35-1 The National Institute of Medicine’s Guidelines for Weight Gain in Pregnancy

Pre-pregnancy BMI	Recommended Weight Gain in kg/(lb)
<19.8 (low)	12.5–18 (28,29,30,31,32,33,34,35,36,37,38,39,40)
19.8–26.0 (normal)	11.5–16 (25,26,27,28,29,30,31,32,33,34,35)
26.1–29.0 (overweight)	7–11.5 (15,16,17,18,19,20,21,22,23,24,25)
>29 (obese)	≤6 (≤15)
Adapted with permission from: Stotland NE. Obesity and pregnancy. BMJ 2009;338:107–110.

During the third trimester of pregnancy, gravid uterus pushes the diaphragm in a cephalad direction.

It has been shown that the closing volume (CV) does begin to impinge on FRC as pregnancy advances. This is most likely from a reduction in RV and ERV (14). However, in contrast to obese parturients, this change does not worsen in normal-weight parturients upon taking the supine position (14). When the mass loading effect of obesity reduces FRC, it may fall at or below closing capacity leading to airway closure during tidal ventilation, especially in the dependent regions causing intrapulmonary shunting (15,16). Assumption of supine, lithotomy, or Trendelenburg position, use of abdominal straps to retract the panniculus cephalad, and induction of general anesthesia results in further reduction in FRC in the obese parturient (Fig. 35-2).

Shunt fractions of 10% to 25% of cardiac output have been reported in obesity (15). Therefore, unlike in normal-weight pregnancy, in obese parturients there is mismatching of ventilation–perfusion ratio with concomitant increase in
alveolar to arterial oxygen tension difference, especially in the supine position. Oxygen saturation measured in the sitting and supine position during normal ventilation may provide evidence of airway closure and the degree of pulmonary reserve.

Table 35-2 Blood Gas Measurements by Pregnancy and Obesity Status

	PaO₂ (SD) mm Hg	PaCO₂ (SD) mm Hg	pH (SD)	Mean BMI (n)
Normal-weight–term pregnant	101.8 (1.0)	30.4 (0.06)	7.43 (0.006)	23.6 (20)
Obese term pregnant	85 (5.0)	29.7 (2.8)	7.44 (0.04)	43.5 (12)
Obese postpartum	86 (10)	35.5 (3)	7.44 (0.04)	41.4 (12)
Obese nonpregnant	76.7 (16.1)	41.3 (5.7)	Not available	39.5 (62)
Obese nonpregnant with sleep apnea	70.9 (11.7)	42.8 (5.0)	Not available	39.6 (40)
Reprinted with permission from: Mhyre JM. Anesthetic management for the morbidly obese pregnant woman. Int Anesthesiol Clin 2007;45: 51–70.

Holley et al. (17) reported that in obese subjects with ERV less than 0.4 L (21% predicted), the distribution of a normal tidal breath was predominantly to the upper zones. This distribution pattern is similar to what is found in normal weight subjects at low lung volumes, i.e., upper lungs are predominantly ventilated at low lung volumes and opposite occurs at high lung volumes. Distribution of perfusion, on the other hand, remains gravity dependent and perfusion index increases approximately linearly with vertical distance down the lungs similar to normal-weight subjects (18). Thus, in obese subjects there is an abnormally low V/Q ratio in lower lung zones, which depends more on the amount of ERV reduction than to the degree of obesity. Even a very large increase in weight is not necessarily associated with severe decrease in ERV due to the fact that the increase in body mass may occur in lower half of the body, which would not interfere with the ERV (17). However, if the fat deposition occurs in the abdominal wall, this would cause an increase in abdominal pressure, and cause a considerable decrease in ERV. The value of ERV may be taken as an approximate indicator as to whether a defect in ventilation distribution is likely in the parturient.

Figure 35-2 Effect of position change on lung volumes in nonobese compared with markedly obese subjects. FRC, functional residual capacity; RV, residual volume; CC, closing capacity. Adapted with permission from: Vaughan RW. Pulmonary and cardiovascular derangements in the obese patient. In: Brown BR Jr, ed. Anesthesia and the Obese Patient. Philadelphia, PA: Davis. 1982:26.

Classically, spirometric values other than maximum voluntary ventilation (MVV) are not affected in obesity. Therefore, an abnormal pulmonary function test (PFT) value should be considered as an indication of intrinsic lung disease and not caused by obesity, unless in extreme obesity where a significant reduction in vital capacity (VC) and total lung capacity (TLC) can be seen (19). The pulmonary diffusion capacity remains unchanged during pregnancy and is well preserved in obesity as well.

The lung parenchyma in obese subjects is essentially normal and the above-mentioned changes in pulmonary values reflect changes due to chest wall mechanics and low lung volumes. Obesity alters the relationship between the lungs, the chest wall, and the diaphragm (Table 35-3).

Work of Breathing

Early in pregnancy, the alveolar ventilation is increased, which is attributed to the respiratory stimulant effect of progesterone rather than a response to increased metabolism. In obesity, hyperventilation at rest occurs due to increased oxygen requirement and CO₂ production by the excess fat that is deposited in the body. Dempsey et al. (20) demonstrated that excess body weight increases oxygen consumption and CO₂ production in a linear fashion. Achieving this augmented ventilation imposes an additional physiologic burden, and work of breathing is increased tremendously in obesity. In patients with simple obesity, the total work of breathing may be increased up to twice normal. In patients with OHS, it is increased about 3 times above that of normal individual (21). The oxygen consumption in obesity is increased even more than the mechanical work of breathing, ranging 4 to 12 times normal thus reducing the efficiency of respiratory muscles in obesity (22).

Compared to normal pregnancy, the most significant pulmonary mechanics change in obesity, is that the chest compliance is reduced to a much greater extent. This change is due to the increased weight of the chest and abdominal wall from accumulation of fat in and around the ribs, the diaphragm, and the abdomen. It has been estimated that 33% of the increased work of breathing in obese subject is due to elastic work done on the chest wall (22). Sharp et al. (21) showed that in obesity the total respiratory compliance is reduced to one-third of normal. Naimark et al. (23) reported further significant reduction in respiratory compliance in obese subjects when assuming supine position as compared to normal-weight patients. Another factor that may contribute to increased work of breathing in obesity is due to an increase in total airway resistance, secondary to the lower lung volumes (24).

Table 35-3 Resting Respiratory Changes in Pregnancy, Obesity, and Pregnancy and Obesity Combined

Parameter	Pregnancy	Obesity	Combined
Tidal volume	↑	↓	↑
Respiratory rate	↑	↑	↑
Minute volume	↑	↓ or ↔	↑
Inspiratory reserve volume	↑	↓	↑
Expiratory reserve volume	↓	↓ ↓	↓
Residual volume	↓	↓ or ↔	↓
Functional residual capacity	↓ ↓	↓ ↓ ↓	↓ ↓
Vital capacity	↔	↔ or ↓	↔ or ↓
FEV₁	↔	↓ or ↔	↔
FEV₁/VC	↔	↔	↔
Total lung capacity	↓	↓ ↓	↓
Compliance	↔	↓ ↓	↓
Work of breathing	↑	↑ ↑	↑
Airway resistance	↓	↑	↓
V/Q mismatch	↑	↑	↑ ↑
DLCO	↔	↔	↔
PaO₂	↑	↓ ↓	↓
PaCO₂	↓	↑	↓
A–a gradient	↔	↑	↑ ↑
↑, increase; ↓, decrease; ↔, no change (multiple arrows represent the degree of intensity). CO₂, carbon dioxide; FEV₁, forced expiratory volume in 1 s; V/Q, ratio of ventilation to perfusion; DLCO, diffusion capacity of lung for carbon monoxide; PaO₂, partial pressure of oxygen; PaCO₂, = partial pressure of carbon dioxide. Modified with permission from: Sarvanakumar et al. Obesity and obstetric anaesthesia. Anesthesia 2006;61: 36–48, from Blackwell Publishing.

During pregnancy, resting minute ventilation increases primarily due to increase in tidal volume. In contrast, obese individuals with increased chest wall mass show a tendency to rapid shallow breathing pattern. This particular breathing pattern optimizes the work of breathing thus avoiding diaphragmatic muscle fatigue (25). However, in obesity, with increasing ventilation when breathing frequency and dead space increases, rapid breathing may become uneconomical leading to ventilatory failure (26).

The adverse changes in the respiratory system illustrate that the obese parturient has minimal or absent pulmonary reserve and can develop hypoxemia rapidly.

Obstructive Sleep Apnea

Obesity is linked to many respiratory conditions which include asthma, OSA, OHS, pulmonary embolism, and aspiration pneumonia. With increased prevalence, obesity is now considered an emerging cause of chronic respiratory failure (27).

The prevalence of OSA in pregnancy is unknown and in many cases may be undiagnosed. It has been suggested that pregnancy may precipitate or exacerbate this condition (28). During normal pregnancy it is not uncommon to have upper airway congestion and edema; which in the obese parturient at risk can precipitate OSA. OSA is characterized by periodic apnea during sleep that produces hypoxia and sleep disruption. Obesity in pregnancy complicated by OSA can have adverse effects on the mother and the fetus. Repetitive significant hypoxemia episodes concurrent with apneic episodes results in maternal hemodynamic consequences, such as elevation of maternal systemic and pulmonary artery pressures, right-sided heart failure and cardiac arrhythmias. Pulmonary vasoconstriction secondary to hypoxia and hypercapnia is believed to be the pathophysiology of this process. Pulmonary hypertension when superimposed by the physiologic changes of pregnancy and labor produces a lethal condition (29).

Maternal oxygen desaturation during apnea can result in fetal hypoxia as demonstrated by resultant fetal heart rate abnormalities. Episodic fetal hypoxia may result in intrauterine fetal growth retardation (30).

Careful history taking and prompt diagnosis by polysomnography would allow early treatment of OSA. Since daytime fatigue is very common in normal pregnancy, OSA is easily missed in this patient population. A recent systemic review and meta-analysis of clinical screening tests for OSA reported that the STOP questionnaire (S = Snoring, T = Tiredness, O = Observed apnea, P = Elevated blood pressure) is an excellent screening test for moderate-to-severe OSA (31) and must be ascertained preoperatively in the morbidly obese parturients. Patients who present with combination of high screening score, recurrent apneic episodes, and/or desaturations during immediate postoperative period were shown to be at increased risk of recurrent postoperative respiratory events (odds ratio = 21) (32). Therefore, these patients require close surveillance and postoperative monitoring to prevent adverse catastrophic respiratory events.

Nasal CPAP is the mainstay of therapy for OSA. Diagnosis of OSA early in the prenatal period allows initiation of CPAP therapy. CPAP has been used successfully with improved perinatal outcome, with no adverse effects during pregnancy (33).

Cardiovascular Changes

The blood volume and cardiac output increases during pregnancy beginning early first trimester. Obesity, on the other hand, independently increases blood volume and cardiac output to double that of pregnancy. The increased cardiac output is required to meet high metabolic demands related to increased fat and increased work of breathing. Cardiac output increases by 30 to 35 mL/min for every 100 g of fat tissue (34).

During normal pregnancy there is additional elevation of cardiac output during labor, and immediate postpartum period (125% increased from pre-pregnancy values). Obese parturients with reduced functional reserves may not be able to tolerate this dramatic increase in cardiac demand and is therefore at much higher risk during the peripartum period. In addition, obesity is a risk factor for peripartum cardiomyopathy, a potentially lethal disease (35).

The systemic vascular resistance decreases during normal pregnancy, and is about 20% below pre-pregnancy value at term (36). In an obese or morbidly obese parturient, due to generalized atherosclerosis, the arterial walls can be less compliant, thus the normal pregnancy–associated afterload reduction, may not occur to the same extent (37).

The combination of higher afterload and increased cardiac output contributes to the significant left ventricular hypertrophy that is found in obese parturients (37). In normal pregnancy, there is an increase in left ventricular diameter (38). However, this increase occurs without a corresponding enlargement in wall thickness. In contrast, cardiac adaptation to obesity results in left ventricular dilatation as well as ventricular hypertrophy (eccentric hypertrophy). Veille et al. (37) demonstrated significantly greater left ventricular posterior wall thickness and interventricular septal thickness with smaller radius-to-wall thickness in obese pregnant patients. This adaptation seems to be important to maintain normal systolic function in obese pregnant patients (Fig. 35-3).

In spite of hypertrophy, left ventricular size and function are shown to be normal in otherwise healthy obese pregnant women during the third trimester of pregnancy (37).

Up to about 15% of pregnant women at term experience a significant drop in blood pressure and bradycardia when they assume the supine position, the so-called supine hypotensive syndrome. This phenomenon is more pronounced in obese parturients since the fat pannus further contributes to pressure on the inferior vena cava in the supine position. Although left uterine decubitus (LUD) position is usually an effective measure to improve venous return, it may be very hard to achieve the LUD position in obese women due to the extra weight.

Tamoda et al. (39) studied the effects of obesity on maternal hemodynamic changes. They concluded that obesity during pregnancy is clearly a risk factor for hypertension, hemoconcentration, and poor cardiac function. Obese parturients secrete excess insulin from the pancreas since adipose tissue is resistant to insulin. This hyperinsulinemia is considered to be the main cause of hypertension (40). During pregnancy, hyperinsulinemia will be more severe due to the fat deposition and enhanced insulin secretion due to estrogen (41). The possible mechanism for hemoconcentration is also thought to be due to sympathetic nervous activity caused by hyperinsulinemia. Pre-pregnancy obesity is a significant risk factor for preeclampsia (42).

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