A 32-year-old man, weighing 396 lb (180 kg) and standing 5 feet 7 inches (170 cm) tall, presented for laparoscopic sleeve gastrectomy. He had a past medical history of hypertension, diabetes mellitus, asthma, and gastroesophageal reflux disease. He used bilevel positive airway pressure (BiPAP) for obstructive sleep apnea (OSA) at night.
How is body mass index defined?
According to the World Health Organization, obesity is defined as abnormal or excessive fat accumulation that presents a risk to health. Differences in weight among individuals are due only partly to variations in body fat. Total body weight, although easy to obtain, is a limited measure of obesity. In 1832, Quetelet, a Belgian mathematician, defined the relationship between weight and height and created the Quetelet index, which eventually became known as the body mass index (BMI), so named by Keys in 1972.
BMI is an index of weight-for-height that is commonly used to classify obesity. It is defined as weight in kilograms divided by the square of height in meters (kg/m 2 ). Although also applicable to children, age is an additional factor. BMI values of ≥40 are commonly considered an indication for bariatric surgery. Patients with a BMI >35 and significant comorbidities (e.g., diabetes) are also candidates for bariatric surgery. Another indication for bariatric surgery is a desire to become pregnant in a nulliparous, obese woman.
Although several classifications of obesity exist, the most widely accepted is from the World Health Organization and is based on BMI ( Table 37-1 ). More recently, with the increase of bariatric procedures, a slightly different classification has been introduced to the surgical literature ( Table 37-2 ). The BMI of our patient is 62 (180 kg/1.7 m 2 ), and he is classified as super-superobese.
|BMI (kg/m 2 )||Classification|
|30–34.9||Class I obesity|
|35–39.9||Class II obesity|
|≥40||Class III obesity|
|BMI (kg/m 2 )||Classification|
As noted earlier, in children, because of ongoing growth and differences in distribution of fat and muscle that is age dependent and gender dependent, the calculated BMI is measured against other children of the same age and gender ( Figure 37-1 ). The calculated BMI is plotted on growth charts from the U.S. Centers for Disease Control and Prevention that are based on age and gender. A BMI percentile for age is determined. The percentile determines the classification of obesity ( Table 37-3 ).
BMI calculations without taking into consideration body habitus may be misleading in certain patient populations. For example, in a muscular person, BMI may suggest obesity but in fact reflects additional muscle mass. Also, in a person with degenerative loss of skeletal muscle mass, BMI may not account for the relative increased percentage in fat. Calculation of body fat percentage may help differentiate between obesity from excess body fat and increased muscle mass. Body fat percentage is calculated as follows:
1.2 (BMI) + 0.23 (age) − 10.8 (sex) − 5.4
Sex is assigned a value of 1 for males and 0 for females. Men who have a body fat percentage >25% are classified as obese ( Table 37-4 ). Our patient’s body fat percentage is 75.16%.
|Description/Status||Women (Fat %)||Men (Fat %)|
What cardiopulmonary changes occur with superobesity?
Superobesity affects multiple organ systems. Effects on the respiratory system involve the upper and lower airways and lung mechanics. Patients are prone to upper airway obstruction, particularly during sleep. OSA, defined by the number of apnea and hypopnea events per hour of sleep, occurs in approximately 3%–7% of all men and 2%–5% of all women (see Question 4 for details). However, the prevalence of OSA is >50% higher in obese individuals. Both chest wall and lung compliance are decreased secondary to fat accumulation over the thorax and abdomen. The decrease in lung compliance is also due to increased pulmonary blood flow secondary to increased cardiac output and polycythemia seen in chronically hypoxemic patients.
A decrease in lung compliance leads to a decrease in functional residual capacity (FRC), at the expense of expiratory reserve volume, vital capacity, and total lung capacity. Closing capacity is unchanged, but reduced FRC could result in normal tidal volumes occurring at lung volumes below closing capacity. Small airway closure, absorption atelectasis, ventilation/perfusion mismatch, and hypoxemia result. These changes are exacerbated during general anesthesia and in the supine position.
Total blood volume is increased, but the total blood volume per total body weight measurement is decreased (i.e., 50 mL/kg). As weight increases, so does cardiac output, with shunting to adipose tissue. The increase in cardiac output is the result of left ventricular hypertrophy and increased stroke volume. Ultimately, left ventricular hypertrophy, decreased left ventricular compliance, and impaired filling (i.e., diastolic dysfunction) occur. The endpoint is systolic dysfunction and left ventricular failure.
Right-sided heart changes are secondary to chronic hypoxemia, particularly in patients with OSA. Chronic hypoxemia and increased pulmonary blood volume lead to pulmonary hypertension, right ventricular hypertrophy, and ultimately right ventricular failure.
Development of atherosclerosis is accelerated. However, it is difficult to detect the presence of coronary artery disease by history alone because obese patients tend to have sedentary lifestyles. A high index of suspicion and diagnostic testing are indicated. Hypertension and arrhythmias are frequent complications.
What comorbidities are associated with superobesity?
Many comorbidities involving multiple organ systems occur in patients who are superobese ( Table 37-5 ). The death risk is increased. The relative risk for coronary heart disease is 1.72 in patients with a BMI of 25–28.9 kg/m 2 and progressively increases with increasing BMI. Similar trends have been shown in the relationship between obesity and stroke or congestive heart failure. Overall, the estimated increase in cardiovascular mortality rate is fourfold and the estimated increase in cancer-related mortality rate is 2-fold in obese patients. The incidence of polycystic ovarian disease is also increased. As a group, people who are superobese have a 6-fold to 12-fold increase in all-cause mortality rates.