Anesthesia in the patient with extreme obesity

Published on 13/02/2015 by admin

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Anesthesia in the patient with extreme obesity

James P. Conterato, MD

General

Obesity has rapidly become an endemic disorder of Western society. Its presentation is now a daily phenomenon for the practicing anesthesia provider. Obesity is a condition of excess body fat, its derivation coming from the Latin word obesus, meaning fattened by eating. Body fat is a relative state, but in healthy Western societies, body fat averages for women are 20% to 30%, for men 18% to 25%, and for ultrafit marathoners approximately 7%. Obesity is a disorder that has genetic, socioeconomic, and endocrine causes. In developing countries, it correlates with a higher socioeconomic status, whereas in Western society, it more frequently occurs in lower socioeconomic classes. The original definitions of obesity are derived from the concept of ideal body weight calculations, developed by insurance companies to describe those population groups with the lowest mortality rates for age, and calculated as follows:

< ?xml:namespace prefix = "mml" />Ideal body weight (kg) = height (cm) – x

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where x equals 105 for women and 100 for men. Body mass index (BMI) is a more relevant measure of height-weight relationships and is the currently accepted standard used to stratify obesity, although evidence has accumulated that the distribution of fat (central and intra-abdominal vs. peripheral) may best correlate with morbidity and mortality rates, recognizing that central intra-abdominal fat is a more metabolically active, proinflammatory substrate. BMI is calculated as body weight (in kilograms) divided by height (in meters) squared. The World Health Organization and the Centers for Disease Control and Prevention have defined levels of obesity (Table 163-1). Obesity can be further subdivided into morbid obesity (defined as a BMI >35 and <54.9) and super or extreme morbid obesity (BMI >55).

Table 163-1

Classification of Weight by Body Mass Index (BMI)

Category BMI (kg/m2) Obesity Class
Underweight <18.5  
Normal weight 18.5-24.9  
Overweight 25.0-29.9  
Obesity 30.0-34.9 Obesity class I
  35.0-39.9 Obesity class II
Extreme obesity ≥40 Obesity class III

Adapted from Obesity: Preventing and Managing the Global Epidemic. Geneva, Switzerland, World Health Organization; 1997. Report No. 894.

The inflection point for risk is a BMI greater than 30, at which point an exponential increase occurs in multiple risks for morbidity and mortality. Fat-distribution analyses suggest that the waist-to-hip ratio may correlate best with risk and dramatically increases at values of greater than 1 for women and greater than 0.8 for men.

The literature is replete with documentation that the morbidly obese are at increased risk for developing a wide variety of comorbid conditions, including a threefold to fourfold increased incidence of the age-related risks for diabetes, hypertension, cerebrovascular disease, and ischemic heart disease. Obesity predisposes an individual to develop the now well-recognized metabolic syndrome, consisting of hypertension, insulin resistance with adult-onset diabetes (type 2), and hyperlipidemia. It represents a proinflammatory and prothrombotic state associated with vascular endothelial dysfunction, which dramatically increases one’s risk of developing atherosclerotic disease. Additionally, meta-analyses demonstrate increased incidences of essentially all solid-tissue cancers except esophageal cancer, and of deep venous thrombosis and thromboembolism, osteoarthritis, gout, chronic back pain, asthma, infertility, impotence, and gallbladder disease in obese people. Other potentially key considerations are the cardiorespiratory complications of obstructive sleep apnea, apnea-hypoventilation syndrome (pickwickian syndrome), and cardiomyopathy of obesity.

The anesthesia provider faces potential issues in caring for obese patients that encompass these comorbid conditions and impact airway management, cardiorespiratory physiology, pharmacokinetics and pharmacodynamics of drugs, and positioning concerns, to name a few.

Physiology and pathophysiology of morbid obesity

Cardiovascular effects

Each kilogram of fat develops approximately 3000 m of blood vessels and requires a progressive increase in cardiac output that averages 100 mL/min. As a result, circulating blood volumes in the systemic and pulmonary circuits increase, resulting in increased cardiac preload and afterload. Ventricular dilatation and increased stroke volume develop, which eventually elicit ventricular hypertrophy, all of which increase cardiac work. The systemic hypertension and cardiomegaly seen are a result of increases in circulating blood volumes and cardiac output, as are the development of hyperinsulinemia-induced sympathetic activity and tone and progressive peripheral insulin resistance eliciting increased pressor effects of renin and angiotensin II. The development of pulmonary hypertension is a result of increased circulating blood volume, increased sympathetic tone, and chronic arterial hypoxemia (see following discussion under “Airway and Pulmonary Effects”).

The constellation of events that lead to hypertrophy-induced diastolic dysfunction can eventually result in the failure of hypertrophy compensating for ventricular dilatation, resulting in eventual systolic dysfunction—what is described as obesity-induced cardiomyopathy. Patients lose the ability to compensate for additional work stress on the cardiovascular system, relying more on increases in heart rate than stroke volume. Studies have documented an impaired response to exercise in the morbidly obese, with imageO2 max rarely reaching above 25 mL of O2 per kilogram per minute, indicating that levels of work that are submaximal in normal patients can only be met by an increased anaerobic debt in morbidly obese individuals.

Airway and pulmonary effects

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