Key points
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Obesity is a common disease. The number of overweight, obese, and morbidly obese persons has increased alarmingly in the last three decades.
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Body mass index (BMI) is only one measure of obesity; some patients with high BMI are in good health.
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Distribution of fat is a better predictor of health risk than weight alone; gynecoid (gluteofemoral) fat distribution predicts better risk than android (abdominal) distribution. Fat tissue is an active endocrine organ.
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Hypertension, diabetes, cardiac disease, dyslipidemia, arthritis, and back pain are common problems in obese patients, who are also at increased risk for depression and cancer, as well as social discrimination.
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Obese women may have more menstrual irregularities, subfertility, stress incontinence, and hirsutism.
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Obstructive sleep apnea (OSA) is a common problem among obese persons, with many negative anesthetic implications and insufficient screening of surgical patients.
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Ventilation is more difficult in obese patients; OSA, BMI, and large neck circumference also can make intubation challenging. A consistent approach with head elevation and preoxygenation can increase apnea time significantly.
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Drug dosing in the obese patient must consider total, lean, and ideal body weight, along with lipophilic drug characteristics.
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Nutrition disorders can significantly impact surgical outcomes, especially postoperative infections.
Obesity
Obesity is a common disease, at least in most of the developed world; parts of the developing world, such as China and Egypt, also have increasing overweight and obesity rates. With one third of the U.S. adult population and one sixth of U.S. children classified as obese, obesity is now the second most common cause of preventable deaths in the United States, second only to smoking. In the 1970s, 15% of the U.S. population was classified as obese; this has steadily increased to 33% and for the first time has now leveled off in the past few years. Clinically, minority populations have a much higher incidence of obesity.
Alarmingly, the incidence of childhood obesity has tripled since 1980 and had reached 17% in 2008, with no signs of abating. Long-term health and social consequences for these children are substantial. They have a significantly greater chance of developing associated medical problems, such as diabetes, hypertension, and heart disease, and at a much younger age. As they grow into obese teenagers and young adults, they are the same children who are much more likely to suffer from depression and social isolation.
In economic terms, the estimated medical cost of obesity in the United States is a staggering $147 billion. Globally, the incidence of obesity has more than doubled since 1980, with more than 1 in 10 adults now classified as obese; obesity is now the fifth leading risk of death. According to the World Health Organization, “Once considered a high-income country problem, overweight and obesity are now on the rise in low- and middle-income countries, particularly in urban settings. Overweight and obesity are linked to more deaths worldwide than underweight.” Perhaps for the first time in human history, there are more overweight than underweight people in the world.
Pathophysiology
Obesity is a function of a person’s weight being disproportionately greater than their height. There are different ways of classifying a person as overweight or obese and even morbidly obese. For example, a person who is 100 pounds above their ideal body weight is considered morbidly obese. A patient with a body mass index (BMI) of 30 kg/m 2 or more is classified as being obese. BMI is calculated by using the person’s weight in kilograms (kg) divided by the person’s height in meters squared (m 2 ). Table 6-1 lists other weight classifications based on BMI.
| BMI | Weight Status |
|---|---|
| < 18.5 | Underweight |
| 18.5-24.9 | Normal |
| 25.0-29.9 | Overweight |
| 30.0-39.9 | Obese |
| 40.0-49.9 | Morbidly obese |
| 50.0-69.9 | Super morbidly obese |
| > 70.0 | Ultra-obese |
Although one of many methods for estimating body fat, BMI does not correlate well with the distribution of fat (android or “apple” vs. gynecoid or “pear”). BMI also does not take into account the amount of pre-existing muscle mass often seen in some athletes or even weightlifters. Other methods used to estimate body fat and distribution include measurements of skin fold, waist circumference, waist-to-hip circumference ratios, or radiographic studies such as computed tomography (CT), ultrasound, and magnetic resonance imaging (MRI). For adult patients with a BMI of 25 to 34.9 kg/m 2 , waist circumference should be used in addition to BMI to identify risk factors, with higher risks associated with males with a waist size greater than 40 inches and females with a waist size more than 35 inches .
Many factors contribute to overweight and obesity. On a basic level, an energy imbalance between the caloric intake and caloric expenditure—in which caloric intake exceeds calories consumed in basal metabolic demand, work, or exercise—leads to overweight and ultimately obesity. As excess calories are stored in the body as fat, obesity can result from overconsumption of food, insufficient physical activity, or other factors ( Table 6-2 ). A 2% differential in this balance can lead to a 5-pound (2.2-kg) increase in weight every year.
| Etiologic Category | Examples |
|---|---|
| Familial/genetics | Bardet-Biedl syndrome Prader-Willi syndrome |
| Diseases | Hypothyroidism Cushing’s disease Polycystic ovary syndrome Depression Eating disorders |
| Medications | Antidepressants Steroids |
| Societal factors | Poor access to healthy foods Larger food portions |
Comorbidities
Obesity is associated with an increased incidence of several diseases. Higher morbidity caused by overweight and obesity has been observed for hypertension, type 2 diabetes, coronary heart disease, cerebrovascular accident (stroke), gallbladder disease, osteoarthritis, sleep apnea and respiratory problems, and endometrial, breast, prostate, and colon cancer. Obesity is also associated with complications of pregnancy, menstrual irregularities, hirsutism, stress incontinence, and psychological disorders such as depression.
Fat distribution also plays an important role in the type of associated disease. Visceral fat, typically seen in males with an android (truncal) fat distribution, represent a risk factor for the development of cardiovascular disease and type 2 diabetes. Visceral adipose tissue mass frequently correlates with the development of insulin resistance. This is not the case with total or subcutaneous adipose tissue mass. It is now known that the adipocytes of visceral fat tissue are more lipolytically active than subcutaneous adipocytes and contribute more to the plasma free fatty acid (FFA) level. Subcutaneous adipose tissue (SAT) is divided into superficial subcutaneous adipose tissue (sSAT) and deep subcutaneous adipose tissue (dSAT) by the layer of fascia superficialis. Deep SAT is strongly linked to insulin resistance, particularly in obese males. Interestingly, subcutaneous leg and hip adipose tissue have a protective role against diabetes and cardiovascular disease.
Obesity affects many organ systems ( Table 6-3 ). During the perioperative period, the anesthesiologist is primarily concerned with cardiovascular, respiratory, and gastrointestinal diseases.
| Disease Category | Select Comorbidities |
|---|---|
| Cardiovascular | Obesity cardiomyopathy Hypertension Ischemic heart disease Hyperlipidemia Sudden cardiac death |
| Respiratory | Obstructive sleep apnea (OSA) Obesity hypoventilation syndrome (OHS) Restrictive lung disease |
| Endocrine | Diabetes Cushing’s disease Hypothyroidism Polycystic ovary syndrome (PCOS) Infertility |
| Gastrointestinal | Gastroesophageal reflux disease (GERD) Fatty liver Gallstones |
| Genitourinary | Menstrual abnormalities Female urinary incontinence Renal calculi |
| Malignancy | Breast, prostate, colorectal, cervical, renal, and endometrial cancer |
| Musculoskeletal | Osteoarthritis of weight-bearing joints Back pain |
Obesity-hypoventilation syndrome
Between 10% and 20% of OSA patients eventually develop obesity-hypoventilation syndrome (OHS), also known as pickwickian syndrome. OHS is defined as a combination of obesity (BMI ≥ 30 kg/m 2 ) and chronic hypercapnia (Pa co 2 ≥ 45 mm Hg) accompanied by sleep-disordered breathing. Patients typically present with daytime hypersomnolence as well. Patients with severe OHS may develop polycythemia, pulmonary hypertension, and right-sided heart failure. Obstructive sleep apnea causes hypoventilation, leading to hypoxia and hypercapnia, with metabolic alkalosis to compensate for respiratory acidosis. Initially the acid-base disturbance is limited to nocturnal periods, with a return to homeostasis during the day. Over time, however, the central respiratory centers become desensitized to hypercapnia, and nocturnal episodes of apnea occur. Gradually, an increased reliance on hypoxic drive for ventilation develops (see Airway Considerations ).
Patients with OHS are more sensitive to the respiratory depressive effects of opioids and hypnotics. Because of the added complexity of arterial hypoxia, hypercapnia, pulmonary hypertension, and right-sided heart failure, invasive monitoring should be considered in obese patients along with baseline arterial blood gas (ABG) levels as a reference point for further management.
Respiratory Effects
Obese patients have an increased amount of chest wall adipose tissue, causing a mass effect on the thoracic cage and abdomen. This extra weight impedes the normal diaphragmatic motion, especially in a supine position, resulting in splinting of the diaphragm. This causes a decrease in functional residual capacity (FRC), expiratory reserve volume (ERV), and total lung capacity (TLC). The FRC may decrease to the point that small-airway closure occurs with resulting ventilation/perfusion mismatch, right-to-left shunting, and arterial hypoxemia. General anesthesia further decreases the FRC in an obese patient (~ 50%) compared with a nonobese patient (~ 20%), leading to a decrease tolerance of apnea. Preoxygenation with anesthesia induction helps prolong the apnea period, although arterial hypoxia is still quite common during direct laryngoscopy. The addition of continuous positive airway pressure (CPAP) helps improves FRC at the expense of cardiac output and oxygen (O 2 ) delivery.
The extra weight around the chest wall also causes decreased lung compliance, resulting in rapid, shallow breathing patterns in obese patients. This increases the work of breathing, causing increased O 2 consumption and increased carbon dioxide production. Therefore, obese patients have increased CO 2 production and increased O 2 consumption partly because of increased effort to mobilize and increased energy requirement for breathing in trying to move the chest wall, causing up to a 70% increase in the energy expenditure for breathing.
Cardiovascular Effects
The risk of comorbidities rises with increasing BMI. Even though exertional dyspnea and lower-extremity edema are common and nonspecific, even electrocardiography and physical examination can underestimate the degree of cardiac dysfunction in the obese patient group. The increased length of assisted ventilation, longer hospital stay, and increased risk of renal dysfunction are more often seen than increased mortality, at least in cardiac surgery patients.
Adipose tissue is highly vascular, with each kilogram of fat containing 3000 m of blood vessels. This causes cardiac output to increase 0.1 L/min for each kilogram of excess weight related to adipose tissue. The result is that 50% to 60% of obese patients also have hypertension from hypervolemia caused by excess extracellular fluid volume and increased cardiac output. Systemic hypertension could eventually lead to concentric left ventricular hypertrophy (LVH), ultimately leading to congestive heart failure (CHF). The right side of the heart is frequently affected because of CHF from the left ventricle or pulmonary hypertension from chronic arterial hypoxemia or increased pulmonary blood volume.
Obese patients often have poor exercise tolerance. Because of LVH and a stiffened left ventricle during exercise, cardiac output can only be increased by increasing heart rate, without a corresponding increase in stroke volume or ejection fraction.
In addition to these cardiac issues, obesity (especially central obesity) is also an independent risk factor for the development of ischemic heart disease. Acid-base and electrolyte disturbances, volume overload, and coronary heart disease also put obese patients at higher risk for arrhythmias, especially atrial fibrillation.
In evaluating risk of perioperative morbidity and mortality, the anesthesiologist focuses on age, gender, cardiac and respiratory fitness, electrolyte imbalances, and heart failure as predictors. The American Heart Association (AHA) provides recommendations for evaluation of obese surgical patients.
Gastrointestinal and Metabolic Effects
Gastroesophageal reflux disease
Contrary to popular belief, obese patients without symptoms of gastroesophageal reflux disease (GERD) have a resistance gradient between the stomach and gastroesophageal junction similar to that in the nonobese population, in both the supine and the upright position. Although obese patients have 75% greater gastric volume than nonobese persons, a faster gastric emptying time compensates for most of this extra volume. This implies that the risk of aspiration at anesthesia induction is probably overestimated by most clinicians.
Diabetes mellitus
Obesity is an important independent risk factor for type 2 diabetes mellitus. All obese patients should have a random glucose test preoperatively and if indicated, a glucose tolerance test. The stress response of surgery may trigger hyperglycemia and necessitate exogenous insulin in the perioperative period. Preoperative blood glucose levels are obtained, with hourly follow-ups operatively as well as in the immediate postoperative period.
Metabolic syndrome
Metabolic syndrome, sometimes referred to as “insulin resistance syndrome” or syndrome X, seems to result from the maladaptation to overnutrition of genes selected to survive undernutrition. Medicine traditionally viewed the relationship between insulin and glucose as confined to diabetes. In fact, the hyperinsulinemia of insulin resistance is associated with a range of apparently unconnected disturbances that include hyperglycemia, hypercholesterolemia, hypertriglyceridemia, hypertension, hyperviscosity (increased hematocrit), hypercoagulability and hyperuricemia. Each of these disturbances poses a cardiovascular risk to the patient, but in concert, they are deadly to the macrovascular system. Although Reaven first elucidated the relationship between insulin resistance and metabolic disturbance in 1988, Himsworth had observed almost five decades earlier that some diabetic patients required increasing amounts of insulin and appeared to become increasingly insensitive or “resistant.”
Weight gain and insulin resistance are the primary causes of metabolic syndrome. Fat distribution also seems to be involved in cardiovascular risk differences in patients. Upper abdominal fat (around the digestive organs), usually in the male, and gluteofemoral (subcutaneous) in the female patient explain some of the disparate risk. Fat, the largest endocrine organ in the body, produces many inflammatory mediators, including adiponectin, which appears to play a significant role in insulin resistance. Adiponectin has an inverse relationship with obesity, with levels decreasing with increasing obesity, and negatively with glucose, insulin, triglycerides, and increasing BMI.
Thromboembolic events
The risk of deep vein thrombosis (DVT) in obese patients undergoing nonmalignant abdominal surgery is approximately twice that of nonobese patients, with a similarly increased risk of pulmonary embolus or embolism (PE). Stein et al. showed that in the nonsurgical population, the relative risk of DVT and PE was 2.5 and 2.21, respectively, comparing obese patients with nonobese patients. Obese females under age 40 were noted to be the highest-risk group for DVT and PE. The use of subcutaneous heparin and pneumatic devices has helped decrease incidence and thereby improve outcomes in these patients.
Airway Considerations
The pharynx is a collapsible tube that is controlled by more than 20 pairs of pharyngeal muscles. The pharyngeal airway size is determined by the structural properties of the airway and neural regulation of the pharyngeal dilating muscles. Anatomically, the pharyngeal airway is formed by the space surrounded by soft tissue such as the tongue and soft palate. The soft tissue is itself enclosed in a rigid craniofacial bony structure that limits its outward expansion. Therefore, an increase in soft tissue surrounding the airway or a decrease in the rigid bony structures surrounding the soft tissue would reduce the amount of space for the airway. The pharynx further narrows or closes when the neural control mechanism is diminished during sleep or general anesthesia, leading to obstruction of the airway.
Obstructive sleep apnea
Cessation of airflow of more than 10 seconds, characterized by frequent episodes of apnea or hypopnea during sleep, defines obstructive sleep apnea . OSA is seen in 38% of obese men and 28% of obese women; odds ratio (OR) is 6.7 in heavy smokers. In the general population, 11.4% of males and 4.7% of females have moderately severe OSA. This number increases with age, with OR increasing 1.8 with each decade of life.
Clinical diagnosis of OSA is made when the frequency of apnea or hypopnea per hour of sleep (apnea-hypopnea index [AHI]) is > 5/hr in adults. Severity of OSA is determined by the AHI: mild (6-15/hr), moderate (16-30/hr), and severe OSA (AHI > 30/hr). OSA is now recognized as an independent risk factor for the development of hypertension, cardiovascular morbidity and mortality, and sudden death.
Obesity is a common feature of OSA patients. Alternately, not all obese patients have OSA, and not all patients with OSA are obese. Obesity has two distinct mechanisms affecting pharyngeal airway collapsibility. First, obesity increases soft tissue mass surrounding the pharynx, leading to a smaller upper airway. This is especially true for patients with a large neck circumference, which represents regional obesity near the pharyngeal airway, and thus has a stronger correlation to OSA severity than BMI. Second, obesity, particularly central obesity, decreases lung volume through an increase in visceral fat volume. The decrease in lung volume causes pharyngeal wall collapsibility from “decreased longitudinal tracheal traction.” Recent studies show that waist circumference may be an even better predictor for OSA than neck circumference or BMI.
Perioperative airway management starts with the preoperative interview. There is a high prevalence (> 24%) of undiagnosed OSA in the surgical patients, and appropriately, it is even higher in the obese surgical patient. All obese patients undergoing surgery should therefore be suspected of having OSA preoperatively. During the airway evaluation, a modified Mallampati class 3 or 4, or excessive submandibular soft tissue, also indicates anatomic imbalance, which may suggest OSA. With OSA as a primary risk factor, Langeron et al. reported five independent risk factors for potential difficult mask ventilation (age > 55; BMI > 26 kg/m 2 ; snoring; beard; lack of teeth). The relationship among OSA, obesity, and difficult tracheal intubation is more controversial. Siyam and Benhamou showed a higher incidence of difficult intubations in OSA versus non-OSA patients (21.9% vs. 2.6%), whereas Neligan et al. showed that in morbidly obese patients, there was no relationship between the presence and severity of OSA, BMI, or neck circumference and difficulty of intubation or laryngoscopy grade. Chung et al. cited the STOP-BANG questionnaire as an ideal screening tool for OSA: s noring, t iredness, o bserved apnea, high blood p ressure, high B MI, advanced a ge, large n eck circumference, and male g ender ( Box 6-1 ).
- 1.
Snoring: Do you snore loudly (louder than talking or loud enough to be heard through closed doors)?
- 2.
Tired: Do you often feel tired, fatigued, or sleepy during the daytime?
- 3.
Observed: Has anyone observed that you stopped breathing during your sleep?
- 4.
Blood pressure: Do you have, or are you being treated for, high blood pressure?
- 5.
Body mass index: BMI greater than 35 kg/m 2 ?
- 6.
Age: Older than 50?
- 7.
Neck circumference: Greater than 40 inches?
- 8.
Gender: Are you male?
High risk of OSA: “Yes” to three or more items.
Low risk of OSA: “Yes” to less than three items.
Modified from Chung F, et al: Anesthesiology 108:812-821, 2008.
During anesthesia induction, the obese OSA patient should be placed on a “ramped position,” with elevation of torso and head combined with the semiupright position ( Fig. 6-1 ). This position increases lung volume, decreases pharyngeal closing pressure by improving the pharyngeal anatomic disparity, and improves the alignment of the oral, laryngeal, and pharyngeal axes when combined with placing the patient in a “sniffing” position. Preoxygenation with 100% O 2 by a tight-fitting mask using CPAP can increase apnea tolerance time and oxygenation (see Fig. 6-1 ). At our institution, this consistent approach has resulted in no incidences of “could not intubate, could not ventilate” scenarios over the last 2000 + morbidly obese cases.
Airway maneuvers such as mandible advancement, neck extension, and mouth opening (triple airway maneuver), in addition to use of an oral airway, often aid in oxygenation and prevention of airway obstruction. About 10% of obese patients are difficult to ventilate, and about 1% are difficult to intubate. There are multiple reasonable approaches to the airway in the obese and morbidly obese patient. Direct laryngoscopy with a class 1 airway combined with a ramped position has a high degree of success. Intubating laryngeal mask airway (LMA), awake fiberoptic intubation, and video laryngoscopy also have high success rates.
Importantly, the clinician should not become fixated on intubating or on just one approach to the airway. The anesthesiologist should be prepared to stop, re-evaluate, and change equipment, position of head, or person intubating. Use of short-acting neuromuscular blockade (succinylcholine or rocuronium with Sugamadex availability) allows the patient to return to spontaneous respiration. Clearly the American Society of Anesthesiologists (ASA) “difficult airway algorithm” still applies for obese patients in case of difficulties with mask ventilation or intubation. Awake intubation should be considered when any element of the triple airway maneuver is disturbed in obese patients with severe OSA. Kheterpal et al. showed that limited mandible advancement is an independent risk factor for impossible mask ventilation. During an awake intubation, upper airway anesthesia by local anesthetic could blunt the reflexive increase of pharyngeal dilator muscles as a response to pharyngeal narrowing or obstruction. Preservation of the neural compensatory mechanism is important, and thus deep sedation should be avoided.
Airway maintenance
Ventilator settings can be challenging, potentially with increasing CO 2 , decreasing oxygen saturation (SaO 2 ), and intolerable peak pressures in the airway. The starting settings may be positive end-expiratory pressure (PEEP) of 8 to 10 cm H 2 O, tidal volume of 10 to 12 mL/kg of ideal body weight, and respiratory rate of 12 to 14/min. These values may need to be adjusted, along with inspiratory/expiratory (I:E) ratio, until satisfactory peak pressures, SaO 2 and end-tidal CO 2 are achieved. An easy way to re-establish saturation after induction, or at any time during anesthesis, is a recruitment maneuver (e.g., applying CPAP), 30 cm H 2 O for 30 seconds, or even 40 cm H 2 O for 40 seconds. A high index of suspicion for suboptimal tube position, which can be checked using a fiberoptic scope, can be critical. Volatile agents are usually chosen based on solubility; desflurane was shown to be better than isoflurane, propofol, or sevoflurane, but these data are now questionable.
Pharmacologic Issues
The physiologic changes associated with obesity alter the pharmacokinetic and pharmacodynamic properties of many drugs. Obese patients have an increased amount of both fat and lean body weight compared with nonobese patients of similar age, height, and gender. These changes affect the volume of distribution of some drugs ( Table 6-4 ).
| Drug | Dosing Scalar * | Altered Pharmacokinetics |
|---|---|---|
| Hypnotics | ||
| Thiopental | Induction: LBW Maintenance: TBW | Increased central volume of distribution and clearances; induction dose adjusted to LBW results in same peak plasma concentration as dose adjusted to cardiac output |
| Propofol | Induction: LBW Maintenance: TBW | During induction, similar time of loss of consciousness exists between obese subjects given LBW dose and nonobese subjects given TBW dose. Propofol has high affinity for excess fat, so systemic clearance and volume of distribution at steady state correlate better to TBW |
| Midazolam, diazepam | Induction: TBW Maintenance: TBW | Central volume of distribution increases along with body weight; prolonged duration of action because larger initial doses are needed |
| Opioids | ||
| Fentanyl/Sufentanil | Induction: TBW Maintenance: IBW | Increased volume of distribution and elimination half-life as related to obesity |
| Alfentanil | Induction: LBW Maintenance: LBW | Prolonged elimination |
| Remifentanil | Induction: LBW Maintenance: LBW | Infusion based on LBW in obese patients resulted in similar plasma concentration as TBW for nonobese patients |
| Morphine | No information available | |
| Neuromuscular Blocking Agents | ||
| Succinylcholine | Induction: TBW | Doses based on 1 mg/kg of TBW resulted in better intubating conditions compared with dosing based on IBW or LBW |
| Atracurium/Cisatracurium | Induction: TBW Maintenance: TBW | Absolute clearance, volume of distribution, and elimination half-life unchanged because of organ-independent Hoffman elimination |
| Vecuronium | Induction: IBW Maintenance: IBW | Doses based on TBW may result in prolonged duration of action from increased volume of distribution and impaired hepatic clearance |
| Rocuronium | Induction: IBW Maintenance: IBW | |
| Pancuronium | Induction: IBW Maintenance: IBW | Low lipid solubility; shorter-acting neuromuscular blockers are preferred for obese patients |
| Local Anesthetics | ||
| Lidocaine | Intravenous: TBW Epidural: 75% TBW | Increased epidural fat content and epidural venous engorgement |
* LBW, Lean body weight; TBW, total body weight; IBW, ideal body weight.
In addition, increases in cardiac output and total blood volume and changes in regional blood flow can also affect peak plasma concentration, clearance, and elimination half-life of many anesthetic agents. With increasing obesity, the less vascular fat mass starts accounting for an increasing amount of total body weight (TBW). Therefore, drug dosing based on TBW may result in overdose of an obese patient. To compensate for some of the obesity-related physiologic changes, dosing scalars other than TBW are frequently used, including lean body weight (LBW), ideal body weight (IBW), and adjusted body weight (ABW).
Lean body weight
Lean body weight is the difference between TBW and fat mass. In obese patients, LBW increases, although at a slower rate of increase compared with TBW. LBW represents the highly vascular portion of the body and is significantly correlated to cardiac output (CO), which is an important determinant in the early distribution kinetics of drugs. LBW is often calculated using the following formula :
LBW ( men ) = ( 1.10 × Weight [ kg ] ) − 128 ( Weight 2 / ( 100 × Height [ m ] ) 2 ) LBW ( men ) = ( 1.07 × Weight [ kg ] ) − 148 ( Weight 2 / ( 100 × Height [ m ] ) 2 )
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