Chapter 23. Evaluation of the Obese Patient

1. Expiratory reserve volume (ERV) is the most sensitive indicator of the effect of obesity on pulmonary function testing.

2. Plasminogen activator inhibitor-1 (PAI-1), secreted by the endothelium, vascular smooth muscle cells, hepatocytes, and adipocytes, is associated with visceral obesity and inhibits the fibrinolytic system. PAI-1 decreases fibrinolysis and increases the risk of coronary artery disease.

3. Gastric emptying may be delayed in obese patients because of increased abdominal mass causing antral distension, gastrin release, and a decrease in pH with parietal cell hypersecretion. However, emptying has been documented to be faster, with high energy content intake such as fat emulsions, but residual volume (RV) is increased because of their larger gastric volume (up to 75% larger). They should follow the same fasting guidelines as nonobese patients.

4. Rhabdomyolysis has been documented in morbidly obese patients undergoing prolonged procedures. Elevations in serum creatinine and creatine phosphokinase (CPK) levels unexplained by other reasons and complaints of buttock, hip, or shoulder pain in the postoperative period should raise the suspicion of rhabdomyolysis.

5. Difficult laryngoscopy and intubation correlates well with increased age, male sex, temporomandibular joint (TMJ) pathology, Mallampati classes 3 and 4, history of obstructive sleep apnea (OSA), and abnormal upper teeth, not the magnitude of body mass index (BMI).

6. Neck circumference has been identified as the single biggest predictor of problematic intubation in morbidly obese patients.

7. Preoxygenation in the head-up or sitting position is more effective and provides the longest safe apnea period (SAP) during induction of anesthesia in obese patients.

8. The head-elevated laryngoscopy position (HELP) position significantly elevates the obese patient's head, neck, upper body, and shoulders above the chest to a point where an imaginary horizontal line can be drawn from the sternal notch to the external ear to better improve laryngoscopy and intubation.

9. Positive end-expiratory pressure (PEEP) is the only ventilatory parameter that has consistently been shown to improve respiratory function in obese subjects, but it decreases venous return, cardiac output, and subsequent oxygen delivery.

10. Postoperative continuous positive airway pressure (CPAP) does not increase the incidence of major anastomotic leakage after gastric bypass surgery despite the theoretical risk of anastomotic injury from pressurized air delivered by CPAP.

The worldwide epidemic status of obesity is a key factor in the increased incidence of type 2 diabetes mellitus and cardiovascular diseases such as high blood pressure, and stroke.1 Obesity is defined as an abnormally high percentage of body weight as fat. Overweight is an increase in weight relative to a standard. Approximately 65%, or 2 of every 3 adults, in the United States are overweight or obese.2

Approximately 85% of the economic burden of obesity can be accounted for by obesity-related diseases (coronary artery disease, stroke, type 2 diabetes mellitus, hypertension, hyperlipidemia) and prescription drugs.3 The anatomic distribution of body fat is associated with varying pathophysiologic consequences. Android (central) obesity is commonly seen in men and associated with increased oxygen consumption and increased incidence of cardiovascular disease with a truncal or upper body distribution of the adipose tissue. Visceral fat is particularly associated with cardiovascular disease and ventricular dysfunction. Alcohol encourages deposition of central (android pattern) body fat. Gynecoid (peripheral) obesity, typically seen in women, locates adipose tissue predominantly in the hips, buttocks, and thighs and is less closely associated with cardiovascular disease because it is less metabolically active. Waist circumference (WC), waist-to-stature ratio (WSR), and waist-to-hip ratio (WHR) are body circumference (anthropometric) indices that identify patterns of obesity and correlate strongly with mortality and the development of obesity-related diseases. WC generally represents abdominal fat and is an independent predictor of disease. A WHR greater than 0.9 in women and greater than 1.0 in men is associated with a higher risk of morbidity and mortality than is a more peripheral pattern of body fat distribution (WHR <0.75 in women and <0.85 in men). A WC greater than 102 cm (40 in) in men and 88 cm (35 in) in women increases the risk of obesity-related diseases, including cardiovascular diseases, diabetes mellitus, and dyslipidemia (Table 23-1). WSR is the best simple anthropometric index in predicting a wide range of cardiovascular risk factors and related health conditions. It is recommended that a person's WC not exceed half the stature to minimize the incidence of these diseases.4

Ideal body weight (IBW) is the weight associated with the lowest mortality rate for a given height and gender. It is estimated using the Broca's index: IBW (kg) = height (cm) – x; where x is 100 for adult males and 105 for adult females. BMI is more appropriate for clinical use. It estimates the degree of obesity using this equation:

A BMI of 18.5 to 24.9 is within normal weight range; 25.0 to 29.9 is overweight, and BMIs more than 30 and more than 40 kg/m2 are considered obesity and extreme obesity, respectively (Table 23-2). BMI reliably measures body fat, but it cannot distinguish overweight from overfat because heavily muscled people can be easily classified as overweight using BMI.

Lean body weight (LBW) is the total body weight (TBW) minus the adipose tissue. It is a combination of body cell mass, extracellular water, and nonfat connective tissue. It approximates 80% of TBW in males and 75% in females. In morbidly obese subjects, decreasing the TBW by 20% to 30% gives an estimate of LBW. In nonobese and not overtly muscular individuals, TBW approximates IBW.5,6

A simple reversal of the BMI equation can be used to estimate IBW by relating "normal" BMI average of 22 (normal = 18.5-24.9) to a known height so that when the equation is rearranged, it reads: IBW = 22 × height2. This equation yields weights that fall midway within the range of values obtained with other IBW formulas.7

See Table 23-3.

Respiratory System

Morbidly obese patients have an increased work of breathing due to reduced chest wall compliance associated with the accumulation of fat on the chest wall, diaphragm, and abdomen. There is some contribution from obesity-related respiratory muscle dysfunction. Decreases in functional residual capacity (FRC) and ERV are the most commonly reported abnormalities of pulmonary function in obese subjects.8 Decreased respiratory compliance leads to decreased FRC, vital capacity (VC), and TLC. These parameters are significantly lower in individuals with upper body fat distribution (central obesity). The reduction in FRC is due to decreased ERV. Reduction in ERV is due to encroachment of abdominal contents on the diaphragm, decrease in respiratory system compliance by chest wall fat, and impairment of respiratory muscle strength. ERV is the most sensitive indicator of the effect of obesity on pulmonary function testing. Each kilogram of weight gained results in approximately a 26 mL reduction in VC.9 RV remains normal. Decreased FRC can result in lung volumes below closing capacity during normal tidal ventilation leading to small airway closure, V/Q mismatch, right-to-left shunting, and hypoxemia (Fig. 23-1). Anesthesia worsens the situation such that up to a 50% reduction in FRC occurs in the obese anesthetized patient compared with 20% in the nonobese. Reduction in FRC impairs the ability of the obese patient to tolerate even minimal periods of apnea; hence the rapid desaturation after induction of anesthesia despite adequate preoxygenation.

Obesity increases total oxygen consumption and carbon dioxide production even at rest. This is due to the metabolic activity of excess body fat and increased workload on supportive tissues. Basal metabolic activity in relation to body surface area is usually within normal limits, and an increase in minute ventilation usually maintains normocapnia. The increase in minute ventilation requires an increase in oxygen consumption because most obese patients retain their normal response to hypoxemia and hypercapnia. Morbidly obese patients do extra work to maintain their augmented ventilation; therefore they have to dedicate a high percentage of their total oxygen utilization to perform respiratory work even during regular respiration.10 Dynamic lung volumes, including the forced expiratory volume in 1 second (FEV1) and the forced vital capacity (FVC) both, decline with increasing body mass, resulting in an unchanged ratio of FEV1 to FVC. Significant hypoxemia is attributed in part to the closure of dependent airways within the range of normal tidal ventilation. Substantial weight loss results in gas exchange improvement as evidenced by an increase in Pao2. Morbid obesity is associated with a reduction in forced expiratory flow during midexpiratory phase and maximum voluntary ventilation (MVV) while the diffusing capacity remains normal.11 MVV, an index of respiratory muscle strength, is decreased in extreme obesity. Respiratory muscle efficiency is suboptimal in obese patients. Inefficiency is suggested by a sharper increase in oxygen consumption during exercise when compared with nonobese patients. Supine position reduces FRC due to cephalad displacement of the diaphragm. This effect is exaggerated in the obese, leading to a further reduction in FRC, further small airway closure, and increased work of breathing. Clinically significant increases in intrapulmonary shunting and oxygen consumption have been documented in obese patients while changing from a sitting to a supine position. Chest wall and lung compliance are both decreased by fat accumulation on the thorax and abdomen. Increased pulmonary blood volume, which is part of an overall increase in total blood volume, partially explains the decreased lung compliance. Chronic hypoxemia causes polycythemia, which contributes to the increased blood volume. Morbidly obese patients breathing room air have lower arterial oxygen tensions (Pao2) than that predicted for similar-age nonobese subjects in both sitting and supine positions. Chronic hypoxemia can eventually lead to pulmonary hypertension and cor pulmonale.

Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is defined as a cessation of airflow for more than 10 seconds 5 or more times per hour of sleep despite continuous respiratory effort against a closed glottis in combination with a decrease in arterial oxygen saturation of greater than 4% (Fig. 23-2). Obstructive sleep hypopnea is a decrease in airflow of more than 50% for more than 10 seconds, 15 or more times per hour of sleep; it is usually associated with snoring and arterial oxygen desaturation greater than 4%. The upper airway resistance syndrome is characterized by arousal in response to increased upper airway resistance without an elevated apnea-hypopnea index (AHI). AHI is the total number of apneas and hypopneas per hour and used to quantify the severity of OSA.12 The AHI is the total number of apneas and hypopneas per hour. An AHI index higher than 30 signifies severe OSA; values of 5 to 15 and 16 to 30 define mild and moderate OSA, respectively. The total arousal index (AI) is the total number of arousals per hour. The sum of the AHI and total AI is known as the respiratory disturbance index.13

Predisposing factors to OSA include male gender, middle age, and obesity. Alcohol consumption or night sedation worsens the situation. BMI higher than 30 kg/m2 and collar size more than 16.5 in correlate with severe OSA. Resulting physiologic abnormalities include hypoxemia, hypercapnia, and generalized (pulmonary and systemic) vasoconstriction. Secondary polycythemia due to recurrent hypoxemia increases the risk of cerebrovascular and ischemic heart disease. Right ventricular failure is a potential consequence of chronic hypoxic pulmonary vasoconstriction. Electrocardiogram (ECG) pattern of right ventricular hypertrophy or echocardiographic evidence of hypofunction may be seen. Initially, respiratory acidosis occurs only during sleep with return to normal homeostasis when awake. Hypoxemia during apnea can lead to bradycardia, long sinus pauses, second-degree heart block, and ventricular dysrhythmias with markedly increased severity if arterial oxygenation decreases below 60%. The higher incidence of nocturnal angina and myocardial infarction in OSA patients may be explained by the increased incidence of arrhythmias in these patients. Activation of the sympathetic nervous system occurs in response to hypoxemia due to apneic and hypopneic events, which may explain the increased incidence of hypertension in obese OSA patients. As obesity worsens, pharyngeal area decreases due to adipose tissue deposition into pharyngeal tissues including the uvula, tonsils, tonsillar pillars, tongue, aryepiglottic folds, and the lateral pharyngeal walls where it is most pronounced, correlating well with the severity of OSA (Fig. 23-3). Weight loss improves the pharyngeal and glottic function of patients with OSA.14 The upper airway can be compressed externally by superficially located fat masses that increase the pharyngeal extraluminal pressure. This situation is evidenced by a significantly larger neck in the obese patient with OSA when compared to those without OSA and the fact that the severity of OSA correlates better with larger neck circumference than with general obesity.

Central depressant anesthetic drugs (benzodiazepines, opioids, and induction agents such as thiopental and propofol) reduce the action of pharyngeal dilator muscles in obese OSA patients causing pharyngeal collapse. Precurarizing doses of muscle relaxants and nitrous oxide also reduce their action. Addition of opioids will depress ventilation and result in poor response to the ensuing hypoxemia and hypercapnia. OSA is associated with difficult mask ventilation and difficult laryngoscopy, which when combined with decreased FRC and reduced oxygen stores requires anticipation and preparation for an airway emergency.

A significant number of patients with OSA are undiagnosed, which poses various perioperative challenges for the anesthesiologist. The STOP questionnaire, the initial portion of the STOP-BANG scoring model (Table 23-4), is a concise and easy-to-use screening tool for OSA. Incorporating BMI, age, neck size, and gender with the STOP questionnaire (STOP-BANG scoring model) significantly increases screening sensitivity especially for patients with moderate to severe OSA.15

Obesity-Hypoventilation Syndrome

Obesity-hypoventilation syndrome (OHS) is a combination of obesity and chronic hypoventilation that ultimately results in pulmonary hypertension and cor pulmonale.14 It can also be defined as a combination of obesity (BMI >30 kg/m2) and awake arterial hypoxemia (Paco2 >45 mm Hg) in the absence of known causes of hypoventilation. OHS is seen in up to 10% of morbidly obese patients. Clinical features are similar to those seen with OSA including excessive daytime somnolence, fatigue, and morning headaches. In addition, there is daytime hypercapnia and hypoxemia that are associated with pulmonary hypertension and right-sided congestive heart failure (cor pulmonale), resulting in substantial morbidity and mortality.16

OHS patients have an increased sensitivity to the respiratory depressant effects of general anesthetics. Episodes of central apnea from progressive desensitization of respiratory centers to hypercapnia are initially limited to sleep but eventually leads to a progressive reliance on hypoxic drive for ventilation. Pickwickian syndrome,17 characterized by obesity, hypersomnolence, hypoxia, hypercapnia, right ventricular failure, and polycythemia, is the end result of OHS. Chronic daytime hypoxemia may be a better predictor of pulmonary hypertension and cor pulmonale than the presence and severity of OSA.18 There is a strong correlation between increasing BMI (>40 kg/m2) and the likelihood of developing OHS.19 Many obese patients with OHS also have OSA, but the reverse is not always true, suggesting that OHS is an autonomous disease.20

Arterial blood gas (ABG) analysis should be obtained in any morbidly obese patient with unexplained hypoxemia or features of cor pulmonale because pulse oximetry detects oxyhemoglobin desaturation without consideration for the presence of hypercapnia. This results in inappropriate treatment with supplemental oxygen alone that does not reverse the hypoventilation.15 ABG confirms the presence of daytime hypercapnia and usually reveals compensated respiratory acidosis and hypoxemia. Elevated bicarbonate level is consistent with chronic hypercapnia.

Treatment of OHS with weight reduction, tracheostomy, or nocturnal positive-pressure support improves daytime hypercapnia and hypoxia without changing the abnormal ventilatory responses.

Cardiovascular System

The increased morbidity and mortality of obesity is largely due to cardiovascular problems, including hypertension, ischemic heart disease, cardiac failure, cardiomyopathy, arrhythmias, dyslipidemia, and sudden cardiac death.21 Total blood volume is increased in the obese, but it is less than that in nonobese individuals when compared on a volume-to-weight basis (50 mL/kg compared with 70 mL/kg). Most of the extra blood volume supplies adipose tissue. Excess adiposity requires an increase in cardiac output to parallel the increase in oxygen consumption, leading to a systemic arteriovenous oxygen difference that remains normal or slightly above normal. Cardiac output increases with increasing weight (20-30 mL/kg of excess adipose tissue) because of ventricular dilatation and an increase in stroke volume. Left ventricular dilatation results in increased left ventricular wall stress leading to eccentric hypertrophy that leads to reduced left ventricular compliance, impairment of left ventricular filling (diastolic dysfunction) elevation of left ventricular end diastolic pressure (LVEDP), and eventual pulmonary edema. The dilated left ventricle has a limited capacity to hypertrophy, so when left ventricular wall thickening fails to keep pace with dilatation, systolic dysfunction ("obesity cardiomyopathy") results with eventual biventricular failure (Fig. 23-4). Obese subjects compensate by using cardiac reserve, especially in the presence of hypertension. Systemic vascular resistance (SVR) is usually within normal limits in morbidly obese patients, suggesting that hypertension and obesity can coexist with a normal SVR.

Obesity accelerates atherosclerosis; however, because of reduced mobility, morbidly obese patients appear asymptomatic in the face of significant cardiovascular disease; symptoms such as angina or exertional dyspnea only occur during periods of significant physical activity.22 Cardiac output rises faster in response to exercise in the morbidly obese and is often associated with a rise in left ventricular end-diastolic pressure and pulmonary capillary wedge pressure. Increase in cardiac output during exercise is achieved by increases in heart rate without a concomitant increase in stroke volume or ejection fraction but with an increase in filling pressures. Similar changes occur during the perioperative period. With the exception of renal and splanchnic blood flows that increase with obesity, organ blood flow does not change significantly because the additional cardiac output is diverted to perfuse excess fat. Blood volume and cardiac output are approximately twice the values predicted for those with ideal body weight, but when it is normalized for body surface area, it is within normal limits or slightly below normal. Chronically increased cardiac output and blood volume may cause the SVR to increase over time. A high SVR and high preload combination may lead to an early left ventricular dysfunction and congestive heart failure.

Obesity is an independent risk factor for ischemic heart disease and eventual heart failure and is strongly associated with central (android) distribution of fat. Angina may actually be a direct symptom of obesity because a significant number of obese patients with angina do not have demonstrable coronary artery disease.23 The risk of heart failure increases by 5% for men and 7% for women for every increment of 1 kg/m2 in BMI.24 Coronary blood flow reserve in obese patients is limited because of ventricular mass and metabolic demands of the myocardium. Intraoperative cardiac failure can occur from rapid intravenous fluid administration (indicating left ventricular diastolic dysfunction), negative inotropy of anesthetic agents, or pulmonary hypertension precipitated by hypoxia or hypercapnia.

Cardiac arrhythmias can be precipitated by fatty infiltration of the conduction system, hypoxia, hypercapnia, electrolyte imbalance, coronary artery disease, increased circulating catecholamines, OSA, and myocardial hypertrophy. ECG findings frequently seen in morbidly obese patients include low QRS voltage, multiple criteria for left ventricular hypertrophy (LVH) and left atrial enlargement, and T-wave flattening in the inferior and lateral leads.25 In addition, there is a leftward shift of the P-wave, QRS complex, and T-wave axes, lengthening of the corrected QT interval, and prolonged QT interval duration. Echocardiography usually shows an increased cardiac output, increased LVEDP, and LVH in otherwise healthy obese subjects.

Mild to moderate hypertension is common in obese patients. There is a 3 to 4 mm Hg increase in systolic and a 2 mm Hg increase in diastolic arterial pressure for every 10 kg of weight gained. SVR is usually within normal limits, suggesting that hypertension and obesity can coexist with a normal SVR. Their expanded blood volume causes an increased cardiac output with a lower calculated SVR for the same level of arterial blood pressure. The renin-angiotensin system has been implicated in the hypertension of obesity. Increases in circulating levels of angiotensinogen, aldosterone, and angiotensin-converting enzyme occur. With obesity, most tissues have normal to increased level of sympathetic nervous system activity. An increased basal level of sympathetic activity predisposes to insulin resistance, dyslipidemia, and hypertension.26 Obesity-induced insulin resistance enhances the pressor activity of norepinephrine and angiotensin II.27 Hyperinsulinemia further activates the sympathetic nervous system causing sodium retention and contributing to the hypertension of obesity.28 Hypertension causes concentric hypertrophy of the ventricle in normal weight individuals but causes eccentric dilatation in obese subjects.29 The combination of obesity and hypertension causes left ventricular wall thickening and a larger heart volume and therefore increased likelihood of cardiac failure (Fig. 23-5).

A hypofibrinolytic and hypercoagulable state predisposes the obese patient to cardiovascular disease. Obese patients have higher levels of fibrinogen (a marker for the inflammatory process of atherosclerosis) factor VII, factor VIII, von Willebrand factor, and PAI-1 produced by adipose tissue.30 Increased fibrinogen, factor VII, factor VIII, and hypofibrinolysis due to increased PAI-1 levels are associated with hypercoagulability and an increased risk of coronary artery disease. High factor VIII coagulant activity levels are associated with increased cardiovascular mortality. Visceral (abdominal) fat is associated with increased levels of PAI-1, factor VIII, and von Willebrand factor. Endothelial dysfunction induced by insulin increases von Willebrand factor and factor VIII levels, predisposing to fibrin formation.

Gastrointestinal/Hepatic System

Gastric volume and acidity are increased, hepatic function altered, and drug metabolism adversely affected by obesity. A significant number of fasted morbidly obese patients have gastric volumes in excess of 25 mL and gastric pH less than 2.5, which are the generally accepted volume and pH indicative of high risk for pneumonitis in the event of regurgitation and aspiration. Gastric emptying can be delayed in obese patients because of increased abdominal mass that causes antral distension, gastrin release, and a decrease in pH with parietal cell hypersecretion. However, emptying may be faster, with high-energy content intake such as fat emulsions, but RV is increased because of their larger gastric volume (up to 75% larger). Accelerated gastric emptying induces hunger and frequent eating by reducing the negative feedback satiety signal produced by the presence of nutrients inside the stomach, thus precipitating a feeling of hunger and shortening the interval between consecutive meals.31

An increased incidence of hiatal hernia and gastroesophageal reflux (GERD) increases aspiration risk. Fasting nonpremedicated, nondiabetic obese surgical patients who have no significant gastroesophageal pathology are not more likely to have high-volume, low pH gastric contents than lean patients at the time of general anesthetic induction after routine preoperative fasting.32 They should follow the same guidelines as nonobese patients and be allowed to drink clear liquids (up to 300 mL) until 2 hours before elective surgery, a quantity that has been shown not to affect gastric pH and volume at induction of anesthesia adversely.33 One mechanism of increased risk of GERD is via mechanical factors whereby abdominal obesity increases intragastric pressure, increasing the frequency of transient lower esophageal sphincter relaxation and/or formation of hiatal hernia. A greater than 3.5 kg/m2 increase in BMI is associated with a 2.7-fold increase in risk for developing new reflux symptoms.34 The combination of hiatus hernia, GERD, and delayed gastric emptying, coupled with increased intra-abdominal pressure and a high volume-low pH gastric content, increases the incidence of severe pneumonitis should aspiration occur.

Peculiar morphologic and biochemical abnormalities of the liver associated with obesity include fatty infiltration, inflammation, focal necrosis, and cirrhosis. Fatty infiltration reflects the duration rather than the degree of obesity. Histologic and liver function test abnormalities are relatively common in the obese, but clearance is usually not reduced. Abnormal liver function tests are seen in up to a third of obese patients who have no evidence of concomitant liver disease; increased alanine aminotransferase is most frequently seen. Despite these histologic and enzymatic changes, no clear correlation exists between routine liver function tests and the capacity of the liver to metabolize drugs.35 Hepatic decompensation can occur after Roux-en-Y gastric bypass (RYGB), which necessitates careful assessment for preexisting liver disease in candidates scheduled to undergo this procedure because of a high prevalence (63%) of nonalcoholic fatty liver disease (NAFLD) and cirrhosis.36 NAFLD is a group of liver abnormalities associated with obesity and insulin resistance. Hepatomegaly, elevated liver enzymes, and abnormal liver histology (including steatosis, steatohepatitis, fibrosis, and cirrhosis) are an intrinsic part of this disease.37 Up to 95% of morbidly obese patients have nonalcoholic steatohepatitis (NASH).38 NASH is an aggressive form of NAFLD that can progress to cirrhosis or hepatocellular carcinoma. The incidence of gallbladder disease, including cholelithiasis, is significantly increased in morbidly obese subjects; the relative risk appears to be positively correlated with increasing BMI.39 Abnormal cholesterol metabolism is partially to blame.

Renal, Endocrine, and Metabolic Systems

Impaired glucose tolerance in the morbidly obese is reflected by a high prevalence of type 2 diabetes mellitus due to the resistance of peripheral fatty tissues to insulin. A significant number of obese patients have an abnormal glucose tolerance test that predisposes them to wound infection and an increased risk of myocardial infarction.40 Exogenous insulin may be required perioperatively, to oppose the catabolic response to the stress of surgery, even in obese patients on oral hypoglycemic agents. Gastric bypass surgery improves or even cures type 2 diabetes mellitus by substantially improving insulin resistance through an unknown mechanism.41 Subclinical hypothyroidism occurs in about 25% of all morbidly obese patients.42 Thyroid stimulating hormone levels are frequently elevated, suggesting the possibility that obesity leads to a state of thyroid hormone resistance in peripheral tissues.43,44 Hypothyroidism should be considered in any obese patient who displays perioperative cardiovascular or respiratory instability. Hypoglycemia, hyponatremia, and impaired hepatic drug metabolism are other adverse consequences of hypothyroidism. Reduction in thyroxine requirements is seen with a decrease in BMI.45

Obesity is a major risk factor for end-stage renal disease and essential hypertension. It induces high blood pressure through increased renal tubular sodium reabsorption, impaired pressure natriuresis, and volume expansion due to the activation of the sympathetic nervous system and renin-angiotensin system, and by physical compression of the kidneys especially when visceral obesity is present. Chronic obesity results in increasing urinary protein excretion and gradual loss of nephron function that worsens with time and exacerbates hypertension. Obesity-related glomerular hyperfiltration decreases after weight loss, which decreases the incidence of overt glomerulopathy.46 Obesity-related glomerulopathy is defined as focal segmental glomerulosclerosis and glomerulopathy or glomerulopathy alone.

The Metabolic Syndrome

According to the International Diabetes Federation, diagnostic criteria for metabolic syndrome include central obesity (defined as WC >94 cm for men and >80 cm for women); plus any 2 of the following 4 factors: raised serum triglyceride, low serum high-density lipoprotein-cholesterol level, high blood pressure or treatment of previously diagnosed hypertension, and abnormal fasting plasma glucose or previously diagnosed type 2 diabetes mellitus.47 It is a cluster of metabolic abnormalities including diabetes (or prediabetes), abdominal obesity, and changes in cholesterol and high blood pressure. People with this syndrome have up to a 5-fold greater risk of developing type 2 diabetes mellitus (if not already present) and are also twice as likely to die from and 3 times more likely to have a heart attack or stroke compared with people without the syndrome.

General pharmacokinetic principles dictate that drug dosing should take into consideration the volume of distribution (VD) for administration of the loading dose and or the clearance for the maintenance dose.48 A drug that is mainly distributed to lean tissues should have the loading dose calculated based on LBW, whereas dosing should be calculated based on TBW if the drug is equally distributed between adipose and lean tissues. For maintenance, a drug with similar clearance values in both obese and nonobese individuals should have the maintenance dose calculated based on LBW; a drug whose clearance increases with obesity should have the maintenance dose calculated according to TBW.

The volume of the central compartment in which drugs are first distributed remains unchanged in obese patients, but absolute body water content is decreased and lean body adipose tissue mass is increased, affecting lipophilic and polar drug distribution (Fig. 23-6). The VD in obese patients is affected by reduced total body water, increased total body fat, increased LBM, altered protein binding, increased blood volume, increased cardiac output, increased serum concentrations of free fatty acids, triglycerides, cholesterol, and α1-acid glycoprotein, lipophilicity of the drug, and organomegaly.49 Lipophilic compounds are associated with increases in VD with some exceptions such as digoxin, procainamide, and cyclosporine that are highly lipophilic substances but have comparable volumes of distribution in obese and nonobese subjects.49

The major plasma proteins are albumin (primarily responsible for binding acidic drugs), α1-acid glycoprotein (primarily responsible for binding basic drugs) and lipoproteins. Plasma protein binding of acidic drugs may decrease because of the obesity-associated decrease in albumin levels and an increase in concentration of α1-acid glycoprotein. Hyperlipidemia and an increased concentration of α1-acid glycoprotein affect protein binding and lead to a reduction in free drug concentration. Drugs that are primarily bound to albumin (eg, thiopentone, phenytoin) show no significant changes in protein binding in obese individuals, whereas binding of drugs to α1-acid glycoprotein increases. Lipoprotein levels may be elevated in obese individuals due to higher triglyceride and cholesterol levels. Histologic and liver function abnormalities are common in the obese with concomitant deranged liver function tests; metabolism and clearance, however, are usually not adversely affected. Drugs that depend on the kidneys for elimination face consistently higher clearance rate in obese patients.50 Orally administered medications are expected to have decreased bioavailability in obese patients because of increased splanchnic blood flow, but there is no evidence to suggest a significant difference in the absorption and bioavailability of orally administered drugs when compared with nonobese subjects.

Increased blood volume in the obese patient decreases the plasma concentrations of rapidly injected intravenous drugs. Fat, however, has poor blood flow; therefore doses calculated on actual body weight could lead to excessive plasma concentrations. A reasonable approach is to calculate the initial doses based on LBW and subsequent doses determined by pharmacologic response to the initial dose. Repeated injections accumulate in fat leading to prolonged response due to subsequent release from this large fat depot.

See Table 23-5.

Thiopental

Thiopental is highly lipophilic and has a larger VD in obese patients; prolonged somnolence is expected. Increased blood volume and cardiac output and increased muscle mass necessitate an increase in the initial induction dose. The volume of distribution is larger in obese than in nonobese patients; elimination half-life is significantly longer. They are more sensitive to the effects of thiopental dosed according to TBW.51 Continuous infusion results in longer elimination half-life due to a larger VD; clearance, however, remains unaltered.

Propofol

Both the VD and clearance of propofol in obese and nonobese subjects correlate well with TBW without signs of accumulation and prolongation of action because the half-life is similar in obese and nonobese subjects due to the increase in both VD and clearance.52 Induction and maintenance dosing for propofol in both obese and nonobese individuals may be based on TBW, but the negative cardiovascular effects of large doses of propofol combined with the negative physiologic effects of obesity on the cardiovascular system should prompt a somewhat reduced total dose.

Midazolam

There is a significant increase in both VD and elimination half-life in obese patients. Midazolam is relatively shorter acting compared with other benzodiazepines; therefore the intensity and duration of its sedative side effects after a single intravenous dose correlate better with the extent of distribution of the drug than on the rate of elimination and clearance.53 The total VD and elimination half-life of midazolam in the obese are up to 3 times larger and 3 times more prolonged than those in nonobese subjects with no difference in the clearance rates. A single intravenous dose of midazolam should be administered based on TBW, but continuous infusion dosing should be adjusted according to LBW rather than TBW. Even though midazolam is considered short acting, it has the potential to accumulate and cause prolonged sedation in obese patients because larger initial doses are required to achieve adequate serum concentrations.

Neuromuscular Blocking Agents

Muscle relaxants are polar and hydrophilic drugs that are distributed poorly into excess adipose tissue. Obese individuals have a larger absolute lean body mass in conjunction with extra adipose tissue and a decreased proportion of muscle mass and body water when compared with nonobese subjects.35 Therefore drugs with weak or moderate lipophilicity have fairly predictable effects in obese patients due to their distribution mainly into lean tissues; they should therefore be dosed based on LBW rather than TBW.54

Succinylcholine

Succinylcholine should be dosed based on TBW. Larger extracellular fluid compartment and a linear increase in pseudocholinesterase activity with weight gain necessitate an increase in dosage of succinylcholine in obese patients. The potency estimates for succinylcholine in obese adolescents with BMI more than 30 kg/m2 are similar to those of nonobese adolescents in the same age group when calculated based on TBW.55

Nondepolarizing Muscle Relaxants

Nondepolarizing muscle relaxants should be administered according to lean body mass to prevent delayed recovery due to increased VD and impaired hepatic clearance. There is no alteration in the pharmacokinetics and pharmacodynamics of rocuronium in obese female patients when compared with normal weight patients. The duration of action of rocuronium in obese patients is significantly longer when dosed according to TBW; therefore, rocuronium should be dosed according to LBW.56 Vecuronium pharmacokinetics and pharmacodynamics in obese patients is consistent with dosing on the basis of LBW because the VD, plasma clearance, and elimination half-life of vecuronium are not different between obese and nonobese patients.57 Vecuronium action is prolonged, however, when dosed according to TBW because of the excess dose administered. The VD, absolute clearance, and elimination half-life of atracurium are unchanged by obesity. However, if dosed according to TBW, atracurium concentrations are higher in obese patients than in the nonobese with no increase in recovery times. The median effective dose is higher; therefore dosing can be based on TBW with some reduction in the total dose.58 The duration of action of cisatracurium is prolonged in the morbidly obese when dosed according to TBW, suggesting that dosing based on LBW is optimal in this group of patients.59

Prompt early reversal but slow full recovery has been documented in overweight and obese patients during neostigmine-induced reversal of vecuronium dosed according to TBW.60 Sugammadex, a modified γ-cyclodextrin compound that encapsulates rocuronium, and other steroid-based neuromuscular blockers to a lesser extent, may prove invaluable for more rapid and complete neuromuscular blockade reversal in obese patients.61

Opioids

All synthetic opioids are highly lipophilic drugs. Application of non-weight-based pharmacokinetic models for fentanyl derived from normal weight patients overestimates the plasma concentration of fentanyl as body weight increases from normal to morbid obesity. Fentanyl dosing based a derived "pharmacokinetic mass" (derived pharmacokinetic body weight for dosing that reflects the influence of TBW on clearance) is clinically more useful than that based on TBW because of the strong linear correlation between this derived mass and total body clearance and also a strong correlation with dosing for postoperative analgesia.62,63 Administration of fentanyl according to TBW overestimates fentanyl dose requirements in obese patients. Sufentanil, a highly lipid soluble opioid, distributes extensively in body fat as well as in lean tissues, and it has an increased VD and a prolonged elimination half-life that correlates positively with the degree of obesity. Plasma clearance, however, is similar in obese and nonobese patients; therefore loading dose should account for TBW while maintenance and infusion dosing should be reduced and dosed according to LBW. Pharmacokinetic parameters derived from nonobese subjects accurately predict plasma sufentanil concentrations in morbidly obese subjects, but at the morbidly obese range (BMI >40 kg/m2), overestimation of plasma sufentanil concentration rises.64 Remifentanil, a fentanyl congener, is hydrolyzed by blood and tissue esterases leading to rapid metabolism and inactive products. There is no difference in VD estimate of remifentanil between obese and nonobese subjects, and remifentanil pharmacokinetics is more closely related to LBW than to TBW; therefore, dosing should be based on LBW.65

Dexmedetomidine

Dexmedetomidine is a highly selective α2-adrenergic agonist with sedative-hypnotic, anesthetic-sparing, analgesic, and sympatholytic properties but lacks significant effects on respiration, making it ideally suitable as an analgesic adjuvant in morbidly obese subjects in whom opioid-induced respiratory depression may be a risk.66 At infusion rates of 0.2 to 0.7 μg/kg per hour, dexmedetomidine produces clinically effective sedation with decreased analgesic and anesthetic requirements.

Antiobesity medications are formulated to reduce energy intake, increase energy utilization, or decrease absorption of nutrients. Indications for drug treatment include a BMI 30 kg/m2 or higher or a BMI between 27 and 29.9 kg/m2 in conjunction with an obesity-related medical complication. The combination of phentermine and fenfluramine (Phen-Fen) was previously popular for obesity treatment until evidence indicated its association with valvular heart disease and pulmonary hypertension. Sibutramine and orlistat are antiobesity medications for long-term use that have not yet been associated with such detrimental side effects. Sibutramine inhibits the reuptake of both serotonin and norepinephrine to increase satiety after the onset of eating rather than reduce appetite; it does not promote the release of serotonin, unlike fenfluramine and dexfenfluramine that primarily increase the release of serotonin in brain synapses and also inhibit reuptake to produce anorexia. Sibutramine does not deplete the neural synapses of catecholamines; therefore, dangerous hypotension that is unresponsive to indirectly acting vasopressors, seen with fenfluramine and dexfenfluramine, does not occur. Orlistat blocks the absorption and digestion of dietary fat by binding lipases in the gastrointestinal tract. It improves cardiovascular risk factors associated with obesity such as hypertension, WC, fasting blood glucose levels, and lipid profile.67 Low-density lipoprotein and total cholesterol levels also decrease. An increase in warfarin's anticoagulant effect is seen with chronic dosing of orlistat because of its side effect of decreasing absorption of fat-soluble vitamins, including vitamin K.68 This results in an abnormal plasma thromboplastin time due to deficiency of clotting factors II, VII, IX, and X. Rimonabant, a selective cannabinoid-1 receptor antagonist, induces weight loss, reduces WC, and improves lipid profile and glucose management by decreasing appetite, with a concomitant reduced incidence of the metabolic syndrome.69 Significant side effects that should be considered during the perioperative period include psychiatric disorders, anxiety, and depression. Nausea, dizziness, diarrhea, arthralgia, and back pain are also seen.

Obesity (bariatric) surgery is generally classified into malabsorptive, restrictive, or combined. Malabsorptive procedures that include jejunoileal bypass and biliopancreatic diversion are rarely used presently. Restrictive procedures include the vertical banded gastroplasty and the adjustable gastric banding (ABG). The RYGB combines gastric restriction with a minimal degree of malabsorption. RYGB is the most commonly performed and the most effective bariatric procedure in the United States today. It involves anastomoses of the proximal gastric pouch to a segment of the proximal jejunum, bypassing most of the stomach and the entire duodenum. RYGB patients lose an average of 50% to 60% excess body weight and decrease their BMI by approximately 10 kg/m2 during the first 12 to 24 postoperative months. Type 2 diabetes mellitus resolves in more than 90% of post-RYGB patients.70 AGB requires that an adjustable inflatable band be placed around the proximal stomach to limit the stomach capacity. Adjustments can be made to meet a patient's individual needs by adding to or removing saline from the silicone band, making it tighter or less so.

Rhabdomyolysis has been documented in morbidly obese patients undergoing prolonged procedures such as laparoscopic bariatric surgery; the main risk factor is prolonged duration of surgery. Elevations in serum creatinine and CPK levels unexplained by other reasons and complaints of buttock, hip, or shoulder pain in the postoperative period should raise the suspicion of rhabdomyolysis. Measurement of serum CPK pre- and postoperatively aids in early diagnosis and treatment. Myoglobinuric acute renal failure can be as high as 30% when serum CPK is higher than 5000 IU/L.71 Efforts to determine whether liberal intraoperative intravenous fluid administration used to treat rhabdomyolysis can also be used to prevent it did not show favorable results. Both conservative (15 mL/kg) and liberal (40 mL/kg) fluid administration did not affect the incidence of rhabdomyolysis in obese patients undergoing laparoscopic bariatric surgery.72

Previous experiences as detailed by the patient and anesthetic records are useful sources of information. Obese patients should be evaluated for systemic and pulmonary hypertension, signs of right and/or left ventricular or congestive cardiac failure, and ischemic heart disease. Excess adiposity may make signs of congestive cardiac failure difficult to elucidate. The chronicity of pulmonary impairment including OSA and OHS makes pulmonary hypertension common in morbidly obese patients. Tricuspid regurgitation on echocardiography is the most useful confirmatory test of pulmonary hypertension but should be combined with clinical features such as exertional dyspnea, fatigue, and syncope that reflect the inability to increase cardiac output in response to activity.73 Features of right ventricular hypertrophy such as tall precordial R waves, right axis deviation, and right ventricular strain pattern may be seen on ECG. Sensitivity of the ECG features correlates well with the degree of pulmonary hypertension. Chest radiographs may show evidence of underlying lung disease and prominent pulmonary arteries. In patients with significant cardiopulmonary disease or abnormal ECG, preoperative echocardiography, spirometry, and arterial blood gas analysis are strongly recommended.74

Patients who have previously undergone bariatric surgery should be investigated for long-term metabolic and nutritional abnormalities during the preoperative visit. Common deficiencies include vitamin B12, iron, calcium, and folic acid. A collective form of postoperative polyneuropathy known as acute postgastric reduction surgery (APGARS) neuropathy could result from these deficiencies.75 Patients with APGARS neuropathy present with protracted postoperative vomiting, hyporeflexia, and muscular weakness. Differential diagnoses of this disorder include thiamine deficiency (Wernicke encephalopathy, beriberi), vitamin B12 deficiency, and Guillain-Barré syndrome. Because of the associated hyporeflexia and muscular weakness, close attention should be paid to dosing and monitoring of neuromuscular blocking agents.76 Electrolyte and coagulation indices should be checked before surgery, particularly in patients on chronic diuretics treatment and weight loss medications and also in the acutely ill or those poorly compliant with vitamin and nutritional supplements. Chronic vitamin K deficiency can result in coagulation abnormalities requiring vitamin K analog or fresh-frozen plasma.

OSA and OHS are frequently associated with difficult laryngoscopy and intubation. Inquiry should be made about the signs and symptoms during preoperative evaluation. History of hypertension or neck circumference greater than 40 cm correlates with an increased probability of OSA. OSA is a legitimate reason to delay surgery to get a proper workup.13 A formal sleep study helps quantify its severity. Those requiring general anesthesia should be treated as having severe OSA. Regional anesthesia should be considered if it is technically feasible. OSA patients should generally be treated as inpatients; however, outpatient surgery can be considered in the following circumstances: mild OSA, local or regional anesthesia with minimal or no sedation, 23-hour observation postanesthesia care unit following surgery, and patients on oral medication at the time of discharge. Patients on a CPAP device at home should be encouraged to bring them to the hospital for postoperative use. The possibility of invasive monitoring, prolonged endotracheal intubation, and postoperative mechanical ventilation at preoperative evaluation should be discussed. Specialized tests such as pulmonary function tests and liver function tests need not be routinely obtained because they are not cost-effective in the asymptomatic morbidly obese patient. Blood glucose abnormalities should be corrected if present.

Preoperative Medications

All current medications should be continued until the time of surgery; with the possible exception of insulin and oral hypoglycemic agents. Antibiotic prophylaxis is important because of an increased incidence of wound infection in obese patients partly due to a decrease in tissue oxygenation.77 Oral benzodiazepines are reliable for anxiolysis and mild sedation; intravenous midazolam can be titrated in small doses during the immediate preoperative period. Prophylaxis against both aspiration pneumonitis and deep vein thrombosis (DVT) should be addressed during the preoperative period. H2 receptor antagonists, nonparticulate antacids, and proton pump inhibitors all reduce gastric volume, acidity, or both, reducing the risk and severity of aspiration pneumonitis.

Obesity is a major independent risk factor for deep vein thrombosis (DVT) and subsequent morbidity and mortality from postoperative pulmonary embolism (PE).78,79 Minidose subcutaneous heparin 5000 IU administered before surgery and repeated every 8 to 12 hours until the patient is fully mobile reduces this risk. The incidence of clinically evident DVT after laparoscopic RYGB is low when the procedure is accomplished in a relatively short time, with the initiation of calf-length pneumatic compression hose before induction of anesthesia and with routine early ambulation.80 Prophylactic inferior vena caval (IVC) filter placement is recommended for bariatric surgery patients with prior pulmonary embolus, prior DVT, evidence of venous stasis, or a hypercoagulable state.81 Four important risk factors that may necessitate prophylactic IVC filter placement include venous stasis disease, BMI 60 or higher, truncal obesity, and obesity hypoventilation/sleep apnea syndrome (OHS/SAS).82 Many bariatric surgeons prefer low-dose unfractionated heparin as their primary method of thromboprophylaxis.83 The use of a protocol for heparin dosing in gastric bypass patients as opposed to a fixed dose is the preferred method. Dose calculations based initially on height and weight that is later adjusted according to peak anti–factor Xa activity results in better thromboprophylaxis and few side effects.84 Low-molecular-weight heparins have better bioavailability when injected subcutaneously.

Anatomic changes of obesity that contribute to a potentially difficult airway include limitation of movement of the atlantoaxial joint and cervical spine by upper thoracic and low cervical fat pads, excessive tissue folds in the mouth and pharynx, short thick neck, suprasternal, presternal, and posterior cervical fat, and a very thick submental fat pad. Obese patients with OSA are significantly more difficult to intubate than those without OSA; however there is no relationship between the severity of sleep apnea and the occurrence of difficult intubation.85 A short thick neck is significantly more related to difficult intubation, whereas obesity and a short thick neck are significantly related to each other, in addition to both being related to OSA. Patients with OSA have excess adipose tissue deposited in their pharyngeal area, including the tonsils, tonsillar pillars, uvula, tongue, aryepiglottic folds, and the lateral pharyngeal walls.13 This fat deposition is most pronounced in the lateral pharyngeal walls, and it may not be noticed during routine airway examination. Even with the presence of these anatomic changes and pathology, the magnitude of BMI does not have much influence on the difficulty of laryngoscopy. Such difficulty correlates better with increased age, male sex, TMJ pathology, Mallampati classes 3 and 4, history of OSA, and abnormal upper teeth.86 Neck circumference has been identified as the single biggest predictor of problematic intubation in morbidly obese patients.87 A larger neck circumference is associated with the male sex, higher Mallampati score, grade 3 views at laryngoscopy, and OSA. The probability of a problematic intubation is approximately 5% with a 40-cm neck circumference compared with a 35% probability at a 60-cm neck circumference.87

The Royal College of Surgeons of England issued guidelines in 1992 that deemed patients with BMI 30 kg/m2 or higher unsuitable for ambulatory surgery.88 Subsequent evaluation of adherence to these guidelines discovered that greater than 85% of ambulatory surgery units in England and a significant number in other countries continued routinely to anesthetize patients with BMI higher than 30 kg/m2.89,90 Many anesthesiologists believe that morbidly obese patients with comorbidities and no patient escort are unsuitable for ambulatory anesthesia because many of them are in suboptimal health. The presence of cardiovascular or respiratory comorbidity significantly reduces the willingness of anesthesiologists to provide ambulatory care to the obese.91,92 An excess of adverse perioperative cardiovascular events has not been found in obese patients undergoing ambulatory surgery despite a prevalence of cardiovascular disease in this patient population; however, adverse intraoperative and postoperative respiratory events, including arterial oxygen desaturation and bronchospasm, are quite common.93 Individual evaluation should dictate which obese patients can undergo ambulatory anesthesia and surgery. Proper equipment and procedures for positioning and monitoring should be readily available, including difficult airway and resuscitation equipment. Arrangements for transfer to a 24-hour observation unit or full admission unit should be in place. Ambulatory anesthesia for morbidly obese patients without significant comorbidities is safe. Obese patients do not have a higher incidence of contact with health care professionals after discharge from the ambulatory surgery unit, neither do they have a higher postambulatory surgery unplanned hospital admission rate than the general population.94 Obesity is associated with a higher regional block failure and complication rates during ambulatory regional anesthesia. The rate of successful blocks and overall satisfaction, however, is high; therefore, obese patients should not be excluded from ambulatory regional anesthesia procedures.95

Positioning

Obese patients may require specially designed tables or 2 regular operating tables for safe anesthesia and surgery. Regular operating tables have a maximum weight limit of approximately 205 kg, but wider and higher-capacity operating tables are also available that can hold up to 450-kg patients and accommodate the extra girth. Electrically operated or motorized tables facilitate maneuvering into various surgically favorable positions. The use of belts and straps and malleable bean bags helps keep obese patients from falling off the operating table. Pressure areas on the body should be protected with care to avoid neural injuries and possible pressure necrosis. Brachial plexus and lower extremity nerve injuries are frequent. A documented association between ulnar neuropathy and increasing BMI quoted a greater than 30% incidence of ulnar neuropathy in patients with a BMI 38 kg/m2 or higher compared with only 1% in the control group.96 Peripheral neuropathy occurs more frequently after bariatric surgery than after other abdominal surgery. Intraoperative neural compression or stretching from improper positioning is one of the most common etiologies. Malnutrition may be an important contributing factor; inflammation and altered immunity also play some role.97 Other associated risk factors include greater absolute weight loss, a faster rate of weight loss, lower serum albumin and transferrin concentrations, prolonged postoperative gastrointestinal symptoms (nausea and vomiting, diarrhea, and dumping syndrome), and reduced vitamin and calcium supplementation.97 Attention to patient positioning and duration of immobility during surgery helps reduce the incidence of compression injuries and rhabdomyolysis during bariatric surgery. Micronutrient deficiencies such as vitamins B6, B12, D, E, folate, and minerals such as calcium, magnesium, phosphorus, selenium, and copper contribute to nonmechanical peripheral neuropathies, especially in nutritionally noncompliant patients undergoing postbariatric surgery procedures.98

Supine positioning of the obese patient causes aortic and IVC compression and also leads to ventilatory impairment with further decrease in FRC and oxygenation. Trendelenburg positioning, when required, further worsens FRC and should be avoided whenever possible. A simple change from the supine to sitting position in the obese patient causes a significant increase in cardiac output, oxygen consumption, and pulmonary artery pressure. The head-up (semirecumbent) or reverse Trendelenburg (semi-Fowler) position unloads the weight of the intra-abdominal contents from the diaphragm leading to increased pulmonary compliance and better values for FRC and oxygenation. Both intraoperative PEEP and reverse Trendelenburg positions significantly decrease alveolar-arterial oxygen tension difference and increase total respiratory compliance to a similar degree in the obese, but reverse Trendelenburg position results in lower airway pressures. Both maneuvers decrease cardiac output significantly, however, which partially counteracts their beneficial effects on oxygenation.99 Prone positioning in the obese patient should be correctly performed with freedom of abdominal movement to prevent detrimental effects on lung compliance, ventilation, and arterial oxygenation. Prone positioning increases intra-abdominal pressure, worsening IVC and aortic compression and further decreasing FRC. Lateral decubitus positioning allows for good diaphragmatic excursion during mechanical ventilation because the panniculus is displaced off the abdomen reducing intra-abdominal pressure.100 Changing from a sitting to a lateral decubitus position after placing an epidural catheter may cause catheter dislodgment, resulting in inadequate analgesia because movement from sitting to lateral position increases the distance from the skin to the epidural space.101

Monitoring

Noninvasive blood pressure measurements can be falsely elevated if a cuff is too small for the limb. The blood pressure cuff bladder should encircle a minimum of 75% of the upper arm circumference or, preferably, the entire arm. Forearm blood pressure is a fairly good predictor of upper arm blood pressure in most patients; however, forearm measurements with a standard cuff may overestimate both systolic and diastolic blood pressures in obese patients.102 Invasive arterial pressure monitoring may be indicated for the morbidly obese with severe cardiopulmonary disease and for those with poor fit of the noninvasive blood pressure cuff. Central venous and pulmonary artery catheters may be indicated for extensive surgery and in patients with significant cardiopulmonary impairment. Difficult intravenous access is an indication for central venous catheterization. A central venous line need not be routinely inserted in obese patients because insertion of peripheral lines is almost always successful.103

Induction, Intubation and Maintenance

Obese patients desaturate very rapidly after loss of consciousness because of increased oxygen consumption and decreased FRC; therefore, adequate preoxygenation is vital before the induction of anesthesia. Application of positive pressure ventilation during preoxygenation decreases atelectasis formation and improves oxygenation.104 Four VC breaths with 100% oxygen within 30 seconds have been suggested as superior to the usually recommended 3 minutes of 100% preoxygenation in obese patients.105 Preoxygenation in the head-up or sitting position provides the longest SAP and is more effective and significantly extends the tolerance to apnea in obese patients when compared with the supine position.106-108

Obese patients may require larger doses of induction agents because blood volume, muscle mass, and cardiac output increase linearly with the degree of obesity. Cardiovascular and respiratory depression may result from larger doses, however. An increased dose of succinylcholine is indicated because of an increase in pseudocholinesterase activity. Myalgia following succinylcholine is not frequently seen in morbidly obese patients so it is highly recommended for tracheal intubation.109 If difficult intubation is anticipated, awake intubation under topical or regional anesthesia is a prudent approach. During awake intubation, sedative-hypnotic medications should be reduced to a minimum, to prevent cardiorespiratory depression. An immediately available experienced colleague is invaluable during induction and airway management. If endotracheal intubation under general anesthesia is selected, hypoxia and aspiration of gastric contents should be prevented at all costs. Preparation should be made for the possibility of difficult intubation, and a surgeon capable of rapidly surgically accessing the airway should be readily available. Towels or folded blankets under the shoulders and head can compensate for the exaggerated flexed position of posterior cervical fat (Fig. 23-7). The object of this maneuver, known as "stacking," is to position the patient so that the tip of the chin is at a higher level than the chest to facilitate laryngoscopy and intubation. The HELP, or "ramped" position,110,111 is a step beyond stacking. It significantly elevates the obese patient's head, neck, upper body, and shoulders above the chest to a point where an imaginary horizontal line can be drawn from the sternal notch to the external ear to better improve laryngoscopy and intubation. To facilitate proper HELP placement, the preformed Troop Head Elevation Pillow (C&R Enterprises, Frisco, TX, USA) in combination with a standard intubation pillow can be used in place of folded towels or blankets (Fig. 23-8A-C). The advantage of the preformed pillow is that it can be prepositioned, inserted, and removed much faster with less effort than that required to build and dismantle a ramp made from blankets and towels.112 The need for additional lifting can be eliminated by using an inflatable multichambered pillow to facilitate HELP placement more easily113 (Fig. 23-9).

Continuous infusion of a short-acting intravenous agent such as propofol or any of the inhalational agents or a combination may be used to maintain anesthesia. Desflurane, sevoflurane, and isoflurane are minimally metabolized and are therefore useful choices in obese patients. Desflurane may provide better hemodynamic stability.114 Sevoflurane provides rapid recovery, good hemodynamic control, prompt regaining of psychological and physical functioning, and infrequent incidence of nausea and vomiting when compared with isoflurane.115 An insignificant difference exists between sevoflurane and desflurane with respect to emergence and cognitive psychomotor recovery characteristics when careful anesthetic titration is used.116 Morbidly obese patients awake and regain protective airway reflexes significantly faster after desflurane than after sevoflurane anesthesia and also record higher oxygen saturation on arrival in the postanesthesia care unit (PACU).117-119 Propofol-nitrous oxide anesthesia adjusted to a Bispectral Index Sensor level of approximately 60 combined with thoracic epidural analgesia provides intraoperative hemodynamic stability and prompts recovery during laparotomy for gastric bypass surgery.120 Metabolism of volatile anesthetics is greater in obese than in normal weight patients, which is reflected by a greater increase in serum inorganic fluoride, including during anesthesia with sevoflurane, whose biotransformation has not been shown to result in significant differences in plasma fluoride levels or differences in pre- and postoperative liver function and renal function tests between obese and nonobese patients.121 A potentially hepatotoxic reductive pathway metabolizes halothane in obese patients, resulting in an increased incidence of "halothane hepatitis." Fortunately, halothane is rarely needed in modern-day practice. Rapid elimination and analgesic properties make nitrous oxide an attractive choice for anesthesia in obese patients, but high oxygen demand in this patient population limits its use. Short-acting opioids such as remifentanil at the lowest possible dose, combined with a low-solubility inhalation anesthetic, facilitates a more rapid emergence without increasing opioid-related side effects.122 Cisatracurium possesses an organ-independent elimination profile and is a favorable nondepolarizing muscle relaxant for maintenance of anesthesia in the obese patient with a high prevalence of renal and hepatic compromise. Vecuronium and rocuronium are also useful choices. Dexmedetomidine, an α2 agonist with sedative and analgesic properties, provides hemodynamic stability without myocardial depression; it has no clinically significant adverse effects on respiration, which makes it an attractive agent for use as an anesthetic adjunct in obese patients. Furthermore, it reduces the postoperative opioid analgesic requirements and their subsequent detrimental respiratory depressant effects.66,123

Ventilatory tidal volumes greater than 13 mL/kg offer no added advantages during ventilation of morbidly obese patients during anesthesia because larger volumes increase airway pressures and lung compliance without significantly improving arterial oxygen tension but results in severe hypocarbia that increases shunt fraction at a Paco2 less than 30 mm Hg.124 Arterial oxygenation during laparoscopy in morbidly obese patients is affected mainly by body weight and not body position, pneumoperitoneum, or mode of ventilation, and oxygenation is not significantly improved by increasing either the respiratory rate or tidal volume.125 PEEP is the only ventilatory parameter that has consistently been shown to improve respiratory function in obese subjects, but it may decrease venous return, cardiac output, and subsequent oxygen delivery.126

Blood loss is usually greater in the obese than in the nonobese for the same type of surgery because technical difficulties of accessing the surgical site requires larger incisions and more extensive dissection. Early infusion of colloids and blood products may be necessary because obese patients are less able to compensate for small volumes lost, but rapid infusion of excessive amounts should be avoided because of high prevalence of preexisting congestive cardiac failure.

Regional Anesthesia

A regional technique is a useful alternative or adjunct to general anesthesia in the morbidly obese because it may help avoid potential intubation difficulties and assist with postoperative pain control and physical therapy. It can be technically difficult, however, because of the inability to easily identify usual bony landmarks. A peripheral nerve stimulator with or without ultrasound guidance helps with the success of regional anesthesia. Central neuraxial block is easier in the lumbar region because the midline in this area has a thinner layer of fat than other areas of the spinal column. Longer needles and the sitting position are other useful tools that facilitate induction of central neuraxial anesthesia. Ultrasound127 and fluoroscopy128,129 can be used to guide a needle or continuous infusion catheter into the spinal or epidural space. Low-current electrical stimulation through an epidural catheter, to achieve trunk or limb movement, can also be used for confirmation of epidural catheter placement.130 Epidural vascular engorgement and fatty infiltration reduce the volume of the space, making dose requirements of local anesthetics for epidural anesthesia 20% to 25% less in obese patients. Subarachnoid blocks are not technically as difficult as epidural blocks, but the height of a subarachnoid block in obese patients can be unpredictable because it may spread considerably upward within a short time causing cardiovascular and respiratory embarrassment. tContinuous catheter subarachnoid block allows titration of the local anesthetic to the desired effect and level.131 Combined epidural and balanced general anesthesia allows for better titration of anesthetic drugs, use of larger oxygen concentration, and optimal muscle relaxation. It also allows for continuation of postoperative analgesia through the same catheter used to provide surgical anesthesia, thereby facilitating early postoperative mobilization.

Emergence

Prompt extubation prevents the morbidly obese patient from becoming ventilator dependent. Tracheal extubation should be considered only when there is complete reversal of neuromuscular blockade and full recovery from the effects of anesthetics. The patient should be preferably extubated in the semirecumbent position, which has less adverse effect on the respiratory system. Supplemental oxygen should be administered after extubation. Lifting devices such as the HoverMatt (Patient Handling Technologies; Allentown, PA, USA) and the Patient Transfer Device (PTD; AliMed; Dedham, MA, USA) are useful for transporting morbidly obese patients onto or off the operating table. The PTD can be combined with the Walter Henderson Maneuver (Fig. 23-10) to transfer obese patients safely and gently onto their postoperative beds.132

Risk of airway obstruction at extubation is increased in the obese OSA patient; up to 5% incidence of life-threatening postextubation obstruction is seen. Negative pressure pulmonary edema can occur from postextubation obstruction and is best treated by reintubation, which can be difficult in a patient with OSA. Extubation in the fully awake state is advocated. Any regional technique, if instituted for postoperative analgesia, should be operative at the time of extubation.

Patients on preoperative CPAP should continue on it postoperatively. CPAP should not be immediately applied to obese OSA patients upon arrival in the PACU because it impairs access to suctioning and dealing with postoperative nausea and vomiting; it also impairs communication between patient and caregiver, and interferes with monitoring of facial color. Furthermore, intraoperative and postoperative events such as facial edema may change mask fit, and also CPAP requirements may change significantly because it is meant to be used for natural, not drug-induced sleep.13 Another indication for CPAP is an increased incidence of postoperative atelectasis in morbidly obese patients after general anesthesia.133 Postoperative CPAP does not increase the incidence of major anastomotic leakage after gastric bypass surgery despite the theoretical risk of anastomotic injury from pressurized air delivered by CPAP.134 The obese patient may avoid taking deep breaths due to pain after abdominal surgery. Adequate analgesia and a properly fitted elastic binder for abdominal support may encourage them to cooperate with early ambulation and deep breathing exercises with the aid of incentive spirometry. Pulse oximetry and arterial blood gases should be monitored appropriately.

Postoperative Analgesia

Perioperative use of regional anesthesia and analgesia reduces the incidence of postoperative respiratory complications. Epidural analgesia with local anesthetics, opioids, or both, or intrathecal opioid are viable options. Potential advantages of epidural analgesia in obese patients include prevention of DVT, improved analgesia, and earlier recovery of intestinal motility. Lesser oxygen consumption and decreased left ventricular stroke work are other benefits. Patient-controlled analgesia (PCA) with morphine may be equivalent to low thoracic/high lumbar continuous infusions of bupivacaine/fentanyl epidural analgesia in morbidly obese patients undergoing gastric bypass surgery with regard to the quality of pain control at rest, the frequency of nausea and pruritus, the time to ambulation, time to return of gastrointestinal function, and the length of hospital stay.135 Incisional local anesthetic infiltration plus PCA produces lower pain scores when compared with epidural anesthesia and analgesia and postoperative PCA for gastric bypass surgery. In addition, infiltration analgesia as part of a multimodal regimen offers a simple, safe, and inexpensive alternative to epidural analgesia alone.136,137 A combination of intraoperative nonopioid analgesics and anesthetic adjuvants (ketorolac, clonidine, ketamine, lidocaine, magnesium sulfate, and methylprednisolone) decreases sedation during recovery from anesthesia and reduces postoperative morphine requirements when compared with intraoperative fentanyl anesthesia in morbidly obese patients.138 Delayed respiratory depression from neuraxial opioids coupled with a potentially difficult airway in the obese patient necessitates closer monitoring in a stepdown or intensive care unit. Increased analgesic requirements during the first 3 postoperative days increase the danger of life-threatening apnea during drug-induced sleep. The first postoperative week is a period of increased risk of prolonged apnea during sleep for the postoperative obese patient, especially those with OSA.13

Chest compressions may not be effective when improperly performed. Mechanical compression devices may be required. The maximum 400 J of energy on regular defibrillators is sufficient for the morbidly obese because their chest wall is usually not much thicker, but the higher trans-thoracic impedance from fat may obligate several attempts.139 Mask ventilation is more difficult because of poor mask fit, redundant oropharyngeal tissues, and reduced chest wall compliance. Intubation may be difficult. The gum-elastic bougie may help facilitate successful intubation in emergency situations. The intubating and ProSeal laryngeal mask airways and the esophageal tracheal Combitube are useful temporary supraglottic airway devices. Transtracheal jet ventilation and retrograde wire intubation may be difficult to establish due to difficulty in palpating anatomic landmarks. Tracheostomy and percutaneous cricothyrotomy should be reserved as final options and should be performed by experienced practitioners.140 Pulse oximetry may be unreliable because of increased finger thickness; the earlobe may be a better choice.

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