Anesthesia & Analgesia:
REVIEW ARTICLE: Review Article
Anesthetic Considerations for Bariatric Surgery
Ogunnaike, Babatunde O. MD*,; Jones, Stephanie B. MD*,; Jones, Daniel B. MD, FACS†,; Provost, David MD, FACS‡, and; Whitten, Charles W. MD*
*Department of Anesthesiology and Pain Management, †Southwestern Center for Minimally Invasive Surgery, and ‡Bariatric Program, University of Texas Southwestern Medical Center at Dallas
July 15, 2002.
Address correspondence and reprint requests to Babatunde O. Ogunnaike, MD, Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75390-9068. Address e-mail to firstname.lastname@example.org.
According to the National Institutes of Health, obesity is a major health problem with clearly established health implications, including an increased risk for coronary artery disease, hypertension, dyslipidemia, diabetes mellitus, gallbladder disease, degenerative joint disease, obstructive sleep apnea, and socioeconomic and psychosocial impairment (1). The risk of developing one or more of these obesity-related conditions is based on body mass index (BMI), with 25–30 kg/m2 being low risk and >40 kg/m2 being very high risk (2). The prevalence of obesity in the 18- to 29-yr-old group increased from 12% in 1991 to 18.9% in 1999 (3).
Bariatric surgery encompasses a variety of surgical weight loss procedures used to treat morbid obesity. Obesity is clinically expressed in terms of BMI or Quetelet’s index (4), which is derived by dividing weight by the square of height to estimate the degree of obesity. Thus, BMI = body weight (kg)/height2 (m2). Morbid obesity is a BMI more than 35 kg/m2, and super morbid obesity is BMI more than 55 kg/m2.
The indications for surgical treatment of severe obesity, as outlined in the 1991 National Institutes of Health Consensus Development Conference Panel, include an absolute BMI more than 40 kg/m2 or BMI more than 35 kg/m2 in combination with life-threatening cardiopulmonary problems or severe diabetes mellitus (1).
Patients seeking surgical weight loss must have proven attempts at medically supervised weight loss. Documentation of loss of <5% to 10% excess body weight or weight gain after at least 6 mo of diet modification, exercise, and medical therapy or nonimprovement in comorbid conditions during this period indicates failure. Studies have shown that weight loss of 5%–10% of initial body weight improves glucose intolerance and Type II diabetes, hypertension, and dyslipidemia (5–7).
The average expenditure is approximately $7000 per year per patient on weight loss programs and equipment. Unfortunately, long-term weight loss is the exception, and most patients regain weight, sometimes more than they initially lost.
Surgical Treatment of Obesity
Surgical approaches designed to treat obesity can be classified as malabsorptive or restrictive (8,9). Malabsorptive procedures, which include jejuno-ileal bypass and biliopancreatic bypass, are rarely used at present. Restrictive procedures include the vertical banded gastroplasty (VBG) and gastric banding, including adjustable gastric banding (AGB). RYGB, the “gold standard” of bariatric operations, combines gastric restriction with a minimal degree of malabsorption. VBG, AGB, and RYGB can all be performed laparoscopically (10,11).
At our institution, laparoscopic Roux-en-Y gastric bypass (RYGB) is routinely performed on patients weighing <160 kg without other contraindications to laparoscopy, including uncorrected coagulopathy and inability to tolerate laparotomy. Technical considerations and instrumentation technology currently make laparoscopic bariatric surgery difficult in patients weighing >180 kg (8,12).
Gastric restriction, or gastroplasty, separates the stomach into a small upper pouch (15–30 mL), which restricts food intake. This pouch communicates with the remainder of the stomach through a narrow channel, or stoma.
RYGB (Fig. 1), the most commonly performed bariatric procedure in the United States, involves anastomosing the proximal gastric pouch to a segment of the proximal jejunum, bypassing most of the stomach and the entire duodenum. It is the most effective bariatric procedure to produce safe short-term and long-term weight loss in severely obese patients (13). With RYGB, patients lose an average of 50%–60% of excess body weight and show a decrease in BMI of approximately 10 kg/m2 during the first 12 to 24 postoperative months. To the health care provider, the effect of weight loss on associated weight-related comorbidity is more important than absolute weight loss. Studies have shown that Type II diabetes resolves in up to 90% of patients (14).
The variables used to measure surgical outcome include operative time, length of skin incision, estimated blood loss, number of patients requiring intensive care unit stay, length of hospital stay, early and late (>30 days) complications, early (<30 days) reoperation, and weight loss. Using these variables, Nguyen et al. (15) found that, with the exception of length of operative time, laparoscopic RYGB was generally associated with better outcomes and cost-effectiveness than open RYGB. The rate of anastomotic leakage is also slightly more frequent with the laparoscopic approach (8), but it becomes comparable once the learning curve has been mastered (approximately 70 cases) (16). Other advantages of the laparoscopic procedure include reduced hospital stay, more rapid return to normal activity, improved cosmesis, and a marked reduction in the incidence of incisional hernia and wound infection (8,15). There are also smaller postoperative pain medication requirements, less pain intensity during mobilization, and improved pulmonary function.
Complications after RYGB include anastomotic leak, gastric pouch outlet obstruction, jejunostomy obstruction, deep vein thrombosis (DVT), pulmonary embolism (PE), respiratory failure, gastrointestinal (GI) bleeding, and wound infection. Late complications include prolonged nausea and vomiting, cholelithiasis, ventral hernia, anemia, and protein-calorie malnutrition. Nguyen et al. (15) discovered, in a prospective, randomized study, that these complications are more common after open RYGB than after laparoscopic RYGB, except for late anastomotic stricture, which was significantly more common after the laparoscopic approach. The more frequent leak rate with laparoscopic RYGB was thought to be related to the learning curve.
RYGB induces an undesirable “dumping syndrome” if the patient ingests a high-sugar liquid meal (17), with potential side effects of iron and vitamin B12 malabsorption. Dumping syndrome consists of early postprandial abdominal and vasomotor symptoms resulting from fluid shifts and release of vasoactive neurotransmitters (the pathophysiology of which is peripheral) and splanchnic vasodilation, coupled with a relative hypovolemia, leading to diarrhea and abdominal cramps. It occurs in approximately 10% of patients postgastric bypass surgery. Late dumping symptoms are due to reactive hypoglycemia, which results from an exaggerated insulin and glucagon-like peptide 1 release. Symptoms can be relieved with dietary modifications to minimize the ingestion of simple carbohydrates and to exclude fluid intake during ingestion of the solid portion of the meal. Severe cases may respond to agents such as pectin and guar (plant polysaccharide bulking agents that increase the viscosity of intraluminal contents) or to acarbose, an α-glucosidase inhibitor that blunts the rapid absorption of glucose (18,19). Octreotide, a somatostatin analog that alters gut transit and impairs the release of vasoactive mediators, may also be useful in patients refractory to all other therapy (18). It acts through its inhibitory effects on insulin and gut hormone release, a delay of intestinal transit time, and inhibition of food-induced circulatory changes (19).
The AGB (Fig. 2), recently approved by the Food and Drug Administration for use in the United States, is the newest gastric restrictive operation and is usually placed by a minimally invasive laparoscopic approach. It consists of an adjustable inflatable band placed around the proximal stomach to limit oral intake (8). It is a less dynamic operation than RYGB and has a learning curve of 30 operations. Up to 50% ± 28% average excess weight loss has been reported with AGB at 2-yr follow-up, with a complication rate of 19% and a mortality rate of 0.4%(20,21). Band erosion and erosive esophagitis were reported by Westling et al. (22) to be the most common complications requiring repeat surgery over 3 yr. Other complications include herniation of the stomach upward inside of the band and band migration from overfilling (23). In a series of 250 laparoscopic AGB patients by Nehoda et al. (24), the most significant complications were early pouch dilations occurring in the first week; however, the most common complications were disconnections at the portal site between the tube and reservoir. Specific contraindications to AGB include inflammatory diseases of the GI tract (such as severe esophagitis, gastric or duodenal ulcers, or specific inflammation, such as Crohn’s disease), upper GI bleeding (such as esophageal or gastric varices), portal hypertension, congenital or acquired anomalies of the GI tract (e.g., atresias or stenoses), intraoperative gastric injury (e.g., gastric perforation at or near the location of the intended band placement), liver cirrhosis, chronic pancreatitis, and allergy to the materials used to make the band.
Medical Therapy for Obesity
Approved indications for drug treatment include a BMI of ≥30 kg/m2 or a BMI from 27 and 29.9 kg/m2 in conjunction with an obesity-related medical complication. The combination of phentermine and fenfluramine (Phen-Fen) was the most popular treatment for obesity until it became associated with valvular heart disease and pulmonary hypertension. As a result of this, Phen-Fen is no longer approved by the Food and Drug Administration and should never be used for this purpose.
Sibutramine and orlistat are newer antiobesity medications approved for long-term use. Sibutramine inhibits the reuptake of norepinephrine, serotonin, and dopamine, thereby causing anorexia. These mechanisms act synergistically to increase satiety after the onset of eating rather than reduce appetite (25). It does not promote the release of serotonin, unlike fenfluramine and dexfenfluramine, which primarily increase the release of serotonin in brain synapses and also inhibit the reuptake, thereby causing anorexia (26). These differences in mechanisms of action may explain why there have been no reports thus far of sibutramine causing cardiac valvular lesions. Because sibutramine does not deplete the neural synapses of catecholamines, dangerous hypotension unresponsive to indirectly acting vasopressors (seen with fenfluramine and dexfenfluramine) does not generally occur (27).
The most frequent adverse effects of sibutramine treatment include dry mouth, insomnia, anorexia, and constipation (28). Sibutramine also causes transient dose-related increases in both systolic and diastolic blood pressure by a mean of 2–4 mm Hg and induces a small increase in heart rate of 3–5 bpm (29). Although blood pressure decreases with weight loss, this stimulatory effect on blood pressure remains detectable as long as sibutramine is taken. A randomized, controlled trial (30) showed that 13% of those treated with sibutramine, compared with 4% of those treated with placebo, lost ≥10% of their initial weight. Si-butramine results in peak weight loss after approximately 6 mo that is maintained for at least 1 yr (30,31).
Orlistat is a synthetic derivative of a product from Streptomyces toxytricini that inhibits mammalian lipase (32). It blocks digestion and absorption of dietary fat by binding lipases in the GI tract. Serum low-density lipoprotein cholesterol concentrations decrease in addition to the weight loss (33). GI complaints induced by fat malabsorption are the most common. A decrease in serum concentration of fat-soluble vitamins (A, D, E, and K) has been observed in approximately 5%–15% of patients (33–35). Some trials with orlistat achieved an average weight loss of 9% compared with 5% in the placebo group at the end of 1 yr (33–35). In isolated cases, orlistat has been blamed as a causative factor of aggravated hypertension in previously treated hypertensive and normotensive patients, but a cause-effect relationship has not been definitely proven (36–38). Warfarin’s anticoagulant effect may increase because orlistat decreases the absorption of vitamin K (39). Both orlistat and sibutramine induce ≥5% to 10% weight reduction, with maintenance for up to 2 yr (40).
There is a paucity of studies and literature on direct interactions between sibutramine or orlistat and anesthesia medications. However, anesthesiologists should be aware of the side effects of these drugs and their effects on body systems and tailor their anesthesia accordingly.
Histological and liver function test abnormalities are relatively common in the obese, but clearance is usually not reduced. Up to 90% of morbidly obese patients show histological abnormalities of the liver, with one-third of them having fatty change involving more than 50% of hepatocytes (41).
In a prospective study of 127 consecutive morbidly obese patients presenting for bariatric surgery, 75% had histological evidence of hepatic steatosis, which was severe and diffuse in 20%(42). Twenty to thirty percent of obese patients without evidence of concomitant liver disease have increased liver function tests. Increased alanine aminotransferase (ALT) is the most frequent hepatic abnormality in the obese population. For every 1% reduction in body weight, ALT activity improves by 8.1%(43). In a study of 198 patients awaiting gastric banding (44), 18.7% had increased liver enzymes. ALT increased by 14.1%, aspartate aminotransferase by 9.6%, and γ-glutamyl transpeptidase by 6.6% before surgery. ALT and aspartate aminotransferase returned to normal after surgery in all the patients in direct proportion to the extent of weight reduction after gastric banding. Palmer and Schaffner (43) showed that in overweight adults without primary liver disease, a weight reduction of ≥10% corrected abnormal hepatic test results, decreased hepatomegaly, and resolved some stigmata of liver disease. More recently (45), 75 morbidly obese patients who had intraoperative liver biopsies at the time of RYGB had an 84% rate of hepatic steatosis, with only approximately 20% having moderate to severe inflammation and fibrosis. Despite these histologic and enzymatic changes, no clear correlation has been found between routine liver function tests and the capacity of the liver to metabolize drugs (46).
Renal clearance of drugs is increased in obesity because of increased renal blood flow and glomerular filtration rate (GFR) (47). Ribstein et al. (48) assessed the influence of obesity on renal function and urinary albumin excretion in normotensive and hypertensive subjects and found that the GFR and effective renal plasma flow were increased in overweight compared with lean subjects irrespective of the presence of hypertension. Brochner-Mortensen et al. (49) documented up to a 40% increase in GFR in obese patients; this may be an important contributing factor to proteinuria, the most cited renal abnormality in these patients (50). Other studies (51–53) have also independently shown increases in measured GFR in obese compared with normal-weight subjects.
Attention should focus on issues unique to the obese patient, particularly cardiorespiratory status and the airway. Patients presenting for bariatric surgery should be evaluated for systemic hypertension, pulmonary hypertension, signs of right and/or left ventricular failure, and ischemic heart disease. Signs of cardiac failure—such as increased jugular venous pressure, added heart sounds, pulmonary crackles, hepatomegaly, and peripheral edema—may be difficult to detect.
The most common symptoms of pulmonary hypertension include exertional dyspnea, fatigue, and syncope, which reflect an inability to increase cardiac output during activity (54). Identification of tricuspid regurgitation with echocardiography is the most useful confirmation of pulmonary hypertension (55). An electrocardiogram may demonstrate signs of right ventricular hypertrophy, such as tall precordial R waves, right axis deviation, and right ventricular strain. The higher the pulmonary artery (PA) pressure, the more sensitive the electrocardiogram (56). Chest radiograph may show evidence of underlying lung disease and evidence of prominent pulmonary arteries (56). Mild to moderate pulmonary hypertension warrants avoidance of hypoxemia, nitrous oxide, and other drugs that may further worsen pulmonary vasoconstriction. Inhaled anesthetics may be beneficial because they cause bronchodilation and decrease hypoxic pulmonary vasoconstriction (57). With severe pulmonary hypertension, PA catheterization and monitoring may be necessary.
Peripheral and central venous access and arterial cannulation sites should be evaluated during the preoperative examination, and the possibility of invasive monitoring should be discussed with the patient. Baseline arterial blood gas measurements will help evaluate carbon dioxide retention and provide guidelines for perioperative oxygen administration and possible institution of and weaning from postoperative ventilation.
Patients scheduled for repeat bariatric surgery may confront the anesthesiologist days, months, or years after the initial surgery, so the anesthesiologist should be familiar with possible metabolic changes in these patients. Common long-term nutritional abnormalities include vitamin B12, iron, calcium, and folate deficiencies. Vitamin deficiency is uncommon in patients compliant with daily vitamin supplements, especially in patients followed up with regular postoperative visits. With rapid weight loss, patients may also be protein depleted. Electrolyte and coagulation indices should be checked before surgery, particularly if patient compliance has been poor or if the patient is acutely ill. Chronic vitamin K deficiency can lead to an abnormal prothrombin time with a normal partial thromboplastin time because of deficiency of clotting factors II, VII, IX, and X (58). For elective surgery, the administration of a vitamin K analog, such as phytonadione, can be used to correct the coagulopathy within 6–24 h. Fresh frozen plasma will be required for emergency surgery or active bleeding (59).
Concurrent and Preoperative Medications
It is recommended that the patient’s usual medications, except insulin and oral hypoglycemics, be continued until the time of surgery. Antibiotic prophylaxis is important because of increased risk of postoperative wound infection. Published rates of wound infection after gastric operations for obesity are approximately 5%(60), and rates after clean contaminated GI surgery are 2%–3%(61). A metaanalysis of open bariatric surgery quoted the infection rate of restrictive procedures (VBG, silastic ring vertical gastroplasty, and AGB) as 3%–11%, whereas that of combination procedures (RYGB and extended RYGB) was 5.27%(62). Other authors have quoted wound infection rates of 11.7%–15.8% after open gastric bypass (63,64). In a prospective, randomized study, Nguyen et al. (15) found that open RYGB had an approximately 10 times more frequent incidence of wound infection (10.5% versus 1.3%) when compared with the laparoscopic approach. The increased incidence of wound infection is due to longer incisions, generally longer operative times because of obesity, tissue trauma from excessive traction, difficulty in dead-space obliteration, and inability of adipose tissue to resist infection (65). Antibiotic prophylaxis is, however, also recommended by many practitioners for the laparoscopic approach.
Anxiolysis, analgesia, and prophylaxis against both aspiration pneumonitis and DVT should be addressed during premedication. Oral benzodiazepines are reliable for anxiolysis and sedation because they cause little or no respiratory depression. IV midazolam can also be titrated in small doses for anxiolysis during the immediate preoperative period. Pharmacologic intervention with H2-receptor antagonists (e.g., cimetidine, ranitidine, famotidine) and nonparticulate antacids (e.g., sodium bicitrate) and proton pump inhibitors (e.g., omeprazole, lansoprazole, rabeprazole) will reduce gastric volume, acidity, or both, thereby reducing the risk and complications of aspiration.
Morbid obesity is a major independent risk factor for sudden death from acute postoperative PE (66,67). Heparin, 5000 IU subcutaneously, administered before surgery and repeated every 12 h until the patient was fully mobile, reduced the risk of DVT (68). Recently, low molecular weight heparins (LMWH) have gained popularity in thromboembolism prophylaxis because of their bioavailability when injected subcutaneously (69). Two recent studies examined two different doses of two different types of LMWH for use in the prophylaxis of DVT in patients undergoing bariatric surgery. Scholten et al. (70) found that 40 mg every 12 h rather than 30 mg every 12 h of enoxaparin resulted in a decreased incidence of postoperative DVT complications without an increase in bleeding complications. In the second study, Kalfarentzos et al. (71) evaluated two different doses of nadroparin (5700 IU versus 9500 IU) for DVT prophylaxis in patients undergoing RYGB and found that the smaller dose (5700 IU) given once daily is safe and well tolerated and has equal thromboembolism prophylaxis as the larger dose (9500 IU) in high-risk patients. Nadroparin is currently not commercially available in the United States. Studies have shown that unfractionated heparin 5000 IU given subcutaneously three times daily is equivalent to the LMWH enoxaparin given once daily for thromboprophylaxis (72). In a survey of members of the American Society for Bariatric Surgery regarding their current practices for thromboprophylaxis (73), small-dose heparin, 5000 U every 8–12 h, was the most preferred method (50% of members), followed by pneumatic compression stockings (33%), LMWH (13%), and other methods (4%). In combination with subcutaneous heparin, we favor placement of pneumatic compression devices on the feet because knee- or thigh-length devices tend to slip and fall off.
Specially designed tables or two regular tables joined together may be required for safe anesthesia for bariatric surgery. Regular operating room tables have a maximum weight limit of approximately 205 kg, but operating tables capable of holding up to 455 kg, with a little extra width to accommodate the extra girth, are available. Electrically operated or motorized tables facilitate maneuvering into various surgically favorable positions. Bariatric surgical patients are prone to slipping off the operating table during table position changes; therefore, they should be well strapped to the operating table. The use of a bean bag is also recommended. Bean bags (Vac-Pac®; Olympic Medical, Seattle, WA) are soft pads available in various sizes and shapes that are filled with thousands of tiny plastic beads (74). The patient is positioned on the bean bag, which is then molded around the patient, and a suction line is attached to it, creating a vacuum inside the bean bag which allows outside atmospheric pressure to force the beads together so they cannot move. It is worthwhile to note that all materials used to manufacture Vac-Pac® are latex free.
Particular care should be paid to protecting pressure areas, because pressure sores and neural injuries are more common in this group, especially in the super obese and the diabetic. Brachial plexus and sciatic nerve palsies have been reported (75). Stretch injuries may be caused by extreme abduction of the arms, thereby stretching the lower roots of the brachial plexus. The upper roots are most likely stretched by excessive rotation of the head to the opposite side (76). Sciatic nerve palsy may be caused by prolonged ischemic pressure from tilting the table sideways. Lateral femoral cutaneous nerve injury may occur if the lower limb falls and hangs freely. Ulnar neuropathy has been associated with increased BMI. A retrospective study by Warner et al. (77) documented such an association because 29% of patients with ulnar neuropathy in their series had a BMI ≥38 kg/m2, compared with only 1% of the control subjects. The extent and degree to which a nerve is injured should be well documented so that recovery and prognosis can be discussed with the patient. Electromyography and nerve conduction studies provide valuable clinical information in this respect. A mild degree of reversible neural insult that results in impulse conduction failure across the affected segment is termed neuropraxia(76). It is a focal conduction block from local myelin injury of primarily larger fibers, with recovery expected within weeks to months. Axonotmesis describes physical disruption of only the axon, with preservation of endoneurial and other connective tissue structures. There is loss of nerve conduction at the injury site and distally, with disruption of axonal continuity and Wallerian degeneration. Recovery of function depends on the time for the process of Wallerian degeneration and neural regeneration to occur. Prognosis is good because the original end organs are reached (76). Neurotmesis implies complete severance of the nerve, with complete disruption of all supporting connective tissue structures. It carries a poor prognosis for complete functional recovery (76). Gradings of this type help with the discussion of prognosis with patient and family. Despite careful positioning and appropriate padding, nerve injury may still occur in this at-risk population. Fortunately, most resolve with time.
Laparoscopy and Anesthesia
Pneumoperitoneum causes systemic changes during laparoscopy. The gas most often used for this purpose is carbon dioxide. Positioning, such as Trendelenburg, can worsen the systemic changes of pneumoperitoneum (78).
Systemic vascular resistance is increased with increased intraabdominal pressure (IAP). The degree of IAP determines its effects on venous return and myocardial performance (79). There is a biphasic cardiovascular response to increases in IAP. At an IAP <10 mm Hg, there is an increase in venous return, probably from a reduction in splanchnic sequestration of blood, with a subsequent increase in cardiac output and arterial pressure. Hypovolemia, however, blunts this response (80). Compression of the inferior vena cava occurs at an IAP >20 mm Hg, with decreased venous return from the lower body and consequent decreased cardiac output (79). Increased renal vascular resistance at an IAP >20 mm Hg decreases renal blood flow and GFR (81). Femoral venous blood flow can be reduced by both pneumoperitoneum and Trendelenburg positioning, with an increased risk of lower-extremity thrombosis (82). Abdominal viscera further exert weight on the diaphragm during Trendelenburg positioning, causing a reduction in vital capacity, and placement of surgical packs and retractors in the upper abdomen may worsen the situation (83). Sprung et al. (84) studied the effect of morbid obesity, 20 mm Hg pneumoperitoneum, and body posture (30° head down and 30° head up) on respiratory mechanics, oxygenation, and ventilation during laparoscopy. In contrast however, they did not find body position to have any significant effect on respiratory mechanics during laparoscopy. They reported that, whereas arterial oxygen tension was adversely affected only by increased body weight, respiratory mechanics were affected by both obesity and pneumoperitoneum but varied little with body position. We have witnessed situations in which cephalad displacement of the diaphragm and carina from pneumoperitoneum caused a firmly secured endotracheal tube to be displaced into a bronchial mainstem. Hypercarbia and hypoxemia may be caused by ventilation-perfusion mismatch because of restriction of diaphragmatic mobility from pneumoperitoneum that leads to uneven distribution of ventilation to the nondependent part of the lung. Absorption of carbon dioxide can worsen hypercarbia and acidosis, which can be offset by hyperventilation. Catastrophic complications that should be kept in mind include massive gas embolism, pneumothorax, and mediastinal emphysema.
Invasive arterial monitoring should be used for the super morbidly obese with severe cardiopulmonary disease and for those with poor fit of the noninvasive blood pressure cuff because of severe conical shape of the upper arms or unavailability of appropriately sized cuffs. Blood pressure measurements can be falsely increased if a cuff too small for the arm is used (85). Cuffs with bladders that encircle a minimum of 75% of the upper arm circumference or, preferably, the entire arm, should be used (86). Comparable and accurate blood pressure readings can be obtained from the wrist (87) or ankle (88) with appropriately sized blood pressure cuffs in situations in which difficulty occurs with upper-arm noninvasive blood pressure measurement. We use central venous catheters in cases in which peripheral IV access cannot be obtained, whereas PA catheters are reserved for serious cardiopulmonary disease. Another strong indication for central venous catheterization is postoperative IV access, which can be problematic in this patient population and is probably more easily performed in the anesthetized patient.
Induction, Intubation, and Maintenance of Anesthesia
Preparation should be made for the possibility of a difficult intubation, and a surgeon familiar with surgical airways should be readily available. A towel or folded blankets under the shoulders and head can compensate for an exaggerated flexed position from posterior cervical fat (89). 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. Brodsky et al. (90) used a logistic regression model to quantify the relationship between the ease of intubation and patient characteristics. They predicted that odds of a problematic intubation in a particular patient with a neck circumference 1 cm larger than that of another patient are 1.13 times the odds of the patient with a 1-cm-smaller neck circumference. Therefore, the probability of a problematic intubation was approximately 5% with a 40-cm neck circumference, compared with a 35% probability at 60-cm neck circumference. This model identified neck circumference as the single best predictor of problematic intubation.
Highly lipophilic substances (Table 1) (91–102), such as barbiturates and benzodiazepines, show significant increases in volume of distribution (Vd) for obese individuals relative to normal-weight individuals (91,103,104). Less-lipophilic compounds have little or no change in Vd with obesity. Certain exceptions to this rule include digoxin (105), procainamide (106), and remifentanil (101), which are highly lipophilic drugs but which have no systematic relationship between their degree of lipophilicity and their distribution in obese individuals. Consequently, their absolute Vd remains relatively consistent between obese and normal-weight individuals, and their doses should be calculated on the basis of ideal body weight (101,105,106).
Drugs with weak or moderate lipophilicity can be dosed on the basis of ideal body weight (IBW) or, more accurately, lean body mass (LBM). These values are not identical, because 20%–40% of an obese patient’s increase in total body weight can be attributed to an increase in LBM. Adding 20% to the estimated IBW dose of hydrophilic medications is sufficient to include the extra lean mass. Nondepolarizing muscle relaxants can be dosed in this manner. The majority of anesthetic drugs are strongly lipophilic. Increased Vd is expected for lipophilic substances, but this is not consistently demonstrated in pharmacological studies because of factors such as end-organ clearance or protein binding.
Desflurane has been suggested as the inhaled anesthetic of choice in this patient population because of its more rapid and consistent recovery profile (108). Two different studies (109,110) compared sevoflurane with isoflurane for use during bariatric surgery and favored sevoflurane because of its more rapid recovery, good hemodynamic control, infrequent incidence of nausea and vomiting, prompt regaining of psychological and physical functioning, early discharge from the hospital, and small cost. Rapid elimination and analgesic properties make nitrous oxide a good inhaled choice during bariatric surgery, but high oxygen demand in the obese limits its use. Obesity increases oxygen consumption and carbon dioxide production (111). This is due to excess metabolically active tissue and an increased workload on muscles and other supportive tissue. DeDivitiis et al. (112) performed left and right heart catheterization in 10 morbidly obese but otherwise healthy individuals and noted that the mean oxygen consumption was increased by up to 25% and increased linearly with increasing body weight. The arteriovenous oxygen difference was normal, however, suggesting that cardiac output increases primarily to serve the metabolic requirements of excess fat (113).
Complete muscular relaxation is crucial during laparoscopic bariatric procedures to facilitate ventilation and to maintain an adequate working space for visualization and safe manipulation of laparoscopic instruments. Complete relaxation also facilitates the introduction of surgical equipment and extraction of excised tissues. Collapse of pneumoperitoneum may be an early indication that muscle relaxation is inadequate, because muscle tone competes with the pressure limit set for the pneumoperitoneum. Tightening of the musculature around the surgeon’s finger palpating the port site may also be a sign of inadequate paralysis.
Combined epidural and general balanced anesthesia has been advocated to allow better titration of anesthetic drugs, use of a larger oxygen concentration, and optimal muscle relaxation for upper abdominal surgery in the obese (114). This does not reflect current practice, because most bariatric procedures are performed under a minimally invasive laparoscopic approach, with less depression of postoperative pulmonary function, decreased pain, improved oxygenation, and less atelectasis when compared with laparotomy (115). With the introduction of easily titratable drugs such as remifentanil, propofol, and desflurane, decreased intraoperative dosing is not generally required for prompt emergence. Michaloudis et al. (116) described a technique of continuous spinal anesthesia combined with general anesthesia for intraoperative anesthetic management and postoperative analgesia in 27 obese patients undergoing laparotomy for gastroplasty. They found this technique to be safe during surgery and effective for postoperative analgesia.
Tidal volumes of up to 15–20 mL/kg have been recommended as one method to improve functional residual capacity (FRC) in the anesthetized obese patient (117). This has not been shown to improve oxygenation significantly, even though FRC may be increased above closing volume. Bardoczky et al. (118) evaluated the effects of large tidal volume ventilation on oxygenation and ventilation in morbidly obese patients during anesthesia and found that increasing tidal volumes up to 22 mL/kg increased the peak inspiratory airway pressure, end-expiratory (plateau) airway pressure, and compliance of the lungs without significantly improving arterial oxygen tension, but it resulted in severe hypocapnia. They concluded that tidal volumes >13 mL/kg IBW offer no added advantage during ventilation of morbidly obese patients during anesthesia. Also, in light of evidence that the lung can be injured by excessive expansion (volutrauma) from large tidal volumes leading to pulmonary edema and that positive end-expiratory pressure (PEEP) actually reduced lung water content in this type of edema (119), it seems prudent to use moderate levels of PEEP (enough to preserve hemodynamic stability) rather than large tidal volumes in an attempt to improve oxygenation. We routinely use tidal volumes of 10–12 mL/kg to avoid barotrauma and respiratory rates of up to 12–14 breaths/minute to maintain normocapnia during laparoscopic bariatric surgery with carbon dioxide abdominal inflation. We have also successfully used pressure control ventilation with vigilant monitoring of exhaled tidal volumes to achieve adequate oxygenation and normocapnia.
We have found that intraoperative fluid requirements are usually larger if postoperative acute tubular necrosis is to be prevented. Patients usually require up to 4–5 L of crystalloid for an average 2-h operation. This adds up to twice the calculated maintenance fluid requirement plus the calculated deficit based on a 12-h fasting period for an average 70-kg patient for the first hour by using the 4-2-1 formula (4 mL · kg−1 · h−1 for the first 10 kg; 2 mL · kg−1 · h−1 for the next 10 kg; then 1 mL · kg−1 · h−1 for every kilogram thereafter). The next hour usually requires the same amount of crystalloid, after which the amounts are reduced to approximately twice the calculated maintenance requirement, based on LBM, for the next 12 h (200 mL/h overnight).
Other Technical Issues
Anesthesiologists help facilitate proper placement of an intragastric balloon and nasogastric (NG) tube during surgery to help the surgeon size the gastric pouch. They also help perform leak tests with saline and methylene blue to ensure anastomotic integrity. Care should be taken during injection of saline or methylene blue through the NG tube to ensure that the endotracheal tube cuff maintains a tight seal; otherwise, aspiration of methylene blue can occur, leading to chemical pneumonitis. It is also important to completely remove all endogastric tubes (not just merely pull them back into the esophagus) before gastric division, to avoid unplanned stapling and transection of these devices (Fig. 3). After an RYGB pouch is created, the anesthesiologist should not blindly insert the NG tube; in this situation, the monitor should be watched carefully while the NG tube is advanced, to avoid disruption of the anastomosis.
A 45% incidence of atelectasis has been reported in obese patients after upper abdominal surgery (120), and initiation of continuous positive airway pressure (CPAP) treatment has been advocated, starting in the recovery room and continuing overnight, to prevent postoperative acute airway obstruction (121,122). Bilevel positive airway pressure (BiPAP) has also been used to combat nocturnal airway obstruction (123). Joris et al. (124) investigated the effect of BiPAP—a combination of pressure support ventilation and PEEP— on postoperative pulmonary function in obese patients during the first 24 h after gastroplasty. They found that prophylactic BiPAP system therapy with a 12 cm H2O inspiratory positive airway pressure and 4 cm H2O expiratory airway pressure significantly reduced pulmonary dysfunction and accelerated the reestablishment of preoperative pulmonary function. The possibility of stomach inflation, which is probably best avoided early after gastric surgery, was not addressed by this study. However, Huerta et al. (125) recently assessed the efficacy of postoperative CPAP for patients undergoing gastrojejunostomy as part of the RYGB procedure. They did not find any correlation between CPAP use and the incidence of major anastomotic leakage, despite the theoretical risk of anastomotic injury from pressurized air delivered by CPAP.
After a laparotomy for bariatric surgery, patients may avoid taking deep breaths because of pain. Adequate analgesia and a properly fitted elastic binder for abdominal support may encourage patients to cooperate with early ambulation and incentive spirometry. Although incentive spirometry has been recommended by some authors to prevent postoperative atelectasis (126,127), adequate evidence is lacking in this respect. A systematic retrospective review on the use of incentive spirometry in preventing postoperative pulmonary complications did not reveal evidence to support its use during cardiac or upper abdominal surgery (128). Of the 46 articles reviewed, only 1 reported that incentive spirometry, deep breathing, and intermittent positive pressure breathing were equally more effective than no treatment in preventing postoperative pulmonary complications after upper abdominal surgery (129). Current widespread use of laparoscopic techniques for bariatric procedures results in less postoperative pulmonary dysfunction (115), possibly reducing the need for incentive spirometry. Patients with a history of severe sleep apnea may require overnight observation in the intensive care unit because prolonged obstructive apnea is a real possibility, especially when parenteral narcotics are used.
The pain from an open bariatric surgical procedure can be quite significant. Epidural local anesthetics and/or narcotics via the thoracic route are a safe and effective form of postoperative analgesia in these patients. Intrathecal narcotics are also a viable option. Potential advantages of thoracic epidural analgesia in the setting of bariatric surgery include prevention of DVT, improved analgesia, and earlier recovery of intestinal motility. Investigators have been unable to document a difference in the incidence of thrombophlebitis and PE with continuous epidural analgesia (130,131). Less oxygen consumption and decreased left ventricular stroke work have, however, been documented as benefits of local anesthetic epidural analgesia (132).
A recent abstract (133) looked at patient-controlled thoracic epidural analgesia after gastric bypass surgery and found that it provided adequate postoperative pain control with few side effects and no serious complications. Most of the patients were able to start oral intake on the second postoperative day and were discharged home by the fourth postoperative day. Another study on thoracic epidural analgesia (134) found distinct advantages over morphine patient-controlled analgesia (PCA) in providing a superior quality of analgesia and shortening the duration of postoperative ileus. Continuous spinal analgesia has been used for postoperative analgesia after open VBG with demonstrated safety, efficacy, and a small incidence of morbidity (116).
Laparoscopic bariatric surgery induces less postoperative pain and is less likely to interfere with pulmonary mechanics (115). Most laparoscopic bariatric patients do well with local anesthetic wound infiltration and basic parenteral narcotics, such as PCA. In a study of 200 patients who underwent VBG (135), effective postoperative analgesia sufficient to allow mobilization was achieved by IV infusion of opioids or PCA. Choi et al. (136) also prospectively investigated the efficacy of IV morphine PCA in morbidly obese patients undergoing RYGB surgery and found that it provided satisfactory analgesia without deleterious effects on oxygen saturation, blood pressure, heart rate, or respiratory function. Patients can be switched to liquid oral narcotics on the first postoperative day after contrast (Gastrografin) swallow has eliminated anastomotic leaks, or as soon as they can tolerate them. Supplementation with oral or rectal nonnarcotic analgesics may be considered, but chronic nonsteroidal antiinflammatory drugs should be discouraged because of concern about gastric ulcers after bariatric procedures.
Bariatric surgery is a safe and viable option in the management of obese patients when nonsurgical treatment options have been unsuccessful. Anesthetic management of these patients should take into consideration the specific problems associated with obesity and optimize them before surgery. Success of medical therapy is marginal at best, with a loss of only 5%–10% body weight at 6 mo to 1 yr with up to 2 yr of maintenance. Combined gastric restriction and bypass or simple gastric restriction have 30-day morbidity and mortality rates of 1% and 0.3%, respectively (137), with the most common 30-day complications (major and minor) being respiratory in nature, from atelectasis to PE. Laparoscopic morbidity and mortality rates have been quoted as much less frequent (8).
1. NIH conference: gastrointestinal surgery for severe obesity— Consensus Development Conference Panel. Ann Intern Med 1991; 115: 956–61.
2. Bray GA. Pathophysiology of obesity. Am J Clin Nutr 1992; 55 (Suppl): 488–94.
3. Mokdad AH, Serdula MK, Dietz WH, et al. The spread of the obesity epidemic in the United States 1991–1998. JAMA 1999; 282: 1519–22.
4. Quetelet LAJ. A treatise on man and the development of his faculties: Edinburgh 1842, reprinted. Obes Res 1994; 2: 72–85.
5. Wing RR, Koeske R, Epstein LH, et al. Long-term effects of modest weight loss in type II diabetic patients. Arch Intern Med 1987; 147: 1749–53.
6. Stevens V, Corrigan S, Obarzanek E, et al. Weight loss intervention in phase I of the trials of hypertension prevention. Arch Intern Med 1993; 153: 849–58.
7. Dattilo A, Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am J Clin Nutr 1992; 56: 320–8.
8. Provost DA, Jones DB. Minimally invasive surgery for the treatment of severe obesity. Dallas Med J 1999; 87: 110–3.
9. Balsiger BM, Murr MM, Poggio JL, Sarr MG. Bariatric surgery: surgery for weight control in patients with morbid obesity. Med Clin North Am 2000; 84: 477–89.
10. Scott DJ, Provost DA, Jones DB. Laparoscopic Roux-en-Y gastric bypass for morbid obesity. Surg Rounds 2000; 23: 177–89.
11. Wittgrove AC, Clark GW, Schubert KR. Laparoscopic gastric bypass, Roux-en-Y: technique and results in 75 patients with 3–30 months of follow-up. Obes Surg 1996; 6: 500–4.
12. Schirmer BD. Laparoscopic bariatric surgery. Surg Clin North Am 2000; 80: 1253–67.
13. Sugerman HJ, Kellum JM, Engle KM, et al. Gastric bypass for treating severe obesity. Am J Clin Nutr 1992; 55 (Suppl): 560–6.
14. Long SD, O’Brien K, Macdonald KG Jr, et al. Weight loss in severely obese subjects prevents the progression of impaired glucose tolerance to type II diabetes. Diabetes Care 1994; 17: 372–5.
15. Nguyen NT, Goldman C, Rosenquist CJ, et al. Laparoscopic versus open bypass: a randomized study of outcomes, quality of life, and costs. Ann Surg 2001; 234: 279–91.
16. Wittgrove AC, Clark GW. Laparoscopic bypass, Roux-en-Y: 500 patients—technique and results, with 3–60 month follow-up. Obes Surg 2000; 10: 233–9.
17. Capella JF, Capella RF. The weight reduction operation of choice: vertical banded gastroplasty or gastric bypass? Am J Surg 1996; 171: 74–9.
18. Hasler WL. Dumping syndrome. Curr Treat Options Gastroenterol 2002; 5: 139–45.
19. Vecht J, Masclee AA, Lamers CB. The dumping syndrome: current insights into pathophysiology, diagnosis, and treatment. Scand J Gastroenterol 1997; 223 (Suppl): 21–7.
20. Belachew M, Legrand M, Vincent V, et al. Laparoscopic adjustable silicone gastric banding in the treatment of morbid obesity: a preliminary report. Surg Endosc 1994; 8: 1354–6.
21. Kunath U, Susewind M, Klein S, Hofmann T. Success and failure in laparoscopic gastric banding: a report of 3 years experience. Chirurg 1998; 69: 180–5.
22. Westling A, Bjurling K, Ohrvall M, Gustavsson S. Silicone-adjustable gastric banding: disappointing results. Obes Surg 1998; 8: 467–74.
23. Forsell P, Hallerback B, Glise H, Hellers G. Complications following Swedish adjustable gastric banding: a long-term follow-up. Obes Surg 1999; 9: 11–6.
24. Nehoda H, Weiss H, Labeck B, et al. Results and complications after adjustable gastric banding in a series of 250 patients. Am J Surg 2001; 181: 12–5.
25. Heal DJ, Aspley S, Prow MR, et al. Sibutramine: a novel anti-obesity drug—a review of the pharmacological evidence to differentiate it from d-amphetamine and d-fenfluramine. Int J Obes Relat Metab Disord 1998; 22 (Suppl): 18–28.
26. Garattini S, Mennini T, Bendotti C, et al. Neurochemical mechanism of action of drugs which modify feeding via the serotonergic system. Appetite 1986; 7 (Suppl): 15–38.
27. Rich JM, Njo L, Roberts KW, Smith P. Unusual hypotension and bradycardia in a patient receiving fenfluramine, phentermine, and fluoxetine. Anesthesiology 1997; 88: 529–31.
28. McNeely W, Goa KL. Sibutramine: a review of its contribution to the management of obesity. Drugs 1998; 56: 1093–124.
29. Bray GA, Greenway FL. Current and potential drugs for treatment of obesity. Endocr Rev 1999; 20: 805–75.
30. McMahon F, Fujioka K, Singh B, et al. Efficacy and safety of sibutramine in obese white and African-American patients with hypertension: a one-year, double-blind, placebo-controlled, multicenter trial. Arch Intern Med 2000; 160: 2185–91.
31. Apfelbaum M, Vague P, Ziegler O, et al. Long-term maintenance of weight loss after a very low-calorie diet: a randomized blinded trial of the efficacy and tolerability of sibutramine. Am J Med 1999; 106: 179–84.
32. Hadvary P, Lengsfeld H, Wolfer H. Inhibition of pancreatic lipase in vitro by the covalent inhibitor tetrahydrolipostatin. Biochem J 2000; 256: 357–61.
33. Davidson M, Hauptman J, DiGirolamo M, et al. Weight control and risk factor reduction in obese subjects treated for 2 years with orlistat. JAMA 1999; 281: 235–42.
34. Hauptman J, Lucas C, Boldrin M, et al. Long-term treatment of obesity in primary care settings. Arch Fam Med 2000; 9: 160–7.
35. Sjöström L, Rissanen A, Andersen T, et al. Randomized placebo-controlled trial of orlistat for weight loss and prevention of weight regain in obese patients. Lancet 1998; 352: 167–72.
36. Valsecia ME, Malgor LA, Farias EF, et al. Interaction between orlistat and antihypertensive drugs. Ann Pharmacother 2001; 35: 1495–6.
37. Persson M, Vitols S, Yue QY. Orlistat associated with hypertension. BMJ 2000; 321: 87.
38. Johnston GD. Orlistat associated with hypertension: digit preference lays conclusions about orlistat open to doubt [letter]. BMJ 2001; 322: 110.
39. Gotfredsen A, Westergren-Hendel H, Andersen T. Influence of orlistat on bone turnover and body composition. Int J Obes Relat Metab Disord 2001; 25: 1154–60.
40. Scheen AJ. Results of obesity treatment. Ann Endocrinol 2002; 63: 163–70.
41. Clain DJ, Lefkowitch JH. Fatty liver disease in morbid obesity. Gastroenterol Clin North Am 1987; 16: 239–52.
42. Ramsey-Stewart G. Hepatic steatosis and morbid obesity. Obes Surg 1993; 3: 157–9.
43. Palmer M, Schaffner F. Effect of weight reduction on hepatic abnormalities in overweight patients. Gastroenterology 1990; 99: 1408–13.
44. Albert S, Borovicka J, Thurnheer M, et al. Pre- and post-operative transaminase changes within the scope of gastric banding in morbid obesity. Schweiz Rundsch Med Prax 2001; 90: 1459–64.
45. Gholam PM, Kotler DP, Flancbaum LJ. Liver pathology in morbidly obese patients undergoing Roux-en-Y gastric bypass surgery. Obes Surg 2002; 12: 49–51.
46. Cheymol G. Effects of obesity on pharmacokinetics: implications for drug therapy. Clin Pharmacokinet 2000; 39: 215–31.
47. Marik P, Varon J. The obese patient in the ICU. Chest 1998; 113: 492–8.
48. Ribstein J, duCailar G, Mimran A. Combined renal effects of overweight and hypertension. Hypertension 1995; 26: 610–5.
49. Brochner-Mortensen J, Rickers H, Balslev I. Renal function and body composition before and after intestinal bypass operation in obese patients. Scand J Clin Lab Invest 1980; 40: 695–702.
50. Brenner BM. Hemodynamically mediated glomerular injury and the progressive nature of kidney disease. Kidney Int 1983; 23: 647–55.
51. Davis RL, Quenzer RW, Bozigian HP, Warner CW. Pharmacokinetics of ranitidine in morbidly obese women. DICP 1990; 24: 1040–3.
52. Stokholm KH, Brochner-Mortensen J, Hoilund-Carlsen PF. Increased glomerular filtration rate and adrenocortical function in obese women. Int J Obes 1980; 4: 57–63.
53. Dionne RE, Bauer LA, Gibson GA, et al. Estimating creatinine clearance in morbidly obese patients. Am J Hosp Pharm 1981; 38: 841–4.
54. Nauser TD, Stites SW. Diagnosis and treatment of pulmonary hypertension. Am Fam Physician 2001; 63: 1789–98.
55. Schiller NB. Pulmonary artery pressure estimation by Doppler and two-dimensional echocardiography. Cardiol Clin 1990; 8: 277–87.
56. Widimsky J. Noninvasive diagnosis of pulmonary hypertension in chronic lung diseases. Prog Respir Res 1985; 20: 69–75.
57. Konduri GG, Garcia DC, Kazzi NJ, et al. Adenosine infusion improves oxygenation in term infants with respiratory failure. Pediatrics 1996; 97: 295–300.
58. Stoelting RK, Dierdorf SF. Anesthesia and co-existing disease, 4th ed. Philadelphia: Churchill Livingstone, 2002.
59. Consensus conference: fresh-frozen plasma—indications and risks. JAMA 1985; 253: 551–3.
60. Derzie AJ, Silvestri F, Liriano E, Benotti P. Wound closure technique and acute wound complications in gastric surgery for morbid obesity: a prospective randomized trial. J Am Coll Surg 2000; 191: 238–43.
61. Culver DH, Horan TC, Gaynes RP, et al. Surgical wound infection rates by wound class, operative procedure and patient risk index: National Nosocomial Infections Surveillance System. Am J Med 1991; 91 (Suppl): 152–7.
62. Monteforte MJ, Turkelson CM. Bariatric surgery for morbid obesity. Obes Surg 2000; 10: 391–401.
63. Kellum JM, DeMaria EJ, Sugerman HJ. The surgical treatment of morbid obesity. Curr Probl Surg 1998; 35: 791–858.
64. Pories WJ, Swanson MS, McDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg 1995; 222: 339–50.
65. Fisher A, Waterhouse TD, Adams AP. Obesity: its relation to anaesthesia. Anaesthesia 1975; 30: 633–47.
66. Blaszyk H, Wollan PC, Witkiewicz AK, Björnsson J. Death from pulmonary thromboembolism in severe obesity: lack of association with established genetic and clinical risk factors. Virchows Arch 1999; 434: 529–32.
67. Blaszyk H, Björnsson J. Factor V Leiden and morbid obesity in fatal postoperative pulmonary embolism. Arch Surg 2000; 135: 1410–3.
68. Kakkar VV, Howe CT, Nicolaides AN, et al. Deep vein thrombosis of the leg: is there a ”high risk“ group? Ann Surg 1970; 120: 527–32.
69. Pineo GF, Hull RD. Unfractionated and low-molecular weight heparin: comparison and current recommendations. Med Clin North Am 1998; 82: 587–99.
70. Scholten DJ, Hoedema RM, Scholten SE. A comparison of two different prophylactic dose regimens of low molecular weight heparin in bariatric surgery. Obes Surg 2002; 12: 19–24.
71. Kalfarentzos F, Stavropoulou F, Yarmenitis S, et al. Prophylaxis of venous thromboembolism using two different doses of low-molecular weight heparin (nadroparin) in bariatric surgery: a prospective randomized trial. Obes Surg 2001; 11: 670–6.
72. Bergquist D, Eldor A, Thorlacius-Ussing O, et al. Efficacy and safety of enoxaparin versus unfractionated heparin for prevention of deep vein thrombosis in elective cancer surgery: a double-blind randomized multicenter trial with venographic assessment. Br J Surg 1997; 84: 1099–103.
73. Wu EC, Barba CA. Current practices in the prophylaxis of venous thromboembolism in bariatric surgery. Obes Surg 2000; 10: 7–13.
74. Olympic Vac-Pac®
: current sales and instruction manual. Seattle, WA: Olympic Medical, 2002.
75. Jupiter JB, Ring D, Rosen H. The complications and difficulties of nonunion in the severely obese. J Orthop Trauma 1995; 9: 363–70.
76. Sawyer RJ, Richmond MN, Hickey JD, Jarratt JA. Peripheral nerve injuries associated with anaesthesia. Anaesthesia 2000; 55: 980–91.
77. Warner MA, Warner ME, Martin JT. Ulnar neuropathy: incidence, outcome, and risk factors in sedated or anesthetized patients. Anesthesiology 1994; 81: 1332–40.
78. Coşkun F. Anesthesia for gynecologic laparoscopy. J Am Assoc Gynecol Laparosc 1999; 6: 245–58.
79. Chui PT, Gin T, Oh TE. Anaesthesia for laparoscopic surgery. Anaesth Intensive Care 1993; 21: 163–71.
80. Kashtan J, Green JF, Parsons EQ, Holcroft JW. Hemodynamic effects of increased abdominal pressure. J Surg Res 1981; 30: 249–55.
81. Harman PK, Kron IL, McLachlan HD, et al. Elevated intraabdominal pressure and renal function. Ann Surg 1982; 196: 594–7.
82. Rosen DM, Chou DC, North L, et al. Femoral venous blood flow during laparoscopic gynecologic surgery. Surg Laparosc Endosc Percutan Tech 2000; 10: 158–62.
83. Cunningham AJ, Brull SJ. Laparoscopic cholecystectomy: anesthetic implications. Anesth Analg 1993; 76: 1120–33.
84. Sprung J, Whalley DG, Falcone T, et al. The impact of morbid obesity, pneumoperitoneum, and posture on respiratory system mechanics and oxygenation during laparoscopy. Anesth Analg 2002; 94: 1345–50.
85. Maxwell MH, Waks AU, Schroth PC, et al. Error in blood pressure measurement due to incorrect cuff size in obese patients. Lancet 1982; 2: 33–6.
86. Mann GV. The influence of obesity on health. N Engl J Med 1974;291:178–85, 226–32.
87. Emerick DR. An evaluation of non-invasive blood pressure (NIBP) monitoring on the wrist: comparison with upper arm NIBP measurement. Anaesth Intensive Care 2002; 30: 43–7.
88. Block FE, Schulte GT. Ankle blood pressure measurement, an acceptable alternative to arm measurements. Int J Clin Monit Comput 1996; 13: 167–71.
89. McCarroll SM, Saunders PR, Brass PJ. Anesthetic considerations in obese patients. Prog Anesthesiol 1989; 3: 1–12.
90. Brodsky JB, Lemmens HJM, Brock-Utne JG, et al. Morbid obesity and tracheal intubation. Anesth Analg 2002; 94: 732–6.
91. Jung D, Mayersohn M, Perrier D, et al. Thiopental disposition in lean and obese patients undergoing surgery. Anesthesiology 1982; 56: 269–74.
92. Servin F, Farinotti R, Haberer JP, et al. Propofol infusion for maintenance of anesthesia in morbidly obese patients receiving nitrous oxide: a clinical and pharmacokinetic study. Anesthesiology 1993; 78: 657–65.
93. Adams JP, Murphy PG. Obesity in anaesthesia and intensive care. Br J Anaesth 2000; 85: 91–108.
94. Greenblatt DJ, Abernethy DR, Locniskar A, et al. Effect of age, gender, and obesity on midazolam kinetics. Anesthesiology 1984; 62: 27–35.
95. Schwartz AE, Matteo RS, Ornstein E, et al. Pharmacokinetics and pharmacodynamics of vecuronium in the obese surgical patient. Anesth Analg 1992; 74: 515–8.
96. Puhringer FK, Khuenl-Brady KS, Mitterschiffthaler G. Rocuronium bromide: time-course of action in underweight, normal weight, overweight, and obese patients. Eur J Anaesthesiol 1995; 11 (Suppl): 107–10.
97. Puhringer FK, Keller C, Kleinsasser A, et al. Pharmacokinetics of rocuronium bromide in obese female patients. Eur J Anaesthesiol 1999; 16: 507–10.
98. Weinstein JA, Matteo RS, Ornstein E, et al. Pharmacodynamics of vecuronium and atracurium in the obese surgical patient. Anesth Analg 1988; 67: 1149–53.
99. Varin F, Ducharme J, Theoret Y, et al. Influence of extreme obesity on the body disposition and neuromuscular blocking effect of atracurium. Clin Pharmacol Ther 1990; 48: 18–25.
100. Schwartz AE, Matteo RS, Ornstein E, et al. Pharmacokinetics of sufentanil in obese patients. Anesth Analg 1991; 73: 790–3.
101. Egan TD, Huizinga B, Gupta SK, et al. Remifentanil pharmacokinetics in obese versus lean patients. Anesthesiology 1998; 89: 562–73.
102. Minto CF, Schnider TW, Shafer SL. Pharmacokinetics and pharmacodynamics of remifentanil. II. Model application. Anesthesiology 1997; 86: 24–33.
103. Blouin RA, Warren GW. Pharmacokinetic considerations in obesity. J Pharm Sci 1999; 88: 1–7.
104. Abernethy DR, Greenblatt DJ, Divoll M, Shader RI. Prolonged accumulation of diazepam in obesity. J Clin Pharmacol 1983; 23: 369–76.
105. Abernethy DR, Greenblatt DJ, Smith TW. Digoxin disposition in obesity: clinical pharmacokinetic investigation. Am Heart J 1981; 102: 740–4.
106. Christoff PB, Conti DR, Naylor C, Jusko WJ. Procainamide disposition in obesity. Drug Intell Clin Pharm 1983; 17: 516–22.
107. Deleted in proof.
108. Juvin P, Vadam C, Malek L, et al. Postoperative recovery after desflurane, propofol, or isoflurane anesthesia among morbidly obese patients: a prospective randomized study. Anesth Analg 2000; 91: 714–9.
109. Sollazzi L, Perilli V, Modesti C, et al. Volatile anesthesia in bariatric surgery. Obes Surg 2001; 11: 623–6.
110. Torri G, Casati A, Albertin A, et al. Randomized comparison of isoflurane and sevoflurane for laparoscopic gastric banding in morbidly obese patients. J Clin Anesth 2001; 13: 565–70.
111. Luce MJ. Respiratory complications of obesity. Chest 1980; 78: 626–31.
112. De Divitiis O, Fazio S, Pettito M, Petitto M. Obesity and cardiac function. Circulation 1981; 64: 477–82.
113. Rexrode KM, Manson JE, Hennekens CH. Obesity and cardiovascular disease. Curr Opin Cardiol 1996; 11: 490–5.
114. Buckley FP, Robinson NB, Simonowitz DA. Anaesthesia in the morbidly obese: a comparison of anaesthetic and analgesic regimens for upper abdominal surgery Anaesthesia 1983; 38: 840–51.
115. Nguyen NT, Lee SL, Goldman C, et al. Comparison of pulmonary function and postoperative pain after laparoscopic versus open gastric bypass: a randomized trial. J Am Coll Surg 2001; 192: 469–76.
116. Michaloudis D, Fraidakis O, Petrou A, et al. Continuous spinal anesthesia/analgesia for perioperative management of morbidly obese patients undergoing laparotomy for gastroplastic surgery. Obes Surg 2000; 10: 220–9.
117. Cooper JR, Brodsky JB. Anesthetic management of the morbidly obese patient. Semin Anesth 1987; 6: 260–70.
118. Bardoczky GI, Yernault JC, Houben JJ, d’Hollander AA. Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anesthesia. Anesth Analg 1995; 81: 385–8.
119. Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema: respective effects of high airway pressure, high tidal volume and positive end-expiratory pressure. Am Rev Respir Dis 1988; 137: 1159–64.
120. Söderberg M, Thomson D, White T. Respiration, circulation, and anesthetic management in obesity: investigation before and after jejuno-ileal bypass. Acta Anaesthesiol Scand 1977; 21: 55–61.
121. Øberg B, Poulsen TD. Obesity: an anesthetic challenge. Acta Anaesthesiol Scand 1996; 40: 191–200.
122. Sugerman HJ. Pulmonary function in morbid obesity. Gastroenterol Clin North Am 1987; 16: 225–37.
123. Schafer H, Ewig S, Hasper E, Luderitz B. Failure of CPAP therapy in obstructive sleep apnea syndrome: predictive factors and treatment with bilevel-positive airway pressure. Respir Med 1998; 92: 208–15.
124. Joris JL, Sottiaux TM, Chiche JD, et al. Effect of bi-level positive airway pressure (BiPAP) nasal ventilation on the postoperative pulmonary restrictive syndrome in obese patients undergoing gastroplasty. Chest 1997; 111: 665–70.
125. Huerta S, DeShields S, Shpiner R, et al. Safety and efficacy of postoperative continuous positive airway pressure to prevent pulmonary complications after Roux-en-Y gastric bypass. J Gastrointest Surg 2002; 6: 354–8.
126. Yao F-SF, Savarese JJ. Morbid obesity. In: Yao F-SF, ed. Anesthesiology: problem oriented patient management. Philadelphia: Lippincott-Raven, 1998: 1001–18.
127. Byrne TK. Complications of surgery for obesity. Surg Clin North Am 2001; 81: 1181–93.
128. Overend TJ, Anderson CM, Lucy SD, et al. The effect of incentive spirometry on postoperative pulmonary complications: a systematic review. Chest 2001; 120: 971–8.
129. Celli BR, Rodriguez KS, Snider GL. A controlled trial of intermittent positive pressure breathing, incentive spirometry, and deep breathing exercises in preventing pulmonary complications after abdominal surgery. Am Rev Respir Dis 1984; 130: 12–5.
130. Fox GS, Whalley DG, Bevan OR. Anaesthesia for the morbidly obese: experience with 110 patients. Br J Anaesth 1981; 53: 811–6.
131. Rawal N, Sjöstrand U, Christofferson E, et al. Comparison of intramuscular and epidural morphine for postoperative analgesia in the grossly obese: influence on postoperative ambulation and pulmonary function. Anesth Analg 1984; 63: 583–92.
132. Gelman S, Laws HL, Potzick J, et al. Thoracic epidural vs. balanced anesthesia in morbid obesity: an intraoperative and postoperative hemodynamic study. Anesth Analg 1980; 59: 902–8.
133. Otsu I, Thirlby RC, Allen HW. Patient controlled thoracic epidural analgesia after gastric bypass surgery for morbid obesity [abstract]. Reg Anesth Pain Med 2001; 26: A117.
134. Carli F, Trudel JL, Belliveau P. The effect of intraoperative thoracic epidural anesthesia and postoperative analgesia on bowel function after colorectal surgery: a prospective, randomized trial. Dis Colon Rectum 2001; 44: 1083–9.
135. Goulding ST, Hovell BC. Anesthetic experience with vertical banded gastroplasty. Br J Anaesth 1995; 75: 301–6.
136. Choi YK, Brolin RE, Wagner BK, et al. Efficacy and safety of patient-controlled analgesia for morbidly obese patients following gastric bypass surgery. Obes Surg 2000; 10: 154–9.
137. IBSR 2000–2001 winter pooled report. Iowa City: International Bariatric Surgery Registry, 2001: 7–15.
This article has been cited 2 time(s).
Obesity SurgeryRapid Weight Loss Is Associated with Preoperative Hypovolemia in Morbidly Obese PatientsObesity Surgery
Obesity SurgeryMorbid Obesity and Optimization of Preoperative Fluid TherapyObesity Surgery
© 2002 International Anesthesia Research Society