Adrian Alvarez
Juan C. Cendan
Throughout the economically developed world, the incidence of obesity is rising at epidemic proportions. University medical centers are reporting that 25% of routine surgical patients are obese, and at least 10% of all patients are morbidly obese. Given the increasing prevalence of obesity in the general population, it is not surprising that many morbidly obese patients undergoing surgery are treated in intensive care units (ICU). Nevertheless, the real prevalence of critically ill morbidly obese patients, even in the United States, is not known. A retrospective study has allowed researchers to estimate that the incidence rate of morbidly obese patients requiring nonsurgical intensive care treatment approaches 14 cases per 1,000 ICU admissions annually. Bariatric surgical procedures alone have increased in the United States from 37,000 cases in 2000 up to 200,000 in 2006 as reported by the American Society for Bariatric Surgery (1).
The critically ill morbidly obese surgical patient presents the critical care team with many unique problems (2). As a result, every health care provider eventually involved in surgical procedures must be familiar with the management of morbidly obese patients, not only for bariatric procedures, but also for all types of surgery (3,4). Morbidly obese patients have an eightfold higher mortality rate after blunt trauma than nonobese patients presenting with the same diagnosis (5). Retrospective reviews of morbidly obese patients—hospitalized with or without ICU requirements—have shown significant increases in length of ICU stay, mortality, and duration of mechanical ventilation (6,7,8,9).
The pathophysiologic consequences of obesity involve all major organ systems (10). Conditions such as diabetes mellitus and hyperlipidemia are associated with obesity and contribute to chronic morbidity in the obese. However, the main concerns for the intensivist, anesthesiologist, and surgeon have been the same for over three decades: the derangements of the cardiopulmonary system (11,12).
The perioperative care of these patients must be understood as a continuous, indivisible, and dynamic process that requires multidisciplinary involvement from surgeons, anesthesiologists, internists, and intensivists. Collaborative and coordinated activity within the surgical team is vital in these scenarios involving the morbidly obese (13). In this chapter, we will discuss cardiac and respiratory diseases in the morbidly obese patient undergoing a surgical procedure, following the above-mentioned focus, from preoperative assessment to postoperative care.
Specific Surgical Issues
Obese patients undergoing emergency general surgery are particularly challenging for the team managing the patient before and after surgery. These patients occasionally present with more advanced disease than otherwise might be expected due to the obesity causing delays in diagnosis.
The first decision to be made is whether or not the procedure can be performed laparoscopically, or if an open procedure is required. Where possible, it has been our practice to perform emergency surgery laparoscopically in obese patients; there is evidence to support this approach for laparoscopic appendectomy and cholecystectomy. However, these patients require an additional level of expertise in the operating theater, not only from the surgeon and anesthesiologist, but also from the equipment handlers and the assistants. Colon cases and other cases involving more complicated visceral dissection may be detrimental if performed laparoscopically.
Obese patients are at higher risk for wound infection. The worst-case scenario develops when an obese patient eviscerates in the postoperative period. Emergent management will require closure, but this may not be technically feasible. These patients may require leaving the abdomen “open” with packing, and the patient will generally be intubated and paralyzed until the abdominal contents can be reduced or sufficient granulation develops that allows the construct to stabilize.
Cardiovascular Considerations in the Morbidly Obese
Cardiovascular diseases are common in obese individuals, and manifest as ischemic heart disease, hypertension, and cardiac failure. Cardiovascular disease is reported in 37% of adults with a body mass index (BMI) greater than 30 kg/m2, 21% with a BMI of 25 to 30 kg/m2, and only 10% in those with a BMI less than 25 kg/m2. Obesity—defined as a BMI of greater than or equal to 30 kg/m2—has been observed to be an independent risk factor for the development of hypertension. The Framingham Heart Study suggests that 65% of the risk for hypertension in women and 78% of the risk in men can be related to obesity (14). Interestingly, mortality rates were reported to be 3.9 times greater in the overweight group versus the normal-weight group participating in the Framingham study (15).
The relationship between the increase in blood pressure and the risk of cardiovascular disease is considered to be independent of other risk factors. The chances of myocardial infarction, heart failure, stroke, and kidney disease are all greater as a patient's blood pressure increases (16). Obesity is also well recognized as a risk factor for ischemic heart disease. Many obese individuals also suffer from “metabolic syndrome,” which has a strong association as being a precursor in the development of diabetes, cardiovascular disease, and increased mortality rates from cardiovascular disorders. There is also a 5% increased risk of heart failure for men and 7% for women associated with each unit of increase in body mass (15).
Preoperative Considerations
Pathophysiology
In morbidly obese patients, blood volume, cardiac output, systemic and pulmonary artery pressures, and left and right ventricular pressures are all elevated (17,18). These changes manifest clinically as arterial hypertension and, with advancing age, one may note ischemic heart disease and right–left heart failure (19). The incidence of pre-existing, often severe, cardiovascular disease in morbidly obese patients scheduled for elective bariatric surgery is reported to be as great as 20% (20,21). It is the complex interaction of hypertension, ischemic heart disease, and pulmonary hypertension that contribute to the development of global cardiac dysfunction and exacerbates congestive heart failure. This clinical situation is referred to as “obesity cardiomyopathy.”
Arterial Hypertension
The pathogenesis of obesity-related hypertension is complex. There is a continuous relationship between body mass index and systolic/diastolic blood pressures (22,23). Blood pressure is normally regulated by a series of feedback loops (baroreceptors) and by the secretion of vasoactive hormones—renin, angiotensin, aldosterone, and catecholamines. A derangement in any of these feedback loops may lead to hypertension.
Many factors act together to promote vasoconstriction, sodium retention, and volume overload in obesity, and are noted in Table 102.1 (24,25,26,27,28). In the long term, these changes cause glomerular injury, ultimately leading to glomerulosclerosis. A review of 7,000 renal biopsies between the years 1990 and 2000 showed a 10-fold increase in obesity-related glomerulopathy (glomerulomegaly and glomerulosclerosis). Prolonged obesity may lead to a gradual loss of nephron function that worsens with time and exacerbates hypertension (29). Hypertension contributes to a pressure overload of the heart, as well as an expansion of extracellular and blood volume combining to create a volume overload.
Other variables that may also lead to hypertension in obese patients include leptin, free fatty acids, and insulin, which stimulate sympathetic activity and vasoconstriction (24). Furthermore, obesity-induced insulin resistance and endothelial dysfunction may act as amplifiers of the vasoconstrictor response. Obstructive sleep apnea (OSA), which also is more prevalent in obese patients, leads to periods of apnea and hypoxia, triggering a chemoreceptor response, which causes sympathetic activation (24,30,31).
|
Table 102.1 Factors that act together to promote vasoconstriction, sodium retention, and volume overload in the obese patient |
||
|
Ischemic Heart Disease
Obesity is a recognized risk factor for ischemic heart disease (19,32). The risk is proportional to the duration of obesity and distribution of fat. A habitually overweight individual is less likely to be at risk than individuals who exhibit continuous weight gain, and individuals with a central distribution of fat are more at risk than individuals with a peripheral distribution. Additionally, hypertension, diabetes, hypercholesterolemia, and increased levels of low-density lipoproteins (LDLs), which are common in obese patients, further increase the risk of coronary stenosis. Nevertheless, more than 40% of obese patients with angina do not have significant coronary artery disease (30,33,34). Angina would then be attributable to the oxygen supply/demand imbalance due to cardiac hypertrophy and other factors. In the morbidly obese, myocardial oxygen consumption is higher than in normal-weight adults. The ventricular cavity dimension is enlarged due to a chronically augmented preload. An enhanced sympathetic activity and subsequent arterial hypertension and/or increased heart rate promote higher wall tension and ventricular systolic stress. In addition, the ventricular wall is commonly hypertrophic (35,36,37,38,39). Patients suffering chronic hypoxemia (pickwickian syndrome, obesity hypoventilation syndrome, and obstructive sleep apnea syndrome) frequently develop secondary polycythemia and, subsequently, elevated blood viscosity. In these patients, due to the higher blood viscosity, the contractility is augmented, which consequently increases myocardial oxygen requirements (40).
It may be assumed that morbidly obese patients are at a higher risk of myocardial ischemia. In these subjects, reducing myocardial oxygen consumption and ensuring the maximum possible oxygen delivery to the heart must be a major therapeutic target.
Cardiac Failure
There is an increased risk of heart failure of 5% for men and 7% for women per each unit of increase in body mass (15). There is a linear relationship between body weight and cardiac weight gain attributed to concentric and eccentric hypertrophy. This event is secondary to pressure overload, which is due to arterial hypertension and possibly increased blood viscosity. In obese patients, circulating blood volume, plasma volume, and cardiac output increase proportionately with rising weight. For a patient with a fat mass of 50 kg, blood flow to this fat mass accounts for an extra cardiac output of 1.5 to 2.0 L/minute, resulting in both ventricular enlargement and an increase in stroke volume. The hypertrophy that ensues subsequently contributes to a reduction in cardiac compliance and left ventricular diastolic function, which leads to increased left ventricular end-diastolic pressure and possible pulmonary edema (41).
In long-standing obesity, systolic function might be reduced if hypertrophy is unable to keep pace with the increasing demand. A decrease in midwall fiber shortening and a decrease in ejection fraction may thus become evident in developing “obesity cardiomyopathy.” The right ventricle can also exhibit hypertrophy secondary to pulmonary hypertension due to obstructive sleep apnea and subsequent chronic hypoxemia and hypercapnia.
Preoperative Evaluation and Optimization for Surgery
A significant percentage of obese patients who present for intermediate- to high-risk noncardiac surgery is likely to have cardiovascular disease. It is imperative to know if any related impairment actually exists. If so, assessment of its severity, decisions on whether or not any therapeutic measures can be taken prior to surgery, and consideration of any extra intraoperative or postoperative monitoring are of utmost importance for effective treatment of the obese patient.
Arterial Hypertension
The preoperative assessment, optimization, and treatment of arterial hypertension in the obese patient are guided by the same principles as in the nonobese patient. Urgent and emergent surgeries should be evaluated on a case-by-case basis, and aggressive control of blood pressure in the perioperative period is vital.
Acute hypertensive episodes and hypertensive emergencies should also be approached as they would be in the nonobese, but with the strong recommendation for meticulous and adequate monitoring. Careful drug titration is required due to the particular hemodynamic liability of this population, coupled with the fact that for obvious reasons, pharmacokinetics and dynamics might be altered.
In current clinical practice, measurement of blood pressure may be difficult, even to the point of deciding where to make the measurement. Obese individuals—especially women—tend to have a conical shape of the upper arm, termed gynoid obesity, and accurate measurement of blood pressure is difficult with conventional cuffs. As an alternative, the cuff can be placed around the forearm for more predictable cuff pressures. An increasing arm circumference is associated with miscalculation of blood pressure if standard-length cuffs are used. An appropriate-sized cuff that encompasses at least 80% of the arm should be used to ensure accurate measurement of blood pressure in an obese patient (42). If these maneuvers fail to result in adequate and reliable measurements, invasive blood pressure monitoring should then be considered as an alternative.
Ischemic Heart Disease and Cardiac Failure
To date, no specific cardiac risk index has been proposed for obese patients. Preoperative cardiac assessment of obese patients follows the same sequence as for lean patients, and for that reason, the American College of Cardiology/American Heart Association (ACC/AHA) guidelines are thought to be valid for this population (43). However, the guidelines do not take into account the presence of multiple, intermediate, or minor risk factors that are frequently observed in the obese. The presence of multiple cardiac risk factors has been shown to increase the incidence of perioperative cardiac morbidity (44). In addition, surgical risk categories may be modified based on institutional expertise, which is highly dependent on clinical experience, surgical skills, anesthetic care, and nursing quality (45,46). In this regard, there is evidence to suggest significant differences between care and outcomes at different institutions for the same surgical procedure (46,47,48,49). In addition to careful appraisal of arterial hypertension and its consequences, a comprehensive cardiac evaluation in obese patients should focus on assessing both cardiac function and the presence and severity of ischemic heart disease. Evaluation of cardiac function by clinical signs can be extremely difficult in the obese and, for that reason, objective evaluation of ejection fraction and cardiac function by echocardiography and/or left ventriculography is usually necessary.
The ACC/AHA recommendation for preoperative noninvasive evaluation of left ventricular function includes patients with current or poorly controlled heart failure, patients with a history of heart failure, and patients with dyspnea of unknown origin—an extremely frequent finding within this population.
Despite the fact that no randomized study has been performed in obese patients to determine the utility of routine evaluation of right and left ventricular function, it is very probable that such evaluation, guided by symptoms prior to intermediate- and high-risk surgery, will be helpful in guiding intraoperative and postoperative management of obese patients.
Evaluation for ischemic heart disease requires stress testing, although there is no consensus on which type of stress test is optimal. The choice among the various noninvasive tests must be made based on local preferences. The patient's weight must be taken into account not only for logistical reasons—as many diagnostic devices have significant weight limitations—but also because the effect of the patient's body habitus has long been recognized as a factor that may reduce the accuracy of myocardial perfusion studies (50,51).
The first decision to be made is whether or not patients can exercise sufficiently to obtain 85% of predicted maximal heart rate. If they cannot, then a pharmacologic stress test is better indicated (e.g., stress echocardiography after dobutamine or atropine administration [DSE] or a dipyridamole thallium nuclear imaging study [DTS]) (52). Patients who have positive stress test results will require coronary angiography.
If cardiac catheterization is indicated, patient weight has to be taken into account because some tables used to perform this study have weight limits as low as 300 lb. Despite the concerns raised by the size of the patients, cardiac catheterization is considered safe in these patients. Fifty-five percent of the time, cardiac catheterization results in negative findings; when positive, medical management, interventional cardiology therapy, or even cardiac bypass surgery may be indicated (52).
Once ischemic heart disease has been identified and its severity quantified in the morbidly obese patient, three therapeutic options are available prior to elective noncardiac surgery:
· Revascularization by surgery (coronary artery bypass grafting [CABG])
· Revascularization by percutaneous coronary intervention (PCI)
· Optimized medical management (typically with β-blockers or α2-agonists)
There is no irrefutable evidence that indications for preoperative cardiac revascularization are any different for obese patients than for nonobese patients.
Coronary Artery Bypass Grafting
Still a controversial topic, some studies suggest that moderately and morbidly obese patients have a higher rate of deep sternal wound infection, renal failure, prolonged postoperative hospital stay, and operative mortality after coronary artery bypass surgery (53,54,55).
Coronary revascularization is guided by the patient's cardiac condition—that is, is there unstable angina, left main coronary artery disease (CAD), three-vessel disease, decreased left ventricular (LV) function, and/or left anterior descending artery disease?—as well as by the added risk of the coronary intervention and the potential consequences of delaying the noncardiac surgery for recovery after the cardiac intervention (56). It has been demonstrated that when indicated, patients undergoing coronary revascularization prior to major-risk noncardiac surgery did better postoperatively. Comparing this population of preoperatively revascularized patients with those medically managed suggests that the latter patient group had a mortality rate two times higher than the former (57,58).
Percutaneous Coronary Intervention
Evidence suggests that patients who underwent angioplasty prior to elective noncardiac surgery had better outcomes (59,60,61,62). However, angioplasty is now often accompanied by stenting, with postprocedure antiplatelet therapy to prevent acute coronary thrombosis and maintain long-term patency of the intervened vessel. It is strongly suggested that elective noncardiac surgery should be delayed for 4 to 6 weeks after PCI with stenting to allow for complete endothelialization of the stent and completion of aggressive antiplatelet therapy with glycoprotein (GP) IIb/IIIa inhibitors (63).
The introduction of drug-eluting stents may obviate the need for such prolonged systemic anticoagulation, thus allowing patients to undergo noncardiac surgery sooner. The complication rate of PCI in obese patients has not been reported to be different than in nonobese individuals, and similar precautions should also be taken in morbidly obese patients (64).
Medical Management
Perioperative use of β-blockers has been shown to be efficacious in reducing perioperative morbidity and mortality (65,66,67,68). The ACC/AHA guidelines recommend initiating β-blockers as early as possible prior to high-risk surgery and titrating the patient's heart rate to 60 bpm (43). Perioperative β-blocker use is recommended for patients with one or more Revised Cardiac Index risk factors despite a negative stress test and for patients with two minor risk factors, even with a good functional status and/or a negative noninvasive stress test (43,67).
Many morbidly obese patients are already receiving β-blocker therapy when they present for their preoperative assessment. β-Blockers have been used intraoperatively to control hemodynamics, intraoperative ischemia, and cardiac arrhythmias (65). Some studies investigating their prophylactic role have demonstrated decreased intraoperative ischemia (69).
The general consensus appears to be that if β-blockers are indicated perioperatively, they should be given not only intraoperatively but, more appropriately, they should be initiated during the preoperative period and—except in the presence of significant contraindications—should be continued through the postoperative period. The pharmacokinetics of β-blockers are affected by obesity, and there exists significant pharmacodynamic variability. The dosage of β-blockers should be initiated based on lean body mass and then titrated until the desired clinical effect is achieved (70,71).
Intraoperative Considerations
Mechanics
Surgical beds are now available that accommodate patients weighing as much as 500 kg. However, these patients require tremendous preparation on behalf of the operative staff. Even with appropriate beds, the obese patient can be at high risk for falling during sudden motion. This situation can be extremely dangerous to the patient and the supporting staff alike. Institution of a lift team and the availability of both “bean” bags and bed extensions in order to keep the folds of pannus stable are of the utmost importance to the surgical team, and have already become widely used in accredited surgical facilities. Finally, institutional investments in lifting equipment such as ceiling-mounted lifts and beds that oscillate and/or transform into chairs may be necessary to fully deploy the necessary mechanical advantage to care for the obese patient.
Rhabdomyolysis
Rhabdomyolysis is often described in the obese patient. This scenario generally follows prolonged operations and presents as dark urine, representing muscle necrosis from groups on the flanks or buttock. Also termed pressure-induced myoglobinuria, this is more commonly noted among patients with diabetes mellitus (72,73). It is generally attributed to lying on a hard surface, and has been frequently associated with an exaggerated lithotomy position in the operating theater (74). To handle this situation, attending staff should initiate aggressive hydration and monitor creatine phosphokinase (CPK). If CPK exceeds 5,000 IU/L, staff must initiate diuresis with mannitol and alkalinize the urine with sodium bicarbonate (75,76). Acute renal failure may develop, but recovery of renal function is generally expected.
|
Table 102.2 Most frequent and prominent risks of the morbidly obese patient undergoing surgery |
|
|
Anesthetic Technique
No randomized, controlled trial provides unquestionable evidence that one or another anesthetic technique is best for the morbidly obese. Total intravenous anesthesia (TIVA) and inhalational, regional, and combined general/epidural or general/spinal anesthetics have been used safely in these individuals (77,78,79,80,81). Selecting one technique over another will depend upon:
· Patient's clinical status
· Type of surgery the patient requires
· Expertise of the senior anesthesiologist
· Availability of institutional resources
· Patient's verbal and/or written requests and consent
What must be absolutely clear are the pathophysiologic alterations and subsequent risks presented in each individual case. This should guide the physician to define the intraoperative goals. Considering only the potential impairments of the cardiovascular and respiratory systems, we must highlight the potential risks and recommended anesthetic goals.
The classic, most frequent and prominent risks of the morbidly obese patient undergoing surgery are listed in Table 102.2. Accordingly, the basic anesthetic goals should be (77):
· Hemodynamically smooth and rapid induction
· Rapid access and securing of the airway
· Prominent attention paid to hemodynamic stability
· A high level of analgesia to avoid increments in catecholamine activity
· Rapid recovery and early ambulation
Postoperative Considerations
Logistic and Technical Issues
The main diagnostic and therapeutic principles related to cardiovascular diseases and/or complications commonly observed in the ICU setting—such as arrhythmias, cardiac failure, hypertensive or ischemic episodes, and so forth—do not differ significantly when comparing the morbidly obese with lean patients. Therefore, a detailed discussion is not warranted. Nevertheless, we will highlight the few—but in our eyes important—differences to consider when presented with a morbidly obese surgical patient in the ICU setting.
Pathophysiologic Principles for a Rational Therapeutic Approach
Obesity has been likened to “exercise,” that is, a constant state of “exercise.” The morbidly obese patient's cardiovascular system is continuously overdemanded, even at rest, mainly because of chronic intravascular volume overload, blood hyperviscosity, and sympathetic hyperactivity. These are components of a “dysfunctional compensating mechanism,” which tries to satisfy the increased metabolic rate imposed by the excessive adipose tissue. The resulting eccentric left ventricular hypertrophy (LVH) is associated with a reduced LV compliance, causing elevation of LV filling pressure in many morbidly obese persons (18,82).
The additional increase in cardiac output promoted by any perioperative stress may markedly increase LV filling pressure, often exceeding the threshold for pulmonary edema. Respiratory disease, especially obstructive sleep apnea syndrome (OSAS) and the obesity hypoventilation syndrome (OHS), acting on the pulmonary circulation may affect the right heart cavities as well. The heart of a morbidly obese patient may have less tolerance to any kind of cardiovascular stress—hypovolemia, hypervolemia, hypertension, hypotension, and so forth—and is at a higher risk of organ failure. Consequently, the appropriate diagnostic and therapeutic measures should be applied as soon and as accurately as possible to avoid systemic hypoperfusion and inadequate oxygen delivery, which may predispose to multiple organ system failure.
Importance of Coupled Cardiorespiratory Function
It is vital to maintain the best possible ventilation/perfusion (V/Q) balance, since V/Q mismatch is a prominent mechanism that can trigger respiratory and subsequent cardiac dysfunction in the morbidly obese surgical patient. In mechanically ventilated, morbidly obese patients, airway pressure may be elevated. Additionally, morbid obesity is associated with volume and pressure overload. Volume load conditions may fluctuate according to patient positioning. For example, changing position from the “physiologically ideal” reverse Trendelenburg to the supine position can significantly increase venous blood return to the heart and, as a result, augment cardiac output, pulmonary capillary wedge pressure, and mean pulmonary artery pressure, potentially increasing the risk of acute heart failure (83); one would expect this maneuver to increase airway pressure as well due to the increased weight of the chest.
Compression of the inferior vena cava may reduce venous return to the heart, and is thus a possible mechanism of hypotension. This can be avoided by tilting the operating room table or ICU bed by placing a wedge under the patient. These maneuvers are similar to those performed during caesarean section to reduce the pressure of the gravid uterus on the inferior vena cava (84). Considering that the reverse Trendelenburg position significantly improves cardiac and respiratory performance, it should be maintained during the entire perioperative period unless there is a particular contraindication.
Drug Dosing
The distribution, metabolism, protein binding, and clearance of many drugs are altered by the physiologic changes associated with obesity (85,86,87). In addition, the patient's underlying disease may substantially influence the pharmacokinetic properties of a drug (88). The net pharmacologic alteration in any patient is, therefore, often uncertain, especially in those suffering from morbid obesity. Nevertheless, for a number of drugs used in the ICU—most notably digoxin, aminophylline, aminoglycosides, and cyclosporine—drug toxicity may occur if the patients are dosed based on their actual, rather than ideal or adjusted, body weight (70,85,87,89,90,91). For drug dosing, with few exceptions, it is advisable to base drug calculations on ideal body weight (IBW) rather than real weight, and then adjust doses through meticulous monitoring (92).
Respiratory Considerations in the Morbidly Obese
The higher morbidity and mortality of hospitalized obese patients may be related to the increased pulmonary complications with which morbidly obese patients present (93). In the postoperative state, obese individuals are at increased risk of developing atelectasis, aspiration, ventilatory failure, and pulmonary embolism (93).
Clinicians caring for morbidly obese patients must be aware of the significant physiologic changes associated with their obesity, such as reduced lung volumes, increased work of breathing, and alterations in control of breathing and gas exchange. Many factors are involved including, but not limited to, BMI, patient's age, duration of obesity, fat distribution (central or peripheral), and the strong association of certain disorders such as OSAS, OHS, and pickwickian syndrome. In addition, obesity itself has a major detrimental impact on the respiratory system (94).
Preoperative Considerations
Respiratory Disorders
Obstructive Sleep Apnea Syndrome
Morbid obesity is the most common and major risk factor for OSAS (95). While its prevalence in the general U.S. population is 2% to 4%, this increases to 40% to 78% in the morbidly obese (95,96,97,98,99). Notwithstanding these facts, it is thought that 80% to 90% of American sleep apnea sufferers are undiagnosed (100,101).
The detection of OSAS among obese surgical patients is vital for several reasons:
· Obese patients are more sensitive to the depressant effects of hypnotics and opioids (102). Perioperative administration may lead to life-threatening respiratory complications (103,104), especially in face of pre-existing OSAS.
· OSAS is associated with difficult laryngoscopy and mask ventilation (104,105,106,107).
· Obese patients have, in general, a diminished expiratory reserve volume (ERV) with, consequently, reduced oxygen stores; this promotes faster development of desaturation after apnea (108).
If OSAS is present, these effects become exaggerated. The combination of these factors sets the stage for an airway catastrophe, not only during induction of general anesthesia, but also during tracheal extubation, and especially if an emergent intubation becomes necessary in the ICU or during intra- or interhospital transfer.
Obesity Hypoventilation Syndrome
Some obese patients suffer from a disorder characterized by chronic daytime hypoventilation, also known as obesity hypoventilation syndrome (109). These individuals are typically extremely obese, with a BMI greater than 40 kg/m2, and the likelihood of OHS increases as the BMI increases. OHS is associated with chronic daytime hypoxemia—with a PaO2 less than 65 mm Hg—and hypercapnia (107,108,110). It is essential to find out if the obese patient suffers from chronic daytime hypoxemia, as this is a better predictor of pulmonary hypertension and cor pulmonale than the presence and/or severity of OSAS (111,112,113).
Pickwickian Syndrome
Patients suffering OHS who additionally have signs and symptoms of cor pulmonale are termed pickwickian—from the Charles Dickens novel, The Pickwick Papers—and they have an increased perioperative morbidity and mortality (93).
Respiratory Insufficiency
Obesity per se is not a common cause for chronic respiratory insufficiency (109). Significant respiratory dysfunction is more common when chronic obstructive pulmonary disease (COPD) and obesity coexist. When respiratory insufficiency is present, impairment of gas exchange is greater than expected from a simple summation of the alterations caused by each pathophysiologic process (114).
Simple Obesity
Obese patients with minimal or no coexisting pulmonary conditions are classified as “simple” obesity patients. The pathophysiology of simple obesity consists of alterations in daytime gas exchange and pulmonary function, and may result from compression and restriction of the chest wall and diaphragm by excess adipose tissue (115). The ERV and functional residual capacity (FRC) are particularly affected, being reduced to 60% to 80% of normal, respectively.
If ERV decreases below the alveolar closing volume, then airway closure occurs during normal tidal breathing, and dependent alveoli are relatively or completely underventilated. As a consequence, V/Q mismatch, pulmonary shunt, and daytime hypoxemia results. One may see, in formerly obese patients after massive weight loss, a marked improvement in the PaO2 and alveolar–arterial oxygen gradient; thus, this improvement is directly proportional to the increase in the ERV (116,117).
Other mechanisms may further impair respiratory function. Sleep apnea in the obese is usually obstructive, secondary to airway narrowing from abundant peripharyngeal adipose tissue, and an abnormal decrease of upper airway muscle tone during rapid eye movement (REM) sleep (95). Hypopneic and apneic events lead to arousal from REM sleep, oxyhemoglobin desaturation, and sympathetic nervous system activation in response to hypoxemia. This may explain the strong association between OSA and systemic hypertension (118). The precise pathophysiologic mechanism of OHS is unclear (93,109).
Of most importance is that vital capacity, reduced to 90% of normal in simple obesity, decreases to 60% of normal in OHS. This reflects a profound and important decrement in lung volumes in OHS, as compared with simple obesity patients. Thus, one may see:
· A marked increase in distal airway resistance
· A more profound abnormality in V/Q matching
· A more significant impact on the PaO2
· A larger A–a gradient in patients with OHS
Supine positioning further reduces lung volume and, as a result, increases the magnitude of all these alterations (107,115,119).
Diaphragmatic function is also affected due to overstretching and cephalad displacement resulting from increased intra-abdominal pressure. All of these factors combined may lead to chronic respiratory muscle fatigue and the chronic hypoventilation characteristic of OHS (93).
Venous Thromboembolism
Perioperative venous thromboembolism (VTE) occurs in 0.2% to 2.4% of bariatric patients receiving thromboprophylaxis (120). According to the Chest Consensus Statement, obese patients in the ICU will generally fall into either the high or highest risk categories in which, if left untreated, the risk of deep venous thrombosis (DVT) ranges from 20% to 80%. The risk of clinical pulmonary embolus (PE) ranges from 2% to 10%, and fatal PE occurs in 0.4% to 5% of patients (121).
The obese population in the surgical ICU requires thromboprophylaxis; however, the best regimen is not clear. Multiple variables are worthy of mention in regard to this matter. Venous stasis ulcers are more common in the obese, and in turn, are associated with DVT. Prophylactic inferior vena cava filters can be considered, but may also be technically difficult in the heaviest patients. Sequential compression devices (SCDs) are generally recognized as a useful adjunct but, again, may be limited by the patient size. The adequacy of pedal pumps is not clear. Unfractionated or low-molecular-weight heparins are both viable options, though precise dosing regimens and duration of dosage have emerged largely from uncontrolled trials. There are reports in the bariatric literature that 40 mg of enoxaparin every 12 hours may provide better thromboprophylaxis than 30 mg every 12 hours; however, this recommendation came from a retrospective report that coincided with significant changes in patient mobilization and improvements in overall hospital length of stay. It is not clear if it was these improvements in overall patient mobility or the change in medication administered that led to the improved VTE rates (122).
Evaluation and Optimization for Surgery
In simple obesity, preoperative assessment of respiratory function should be similar to that indicated in the assessment of lean and healthy patients. More extensive pulmonary function tests and preoperative treatment may be necessary for the obese patient who smokes or has pulmonary symptoms.
Elements of the history and physical examination can be as important—indeed, more important—as preoperative testing. Obese patients who habitually snore and report daytime somnolence and/or have suffered breath interruptions during sleep should be evaluated with polysomnography, since it is the definitive diagnostic test for OSAS (95). However, morbid obesity and symptoms of OSA are not, per se, indications for preoperative pulmonary function testing and room air arterial blood gas (ABG) analyses. These tests have failed to demonstrate predictive values and/or lead to the optimization of postoperative management or outcomes of bariatric surgery patients, and are not routinely indicated (103,123,124,125). Room air pulse oximetry in both the upright and supine positions may be a useful, noninvasive method for screening patients for daytime hypoxemia. A supine room air SpO2 less than 96% may merit further investigation. An elevated hematocrit may also be a clue of chronic hypoxemia.
If clinical evidence of OHS is present, ABG analyses are indicated because of chronic daytime hypoxemia—PaO2 less than 65 mm Hg, but especially sustained hypercapnia—a PaCO2 greater than 45 mm Hg—in the morbidly obese patient without significant obstructive pulmonary disease is diagnostic for this syndrome.
One must differentiate whether morbid obesity coexists with either OHS or COPD. These combinations often result in chronic daytime hypoxemia and increase the chances for pulmonary hypertension, right ventricular hypertrophy, and/or right ventricular failure. Assessment of these pickwickian patients may require extensive testing to guide preoperative medical optimization and postoperative management, given that their morbidity and mortality rate is increased (93,102,126).
It is unclear if it is appropriate to delay bariatric surgery for aggressive optimization of airway status and oxygenation with continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) therapy. Rennotte et al. observed no major postoperative respiratory complications in 14 patients treated with nasal CPAP for up to 3 weeks prior to surgery (127). Two to three weeks may be necessary not only to maximize medical benefits, but also to allow sufficient time for patients unfamiliar with CPAP or BiPAP therapy to acclimate to the nocturnal use of the device. Three weeks of nightly CPAP treatment prior to bariatric surgery improved left ventricular ejection fraction and afterload in obese patients with coexisting heart failure (128). Eight weeks of preoperative nasal CPAP therapy may be required to treat hypertension secondary to OSA (129).
Intraoperative Considerations
Airway Management
It is still a debatable issue whether or not morbid obesity should be considered a risk factor for difficult airway management. Brodsky et al. observed that neither absolute obesity nor BMI was associated with problematic intubation in morbidly obese patients. They also concluded that only a large neck circumference and a Mallampati score of 3 or more were significantly correlated with a high probability of problematic intubation (130). In our opinion, preoperative airway assessments should be similar in both morbidly obese and lean patients.
Whether or not morbid obesity is considered a risk factor for intubation, issues related specifically to the patient's BMI that impact airway management include:
· Preoxygenation
· Positioning
· Immediate availability to adequate resources, both technical and human (technical: special laryngoscopes, blades, tracheal tubes, oro- and nasopharyngeal cannulae, intubating laryngeal airway [ILA], LMA Fastrach, Combitube, etc.; human: personnel sufficient in both number and expertise) In the perioperative setting, one never knows when an emergent tracheal intubation or reintubation may be necessary, or when an unpredicted difficult mask ventilation and difficult tracheal intubation combination may appear. Indeed, the latter is a common situation in morbidly obese patients suffering from OSAS or OHS. The presence of any of these urgent/emergent events—taking into account the reduced time to hypoxemia after apnea and possible increased risk for gastric aspiration in morbidly obese individuals—will likely result in a life-threatening, although preventable/treatable, respiratory misadventure.
In our opinion, the same American Society of Anesthesiologists algorithm for difficult airway management and indications for conscious tracheal intubation should be considered for both obese and lean patients. If conscious intubation is indicated, it must be remembered that most episodes of gastroesophageal reflux, and the greatest potential for pulmonary aspiration of gastric contents, occur from and during “bucking” on an endotracheal tube; consequently, appropriate preparation of the patient is crucial (131,132).
Meticulous patient explanation, a low infusion rate of remifentanil (0.05 µg/kg IBW/minute) to avoid loss of response to verbally required active ventilation, and/or local anesthesia—such as bilateral blockade of the internal branch of the glossopharyngeal nerve—have shown to be the most effective and safest induction alternative (77). Finally, although somewhat controversial, it is prudent to treat morbidly obese patients with prophylactic measures against gastric aspiration, such as cimetidine, ranitidine, Bicitra, and/or metoclopramide (133); the timing of administration of these agents is, of course, of great significance.
Preoxygenation and Position
Hypoxemia during induction of general anesthesia in obese individuals is, and must be, a real concern for the anesthesiologist and/or intensivist. These patients may experience rapid arterial oxygen desaturation after apnea (134). Compared with supine-positioned obese patients, preoxygenation in the 25- to 30-degree head-up position with 100% oxygen for 3 minutes achieves higher oxygen tensions—in other words, more time and better oxygenation for intubation and airway control, given that as the BMI increases, it has been shown that the amount of time for desaturation in the patient decreases (135). Preoxygenation in the 30-degree reverse-Trendelenburg position provides a longer, safer apnea period than the 30-degree semi-Fowler and supine positions. Consequently, the Trendelenburg position has been recommended as the optimal position for induction of general anesthesia in obese patients (136). The head-up position results in an unloading of the intra-abdominal contents from the diaphragm; thus, pulmonary compliance and FRC increase, and oxygenation returns toward baseline values, as compared to the same patients who were placed in the supine position (137).
Prior to induction of general anesthesia in any setting—whether the operating room, the ICU, or on the hospital floor—the obese patient should be positioned with pillows under the shoulders, with the head and upper body elevated in a semirecumbent or reverse Trendelenburg position. This “ramped” position is strongly recommended in the morbidly obese, as it improves pulmonary function, oxygenation, cardiovascular function, conditions for mask ventilation, laryngoscopic view, and tracheal intubation (130). Extremely obese patients should never be allowed to lie completely flat. Their upper body should be constantly elevated at 25 to 30 degrees in the perioperative period.
Atelectasis
In the perioperative setting, reduction of chest wall and diaphragmatic muscle tone following the induction of general anesthesia and skeletal muscle relaxation impairs oxygenation. In simple obesity, the net effect may reduce ERV and FRC to less than 50% of preinduction values, excluding even more alveoli from effective gas exchange (115). As reduction of ERV and FRC increases exponentially with increasing BMI, the combination of these factors predisposes the morbidly obese patient to suffer atelectasis not only during anesthesia and surgery, but also in the postoperative period. The importance of this topic will be developed in the postoperative section.
Mechanical Ventilation: Invasive Positive Pressure Ventilation
Respiratory physiology must be taken into account when considering mechanical ventilation. Oxygen consumption and carbon dioxide production increase due to a higher metabolic rate promoted by excessive fat and an augmented workload on supportive tissues (138). Normocapnia is maintained by increased minute ventilation. Regarding mechanics, total compliance of the respiratory system declines exponentially with increasing BMI, as do FRC, ERV, and total lung capacity (139). Clinical correlates of these changes are increased work of breathing, small airway closure, ventilation/perfusion mismatch, pulmonary shunt, and hypoxemia. Sedation, anesthesia, and positioning supine further reduce FRC in the obese as compared to nonobese subjects, and consequently worsen respiratory performance (140).
Considering these factors, the initial tidal volume should be based on ideal body weight rather than actual body weight, and adjustments made according to airway pressures and appropriate respiratory monitoring (141). As lung volumes are reduced and airway resistance is increased, a tidal volume based on the patients' actual body weight would probably result in high airway pressures, alveolar overdistention, and barotrauma. Some data suggest, as a lung-protective strategy, the use of smaller tidal volumes and adequate positive end-expiratory pressure (PEEP)/CPAP (142) to prevent airway closure (143). Although this technique may result in decreased cardiac output, fluid loading will correct the problem. Additionally, in an attempt to improve ventilator–patient synchrony and reduce airway pressure, the patient's spontaneous respiratory effort should be maintained and assisted with pressure support ventilation as needed (144).
Tracheal Extubation and Intrahospital Transfer
As a result of the increased work of breathing and impaired respiratory mechanics, morbid obesity has been associated with prolonged mechanical ventilation, extended weaning periods, and longer ICU and hospital lengths of stay (6). Strategies suggested for facilitating the weaning process include positioning of the patient in a 45-degree reverse Trendelenburg position—thus optimizing lung mechanics, increasing tidal volume, and reducing respiratory rate (145)—and BiPAP post extubation (146).
If hemodynamic stability has been achieved, the trachea should be extubated with the patient's upper body elevated between 30 and 45 degrees. The patient should be transferred from the operating room while in a semirecumbent or tilted reverse Trendelenburg position (147). As obese patients have greater reduction in lung volumes than normal-weight counterparts following abdominal surgery (115), it comes as no surprise that the recovering patient should be kept in a head-up position in order to minimize intrapulmonary shunting (148). On days 1 and 2 postoperatively, a change from the semi-recumbent to the supine position may result in significant decreases in PaO2. Consequently, obese patients should convalesce in the semirecumbent position while receiving supplemental oxygen (148), if at all possible. Intrahospital transfer of a morbidly obese patient is best and most safely accomplished if the patient remains in his or her own hospital bed.
Ideal FiO2 (Supplemental Oxygen)
It should go without saying that one uses the highest concentration of oxygen necessary to maintain life. Nonetheless, high oxygen concentrations have often been associated with atelectasis formation and recurrence (149). In order to avoid this consequence, using as low an oxygen concentration as possible has been recommended. When 100% oxygen is delivered, shunt increases significantly due to atelectasis development, while with 30% oxygen delivery, shunt and atelectasis are minimal (150). Finally, without any preoxygenation, no atelectasis develops after induction (151,152), although there may be other problems unrelated to atelectasis.
Nevertheless, supplemental oxygen carries clear benefits for patients, especially the morbidly obese. There is evidence that suggests that an FiO2 of 0.8 ensures appropriate oxygenation without increasing the risk of absorptive atelectasis, reduces the incidence of postoperative nausea and vomiting (PONV) in patients with an increased risk of gastric aspiration, and improves the host's defense mechanisms against infection. The improvement can be seen not only in the wound site, but also in the respiratory system (153,154,155,156). Although not proven in morbidly obese surgical patients, this possible benefit should not be ignored. Ideal FiO2 should, then, result from a balance between a supplemental quantity of oxygen that is sufficient enough to avoid hypoxemia, reduce postoperative infections, and reduce PONV, but not so high as to facilitate the development and maintenance of atelectasis.
Our recommendation is to deliver 100% oxygen before induction of anesthesia to retard the development of hypoxemia after apnea and, once tracheal intubation is confirmed, reduce the FiO2 to 0.8, if possible, according to respiratory monitoring.
Monitoring
FRC is reduced in the morbidly obese patient; if it drops below closing capacity (CC), the dependent small airways will collapse, promoting:
· Ventilation/perfusion mismatch
· Gas exchange deterioration
· An increase in the shunt fraction
· An increase in the alveolar–arterial oxygen gradient
Consequently, the more obese the patient—the greater will be the alveolar–arterial gas difference, in other words, the less the expiratory gas measurements will correlate with arterial blood gas analysis.
A morbidly obese patient will not be able to reach the same PaO2/FiO2 ratio as the normal-weight patient, even if higher inspiratory oxygen concentrations are delivered. Morbid obesity decreases the arterial oxygenation index even further, yet leaves PaCO2 values unaffected if the patient does not suffer from either OHS or pickwickian syndrome (115); this effect is mainly due to intrapulmonary shunts in the atelectatic-dependent lung areas. In this scenario, arterial blood gas analysis becomes increasingly important because blood gases reflect the respiratory status more accurately than expiratory gas measurements. This does not mean that morbidly obese patients routinely require invasive or special monitoring of respiration (157), but morbid obesity, the presence of comorbidities, and the type of surgery, among other factors, should influence the decision of which monitoring devices need be used. Routine noninvasive monitoring will be sufficient in simple obesity cases, while the presence of OSAS, OHS, pickwickian syndrome, daytime hypoxemia, and/or associated COPD should alert the anesthesiologist or intensivist to modify not only the intra- and postoperative respiratory monitoring, but also narcotic use (158). It is a good practice to obtain pulse oximetry or even arterial blood gas analysis values in the awake obese patient prior to any anesthetic premedication in order to obtain a reference reading, and thereby allow a comparison of preoperative values with intra- and postoperative values.
Anesthesia and controlled mechanical ventilation will almost always have a negative impact on oxygenation and alveolar ventilation. In surgeries where large fluid shifts occur, long intraoperative hypotensive episodes are possible, and satisfactory tissue oxygenation cannot be assessed by pulse oximetry or PaO2 alone. In these cases, decreasing pH values or increasing anionic gap or lactate values may be indicative of inadequate oxygen delivery (159). Inadequate oxygen delivery may be reflected in increased, and sometimes “unexplained,” postoperative complications. The degree and duration of postoperative surveillance depend on the surgical intervention, the course of anesthesia, and the patient's condition. Monitoring should at least include pulse oximetry, respiratory rate, cardiac rhythm monitoring, and blood pressure measurement in the immediate postoperative period. In patients with decreasing oxygen saturations, ABG analysis and chest radiographs may be useful in sorting out the differential diagnosis. Sudden onset of respiratory distress, chest pain, and dyspnea may be indicative not only of a cardiac event, but also of pulmonary embolism; most mortality in the 30-day postoperative period after bariatric surgery is due to pulmonary embolism (160).
Obese patients have increased risk of respiratory-related complications in the postoperative period. In one study, the overall rate of critical respiratory events in obese patients was 3% (8). Interestingly, however, another study showed no significant increase of adverse perioperative events, even in patients with confirmed OSAS when the levels of wakefulness were carefully maintained (161). This reflects the importance of the anesthetic and analgesic management on the speed and quality of recovery of central nervous system (CNS) function. It is of utmost importance to take this into account when considering the anesthetic/analgesic strategy. Combined thoracic epidural/general anesthesia techniques may be quite suitable in these major cases.
Patients with confirmed or suspected OSAS, OHS, and pickwickian syndrome require more stringent observation. In the postoperative period, this may warrant prolonged surveillance in the postanesthesia care unit or even admission to the ICU in selected cases, especially in those with surgery lasting for more than 4 hours and in patients with critical comorbidities. The main reasons for ICU admission in morbidly obese patients are disturbances in pulmonary gas exchange, which can be prevented by more prolonged one-on-one surveillance combined with meticulous medical care (162).
Postoperative Considerations
Hypoxemia and Associated Postoperative Respiratory Disorders
Following major open abdominal surgery without postoperative oxygen supplementation, even normal patients experience hypoxemia (SpO2 less than 90%) (163). On the first postoperative day following open bariatric surgery, 75% of morbidly obese patients had a PaO2 less than 60 mm Hg, which usually persisted and worsened in the following days (12). Many clinical processes may be suggested to explain this phenomenon. The most frequently observed is atelectasis, but pulmonary aspiration of oral or gastric secretions, pneumonia, acute lung injury, and acute respiratory distress syndrome (ARDS) should also be considered as possible and relatively common respiratory complications of postsurgical morbidly obese patients.
Finally, it is important to remember tracheal tube displacement as a mechanism of perioperative hypoxemia. Abdominal insufflation, as well as changes in operating room table position—usually to the Trendelenburg position—can cause cephalad movement of the diaphragm, and can lead to migration of an initially correctly positioned endotracheal tube (164,165). This phenomenon in morbidly obese patients undergoing laparoscopy can result in right endobronchial intubation and intraoperative hypoxemia. This mechanism should be considered in the intubated ICU patient because of the frequent, necessary changes in the patient's position during care (166).
Atelectasis
General anesthesia may impair pulmonary gas exchange, and consequently decrease oxygenation in the general population; atelectasis is a major cause of this kind of impairment (167,168,169,170). Alterations in respiratory mechanics induced by general anesthesia, such as decreased chest wall and lung compliance, and a reduction in functional residual capacity promote atelectasis in nonobese patients. Conscious morbidly obese patients already have prominent alterations of their respiratory mechanics (171), and these patients are, in fact, particularly prone to intra- and postoperative atelectasis. During general anesthesia, as well as during the immediate postoperative period, morbidly obese patients are more likely to have significant impairment of pulmonary gas exchange and respiratory mechanics (115,172,173). Thus, it has been noted, even before the induction of anesthesia, that morbidly obese patients had more atelectasis, expressed in the percentage of the total lung area, than nonobese patients. After tracheal decannulation, atelectasis increased in both groups, but remained significantly more severe in the morbidly obese. Finally, 24 hours postoperatively, a complete re-expansion of the lung parenchyma occurred in nonobese patients, while the amount of atelectasis remained unchanged in the morbidly obese (94).
|
Table 102.3 Vital measures to prevent or reduce the severity and duration of atelectasis in the obese patient |
||
|
The increased atelectasis found in morbidly obese patients explains, at least partially, postoperative pulmonary complications. Various mechanisms have been suggested for the development of atelectasis in the morbidly obese, such as lung parenchyma compression, absorption of alveolar gas in completely or partially collapsed airways, and alterations in surfactant production, function, and/or distribution (174). Our conclusion is that all possible measures to prevent or reduce the severity and duration of atelectasis in this patient population are vital and are listed in Table 102.3.
While some bariatric groups use noninvasive positive pressure ventilation (NIPPV) routinely in the postoperative care of morbidly obese patients immediately after extubation, others are reluctant because of the fear of anastomotic disruption; there are no data to support this concern. Commonly, morbidly obese patients use some form of NIPPV (CPAP or BiPAP) chronically for the treatment of OSA. Postoperatively, morbidly obese patients are at risk for prolonged depressant effects of the drugs administered during surgery. This situation may promote airway collapse not only in those morbidly obese patients with diagnosed OSAS and already under preoperative treatment, but also in previously undiagnosed morbidly obese patients (175,176). Airway collapse is most frequent during REM sleep, which is brief in the initial postoperative period, but significantly longer on the third to fifth postoperative nights. The risk for airway collapse increases even days after surgery. This means that oximetric monitoring and supplementary oxygen must continue to be administered during this dangerous period (177).
A prospective study of 1,067 bariatric patients evaluated the risk of developing anastomotic leaks and pulmonary complications after gastric bypass. Of the 1,067 patients, 420 had OSAS and 159 were dependent on CPAP. There were 15 major anastomotic leaks, two of which occurred in CPAP-treated patients. No correlation between CPAP utilization and incidence of major anastomotic leakage was demonstrated. No episodes of pneumonia were diagnosed in either group. Based on this study, the conclusion was that CPAP is a useful modality for treating hypoventilation after gastric bypass surgery without increasing the risk of developing postoperative anastomotic leaks (178).
Regarding BiPAP, it appears that when used prophylactically during the first 24 hours postoperatively, it significantly reduces pulmonary dysfunction after gastroplasty in morbidly obese patients and accelerates the re-establishment of preoperative pulmonary function (146).
Pulmonary Aspiration
Even though many mechanisms were classically associated with an increased risk of gastric content aspiration in the morbidly obese, this topic remains controversial. While it is still recommended to take precautions against acid aspiration, massive pulmonary aspiration in morbidly obese patients is a rare event in current anesthesia practice, and the occurrence of unwitnessed “microaspirations” in the postoperative period is difficult to assess because of the diagnostic problems observed within this population (144). While massive aspiration is uncommon, the following cautionary list should be carefully noted:
· While in bed, the patient must be adequately positioned in a semirecumbent or reverse Trendelenburg position at all times.
· The care team must be ready for bag-valve-mask ventilation and tracheal intubation in a ramped position, as well as have technical and adequate human resources.
· Drug dosing must be meticulously titrated according to monitoring parameters and clinical response, and based on the IBW.
· Consider the importance of a sufficient and safe analgesic strategy. It will improve the tolerance and cooperation of the patient with the therapeutic measures required for an expeditious recovery.
Radiographic Evaluation and Complications
Radiographic evaluation of the surgically obese patient is complicated and made difficult by the weight limitations of modern scanners and the patient's inability to cooperate with the transfer. Several radiographic tests, including the upper gastrointestinal series, may require the patient to stand for extended periods of time. Although tomographic tables now routinely handle patients weighing 400 lb. (182 kg), these weight limits vary by institutional device. Surgeons and caregivers that are in a position to affect patient selection should consider this when planning operative interventions for obese patients. Further consideration for tables that handle heavier patients should be entertained when new equipment is being purchased. In the absence of excellent radiographic capabilities, these patients may require surgical exploration, and both patients and surgical team members must assume those additional risks.
Venous, Arterial, and Nutritional Access
Venous access is difficult in this population. When peripheral access is inadequate, the point of choice may be the jugular vein. Gilbert et al. found this location to have fewer complications and to require fewer conversions to different locations (179). Arterial access is generally recommended as noninvasive blood pressure cuffs can give inaccurate measurements in this patient population. Nutritional access in critically ill obese patients is imperative; despite their weight, these patients can be relatively malnourished. There is evidence from the trauma literature that obese patients preferentially mobilize protein instead of fats as compared to lean patients (180). As a result of this mobilization, the obese patient will need additional nutrition. Optimally, if the patient requires reoperative interventions, a feeding gastrostomy or jejunostomy can be placed. Although not impossible, achieving percutaneous gastric access can be extremely difficult, especially in a patient following a gastric bypass procedure. In these circumstances, it is a good time to reiterate the importance of communication between the surgical and critical care physicians and staff.
Analgesia
Overview
Acute pain can result in reduced tidal volume, vital capacity, functional residual capacity, and alveolar ventilation (181,182). These factors contribute to atelectasis, V/Q mismatch, hypoxemia, and hypercapnia. Pain-related muscle splinting interferes with the patient's ability to cough, clear secretions, and efficiently participate in chest physiotherapy, all of which increase the chances for pulmonary complications (182).
A major component of segmental and suprasegmental reflex responses is enhanced general sympathetic tones (183). Results of this tone are increased peripheral resistance, stroke volume, and heart rate, which lead to an increase in cardiac output. High blood pressure results in increased myocardial work and myocardial oxygen consumption (181). The rise in heart rate causes decreased diastolic filling time, possibly resulting in reduced oxygen delivery to the myocardium, with a risk of ischemia (181). All of these alterations could result in devastating respiratory and/or cardiovascular complications in at-risk individuals such as the morbidly obese, who commonly are at a higher risk of suffering variable degrees of impaired function affecting both systems.
Every health care provider knows that the efficacy of analgesia must be measured by the ability to cough and move without pain or discomfort, and not only by the absence of pain while in a resting state. All the potential consequences of poor pain control are serious problems in a general population, but they are of outstanding importance in the morbidly obese surgical patient. Early mobilization without discomfort should be considered a major anesthetic target in this population due to the fact that deep vein thrombosis and pulmonary embolism are some of the most frequent causes of mortality during the first 30 postoperative days. In addition, sufficient and safe postoperative pain control would result in a more effective and tolerable respiratory physiotherapy—a critical maneuver in this context—which would certainly reduce the possibilities for other respiratory complications such as atelectasis. Nevertheless, most morbidly obese patients with surgical pain do not receive adequate pain relief (184).
Analgesic Strategies (Intravenous, Thoracic Epidural, Multimodal Approach)
Unfortunately, uncertainty remains as to the superiority of one pain treatment modality versus another (185). Open versus laparoscopic surgical techniques, personal skills, and experience may influence the patient's and anesthesiologist's choice of pain treatment. Pain management strategies may offer specific advantages for specific patient outcomes, such as a reduced rate of pulmonary complications after abdominal surgery and superior pain control with thoracic epidural analgesia (TEA) (185,186,187,188). Postoperative epidural analgesia, using either local anesthetics or opioids, may be the route of choice for postoperative analgesia in morbidly obese patients, as it allows a more vigorous cough and chest physiotherapy, better diaphragmatic function, more powerful leg exercise, and earlier ambulation and discharge from hospital (11,189,190). These advantages may lead to a more benign postoperative course, as previously noted in other populations who had earlier walking, earlier feeding, a lower incidence of pulmonary alveolar collapse, and fewer thromboembolic complications (11,189,190). TEA can be improved by adding opioids and possibly epinephrine to the epidural solution (191,192).
Thoracic epidural anesthesia/analgesia may be particularly beneficial in the pathophysiologic context observed in morbid obesity. For example, left ventricular work conditions (both preload and afterload) may be improved by the sympathetic blockade, thus reducing the chances for developing heart failure (193,194). Myocardial oxygen balance may be improved as well due to a decrease in oxygen demand and augmented myocardial perfusion induced by coronary vasodilatation, both secondary to sympathetic block, thereby reducing the risk of ischemia (195,196,197,198,199,200,201,202). TEA does not affect chest wall compliance in the postsurgical state, and allows for better diaphragmatic function when compared with general anesthesia alone (190,203,204,205,206,207,208,209). Alterations in chest wall compliance and diaphragmatic performance can be considered major determinants of postoperative respiratory dysfunction in most patients, but especially in the morbidly obese after upper open abdominal procedures (182,210,211,212,213,214,215,216,217,218,219).
Regarding intravenous analgesia, improved efficacy and safety have been shown when patient-controlled anesthesia management includes adjunct analgesics such as nonsteroidal anti-inflammatory medications and local anesthetic wound infiltration in a multimodal approach (220,221). It must be remembered in the most emphatic way that a continuous and efficient analgesic scheme would certainly improve patient satisfaction and comfort, and very probably—even though still not proven in the morbidly obese—would reduce morbidity and mortality.
References
1. James PT, Leach R, Kalamara E, et al. The worldwide obesity epidemic. Obes Res. 2001;9(Suppl 4):228S–233S.
2. Marik FB. Management of the obese critically ill patient in intensive care unit. In: Alvarez A, ed. Morbid Obesity Peri-operative Management. Cambridge, UK: Cambridge University Press; 2004:363–368.
3. Dindo D, Muller MK, Weber M, et al. Obesity in general elective surgery. Lancet. 2003;361:2032–2035.
4. McTigue KM, Harris R, Hemphill B, et al. Screening and interventions for obesity in adults: summary of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2003;139:933–949.
5. Choban PS, Weireter LJ Jr, Maynes C. Obesity and increased mortality in blunt trauma. J Trauma. 1991;31:1253–1257.
6. El-Solh A, Sikka P, Bozkanat E, et al. Morbid obesity in the medical ICU. Chest. 2001;120:1989–1997.
7. Goldhaber SZ, Grodstein F, Stampfer MJ, et al. A prospective study of risk factors for pulmonary embolism in women. JAMA. 1997;277:642–645.
8. Rose DK, Cohen MM, Wigglesworth DF, et al. Critical respiratory events in the postanesthesia care unit. Patient, surgical, and anesthetic factors. Anesthesiology. 1994;81:410–418.
9. Yaegashi M, Jean R, Zuriqat M, et al. Outcome of morbid obesity in the intensive care unit. J Intensive Care Med. 2005;20:147–154.
10. Fontaine KR, Redden DT, Wang C, et al. Years of life lost due to obesity. JAMA. 2003;289:187–193.
11. Fox GS, Whalley DG, Bevan DR. Anaesthesia for the morbidly obese. Experience with 110 patients. Br J Anaesth. 1981;53:811–816.
12. Taylor RR, Kelly TM, Elliott CG, et al. Hypoxemia after gastric bypass surgery for morbid obesity. Arch Surg. 1985;120:1298–1302.
13. Friederich JA, Heyneker TJ, Berman JM. Anesthetic management of a massively morbidly obese patient. Reg Anesth. 1995;20:538–542.
14. Garrison RJ, Kannel WB, Stokes J III, et al. Incidence and precursors of hypertension in young adults: the Framingham Offspring Study. Prev Med. 1987;16:235–251.
15. Kenchaiah S, Evans JC, Levy D, et al. Obesity and the risk of heart failure. N Engl J Med. 2002;347:305–313.
16. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560–2572.
17. Whyte HM. Blood pressure and obesity. Circulation. 1959;19:511–516.
18. Alexander J. Obesity and cardiac performance. Am J Cardiol. 1964;14:860–865.
19. Kannel WB, LeBauer EJ, Dawber TR, et al. Relation of body weight to development of coronary heart disease. The Framingham study. Circulation. 1967;35:734–744.
20. Buckley FP, Robinson NB, Simonowitz DA, et al. Anaesthesia in the morbidly obese. A comparison of anaesthetic and analgesic regimens for upper abdominal surgery. Anaesthesia. 1983;38:840–851.
21. Dominguez-Cherit G, Gonzalez R, Borunda D, et al. Anesthesia for morbidly obese patients. World J Surg. 1998;22:969–973.
22. Jones DW, Kim JS, Andrew ME, et al. Body mass index and blood pressure in Korean men and women: the Korean National Blood Pressure Survey. J Hypertens. 1994;12:1433–1437.
23. Jones DW. Body weight and blood pressure. Effects of weight reduction on hypertension. Am J Hypertens. 1996;9:50s–54s.
24. Montani JP, Antic V, Yang Z, et al. Pathways from obesity to hypertension: from the perspective of a vicious triangle. Int J Obes Relat Metab Disord. 2002;26(Suppl 2):S28–38.
25. DiBona GF, Kopp UC. Neural control of renal function. Physiol Rev. 1997;77:75–197.
26. Engeli S, Sharma AM. The renin-angiotensin system and natriuretic peptides in obesity-associated hypertension. J Mol Med. 2001;79:21–29.
27. Dessi-Fulgheri P, Sarzani R, Tamburrini P, et al. Plasma atrial natriuretic peptide and natriuretic peptide receptor gene expression in adipose tissue of normotensive and hypertensive obese patients. J Hypertens. 1997;15:1695–1699.
28. Endre T, Mattiasson I, Berglund G, et al. Insulin and renal sodium retention in hypertension-prone men. Hypertension. 1994;23:313–319.
29. Hall JE. Mechanisms of abnormal renal sodium handling in obesity hypertension. Am J Hypertens. 1997;10:49S–55S.
30. Adams JP, Murphy PG. Obesity in anaesthesia and intensive care. Br J Anaesth. 2000;85:91–108.
31. Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA. 2003;290:1906–1914.
32. Hubert HB, Feinleib M, McNamara PM, et al. Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation. 1983;67:968–977.
33. McNulty PH, Ettinger SM, Field JM, et al. Cardiac catheterization in morbidly obese patients. Catheter Cardiovasc Interv. 2002;56:174–177.
34. Bahadori B, Neuer E, Schumacher M, et al. Prevalence of coronary artery disease in obese versus lean men with angina pectoris and positive exercise stress test. Am J Cardiol. 1996;77:1000–1001.
35. Alpert MA, Terry BE, Kelly DL. Effect of weight loss on cardiac chamber size, wall thickness and left ventricular function in morbid obesity. Am J Cardiol. 1985;55:783–786.
36. Kasper EK, Hruban RH, Baughman KL. Cardiomyopathy of obesity: a clinicopathologic evaluation of 43 obese patients with heart failure. Am J Cardiol. 1992;70:921–924.
37. Merlino G, Scaglione R, Paterna S, et al. Lymphocyte beta-adrenergic receptors in young subjects with peripheral or central obesity: relationship with central haemodynamics and left ventricular function. Eur Heart J. 1994;15:786–792.
38. Warnes CA, Roberts WC. The heart in massive (more than 300 pounds or 136 kilograms) obesity: analysis of 12 patients studied at necropsy. Am J Cardiol. 1984;54:1087–1091.
39. Alexander JK, Pettigrove JR. Obesity and congestive heart failure. Geriatrics. 1967;22:101–108.
40. Avellone G, Di G, V, Cordova R, et al. Coagulation, fibrinolysis and haemorheology in premenopausal obese women with different body fat distribution. Thromb Res. 1994;75:223–231.
41. Herrera MF, Oseguera J, Gamino R, et al. Cardiac abnormalities associated with morbid obesity. World J Surg. 1998;22:993–997.
42. Iyriboz Y, Hearon CM, Edwards K. Agreement between large and small cuffs in sphygmomanometry: a quantitative assessment. J Clin Monit. 1994;10:127–133.
43. Eagle KA, Brundage BH, Chaitman BR, et al. Guidelines for perioperative cardiovascular evaluation for noncardiac surgery. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). J Am Coll Cardiol. 1996;27:910–948.
44. Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100:1043–1049.
45. Pronovost PJ, Jenckes MW, Dorman T, et al. Organizational characteristics of intensive care units related to outcomes of abdominal aortic surgery. JAMA. 1999;281:1310–1317.
46. Dimick JB, Pronovost PJ, Cowan JA Jr, et al. Postoperative complication rates after hepatic resection in Maryland hospitals. Arch Surg. 2003;138:41–46.
47. Begg CB, Cramer LD, Hoskins WJ, et al. Impact of hospital volume on operative mortality for major cancer surgery. JAMA. 1998;280:1747–1751.
48. Hannan EL, O'Donnell JF, Kilburn H Jr, et al. Investigation of the relationship between volume and mortality for surgical procedures performed in New York State hospitals. JAMA. 1989;262:503–510.
49. Hannan EL. The relation between volume and outcome in health care. N Engl J Med. 1999;340:1677–1679.
50. Dunn RF, Wolff L, Wagner S, et al. The inconsistent pattern of thallium defects: a clue to the false positive perfusion scintigram. Am J Cardiol. 1981;48:224–232.
51. Goodgold HM, Rehder JG, Samuels LD, et al. Improved interpretation of exercise Tl-201 myocardial perfusion scintigraphy in women: characterization of breast attenuation artifacts. Radiology. 1987;165:361–366.
52. Brusco L Jr. Peri-operative risks and frequent complications. In: Alvarez A, ed. Morbid Obesity Peri-operative Management. Cambridge, UK: Cambridge University Press; 2004:13–23.
53. Kuduvalli M, Grayson AD, Oo AY, et al. Risk of morbidity and in-hospital mortality in obese patients undergoing coronary artery bypass surgery. Eur J Cardiothorac Surg. 2002;22:787–793.
54. Reeves BC, Ascione R, Chamberlain MH, et al. Effect of body mass index on early outcomes in patients undergoing coronary artery bypass surgery. J Am Coll Cardiol. 2003;42:668–676.
55. Prabhakar G, Haan CK, Peterson ED, et al. The risks of moderate and extreme obesity for coronary artery bypass grafting outcomes: a study from the Society of Thoracic Surgeons' database. Ann Thorac Surg. 2002;74:1125–1130.
56. Eagle KA, Berger PB, Calkins H, et al. ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery–Executive Summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg. 2002;94:1052–1064.
57. Eagle KA, Rihal CS, Mickel MC, et al. Cardiac risk of noncardiac surgery: influence of coronary disease and type of surgery in 3368 operations. CASS Investigators and University of Michigan Heart Care Program. Coronary Artery Surgery Study. Circulation. 1997;96:1882–1887.
58. Hassan SA, Hlatky MA, Boothroyd DB, et al. Outcomes of noncardiac surgery after coronary bypass surgery or coronary angioplasty in the Bypass Angioplasty Revascularization Investigation (BARI). Am J Med. 2001;110:260–266.
59. Allen JR, Helling TS, Hartzler GO. Operative procedures not involving the heart after percutaneous transluminal coronary angioplasty. Surg Gynecol Obstet. 1991;173:285–288.
60. Posner KL, Van Norman GA, Chan V. Adverse cardiac outcomes after noncardiac surgery in patients with prior percutaneous transluminal coronary angioplasty. Anesth Analg. 1999;89:553–560.
61. Elmore JR, Hallett JW Jr, Gibbons RJ, et al. Myocardial revascularization before abdominal aortic aneurysmorrhaphy: effect of coronary angioplasty. Mayo Clin Proc. 1993;68:637–641.
62. Gottlieb A, Banoub M, Sprung J, et al. Perioperative cardiovascular morbidity in patients with coronary artery disease undergoing vascular surgery after percutaneous transluminal coronary angioplasty. J Cardiothorac Vasc Anesth. 1998;12:501–506.
63. Wilson SH, Fasseas P, Orford JL, et al. Clinical outcome of patients undergoing non-cardiac surgery in the two months following coronary stenting. J Am Coll Cardiol. 2003;42:234–240.
64. Powell BD, Lennon RJ, Lerman A, et al. Association of body mass index with outcome after percutaneous coronary intervention. Am J Cardiol. 2003;91:472–476.
65. Akhtar S, Barash PG. Perioperative use of beta-blockers: past, present, and future. Int Anesthesiol Clin. 2002;40:133–157.
66. Zaugg M, Schaub MC, Pasch T, et al. Modulation of beta-adrenergic receptor subtype activities in perioperative medicine: mechanisms and sites of action. Br J Anaesth. 2002;88:101–123.
67. Auerbach AD, Goldman L. beta-Blockers and reduction of cardiac events in noncardiac surgery: clinical applications. JAMA. 2002;287:1445–1447.
68. Stevens RD, Burri H, Tramer MR. Pharmacologic myocardial protection in patients undergoing noncardiac surgery: a quantitative systematic review. Anesth Analg. 2003;97:623–633.
69. Wallace A, Layug B, Tateo I, et al. Prophylactic atenolol reduces postoperative myocardial ischemia. McSPI Research Group. Anesthesiology. 1998;88:7–17.
70. Cheymol G, Poirier JM, Carrupt PA, et al. Pharmacokinetics of beta-adrenoceptor blockers in obese and normal volunteers. Br J Clin Pharmacol. 1997;43:563–570.
71. Cheymol G. Effects of obesity on pharmacokinetics implications for drug therapy. Clin Pharmacokinet. 2000;39:215–231.
72. Bostanjian D, Anthone GJ, Hamoui N, et al. Rhabdomyolysis of gluteal muscles leading to renal failure: a potentially fatal complication of surgery in the morbidly obese. Obes Surg. 2003;13:302–305.
73. Torres-Villalobos G, Kimura E, Mosqueda JL, et al. Pressure-induced rhabdomyolysis after bariatric surgery. Obes Surg. 2003;13:297–301.
74. Guzzi LM, Mills LM, Greenman P. Rhabdomyolysis, acute renal failure, and the exaggerated lithotomy position. Anesth Analg. 1993;77:635–637.
75. Zager RA, Foerder C, Bredl C. The influence of mannitol on myoglobinuric acute renal failure: functional, biochemical, and morphological assessments. J Am Soc Nephrol. 1991;2:848–855.
76. Abassi ZA, Hoffman A, Better OS. Acute renal failure complicating muscle crush injury. Semin Nephrol. 1998;18:558–565.
77. Alvarez AO, Cascardo A, Albarracin MS, et al. Total intravenous anesthesia with midazolam, remifentanil, propofol and cisatracurium in morbid obesity. Obes Surg. 2000;10:353–360.
78. Pizzirani E, Pigato P, Favretti F, et al. The Post-anaesthetic Recovery in Obesity Surgery: comparison between two anaesthetic techniques. Obes Surg. 1992;2:91–94.
79. Shenkman Z, Shir Y, Brodsky JB. Perioperative management of the obese patient. Br J Anaesth. 1993;70:349–359.
80. von Ungern-Sternberg BS, Regli A, Reber A, et al. Effect of obesity and thoracic epidural analgesia on perioperative spirometry. Br J Anaesth. 2005;94:121–127.
81. 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;10:220–229.
82. Backman L, Freyschuss U, Hallberg D, et al. Cardiovascular function in extreme obesity. Acta Med Scand. 1973;193:437–446.
83. Paul DR, Hoyt JL, Boutros AR. Cardiovascular and respiratory changes in response to change of posture in the very obese. Anesthesiology. 1976;45:73–78.
84. Brodsky JB. Positioning the morbid obese patient for surgery. In: Alvarez A, ed. Morbid Obesity Peri-Operative Management. Cambridge, UK: Cambridge University Press; 2004:274–283.
85. Abernethy DR, Greenblatt DJ. Drug disposition in obese humans. An update. Clin Pharmacokinet. 1986;11:199–213.
86. Cheymol G. Clinical pharmacokinetics of drugs in obesity. An update. Clin Pharmacokinet. 1993;25:103–114.
87. Blouin RA, Kolpek JH, Mann HJ. Influence of obesity on drug disposition. Clin Pharm. 1987;6:706–714.
88. Li L, Miles MV, Lakkis H, et al. Vancomycin-binding characteristics in patients with serious infections. Pharmacotherapy. 1996;16:1024–1029.
89. Zahorska-Markiewicz B, Waluga M, Zielinski M, et al. Pharmacokinetics of theophylline in obesity. Int J Clin Pharmacol Ther. 1996;34:393–395.
90. Flechner SM, Kolbeinsson ME, Tam J, et al. The impact of body weight on cyclosporine pharmacokinetics in renal transplant recipients. Transplantation. 1989;47:806–810.
91. Traynor AM, Nafziger AN, Bertino JS Jr. Aminoglycoside dosing weight correction factors for patients of various body sizes. Antimicrob Agents Chemother. 1995;39:545–548.
92. Luc EC De Baerdemaeker M, Mortier EP, et al. Pharmacokinetics and pharmacodynamics. Essential guide for anesthetic drugs administration. In: Alvarez A, ed. Morbid Obesity Peri-operative Management. Cambridge, UK: Cambridge University Press; 2004:211–220.
93. Koenig SM. Pulmonary complications of obesity. Am J Med Sci. 2001;321:249–279.
94. Eichenberger A, Proietti S, Wicky S, et al. Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Anesth Analg. 2002;95:1788–1792, table.
95. Strollo PJ Jr, Rogers RM. Obstructive sleep apnea. N Engl J Med. 1996;334:99–104.
96. Rajala R, Partinen M, Sane T, et al. Obstructive sleep apnoea syndrome in morbidly obese patients. J Intern Med. 1991;230:125–129.
97. Ferretti A, Giampiccolo P, Cavalli A, et al. Expiratory flow limitation and orthopnea in massively obese subjects. Chest. 2001;119:1401–1408.
98. Resta O, Foschino-Barbaro MP, Legari G, et al. Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects. Int J Obes Relat Metab Disord. 2001;25:669–675.
99. Vgontzas AN, Bixler EO, Chrousos GP. Obesity-related sleepiness and fatigue: the role of the stress system and cytokines. Ann N Y Acad Sci. 2006;1083:329–344.
100. Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328:1230–1235.
101. Silverberg DS, Iaina A, Oksenberg A. Treating obstructive sleep apnea improves essential hypertension and quality of life. Am Fam Physician. 2002;65:229–236.
102. Dhonneur G, Combes X, Leroux B, et al. Postoperative obstructive apnea. Anesth Analg. 1999;89:762–767.
103. Boushra NN. Anaesthetic management of patients with sleep apnoea syndrome. Can J Anaesth. 1996;43:599–616.
104. Ostermeier AM, Roizen MF, Hautkappe M, et al. Three sudden postoperative respiratory arrests associated with epidural opioids in patients with sleep apnea. Anesth Analg. 1997;85:452–460.
105. Hiremath AS, Hillman DR, James AL, et al. Relationship between difficult tracheal intubation and obstructive sleep apnoea. Br J Anaesth. 1998;80:606–611.
106. Siyam MA, Benhamou D. Difficult endotracheal intubation in patients with sleep apnea syndrome. Anesth Analg. 2002;95:1098–1102, table.
107. Biring MS, Lewis MI, Liu JT, et al. Pulmonary physiologic changes of morbid obesity. Am J Med Sci. 1999;318:293–297.
108. Langeron O, Masso E, Huraux C, et al. Prediction of difficult mask ventilation. Anesthesiology. 2000;92:1229–1236.
109. Kessler R, Chaouat A, Schinkewitch P, et al. The obesity-hypoventilation syndrome revisited: a prospective study of 34 consecutive cases. Chest. 2001;120:369–376.
110. Akashiba T, Kawahara S, Kosaka N, et al. Determinants of chronic hypercapnia in Japanese men with obstructive sleep apnea syndrome. Chest. 2002;121:415–421.
111. Blankfield RP, Hudgel DW, Tapolyai AA, et al. Bilateral leg edema, obesity, pulmonary hypertension, and obstructive sleep apnea. Arch Intern Med. 2000;160:2357–2362.
112. Bradley TD, Rutherford R, Grossman RF, et al. Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis. 1985;131:835–839.
113. Al-Mobeireek AF, Al-Kassimi FA, Al-Majed SA, et al. Clinical profile of sleep apnea syndrome. A study at a university hospital. Saudi Med J. 2000;21:180–183.
114. Chaouat A, Weitzenblum E, Krieger J, et al. Association of chronic obstructive pulmonary disease and sleep apnea syndrome. Am J Respir Crit Care Med. 1995;151:82–86.
115. Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol. 1997;82:811–818.
116. Vaughan RW, Cork RC, Hollander D. The effect of massive weight loss on arterial oxygenation and pulmonary function tests. Anesthesiology. 1981;54:325–328.
117. Hakala K, Maasilta P, Sovijarvi AR. Upright body position and weight loss improve respiratory mechanics and daytime oxygenation in obese patients with obstructive sleep apnoea. Clin Physiol. 2000;20:50–55.
118. Peppard PE, Young T, Palta M, et al. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342:1378–1384.
119. Rochester DF. Obesity and pulmonary function. In: Alpert MA, Alexander JK, eds. The Heart and Lung in Obesity. Armonk, NY: Futura Publishing Company; 1998:108–132.
120. Eriksson S, Backman L, Ljungstrom KG. The incidence of clinical postoperative thrombosis after gastric surgery for obesity during 16 years. Obes Surg. 1997;7:332–335.
121. Geerts W, Selby R. Prevention of venous thromboembolism in the ICU. Chest. 2003;124:357S–363S.
122. 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.
123. Hnatiuk OW, Dillard TA, Torrington KG. Adherence to established guidelines for preoperative pulmonary function testing. Chest. 1995;107:1294–1297.
124. Roche N, Herer B, Roig C, et al. Prospective testing of two models based on clinical and oximetric variables for prediction of obstructive sleep apnea. Chest. 2002;121:747–752.
125. Crapo RO, Kelly TM, Elliott CG, et al. Spirometry as a preoperative screening test in morbidly obese patients. Surgery. 1986;99:763–768.
126. Tung A, Rock P. Perioperative concerns in sleep apnea. Curr Opin Anaesthesiol. 2001;14:671–678.
127. Rennotte MT, Baele P, Aubert G, et al. Nasal continuous positive airway pressure in the perioperative management of patients with obstructive sleep apnea submitted to surgery. Chest. 1995;107:367–374.
128. Tkacova R, Rankin F, Fitzgerald FS, et al. Effects of continuous positive airway pressure on obstructive sleep apnea and left ventricular afterload in patients with heart failure. Circulation. 1998;98:2269–2275.
129. Wilcox I, Grunstein RR, Hedner JA, et al. Effect of nasal continuous positive airway pressure during sleep on 24-hour blood pressure in obstructive sleep apnea. Sleep. 1993;16:539–544.
130. Brodsky JB, Lemmens HJ, Brock-Utne JG, et al. Morbid obesity and tracheal intubation. Anesth Analg. 2002;94:732–736.
131. Illing L, Duncan PG, Yip R. Gastroesophageal reflux during anaesthesia. Can J Anaesth. 1992;39:466–470.
132. Hardy JF, Lepage Y, Bonneville-Chouinard N. Occurrence of gastroesophageal reflux on induction of anaesthesia does not correlate with the volume of gastric contents. Can J Anaesth. 1990;37:502–508.
133. Beers RA, Roizen MF. Pre-operative evaluation of the patient for bariatric surgery. In: Alvarez A, ed. Morbid Obesity Peri-operative Management. Cambridge, UK: Cambridge University Press; 2004:113–125.
134. Berthoud MC, Peacock JE, Reilly CS. Effectiveness of preoxygenation in morbidly obese patients. Br J Anaesth. 1991;67:464–466.
135. Dixon BJ, Dixon JB, Carden JR, et al. Preoxygenation is more effective in the 25 degrees head-up position than in the supine position in severely obese patients: a randomized controlled study. Anesthesiology. 2005;102:1110–1115.
136. Boyce JR, Ness T, Castroman P, et al. A preliminary study of the optimal anesthesia positioning for the morbidly obese patient. Obes Surg. 2003;13:4–9.
137. Perilli V, Sollazzi L, Bozza P, et al. The effects of the reverse Trendelenburg position on respiratory mechanics and blood gases in morbidly obese patients during bariatric surgery. Anesth Analg. 2000;91:1520–1525.
138. Luce JM. Respiratory complications of obesity. Chest. 1980;78:626–631.
139. Pelosi P, Croci M, Ravagnan I, et al. The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg. 1998;87:654–660.
140. Damia G, Mascheroni D, Croci M, et al. Perioperative changes in functional residual capacity in morbidly obese patients. Br J Anaesth. 1988;60:574–578.
141. Marik P, Varon J. The obese patient in the ICU. Chest. 1998;113:492–498.
142. The ARDS Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342:1301–1308.
143. Pelosi P, Ravagnan I, Giurati G, et al. Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology. 1999;91:1221–1231.
144. Marko P, Gabrielli A, Caruso LJ, et al. Digestive physiology and gastric aspiration. In: Alvarez A, ed. Morbid Obesity Peri-operative Management. Cambridge, UK: Cambridge University Press; 2004:89–106.
145. Burns SM, Egloff MB, Ryan B, et al. Effect of body position on spontaneous respiratory rate and tidal volume in patients with obesity, abdominal distension and ascites. Am J Crit Care. 1994;3:102–106.
146. 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;111:665–670.
147. Brodsky JB. Morbid obesity. Curr Anaesth Crit Care. 1998;9:249–254.
148. Vaughan RW, Bauer S, Wise L. Effect of position (semirecumbent versus supine) on postoperative oxygenation in markedly obese subjects. Anesth Analg. 1976;55:37–41.
149. Rothen HU, Sporre B, Engberg G, et al. Reexpansion of atelectasis during general anaesthesia may have a prolonged effect. Acta Anaesthesiol Scand. 1995;39:118–125.
150. Rothen HU, Sporre B, Engberg G, et al. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology. 1995;82:832–842.
151. Reber A, Engberg G, Wegenius G, et al. Lung aeration. The effect of pre-oxygenation and hyperoxygenation during total intravenous anaesthesia. Anaesthesia. 1996;51:733–737.
152. Rothen HU, Sporre B, Engberg G, et al. Prevention of atelectasis during general anaesthesia. Lancet. 1995;345:1387–1391.
153. Goll V, Akca O, Greif R, et al. Ondansetron is no more effective than supplemental intraoperative oxygen for prevention of postoperative nausea and vomiting. Anesth Analg. 2001;92:112–117.
154. Greif R, Laciny S, Rapf B, et al. Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Anesthesiology. 1999;91:1246–1252.
155. Greif R, Akca O, Horn EP, et al. Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. Outcomes Research Group. N Engl J Med. 2000;342:161–167.
156. Kotani N, Hashimoto H, Sessler DI, et al. Supplemental intraoperative oxygen augments antimicrobial and proinflammatory responses of alveolar macrophages. Anesthesiology. 2000;93:15–25.
157. Capella JF, Capella RF. Is routine invasive monitoring indicated in surgery for the morbidly obese? Obes Surg. 1996;6:50–53.
158. Esclamado RM, Glenn MG, McCulloch TM, et al. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope. 1989;99:1125–1129.
159. Tucci M, Bansal V, Camporesi EM. Respiratory monitoring. In: Alvarez A, ed. Morbid Obesity Peri-operative Management. Cambridge, UK: Cambridge University Press; 2004:89–106.
160. Sapala JA, Wood MH, Schuhknecht MP, et al. Fatal pulmonary embolism after bariatric operations for morbid obesity: a 24-year retrospective analysis. Obes Surg. 2003;13:819–825.
161. Sabers C, Plevak DJ, Schroeder DR, et al. The diagnosis of obstructive sleep apnea as a risk factor for unanticipated admissions in outpatient surgery. Anesth Analg. 2003;96:1328–1335, table.
162. Schroder T, Nolte M, Kox WJ, et al. [Anesthesia in extreme obesity]. Herz. 2001;26:222–228.
163. Rosenberg J, Ullstad T, Rasmussen J, et al. Time course of postoperative hypoxaemia. Eur J Surg. 1994;160:137–143.
164. Yap SJ, Morris RW, Pybus DA. Alterations in endotracheal tube position during general anaesthesia. Anaesth Intensive Care. 1994;22:586–588.
165. Lobato EB, Paige GB, Brown MM, et al. Pneumoperitoneum as a risk factor for endobronchial intubation during laparoscopic gynecologic surgery. Anesth Analg. 1998;86:301–303.
166. Ezri T, Hazin V, Warters D, et al. The endotracheal tube moves more often in obese patients undergoing laparoscopy compared with open abdominal surgery. Anesth Analg. 2003;96:278–282, table.
167. Hedenstierna G, Tokics L, Strandberg A, et al. Correlation of gas exchange impairment to development of atelectasis during anaesthesia and muscle paralysis. Acta Anaesthesiol Scand. 1986;30:183–191.
168. Moller JT, Johannessen NW, Berg H, et al. Hypoxaemia during anaesthesia—an observer study. Br J Anaesth. 1991;66:437–444.
169. Bendixen HH, Hedley-Whyte J, Laver MB. Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation. A concept of atelectasis. N Engl J Med. 1963;269:991–996.
170. Brismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with muscular relaxation-a proposal of atelectasis. Anesthesiology. 1985;62:422–428.
171. Zerah F, Harf A, Perlemuter L, et al. Effects of obesity on respiratory resistance. Chest. 1993;103:1470–1476.
172. Pelosi P, Croci M, Ravagnan I, et al. Total respiratory system, lung, and chest wall mechanics in sedated-paralyzed postoperative morbidly obese patients. Chest. 1996;109:144–151.
173. Tweed WA, Phua WT, Chong KY, et al. Tidal volume, lung hyperinflation and arterial oxygenation during general anaesthesia. Anaesth Intensive Care. 1993;21:806–810.
174. Magnusson L, Spahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth. 2003;91:61–72.
175. Millman RP, Meyer TJ, Eveloff SE. Sleep apnea in the morbidly obese. R I Med. 1992;75:483–486.
176. Douglas NJ, Polo O. Pathogenesis of obstructive sleep apnoea/hypopnoea syndrome. Lancet. 1994;344:653–655.
177. Murphy PG. Obesity. In: Hemmings HC, Hopkins PM, eds. Foundation of Anaesthesia. Basic Clinical Sciences. Philadelphia: Mosby; 2000:703–711.
178. 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;6:354–358.
179. Gilbert TB, Seneff MG, Becker RB. Facilitation of internal jugular venous cannulation using an audio-guided Doppler ultrasound vascular access device: results from a prospective, dual-center, randomized, crossover clinical study. Crit Care Med. 1995;23:60–65.
180. Jeevanandam M, Young DH, Schiller WR. Obesity and the metabolic response to severe multiple trauma in man. J Clin Invest. 1991;87:262–269.
181. Cousins M, Power I. Acute and postoperative pain. In: Wall PD, Melzack R, eds. Textbook of Pain. Philadelphia: Elsevier; 1999:447–491.
182. Craig DB. Postoperative recovery of pulmonary function. Anesth Analg. 1981;60:46–52.
183. Fine PC, Ashburn MA. Functional neuroanatomy and nociception. In: Ashburn MA, Rice LJ, eds. The Management of Pain. Philadelphia: Churchill Livingstone; 1998:1–16.
184. Rawal N. 10 years of acute pain services–achievements and challenges. Reg Anesth Pain Med. 1999;24:68–73.
185. Provenzano D, Grass J. Is epidural analgesia superior to IV-PCA? In: Fleisher L, ed. Evidence-Based Practice of Anesthesiology. Philadelphia: Saunders, Elsevier Inc.; 2004:441–448.
186. Rigg JR, Jamrozik K, Myles PS, et al. Epidural anaesthesia and analgesia and outcome of major surgery: a randomised trial. Lancet. 2002;359:1276–1282.
187. Block BM, Liu SS, Rowlingson AJ, et al. Efficacy of postoperative epidural analgesia: a meta-analysis. JAMA. 2003;290:2455–2463.
188. Schumann R, Shikora S, Weiss JM, et al. A comparison of multimodal perioperative analgesia to epidural pain management after gastric bypass surgery. Anesth Analg. 2003;96:469–474, table.
189. Brodsky JB, Merrell RC. Epidural administration of morphine postoperatively for morbidly obese patients. West J Med. 1984;140:750–753.
190. Rawal N, Sjostrand U, Christoffersson 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;63:583–592.
191. Niemi G, Breivik H. Epidural fentanyl markedly improves thoracic epidural analgesia in a low-dose infusion of bupivacaine, adrenaline and fentanyl. A randomized, double-blind crossover study with and without fentanyl. Acta Anaesthesiol Scand. 2001;45:221–232.
192. Niemi G, Breivik H. The minimally effective concentration of adrenaline in a low-concentration thoracic epidural analgesic infusion of bupivacaine, fentanyl and adrenaline after major surgery. A randomized, double-blind, dose-finding study. Acta Anaesthesiol Scand. 2003;47:439–450.
193. Blomberg S, Emanuelsson H, Ricksten SE. Thoracic epidural anesthesia and central hemodynamics in patients with unstable angina pectoris. Anesth Analg. 1989;69:558–562.
194. Saada M, Catoire P, Bonnet F, et al. Effect of thoracic epidural anesthesia combined with general anesthesia on segmental wall motion assessed by transesophageal echocardiography. Anesth Analg. 1992;75:329–335.
195. Tevelenok I. [Peridural anesthesia in the acute period of myocardial infarct]. Anesteziol Reanimatol. 1977;36–39.
196. Toft P, Jorgensen A. Continuous thoracic epidural analgesia for the control of pain in myocardial infarction. Intensive Care Med. 1987;13:388–389.
197. Blomberg SG. Long-term home self-treatment with high thoracic epidural anesthesia in patients with severe coronary artery disease. Anesth Analg. 1994;79:413–421.
198. Kataja J. Thoracolumbar epidural anaesthesia and isoflurane to prevent hypertension and tachycardia in patients undergoing abdominal aortic surgery. Eur J Anaesthesiol. 1991;8:427–436.
199. Baron JF, Coriat P, Mundler O, et al. Left ventricular global and regional function during lumbar epidural anesthesia in patients with and without angina pectoris. Influence of volume loading. Anesthesiology. 1987;66:621–627.
200. Diebel LN, Lange MP, Schneider F, et al. Cardiopulmonary complications after major surgery: a role for epidural analgesia? Surgery. 1987;102:660–666.
201. Yeager MP, Glass DD, Neff RK, et al. Epidural anesthesia and analgesia in high-risk surgical patients. Anesthesiology. 1987;66:729–736.
202. Her C, Kizelshteyn G, Walker V, et al. Combined epidural and general anesthesia for abdominal aortic surgery. J Cardiothorac Anesth. 1990;4:552–557.
203. Meyers JR, Lembeck L, O'Kane H, et al. Changes in functional residual capacity of the lung after operation. Arch Surg. 1975;110:576–583.
204. Spence AA, Smith G. Postoperative analgesia and lung function: a comparison of morphine with extradural block. Br J Anaesth. 1971;43:144–148.
205. Brown D, Neal J. Chronic obstructive pulmonary disease and perioperative analgesia. In: Brown DL, ed. Problems in Anesthesia. Philadelphia: JB Lippincott; 1988:422–434.
206. Hickey RF, Visick WD, Fairley HB, et al. Effects of halothane anesthesia on functional residual capacity and alveolar-arterial oxygen tension difference. Anesthesiology. 1973;38:20–24.
207. Garibaldi RA, Britt MR, Coleman ML, et al. Risk factors for postoperative pneumonia. Am J Med. 1981;70:677–680.
208. Hendolin H, Lahtinen J, Lansimies E, et al. The effect of thoracic epidural analgesia on respiratory function after cholecystectomy. Acta Anaesthesiol Scand. 1987;31:645–651.
209. Cuschieri RJ, Morran CG, Howie JC, et al. Postoperative pain and pulmonary complications: comparison of three analgesic regimens. Br J Surg. 1985;72:495–498.
210. Pansard JL, Mankikian B, Bertrand M, et al. Effects of thoracic extradural block on diaphragmatic electrical activity and contractility after upper abdominal surgery. Anesthesiology. 1993;78:63–71.
211. Duggan J, Drummond GB. Activity of lower intercostal and abdominal muscle after upper abdominal surgery. Anesth Analg. 1987;66:852–855.
212. Ali J, Weisel RD, Layug AB, et al. Consequences of postoperative alterations in respiratory mechanics. Am J Surg. 1974;128:376–382.
213. Tarhan S, Moffitt EA, Sessler AD, et al. Risk of anesthesia and surgery in patients with chronic bronchitis and chronic obstructive pulmonary disease. Surgery. 1973;74:720–726.
214. Rademaker BM, Ringers J, Odoom JA, et al. Pulmonary function and stress response after laparoscopic cholecystectomy: comparison with subcostal incision and influence of thoracic epidural analgesia. Anesth Analg. 1992;75:381–385.
215. Sydow FW. The influence of anesthesia and postoperative analgesic management of lung function. Acta Chir Scand Suppl. 1989;550:159–165; discussion 165–168
216. Nunn JF. Effects of anaesthesia on respiration. Br J Anaesth. 1990;65:54–62.
217. Weller R, Rosenblum M, Conard P, et al. Comparison of epidural and patient-controlled intravenous morphine following joint replacement surgery. Can J Anaesth. 1991;38:582–586.
218. McCarthy GS. The effect of thoracic extradural analgesia on pulmonary gas distribution, functional residual capacity and airway closure. Br J Anaesth. 1976;48:243–248.
219. Groeben H. Effects of high thoracic epidural anesthesia and local anesthetics on bronchial hyperreactivity. J Clin Monit Comput. 2000;16:457–463.
220. Ballantyne J, Carwood C. Optimal postoperative analgesia. In: Fleisher L, ed. Evidence-Based Practice of Anesthesiology. Philadelphia: Saunders, Elsevier Inc.; 2004:449–458.
221. Meyer R. Rofecoxib reduces perioperative morphine consumption for abdominal hysterectomy and laparoscopic gastric banding. Anaesth Intensive Care. 2002;30:389–390.