Chapter 109. The Obesity Epidemic and Critical Care

• Morbid obesity presents unique cardiorespiratory challenges in the intensive care unit and frustrates the delivery of routine care. Whether or not obesity itself influences the outcome of critical illness is unclear.
• Morbid obesity leads to heart disease through a number of diverse mechanisms. Therefore, a high index of suspicion for its presence is warranted in the critically ill patient.
• An increased risk of venous thromboembolism in obesity merits an aggressive approach to prophylaxis.
• Cor pulmonale occurs in individuals with nocturnal and diurnal hypoxemia related to the obesity hypoventilation syndrome or coexisting obstructive sleep apnea and obstructive lung disease.
• Although simple obesity has relatively minor effects on pulmonary function, morbid obesity may be associated with reductions in forced vital capacity, forced expiration volume in 1 second, and total lung capacity. An increase in mid to late expiratory flow may be seen.
• Morbid obesity is associated with a significant increase in the percentage of oxygen consumption attributable to the work of breathing. This decreased respiratory reserve results in a predisposition to the development of respiratory failure even after trivial insults.
• Atelectasis is common in the morbidly obese postoperative patient and, in addition to any accompanying sleep-disordered breathing, may lead to respiratory failure. Although conclusive data are lacking, the early use of noninvasive ventilation in the high-risk postoperative patient may prevent the development of respiratory failure.
• Intubation of the morbidly obese patient may be technically challenging because of poor visibility of the glottis and decreased oxygen stores in alveoli from a reduced functional residual capacity.
• Morbidly obese patients should be ventilated in the upright or semi-upright position to improve respiratory system compliance and reduce the work of breathing. Positive end-expiratory pressure between 8 and 15 cm H2O may be necessary to prevent atelectasis.
• Because the compliance of the chest wall is diminished in morbid obesity, a high plateau pressure does not necessarily indicate alveolar overdistention. When using low tidal volume ventilation in the management of the acute respiratory distress syndrome, a plateau pressure of 35 to 40 cm H2O may be acceptable in some patients.
• Ultrasound guidance may be useful in establishing vascular access in the morbidly obese patient.
• Numerous unpredictable alterations in pharmacokinetics have been described in obesity. Reference to published guidelines for individual drugs and close monitoring of clinically available serum drug levels are recommended.
• Attempts by clinicians to accelerate a program of weight loss during the course of critical illness are misguided and may interfere with immune function, wound healing, and respiratory muscle strength. Carefully balanced hypocaloric regimens may be safe.

An ever-increasing percentage of the inhabitants of developed countries is obese or overweight. This trend includes men and women and spans all age groups, including children. Obesity is associated with diabetes mellitus, cardiovascular disease, hypertension, and cancer and confers a reduced life expectancy, particularly in younger and severely obese individuals. Extreme obesity is frequently associated with life-threatening cardiopulmonary disease and presents substantial obstacles to the delivery of routine care. We present a summary of the challenges inherent in the care of the morbidly obese critically ill patient and highlight physiological principles important to the care of such patients.

Defining Obesity

Due to the impracticality of determining body fat composition in the clinical setting, obesity is typically defined as excessive weight relative to body surface area as determined by calculation of the body mass index (BMI), calculated as weight in kilograms divided by height in square meters. The correlation between BMI and obesity in most middle-age adults is very good, although using BMI as a proxy for body fat is misleading in individuals engaged in weight training who have increased muscle mass, and when significant edema is present. The World Health Organization and National Institutes of Health recommend the following definitions of overweight and obesity: overweight is defined as a BMI greater than 25 kg/m2, obesity is defined as a BMI greater than 30 kg/m2, and morbid obesity is defined as a BMI greater than 40 kg/m2. Some authorities have extended the definition of morbid obesity to individuals with a BMI greater than 35 kg/ m2 if they have serious medical comorbidities.

The Magnitude of the Problem

Data from the 1999–2000 National Health and Nutrition Examination Survey show a continued increase in the prevalence of overweight and obesity in the United States over the past 15 years. Relative to the 1988–1994 survey, the prevalence of overweight individuals has increased from 55.9% to 64.5%, obesity has increased from 22.9% to 30.5%, and morbid obesity has increased from 2.9% to 4.7%.1 Non-Hispanic black women have the highest prevalence of obesity and overweight, but increases were found across all ethnic groups and in men and women. Perhaps of greatest concern is an increase in the prevalence of overweight and obesity among children, particularly Mexican American and non-Hispanic black adolescents.2,3

There are many potential explanations for the increasing number of persons who are overweight or obese. Technologic advances have decreased the cost of food production, thereby making food more affordable, and decreased the energy expended by the typical worker.4 Leisure time is increasingly dominated by sedentary activities such as watching television or using the computer. Television viewing is associated with increased food intake and a decrease in metabolic rate even when compared with other sedentary activities such as reading or sewing.5 The risks of obesity and type II diabetes mellitus have been positively correlated with the amount of television watched,6 and children randomized to an intervention discouraging television viewing had significant reductions in relative BMI compared with controls.7 Other possible explanations for the obesity epidemic include an increased percentage of meals eaten outside the home, the serving of larger portions at commercial establishments, and the widespread consumption of diets low in vegetables and fibers and high in refined sugars. Individual susceptibility to these influences is poorly understood but likely includes a genetic component.

Unfortunately, the obesity epidemic is not confined to highly developed countries. The World Health Organization estimates that 1 billion people worldwide are overweight or obese. Worse, most indications are that the epidemic has not yet peaked: obesity is increasing in prevalence in developing countries coincident with decreased physical activity and the replacement of traditional fruits and whole grains in the diet with calorie-dense, processed foods.

Obesity is associated with a shortened life expectancy, particularly in severely obese younger individuals.8 This section summarizes important physiologic derangements associated with obesity, with an emphasis on those germane to the care of the morbidly obese critically ill patient.

Cardiovascular Effects

The risk of death from cardiovascular disease rises steeply above a BMI of 30 kg/m2.9 There are several mechanisms through which obesity can cause cardiovascular disease. First, obesity increases the risk of coronary atherosclerosis by inducing several risk factors in parallel. For example, obesity is associated with hypertension, insulin resistance, dyslipidemia, and coagulation abnormalities, which separately and collectively promote the development of cardiovascular disease.

There are other mechanisms through which obesity causes heart disease. Obesity may impair cardiac function through chronic pressure and volume overload.10 Cardiac output is increased in obesity as a result of increased extracellular volume and increased blood flow to most tissue beds. This increased cardiac output is associated with increased preload and cardiac dilatation, with the subsequent development of eccentric left ventricular hypertrophy. This chronic volume-overloaded state, when combined with increased left ventricular afterload from concurrent hypertension, may result in marked left ventricular hypertrophy. Over time, left ventricular hypertrophy leads to impaired ventricular filling and diastolic heart failure. Systolic heart failure may result from ischemic heart disease, microvascular disease from diabetes mellitus, longstanding hypertension, or, in severe, longstanding obesity, a decrease in mid-wall fiber shortening and ejection fraction.9

Pulmonary hypertension with right ventricular hypertrophy and dilation may accompany obesity. When not caused by left ventricular failure, pulmonary hypertension in these patients typically arises from conditions that cause nocturnal and diurnal hypoxemia. A relatively common presentation of this problem is that of the patient with obstructive sleep apnea who has coexisting chronic obstructive pulmonary disease. Cor pulmonale may also develop in patients with the obesity hypoventilation syndrome (OHS). This poorly understood disorder is associated with daytime hypercapnia and hypoxemia, with the latter arising from alveolar hypoventilation and poor ventilation of the basal lung due to airway closure and atelectasis. Hypercapnia and hypoxemia elicit pulmonary vasoconstriction. Eventually, this may lead to vascular remodeling with resulting irreversible pulmonary hypertension and cor pulmonale. Individuals with the OHS frequently, but not always, have coexisting obstructive sleep apnea.

Plasminogen activator inhibitor I and fibrinogen levels are elevated in most patients with obesity, suggesting a role for hypercoagulability and impaired fibrinolysis in cardiac and cerebrovascular diseases. Elevated proinflammatory cytokines, for example, interleukin 6 and C-reactive protein, potentially indicate the presence of a low-grade inflammatory state in this condition.9

What are the clinical implications of this susceptibility to such a range of cardiovascular disorders? First, the intensivist caring for the morbidly obese patient should have a high index of suspicion for the presence of ischemic heart disease from coronary artery or microvascular disease. Second, abnormal cardiac function, diastolic or systolic, may be present, even if other risk factors for heart disease are absent. Particular sensitivity to changes in intravascular volume may result. Third, pulmonary hypertension and right ventricular failure should be suspected when obstructive lung disease and/or daytime hypoxemia or hypercapnia are present. The diagnosis of these conditions is complicated by poor sensitivity of physical examination and transthoracic echocardiography in morbidly obese individuals. In selected patients, transesophageal echocardiography or invasive hemodynamic monitoring may be necessary.

Pulmonary Effects

Mechanics of the Respiratory System

The effect of obesity on pulmonary function varies considerably between individuals, ranging from trivial to profound impairment, but generally increases in severity with the BMI.11,12 The overall compliance of the respiratory system is reduced, mildly so in simple obesity and as low as 45% of normal in patients with OHS. Some studies have suggested that decreased chest wall compliance from the mechanical effect of adipose tissue on the thoracic cage is the principal cause of this abnormality, whereas other investigators have implicated reduced lung compliance as an additional factor, probably from a decrease in functional residual capacity. Airway resistance has been found to be increased, and a reduction in mid to late expiratory flows has been noted; because the ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) is typically normal or even elevated in obesity, a reduction in small airway caliber is likely responsible.

Pulmonary Function

The most frequent abnormality in pulmonary function in obesity is a decrease in the expiratory reserve volume attributable to cephalad displacement of the diaphragm by adipose tissue. In severely obese individuals and in those with the OHS, total lung capacity and vital capacity may be reduced. In such patients, the residual volume may actually be increased relative to total lung capacity because of small airway closure and gas trapping. This is supported by the finding of larger total lung capacity by body box plethysmography than by helium dilution.13 Similarly, spirometry is typically normal in simple obesity, whereas severely obese individuals or those with the OHS may exhibit reductions in FEV1 and FVC, even though the ratio of these two variables is preserved or even increased.

Why do some individuals exhibit diminished pulmonary function and/or the OHS, whereas comparably overweight individuals may be little affected? Some, but not all, data suggest that the distribution of body fat may be an important determinant of pulmonary function; simply put, adipose tissue that is more centrally located is more likely to negatively influence pulmonary function. There are also important differences in respiratory muscle strength between patients with simple obesity and those with the OHS, with the latter exhibiting decreased inspiratory muscle strength. Weakness may be considered absolute, a result of mechanical disadvantage from diaphragm malposition, and relative, when the increased work of breathing from morbid obesity is considered (see below).

Gas Exchange

Morbid obesity causes closure of small peripheral airways in the dependent regions of the lung, resulting in mismatching of ventilation and perfusion.14 The result may be a widened alveolar to arterial oxygen gradient and mild to moderate hypoxemia that worsens in the supine position. Severe hypoxemia may be present in individuals with the OHS because of the additional contribution of hypoventilation. The diffusing capacity for carbon monoxide is typically normal and may be elevated when indexed to alveolar volume.

Control of Breathing

Ventilatory drive is increased in simple obesity as assessed by the mouth occlusion pressure and diaphragm electrical activity in response to carbon dioxide inhalation. In contrast, mouth occlusion pressure response to carbon dioxide is reduced in OHS compared to normal individuals and to patients with simple obesity. Diaphragm electrical activity in response to carbon dioxide is inappropriately low in OHS.

Perioperative and Other Pulmonary Considerations in Obesity

The reduced functional residual capacity associated with severe obesity encroaches on the closing capacity, the lung volume at which small airways in the lung bases begin to close. This places severely obese patients at significant risk for atelectasis in the perioperative period, particularly where upper abdominal or thoracic operations are concerned. Hypoxemia may result and may be marked in the setting of a relatively unremarkable chest radiograph. Pulmonary embolism should always be considered in the differential diagnosis of such patients. Treatment involves adequate analgesia, avoidance of oversedation, early mobilization, and vigorous pulmonary toilet. Sleep-disordered breathing may worsen in the postoperative period, thereby increasing the risk of respiratory failure. Early application of noninvasive ventilation may decrease the incidence of postoperative pulmonary complications. The risk of aspiration of gastric contents is generally felt to be increased in obesity, and efforts to minimize this occurrence should be taken at the time of intubation (see below).

Not surprisingly, the risk of obstructive sleep apnea increases significantly with obesity, to as high as 40% when the BMI exceeds 40 kg/m2. Patients who successfully lose a significant amount of weight, usually via surgical approaches to weight reduction, may exhibit significant improvements in lung volumes, gas exchange, and work of breathing, and sleep-disordered breathing may improve or even resolve.

Other Effects of Obesity

An intriguing association between obesity and progressive renal insufficiency is becoming apparent.10,15 Obesity is associated with increased renal blood flow, glomerular filtration rate, and microalbuminuria. Glomerular hyperfiltration may subsequently lead to glomerular sclerosis in a manner analogous to diabetes, even in obese patients without this diagnosis. Several potential mechanisms for this process have been suggested, ranging from hyperleptinemia to insulin resistance to a chronic state of low-grade inflammation induced by obesity. Apart from the direct effects of obesity on the kidney, a significant proportion of cases of end-stage renal disease may be attributable to the diabetes and hypertension associated with obesity.

The risk of venous thromboembolism is greatly increased in obese patients (BMI >30 kg/m2). Inactivity, venous stasis, and hypercoagulability likely contribute to this risk. The risk of death from cancer is substantially increased in individuals with a BMI greater than 40 kg/m2.16

Pathophysiology of Respiratory Failure in Morbid Obesity

Morbidly obese patients may be particularly susceptible to respiratory failure. Under normal conditions, very little (<5%) of the body's total oxygen consumption (VO2) is attributable to the work of breathing. Emphysema and other forms of chronic lung disease increase the oxygen consumed by the respiratory muscles (VO2RESP) by increasing the load on the respiratory muscles. In such conditions, the strength of the respiratory system may be just adequate for the load on the system, and further insults, however trivial, may provoke respiratory failure.

Evidence suggests that morbidly obese patients may be similarly compromised. Baseline VO2RESP averaged 16% in a group of morbidly obese (average BMI = 53 kg/m2) patients scheduled for gastric bypass surgery.17 Further, obesity is associated with a disproportionate rise in VO2RESP for a given increase in minute ventilation, similar to emphysema.18 Together these data suggest reduced respiratory reserve in morbid obesity, thereby increasing the risk of respiratory failure even from seemingly trivial insults (e.g., viral infection or, particularly in the postoperative patient, atelectasis) in a manner analogous to emphysema or other chronically compensated forms of respiratory failure.

Evaluation of Respiratory Failure

The evaluation of morbidly obese patients with critical illness and with respiratory failure, in particular, is challenging. Physical examination is difficult, and chest radiography is commonly unhelpful. Computed tomography or other similar diagnostic studies are impossible if the patient exceeds the weight limit or width of the scanner table. Even when such studies are possible, there are enormous technical and safety challenges that accompany the transfer of such patients throughout the hospital. Frequently, diagnoses must by necessity be made on the basis of other clinical criteria.

The diagnosis of pulmonary edema is often frustrated by uncertainty regarding the presence of edema on the chest radiograph. Soft tissue shadows on portable chest radiographs are often difficult to distinguish from airspace edema. When suspected, other clinical signs may assist in making a diagnosis. For example, abundant frothy secretions from the endotracheal tube commonly accompany pulmonary edema. Analysis of the protein content of the initial secretions may permit a distinction between high- and low-pressure edema, as the latter is associated with a protein content greater than one-half that of serum.19 Measurement of a frankly elevated pulmonary capillary wedge pressure usually indicates that pulmonary edema is present. Similarly, pulmonary edema may be diagnosed in the patient with hypoxemia refractory to high-flow oxygen who also has an elevated right atrial pressure and abnormal left ventricular systolic or diastolic function, although this approach also makes an inference that pulmonary edema necessarily results from abnormal pump function. Acute lung injury may be diagnosed on the basis of appropriate setting (e.g., aspiration after the administration of sedation) and hypoxemia refractory to high-flow oxygen. Although differentiating this condition from atelectasis can be difficult, noting abundant protein-rich endotracheal secretions may be helpful.

Pulmonary embolism is another serious condition that is particularly difficult to diagnose in the morbidly obese patient. Computed tomography of the chest and pulmonary angiography may be technically unfeasible. Serial lower extremity Doppler examinations should be performed, although pulmonary embolism is not disproved solely through this approach. A normal D-dimer as determined by enzyme-linked immunosorbent assay reliably excludes the diagnosis, but such a result is unlikely in the critically ill population, given the multitude of conditions associated with elevations in D-dimer levels. Echocardiography may suggest the diagnosis by demonstrating acute right heart dysfunction, but this finding lacks specificity given the range of disorders precipitating respiratory failure (e.g., acute lung injury or severe, untreated sleep disordered breathing) that cause this. Because there are no good data to guide the clinician, our approach is to initiate therapeutic anticoagulation in the setting of significant pulmonary hypertension (mean pulmonary artery pressure >40 mm Hg), if acute right heart dilation without another satisfactory cause is present, or when historical features (e.g., acute onset of chest pain and dyspnea) suggest the diagnosis.

Management of Respiratory Failure

Noninvasive positive pressure ventilation has several potential benefits in the initial management of morbidly obese patients with respiratory failure, including unloading the respiratory muscles, decreasing atelectasis, and treating any underlying sleep-disordered breathing. It may also have a role in preventing respiratory complications in the postoperative period. Joris et al demonstrated the utility of noninvasive positive pressure ventilation in reducing the postoperative decrease in FVC and FEV1 when applied to morbidly obese patients in the first 24 hours after gastroplastly.20 We recommend the early use of noninvasive positive pressure ventilation in morbidly obese patients who have developed respiratory failure. Extubation to noninvasive ventilation may also be considered for morbidly obese patients at high risk for respiratory failure after thoracic or abdominal surgery, although this approach is unproven. Noninvasive ventilation is discussed in greater detail in Chap. 33.

Intubation of the morbidly obese patient can be problematic.21 The view afforded the operator may be suboptimal because of extensive soft tissue in the hypopharynx. Reduced functional residual capacity from morbid obesity and from sedation diminishes the oxygen stores available for the patient during apnea. The risk of aspiration of gastric contents may be increased in this population, and obese patients should be considered to have “full stomachs” during airway manipulation. For these reasons, we recommend that intubation be performed in the presence of an experienced operator, if possible. Once the decision has been made to intubate, appropriate planning should commence without delay. Early planning allows for the consultation of an experienced operator and an opportunity to perform an awake intubation, with or without fiberoptic assistance. If the patient is too unstable to attempt this, we recommend the routine use of cricoid pressure to minimize the risk of aspiration.

Several factors promote the development of atelectasis in the morbidly obese patient who is intubated for respiratory failure. These include the supine position, administration of sedatives and narcotics, and translaryngeal intubation. As a result, extremely obese patients frequently require increased levels of positive end-expiratory pressure to prevent atelectasis and maintain adequate oxygenation, even in the absence of acute lung injury. In our experience, a positive end-expiratory pressure of 8 to 15 cm H2O is frequently necessary. Because of atelectasis, significant hypoxemia may be present at the time that the patient is otherwise ready to sustain spontaneous breathing. Extubation to noninvasive positive pressure ventilation (NIPPV) may facilitate this transition and may maintain upper airway patency when residual sedation promotes obstructive respiratory events, although the routine use of NIPPV for post-extubation respiratory failure cannot currently be supported.21a If possible, morbidly obese patients should be ventilated and undergo spontaneous breathing trials in the reverse Trendelenburg position, a maneuver that improves respiratory system compliance by shifting the abdominal contents off the chest wall.

Lung protective ventilatory strategies are challenging to apply in the morbidly obese patient with acute lung injury because of the difficulty in diagnosing alveolar overdistension in this population. The plateau pressure represents the pressure required to inflate the lung against the elastic recoil of the lung and chest wall. Because the compliance of the chest wall is diminished in morbid obesity, a high plateau pressure does not necessarily indicate alveolar overdistension. Thus, when using low tidal volume ventilation in the management of acute lung injury or the acute respiratory distress syndrome, the delivery of a tidal volume of 6 mL/kg ideal body weight may result in a plateau pressure easily exceeding 30 cm H2O but not necessarily overdistend alveoli. Given the lack of convincing utility of pressure-volume curves in the management of acute lung injury, we do not advocate their use in such cases. We recommend measurement of the plateau pressure in the upright or semi-upright position to minimize the contribution of increased intraabdominal pressure from obesity and at times accepting an arbitrarily higher plateau pressure, for example, up to 35 to 40 cm H2O in the extremely obese patient, if necessary.

Tracheostomy

Although firm data are lacking, we have found early tracheostomy to be useful in the management of many morbidly obese patients with respiratory failure. We recommend that consideration be given to early tracheostomy in the following settings: (1) when severe obstructive sleep apnea that is refractory to medical therapy is present, (2) when long-term nocturnal ventilation for the treatment of obesity hypoventilation syndrome is planned, and (3) when the course of recovery is expected to be prolonged.

Establishing Vascular Access

Establishing intravenous access may be particularly difficult in the morbidly obese patient, beginning with the frequent inability to place a peripheral intravenous line. The increased distance from skin to blood vessel makes any attempt to cannulate a central vein more difficult, and the sharp angle required, particularly to enter the subclavian vein, may make it impossible for the operator to pass the wire and/or dilator. In some patients, the needle and the introducer may be too short for the subclavian site. The femoral site should be used as a last resort because of the increased risk of infection and thrombosis associated with this site; in addition, this site is frequently inaccessible because of intertrigo. The internal jugular vein is therefore generally the site of choice for extremely obese patients, even with the difficulties imposed by a short, thick neck.

There is very little information regarding the practice of central venous catheterization in the morbidly obese. Because bedside ultrasound has been shown to decrease the risk of insertion complications in high-risk patients,22 we recommend its use in the morbidly obese patient with poor landmarks.

Nutritional Support

Critically ill obese patients exhibit less lipolysis and fat oxidation than nonobese subjects.23 This decreased ability to mobilize fat increases protein breakdown to fuel gluconeogenesis and, hence, ensure adequate carbohydrates for energy. An increased risk for protein malnutrition results, with potentially detrimental effects on immune function, wound healing, and lean muscle mass. Thus, the clinician should avoid the temptation to starve the patient in a misguided attempt to accelerate a program of weight loss during the course of critical illness. In contrast, several trials of carefully controlled hypocaloric nutritional support in which adequate protein was supplied demonstrated that chronically critically ill patients receiving such a regimen had nitrogen balance comparable to those patients receiving conventional total parenteral nutrition.24

We recommend the provision of not less than 60% of the measured energy expenditure with 1.5 to 2.0 g /kg ideal body weight as protein, or less if renal insufficiency is present, to ensure adequate carbohydrates for energy and prevent protein malnutrition. Indirect calorimetry should be used to guide nutritional support because of the unreliability of conventional equations in this setting.

Drug Dosing

Different alterations in pharmacokinetics have been described in obese patients.25 In general, the volume of distribution for drugs with greater lipophilicity is increased. There are notable exceptions, however, thus illustrating the importance of other factors, such as plasma protein binding, in the distribution of drugs. Some studies have shown an increase in protein binding of some drugs because of increased levels of α1-acid glycoprotein in obesity, whereas other studies have shown decreased protein binding related to elevated triglycerides, lipoproteins, cholesterol, and free fatty acids.23 Variable alterations in enzymatic and antioxidant systems have been described, and increased and decreased renal clearance rates have been found.

This tremendous intersubject variability, combined with important differences between drugs make generalizations about the dosing of individual medications impossible. Drugs with a narrow therapeutic window such as theophylline and digoxin may confer toxicity when dosed according to total body weight. Reference to published guidelines for individual drugs is recommended, as is close monitoring of clinically available serum drug levels. Because of data indicating an increased volume of distribution and prolonged half-life for midazolam in obese subjects and an apparent lack of accumulation for propofol when given as a general anesthetic, we prefer propofol as a continuous intravenous sedative, when this method of administration is indicated.26,27 A strategy to prevent any potential accumulation of this sedative or the accompanying analgesic is still desirable, whether it be by daily interruption of continuous intravenous sedation or conversion to a validated regimen of intermittent sedative administration.

Minimizing Complications of Critical Illness

Because of the significantly elevated risk of venous thromboembolism in obesity, we recommend an aggressive approach to prophylaxis. Unfortunately, data on this subject are lacking, and a survey of surgeons who perform bariatric surgery showed wide variation in practice.28 Without good data to guide the clinician, we suggest the joint use of pneumatic compression boots and increased-dose subcutaneous heparin (7500 U twice per day).

Most studies suggest that the risk of aspiration of gastric contents is increased in the obese patient due to increased intraabdominal pressure and the high volume and low pH of gastric contents in such patients. This has implications not only for intubation (see above) but also for routine nursing and feeding. We recommend that all morbidly obese patients be fed and nursed in the semi-upright position.

Nursing Issues

The patient should be nursed in the semi-upright position to improve respiratory function and decrease the risk of aspiration. Special beds are available that accommodate extremely large patients. Hoists can be obtained that assist in lifting and turning the patient. The services of a lift team, if available, should be employed whenever moving the patient to minimize the risk of injury to staff members. Careful attention to the development of bed sores should be paid, because of patient immobility and the difficulty of examining and moving the patient.

Recovery from critical illness related to morbid obesity provides an opportunity to engage the patient in a long-term plan to achieve weight loss. Referral to a weight-loss specialist is indicated. In addition to dietary counseling and physical activity (insofar as possible), available medical therapies include a variety of appetite-suppressant and anti-absorptive medications. Unfortunately, although short-term success is frequent, significant long-term weight loss is uncommon in this population. Therefore, careful consideration should be given to the option of surgical therapy for obesity. Currently favored techniques such as the Roux-en-Y gastric bypass and the biliopancreatic diversion with duodenal switch combine gastric restriction with different degrees of malabsorption. Improvement in or resolution of insulin resistance, obstructive sleep apnea, hypertension, left ventricular systolic dysfunction, and left ventricular hypertrophy have been reported.29 Properly selected patients have a low (≤1%) perioperative mortality rate, although anemia and vitamin deficiency are common in the first year after the procedure. Mean excess weight loss exceeded 50% at 14 years after surgery in a large cohort of patients who had undergone gastric bypass.30 A randomized trial comparing open versus laparoscopic Roux-en-Y gastric bypass surgery demonstrated less deterioration in pulmonary function postoperatively when using the laparoscopic approach.31 Noninvasive positive pressure ventilation may be useful in preventing postoperative respiratory failure in patients with marginal pulmonary function.

Until a large trial comparing medical with surgical approaches to morbid obesity is performed, we believe that properly motivated morbidly obese patients who have failed nonsurgical attempts at weight loss should be considered for bariatric surgery. Careful preoperative evaluation is necessary to exclude patients in whom the potential benefit is exceeded by the risk (e.g., older patients with cor pulmonale).

Obesity has obviously detrimental effects on health across many domains, including an increase in the rate of malignancies and an increase in mortality rate. The influence of obesity on outcome of patients undergoing intensive care is less clear. Whereas some investigators have found an increased mortality rate with morbid obesity,32 others have not.33 Conceivably, increased nutritional reserve could provide a protective effect from overweight in the setting of prolonged critical illness, although further studies are needed to reconcile the different reports of outcome from the studies to date.