Nutritional diseases: Obesity and malnutrition

Metabolic syndrome.

Increasing abdominal adiposity is the primary driver of the multidimensional obesity disease continuum. This visceral fat, located intraabdominally, and later ectopic fat, deposited around lean organs, reacts to anabolic signals beyond the physiologic limits of adipocyte accommodation. These cells release a proinflammatory, hyperinsulinemic, and immunogenic response with actions systemically. If the inflammatory state is prolonged, as in chronic overnutrition, individuals with epigenetic or existing environmental vulnerabilities can develop multisystem dysfunction known as metabolic syndrome (MetS). The diagnostic criteria include at least three of the following: (1) excess central obesity, (2) atherogenic dyslipidemia, (3) hypertension, and (4) dysglycemia. The individual definitions commonly in use are reported in Table 19.3 . Patients in this state exhibit closely coupled disease processes that are strong risk factors for cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). Metabolic syndrome is also associated with a higher incidence of adverse perioperative outcomes, including higher infection and mortality rates, increased postoperative atelectasis, longer hospitalizations, and increased need for critical care and mechanical ventilation. Due to its wide range of adverse outcomes, it is important to preoperatively evaluate for any component of MetS and to treat each component individually.

Glucose intolerance and T2DM.

Obesity is an important risk factor for the development of noninsulin-dependent (type 2) diabetes mellitus. Increased adipose tissue leads to increased resistance of peripheral tissues to the effects of insulin, which ultimately results in glucose intolerance and overt diabetes mellitus. Events that increase stress levels in these patients (e.g., surgery) may necessitate the use of exogenous insulin. Resolution of T2DM can be achieved in more than 75% of patients with obesity simply by weight loss.

Systemic hypertension.

Mild to moderate systemic hypertension is seen in approximately 50% to 60% of patients with obesity. The development of hypertension in obesity is multifactorial ( Fig. 19.3 ). Obesity-induced hypertension is related to insulin’s effects on the sympathetic nervous system and extracellular fluid volume. Hyperinsulinemia appears to increase circulating levels of norepinephrine, which has direct pressor activity and increases renal tubular reabsorption of sodium, resulting in hypervolemia. Cardiac output increases by an estimated 100 mL/min for each kilogram of adipose tissue weight gain. At the cellular level, insulin activates adipocytes to release angiotensinogen, which activates the renin-angiotensin-aldosterone pathway; this in turn leads to sodium retention and development of hypertension. An increase in circulating cytokines is seen in obesity, and this may cause damage to and fibrosis of the arterial wall, increasing arterial stiffness. If hypertension is not well controlled, a mixed eccentric and concentric left ventricular hypertrophy can develop that eventually leads to heart failure and pulmonary hypertension. Weight loss can significantly improve or even completely resolve this hypertension . In general, a decrease of 1% in body weight can decrease systolic blood pressure by 0.6 mm Hg and diastolic blood pressure by 0.2 mm Hg.

Heart failure.

Obesity is an independent risk factor for heart failure. In its staging of heart failure, the American College of Cardiology and the American Heart Association lists MetS and obesity as stage A of heart failure. This is defined as heart failure risk factors without symptoms or overt evidence of heart failure. Possible mechanisms for the development of heart failure are structural and functional modifications of the heart resulting from volume overload and vascular stiffness. These changes cause pressure overload that leads to concentric left ventricular hypertrophy, a progressively less compliant left ventricle that develops diastolic dysfunction, and finally systolic dysfunction. Increased metabolic demands and a larger circulating blood volume result in a hyperdynamic circulation. Right ventricular afterload may be increased because of associated sleep-disordered breathing and changes in right ventricular function ( Fig. 19.4 ). Insulin resistance also appears to play a significant role in the development of heart failure. Cardiac steatosis, lipoapoptosis, and activation of specific cardiac genes that promote left ventricular remodeling and cardiomyopathy may contribute to obesity-related cardiomyopathy. The increased demands placed on the cardiovascular system by obesity decrease cardiovascular reserve and limit exercise tolerance. Cardiac dysrhythmias in obese individuals may be precipitated by arterial hypoxemia, hypercarbia, ischemic heart disease, obesity hypoventilation syndrome, or fatty infiltration of the cardiac conduction system. It is important to note that ventricular hypertrophy and dysfunction worsen with the duration of obesity. However, some of these structural and functional changes can be reversed with significant weight loss.

Lung volumes.

Obesity can produce a restrictive pattern of ventilation due to the added weight of the thoracic cage, chest wall, and abdomen. The added weight impedes motion of the diaphragm, especially in the supine position, which results in an overall decrease in functional residual capacity (FRC), expiratory reserve volume, and total lung capacity. FRC declines exponentially with increasing BMI and may decrease to the point that small airway closure occurs (i.e., closing volume becomes greater than FRC) during normal tidal volume breathing. This results in ventilation/perfusion mismatching, right-to-left intrapulmonary shunting, and arterial hypoxemia. General anesthesia accentuates these changes. A 50% decrease in FRC occurs in anesthetized patients who are obese compared with a 20% decrease in nonobese individuals. Application of positive end-expiratory pressure (PEEP) can improve FRC and arterial oxygenation but at the potential expense of reducing venous return and cardiac output.

This decrease in FRC impairs the ability of patients to tolerate prolonged periods of apnea, such as during direct laryngoscopy for endotracheal intubation. They are more likely to experience oxygen desaturation following induction of anesthesia, even with adequate preoxygenation. This phenomenon reflects a decreased oxygen reserve due to the reduced FRC and increased oxygen consumption resulting from the increased metabolic activity of excess adipose tissue.

Gas exchange and work of breathing.

Because of the obese patient’s increased body mass, oxygen consumption and carbon dioxide (CO ₂ ) production are increased. To maintain normocapnia, patients with obesity must increase minute ventilation, which also increases their work of breathing. Patients with obesity typically increase their minute ventilation by rapid, shallow breathing because this pattern uses the least amount of energy and helps prevent fatigue from the increased work of breathing. Individuals with clinically severe obesity may exhibit only modest decreases in arterial oxygenation and modest increases in the alveolar-arterial oxygen gradient. The Paco ₂ and ventilatory response to CO ₂ remains within the normal range in obese patients, which reflects the high diffusing capacity and favorable characteristics of the CO ₂ dissociation curve. However, arterial oxygenation may deteriorate markedly during induction of anesthesia (a period of increased oxygen consumption and decreased oxygen reserve) so that a higher fraction of inspired oxygen (Fio ₂ ) is required to maintain an acceptable level of oxygen saturation.

Lung compliance and airway resistance.

Increased BMI is associated with decreased lung compliance and increased airway resistance. The decrease in lung compliance is due to accumulation of adipose tissue in and around the chest wall and abdomen as well as the added effect of an increased pulmonary blood volume. The decrease in lung compliance is associated with a decrease in FRC and impaired gas exchange. These changes are most evident when obese individuals assume the supine position.

Obstructive sleep apnea.

Obstructive sleep apnea (OSA) is defined as cessation of breathing during sleep for periods lasting longer than 10 seconds. There may be frequent episodes of apnea and hypopnea during sleep. Hypopnea is a reduction in the size or number of breaths compared with normal ventilation and is associated with some degree of arterial desaturation. Apnea occurs when the pharyngeal tissues collapse. Pharyngeal patency depends on the action of dilator muscles that prevent upper airway collapse. Pharyngeal muscle tone is decreased during sleep, and in many individuals this reduction in tone leads to significant narrowing of the upper airway, resulting in turbulent airflow and snoring. In susceptible individuals, this may progress to severe snoring and ultimately to sleep apnea. Sleep fragmentation is the most likely explanation for daytime somnolence, which is associated with impaired concentration, memory problems, and an increase in motor vehicle accidents. Airway obstruction may induce physiologic changes that include arterial hypoxemia and hypercarbia, polycythemia, systemic hypertension, pulmonary hypertension, and right ventricular dysfunction. In addition, patients may complain of morning headaches caused by nocturnal CO ₂ retention and cerebral vasodilation. OSA is diagnosed using polysomnography, where episodes of apnea can be observed and quantified. The average number of incidents per hour measures the severity of OSA. More than five incidents per hour is considered evidence of sleep apnea syndrome. The main predisposing factors for development of OSA are male gender, middle age, and a BMI of 30 kg/m ² or above. Additional factors such as evening alcohol consumption or use of pharmacologic sleep aids can worsen the problem. Treatment of OSA aims to apply enough positive airway pressure through a mask to sustain patency of the upper airway during sleep. Patients treated with positive airway pressure demonstrate improved neuropsychiatric function and reduced daytime somnolence. Patients with mild OSA who do not tolerate positive airway pressure may benefit from nighttime application of oral appliances designed to enlarge the airway by keeping the tongue in an anterior position or by displacing the mandible forward. Nocturnal oxygen therapy is another possibility for individuals who experience significant oxygen desaturation. In severe cases of sleep apnea, surgical treatment, including uvulopalatopharyngoplasty, tracheostomy, or maxillofacial surgery (i.e., genioglossal advancement) may be performed. In many instances, weight loss results in a significant improvement in or even complete resolution of OSA symptoms.

Obesity hypoventilation syndrome.

Obesity hypoventilation syndrome (OHS) is the long-term consequence of OSA. It is defined as a combination of obesity, chronic daytime hypercapnia (Paco ₂ >45 mm Hg), and sleep-disordered breathing. Severe cases of OHS can be characterized by obesity, daytime hypersomnolence, hypoxemia, hypercarbia, polycythemia, respiratory acidosis, pulmonary hypertension, and right ventricular failure. Even light sedation can cause complete airway collapse and/or respiratory arrest in a patient with OHS. All patients with a history of OSA or OHS must be thoroughly evaluated preoperatively. Obese patients without a documented history of sleep apnea should be screened preoperatively with a tool such as the STOP-Bang Questionnaire.

Nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.

Obesity is the most important risk factor associated with nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Obesity causes an excess of intrahepatic triglycerides, impaired insulin activity, and additional release of inflammatory cytokines. These factors can lead to destruction of hepatocytes and disruption of hepatic physiology and architecture. Because of the increasing prevalence of obesity, NASH has become one of the most common causes of end-stage liver disease in the United States. Approximately one-third of overweight children, adolescents, and adults have NAFLD, and 85% of severely obese adults have NAFLD. In most cases this form of hepatitis follows a benign course. However, in severe cases it may progress to cirrhosis, portal hypertension, and/or hepatocellular carcinoma requiring liver transplantation. Most patients are asymptomatic, but some may experience fatigue and abdominal discomfort. Liver function test results may be abnormal. Among patients with NAFLD, 22% also develop diabetes mellitus, 22% develop systemic hypertension, and 25% die of coronary heart disease within 5 to 7 years. Weight reduction, especially bariatric surgery–induced weight loss, has been shown to significantly improve the metabolic abnormalities associated with fatty liver disease or even cure this form of hepatic inflammation.

Gallbladder disease.

Gallbladder disease is closely associated with obesity. Most commonly, patients with obesity have cholelithiasis resulting from supersaturation of bile with cholesterol due to abnormal cholesterol metabolism. Women with a BMI of more than 32 kg/m ² have a three times higher risk of developing gallstones, and those with a BMI of more than 45 kg/m ² have a seven times higher risk of gallstones than lean women. Paradoxically, rapid weight loss, especially after bariatric surgery, increases the risk of gallstones.

Gastric emptying and gastroesophageal reflux disease.

Obesity per se is not a risk factor for delayed gastric emptying or gastroesophageal reflux disease (GERD). In the absence of gastroparesis or other comorbidities that affect gastric transit time and emptying, patients with obesity do not have delayed gastric emptying or higher gastric volumes compared to patients with normal BMIs. Standard preoperative fasting guidelines should be followed, and the routine use of pharmacologic agents to decrease aspiration risk is not recommended. If a fasting state is in question (e.g., active liraglutide therapy) or a nonfasting state is unavoidable (e.g., trauma), standard practice rapid-sequence intubation should be considered. Gastric point-of-care ultrasound (PoCUS) has demonstrated rapid, accurate identification of intragastric contents.