Statistics

The prevalence of obesity around the world continues to rise, and in the United States, millions of Americans are considered to be severely obese. Current estimates are that 200 million or 66% of U.S. adults are classified as overweight or obese, and more than 34% of adults are classified as obese. In nationwide data from 2004, 7% of women and 3% of men were extremely obese.⁷ There are an estimated 26 million people in the United States with a body mass index (BMI) of no less than 35 kg/m², and 15 million with a BMI of 40 kg/m² or higher.^1,4

For persons ages 20 years and older, there has been an increase in the proportion of obese adults from a previous level of 23% in 1994 to a new level of approximately 35% (Figure 43-1).

Obesity is not confined to the United States; it is a health problem that is increasing at an alarming rate throughout the world. Globally there are approximately 2 billion individuals documented as overweight (BMI of 25 kg/m² to 29.9 kg/m²), which approximates the number of individuals who are starving worldwide.8.9 It is estimated that there are more than 300 million obese people worldwide,¹⁰ and three countries report that more than 50% of their population is obese. The World Health Organization (WHO) has predicted that the number of severely overweight adults is expected to double by 2025. Concerns about the global obesity crisis are growing, and WHO reports that obesity accounts for more than 400,000 deaths annually, second only to tobacco-related disease as a cause of preventable and premature death.¹¹

In the United States, individuals who are obese have a 10% to 50% percent greater risk of death from all causes, compared with healthy-weight individuals (BMI 18.5 to 24.9). Obesity is associated with about 112,000 excess deaths per year.¹² Most of the increased risk is due to cardiovascular causes.¹³

Cost of Obesity

Public awareness of the problems that arise from obesity is corroborated by the $147 billion spent annually on medical treatment, weight-reduction programs, exercise equipment, low-fat diet products, pharmacologic agents, advertising, and marketing.⁴ Obesity is a major health concern, and obese patients admitted for surgery may exhibit one or more medical conditions in addition to the primary underlying problem.¹⁴ Clearly, identification of obesity-related conditions is vital to the safe administration of an anesthetic.

Definitions

BMI is the accepted measure of body habitus that normalizes adiposity for height.¹ BMI can be calculated according to the following formulas:

Overweight is defined as a BMI of 25 to 29 kg/m², and obesity as a BMI of 30 kg/m².1–3 The rationale for these definitions is based on epidemiologic data that reveal increasing mortality with BMIs over 25 kg/m².⁶ For individuals with a BMI greater than 30 kg/m², mortality rates for a number of conditions, especially those associated with cardiovascular disease, are increased 50% to 100% above rates in individuals of normal weight. A person’s degree of obesity is commonly defined using the body mass index, as classified in Table 43-1. A BMI greater than or equal to 25 is considered “overweight,” a BMI of greater than or equal to 30 is considered “obese,” and a BMI greater than or equal to 40 is classified as “morbidly obese.” We are now seeing references to “super-obese” (BMI greater than 50) and “super-super-obese” (BMI greater than 60).¹⁵

Ideal body weight (IBW) is a term used interchangeably with the terms normal weight and desirable weight.1–3 IBW is a measurement of height and body mass that exhibits the lowest morbidity and mortality for a given population.² Determination of IBW is especially useful in calculating drug and intravenous infusion doses in morbidly obese patients. Certain drugs, if administered according to actual body weight, can produce toxicity, renal damage, or hemodynamic instability. Conversely, some drugs must be given according to actual body weight if therapeutic effects are to be achieved. Simplified weight calculations for ideal and lean body weight (LBW) are as follows:

Risk Factors

Obesity is associated with an increase in the incidence of many medical conditions (Box 43-1). The risk for cardiovascular disease, certain cancers, diabetes, and overall mortality is linearly related to weight gain. Type 2 diabetes, coronary heart disease, hypertension, and hypercholesterolemia are prominent conditions in overweight and obese patients.^1–3 With increasing weight gain and increased adiposity, glucose tolerance deteriorates, blood pressure rises, and the lipid profile becomes more atherogenic.² Using BMI, age, and gender as independent variables, a multiple logistic regression model established that males (P = 0.021), those with higher BMI (P <0.0001), and those of older age (P <0.0001) tended to have more comorbid illness. These data suggest that age, male gender, and extent of obesity are risk factors because they are markers for sicker patients.¹⁶ Hormonal and nonhormonal mechanisms contribute to the greater risk of breast, gastrointestinal, endometrial, and renal cell cancers.⁶ Psychological health risks often stem from social ostracism, discrimination, and impaired ability to participate fully in activities of daily living. Coexistent feelings of worthlessness and low self-esteem can lead to depression that not only magnifies anesthetic morbidity, but also contributes to an increased incidence of suicide among morbidly obese persons.

Body Fat Distribution

In early childhood, fat-cell formation occurs rapidly.² Overfeeding during this time accelerates fat storage and triggers hyperproliferation of fat cells. During adolescence, the number of fat cells stabilizes and remains constant throughout adult life. Children become obese through an increase in fat-cell numbers, whereas adults become obese through hypertrophy of existing fat cells.^2,3 The distribution of body fat, however, is a clearer indicator of increased health risk.¹⁸

Central, android, or abdominal visceral obesity (“apple” shape), with a waist/hip ratio greater than 0.85 in men and 0.92 in women, is perceived as a malignant form of fat accumulation2,19 (Figure 43-2, A). Waist/hip ratio is calculated by dividing the narrowest waist measurement by the broadest hip measurement while the patient is standing.² Waist circumference is the newly established standard used as a marker for abdominal obesity. In men a waist circumference greater than 102 cm (40 inches) and in women a waist circumference of 88 cm (35 inches) denote increased risk for certain diseases and conditions.^2,17 These include ischemic heart disease, diabetes mellitus, hypertension, dyslipidemia, and death.^1–3

Peripheral gynecoid, or gluteal femoral obesity (“pear” shape), with a waist/hip ratio below 0.76 is associated with varicose vein development, joint disease, and reduced incidence of non–insulin-dependent diabetes mellitus (Figure 43-2, B). Medical risks accompanying gynecoid fat deposition are less perilous than those associated with the android pattern.^1,20

Differences in morbidity between android and gynecoid fat distribution are caused by metabolic attributes of the adipose and tissues adjacent to it. Gynecoid repositories of fat, found primarily in women, are metabolically static and are proposed to function as energy depots for pregnancy and lactation.3,20 Android fat distribution, typically seen in males, is metabolically active with regard to free fatty acid (FFA) release.² When elevated levels of FFAs are mobilized from adipose tissue, portal venous drainage delivers high concentrations of FFAs to the liver. Continual delivery of excessive FFAs stimulates hepatic synthesis of very-low-density lipoproteins (VLDLs) and circulation of low-density lipoproteins (LDLs). Hepatic exposure to high concentrations of FFAs also increases gluconeogenesis and inhibition of insulin uptake, which induces non–insulin-dependent diabetes mellitus. Although VLDLs, LDLs, and hyperglycemia are catalysts for the formation of associated cardiovascular and cerebrovascular disease, some studies support the possibility that hyperinsulinemia alone may cause hypertension.^2,3

Cardiovascular Considerations

Cardiovascular considerations are predominantly a reflection of the progressive compensatory processes that evolve to meet the increased metabolic demands of the fat organ.23,24 Cardiovascular disease dominates the morbidity and mortality in obesity and manifests in the form of ischemic heart disease, hypertension, and cardiac failure.¹⁴ Development and sustenance of the fat mass necessitates formation of extra blood vessels and increased circulatory, pulmonary, central, and peripheral blood volume.^2–4 For every 13.5 kg of fat gained, an estimated 25 miles of neovascularization occurs to provide blood flow at a rate of 2 to 3 mL/100 g of tissue per minute. This represents an increased cardiac output of 0.1 L/min for each kilogram of fat acquired.³ Expansion of blood volume, stimulated by hypoxia-induced chronic respiratory insufficiency, is seen in severe obesity. Accelerated renin-angiotensin activity and the perfusion requirements of the fat organ further increase the vascular fluid compartment.^2–4,23,24

Movement of the expanded blood volume through extensive vascular tissue, under compression by adipose tissue, places greater demand on the myocardium. Increased workload caused by elevation of the basal metabolic rate is reflected in increased cardiac output, increased oxygen (O₂) consumption, increased carbon dioxide production, and normal or slightly abnormal arteriovenous O₂ difference.2,25 Chronically elevated cardiac output precedes increased left-sided heart pressures and left ventricular hypertrophy. Because heart rate usually remains the same, cardiac output must be augmented by an increase in stroke volume. Therefore, cardiomegaly, atrial and biventricular dilation, and biventricular hypertrophy ensue. These contribute to the development of hypertension and eventual congestive heart failure.^2–4,26

Hypertension is defined as a systolic pressure greater than 140 mmHg, a diastolic pressure greater than 90 mmHg, or both.³ The prevalence rates of hypertension in obese patients are more than twice as high as those in lean men and women.^26,27 Blood pressure has been shown to increase 6.5 mmHg for every 10% increase in body weight.²⁸ In the nonhypertensive remainder of the severely obese, decreased systemic vascular resistance may serve to facilitate forward blood flow through the doubled body habitus.^2,4 Hypertension is precipitated by increased blood viscosity, catecholamine kinetics, and possibly increased estrogen concentrations. Hyperinsulinemia, elevated mineralocorticoids, and abnormal sodium reabsorption are also implicated as causes of hypertension. Hypercholesterolemia (i.e., cholesterol levels greater than 240 mg/dL) often coexists with hypertension, thereby predisposing obese patients to atherosclerosis and cerebrovascular accident.25,27 Arrhythmias may occur as a result of hypoxemia, hypercapnia, electrolyte disorders, sleep apnea, ventricular hypertrophy, hypertension, and coronary artery disease.^23,24

Coronary artery disease in the obese is a frequently associated but independent risk factor. It appears with or without hypertension, hypercholesterolemia, diabetes mellitus, hyperlipidemia, or sedentary lifestyle.2–4,29 Obesity coincident with coronary artery disease results in frequent angina, congestive heart failure, acute myocardial infarction, and sudden death.^14,25,26 Ischemic heart disease is more common in those obese individuals with a central distribution of fat.²⁵

Respiratory Considerations

Compromise of respiratory function results from the compression of fat on abdominal, diaphragmatic, and thoracic structures. Over time, thoracic kyphosis and lumbar lordosis develop, resulting in impaired rib movement and fixation of the thorax in an inspiratory position.1,3 As a result, chest wall, lung, parenchyma, and pulmonary compliance is reduced to 35% of predicted values.^29,30 Metabolic needs of the fat organ and the greater mechanical work of breathing stimulate increased myocardial O₂ consumption. Increases in carbon dioxide production and retention, coupled with decreased ventilation, coincide with reduced respiratory muscle efficiency.² Lung inflation is inhibited, which causes declinations in functional residual capacity (FRC) to less than closing capacity. Premature airway closure increases dead space and causes carbon dioxide retention, ventilation-perfusion mismatch, shunting, and hypoxemia.^1,19 Morbid obesity is associated with reductions in FRC, expiratory reserve volume (ERV), and total lung capacity.^29–31 FRC declines exponentially with increasing BMI.² A recent study of pulmonary function in morbidly obese patients indicates that forced vital capacity varies inversely with BMI, and patients with a very high BMI, even when asymptomatic, will have major reductions in lung function.³²

Concomitant diminution of vital capacity, total lung capacity, ERV, and inspiratory capacity are demonstrated by rapid, shallow breathing. These ventilation patterns are characteristic of restrictive lung disease.2,30,31 Eventual hypoventilation, hypercarbia, and acidosis result from depression of central nervous system responsiveness to chronic hypoxia.³ Recurrent hypoxemia leads to secondary polycythemia and is associated with an increased risk of coronary artery disease and cerebrovascular disease.¹⁸ Respiratory muscle dysfunction also has been reported with obesity³³ and may result from an inefficiency secondary to changes in chest-wall compliance or the lower lung volumes found in obesity. These abnormalities predispose obese patients to respiratory failure in the setting of even mild pulmonary or systematic insults.³⁴

Obstructive Sleep Apnea

Obesity is a well-established risk factor for sleep apnea, with the incidence of obstructive sleep apnea (OSA) increasing in direct proportion with the level of obesity. Patients characterized with OSA have a BMI greater than 30 kg/m², abdominal fat distribution, and a large neck girth (greater than 17 inches in men and greater than 16 inches in women).² For patients with clinically severe obesity (BMI 35 kg/m² or greater) who present for bariatric surgery, the incidence of sleep apnea ranges from 71% to 77%.^35–57

OSA is characterized by excessive episodes of apnea (10 seconds) and hypopnea during sleep that are caused by complete or partial upper airway obstruction.³⁸ Up to 25% of all surgical patients are at risk of OSA.³⁹ Obstructive sleep apnea is characterized by intermittent closure or narrowing of the upper airway during sleep, which leads to episodes of apnea-hypopnea, arousal, and oxygen desaturation.⁴⁰ This disorder is pervasive and affects nearly 18 million Americans.⁴¹ As many as 80% to 95% of persons with OSA are undiagnosed.⁴²

Apnea is the cessation of airflow at the nose and mouth for more than 10 seconds.⁴³ Apnea is considered obstructive if there is continued respiratory effort despite airflow cessation. Hypopnea is defined as a 50% reduction in airflow for 10 seconds for 15 or more times per hour of sleep associated with snoring and a 4% decrease in oxygen saturation. It connotes a transient reduction in airflow caused by increased upper airway resistance.⁴² OSA syndrome is diagnosed by polysomnography using an apnea-hypopnea index (AHI).⁴⁴ There are different definitions of OSA. The AHI is the number of abnormal respiratory events per hour of sleep. Classically, the accepted minimal clinical diagnostic criteria for OSA are an AHI of 10 plus symptoms of excessive daytime sleepiness. The American Academy of Sleep Medicine defines mild OSA as AHI between 5 and 15, moderate OSA as AHI between 15 and 30, and severe OSA as AHI more than 30. The Medicare guidelines diagnose OSA with an AHI of 15, or an AHI of 5 with 2 comorbidities.³⁵

The pathogenesis of OSA is likely multifactorial.⁴⁵ Contributing factors include airway anatomy, the state-dependent control of the upper airway dilator muscles, and ventilatory stability. The site of upper airway obstruction typically lies in the pharynx. The pharyngeal luminal area during inspiration reflects a balance between collapsing intrapharyngeal negative suction pressure and dilating forces provided by the pharyngeal muscles.⁴⁶ In awake human subjects, the patency is maintained by the central nervous system’s continually mediated contraction of the tensor muscles. These dilator muscles oppose the negative collapsing force developed during inspiration.⁴² This activation of muscle tone is typically reduced during sleep and in many individuals leads to compromised patency of the upper airway with turbulent airflow and snoring. In obese patients, more adipose tissues in the pharyngeal structures increase the likelihood that relaxation of the upper airway muscles will cause collapse of the soft-walled oropharynx between the uvula and the epiglottis. Extraluminal pressure is increased by superficially located masses, and the upper airway is compressed externally.^40,42,47,48

While sleeping, any and all of these mechanical, neural, and structural factors may contribute to upper airway collapse that either interferes with or eliminates ventilation, which results in a surge of pharyngeal dilator muscle activity that subsequently opens the airway. A period of hyperventilation then follows, which reverses hypercarbia, and then correspondingly the central respiratory drive is reduced. The process can repeat itself continually throughout the night, causing intermittent hypoxia and hypercarbia, fragmenting sleep, and triggering adrenergic surges with each cycle.42,43,46 Clinically significant episodes of 5 or more per hour or more than 30 per night result in hypoxia, hypercapnia, systemic and pulmonary hypertension, and cardiac arrhythmias.^20,30,31,38

Patients undergoing electrocardiogram (ECG) Holter monitoring showed that nocturnal paroxysmal asystole, episodic bradycardia, and sinus node dysfunction were more prevalent in patients with OSA.⁴⁹ Study of OSA patients with permanent atrial pacemakers demonstrated that subjects had fewer episodes of OSA if their pacemakers were set to increase their heart rate during the night. It is hypothesized that the increased vagal tone accompanying bradycardia also affects airway patency.⁵⁰

Patients with OSA also have a higher incidence of comorbidities. Approximately 50% to 60% of patients with OSA are hypertensive, and an estimated 50% of hypertensive patients have sleep apnea.⁵¹

Because 80% to 95% of all patients with OSA are undiagnosed and untreated, many patients who present for surgery will not be diagnosed. During preanesthetic evaluation, patients should be asked about their sleeping patterns, and anesthesia providers should have a high index of suspicion for OSA in all obese patients.⁵² Some advocate that all obese patients, or those who observe them while they sleep, be routinely asked about nocturnal snoring or apnea, arousals, and diurnal sleepiness.⁵³ Several screening tools have been developed for preoperative use. The STOP-Bang screening tool (Box 43-2) is easy to use and has a sensitivity of up to 93%.^39,54,55

Suggestions for the management of obstructive sleep apnea patients are listed in Table 43-2.

Obesity Hypoventilation (Pickwickian) Syndrome

Obesity hypoventilation syndrome (OHS), or pickwickian syndrome, is a complication of extreme obesity characterized by OSA, hypercapnia, daytime hypersomnolence, arterial hypoxemia, cyanosis-induced polycythemia, respiratory acidosis, pulmonary hypertension, and right-sided heart failure. At its extreme, there is evidence of nocturnal episodes of central apnea, apnea without respiratory efforts, reflecting progressive desensitization of the respiratory centers to nocturnal hypercarbia.30,31,38,47

OHS is defined as obesity (body mass index greater than 30 kg/m2), daytime hypoventilation with awake Pco₂ greater than 45 mmHg, and sleep-disordered breathing in the absence of other causes of hypoventilation. About 90% of patients with OHS also have OSA. The prevalence of OHS in patients with OSA is uncertain but is estimated to be between 4% and 20%.⁵⁶

OHS, which occurs in 8% of the obese population, is clinically distinct from simple obesity.³¹ With simple obesity, the partial pressure of arterial carbon dioxide, pH, and pulmonary compliance are within normal ranges.²⁹ Hypoxia may be present, but no evidence of cardiac failure or arterioalveolar O₂ difference exists. In contrast, OHS is diagnosed when the morbidly obese patient exhibits inappropriate and sudden somnolence, sleep apnea, hypoxia, and hypercapnia.³ A Pco₂ greater than 45 during wakefulness on arterial blood gas testing with compensatory metabolic compensation and hypoxemia (Po₂ less than 70) is suggestive of OHS.⁵⁶ Alveolar ventilation is reduced because of shallow and inefficient ventilation related to decreased tidal volume, inadequate inspiratory strength, and inadequate elevation of the diaphragm. Cardiac enlargement, cyanosis, polycythemia, and twitching also are evident on physical examination.⁴ Activities of daily living are altered by the somnolent episodes. Operating machinery or driving a vehicle may cause injury or death.

Gastrointestinal Disease

The incidence of gastroesophageal reflux disease, gallstones, and pancreatitis increases with obesity. Obesity is associated with a number of liver abnormalities referred to as nonalcoholic fatty liver disease (NAFLD).⁵⁷ NAFLD includes steatosis, steatohepatitis, fibrosis, cirrhosis, hepatomegaly, and abnormal liver biochemistry. Patients with NAFLD are at risk for developing cirrhosis, hepatic decompensation, and hepatocellular carcinoma. The pathogenesis of NAFLD is not fully understood, although researchers have found that a combination of environmental, genetic, and metabolic factors lead to advanced disease. There have been improvements in noninvasive radiographic methods to diagnose NAFLD—especially for advanced disease. However, liver biopsy is still the standard method of diagnosis for NAFLD.⁵⁸

The prevalence of NAFLD is up to 30% in developed countries and nearly 10% in developing nations, making NAFLD the most common liver condition in the world. The pathogenesis of NAFLD is related to insulin resistance and it is frequently found in individuals who have central obesity or diabetes. Insulin resistance and excess adiposity are associated with increased lipid influx into the liver and increased hepatic triglyceride accumulation. Defects in lipid use via mitochondrial oxidation and lipid export also may contribute to hepatic lipid build-up. Clinically, NAFLD is commonly asymptomatic and usually detected incidentally by liver function tests or imaging performed for other reasons. Subjects with NAFLD have a higher mortality rate than the general population and are at increased risk of developing cardiovascular disease and diabetes in the future.⁵⁷ In obese patients, the mortality rate from liver cirrhosis is 1.5 to 2.5 times higher than in nonobese persons.¹⁸

Gallstones

Gallstones are 30% more prevalent in obese than nonobese women, and this prevalence increases linearly with BMI.⁴ Higher concentrations of cholesterol in the bile and an increased ratio of bile salts to lecithin are responsible for the development of gallstones.⁵⁹ Jaundice also may accompany bile duct obstruction. Laparoscopic and open cholecystectomies are commonly performed in this group of patients because of the increased incidence of gallbladder disease in the obese. Although technically more difficult for both surgical and anesthesia teams, the benefits of laparoscopic gallbladder removal (e.g., reduced postoperative pain, shorter hospitalization, earlier return to activities of daily living) outweigh the risks.

Endocrine and Metabolic Disease

Obesity is seldom the result of primary endocrine dysfunction. Thyroid, adrenocortical, and pituitary function should be investigated with obesity that manifests atypical symptoms.³ Menstrual problems such as oligomenorrhea, amenorrhea, menorrhagia, and the presence of hirsutism may herald hypothalamic-pituitary abnormalities. Obese men may experience decreased libido or impotence indicative of hypogonadism. Low serum follicle-stimulating hormone and testosterone levels are frequently evident.²⁰

Within groups of individuals demonstrating non–insulin-dependent diabetes mellitus, 80% are obese. The risk of type 2 diabetes increases linearly with BMI.²⁰

There is a 35% to 40% prevalence of the metabolic syndrome in the U.S. population. Patients with obesity and metabolic syndrome may have complicated medical histories including diabetes, heart disease, and OSA. Metabolic syndrome comprises an array of conditions including glucose intolerance and/or type 2 diabetes mellitus, hypertension, dyslipidemia, and cardiovascular diseases. Patients with the metabolic syndrome have increased risks for developing coronary artery disease, stroke, peripheral vascular disease, and type 2 diabetes mellitus, and greater mortality from coronary disease and other causes. These patients also have a proinflammatory and prothrombotic state. Whether this syndrome is a disease itself or is composed of discrete disorders is the subject of much investigation and controversy. Individuals with the metabolic syndrome have a cardiovascular risk 50% to 60% higher than normal. The definition and characteristics of metabolic syndrome is noted in Box 43-3.⁶⁰

Orthopedic and Joint Disease

Obese persons often develop osteoarthritis from continued mechanical stress on weight-bearing joints. A linear relationship between degree of arthritis and weight exists.2–4 Ankles, hips, knees, and lumbar spine are frequently burdened. Bone resorption secondary to limited physical activity also may reduce bone density and contribute to stress fractures. Reduction of weight can curb orthopedic injury and lessen the discomfort in the back and lower extremities.

• Obese adolescents have a 70% to 80% chance of being obese adults.⁶⁴

• Childhood obesity is associated with a higher chance of premature death and disability in adulthood, particularly in urban areas.⁶⁵

• Childhood and adolescent overweight and obesity are linked with adult cardiovascular and endocrine problems.⁶⁶

• Obese children are three to five times more likely to suffer a heart attack or stroke before they reach the adult age of 65.⁶⁶

• Being overweight as young as age 18 could be the strongest predictor of future hip replacement because of osteoarthritis.⁶⁷

• Pediatric obesity is more common than diabetes, human immunodeficiency virus (HIV), cystic fibrosis, and all childhood cancers combined.

• Primary hypertension in children has become increasingly common in association with obesity and risk factors such as a family history of hypertension and an ethnic predisposition to hypertensive disease. Obese children are at approximately a three-fold higher risk for hypertension than nonobese children.⁶⁹

• Most children with type 2 diabetes are overweight or obese at diagnosis and usually have a family history of type 2 diabetes. Americans of African, Hispanic, Asian, and American Indian descent are disproportionately represented.⁷⁰

• OSA sleep disorder was very common in a clinical sample of overweight children. OSA is not associated with abdominal obesity. On the contrary, higher levels of abdominal obesity and fat mass are associated with central sleep apnea.

• Bariatric surgery may be useful but only with carefully selected obese children with serious comorbidities and unresponsiveness to interventions. The biggest barrier seems to be the psychosocial aspect, although complications from child bariatric surgery may include leaks, deep vein thrombi, micronutrient deficiency, bleeding, and infection.⁷¹

• Psychosocial disorders may result when obese children are treated differently. This may be the most devastating effect of obesity on children. They may feel isolated and lonely and have self-esteem and identity problems. It is important for the healthcare professional to be sensitive to this issue and understand that an individual’s confidence, especially a child’s, is affected by self-image and perceptions of peers.⁷²

• Cesarean delivery and associated morbidity (approaches 40% in severely obese)

• Difficult placement of epidural and spinals, requiring multiple attempts

• Difficult intubation risk, usually in an emergent setting (twice the risk of nonobese women)

• Decreased ability of ultrasound to detect cardiac and craniospinal abnormalities

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