Morbid Obesity, Obstructive Sleep Apnea, and Bariatric Anesthesia
Jon D. Samuels
Fun-Sun F. Yao
A 46-year-old woman was scheduled for elective laparoscopic sleeve gastrectomy. She had a past medical history significant for morbid obesity (MO) (height, 162.5 cm; weight, 176 kg; body mass index [BMI], 66.6 kg per m2), Pickwickian habitus, mild rheumatoid arthritis, osteoarthritis, mild asthma, hypertension, adult-onset diabetes mellitus, peptic ulcer disease with symptomatic gastroesophageal reflux, and obstructive sleep apnea (OSA). She experienced daytime somnolence, heavy nighttime snoring, and had slept in a seated position for the previous 2 years. She was able to walk around the house with a cane but was unable to climb any stairs. A preoperative diagnostic polysomnogram was performed, and an apnea-hypopnea index (AHI) of 42 was calculated. Two weeks prior to surgery, home oxygen therapy with bilevel positive airway pressure (BIPAP) settings had been started at the following settings, with symptomatic improvement: FIO2 of 0.40, respiratory rate 10 breaths per minute, inspired positive airway pressure (IPAP) of +12 cm H2O, and expired positive airway pressure (EPAP) of +4 cm H2O, spontaneous mode. Cardiology clearance was obtained as a high-risk candidate, after an echocardiogram revealed mild right-sided cardiomegaly and mild pulmonary hypertension. The patient’s blood pressure was 155/82 mm Hg, pulse 60 beats per minute, and respirations 20 breaths per minute. The patient was determined to have a difficult airway based on a poor Mallampati score (class 3).
A. Medical Disease and Differential Diagnosis
What problems exist with this patient? This patient asks you if she is high-risk. What is the evidence?
Define the terms overweight, obesity, morbid obesity (MO), super obesity (SO), normal weight, and ideal body weight (IBW).
What is obstructive sleep apnea (OSA)? What are the risk factors for OSA?
How is OSA diagnosed? What is a sleep study, or polysomnogram (PSG)? How are results obtained from a PSG used to grade the severity of OSA?
How does OSA differ in the pediatric population in clinical presentation and pathogenesis?
What is the Pickwickian syndrome (PS)? What is the pathogenesis of severe OSA?
What is the association between obesity and OSA? What is the etiology of pharyngeal pathology in severe obesity?
What are the anesthetic implications of OSA?
What type of metabolic problems would you expect to find in morbidly obese patients? What is the role of leptin in obesity?
Describe the changes that occur in the following respiratory parameters in morbidly obese patients:
Pulmonary mechanics: tidal volume (VT), functional residual capacity (FRC), residual volume (RV), vital capacity (VC), inspiratory reserve volume (IRV), expiratory reserve volume (ERV), and total lung capacity (TLC)
Flow volume loops
Pressure volume loops
Diffusing capacity for carbon monoxide (DLCO)
Compliances: lung (CL), chest wall (CCW), and total (CRS)
Resistance: airway and total respiratory system
Closing capacity (CC)
Work of breathing (WOB)
What changes occur in PaO2 and PaCO2 in morbidly obese patients?
What changes occur in intrapulmonary shunt (QS/QT) and dead space (VD/VT)? Describe the equations.
What changes occur in the cardiovascular system of the obese patient? Discuss cardiac output, blood volume, blood pressure, and pulmonary arterial pressure.
Are there any other disease entities commonly associated with obesity? What is their relationship?
What anatomic changes that affect the airway are associated with MO?
What derangements of the gastrointestinal system are associated with MO?
B. Preoperative Evaluation and Preparation
How would you prepare this patient preoperatively? Would you use preoperative screening questionnaires to diagnose OSA?
How would you premedicate this patient? Why?
How would you adjust doses of anesthetics in the morbidly obese?
C. Intraoperative Management
How would you monitor this patient?
The American Society of Anesthesiologists’ (ASA) Difficult Airway Algorithm provides a guideline for management of the difficult airway. How do the comorbidities of MO and OSA modify implementation of the algorithm?
How would you induce anesthesia? Describe the intubation technique.
Why is it important to preoxygenate the obese patient? How would you do it? Compare the effectiveness of the four-maximum-breath and 3-minute techniques.
There are many new airway devices on the marketplace. Which of these devices have been particularly successful on the morbidly obese or OSA patient?
How would you maintain general anesthesia? What agents would you choose? How would you prepare for emergence?
Which muscle relaxants would you use?
Can regional anesthesia be used intraoperatively and postoperatively to decrease opioid requirements for bariatric surgery? What are the advantages and disadvantages of regional anesthesia? What are some of the newer techniques available?
What is the pathophysiology of pneumoperitoneum (PNP)? What is the effect on the cardiopulmonary system? How does it change perioperative care? What are the optimal ventilator strategies for morbidly obese patients undergoing bariatric surgery?
What are the devices that anesthesiologists place in the upper gastrointestinal canal during laparoscopic bariatric surgery? Are there risks associated with placement and management of these devices?
When will you extubate this patient? What are the extubation criteria?
What is apneic oxygenation?
What is diffusion hypoxia? How do you prevent it?
D. Postoperative Management
What are the major early postoperative complications in the morbidly obese patient?
How does position affect respiratory function in the obese patient?
How would you prevent postoperative atelectasis?
How long would you prescribe supplementary oxygen postoperatively?
How would you control postoperative pain?
A. Medical Disease and Differential Diagnosis
A.1. What problems exist with this patient? This patient asks you if she is high-risk. What is the evidence?
Preoperative significant past medical history in this patient consists of MO, OSA, possible PS, right ventricular hypertrophy, mild pulmonary hypertension, systemic hypertension, adultonset diabetes mellitus, osteoarthritis, mild rheumatoid arthritis, and severe gastroesophageal reflux disease (GERD). Epidemiologically, this patient is at increased risk of coronary artery disease, cardiac arrhythmias, left- and right-sided congestive heart failure, peripheral vascular disease, venous thrombosis and pulmonary emboli, cerebrovascular disease, biliohepatic disease, hepatic steatosis, hepatic cirrhosis, degenerative joint disease, metabolic syndrome, and socioeconomic and psychosocial impairment.
This is a high-risk patient, with increased risk of both perioperative morbidity and mortality. Major anesthetic concerns include risk of difficult airway, difficult mask ventilation, decreased apneic threshold to trace amount of anesthetics, sedatives and narcotics, prolonged anesthesia emergence, postemergence resedation, positional ventilatory collapse, restrictive and obstructive lung disease, ventilation/perfusion mismatch, and worsening of reactive pulmonary hypertension and cor pulmonale. This patient must receive continuation of her preoperative oxygen therapy with continuous positive airway pressure (CPAP) in the immediate recovery period, at the values determined by her sleep study (PSG), or greater. Additional anesthetic concerns include difficult monitoring, difficult vascular access, and positioning issues. Additionally, there is a rare risk of postoperative massive pharyngeal collapse, rhabdomyolysis with renal failure, increased risk of infection including pneumonia, and positional injuries. Meticulous attention to acute pain management is essential.
Safe perioperative care for this patient requires triage to a specialized facility, additional personnel, surgeons with advanced laparoscopic training, and anesthesiologists with advanced airway skills and optimal equipment.
Alvarez A, Brodsky JB, Lemmens HJM, et al, eds. Morbid Obesity Peri-operative Management. 2nd ed. Cambridge, United Kingdom: Cambridge University Press; 2010:208-212.
American Society of Bariatric Surgery. The largest dedicated site to weight reduction surgery. http://www.asbs.org. Accessed October 22, 2015.
Kaw R, Chung F, Pasupuleti V, et al. Meta-analysis of the association between obstructive sleep apnoea and postoperative outcome. Br J Anaesth. 2012;109(6):897-906.
Kopelman PG, Caterson ID, Dietz WH, eds. Clinical Obesity in Adults and Children. 3rd ed. West Sussex, United Kingdom: Wiley-Blackwell; 2010;228-243, 267-274.
Leykin Y, Brodsky JB, eds. Controversies in the Anesthetic Management of the Obese Surgical Patient. Milan, Italy: Springer-Verlag Italia; 2013:33-40.
A.2. Define the terms overweight, obesity, morbid obesity (MO), super obesity (SO), normal weight, and ideal body weight (IBW).
Obesity is a multifactorial chronic disease involving social, cultural, physiologic, psychological, metabolic, endocrine, genetic, and behavioral components, resulting in excess adipose and tissue mass. The modern basis for the determination of demographics is the BMI, or Quetelet’s
Index, after the Belgian statistician, Adolphe Quetelet, published in 1842, and is measured in body weight in kilograms divided by the height in meters squared (kg per m2). The standard for ideal body weight (IBW), the sex-specific desirable weight for persons with small, middle, and large frames, is published in the Metropolitan Life insurance tables.
Index, after the Belgian statistician, Adolphe Quetelet, published in 1842, and is measured in body weight in kilograms divided by the height in meters squared (kg per m2). The standard for ideal body weight (IBW), the sex-specific desirable weight for persons with small, middle, and large frames, is published in the Metropolitan Life insurance tables.
Anorexia is defined as a BMI of less than 17.5 in males or females.
Underweight is defined as a BMI of 17.6 to 19.0 in females or 17.6 to 20.6 in males.
Ideal (normal) weight is defined as a BMI of 19.1 to 25.8 in females and 20.7 to 26.4 in males.
Marginally overweight is defined as a BMI of 25.9 to 27.2 in females and 26.5 to 27.8 in males.
Overweight is defined as a BMI of 27.3 to 32.3 in females and 27.9 to 31.1 in males.
Obesity is defined as a BMI of greater than 20% of IBW, 32.4 to 34.9 in females and 31.2 to 34.9 in males.
Severe obesity is defined as a BMI of 35.0 to 39.9 in both sexes.
Morbid obesity is defined as a BMI of greater than 40 or greater than 35 with associated comorbidites such as hypertension and diabetes mellitus.
Super obesity, a relatively new term, is defined as a BMI greater than 50.
There exist imperial and metric system BMI tables and web-based calculators.
Occasionally, an approximate, non-sex-specific system is used. In this system, a healthy (normal) weight is a BMI of 18.6 to 24.9, overweight is a BMI of 25 to 29.9, obesity is a BMI of 30 to 34.9, severe obesity is a BMI of 35 to 39.9, morbid obesity is a BMI of more than 40.0.
The older definitions of obesity may occasionally suffice. Overweight was formerly defined as a body weight of up to 20% greater than the predicted ideal weight, and obesity of more than 20%. MO was formerly defined as a body weight of 100 lb above the IBW, or alternatively, of twice the IBW. These definitions involved value judgments and inaccuracies and were later abandoned in favor of more objective terminology.
Alternative systems for the determination of obesity exist. In the triceps skinfold thickness test, for example, obesity is defined as a value of greater than 23 mm in males or greater than 30 mm in females. In the Broca’s index (height in centimeters minus 100 for males and minus 105 for females), the IBW is calculated in kilograms.
Males: ideal body weight (kg) = height (cm) – 100
Females: ideal body weight (kg) = height (cm) – 105
There are different patterns of distribution of obesity. In peripheral obesity (e.g., gynoid or gluteal pattern), the individual has a pear shape, and adipose tissue deposition is predominantly in the lower body. In central obesity (e.g., android, or cushingoid), and especially upper body obesity, the individual has an apple shape, and adipose tissue deposition occurs predominantly in the upper body. Central obesity has greater associations with perioperative risk and OSA.
Halls SB. The “Metropolitan Life” tables. http://www.halls.md/met-life-ideal-weight/. Accessed July 1, 2015.
Kopelman PG, Caterson ID, Dietz WH, eds. Clinical Obesity in Adults and Children. 3rd ed. West Sussex, United Kingdom; Wiley-Blackwell; 2010:3-14.
The New Image Weight Loss Center. Imperial system BMI calculator. http://www.newimageweightloss.com. Accessed July 1, 2015.
What Health. Metric system BMI calculator. http://www.whathealth.com/bmi/chart-metric2.html. Accessed July 1, 2015.
A.3. What is obstructive sleep apnea (OSA)? What are the risk factors for OSA?
OSA is a sleep disorder. Sleep disorders may be grouped into the following types: conditions with excessive daytime somnolence (e.g., OSA), conditions with disorders initiating and maintaining sleep (e.g., insomnia), and circadian rhythm disorders (e.g., jet lag).
In the older terminology, OSA referred to both OSA proper and to obstructive sleep hypopnea (OSH) syndrome, a milder variant. Today, it is more precise to refer to obstructive sleep apnea and hypopnea syndrome (OSAHS) when naming the general condition.
OSA is defined as cessation of airflow for more than 10 seconds despite continuing ventilatory effort, five or more times per hour of sleep, associated with a decrease in arterial oxygen saturation (SpO2) of greater than 4%. OSH is defined as a decrease in airflow of more
than 50% for more than 10 seconds, 15 or more times per hour of sleep, associated with a decrease in SpO2 of greater than 4%. Both forms of OSAHS are usually associated with snoring, sleep disruption from increased ventilatory effort-induced arousal, hypersomnolence (daytime sleepiness), altered cardiovascular function, and pathophysiologic alterations, of which hypoxemia and hypercarbia are primary events, and polycythemia, systemic and pulmonary hypertension, various cardiac arrhythmias, myocardial ischemia, right and left ventricular hypertrophy, and eventually failure are secondary events.
than 50% for more than 10 seconds, 15 or more times per hour of sleep, associated with a decrease in SpO2 of greater than 4%. Both forms of OSAHS are usually associated with snoring, sleep disruption from increased ventilatory effort-induced arousal, hypersomnolence (daytime sleepiness), altered cardiovascular function, and pathophysiologic alterations, of which hypoxemia and hypercarbia are primary events, and polycythemia, systemic and pulmonary hypertension, various cardiac arrhythmias, myocardial ischemia, right and left ventricular hypertrophy, and eventually failure are secondary events.
Severe obesity is a strong independent risk factor for OSAHS. Other risk factors include male gender, middle age, evening ingestion of alcohol, and drug-induced sleep. In nonobese individuals, risk factors are craniofacial dysostoses, particularly micrognathia (absolute or relative), cartilaginous abnormalities (e.g., lingual tonsillar hyperplasia), chronic nasal obstruction, and tonsillar hypertrophy.
Alvarez A, Brodsky JB, Lemmens HJM, et al, eds. Morbid Obesity Peri-operative Management. 2nd ed. Cambridge, United Kingdom: Cambridge University Press; 2010:19-27.
Sugerman HJ, Nguyen NT, eds. Management of Morbid Obesity. New York; Taylor and Francis; 2006:14, 52.
A.4. How is OSA diagnosed? What is a sleep study, or polysomnogram (PSG)? How are results obtained from a PSG used to grade the severity of OSA?
OSA may be suspected by history, physical examination, or comorbidities, but definitive diagnosis requires a sleep study. The hallmark of OSA is a history of heavy snoring. Nocturnal apnea, arousal during sleep, and daytime somnolence are commonly reported. Most adults with OSA have upper body obesity, increased neck circumference, micrognathia, and poor Mallampati scores on physical examination. Patient characteristics typically associated with OSA are a higher BMI, hypertension, and certain cephalometric measurements. In 90% of cases, the patient has a BMI in excess of 28 kg per m2. OSA, however, may result from any condition that predisposes to upper airway obstruction. Some examples are pregnancy, upper airway abnormalities (e.g., deviated nasal septum, hypertrophic tonsils, and adenoids), cartilaginous abnormalities (e.g., lingual tonsillar hyperplasia), craniofacial dysostoses, certain congenital and genetic conditions (e.g., Prader-Will syndrome, Down syndrome, Marfan syndrome, Pierre Robin sequence, acromegaly, muscular dystrophy), as well as certain medical conditions (hypothyroidism). The absence of a typical or compelling presentation, however, does not rule out the possibility of OSAHS.
Definitive diagnosis of OSA is made by sleep specialists with a formal sleep study or a PSG. A PSG is an involved study, performed at sleep study centers, that examines nocturnal sleeping patterns by monitoring physiologic parameters. In its most comprehensive form, the following parameters are studied: two to six electroencephalographic (EEG) channels to measure electrical activity of the brain and to document sleep cycles, two electrooculogram (EOG) channels to distinguish rapid eye movement (REM) from non-REM sleep, chin electromyogram (EMG) to monitor arousal and activity of the upper airway (genioglossus and digastric muscles), an airway microphone to monitor airflow from the nose and mouth, elastic belts placed on the chest and abdomen to monitor respiratory effort, an infrared video camera to monitor body position, one channel of electrocardiogram (ECG) to monitor cardiac activity, a pulse oximeter to monitor oxygen saturation, and two-leg EMG channels to monitor leg movements. A PSG may be ordered to definitively diagnose a sleep disorder, as part of medical management, or in the surgical work-up of a high-risk population (e.g., preoperative screening of bariatric surgical candidates).
A PSG will diagnose the presence of OSAHS, type (central, peripheral, or mixed), and grade severity. Results are reported in as the total number of apneas and hypopneas per hour of sleep or the AHI. AHI values correspond to OSA severity as follows: 6 to 20 (mild), 21 to 40 (moderate), and greater than 40 (severe). The total number of arousals hourly is the Arousal Index (AI), which is the number of hourly arousals. The sum of the AHI and the AI is the Respiratory Disturbance Index (RDI).
As the PSG is an expensive and time-consuming study that not covered by all insurance plans, simpler tests have been proposed, such as a partial (level 2) portable polysomnography and nocturnal oximetry. OSA is primarily a clinical diagnosis. Because only a very small
percentage of patients presenting for surgery have been tested, have available results, and are compliant with recommendations, great importance is placed on preoperative sleep apnea screening tools and questionnaires.
percentage of patients presenting for surgery have been tested, have available results, and are compliant with recommendations, great importance is placed on preoperative sleep apnea screening tools and questionnaires.
Abishami A, Khajehdehi A, Chung F. A systematic review of screening questionnaires for obstructive sleep apnea. Can J Anaesth. 2010;57:423-438.
American Sleep Apnea Association. http://www.sleepapnea.org/learn/sleep-apnea.html. Accessed July 1, 2015.
Kopelman PG, Caterson ID, Dietz WH, eds. Clinical Obesity in Adults and Children. 3rd ed. West Sussex, United Kingdom: Wiley-Blackwell; 2010:251-253.
Leykin Y, Brodsky JB, eds. Controversies in the Anesthetic Management of the Obese Surgical Patient. Milan, Italy: Springer-Verlag Italia; 2013:103-104.
National Heart, Lung, and Blood Institute. Introduction to types of polysomnograms. http://www.nhlbi.nih.gov/health/health-topics/topics/slpst/types.html. Accessed July 1, 2015.
Practice Guidelines for the Perioperative Management of Patients with Obstructive Sleep Apnea. Washington, DC: American Society of Anesthesiologists; 2005.
A.5. How does OSA differ in the pediatric population in clinical presentation and pathogenesis?
Sleep-disordered breathing in children and adults is distinct in pathophysiology, clinical presentation, and therapy.
Childhood OSA (COSA) consists of a continuum from snoring, to upper airway resistance syndrome, to the fully expressed syndrome. The pathophysiology of COSA is most commonly peripheral in origin due to nocturnal airway blockage from nasal pathophysiology, hypertrophic tonsils and adenoids, or craniofacial dysostoses. The symptomatology in COSA consists of snoring (usually continuous), rare daytime sleepiness, and frequent behavioral disturbances (e.g., attention deficit hyperactivity disorder [ADHD]). It is distinguished from adult OSA by the following: Snoring is more continuous, there is no sex predilection, and surgery (commonly adenotonsillectomy, rarely uvulopalatopharyngoplasty [UPPP]) is curative. There is no gold standard for the PSG diagnosis in children.
Adult OSA or OSAHS consists of a continuum from asymptomatic, to paroxysmal snoring, to severe nocturnal airway closure, requiring the patient to sleep in a sitting position, and daytime somnolence. The pathophysiology of OSAHS is central, peripheral, or mixed. Peripheral disease is caused by redundant adipose tissue in the upper airway, in the setting of severe obesity, sometimes with a superimposed craniofacial dysostosis. The symptomatology of OSAHS consists of intermittent snoring, apneic episodes, with daytime somnolence. OSH, a milder form of OSA, may be clinically indistinguishable. Obesity-hypoventilation syndrome (OHS) is severe OSA with chronic daytime hypoventilation, super obesity, and hypercapnia not related to pulmonary disease. Pickwickian syndrome is OHS with cor pulmonale.
Alvarez A, Brodsky JB, Lemmens HJM, et al, eds. Morbid Obesity Peri-operative Management. 2nd ed. Cambridge, United Kingdom: Cambridge University Press; 2010:222-232.
Kopelman PG, Caterson ID, Dietz WH, eds. Clinical Obesity in Adults and Children. 3rd ed. West Sussex, United Kingdom: Wiley-Blackwell; 2010:392-407.
A.6. What is the Pickwickian syndrome (PS)? What is the pathogenesis of severe OSA?
The PS was so named by Burwell in 1956, as a reference to Joe, an obese, somnolent boy in the Posthumous Papers of the Pickwick Club, written in 1837 by Charles Dickens. In Joe, Dickins provided the first accurate description of the most severe type of OSA, consisting of a BMI over 50 kg per m2 or SO, alveolar hypoventilation (hypoxemia and hypercarbia), heavy nighttime snoring with periodic respiration, hypersomnolence (daytime somnolence), secondary polycythemia, right and left ventricular hypertrophy, and right-sided heart failure. This syndrome may occur with or without pulmonary hypertension.
In these individuals with PS, there are repeated cycles of sleep, arousal, and sleep, accompanied by obstructed breathing, with snoring and restlessness. Hypoxemia and hypercarbia result from disruption of a normal sleep pattern, with loss of REM sleep and cardiovascular changes. Loss of REM sleep induces hypersomnolence, personality, behavior, and cognitive changes, and predisposes these individuals to be accident-prone. Eventually, severe
OSA leads to OHS, with nocturnal, and later diurnal alterations in the control of breathing, manifested as central apneic events, or apnea without ventilatory efforts. They also develop an alveolar-arterial oxygen gradient by ventilation/perfusion mismatch. The major factor in the pathogenesis of this syndrome is unknown but may be due to decreased hypoxic and hypercarbic ventilatory drive. Late in the disease process, there is progressive daytime hypoxia and hypercarbia. When cor pulmonale supervenes, PS is complete. Recently, the term Pickwickian syndrome has been abandoned in favor of obesity hypoventilation syndrome.
OSA leads to OHS, with nocturnal, and later diurnal alterations in the control of breathing, manifested as central apneic events, or apnea without ventilatory efforts. They also develop an alveolar-arterial oxygen gradient by ventilation/perfusion mismatch. The major factor in the pathogenesis of this syndrome is unknown but may be due to decreased hypoxic and hypercarbic ventilatory drive. Late in the disease process, there is progressive daytime hypoxia and hypercarbia. When cor pulmonale supervenes, PS is complete. Recently, the term Pickwickian syndrome has been abandoned in favor of obesity hypoventilation syndrome.
There are several cardiovascular changes in severe OSA, all related to the episodic airway closure, with hypoxemia and hypercarbia. Hypoxemia and alterations in autonomic tone may induce bradycardia during apneic episodes; in half of these patients, long sinus pauses, second-degree heart block, and ventricular ectopy may result. These arrhythmias may lead to nocturnal angina and myocardial infarction in susceptible individuals. Pulmonary hypertension may be caused directly by hypoxic pulmonary vasoconstriction, or indirectly by either increased transmural pulmonary artery pressures from negative thoracic pressure created by a sustained ventilatory effort against the upper airway obstruction, or by increases in pulmonary artery tone from increased sympathetic tone created by episodic hypoxemia. Pulmonary hypertension initially causes right ventricular hypertrophy, resulting in a higher right ventricular end-diastolic pressure (RVEDP), and later culminates in right ventricular failure, or cor pulmonale. The systemic circulation is also affected by episodic increases in sympathetic tone, with systemic hypertension presenting early, and left ventricular hypertrophy, followed by left ventricular failure, presenting much later. Systemic hypertension may also lead to increased stroke volume.
Chau EHL, Lam DB, Wong J, et al. Obesity hypoventilation syndrome: a review of epidemiology, pathophysiology, and perioperative considerations. Anesthesiology. 2012;117(1):188-205.
A.7. What is the association between obesity and OSA? What is the etiology of pharyngeal pathology in severe obesity?
Obesity and OSAHS are both common, coexisting diseases. Obesity has reached epidemic proportions in the industrialized world and currently poses a greater worldwide health risk than malnourishment. In the United States alone, obesity is annually responsible for 300,000 premature deaths and an annual health care cost of $100 billion dollars. Sixty-five percent of the U.S. population, or 127 million adults, are obese. The prevalence of severe obesity, a strong risk factor for OSAHS, is 3.15% in males and 6.70% in females, according to U.S. population data.
Incidence and severity of OSAHS correlates loosely with BMI, better with neck circumference, and most closely with waist circumference. OSAHS is 2.6 times more likely when the waist-to-hip ratio exceeds 1.0 in obese males and 0.85 in obese females.
Sixty percent to 90% of OSA patients are obese, and it has been estimated that 9% of women and 24% of men in the United States suffer from the syndrome, a total of 18 million individuals, of which 2% of women and 4% of men are symptomatic. These figures will almost certainly increase, as the demographics shift toward an older and more obese population. Many of these patients are undiagnosed at the time of surgery, representing potential perioperative complications. The prevalence of OSA in morbidly obese patients presenting for weight loss surgery is 78%.
There are three reasons why severe obesity per se may cause or exacerbate OSAHS. First, there is an inverse relationship between obesity and pharyngeal volume. The pharyngeal area decreases in obesity from deposition of adipose tissue into pharyngeal structures, in particular, the uvula, the tonsils, the tonsillar pillars, the tongue, the aryepiglottic folds, and, most importantly, the lateral pharyngeal walls. The volume of adipose in the lateral pharyngeal walls correlates with the clinical severity of airway obstruction. Increased deposition of pharyngeal adipose increases the likelihood that relaxation of the upper airway muscles will result in collapse of the soft-walled retroglossal space, or the oropharynx, between the uvula and the epiglottis. The shape of the pharynx remodels from an ellipse with the long axis transverse to an ellipse with the long axis anterior-posterior. The muscles that open the collapsible pharynx on expiration during sleep (e.g., tensor palatini, genioglossus, hyoid
muscles) in response to stretch receptors in the pharynx are located in the anterior pharynx, and do not function well with a remodeled pharynx.
muscles) in response to stretch receptors in the pharynx are located in the anterior pharynx, and do not function well with a remodeled pharynx.
Second, patency of the collapsible pharynx is determined by the transmural pressure (the difference between the extraluminal and intraluminal pressure) and compliance of its wall. If the compliance of the pharyngeal wall and intraluminal pressure (inspiratory pressure) is constant, then the remaining important determinant of upper airway patency is extraluminal pressure. In obese patients, extraluminal pressure is increased by superficially located fat masses; that is, the upper airway is compressed externally. Therefore, neck circumference is greater in obese patients with OSAHS compared with obese non-OSAHS patients.
Third, pharyngeal patency is partially determined by lung volume. The collapsible (particularly in a supine position), soft-walled pharynx is kept patent during sleep by lung volumes above the FRC, which pulls on the carina, tenting open the pharynx. This is known as the lung volume hypothesis. Smaller lung volumes allow a cephalad displacement of the carina, approximately 0.5 to 1.5 cm, resulting in collapse or even telescoping of the pharynx, with a smaller circumferential area.
Amatoury J, Kairaitis K, Wheatley JR, et al. Peripharyngeal tissue deformation and stress distributions in response to caudal tracheal displacement: pivotal influence of the hyoid bone? J Appl Physiol (1985). 2014;116(7):746-756.
Hillman DR, Walsh JH, Maddison KJ, et al. The effect of diaphragm contraction on upper airway collapsibility. J Appl Physiol (1985). 2013;115(3):337-345.
Lopez PP, Stefan B, Schulman CI, et al. Prevalence of sleep apnea in morbidly obese patients who presented for weight loss surgery evaluation: more evidence for routine screening for obstructive sleep apnea before weight loss surgery. Am Surg. 2008;74:834-838.
Martinez-Rivera C, Abad J, Fiz JA, et al. Usefulness of truncal obesity indices as predictive factors for obstructive sleep apnea syndrome. Obesity (Silver Spring). 2008;16:113-118.
Squier SB, Patil SP, Schneider H, et al. Effect of end-expiratory lung volume on upper airway collapsibility in sleeping men and women. J Appl Physiol (1985). 2010;109:977-985.
A.8. What are the anesthetic implications of OSA?
Management of anesthesia in patients with severe OSAHS poses significant risks. These patients are extremely sensitive to minimal doses of central nervous system-depressant drugs, such as anesthetics, sedatives, and analgesics, and may exhibit prolonged sedation, resedation, or apnea as well as upper airway obstruction or, rarely, massive pharyngeal collapse. For these reasons, premedication with benzodiazepines or narcotics is used sparingly if at all, and sedation is generally reserved for painful or unpleasant situations (e.g., placement of invasive lines) where the patient is under the direct observation of a trained clinician.
Difficult tracheal intubation is expected in 13% to 24% of obese patients with OSAHS. In this particular case, the patient presents for laparoscopic bariatric surgery. Although the “ideal general anesthetic” regimen for these patients is a matter of some discussion, the literature does support the following: a safe induction, a deep maintenance anesthetic with muscle relaxants, and a smooth emergence with rapid offset devoid of active metabolites or trace anesthetic. Anesthetic gases should be insoluble, resistant to metabolic degradation, and without lipid depot compartmentalization, combined with rapid return of airway reflexes. The only weak inhalation anesthetic, nitrous oxide (N2O), has the advantage of being relatively insoluble, as measured by blood-gas solubility coefficient (0.46), but it causes intestinal inflation, may be emetic, and is not recommended in the presence of pulmonary hypertension, a condition that is more common in MO. Of the available potent inhalation anesthetics (desflurane, sevoflurane, and isoflurane), desflurane combines the quickest wake-up, fastest return of airway reflexes, lowest solubility, as measured by the blood-gas solubility coefficient (desflurane, 0.45; sevoflurane, 0.65; isoflurane, 1.4), and lowest percentage of hepatometabolization (desflurane, 0.02%; isoflurane, 0.2%; sevoflurane, 2% to 3%). Intravenous agents should be either lipophobic (hydrophilic), spontaneously degrade in vivo or be ultrashort-acting.
Sedation or awake fiberoptic intubation: Ketamine and dexmedetomidine are optimal agents. Induction of general anesthesia: All agents have been utilized. Maintenance agents: air/oxygen mixtures, desflurane, cisatracurium, and remifentanil. Last hour of general anesthesia
and emergence: nitrous oxide (except in the presence of pulmonary hypertension), remifentanil, and morphine sulfate.
and emergence: nitrous oxide (except in the presence of pulmonary hypertension), remifentanil, and morphine sulfate.
When feasible, regional anesthesia is useful. Tracheal extubation is considered only when patients are fully awake with intact upper airway reflexes. Episodic arterial hypoxemia may occur early, in the first 24 hours, or late, from the second to the fifth day, postoperatively.
Discharge from the postanesthetic care unit (PACU) may be made in the morbidly obese OSA, per protocol, after they have been started on CPAP or BIPAP, and have been observed for at least 30 minutes, without stimulation, and found to be free of respiratory arrests. If they have even one respiratory arrest, PACU stay is extended for an additional 3 hours, and consideration is made to transfer the patient to a monitored bed.
Intravenous patient-controlled analgesia (PCA) appears to be well tolerated in the morbidly obese, without deleterious effects on oxygen saturation, respiratory function, blood pressure, or heart rate. Dosing is based on IBW, without continuous rate. The most common drug used is morphine sulfate, starting at 20 µg per kg every 10 minutes with a 4-hour dose of 80% of the calculated maximum dose. Hydromorphone is an excellent second-line agent. It is important to individualize therapy. There is a paucity of literature on the safety and efficacy of intravenous PCA in the morbidly obese severe OSAHS patient. There are case reports of respiratory complications in this population; postoperative pain management must take into account the exquisite sensitivity of these patients to the ventilatory-depressant effects of opioids.
American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology. 2014;120:268-286.
Apfelbaum JL, Hagberg CA, Caplan RA, et al. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology. 2013;118:251-270.
A.9. What type of metabolic problems would you expect to find in morbidly obese patients? What is the role of leptin in obesity?
In MO, there is an increase in both low metabolically active tissue (e.g., adipose) and normally active tissue (e.g., muscle). In general, lean body weight (LBW) is equal to IBW plus 20% to 40% IBW. IBW is a value, based on population demographics, which could never be realized through weight reduction, in a severely obese individual.
Morbidly obese individuals have an increase in total oxygen consumption and carbon dioxide production due to an increased tissue mass. Increased metabolism demonstrates a linear relation with body weight and body surface area. Basal metabolic rate, however, remains normal in obese individuals.
Severely obese patients often have nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH), increasing long-term risk of hepatic cirrhosis, dyslipidemia, inflammation, insulin resistance, and atherosclerosis. Metabolic syndrome, defined as a collection of central obesity, hypertension, dyslipidemia, and impaired glucose tolerance, is present in severe cases and increases perioperative risk of morbidity and death. Metabolic syndrome is mediated through adipocytokines, such as acute phase reactants (increases in C-reactive protein and serum amyloid A [SAA]), adipokines (decreased adiponectin, or increases in leptin or resistin), macrophage-derived factors (increased resistin or interleukin-1 beta [IL-1β beta]), proinflammatory cytokines and chemokines (increases in tissue necrosis factor-alpha [TNF-α], several interleukins [IL-1, IL-6, IL-8, IL-10, IL-18]), chemokine [C-C motif], and prothrombotic factors (increases in plasminogen activator inhibitor-1 [PAI-1], fibrinogen and Factor VII).
Leptin is a satiety hormone secreted by adipocytes. Most obese adults have high inappropriate leptin levels or hyperleptinemia. Leptin levels are increased by overfeeding, insulin, glucocorticoids, endotoxin, and cytokines and are decreased by fasting, testosterone, thyroid hormone, and exposure to cold temperature. In the heart, increased leptin expression is seen following reperfusion after ischemia, and leptin concentration in cardiomyocyte culture serum is increased with endothelin (ET)-1 and angiotensin II treatment. Congenital leptin
deficiency is a rare cause of obesity, caused by mutations in the LEP gene in an autosomal recessive pattern.
deficiency is a rare cause of obesity, caused by mutations in the LEP gene in an autosomal recessive pattern.
Genetics Home Reference. http://ghr.nlm.nih.gov/condition/congenital-leptin-deficiency. Reviewed December 2013. Accessed July 1, 2015.
Martyn JA, Kaneki M, Yasuhara S. Obesity-induced insulin resistance and hyperglycemia: etiologic factors and molecular mechanisms. Anesthesiology. 2008;109:137-148.
Matsuzawa Y. Therapy insight: adipocytokines in metabolic syndrome and related cardiovascular disease. Nat Clin Pract Cardiovasc Med. 2006;3:35-42.
Yang R, Barouch LA. Leptin signaling and obesity: cardiovascular consequences. Circ Res. 2007;101:545-559.
A.10. Describe the changes that occur in the following respiratory parameters in morbidly obese patients:
Pulmonary mechanics: tidal volume (VT), functional residual capacity (FRC), residual volume (RV), vital capacity (VC), inspiratory reserve volume (IRV), expiratory reserve volume (ERV), and total lung capacity (TLC)
Flow volume loops
Pressure volume loops
Diffusing capacity for carbon monoxide (DLCO)
Compliances: lung (CL), chest wall (CCW), and total (CRS)
Resistance: airway and total respiratory system
Closing capacity (CC)
Work of breathing (WOB)
Morbidly obese patients have reduced lung volumes, increased WOB, and alterations in control of breathing and gas exchange. Body fat distribution, as well as BMI, determines the effect of obesity on pulmonary function.
Pulmonary mechanics. Pulmonary function tests (PFTs), or lung volumes, are uniformly altered in obesity. VT is normal or increased in the obese and is decreased in Pickwickian obesity. IRV is decreased. ERV is markedly decreased because the increased weight of the torso decreases the normal expansive tendency of the rib cage and pulmonary parenchyma. RV is normal. FRC or ERV plus RV is markedly decreased because of the decrease in ERV. VC or ERV + VT + IRV is decreased because of decreased ERV. TLC or RV + ERV + VT + IRV is decreased for the same reason as VC. Individuals with central, as opposed to peripheral fat distribution, have greater decreases in the forced vital capacity (FVC), forced expiratory volume (FEV), and TLC. The maximum voluntary ventilation (MVV) may also be reduced.
Diffusing capacity for carbon monoxide. The DLCO is usually normal in individuals with obesity and mildly reduced in those with OHS because the lung parenchyma is normal, and changes in PFTs are due to abnormal chest wall mechanics and lower lung volumes. DLCO is a useful test to separate intrinsic lung pathology from obesity.
Compliance. There is a decrease in the total respiratory system compliance (1 / CRS = 1 / CL + 1 / CCW), where CRS is the total compliance, CL is the compliance of the lung, and CCW is the compliance of the chest wall. Total compliance is always decreased because of the weight of the torso and abdominal contents pressing against the diaphragm creating a restrictive component, markedly decreasing the chest wall compliance. Lung compliance is often normal but is decreased when pulmonary and circulatory comorbidities are present (e.g., pulmonary hypertension).
Resistance. There are increases both in the airway resistance (reduced elastic tension of the lung) and in the total respiratory system resistance (increased elastic tension of chest wall) at lower lung volumes, which leads to reduction in the caliber of the smaller airways. The increase in total resistance is approximately 30% in simple obesity and 100% in OHS. Resistance increases further in the supine position, possibly due to extrinsic adipose pressure of the supralaryngeal airway, and a decreased FRC.
Closing capacity. FRC is reduced in the morbidly obese patient and may be below the closing capacity (CC), resulting in small airway closure, ventilation/perfusion mismatch, right-to-left shunting, and possibly hypoxemia, the so-called positional ventilatory collapse. This may be worsened in the supine position, Trendelenburg position, by general anesthesia
and muscle relaxants, and improved by the use of lung recruitment strategies (e.g., positive end-expiratory pressure [PEEP]), and reverse Trendelenburg position.
and muscle relaxants, and improved by the use of lung recruitment strategies (e.g., positive end-expiratory pressure [PEEP]), and reverse Trendelenburg position.
Increased work of breathing. MO is associated with a 70% increase in the work of breathing, and a fourfold increase in the oxygen cost of breathing (oxygen consumed by the respiratory muscles per liter of ventilation, used as a surrogate for the energy cost of breathing). This is due to decreased lung compliance, increased respiratory resistance, and threshold inspiratory load from adipose tissue mass. Obese individuals with obstructive sleep apnea syndrome (MO-OSAHS) have elevated pharyngeal and nasopharyngeal resistance, raising the work of breathing 60% above the obese and 250% above the nonobese.
Al Ghobain M. The effect of obesity on spirometry tests among healthy non-smoking adults. BMC Pulm Med. 2012;12:10.
Lumb AB, ed. Nunn’s Applied Respiratory Physiology. 7th ed. Philadelphia, PA: Churchill Livingstone Elsevier; 2010:28-40, 43-55, 92-96.
Salome CM, King GG, Berend N. Physiology of obesity and effects on lung function. J Appl Physiol (1985). 2010;108:206-211.
A.11. What changes occur in PaO2 and PaCO2 in morbidly obese patients?
In the awake patient, positional reduction in lung volume and respiratory system compliance occur when moving from an upright position to a supine position. These changes are exaggerated in the severely obese patient, particularly ERV and FRC. FRC declines both with obesity and with induction of general anesthesia.
Hypoxemia is the most common blood gas abnormality in the severely obese patient. The etiology is most commonly due to a low ventilation/perfusion ratio ([V with dot above]/[Q with dot above]) and less commonly as a result of hypoventilation. Pulmonary perfusion is increased in the obese as a result of increased cardiac output, increased circulating blood volume, and, occasionally, pulmonary hypertension. Alveolar ventilation is decreased in the obese as a result of upper airway closure, and spirometric changes (decreased ERV and FRC). In addition, the closing volume is often greater than the expiratory reserve volume, particularly in the supine position, causing airway closure, resulting in right-to-left shunt and hypoxemia. These patients frequently develop atelectasis, both from cephalad position of the diaphragm and increased weight of thoracic adipose tissue. Many obese patients develop a restrictive respiratory pattern, with mild small volume tachypnea, and increased use of accessory muscles of respiration.
The second most common blood gas abnormality in the severely obese is a variable change in the carbon dioxide tension (PaCO2), not related to lung disease, and dependent on the alveolar ventilation. There are three patterns of ventilatory derangement described:
Alveolar hyperventilation in response to a hypoxic drive. This occurs in young, active subjects. PaCO2 is approximately 35 mm Hg.
Periodic, nocturnal, alveolar hypoventilation with normal daytime values. This is the hallmark of OSAHS.
Daytime, or constant, alveolar hypoventilation. This occurs in OHS and PS.
In addition, lung disease, such as asthma and chronic obstructive pulmonary disease (COPD), is more common in the obese patient population, when compared with age- and sex-matched controls. Preexisting lung disease may become exacerbated perioperatively.
Alvarez A, Brodsky JB, Lemmens HJM, et al, eds. Morbid Obesity Peri-operative Management. 2nd ed. Cambridge, United Kingdom: Cambridge University Press; 2010:125-126.
A.12. What changes occur in intrapulmonary shunt (QS/QT) and dead space (VD/VT)? Describe the equations.
QS/QT is normally less than 5%. In the MO, this is increased, because of the following:
Related posts:
Full access? Get Clinical Tree
