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Over the past 3 decades, the world has experienced an obesity epidemic. Obesity is increasing rapidly in almost every part of the world; overweight and obesity rates are higher in the United States than in any other developed country. A recent report from the National Health and Nutrition Examination Survey—which examined a nationally representative sample of the U.S. population—revealed that more than two-thirds of the adult population (>20 years) was either overweight (body mass index [BMI] >25 kg/m 2 ) or obese (BMI >30 kg/m 2 ). Anesthesiologists now must manage increasing numbers of obese patients. These patients undergo a variety of procedures, both within and outside the operating suite. The presence and the degree of obesity is usually defined by BMI. BMI is calculated by dividing the patient’s weight in kilograms (kg) by the square of their height in meters (m) (BMI = kg/m 2 ). BMI is not a measure of body fat but rather a measure of actual weight. As such, an elevated BMI can present for reasons other than increased adiposity. Extreme or morbid obesity (MO) is considered to be present when a patient has a BMI over 40 kg/m 2 . Based on this definition, more than 8% of Americans are now morbidly obese. The anesthetic management of obese patients differs in many aspects from that of normal-weight patients. Obesity alters each patient’s anatomy and physiology and is associated with many medical comorbidities. Obstructive sleep apnea (OSA) is very common in obese patients and further complicates their care. This chapter considers the anesthetic management of the obese patient undergoing thoracic procedures with an emphasis on patients with sleep-disordered breathing.
During each patient’s preoperative examination, the indications for the proposed surgery are reviewed and evaluated. In addition, all other associated medical conditions must be considered. For obese patients these frequently include hypertension, cardiovascular disease, type II diabetes, sleep-disordered breathing, and osteoarthritis. The preoperative diagnosis and management of each of these comorbidities often referred as “hypermetabolic syndrome,” have been extensively reviewed elsewhere.
Preoperative documentation of the patient’s height and weight is extremely important because anesthetic drugs doses are based on weight scalars, either by measured actual or total body weight (TBW), or by calculating ideal body weight (IBW) and lean body weight (LBW). In normal-weight patients (defined as BMI range between 18.5 and 24.9 kg/m 2 ) IBW approximates TBW. This obviously is not the case for obese patients. The formula IBW = 22 × height 2 (meters) can be used to estimate IBW for both obese men and women.
Both TBW and LBW increase as obesity increases. LBW equals TBW minus the weight of fat. LBW is composed of muscles, bones, tendons, ligaments, and body water. In normal-weight patients LBW can be estimated as 80% of TBW for males and 75% of TBW for females. The increase in LBW in obesity is mainly because of muscle and body water, both of which increase to a much lesser extent than does fat. Because LBW is difficult to measure clinically, in a MO patient it can be roughly estimated by adding 20% or 30% to the patient’s calculated IBW.
During the preanesthetic visit, predictors of potential problems with airway management are sought. The most frequently performed tests and measurements include assigning a Mallampati score, measuring sternomental and thyromental distances, measuring neck circumference, performing an upper lip bite test, noting the presence or absence of teeth and the general state of dentition, assessing cervical range of motion, noting the presence of a receding mandible and an interincisor gap, and measuring the width of mouth opening. Unfortunately, those screening tests thought to be helpful in predicting difficulty with tracheal intubation are inconsistent and have poor predictive value in obesity. Roth et al. estimated the diagnostic accuracy of commonly used bedside examination tests for assessing the airway in adult patients without apparent anatomic abnormalities scheduled to undergo general anesthesia. They included 133 studies involving 844,206 participants. They evaluated the Mallampati test, modified Mallampati test, Wilson risk score, thyromental distance, sternomental distance, mouth opening test, and the upper lip bite test. They found that all index tests had relatively low sensitivities, with high variability. Although the upper lip bite test showed the most favorable diagnostic test accuracy properties, none of the common bedside screening tests is well suited for detecting unanticipated difficult airways, as many of them are missed.
Conversely, the “negative” predictive values of such tests can be helpful. If a MO patient has a combination of a Mallampati score of I or II, a neck that is not thick or short, has full cervical range of motion and normal thyromental and sternomental distances, there is usually no difficulty encountered with direct laryngoscopy (DL) for tracheal intubation. Adipose distribution is different between males and females, and this reassuring clinical presentation is more often present in female patients.
Preoperatively, MO men with a combination of a very large neck circumference (>65 cm) combined with a high Mallampati scores (III or IV) and a history of OSA can be expected to experience problems with some aspect of their airway management. A history of airway management difficulties during a previous anesthetic is probably the best means for anticipating a difficult DL and tracheal intubation ( Fig. 49.1 ).
General anesthesia has a significant effect on impairing pulmonary function. These effects have also been studied in patients undergoing thoracic surgical procedures, but without a focus on the obese patient. Chest wall and total pulmonary compliance decrease as patients increase in weight, leading to increased airway resistance and increased work of breathing in the spontaneously breathing MO patient. As BMI increases, pulmonary function tests reveal a restrictive ventilatory pattern with progressive decreases in functional residual capacity (FRC), which is mainly because of a decrease in expiratory reserve volume (ERV). In the supine position, these changes are associated with small airway collapse within the tidal breathing, which in turn results in air trapping, ventilation/perfusion (V/Q) mismatch, an increase in shunt fraction, and a much lower arterial partial pressure of oxygen (PaO2) than would occur in a normal weight patient.
Preoperative pulmonary function testing has been used to help predict which patients can safely tolerate lung resection. , In nonobese patients, the values of 40% for both forced expiratory volume in 1 second (FEV 1 ) and diffusion capacity serve as acceptable guidelines for proceeding with lung resection. Carbon monoxide diffusion capacity consistently appears to be the best predictor for postoperative complications. These predictors are not validated in the MO patient and no predictive baseline spirometry studies in this population are currently available. For all patients, lung function decreases following surgery. With increasing BMI, postoperative values for FEV 1 and FVC decrease proportionally. It is reasonable to expect even greater reductions in postoperative pulmonary function occur with the combination of thoracic operation and obesity compared with lean patients.
Snoring, hypopnea, OSA, OSA-hypopnea syndrome and upper airway resistance syndrome (UARS) are all disorders that fall under the umbrella of sleep-disordered breathing. OSA is characterized by repetitive collapse of the upper airway during sleep with complete cessation (apnea, lasting at least 10 seconds) or near complete cessation (hypopnea, defined as a decrease of ≥50% in airflow or ≤50% decrease for at least 10 seconds) of airflow. These events are associated with oxygen desaturation and sympathetic activation resulting in brief cortical arousals or complete awakening. If there is increasing respiratory effort, apnea is described as “obstructive.” In central sleep apnea there is no breathing effort.
The preoperative identification of patients who have OSA has important clinical implications. OSA is associated with day-time drowsiness, morning headaches, irritability, personality changes, depression, cognitive impairment, and visual incoordination. With severe OSA there is sleep fragmentation, transient hypoxemia and hypercapnia, large negative intrathoracic pressure swings, and marked elevations in blood pressure. Recurrent hypoxic pulmonary vasoconstriction eventually results in pulmonary hypertension and right and left ventricular hypertrophy. In addition, patients with OSA may have “difficult” airways from an increased tissue mass of the oropharyngeal track. Periods of apnea or hypoventilation often result in hypercapnia and subsequent metabolic changes. This may lead to elevation in serum bicarbonate levels as a compensatory mechanism for acute respiratory acidosis.
The definitive diagnosis of OSA is made by polysomnography. Measurements during sleep include the Apnea Index (AI) (number of apneas/hour) and the Hypopnea Index (HI) (number of hypopneas/hour). The sum of the AI and HI is the Apnea-Hypopnea Index (AHI). The Arousal Index (ARI) is the number of arousals/hour that do not meet the definitions of apnea or hypopnea. The combination of ARI and AHI is the Respiratory Disturbance Index (RDI), a measure that significantly correlates with excessive daytime sleepiness. An AHI over 5 in combination with clinical symptoms is diagnostic of OSA. Bicarbonate elevation correlates with AHI, and when used in conjunction with the STOP-Bang score, the diagnosis of moderate to severe OSA significantly increases.
The severity of the OSA is defined by the AHI score: moderate (AHI>5) in surgical patients, moderate to severe OSA (AHI>15) or severe (AHI >30). The prevalence of moderate to severe OSA (defined as AHI ≥15 events/hour) may be as high as 70% or even greater in MO patients, which represents a 5-fold increase compared with the general population. In the absence of a formal sleep study, the STOP and STOP-Bang Questionnaires were developed as OSA screening tools in preoperative clinics. The STOP questionnaire includes four questions related to snoring, tiredness, observed apnea, and high blood pressure. The STOP-Bang questionnaire includes the four questions used in the STOP questionnaire plus four additional demographic queries, for a total of eight questions related to features of sleep apnea (snoring, tiredness, observed apnea, high blood pressure, BMI, age, neck circumference and male gender). The total score ranges from 0 to 8 which can be used to classify OSA risk. The sensitivity of a STOP-Bang score of 3 or more to detect moderate to severe OSA (AHI >15) and severe OSA (AHI >30) is 93% and 100%, respectively.
Moderate to severe OSA can be effectively treated with continuous positive airway pressure (CPAP). CPAP provides a pneumatic stent that opens the upper airway and maintains its patency. For patients requiring high levels of CPAP or those with chronic obstructive pulmonary disease, bilevel positive airway pressure (BiPAP) allows for independent adjustment of inspiratory and expiratory positive airway pressure. CPAP treatment improves many of the associate comorbidities of OSA and should be encouraged preoperatively as early as possible. After several weeks of CPAP, benefits include the stabilization of congestive heart failure (HF), hypertension, pulmonary hypertension, and perhaps improved airway management through the reduction of tongue volume and increased pharyngeal space.
Because OSA is so common in the obese population, all MO patients should be presumed to have OSA and should be managed accordingly. The American Society of Anesthesiologists consensus guideline for the perioperative management of patients with OSA and the Society of Anesthesia and Sleep Medicine Guideline on Intraoperative Management of Adult Patients With Obstructive Sleep Apnea are useful resources for planning the management of any MO patient undergoing thoracic surgery.
Obesity hypoventilation syndrome (OHS) is another breathing disorder that is estimated to occur between 5% and 10% of MO patients with OSA with the highest occurrence is in superobese (BMI >50 kg/m 2 ) patients. OHS is defined by daytime hypercapnia (PaCO2 >45 mm Hg) and hypoxemia (PaO2 <70 mm Hg) in an obese patient (BMI >30 kg/m 2 ) with sleep-disordered breathing in the absence of any other cause of hypoventilation. In OHS there is a diminished central ventilatory drive despite elevated PaCO2. Severe OHS has been termed “Pickwickian syndrome.” OHS patients have the same symptoms as OSA patients but have greater daytime hypoxemia and is associated with more severe pulmonary hypertension.
Patients with OHS have both elevated PaCO2 and bicarbonate levels on preoperative room air arterial blood gas samples. These patients have higher risk, compared with eucapnic MO patients with OSA, of developing serious cardiovascular disease. Electrocardiographic evidence of right heart strain and hypertrophy is common. Chronic hypoxemia leads to polycythemia, further increasing an already elevated risk for postoperative pulmonary embolism.
For anesthesiologists, the management of MO patients with OHS represent one of the most challenging patient populations they will encounter. Thorough preoperative assessment with early optimization can have a significant impact in the reduction of perioperative adverse events. For OHS patients, both preoperative CPAP and noninvasive ventilation (NIV) improve clinical symptoms, gas exchange, and quality of life. , The American Thoracic Society Practice Guideline on Evaluation and Management of Obesity Hypoventilation Syndrome can be a useful resource for anesthesiologists interested in optimizing the management of these challenging patients. The guideline encourages clinicians to test serum bicarbonate levels and blood gas samples to assist in the diagnosis of OHS. Stable ambulatory patients with OHS and severe OSA should receive CPAP rather than NIV as first-line treatment. Patients hospitalized with respiratory failure and suspected of having OHS should be discharged with NIV until they undergo outpatient diagnostic procedures and positive airway pressure titration in a sleep laboratory (ideally within 2–3 months). Patients with OHS are recommended to use weight-loss interventions that produce sustained weight loss of 25% to 30% of body weight. To achieve resolution of OHS by weight loss many of these patients are suggested to undergo bariatric surgery.
MO patients with OSA and/or OHS have an elevated risk of developing cardiac disease, that should be presumed present unless excluded by testing. MO patients frequently develop systemic hypertension because of the increase in absolute blood volume and cardiac output (hypermetabolic syndrome). The presence of OSA further increases the risks of pulmonary hypertension. Obesity is a risk factor for HF in both men and women. Severe obesity produces hemodynamic alterations that predispose to changes in cardiac morphology and ventricular function, which may lead to the development of HF. The presence of systemic hypertension, sleep apnea, and hypoventilation, comorbidities that occur commonly with severe obesity, may contribute to HF in such patients. In older MO patient’s eccentric right ventricular hypertrophy, left ventricular hypertrophy, and right and left HF (“obesity cardiomyopathy”) develops.
A routine electrocardiogram is usually adequate for most MO patients, even those with arterial hypertension. Given that echocardiography demonstrates some degree of right ventricular dysfunction in asymptomatic patients, the presence of angina or any additional cardiac symptoms is a red flag that requires a more thorough cardiac evaluation. Moderate or severe left ventricular diastolic dysfunction was found in 50% of patients with moderate or severe OSA. Long-standing or severe OSA should alert the clinician to the presence of pulmonary hypertension and potential right ventricular failure and prompt further investigations.
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