Thoracic Anesthesia inthe Morbidly Obese Patient: Obstructive Sleep Apnea




Thoracic Anesthesia inthe Morbidly Obese Patient: Obstructive Sleep Apnea



George W. Kanellakos, Jay B. Brodsky



Abstract


The anesthetic management of obese patients differs from that of normal-weight patients. Obesity alters anatomy and physiology and is associated with numerous medical comorbidities. Obstructive sleep apnea (OSA) and obesity hypoventilation syndrome are common and fall under the umbrella of sleep-disordered breathing. OSA should be identified preoperatively and treated with continuous positive airway pressure. Morbidly obese (MO) patients should never be allowed to lie flat for induction of anesthesia. Obese patients should be positioned in the “ramped” or “head elevated laryngoscopy position.” Inadequate arm support can result in brachial plexus injury. The lateral position requires larger axillary rolls and beanbags. Obesity is a factor for a difficult airway but not a single study has demonstrated a direct relationship between increasing weight with increasing tracheal intubation difficulty. There is a subset of patients that often present with challenging airways. This group consists of MO men, often with OSA, who have thick necks and high Mallampati scores. Emergence from anesthesia should also be in an upper-body elevated position. MO patients can maintain adequate oxygenation during one-lung ventilation, but arterial oxygen tension remains significantly lower than in normal-weight patients. Postthoracotomy pain control in MO patients should include thoracic epidural or paravertebral regional anesthesia. Systemic opioids, in general, should be limited or avoided. This chapter considers the anesthetic management of the obese patient undergoing thoracic procedures with an emphasis on patients with sleep-disordered breathing.


Keywords


Thoracic anesthesia; preoperative considerations; morbid obesity (MO); airway management; obstructive sleep apnea (OSA); obesity hypoventilation syndrome (OHS); obesity supine death syndrome; one-lung ventilation (OLV); patient positioning; complications; pain control



Introduction


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/m2) or obese (BMI >30 kg/m2).1 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/m2). 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/m2. 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.2 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.



Preoperative Considerations


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.3–5


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/m2) IBW approximates TBW. This obviously is not the case for obese patients. The formula IBW = 22 × height2 (meters) can be used to estimate IBW for both obese men and women.6


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,7 in a MO patient it can be roughly estimated by adding 20% or 30% to the patient’s calculated IBW.



Airway Concerns


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.8 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.9


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.10 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).


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• Fig. 49.1 Morbidly obese patients, particularly men with a very large neck circumference and a high Mallampati score (III or IV) will usually have obstructive sleep apnea. These patients can be anticipated to have difficulty with some aspect of their airway management. The presence of a beard further increases the chance of difficult mask ventilation.


Pulmonary Function


General anesthesia has a significant effect on impairing pulmonary function. These effects have also been studied in patients undergoing thoracic surgical procedures,11 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.12


Preoperative pulmonary function testing has been used to help predict which patients can safely tolerate lung resection.13,14 In nonobese patients, the values of 40% for both forced expiratory volume in 1 second (FEV1) and diffusion capacity serve as acceptable guidelines for proceeding with lung resection.15 Carbon monoxide diffusion capacity consistently appears to be the best predictor for postoperative complications.16 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.17 With increasing BMI, postoperative values for FEV1 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.



Sleep-Disordered Breathing


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.18 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.19 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.20


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.21–23


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.24 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 OSA17 and the Society of Anesthesia and Sleep Medicine Guideline on Intraoperative Management of Adult Patients With Obstructive Sleep Apnea25 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/m2) patients. OHS is defined by daytime hypercapnia (PaCO2 >45 mm Hg) and hypoxemia (PaO2 <70 mm Hg) in an obese patient (BMI >30 kg/m2) with sleep-disordered breathing in the absence of any other cause of hypoventilation.26 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.27,28 The American Thoracic Society Practice Guideline on Evaluation and Management of Obesity Hypoventilation Syndrome29 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.




Cardiovascular Function


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.30


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.31 Long-standing or severe OSA should alert the clinician to the presence of pulmonary hypertension and potential right ventricular failure and prompt further investigations.



Intraoperative Management



Patient Position


An awake, spontaneously breathing MO patient should not be allowed to lie flat for induction of anesthesia. In the supine position, MO patients experience a further reduction in their already reduced FRC and this can result in dangerous hypoxemia, especially if they are breathing air.


The “safe apnea period” (SAP) is the duration of time between onset of apnea following preoxygenation and the administration of a neuromuscular blocking agent until pulse oximeter saturation (SpO2) falls below a safe level (usually 88%–92% in different studies). Proper patient positioning before and during the induction of general anesthesia is one of the most important means of lengthening SAP. Obese patients preoxygenated in the sitting position have significantly extended tolerance to apnea after muscle paralysis when compared with similar obese patients preoxygenated in the conventional supine position. Altermatt et al. studied 40 obese patients (BMI >35 kg/m2) undergoing surgery with general anesthesia were randomly assigned to one of two groups: group 1 (sitting, n = 20) or group 2 (supine, n = 20). In the predetermined body position, preoxygenation was achieved with eight deep breaths within 60 s and an oxygen flow of 10 L/min. After rapid sequence ­induction and tracheal intubation, the patient was left apneic and disconnected from the anesthesia circuit until SpO2 decreased to 90%. Oxygen and carbon dioxide (CO2) tensions were similar between groups, both at baseline and after preoxygenation. However, the mean time to desaturation to 90% was significantly longer in the sitting group compared with the supine group (mean [standard deviation {SD}: 214 [28] vs. 162 [38] s, P < .05).32


MO patients should always be positioned in the “ramped” or “head elevated laryngoscopy position” (HELP) before anesthetic induction. It facilitates alignment of the pharyngeal, laryngeal, and oral axis of the airway during difficult laryngoscopy, especially in the large patient. In the MO patient, the goal is for the upper body and head to be elevated to a point that the sternum and ear are aligned in a horizontal line therefore easing the work of breathing and improving oxygen reserves.33 In addition, if the patient is hemodynamically stable, the operating room table should be in the reverse Trendelenburg position (RTP).34 The semi-Fowler position with the patient’s upper body elevated 25 to 30 degrees also extends SAP but the 30 degrees RTP is better.35,36 With the upper body elevated and the table in RTP the patient’s diaphragm is “unloaded,” diaphragmatic excursion is increased and the view during DL is improved. A recent study with MO volunteers confirmed that FRC is greatest in the RTP, less so in the semi-Fowler position, and least with the patient supine37 (Fig. 49.2).


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• Fig. 49.2 Obese patients should always be positioned in the “ramped” or “head elevated laryngoscopy position” (HELP) before anesthetic induction. In this position, the upper body and head are elevated so that the sternum and ear are aligned in a horizontal line. If the patient is hemodynamically stable the operating room table should be tilted in the reverse Trendelenburg position. This arrangement will allow greater diaphragmatic excursion and improve the view during direct laryngoscopy.

Besides maintaining the patient in a head-up, body elevated position, other strategies can be applied to the obese patient to prolong SAP. Adequate preoxygenation is most essential. Tidal volumes in a spontaneously breathing obese patient are too small to recruit lung volume. The patient must take deep vital capacity breaths. For the patient with an anticipated difficult airway, application of apneic or “diffusion” oxygenation should be considered.


During apnea metabolism continues and the body consumes approximately 250 mL O2/min and produces 200 mL CO2/min. Most CO2 (up to 90%) stays in the blood and will cause a respiratory acidosis. The O2 continues to be consumed from alveoli with a loss of lung volume. The resulting pressure differential allows mass movement of gas from upper airways into alveoli. Delivering a high fraction of inspired oxygen (FiO2) at any level of the airway (pharynx, trachea, alveoli) can increase alveolar O2 and thereby increase SAP. Nasal delivery of oxygen by transnasal humidified rapid-insufflation ventilatory exchange (THRIVE),38 through high-flow nasal cannulae,39 and/or by the buccal route through modified endotracheal tubes (ETTs)40 have each been used in obese patients for preoxygenation and to prevent hypoxemia during periods of apnea during upper airway procedures before the trachea being intubated. Apneic oxygenation cannot compensate for ineffective preoxygenation. The upper airway must remain patent. A nonpatent airway results in alveolar collapse with rapid desaturation. To keep the airway open the patient may require head elevation, jaw thrust, nasal prongs, or an oral airway.


Lying flat usually increases venous blood return to the heart. Cardiac output (CO), pulmonary blood flow, and an increase in arterial blood pressure can occur. The supine obese patient will experience significant increases in metabolic oxygen demand and CO2 production combined with the increases in CO and arterial and pulmonary artery pressures. For the supine MO patient with preexisting limited physiologic reserves acute and sometimes fatal cardiorespiratory decompensation, termed the “obesity supine death syndrome,” can result (Fig. 49.3).


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• Fig. 49.3 When a morbidly obese patient lies flat, there is an increase in venous blood return to the heart. A further loss of functioning lung volume occurs resulting in a decrease in oxygenation, especially when breathing room air. The supine obese patient will also experience significant increases in oxygen demand and carbon dioxide production. These changes combined with increases in cardiac output and arterial and pulmonary artery pressures that occur in the supine patient can result in acute cardiorespiratory decompensation, termed the “obesity supine death syndrome.” The syndrome may present not only in the operating room, but at other locations outside the operating suite, including the endoscopy unit, at imaging and interventional radiology, or even during patient transport.

Although this syndrome was first described in 1977 in two massively obese patients who were forced to lie down for medical procedures,41 many physicians remain unaware of the great danger of placing an anesthetized or sedated obese patient in the supine position. It is postulated that the obesity supine death syndrome is the cause of unexplained deaths occurring not only in the operating room, but also at other locations, such as endoscopy, imaging, interventional radiology, or even during patient transport.42 Unexplained deaths occur much more frequently in MO patients and in the absence of positive findings at autopsy the death is usually attributed to cardiac arrhythmia.43 Patients at greatest risk are usually men with central obesity who have massive abdomens and who complain of shortness of breath when lying flat. When the syndrome does occur, the first response should be immediately returning the patient to a sitting or table-upright position. It is likely that in the patient with significant central obesity in the supine position the inferior vena cava can be compressed reducing venous return to the heart and causing hypotension.


Moving an anesthetized MO patient in the operating room can cause numerous injuries to the patient and is beyond the scope of this chapter. In this population, there is an additional risk to injury to the staff attempting to move the patient. The lateral position for thoracic surgery requires additional physical assistance and equipment. In that position, in addition to padding all the pressure points, special care must be taken to maintain the patient’s head in a position to avoid brachial plexus stretch injuries. Because MO patients can have a short neck, supporting the head often requires extra blankets strategically placed to maintain a neutral position.


In any nonphysiologic position in an obese patient, inadequate arm support can result in brachial plexus injury. Changing to the lateral position requires larger axillary rolls and beanbags for support. The beanbag may not be large enough to adequately hold the patient. Belts or tape across the pelvis may be required to help stabilize a patient’s position and special precaution should be taken when tilting the operating room table laterally (Fig. 49.4).


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• Fig. 49.4 The morbidly obese patient in the lateral position for thoracic surgery requires large axillary rolls and a beanbag for support. Conventional size beanbags may not be large enough to adequately hold the obese patient in place. Additional belts and tape across the pelvis are required to help stabilize the patient in the proper position.


Airway Management


By definition, a “difficult airway” is present when a conventionally trained anesthesia provider experiences problems to get control of the patients airway which can be either bag-mask ventilation, tracheal intubation, and/or the insertion of a supraglottic airway device (SGD).44 The association between obesity and “difficult airway” remains unresolved because the medical literature on this subject consists of heterogeneous studies with conflicting results.45 What constitutes “problems” is not well defined and depends on what aspect of airway management is being considered and what criteria are being used to define difficulty. The reported ­incidence of “difficult” tracheal intubation in published studies widely ranges from of 1.9% to 44.4% in MO patients and from 3.2% to 20.4% in obese patients.46


An MO patient, especially with a history or symptoms of OSA may have a diminution of the pharyngeal space secondary to an increase in fat deposition in the pharyngeal wall, which can make airway access and bag-mask ventilation difficult. Most studies do agree that difficulty with bag-mask ventilation (DMV) is very common in obese patients. The weight of the chest wall, especially when the patient is supine, coupled with other factors, such as a poorly fitting face-mask, the presence of a beard, poor dentition, and the frequent association of OSA all complicate mask ventilation. If any concern exists regarding the possibility of adequate mask ventilation in the patients, an awake fiberoptic intubation should be considered.


DMV is usually defined as either mask ventilation that is inadequate to maintain oxygenation saturation SpO2 over 92%, unstable mask ventilation, or mask ventilation requiring two providers. Impossible mask ventilation is defined as the absence of end-tidal CO2 measurements and lack of perceptible chest wall movement during positive-pressure ventilation attempts despite airway adjuvants (oral or nasopharyngeal airway) and additional personnel. Obesity (BMI >30 kg/m2) is one of many independent predictors of DMV. Other factors include age (>46 years), male gender, Mallampati score of III or IV, neck mass or radiation, limited thyromental distance, OSA, presence of teeth or beard, neck circumference >43 cm, limited cervical spine mobility and limited jaw protrusion.47 Unlike the inconclusive data regarding obesity and difficult tracheal intubation (see later), the consistent findings from published studies is that obesity is associated with DMV.


In the past bag-mask ventilation during anesthetic induction was avoided because of concerns that insufflation of the stomach would increase the risk of aspiration. Clinically significant gastric distention does not occur during normal bag-mask ventilation, especially if peak pressures are kept low. Unless at high risk for aspiration, the anesthetic induction of the obese patient should include positive-pressure bag-mask ventilation with the application of CPAP or positive end-expiratory pressure (PEEP). Bag-mask ventilation will decrease atelectasis and increase SAP by as much as 50% in MO patients.48


Obesity is often listed as a factor for difficult tracheal intubation. Not a single study has ever demonstrated a direct relationship between increasing weight and/or BMI with increasing intubation difficulty.


The Intubation Difficulty Scale (IDS) has been used as a measure of intubation difficulty. It is based on seven variables.49 Points are assigned as follows:


N1, number of additional intubation attempts;


N2, number of additional operators;


N3, number of alternative intubation techniques used (e.g., SGD, change of laryngoscope blade, bougie);


N4, glottic exposure as defined by Cormack and Lehane50 (grade 1, N4 = 0; grade 2, N4 = 1; grade 3, N4 = 2; and grade 4, N4 = 3);


N5, lifting force applied during laryngoscopy (N5 = 0 if “inconsiderable” and N5 = 1 if “considerable”) (as assessed subjectively by the laryngoscopist);


N6, need to apply external laryngeal pressure to improve glottic pressure (N6 = 0 if no external pressure or only the Sellick maneuver applied and N6 = 1 if external laryngeal pressure was used); and


N7, position of the vocal cords at intubation (N7 = 0 if abducted or not visible and N7 = 1 if adducted). The IDS score is the sum of N1 through N7. An IDS of 0 indicates intubation performed on the first attempt by the first operator using a single technique and applied minimal force to insert the ETT through a fully visualized glottis. An IDS score from 1 to 5 indicates slight difficulty, and an IDS score over 5 indicates moderate to major difficulty.


In a study of 134 lean (BMI <30 kg/m2) and 129 obese (BMI >35 kg/m2) patients an IDS of 5 or more occurred in three lean (2.2%) and 20 obese (15.5%) patients during intubation by DL.51 The conclusion was that difficult tracheal intubation is more common in obese patients based on an IDS of 5 or more. Most IDS studies consider a score of 5 to represent only “slight” difficulty. It is also important to note that the incidence of poor glottic view during laryngoscopy (Cormack-Lehane class 3 or 4) was identical between lean (10.4%) and obese (10.1%) groups, and all patients in both groups were successfully intubated by DL. A Mallampati score of III or IV was the only independent risk factor for the increased “difficulty” in the obese group and there was no relationship between increasing BMI and increasing difficulty. A similar study of 70 obese (BMI >30 kg/m2) and 61 lean (BMI <30 kg/m2) reported an IDS greater than 5 in 14.3% of obese and 3.0% of lean patients.52


These studies assessed difficult intubation by IDS criteria. By contrast, other studies using different criteria for ­“difficulty” have reached different conclusions. In a study of 100 consecutive MO patients (BMI >40 kg/m2) scheduled for bariatric surgery, tracheal intubation was classified as “easy” if the product of the Cormack-Lehane graded laryngoscopy view times the number of intubation attempts was less than 3, and was classified as “problematic,” that is potentially difficult, when it was 3 or more.53 All but one patient was successfully intubated by DL without using any adjuncts. Neck circumference (>65 cm) and Mallampati score (III or IV) were the only predictors of potential difficulty with intubation. Neither absolute weight nor BMI were associated with problematic intubation.


If obesity by itself was the major factor, one would expect to see a direct relationship between increasing weight and increasing intubation difficulty and failure. None of the many studies on airway management in obesity has demonstrated such a relationship. For example, a recent study found that at a BMI greater than 30 kg/m2, the odds of DL, simply defined as requiring more than one attempt, were greater in obese compared with lean patients. However, there was no increase in the number of intubation attempts as BMI increased. Difficult intubation was no more likely to occur in an MO patient than in a moderately obese patient. This study, like all the previous reports found that more obesity does not convey more intubation difficulty.54


There are many problems with these studies. The view obtained during DL is often used as a measure for difficult or failed intubation; however, an ETT may be easy to place despite a poor laryngoscopic view, and even with a reasonable view there can be difficulty passing an ETT. The IDS considers factors that are subjective and may lead to bias (lifting force during laryngoscopy) and factors unrelated to obesity (adduction of the vocal cords, a measure of the degree of muscle relaxation). If the laryngoscopic view and success rate with conventional laryngoscopy are used as the measure of intubation difficulty, there is little difference between lean, obese, and MO patients.


All these studies define obesity by absolute weight or BMI and fail to consider that the distribution of fat, not weight itself, can contribute to difficulty with laryngoscopy. The results can also be biased because many superobesity patients undergo elective awake fiberoptic intubation (FOI) or video-laryngoscopy (VL) and are thus excluded from the series reporting experience with DL. Finally, many of the studies are from patients undergoing bariatric surgery, which typically include a much a higher percentage of women than men.


There is a subset of obese patients that exhibit a distribution of excess adipose tissue that does directly affect airway management. This group of patients consists mostly of MO men, often with OSA, who have very thick necks and high Mallampati scores. No study has considered these patients separately in airway studies in obesity. Whereas the majority of obese and MO patients are usually not difficult to intubate, these subsets of patients can present challenging airways.


Tracheal intubation in MO patients is managed differently than in lean patients. The standard sniffing position for tracheal intubation is achieved in nonobese patients by raising their occiput 8 to 10 cm with a pillow or headrest. Obese patients, on the other hand, require much greater elevation of their head, neck, and shoulders (HELP) to produce the same alignment of axes for intubation. In studies of MO patients where the head position is suboptimal, that is not in the HELP, there are higher incidences of grade 3 and 4 Cormack–Lehane views with potentially increasing difficulty with DL.


For patients with an anticipated difficult intubation and in those in which difficult DL is encountered following induction of anesthesia, alternative methods to establish the airway should be considered. Awake FOI was once considered the “gold standard” for difficult intubation.55 However, with the development of new airway equipment, particularly with the readily available video-laryngoscopes, FOI is now being performed less frequently.56 FOI can be difficult in MO patients because of reduced pharyngeal space and the increase in redundant tissue which can restrict field of view, especially in the anesthetized patient when loss of pharyngeal tone further complicates the bronchoscopist’s view. An “asleep FOI” compares unfavorably with other airway devices, such as video-laryngoscopes for first-intubation success. If a difficult airway is identified in an obese patient and FOI is planned, an awake FOI should be performed.57 Even as a rescue strategy in the unanticipated difficult airway, FOI has now been replaced by readily available VL.


Because conventional DL is successful in the great majority of obese and MO patients, it remains unclear whether VL is superior and should be the default means for establishing an airway in obese patients.58 A Cochrane review of 64 randomized controlled trials comparing 7044 adult patients found “moderate quality” evidence that video-scopes may reduce the number of failed intubations by improving glottic view, especially for patients with an anticipated difficult airway. Video-laryngoscopes may also reduce airway trauma and hoarseness, but there was no evidence of reduced episodes of hypoxia or mortality. Intubation success rates differed between different video-laryngoscopes. Only the C-MAC blade showed a statistically significant reduction in failed intubations, with no difference in success rates for the Glidescope, Pentax and McGrath instruments when compared with conventional DL. Although there is growing body of evidence that VL improves glottic view and reduces intubation attempts compared with Macintosh DL in obese patients, however, it is up to the practitioner to decide if to select it as a first-line use for all obese patients. Until a large, randomized trial in obese patients is performed to help determine if the routine use of VL in the obese is better than DL, factors such as provider comfort and anticipated airway difficulty should be considered when VL is used as the primary approach to intubate the trachea in obese adults. There is no strong evidence that VL reduced the number of intubation attempts, reduced the time to successful tracheal intubation, or influenced the incidence of hypoxia or respiratory complications compared with DL.59 The success rate of VL compared with DL in obesity was not considered in this study. Another review reported weak evidence that VL may improve glottic view, reduce the number of intubation attempts, and increase the intubation success rate in obese patients. There was no evidence it reduced the time to successful intubation, a critically important concern given the short SAP in obese patients.60


During the past decade, there has been a steady increase in use of supraglottic devices (SGD’). The introduction of second-generation SGDs with improved oropharyngeal leak pressure and a channel for inserting a gastric tube has led to a widening of the indications for their use. The potential advantages of SGDs include ease of placement and less airway injury than an ETT. However, there is still disagreement about the role of SGDs in obese surgical patients, and their safe use in MO patients remains controversial.


The Fourth National Audit Project (NAP-4) examined the records of 2.9 million anesthetics performed in the United Kingdom. Obese and MO patients had a disproportionate incidence of airway complications.61 Of the patients who experienced a major airway complication (death, brain damage, emergency surgical airway, or intensive care unit [ICU] admission) 42% were obese. Furthermore, patients with severe obesity were four times more likely to experience these airway problems. Regurgitation and pulmonary aspiration, which accounted for 50% of the deaths in NAP-4 occurred more frequently in MO patients. Although the use of SGDs in obesity did not differ from nonobese patients, the obese patients had an increased frequency of aspiration associated with use of an SGD. The study stated that the use of these devices in MO patients indicated “failure to respect the risks associated with airway management in obesity.” Following publication of the NAP-4 report, the Society of Bariatric Anaesthetists in the United Kingdom recommended intubation with an ETT as the default airway management strategy for patients with BMI >35 kg/m2.62 Since NAP-4 was published, second generation SGDs have been introduced. They may have an increased role in obesity but their safe use in this population presently remains unknown.


There are indications for using an SGD in obesity. An SGD remains an important rescue tool during “cannot ventilate, cannot intubate” situations,63 and is especially helpful in obese and MO patients as a life-saving bridge until an ETT can be placed or until a surgical airway is attempted.64 SGDs have been used to preoxygenate obese patients to increase SAP before laryngoscopy.65

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Oct 6, 2021 | Posted by in ANESTHESIA | Comments Off on Thoracic Anesthesia inthe Morbidly Obese Patient: Obstructive Sleep Apnea
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