A 67-year-old woman presents to the emergency department (ED) by ambulance with a 3-hour history of increasing dyspnea associated with chest pain. She has a history of coronary artery disease, hypertension, and hyperlipidemia, but no known allergies. Her medications include atenolol, low-dose aspirin, atorvastatin, acetaminophen with codeine, and nitroglycerin spray as needed. Prior to notifying the emergency medical services (EMS), the patient had used three sprays of nitroglycerin every 5 to 10 minutes with no relief.

She is placed on 10 L·min⁻¹ oxygen by face mask and is transported to the hospital. On examination after the arrival at the ED, her vital signs are: heart rate 113 beats per minute and irregular, respiration rate 31 breaths per minute, blood pressure 85/45 mm Hg, and SaO₂ 86%. She appears to be in severe respiratory distress and is unable to speak more than three to four words in one breath. She is morbidly obese with an estimated weight of over 137 kg (300 pounds) and is 151 cm (5 feet) tall with a body mass index (BMI) 60 kg·m⁻². Chest auscultation reveals faint breath sounds with crackles over the entire lung fields, a significant decrease in air entry in both bases combined with mild wheezing. Other findings include 1+ bilateral ankle edema, S₄ heart sound, and a grade III/VI systolic murmur radiating to the axilla. Her jugular venous pressure (JVP) cannot be assessed because of her marked obesity and short neck. Her electrocardiogram on admission to the ED reveals a pattern consistent with an acute antero-lateral myocardial infarction. The chest x-ray shows poor inflation and is also consistent with pulmonary edema.

Following the initial assessment, it is noticed that the SaO₂ decreases to 81% and her respirations increasing to 35 to 40 breaths per minute. Pink froth appears from her mouth.

As you prepare for airway intervention, she loses consciousness. The monitor shows pulseless ventricular tachycardia.

Define Obesity

Obesity is the presence of an excess of body fat when compared to average values for age and gender. When the percentage of body fat exceeds 15% to 18% in men, or 20% to 25% in women, the individual is considered obese. Unfortunately, measuring body fat is not practical, as it requires sophisticated techniques.

The ideal body weight (IBW) has been used frequently in clinical settings to define obesity:

IBW ( kg ) = height ( cm ) − x where x is 100 for males and 105 for females.

Patients who weigh 20% above IBW are considered overweight, and they are considered morbidly obese if their weight is 200% above the calculated IBW.¹

The World Health Organization (WHO) specifies the use of BMI as the international method of classifying obesity.² It has become the standard method for defining obesity.

BMI 3 = body weight ( kg ) / height 2 ( m )

Using the BMI, obesity is categorized as follows³:

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  A person is considered overweight with a BMI of 25 to 29.9 kg·m⁻².

  
  
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  Obese individuals have a BMI>30 kg·m⁻².

  
  
  
  
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    Obesity Class I: BMI 30 to 34.99

    
    
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    Obesity Class II: BMI 35 to 39.99

    
    
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    Obesity Class III: BMI≥40

  
  

It has been well established that obesity is associated with multiple medical issues including: hypertension, heart disease, congestive heart failure, diabetes mellitus, stroke, obstructive sleep apnea (OSA), an increased incidence of perioperative wound infection, and respiratory complications.

Recently, a more important predictor of long-term outcome has been shown to be the type of fat distribution, rather than BMI. “Male” or android pattern central obesity (trunk and abdomen) has been shown to correlate more with negative outcomes than “female pattern” gynecoid obesity (peripheral), including metabolic complications, risk of cardiac disease, and premature death.

“Metabolic syndrome” (Syndrome X) is defined as central obesity, as described by ethnicity-specific waist circumferences measurements, and any two of the following four criteria: hypertriglyceridemia, reduced HDL-cholesterol, glucose intolerance, and hypertension.⁴ This syndrome is associated with Type 2 Diabetes, microalbuminuria, prothrombotic states, and proinflammatory states (e.g., elevated C-reactive protein), and represents a particularly high-risk group for the development of cardiovascular and cerebrovascular diseases.^5,6

Reducing the degree of obesity has been shown to favorably impact the progression of these disorders.^7,8

What Are the Anatomic and Physiologic Factors That Might Contribute to the Difficulty of Airway Management in the Morbidly Obese Patient?

In this population, numerous factors have been implicated in increasing the difficulty of bag-mask-ventilation (BMV), of extraglottic device (EGD) placement, of performing laryngoscopic intubation, and of obtaining a surgical airway. These include: large breasts (male and female), excess adipose tissue in the face and cheeks, short and thick neck, large tongue, redundant palatal and pharyngeal tissue, superior and anterior larynx, limited mouth opening, limited access to the anterior neck, and limited cervical spine mobility due to occipital adipose tissue accumulation.³

The ASA definition of the difficult airway is “the clinical situation in which a conventionally trained anesthesiologist experiences difficulty with face mask ventilation, tracheal intubation, or both.”⁹ Experience and the literature suggest that obesity may contribute to a “difficult airway,” as discussed below (see Chapter 1). However, even when a morbidly obese patient has favorable airway assessment parameters (i.e., Mallampati I, full range of motion of neck, adequate mouth opening, etc.), other factors can make airway intervention more challenging.

There is a significant decrease in tolerable apnea time in obese, compared with that of non-obese, patients. This decrease occurs in a linear fashion as obesity increases and relates to both a decreased respiratory reserve and an increase in metabolic requirements.¹⁰ This decreased “respiratory reserve” is the result of a decrease in functional residual capacity (FRC) combined with a closing capacity that intrudes on tidal volume ventilation.^10,11 Furthermore, the high FiO₂ employed in all intubations induces absorption atelectasis, further reducing the amount of lung tissue available for gas exchange. Because of these factors, precipitous oxygen desaturation occurs when the patient is rendered apneic during airway management.¹¹ Data from Jense et al.¹⁰ suggest that, during rapid-sequence induction (RSI) in the morbidly obese patient, hypoxemia can occur quickly (in as little as 95 seconds), and so only one intubation should be attempted.

The morbidly obese patient also has a restrictive lung defect resulting in a decreased vital capacity, expiratory reserve volume, and inspiratory capacity.^10,12 Auler et al.¹³ found that morbidly obese patients under general anesthesia show a higher resistance throughout the respiratory system.

The presence of morbid obesity is considered by many to be a predictor of difficult mask-ventilation.^3,10,14 Adequate BMV requires an open airway and a tight mask seal. Creating a patent airway, and maintaining a competent mask seal in order to overcome elevated airway pressures in these patients with a restrictive lung defect due to obesity, render more difficult effective BMV. Langeron et al.¹⁴ found that the odds ratio of difficult BMV in obese patients was 2.75 (1.64–4.62, p<0.001). Anterior translation of the mandible (jaw thrust) to effect airway opening has been shown to be more difficult and less effective in the obese.¹⁵ In this study, nine non-obese and nine obese subjects were anesthetized and given neuromuscular blocking agents. Once apneic, and with steady airway pressure applied via a nasal device, the oropharynx and velopharynx (nasopharynx) were visualized with an endoscope. The cross-sectional areas were measured, both in the resting state and with a jaw thrust applied. In both groups of patients, the jaw thrust improved the cross-sectional area of the oropharynx. However, although an improvement with the jaw thrust maneuver occurred in the measurements of the velopharynx in the non-obese population, no improvement was seen with this maneuver in the obese patients. The authors found that obstruction persisted in the lateral plane rather than in the A-P dimension, and postulated that this was due to the redundant soft tissue around the tonsillar pillars closing in from the sides as the tonsillar pillars were stretched antero-posteriorly. This may explain why CPAP or PEEP augments ventilation in the obese patient, as both laterally splint the airway.^15,16 It may also explain why the Laryngeal Mask Airway (LMA) has been found to be an effective rescue device in the obese population. (See Section “How Effective Is the LMA in the Obese Patient.”)

What Are the Special Considerations in Patients with Obstructive Sleep Apnea?

About 5% of morbidly obese patients have OSA.³ In studying over 6000 subjects, Nieto et al.¹⁷ reported that most patients with OSA are not obese. Consequently, questioning patients regarding OSA should not be reserved for only the obese. The presence of snoring may be the only indicator of OSA in the general population. Snoring and obesity are important predictors of difficult BMV.¹⁴

Although difficult to quantify, a direct correlation may exist between difficult tracheal intubation and OSA.¹⁸ Some controversy exists however, and opposing data are present in the literature. In their study, Neligan et al. showed that OSA is not a risk factor for difficult intubation. They did show, however, that male gender as well as high Mallampati scores (≥III) did predict difficulty in establishing an airway.¹⁹ Chung et al. followed up with sleep studies on a number of patients who were found to have difficult or failed intubations at the time of surgery. Sixty-six percent of these were subsequently diagnosed with OSA.²⁰

In patients with OSA, airway patency is disturbed by relaxation of pharyngeal dilator muscles during sleep. The upper airway is soft, pliable, and narrow in these patients, which makes it collapse during sleep. Turbulent air flow through these structures produces vibrations (snoring) and collapse (apnea).²¹ This obstruction continues until the level of sleep is interrupted and the individual regains pharyngeal muscle tone. Drugs or alcohol can exacerbate this snoring/obstruction/apnea cycle. Consequently, sedatives, particularly the long-acting agents given in the perioperative period, can have a pronounced deleterious effect on the ability of this patient population to maintain airway patency when asleep.³ There is little question that these factors lead to increased perioperative risk for morbidity and mortality. Numerous papers address the management issues surrounding the perioperative care of this patient population.²² Unfortunately, most recommendations appear to be based on expert opinion rather than evidence. A useful reference is the “Practice Guidelines” published by the American Society of Anesthesiologists.²³ Again, these are positions based primarily on the consensus of experts.

The obesity hypoventilation syndrome (OHS), also known as Pickwickian syndrome, is characterized by chronic respiratory insufficiency, with both obstructive and restrictive features based on pulmonary function testing. Chronic hypoxemia and hypercarbia, polycythemia, somnolence, pulmonary hypertension, and right ventricular dysfunction (cor pulmonale) characterize this condition. These patients all exhibit a marked reduction in hypoxic and hypercarbic drives, measuring 1/6 and 1/3 the response to that of controls.²⁴ Although some similarities exist between OSA and OHS, they are not the same disease. As pointed out above, not all patients with OSA are obese, and patients with OHS do not necessarily have OSA. Due to the significant underlying pulmonary and cardiac dysfunction with the OHS population, they represent an increased perioperative risk.

Is Tracheal Intubation More Difficult in Morbidly Obese Patients?

There is some disagreement as to whether morbid obesity is predictive of difficult intubation. The incidence of difficult intubation in the morbidly obese population has been reported to be approximately 13% to 20%.^25–27 This wide range is likely related to the inconsistent definitions of “difficult intubation” in the literature.

In a study of 100 morbidly obese patients with BMIs of >40 kg·m⁻², Brodsky et al.²⁸ concluded that obesity, per se, was not a predictive factor in determining difficulty of intubation. Of the many parameters measured in the study population, the only two that correlated with difficult laryngoscopy following RSI with cricoid pressure were large neck circumference and high Mallampati scores. A neck circumference (measured at the level of the thyroid cartilage) of 40 cm was associated with a 5% incidence of difficult intubation. In the same study, difficult intubations were encountered in 35% of patients with a neck circumference of 60 cm.²⁸ Of interest, larger neck circumference has also been associated with increasing severity of OSA.²⁹

In a separate study, Ezri et al.³⁰ also found that obesity, by itself, was not a predictor of difficult intubation.

In both of the above studies, laryngoscopic view was used as a predictor for difficult intubation. Alternatively, the Intubation Difficulty Scale (IDS) has been validated and used to provide a more comprehensive assessment of intubation difficulty.³¹ In addition to laryngoscopic grade, the IDS scores the number of intubation attempts, different techniques tried, lifting force applied during laryngoscopy, need for external laryngeal pressure, and position of the vocal cords at intubation. Studies employing this tool suggest an increased incidence of difficult intubation (IDS>5) in obese patients.^32–34 That being said, BMI itself was not shown to be an independent predictor of difficulty in these cases. It is important to note that the vast majority of obese patients, with proper positioning and preparation, do not present an airway problem.

The above is clearly stated in the NAP4 study which recognized obesity as representing a high proportion of patients who have difficulty, with particular emphasis on the morbidly obese.³⁵ The Executive Summary stated:

Are Obese Patients at Increased Risk of Aspiration?

Obesity has been frequently listed as a risk factor for aspiration. However, recently this assumption has been challenged by a number studies that have found no increase in gastric volumes or acidity in obese subjects.^36,37 Maltby et al.³⁸ demonstrated that gastric emptying was no different in obese than in non-obese patients and suggested that the same guidelines for fasting can be applied to both patient populations. Aspiration risks and prophylaxis should be applied in the obese patients using the same criteria as in the non-obese. For a detailed discussion of aspiration and risks, see Chapter 5.

How Should the Morbidly Obese Patient be Positioned for Airway Management?

Because of the decreased oxygen reserve in this patient population, it is crucial to position these patients carefully for airway intervention prior to induction of anesthesia. Appropriate positioning prior to the induction of anesthesia can significantly reduce the apnea time required for intubation as well as increase the oxygen reserve. While recent literature has questioned the advantage of the sniffing position over simple head extension,³⁹ these studies still advocate the sniffing position for obese patients. Proper sniffing position has been defined as head extension and a 35-degree flexion of the neck onto the chest.⁴⁰

Achieving adequate sniffing position in a patient of IBW may include placement of a pillow under the neck and extending the head. However, in the morbidly obese patient, optimal positioning requires building a ramp of sheets or towels under the shoulders, neck, and head (Figures 20–1 and 20–2). This is referred to as “extreme sniffing” or “ramped” position or the “head-elevated laryngoscopy position” (HELP) where the external auditory meatus is in line with the sternal notch. As an alternative to blankets, towels, and pillows, the Troop^® Elevation Pillow can be used (see Figure 51–2). In several studies, this position has been shown to significantly improve laryngoscopic view when compared to supine positioning. For example, a comparative study of 60 morbidly obese patients by Collins et al.⁴¹ demonstrated a significant improvement of laryngoscopic grade in patients in the “ramped” position. Determinants of proper “ramped” positioning have been described as follows: at least a 90-degree angle between the mandible and chest; the face higher than the chest; external auditory meatus at the same horizontal level as the sternal angle.⁴¹

A second and important positioning principle involves the use of the reverse Trendelenburg position. Bed placement of 30-degree head up tilt increases FRC and compliance (both lung and chest wall) thereby permitting greater degrees of pulmonary oxygen reserve⁴² and prolonging apneic oxygen desaturation time in obese patients.^43,44 Adding continuous positive airway pressure (CPAP) of 10 cm of H₂O pressure has been shown to be an effective maneuver in reducing the degree of atelectasis associated with induction. Patients receiving positive end-expiratory pressure (PEEP)/CPAP prior to induction can be expected to have higher PaO₂ values than control groups that have not undergone the maneuver.^45,46 However, the morbidly obese patient will still have more rapid oxygen desaturation once apneic when compared to the non-obese patients, even with CPAP. Passive oxygenation has been shown to be an important technique in significantly prolonging safety after apnea occurs. (See section “What Is the Role of Passive Oxygenation During the Management of the Difficult Airway in the Obese Patient?” in this chapter for the discussion of this topic.)

How Should Medications be Dosed in the Morbidly Obese Patient?

Though there is a lack of consensus regarding dose adjustments in obese patients, both the IBW and lean body weight (LBW) have been used instead of total body weight (TBW). The LBW is a measured value, but can be estimated by the formula:

The IBW (as presented above) can be approximated by a simple formula.

IBW ( kg ) = height ( in cm ) − x where x is 100 for males and 105 for females

Another suggested way to calculate the dose of these agents is to employ the adjusted body weight (ABW)⁴⁸:

ABW = IBW + 0.4 ( TBW − IBW )