Obesity, Sleep Apnea, the Airway, and Anesthesia

Key Points

• A high body mass index (BMI) is a weak but statistically significant predictor of difficult intubation (DI) and difficult mask ventilation (DMV). Body fat distribution, rather than the BMI value, may be a better predictor of difficult laryngoscopy. Measuring the neck circumference at the thyroid cartilage level is a useful addition to the normal daily practice of measuring weight or BMI during preoperative airway evaluation.

• For those suspected of having obstructive sleep apnea (OSA) based on clinical criteria, anesthesiologists may elect to proceed with a presumptive OSA diagnosis unless the patient has significant comorbidities.

• General anesthesia with a secure airway is preferable to deep sedation without an airway for superficial procedures and patients with OSA undergoing procedures involving the upper airway. Intraoperative positive airway pressure (PAP) or high-flow nasal cannula (HFNC) can be used in the patient with morbid obesity and OSA to augment spontaneous ventilation and provide good sedation for surgery.

• Intubation under general anesthesia should be carried out with the patient fully preoxygenated to prevent hypoxia. The relatively low functional residual capacity (FRC) found in patients with obesity causes them to desaturate more rapidly. Extension of apnea time during laryngoscopy through apneic oxygenation can prolong the safe apnea time and increase first-pass intubation success.

• The head-elevated laryngoscopy position (HELP) significantly elevates the head, upper body, and shoulders above the chest so that an imaginary horizontal line connects the sternal notch with the external auditory meatus to create a better alignment among the three axes to improve laryngoscopy conditions.

• Rapid sequence intubation (RSI) is often recommended in patients with obesity because of the high prevalence of lower esophageal sphincter hypotonia, which increases the prevalence of gastroesophageal reflux disease. Still, the benefits should be weighed against the risks of DMV or DI.

• Pressure-controlled ventilation volume-guaranteed (PCV-VG) may be advantageous in the patient with obesity because it ensures a minimum tidal volume with lower peak inspiratory pressures.

• The endotracheal tube (ETT) should be left in place, or extubation should be carried out over an airway exchange catheter if any doubt exists about the patient’s ability to breathe spontaneously or the practitioner’s ability to reintubate in an emergency.

• Tracheal extubation should occur in the semi-upright or head-up position only after the patient with obesity and OSA regains full consciousness after general anesthesia and after confirming airway patency and verification of complete reversal of neuromuscular blockade.

• Patients with obesity and OSA may need a higher level of monitoring postoperatively due to an increased risk of opioid-induced postoperative upper airway obstruction.

Introduction

The prevalence of obstructive sleep apnea (OSA) among patients with obesity ranges from 35% up to as high as 94%, with a majority of studies reporting a prevalence of at least 60%. With obesity at epidemic proportions worldwide, OSA remains a major contributing factor to airway management difficulties. Surgical patients with OSA have been found to have a higher incidence of pulmonary and airway complications, ^, and numerous studies have reported major respiratory complications, including brain damage and death. These devastating outcomes can result from failure to secure the airway during the induction of anesthesia, airway obstruction immediately following tracheal extubation, and respiratory arrest after the administration of opioids or sedation in the postoperative period.

The prevalence of OSA globally is estimated to be 18.6% in adults (age 30–69). In the US adult population (age 30–70), its prevalence is estimated to be 26%, and it is the most common type of sleep-disordered breathing (SDB). It occurs due to partial or complete airway obstruction during sleep, and it is associated with episodic hypoxemia and hypercarbia. However, with the US population aging and becoming more obese, the prevalence of OSA is expected to increase significantly. Among the surgical population, patients with morbid obesity and OSA tend to be overrepresented because of the higher rates of obesity and OSA-related complications requiring surgical therapy. However, a significant proportion of these patients are often undiagnosed or untreated for OSA.

Definitions of Obesity and Obstructive Sleep Apnea

In 2013, the American Medical Association and several other organizations officially recognized obesity as a disease requiring treatment and prevention efforts. The Obesity Medical Association defines obesity as a “chronic, relapsing, and treatable multi-factorial, neurobehavioral disease, wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces, resulting in adverse metabolic, biomechanical, and psychosocial health consequences.” When utilized as a tool to categorize individuals based on relative weight and assess population-level measurements of risk factors, obesity is defined as a body mass index (BMI) or weight in kilograms (kg) divided by height in meters (m ² ) >29.9, and overweight is defined as a BMI of 25 to 29.9 kg/m ² . ^, Morbid obesity is classified as a BMI of ≥40 and a BMI of ≥50 kg/m ² designates super morbid obesity. Obesity and morbid obesity are associated with increased risk for several chronic medical comorbidities, including cardiovascular disease, diabetes, and chronic kidney disease, ^, which may influence perioperative morbidity and mortality. ^,

OSA is a sleep disorder characterized by repetitive upper airway collapse during which airflow ceases for more than 10 seconds, five or more times per hour, despite continuing ventilatory effort. It is usually associated with decreased arterial oxygen saturation (Sao ₂ ) of more than 4%. Obstructive sleep hypopnea is defined as a decrease in airflow, ranging from ≥30 to 50%, associated with a decrease in arterial saturation ≥3% to 4% for ≥10 seconds occurring five times or more per hour of sleep. ^,

Pathophysiology of Obstructive Sleep Apnea

Pharyngeal Muscle Activity and Airway Patency

Three pharyngeal segments—the nasopharynx (i.e., retropalatal pharynx), oropharynx (i.e., retroglossal pharynx), and laryngopharynx (i.e., retroepiglottic pharynx)—form the upper airway, which is a long, soft-walled tube that lacks bony support on the anterior and lateral walls, making it collapsible ( Fig. 40.1 ). The transmural pressures across the pharyngeal walls (i.e., the difference between extraluminal and intraluminal pressure) determine the upper airway’s patency. Activation of pharyngeal dilator muscles, the tensor veli palatini, the genioglossus, and the hyoid bone’s muscles (geniohyoid, sternohyoid, and thyrohyoid) during inspiration counteracts the narrowing effects of reduced intraluminal pressure associated with inspiration. In addition to this inspiration-associated activation, the tonic activity of these muscles during wakefulness helps stabilize the pharyngeal walls.

The cause of upper airway collapse is multifactorial and can be attributed to several factors. A reduction in pharyngeal dilator muscle activation, which likely results from the loss of the stimulatory effect of wakefulness (i.e., during sleep), reduction in respiratory drive, depression of negative pressure reflexes, loss of lung volume, and overaction of the respiratory pump muscles, decreases longitudinal traction on the pharyngeal walls and increases the likelihood of upper airway collapse. ^, Loop gain is a term utilized to describe the stability of a feedback control system, and patients with severe OSA have been shown to have high loop gain, rapidly and aggressively responding to minimal changes in CO ₂ , which leads to a higher tendency of periodic breathing. ^,

Patients with OSA also tend to have a reduced respiratory-tract diameter. The pharynx has a round shape, compared to an oval shape, attributing to a larger anteroposterior diameter rather than a larger transversal diameter. This ultimately generates a hindrance in the mechanics of the dilator muscles of the pharynx.

Sleep Pattern, Airway Obstruction, and Arousal

Normal sleep consists of four to six cycles of non-rapid-eye-movement (NREM) sleep, followed by rapid-eye-movement (REM) sleep. The four stages of NREM sleep and one stage of REM sleep represent a progressive slowing of the electroencephalographic waves. Rhythmic activity of the upper airway muscles decreases during deeper sleep stages, which accompanies a significant increase in upper airway resistance and consequent upper airway collapse. Patients with OSA have a decreased or even absent airway reflex during non-REM sleep. REM sleep is associated with impaired respiratory arousal and an increase in nocturnal hypoxemia episodes. ^,

Contraction of the diaphragm during inspiration creates a subatmospheric pressure within the airway that may narrow the collapsible segments of the pharynx. As pharyngeal pressure becomes more negative, pharyngeal collapse increases progressively. The most compliant and common pharyngeal collapse site is the lateral pharyngeal walls, a significant pharyngeal adipose tissue deposition site. In patients with obesity, deposition of fat around the pharyngeal walls narrows the upper airway and increases the extraluminal pressure and risk of collapse. ^{, ,} Increased fat deposits, in addition to the gravitational effects of being in the supine position, also lead to increased compression to the retropalatal airway and retroglossal airway, which tend to be smaller in this patient population. For a given degree of loss of pharyngeal muscle tone and pharyngeal muscle collapse, a greater degree of pharyngeal obstruction is observed in patients with a posteriorly set tongue (caused by micrognathia and retrognathia or a receding mandible), displacement of the hyoid bone often associated with obesity, a large tongue, large tonsils, and nasal obstruction. Other factors that contribute to upper airway narrowing and subsequent collapse during sleep include large neck circumference, anatomic or craniofacial abnormalities affecting the airway, gender, and age. ^{, , ,}

Airway collapse leads to obstructive apnea and consequently causes a decrease in arterial oxygen tension (Pao ₂ ) and an increase in arterial carbon dioxide tension (Paco ₂ ), which increases neural traffic in the reticular activating system, progressively increasing ventilatory efforts ^, and causing arousal from sleep. Arousal, expressed as extremity twitching, gasping or snorting, vocalization, and increased electroencephalographic activity, reactivates the pharyngeal muscles and opens the upper airway. As the upper airway opens, an increase in diaphragm activity leads to hyperventilation, reversing the blood gas disturbance, correcting hypoxia and hypercarbia, and decreasing the central drive. The cycle repeats itself when the patient falls asleep again ( Fig. 40.2 ).

Frequent arousals and the subsequent cycle of wake and sleep prevent deep restorative sleep phases and lead to excessive daytime somnolence, which has been shown to exist in up to 32% of highly compliant patients with continuous positive airway pre­ssure (CPAP) during the night. Oxygen desaturation, sympathetic hyperactivity, and a systemic inflammatory response may contribute to cardiovascular comorbidities such as systemic hypertension, cardiac arrhythmias, myocardial ischemia, pulmonary hypertension, and heart failure.

Diagnosis of Obstructive Sleep Apnea

Because OSA is undiagnosed in up to 80% of patients at the time of surgery and failure to recognize OSA preoperatively is one of the major causes of perioperative complications, all perioperative patients should be screened for OSA. Obtaining a thorough history and physical examination helps to determine a presumptive diagnosis of OSA. However, only polysomnography can confirm the diagnosis and severity of OSA and determine the need for and level of CPAP needed.