Obesity, Obstructive Sleep Apnea, and Sleep

Patients with obesity (see Chapter 27 ) and obstructive sleep apnea (OSA) may be at higher risk for postoperative complications. Obesity and OSA are separate disease states, but there is some association between the two, because OSA occurs in a relatively higher percentage of obese than nonobese patients.^[449] Although some data suggest that epidural analgesia may decrease postoperative complications in the obese patient, ^{[168] [450]} the optimal postoperative analgesic and monitoring regimen for patients with OSA is not clear. Data suggest that sleep is disrupted in the immediate postoperative period and may influence postoperative morbidity and patient-oriented outcomes.

Obesity is defined as a body mass index (BMI) of more than 30 kg/m² , with morbid and supermorbid obesity defined as a BMI of more than 35 kg/m² and 55 kg/m² , respectively. The prevalence of obesity has increased to

2749

Because obese patients are at higher risk for development of postoperative pulmonary complications and hypoxia, in part because of reductions in functional residual capacity, expiratory reserve volume, and total lung capacity and a predisposition to atelectasis,^{[451] [455]} special consideration for the management of postoperative pain is essential to allow these patients to actively participate in postoperative physiotherapy that may decrease pulmonary complications.^{[456] [457]} Although intravenous PCA with opioids may provide effective postoperative analgesia in morbidly obese patients,^[458] use of epidural morphine analgesia has been shown to reduce the incidence of pulmonary complications compared with intramuscular opioids.^[450] Other randomized data also suggest that high-risk subjects, such as obese patients, undergoing upper abdominal surgery may have a lower incidence of respiratory failure with the use of a local anesthetic-based epidural regimen compared with the use of systemic opioids.^[168] Unfortunately, there is a paucity of randomized clinical trial data specifically examining various analgesic regimens and outcomes in obese patients; however, it appears that the use of epidural analgesia can provide superior analgesia and may decrease pulmonary complications in obese patients, especially those undergoing upper abdominal procedures.^{[168] [450]}

Although obese patients do not necessarily have OSA, obesity is the most important physical characteristic associated with OSA. Approximately 60% to 90% of OSA patients are obese, and at least 5% of morbidly obese patients have OSA, which is defined as more than five episodes per hour of cessation of airflow for more than 10 seconds despite continued ventilatory effort.^{[449] [451]} It is estimated that approximately 4% of men and 2% of women (18 million Americans overall) have OSA and that up to 95% of persons with OSA are underdiagnosed.^[449] Patients with OSA are generally at higher risk for chronic cognitive impairment, pulmonary hypertension, cardiomyopathy, systemic hypertension, and possibly for myocardial infarction.^{[459] [460] [461] [462] [463] [464]} The pathophysiology of airflow obstruction is related primarily to upper airway pharyngeal collapse, including the retropalatal, retroglossal, and retroepiglottic pharynx, during sleep, especially during rapid eye movement (REM) sleep.^{[449] [465]} During these obstructive episodes, OSA patients may exhibit hypoxia, bradyarrhythmias or tachyarrhythmias, myocardial ischemia, abrupt decreases in left ventricular stroke volume and cardiac output, or increases in pulmonary and systemic blood pressure.^{[461] [466] [467]}

Based on our understanding of the pathophysiology of OSA, it is easy to see how postoperative pain management can be difficult in this population. Patients with OSA are at higher risk for respiratory arrest.^{[465] [468]} Use of sedative doses of benzodiazepines and opioids may result in frequent hypoxemia and apnea, which may be especially dangerous in the OSA patient.^{[465] [469] [470]} Avoiding respiratory depressants by optimizing use of NSAIDs and epidural analgesia with a local anesthetic-based regimen may attenuate the risk for respiratory depression and arrest because the use of epidural and systemic opioids is associated with sudden postoperative respiratory arrest.^{[465] [467]} Use of a local analgesic solution alone should not be considered without risk because local anesthetics may also depress the hypoxic ventilatory drive.^[471] If opioids are to be used for postoperative analgesia in patients with OSA, careful titration of analgesia and close monitoring (possibly in an intensive care unit or other monitored setting) may be necessary, although there is no consensus on the criteria for postoperative monitoring of OSA patients. Observational data suggest that use of nasal continuous positive airway pressure (CPAP) in OSA patients may allow the use of systemic analgesic agents and reduce hemodynamic changes,^{[472] [473] [474]} but additional randomized clinical trials are required to further define the role of CPAP in this setting.

The normal architecture of sleep is disrupted after surgery, with suppression of REM sleep during the first 1 or 2 nights postoperatively, followed by a rebound of increased, intense REM sleep, which may be associated with hypoxemia. ^{[449] [475] [476] [477]} The basis for the sleep disruption is not clear, but it may be a reflection of the extent of surgery (e.g., laparoscopic versus open procedures)^{[478] [479]} rather than the anesthetic itself.^{[480] [481]} Poor pain control may generally affect sleep postoperatively,^{[482] [483]} although a direct correlation between the severity of pain and quality of sleep has not been confirmed,^[484] and the extent of its input to postoperative sleep disruption has not been elucidated. Analgesic agents such as opioids may interfere with REM sleep,^[485] but the use of local anesthetic-based epidural analgesia may not necessarily improve postoperative sleep disruption.^[484]

Although postoperative sleep disruption affects all surgical patients, OSA patients may be especially vulnerable to postoperative complications and the physiologic changes associated with the rebound in REM sleep.^{[449] [486] [487] [488]} Late postoperative hypoxemia (i.e., beyond the first 2 postoperative nights) related to the rebound in REM sleep is well documented.^{[476] [477] [489] [490]} REM sleep is associated with profound sympathetic activation and release of catecholamines, ^{[491] [492]} which in combination with cardiovascular responses and hypoxemia from apnea may lead to myocardial ischemia, arrhythmias, infarction, and death.^{[488] [493] [494] [495]} Oxygen therapy postoperatively may increase mean oxygen saturation but does not alter the basic mechanism of apnea causing the hypoxic episodes.^[496]