Perianesthesia implications of obstructive sleep apnea.

Crit Care Nurs Q Vol. 38, No. 1, pp. 97–108 c 2015 Wolters Kluwer Health | Lippincott Williams & Wilkins Copyright

Perianesthesia Implications of Obstructive Sleep Apnea Penelope Z. Strauss, PhD, CRNA, RRT Obstructive sleep apnea (OSA) is a complex medical condition that affects not only the airway but also the cardiopulmonary, endocrine, and central nervous systems. Obstructive sleep apnea can usually be identified with a focused history and physical examination and is commonly associated with obese, middle-aged men with hypertension and glucose intolerance. A high index of suspicion for OSA should arise when reports of loud snoring, nighttime arousal, and acid reflux accompanied by a history of stroke, atrial fibrillation, or congestive heart failure are elicited during a perianesthesia evaluation. Perianesthesia risk in OSA patients includes the potential for difficult airway management, cardiovascular instability, and abnormal sensitivity to sedation and analgesia. Typical doses of respiratory depressants may cause profound hypoventilation, apnea, or cardiopulmonary arrest in OSA patients. Central axial opioids and continuous intravenous opioid infusions should be avoided while nonopioid and non–centrally acting analgesics are recommended. Careful postoperative monitoring is important to preventing serious morbidity. Early identification of OSA and its comorbidities is key to developing a safe anesthesia and postoperative treatment plan. Key words: obstructive/complications, sleep apnea syndromes, sleep apnea

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BSTRUCTIVE SLEEP APNEA (OSA) syndrome has emerged as a chronic disease that has been identified primarily in middleaged men and postmenopausal women with prevalence from 3% to 18% and 0.6% to 7%, respectively, with higher prevalence at ages greater than 60 years.1 Obstructive sleep apnea is a complex medical condition, named for the clinical sign of partial or complete airway obstruction during sleep. Although OSA is associated with abnormal anatomy in the upper airway in all age groups, it is most commonly associated with excess adiposity in adults. In children, OSA peaks in the preschool-age group, is equally distributed

Author Affiliation: Department of Acute and Continuing Care, The University of Texas Health Science Center at Houston, Houston, Texas. The author has disclosed that she has no significant relationships with, or financial interest in, any commercial companies pertaining to this article. Correspondence: Penelope Z. Strauss, PhD, CRNA, RRT, Department of Acute and Continuing Care, The University of Texas Health Science Center at Houston, 6901 Bertner Ave, SON 682, Houston, TX 77030 ([email protected]). DOI: 10.1097/CNQ.0000000000000044

among the sexes, and is almost exclusively associated with adenotonsillar hypertrophy and/or craniofacial abnormalities.2 Obstructive sleep apnea is a public health issue because of its independent association with hypertension, coronary events, stroke, and the risk of motor vehicle accidents.3 OSA patients have increased perianesthesia risks in the areas of airway management, coexisting cardiovascular and metabolic disorders, and altered responses to central nervous system (CNS) depressants. In addition, the potential aberrant responses of an OSA patient to sedation and anesthesia can increase the incidence of adverse events in the postanesthesia period and prolong the length of stay in postanesthesia care units.4 The “gold standard” for diagnosis of sleep apnea is polysomnography, an elaborate overnight examination that involves monitoring sleep stage, respiratory effort, and airflow.5 Respiration is detected by nasal and oral thermistors or capnography. Respiratory effort is monitored with strain gauges placed on the thorax and abdomen or with a respiratory inductive plethysmograph. The presence or absence of respiratory effort differentiates 97

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CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2015

centrally mediated from obstructive apnea. The apnea-hypopnea index (AHI) is determined by the number of apnea and hypopnea episodes per hour of sleep. General criteria to advance the diagnosis of sleep apnea include an AHI of more than 10, along with evidence of disturbed or unrefreshing sleep, daytime sleepiness, or other daytime symptoms. Using the American Academy of Sleep Medicine criteria, mild, moderate, and severe OSA are defined by an AHI ≥5 up to 15, ≥15 to 30, and ≥30, respectively. Obstructive sleep apnea is usually associated with hemoglobin desaturation of 4% or more. Because a polysomnogram is expensive and time-consuming, however, a majority of patients may be undiagnosed. Clinical pathognomonic symptoms of OSA in adults include heavy snoring, excessive daytime sleepiness, sudden awakenings associated with choking, and/or witnessed apneas during sleep.6 Increasing body mass index (BMI) is highly correlated with the number of symptoms of OSA7 ; therefore, all high-risk patients (BMI >30 kg/m2 ) should have a focused preoperative interview, if possible, with the bed partner present to report nighttime sleep events. The classical signs of OSA vary between the sexes with both exhibiting witnessed apnea during sleep and/or loud snoring. However, women often describe fatigue and lack of energy, while men report fitful sleep, awakening with gasping or choking, and excessive daytime sleepiness.8 CHRONIC AIRWAY OBSTRUCTION LEADS TO CHRONIC HYPOXIA AND HYPERCARBIA Airway obstruction in OSA has both anatomical and physiological roots.9 During inspiration while awake, the dilating actions of the pharyngeal muscles brace the collapsible pharyngeal walls against negative transmural pressure that normally narrows the airway. The underlying pathology of OSA involves 2 events that occur during inspiration while asleep: a reduction in neuromuscular tone and altered CNS control of respiration. Tonic muscle activity in the pharyngeal muscles is de-

creased or completely absent during sleep. A sleep-induced increase in upper airway resistance creates more negative pharyngeal pressure during diaphragmatic contraction, leading to airway narrowing or collapse.10 The key sites of collapse are the lateral pharyngeal walls, which are also the predominant site of fat deposition in OSA patients. Continuing diaphragmatic efforts coupled with complete airway obstruction leads to the development of hypoxia and hypercarbia. The association between obesity and airway obstruction can be partially explained by the decreased functional residual capacity that accompanies obesity. An increased lung volume is thought to exert caudal traction on the upper airway, preventing its collapse.11 Maneuvers that increase the functional residual capacity such as sleeping on an incline can reduce pharyngeal collapse and potentially decrease airway collapse and/or the amount of positive airway pressure necessary to maintain airway patency. These principles can be applied to perioperative practice by using Fowler’s position, reverse Trendelenburg position or “ramping” the upper torso of the obese patient. Some patients have a positional variation of OSA severity in the supine versus lateral position—that is, lateral positioning relieves the airway obstruction. This may be the case in from 20% to 55% of OSA patients.12 These patients tend to be younger, less overweight, and have a lower AHI. The differential effect of sleep position is lost in severe OSA and in the morbidly obese (BMI >40). However, if effective, lateral positioning is the least obtrusive of the available treatments and can be used in postanesthesia care units and on the hospital ward. OSA ALTERS CENTRAL NERVOUS SYSTEM RESPONSIVENESS Neural activity in the hypoglossal nerve is highly coordinated with phrenic nerve activity, so that genioglossus muscle activation coincides with diaphragmatic contraction. Genioglossus muscle activity is partly due


Perianesthesia Implications OSA to a reflex response to negative pharyngeal pressure so that as inspiration begins, the tongue’s muscle tone increases to maintain an open airway. In addition, the activities of both the diaphragm and the genioglossus muscles are heightened in the presence of hypoxia and hypercarbia.6 The activity of these motor neurons is uncoupled when exposed to alcohol, benzodiazepines, anesthesia, and brain hypoxia, contributing to the potential for airway obstruction in any of these scenarios. The CNS is typically very sensitive to low oxygen and high carbon dioxide levels, increasing minute ventilation if these conditions occur. However, in airway obstruction during rapid eye movement sleep, the CNS response to the hypoxia is reduced and the hypercapneic response is all but eliminated. In anywhere from 20 seconds to 3 minutes, hypoxia will become profound enough to cause brief arousal that restores upper airway muscle tone and relieves airway obstruction. In the presence of severe OSA, this cycle of breathing cessation, arousal, and resumption

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of breathing may occur up to 400 to 600 times in an 8-hour sleep period. In the context of sleep, arousal is a valid and appropriate response to episodes of obstructive apnea associated with hypoxia and hypercarbia.13 Unfortunately, the chronic hypoxemia and hypercarbia that occur during OSA alter normal neural thresholds for arousal, impairing the arousal response. Untreated sleep disturbances tend to progress as chemoreceptors will “reset” their sensitivity so that arousal does not occur as frequently. This initiates a vicious cycle in which hypoxia and hypercarbia must become more and more profound before arousal and airway opening occur. Upper airway responses in OSA are remarkably similar to the upper airway under deep sedation or general anesthesia. Because both chronic OSA and perianesthesia drugs shift the carbon dioxide and oxygen response curves, OSA patients may be markedly sensitive to respiratory depressant effects of anesthesia, sedatives, or opioids.14 Figure when

Figure. The effects of sleep, narcotics, chronic pulmonary obstructive pulmonary disease, deep anesthesia, and metabolic acidosis on the ventilatory response to carbon dioxide. From MG Levitzky, Pulmonary Physiology, 5th ed. Reproduced with permission of McGraw-Hill Education.


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combined with postoperative analgesia, including epidural morphine and fentanyl, altered arousal responses can lead to severe hypoxemia, hypercarbia, and respiratory or cardiac arrest in the postoperative period.15,16 Intravenous (IV) analgesia, intramuscular (IM) analgesia, patient-controlled analgesia with and without a continuous background infusion, and epidural and spinal analgesia have been implicated in adverse respiratory responses to opioids in OSA patients. In a recent retrospective study in a single institution, 32 life-threatening critical respiratory events were identified over a 6-year period.16 Four deaths occurred, with 3 of the 4 in the first 24 hours postoperatively and between midnight and 6 AM. Significant risk factors for adverse respiratory events were OSA, hypertension, coronary artery disease, diabetes, and history of congestive heart failure and cardiac dysrhythmias. Obstructive sleep apnea, hydromorphone use, and deep sedation were observed in the patients who died.16 Multiple prospective studies have also demonstrated increases in apneic events and desaturation when OSA patients receive opioid therapy.17 UNTREATED OSA HAS PROFOUND CARDIOVASCULAR SEQUELAE The repetitive obstructive events that occur in OSA are equivalent to experiencing “fight or flight” responses all night instead of achieving restorative sleep. Chronic episodes of hypoxia, arousal, and sympathetic nervous system activation may lead to sustained hypertension and cardiovascular remodeling. These events can alter baroreceptor responses such that cardiovascular response under anesthesia is attenuated.18 Chronic sympathetic stimulation is also known to be associated with depression of immune function, the acceleration of atherosclerosis, and, if severe, an elevated pulmonary artery pressure and right ventricular hypertrophy with possible heart failure and stroke. Short-term treatment (60 days) with nasal continuous positive airway pressure (CPAP) has demonstrated both

statistically significant and clinically relevant reductions in blood pressure and daytime catecholamine levels.19 Bradycardia is a common feature of sleep apnea or hypopnea with associated hypoxia and can be relieved with nighttime oxygen administration.20 Treatment with nasal CPAP ends bradydysrhythmias; however, this effect dissipates within several days of discontinuing treatment. Heart block has been identified in up to 20% of severe OSA patients.21 The OSA patients with heart block are likely to be more obese and to desaturate to a greater extent than those without heart block. Ventricular tachycardia occurs in up to 13% of OSA patients, with as many as 67% of patients presenting with frequent premature ventricular contractions.22 OSA patients are 4 times more likely to have atrial fibrillation than those without OSA; postcardioversion, treated OSA patients have a lower rate of recurrence than untreated OSA patients.23 Along with cardiovascular disease and dysrhythmias, OSA is highly associated with cerebral vascular accidents. As many as 60% to 80% of stroke patients are estimated to have undiagnosed and untreated OSA.24 In OSA patients who have endured an ischemic stroke, treatment with CPAP reduces the risk of a new stroke event from 36% to 6% compared with patients who did not tolerate CPAP.25 METABOLIC AND NEUROPSYCHOLOGICAL SYMPTOMS MAY OCCUR Obstructive sleep apnea and daytime somnolence are associated with a metabolic syndrome in which insulin and leptin levels are elevated independent of obesity.26 Leptin is a hormone released from adipocytes that correlates with fat mass; increased circulating leptin may contribute to sympathetic activation. OSA patients also have elevated levels of interleukin-6 and tumor necrosis factor α, inflammatory cytokines involved in sleep regulation and fatigue. In addition, plasma insulin and glucose levels are


Perianesthesia Implications OSA increased in OSA compared with obese controls. The relationship between insulin resistance and sleep disordered breathing is maintained even in mild OSA and seems to be related to the presence of visceral adipose tissue. OSA patients with diabetes demonstrate improved insulin resistance after treatment with nasal CPAP. Neuropsychological consequences of OSA may be due to altered sleep architecture and sleep quality. Outcome measures of these effects include altered cognitive function, quality of life, and an increased rate of motor vehicle and occupational accidents.27 Various studies have found weak associations between OSA and diminished psychomotor efficiency, self-assessed concentration problems, and memory impairment. Patients with an AHI of more than 15 are 7 times more likely to experience multiple motor vehicle crashes over 5 years, even when adjusted for age and annual miles driven.28,29 OSA patients are 2 to 3 times more likely to have an occupational injury than normal controls.30 PERIANESTHESIA IMPLICATIONS OF OSA Due to these significant systemic comorbidities, both untreated and treated OSA patients are at risk for increased drug-related morbidity and mortality during the perioperative period. Some OSA patients will exhibit markedly altered responses to hypoxia and hypercarbia; have increased sensitivity to sedatives, opioids, and anesthetics; and be at extreme risk for postoperative respiratory depression. Identifying these individuals preoperatively and creating a safe perianesthetic plan is crucial to preventing OSA-related critical incidents. PREOPERATIVE EVALUATION IN ADULT OSA In general, as BMI increases, there are increases in both the number of OSA symptoms and the severity of OSA.31 Because increased BMI is highly correlated with OSA, all highrisk patients (BMI >30 kg/m2 ) should have

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a preoperative interview seeking the OSA diagnosis.32 In the absence of a polysomnogram, a targeted history and physical examination can provide a presumptive clinical diagnosis of OSA. Signs and symptoms that support the diagnosis can be evaluated by system (Table 1). In addition, the presence of multiple highly prevalent comorbidities of Table 1. Signs/Symptoms That Support a Diagnosis of Adult Obstructive Sleep Apnea Syndrome Anthropometric Obesity (body mass index >30 kg/m2 ) Waist circumference >40 inches in men; >35 inches in women Neck circumference >17 inches in men; >16 inches in women Airway/respiratory Intermittent snoring with apneas “Difficult airway” on examination Nocturnal choking Dry mouth/sore throat on awakening Adenotonsillar hypertrophy/nasal obstruction Cardiovascular Atrial fibrillation Cerebral vascular accident Congestive heart failure Treatment-refractory hypertension Nocturnal chest pain, palpitations, or diaphoresis Lower extremity edema of unknown origin Central nervous system Frequent arousals from sleep Fatigue despite “adequate sleep” Falls asleep in nonstimulating environment Morning cephalgia or confusion On-the-job injury/motor vehicle accident victim Endocrine Glucose intolerance/insulin resistance Metabolic syndrome/syndrome X Polycystic ovarian syndrome Gastrointestinal/genitourinary Gastrointestinal reflux Decreased libido/impotence Nocturia, enuresis


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OSA will further support the presumptive diagnosis and may indicate that the patient has more severe disease. Comorbidities that are highly prevalent in OSA patients include treatment-resistant hypertension, congestive heart failure, pulmonary hypertension, first stroke, morbid obesity, and gastroesophageal reflux disease.33 In the most severe cases, chronic nighttime hypoxemia is evidenced by polycythemia.16 Notably, a subset of patients with severe OSA has been identified who report minimal daytime sleepiness.34 “Nonsleepy” patients tend to be older, have lower BMI, lower AHI, quieter snoring, and a higher minimum oxygen saturation during sleep but still present with common OSA comorbidities. PREOPERATIVE EVALUATION IN PEDIATRIC OSA Obstructive sleep apnea occurs in the pediatric population peaking in the 2- to 8-year-old age group and paralleling the growth of lymphoid tissue during these years.35 Pediatric OSA should be suspected if enuresis reappears after toilet training had been successfully accomplished and/or with the development of learning difficulties, poor performance in school, or hyperactivity disorders.36 Pediatric OSA is almost exclusively associated with adenotonsillar hypertrophy and/or craniofacial abnormalities, although childhood obesity is beginning to play a larger role. Pediatric patients may adopt unusual sleeping positions that improve airway patency (knee-chest, kneeling, upright, use of multiple pillows); it is helpful to identify a preferred sleep position preoperatively. Daytime sleepiness is relatively uncommon unless the child is obese; poor somatic growth and failure to thrive is a feature of advanced disease. Upper airway obstruction is becoming the most common indication for tonsillectomy and adenoidectomy in children although polysomnography is rarely used to diagnose these children.37 Excess adenoid and tonsillar tissue is not always the source of obstruction;

many syndromes are associated with a narrow epipharyngeal space and poorly developed maxillary and mandibular structures. A large number of rare syndromes are associated with OSA (eg, Pierre Robin, Treacher Collins, Crouzon, and many more).38 Children with Down syndrome have a high probability of developing OSA, while up to 75% of patients with achondroplasia present with sleep apnea of both obstructive and central origin. Supporting evidence for the presence of pediatric OSA syndrome is listed in Table 2. A crucial difference between untreated adult versus pediatric OSA is that adults generally die during sleep or of cardiovascular disease, while children usually die perioperatively.39 Complication rates known in the pediatric OSA population are as high as 23%. Pediatric OSA patients undergoing adenotonsillectomy Table 2. Signs/Symptoms That Support a Diagnosis of Pediatric Obstructive Apnea Syndrome Anthropometric >95th percentile for age and gender or Delayed growth with impaired weight gain Failure to thrive Airway/respiratory Continuous snoring Craniofacial abnormality Tonsils touching or nearly touching Parental report of difficulty breathing or struggling respiratory efforts during sleep Nasal obstruction Central nervous system Parental report of restless sleep Signs of attention deficit disorder Child often difficult to arouse at usual awakening time Nocturnal diaphoresis Odd sleeping positions Parent or teacher comments that child appears sleepy during the day Gastrointestinal/genitourinary Obesity (school age, adolescents) Nocturnal enuresis


Perianesthesia Implications OSA have a lower risk of postoperative respiratory complications if operated on in the morning rather than after 1 PM.40 Morning anesthetics allow for a longer period before the first nocturnal sleep and may provide for a higher degree of postoperative care by the day staff and more alert parents. Not all children with OSA will have symptomatic resolution following tonsillectomy; success rates depend largely on patient selection.41 It is also notable that, in both adults and children, the altered central chemoreceptor responses to hypoxia and hypercarbia are not immediately cured by surgical intervention. It may take days or weeks for the respiratory centers in the medulla to “reset” and for response patterns to become normal. Health care providers must remain vigilant for episodes of apnea, hypoxia, and hypercarbia in the postoperative period. A recent meta-analysis demonstrated that adenotonsillectomy in obese pediatric patients reduces the severity of OSA but rarely cures it.42 In addition, only 51% of pediatric OSA patients treated with adenotonsillectomy received a surgical “cure” when evaluated as late as 5 months postoperatively.43 PREOPERATIVE OSA ASSESSMENT TOOLS The STOP-BANG questionnaire is an efficient and valuable assessment tool for a presumptive diagnosis of OSA, in particular, the higher-risk moderate to severe OSA categories (Table 3). It has been validated for a high sensitivity and specificity against AHI severity evaluated by polysomnography. Using this tool, if 3 or more “yes” answers are elicited, there is a high risk of moderate to severe obstructive sleep apnea. If a shorter albeit slightly less sensitive screen is necessary, the STOPBANG questionnaire may be truncated after the first 4 questions (STOP).44 In this case, 2 or more “yes” answers indicate a high risk of OSA. In a recent systematic review of patient questionnaires that are designed to predict OSA, the STOP and STOP-BANG questionnaires were found to have the highest method-

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ological validity, reasonable accuracy, and the best usability.45 Based on the use of the STOP or STOPBANG and sufficient knowledge of the comorbidities of OSA, several authors have published guidelines for the preoperative evaluation and treatment of the suspected or known OSA patient.31,33 Patients who have presumptive or proven OSA are recommended to receive perioperative OSA precautions. Some patients might benefit from perioperative positive airway pressure treatment if the surgery is emergent or delay in the case of elective surgery while appropriate treatment is arranged. Perianesthesia-related OSA safety measures include opioid avoidance or the use of short-acting opioids, multimodal analgesia (nonsteroidal anti-inflammatory drugs, acetaminophen, ketamine, gabapentin, or pregabalin), regional anesthesia, full neuromuscular blockade reversal, awake extubation, and extubation and recovery in a semiFowler’s, Fowler’s, or lateral position.33 Recommendations for the preoperative medication of OSA patients include slow titration of sedation or analgesia, if any, in the holding area.46 Monitoring with either continuous pulse oximetry with alarms turned on or within line-of-sight of an educated nursing staff is recommended if a sedative is administered. The OSA patient should not be exposed to beginning trainees without the direct supervision of an experienced provider. “Routine” preoperative sedation given without adequate understanding of the pathophysiology of OSA can increase patient’s morbidity. AIRWAY MANAGEMENT IN OSA A thorough preoperative airway assessment should be conducted because the diagnosis of OSA implies that an inherently small space is available in the upper airway. This space will shrink with supine positioning, sedation, anesthesia, and muscle paralysis. Difficult airway adjuncts (minimally oral, nasal, and laryngeal mask airways) should be available in


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Table 3. STOP-BANG Questionnairea44 S (snore) T (tired) O (observed) P (blood pressure) B (BMI) A (age) N (neck) G (gender)

Do you snore loudly (louder than talking or loud enough to be heard through closed doors)? Do you often feel tired, fatigued, or sleepy during daytime? Has anyone observed you stop breathing during sleep? Do you have or are you being treated for high blood pressure? BMI >35 kg/m2 ? Age >50 y? Neck circumference >40 cm (15.7 in)? Gender male?

Abbreviation: BMI, body mass index. a High risk of obstructive sleep apnea: Answering Yes on 3 or more items. Adapted with permission from Chung et al.44

both the induction room and the recovery unit. The use of a “ramped” position generally improves both oxygenation and visualization of the glottic aperture during intubation. The difficulty of repositioning a morbidly obese patient during a failed intubation should not be underestimated.46 Appropriate choices for advanced airway management techniques are providerspecific, depending upon the preferences and experience of the provider. In one study, approximately two-thirds of patients with an unanticipated difficult intubation were subsequently discovered to have OSA.47 Nevertheless, the presence of OSA does not always predict a difficult intubation, at least in a carefully assessed sample of morbidly obese patients placed in a “ramped” position.48 It is relevant for the postanesthesia care unit (PACU) nursing staff to be familiar with any difficulties that may have occurred in securing the airway. INTRAOPERATIVE MANAGEMENT OF OSA PATIENTS Several principles of pharmacologic management have been suggested that serve to reduce morbidity in this population during operation. The severity of the CNS impairment in an OSA patient is not predictable; therefore, health care providers should consider administering drugs with short half-lives to mini-

mize the depression of ventilatory responses. The CO2 response curve is shifted by both severe OSA and anesthetics; even small doses of administered opioids (fentanyl 0.5 μg/kg) can cause a decreased minute ventilation or apnea in this population.49 Small doses of ketamine (0.5 mg/kg) have morphine-sparing effects in the pediatric tonsillectomy population and should be considered.50 Other nonopioid analgesics should be considered including acetaminophen, dexmedetomidine or other α-2 agonists, and nonsteroidal antiinflammatory agents.17 If opioids are deemed necessary, only short-acting agents should be used unless a clear plan for postoperative ventilation is in place. Neuromuscular paralysis should be avoided when possible and full reversal of neuromuscular function should be verified quantitatively (train-of-four [TOF] ratio >0.9) prior to extubation.51 OSA patients are at high risk for postoperative airway obstruction, including the risk of developing postobstructive pulmonary edema. Up to 5% of OSA patients require immediate reintubation in the operating suite; providers should have emergency reintubation supplies and devices available prior to extubation whether in the suite or in the postanesthesia recovery area. OSA patients should be positioned in semi- to full Fowler’s position before extubation; this is especially important if the patient has undergone reconstructive airway surgery. Fowler’s positioning


Perianesthesia Implications OSA reduces airway swelling and edema that will worsen airway obstruction, and increases lung volume that helps splint the upper airways open. Regional anesthesia with local anesthetics or peripheral nerve blocks should be considered instead of general anesthesia whenever possible. It is well established that neuraxial analgesia with opioids can cause respiratory depression equivalent to either IV or IM opioid administration. All opioids spread cephalically after intrathecal or epidural injection with similar peak levels; however, fentanyl is cleared from the spinal fluid substantially faster than morphine.52,53 This makes patients who receive neuraxial morphine more susceptible to delayed respiratory depression as the drug reaches the central respiratory centers in the brainstem. Epidural analgesia with opioids augments the detrimental physiologic effects of sleep, suppresses the arousal response, and depresses ventilatory responses to hypoxia and hypercarbia. Therefore, central axial opioids pose risks similar to IV, IM, or patient-controlled analgesia administration of opioids and should be avoided in the presence of moderate to severe OSA.54 If patientcontrolled analgesia (IV or epidural) is required, the background infusion should not contain opioids; lowered doses of short-acting opioids are recommended for bolus dosing.31 It should be noted that the first sign of respiratory depression due to opioids is somnolence, a common condition in a postoperative patient. Therefore, the recognition of respiratory depression may be delayed, as a slowed respiratory rate is a later sign of opioidinduced respiratory depression. POSTOPERATIVE MANAGEMENT OF OSA PATIENTS Current recommendations are based on the expert opinions of anesthesia and surgical specialists after extensive literature review of case reports, prospective and retrospective studies, and available randomized controlled trials. Patients with OSA appear to have more frequent episodes of hypoxia in the PACU,

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higher levels of residual neuromuscular blockade, and longer hospital lengths of stay.55 The principal risk for the OSA patient is that once discharged from a higher acuity postanesthesia care unit, the level of nursing surveillance necessarily decreases. There is agreement that OSA patients require an increased degree of monitoring in the postoperative period; however, the literature offers no definitive guidance about what type or how long monitoring is required.32,51 Many reported cases of OSA patients with respiratory or cardiac arrest have occurred in unmonitored units.56 Therefore, current recommendations state that OSA patients need observation by an educated staff and continuous pulse oximetry with audible alarm systems, either in a step-down unit or via telemetry. Intermittent vital signs checks are insufficient to detect periods of hypoventilation and apnea that lead to respiratory and/or cardiac arrest. While the drug oxygen is recommended to maintain normal arterial oxygen saturation, the use of oxygen alone is not sufficient therapy for OSA patients. Supplemental oxygen masks hypoventilation and, by increasing arterial oxygen levels, delays the recognition of obstruction and/or apnea by pulse oximetry. Patients who use home CPAP or bilevel positive airway pressure devices should bring them for use whenever napping or asleep, including in the immediate postoperative period. However, the use of these devices is not meant to preclude adequate monitoring as previously described. The postoperative period is generally not an appropriate time to introduce CPAP therapy, unless it is medically warranted to treat impending respiratory failure and prevent intubation on a short-term basis. It was recently reported that both OSA and non-OSA patients have altered sleep architecture after surgery, with the AHI increasing in both groups after an anesthetic.57 The OSA patients’ AHI increased from 19 to 28 on postoperative day 3. This suggests an increased risk in the OSA patient on postoperative day 3—a recognized time when REM sleep rebounds after surgery.58


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Clearly, some patients may require overnight monitoring rather than day case management; this is more likely the case in OSA patients who have a high AHI or high levels of desaturation either pre- or postoperatively. There is consensus that adults with OSA who undergo airway reconstructive surgery and children younger than 3 years undergoing tonsillectomy should stay overnight with adequate monitoring. Minor or superficial surgery performed under local or regional anesthesia would be conducive to same day discharge in OSA patients as long as the patient does not become hypoxemic or obstructed during the PACU period. It is important to either personally observe or interview nursing personnel who have observed the postoperative patient while asleep prior to discharge. In selected patients, arranging for an overnight stay is a more cautious and a safer approach to perioperative management. Along with respiratory complications, OSA patients are more likely to exhibit sustained dysrhythmias, conduction abnormalities, and hypertension than non-OSA patients. Telemetry monitoring should be considered for patients with a cardiac history because of the high risk of dysrhythmias in this group. Because cardiac dysrhythmias during OSA are directly related to low oxygen saturation, patients who continue to require oxygen in the PACU should be evaluated for transfer to a telemetry unit rather than a ward. Notably, there are case reports of symptomatic respiratory depression well after the typical 12-hour hazard limit in OSA patients who received neuraxial opioids. A very thoughtful risk-benefit analysis should be performed before neuraxial or PCA opioids are administered to OSA patients. Continuous background infusions that contain opioids should be avoided or used with extreme caution. If neuraxial or PCA opioids are deemed necessary, the patient should be in a high acuity, monitored unit with airway support immediately available. Concurrent use of sedatives should be avoided. If OSA patients are placed on a ward, monitoring with continuous pulse oximetry and

functional alarms is recommended along with placement close to the nursing station with provisions for immediate ventilatory support. If this level of care is not available, these patients should be nursed in a monitored care unit. SUMMARY Careful and conservative preoperative management of high-risk patients includes a focused history and physical examination to determine the presence or extent of OSA, very careful airway assessment and difficult airway planning, and either avoidance of or minimal preoperative sedation unless the patient is monitored by remote telemetry or directly by an educated nursing staff. Intraoperative management should focus on the use of shortacting and non-lipid soluble drugs, minimal use of neuromuscular blocking agents with mandatory peripheral nerve monitoring, full neuromuscular reversal to a TOF ratio of more than 0.9 prior to extubation, and avoidance of opioids by any route when possible. The postoperative period is most fraught with danger for the OSA patient; respiratory depression, apnea, and respiratory or cardiac arrest are possibilities in the immediate and later postoperative period. Postoperative care is multidisciplinary and should involve an educated PACU, step-down unit, or ward nursing staff. Patients should be recovered in the Fowler’s or lateral position, avoiding supine positioning unless the airway remains secured and mechanical ventilation is in use. Emergency ventilation equipment and supplies, and the personnel trained to use them, should be immediately available. The administration of opioid-based analgesics should be avoided, and when administered via any route, strict attention should be paid to appropriate patient monitoring. Postanesthesia OSA patients should be monitored with continuous pulse oximetry with alarms set and audible, preferably within the line of sight of the nursing station. Patients with severe OSA and those undergoing upper airway surgery should stay overnight in


Perianesthesia Implications OSA an adequately monitored unit. Pediatric OSA patients younger than 3 years who undergo tonsillectomy should be monitored overnight prior to discharge. Any OSA patient who is

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unable to maintain adequate oxygenation on room air during the recovery period should be thoughtfully evaluated for remaining in a monitored care unit until stable.

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Obstructive Sleep Apnea: Women's Perspective.

[Obstructive sleep apnea in women].

Asthma and Obstructive Sleep Apnea.

Obstructive sleep apnea in adults.

Treatments for Obstructive Sleep Apnea.

Obstructive sleep apnea: therapeutic alternatives.

Secondary hypertension: obstructive sleep apnea.

Diagnosis and treatment for obstructive sleep apnea: Fundamental and clinical knowledge in obstructive sleep apnea.

Obstructive sleep apnea during rapid eye movement sleep: clinical relevance and therapeutic implications.

Fabrication of an obstructive sleep apnea prosthesis.

Effect of clonidine in obstructive sleep apnea.

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Diagnosis of obstructive sleep apnea in adults.

Obstructive Sleep Apnea: Role of an Otorhinolaryngologist.

Diagnosis of obstructive sleep apnea in adults.

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