Anesthesia & Analgesia:
Ambulatory Anesthesiology: Review Article
A Systemic Review of Obstructive Sleep Apnea and Its Implications for Anesthesiologists
Chung, Sharon A. PhD*; Yuan, Hongbo PhD†; Chung, Frances FRCPC†
Section Editor(s): Glass, Peter S. A.
Continued Medical Education
From the *Department of Psychiatry and the Sleep Research Unit, and †Department of Anesthesia, Toronto Western Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Accepted for publication July 22, 2008.
Supported by the University Health Network Foundation and Department of Anesthesia, University Health Network and Mount Sinai Hospital, University of Toronto.
Address correspondence and reprint requests to Dr. Frances Chung, Department of Anesthesia, McL 2-405, Toronto Western Hospital, 399 Bathurst St., Toronto, Ontario, Canada M5T 2S8. Address e-mail to email@example.com.
BACKGROUND: Obstructive sleep apnea (OSA) is present in a significant proportion of the population, but the majority of patients remain undiagnosed. It is crucial that anesthesiologists and surgeons recognize the increased perioperative risks associated with undiagnosed OSA. We present a systematic review of the literature on the perioperative management of surgical patients with OSA.
METHODS: The scope of this review is restricted to publications in all surgical specialties and in the adult patient population. The main search key words were: “perioperative care,” “sleep apnea,” “obstructive sleep apnea,” “perioperative risk,” and “perioperative care.” The databases Medline, Embase, Biological Abstract, Science Citation Index, and Healthstar were searched for relevant English language articles from 1966 to March 2007.
RESULTS: The literature supports an increased perioperative risk in OSA patients. The American Society of Anesthesiologists guidelines support the routine screening for OSA during preoperative assessment, and methods of OSA screening are discussed in this review. This review suggests a number of perioperative management strategies to reduce surgical risk in patients with OSA. However, apart from the consensus-based American Society of Anesthesiologists guidelines, it is important to note that evidence-based recommendations are lacking in the literature.
CONCLUSIONS: This review suggests ways to screen for OSA in the preoperative setting and proposes perioperative management strategies. The ultimate goal is to reduce the perioperative risk of OSA patients but, to realize that goal, research will be needed to determine whether screening for OSA and/or adapting specific perioperative management approaches translates into a lessening of adverse events in surgical patients with undiagnosed OSA.
Obstructive sleep apnea (OSA) is a common sleep disorder caused by repetitive partial or complete obstruction of the upper airway and is characterized by episodes of cessation of breathing during sleep lasting for more than 10 s. Population-based epidemiologic studies have shown a frequent prevalence of undiagnosed OSA, and even mild OSA is associated with significant morbidity1 and mortality.2 The American Society of Anesthesiologists (ASA) recently issued practice guidelines for the perioperative management of OSA patients.3 The purpose of the guidelines was to reduce the risk of adverse outcomes in patients with OSA and to improve perioperative care. The development of the guidelines was built on the scientific evidence derived from the research literature and opinion-based evidence obtained from the ASA task force and consultants. The guidelines indicate that the literature lacked sufficient evidence-based findings to enable clinicians to formulate strategies for preoperative evaluation and postoperative management of OSA. Relevant recommendations were primarily based on the consensus of consultants’ opinions. Identification of shortfalls in the research literature is warranted to promote future research. The purpose of this review is to examine the current evidence on the perioperative risk of sleep apnea, its implication for perioperative management, and to identify the gaps in knowledge regarding this important issue in anesthesia care. The objectives of this review are to discuss the following issues: 1) Does evidence from pathophysiologic studies, pharmacodynamic models, and methodologically sound cohort studies point towards OSA, posing a special challenge to anesthesiologists? 2) Are surgical patients with OSA especially vulnerable with sedation, anesthesia and analgesia? 3) Can episodic sleep-related oxygen desaturations, incidences of unexplained cardiorespiratory events or sudden, unexpected death in a number of perioperative patients be attributed to undiagnosed OSA? 4) Is it possible to screen for OSA preoperatively? 5) What considerations (e.g., identification of contributors to increased perioperative risk, choice of sedatives, anesthetics and analgesics) are needed to develop a perioperative management plan for OSA patients?
The scope of this review is restricted to studies in all surgical specialties and in the adult patient population with an emphasis on outcome in patients who were previously or subsequently diagnosed with sleep apnea. The following key words were used for literature search: “perioperative care,” “sleep apnea,” “obstructive sleep apnea,” and “perioperative risk.” The medical subject heading index terms on Medline were “Perioperative Care,” “Sleep apnea,” and “Perioperative Care and Obstructive Sleep apnea.” We also used “perioperative risk” and “sleep apnea” as index terms to capture data relating to themes of “sleep apnea,” “risk,” and “perioperative care.” Other search areas included “sleep apnea” combined with “etiology” or “prevalence,” “screening instruments,” “sedation,” “anesthesia,” and “analgesia.” The databases Medline, Embase, Biological Abstract, Science Citation Index and Healthstar, as listed below, were thoroughly searched for relevant articles. Studies focusing on central sleep apnea were excluded by including “NOT central sleep apnea” in the search string.
1. Ovid MEDLINE(R) 1966 to March 2007
2. Ovid CINAHL—Cumulative Index to Nursing & Allied Health Literature (1982–March 2007)
3. EMBASE (1980–2007)
4. Cochrane Database of Systematic Reviews (1st Quarter 2007)
5. ACP Journal Club (1991–March 2007)
6. Database of Abstracts of Reviews of Effects (1st Quarter 2007)
The databases of the Cochrane Library were used to verify the completeness of the search. The time period searched was from 1966 to 2007. Classification of relevant articles was judged according to whether they contributed primary empirical evidence to the review topics. Critical appraisal of each paper was conducted by the authors. All the papers were classified according to the Oxford Centre for Evidence-based Medicine Levels of Evidence.4 The appraisal process focused on the strength of the study design. The classification was as follows: Level I: blinded, randomized controlled trial with narrow confidence intervals; Level II: nonblinded randomized controlled trial; Level III: nonrandomized controlled or cohort, case-control studies; and Level IV: nonrandomized case-series report.
The search strategy resulted in 8897 articles. Whenever possible, Level I and II papers were preferentially used, however, Level III and IV papers were used whenever Level I and II papers were unavailable. Information from reviews and abstracts was also included in cases where reports of a higher evidence level were unavailable. Limiting those articles to English Language and Adult population (19+ yr) reduced the number to 3974. Further limitation of search results to evidence level I and II articles (clinical trials, meta-analyses, practice guidelines and randomized controlled trials) netted 411 available articles. Nine of these articles were excluded as they were not available at the University of Toronto, the University Health Network or through the Consortium of Toronto Area Hospitals. Of those remaining, 198 studies were selected based on content and suitability for this review. Despite the lack of adequate blinding, a control group or randomization, 18 articles of evidence level III and IV had to be included in this review due to a lack of studies at a higher evidence level.
What Is the Prevalence of OSA?
For OSA to represent a problem in the perioperative setting, there would have to be a substantial number of surgical patients with OSA. The prevalence of OSA varies widely depending on the demographics of the population studied, the definitions of the disorder and the methods of diagnosis. The accepted minimal clinical diagnostic criteria for OSA is an apnea hypopnea index (AHI) of 10 plus symptoms of excessive daytime sleepiness.5 AHI is the number of episodes of apnea or hypopnea per hour during sleep.
Many epidemiological studies6–9 estimated the OSA prevalence using polysomnography (PSG) as the “gold standard” for diagnosis (Table 1). In primary care practice, about 38% of men and 28% of women are at high risk of having sleep apnea.10 Other patient populations at greater risk for or having a higher prevalence of OSA include patients who smoke (OR 6.7 for heavy smokers)11 and those with medical conditions such as diabetes (prevalence of 36%),12 treatment-resistant hypertension (63%),13 overweight men and older women with congestive heart failure (men: OR for a Body Mass Index [BMI] >35 kg/m2, 6.10; 95% CI 2.86–13.00; women: OR for age >60 yr, 6.04; 95% CI 1.75–20.0),14 during the acute phase of first-ever stroke (prevalence of 71%),15 primary open angle glaucoma (prevalence of 20%),16 hypothyroidism (prevalence of 45%),17 alcoholism (prevalence of 17% in subjects aged 40–59 yr)18 and head and neck cancer (prevalence of 76%).19 These medical disorders are of particular importance to tertiary care centers that typically provide care for a sicker patient population.
In the general population, moderately severe OSA (AHI >15) is present in 11.4% and 4.7% of men and women, respectively.7,8,20 Apart from a significant male gender predominance, an elevated AHI is significantly associated with age (Odds Ratio, per 10-yr increase, 1.79 (95% CI: 1.41–2.27).21 OSA is also more prevalent in obese individuals.22 In a follow-up to the Wisconsin Sleep Cohort Study,23 the percentage of obese subjects (BMI >40 kg/m−2) with an AHI ≥15 is 42%–55% of men and 16%–24% of women.23 Further, in older adults, logistic regression points to BMI as the strongest, independently significant predictor of having OSA (dependent variable AHI ≥10, BMI factor, logistic regression coefficient 0.0869, P = 0.0067).20
No epidemiologic studies have been conducted to determine the prevalence of OSA in the general surgical population. However, a few studies24–27 have used PSG to determine the frequency of OSA in the surgical population (Table 2). In most instances, the frequency of OSA in these surgical populations is substantially higher than the incidence in the general population (Table 1), and it varies with the surgical population. In particular, about 7 of every 10 patients undergoing bariatric surgery were found to have OSA,24 presumably due to the high level of obesity in this surgical population. Of even greater concern, despite OSA being present in the majority of patients presenting for bariatric surgery,24,28most cases were not diagnosed unless careful screening was implemented before surgery.28 Further studies of OSA prevalence in general surgical patients are needed. One problem with undertaking such a study is that it is difficult to recruit surgical patients to undergo PSG studies. As illustrated in the study by Fidan et al.,27 less than half (18 of 41, 44%) of the patients identified as being at risk for OSA agreed to undergo a sleep study. More importantly, of the patients agreeing to a PSG, the majority (78%) were found to have AHI >5.
Consistent with the above figures, in a nationwide survey of Canadian anesthesiologists, 67% of respondents reported that they provided care for 1 to 5 patients with OSA each month.29 Another study of patients undergoing total joint arthroplasty reported that, by asking patients to complete a few screening questionnaires on OSA, they were able to identify 10 cases of undiagnosed OSA out of 254 patients.30 Recently, we have studied patients undergoing elective surgery and 24% were identified preoperatively at high risk for OSA using the Berlin questionnaire (BQ).31 In North America, OSA affects millions of middle-aged men and women,6 and it has been estimated that, of these, more than 80% of men and 90% of women are not clinically diagnosed and, hence, remain untreated.32 In short, the magnitude of the problem may have profound implications for anesthesiologists in the perioperative care of patients with previously unrecognized OSA.
What Are the Effects of Sedatives, Anesthetics and Analgesics on Respiratory Function?
Impact of Sedatives and Anesthesia on Respiration
The dose-dependent depression of muscle activity of the upper airway by general anesthesia has been well established.33–36 An increasing depth of propofol anesthesia is associated with the increased collapsibility of the upper airway.36 This dose-related inhibition is likely to be the combined result of the depression of central respiratory output to the upper airway dilator muscles and the upper airway reflexes.36 In addition, most anesthetics or opioids used for analgesia can alter the control of breathing by affecting the chemical, metabolic or behavioral control of breathing. For example, halothane depresses ventilation by abolishing peripheral drive from the chemoreceptors at the carotid bodies and by general depression of respiratory centers in the central nervous system. Halothane also depresses ventilation by suppression of the function of intercostal muscles and the diaphragm.34,37–39 Other sedative and anesthetics also affect the upper airway. Thiopental administration has been shown to result in the loss of tonic activity in the sternothyroid and sternohyoid muscles in surgical patients.40 In normal subjects, propofol anesthesia was shown to produce a dose-dependent inhibition of genioglossus muscle activity resulting in greater collapsibility of the upper airway.36 Midzolam is commonly used in combination with other sedative and anesthetic drugs,41–43 so it is difficult to ascertain from the literature if obstructive events, when they occur, are a direct consequence of midozolam, the other sedatives or anesthetic drugs, or the combination of drugs. However, there is evidence from one study suggesting that midozolam, when administered at sedative doses, can increase supraglottic airway resistance leading to obstructive episodes.44
A few papers have documented the benefits of using dexmedetomidine as a sedative and anesthetic in OSA patients because of the lack of respiratory depression associated with dexmedetomidine use.45,46 Further, dexmedotomidine’s analgesic properties allow for reduced administration or avoidance of opioid drugs in the perioperative period.45,46 Of note, one case report has cautioned that dexmedetomidine can enhance respiratory depression when co-administered with opioids.47 Further investigations on the utility of using dexmedetomidine in surgical patients with OSA are needed.
Impact of Opioids on Respiration
Opioids can impair respiratory function. In the animal model, morphine has been shown to have a direct action on the respiratory motor activity of the hypoglossal and phrenic nerve.48 Weil et al. first reported a decreased ventilatory response to hypoxia and hypercapnia after morphine in healthy subjects in 1975.49
Factors such as ethnicity and gender can also influence the ventilatory response to morphine. In contrast to Caucasians, North American Aboriginal Indians have been observed to have an 18% greater reduction in the ventilatory response to morphine administration.50 Morphine has an effect on the apneic threshold in men, but not women; however, morphine decreases the hypoxic sensitivity in females, but not in males.51 Opioids may profoundly impair respiration in the postoperative period leading to obstructive apneas and drastic oxygen desaturation.52,53 There are clinical trials52,53 comparing the respiratory effects of IV morphine versus extradural bupivacaine in patients undergoing hip and abdominal surgery. Compared to those in the regional anesthesia group, patients receiving morphine experienced postoperative obstructive apneas, ventilation disturbances, acute oxygen desaturation and elevated end-tidal CO2.52,53A greater frequency of tachyarrhythmia and ventricular ectopic beats were also noted in the morphine group.53 The obstructive apneas and oxygen desaturation were found to occur only when the patients were asleep, and the vast majority of the hypoxic episodes occurred within 6 to 8 h after surgery.52 Depression of the tonic activity of the upper airway muscles is well documented in sleep.54,55 It was proposed that the deleterious respiratory effect of morphine may be enhanced in sleep because of the diminution in airway function.52 Further studies are necessary to assess the effect of long-term opioid treatment on respiration during sleep, the interaction of opioids with other medications and the risk factors predisposing patients to sleep breathing disorders with opioid use.56
Is There a Greater Impact on Ventilation of Sedation, Anesthesia and Analgesia in OSA Patients?
Impact of Upper Airway Dynamics
Although the etiology of OSA remains uncertain, the general consensus is that upper airway obstruction occurs when the negative pressure generated by the inspiratory muscles exceeds the capacity of the upper airway dilator muscles to maintain airway patency.57 In general, the negative pressure generated by inspiration is counterbalanced by the contraction of the pharyngeal muscles. However, medications or conditions (such as fat deposits in obesity) that reduce lumen diameter or impair the ability of the upper airway muscles to overcome the negative forces of inspiration will result in greater upper airway resistance during breathing, thus predisposing the patient to obstructive events. These factors are of particular importance in OSA patients since, during both wake and sleep, they seem to have a reduced upper airway diameter, especially in the retropalatal region.58–60 To complicate matters, research also suggests that OSA patients may also have a primary myopathy of their genioglossus muscles.61,62 Thus, OSA patients may have a lowered threshold in their ability to overcome factors that predispose them to increased negative pharyngeal pressures during inspiration or that reduce upper airway muscle tone.
There is evidence that a compromised upper airway can be exacerbated by opioids. In a paper describing two case reports of patients with upper airway narrowing due to enlarged tonsils or tumor,63 both patients died after morphine use. In both cases, death was due to the effects of severe upper airway narrowing coupled with the respiratory depressant action of morphine. The authors highlighted the dangers of using morphine in individuals with a compromised upper airway. The evidence suggests that OSA patients are in this category since they have a narrowed airway and perhaps a primary pharyngeal myopathy. In addition, sleep can be a dangerous time for OSA patients. The decline in electromyographic activity in the pharyngeal dilator muscles at sleep onset is much greater in OSA patients than in controls.64 There is enhanced neuromuscular activity during wakefulness in OSA patients that offsets deficiencies in their airway anatomy or functioning. However, in sleep, this neuromuscular compensation is lacking. This finding indicates that upper airway patency during sleep is particularly compromised in OSA patients.
OSA patients also seem more vulnerable to respiratory depressants. Alcohol ingestion in patients with mild OSA results in an increased number and duration of hypoxic events and almost triple the number of episodes of oxygen desaturation.65 Furthermore, the hypoxic episodes occur earlier in the sleep period and SaO2 levels may not return to normal after the long apneas that were induced by alcohol consumption. It was proposed that alcohol has a depressant effect on the respiratory centers that control pharyngeal muscle tone, thus increasing the likelihood of pharyngeal collapse during sleep.65 This reduction in pharyngeal tone with alcohol ingestion is coupled with the prolongation of time to arousal after airway occlusion.66 A similar reduction in pharyngeal tone and increased arousal threshold to hypoxia occurs after administration of sedatives, anesthetics and analgesics. Investigation of the actions of sedatives, anesthetics and analgesics points to the pharynx as a primary site of obstruction after anesthesia.67–70 It has been proposed that airway obstruction with sedation and anesthesia follows a similar course as that seen with obstructive apneas during sleep; that is, increased airway collapsibility due to an increase in the critical closing pressure,36 loss of tonic activity in pharyngeal muscle41 and failure of the phasic activation of upper airway muscles before diagphragmatic activity.71 This suggests that respiration in OSA patients may also be more susceptible to drugs used during the perioperative period.
Effects of Opioids
A differential effect of opioid administration in individuals with and without OSA is evident from the literature. Oral hydromorphone administration in healthy adults without a history of OSA does not significantly alter the number of apneic or hypopnea episodes.72 A greater number of apneic episodes at higher doses of hydromorphone (4 mg) predominantly occurred in patients with a larger baseline number of obstructive events.72 Similarly, in the postoperative setting, analgesia with oxycodone in healthy, nonobese ASA class I-II females without a history of OSA did not result in apnea. In this study, SaO2 was decreased during the first postoperative night but levels above 90% were maintained.73
An important study by Brown et al. showed that the total analgesic opiate dose in children with OSA and recurrent hypoxemia was one-half of that required in children without such a history.74 Previous recurrent hypoxemia in OSA children is associated with a greater analgesic sensitivity to morphine administration. There are no studies investigating whether adult OSA patients require less opioids.
There are only case reports of the effects of opioids in adult patients with OSA. A compilation of case reports of patients with OSA receiving sustained-release opioids treatment for chronic pain has demonstrated that these patients have longer apnea duration, more severe hypoxia, irregular respiratory pauses and gasping, and periods of obstructive hypoventilation lasting for 5 min or longer.56 Postoperative epidural morphine in a patient with a history suggestive of OSA was documented to result in apneas, respiratory depression and cyanosis.75
As outlined above, sedatives, anesthetics and analgesics seem to selectively compromise respiratory function in OSA patients. Although there remains a lack of good evidence in the literature of the effect of opioids administration on respiration in OSA patients, the general recommendation is that opioids and other drugs with central respiratory and sedating effects should be avoided, if possible. The compromised airway in OSA patients may exacerbate the respiratory-depressive effects of these drugs.76 However, preoperative screening for OSA is not routinely performed, and use of analgesics is common in the postoperative period. At the very least, use of any sedative and analgesic in OSA patients should be done with extreme caution.
After sedation, anesthesia or analgesia, the resulting hypoventilation or hypoxia may produce central instability in respiratory control resulting in low levels of oxygen saturation. However, there is evidence that airway obstruction is a major contributor to oxygen desaturation in the perioperative period. In surgical patients without a diagnosis of OSA, decreases in SaO2 <80% were observed to be primarily associated with obstructive apnea and paradoxical breathing,52 and no correlation was found between the duration of anesthesia and postoperative SaO2 levels52 after postoperative morphine. In support of that hypothesis, administration of oxygen in surgical patients who did not have a prior OSA diagnosis was found to improve the oxygen saturation, but not to alter the number and severity of obstructive apneic or hypopnic events.77 Moreover, increased numbers and duration of apneic events is observed in healthy volunteers and asymptomatic nonsurgical patients78–80 after sedation with various sedative medications such as midazolam, fentanyl,78,79 and flurazepam.80 A careful study of sedative medications in OSA patients has not been conducted, but the aforementioned suggestion of a compromised upper airway (reduced diameter and myopathy of pharyngeal muscles) would likely more greatly predispose OSA patients to the deleterious effects of sedatives.
The respiratory-depressant effects of sedatives, anesthetics and analgesics have direct clinical relevance for the perioperative management of a patient with OSA, but our knowledge at present is inadequate to propose evidence-based anesthetic procedures that can minimize the impact of the anesthesia or sedation on OSA.
Can OSA Affect Perioperative Outcome and Are Patients with OSA at an Increased Risk for Perioperative Complications?
It is well-established that untreated OSA results in greater morbidity and an increased mortality rate.1,2,81–83 Untreated OSA patients are at a greater risk of developing cardiovascular disease (OR 3.1, 95% CI 1.2–8.3),84 including heart failure,85 arrhythmias (2–4 fold increase),86 hypertension (10-fold increase),87 and stroke (OR 4.33, 95% CI 1.32–14.24, P < 0.02).88 Furthermore, OSA is independently linked (OR 9.1, 95% CI, 2.6–31.2, P < 0.0001) to the development of metabolic syndrome characterized by insulin resistance, impaired glucose tolerance and dyslipidemia.89 The impact of OSA is also seen on Paco2 levels and the coagulation systems.90–92 In a large observational cohort study,93 untreated OSA significantly and independently increased the risk (HR 1.97, CI 95%, 1.12–3.48, P = 0.01) of stroke or death from any cause.
In determining whether OSA patients are at greater risk perioperatively, one needs to determine if the presence of OSA directly or indirectly translates to greater incidences of adverse events in the perioperative setting. That is, are untreated OSA patients at a greater risk of having respiratory adverse events in the perioperative period? Further, the underlying morbidity associated with longstanding untreated OSA, particularly those of a cardiovascular nature, may predispose OSA patients to severe perioperative adverse events or may reduce the patients’ ability to cope should adverse events occur. However, it is possible that even patients with treated OSA are at a greater perioperative risk compared to normal patients due to the etiology of the disease including upper airway pathology or upper body obesity.
The presence of sleep apnea in the postoperative period as indicated by frequent episodes of oxygen desaturation has been reported. Ten of 16 surgical non-OSA patients receiving morphine infusion had a total of 456 episodes of pronounced oxygen desaturation (SaO2 <80%) when they were monitored for 16 h after surgery.50 These occurred only while the patients were asleep and were associated with disturbances in ventilatory pattern such as obstructive apnea (144 episodes), paradoxic breathing and periods of slow ventilatory rate.52,75,94 In patients with OSA-associated severe postoperative respiratory events, the need for postoperative reintubation has been documented.95 However, since OSA is a risk factor for increased difficulty with tracheal intubation,96 problems with postoperative reintubation could seriously impact patient morbidity.
It seems that the preoperative values of the apnea index and minimal level of oxygen saturation can be used to help predict the postoperative occurrence of obstructive apneas and adverse respiratory events.97 In OSA patients undergoing uvulopalatopharyngoplasty (UPPP), predisposing factors for respiratory complications included a higher preoperative AHI (AHI 69 vs 43, P < 0.008) and lower minimal levels of oxygen saturation (minimal O2 Sat 71.9% vs 77.8%, P < 0.01).98 Esclamado et al. retrospectively reviewed 135 patients with OSA after UPPP and associated procedures. They compared 18 patients with complications with 117 patients without complications. Preoperative AHI more than 70 or minimal oxygen saturation <80 was considered a risk factor for the development of complications.99 Pang et al.100 in a retrospective review of 118 OSA patients for upper airway surgery, concluded that patients with severe OSA AHI >60 and minimal oxygen saturation <80% were at high risk of postoperative oxygen desaturation (Table 3). Two studies, however, found no significant difference between those with and without complications regarding the severity of AHI in patients undergoing tonsillectomy or UPPP (Table 3).
For 24,157 surgical patients given general anesthesia, but not specifically diagnosed with OSA, the risk of a critical respiratory event in the postanesthesia care unit (PACU) was 1.3% (hypoxemia 0.9%, hypoventilation 0.2%, airway obstruction 0.2%).103 Significant risk factors for adverse respiratory events postoperatively were older age, male gender, diabetes, and obesity. The choice of anesthetic drug was also an important contributing factor. Use of opioids, fentanyl, atracurium or thiopental, either alone or in combination, were associated with greater anesthetic risk with odds ratios ranging from 1.6 to 2.5.103 However, the risk factor of an OSA diagnosis was not studied in this population.103
Apart from respiratory complications, sustained arrhythmias and hypertension104 are commonly reported in association with OSA and may have implications for postoperative outcome in OSA patients. Arrhythmias and conduction abnormalities resulting from sleep apnea-associated hypoxemia105 have been reported in OSA patients undergoing gastric bypass surgery.106 The hemodynamic instability associated with arrhythmias can significantly affect postoperative morbidity. Morphine infusion in asymptomatic surgical patients has been shown to increase the incidence of conduction abnormalities.53 Furthermore, a preoperative diagnosis of OSA has been shown to be an independent predictor of atrial fibrillation after coronary bypass surgery.107
There are numerous case reports (Table 3) indicating that adverse perioperative outcomes have been reported in OSA patients, including respiratory and cardiac arrest leading to death.75,108–113 These patients all received opioids. There was no preoperative screening for OSA, although, in most cases, the patient had a history suggestive of OSA or there was an established diagnosis of OSA before surgery. Unfortunately, the postoperative management plan did not include frequent monitoring of vital signs and oximetry. In these case reports, the use of perioperative opioids in these OSA patients might have contributed to the compromised respiration, however, this has not been clearly established. A retrospective review of OSA patients undergoing cardiac surgery also noted more postoperative adverse events and a longer intensive care unit (ICU) stay.114 Two reviews on anesthesia in OSA patients emphasize that these patients are at greater risk of perioperative adverse events.115,116 A major limitation of the aforementioned studies that provide information on the relationship between OSA and postoperative outcome (Table 3) is that, in general, they have a poor level of evidence.
Not all studies have endorsed a greater perioperative risk in OSA patients. A retrospective study of 234 OSA patients versus control group117 concluded that a preoperative diagnosis of OSA was not a risk factor for unanticipated admissions (23.9% vs 18.8%, odds ratio 1.4 95% CI 0.8–2.5). However, this study had a number of serious limitations that bring their findings into question. The study patients were scheduled for outpatient surgery implying that these OSA patients may have had less preexisting morbidity. Other limitations included a lack of information on the screening process and whether the anesthesia and surgical team altered their perioperative management based on the OSA diagnosis. A further confound was that the majority of OSA patients were using continuous positive airway pressure (CPAP) treatment. In addition, the incidence of unanticipated admission was an exceptionally high 19%–24% in both OSA and control groups, whereas the rate of unanticipated admission in ambulatory surgical surgery is normally around 1%–2%.118
In contrast to the above findings, a retrospective matched case-controlled study of OSA patients undergoing hip or knee replacement surgery95 reported longer hospital stays (OSA vs control 6.8 days vs 5.1 days, P < 0.007) and 2.5 times the number of serious postoperative complications (OSA vs control 24% vs 9%, P < 0.04). These serious complications included the need for urgent respiratory support and more ICU transfer. Despite the different findings, this study95 suffers from many of the same limitations as the above study117 given the retrospective nature and the inability to exclude a diagnosis of OSA in their control groups.
There are also a number of reports of OSA patients undergoing upper airway surgery, including UPPP, for surgical management of their sleep apnea.98,100–102,119–122 Postoperatively, there are reports of increased obstructions and desaturations98,119,121 and changes in systolic and diastolic blood pressure.119 It was further documented that postoperative complications were more frequent in OSA patients that had an increased AHI and higher levels of desaturation preoperatively (Table 3).98,102,121
Most studies are case reports, retrospective reviews or noncontrolled observational studies. This may contribute to the varied findings, i.e., why some studies, but not others, report more perioperative adverse events. Thus, although multiple case reports support increased perioperative risk of patients with OSA, there remains insufficient level 1 or 2 evidence to clarify if treated or untreated OSA patients are at increased risk during the perioperative period for either respiratory or cardiovascular adverse events. As level 1 studies may be difficult to perform, we may have to accept that these case reports or retrospective studies are sufficient evidence that OSA patients are at greater risk for perioperative adverse outcomes and greater emphasis should be placed on diagnosing patients with OSA and determining best practices during the perioperative period to reduce the risk for adverse outcomes.
Perioperative OSA-Associated Complications
Relationship Between Acute Hypoxemia and Cardiovascular Events
Apart from respiratory complications, sustained arrhythmias, and hypertension104 are commonly reported in association with OSA and may have implications for postoperative outcome in OSA patients. Arrhythmias and conduction abnormalities resulting from sleep apnea-associated hypoxemia105 have been reported in OSA patients undergoing gastric bypass surgery.106 The hemodynamic instability associated with arrhythmias can significantly impact postoperative morbidity. Morphine infusion in asymptomatic surgical patients has been shown to increase the incidence of conduction abnormalities.53 Further, a preoperative diagnosis of OSA has been shown to be an independent predictor of atrial fibrillation after coronary bypass surgery.107
Apneas and hypopneas have been shown to produce acute changes in systolic and diastolic blood pressure123 in patients not undergoing surgery. In a population of middle-aged adults with subclinical sleep-disordered breathing, large fluctuations in systolic blood pressure (23 ± 10 mm Hg) and diastolic pressure (13 ± 6 mm Hg) were observed during and after apneic events. Transient changes in heart rate mirror the acute arterial blood pressure responses to apneas; bradycardia develops during the obstructive event and is followed by abrupt tachycardia and decreases in left ventricular stroke volume immediately after apnea termination.124,125
As a consequence of the OSA-related increases in systolic blood pressure, high levels of myocardial blood flow are required to maintain the oxygen balance in heart muscles.126 In an animal model of limited coronary flow reserve, oxygen desaturation can result in myocardial ischemia, thus subsequently impairing left ventricular function.127 Preoperative hypoxemia, especially in OSA patients has been found to be a predictor of severe postoperative hypoxemia98,119,121 while decreases in arterial oxygen saturation (Spo2) have been found to be significantly higher on postoperative nights than preoperatively128,129 (Table 3). Thus patients with moderate to severe OSA may be at increased risk for myocardial infarction or congestive cardiac failure in the postoperative period.
There are numerous reports that support the link between OSA and cardiac arrhythmias and conduction disturbances.130–135 In a retrospective analysis of 400 nonsurgical OSA patients, sinus bradycardia was seen in 7%, second degree atrioventricular conduction block in 8%, and sinus arrest in 11% of these patients.104,133 Another study130 confirms 7% frequency of heart block (sinus arrest, II and III atrioventricular block) in nonsurgical OSA patients. Earlier studies suggested that heart block occurred exclusively with arterial oxygen desaturation below 72%,104 however, heart block with oxygen desaturation exceeding 4% has been noted.133 In 121 coronary artery bypass surgery patients, atrial fibrillation was more common in OSA patients and preoperative OSA with nocturnal hypoxemia was an independent predictor of postoperative atrial fibrillation.107
Pulmonary hemodynamics are also acutely altered during apneas resulting in oscillations in pulmonary artery pressure with each apnea.136 Prolonged severe hypoxemia results in greater changes in intrathoracic pressure and larger swings in pulmonary artery pressure. Greater inspiratory effort during the apnea in OSA patients promotes an increase in pulmonary capillary wedge pressure resulting in decreased right ventricular stroke volume. This reduction in ventricular stroke volume, in turn, leads to a diminished cardiac output at apnea resolution which occurs regardless of the postapneic tachycardia. In the animal model, pulmonary edema and deterioration of gas exchange has been shown to occur after 8 h of recurrent obstructive apneas.137 Incidences of fatal pulmonary edema have been reported in the postoperative setting138,139 and particularly in patients with OSA.140 With the increased risk of prolonged hypoxia in OSA patients, there is the distinct possibility of pulmonary edema occurring in the perioperative period.
Increased Risk of Difficulty with Tracheal Intubation
Difficult tracheal intubation is a significant concern for anesthesiologists. Difficult tracheal intubation and OSA seem to share similar etiological pathways of predisposing upper airway abnormalities. A retrospective case-controlled study of 253 patients was conducted to determine the occurrence of difficult intubation in OSA patients.96 The OSA patients were matched with controls of the same age, gender, and type of surgery. Difficult intubation was assessed by laryngoscopy using the Cormack and Lehane classification.141 Difficult intubation was found to occur 8 times as often in OSA patients versus controls (21.9% vs 2.6%, P < 0.05).96 In OSA patients undergoing ear, nose, and throat surgery, a 44% prevalence of difficult intubation had similarly been reported.142 Furthermore, patients with severe OSA (AHI ≥40) were found to have a much higher prevalence of difficult intubation.143 A study of more than 1500 nonobese and obese patients concluded that increased age, male gender, pharyngo-oral pathology, and the presence of OSA are all associated with a more frequent occurrence of difficult intubation.144 The corollary of the relationship is also true, that is, patients with difficult tracheal intubation have also been shown to be at greater risk of having OSA.145 In a small retrospective study of 15 patients with difficult intubation, 53% (8 of 15) of patients were diagnosed with OSA.145 In a prospective study, 66% of patients with difficult intubation were subsequently found to have AHI >5.146 These reports suggest that anesthesiologists should refer patients with difficult intubation for PSG sleep investigation of OSA.
Apart from the above-mentioned studies, there is no research investigating the causal and anatomical relationship between OSA and difficult tracheal intubation and the implications for perioperative management. It can be assumed, but has yet to be proven, that a combination of the two conditions would increase the perioperative risk of patients. Despite the higher prevalence of OSA in patients with difficult intubation, it needs to be determined whether it is cost effective for all patients with difficult intubation to undergo a diagnostic sleep study and if preoperative CPAP treatment could ameliorate the difficulty with tracheal intubation.
What Is the Evidence Suggesting That Perioperative CPAP Treatment May Decrease the Risk of Perioperative Complications in OSA Patients?
Nasal application of CPAP is the most widely used treatment for OSA because of its efficacy and low level of invasiveness.147 CPAP acts as a pneumatic splint to prevent occlusion of the airway during sleep, thereby significantly reducing apneas and hypopneas and the associated hypoxic and hypercapnic events. CPAP has been shown unequivocally to alleviate the symptoms of OSA including: amelioration of excessive daytime sleepiness,148 restoration of quality of life,149 improvement in vigilance,150 concentration and memory,151 lessening of fatigue,152 reduction in health care usage,1 and a decrease in traffic accidents.148
The efficacy of CPAP has not been established in the perioperative setting. There is insufficient evidence from the literature to evaluate whether the perioperative use of CPAP may reduce adverse events in OSA patients undergoing surgery. It is not known whether CPAP can reduce the risk of perioperative cardiorespiratory events in OSA patients when the upper airway is further compromised by sedation, anesthesia or analgesia. There are no randomized controlled studies that specifically address this issue. The following is a summary of the possible potential beneficial effects of CPAP in OSA patients undergoing surgery.
Acute Effect of CPAP on Hemodynamics
In general, acute elevation in arterial blood pressure is a common adverse event in the perioperative setting that accounts for more than 10% of the complications in the PACU.153 There are a number of reports of serious postoperative hypertensive events in OSA patients.100,112,119 The efficacy of long-term CPAP treatment in reducing arterial blood pressure in OSA patients not undergoing surgery has been demonstrated.154–157 Acute CPAP use for 1–3 days in nonsurgical OSA patients with hypertension can lead to a reduction of arterial blood pressure (systolic blood pressure from 125 ± 15 mm Hg to 120 ± 10 mm Hg, diastolic pressure from 86 ± 16 mm Hg to 83 ± 12 mm Hg).158,159 However, the literature is not without controversy as others160 have reported that acute CPAP does not alter blood pressure. Apart from one case report112 documenting the beneficial effects of CPAP in treating hypertension in the postoperative period, there is no available evidence from randomized controlled studies. Evidence that acute CPAP treatment can reduce blood pressure perioperatively is required before the use of CPAP in the perioperative setting can be considered.
With regards to cardiac rhythm abnormalities, CPAP treatment reduces the number of apnea-associated cardiac arrhythmias133,161,162 and the beneficial effects of CPAP on sinus arrest and episodes of heart block during sleep have been reported.163 In a study of 17 patients, CPAP treatment reduced the number of arrhythmias from 1575 to 165 episodes per night (P < 0.01).163 These studies provide preliminary support for the use of CPAP for perioperative cardiac rhythm abnormalities among OSA surgical patients.
Cardiovascular adverse events with OSA patients in the perioperative setting are a growing concern. CPAP has been shown to improve cardiac function with long-term use164–166 but evidence of a beneficial cardiovascular effect with short-term CPAP use is required. A single night of CPAP was documented to reduce the variability in systolic and diastolic blood pressure and pulse interval during sleep.167 Also, a 10-min application of CPAP in patients with congestive heart failure was found to improve oxygen saturation, significantly decrease left ventricular stroke volume, reduce myocardial oxygen consumption, and reduce cardiac output.168 A favorable hemodynamic effect within a few minutes of application suggests a potential role for postoperative CPAP.
Research Studies Using Postoperative CPAP: What Is the Strength of Evidence?
The level of evidence is poor regarding the benefits of postoperative CPAP. There are only three studies on the benefits of postoperative CPAP in OSA patients: a small prospective study,169 one case report109 and one retrospective study.95 The findings of these studies suggest that CPAP can alleviate postoperative airway obstruction, decrease major postoperative complications, and reduce the length of hospital stay in OSA patients undergoing surgery. However, all three studies have low evidence levels and suffer from methodological problems, including small sample sizes and the lack of an appropriate prospective, randomized, controlled design, thus, limiting the ability to generalize the results of these studies.
A randomized, controlled and nonblinded study was conducted in abdominal surgery patients without a diagnosis of OSA. Either routine oxygen or a trial of CPAP plus oxygen was administered to these non-OSA patients who developed severe postoperative hypoxemia.170 Patients using CPAP were found to have decreased need of reintubation to treat respiratory failure and less postoperative complications. Conversely, two studies, one in nonsurgical non-OSA patients admitted to intensive care171 and another in abdominal surgery patients without a history of OSA,172 found no benefit of postoperative CPAP use.
Well-designed research studies on the postoperative effect of CPAP in OSA surgical patients are lacking. Such studies would need to be geared towards evidence-based medicine and would have to address the following questions: how long should CPAP be applied, preoperatively and/or postoperatively, for optimum efficacy, what type of surgery would benefit most from CPAP treatment, should OSA severity influence the decision to use CPAP postoperatively, would use of preoperative prophylactic CPAP confer a reduced postoperative risk, and would CPAP allow for safer administration of analgesics?
Perioperative Risk Management–a Significant Challenge in OSA Patients
The evidence of the potential deleterious effect of sedatives, anesthesia and analgesics in OSA patients and the increased risk of perioperative adverse events implies that clinical management strategies need to be specifically tailored. It is important for anesthesiologists to meet the challenge of maintaining upper airway patency and preventing perioperative complications in these patients. The recently developed ASA guidelines3 emphasize the importance of evaluation, detection and preparation in the preoperative workup and the necessity of using forethought and vigilance when developing perioperative management for OSA patients undergoing surgery. The following questions arise: is it feasible for anesthesiologists to identify patients with undiagnosed OSA in the preoperative clinic, can we identify factors that may increase the perioperative risk in OSA patients, is it possible to modify anesthetic techniques to reduce perioperative risk in OSA patients, are there safer alternatives to opioid analgesics for postoperative pain control, and finally, what are the optimal postoperative management strategies for OSA patients?
Is It Feasible to Identify OSA in the Preoperative Clinic?
The current “gold standard” in the clinical diagnosis of OSA is an overnight sleep laboratory study with PSG.173 PSG is a highly reliable diagnostic tool but screening of every surgical patient is not feasible due to the time-commitment, expense and burden on the health care system. Moreover, PSG is not practical for rapid screening in a fast-paced preoperative clinic. A number of questionnaire-based screenings are available in the literature.174–177 In general, the problem is that these questionnaires ask a variety of questions about sleep that are not specifically geared towards identifying which patients have OSA. To complicate matters, 2 of the questionnaires contain 100 or more items, thereby reducing their practicality.
The BQ is a self-report instrument specifically designed to identify undiagnosed OSA. It has been shown to perform well in a large population of 744 primary care patients with a sensitivity of 0.89 and specificity of 0.71.10,178 The BQ has also been validated in atrial fibrillation patients and shown to perform with a similar sensitivity (0.86) and specificity (0.89). The 10-item BQ is comprised of 5 questions on snoring, 3 on excessive daytime sleepiness, 1 on sleepiness while driving, and 1 inquiring about a history of hypertension. Details of age, gender, weight, height, and neck circumference are also recorded. The BQ stratifies patients into high or low risk of having OSA based on their endorsement of symptom severity.
The BQ has been shown to be a valuable tool for OSA screening in primary care and atrial fibrillation patients, but its usefulness in determining which surgical patients are at greater risk of having OSA has yet to be established. Recently, we screened 318 patients using BQ at our hospital and 24% (n = 76, 95% CI 19%–29%) were found to be at high risk of having OSA.31
The number of questions and the complicated scoring procedure of BQ may be too cumbersome for anesthesiologists and their patients. To facilitate the widespread usage of an OSA screening tool, we developed a shorter 4-item OSA screening questionnaire (STOP). The STOP questionnaire contains four questions: S: “Do you snore loudly, loud enough to be heard through closed door,” T: “Do you feel tired or fatigued during the daytime almost every day,” O: “Has anyone observed that you stop breathing during sleep,” and P: “Do you have a history of high blood pressure with or without treatment”? Patients answering “yes” to two or more questions were assigned as being at high risk of having OSA. The sensitivity of the STOP questionnaire at AHI >5, >15, and >30 cutoff levels was 65.6%, 74.3%, and 79.3%, respectively.179 When incorporating BMI more than 35 kg/m−2 (B), age over 50 yr (A), neck circumference larger than 40 cm (N) and male gender (G) into the STOP questionnaire, STOP-BANG, the sensitivity was increased to 83.6%, 92.9%, and 100% for the same AHI cutoffs above.179
The ASA taskforce on OSA3 also developed a 16-item checklist to assist anesthesiologists in identifying OSA. The checklist is comprised of three categories of predisposing physical characteristics, symptoms and complaints attributable to OSA. Patients endorsing symptoms or signs in two or more of the categories are to be considered at high risk of having OSA. The major drawback to this screening tool is time commitment because the checklist needs to be completed by the clinician.
With the development of the BQ, STOP, and ASA checklist, a necessary step before their use as an OSA screening tool in the preoperative clinic is the determination of their validity. We have conducted a study to compare the validity of the BQ, STOP, and ASA checklist in 177 surgical patients who were concurrently studied with PSG.180 The sensitivity of the BQ, the ASA checklist, and the STOP questionnaire was 68.9%, 72.1%, and 65.6% at AHI > 5; 78.6%, 78.6%, and 74.3% at AHI >15; 87.2%, 87.2%, and 79.5% at AHI >30, respectively. There is no significant difference in the predictive parameters of the three screening tools.180 The STOP questionnaire is a concise and easy to use screening tool for OSA. It has been validated in surgical patients at the preoperative clinic and is equivalent to the BQ and ASA checklist. Incorporating BMI, age, neck size, and gender with the STOP questionnaire, STOP-BANG, will give a higher sensitivity and negative predictive value for patients with moderate to severe OSA.180 A recent study found that the percentage of patients with oxygen desaturation index (the number of times per hour the oxygen saturation decreases by ≥4% from baseline) >10 was significantly higher in patients identified as being at high risk of having OSA and having recurrent PACU respiratory events.181 The anesthesiologist may be the first health professional to inquire about sleep, and therefore, will have an important role in identifying these patients and preventing both short and long-term complications. Use of a practical screening tool in the preoperative clinic is highly recommended.
Possible Factors Contributing to Increased Perioperative Risk in OSA Patients
Certainly, not all OSA patients undergoing surgery have serious adverse perioperative events and of those who do, the time course of the serious adverse events varies greatly (Table 3). A review of the findings points to possible multiple factors in surgical patients with OSA that could lead to perioperative adverse events. Further research in this area is needed, not only to identify these factors, but to elucidate their level of involvement by determining the varying odds ratios. The impact of anesthetics and analgesics in OSA patients is a definite consideration in determining risk. These will be discussed below.
Other factors related directly to the etiology of OSA or the associated morbidity also merit consideration. Studies of patients undergoing surgical treatment for their OSA98–100,119,121 or major surgery, excluding upper airway procedures, have documented that patients with a preoperative history of more severe OSA tend to have more perioperative complications (Table 3). These findings would imply that preoperative screening and identification of those patients with more severe OSA would allow for better preparation for perioperative complications. However, these studies are either retrospective or observational and are of too low evidence level (Level IV) to enable firm conclusions Moreover, two other studies102,117 at the same evidence level found that higher AHI and lower SaO2 levels preoperatively were not correlated with postoperative complications (Table 3). Therefore, more research is needed to correlate AHI and preoperative oxygen level with perioperative complications.
Further information on this matter can be gleaned from studies of obese surgical patients with a high prevalence of OSA. While obesity is associated with a greater risk of perioperative complications,182,183 multivariate analyses do not implicate a history of OSA as a risk factor for increased surgical complications in patients undergoing gastric bypass surgery.184 Rather, it seems that preexisting pulmonary disorders are more predictive of the need for postoperative ICU monitoring and longer hospital stay.185 This suggests that it is not the obesity per se, but the associated morbidity that increases perioperative risk. That OSA may not feature prominently as a cause of postoperative complications may also be explained by the fact that bariatric surgery candidates undergo extensive preoperative medical examination before being allowed to undergo surgery.186 Overnight PSG screening for OSA is also commonly included in the preoperative work-up so that OSA can be identified and treated before surgery. It remains to be determined whether preoperative treatment of OSA could significantly reduce the perioperative risk in these patients.
An alternative hypothesis is that long-standing untreated OSA is associated with greater morbidity and preoperative morbidity may be a more sensitive indicator of perioperative complications. A retrospective study of 311 patients undergoing bariatric surgery for weight reduction reported that OSA was associated with a longer length of hospital admissions (OR 5.5) but that stronger predictors of longer hospitalization included coronary artery disease (OR 8.7) and the presence of the metabolic syndrome (OR 6.7–10.2).187
The change in sleep architecture with surgery could possibly contribute to a greater postoperative risk in OSA patients. Among patients undergoing abdominal surgery, anesthesia initially suppresses rapid eye movement (REM) sleep but there is intense REM rebound towards the middle of the first postoperative week.188 This alteration in sleep architecture can have a substantial impact on the respiratory variables in OSA patients. In REM sleep, upper airway muscle activity in the late apneic phase is reduced189 and, consequently, apneas are of larger duration and are associated with a greater degree of hypoxemia during REM sleep than non-REM sleep.190 Hemodynamic changes are also evident in REM sleep as REM-related incidences of desaturation were found to be linked to significantly higher postapnea increases in arterial blood pressure.191 Coincidentally, numerous ventilatory disturbances, including apneas and hypopneas, have been observed on the second and third postoperative nights.192 There are no studies directly linking changes in sleep stage with ventilatory disturbances during the postoperative period.
There are also reports of numerous obstructive hypopnic and/or apneic events within the first 12 h postoperatively.77 Moreover, the respiratory disturbances in the early postoperative period have been reported to occur mainly in Stages 1 and 2 sleep since most patients did not have slow wave sleep or REM sleep in the early postoperative period.52 More recent studies have documented that the more serious complications occurred within the first 24 h after surgery in OSA patients.95 In a study of non-OSA surgical patients,193 more than 75% of postoperative patients had respiratory events within 13 to 24 h after surgery and significant risk factors included older age, having more than one comorbidity and whether hydromorphone was administered for analgesia. Similar studies in OSA patients undergoing surgery are needed to determine if the timing of respiratory events is similar and which risk factors are significant for this population. The time course of adverse postoperative events suggests the involvement of other factors than sleep architecture, but it may help to elucidate the period of greatest postoperative risk. That is, the REM-related impact on respiratory events would take place a number of days postoperatively and may represent a second period of greater risk of postoperative respiratory complications. However, the above studies suggest that postoperative complications are quite common within the first 24 h postoperatively.
Can Choice of Anesthetics or Anesthetic Technique Reduce Perioperative Risk in OSA Patients?
There are numerous reviews on the subject of anesthetic management of OSA patients111,113,194–197 that emphasize that the type of anesthesia may have differential impact on the respiration of patients. Despite these reviews, there are no randomized controlled trials of the safety of various anesthetics in the perioperative period. As mentioned previously, different analgesics have different margins of safety and result in varying levels of respiratory depression. A relatively recent study36 has documented the impact of propofol on upper airway collapsibility by investigating the relationship between varying concentrations and the critical airway closing pressure. The use of healthy individuals, and not patients with OSA, as subjects coupled with the lack of a randomized controlled design, are significant limitations of this study. Nevertheless, the findings highlight that a carefully chosen concentration of anesthetic may play an important role in the airway management of OSA patients.
An important consideration in the choice of inhaled anesthesia is the presence of any carryover anesthetic effects into the postoperative period that could impair respiration and/or enhance the deleterious respiratory effects of analgesics. In OSA patients undergoing UPPP, there was delayed recovery in those patients receiving isoflurane versus propofol. Propofol anesthesia was found to result in better oxygen saturation in the first postoperative hour and more rapid recovery of spontaneous breathing versus isoflurane.97 However, these studies were not done on OSA patients. Short-acting anesthetics, such as remifentanil, have also been shown to result in a rapid postoperative recovery, better oxygen saturation profile and shorter postoperative length of stay.198,199 Also, morbidly obese patients who underwent major abdominal surgery awoke significantly faster after desflurane than after sevoflurane anesthesia. The patients anesthetized with desflurane had higher oxygen saturation on entry to the PACU.200
Premedication sedatives, especially benzodiazepines, such as flunitrazepam or midazolam, have been shown to cause postoperative airway obstruction.41 In this study, 12 patients did not have a premorbid history of OSA but were observed to snore loudly postoperatively. Conversely, some premedication drugs have been shown to be beneficial in OSA patients. In a case report of a morbidly obese woman with tracheal stenosis, dexmedetomidine, an α-2 adrenergic agonist, was used as a premedication due its anxiolytic and sedative properties. The benefit of dexmedetomidine is the lack of significant respiratory depression within the clinical dose range. Similarly, in a randomized controlled trial, orally administered clonidine was found to reduce the propofol dose required for induction of anesthesia.201 Unfortunately, there are no trials of the efficacy of varying premedication drugs in OSA patients undergoing surgery, but the above studies illustrate their importance.
Are There Safer Alternatives to Opioid Analgesics for Postoperative Pain Control?
Postoperative analgesia is another factor that can influence respiration in surgical patients with OSA. In a retrospective study of 1600 patients, not specifically OSA patients, who had received postoperative patient-controlled analgesia with IV opioids, 8 cases of serious respiratory depression were reported.202 Contributing factors were the concurrent use of a background infusion of opioids, advanced age, concomitant administration of sedative or hypnotic medications and a preexisting history of sleep apnea. Two retrospective reviews of more than one-thousand surgical patients indicated that postoperative respiratory depression after morphine-based patient-controlled analgesia was observed to occur in about 1%–2% of patients.203,204 This respiratory depression occurred between 2 to 31 h after initiation of the IV patient-controlled analgesia203 indicating the need for long-term diligent patient monitoring.
A review conducted to identify the risk factors for respiratory depression subsequent to patient-controlled analgesia concluded that there is no single indicator for respiratory depression but that OSA, whether suspected or verified by patient history, is one of the risk factors for respiratory depression. Other factors include older age, hepatic, pulmonary or cardiac disease, concurrent use of central depressants, obesity, and higher bolus doses of patient-controlled analgesia.205 There are no prospective randomized studies examining the respiratory effect of patient-controlled analgesia in OSA patients.
In general, the consensus is that opioids are to be avoided in OSA patients, if possible, especially when they undergo upper airway surgical treatment for OSA.206 The ASA guidelines recommend regional anesthesia to reduce the possibility of negative adverse events associated with systemic opioids.3 A multimodal approach with combinations of analgesics from different classes and different sites of analgesic administration is a prudent strategy for perioperative pain management.207–209 The use of nonsteroidal antiinflammatory analgesics210 is strongly recommended.3 Drugs such as acetaminophen, tramadol, and other nonopioid analgesics and their combination can be used to provide effective pain relief and reduce opioid consumption, thus alleviating the opioid-related adverse effect of respiratory depression. Other novel approaches, such as ketamine, clonidine, or gabapentin can be used.201,207–209 In a case report, the nonopioid sedative dexmedetomidine45 has been shown to reduce the need for postoperative opioids. Other techniques that avoid medication, such as transcranial magnetic stimulation,211 are also being investigated. The opiate-sparing strategies geared towards OSA patients are summarized (Table 4). A major drawback of these studies is that they are predominantly case reports. Unfortunately, there are no studies comparing the safety and efficacy of different anesthesia technique, general anesthesia, regional anesthesia or monitored anesthesia care in OSA patients undergoing surgery or studies on different analgesic or adjuvants.
Postoperative Management Strategies for OSA Patients
Clearly, anesthesiologists need to develop effective management strategies to minimize perioperative risk for patients with OSA undergoing surgery. To that end, the ASA recently published guidelines,3 a Level IV evidence document based on expert consensus report, that propose strategies for overall perioperative care of OSA patients. The clinical practice review committee of the American Academy of Sleep Medicine also indicated that the scientific literature regarding the perioperative risk and best management techniques for OSA patients was scanty and of limited quantity. They used the available data to make a statement on the perioperative management of OSA patients instead of standards of practice recommendations.212
Due to the high risk of complications and morbidity associated with upper airway surgery for OSA treatment, suggestions for perioperative monitoring in OSA patients undergoing upper airway surgery were initially introduced 15 yr ago,76 however, no consensus-based guidelines for the perioperative management of OSA patients undergoing airway surgery were formulated. Moreover, the upper airway surgical literature is specifically oriented towards upper airway procedures thus lessening the applicability of these management strategies to other types of surgery. For example, steps to minimize upper airway edema with topical corticosteroids213 are crucial with upper airway surgery but have much less applicability to other types of surgery. Nonetheless, a closer examination of management strategies for upper airway surgery may help to provide information that is applicable to OSA patients undergoing surgery.
Pertinent information can also be gleaned from reports of patients undergoing bariatric surgery for obesity. A major confound with the bariatric surgery population is the presence of obesity and the added risk of the associated morbidity184 that render it difficult to extrapolate these findings to the general surgical population. Of positive note, it was shown that anesthesia need not be associated with postoperative complications in obese patients with OSA undergoing bariatric surgery.214 With careful postoperative monitoring in the PACU and the ward, surgery was reported to be safe in this high-risk group of patients.
Surgery in OSA patients is associated with significant perioperative risk. As mentioned earlier, cardiovascular morbidity is common in patients with long-standing untreated OSA thus further increasing the likelihood of adverse perioperative events. The incidence of perioperative complications associated with upper airway surgery for OSA is about 3.5% (range, 0.6–8.9),215 and a 0.4% to 1.6% incidence of mortality has been reported.216,217 Airway-related postoperative complications occur in about 6% of patients, oxygen desaturations in 9% and electrocardiogram changes in 1%.98 Others have documented that about one-third of the complications involve the airway.102 Cardiac complications, such as hypertension, have also been commonly reported.122 Alerting surgeons, anesthesiologists, and nurses to the potential perioperative complications associated with surgery in OSA patients is a first step to reducing the rate of morbidity and mortality.
The ASA guidelines3 recommend that the preoperative evaluation be conducted well in advance of the surgery in patients suspected of having OSA. This procedure would allow for the necessary preoperative evaluation and development of an appropriate perioperative management plan. However, patients with undiagnosed OSA would likely be identified at the time of the preoperative visit when there may not be time to do further testing before surgery. In this event, the ASA guidelines recommend that a presumptive diagnosis of OSA be made from criteria based on the signs and symptoms of OSA.3
As maintenance of upper airway patency in OSA patients is a major consideration, caution is needed to ensure that extubation should only be done after the patient is fully conscious and airway patency is ensured. However, the ASA guidelines state that this need be the case only for patients at increased perioperative risk from OSA.3 The use of postoperative supplemental oxygen has been suggested76 for OSA patients undergoing upper airway surgery to maintain appropriate oxygen saturation. The ASA guidelines caution that oxygen supplementation should be used only until patients are able to maintain baseline oxygen saturation with room air.3 A side effect of the use of prolonged supplemental oxygen in patients with chronic obstructive pulmonary disease is the increased duration of obstructive apneas or hypopneas.218 The ASA guidelines further recommend that continuous oximetry may be used in the step down unit in patients with increased perioperative risk from OSA, but it does not support the need of continuous oxygen monitoring in all patients. There is no evidence-based determination if the cost of routine monitoring is warranted as there are no studies examining whether such monitoring reduces the postoperative risk in OSA patients.
Other postoperative strategies for reducing postoperative risk, such as the influence of sleep position on OSA, also warrant investigation. Lateral position is reported to improve the maintenance of the passive pharyngeal airway in patients with OSA.219 The lateral position improves upper airway stability during sleep which may allow reduction of the therapeutic levels of CPAP.220 The study by Penzel et al. also supported the idea that lower CPAP pressure was needed during lateral positions versus supine positions.221 However, the ASA guidelines recommend a semi-upright position for extubation and recovery in OSA patients3 and the use of a nonsupine position postoperatively. However, this position may not be feasible for certain orthopedic procedures.
Several nonrandomized follow-up studies in patients with upper airway surgery101,183 have assessed the effect of the appropriate setting of surgery for OSA patients. Based on these studies, it is recommended that OSA patients at low risk for adverse outcomes may be discharged home without ICU admission. One study proposed that upper airway surgery may be safely done as outpatient surgery and that more than 80% were discharged on the same day of surgery.120 A limitation of this study was that there was no information regarding postoperative follow-up and whether respiratory complications occurred in the days after surgery. Other studies, however, support the notion that ICU admission is not required and that respiratory complications, if they occur, do so a few hours after surgery.102,122,222 It is important to note that all OSA patients are carefully screened before undergoing upper airway surgery to improve the success of the treatment. As part of this screening process, younger nonobese OSA patients with AHI <40 are generally selected.223,224
From the consultants in the ASA guidelines,3 there is an overall agreement that the level of perioperative risk is a function of OSA severity and type of surgery. The guidelines propose that the following types of surgeries can be performed safely on an outpatient basis: superficial surgeries using local or regional anesthesia, minor orthopedic surgery with local or regional anesthesia and lithotripsy. The consultants were equivocal or in disagreement regarding the other types of surgeries,3 particularly with regards to upper airway surgery. The ASA guidelines further propose that the following factors need to be considered when determining outpatient care and the degree of postoperative risk: status of sleep apnea (e.g., treated or untreated), anatomical and physiologic abnormalities, level of co-morbidity (e.g., Are there OSA-associated comorbidities such as cardiovascular disorders and have these been appropriately managed?), type of surgery, anesthesia modality, postoperative opioid use (dosage, duration and length of administration, etc), patient age, how patients will be monitored after discharge and what facilities are available for outpatient monitoring.
The ASA3 guidelines emphasize the importance of increased perioperative risk in OSA patients and that additional measures of perioperative management need to be instituted in these patients. The guidelines identify several factors (above) that could increase the risk but there is no further elucidation of the degree of contribution of each factor. Certainly, surgeons and anesthesiologists have to treat each patient on a case-by-case basis, but an evidence-based algorithm to determine the actual level of risk would be a useful starting point. However, no clear definitions or grading schemes for “high” versus “low” risk for perioperative management are available in the literature and further studies are urgently needed in this area. The purpose of such research would be to identify and quantify the required measures in specifically assigning perioperative risk status in OSA patients. The appropriate classification and definition of level of perioperative risk would be an important step towards a concrete discernment of the degree of necessary perioperative monitoring and whether outpatient surgery could be conducted. Above all, the pressures to reduce health care expenditure dictate that the perioperative care of patients needs to be optimized to prevent unnecessary monitoring and depletion of limited resources.
A summary of the recommendations for OSA surgery from the ASA guidelines3 is shown in Table 5. The strength of the ASA guidelines is their use of expert-based consensus. However, it is important to note that their recommendations are not evidence-based and there is a paucity of research to substantiate the efficacy of these measures in improving perioperative outcome.
There is a frequent prevalence of undiagnosed OSA. Also, the severity of OSA varies among patient groups and perioperative complications are probably related to the interaction of the severity of the diseases and the degree of respiratory depression induced by opioids. Sleep apnea is associated with other preexisting medical conditions such as obesity, hypertension, coronary artery disease, and diabetes that negatively impact perioperative outcomes. It may be difficult to separate the impact of OSA per se from the other associated conditions.
Surgical patients with OSA may be vulnerable to sedation, anesthesia and analgesia. Episodic sleep-related desaturation and incidence of unexplained cardiorespiratory arrest may be attributable to undiagnosed OSA in surgical patients, but this connection needs to be tested within randomized, controlled trials. It also remains to be determined whether the perioperative risk of OSA patients could be reduced by appropriate screening to detect undiagnosed OSA and implementation of a perioperative management plan for OSA. Evidence-based research on perioperative management of OSA patients is sorely lacking.
1.Bahammam A, Delaive K, Ronald J, Manfreda J, Roos L, Kryger MH. Health care utilization in males with obstructive sleep apnea syndrome two years after diagnosis and treatment. Sleep 1999;22:740–7
2.He J, Kryger MH, Zorick FJ, Conway W, Roth T. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest 1988;94:9–14
3.Gross JB, Bachenberg KL, Benumof JL, Caplan RA, Connis RT, Cote CJ, Nickinovich DG, Prachand V, Ward DS, Weaver EM, Ydens L, Yu S. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology 2006;104:1081–93
4.Sackett DL. Rules of evidence and clinical recommendations for the management of patients. Can J Cardiol 1993;9:487–9
5.Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 1999;22:667–89
6.Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230–5
7.Bixler EO, Vgontzas AN, Ten HT, Tyson K, Kales A. Effects of age on sleep apnea in men: I. Prevalence and severity. Am J Respir Crit Care Med 1998;157:144–8
8.Bixler EO, Vgontzas AN, Lin HM, Ten HT, Rein J, Vela-Bueno A, Kales A. Prevalence of sleep-disordered breathing in women: effects of gender. Am J Respir Crit Care Med 2001;163:608–13
9.Duran J, Esnaola S, Rubio R, Iztueta A. Obstructive sleep apnea-hypopnea and related clinical features in a population-based sample of subjects aged 30 to 70 yr. Am J Respir Crit Care Med 2001;163:685–9
10.Netzer NC, Hoegel JJ, Loube D, Netzer CM, Hay B, varez-Sala R, Strohl KP. Prevalence of symptoms and risk of sleep apnea in primary care. Chest 2003;124:1406–14
11.Wetter DW, Young TB, Bidwell TR, Badr MS, Palta M. Smoking as a risk factor for sleep-disordered breathing. Arch Intern Med 1994;154:2219–24
12.Elmasry A, Lindberg E, Berne C, Janson C, Gislason T, Awad TM, Boman G. Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study. J Intern Med 2001;249:153–61
13.Logan AG, Perlikowski SM, Mente A, Tisler A, Tkacova R, Niroumand M, Leung RS, Bradley TD. High prevalence of unrecognized sleep apnoea in drug-resistant hypertension. J Hypertens 2001;19:2271–7
14.Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir Crit Care Med 1999;160:1101–6
15.Parra O, Arboix A, Bechich S, Garcia-Eroles L, Montserrat JM, Lopez JA, Ballester E, Guerra JM, Sopena JJ. Time course of sleep-related breathing disorders in first-ever stroke or transient ischemic attack. Am J Respir Crit Care Med 2000;161:375–80
16.Mojon DS, Hess CW, Goldblum D, Bohnke M, Korner F, Mathis J. Primary open-angle glaucoma is associated with sleep apnea syndrome. Ophthalmologica 2000;214:115–18
17.Hira HS, Sibal L. Sleep apnea syndrome among patients with hypothyroidism. J Assoc Physicians India 1999;47:615–18
18.Aldrich MS, Brower KJ, Hall JM. Sleep-disordered breathing in alcoholics. Alcohol Clin Exp Res 1999;23:134–40
19.Payne RJ, Hier MP, Kost KM, Black MJ, Zeitouni AG, Frenkiel S, Naor N, Kimoff RJ. High prevalence of obstructive sleep apnea among patients with head and neck cancer. J Otolaryngol 2005;34:304–11
20.Ancoli-Israel S, Kripke DF, Klauber MR, Mason WJ, Fell R, Kaplan O. Sleep-disordered breathing in community-dwelling elderly. Sleep 1991;14:486–95
21.Tishler PV, Larkin EK, Schluchter MD, Redline S. Incidence of sleep-disordered breathing in an urban adult population: the relative importance of risk factors in the development of sleep-disordered breathing. JAMA 2003;289:2230–7
22.Resta O, Foschino-Barbaro MP, Legari G, Talamo S, Bonfitto P, Palumbo A, Minenna A, Giorgino R, De PG. Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects. Int J Obes Relat Metab Disord 2001;25:669–75
23.Young T, Peppard PE, Taheri S. Excess weight and sleep-disordered breathing. J Appl Physiol 2005;99:1592–9
24.Frey WC, Pilcher J. Obstructive sleep-related breathing disorders in patients evaluated for bariatric surgery. Obes Surg 2003;13:676–83
25.Malow BA, Levy K, Maturen K, Bowes R. Obstructive sleep apnea is common in medically refractory epilepsy patients. Neurology 2000;55:1002–7
26.Pollak L, Shpirer I, Rabey JM, Klein C, Schiffer J. Polysomnography in patients with intracranial tumors before and after operation. Acta Neurol Scand 2004;109:56–60
27.Fidan H, Fidan F, Unlu M, Ela Y, Ibis A, Tetik L. Prevalence of sleep apnoea in patients undergoing operation. Sleep Breath 2006;10:161–5
28.O’Keeffe T, Patterson EJ. Evidence supporting routine polysomnography before bariatric surgery. Obes Surg 2004;14:23–6
29.Turner K, VanDenKerkhof E, Lam M, Mackillop W. Perioperative care of patients with obstructive sleep apnea - a survey of Can anesthesiologists: [La prise en charge perioperatoire des patients atteints d’apnee du sommeil d’origine obstructive - une enquete aupres des anesthesiologistes canadiens]. Can J Anaesth 2006;53:299–304
30.Harrison MM, Childs A, Carson PE. Incidence of undiagnosed sleep apnea in patients scheduled for elective total joint arthroplasty. J Arthroplasty 2003;18:1044–7
31.Chung F, Ward B, Ho J, Yuan H, Kayumov L, Shapiro C. Preoperative Identification of Sleep Apnea Risk in Elective Surgical Patients Using The Berlin Questionnaire. J Clin Anesth 2007;19:130–4
32.Young T, Evans L, Finn L, Palta M. Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women. Sleep 1997;20:705–6
33.Bouillon T, Schmidt C, Garstka G, Heimbach D, Stafforst D, Schwilden H, Hoeft A. Pharmacokinetic-pharmacodynamic modeling of the respiratory depressant effect of alfentanil. Anesthesiology 1999;91:144–55
34.Dahan A, van den Elsen MJ, Berkenbosch A, DeGoede J, Olievier IC, van Kleef JW, Bovill JG. Effects of subanesthetic halothane on the ventilatory responses to hypercapnia and acute hypoxia in healthy volunteers. Anesthesiology 1994;80:727–38
35.Drummond GB. Effects of extradural sufentanil and morphine on ventilation. Br J Anaesth 1995;74:492–3
36.Eastwood PR, Platt PR, Shepherd K, Maddison K, Hillman DR. Collapsibility of the upper airway at different concentrations of propofol anesthesia. Anesthesiology 2005;103:470–7
37.Knill RL, Clement JL. Site of selective action of halothane on the peripheral chemoreflex pathway in humans. Anesthesiology 1984;61:121–6
38.Knill RL, Clement JL. Ventilatory responses to acute metabolic acidemia in humans awake, sedated, and anesthetized with halothane. Anesthesiology 1985;62:745–53
39.Teppema LJ, Nieuwenhuijs D, Sarton E, Romberg R, Olievier CN, Ward DS, Dahan A. Antioxidants prevent depression of the acute hypoxic ventilatory response by subanaesthetic halothane in men. J Physiol 2002;544:931–8
40.Drummond GB. Influence of thiopentone on upper airway muscles. Br J Anaesth 1989;63:12–21
41.Dhonneur G, Combes X, Leroux B, Duvaldestin P. Postoperative obstructive apnea. Anesth Analg 1999;89:762–7
42.Kovoor P, Porter R, Uther JB, Ross DL. Efficacy and safety of a new protocol for continuous infusion of midazolam and fentanyl and its effects on patient distress during electrophysiological studies. Pacing Clin Electrophysiol 1997;20:2765–74
43.Miller RJ, Gerhardt MA. Uvular edema secondary to snoring under deep sedation. Anesth Prog 2006;53:13–16
44.Montravers P, Dureuil B, Desmonts JM. Effects of i.v. midazolam on upper airway resistance. Br J Anaesth 1992;68:27–31
45.Hofer RE, Sprung J, Sarr MG, Wedel DJ. Anesthesia for a patient with morbid obesity using dexmedetomidine without narcotics. Can J Anaesthesia 2005;52:176–80
46.Ramsay MA, Saha D, Hebeler RF. Tracheal resection in the morbidly obese patient: the role of dexmedetomidine. J Clin Anesth 2006;18:452–4
47.Ho AM, Chen S, Karmakar MK. Central apnoea after balanced general anaesthesia that included dexmedetomidine. Br J Anaesth 2005;95:773–5
48.Bartlett D Jr, St John WM. Influence of morphine on respiratory activities of phrenic and hypoglossal nerves in cats. Respir Physiol 1986;64:289–94
49.Weil JV, McCullough RE, Kline JS, Sodal IE. Diminished ventilatory response to hypoxia and hypercapnia after morphine in normal man. N Engl J Med 1975;292:1103–6
50.Cepeda MS, Farrar JT, Roa JH, Boston R, Meng QC, Ruiz F, Carr DB, Strom BL. Ethnicity influences morphine pharmacokinetics and pharmacodynamics. Clin Pharmacol Ther 2001;70:351–61
51.Dahan A, Sarton E, Teppema L, Olievier C. Sex-related differences in the influence of morphine on ventilatory control in humans. Anesthesiology 1998;88:903–13
52.Catley DM, Thornton C, Jordan C, Lehane JR, Royston D, Jones JG. Pronounced, episodic oxygen desaturation in the postoperative period: its association with ventilatory pattern and analgesic regimen. Anesthesiology 1985;63:20–8
53.Clyburn PA, Rosen M, Vickers MD. Comparison of the respiratory effects of i.v. infusions of morphine and regional analgesia by extradural block.[see comment]. Br J Anaesth 1990;64:446–9
54.Wiegand DA, Latz B, Zwillich CW, Wiegand L. Geniohyoid muscle activity in normal men during wakefulness and sleep. J Appl Physiol 1990;69:1262–9
55.Tangel DJ, Mezzanotte WS, White DP. Influence of sleep on tensor palatini EMG and upper airway resistance in normal men. J Appl Physiol 1991;70:2574–81
56.Farney RJ, Walker JM, Cloward TV, Rhondeau S. Sleep-disordered breathing associated with long-term opioid therapy. Chest 2003;123:632–9
57.McNicholas WT, Ryan S. Obstructive sleep apnoea syndrome: translating science to clinical practice. Respirology 2006;11:136–44
58.Ciscar MA, Juan G, Martinez V, Ramon M, Lloret T, Minguez J, Armengot M, Marin J, Basterra J. Magnetic resonance imaging of the pharynx in OSA patients and healthy subjects. Eur Respir J 2001;17:79–86
59.Horner RL, Shea SA, McIvor J, Guz A. Pharyngeal size and shape during wakefulness and sleep in patients with obstructive sleep apnoea. Q J Med 1989;72:719–35
60.Schwab RJ, Gupta KB, Gefter WB, Metzger LJ, Hoffman EA, Pack AI. Upper airway and soft tissue anatomy in normal subjects and patients with sleep-disordered breathing. Significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995;152:1673–89
61.Carrera M, Barbe F, Sauleda J, Tomas M, Gomez C, Agusti AG. Patients with obstructive sleep apnea exhibit genioglossus dysfunction that is normalized after treatment with continuous positive airway pressure. Am J Respir Crit Care Med 1999;159:1960–6
62.Series F, Cote C, Simoneau JA, Gelinas Y, St Pierre S, Leclerc J, Ferland R, Marc I. Physiologic, metabolic, and muscle fiber type characteristics of musculus uvulae in sleep apnea hypopnea syndrome and in snorers. J Clin Invest 1995;95:20–5
63.Byard RW, Gilbert JD. Narcotic administration and stenosing lesions of the upper airway–a potentially lethal combination. J Clin Forensic Med 2005;12:29–31
64.Mezzanotte WS, Tangel DJ, White DP. Influence of sleep onset on upper-airway muscle activity in apnea patients versus normal controls. Am J Respir Crit Care Med 1996;153:1880–7
65.Scrima L, Broudy M, Nay KN, Cohn MA. Increased severity of obstructive sleep apnea after bedtime alcohol ingestion: diagnostic potential and proposed mechanism of action. Sleep 1982;5:318–28
66.Berry RB, Bonnet MH, Light RW. Effect of ethanol on the arousal response to airway occlusion during sleep in normal subjects. Am Rev Respir Dis 1992;145:445–52
67.Hudgel DW, Hendricks C. Palate and hypopharynx–sites of inspiratory narrowing of the upper airway during sleep. Am Rev Respir Dis 1988;138:1542–7
68.Boidin MP. Airway patency in the unconscious patient. Br J Anaesth 1985;57:306–10
69.Abernethy LJ, Allan PL, Drummond GB. Ultrasound assessment of the position of the tongue during induction of anaesthesia. Br J Anaesth 1990;65:744–8
70.Shorten GD, Opie NJ, Graziotti P, Morris I, Khangure M. Assessment of upper airway anatomy in awake, sedated and anaesthetised patients using magnetic resonance imaging. Anaesth Intensive Care 1994;22:165–9
71.Brouillette RT, Thach BT. A neuromuscular mechanism maintaining extrathoracic airway patency. J Appl Physiol 1979;46:772–9
72.Robinson RW, Zwillich CW, Bixler EO, Cadieux RJ, Kales A, White DP. Effects of oral narcotics on sleep-disordered breathing in healthy adults. Chest 1987;91:197–203
73.Tallila T, Polo O, Aantaa R, Lepisto M, Lahdenpera A, Scheinin H. Nocturnal body movements and hypoxemia in middle-aged females after lower abdominal surgery under general anesthesia: a study with the static-charge-sensitive bed (SCSB). J Clin Monit Comput 1998;14:239–44
74.Brown KA, Laferriere A, Lakheeram I, Moss IR. Recurrent hypoxemia in children is associated with increased analgesic sensitivity to opiates. Anesthesiology 2006;105:665–9
75.Lamarche Y, Martin R, Reiher J, Blaise G. The sleep apnoea syndrome and epidural morphine. Can Anaesth Soc J 1986;33:231–3
76.Connolly LA. Anesthetic management of obstructive sleep apnea patients. [Review] [43 refs]. J Clin Anesth 1991;3:461–9
77.Jones JG, Jordan C, Scudder C, Rocke DA, Barrowcliffe M. Episodic postoperative oxygen desaturation: the value of added oxygen. J R Soc Med 1985;78:1019–22
78.Bailey PL, Pace NL, Ashburn MA, Moll JW, East KA, Stanley TH. Frequent hypoxemia and apnea after sedation with midazolam and fentanyl. Anesthesiology 1990;73:826–30
79.Alexander CM, Gross JB. Sedative doses of midazolam depress hypoxic ventilatory responses in humans. Anesth Analg 1988;67:377–82
80.Dolly FR, Block AJ. Effect of flurazepam on sleep-disordered breathing and nocturnal oxygen desaturation in asymptomatic subjects. Am J Med 1982;73:239–43
81.Bixler EO, Vgontzas AN, Lin HM, Ten HT, Leiby BE, Vela-Bueno A, Kales A. Association of hypertension and sleep-disordered breathing. Arch Intern Med 2000;160:2289–95
82.Dyken ME, Somers VK, Yamada T, Ren ZY, Zimmerman B. Investigating the relationship between stroke and obstructive sleep apnea. Stroke 1996;27:401–7
83.Hung J, Whitford EG, Parsons RW, Hillman DR. Association of sleep-apnea with myocardial-infarction in men. Lancet 1990;336:261–4
84.Peker Y, Kraiczi H, Hedner J, Loth S, Johansson A, Bende M. An independent association between obstructive sleep apnoea and coronary artery disease. Eur Respir J 1999;14:179–84
85.Sin DD, Fitzgerald F, Parker JD, Newton GE, Logan AG, Floras JS, Bradley TD. Relationship of systolic BP to obstructive sleep apnea in patients with heart failure. Chest 2003;123:1536–43
86.Mehra R, Benjamin EJ, Shahar E, Gottlieb DJ, Nawabit R, Kirchner HL, Sahadevan J, Redline S. Association of nocturnal arrhythmias with sleep-disordered breathing: The Sleep Heart Health Study. Am J Respir Crit Care Med 2006;173:910–16
87.Ohayon MM, Guilleminault C, Priest RG, Zulley J, Smirne S. Is sleep-disordered breathing an independent risk factor for hypertension in the general population (13,057 subjects)? J Psychosom Res 2000;48:593–601
88.Arzt M, Young T, Finn L, Skatrud JB, Bradley TD. Association of sleep-disordered breathing and the occurrence of stroke. Am J Respir Crit Care Med 2005;172:1447–51
89.Coughlin SR, Mawdsley L, Mugarza JA, Calverley PM, Wilding JP. Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome. Eur Heart J 2004;25:735–41
90.Chin K, Ohi M, Kita H, Noguchi T, Otsuka N, Tsuboi T, Mishima M, Kuno K. Effects of NCPAP therapy on fibrinogen levels in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 1996;153:1972–6
91.Chin K, Kita H, Noguchi T, Otsuka N, Tsuboi T, Nakamura T, Shimizu K, Mishima M, Ohi M. Improvement of factor VII clotting activity following long-term NCPAP treatment in obstructive sleep apnoea syndrome. QJM: 1998;91:627–33
92.Chin K, Ohi M. New insights into the therapy and pathophysiology of patients with obstructive sleep apnoea syndrome. Respirology 1998;3:139–43
93.Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med 2005;353:2034–41
94.Samuels SI, Rabinov W. Difficulty reversing drug-induced coma in a patient with sleep apnea. Anesth Analg 1986;65:1222–4
95.Gupta RM, Parvizi J, Hanssen AD, Gay PC. Postoperative complications in patients with obstructive sleep apnea syndrome undergoing hip or knee replacement: a case-control study. Mayo Clin Proc 2001;76:897–905
96.Siyam MA, Benhamou D. Difficult endotracheal intubation in patients with sleep apnea syndrome. Anesth Analg 2002;95:1098–102 table of contents
97.Hendolin H, Kansanen M, Koski E, Nuutinen J. Propofol-nitrous oxide versus thiopentone-isoflurane-nitrous oxide anaesthesia for uvulopalatopharyngoplasty in patients with sleep apnea. Acta Anaesthesiol Scand 1994;38:694–8
98.Kim JA, Lee JJ, Jung HH. Predictive factors of immediate postoperative complications after uvulopalatopharyngoplasty. Laryngoscope 2005;115:1837–40
99.Esclamado RM, Glenn MG, McCulloch TM, Cummings CW. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope 1989;99:1125–9
100.Pang KP. Identifying patients who need close monitoring during and after upper airway surgery for obstructive sleep apnoea. J Laryngol Otol 2006;120:655–60
101.Gessler EM, Bondy PC. Respiratory complications following tonsillectomy/UPPP: is step-down monitoring necessary? Ear Nose Throat J 2003;82:628–32
102.Mickelson SA, Hakim I. Is postoperative intensive care monitoring necessary after uvulopalatopharyngoplasty? Otolaryngol Head Neck Surg 1998;119:352–6
103.Rose DK, Cohen MM, Wigglesworth DF, DeBoer DP. Critical respiratory events in the postanesthesia care unit. Patient, surgical, and anesthetic factors. Anesthesiology 1994;81:410–18
104.Guilleminault C, Connolly SJ, Winkle RA. Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 1983;52:490–4
105.Alonso-Fernandez A, Garcia-Rio F, Racionero MA, Pino JM, Ortuno F, Martinez I, Villamor J. Cardiac rhythm disturbances and ST-segment depression episodes in patients with obstructive sleep apnea-hypopnea syndrome and its mechanisms. Chest 2005;127:15–22
106.Peiser J, Ovnat A, Uwyyed K, Lavie P, Charuzi I. Cardiac arrhythmias during sleep in morbidly obese sleep-apneic patients before and after gastric bypass surgery. Clin Cardiol 1985;8:519–21
107.Mooe T, Gullsby S, Rabben T, Eriksson P. Sleep-disordered breathing: a novel predictor of atrial fibrillation after coronary artery bypass surgery. Coron Artery Dis 1996;7:475–8
108.Cullen DJ. Obstructive sleep apnea and postoperative analgesia–a potentially dangerous combination. J Clin Anesth 2001;13:83–5
109.Vidhani K, Langham BT. Obstructive sleep apnoea syndrome: is this an overlooked cause of desaturation in the immediate postoperative period? Br J Anaesth 1997;78:442–3
110.Lofsky A. Sleep apnea and narcotic postoperative pain medication: a morbidity and mortality risk. APSF Newsletter 2002;17:24–5
111.Ostermeier AM, Roizen MF, Hautkappe M, Klock PA, Klafta JM. Three sudden postoperative respiratory arrests associated with epidural opioids in patients with sleep apnea. Anesth Analg 1997;85:452–60
112.Reeder MK, Goldman MD, Loh L, Muir AD, Casey KR, Gitlin DA. Postoperative obstructive sleep apnoea. Haemodynamic effects of treatment with nasal CPAP. Anaesthesia 1991;46:849–53
113.Block M, Jacobson LB, Rabkin RA. Heart block in patients after bariatric surgery accompanying sleep apnea. Obes Surg 2001;11:627–30
114.Kaw R, Golish J, Ghamande S, Burgess R, Foldvary N, Walker E. Incremental risk of obstructive sleep apnea on cardiac surgical outcomes. J Cardiovasc Surg (Torino) 2006;47:683–9
115.Benumof JL. Obesity, sleep apnea, the airway and anesthesia. Curr Opin Anaesthesiol 2004;17:21–30
116.Hillman DR, Loadsman JA, Platt PR, Eastwood PR. Obstructive sleep apnoea and anaesthesia. Sleep Med Rev 2004;8:459–71
117.Sabers C, Plevak DJ, Schroeder DR, Warner DO. The diagnosis of obstructive sleep apnea as a risk factor for unanticipated admissions in outpatient surgery. Anesth Analg 2003;96:1328–35 table of contents
118.Fortier J, Chung F, Su J. Unanticipated admission after ambulatory surgery–a prospective study. Can J Anaesth 1998;45:612–19
119.Araujo MT, Ouayoun M, Poirier JM, Bayle MM, Vasquez EC, Fleury B. Transitory increased blood pressure after upper airway surgery for snoring and sleep apnea correlates with the apnea-hypopnea respiratory disturbance index. Braz J Med Biol Res 2003;36:1741–9
120.Hathaway B, Johnson JT. Safety of uvulopalatopharyngoplasty as outpatient surgery. Otolaryngol Head Neck Surg 2006;134:542–4
121.Isono S, Sha M, Suzukawa M, Sho Y, Ohmura A, Kudo Y, Misawa K, Inaba S, Nishino T. Preoperative nocturnal desaturations as a risk factor for late postoperative nocturnal desaturations. Br J Anaesth 1998;80:602–5
122.Terris DJ, Fincher EF, Hanasono MM, Fee WE Jr, Adachi K. Conservation of resources: indications for intensive care monitoring after upper airway surgery on patients with obstructive sleep apnea. Laryngoscope 1998;108:784–8
123.Morgan BJ, Dempsey JA, Pegelow DF, Jacques A, Finn L, Palta M, Skatrud JB, Young TB. Blood pressure perturbations caused by subclinical sleep-disordered breathing. Sleep 1998;21:737–46
124.Vanninen E, Tuunainen A, Kansanen M, Uusitupa M, Lansimies E. Cardiac sympathovagal balance during sleep apnea episodes. Clin Physiol 1996;16:209–16
125.Weiss JW, Remsburg S, Garpestad E, Ringler J, Sparrow D, Parker JA. Hemodynamic consequences of obstructive sleep apnea. Sleep 1996;19:388–97
126.Egan B, Schmouder R. The importance of hemodynamic considerations in essential hypertension. Am Heart J 1988;116:594–9
127.Chen L, Scharf SM. Systemic and myocardial hemodynamics during periodic obstructive apneas in sedated pigs. J Appl Physiol 1998;84:1289–98
128.Bowdle TA. Nocturnal arterial oxygen desaturation and episodic airway obstruction after ambulatory surgery. Anesth Analg 2004;99:70–6
129.Gentil B, Lienhart A, Fleury B. Enhancement of postoperative desaturation in heavy snorers. Anesth Analg 1995;81:389–92
130.Becker HF, Koehler U, Stammnitz A, Peter JH. Heart block in patients with sleep apnoea. Thorax 1998;53:S29–S32
131.Hoffstein V, Mateika S. Cardiac-arrhythmias, snoring, and sleep-apnea. Chest 1994;106:466–71
132.Koehler U, Schafer H. Is obstructive sleep apnea (OSA) a risk factor for myocardial infarction and cardiac arrhythmias in patients with coronary heart disease (CHD)? Sleep 1996;19:283–6
133.Koehler U, Fus E, Grimm W, Pankow W, Schafer H, Stammnitz A, Peter JH. Heart block in patients with obstructive sleep apnoea: pathogenetic factors and effects of treatment. Eur Respir J 1998;11:434–9
134.Miller WP. Cardiac arrhytmias and conduction disturbances in the sleep apnea syndrome: prevalence and significance. Am J Med 1982;73:317–21
135.Tilkian AG, Guilleminault C, Schroeder JS, Lehrman KL, Simmons FB, Dement WC. Sleep-induced apnea syndrome. Prevalence of cardiac arrhythmias and their reversal after tracheostomy. Am J Med 1977;63:348–58
136.Marrone O, Bonsignore MR. Acute and chronic influences of obstructive sleep apnoea on the pulmonary circulation. Monaldi Arch Chest Dis 1997;52:263–7
137.Fletcher EC, Proctor M, Yu J, Zhang J, Guardiola JJ, Hornung C, Bao G. Pulmonary edema develops after recurrent obstructive apneas. Am J Respir Crit Care Med 1999;160:1688–96
138.Arieff AI. Fatal postoperative pulmonary edema: pathogenesis and literature review. Chest 1999;115:1371–7
139.Scarbrough FE, Wittenberg JM, Smith BR, Adcock DK. Pulmonary edema following postoperative laryngospasm: case reports and review of the literature. Anesth Prog 1997;44:110–16
140.Burke AJ, Duke SG, Clyne S, Khoury SA, Chiles C, Matthews BL. Incidence of pulmonary edema after tracheotomy for obstructive sleep apnea. Otolaryngol Head Neck Surg 2001;125:319–23
141.Cormack RS, Lehane J. Difficult tracheal intubation in obstetrics. Anaesthesia 1984;39:1105–11
142.Gentil B, Delarminat JM, Boucherez C, Lienhart A. Difficult intubation and obstructive sleep-apnea syndrome. Br J Anaesth 1994;72:368
143.Kim JA, Lee JJ. Preoperative predictors of difficult intubation in patients with obstructive sleep apnea syndrome. Can J Anaesth 2006;53:393–7
144.Ezri T, Medalion B, Weisenberg M, Szmuk P, Warters RD, Charuzi I. Increased body mass index per se is not a predictor of difficult laryngoscopy. Can J Anaesth 2003;50:179–83
145.Hiremath AS, Hillman DR, James AL, Noffsinger WJ, Platt PR, Singer SL. Relationship between difficult tracheal intubation and obstructive sleep apnoea. Br J Anaesth 1998;80:606–11
146.Chung F, Herrera F, Shenderey A, Yegneswaran B, Shapiro C. Should surgical patients with difficult intubation be referred to sleep clinic for polysomnography? Anesthesiology 2006; 105:A986 Ref type: Abstract
147.Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1981;1:862–5
148.Yamamoto H, Akashiba T, Kosaka N, Ito D, Horie T. Long-term effects nasal continuous positive airway pressure on daytime sleepiness, mood and traffic accidents in patients with obstructive sleep apnoea. Respir Med 2000;94:87–90
149.Bolitschek J, Schmeiser-Rieder A, Schobersberger R, Rosenberger A, Kunze M, Aigner K. Impact of nasal continuous positive airway pressure treatment on quality of life in patients with obstructive sleep apnoea. Eur Respir J 1998;11:890–4
150.Munoz A, Mayoralas LR, Barbe F, Pericas J, Agusti AG. Long-term effects of CPAP on daytime functioning in patients with sleep apnoea syndrome. Eur Respir J 2000;15:676–81
151.Borak J, Cieslicki JK, Koziej M, Matuszewski A, Zielinski J. Effects of CPAP treatment on psychological status in patients with severe obstructive sleep apnoea. J Sleep Res 1996;5:123–7
152.Derderian SS, Bridenbaugh RH, Rajagopal KR. Neuropsychologic symptoms in obstructive sleep apnea improve after treatment with nasal continuous positive airway pressure. Chest 1988;94:1023–7
153.Tarrac SE. A description of intraoperative and postanesthesia complication rates. J Perianesth Nurs 2006;21:88–96
154.Faccenda JF, Mackay TW, Boon NA, Douglas NJ. Randomized placebo-controlled trial of continuous positive airway pressure on blood pressure in the sleep apnea-hypopnea syndrome. Am J Respir Crit Care Med 2001;163:344–8
155. Dhillon S, Chung SA, Fargher T, Huterer N, Shapiro CM. Sleep apnea, hypertension, and the effects of continuous positive airway pressure. Am J Hypertension 2005;18:594–600
156. Hla KM, Skatrud JB, Finn L, Palta M, Young T. The effect of correction of sleep-disordered breathing on BP in untreated hypertension. Chest 2002;122:1125–32
157. Pepperell JCT, Ramdassingh-Dow S, Crosthwaite N, Mullins R, Jenkinson C, Stradling JR, Davies RJO. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 2002;359:204–10
158. Akashiba T, Minemura H, Yamamoto H, Kosaka N, Saito O, Horie T. Nasal continuous positive airway pressure changes blood pressure ‘non- dippers’ to ‘dippers’ in patients with obstructive sleep apnea. Sleep 1999;22:849–53
159. Minemura H, Akashiba T, Yamamoto H, Akahoshi T, Kosaka N, Horie T. Acute effects of nasal continuous positive airway pressure on 24-hour blood pressure and catecholamines in patients with obstructive sleep apnea. Intern Med 1998;37:1009–13
160. Dursunoglu N, Dursunoglu D, Cuhadaroglu C, Kilicaslan Z. Acute effects of automated continuous positive airway pressure on blood pressure in patients with sleep apnea and hypertension. Respiration 2005;72:150–5
161. Liston R, Deegan PC, McCreery C, McNicholas WT. Role of respiratory sleep disorders in the pathogenesis of nocturnal angina and arrhythmias. Postgrad Med J 1994;70:275–80
162. Randazzo DN, Winters SL, Schweitzer P. Obstructive sleep apnea-induced supraventricular tachycardia. J Electrocardiol 1996;29:65–7
163. Becker H, Brandenburg U, Peter JH, von Wichert P. Reversal of sinus arrest and atrioventricular conduction block in patients with sleep apnea during nasal continuous positive airway pressure. Am J Respir Crit Care Med 1995;151:215–18
164. Belozeroff V, Berry RB, Sassoon CS, Khoo MC. Effects of CPAP therapy on cardiovascular variability in obstructive sleep apnea: a closed-loop analysis. Am J Physiol Heart Circ Physiol 2002;282:H110–H121
165. Krieger J, Grucker D, Sforza E, Chambron J, Kurtz D. Left ventricular ejection fraction in obstructive sleep apnea. Effects of long-term treatment with nasal continuous positive airway pressure. Chest 1991;100:917–21
166. Mansfield DR, Gollogly NC, Kaye DM, Richardson M, Bergin P, Naughton MT. Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure. Am J Respir Crit Care Med 2004;169:361–6
167. Bonsignore MR, Parati G, Insalaco G, Castiglioni P, Marrone O, Romano S, Salvaggio A, Mancia G, Bonsignore G, Di RM. Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP. Eur Respir J 2006;27:128–35
168. Kaye DM, Mansfield D, Naughton MT. Continuous positive airway pressure decreases myocardial oxygen consumption in heart failure. Clin Sci (Lond) 2004;106:599–603
169. Rennotte MT, Baele P, Aubert G, Rodenstein DO. Nasal continuous positive airway pressure in the perioperative management of patients with obstructive sleep apnea submitted to surgery. Chest 1995;107:367–74
170. Squadrone V, Coha M, Cerutti E, Schellino MM, Biolino P, Occella P, Belloni G, Vilianis G, Fiore G, Cavallo F, Ranieri VM. Continuous positive airway pressure for treatment of postoperative hypoxemia: a randomized controlled trial. JAMA 2005;293:589–95
171. Delclaux C, L’Her E, Alberti C, Mancebo J, Abroug F, Conti G, Guerin C, Schortgen F, Lefort Y, Antonelli M, Lepage E, Lemaire F, Brochard L. Treatment of acute hypoxemic nonhypercapnic respiratory insufficiency with continuous positive airway pressure delivered by a face mask: a randomized controlled trial. JAMA 2000;284:2352–60
172. Drummond GB, Stedul K, Kingshott R, Rees K, Nimmo AF, Wraith P, Douglas NJ. Automatic CPAP compared with conventional treatment for episodic hypoxemia and sleep disturbance after major abdominal surgery. Anesthesiology 2002;96:817–26
173. Practice parameters for the indications for polysomnography and related procedures. Polysomnography task force, am sleep disorders association standards of practice committee. Sleep 1997;20:406–22
174. Douglas NJ, Polo O. Pathogenesis of obstructive sleep apnoea/hypopnoea syndrome. Lancet 1994;344:653–5
175. Gurubhagavatula I, Maislin G, Pack AI. An algorithm to stratify sleep apnea risk in a sleep disorders clinic population. Am J Respir Crit Care Med 2001;164:1904–9
176. Kump K, Whalen C, Tishler PV, Browner I, Ferrette V, Strohl KP, Rosenberg C, Redline S. Assessment of the validity and utility of a sleep-symptom questionnaire. Am J Respir Crit Care Med 1994;150:735–41
177. Maislin G, Pack AI, Kribbs NB, Smith PL, Schwartz AR, Kline LR, Schwab RJ, Dinges DF. A survey screen for prediction of apnea. Sleep 1995;18:158–66
178. Strauss R, Browner W. Letter to the Editor: Sensitivity, specificity and positive predictive value of Berlin Questionnaire. Ann Intern Med 2000;132:758–9
179. Chung F, Yegneswaran B, Liao P, Chung SA, Vairavanathan S, Islam S, Khajehdehi A, Shapiro CM. STOP questionnaire: a tool to screen patients for obstructive sleep apnea. Anesthesiology 2008;108:812–21
180. Chung F, Yegneswaran B, Liao P, Chung SA, Vairavanathan S, Islam S, Khajehdehi A, Shapiro CM. Validation of the Berlin questionnaire and American Society of Anesthesiologists checklists as screening tools for obstructive sleep apnea in surgical patients. Anesthesiology 2008;108:822–30
181. Gali B, Whalen FX Jr, Gay PC, Olson EJ, Schroeder DR, Plevak DJ, Morgenthaler TI. Management plan to reduce risks in perioperative care of patients with presumed obstructive sleep apnea syndrome. J Clin Sleep Med 2007;3:582–8
182. Biro P, Kaplan V, Bloch KE. Anesthetic management of a patient with obstructive sleep apnea syndrome and difficult airway access. J Clin Anesth 1995;7:417–21
183. Ulnick KM, Debo RF. Postoperative treatment of the patient with obstructive sleep apnea. Otolaryngol Head Neck Surg 2000;122:233–6
184. Gonzalez R, Haines K, Nelson LG, Gallagher SF, Murr MM. Predictive factors of thromboembolic events in patients undergoing Roux-en-Y gastric bypass. Surg Obes Relat Dis 2006;2:30–5
185. Helling TS. Operative experience and follow-up in a cohort of patients with a BMI > or =70 kg/m2
. Obes Surg 2005;15:482–5
186. Safadi BY, Kieran JA, Hall RG, Morton JM, Bellatorre N, Shinoda E, Johnson PJ, Curet MJ, Wren SM. Introducing laparoscopic Roux-en-Y gastric bypass at a Veterans Affairs medical facility. Am J Surg 2004;188:606–10
187. Ballantyne GH, Svahn J, Capella RF, Capella JF, Schmidt HJ, Wasielewski A, Davies RJ. Predictors of prolonged hospital stay following open and laparoscopic gastric bypass for morbid obesity: body mass index, length of surgery, sleep apnea, asthma, and the metabolic syndrome. Obes Surg 2004;14:1042–50
188. Knill RL, Moote CA, Skinner MI, Rose EA. Anesthesia with abdominal surgery leads to intense REM sleep during the first postoperative week. Anesthesiology 1990;73:52–61
189. Okabe S, Hida W, Kikuchi Y, Taguchi O, Takishima T, Shirato K. Upper airway muscle activity during REM and non-REM sleep of patients with obstructive apnea. Chest 1994;106:767–73
190. Findley LJ, Wilhoit SC, Suratt PM. Apnea duration and hypoxemia during REM sleep in patients with obstructive sleep apnea. Chest 1985;87:432–6
191. Garpestad E, Ringler J, Parker JA, Remsburg S, Weiss JW. Sleep stage influences the hemodynamic response to obstructive apneas. Am J Respir Crit Care Med 1995;152:199–203
192. Rosenberg J, Rasmussen GI, Wojdemann KR, Kirkeby LT, Jorgensen LN, Kehlet H. Ventilatory pattern and associated episodic hypoxaemia in the late postoperative period in the general surgical ward. Anaesthesia 1999;54:323–8
193. Taylor S, Kirton OC, Staff I, Kozol RA. Postoperative day one: a high risk period for respiratory events. Am J Surg 2005;190:752–6
194. Boushra NN. Anaesthetic management of patients with sleep apnoea syndrome. Can J Anaesth 1996;43:599–616
195. Chung F, Imarengiaye C. Management of sleep apnea in adults. Can J Anaesth 2002;49:R1–R6
196. Jain SS, Dhand R. Perioperative treatment of patients with obstructive sleep apnea. Curr Opin Pulm Med 2004;10:482–8
197. Kaw R, Michota F, Jaffer A, Ghamande S, Auckley D, Golish J. Unrecognized sleep apnea in the surgical patient: implications for the perioperative setting. Chest 2006;129:198–205
198. Guggenberger H, Schroeder TH, Vonthein R, Dieterich HJ, Shernan SK, Eltzschig HK. Remifentanil or sufentanil for coronary surgery: comparison of postoperative respiratory impairment. Eur J Anaesthesiol 2006;23:832–40
199. Wuesten R, Van AH, Glass PS, Buerkle H. Assessment of depth of anesthesia and postoperative respiratory recovery after remifentanil- versus alfentanil-based total intravenous anesthesia in patients undergoing ear-nose-throat surgery. Anesthesiology 2001;94:211–17
200. Strum EM, Szenohradszki J, Kaufman WA, Anthone GJ, Manz IL, Lumb PD. Emergence and recovery characteristics of desflurane versus sevoflurane in morbidly obese adult surgical patients: a prospective, randomized study. Anesth Analg 2004;99:1848–53, table of contents
201. Pawlik MT, Hansen E, Waldhauser D, Selig C, Kuehnel TS. Clonidine premedication in patients with sleep apnea syndrome: a randomized, double-blind, placebo-controlled study. Anesth Analg 2005;101:1374–80
202. Etches RC. Respiratory depression associated with patient-controlled analgesia: a review of eight cases. Can J Anaesth 1994;41:125–32
203. Shapiro A, Zohar E, Zaslansky R, Hoppenstein D, Shabat S, Fredman B. The frequency and timing of respiratory depression in 1524 postoperative patients treated with systemic or neuraxial morphine. J Clin Anesth 2005;17:537–42
204. Sveticic G, Eichenberger U, Curatolo M. Safety of mixture of morphine with ketamine for postoperative patient-controlled analgesia: an audit with 1026 patients. Acta Anaesthesiol Scand 2005;49:870–5
205. Hagle ME, Lehr VT, Brubakken K, Shippee A. Respiratory depression in adult patients with intravenous patient-controlled analgesia. Orthop Nurs 2004;23:18–27
206. Virtaniemi J, Kokki H, Nikanne E, Aho M. Ketoprofen and fentanyl for pain after uvulopalatopharyngoplasty and tonsillectomy. Laryngoscope 1999;109:1950–4
207. Pyati S, Gan TJ. Perioperative pain management. CNS Drugs 2007;21:185–211
208. White PF. The changing role of non-opioid analgesic techniques in the management of postoperative pain. Anesth Analg 2005;101:S5–S22
209. Joshi GP. Multimodal analgesia techniques for ambulatory surgery. Int Anesthesiol Clin 2005;43:197–204
210. Nikanne E, Virtaniemi J, Aho M, Kokki H. Ketoprofen for postoperative pain after uvulopalatopharyngoplasty and tonsillectomy: two-week follow-up study. Otolaryngol Head Neck Surg 2003;129:577–81
211. Borckardt JJ, Weinstein M, Reeves ST, Kozel FA, Nahas Z, Smith AR, Byrne TK, Morgan K, George MS. Postoperative left prefrontal repetitive transcranial magnetic stimulation reduces patient-controlled analgesia use. Anesthesiology 2006;105:557–62
212. Meoli AL, Rosen CL, Kristo D, Kohrman M, Gooneratne N, Aguillard RN, Fayle R, Troell R, Kramer R, Casey KR, Coleman J Jr. Upper airway management of the adult patient with obstructive sleep apnea in the perioperative period–avoiding complications. Sleep 2003;26:1060–5
213. Williams PM, Strome M, Eliachar I, Lavertu P, Wood BG, Vito KJ. Impact of steroids on recovery after uvulopalatopharyngoplasty. Laryngoscope 1999;109:1941–6
214. Ezri T, Muzikant G, Medalion B, Szmuk P, Charuzi I, Susmallian S. Anesthesia for restrictive bariatric surgery (gastric bypass not included): laparoscopic vs open procedures. Int J Obes Relat Metab Disord 2004;28:1157–62
215. Kezirian EJ, Weaver EM, Yueh B, Khuri SF, Daley J, Henderson WG. Risk factors for serious complication after uvulopalatopharyngoplasty. Arch Otolaryngol Head Neck Surg 2006;132:1091–8
216. Harmon JD, Morgan W, Chaudhary B. Sleep apnea: morbidity and mortality of surgical treatment. South Med J 1989;82:161–4
217. Kezirian EJ, Weaver EM, Yueh B, Deyo RA, Khuri SF, Daley J, Henderson W. Incidence of serious complications after uvulopalatopharyngoplasty. Laryngoscope 2004;114:450–3
218. Damato S, Frigo V, Dell’Oca M, Negretto GG, Tarsia P. Utility of monitoring breathing during night hours in COPD patients undergoing long-term oxygen therapy. Monaldi Arch Chest Dis 1997;52:106–11
219. Isono S, Tanaka A, Nishino T. Lateral position decreases collapsibility of the passive pharynx in patients with obstructive sleep apnea.[see comment]. Anesthesiology 2002;97:780–5
220. Neill AM, Angus SM, Sajkov D, McEvoy RD. Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea. Am J Respir Crit Care Med 1997;155:199–204
221. Penzel T, Moller M, Becker HF, Knaack L, Peter JH. Effect of sleep position and sleep stage on the collapsibility of the upper airways in patients with sleep apnea. Sleep 2001;24:90–5
222. Spiegel JH, Raval TH. Overnight hospital stay is not always necessary after uvulopalatopharyngoplasty. Laryngoscope 2005;115:167–71
223. Dundar A, Gerek M, Ozunlu A, Tetiser S. Patient selection and surgical results in obstructive sleep apnea. Eur Arch Otorhinolaryngol 1997;254:S157–S161
224. Millman RP, Carlisle CC, Rosenberg C, Kahn D, McRae R, Kramer NR. Simple predictors of uvulopalatopharyngoplasty outcome in the treatment of obstructive sleep apnea. Chest 2000;118:1025–30
This article has been cited 15 time(s).
Anasthesiologie Intensivmedizin Notfallmedizin SchmerztherapiePssst ... AINS-Secrets! Today in General SurgeryAnasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie
Revista Portuguesa De PneumologiaPatients with a high risk for obstructive sleep apnea syndrome: Postoperative respiratory complicationsRevista Portuguesa De Pneumologia
Journal of Physiology and Pharmacology
Remifentanil Reversibly Abolished Phrenic Long Term Facilitation in Rats Subjected to Acute Intermittent Hypoxia
Journal of Physiology and Pharmacology, 64(4):
Sleep and BreathingPostoperative complications in obstructive sleep apneaSleep and Breathing
Revue Des Maladies RespiratoiresEvaluation of preoperative non-invasive ventilation in thoracic surgery for lung cancer: The preOVNI study GFPC 12-01Revue Des Maladies Respiratoires
Digestive Diseases and SciencesProne Positioning of Obese Patients for Colonoscopy Results in Shortened Cecal Intubation Times: A Randomized TrialDigestive Diseases and Sciences
Respiratory Physiology & NeurobiologyEffects of clonidine on breathing during sleep and susceptibility to central apnoeaRespiratory Physiology & Neurobiology
Obesity SurgerySugammadex Allows Fast-Track Bariatric SurgeryObesity Surgery
Sleep and BreathingSubjective sleepiness and daytime functioning in bariatric patients with obstructive sleep apneaSleep and Breathing
Sleep MedicineObstructive sleep apnea screening and postoperative mortality in a large surgical cohortSleep Medicine
British Journal of AnaesthesiaProportion of surgical patients with undiagnosed obstructive sleep apnoeaBritish Journal of Anaesthesia
Chronic Respiratory DiseaseThe use of practice guidelines by the American Society of Anesthesiologists for the identification of surgical patients at high risk of sleep apneaChronic Respiratory Disease
Respiratory Physiology & NeurobiologyThe effects of a single mild dose of morphine on chemoreflexes and breathing in obstructive sleep apneaRespiratory Physiology & Neurobiology
American Journal of MedicinePortable Monitoring for Obstructive Sleep Apnea: The Horse Is Out of the Barn-Avoiding PitfallsAmerican Journal of Medicine
Sleep MedicineClinical significance of sleep-disordered breathing induced by sedatives during ablation of atrial fibrillationSleep Medicine
© 2008 International Anesthesia Research Society
What does "Remember me" mean?
By checking this box, you'll stay logged in until you logout. You'll get easier access to your articles, collections,
media, and all your other content, even if you close your browser or shut down your
To protect your most sensitive data and activities (like changing your password),
we'll ask you to re-enter your password when you access these services.
What if I'm on a computer that I share with others?
If you're using a public computer or you share this computer with others, we recommend
that you uncheck the "Remember me" box.
Data is temporarily unavailable. Please try again soon.
Readers Of this Article Also Read