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Obstructive sleep apnoea and anaesthesia
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Obstructive sleep apnoea and anaesthesia
Learning objectives After reading this article, you should be able to: C understand the pathophysiology of obstructive sleep apnoea and its treatment C recognize the patient at risk presenting for surgery C plan an appropriate approach to safe anaesthesia and postoperative care
Peter JH Venn
Abstract Obstructive sleep apnoea (OSA) is a common condition affecting approximately 4% of middle-aged individuals. The condition is more common in men with a history of snoring. Patients experience fragmented sleep caused by repetitive obstruction of the upper airway during sleep. There is mounting evidence that OSA is associated with metabolic syndrome. Metabolic syndrome comprises hypertension and type 2 diabetes, with associated disturbances of lipid metabolism and central obesity that predisposes to cardiovascular disease. Sleep disruption causes excessive daytime sleepiness and patients may be a danger to themselves or others, especially when driving. Anaesthetists meet the condition frequently, and should have a high index of suspicion when assessing overweight middle-aged patients for surgery. Patients may present for ENT or maxillofacial surgery as part of the management of the condition, but the group at greatest risk comprises those who are unrecognized and therefore untreated, who present for surgery for an unrelated condition. Recent screening questionnaires have been developed to aid the anaesthetist in spotting at risk patients, and in predicting the likelihood of postoperative complications. Difficulty with intubation is common, and airway obstruction may occur under anaesthesia if opioid and sedative drugs are used without caution. Many patients also suffer from acid reflux, which may complicate induction of anaesthesia. A plan for difficult airway management is essential, and consideration should be given to carrying out an awake intubation under topical anaesthesia of the upper airway. Knowledge of treatment with nasal continuous positive airway pressure is necessary, and all staff involved should be experienced in the management of such patients during the perioperative period.
Definition and presentation of obstructive sleep apnoea OSA is a repetitive obstruction of the upper airway during sleep that causes arterial hypoxaemia, and often leads to a reduced quality of sleep. When excessive daytime sleepiness (EDS) ensues, the condition is referred to as obstructive sleep apnoea syndrome (OSAS). Typically, there is a history of worsening snoring over the preceding few years, often causing patients and partners to sleep separately. Airway obstruction may arise from a number of discrete anatomical features in the upper airway but, in the absence of abnormal anatomy, it is relaxation of the genioglossus and pharyngeal constrictor muscles during sleep that allows collapse of the airway. There is evidence that these muscles are hypertonic during wakefulness, unmasking fatigue during sleep with excessive relaxation. Physical associations with OSA include being male, a collar size of 17 inches (43 cm) or greater, a wide tongue base and often some degree of retrognathia. The association with a high body mass index (BMI) means that these patients are potentially difficult to intubate. Medical associations include hypothyroidism, acromegaly and glycogen storage diseases, whilst congenital causes include Down’s syndrome, Pierre-Robin sequence and other facial anomalies. Obstruction from hypertrophied tonsils should always be considered. There is now good evidence that OSA is associated with the development of metabolic syndrome. This is sometimes referred to as syndrome Z. The World Health Organization has developed criteria for the diagnosis of metabolic syndrome, and these are listed in Table 2. The International Diabetes Federation (IDF) and the National Cholesterol Education Program (NCEP) in the USA have reiterated these criteria, each with minor alterations. All relate insulin resistance and increased risk of developing type 2 diabetes to cardiovascular risk. Sleep deprivation has recently been shown to cause increased resistance to the action of insulin in healthy young male volunteers. The incidence of the syndrome worldwide is rising at an alarming rate, with estimates of 50 million sufferers in the USA. The British Nutrition Foundation suggests that 25% of adults in the UK show evidence of the syndrome. Physiologically, there is mounting evidence that cyclical alterations in arterial oxygen saturation caused by OSA lead to hypoxia/reperfusion injury. This causes excessive release of oxygen radicals, which outstrips the ability of naturally occurring intracellular anti-oxidants with consequent lipid peroxidation in the cell membrane. There is evidence that this leads to cellular damage and the development of endothelial damage and atheroma formation. Thus, recurrent night-time hypoxaemia can lead to several cardiovascular complications, including arterial and pulmonary hypertension, cor pulmonale, and an increased incidence of heart
Keywords Body mass index; CPAP; metabolic syndrome; obstructive sleep apnoea
Worldwide, obstructive sleep apnoea (OSA) is the most common medical disorder of sleep, affecting 4e5% of middle-aged men and 2e4% of middle-aged women. Sleep disorders have been classified by the American Sleep Disorders Association (Table 1). Anaesthetists are frequently involved with patients presenting either for surgery to treat the condition itself, or for unrelated surgery. This article reviews the presenting features, investigations and treatment of OSA in adults. It concludes with management during the perioperative period.
Peter JH Venn FRCA is a Consultant Anaesthetist at the Queen Victoria Hospital, East Grinstead, UK and Clinical Director of the Sleep Disorder Centre, East Grinstead, West Sussex, UK. Conflicts of interest: none declared.
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disease and cerebrovascular events. Furthermore, patients with diagnosed metabolic syndrome have a sixfold increase in cardiovascular risk compared with age-matched controls. Preoperative assessment of patients with OSA must therefore include an evaluation of the patient’s metabolic and cardiovascular status, with the increased risks brought to the attention of the patient and the surgical team. There is unequivocal evidence that treating OSA reduces raised arterial blood pressure. To meet the criteria for diagnosis of OSA, complete obstruction of the airway should occur repeatedly during sleep for more than 10 seconds in the presence of continued movement of the diaphragm, leading to a reduction of more than 4% in arterial oxygen saturation (SaO2) from the baseline. Attempted inspiration becomes increasingly vigorous as arterial oxygen desaturation progresses, finally leading to a partial arousal from sleep with sudden reopening of the airway. This causes an explosive intake of breath, which is usually accompanied by some movement of the body or twitching of the limbs as partial arousal from sleep occurs. Hyperventilation follows for a short time, but as sleep deepens again airway obstruction returns, causing the cycle to restart. The worst cases may have up to 60 of these cycles per hour (apnoea index) giving 400e500 episodes in a sleep period of 8 hours, with each dip in oxygen saturation as low as 60%. The resulting fragmentation of sleep leads to a lack of refreshment on awakening with EDS as measured by the Epworth sleepiness score (Figure 1). Epworth scores above 8 out of the maximum 24 possible are regarded as above normal, and a score of greater than 12 affects social and family life as well as daytime performance e particularly driving ability. Sufferers are consequently a potential danger to themselves and to others. Drivers of large goods vehicles are predisposed to the condition partly as a result of their typical lifestyle. Some individuals experience lesser degrees of upper airway obstruction that does not lead to overt arterial oxygen desaturation. Sleep arousals may still occur, probably because of the increased upper airway resistance causing increased diaphragmatic work. The resulting reduction in tidal volume is called hypopnoea, and often results in EDS in the absence of defined OSA. Cessation of diaphragm movement resulting in absence of ventilation is called central sleep apnoea (CSA), equivalent to Cheynes Stokes respiration, and is more likely in elderly patients with left ventricular dysfunction. Central sleep apnoea can also co-exist with obstructive apnoeas owing to alterations in the gain of the feedback loop, and the combination of the two has recently been termed complex sleep apnoea. The combination of the two often leads to a greater fall in oxygen saturation. CSA is more likely to occur episodically in patients with obesity hypoventilation syndrome.
Classification outline of sleep disorders published by the American Academy of Sleep Medicine 1 Dyssomnias A. Intrinsic sleep disorders B. Extrinsic sleep disorders C. Circadian rhythm sleep disorders
2 Parasomnias A. B. C. D.
Arousal disorders Sleep-wake transition disorders Parasomnias usually associated with REM sleep Other parasomnias
3 Medical/psychiatric sleep disorders A. Associated with mental disorders B. Associated with neurological disorders C. Associated with other medical disorders
1A Intrinsic sleep disorders 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.
Psychophysiological insomnia Sleep state misperception Idiopathic insomnia Narcolepsy Recurrent hypersomnia Idiopathic hypersomnia Post-traumatic hypersomnia Obstructive sleep apnoea syndrome Central sleep apnoea syndrome Central alveolar hypoventilation syndrome Periodic limb movement disorder Restless legs syndrome
REM, rapid eye movement.
Table 1
Criteria for diagnosis of metabolic syndrome as laid down by the World Health Organization (1999) The presence of either diabetes mellitus or impaired glucose tolerance, impaired fasting glucose and insulin resistance are necessary, together with two or more of the following: Criterion Value Body weight W/H ratio >0.9 in males Raised waist/hip W/H ratio >0.85 in females (W/H) ratio Central obesity and increased intraabdominal fat Body mass index >30 kg/m2 High-density lipoprotein <1.7 mmol/litre Low-density lipoprotein >0.9 mmol/litre Arterial blood pressure >140/90 mmHg Micro-albuminuria Urine albumin excretion >20 mg/minute Inflammatory state Elevated C-reactive protein
Clinical presentation History The symptoms of snoring, apnoea and EDS usually lead to consultations with ENT surgeons, but other medical complications may precipitate alternative presentations to chest physicians, neurologists or cardiologists. Furthermore, daytime sleepiness can mimic clinical depression and lead to psychiatric referral.
Table 2
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The Epworth sleepiness score How likely are you to fall asleep or doze in the situations described in the boxes below, in contrast to just feeling tired? Use the following scale to choose the most appropriate number for each situation. Not at all Slight chance Moderate chance High chance
0 1 2 3
Activity
Score
Sitting and reading Watching TV Sitting inactive in a public place (e.g. in a theatre or meeting) Sitting quietly after lunch without alcohol Sitting in a car as a passenger for 1 hour without a break Lying down to rest in the afternoon when circumstances permit Figure 2 The typical facial features of a patient with obstructive sleep apnoea. Notice the width of the neck.
Talking to someone In a car, while stopped for a few minutes in traffic
become necessary as part of the ongoing management of the condition.
Total
Examination A full examination of the upper airway should be undertaken, with attention to the collar size, Mallampati score, dental occlusion and pharyngeal volume. Tonsillar hypertrophy should be recorded because this may be the underlying problem, and usually is so in children presenting with OSA. Any retrognathia should be recorded. The tongue may have crenulations at the side e small indentations on the lateral borders made by the teeth e which indicate that it is being squeezed inwards and backwards into the pharyngeal space when the mouth is closed. The pharyngeal volume is often reduced with redundant mucosal folds limiting the lateral diameter (Figure 3). Ability to sublux the jaw forwards should be measured because good degrees of movement of greater than 5 mm may allow treatment with mandibular advancement devices rather than continuous positive airway pressure devices.
Figure 1 The Epworth Sleepiness Score, used to assess the amount of daytime dysfunction due to fragmented sleep at night. This is the most widely used scoring system in the world at the present time, although other scoring systems are becoming popular.
Although the clinical presentation varies, the typical patient is male, with a current BMI of 30 kg/m2 or more, and an increase in collar size of 1.5 inches (4 cm) to around 17 inches (43 cm) over adulthood (Figure 2). There is a history of increasing snoring in all positions during sleep, with reports of sleep apnoea and daytime sleepiness. A full medical history should include details of the presenting complaint, as well as enquiry about nocturia, loss of libido, nightmares and sudden awakening in the night with fear, all of which are associated. Gastro-oesophageal reflux is common in this group and may lead to sudden awaking with choking and dyspnoea. A detailed cardiovascular history, including the pathological end-organ consequences of hypertension, should be sought, as well as prescribed and non-prescribed drugs, tobacco and alcohol consumption. Many patients will be taking antihypertensive drugs, hypocholesterolaemics and aspirin. Unfortunately, some patients present on night sedatives, their morning lack of refreshment being attributed to insomnia. Benzodiazepines, particularly, tend to worsen pharyngeal relaxation, and exacerbate the situation. A commonly associated feature is poor subjective ability to breathe through the nose, and previous nasal surgery may already have been carried out, or
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Investigations Investigations include blood tests to exclude other causes of EDS such as hypothyroidism and narcolepsy, but the diagnosis is readily confirmed by carrying out a sleep study called a polysomnogram. Full polysomnography includes monitoring of the chest movement, airflow dynamics, heart rate and blood pressure, arterial oxygen saturation and the electroencephalogram (EEG), all during sleep. EEG monitoring is used to assess the stage of sleep (stages I, II, III, IV non-rapid eye movement (NREM), or REM sleep) and is a valuable tool in the diagnosis of complex sleep disorders. REM sleep is also staged by recording
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supervision while the correct level of airway pressure measured in centimetres of water (cmH2O) is set for the individual, although there are now machines that detect reduced airflow and adjust the pressure automatically. While the pressure energy should be high enough to overcome the pharyngeal collapse, it should not be so high as to reach the lower airway and raise the functional residual capacity, because this in itself disrupts sleep. Pressure requirements range from as low as 5 cmH2O to as high as 15e20 cmH2O depending on severity. Figure 5 shows the beneficial effect on the arterial oxygen saturation of commencing CPAP in a patient with OSA. Compliance to treatment of patients who use CPAP at home has been studied. Clearly, non-compliance brings no benefit or relief from symptoms but every clinic has its group of such patients. Good compliance predictors include self-referral due to EDS (as opposed to referral due to snoring under pressure from partners), a patent nasal airway and, most importantly, relief of daytime sleepiness on nCPAP with an improved quality of life. It remains unclear why, despite adequate compliance, about 10% of patients remain excessively sleepy by day. Compliance is recorded in hours of usage by a metre built into the device, and at least 4 hours of use per night is necessary for a reduction in EDS as evaluated by pre- and post-treatment Epworth scores. There are no serious side effects of nCPAP treatment, but minor side effects may decrease compliance and benefit. Of these, inflammation of the nasal mucosa from the pressurized airflow often leads to symptoms of rhinitis and nasal blockage that can be troublesome during early treatment, and is sometimes a reason for reduced or non-compliance. Nasal blockage may result in mouth breathing with loss of pharyngeal pressure, causing airflow entering through the nose to escape through the mouth. Such patients awaken with sore and dry throats that may
Figure 3 The crowded oropharynx of a patient with obstructive sleep apnoea. Crenulations (indentations) are apparent on the side of the tongue (a), and the uvula (b) is reddened and swollen from snoring.
the electro-oculogram and the sub-mental electromyogram, which show activity and lack of activity, respectively. However, cardiorespiratory monitoring alone is adequate to diagnose OSA. Infrared video recording combined with sound is a very useful supplement. The arterial oxygen saturation trace from a patient with florid OSA is shown in Figure 4.
Treatment of OSA The gold standard of treatment for OSA is to submit the patient to nasal continuous positive airway pressure (nCPAP) whilst asleep. Throughout the breathing cycle, CPAP is applied to the pharynx to overcome the obstructive forces due to pharyngeal collapse. CPAP is best initiated in hospital for one night under
Oximetry trace from a patient with obstructive sleep apnoea
Oximetry trace from a patient with severe obstructive sleep apnoea Index number: SS123456C Date of birth: 14/06/1955
Index number: SS789123C Date of birth: 16/03/1961
Date of study: 20/12/2007 Start time: 13:00:38 Duration: 03:57:42
Hour 1
Hour 1
2
2
3
3
4
4
5
5
6
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7
Date of study: 30/11/2007 Start time: 00:04:20 Duration: 06:33:56
A
8
8 0
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0
60
10
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Minutes
Minutes
y-axis from 70% to 100%
y-axis from 70% to 100%
Each line represents 1 hour of sleep. There are repetitive dips in the saturation throughout the period of sleep
Continuous positive airway pressure was commenced at point A, resulting in an immediate improvement in arterial oxygenation
Figure 4
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Figure 5
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be distressing. Nasal blockage can be treated with topical steroid sprays, but responds better to humidification of the pressurized airflow, the humidifier often being an integral part of the machine design. When the nasal airway persistently blocks despite simple measures, a full face-mask covering the nose and mouth may be helpful, with resort to nasal surgery if all else fails. Other problems of using nCPAP include noise emission from the device disturbing the sleep of the partner or patient, discomfort from the mask and feelings of claustrophobia. Although the most noticeable effect of nCPAP is to reduce daytime sleepiness, physiological benefits also occur. Hypertensive patients treated with nCPAP show a beneficial reduction in both systolic and diastolic blood pressure, the effect of which appears to increase with time. The strong association of asthma with OSA also benefits, as does nocturia, the reduction of which improves sleep quality in itself. With time, patients become very adept in managing their nCPAP therapy, putting the mask on, adjusting it and going to sleep within only a few minutes. Some patients can be treated for mild OSA with mandibular advancement devices, which posture the mandible forwards, pulling the tongue away from the posterior pharyngeal wall via the suprahyoid muscles. Mandibular advancement depends upon a partial dislocation of the temporomandibular joint. Patients who benefit most from this treatment tend to be retrognathic with a class II dental malocclusion. They have snoring predominantly from behind the tongue that may cause varying degrees of upper airway obstruction during sleep, even in the absence of true OSA. More recently radiofrequency coagulation of the palate (somnoplasty) and ablation of the base of the tongue have been used with some success in the treatment of palatal snoring, having replaced the unpleasant operation of uvulopalatopharyngoplasty (UPPP). There is no place for UPPP in the management of sleep apnoea; postoperative infection and the later and more serious complication of velopharyngeal incompetence combined with poor results having led to a sharp decline in its use. Laser-assisted palatoplasty is still carried out on the unwary, and many patients present to sleep clinics with OSA who have previously undergone such surgery. Selected patients may benefit from bimaxillary osteotomy which advances the mid-face and mandible to increase space in the nasopharynx and oropharynx. In the author’s department, all patients referred to orthodontics for advice about treatment with mandibular splints, are given the opportunity to see a maxillofacial surgeon also, to discuss this as a permanent solution.
sleep studies prior to admission. However, the undiagnosed patient presenting for unrelated surgery poses the greatest risk, and when there is a suspicion of sleep apnoea, elective surgery should be postponed until the patient has been fully investigated and treated. A scoring system has recently been proposed and validated by the American Society of Anesthesiologists (ASA) to help anaesthetists to screen patients for the likelihood of OSA in the absence of previous formal investigations. STOPB-ang comprises a short eightpoint questionnaire (Box 1), which shows a sensitivity of 100% in predicting an apnoea/hypopnoea index (AHI) of greater than 30 events per hour, thus indicating significant OSA. The outcome after surgery is more likely to be complicated in patients with high AHIs, and further predictive scoring has been developed (Box 2). Where OSA is suspected, planning for surgery should begin before admission because special investigations may be needed as part of the perioperative work-up. Previous anaesthetic records are invaluable if available. All patients using CPAP at home should be instructed to bring their device with them on the day of admission for use during their hospital stay, and the staff looking after them on the ward and in the recovery room should be familiar with CPAP. Assessment of the airway should always include a history of snoring or apnoea during sleep. Most patients will be aware of the disharmony in the bedroom due to their condition even if no medical help has previously been sought. Daytime sleepiness suggests some degree of airway obstruction during sleep that may well be transposed to anaesthesia. Examination and prediction of the difficult airway has been extensively documented in the anaesthetic literature, and the degree of mouth opening, Mallampati score and thyromental distance should be recorded, together with a Wilson summation score. A frank discussion with the patient is necessary about the increased risk of general anaesthesia and should include a detailed explanation of the anaesthetic technique deemed appropriate. Obesity and acid reflux may affect the planning of the anaesthetic. Premedication with sedatives and opioids should be avoided or used with extreme caution if deemed absolutely necessary. Constant vigilance is required once these drugs have been
The STOPB-ang questionnaire developed by the ASA to help anaesthetists recognize patients at risk from OSA. If three or more points are positive, OSA is likely
Obstructive sleep apnoea and anaesthesia S e Snoring (observed during sleep) T e Tiredness (in the daytime) O e Observed (sleep disordered breathing by sleeping partner) P e Pressure (hypertension) B e Body mass index (greater than 35 kg/m2) a e age (above 50 years) n e neck (collar size greater than 16.5 inches) g e gender (male)
Preoperative assessment The most serious risk for patients with OSA is loss of the airway owing to anaesthetic, sedative and opioid drugs, and increased risk of anaesthesia from clinical obesity and the consequences of hypertension. Most sufferers remain undiagnosed, and therefore reliance cannot be put upon patients to volunteer information about their symptoms. Patients may present for surgery as part of the overall management of their sleep apnoea, most often on the nasal airway, palate, tongue or tonsils, with the added complication of shared airway anaesthesia. An increasing number of patients now present for bariatric surgery, either gastric banding or bypass, and most surgeons now refer these patients for formalized
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ASA, American Society of Anesthesiologists; OSA, obstructive sleep apnoea.
Box 1
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Intraoperative local anaesthesia for pain relief will allow sparing administration of opioid drugs, and regional techniques using infusions are useful adjuncts in the postoperative period. Although avoidance of sedative and opioid drugs during the perioperative period is the recommended practice, sedatives and opioids have reportedly been used in conjunction with CPAP therapy without complication in the postoperative period.
Likelihood of complications arising in the postoperative period in patients with diagnosed OSA A: Severity of sleep apnoea based on sleep study (ie, AHI) or clinical indicators if sleep study not available None ¼ 0; Mild OSA ¼ 1; Moderate OSA ¼ 2; Severe OSA ¼ 3 Subtract 1 point in patients using CPAP or bilevel pressure ventilation preoperatively and postoperatively, and add 1 point in a patient with PaCO2 >50 mmHg
Postoperative management The patient’s CPAP device should be sent to the recovery room for use immediately on emergence from anaesthesia. Under no circumstances should the patient be left unattended or without cardiorespiratory monitoring until fully awake, and even then consideration should be given to the enterohepatic circulation of any sedative or opioid drugs. Up to 20% of patients require major medical intervention including re-intubation in the immediate postoperative period. Nursing staff should be familiar with such complications and ready to maintain a difficult airway if needed, and the anaesthetist should obviously be immediately available. Subsequent management in an intensive care or highdependency unit should be considered for any major surgical intervention, especially vascular surgery, in which significant oxygen desaturation has been recorded during the first two postoperative nights, possibly because of rebound levels of REM sleep following anaesthesia. A
B: Invasiveness of surgery and anaesthesia Superficial surgery under local or peripheral nerve block anaesthesia without sedation ¼ 0 Superficial surgery with moderate sedation or general anaesthesia or peripheral surgery under spinal or epidural anaesthesia (with no more than moderate sedation) ¼ 1 Peripheral surgery with general anaesthesia or airway surgery with moderate sedation ¼ 2 Major surgery or airway surgery under general anaesthesia ¼ 3 C: Requirement for postoperative opioid None ¼ 0 Low-dose oral opioids ¼ 1 High-dose oral opioids or parenteral or neuraxial opioids ¼ 3 D: Estimation of perioperative risk Overall score ¼ score of A þ greater score of either B or C Patients with overall score 4 may be at increased perioperative risk from OSA. Patients with a score ¼ 5 may be at significantly increased perioperative risk from OSA
FURTHER READING 1 Logan AG, Tkacova R, Perlikowski SM, et al. Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreceptor reflex. Eur Respir J 2003 Feb; 21: 241e7. 2 Ezri E, Medalion B, Weisenberg M, Szmuk P, Warters RD. Increased body mass index per se is not a predictor of difficult laryngoscopy. Can J Anaesth 2003; 50: 179e83. 3 Parish AM, Adam T, Facchiano L. Relationship of metabolic syndrome and obstructive sleep apnea. J Clin Sleep Med 2007; 3: 467e72. 4 Lavie L, Vishnevski A, Lavie P. Evidence for lipid peroxidation in obstructive sleep apnoea. Sleep 2004; 27: 123e8. 5 Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire: a tool to screen patients for obstructive sleep apnea. Anesthesiology 2008; 108: 812e21. 6 Gross JB, Bachenberg KL, Benumof JL, et al. American Society of Anesthesiologists Task Force on Perioperative Management. 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: 1081e93. 7 Benumof JL. Obstructive sleep apnea in the adult obese patient: implications for airway management. Anesthesiol Clin North America 2002; 20: 789e811. 8 Eastwood PR, Szollosi I, Platt PR, Hillman DR. Comparison of upper airway collapse during general anaesthesia and sleep. Lancet 2002; 359: 1207e9. 9 Adenotonsillectomy for obstructive sleep apnoea in children. Cochrane Database Syst Rev 2003. CD003136. 10 Brown KA, Morin I, Hickey C, Manoukian JJ, Nixon GM, Brouillett RT. Urgent adenotonsillectomy: an analysis of risk factors associated with postoperative respiratory morbidity. Anesthesiology 2003; 99: 586e95.
AHI, apnoea/hypopnoea index; CPAP, continuous positive airway pressure; OSA, obstructive sleep apnoea.
Box 2
administered, and monitoring of the arterial oxygen saturation should be considered. Anaesthetic technique These patients present a formidable challenge in terms of intubation, extubation and postoperative analgesia, and the service of an experienced and senior anaesthetist is advisable. Although morbid obesity in itself is not a predictor of difficult direct laryngoscopy, a history of OSA is so, with Cormick and Lehane grade III and IV views in 90% of OSA patients in one study. No global rules can be applied to anaesthetic technique, and patients should each be considered according to their individual needs. However, induction under full monitoring is required and most agree that tracheal intubation is preferable to use of the laryngeal mask airway. A full range of aids for difficult intubation should be ready and attendant staff should be familiar with the use of such equipment. Awake fibre-optic intubation under topical anaesthesia has been suggested for all patients with OSA, although obtunded airway reflexes after local anaesthesia have been reported to cause increased levels of obstruction in the postoperative period. Whatever technique is chosen for induction and intubation, at least two plans should be made to maintain the airway in the event of failure of the first. Extubation should not be undertaken until the patient is awake.
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Obstructive sleep apnoea and anaesthesia
Learning objectives After reading this article, you should be able to: C understand the pathophysiology of obstructive sleep apnoea and its treatment C recognize the patient at risk presenting for surgery C plan an appropriate approach to safe anaesthesia and postoperative care
Peter JH Venn
Abstract Obstructive sleep apnoea (OSA) is a common condition affecting approximately 4% of middle-aged individuals. The condition is more common in men with a history of snoring. Patients experience fragmented sleep caused by repetitive obstruction of the upper airway during sleep. There is mounting evidence that OSA is associated with metabolic syndrome. Metabolic syndrome comprises hypertension and type 2 diabetes, with associated disturbances of lipid metabolism and central obesity that predisposes to cardiovascular disease. Sleep disruption causes excessive daytime sleepiness and patients may be a danger to themselves or others, especially when driving. Anaesthetists meet the condition frequently, and should have a high index of suspicion when assessing overweight middle-aged patients for surgery. Patients may present for ENT or maxillofacial surgery as part of the management of the condition, but the group at greatest risk comprises those who are unrecognized and therefore untreated, who present for surgery for an unrelated condition. Recent screening questionnaires have been developed to aid the anaesthetist in spotting at risk patients, and in predicting the likelihood of postoperative complications. Difficulty with intubation is common, and airway obstruction may occur under anaesthesia if opioid and sedative drugs are used without caution. Many patients also suffer from acid reflux, which may complicate induction of anaesthesia. A plan for difficult airway management is essential, and consideration should be given to carrying out an awake intubation under topical anaesthesia of the upper airway. Knowledge of treatment with nasal continuous positive airway pressure is necessary, and all staff involved should be experienced in the management of such patients during the perioperative period.
Definition and presentation of obstructive sleep apnoea OSA is a repetitive obstruction of the upper airway during sleep that causes arterial hypoxaemia, and often leads to a reduced quality of sleep. When excessive daytime sleepiness (EDS) ensues, the condition is referred to as obstructive sleep apnoea syndrome (OSAS). Typically, there is a history of worsening snoring over the preceding few years, often causing patients and partners to sleep separately. Airway obstruction may arise from a number of discrete anatomical features in the upper airway but, in the absence of abnormal anatomy, it is relaxation of the genioglossus and pharyngeal constrictor muscles during sleep that allows collapse of the airway. There is evidence that these muscles are hypertonic during wakefulness, unmasking fatigue during sleep with excessive relaxation. Physical associations with OSA include being male, a collar size of 17 inches (43 cm) or greater, a wide tongue base and often some degree of retrognathia. The association with a high body mass index (BMI) means that these patients are potentially difficult to intubate. Medical associations include hypothyroidism, acromegaly and glycogen storage diseases, whilst congenital causes include Down’s syndrome, Pierre-Robin sequence and other facial anomalies. Obstruction from hypertrophied tonsils should always be considered. There is now good evidence that OSA is associated with the development of metabolic syndrome. This is sometimes referred to as syndrome Z. The World Health Organization has developed criteria for the diagnosis of metabolic syndrome, and these are listed in Table 2. The International Diabetes Federation (IDF) and the National Cholesterol Education Program (NCEP) in the USA have reiterated these criteria, each with minor alterations. All relate insulin resistance and increased risk of developing type 2 diabetes to cardiovascular risk. Sleep deprivation has recently been shown to cause increased resistance to the action of insulin in healthy young male volunteers. The incidence of the syndrome worldwide is rising at an alarming rate, with estimates of 50 million sufferers in the USA. The British Nutrition Foundation suggests that 25% of adults in the UK show evidence of the syndrome. Physiologically, there is mounting evidence that cyclical alterations in arterial oxygen saturation caused by OSA lead to hypoxia/reperfusion injury. This causes excessive release of oxygen radicals, which outstrips the ability of naturally occurring intracellular anti-oxidants with consequent lipid peroxidation in the cell membrane. There is evidence that this leads to cellular damage and the development of endothelial damage and atheroma formation. Thus, recurrent night-time hypoxaemia can lead to several cardiovascular complications, including arterial and pulmonary hypertension, cor pulmonale, and an increased incidence of heart
Keywords Body mass index; CPAP; metabolic syndrome; obstructive sleep apnoea
Worldwide, obstructive sleep apnoea (OSA) is the most common medical disorder of sleep, affecting 4e5% of middle-aged men and 2e4% of middle-aged women. Sleep disorders have been classified by the American Sleep Disorders Association (Table 1). Anaesthetists are frequently involved with patients presenting either for surgery to treat the condition itself, or for unrelated surgery. This article reviews the presenting features, investigations and treatment of OSA in adults. It concludes with management during the perioperative period.
Peter JH Venn FRCA is a Consultant Anaesthetist at the Queen Victoria Hospital, East Grinstead, UK and Clinical Director of the Sleep Disorder Centre, East Grinstead, West Sussex, UK. Conflicts of interest: none declared.
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disease and cerebrovascular events. Furthermore, patients with diagnosed metabolic syndrome have a sixfold increase in cardiovascular risk compared with age-matched controls. Preoperative assessment of patients with OSA must therefore include an evaluation of the patient’s metabolic and cardiovascular status, with the increased risks brought to the attention of the patient and the surgical team. There is unequivocal evidence that treating OSA reduces raised arterial blood pressure. To meet the criteria for diagnosis of OSA, complete obstruction of the airway should occur repeatedly during sleep for more than 10 seconds in the presence of continued movement of the diaphragm, leading to a reduction of more than 4% in arterial oxygen saturation (SaO2) from the baseline. Attempted inspiration becomes increasingly vigorous as arterial oxygen desaturation progresses, finally leading to a partial arousal from sleep with sudden reopening of the airway. This causes an explosive intake of breath, which is usually accompanied by some movement of the body or twitching of the limbs as partial arousal from sleep occurs. Hyperventilation follows for a short time, but as sleep deepens again airway obstruction returns, causing the cycle to restart. The worst cases may have up to 60 of these cycles per hour (apnoea index) giving 400e500 episodes in a sleep period of 8 hours, with each dip in oxygen saturation as low as 60%. The resulting fragmentation of sleep leads to a lack of refreshment on awakening with EDS as measured by the Epworth sleepiness score (Figure 1). Epworth scores above 8 out of the maximum 24 possible are regarded as above normal, and a score of greater than 12 affects social and family life as well as daytime performance e particularly driving ability. Sufferers are consequently a potential danger to themselves and to others. Drivers of large goods vehicles are predisposed to the condition partly as a result of their typical lifestyle. Some individuals experience lesser degrees of upper airway obstruction that does not lead to overt arterial oxygen desaturation. Sleep arousals may still occur, probably because of the increased upper airway resistance causing increased diaphragmatic work. The resulting reduction in tidal volume is called hypopnoea, and often results in EDS in the absence of defined OSA. Cessation of diaphragm movement resulting in absence of ventilation is called central sleep apnoea (CSA), equivalent to Cheynes Stokes respiration, and is more likely in elderly patients with left ventricular dysfunction. Central sleep apnoea can also co-exist with obstructive apnoeas owing to alterations in the gain of the feedback loop, and the combination of the two has recently been termed complex sleep apnoea. The combination of the two often leads to a greater fall in oxygen saturation. CSA is more likely to occur episodically in patients with obesity hypoventilation syndrome.
Classification outline of sleep disorders published by the American Academy of Sleep Medicine 1 Dyssomnias A. Intrinsic sleep disorders B. Extrinsic sleep disorders C. Circadian rhythm sleep disorders
2 Parasomnias A. B. C. D.
Arousal disorders Sleep-wake transition disorders Parasomnias usually associated with REM sleep Other parasomnias
3 Medical/psychiatric sleep disorders A. Associated with mental disorders B. Associated with neurological disorders C. Associated with other medical disorders
1A Intrinsic sleep disorders 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.
Psychophysiological insomnia Sleep state misperception Idiopathic insomnia Narcolepsy Recurrent hypersomnia Idiopathic hypersomnia Post-traumatic hypersomnia Obstructive sleep apnoea syndrome Central sleep apnoea syndrome Central alveolar hypoventilation syndrome Periodic limb movement disorder Restless legs syndrome
REM, rapid eye movement.
Table 1
Criteria for diagnosis of metabolic syndrome as laid down by the World Health Organization (1999) The presence of either diabetes mellitus or impaired glucose tolerance, impaired fasting glucose and insulin resistance are necessary, together with two or more of the following: Criterion Value Body weight W/H ratio >0.9 in males Raised waist/hip W/H ratio >0.85 in females (W/H) ratio Central obesity and increased intraabdominal fat Body mass index >30 kg/m2 High-density lipoprotein <1.7 mmol/litre Low-density lipoprotein >0.9 mmol/litre Arterial blood pressure >140/90 mmHg Micro-albuminuria Urine albumin excretion >20 mg/minute Inflammatory state Elevated C-reactive protein
Clinical presentation History The symptoms of snoring, apnoea and EDS usually lead to consultations with ENT surgeons, but other medical complications may precipitate alternative presentations to chest physicians, neurologists or cardiologists. Furthermore, daytime sleepiness can mimic clinical depression and lead to psychiatric referral.
Table 2
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The Epworth sleepiness score How likely are you to fall asleep or doze in the situations described in the boxes below, in contrast to just feeling tired? Use the following scale to choose the most appropriate number for each situation. Not at all Slight chance Moderate chance High chance
0 1 2 3
Activity
Score
Sitting and reading Watching TV Sitting inactive in a public place (e.g. in a theatre or meeting) Sitting quietly after lunch without alcohol Sitting in a car as a passenger for 1 hour without a break Lying down to rest in the afternoon when circumstances permit Figure 2 The typical facial features of a patient with obstructive sleep apnoea. Notice the width of the neck.
Talking to someone In a car, while stopped for a few minutes in traffic
become necessary as part of the ongoing management of the condition.
Total
Examination A full examination of the upper airway should be undertaken, with attention to the collar size, Mallampati score, dental occlusion and pharyngeal volume. Tonsillar hypertrophy should be recorded because this may be the underlying problem, and usually is so in children presenting with OSA. Any retrognathia should be recorded. The tongue may have crenulations at the side e small indentations on the lateral borders made by the teeth e which indicate that it is being squeezed inwards and backwards into the pharyngeal space when the mouth is closed. The pharyngeal volume is often reduced with redundant mucosal folds limiting the lateral diameter (Figure 3). Ability to sublux the jaw forwards should be measured because good degrees of movement of greater than 5 mm may allow treatment with mandibular advancement devices rather than continuous positive airway pressure devices.
Figure 1 The Epworth Sleepiness Score, used to assess the amount of daytime dysfunction due to fragmented sleep at night. This is the most widely used scoring system in the world at the present time, although other scoring systems are becoming popular.
Although the clinical presentation varies, the typical patient is male, with a current BMI of 30 kg/m2 or more, and an increase in collar size of 1.5 inches (4 cm) to around 17 inches (43 cm) over adulthood (Figure 2). There is a history of increasing snoring in all positions during sleep, with reports of sleep apnoea and daytime sleepiness. A full medical history should include details of the presenting complaint, as well as enquiry about nocturia, loss of libido, nightmares and sudden awakening in the night with fear, all of which are associated. Gastro-oesophageal reflux is common in this group and may lead to sudden awaking with choking and dyspnoea. A detailed cardiovascular history, including the pathological end-organ consequences of hypertension, should be sought, as well as prescribed and non-prescribed drugs, tobacco and alcohol consumption. Many patients will be taking antihypertensive drugs, hypocholesterolaemics and aspirin. Unfortunately, some patients present on night sedatives, their morning lack of refreshment being attributed to insomnia. Benzodiazepines, particularly, tend to worsen pharyngeal relaxation, and exacerbate the situation. A commonly associated feature is poor subjective ability to breathe through the nose, and previous nasal surgery may already have been carried out, or
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Investigations Investigations include blood tests to exclude other causes of EDS such as hypothyroidism and narcolepsy, but the diagnosis is readily confirmed by carrying out a sleep study called a polysomnogram. Full polysomnography includes monitoring of the chest movement, airflow dynamics, heart rate and blood pressure, arterial oxygen saturation and the electroencephalogram (EEG), all during sleep. EEG monitoring is used to assess the stage of sleep (stages I, II, III, IV non-rapid eye movement (NREM), or REM sleep) and is a valuable tool in the diagnosis of complex sleep disorders. REM sleep is also staged by recording
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supervision while the correct level of airway pressure measured in centimetres of water (cmH2O) is set for the individual, although there are now machines that detect reduced airflow and adjust the pressure automatically. While the pressure energy should be high enough to overcome the pharyngeal collapse, it should not be so high as to reach the lower airway and raise the functional residual capacity, because this in itself disrupts sleep. Pressure requirements range from as low as 5 cmH2O to as high as 15e20 cmH2O depending on severity. Figure 5 shows the beneficial effect on the arterial oxygen saturation of commencing CPAP in a patient with OSA. Compliance to treatment of patients who use CPAP at home has been studied. Clearly, non-compliance brings no benefit or relief from symptoms but every clinic has its group of such patients. Good compliance predictors include self-referral due to EDS (as opposed to referral due to snoring under pressure from partners), a patent nasal airway and, most importantly, relief of daytime sleepiness on nCPAP with an improved quality of life. It remains unclear why, despite adequate compliance, about 10% of patients remain excessively sleepy by day. Compliance is recorded in hours of usage by a metre built into the device, and at least 4 hours of use per night is necessary for a reduction in EDS as evaluated by pre- and post-treatment Epworth scores. There are no serious side effects of nCPAP treatment, but minor side effects may decrease compliance and benefit. Of these, inflammation of the nasal mucosa from the pressurized airflow often leads to symptoms of rhinitis and nasal blockage that can be troublesome during early treatment, and is sometimes a reason for reduced or non-compliance. Nasal blockage may result in mouth breathing with loss of pharyngeal pressure, causing airflow entering through the nose to escape through the mouth. Such patients awaken with sore and dry throats that may
Figure 3 The crowded oropharynx of a patient with obstructive sleep apnoea. Crenulations (indentations) are apparent on the side of the tongue (a), and the uvula (b) is reddened and swollen from snoring.
the electro-oculogram and the sub-mental electromyogram, which show activity and lack of activity, respectively. However, cardiorespiratory monitoring alone is adequate to diagnose OSA. Infrared video recording combined with sound is a very useful supplement. The arterial oxygen saturation trace from a patient with florid OSA is shown in Figure 4.
Treatment of OSA The gold standard of treatment for OSA is to submit the patient to nasal continuous positive airway pressure (nCPAP) whilst asleep. Throughout the breathing cycle, CPAP is applied to the pharynx to overcome the obstructive forces due to pharyngeal collapse. CPAP is best initiated in hospital for one night under
Oximetry trace from a patient with obstructive sleep apnoea
Oximetry trace from a patient with severe obstructive sleep apnoea Index number: SS123456C Date of birth: 14/06/1955
Index number: SS789123C Date of birth: 16/03/1961
Date of study: 20/12/2007 Start time: 13:00:38 Duration: 03:57:42
Hour 1
Hour 1
2
2
3
3
4
4
5
5
6
6
7
7
Date of study: 30/11/2007 Start time: 00:04:20 Duration: 06:33:56
A
8
8 0
10
20
30
40
50
0
60
10
20
30
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50
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Minutes
Minutes
y-axis from 70% to 100%
y-axis from 70% to 100%
Each line represents 1 hour of sleep. There are repetitive dips in the saturation throughout the period of sleep
Continuous positive airway pressure was commenced at point A, resulting in an immediate improvement in arterial oxygenation
Figure 4
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Figure 5
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be distressing. Nasal blockage can be treated with topical steroid sprays, but responds better to humidification of the pressurized airflow, the humidifier often being an integral part of the machine design. When the nasal airway persistently blocks despite simple measures, a full face-mask covering the nose and mouth may be helpful, with resort to nasal surgery if all else fails. Other problems of using nCPAP include noise emission from the device disturbing the sleep of the partner or patient, discomfort from the mask and feelings of claustrophobia. Although the most noticeable effect of nCPAP is to reduce daytime sleepiness, physiological benefits also occur. Hypertensive patients treated with nCPAP show a beneficial reduction in both systolic and diastolic blood pressure, the effect of which appears to increase with time. The strong association of asthma with OSA also benefits, as does nocturia, the reduction of which improves sleep quality in itself. With time, patients become very adept in managing their nCPAP therapy, putting the mask on, adjusting it and going to sleep within only a few minutes. Some patients can be treated for mild OSA with mandibular advancement devices, which posture the mandible forwards, pulling the tongue away from the posterior pharyngeal wall via the suprahyoid muscles. Mandibular advancement depends upon a partial dislocation of the temporomandibular joint. Patients who benefit most from this treatment tend to be retrognathic with a class II dental malocclusion. They have snoring predominantly from behind the tongue that may cause varying degrees of upper airway obstruction during sleep, even in the absence of true OSA. More recently radiofrequency coagulation of the palate (somnoplasty) and ablation of the base of the tongue have been used with some success in the treatment of palatal snoring, having replaced the unpleasant operation of uvulopalatopharyngoplasty (UPPP). There is no place for UPPP in the management of sleep apnoea; postoperative infection and the later and more serious complication of velopharyngeal incompetence combined with poor results having led to a sharp decline in its use. Laser-assisted palatoplasty is still carried out on the unwary, and many patients present to sleep clinics with OSA who have previously undergone such surgery. Selected patients may benefit from bimaxillary osteotomy which advances the mid-face and mandible to increase space in the nasopharynx and oropharynx. In the author’s department, all patients referred to orthodontics for advice about treatment with mandibular splints, are given the opportunity to see a maxillofacial surgeon also, to discuss this as a permanent solution.
sleep studies prior to admission. However, the undiagnosed patient presenting for unrelated surgery poses the greatest risk, and when there is a suspicion of sleep apnoea, elective surgery should be postponed until the patient has been fully investigated and treated. A scoring system has recently been proposed and validated by the American Society of Anesthesiologists (ASA) to help anaesthetists to screen patients for the likelihood of OSA in the absence of previous formal investigations. STOPB-ang comprises a short eightpoint questionnaire (Box 1), which shows a sensitivity of 100% in predicting an apnoea/hypopnoea index (AHI) of greater than 30 events per hour, thus indicating significant OSA. The outcome after surgery is more likely to be complicated in patients with high AHIs, and further predictive scoring has been developed (Box 2). Where OSA is suspected, planning for surgery should begin before admission because special investigations may be needed as part of the perioperative work-up. Previous anaesthetic records are invaluable if available. All patients using CPAP at home should be instructed to bring their device with them on the day of admission for use during their hospital stay, and the staff looking after them on the ward and in the recovery room should be familiar with CPAP. Assessment of the airway should always include a history of snoring or apnoea during sleep. Most patients will be aware of the disharmony in the bedroom due to their condition even if no medical help has previously been sought. Daytime sleepiness suggests some degree of airway obstruction during sleep that may well be transposed to anaesthesia. Examination and prediction of the difficult airway has been extensively documented in the anaesthetic literature, and the degree of mouth opening, Mallampati score and thyromental distance should be recorded, together with a Wilson summation score. A frank discussion with the patient is necessary about the increased risk of general anaesthesia and should include a detailed explanation of the anaesthetic technique deemed appropriate. Obesity and acid reflux may affect the planning of the anaesthetic. Premedication with sedatives and opioids should be avoided or used with extreme caution if deemed absolutely necessary. Constant vigilance is required once these drugs have been
The STOPB-ang questionnaire developed by the ASA to help anaesthetists recognize patients at risk from OSA. If three or more points are positive, OSA is likely
Obstructive sleep apnoea and anaesthesia S e Snoring (observed during sleep) T e Tiredness (in the daytime) O e Observed (sleep disordered breathing by sleeping partner) P e Pressure (hypertension) B e Body mass index (greater than 35 kg/m2) a e age (above 50 years) n e neck (collar size greater than 16.5 inches) g e gender (male)
Preoperative assessment The most serious risk for patients with OSA is loss of the airway owing to anaesthetic, sedative and opioid drugs, and increased risk of anaesthesia from clinical obesity and the consequences of hypertension. Most sufferers remain undiagnosed, and therefore reliance cannot be put upon patients to volunteer information about their symptoms. Patients may present for surgery as part of the overall management of their sleep apnoea, most often on the nasal airway, palate, tongue or tonsils, with the added complication of shared airway anaesthesia. An increasing number of patients now present for bariatric surgery, either gastric banding or bypass, and most surgeons now refer these patients for formalized
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ASA, American Society of Anesthesiologists; OSA, obstructive sleep apnoea.
Box 1
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Intraoperative local anaesthesia for pain relief will allow sparing administration of opioid drugs, and regional techniques using infusions are useful adjuncts in the postoperative period. Although avoidance of sedative and opioid drugs during the perioperative period is the recommended practice, sedatives and opioids have reportedly been used in conjunction with CPAP therapy without complication in the postoperative period.
Likelihood of complications arising in the postoperative period in patients with diagnosed OSA A: Severity of sleep apnoea based on sleep study (ie, AHI) or clinical indicators if sleep study not available None ¼ 0; Mild OSA ¼ 1; Moderate OSA ¼ 2; Severe OSA ¼ 3 Subtract 1 point in patients using CPAP or bilevel pressure ventilation preoperatively and postoperatively, and add 1 point in a patient with PaCO2 >50 mmHg
Postoperative management The patient’s CPAP device should be sent to the recovery room for use immediately on emergence from anaesthesia. Under no circumstances should the patient be left unattended or without cardiorespiratory monitoring until fully awake, and even then consideration should be given to the enterohepatic circulation of any sedative or opioid drugs. Up to 20% of patients require major medical intervention including re-intubation in the immediate postoperative period. Nursing staff should be familiar with such complications and ready to maintain a difficult airway if needed, and the anaesthetist should obviously be immediately available. Subsequent management in an intensive care or highdependency unit should be considered for any major surgical intervention, especially vascular surgery, in which significant oxygen desaturation has been recorded during the first two postoperative nights, possibly because of rebound levels of REM sleep following anaesthesia. A
B: Invasiveness of surgery and anaesthesia Superficial surgery under local or peripheral nerve block anaesthesia without sedation ¼ 0 Superficial surgery with moderate sedation or general anaesthesia or peripheral surgery under spinal or epidural anaesthesia (with no more than moderate sedation) ¼ 1 Peripheral surgery with general anaesthesia or airway surgery with moderate sedation ¼ 2 Major surgery or airway surgery under general anaesthesia ¼ 3 C: Requirement for postoperative opioid None ¼ 0 Low-dose oral opioids ¼ 1 High-dose oral opioids or parenteral or neuraxial opioids ¼ 3 D: Estimation of perioperative risk Overall score ¼ score of A þ greater score of either B or C Patients with overall score 4 may be at increased perioperative risk from OSA. Patients with a score ¼ 5 may be at significantly increased perioperative risk from OSA
FURTHER READING 1 Logan AG, Tkacova R, Perlikowski SM, et al. Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreceptor reflex. Eur Respir J 2003 Feb; 21: 241e7. 2 Ezri E, Medalion B, Weisenberg M, Szmuk P, Warters RD. Increased body mass index per se is not a predictor of difficult laryngoscopy. Can J Anaesth 2003; 50: 179e83. 3 Parish AM, Adam T, Facchiano L. Relationship of metabolic syndrome and obstructive sleep apnea. J Clin Sleep Med 2007; 3: 467e72. 4 Lavie L, Vishnevski A, Lavie P. Evidence for lipid peroxidation in obstructive sleep apnoea. Sleep 2004; 27: 123e8. 5 Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire: a tool to screen patients for obstructive sleep apnea. Anesthesiology 2008; 108: 812e21. 6 Gross JB, Bachenberg KL, Benumof JL, et al. American Society of Anesthesiologists Task Force on Perioperative Management. 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: 1081e93. 7 Benumof JL. Obstructive sleep apnea in the adult obese patient: implications for airway management. Anesthesiol Clin North America 2002; 20: 789e811. 8 Eastwood PR, Szollosi I, Platt PR, Hillman DR. Comparison of upper airway collapse during general anaesthesia and sleep. Lancet 2002; 359: 1207e9. 9 Adenotonsillectomy for obstructive sleep apnoea in children. Cochrane Database Syst Rev 2003. CD003136. 10 Brown KA, Morin I, Hickey C, Manoukian JJ, Nixon GM, Brouillett RT. Urgent adenotonsillectomy: an analysis of risk factors associated with postoperative respiratory morbidity. Anesthesiology 2003; 99: 586e95.
AHI, apnoea/hypopnoea index; CPAP, continuous positive airway pressure; OSA, obstructive sleep apnoea.
Box 2
administered, and monitoring of the arterial oxygen saturation should be considered. Anaesthetic technique These patients present a formidable challenge in terms of intubation, extubation and postoperative analgesia, and the service of an experienced and senior anaesthetist is advisable. Although morbid obesity in itself is not a predictor of difficult direct laryngoscopy, a history of OSA is so, with Cormick and Lehane grade III and IV views in 90% of OSA patients in one study. No global rules can be applied to anaesthetic technique, and patients should each be considered according to their individual needs. However, induction under full monitoring is required and most agree that tracheal intubation is preferable to use of the laryngeal mask airway. A full range of aids for difficult intubation should be ready and attendant staff should be familiar with the use of such equipment. Awake fibre-optic intubation under topical anaesthesia has been suggested for all patients with OSA, although obtunded airway reflexes after local anaesthesia have been reported to cause increased levels of obstruction in the postoperative period. Whatever technique is chosen for induction and intubation, at least two plans should be made to maintain the airway in the event of failure of the first. Extubation should not be undertaken until the patient is awake.
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