Elsevier

Sleep Medicine Reviews

Volume 8, Issue 6, December 2004, Pages 459-471
Sleep Medicine Reviews

Clinical Review
Obstructive sleep apnoea and anaesthesia

https://doi.org/10.1016/j.smrv.2004.07.002Get rights and content

Summary

Upper airway obstruction is common during both anaesthesia and sleep, as a result of loss of muscle tone present during wakefulness. Patients with obstructive sleep apnoea (OSA) are vulnerable during anaesthesia and sedation as the effects of loss of wakefulness are compounded by drug-induced depression of muscle activity and of arousal responses, so that they cannot respond to asphyxia. Conversely, those with ‘difficult’ airways during anaesthesia, either because of problems with maintenance of airway patency without tracheal intubation or because intubation itself is problematic, are at increased risk of OSA. These relationships have clinical importance. On the one hand identification of patients with OSA forewarns the anaesthetist of potential difficulty with airway maintenance intra- and postoperatively, influencing choice of anaesthetic technique and postoperative nursing environment. On the other hand difficulty with airway maintenance during anaesthesia should prompt further investigation for the possibility of OSA.

Introduction

Maintenance of upper airway patency is a shared obsession of anaesthetists and sleep physicians as anaesthesia and sleep both predispose to upper airway obstruction, largely because of the loss of wakeful pharyngeal muscle tone. If the states are compared, anaesthesia could be considered a ‘worst case’ for the upper airway because it is a state of unrousable unconsciousness with a relatively homogeneous and profound loss of muscle tone once surgical anaesthesia has been established. Asphyxia results if upper airway obstruction occurs during anaesthesia and is unrecognised or untreated. In contrast, sleep is an inhomogeneous state with varying stages and associated variations in muscle tone and severity of obstructive sleep apnoea (OSA). Unlike anaesthesia, sleep is a state of rousable unconsciousness and upper airway obstructions are terminated by arousals, which provide some protection but momentarily disrupt sleep and are responsible for associated daytime lethargy and sleepiness.

Perhaps not surprisingly, because it is anatomical narrowing that renders the airway vulnerable to loss of muscle tone in either state, the tendencies to obstruct during anaesthesia and sleep appear to be related in individuals.1 This association is clinically important: an airway that is prone to collapse during anaesthesia indicates a predisposition to OSA and vice versa. Furthermore, as OSA is associated with upper airway narrowing its presence may indicate increased difficulty with tracheal intubation.2 The reverse is certainly true: those who prove difficult to intubate are at substantially increased risk of OSA.3 The implications of these relationships are significant: the presence of OSA should be considered in patients with ‘difficult airways’ under anaesthesia, either because of difficulty maintaining patency without tracheal intubation or because intubation itself is problematic. Conversely, the possibility of such difficulties should be considered in patients with OSA.

This common ground has inferences for clinical assessment. Signs that anaesthetists use to predict difficult intubation (such as mandibular size and angulation and pharyngeal appearances) have predictive value for OSA3, 4 and are therefore of value to sleep physicians in assessing their patients. Equally, preoperative assessment of patients for anaesthesia is enhanced by the simple addition of questions that elicit the cardinal symptoms of OSA (habitual snoring, witnessed apnoeas, and excessive daytime sleepiness) because they raise the possibility of a ‘difficult airway’ requiring specific perioperative management. An additional benefit is the opportunity to diagnose OSA itself, which while common remains notoriously under-diagnosed.5

While we have reviewed these problems in the past from point of view of anaesthesia6, 7 (and have drawn, with permission, on this work) the purpose of the present review is to explore and develop the common ground that should exist between anaesthetists and sleep physicians in their efforts to understand and manage upper airway obstruction. Relevant considerations include the pathogenetic mechanisms underlying obstruction during anaesthesia and sleep and their interrelationship, sites of obstruction in both states, shared predisposing factors, and peri-operative management of patients with known or suspected OSA, where there is a coalescence of clinical interest.

Section snippets

Pathogenesis of upper airway obstruction during anaesthesia and sleep

From the posterior nares to the larynx the upper airway is unprotected by bone or cartilage and is susceptible to obstruction.8 Pharyngeal muscle tone prevents this during wakefulness. However, tone decreases with both sleep and anaesthesia primarily because of reduced central drive, which is largely attributable to decreased cortical influences and chemosensitivity seen in both states. Upper airway activity is also partly dependent on reflexes originating within the upper airway which are also

Sites of upper airway obstruction during anaesthesia and sleep

Upper airway collapse tends to occur at the site(s) of maximal narrowing or flaccidity. In children tonsillar hypertrophy is a common cause of pharyngeal narrowing and OSA, with craniofacial abnormality a much less usual contributor. In adults discrete pathological lesions in the upper airway are infrequent causes of OSA. Usually it is attributable to an airway that is narrow because of predisposing changes in craniofacial morphology, pharyngeal configuration and/or obesity, compounded by the

Patient factors predisposing to upper airway collapse

Vulnerability to obstruction of the pharynx during sleep or anaesthesia increases wherever factors are present that narrow it, increase pressure around it, reduce pressure within it, or increase compliance of its walls. While, as already noted, specific discrete pathological lesions are uncommon causes of such a tendency in adults they should be looked for along with other more general morphological predispositions. Narrowing may occur as the result of abnormalities intraluminally (e.g. a

Perioperative management of patients with OSA

OSA is common and so anaesthetists will often deal with patients with this problem. A substantial proportion of them will not have been previously diagnosed, as OSA is a notoriously under-diagnosed condition. Indeed, as 1 in 5 adults have at least mild OSA5 and approximately 10% of the population have a general anaesthetic each year in developed nations, it is likely that many OSA sufferers have been submitted to this procedure and treated for postoperative pain with their OSA remaining

Conclusion

The difficult upper airway manifests itself as problems with maintenance of airway patency and/or instrumentation under anaesthesia. The skeletal and neuromuscular characteristics that predispose to these difficulties also predispose to upper airway obstruction during sleep. Behaviour of the upper airway during sleep can provide important information regarding its likely behaviour during anaesthesia, where the effects of loss of wakefulness are compounded by specific anaesthesia-induced

Acknowledgements

This work was supported, in part, by grants from the National Health and Medical Research Council of Australia (Grants 109903 and 303218), the Australian Lung Foundation, and the Sir Charles Gairdner Hospital Research Fund.

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