Clinical ReviewObstructive sleep apnoea and anaesthesia
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.
References* (71)
- et al.
Comparison of upper airway collapse during general anaesthesia and sleep
Lancet
(2002) - et al.
Relationship between difficult tracheal intubation and obstructive sleep apnoea
Br J Anaesth
(1998) - et al.
Anaesthesia and sleep apnoea
Br J Anaesth
(2001) - et al.
The upper airway during anaesthesia
Br J Anaesth
(2003) - et al.
Identifying the patient with sleep apnea: upper airway assessment and physical examination
Otolaryngol Clin North Am
(1998) - et al.
Effects of halothane, enflurane, and isoflurane on laryngeal receptors in dogs
Respir Physiol
(1993) - et al.
The pharyngeal critical pressure
Chest
(1996) - et al.
Is obstructive sleep apnoea a rapid eye movement predominant phenomenon?
Br J Anaesth
(2000) - et al.
Effect of general anaesthesia on the pharynx
Br J Anaesth
(1991) - et al.
Sleep-disordered breathing and obesity
Ballieres Clin Endocrinol Metab
(1994)
Influence of maxillary constriction on nasal resistance and sleep apnea severity in patients with Marfan's syndrome
Chest
Obstructive sleep apnea, control of ventilation, and anesthesia in children
Pediatr Clin North Am
Postoperative complications in patients with obstructive sleep apnea syndrome undergoing hip or knee replacement: a case-control study
Mayo Clin Proc
Obstructive sleep apnea and death associated with surgical correction of velopharyngeal incompetence
J Pediatr
Anesthetic management of obstructive sleep apnea patients
J Clin Anesth
Nasal continuous positive airway pressure in the perioperative management of patients with obstructive sleep apnea submitted to surgery
Chest
Comparison of the effects of mivacurium on the diaphragm and geniohyoid muscles
Br J Anaesth
Comparison of sedation with midazolam and ketamine: effects on airway muscle activity
Br J Anaesth
Influence of morphine on respiratory activities of phrenic and hypoglossal nerves in cats
Respir Physiol
Positional treatment vs continuous positive airway pressure in patients with positional obstructive sleep apnea syndrome
Chest
The laryngeal mask—a new concept in airway management
Br J Anaesth
Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares
Lancet
Difficult endotracheal intubation in patients with sleep apnea syndrome
Anesth Analg
High Mallampati score and nasal obstruction are associated risk factors for obstructive sleep apnoea
Eur Respir J
Epidemiology of obstructive sleep apnea: a population health perspective
Am J Respir Crit Care Med
Pharyngeal pressure and flow effects on genioglossus activation in normal subjects
Am J Respir Crit Care Med
Collapsibility of the upper airway during anesthesia with isoflurane
Anesthesiology
Effects of volatile anesthetics on the activity of laryngeal drive receptors in anesthetized dogs
J Vet Med Sci
Upper airway pressure–flow relationships in obstructive sleep apnea
J Appl Physiol
Motor control of the pharyngeal musculature and implications for the pathogenesis of obstructive sleep apnoea
Sleep
Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism)
J Clin Invest
Anatomy of pharynx in patients with obstructive sleep apnea and in normal subjects
J Appl Physiol
Effect of nasal airway positive pressure on upper airway size and configuration
Am Rev Respir Dis
Static mechanics of the velopharynx of patients with obstructive sleep apnea
J Appl Physiol
Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea
Am Rev Respir Dis
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The most important references are denoted by an asterisk.