Obstructive sleep apnoea: Diagnostics and management

Snoring is the noise caused by the turbulent flow of air in the upper airway. It ranges in severity from mild snoring to so called ‘heroic’ or ‘Olympic’ snoring. According to the Guinness Book of World Records (McWhirter 1986), the loudest recorded snore measured 87.5 decibels, equivalent to the sound of traffic in a busy street. The word ‘apnoea’ originates from the Greek word meaning ‘want of breath’ (Shemwell and Wilson 1994). An apnoeic episode occurs when no air passes through the nose or mouth in a period of ten seconds. Sleep apnoea is characterised by periods of loud, gasping snoring followed by silence. This typically lasts between 30 and 100 seconds, during which struggling motions of the thorax and abdomen may be observed (Tobin et al 1983). Sleep apnoea syndrome is generally defined as 30 or more apnoeic episodes during a seven- hour sleep, or when there are five or more apnoeic episodes per hour.

Sleep apnoea may be characterised as:
• Central apnoea, caused by a lack of central drive from the respiratory centre found in the lower brainstem
• Obstructive sleep apnoea, when air is unable to pass the lips or nose, despite a respiratory effort being made
• Mixed apnoea, a combination of the two

The focus of this article is obstructive sleep apnoea.

To understand the mechanisms behind snoring and sleep apnoea, some knowledge of the neuro-physiology of sleep and alteration of body functions that occur during sleep is essential. There are two major sleep states, each with its own characteristic physiological and electrophysiological features. Normal sleep is a cyclical progression from sleep without rapid eye movements (non-REM sleep) to REM sleep through a period of between 90 and 120 minutes. Respiration during wakefulness and sleep differs, with wakefulness in itself being a powerful respiratory drive. The arousal system during non-REM sleep is very active, and asphyxia results in a rapid return to wakefulness. In comparison, arousal from REM sleep may be slow, as the arousal mechanisms are inhibited, and much lower levels of oxygen saturation are reached before arousal occurs. Thus in REM sleep there is a diminished response to airway obstruction, with a strong possibility of irregular respirations and occasional apnoeic episodes (Gray and Rutka 1988).

Respiratory response. Also during sleep, reduced respiratory centre output to the muscles of the upper airway which normally dilate the oropharynx and larynx on inspiration – produces an increase in upper airway resistance. Relative hypotonia of the soft palate, genioglossus muscle, and posterior pharynx may cause a passive collapse of the upper airway (Orr and Martin 1981). The arterial oxygen level drops, and the respiratory centre responds by increasing inspiratory drive. When the arousal is sufficient, the palate and pharyngeal tissues are pulled out of the way, and the apnoeic episode ends with a gasp.

Pulmonary response. The response of the pulmonary circulation to hypoxia is vasoconstriction. Pulmonary hypertension, arrhythmia and (rarely) myocardial infarction are the sequelae to repeated hypoxic episodes (O’Donoghue et al 1992).

Simmons et al (1983) showed that snorers given alcohol or sedatives develop obstructive sleep apnoea. It is also thought that all snorers predispose to the development of obstructive sleep apnoea because stronger breathing efforts are needed to maintain adequate gas exchange. Chronic respiratory stimulation repeated nightly over a period of years may induce irreversible airway narrowing until the pharyngeal dilator muscles can no longer prevent the airways from complete collapse during sleep. This theory appears quite feasible, as the prevalence of sleep apnoea has been shown to be age-related, usually occurring in middle-aged subjects.

Other identified predisposing factors to the syndrome are shown below (Bomwiecki and Sassin 1983, Douglas 1963, Tobin at al 1983):

• Smoking
• Enlarged uvula
• Increasing age
• Enlarged oropharyngeal tissue
• Retrognathia
• Micrognathia
• Hypertrophic palatine tonsils
• Nasal deformity
• Macroglossia
• Marfan’s syndrome
• Iatrogenic stenosis
• Acromegaly
• Pharyngeal neoplasms
• Myxoedema
• Craniofacial disproportions
• Down’s syndrome
• Scheie’s syndrome
• Platybasia
• Lymphoma
• Prader-Willi syndrome
• Myotonic dystrophy
• Guillain-Barré syndrome

When a patient initially presents at our ear, nose and throat department with obstructive sleep apnoea, the following investigations are made:

• Height and weight measurement – to calculate body mass, and collar size
• Temperature, pulse and blood pressure
• Electrocardiography
• Peak flow recordings
• Flow volume loop testing (Haraldsson et al 1995, O’Donoghue et al 1992)
• Extensive otorhinolaryngologic examination
• Overnight monitoring

Otorhinolaryngologic examination. The examination includes fibre optic rhinolaryngoscopy during voluntary snoring, and Muller’s manoeuvre (Haraldsson et al 1995). In this manoeuvre, the nasendoscope is passed into the postnasal space under local anaesthetic. The patient is asked to take a deep inspiratory effort with a closed nose and mouth in an attempt to simulate snoring conditions (Carney and Robinson 1995). To create a more natural snoring environment, a sleep nasendoscopy can be performed using intra-venous midazolam. Anaesthetic monitoring is necessary throughout and this is a time- consuming and expensive investigation.

Overnight monitoring. Sleep studies are essential for a firm diagnosis of sleep apnoea. The ultimate investigation is polysomnography which records the pattern of sleep and arousal measured by (Douglas 1993):

• Electro-encephalography (EEG)
• Electromyography (EMG)
• Recording thoraco-abdominal movements
• Recording oro-nasal flow
• Oximetry
• Electrocardiography (ECG)

This is a very expensive investigation, with few centres able to offer it routinely for all snorers. A ‘mini’ sleep study is more usual, consisting of pulse oximetry, pulse rate recording and nursing observation. Patients with impairment – nocturnal desaturation without obvious episodes of sleep apnoea – are offered more detailed studies.

Management of obstructive sleep apnoea depends largely on the site of obstruction:

• Nose – nasal polyps or packing, deviated septum
• Pharynx – enlarged tonsils and adenoids, nasopharyngeal tumours, retropharyngeal masses, macroglossia and micrognathia, acromegaly, dysfunction of pharyngeal airway
• Larynx – tumours, laryngeal oedema

Self-help. Initially, patients are advised to lose weight (if appropriate), avoid alcohol and sedatives, and avoid the supine position. Use of stimulants such as coffee and tea, and allowing the snorer’s bed partner to get to sleep first before the discordant snoring begins, may be advocated. (Pelausa and Tarshis 1989).
Nasal dilation. Hoijer et al (1992) and Petruson (1990) found that nasal dilating clips decreased both the frequency and severity of obstructive breathing events in patients with obstructive sleep apnoea. However, their use has not been widely adopted.

Drug treatment. Protriptyline, aminophylline, clomipramine hydrochloride, and acetazolamide all theoretically reduce the amount of REM sleep and hence the number of apnoeic episodes (Gray and Rutka 1988, Tobin et al 1983). However, none has had a therapeutic impact and there are significant side effects, including insomnia, prolonged nightmares, constipation, impotence, urinary retention and cardiac arrhythmia. Strychnine sulphate has been used (Remmers and Anch 1981) in an attempt to increase airway tone by preferentially increasing upper airway muscle activity over diaphragmatic activity. However, the high toxicity/therapeutic ratio of the drug renders it of little value in the treatment of snoring or sleep apnoea.

Continuous positive airways pressure. This is a widely used conservative intervention. It consists of a small mask connected to a pump that supplies positive pressure to the pharyngeal airway, acting as a pneumatic splint and preventing collapse (O’Donoghue at al 1992). However, it is cumbersome, expensive and often poorly tolerated (Carney and Robinson 1995, Gray and Rutka 1988). Long term compliance is reported to be only 58-69 per cent (Haraldsson et al 1995, Larsson et al 1994). Theoretical disadvantages of continuous positive airways pressure include reduced cardiac output and renal function (Sullivan et al 1981). Other respiratory complications, such as pneumothorax, have also been documented (Stradling 1993).

Nasal surgery. Results of nasal surgery are largely controversial. It appears to be widely accepted that underlying nasal pathology, such as hypertrophic inferior turbinates, nasal polyps or deviated nasal septum, should be treated and the patient re-assessed before considering palatal surgery (Carney and Robinson 1995).

Craniofacial surgery. Advancement mandibular osteotomy and maxillary osteotomy have also been reported (Borowiecki and Sassin 1983, Douglas 1993), but are only used for congenital craniofacial defects such as retrognathia.

Expansion hyoidoplasty. In cases where the tongue is the main site of obstruction, expansion hyoidoplasty and base of tongue resection have been developed (Gray and Hawthorne 1992).

Tracheostomy. Permanent tracheostomy was once the only effective treatment for those patients in whom no corrective pathology could be identified (Sher et al 1985). It was first used for treatment of obstructive sleep apnoea syndrome in 1969, in a patient with Pickwickian syndrome (Borowiecki and Sassin 1983, Guilleminault et al 1981). Cotton (1983) stated that: ‘ln our present state of knowledge, tracheostomy is the only certain cure for life-threatening obstructive sleep apnoea in adults.’ Although technology has advanced considerably, cases of obstructive sleep apnoea still exist in which a permanent tracheostomy is indicated to ensure the patient survival. A tracheostomy can have a devastating impact on the patient, leaving him or her aesthetically disfigured and requiring strict hygienic care. It can result in inadequate voice production and exposes the patient to the risk of iatrogenic tracheal stenosis (Borowiedti and Sassin 1983, Zohar et al 1993).

Uvulopalatopharyngoplasty (UVPP). This involves:
• Removal of the tonsils (if present)
• Removal of the redundant folds of tissue around the palatopharyngeus and palatoglossus muscles
• Resection of the distal 1cm of soft palate and related uvula. The technique causes scarring and increased rigidity in the palatopharyngeus isthmus (Gray and Rutka 1988, O’Donoghue et al 1992).

Patients must be carefully selected – many of them will already have intermittent airway obstruction, be overweight and may have coexisting respiratory or cardiovascular disease. They are at risk of post-operative oedema and of increased mortality or morbidity. If nasal surgery is performed at the same time, nasal packing may be required which will further compromise the airway (Camey and Robinson 1995). UVPP has a number of complications and side-effects (below – Cotton 1983, Friberg et al 1995, Haavisto and Suonoaa 1994, Simmons et al 1983) and there have been fatalities (Haavisto and Suonoaa 1994).

• Post-operative pain
• Palatal stenosis
• Velopharyngeal insufficiency (manifested as nasal regurgitation and changes in voice quality)
• Hypernasality
• Pharyngeal dryness
• Secondary haemorrhage
• Breakdown of surgical closure
• Dysphagia
• Loss of taste
• Airway problems

Laser palatoplasty. A less radical surgical treatment, laser palatoplasty, is now being used in some centres. This apparently reduces snoring in 85 per cent of cases (Carney and Robinson 1995). A strip of inferior soft palate is excised, causing fibrosis and palatal stiffening. This procedure is said to have fewer side effects than UVPP.