Obstructive Sleep Apnoea (OSA)

Synonyms: Obstructive Sleep Apnoea/Hypopnoea Syndrome, OSAHS, OSA
(N.B. Sometimes 'apnoea' is spelt 'apnea')

The widely-accepted definition of obstructive sleep apnoea (OSA) is a clinical condition in which there is intermittent and repeated upper airway collapse during sleep. This results in irregular breathing at night and excessive sleepiness during the day.

• Complete apnoea is defined as a ten second pause in breathing activity.
• Partial apnoea, also known as hypopnoea, is characterised by a ten second period in which ventilation is reduced by at least 50%.¹
• OSA was discovered only some forty years ago.²
• Recent work suggests that the relationship between upper airways obstruction, night-time arousal from sleep and daytime sleepiness is by no means as clear-cut as was originally thought.³
• Current research is focussing on the concept of sleep fragmentation (the poor quality sleep produced by repeated episodes of apnoea or hypopnea) and objective measurements of upper airways obstruction.

OSA is a worldwide phenomenon. Studies suggest a prevalence in Western countries of 2-4% of middle-aged men and 1-2% of middle-aged women. The quoted figures vary considerably in the literature, depending on the criteria used to define the condition.³

Risk factors include:^2,4

• Male gender
• Middle age (55 to 59 in men, 60-64 in women)
• Smoking
• Obesity
• Sedative drugs
• Excess alcohol consumption
• Possibly genetic tendency related to jaw morphology

History

The following may be suggestive of OSA:

• Excessive daytime sleepiness
• Impaired concentration
• Snoring
• Unrefreshing sleep
• Choking episodes during sleep
• Witnessed apnoeas
• Restless sleep
• Irritability/personality change
• Nocturia
• Decreased libido

Symptoms such as personality change, episodes of apnoea, irritability and restlessness at night may be better elicited by taking a history from a partner.

Daytime sleepiness is sometimes assessed using the Epworth Sleepiness Scale^1,5 (see our dedicated record).

Examination

There are no specific diagnostic findings on examination, but the following may be noteworthy:

• Obesity is an important risk factor, although 50% of patients are not clinically obese (BMI>30 kg²).
• Fat deposition anterolateral to the upper airway may signify obstruction.
• Neck circumference is a strong predictor of OSA (<37cm low risk, >48cm high risk).
• Certain craniofacial or pharyngeal abnormalities are associated with OSA e.g. retrognathia, micrognathia, enlarged tonsils.⁶

• Fragmented sleep (quality of sleep)
• Sleep deprivation (quantity of sleep)
• Shift work
• Depression
• Narcolepsy
• Hypothyroidism
• Restless leg syndrome /periodic limb movement disorder
• Drugs
  • Sedatives
  • Stimulants (caffeine, theophyllines, amphetamines)
  • Beta-blockers
  • Selective serotonin reuptake inhibitors (SSRIs)
  • Idiopathic hypersomnolence
  • Excess alcohol.
• Neurological conditions
  • Dystrophica myotonica
  • Previous encephalitis
  • Previous head injury
  • Parkinsonism

Clinical assessment is not sufficient to make a diagnosis of OSA. One study showed that sleep experts have been wrong 50% of the time when making a diagnosis based on history and examination alone.⁷ A combination of loud snoring and witnessed apnoeas is however highly suggestive and has a specificity of 67% and a sensitivity of 78%.⁶

Laboratory tests

• Thyroid function tests may be appropriate in patients in whom hypothyroidism is suspected.
• Arterial blood gases may be required in patients presenting with symptoms of cor pulmonale, to rule out daytime hypoxia or hypercapnoea.

Polysomnography (PSG)

This has been the traditional gold standard investigation. Various physiological recordings are taken whilst the patient is asleep. Techniques vary widely, but international standards dictate that a PSG involves at least an electro-encephalogram (EEG), two electro-oculograms (EOG) to measure horizontal and vertical eye movements and an electromyelogram (usually placed on the chin) to monitor muscle movement.⁸

At the end of the investigation, the number of apnoea/hypopnoea episodes whilst asleep is quoted as the Apnoea/Hypopnoea Index (AHI).⁵

• Mild: AHI = 5-15 per hour
• Moderate: AHI = 15-30 per hour
• Severe: AHI >30 per hour

PSG has been criticised in recent years for its lack of evidence base, its cost and - considering it is meant to be a gold standard test - its lack of reproducibility.

This has led to the search for less invasive and expensive techniques, centering on the physiological changes experienced during an apnoeic or hypopnoeic episode. Methods explored include pulse oximetry, finger plethysmography to detect changes in peripheral vasoconstriction and analysis of very low frequency components of heart rate activity.⁶

• Hypertension
• Cardiovascular disease - ischaemic heart disease, stroke, congestive heart failure.
• Obesity
• Metabolic syndrome
• Diabetes
• Asthma - there is some evidence that patients who snore and have severe asthma have an increased risk of developing OSA¹⁰

The recommendations from SIGN, based on randomised trials, is that the patients most likely to benefit from treatment are those with an AHI of 15 or more and a 4% oxygen saturation dip rate (as measured by pulse oximetry during periods of sleep apnoea or hypopnoea) of >10 per hour.

Benefits may be seen in reduction in daytime sleepiness, simulated driving performance, quality of life, blood pressure and mood. Apart from CPAP, there is no diminution of vascular risk in patients without daytime sleepiness, or in asymptomatic patients. It is important to communicate to patients exactly what can be achieved, as well as what the treatments involve.

There are four main management options:

Behavioural interventions

Lifestyle changes should be discussed.

• Weight loss is appropriate if obesity is an issue and gastric surgery may be appropriate in some patients who fit the criteria for this type of treatment. There is however no close correlation between weight loss and improvement of OSA symptoms, nor is there any guarantee that OSA will not return after gastric surgery.
• Smoking cessation should be advocated from a general health perspective, but again there is no guarantee that this will alleviate OSA symptoms.
• Alcohol should be avoided in the evening, as should sedative and hypnotic medication, as these all decrease airway dilator function.

Continuous positive airway pressure (CPAP)

This acts as a pneumatic splint, maintaining upper airway patency. A flow generator delivers pressure through air tubing to a nasal or facial mask worn overnight. Most patients require lifelong therapy.

CPAP is a well established treatment with a solid evidence base, most suitable for patients with moderate to severe OSA. Some patients, particularly those with respiratory failure, require a bi-level system in which the pressure in the inspiratory phase can be adjusted independently of the expiratory phase. One study of patients on CPAP found that good compliance was associated with a reduction in serum cardiovascular risk factors (e.g. high-sensitivity C-reactive protein (hs-CRP), homocysteine, total cholesterol, triglycerides).¹¹

Intra-oral devices

These are a range of devices which sit in the mouth and act mainly by producing anterior displacement of the mandible, thereby increasing upper airway diameter. Randomised trials suggest they are of most benefit in snorers and in patients with mild OSA and normal daytime alertness.

Pharmacological treatments

The role of pharmacological agents is limited. Modafinil may afford some benefit in patients with daytime sleepiness who are compliant with CPAP treatment, but longer-term studies are needed.

Surgery

Various techniques have been tried, but assessment is difficult due to inconsistency of trial methodology. The evidence base is at best equivocal.

The procedures evaluated include:

• Uvulopalatopharyngoplasty (UPPP) - patients may be unable to use CPAP subsequently
• Laser-assisted uvulopalatopharyngoplasty (LUAP)
• Mandibular advancement
• Maxillary advancement
• Tonsillectomy - appropriate for tonsillar enlargement
• Tracheostomy - may be necessary in severe OSA where other treatments fail

One study using multiple minimally-invasive surgical techniques (nasal surgery, palatal stiffening by Pillar implant technique and radiofrequency volume reduction of the tongue base) achieved good results in 125 patients in patients with moderate OSA.¹²

• Excessive daytime sleepiness may cause accidents in the home, at work and whilst driving.
• Irritability, depression and other psychological consequences may ensue.
• Cardiovascular complications include hypertension, coronary artery disease, congestive cardiac failure and stroke.

For patients who respond to CPAP, the short-term prognosis is excellent. Placebo-controlled studies have show a positive benefit in terms of reduction in daytime sleepiness, snoring and an improvement in cognitive function and general health status after 4-8 weeks treatment.

The long-term prognosis in terms of cardiovascular complications is as yet unknown.