Epidemiology

OSA is a worldwide phenomenon. Studies suggest a prevalence in Western countries of 3-7% of middle-aged men and 2-5% of middle-aged women.
Risk factors include:

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

• There is evidence that regular snoring and OSA are independently associated with alterations in glucose metabolism.^[1] Thus, OSA might be a risk factor for the development of type 2 diabetes.

The prevalence of OSA is much higher in patients with cardiac or metabolic disorders than it is in the general population.^[2]

Presentation^[3]

History

Snoring is the simplest form of sleep-disordered breathing (SDB). 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.^[3][4]A score greater than 10 should prompt referral.

Examination

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

• Obesity is an important risk factor.
• Fat deposition anterolateral to the upper airway may signify obstruction.
• Neck circumference is a strong predictor of OSA (<37 cm is low-risk, >48 cm is high-risk).
• Certain craniofacial or pharyngeal abnormalities are associated with OSA - eg, retrognathia, micrognathia, enlarged tonsils, macroglossia, thickening or lengthening of the soft palate or uvula.
• Assess for presence of nasal polyps, rhinitis or any deformity of the nose.

Differential diagnosis^[3]

• 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, amfetamines).
  • Beta-blockers.
  • Selective serotonin reuptake inhibitors (SSRIs).
  • Idiopathic hypersomnolence.
  • Excess alcohol.
• Neurological conditions:
  • Dystrophica myotonica.
  • Previous encephalitis.
  • Previous head injury.
  • Parkinsonism.

Diagnosis

OSA is defined by five or more respiratory events (apnoeas, hypopnoeas or arousals) per hour, in association with symptoms of SDB.

Clinical assessment is not sufficient to make a diagnosis of OSA.

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 electroencephalogram (EEG), two electro-oculograms (EOGs) to measure horizontal and vertical eye movements and an electromyogram (usually placed on the chin) to monitor muscle movement.^[5]

At the end of the investigation, the number of apnoea/hypopnoea episodes whilst asleep is quoted as the Apnoea/Hypopnoea Index (AHI).The AHI is used to measure the severity of OSA and is calculated by the sum of apnoeas and hypopnoeas divided by the number of hours of sleep.

• Mild: AHI = 5-14 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.

Other invesitgations

• A nasolaryngoscopy is usually performed for visualisation of the airway and may also help identify the level of obstruction.
• TFTs 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.

Associated diseases

• 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 OSA.^[6]

Management^[3]

• The recommendations from the Scottish Intercollegiate Guidelines Network (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 continuous positive airway pressure (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.
• The evidence base for non-surgical and surgical management is limited, however, as very few long-term randomised controlled trials comparing techniques exist.

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 evidence for improvement of OSA symptoms with weight loss in mild OSA,^[7] but more research is needed.
• Smoking cessation should be advocated from a general health perspective; however, 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.

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. 
• However, patient compliance can be a problem, as it can lead to claustrophobia, rhinitis, nasal irritation and also disturbance to their partners.
• CPAP is currently recommended as a treatment option for adults with mild OSAHS if they have symptoms that affect their quality of life and ability to go about their daily activities and lifestyle advice and any other relevant treatment options have been unsuccessful or are considered inappropriate.^[8] 

Intra-oral devices

• This is 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.
• Current evidence on soft-palate implants for obstructive sleep apnoea (OSA) raises no major safety concerns, but there is inadequate evidence that soft-palate implants are efficacious in the treatment of tobstructive sleep apnoea. NICE recommends that soft-palate implants should not be used in the treatment of this condition.^[9] 

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.
• The European Respiratory Society have stated that drugs, nasal dilators and apnoea triggered muscle stimulation cannot be recommended as effective treatments of OSA at the moment.^[10]  

Surgery

• Various techniques have been tried; however, 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 (LAUP).
• Mandibular advancement.
• Maxillary advancement.
• Tonsillectomy - appropriate for tonsillar enlargement.
• Tracheostomy - may be necessary in severe OSA where other treatments fail.

Complications

• 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.
• OSA has also been identified as an independent risk factor for stroke and all-cause mortality.^[11] 
• There is an increased risk of cor pulmonale and type 2 respiratory failure.
• There is an increased risk of metabolic disturbances, such as insulin resistance in patients with OSA.^[12]

Obstructive sleep apnoea and driving

All patients with OSA causing excessive daytime or awake time sleepiness need to cease driving until satisfactory control of symptoms has been attained.^[13]Those with Group 2 entitlement should also cease driving until satisfactory control of symptoms has been attained, with ongoing compliance with treatment, confirmed by a consultant or specialist opinion.^[13]

Prognosis

• Untreated OSA can lead to significant neurocognitive and also cardiovascular morbidity. The cognitive impairment can lead to reduced concentration, accidents and also memory problems.
• For patients who respond to CPAP, the short-term prognosis is excellent. Placebo-controlled studies have shown a positive benefit in terms of reduction in daytime sleepiness and in snoring, and an improvement in cognitive function and general health status after 4-8 weeks of treatment. 
• Treatment can significantly decrease cardiovascular complications, especially in those patients with severe OSA.