Section 1. Epidemiology and aetiology
Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is part of a disease spectrum referred to as sleep disordered breathing (SDB). Prevalence is approximately 3 to 7% of middle-aged men and 2 to 5% of middle-aged women.1
The majority of patients remain undiagnosed, with a large community survey from the US demonstrating up to 82% of men and 92 per cent of women with moderate or severe OSAHS were undiagnosed.2
Snoring is the simplest form of SDB, which by definition is not associated with symptoms of OSAHS nor is it associated with arousals, desaturations or airflow limitation.
Apnoea is defined as a cessation of airflow for at least 10 seconds. Hypopnoea is variably defined but a recent consensus conference provided the definition as:
- Reduction in airflow of >50 per cent, or
- Reduction in airflow less than 50 % with desaturation less than 3%, or
- Reduction in airflow less than 50 % with electroencephalographic evidence of arousal.3
OSAHS is defined by five or more respiratory events (apnoeas, hypopnoea or arousals) per hour, in association with symptoms of SDB.
The apnoea-hypopnoea index (AHI) is used to measure the severity of OSAHS and is calculated by the sum of apnoeas and hypopnoeas divided by the number of hours of sleep.
- Mild: AHI five to 14 per hour.
- Moderate: AHI 15 to 30 per hour.
- Severe: AHI >30 per hour.
Upper airway resistance syndrome describes patients who experience excessive daytime somnolence as a result of frequent arousals secondary to increased respiratory effort.
During sleep the pharyngeal dilator muscles are normally relaxed. Structural abnormalities can narrow the pharyngeal airway and lead to a greater propensity for its collapse, which can be total obstruction of the airway (apnoea) or partial obstruction (hypopnoea).
The increased respiratory effort leads to transient arousal in order to maintain pharyngeal patency, causing fragmentation of sleep, reduced quality of sleep and activation of the sympathetic nervous system.
Obesity is the major risk factor, present in around 70%.4 Fat deposition reduces the pharyngeal airway and the lung volume, and therefore reduces the functional residual capacity. A neck circumference greater than 17 inches is associated with an increased risk.
Men are two to three times more likely to have OSAHS than women. Age is directly linked to prevalence, with an initial peak in childhood followed by a rise in incidence with age.5 Post-menopausal women experience a greater number of apnoeas.
Smoking, alcohol and sedating medication may increase the risk of OSAHS. Smoking may lead to inflammation in the pharynx and fluid retention.
Alcohol and sedatives cause relaxation of the pharyngeal muscles and therefore airway collapse during sleep. Nasal obstruction can contribute to the problem but is unlikely to be the primary cause.
Craniofacial abnormalities including retrognathia and maxillary projection are associated with OSAHS and appear to be the dominant contributing factor in the non-white ethnic groups.
Section 2. Making the diagnosis
Clinical features vary between patients (see box right) and some may not even recognise that they have symptoms other than snoring. A collateral history from a partner is therefore invaluable.
Abnormal craniofacial features such as retrognathia may be present (Photograph: SPL)
Differential diagnoses should be considered in the patient who presents with snoring and daytime sleepiness, because without supportive investigations, the symptoms alone do not carry a high positive predictive value for OSAHS.6 Many other conditions can manifest in similar ways, such as:
- Sleep disturbance due to pain.
- Poor sleep hygiene.
- Neurological disorders (Parkinson's disease, head injury).
- Restless leg syndrome.
- Alcohol abuse.
Primary care assessment
Clinical examination should start at the nose, which may exhibit signs of external and internal deformity, nasal polyps or evidence of rhinitis.
Tongue size is significant and signs of macroglossia may be evident, such as ridging. Tonsils should be assessed for hypertrophy. The soft palate and uvula may appear thicker and longer. The Mallampati score has a role in predicting the severity of OSAHS6 and is measured by observing the relationship between the tongue and the soft palate. The score is graded one to four, with the higher grades related to increased risk.
Abnormal craniofacial characteristics may be present, such as retrognathia, micrognathia, a short and thick neck and abnormal positioning of the hyoid.
Severe OSAHS can be associated with hypertension, coronary artery disease, congestive cardiac failure and diabetes mellitus. The patient's BMI and neck collar size should be documented. Patients should fill in an Epworth sleepiness scale (ESS).7 This comprises eight questions with a total score ranging from zero to 24. A score greater than 10 should prompt referral.
Secondary care assessment
Further examination with nasolaryngoscopy is usually performed, which allows visualisation of the airway and may help identify the level of obstruction.
The gold standard test for diagnosis is nocturnal polysomnography, which measures specific parameters including electroencephalogram, electro-oculogram, ECG, airflow, thoraco-abdominal effort and oximetry. It is usually carried out in a sleep centre but ambulatory kits are available. This can be organised through a sleep laboratory or respiratory team. Sleep studies or overnight pulse oximetry can confirm the diagnosis but are unable to exclude it.
|Symptoms of OSAHS|
Section 3. Managing the condition
Referral to secondary care (ENT or respiratory medicine) should be promptly initiated if OSAHS is suspected, especially if the ESS score is >10 or there is a history of sleepiness in dangerous situations.
If applicable, weight loss advice should be given with referral to a dietitian. Reducing the BMI is important although the daytime sleepiness can make this difficult to achieve.
Smoking cessation advice should be given and alcohol should be avoided in the evenings. Sedatives and sleeping tablets should be avoided.
Road traffic accidents are more frequent in patients with OSAHS, with driving performance in these patients comparable to those under the influence of alcohol.8
Whether OSAHS is suspected or confirmed, patients have a legal obligation to inform the DVLA and their insurance company.
Treatment can be divided into non-surgical and surgical treatment and will be offered depending on the level of obstruction, patient preference and comorbidities.
Mild disease without excessive daytime sleepiness in the absence of other comorbidities does not usually need treatment beyond lifestyle changes.
Continuous positive airway pressure (CPAP) is considered the gold standard treatment for OSAHS and is widely used as a first-line intervention. This works by preventing the upper airway collapse during respiration and has a greater effect in moderate to severe OSAHS.
Patient compliance can be an issue due to complaints of claustrophobia, rhinitis, nasal irritation and disturbance to their partner.
A mandibular advancement splint may assist those with mild-moderate OSAHS and tends to be better tolerated than CPAP but can be associated with jaw and toothache and excessive salivation. A dentist can supply these devices or they may be purchased privately. In mild cases the efficacy can be comparable with that of CPAP.
External nasal splints and nasal drops may assist with snoring but no studies have proven their efficacy in OSAHS.
Surgical treatment of OSAHS is tailored towards the level of obstruction, which may be identified from clinical examination and during sedation nasendoscopy. The various procedures may be carried out individually, synchronously or sequentially depending on the site of anatomical narrowing.
In obese patients, consultation with a bariatric surgeon may be considered, because evidence has now emerged suggesting weight loss surgery can significantly improve symptoms in obesity-related OSAHS.9
Surgical procedures are outlined in the box below.
Section 4. Prognosis
Untreated OSAHS can lead to significant neurocognitive and cardiovascular morbidity. The cognitive impairment and sleepiness can lead to accidents at work or on the road, reduced concentration and memory problems. Reduced libido and snoring can cause relationship problems.
Adverse cardiovascular events are significantly higher in those with untreated severe OSAHS, with mild-moderate severity posing a reduced risk even in the absence of obesity. Such events include MI, stroke and acute coronary insufficiency, as well as cardiovascular death.
In addition there is an increased risk of hypertension, cor pulmonale and type 2 respiratory failure.
Treatment can significantly decrease cardiovascular risk especially in those with severe OSAHS. CPAP alone can reduce risk to that of an equivalent person with simple snoring. When oral devices are used as an alternative the efficacy rate may drop although they are still of benefit in selected patients.
Surgical management has variable outcomes and success is determined by patient selection and treatment of other comorbidities.
Patients in whom surgery is successful are at risk of developing recurrence of OSAHS, particularly when adequate weight control has not been maintained.
Follow-up appointments after initiation of CPAP are required to assess response to the treatment and compliance with the machine, and to continue modification of any other risk factors.
Section 5. Case study
KH is a 52-year-old office worker who presents with a history of general lethargy and poor concentration. He has type-2 diabetes with mild hypertension and gastro-oesophageal reflux. He has a wife and three children at home and has little time to exercise. He has no mental health problems and maintains a positive outlook on life. He claims to have a well-balanced diet, maintaining his weight.
Despite this, for the past two years he has struggled to keep his HbA1c below 8.5%. He drinks an occasional glass of wine with his evening meal and is a non-smoker.
Referral to ENT
He attends with his wife who is concerned about his snoring. She has resorted to sleeping in the spare room and is not aware of any breath-holding attacks at night. He sleeps for around eight hours a night.
This patient was referred to his local ENT department for further assessment. On examination, the patient has a BMI of 30.9 kg/m2. His collar size is 16.5. His ESS was 14 out of 24.
Examination of the oropharynx revealed a long uvula but no other abnormality with a Mallampati grade 1 view. Flexible nasolaryngoscopy revealed large lingual tonsils.
He was referred for sleep studies and consideration of CPAP because surgical intervention at this stage was unlikely to result in long-term success due to the obesity.
The patient was given an overnight pulse oximetry kit to take home to monitor his saturations, which demonstrated an AHI of 19 per hour with saturations falling as low as 76 per cent. He was then issued with a CPAP machine as first-line management.
After six months of using CPAP he had noted an improvement in his energy levels and his diabetic control had improved, with his HbA1c reducing to 7.5%t.
He had managed to engage in mild physical activity, helping to reduce his BMI to 28kg/m2.
His wife was still sleeping separately because of the noise from the CPAP machine.
Section 6. Evidence base
The evidence base for non-surgical and surgical management is limited, because only a few long-term RCTs comparing techniques exist.
A Cochrane review was only able to identify 12 studies for surgical intervention in OSAHS.10 The heterogeneity of the data prevented pooled analysis; however, the number of RCTs is increasing and evidence is emerging.
A recent RCT by a Stockholm group has demonstrated that low-calorie diet modification in obese men with severe obstructive sleep apnoea can reduce the AHI.11 Five out of the 30 patients were disease free after nine weeks, with the remainder improving from severe OSAHS to mild OSAHS.
A further large RCT demonstrated significant improvement after one year, especially in those with a high AHI and those who lost more than 10kg in weight.12 Longer-term studies are required but this evidence is compelling.
- NICE. Continuous positive airway pressure for the treatment of obstructive sleep apnoea/hypopnoea syndrome. TA139. London, NICE, 2008.
These guidelines recommend the use of CPAP for moderate to severe OSAHS because several RCTs have demonstrated an improvement in patients' ESS and levels of daytime sleepiness.
Comparison with dental devices did not conclude one was more effective than the other with regard to the ESS; however, CPAP led to a greater improvement in the AHI.
- SIGN. Management of obstructive sleep apnoea/hypopnoea syndrome in adults. Guideline 73, 2003.
This topic is covered in the GP curriculum in statement 15.8: Respiratory problems
- The British Snoring and Sleep Apnoea Association website provides very useful information for patients and partners. www.britishsnoring.co.uk
- Obstructive sleep apnoea and driving guidelines are available from the DVLA. www.direct.gov.uk/en/Motoring/DriverLicensing/MedicalRulesForDrivers
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