Obstructive Sleep Apnea
Introduction
Obstructive sleep apnea (OSA) is a common condition caused by repetitive collapse of the upper airway during sleep, which continually disturbs sleep overnight, leading to poor quality sleep and daytime sleepiness. It has significant physiological effects during sleep and is associated with hypertension, cardiovascular disease and stroke. Obesity is a major risk factor and prevalence is increasing. Untreated OSA leads to significant daytime impairment, loss of productivity and increased motor vehicle accidents. It can be readily treated with continuous positive airway pressure (CPAP), and therefore recognising and treating this condition can have benefits both to individuals and at a population level.
Epidemiology
In 2014, the British Lung Foundation estimated that 330,000 people in the UK were diagnosed with OSA, with a further 1.5 million undiagnosed. Current estimates suggest that figure is at least 2.5 million, largely due to increasing obesity rates. Epidemiological studies estimate that 14% of men have clinically significant OSA, with a larger proportion having the condition without significant symptoms.
Risk factors include obesity, increasing age, family history and sedative medications. It is more common in patients with hypertension, cardiovascular disease, heart failure and diabetes, although these groups may not have significant sleep symptoms.
Pathogenesis
The upper airway (UA) is kept open during wakefulness by the activity of the UA muscles. Their activity falls at sleep onset, which may predispose to UA collapse in someone with an anatomically narrowed airway. Increased tissue around the UA, such as fat or fluid, or a small bony cage (e.g retrognathia) are factors associated with a more collapsible UA.
During an episode of UA collapse, there are continued respiratory movement against a closed airway, causing significant intrathoracic pressure swings, oxygen desaturation and eventually an arousal from sleep that reactivates the UA muscles and opens the airway, only for the cycle to begin again. The arousal is associated with surges in sympathetic activity, resulting in rises in heart rate and blood pressure.
OSA may be worse in the supine position, due to increased narrowing of the airway, or during REM sleep due to even greater reductions in UA muscle activity.
Symptoms
The NICE guidelines recommend assessing patients for OSA if they have two or more of the following symptoms:
Snoring
Witnessed apneas
Sleep fragmentation and insomnia (which may coexist with OSA)
Waking up choking or gasping from sleep
Excessive daytime sleepiness (although some patients will complain of feeling tired without being sleepy)
Nocturia
Memory impairment
Assessment
In addition to asking about the above symptoms, a sleep history should be taken detailing the following:
Bedtime
Sleep onset latency
Awakenings during the night
Waking up time
Naps
Shift patterns (if relevant)
Caffeine intake
It’s helpful to distinguish between actual sleepiness (falling or nearly falling asleep unintentionally) and a feeling of tiredness or fatigue, which may be described as lacking in energy, as the latter is commonly associated with many other medical conditions and medications.
Medications associated with daytime sleepiness include benzodiazepines, beta blockers, opiates, gabapentinoids, antidepressants and antipsychotics. It’s worth reviewing doses as reduction may improve sleepiness.
The Epworth Sleepiness Score (ESS) gives an indication of sleepiness (>11 indicting excessive sleepiness), but bear in mind many patients with symptomatic OSA have a normal ESS.
The STOP-BANG questionnaire is a useful screening tool, commonly used in pre-operative assessment, but a low score should not stop referral for a sleep study if there is clinical suspicion of OSA.
Diagnosis
An overnight sleep study is required to diagnose OSA, but to have OSA syndrome the patient must also have significant symptoms that warrant treatment.
There are different types of sleep study:
Overnight oximetry – this records oxygen saturations and pulse rate. It is a useful screening test but may miss mild OSA in patients who do not desaturate during airway obstruction.
Respiratory polygraphy (semi-polysomnogram) – this records several channels, including saturations, nasal airflow, respiratory movements, pulse rate and leg movements. It can be done at home or in hospital, and may be used first line or after oximetry if the diagnosis is not clear.
Full polysomnography – this records the same measurements as polygraphy, plus EEG and other channels to determine sleep stages. It is the gold standard sleep test but requires a night in hospital, and takes several hours to interpret, so in the UK it is usually reserved for patients in whom there is a suspicion of another sleep disorder, or who do not respond to treatment for OSA.
Definitions
Different terms are used depending on the type of sleep test performed:
Apnoea = ≥90% reduction in airflow for >10 seconds
Hypopnoea = ≥ 30% reduction of airflow associated with ≥3% desaturation or arousal from sleep
Apnoea-hypopnoea index (AHI) = number of apnoeas and hypopnoeas per hour of sleep.
This determines the severity of OSA:
<5 - normal
5-15 - mild
15-30 - moderate
> 30 – severe
Oxygen desaturation index (ODI) = number of desaturations of ≥4% per hour, and may be used instead of AHI.
Treatment
Lifestyle measures
All patients with OSA should be given lifestyle advice, both for management of OSA as well as associated conditions such as hypertension:
Weight loss (including referral to Tier 2 or 3 weight management services)
Smoking cessation
Alcohol reduction
Weight loss alone may be enough to resolve mild OSA, but for moderate to severe OSA, or those with significant symptoms, other treatments are usually needed.
CPAP
This is the most commonly used and most effective treatment for OSA. Patients wear a small mask (either nasal or full face mask) that connects by tubing to the CPAP machine that blows air at a low pressure through the upper airway, splinting it open. The CPAP pressure may be fixed, or an auto-titrating machine can be used that adjusts the pressure according to the upper airway resistance.
CPAP is very effective at treating OSA and improves symptoms almost immediately. The aim is for it to be used all night, every night, as symptoms improve in a linear fashion with increased usage. However, more than 4 hours per night on average, or usage for more than 4 hours on at least 70% of nights is considered to be good compliance. Data recorded on the CPAP machine gives detailed information on usage, as well as mask leak and residual OSA. This can be obtained remotely via a modem from most new machines, or physically from an SD card.
Around 70% of patients will continue using CPAP regularly, with usage in the first month predicting long term usage. Poor mask fit is a common problem that can easily be addressed to improve usage, along with addition of a humidifier to address dryness. Residual sleepiness despite optimising CPAP may be due to a coexistent sleep disorder (such as periodic limb movements or insomnia), medications (see above) or comorbidities.
Mandibular Advancement Devices
Mandibular Advancement devices (MAD), also known as oral appliances, are like gumshields that fit over the upper and lower teeth, and clip together to protrude the lower jaw thus opening the airway. The NICE guidelines now recommend MADs as a potential first line alternative to CPAP, or in those intolerant of CPAP. MADs that are custom-made by a dentist are probably most effective, although can be costly. Access to NHS dental services that provide MADs varies across the country, so some patients may have to obtain them privately. They are generally recommended for mild to moderate OSA, but less likely to control severe OSA.
Newer treatments
The following treatments are either undergoing trials or only available in specialised centres
Oral muscle exercises
Postural devices – vibrating devices that alert the patient when they lie on their back, to train them to sleep on their side. May be used in positional OSA
Hypoglossal nerve stimulation – an implanted device that stimulates the hypoglossal nerve to open the airway
Transcutaneous hypoglossal nerve stimulation