As promised last month, we will now look at Obstructive Sleep Apnoea (OSA) – the most extreme cause of snoring and perhaps the most overlooked with an estimated 80% undiagnosed. It occurs in both sexes and any body shape although typically is more common in overweight males.
In OSA, breathing temporarily stops (apnoea) in deep sleep when the muscle tone is at its lowest, causing airway tissue to collapse to the point of blocking all air inflow for more than 10 seconds at a time.
This results in a drop of blood oxygen levels, which in turn triggers special chemical sensors in the blood to send feedback to the brain to increase muscle tone in tissues and inspire harder to overcome the blockage and get oxygen in. This process leads to the intermittent classical extra loud snore or waking gasp for air.
(A small group of patients with brain or nerve damage suffer from a different variation called central sleep apnoea, in which their brain cannot increase their drive to breath in response to the reduced air inflow.)
OSA is therefore often first picked up by the partner or others who notice the loud gasp or snore. The sufferer themselves may also feel unrefreshed, mentally dull and tired during the day to the point of falling asleep when reading, watching TV or driving. This is the basis for the main screening tool for diagnosis called the Epworth Sleepiness Score in which a score of >10 is suggestive of OSA.
Diagnosis is then officially made through a combination of the Epworth score, symptoms and confirmed laboratory recordings of greater than 5 apnoeic episodes per hour.
So, to investigate for potential OSA, a patient will have their sleep monitored for their oxygen levels, breathing rate and snore. A full comprehensive sleep study (polysomnography) will in addition also record brain waves, heart electrics, muscle signals and eye movements. This allows calculation of sleep latency (time to fall asleep), sleep efficiency (time on bed actually asleep) and apnoeic episodes per hour.
These sleep recordings also help to exclude other possible causes of inefficient sleep (as mentioned last month) such as sleep cycle abnormalities, mood disorders, nerve disorders and restless legs.
By negatively impacting sleep quality and subsequent daytime functioning alongside the stigma of snoring, OSA can cause anxiety and depression in those who have it.
Moreover, the repeated drop in oxygen levels has other serious consequences, most notably increasing the risk for heart disease through increasing risk for high blood pressure, high cholesterol and diabetes. OSA is also an independent risk factor for reduced quality of erection and reduced libido.
The methods discussed to deal with snoring last month can equally be trialled with OSA but given the severity of obstruction to breathing, simple measures such as adjusting sleep position and losing weight are unlikely to be enough.
Most patients with > 5 apnoeic episodes or troublesome symptoms are offered a mask device with high pressure airflow called CPAP (continuous positive pressure ventilation) to overcome the obstruction from collapsing airway tissue. However, the device is uncomfortable to wear all night and the benefits are most noticeable only in the first month. Furthermore, whilst it does help with disturbed sleep and snoring, it does not alter the resulting risk of heart and artery disease from OSA.
For some patients even CPAP does not help achieve refreshing sleep. In such cases, Modafinil (a stimulant drug to counter the daytime sleepiness) is now licensed in the UK to be used in addition -but not in place of – CPAP.
If CPAP doesn’t prove successful, then the surgical methods to treat snoring by removing the obstructing tissue discussed last month are the last resort option.