Obstructive Sleep Apnoea: Repeated Airway Closure During Sleep

Obstructive sleep apnoea occurs when the upper airway repeatedly narrows or closes during sleep. Breathing falls or stops, oxygen can drop and sleep repeatedly lightens. Some people snore or feel very sleepy, while others have few recognised symptoms despite clinically important disease.

What obstructive sleep apnoea is Obstructive sleep apnoea is usually shortened to OSA. During sleep, the upper airway repeatedly narrows or closes even though the body continues trying to breathe. A partial obstruction causes reduced breathing, called hypopnoea. A complete obstruction causes a pause in airflow, called apnoea. OSA and OSAHS NICE commonly uses the term obstructive sleep apnoea or hypopnoea syndrome, shortened to OSAHS. The syndrome combines obstructive breathing events with effects such as disrupted sleep, sleepiness or impaired daytime function. In ordinary clinical speech, OSA is often used as the shorter umbrella term. A sleep study number must still be interpreted with symptoms and health consequences. The upper airway The upper airway includes the nose, mouth, soft palate, tongue and throat. Unlike the windpipe, the throat has no rigid supporting rings. Its openness depends on anatomy, muscle activity and the pressure created during breathing. This flexibility allows speech and swallowing but also permits collapse during sleep. What changes during sleep Muscles supporting the tongue and throat relax during normal sleep. The airway becomes narrower in everyone to some degree. In a susceptible person, the walls move together enough to restrict or stop airflow. The risk can be greatest during rapid eye movement sleep and when lying on the back. Breathing effort continues OSA is called obstructive because the person continues making breathing efforts against a blocked airway. The chest and abdomen may move while little or no air reaches the lungs. This differs from central sleep apnoea, where breathing effort temporarily stops because the brain does not send the usual signal. The distinction is made through a sleep study. How an episode ends Falling oxygen, rising carbon dioxide and increasing breathing effort activate the brain. The person briefly wakes or moves into lighter sleep. Throat muscle activity increases, the airway opens and breathing resumes, sometimes with a gasp or snort. The person often returns to sleep without remembering the event. Repeated sleep fragmentation These brief arousals can occur many times each hour. They interrupt normal progression through restorative sleep stages. A person may spend enough hours in bed but still wake unrefreshed. Sleep fragmentation can impair attention, memory, mood and reaction time. Intermittent hypoxia Intermittent hypoxia means repeated episodes of reduced blood oxygen separated by recovery. The depth of each fall depends on the obstruction, its duration and underlying heart or lung disease. Not every respiratory event produces the same oxygen change. Oxygen burden provides information beyond the event count alone. Stress responses during each event An obstructive event increases breathing effort and changes pressure inside the chest. The brain activates the sympathetic nervous system to reopen the airway. Heart rate and blood pressure can surge as breathing restarts. Repeated surges may contribute to cardiovascular and metabolic stress over time. OSA is not ordinary snoring Snoring is sound produced by vibration of relaxed upper airway tissues. Many people snore without repeated clinically important airway closure. Some people with OSA do not produce dramatic snoring. Snoring therefore raises suspicion but neither confirms nor excludes OSA. OSA is not simply poor sleep habits Insufficient sleep, shift work and insomnia can also cause daytime sleepiness. OSA is a breathing disorder that fragments sleep even when sleep opportunity appears adequate. More than one sleep problem can coexist. The assessment should not stop after identifying one possible contributor. Risk factors interact OSA usually results from a combination of anatomy, tissue load and reduced airway muscle effectiveness during sleep. One person may have obesity and a relatively narrow jaw. Another may have enlarged tonsils despite a lower body weight. Risk factors change probability rather than proving the diagnosis. Obesity Obesity is an important modifiable risk factor for OSA. Fat around the neck and tongue can narrow the upper airway. Abdominal obesity can reduce lung volume, making the throat more likely to collapse. However, OSA also occurs in people who are not living with obesity. Neck circumference A larger neck circumference can reflect increased soft tissue around the airway. It forms part of some screening tools, including STOP Bang. There is no single neck measurement that diagnoses OSA across every sex, body shape and ethnic group. It should be interpreted with the rest of the sleep history. Upper airway anatomy A small or set back lower jaw can reduce space behind the tongue. A large tongue, long soft palate or enlarged tonsils can also narrow the airway. Nasal obstruction can increase breathing resistance and affect treatment comfort. Anatomy helps explain susceptibility but does not show how often collapse occurs during sleep. Older age OSA becomes more common with increasing age. Changes in muscle responsiveness and upper airway structure may contribute. Older adults may report fatigue, nocturia, cognitive change or falls rather than obvious sleepiness. Age should increase awareness without making symptoms inevitable or harmless. Sex and hormonal factors OSA is diagnosed more often in men, particularly during middle age. Risk in women increases after menopause. Women can present with insomnia, fatigue, morning headache or mood symptoms rather than reporting classic sleepiness. The condition should not be dismissed because a person does not match a stereotyped presentation. Alcohol Alcohol relaxes upper airway muscles and reduces the brain's response to obstruction. Drinking near bedtime can worsen snoring, event duration and oxygen falls. Heavy or regular alcohol use also contributes to weight gain and poor sleep quality. Reducing alcohol can help but does not replace testing when OSA is suspected. Sedatives and opioids Sedative medicines can reduce airway muscle activity and arousal responses. Opioids can also suppress breathing drive and cause central or obstructive sleep related breathing problems. The effect varies between medicines and people. Prescribed treatment should be reviewed rather than stopped abruptly without clinical advice. Smoking Smoking can inflame the nose and throat and worsen upper airway symptoms. It also increases cardiovascular and respiratory risk independently of OSA. Stopping smoking benefits sleep, lung health and blood vessels. Sleeping position Gravity can move the tongue and soft palate backwards when a person lies on their back. Some people have many more respiratory events while supine than while sleeping on their side. This is called positional OSAHS. Position is only one contributor and is less useful as the sole treatment for severe disease. Nasal obstruction Allergic rhinitis, vasomotor rhinitis and structural nasal blockage can impair nasal airflow. Congestion can worsen snoring and make a nasal CPAP mask harder to tolerate. Treating rhinitis can improve comfort and adherence. It does not reliably cure obstruction lower within the throat. Enlarged tonsils Large tonsils can occupy substantial space within the throat. They are a particularly important cause in children but can also contribute in adults. NICE considers tonsillectomy for selected adults with large obstructive tonsils and a body mass index below 35 kg per square metre. Craniofacial and genetic conditions Down's syndrome, acromegaly and some craniofacial conditions increase OSA risk. The mechanisms include airway anatomy, muscle tone and soft tissue enlargement. Assessment and treatment may need reasonable adjustments and tailored support. Pregnancy Pregnancy can increase nasal congestion, weight and upper airway narrowing. NICE prioritises pregnant people with suspected OSAHS for rapid sleep service assessment. Untreated symptoms should not be attributed automatically to ordinary pregnancy fatigue. Common associated conditions OSAHS is more common in people with treatment resistant hypertension, type 2 diabetes and atrial fibrillation. It is also associated with stroke, TIA, chronic heart failure and moderate or severe asthma. These associations should increase clinical suspicion. They do not prove that OSA caused an individual's condition. Idiopathic or unexplained OSA Sometimes no dominant anatomical or metabolic contributor is identified. The person can still have genuine obstructive events and benefit from treatment. The absence of obesity or a visible throat abnormality does not exclude OSA. Loud snoring Loud habitual snoring is a common clue. It may vary with sleep stage, alcohol and body position. A bed partner may notice irregular silence followed by gasping. The loudness of snoring does not reliably indicate disease severity. Witnessed apnoeas A partner may see breathing stop, the chest struggle or the person appear to choke. Breathing then restarts with a snort, gasp or body movement. Witnessed events increase suspicion but cannot determine whether they are obstructive, central or clinically significant. Choking and gasping during sleep Some people wake abruptly feeling unable to breathe. Reflux, panic, laryngospasm and asthma can cause similar episodes. Repeated choking with snoring or witnessed pauses supports formal sleep assessment. Excessive daytime sleepiness Excessive sleepiness means difficulty maintaining wakefulness during situations in which wakefulness is expected. A person may doze while reading, watching television, sitting in meetings or travelling as a passenger. More severe sleepiness can affect driving or safety critical work. Sleepiness is different from feeling tired without an urge to sleep. Unrefreshing sleep A person can sleep for many hours but wake feeling as though they have not rested. Repeated arousals prevent consolidated restorative sleep. Unrefreshing sleep is common but non specific. Insomnia, pain, depression and restless legs can produce a similar experience. Morning headache Morning headache can occur after fragmented sleep, oxygen changes or carbon dioxide retention. It is usually non specific and may also result from migraine, bruxism or medication. Persistent morning headache with obesity, low resting oxygen or daytime drowsiness can raise concern about obesity hypoventilation syndrome. Fatigue Fatigue describes reduced energy rather than a tendency to fall asleep. Some people with OSA report fatigue as their main problem. Anaemia, thyroid disease, infection, heart failure, depression and insufficient sleep remain alternative causes. Cognitive effects Fragmented sleep can impair concentration, working memory and decision making. A person may make errors, forget appointments or struggle with complex tasks. These symptoms can be subtle and may be misattributed to stress or ageing. Mood and relationships Untreated OSA can contribute to irritability, low mood and reduced emotional regulation. Loud snoring and witnessed choking can disturb a partner's sleep. Relationship strain can become part of the clinical burden. OSA should not be assumed to explain every mood symptom without broader assessment. Nocturia Repeated arousals and changes in heart pressure can increase night time urination. Nocturia also occurs with prostate disease, diabetes, diuretics and bladder conditions. Its presence can support suspicion but is not diagnostic. Dry mouth and sore throat Mouth breathing and snoring can cause morning dryness. Nasal obstruction and mask leak can also contribute after CPAP begins. The symptom provides information about airway route and treatment comfort rather than severity. Symptoms can be absent Some people with moderate or severe OSA report little sleepiness. They may have adapted to chronic impairment or have symptoms expressed as fatigue or poor concentration. NICE advises not using the Epworth Sleepiness Scale alone to decide whether referral is needed. Daytime function OSA can reduce work performance, learning, reaction time and physical stamina. Accidents can occur at work or during travel. Treatment decisions therefore consider daytime activities and safety, not only the sleep study category. Driving risk Excessive sleepiness slows reaction time and can cause microsleeps. A microsleep is a brief unintended episode of sleep that may last only seconds. At road speed, a few seconds without effective attention can be fatal. A driver must not wait for an actual crash before treating sleepiness as unsafe. When to suspect OSAHS NICE advises assessment when two or more characteristic features are present. These include snoring, witnessed apnoeas, unrefreshing sleep and waking headaches. Other features include excessive sleepiness, fatigue, nocturia, choking, fragmented sleep and cognitive difficulty. Clinical judgement remains important when one feature is particularly concerning. The sleep history The clinician asks about usual bedtime, sleep duration, shift work and insomnia. They explore snoring, witnessed pauses, choking and body position. Daytime questions cover sleepiness, near misses, work risk and concentration. A partner's observations can be valuable when the person is unaware of events. Medical and medicine details Assessment includes blood pressure, weight, neck size and upper airway examination. The clinician reviews heart disease, stroke, diabetes, lung disease and thyroid symptoms. Alcohol, smoking, sedatives, opioids and other medicines are considered. Epworth Sleepiness Scale The Epworth Sleepiness Scale asks how likely someone is to doze in several ordinary situations. It provides a structured description of subjective sleepiness. A low score does not exclude OSA. A high score does not identify OSA as the cause of sleepiness. STOP Bang STOP Bang is a screening questionnaire combining symptoms and risk factors. It includes snoring, tiredness, observed apnoeas and blood pressure. It also considers body mass index, age, neck circumference and sex category. The result estimates risk and supports referral decisions but does not diagnose OSA. Rapid sleep service assessment NICE prioritises vocational drivers and people in safety critical jobs. Rapid assessment also applies with unstable cardiovascular disease, pregnancy or major preoperative assessment. The purpose is to reduce avoidable safety and perioperative risk. It does not mean that every suspected case requires emergency hospital admission. Pulse oximetry while awake A normal daytime oxygen saturation does not exclude OSA. Most people breathe normally while awake. A low resting saturation can indicate lung disease, heart disease or hypoventilation and may change the testing pathway. Home respiratory polygraphy NICE recommends home respiratory polygraphy as the first diagnostic test for suspected OSAHS. The equipment records several channels during sleep or attempted sleep. Typical channels include airflow, breathing effort, oxygen saturation, heart rate, snoring and body position. The test estimates respiratory events in the person's usual sleeping environment. Home oximetry Home oximetry records oxygen saturation and pulse overnight. NICE considers it when respiratory polygraphy access is limited. Repeated saw tooth oxygen falls can support OSA suspicion. Oximetry alone can miss disease and can be difficult to interpret in heart failure or chronic lung disease. Polysomnography Polysomnography is the most detailed sleep study. It adds brain activity, eye movements and muscle tone to respiratory measurements. These signals show when the person is actually asleep and identify sleep stages and arousals. NICE considers it when respiratory polygraphy is negative but significant symptoms continue or another sleep disorder is suspected. Hospital respiratory polygraphy Hospital testing can be used when home testing is impractical or additional monitoring is needed. Examples include disability, technical difficulty or complex cardiorespiratory disease. The setting does not automatically make the condition more severe. A negative test does not always end assessment A person may sleep unusually little during the study. Sensors can detach, or the person may spend less time on their back than usual. Night to night variation can change the recorded event rate. NICE supports further respiratory polygraphy or polysomnography when symptoms remain significant. Apnoea An apnoea is a complete pause in airflow lasting at least ten seconds on a sleep study. An obstructive apnoea occurs despite continuing breathing effort. The definition is technical and should not be timed by a bed partner with a phone. Hypopnoea A hypopnoea is a reduction in breathing lasting at least ten seconds. Scoring also depends on associated oxygen change or sleep arousal under the laboratory's criteria. Hypopnoeas can fragment sleep and affect oxygen even when airflow does not stop completely. Apnoea hypopnoea index The apnoea hypopnoea index is usually shortened to AHI. It is the average number of apnoeas and hypopnoeas per hour of sleep on a multi channel study. AHI is used to classify OSAHS severity. It does not directly measure every consequence of the disorder. Mild, moderate and severe OSAHS NICE defines mild OSAHS as an AHI from 5 to below 15. Moderate OSAHS has an AHI from 15 to below 30. Severe OSAHS has an AHI of 30 or more. These thresholds support treatment pathways but should be interpreted with symptoms, oxygen changes and comorbidities. Respiratory event index Many home studies estimate events per hour of recording rather than confirmed sleep. This can be called a respiratory event index. If the person lies awake for a long time, the calculated number can underestimate events during actual sleep. The sleep service interprets the device and recording method. Oxygen desaturation index The oxygen desaturation index is usually shortened to ODI. It counts oxygen falls per hour. ODI can support diagnosis and treatment monitoring. It does not identify whether each fall resulted from upper airway obstruction, lung disease or hypoventilation. AHI is not the whole severity picture Two people with the same AHI can have different oxygen falls and daytime impairment. One may have long events and cardiovascular disease. Another may have brief events with little sleepiness. The treatment discussion therefore considers the whole clinical effect. Central sleep apnoea Central sleep apnoea involves pauses without normal breathing effort. It can occur with heart failure, neurological disease, high altitude or opioid use. Some people have both central and obstructive events. CPAP selection and specialist evaluation may differ from ordinary OSA. Obesity hypoventilation syndrome Obesity hypoventilation syndrome is usually shortened to OHS. It involves obesity and raised carbon dioxide while awake after other causes are excluded. Most people with OHS also have OSAHS, but OHS is a distinct ventilatory disorder. It can require non invasive ventilation rather than ordinary CPAP alone. Clues to hypoventilation Waking headaches, peripheral oedema and low daytime oxygen can raise concern. Unexplained high red cell concentration may also be a clue. Severe daytime drowsiness, confusion or breathlessness can indicate ventilatory failure. Blood gas testing measures carbon dioxide directly. COPD and OSAHS overlap A person can have both COPD and OSAHS. This is called COPD OSAHS overlap syndrome. Overnight oxygen disturbance can be greater than with either condition alone. Treatment and oxygen decisions require specialist assessment because oxygen alone does not correct upper airway obstruction. Treatment goals Treatment aims to keep the airway open during sleep. It also aims to improve sleepiness, quality of life and safe daytime function. Long term care addresses weight, alcohol, smoking, blood pressure and associated disease. The plan should be effective enough to use consistently. Lifestyle advice for every severity NICE recommends tailored discussion of weight, smoking, alcohol and sleep hygiene for all OSAHS severities. Lifestyle treatment is supportive, not a moral judgement. A person should not be denied effective airway treatment while trying to lose weight. Weight management Weight loss can reduce tissue around the airway and improve lung volume. Even modest sustained loss can reduce OSA severity in some people. The condition may persist despite major weight reduction because anatomy and age still matter. Repeat assessment may be needed before changing established treatment. Weight loss treatment Support can include dietary care, physical activity, behavioural programmes and weight management medicines when indicated. Bariatric surgery can substantially improve OSA in selected people living with severe obesity. Neither medicine nor surgery guarantees complete resolution. CPAP should continue until the sleep service confirms that it is no longer needed. Alcohol reduction Reducing evening alcohol can decrease airway relaxation and sleep fragmentation. People who are dependent on alcohol need medically appropriate support because abrupt withdrawal can be dangerous. Sedative review The prescriber reviews benzodiazepines, sleeping tablets, opioids and other sedating medicines. The aim is to reduce avoidable respiratory and daytime impairment while treating the original condition safely. Abruptly stopping long term sedatives or opioids can cause withdrawal and harm. Sleep hygiene Regular sleep opportunity helps distinguish residual sleepiness from insufficient sleep. Useful measures include a consistent schedule and limiting late stimulants. Sleep hygiene does not mechanically open a collapsing airway. It should not be presented as a cure for moderate or severe OSAHS. Continuous positive airway pressure Continuous positive airway pressure is usually shortened to CPAP. A machine delivers air through a mask at a pressure that splints the upper airway open. CPAP is not simply extra oxygen. It prevents obstruction only while it is being used. Fixed level CPAP Fixed level CPAP delivers a set pressure throughout use. NICE offers it with lifestyle advice for moderate or severe OSAHS. It is also offered for symptomatic mild OSAHS when daytime activities or quality of life are affected and lifestyle advice alone is insufficient or inappropriate. Auto adjusting CPAP Auto CPAP changes pressure within a prescribed range according to detected breathing patterns. NICE considers it when pressure needs vary, fixed pressure is poorly tolerated or local cost and monitoring conditions support it. One mode is not automatically better for every person. CPAP and moderate or severe OSAHS CPAP is the usual first line airway treatment for moderate or severe OSAHS. It can reduce respiratory events, snoring and daytime sleepiness. Benefits depend on correct pressure, mask fit and regular use during sleep. CPAP in mild OSAHS Mild disease without important daytime effects may be managed through lifestyle and sleep measures alone. CPAP is offered when symptoms affect usual activities or quality of life and relevant NICE conditions are met. The AHI label alone does not describe treatment need completely. CPAP use CPAP should be used whenever the person sleeps, including naps. Using it for only the first part of the night leaves later sleep untreated. Rapid eye movement sleep often increases towards morning, when obstruction can be prominent. CPAP is treatment rather than cure The airway can collapse again when CPAP is removed. Symptoms may return after one or several nights without effective treatment. Weight change, surgery or other interventions can alter future need. Any trial without CPAP should be agreed with the sleep service. Masks Masks can cover the nose, the nose and mouth, or use nasal pillows. Choice depends on breathing route, comfort and pressure requirements. Leak can reduce treatment effectiveness and cause dry eyes or noise. A poorly fitting mask should prompt adjustment rather than abandonment of treatment. CPAP side effects Common problems include nasal congestion, dryness, pressure marks and a sensation of claustrophobia. Heated humidification can help nasal or mouth dryness. Gradual practice while awake can improve tolerance. Persistent symptoms should be discussed with the sleep service. Rhinitis treatment NICE recommends assessing nasal congestion for allergic or vasomotor rhinitis. Nasal corticosteroids or antihistamines are used according to the diagnosis. Mask type and humidification can be adjusted because CPAP itself can cause or worsen rhinitis. CPAP monitoring Modern devices can record use, mask leak, pressure and residual respiratory events. Telemonitoring can support early troubleshooting. NICE recommends early follow up, usually within one month, and continued review until symptoms and AHI or ODI are controlled. Device data support rather than replace the person's experience. Mandibular advancement splints A mandibular advancement splint holds the lower jaw forwards during sleep. This increases space behind the tongue and can reduce obstruction. NICE considers a customised or semi customised device when an adult declines or cannot tolerate CPAP and dental health is suitable. Dental suitability The device needs enough healthy teeth and stable gums for support. It may be unsuitable with active periodontal disease, untreated decay or very few teeth. Possible adverse effects include jaw discomfort, tooth movement and bite change. Dental review and adjustment improve safety. Positional therapy A positional modifier discourages sleeping on the back. NICE considers it for mild or moderate positional OSAHS when other treatments are unsuitable or not tolerated. It is unlikely to control severe OSAHS reliably. Effectiveness should be confirmed through symptoms and objective monitoring. Treating enlarged tonsils Tonsillectomy can remove an important anatomical obstruction in selected adults. NICE considers it when tonsils are large and obstructive and BMI is below 35 kg per square metre. Surgery has pain, bleeding and anaesthetic risks. It is not routine treatment for every person who snores. Other upper airway surgery NICE considers specialist oropharyngeal surgical assessment for severe OSAHS when CPAP and a customised mandibular advancement splint cannot be tolerated despite supervised attempts. The procedure depends on the obstruction pattern and anatomy. Surgery may improve disease without eliminating every event. Oxygen is not routine OSA treatment Supplemental oxygen can raise oxygen saturation without preventing airway collapse or sleep fragmentation. It can worsen carbon dioxide retention in susceptible people. Oxygen is prescribed only for a defined additional indication within specialist care. Cardiovascular associations OSAHS is associated with hypertension, atrial fibrillation, stroke and heart failure. Intermittent hypoxia and sympathetic activation provide plausible contributing mechanisms. These relationships are influenced by shared factors including age and obesity. Treating OSA complements rather than replaces standard cardiovascular prevention. Blood pressure CPAP can reduce blood pressure modestly in some people, particularly with good adherence and resistant hypertension. Antihypertensive treatment remains necessary when indicated. A normal blood pressure does not exclude OSA. Atrial fibrillation OSA is common in people with atrial fibrillation and may contribute to rhythm recurrence. Weight management, alcohol reduction and effective OSA treatment support wider AF care. Anticoagulation decisions remain based on stroke risk rather than CPAP use. Stroke Untreated OSA is associated with stroke risk and can be under recognised after a stroke. OSA treatment may improve sleepiness and rehabilitation participation. Antiplatelet, anticoagulant, statin and blood pressure decisions still follow the stroke mechanism. Metabolic associations OSAHS is associated with insulin resistance and type 2 diabetes. Sleep fragmentation and intermittent hypoxia can affect glucose regulation. Weight and other shared factors contribute strongly. CPAP is not a substitute for diabetes treatment or cardiovascular risk management. What treatment can confidently improve Effective CPAP usually reduces obstructive events and snoring. It can improve excessive sleepiness, vigilance and quality of life. It can support safer driving once symptom control and treatment adherence are confirmed. It should not be promised as guaranteed prevention of every heart attack, stroke or metabolic complication. Driving must be addressed directly A person who has excessive sleepiness affecting driving must not drive. This applies while OSAHS is suspected as well as after diagnosis. Driving can resume only when sleepiness is satisfactorily controlled and necessary treatment is being followed. The person should obtain individual advice from the sleep service and DVLA guidance. Confirmed moderate or severe OSAHS and DVLA Current DVLA guidance requires notification when moderate or severe OSAHS is confirmed and causes excessive sleepiness. The person must not drive until the condition is controlled, sleepiness has improved and treatment adherence is demonstrated. Group 1 and Group 2 licences have different ongoing review requirements. Mild or suspected OSAHS with sleepiness Excessive sleepiness from suspected OSAHS or mild OSAHS also means the person must not drive. If satisfactory symptom control cannot be achieved within three months, DVLA must be notified under the current medical standards. Diagnosis without sleepiness affecting driving does not automatically create the same notification rule. Vocational drivers Bus, coach and lorry drivers have stricter licensing oversight because of vehicle size and time on the road. NICE prioritises vocational drivers for rapid sleep service assessment. A professional driver should not conceal sleepiness through fear of work consequences. Early effective treatment can support safe return to driving. Near misses and microsleeps Drifting lanes, missing road signs or waking after travelling part of a route are serious warning signs. Opening a window, increasing music volume or using caffeine does not make continued driving safe. The driver should stop in a safe place and not resume until safe transport and clinical advice are arranged. Safety critical work Sleepiness can endanger people operating machinery, working at height or monitoring critical systems. The occupational risk should be included in referral information. Temporary work modification may be needed until symptoms are controlled. Follow up Follow up reviews symptoms, daytime vigilance and treatment use. For CPAP, clinicians assess residual AHI or ODI, mask leak and pressure needs. Weight, alcohol, medicines and associated conditions are reviewed. Once treatment is optimised, ongoing review is commonly annual and remains accessible between appointments. Residual sleepiness Some people remain sleepy despite apparently effective CPAP. The team checks actual use, mask leak and residual obstruction. Insufficient sleep, shift work, depression, restless legs, narcolepsy and sedating medicines are considered. Persistent sleepiness must not be dismissed as treatment failure without investigation. OSA can change over time Weight gain, menopause, ageing and new medicines can worsen obstruction. Weight loss, airway surgery or treatment of nasal disease can reduce it. Repeat testing may be appropriate when symptoms or clinical circumstances change substantially. Prognosis OSA is usually controllable when it is recognised and treatment is used consistently. Many people notice major improvements in alertness, concentration and quality of life. Untreated disease can continue disrupting sleep and increasing accident risk. Associated cardiovascular and metabolic conditions still need their own active management. Emotional and practical effects A diagnosis can create anxiety about driving, work and long term health. CPAP can initially affect intimacy, travel and sleeping arrangements. Practical mask support and clear licensing advice are more useful than blame. Partners can be involved when the person wishes because they often observe treatment benefit first. What this lesson should not be used for This lesson cannot diagnose OSA from snoring, body size or a smartwatch oxygen trace. Do not calculate an AHI without a validated sleep study or use a screening score as proof. Do not stop prescribed sedatives, opioids or CPAP without clinical advice. Do not drive when excessive sleepiness could impair attention. Call 999 for collapse, stroke symptoms, severe breathing difficulty or another acute emergency.

Obstructive sleep apnoea is repeated upper airway narrowing or closure during sleep, causing breathing events, intermittent oxygen falls and fragmented sleep. Diagnosis requires a sleep study, while treatment combines modifiable contributors with CPAP or another airway intervention. Excessive sleepiness creates an immediate driving safety responsibility.