Obstructive sleep apnoea

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

During sleep, pharyngeal dilator tone falls. In susceptible anatomy, inspiratory negative pressure narrows the upper airway, producing continued effort against partial or complete obstruction. Repeated arousals restore tone but fragment sleep and activate sympathetic responses. The result ranges from loud snoring without daytime impairment to severe sleepiness, resistant hypertension, occupational risk and substantial nocturnal hypoxaemia.

History should include a bed partner when the patient agrees, but absence of a witness is not reassuring. Sleepiness can be underestimated because the person has adapted activity, and fatigue is not synonymous with involuntary sleep propensity. Shift work, insufficient sleep, depression, medicines, restless legs, narcolepsy and medical disease remain alternatives. Urgent pathways are appropriate for vocational drivers, safety-critical workers, pregnancy, unstable cardiorespiratory disease or profound sleepiness where delay creates harm.

CPAP works only while used, splinting the pharynx with positive pressure. Device data can reveal nightly use, leak and residual events but require clinical interpretation. Treatment should also address weight, alcohol near bedtime, smoking, sleep opportunity and nasal obstruction. Tonsillar or craniofacial anatomy may justify ENT or maxillofacial assessment, while bariatric referral follows current obesity guidance rather than being presented as a rapid cure.

Key points

OSAHS is recurrent upper-airway narrowing or collapse during sleep causing apnoeas, hypopnoeas, arousal and often intermittent hypoxaemia.
Ask about witnessed pauses, choking, loud snoring, unrefreshing sleep, morning headache, nocturia, impaired concentration, irritability and daytime sleepiness rather than snoring alone.
Risk rises with obesity, male sex, age, craniofacial or upper-airway anatomy, alcohol, sedatives and endocrine or neurological conditions, but lean people can also have important OSAHS.
Questionnaires estimate pre-test probability and sleepiness; they do not diagnose OSAHS or replace a sleep study.
NICE recommends home respiratory polygraphy as the first-choice diagnostic test for most adults with suspected OSAHS.
A negative home study does not end assessment when symptoms are strong, sleep time was short, sensors failed or another sleep or ventilatory disorder remains possible.
Severity is not the AHI alone: excessive sleepiness, oxygen burden, comorbidity, driving risk and functional impairment change urgency and treatment.
Offer CPAP according to NICE severity and symptom impact, with early troubleshooting of mask, pressure, leak, dryness and nasal obstruction.
A customised mandibular advancement splint is an alternative for suitable people, particularly mild OSAHS or CPAP intolerance, but requires adequate dentition and dental oversight.
Apply current DVLA rules precisely: impaired driving from sleepiness requires stopping driving, and notification duties depend on severity, sleepiness and licence group.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Upper-airway anatomy

A narrow or collapsible pharynx from craniofacial structure, enlarged soft tissue or tonsils predisposes to obstruction during sleep.

Obesity

Fat deposition around the neck and tongue narrows the airway, while abdominal obesity reduces lung volume and stabilising caudal traction.

Reduced neuromuscular tone

Sleep normally lowers pharyngeal dilator activity; alcohol, sedatives and individual control instability can make collapse more frequent or prolonged.

Age and endocrine factors

Risk rises with age and after menopause, while hypothyroidism and acromegaly are uncommon but relevant contributors in a compatible phenotype.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pharyngeal collapse
During sleep, inspiratory negative pressure exceeds the stabilising force of upper-airway muscles, partially or completely obstructing airflow.
2
Intermittent hypoxaemia
Continued respiratory effort against obstruction lowers oxygen and raises carbon dioxide until an arousal restores airway tone.
3
Sleep fragmentation
Repeated micro-arousals disrupt restorative sleep architecture even when the person does not remember waking, contributing to the resulting loss of respiratory reserve.
4
Sympathetic and vascular stress
Cycles of hypoxia, reoxygenation and arousal activate sympathetic, oxidative and inflammatory pathways that raise cardiovascular load.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Nocturnal obstructive pattern

Habitual disruptive snoring, witnessed apnoeas, gasping, choking and restless sleep strongly suggest OSAHS, particularly when daytime impairment or relevant cardiometabolic disease is present.

Excessive sleepinessRed flag

Unintended sleep during conversation, work or driving, near-misses and reduced vigilance indicate functional danger; ask directly because patients may use caffeine or activity to conceal symptoms.

Cardiometabolic presentation

Resistant hypertension, atrial fibrillation, nocturnal arrhythmia, heart failure, stroke or type 2 diabetes may coexist with OSAHS even when classic subjective sleepiness is modest.

Possible hypoventilation overlapRed flag

Marked obesity, daytime hypoxaemia, raised bicarbonate, morning headache, oedema or awake hypercapnia suggests OHS or COPD overlap and requires carbon dioxide assessment rather than simple OSA testing alone.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Sleep and driving history with Epworth or STOP-Bang supportFirst step
Why
Estimate pre-test probability, impairment and urgency.
Interpretation and limitations
Scores structure history but do not diagnose disease. A low Epworth score does not exclude witnessed OSAHS or safety risk, particularly when the patient avoids soporific situations.
02
Home respiratory polygraphy
Why
Measure respiratory events, effort, airflow, oxygen and related channels during sleep time.
Interpretation and limitations
Use technically adequate recording and interpret event index with symptoms and comorbidity. Recording time may exceed true sleep time and underestimate severity; sensor loss can make a negative test uninterpretable.
03
Home overnight oximetry
Why
Provide an alternative when respiratory polygraphy access is limited.
Interpretation and limitations
Repeated saw-tooth desaturation may support OSAHS, but normal oximetry does not exclude arousal-heavy disease and sustained desaturation may represent hypoventilation or lung disease.
04
Hospital respiratory polygraphy or polysomnography
Why
Resolve technically difficult, discordant or complex presentations.
Interpretation and limitations
Consider when home testing is impractical, symptoms remain despite a negative study, parasomnia or another sleep disorder is suspected, or cardiorespiratory and neurological complexity alters interpretation.
05
Awake arterial or arterialised capillary blood gas
Why
Detect daytime ventilatory failure in people at risk.
Interpretation and limitations
Raised PaCO2 is not explained by uncomplicated OSAHS alone and should prompt assessment for OHS, COPD, neuromuscular or chest-wall disease and sedative effects.
06
CPAP device download
Why
Assess adherence, leak and residual events after treatment begins.
Interpretation and limitations
Machine indices are estimates and can be distorted by leak or central events. Relate them to sleepiness, symptoms, mask comfort and technically reliable nightly use.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Primary snoring

Noisy breathing without recurrent obstructive events, oxygen disturbance or clinically important sleep fragmentation does not establish OSA.

Obesity hypoventilation syndrome

Confirmed awake hypercapnia in an obese person indicates broader alveolar hypoventilation rather than OSA alone, and the distinction changes the subsequent clinical pathway.

Central sleep apnoea

Pauses without respiratory effort, often associated with heart failure, opioids or neurological disease, require a different sleep-study interpretation.

Insomnia or insufficient sleep

Short or fragmented sleep from behavioural, mood or environmental causes may explain daytime tiredness without obstructive physiology.

Narcolepsy or other hypersomnolence

Irresistible sleep attacks, cataplexy or persistent sleepiness despite adequate treated breathing events suggests a central sleep-wake disorder.

Additional chapter-specific clues

Alternative sleep disorder

Cataplexy, sleep paralysis, irresistible sleep attacks despite adequate sleep, prominent limb sensations, parasomnia or circadian disruption should broaden specialist assessment beyond obstructive events.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01SuspectIdentify risk and urgencyFirst stepSnoring, witnessed events, non-restorative sleep or daytime impairment suggests OSAHS.

1Document nocturnal events, sleep opportunity, daytime sleepiness, near-misses, occupation, licence group, alcohol, medicines and relevant comorbidity.
2Advise immediate driving cessation when sleepiness could impair driving and explain current DVLA responsibilities without promising a licensing outcome.
3Examine BMI, neck and upper airway, blood pressure and cardiorespiratory signs, looking specifically for awake hypoventilation or structural disease.
4Refer with appropriate priority for home respiratory polygraphy, using hospital testing when home testing is unsuitable or the presentation is complex.

02InterpretReconcile study and symptomsA home sleep-study result becomes available.

1Check recording quality, estimated sleep time, sensor integrity, body position, event type and oxygen pattern before accepting the reported index.
2Grade physiological disease while separately recording sleepiness, quality-of-life effect, cardiovascular comorbidity and driving or occupational risk.
3If the result is negative but suspicion remains high, arrange repeat or more comprehensive testing rather than declaring symptoms psychological.
4If sustained desaturation or suspected hypoventilation appears, measure awake gas and overnight carbon dioxide and move to OHS or overlap assessment.

03TreatChoose a sustainable interventionOSAHS is confirmed and treatment is indicated by severity, symptoms or risk.

1Discuss CPAP, expected benefit and alternatives, then fit an appropriate interface and provide education, humidification or nasal care when needed.
2For suitable mild disease or CPAP intolerance, consider a customised mandibular advancement splint or positional strategy with dental and sleep-service input.
3Address weight without stigma, alcohol near sleep, smoking, sleep duration and sedating medicines, and refer anatomical obstruction selectively.
4Review early enough to solve leak, pressure intolerance, dryness and claustrophobia before the device is abandoned.

04Follow-upDemonstrate control and adherenceCPAP or another OSAHS treatment has started.

1Assess sleepiness, driving safety, snoring, nocturia, cognition and quality of life, alongside nightly use, leak and residual device events.
2Modify interface, humidification, nasal treatment, pressure mode or behavioural support through the sleep service when adherence is limited.
3Confirm current DVLA conditions for return to driving; satisfactory symptom control and treatment adherence must be evidenced where notification applies.
4Repeat diagnostic study only when symptoms, weight, anatomy or treatment response creates a management-changing question.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Splint the pharyngeal airway, reduce obstructive events and improve sleepiness and quality of life.

Continuous positive airway pressure therapy

Use the sleep-service-selected fixed or auto-adjusting pressure every time the person sleeps, with the fitted mask and humidification plan.

CPAP is device therapy rather than oxygen or ventilation for awake hypercapnia. Address leak, pressure sores, aerophagia, dryness and nasal obstruction; do not judge adherence from one night or stop because symptoms improve.

Advance the mandible and upper-airway tissues as an alternative treatment for selected OSAHS.

Customised mandibular advancement splint

Wear the dentist-fitted, progressively titrated device during sleep according to the sleep and dental team's individual schedule.

Requires sufficient healthy teeth and periodontal support; can cause jaw discomfort, salivation and bite change. Over-the-counter devices are not equivalent, and objective response review may be needed.

Avoid ineffective prescribing and reduce medicines that worsen upper-airway obstruction or daytime vigilance.

No routine pharmacotherapy for OSAHS

No medicine dose replaces CPAP or mechanical treatment; review alcohol, opioids, hypnotics and other sedating drugs individually.

Do not abruptly stop dependence-forming medicines. Some patients need essential sedatives or analgesia; balance benefits and risks with the prescriber while treating OSAHS and preserving sleep and mental health.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Road and workplace accidents

Excessive sleepiness and impaired vigilance increase collision and safety-critical occupational risk, creating specific driving responsibilities, and potentially prolonging treatment and functional recovery.

Hypertension and cardiovascular disease

Repeated sympathetic surges and intermittent hypoxia contribute to difficult blood-pressure control, arrhythmia and vascular risk, and increasing the burden of otherwise local respiratory disease.

Metabolic dysfunction

Sleep fragmentation and hypoxia worsen insulin resistance and weight regulation, reinforcing cardiometabolic disease, adding morbidity beyond the initial pulmonary disorder.

Cognitive and mood effects

Poor-quality sleep causes impaired concentration, memory, irritability, low mood and reduced quality of life, adding morbidity beyond the initial pulmonary disorder.

Perioperative respiratory risk

Sedation, opioids and supine positioning increase upper-airway obstruction and postoperative hypoxaemia when OSA is unrecognised or support is interrupted.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review subjective sleepiness, near-misses, driving status, work safety and sleep opportunity at diagnosis and after every material treatment change.
Use CPAP nightly hours, proportion of nights, leak and residual events with symptoms; an excellent device index cannot compensate for minimal use.
Inspect nasal symptoms, mouth leak, skin pressure, aerophagia, mask fit and cleaning, offering timely interface or humidification adjustment.
Track weight, blood pressure and relevant atrial fibrillation, heart failure or metabolic comorbidity without promising CPAP alone will reverse them.
For splints, monitor dental health, temporomandibular symptoms, bite and objective treatment response through coordinated dental and sleep review.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

AHI can underestimate harm

A modest event index with profound sleepiness or occupational driving may be more urgent than a higher index in an asymptomatic non-driver.

Recording is not sleeping

Many home studies divide events by recording time rather than measured sleep time, so prolonged wakefulness can dilute the index and create a false-negative impression.

Oximetry shows pattern not mechanism

Cyclical dips suggest recurrent obstruction, while sustained low oxygen may reflect hypoventilation or lung disease. Neither pattern alone supplies a complete diagnosis.

Driving advice is treatment

Explicitly addressing sleepiness and DVLA duties prevents collisions. Vague advice to 'be careful' is inadequate when the person cannot reliably stay awake.

Early troubleshooting preserves adherence

A different mask, humidifier, ramp or pressure approach in the first weeks often converts apparent intolerance into sustainable therapy.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing OSAHS from snoring, obesity or a questionnaire without an objective sleep study.
02
Reassuring a profoundly sleepy driver because their Epworth score or event index seems modest.
03
Calling a technically inadequate negative home study definitive despite a strong witnessed history.
04
Using oxygen alone for sustained nocturnal desaturation without assessing hypoventilation and PaCO2.
05
Issuing CPAP without early mask, leak, humidification and adherence support.
06
Giving generic DVLA advice without checking current rules, licence group, severity, sleepiness and treatment control.