Obstructive sleep apnoea

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

OSA is recurrent partial or complete upper-airway collapse during sleep with disrupted ventilation or sleep architecture. Paediatric airways are narrow and lymphoid tissue relatively large.

Sleep reduces pharyngeal muscle tone. Adenotonsillar enlargement, obesity-related soft tissue, craniofacial restriction or neuromuscular weakness shifts the airway toward collapse.

Repeated hypoxaemia, carbon-dioxide change and arousal activate sympathetic and inflammatory pathways. Consequences include impaired attention, growth, blood pressure and cardiopulmonary strain.

History should quantify nights per week, pauses, colour, sleep position, restlessness, morning headache, school function and enuresis. A short caregiver video can document sound and effort but cannot grade severity.

Polysomnography distinguishes obstructive from central events and detects hypoventilation. The apnoea-hypopnoea index is interpreted with desaturation, carbon dioxide, sleep stage and comorbidity rather than alone.

Oximetry detects desaturation clusters but misses arousal-based obstruction and mild disease. A negative result is not reassurance in Down syndrome or neuromuscular weakness.

Adenotonsillectomy often improves otherwise healthy children with hypertrophy, yet obesity and multilevel anatomy create residual disease. Plan follow-up before surgery.

Positive pressure splints the airway and bilevel ventilation supports hypoventilation. It requires a child-centred acclimatisation programme rather than simply issuing a machine.

Medical nasal treatment reduces inflammatory obstruction in selected mild cases, not fixed severe collapse. Review response and do not allow indefinite unmonitored treatment.

Communication should avoid blaming weight or behaviour. Sleep fragmentation can itself drive appetite, irritability and reduced activity.

Key points

Ask about habitual snoring, pauses, gasping, restless sleep, unusual positions, sweating, mouth breathing and enuresis. Children often show hyperactivity, irritability and poor concentration rather than obvious daytime sleepiness.
Examine nasal patency, tonsils, palate, jaw, neck, weight and blood pressure. Tonsil size while awake does not reliably grade sleep obstruction.
First-line assessment is a structured sleep history, video when available and risk examination. Primary snoring without gas exchange or functional effect remains a diagnosis of exclusion.
Reference standard: attended overnight polysomnography measuring sleep state, airflow, effort, oxygen, carbon dioxide and arousals. Use age-specific paediatric scoring; adult thresholds are inappropriate.
Overnight oximetry can prioritise obvious moderate-to-severe disease but a normal or inconclusive result does not exclude OSA, especially in a high-risk child.
Adenotonsillectomy is first-line anatomical treatment when significant OSA accompanies adenotonsillar hypertrophy. ENT and anaesthesia assess bleeding, respiratory and postoperative monitoring risk.
Children under 3, severe OSA, obesity, Down syndrome, craniofacial or neuromuscular disease often need inpatient postoperative observation and specialist planning.
Use family-centred weight support when obesity contributes; do not delay treatment of severe obstruction until weight changes.
Intranasal corticosteroid and/or montelukast may be considered by specialists for selected mild disease or residual inflammation; counsel montelukast neuropsychiatric risk and define review.
CPAP or bilevel support is first-line when surgery is unsuitable, obstruction persists or hypoventilation coexists. Mask fit, humidification, desensitisation and family support determine adherence.
Treat allergic rhinitis, avoid smoke and sedating medicines, and provide school and behavioural support while definitive care proceeds.
Repeat symptom and objective assessment after treatment in high-risk children; growth, behaviour and blood pressure are meaningful outcomes beyond snoring.

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

Adenotonsillar enlargement

Lymphoid tissue narrows the common paediatric pharyngeal airway, especially during sleep-related loss of muscle tone. within the child-specific clinical phenotype.

Obesity

Pharyngeal soft tissue, reduced lung volume and altered ventilatory control increase collapsibility and hypoventilation risk. within the child-specific clinical phenotype.

Craniofacial or neuromuscular disease

Small midface or mandible, macroglossia and weak airway dilators create multilevel persistent obstruction. within the child-specific clinical phenotype.

Nasal inflammation

Allergic rhinitis and turbinate swelling increase resistance and mouth breathing, amplifying pharyngeal collapse. within the child-specific clinical phenotype.

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

1
Sleep-related airway collapse
Reduced dilator tone allows inspiratory negative pressure to narrow or close a susceptible pharynx. during progression of the respiratory disorder.
2
Intermittent gas-exchange disturbance
Obstruction produces hypoxaemia and sometimes hypercapnia until arousal restores airway tone and airflow. during progression of the respiratory disorder.
3
Sleep fragmentation
Repeated arousals disrupt restorative sleep even when desaturation is modest, affecting behaviour, learning and quality of life.
4
Cardiometabolic stress
Sympathetic surges and inflammation contribute to hypertension, insulin resistance and pulmonary vascular strain. during progression of the respiratory disorder.

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

Night symptoms

Record snoring frequency, pauses, gasping, colour, sweating, restless positions, mouth breathing and enuresis.

Daytime effect

Assess sleepiness, hyperactivity, irritability, morning headache, learning, growth and family sleep disruption.

Airway examination

Inspect nose, tonsils, palate, tongue and jaw and assess voice and mouth breathing without inferring severity from tonsils alone.

Comorbidity

Measure BMI and blood pressure and identify Down syndrome, craniofacial, neuromuscular, storage and cardiac disease.

Medicine and environment

Review sedatives, opioids, rhinitis treatment, smoke exposure, housing and access to sleep services.

Caregiver evidence

Use a representative sleep video and school observations to supplement, not replace, objective evaluation.

Red flags requiring action

Witnessed prolonged apnoea, cyanosis, gasping or profound desaturation requires expedited paediatric sleep and airway assessment.
Failure to thrive in a young child or rapid obesity-related gain with hypoventilation indicates significant physiological effect.
Pulmonary hypertension, systemic hypertension, morning headache or daytime hypercapnia suggests advanced disease.
Down syndrome, craniofacial difference, achondroplasia, neuromuscular disease and mucopolysaccharidosis increase multilevel obstruction and perioperative risk.
Excessive daytime sleepiness causing dangerous episodes, school failure, severe behaviour change or developmental regression needs timely assessment.
Adenotonsillar surgery does not guarantee cure in obesity or syndromic disease; persistent symptoms require repeat objective evaluation.

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
Reference standard: attended polysomnographyFirst stepReference standard
Why
Measure obstructive events, sleep disruption, gas exchange and hypoventilation across sleep stages.
Interpretation and limitations
Use paediatric scoring and integrate event index with oxygen, carbon dioxide, arousal burden, symptoms and comorbidity.
02
Overnight pulse oximetry
Why
Triage likely moderate-to-severe OSA and prioritise referral where polysomnography is limited.
Interpretation and limitations
Repeated desaturation clusters support obstruction; a normal or incomplete study cannot exclude OSA.
03
Cardiorespiratory sleep study
Why
Assess airflow, effort, heart rate and gas exchange when full polysomnography is not necessary or available.
Interpretation and limitations
It may underestimate arousal-based events because sleep staging is limited; interpret in the specialist pathway.
04
Carbon dioxide monitoring
Why
Detect nocturnal hypoventilation in obesity, neuromuscular or craniofacial disease.
Interpretation and limitations
Sustained elevation changes ventilatory support and perioperative planning even if event count is modest.
05
Targeted ENT and cardiometabolic assessment
Why
Define anatomy and complications before intervention.
Interpretation and limitations
Flexible nasendoscopy, blood pressure, ECG or echocardiography are selected from phenotype, not routine for simple snoring.

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

Primary snoring

Snoring without obstructive events, gas-exchange abnormality or functional consequence requires careful exclusion of evolving disease. when timing, examination and trajectory are integrated.

Central sleep apnoea

Absent respiratory effort during pauses suggests neurological, cardiac, medication or developmental ventilatory-control disease. when timing, examination and trajectory are integrated.

Nocturnal asthma

Cough, expiratory wheeze and variable airflow symptoms differ from inspiratory snoring and obstructive pauses. when timing, examination and trajectory are integrated.

Parasomnia or seizure

Stereotyped movements, confusion or events without obstructive breathing may require neurological or sleep review. when timing, examination and trajectory are integrated.

Sleep restriction and behavioural insomnia

Insufficient or fragmented sleep from routines can produce similar daytime behaviour without airway obstruction. when timing, examination and trajectory are integrated.

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

01AssessBuild a sleep phenotypeFirst stepHabitual snoring, witnessed pauses or daytime impairment is reported.

1Take structured night and day history and examine airway, growth, blood pressure and risk conditions.
2Use video and oximetry for context without allowing a normal result to end high-risk assessment.
3Refer for paediatric sleep or ENT testing according to severity and comorbidity.

02ConfirmChoose the right sleep studyDiagnosis or severity will alter surgery, ventilation or monitoring.

1Reference standardUse attended polysomnography as the reference standard where diagnostic precision is required.
2Use cardiorespiratory study or oximetry only within a pathway that manages inconclusive results.
3EscalationEscalate urgently for profound hypoxaemia, hypoventilation or cardiopulmonary consequences.

03AnatomicalTreat adenotonsillar obstructionSignificant OSA accompanies clinically important adenotonsillar hypertrophy.

1Discuss adenotonsillectomy through ENT with shared benefits and bleeding or respiratory risks.
2Plan inpatient postoperative monitoring for young, severe or comorbid children.
3Reassess symptoms and repeat objective testing when residual disease risk is high.

04PersistentSupport airway and whole childSurgery is unsuitable, incomplete or obstruction is multilevel.

1Initiate CPAP or bilevel ventilation with specialist mask and desensitisation support.
2Treat rhinitis and offer non-stigmatising family weight support without delaying airway care.
3Monitor growth, behaviour, blood pressure, adherence and objective response.

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

Neurobehavioural impairment

Poor attention, hyperactivity, irritability and school difficulty can arise from chronic sleep fragmentation. when recognition or effective treatment is delayed.

Growth and metabolic effects

Increased work and disrupted growth-hormone sleep can impair growth, while obesity-associated disease worsens insulin resistance. when recognition or effective treatment is delayed.

Cardiovascular disease

Systemic and pulmonary hypertension and ventricular strain may develop in severe prolonged obstruction. when recognition or effective treatment is delayed.

Perioperative respiratory events

Severe disease and comorbidity increase obstruction and desaturation after anaesthesia and opioid exposure. when recognition or effective treatment is delayed.

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

Track snoring, apnoea, sleepiness or behaviour, school function, enuresis and quality of life.
Plot growth and BMI and measure blood pressure with appropriate centiles.
After adenotonsillectomy, repeat objective testing in severe, obese, syndromic or persistently symptomatic children.
For CPAP, review mask leak, skin, nasal symptoms, device data and family burden.
Review intranasal or montelukast trials at a defined interval and stop ineffective treatment.
Avoid sedative and opioid exposure where possible and communicate OSA before procedures.
Re-escalate for cyanosis, profound desaturation, morning headache or declining daytime function.

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

Hyperactivity can be sleepiness

A sleep-deprived child may become impulsive and inattentive rather than visibly dozing during the day.

Tonsils do not grade physiology

Small visible tonsils do not exclude multilevel obstruction, and large tonsils do not prove severe gas-exchange disease.

Oximetry can rule in, not out

Characteristic clusters are useful, but arousal-based obstruction can occur with a normal saturation trace.

Surgery may leave residual disease

Obesity, Down syndrome and craniofacial or neuromuscular disease need planned post-treatment objective review.

Weight and airway care run together

Family weight support improves long-term risk but is not a reason to withhold timely treatment for severe obstruction.

11Common pitfallsFrequent interpretation and management errors.

01
Do not diagnose or grade OSA from snoring or tonsil size alone.
02
Do not exclude OSA after normal overnight oximetry in a high-risk child.
03
Do not use adult apnoea thresholds for children.
04
Do not assume daytime sleepiness is required.
05
Do not delay severe airway treatment until weight changes.
06
Do not prescribe sedatives or unmonitored oxygen as primary therapy.
07
Do not omit postoperative monitoring in high-risk disease.
08
Do not assume adenotonsillectomy cures syndromic or obesity-related OSA.