Obstructive Sleep Apnoea in Children
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Direct answer
Snoring on most nights in a child is a symptom to investigate, not background noise: when snoring combines with laboured breathing, witnessed apnoeic pauses, restless sleep, mouth breathing by day and behavioural or growth consequences, obstructive sleep apnoea is confirmed. Adenotonsillar hypertrophy is the dominant cause in children, with obesity now a rising contributor in Indian practice. Overnight polysomnography remains the gold standard, and the paediatric threshold is an apnoea-hypopnoea index above one per hour — not the adult value of five — a distinction examiners reward. First-line treatment is adenotonsillectomy, which resolves the majority; continuous positive airway pressure and anti-inflammatory therapy (nasal steroids, montelukast) cover residual disease, obesity-related OSA and children who cannot have surgery.
What you must remember
- Epidemiology: habitual snoring affects up to roughly one in ten children, whereas OSA affects one to four per cent, peaking between two and eight years when lymphoid tissue is maximal relative to the airway.
- Clinical picture by night and day: snoring, paradoxical chest-abdominal movement, retractions, observed apnoeas, neck extension or odd sleep postures; by day, mouth breathing, hyponasal speech, hyperactivity or inattention (not just sleepiness), morning headache and poor growth.
- Diagnostic standard: polysomnography with paediatric scoring; AHI above 1/hour is abnormal in children (versus 5/hour in adults); oxygen desaturation, hypercapnia and arousals quantify severity.
- Cause ladder: adenotonsillar hypertrophy first; then obesity, allergic rhinitis, craniofacial syndromes (Down, Pierre Robin, Crouzon, achondroplasia), neuromuscular disease, and laryngomalacia or glossoptosis in infants.
- Treatment ladder: adenotonsillectomy is first line and cures the majority of uncomplicated cases; nasal corticosteroids and montelukast shrink residual lymphoid disease; CPAP is the fallback for obesity, syndromic children and post-surgical persistence; tracheostomy is rarely needed.
- Complications to quote: failure to thrive (growth hormone release is disturbed by fragmented sleep), pulmonary hypertension and cor pulmonale, systemic hypertension, learning and behaviour problems, and enuresis.
- High-risk surgical groups: children under three years, severe OSA, obesity, syndromic airways, cerebral palsy and sickle cell disease need overnight monitoring after adenotonsillectomy for post-obstructive pulmonary oedema and bleeding.
- Adenoid facies: long face, open mouth, high arched palate, dental crowding and dull expression from chronic nasopharyngeal obstruction — a classic short-case finding in Indian viva halls.
A typical exam case
A five-year-old is brought for "hyperactivity and poor eating". The mother, unprompted, mentions he snores like an adult and sleeps with his neck extended; on examination he has mouth breathing, hyponasal voice and three-plus tonsils with an adenoid grin. Chart height: he has crossed down two centile lines. The pathway: score symptoms and examine tonsils, adenoids and nose; obtain polysomnography where available (in much of India, oximetry plus audio-video recording serves as a pragmatic screen); confirm AHI above 1; and offer adenotonsillectomy. Counsel the family that snoring may persist for weeks post-operatively and that the hyperactivity, growth and enuresis typically improve within months. Review at three months with repeat assessment; if OSA persists — common in the obese child — add nasal steroids and consider CPAP titration.
Contrast the sleepy adolescent who is obese with a thick neck and morning headaches: adenoids are no longer the story. Weight-linked OSA needs polysomnography, a weight-management plan in parallel, and usually CPAP, because surgery alone resolves only a minority of obesity-driven cases.
How the exam frames it
Three recurring questions dominate. First, the threshold: children are diagnosed at an AHI above 1/hour — quoting the adult cut-off of 5 is the standard error, and one MCQ after another punishes it. Second, the daytime phenotype: children express sleep fragmentation as hyperactivity, inattention and school decline rather than the somnolence adults show, so the "sleepy child" is actually the exception. Third, complications: the favourite sequence is cor pulmonale from chronic nocturnal hypoxaemia in a long-standing case — a child with unexplained pulmonary hypertension should have the tonsils examined before the echo report is believed. In the Indian short-case setting, adenoid facies and mouth breathing link this topic to ENT and to allergic rhinitis management with nasal steroids.
Frequently asked questions
What AHI defines obstructive sleep apnoea in a child?
More than one apnoea or hypopnoea per hour of sleep on polysomnography; the adult threshold of five per hour does not apply to children.
What is the first-line treatment for childhood OSA due to adenotonsillar hypertrophy?
Adenotonsillectomy, which resolves the majority of uncomplicated paediatric cases and also improves behaviour, growth and enuresis.
How does OSA present in children during the day?
Predominantly with hyperactivity, inattention, learning difficulty and morning headache rather than overt daytime sleepiness, plus mouth breathing and hyponasal speech.
Which cardiac complication results from untreated severe OSA?
Pulmonary hypertension progressing to cor pulmonale from sustained nocturnal hypoxaemia and hypercapnia.
When is CPAP preferred over surgery in a child?
Obesity-driven OSA, syndromic or neuromuscular airways, residual disease after adenotonsillectomy, and children in whom surgery is contraindicated.