Obstructive sleep apnoea in children — formative SAQs

SAQ 1 — The preschooler who snores and is not growing (20 marks, ~15 minutes)

A 4-year-old boy is brought in because he snores loudly every night, with his parents describing frightening pauses in his breathing followed by gasping, and he sleeps restlessly with his neck extended. He is a mouth breather with large tonsils, and his weight has drifted from the 50th to the 9th centile over the past year. He is inattentive and hyperactive at preschool. [1]

Questions

1. Give the most likely diagnosis and the features in this history that support it. (5 marks) [1]
2. Name the gold-standard investigation and one pragmatic alternative when it is unavailable, with the key caveat of the alternative. (5 marks) [1] [7]
3. State the first-line treatment and the trial evidence that supports it. (5 marks) [3]
4. Explain why this child's poor growth is relevant and what you expect after treatment. (5 marks) [1]

Model answer (must-hit)

1. The most likely diagnosis is obstructive sleep apnoea from adenotonsillar hypertrophy. Supporting features are loud habitual snoring on most nights, witnessed apnoeas with gasping arousals, restless sleep with neck hyperextension, mouth breathing with large tonsils, faltering growth, and the characteristically behavioural daytime presentation of inattention and hyperactivity rather than sleepiness. [1]
2. The gold standard is overnight attended polysomnography, which measures the obstructive apnoea-hypopnoea index, hypoxaemia and sleep architecture and reliably distinguishes OSA from primary snoring. Where polysomnography is unavailable, nocturnal pulse oximetry is a useful abbreviated test: a positive trace with clusters of desaturation rules OSA in and can expedite treatment, but a normal or non-diagnostic oximetry does not exclude OSA and should prompt full polysomnography if suspicion persists. [1] [7]
3. The first-line treatment is adenotonsillectomy. The Childhood Adenotonsillectomy Trial randomised children with OSA to early surgery or watchful waiting and found significantly greater improvement in behaviour, quality of life and polysomnographic measures with surgery, while noting that around half of the watchful-waiting group with milder disease resolved without an operation. [3]
4. Poor growth is relevant because significant OSA causes failure to thrive through the increased work of breathing during sleep and disruption of the nocturnal growth-hormone surge; it is a marker of disease severity rather than a feeding problem. After effective treatment, catch-up growth is expected, which is one of the clearest demonstrations that the airway was the cause. [1]

SAQ 2 — The obese adolescent with residual symptoms after surgery (20 marks, ~15 minutes)

A 14-year-old with a body mass index on the 98th centile had an adenotonsillectomy 6 months ago for polysomnography-confirmed severe OSA. She continues to snore, remains sleepy and inattentive, and a repeat sleep study shows a persistent moderate obstructive apnoea-hypopnoea index. [6]

Questions

1. Explain why this child has residual OSA despite surgery and which children are at highest risk of this. (6 marks) [6]
2. State the next-line treatment and the single biggest practical barrier to its success. (6 marks) [10]
3. Outline the additional management steps for this child. (8 marks) [1] [6]

Model answer (must-hit)

1. Residual OSA after adenotonsillectomy is common because obesity narrows the airway with soft-tissue deposition and adds a restrictive load that surgery does not address. Bhattacharjee and colleagues' multicentre study showed that while adenotonsillectomy normalises the sleep study in most otherwise healthy children, residual disease is frequent in obese children and in those with severe baseline disease, older age or asthma — which is exactly why post-operative reassessment with a repeat sleep study is needed rather than an assumption of cure. [6]
2. The next-line treatment is continuous positive airway pressure. The single biggest practical barrier is adherence: Marcus and colleagues showed that CPAP is effective when worn but that actual use in children falls well short of the prescribed hours, so success depends on structured support, mask fitting and behavioural strategies. [10]
3. Additional steps are genuine weight management as both cause and barrier to cure; treatment of nasal allergy and use of intranasal corticosteroids or montelukast as adjuncts; attention to metabolic comorbidity; assessment for pulmonary hypertension if the disease has been long-standing; and ongoing sleep and airway follow-up rather than discharge. [1] [6]