# Obstructive Sleep Apnoea Management

> Obstructive sleep apnoea management for NEET-PG ENT: AHI severity bands, polysomnography, CPAP as first line, paediatric adenotonsillectomy and surgery choices.

- Canonical URL: https://prepelephant.com/topics/neet-pg/ent/obstructive-sleep-apnoea-management
- Exam / course: NEET-PG · Subject: ENT
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Obstructive Sleep Apnoea Management", PrepElephant, https://prepelephant.com/topics/neet-pg/ent/obstructive-sleep-apnoea-management

## Direct answer

Polysomnography remains the diagnostic gold standard for obstructive sleep apnoea, and its apnoea–hypopnoea index (AHI) stratifies severity — mild 5–15, moderate 15–30, severe above 30 events per hour — with positive airway pressure (CPAP) the first-line treatment for moderate and severe disease in adults. Management is layered: every patient gets weight reduction, positional therapy and avoidance of sedatives and alcohol; CPAP is titrated and adhered to for moderate-to-severe OSA; oral mandibular advancement appliances serve mild-to-moderate disease and CPAP-intolerant patients; and surgery is selected by level of obstruction — adenotonsillectomy is first-line in children, while adults may need nasal surgery to make CPAP usable, uvulopalatopharyngoplasty for selected retropalatal collapse, tongue base and skeletal procedures (including maxillomandibular advancement) for multilevel disease, and tracheostomy as the definitive bypass in severe cases. Untreated OSA drives systemic and pulmonary hypertension, cardiovascular disease, insulin resistance and road traffic accidents — the reason it is treated, not just snored at.

## What you must remember

- Definition: AHI of 5 or more per hour with symptoms (daytime sleepiness, loud snoring, witnessed apnoeas, unrefreshing sleep) or 15 or more without symptoms; severity bands mild 5–15, moderate 15–30, severe above 30.
- Screening tools: Epworth Sleepiness Scale (score above 10 suggests pathological sleepiness), Berlin and STOP-BANG questionnaires; overnight oximetry is a screening adjunct, not a substitute for polysomnography in complex cases.
- ENT examination checklist: body mass index, neck circumference (roughly above 43 cm in men raises risk), Mallampati class III–IV, retrognathia, tonsillar size, tongue base, nasal obstruction (septum, turbinates, polyps).
- Consequences of untreated OSA: systemic and pulmonary hypertension (cor pulmonale), ischaemic heart disease, stroke, type 2 diabetes, nocturnal arrhythmias, and a several-fold increased risk of road traffic accidents — sleepy drivers must be counselled about driving.
- Adults: CPAP is the most effective therapy across severities but is mandatory-first for moderate-to-severe disease; adherence support (humidification, mask fitting, review) determines success.
- Children: adenotonsillectomy is first-line treatment for paediatric OSA (with adenoid and tonsillar hypertrophy the overwhelming cause), reserving CPAP and further surgery for residual disease, obesity, craniofacial syndromes and neuromuscular disease.
- Adult surgical ladder by site: nasal surgery (septoplasty, turbinate reduction, polypectomy) to improve CPAP tolerance; UPPP (with Friedman staging guiding selection) for retropalatal collapse; tongue base reduction, genioglossus advancement, hyoid suspension, lingual tonsillectomy for retrolingual collapse; maxillomandibular advancement for multilevel disease; hypoglossal nerve stimulation for selected CPAP-intolerant patients; tracheostomy as the definitive bypass.
- Anaesthetic relevance: OSA patients desaturate rapidly and obstruct post-operatively — plan airway, positioning, monitoring and analgesia (avoiding opioids where possible) around the diagnosis.

## How to work through it

A 48-year-old lorry driver, BMI 34, collar 45 cm, snores loudly, has witnessed apnoeas and dozes at traffic lights; Epworth score is 16. Step one, confirm and quantify: polysomnography returns an AHI of 38 with desaturations to 78 per cent — severe OSA. Step two, assess the pharynx: Mallampati IV, a crowded oropharynx with grade 3 tonsils, retrognathia, and a deviated nasal septum with hypertrophic turbinates.

Step three, treat in order of effect. This man's severity makes CPAP the non-negotiable core — titrate it, review adherence at a month, and fix his nasal obstruction (septoplasty with turbinate reduction) if nasal CPAP fails because he cannot breathe through the nose. In the same consultation set the lifestyle agenda: weight target, evening alcohol ban, lateral sleeping, sedative avoidance, and the driving-safety conversation — a sleepy HGV driver is a public-health issue, and in India commercial driving with untreated severe OSA carries real medico-legal weight.

Now contrast the paediatric pathway. A 6-year-old with snoring, restless sleep, mouth breathing and falling school attention has adenotonsillar hypertrophy on examination; a sleep study (or overnight oximetry where polysomnography is inaccessible) confirms the diagnosis. Adenotonsillectomy is first-line and resolves the majority; residual OSA — usually in the obese or syndromic child — goes to CPAP and multidisciplinary review rather than repeated surgery.

The third pattern is the CPAP-intolerant adult with mild-to-moderate disease: a mandibular advancement device (with dental assessment), weight loss and positional therapy are legitimate alternatives; if surgery is chosen, stage the obstruction first — drug-induced sleep endoscopy or awake endoscopy mapping — because UPPP performed for retrolingual collapse fails, and multilevel collapse needs multilevel surgery or skeletal advancement.

## Where students slip

Two errors recur. First, treating OSA as a snoring nuisance rather than a cardiovascular disease — answers must connect AHI severity with systemic hypertension, cor pulmonale and accident risk, and reserve CPAP-first logic for moderate-to-severe disease. Second, applying the adult algorithm to children: paediatric OSA is adenoid and tonsil disease until proved otherwise, and adenotonsillectomy, not CPAP, is the first-line answer. A third slip is offering UPPP uncritically: the exam expects Friedman staging or collapse-pattern assessment before selecting it, plus awareness that UPPP can complicate later CPAP use with oral air leaks. Finally, remember the Epworth threshold (above 10) and the AHI bands (5–15, 15–30, above 30) — pure recall, asked every year.

## Frequently asked questions

### How is obstructive sleep apnoea severity graded on polysomnography?
By the apnoea–hypopnoea index: mild 5–15 events per hour, moderate 15–30, severe above 30, interpreted alongside oxygen desaturation and symptom burden.

### What is the first-line treatment for moderate-to-severe adult OSA?
Continuous positive airway pressure with adherence support, layered on weight reduction, positional therapy and avoidance of alcohol and sedatives.

### What is the first-line surgical treatment of paediatric OSA?
Adenotonsillectomy for adenotonsillar hypertrophy — the cause in the great majority of children — with CPAP reserved for residual disease, obesity or craniofacial syndromes.

### Which conditions are associated with untreated OSA?
Systemic and pulmonary hypertension, coronary disease, stroke, type 2 diabetes, nocturnal arrhythmias, and a substantially raised risk of road traffic accidents.

### When is UPPP offered and what determines its success?
For selected adults with retropalatal collapse, usually Friedman stage I–II anatomy, ideally after sleep endoscopy maps the obstruction; multilevel or retrolingual collapse predicts failure and needs multilevel or skeletal surgery.