How do I know if I might have sleep apnoea?

The most important symptoms are loud snoring, witnessed apnoeas (breathing pauses), choking or gasping arousals, unrefreshing sleep, and daytime sleepiness (Epworth Sleepiness Scale score above 10). Morning headaches, nocturia (two or more overnight trips to the toilet), and difficulty concentrating are also common. Risk is higher with obesity, large neck (over 40 cm), male sex, age over 40, high blood pressure, and a history of atrial fibrillation or type 2 diabetes. If you recognise several of these features, discuss assessment with your GP.

What is the STOP-BANG questionnaire?

STOP-BANG is an eight-item screening tool used in general practice: Snoring, Tired (daytime), Observed apnoea, Pressure (high blood pressure), BMI ≥35, Age ≥50, Neck circumference over 40 cm, and Gender (male). Scoring three or more out of eight indicates high risk and warrants a sleep study. Scoring five or more predicts a high probability of moderate-to-severe OSA. It takes under one minute to administer and can be self-completed in a waiting room.

What is the difference between a home sleep study and polysomnography?

A home sleep apnoea test (HSAT, level 3 or 4) measures airflow, oxygen saturation, effort, and position in your own bed. It is Medicare-rebatable, cheaper, more accessible, and acceptable for high-probability uncomplicated adult OSA. Its limitation is that it can underestimate AHI since it cannot precisely distinguish wake from sleep time. Full polysomnography (PSG, level 1) is an overnight in-laboratory study recording brain waves (EEG), eye movements, muscle activity, ECG, and breathing — it is the gold standard and is required for complex or atypical presentations, paediatric OSA, suspected central apnoea, and commercial driver fitness assessment.

I cannot tolerate CPAP — what are my alternatives?

A custom-made mandibular advancement device (MAD), fitted by a dentist or prosthodontist with sleep medicine training, is an evidence-based alternative for mild-to-moderate OSA (AHI below 30) and for those with moderate-to-severe OSA who cannot use CPAP. It works by advancing the lower jaw to keep the airway open. It is somewhat less effective than CPAP in severe OSA but has similar adherence advantages for many patients. Weight loss (diet, exercise, or GLP-1 medications) is highly effective — a 10% reduction in body weight reduces AHI by approximately 25%. Positional therapy (devices that prevent sleeping on your back) helps positional OSA. Surgical options exist for selected anatomy.

Does sleep apnoea affect my driving licence?

Yes. Under Austroads — Assessing Fitness to Drive, drivers with untreated significant OSA causing excessive daytime sleepiness have an obligation to report this to their state licensing authority. Commercial vehicle drivers (truck, bus, taxi) face stricter requirements — documented CPAP use and evidence of treatment efficacy are typically required before commercial licensing can be maintained. Private vehicle drivers with adequately treated OSA, confirmed by CPAP compliance data and symptom control, generally can drive without restriction. Discuss your specific situation with your GP.

Obstructive sleep apnoea

Obstructive sleep apnoea: diagnosis, CPAP, and the Australian GP approach

By Dr HB Lo, FACRRM Reviewed 27 May 2026 8 min read

Obstructive sleep apnoea (OSA) affects ~25% of Australian adults in mild form, with ~5–10% having moderate-to-severe disease — most undiagnosed. Recurrent upper airway collapse during sleep causes oxygen desaturation, sleep fragmentation, and daytime sleepiness.

CPAP is first-line for moderate-to-severe OSA (AHI ≥15/hour) and for symptomatic mild disease. A mandibular advancement device is an effective alternative for mild-to-moderate disease or for those who cannot tolerate CPAP.

Weight loss is highly therapeutic — a 10% reduction reduces AHI by approximately 25%. Untreated significant OSA with sleepiness must be reported to licensing authorities under Austroads obligations.

What obstructive sleep apnoea is

Obstructive sleep apnoea (OSA) occurs when the upper airway repeatedly collapses during sleep, causing breathing pauses (apnoeas, defined as ≥10 seconds of flow cessation) or partial obstruction (hypopnoeas), oxygen desaturation, and cortical arousals. The apnoea-hypopnoea index (AHI) — the number of events per hour of sleep — defines severity: mild 5–14/hour, moderate 15–29/hour, severe ≥30/hour.

OSA affects approximately 25% of Australian adults in mild form, with 5–10% having moderate-to-severe disease. The large majority are undiagnosed. It is not simply a snoring problem — untreated moderate-to-severe OSA is a major driver of resistant hypertension, atrial fibrillation, ischaemic heart disease, stroke, type 2 diabetes, depression, and motor vehicle accidents. The Sleep Health Foundation estimates OSA-related costs to the Australian economy exceed $26 billion annually.

The primary risk factors are obesity (approximately 60% of OSA attributable), male sex, age over 40, large neck circumference (>43 cm in men, >40 cm in women), retrognathia, alcohol and sedative use, and smoking. Postmenopausal women approach male risk. Aboriginal and Torres Strait Islander populations have high prevalence — often with reduced access to diagnostic and treatment services.

A. Core clinical — the AU general-practice framework

Screening in general practice

The Australasian Sleep Association (ASA) and Thoracic Society of Australia and New Zealand (TSANZ) recommend structured screening with validated tools:

STOP-BANG questionnaire — eight items scored 0 or 1: Snoring, Tired, Observed apnoea, Pressure (hypertension), BMI ≥35, Age ≥50, Neck >40 cm, Gender (male). Score ≥3 = high risk; ≥5 = high probability of moderate-to-severe OSA.

Epworth Sleepiness Scale (ESS) — eight scenarios rated 0–3; total score >10/24 indicates excessive daytime sleepiness.

Screening is appropriate in: snoring with daytime sleepiness; obesity (BMI ≥30); resistant hypertension; atrial fibrillation; type 2 diabetes with poor control; commercial vehicle drivers; patients with witnessed apnoeas; and pre-bariatric surgery assessment (mandatory in most centres).

Symptoms to elicit

Loud snoring (especially partner-reported), witnessed apnoeas or choking arousals, unrefreshing sleep, and daytime sleepiness are the cardinal features. Less-recognised symptoms include nocturia (≥2 overnight voids — OSA-driven via atrial natriuretic peptide), morning headache, dry mouth, difficulty concentrating, mood change, reduced libido, and erectile dysfunction.

Diagnosis

Home sleep apnoea test (HSAT, Level 3/4): Medicare-rebatable (items 12203, 12204), acceptable for high-probability uncomplicated adult OSA. Records airflow, oxygen saturation, respiratory effort, and body position. Can underestimate AHI since it cannot distinguish wake from sleep — AHI is calculated on total recording time, not sleep time.

Polysomnography (PSG, Level 1): In-laboratory overnight study; gold standard. Required for complex or atypical presentations, paediatric OSA, suspected central or mixed apnoea, neuromuscular disease, significant COPD or cardiac failure, and commercial driver fitness-to-drive assessment.

Referral to sleep physician: Arranges sleep study, interprets results in clinical context, and initiates CPAP or mandibular device titration.

Treatment hierarchy

Lifestyle modification — weight loss, alcohol reduction within four hours of bed, smoking cessation, positional therapy for positional OSA.
CPAP — first-line for moderate-to-severe OSA (AHI ≥15) and symptomatic mild OSA plus comorbidity.
Mandibular advancement device (MAD) — alternative for mild-to-moderate or CPAP-intolerant patients.
Surgery — selective anatomical cases; paediatric OSA (adenotonsillectomy).

B. CPAP — the evidence base and practical reality

Therapeutic Guidelines (eTG) and ASA/TSANZ guidelines position CPAP as first-line for moderate-to-severe OSA. CPAP splints the pharyngeal airway open with positive pressure delivered through a mask, eliminating apnoeas and hypopnoeas.

Indications: AHI ≥15/hour (regardless of symptoms); AHI 5–14 with significant symptoms (sleepiness, impaired function), cardiovascular comorbidity, or upcoming surgery; commercial drivers per Austroads.

Setup: Sleep physician or accredited CPAP provider. Auto-titrating CPAP (APAP) is preferred — it adjusts pressure throughout the night (typically 4–20 cmH₂O). Heated humidification reduces nasal dryness and improves adherence. Mask selection (nasal pillow, nasal, full-face) is individual — poor mask fit is the commonest cause of early abandonment.

What CPAP achieves: Robust evidence for improvement in daytime sleepiness, quality of life, blood pressure (particularly resistant hypertension), atrial fibrillation burden, and motor vehicle accident risk. The SAVE trial (McEvoy NEJM 2016) found CPAP did not reduce hard cardiovascular events in secondary prevention — however, patient populations had poor adherence (~3.3 hours/night), and the trial does not challenge CPAP for symptom or comorbidity management.

Adherence: Approximately 60% of patients achieve adequate use (≥4 hours per night on ≥70% of nights). Predictors of better adherence: education before initiation, close support in the first two weeks, troubleshooting mask comfort, and heated humidity.

Troubleshooting common problems:

Mask intolerance — try different mask type; gradual desensitisation.
Dry mouth, nasal congestion — heated humidifier; saline nasal rinse; topical nasal steroid.
Aerophagia (air swallowing) — pressure adjustment; positional change.
Claustrophobia — nasal pillow trial; gradual familiarisation off the machine before sleep.

Cost: Private purchase approximately $1,500–3,000 for machine plus $200–400 for mask; health fund extras cover some costs. NDIS may fund CPAP for eligible participants.

C. Non-CPAP approaches — weight loss, MAD, positional therapy

Weight loss — highly effective

A 10% reduction in body weight reduces AHI by approximately 25%; larger weight loss can resolve mild OSA entirely. Weight management through diet, exercise, and structured support is first-line alongside any device therapy per AMH.

GLP-1 receptor agonists: Semaglutide (Wegovy) and tirzepatide demonstrate significant weight loss with meaningful AHI reduction in clinical trials. In Australia, semaglutide is on the PBS for type 2 diabetes (Ozempic); Wegovy for weight is private script only. Tirzepatide (Mounjaro) is private only — PBS PBAC submission was rejected in April 2026. Bariatric surgery for BMI ≥35 with OSA achieves the most durable weight loss and is a specific OSA indication.

Mandibular advancement device (MAD)

A custom-fitted device advances the lower jaw during sleep to maintain airway patency. It is an ASA-recommended first-line alternative for mild-to-moderate OSA (AHI below 30/hour) and for CPAP-intolerant moderate OSA. Cost approximately $1,000–3,000 through an accredited dentist with sleep medicine training; some health fund coverage. Less effective than CPAP for severe OSA; requires regular dental review to monitor jaw joint and tooth movement.

Positional therapy

Positional OSA — AHI ≥50% higher in the supine position — occurs in approximately 50–60% of OSA patients. Devices preventing supine sleep (positional pillows, vibrating vests, wearable sensors) are an effective adjunct or alternative for selected patients.

Surgical options

Adenotonsillectomy is first-line for paediatric OSA (adenotonsillar hypertrophy — refer ENT). In adults, uvulopalatopharyngoplasty (UPPP) has limited and variable efficacy and has largely been replaced by more selective procedures. Maxillomandibular advancement (MMA) is effective for cephalometrically selected anatomy. Hypoglossal nerve stimulation (Inspire) — TGA-approved, emerging evidence for moderate-to-severe CPAP-intolerant patients — is available at tertiary specialist centres.

D. Australian operations

MBS items: Home sleep apnoea test (items 12203, 12204 — GP-referred for high-probability uncomplicated adult OSA); polysomnography (items 12207, 12210 — specialist referral). Standard consultation items 23, 36, 44. GPCCMP items 965/967 for chronic OSA with comorbidity — enables allied health referral (dietitian, exercise physiologist). Heart Health Check (item 699) — opportunity for OSA discussion in cardiovascular risk assessment. ATSI Health Assessment (715); 75+ Health Assessment (707).

Investigations relevant to GP: TFTs (hypothyroidism as secondary cause of OSA), HbA1c and fasting glucose (T2DM comorbidity), FBC. Echocardiogram for suspected heart failure or pulmonary hypertension from long-standing OSA.

PBS pharmacotherapy: No OSA-specific medications. Modafinil for residual sleepiness despite adequate CPAP (specialist prescription). Weight loss agents as above.

Driving — Austroads obligations: Per Austroads — Assessing Fitness to Drive 2022, patients with significant OSA causing excessive daytime sleepiness have an obligation to self-report to licensing authorities. Commercial vehicle drivers require confirmed treatment compliance and efficacy documentation. Document driving status and advice in the medical record.

Referral pathway: Sleep physician (respiratory or sleep specialist) for sleep study and management. Public sleep clinics at tertiary hospitals; private sleep clinics across metropolitan areas. Telehealth sleep medicine increasingly available for regional and rural patients.

E. Special populations

Pregnancy: Gestational OSA is associated with pre-eclampsia, gestational hypertension, and preterm birth. OSA commonly worsens in pregnancy. CPAP is safe and recommended during pregnancy for known moderate-to-severe OSA — Lung Foundation Australia and ASA support treatment. Re-assess postpartum as OSA may improve with weight loss.

Children: Adenotonsillar hypertrophy is the commonest cause of paediatric OSA. Symptoms include mouth breathing, snoring, restless sleep, behavioural problems, and poor school performance — not typically sleepiness. Refer to ENT for adenotonsillectomy. Full in-lab PSG is required for paediatric assessment.

Elderly: Presentation is often atypical — cognitive decline, falls, mood change, or nocturia rather than sleepiness. Treat per symptoms; lower pressure thresholds acceptable; fall-prevention is a co-benefit of adequate CPAP.

Aboriginal and Torres Strait Islander populations: High prevalence with additional barriers — remote geography, cost, access to specialists, and cultural factors. Telehealth sleep medicine and community health worker support are expanding access.

COMISA — comorbid insomnia and sleep apnoea: Occurs in approximately 30–50% of OSA patients. Sedative hypnotics worsen OSA — CBT-I is preferred for the insomnia component. CPAP adherence is often lower in COMISA; combined CBT-I plus CPAP achieves better outcomes than either alone.

When to escalate

Refer to sleep physician:

STOP-BANG ≥3 with symptoms or comorbidity.
Any commercial vehicle driver with suspected OSA.
Suspected complex (central or mixed) sleep apnoea.
Paediatric OSA — concurrent ENT referral.
OSA in pregnancy — expedite.

Consider urgent assessment:

Respiratory failure or cor pulmonale complicating severe OSA.
Peri-operative risk — known severe OSA with urgent surgery planned.
Severe untreated OSA in a commercial driver who continues to drive.

Review with GP after CPAP initiation:

Two-week review to troubleshoot adherence and mask comfort.
Six-week review with CPAP download to confirm adequate usage (≥4 hours/night).
Annual review for clinical and equipment maintenance.

What this article is and is not

This is general health information drawn from current Australian general practice sources — Therapeutic Guidelines (eTG), AMH, Australasian Sleep Association, TSANZ, Sleep Health Foundation, and Austroads. It is not personal medical advice and does not create a doctor–patient relationship. Sleep study referral, CPAP prescription, and fitness-to-drive assessment are clinical decisions made with your GP and sleep specialist.

For further information: HealthDirect — Sleep apnoea, Sleep Health Foundation, Lung Foundation Australia.

Sources cited

Frequently asked questions

How do I know if I might have sleep apnoea?

The most important symptoms are loud snoring, witnessed apnoeas (breathing pauses), choking or gasping arousals, unrefreshing sleep, and daytime sleepiness (Epworth Sleepiness Scale score above 10). Morning headaches, nocturia (two or more overnight trips to the toilet), and difficulty concentrating are also common. Risk is higher with obesity, large neck (over 40 cm), male sex, age over 40, high blood pressure, and a history of atrial fibrillation or type 2 diabetes. If you recognise several of these features, discuss assessment with your GP.
What is the STOP-BANG questionnaire?

STOP-BANG is an eight-item screening tool used in general practice: Snoring, Tired (daytime), Observed apnoea, Pressure (high blood pressure), BMI ≥35, Age ≥50, Neck circumference over 40 cm, and Gender (male). Scoring three or more out of eight indicates high risk and warrants a sleep study. Scoring five or more predicts a high probability of moderate-to-severe OSA. It takes under one minute to administer and can be self-completed in a waiting room.
What is the difference between a home sleep study and polysomnography?

A home sleep apnoea test (HSAT, level 3 or 4) measures airflow, oxygen saturation, effort, and position in your own bed. It is Medicare-rebatable, cheaper, more accessible, and acceptable for high-probability uncomplicated adult OSA. Its limitation is that it can underestimate AHI since it cannot precisely distinguish wake from sleep time. Full polysomnography (PSG, level 1) is an overnight in-laboratory study recording brain waves (EEG), eye movements, muscle activity, ECG, and breathing — it is the gold standard and is required for complex or atypical presentations, paediatric OSA, suspected central apnoea, and commercial driver fitness assessment.
I cannot tolerate CPAP — what are my alternatives?

A custom-made mandibular advancement device (MAD), fitted by a dentist or prosthodontist with sleep medicine training, is an evidence-based alternative for mild-to-moderate OSA (AHI below 30) and for those with moderate-to-severe OSA who cannot use CPAP. It works by advancing the lower jaw to keep the airway open. It is somewhat less effective than CPAP in severe OSA but has similar adherence advantages for many patients. Weight loss (diet, exercise, or GLP-1 medications) is highly effective — a 10% reduction in body weight reduces AHI by approximately 25%. Positional therapy (devices that prevent sleeping on your back) helps positional OSA. Surgical options exist for selected anatomy.
Does sleep apnoea affect my driving licence?

Yes. Under Austroads — Assessing Fitness to Drive, drivers with untreated significant OSA causing excessive daytime sleepiness have an obligation to report this to their state licensing authority. Commercial vehicle drivers (truck, bus, taxi) face stricter requirements — documented CPAP use and evidence of treatment efficacy are typically required before commercial licensing can be maintained. Private vehicle drivers with adequately treated OSA, confirmed by CPAP compliance data and symptom control, generally can drive without restriction. Discuss your specific situation with your GP.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.

T1 AU primary 10 sources
T2 International primary 1 source
- American Academy of Sleep Medicine — OSA Clinical Practice Guidelines
T3 Named-author reconstruction 1 source
- McEvoy RD et al — SAVE Trial: CPAP for prevention of cardiovascular events in OSA (NEJM 2016)