Lucan · Conditions

Obstructive sleep apnoea

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Australian guidance: Australasian Sleep Association Position Statement on OSA + RACGP

1. Definition and epidemiology

Obstructive sleep apnoea (OSA) is a disorder characterised by repetitive episodes of partial or complete upper airway collapse during sleep, causing oxyhemoglobin desaturation and sleep fragmentation. An estimated 8.3% of Australians have OSA, with obesity as the dominant modifiable risk factor. OSA is significantly underdiagnosed in primary care; prevalence is higher in males, older adults, and people of Pacific Islander and Aboriginal and Torres Strait Islander descent.

2. Pathophysiology

During sleep, reduced neuromuscular tone in the pharyngeal dilator muscles allows the soft tissues of the oropharynx to collapse against the posterior pharyngeal wall. In susceptible individuals, anatomical factors including a narrow pharyngeal lumen (from obesity, macroglossia, retrognathia, or tonsillar hypertrophy) lower the critical closing pressure of the airway. Each apnoeic or hypopnoeic episode generates progressive hypoxia and hypercapnia, which triggers arousal from sleep via central chemoreceptor activation. Arousal restores airway tone and ventilation, then sleep resumes and the cycle repeats. Chronic intermittent hypoxia activates sympathetic pathways, promotes oxidative stress, endothelial dysfunction, and systemic inflammation, which are the mechanistic drivers of the cardiovascular and metabolic complications associated with OSA (Robbins Ch 15).

3. Clinical presentation and diagnostic criteria

Patients typically present with a triad of loud snoring, witnessed apnoeas reported by a bed partner, and excessive daytime somnolence. Other features include morning headache (from nocturnal hypercapnia), nocturia, non-restorative sleep, poor concentration, and mood disturbance. Examination may reveal a crowded oropharynx (Mallampati class III to IV), elevated BMI, increased neck circumference (greater than 40 cm in females, greater than 43 cm in males), and retrognathia. The Epworth Sleepiness Scale (ESS, score 0 to 24) is used to quantify daytime somnolence; a score of 10 or more is clinically significant. The STOP-BANG questionnaire is a validated primary care screening tool; a score of 3 or more indicates high risk and warrants further evaluation.

4. Investigations and AU-specific cutoffs

The diagnostic standard in Australia is overnight polysomnography (PSG), which remains the gold standard for confirming OSA and quantifying severity. For patients with high pre-test probability and no significant comorbidity (such as severe chronic obstructive pulmonary disease, neuromuscular disease, or suspected central sleep apnoea), a home sleep apnoea test (HSAT) using a type 3 or type 4 monitor is an acceptable and more accessible alternative; the Australasian Sleep Association endorses HSAT in this context.

Severity is classified by the apnoea-hypopnoea index (AHI), defined as the number of apnoeas and hypopnoeas per hour of sleep:

An AHI of 5 or more per hour is required for diagnosis in adults with compatible symptoms, or an AHI of 15 or more per hour regardless of symptoms. Overnight oximetry alone is insufficient to diagnose or exclude OSA but may be used when PSG or HSAT is not available. A pre-treatment full blood count and thyroid-stimulating hormone test should be ordered to exclude hypothyroidism and secondary polycythaemia.

5. Management

Management is stratified by severity and symptom burden. All patients with confirmed OSA benefit from lifestyle optimisation, including weight loss (target BMI below 30), avoidance of alcohol and sedatives within four hours of sleep, positional therapy if predominantly supine-dependent OSA is confirmed, smoking cessation, and nasal congestion treatment.

Continuous positive airway pressure (CPAP) is the first-line treatment for moderate to severe OSA and for mild OSA where significant daytime somnolence, hypertension, or cardiovascular disease is present. CPAP prevents airway collapse by delivering a titrated positive pressure via nasal or full-face mask throughout the night. The RACGP recommends CPAP as the definitive primary treatment. A minimum of four hours per night achieves adequate benefit, but six or more hours per night produces maximal improvement in sleepiness scores and cardiovascular outcomes. Auto-titrating CPAP (APAP) is commonly used in Australia for uncomplicated OSA as it adjusts pressure breath to breath.

Mandibular advancement splints (MAS) are an effective alternative for mild to moderate OSA, particularly in patients who are intolerant of CPAP. They are custom-fitted by a dentist with experience in dental sleep medicine and work by advancing the mandible to increase pharyngeal dimensions. MAS are less effective than CPAP for severe OSA.

Upper airway surgery (such as uvulopalatopharyngoplasty or hypoglossal nerve stimulation) is reserved for patients who have failed non-surgical management, and referral to a specialist sleep or ear, nose, and throat service is required. Bariatric surgery in patients with obesity-related severe OSA may result in sustained AHI reduction and, in some cases, OSA remission.

6. Pharmacology and AU PBS notes

There are no first-line pharmacological agents for OSA. Pharmacotherapy targets residual excessive daytime somnolence despite adequate CPAP adherence:

Agents to avoid: benzodiazepines, non-benzodiazepine hypnotics (such as zolpidem), and opioids all reduce upper airway neuromuscular tone and worsen OSA.

7. Complications and monitoring

Untreated OSA carries significant cardiovascular morbidity. Key complications include:

Among people with asthma, OSA co-occurs in an estimated 20 to 40%, and effective CPAP treatment improves both asthma-related quality of life and asthma control.

Monitoring after CPAP initiation:

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Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.