Sleep Apnoea — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Sleep apnoea is a common sleep-related breathing disorder characterised by repeated episodes of partial (hypopnoea) or complete (apnoea) cessation of breathing during sleep, typically lasting 10-30 seconds and occurring 5 or more times per hour. The most common form is obstructive sleep apnoea (OSA), caused by collapse of the upper airway (pharyngeal muscles and soft palate) during sleep. Central sleep apnoea (CSA) — less common — results from failure of the brain to send appropriate respiratory drive signals; occurs in heart failure, after stroke, and with opioid use. Complex (mixed) sleep apnoea combines both. Each apnoea causes arousal from sleep (without conscious awareness), sympathetic activation, oxygen desaturation, and fragmented sleep architecture. OSA is significantly underdiagnosed — estimated 80% of moderate-severe OSA cases are unrecognised. Left untreated, OSA causes hypertension, atrial fibrillation, coronary artery disease, stroke, type 2 diabetes, and depression, with dramatic impairment in quality of life.

Obstructive sleep apnoea results from anatomical narrowing of the upper airway combined with loss of pharyngeal muscle tone during sleep. Risk factors: obesity (most important modifiable risk factor — adipose tissue around the pharynx reduces airway diameter; 10% weight gain increases OSA risk by 32%); large neck circumference (above 43 cm in men, above 40 cm in women — a practical clinical predictor); male sex (testosterone promotes pharyngeal fat deposition; progesterone is protective in premenopausal women); advancing age (muscle tone decreases with age); retrognathia or micrognathia (mandibular anatomy); enlarged tonsils or adenoids (the most common cause of paediatric OSA); nasal obstruction (deviated septum, nasal polyps, chronic rhinitis); hypothyroidism (reduces upper airway muscle tone); acromegaly (macroglossia and soft tissue hypertrophy); alcohol and sedatives (relax pharyngeal musculature); family history; Down syndrome; Marfan syndrome; and pregnancy (particularly third trimester).

The cardinal symptoms of OSA are: loud habitual snoring (reported by a bed partner — present in virtually all OSA patients), witnessed apnoeas (bed partner observes breathing pauses — high specificity for OSA), and excessive daytime sleepiness (EDS — the Epworth Sleepiness Scale, 0-24, quantifies subjective sleepiness; above 10 suggests pathological EDS). Additional symptoms: unrefreshing sleep despite adequate sleep duration, nocturnal awakenings with choking or gasping, nocturia (raised intrathoracic pressure during apnoeas activates atrial natriuretic peptide — causes nocturnal polyuria even without prostatic disease), morning headache (CO2 retention overnight), poor concentration, memory impairment, irritability, and low mood. The STOP-BANG questionnaire (Snoring, Tired, Observed apnoeas, blood Pressure, BMI above 35, Age above 50, Neck circumference above 40 cm, Gender male) is a validated screening tool — a score of 3 or above has 94% sensitivity for moderate-severe OSA. Children with OSA present differently: snoring, restless sleep, nocturnal mouth breathing, growth retardation, behavioural problems, and poor school performance (EDS is less prominent).

Polysomnography (PSG — full overnight sleep study in a sleep laboratory): the gold standard — simultaneously records EEG, EOG, EMG, ECG, airflow (nasal cannula), respiratory effort (thoracic/abdominal belts), oximetry, and body position; characterises sleep architecture and breathing events with full scoring. Severity classification by Apnoea-Hypopnoea Index (AHI — events per hour of sleep): mild 5-14, moderate 15-29, severe 30 or above. Home sleep apnoea testing (HSAT — Level 3 portable monitoring): simplified outpatient study measuring airflow, respiratory effort, and oximetry — appropriate for patients with high pre-test probability of moderate-severe OSA without significant comorbidities; less accurate than PSG as it cannot characterise sleep stages. Overnight oximetry: screening test — oxygen desaturation index (ODI above 15 suggests significant OSA; sensitivity approximately 87% for severe OSA). STOP-BANG questionnaire for initial risk stratification. Clinical examination: BMI, neck circumference, blood pressure (OSA is a reversible cause of hypertension), ENT examination (tonsil size, Mallampati score, nasal patency). Thyroid function tests to exclude hypothyroidism.

Continuous positive airway pressure (CPAP): gold standard treatment for moderate-severe OSA — delivers pressurised air (typically 6-15 cm H2O) through a nasal or full-face mask, maintaining upper airway patency throughout the respiratory cycle; eliminates apnoeas and hypopnoeas in most patients; reverses EDS, reduces blood pressure (systolic BP by 3-5 mmHg), reduces cardiovascular risk, and improves quality of life. Auto-titrating CPAP (APAP) adjusts pressure automatically. Requires consistent nightly use. Mandibular advancement device (MAD): custom-fitted oral appliance worn during sleep — holds the mandible forward, increasing retroglossal airway space; effective for mild-moderate OSA (AHI reduction approximately 40-70%) and snoring; preferred by many patients over CPAP due to portability. Weight loss: even 10-15% weight reduction produces significant AHI improvement; bariatric surgery can lead to near-complete resolution in morbidly obese patients. Positional therapy: for positional OSA (AHI twice as high supine) — position sensors, chest-mounted devices, or specialised pillows. Surgical options: adenotonsillectomy (first-line for children with OSA due to tonsillar hypertrophy — often curative); uvulopalatopharyngoplasty (UPPP); hypoglossal nerve stimulation (Inspire therapy — implanted device, FDA/NICE-approved for CPAP-intolerant patients; activates genioglossus with each inspiration); bimaxillary advancement surgery (highly effective but major procedure). Avoid alcohol and sedatives within 4 hours of bedtime.

Untreated moderate-to-severe OSA causes serious cardiovascular, metabolic, and neurological complications. Systemic hypertension: present in 30-50% of OSA patients; OSA is one of the most common reversible causes of resistant hypertension — repeated sympathetic activation from apnoea arousals drives sustained high blood pressure even during waking hours. Atrial fibrillation: recurrent atrial stretch and hypoxia trigger AF — OSA doubles the risk of AF and significantly reduces the success of cardioversion, ablation, and antiarrhythmic drugs; CPAP treatment reduces AF recurrence by approximately 50%. Coronary artery disease and myocardial infarction: OSA is an independent risk factor with a relative risk of 1.5-2.0 for ischaemic heart disease. Stroke: OSA increases stroke risk 2-3 fold through hypertension, AF, and hypoxia-induced thrombosis. Type 2 diabetes: intermittent hypoxia promotes insulin resistance and impairs glucose tolerance — OSA is present in 40% of type 2 diabetic patients. Non-alcoholic fatty liver disease: hepatic steatosis is worsened by OSA-related hypoxia and metabolic dysregulation. Road traffic accidents: OSA patients have a 3-7 times greater risk of motor vehicle accidents from excessive daytime sleepiness. Cognitive impairment and dementia risk increase with untreated OSA.

Weight management is the single most effective preventive and therapeutic measure for obesity-associated OSA — even a 10 kg weight reduction can eliminate OSA in some patients. Sleep on your side — the supine position worsens OSA by promoting posterior tongue and soft palate displacement; most OSA patients have significantly worse AHI supine. Avoid alcohol and sedatives (benzodiazepines, zopiclone) within 4 hours of bedtime — they preferentially relax upper airway muscles and reduce the arousal response. Treat nasal congestion (allergic rhinitis, polyps) to reduce upper airway resistance. Regular CPAP machine check-ups: pressure adequacy review, mask replacement every 3-6 months, filter maintenance. Annual sleep medicine follow-up including symptoms, CPAP usage data download (adherence monitoring), and blood pressure measurement. OSA patients must inform the DVLA (UK) if they have excessive daytime sleepiness affecting driving ability — driving with untreated severe OSA with EDS is a legal offence.

Consult your GP or a sleep medicine specialist for frequent loud snoring, witnessed breathing pauses during sleep, or excessive daytime sleepiness (falling asleep in sedentary situations — while reading, watching television, or in meetings). The Epworth Sleepiness Scale (available online) can help quantify whether sleepiness warrants professional assessment. Seek urgent assessment if OSA symptoms are accompanied by: newly diagnosed or poorly controlled hypertension (OSA is a reversible secondary cause), cardiac arrhythmias (particularly atrial fibrillation), or recent stroke or TIA. OSA patients experiencing excessive daytime sleepiness should not drive — notify the DVLA and your GP. If OSA has been diagnosed but CPAP is not tolerated, request specialist re-assessment for alternatives (MAD, positional therapy, surgical options) rather than abandoning treatment, given the significant cardiovascular consequences of untreated moderate-severe OSA.