Sleep Apnea — Causes, Symptoms, Diagnosis & CPAP Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Sleep apnea is a sleep-related breathing disorder characterised by repetitive episodes of partial or complete upper airway obstruction during sleep, causing transient hypoxaemia (oxygen desaturation), sleep fragmentation, and physiological stress. The most common form is obstructive sleep apnea (OSA), where anatomical narrowing of the upper airway combined with reduced muscular tone during sleep causes airway collapse. Central sleep apnea (CSA) — less common — results from failure of the brain's respiratory control centres to send appropriate signals to breathing muscles. Complex/mixed sleep apnea has features of both. OSA affects approximately 1 billion adults worldwide, making it one of the most prevalent chronic conditions globally, yet over 80% of moderate-severe cases remain undiagnosed. Severity is measured by the Apnea-Hypopnea Index (AHI — number of apnoeic and hypopnoeic episodes per hour of sleep): mild OSA (5-15 events/hour), moderate (15-30/hour), severe (above 30/hour). OSA is associated with significantly increased risk of hypertension, cardiovascular disease, atrial fibrillation, stroke, type 2 diabetes, motor vehicle accidents (2-7x increased risk from sleepiness), and depression. Untreated severe OSA carries mortality comparable to smoking.

OSA results from anatomical and physiological factors that promote upper airway collapse during sleep. Obesity is the strongest modifiable risk factor — each unit increase in BMI raises OSA risk by 14%; visceral fat deposition increases soft tissue in the pharynx and reduces airway lumen. Anatomical factors: retrognathia (receded jaw), micrognathia, macroglossia (enlarged tongue — Down syndrome, hypothyroidism, acromegaly), enlarged tonsils and adenoids (predominant cause in children), nasal septal deviation, turbinate hypertrophy, and craniofacial abnormalities. Neuromuscular: during sleep, upper airway dilator muscle activity (genioglossus) decreases, particularly in REM sleep. Alcohol and sedatives profoundly worsen OSA by reducing upper airway muscle tone and blunting arousal responses. Supine sleeping position worsens OSA due to gravitational tongue and soft palate displacement. Risk factors: male sex (2-3x higher risk — testosterone reduces airway muscle activity; female hormones are protective; risk equalises post-menopause); advancing age (muscle tone decreases with age); family history (genetic craniofacial anatomy); smoking; nasal congestion; hypothyroidism; acromegaly. In children, adenotonsillar hypertrophy is the predominant cause — peak incidence is 3-6 years.

Symptoms of OSA affect both the patient and their bed partner. Nocturnal symptoms: loud habitual snoring (present in 95% of OSA patients — however most snorers do not have OSA); witnessed apnoeic episodes (bed partner observes the patient stop breathing for 10 seconds or more — the most specific symptom; the patient may gasp, choke, or wake with a start at the end of the apnoeic episode); frequent nocturnal awakenings; nocturia (waking to urinate — from atrial natriuretic peptide release during hypoxic episodes — up to 3-4 times per night); restless sleep; night sweats. Daytime symptoms: excessive daytime sleepiness (EDS) — the most functionally impairing symptom — assessed by the Epworth Sleepiness Scale (score above 10 suggests significant sleepiness); difficulty concentrating and cognitive impairment ('brain fog'); morning headaches (from nocturnal hypercapnia); irritability, mood changes, depression; sexual dysfunction; impaired work and driving performance. Complications: hypertension (in 30-40% of OSA patients — OSA causes sustained sympathetic activation and aldosterone release), atrial fibrillation, heart failure, stroke, and type 2 diabetes are significantly more prevalent in moderate-severe OSA. In children: hyperactivity and behavioural problems (rather than sleepiness), poor school performance, mouth breathing, and failure to thrive.

Clinical suspicion is guided by symptoms and risk factors, supplemented by validated questionnaires. STOP-BANG questionnaire (8-item: Snoring, Tired, Observed apnoea, Pressure/hypertension, BMI over 35, Age over 50, Neck circumference over 40cm, Gender male) — score 3+ suggests moderate-high OSA risk. Epworth Sleepiness Scale (ESS) quantifies daytime sleepiness. Definitive diagnosis requires objective sleep testing. Polysomnography (PSG): the gold standard — overnight laboratory-based study recording EEG (sleep staging), EMG (muscle activity), EOG (eye movements), airflow (nasal-oral thermistor, nasal pressure transducer), respiratory effort (thoracic/abdominal belts), pulse oximetry, ECG, and body position. Calculates AHI, oxygen desaturation index (ODI), and minimum oxygen saturation. Ambulatory (home) sleep apnea testing (HSAT) — Type 3 portable monitors recording airflow, respiratory effort, and oxygen saturation — is suitable for patients with high clinical probability of moderate-severe OSA without significant comorbidities (heart failure, COPD, neuromuscular disease); lower sensitivity than PSG. Upper airway assessment by ENT: nasendoscopy, drug-induced sleep endoscopy (DISE — assess dynamic airway collapse under propofol sedation) for patients considering surgery. Investigations for comorbidities: thyroid function, fasting glucose, HbA1c, fasting lipids, and morning cortisol where indicated.

Continuous Positive Airway Pressure (CPAP) is the gold standard treatment for moderate-severe OSA and first-line for all OSA patients with significant symptoms. CPAP delivers a continuous stream of pressurised air via a mask (nasal, nasal pillow, or full-face) to pneumatically splint the upper airway open, preventing collapse. Treatment pressure is titrated during a CPAP titration polysomnogram or by auto-adjusting CPAP (APAP) devices. Adherence is critical — benefits are proportional to hours of nightly use; at least 4-6 hours per night is considered adequate. CPAP reduces AHI to near-zero, improves EDS and cognitive function, and substantially reduces cardiovascular risk and blood pressure in compliant patients. Adherence challenges (claustrophobia, mask discomfort, nasal congestion, pressure intolerance) must be addressed by experienced CPAP support teams. Mandibular advancement device (MAD/oral appliance): custom-fitted dental device advancing the lower jaw and tongue, reducing pharyngeal collapsibility. Effective in mild-moderate OSA and CPAP-intolerant patients; typically reduces AHI by 50-60%; less effective than CPAP but better tolerated. Weight loss: 10% weight loss reduces AHI by approximately 30-50% in obese patients; bariatric surgery achieves remission of OSA in 75-80% of severely obese patients. Positional therapy: supine-avoidance devices (vibrating alarm, positional pillow) for patients with predominantly positional OSA (AHI >2x higher in supine vs non-supine). Surgical options (for selected patients): uvulopalatopharyngoplasty (UPPP); tongue-based procedures; maxillomandibular advancement (MMA — repositions both jaws — most effective surgical procedure with 90% success rate in selected patients); hypoglossal nerve stimulator (Inspire — implantable device stimulating genioglossus during inspiration — approved for CPAP-intolerant moderate-severe OSA; AHI reduction of 70-80%). Avoid alcohol, sedatives, and opioids. Address nasal obstruction (intranasal corticosteroids, antihistamines, septoplasty).

Untreated moderate-to-severe OSA carries substantial long-term health consequences across multiple organ systems. Cardiovascular disease: OSA is an independent risk factor for systemic hypertension (present in 30-40% of OSA patients; OSA causes 30% of treatment-refractory hypertension), atrial fibrillation (2-4x increased risk), coronary artery disease, heart failure, and stroke (2-3x higher risk). Repetitive nocturnal hypoxaemia and sustained sympathetic nervous system activation drive endothelial dysfunction, platelet aggregation, and systemic inflammation. Metabolic complications: untreated OSA significantly worsens insulin resistance and glycaemic control in type 2 diabetes, and is associated with non-alcoholic fatty liver disease, dyslipidaemia, and metabolic syndrome. Neurocognitive impairment: chronic sleep fragmentation causes impaired attention, executive function, memory, and emotional regulation — cognitive deficits that may be partially reversible with CPAP. Motor vehicle accidents: severe untreated OSA increases road traffic accident risk 2-7 fold from excessive daytime sleepiness — a significant public safety and occupational issue. Mood disorders: depression and anxiety are 2-3x more prevalent in untreated OSA patients. Pulmonary hypertension can develop from repeated hypoxic pulmonary vasoconstriction. Children with untreated OSA may develop behavioural problems, academic difficulties, and growth impairment.

Weight management is the most impactful preventive measure — even modest weight loss (5-10% of body weight) reduces OSA severity significantly. Maintain BMI below 25 kg/m². Avoid alcohol, particularly within 3-4 hours of sleep — even moderate alcohol consumption significantly worsens OSA severity. Avoid sedative medications (benzodiazepines, opioids, sedating antihistamines) which exacerbate airway collapse. Treat nasal congestion (allergic rhinitis, nasal polyps) to improve nasal breathing. Sleeping in the lateral (side) position rather than supine reduces OSA severity in 50-60% of patients with positional OSA. For high-risk preoperative patients: evaluate for OSA before elective surgery, as unrecognised OSA significantly increases perioperative respiratory complications; consider CPAP in the perioperative period. In children, early management of adenotonsillar hypertrophy prevents prolonged OSA and its neurocognitive consequences.

Seek medical evaluation promptly for: witnessed apnoeic episodes during sleep (a bed partner observing breathing stopping is highly specific for OSA and warrants investigation); excessive daytime sleepiness causing safety concerns (particularly if driving — do not drive if experiencing uncontrolled sleepiness, as legal obligations apply in many jurisdictions); waking frequently choking or gasping; loud, habitual snoring combined with any daytime sleepiness; or morning headaches with fatigue despite adequate sleep duration. Seek urgent medical attention for: new-onset loud snoring combined with high blood pressure difficult to control; and symptoms of heart failure (ankle swelling, orthopnoea) in a known OSA patient — CSA complicating heart failure requires urgent specialist review. Children who snore loudly, have witnessed apnoeic episodes, breathe through their mouth consistently, have behavioural problems or poor school performance, or have disrupted sleep should be referred to ENT for assessment.