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

Sleep apnea (sleep apnoea) is a sleep disorder characterised by repeated episodes of partial (hypopneas — airflow reduction of 30% or more for 10 or more seconds with oxygen desaturation) or complete (apneas — cessation of airflow for 10 or more seconds) breathing pauses during sleep. Three types: obstructive sleep apnea (OSA — the most common; 90% of cases — caused by collapse of the pharyngeal upper airway during sleep despite ongoing respiratory effort), central sleep apnea (CSA — failure of the central respiratory drive — absence of both airflow and effort; more common in heart failure, stroke, opioid use), and complex/mixed sleep apnea (combination of OSA and CSA). OSA severity is assessed by the apnea-hypopnea index (AHI — number of breathing events per hour of sleep): mild (5-14), moderate (15-29), severe (30 or above). Untreated moderate-severe OSA significantly increases risk of hypertension (2-3x), stroke (2-3x), type 2 diabetes (2x), cardiac arrhythmia (atrial fibrillation), daytime somnolence (7x increased road traffic accident risk), and reduced quality of life. Approximately 80% of cases remain undiagnosed. CPAP therapy is highly effective when used consistently.

OSA occurs due to collapse of the pharyngeal airway during sleep — sleep causes relaxation of pharyngeal dilator muscles (genioglossus, palatal muscles), and in predisposed individuals the upper airway narrows or collapses with each inspiration, generating the characteristic snoring sound (partial obstruction — turbulent airflow) and apneas (complete obstruction). Anatomical risk factors: obesity (the single most important modifiable risk factor — pharyngeal fat deposition narrows the airway lumen; neck circumference above 43 cm in men, above 38 cm in women correlates strongly with OSA); retrognathia and micrognathia (small or recessed jaw — reduces pharyngeal space); enlarged tonsils and adenoids (particularly in children — the primary cause in paediatric OSA); macroglossia (enlarged tongue — Down syndrome, acromegaly, hypothyroidism); deviated nasal septum (increased nasal resistance increases negative pressure in the upper airway); and craniofacial abnormalities. Physiological risk factors: male sex (testosterone reduces upper airway muscle tone — men are 2-3x more affected than premenopausal women; OSA increases in women after menopause); advancing age (reduced upper airway muscle tone); alcohol, sedatives, and opioids (relax pharyngeal muscles — worsen OSA); hypothyroidism (myxoedema of pharyngeal tissues); nasal congestion. Genetics: first-degree relatives of OSA patients have 2x risk.

Nocturnal (night-time) symptoms: loud habitual snoring (almost universal in OSA — often reported by the bed partner before the patient recognises it); witnessed apneas (bed partner reports breathing stopping, then the sleeper snorts, gasps, or chokes); restless sleep with frequent awakenings; nocturnal choking or gasping (patient may awaken distressed and short of breath); nocturia (waking to urinate — due to increased atrial natriuretic peptide from nocturnal hypoxia); excessive nighttime sweating; and bruxism (tooth grinding). Daytime symptoms: excessive daytime sleepiness (EDS — the cardinal symptom, assessed by Epworth Sleepiness Scale — score above 10 suggests significant sleepiness); morning headaches (from nocturnal carbon dioxide retention); poor concentration, memory problems, and cognitive impairment; irritability, mood disturbance, and depression; and reduced libido. Complications of untreated OSA: systemic hypertension (in up to 50% of OSA patients — often difficult to control without OSA treatment); pulmonary hypertension; atrial fibrillation (2-3x increased risk); heart failure; stroke; type 2 diabetes; non-alcoholic fatty liver disease; and polyuria/nocturia. Paediatric OSA: presents differently — behavioural problems (ADHD-like), school performance difficulties, nighttime enuresis (bedwetting), growth failure, and hyperactivity (rather than daytime sleepiness). Snoring in children is the most common symptom.

Screening: Epworth Sleepiness Scale (ESS) — 8-item questionnaire scoring daytime sleepiness (0-24; above 10 = significant sleepiness). STOP-BANG questionnaire: 8 yes/no questions (Snoring, Tiredness, Observed apneas, Blood Pressure, BMI, Age, Neck circumference, Gender) — scores 3 or above indicate high OSA risk; validated pre-operative screening tool. Overnight oximetry: pulse oximetry worn at home overnight — an oxygen desaturation index (ODI) above 15-20 events per hour is suggestive of OSA; a useful initial screening test. Sleep study — the definitive investigation: Level 1 — attended polysomnography (PSG) in a sleep laboratory: gold standard — measures EEG (sleep stages), airflow, oxygen saturation, heart rate, EMG (leg movements, respiratory effort), and thoracoabdominal movement. Full characterisation of all sleep-disordered breathing events. Level 2 — home sleep apnea testing (HSAT): portable devices measuring airflow, oximetry, and respiratory effort at home — appropriate for patients with high pre-test OSA probability without significant comorbidities; AHI derived from HSAT (may underestimate severity as sleep time is not measured). Diagnosis of OSA: AHI 5 or above with symptoms (or AHI 15 or above regardless of symptoms). CPAP titration: laboratory CPAP titration (manual or autotitrating APAP) determines the optimal therapeutic pressure. Epworth score, clinic blood pressure, and evaluation for cardiac arrhythmia are routine. CT or MRI of the airway for surgical planning.

Lifestyle modification: weight loss — the most impactful intervention for OSA; a 10% weight loss is associated with approximately 26% AHI reduction; low-calorie diet, GLP-1 receptor agonists (semaglutide — significant weight loss reduces OSA severity — SURMOUNT-OSA trial), and bariatric surgery (reduces AHI by 60-80% in morbidly obese patients). Positional therapy: for positional OSA (AHI predominantly worse in supine — back-sleeping position) — positional devices (vibrating belts, shirts with dorsal bumpers), positional pillows; effective for 25-30% of OSA patients. Alcohol and sedative avoidance (especially in the 4 hours before bedtime). Nasal optimisation: treat nasal congestion (intranasal corticosteroids, nasal decongestants) — reduces nasal resistance. CPAP (continuous positive airway pressure): the most effective treatment for moderate-severe OSA (AHI above 15). A mask (nasal, oronasal, nasal pillow) delivers a continuous pneumatic splint to the pharyngeal airway at a pressure of 5-15 cm H2O, preventing collapse. Normalises AHI to below 5, eliminates snoring, resolves daytime somnolence (ESS score improvement 3-4 points), and reduces cardiovascular risk (CPAP reduces ambulatory BP by 2-3 mmHg). Adherence is critical — at least 4-5 hours per night is required for therapeutic benefit; 20-50% of prescribed patients have poor adherence. Autotitrating CPAP (APAP): adjusts pressure breath-by-breath — improves comfort and adherence over fixed CPAP. Mandibular advancement device (MAD): a custom-fitted dental appliance that protrudes the lower jaw during sleep, enlarging the retroglossal space; effective for mild-moderate OSA and CPAP-intolerant patients; less effective than CPAP for severe OSA but better tolerated; side effects — jaw pain, tooth soreness, temporomandibular joint discomfort. Surgical options: Uvulopalatopharyngoplasty (UPPP) — soft palate and uvula resection; effective for selected patients (anatomy-guided); reduces AHI by 50-70% on average but rarely cures severe OSA; less effective than CPAP. Tonsillectomy and adenoidectomy — first-line treatment in children with tonsillar hypertrophy. Hypoglossal nerve stimulation (HNS — Inspire device): an implanted device detects breathing efforts and delivers electrical stimulation to the hypoglossal nerve, advancing the tongue during inspiration; highly effective for moderate-severe CPAP-intolerant OSA (AHI below 65, no significant positional or REM OSA); approved by NICE and FDA. Maxillomandibular advancement (MMA) surgery — most effective surgical option for severe OSA; repositions the jaw forward to permanently enlarge the pharynx. Bariatric surgery: dramatic OSA improvement in morbidly obese patients — often achieves curative resolution. Central sleep apnea: treat underlying cause (heart failure optimisation — CRT pacing if indicated; opioid dose reduction); adaptive servo-ventilation (ASV) for complex sleep apnea (CPAP-related central apneas); supplemental oxygen; acetazolamide (altitude-related central apnea).

Untreated moderate-severe OSA carries serious systemic complications across multiple organ systems. Hypertension: OSA is a major secondary cause of resistant hypertension — present in up to 50% of OSA patients; untreated OSA accounts for a significant proportion of hypertension refractory to three or more antihypertensive drugs. Atrial fibrillation risk is 2–3x elevated; recurrence after electrical cardioversion or catheter ablation is substantially higher without concurrent CPAP treatment. Coronary artery disease and myocardial infarction risk is approximately doubled. Stroke risk is 2–3x elevated from nocturnal hypoxaemia, hypertension, and increased platelet aggregability. Type 2 diabetes: OSA contributes independently to insulin resistance and elevated HbA1c through intermittent hypoxia and sleep fragmentation mechanisms. Motor vehicle accidents are 3–7x more likely from uncontrolled daytime sleepiness — a legal driving impairment in the UK. All-cause mortality is elevated in moderate-severe untreated OSA — meta-analyses confirm cardiovascular mortality is substantially reduced by adherent CPAP therapy. Heart failure exacerbation is worsened by untreated OSA.

Weight management is the most important preventive measure — maintaining a healthy BMI (below 25 kg/m2) significantly reduces OSA risk and severity. For every 10 kg weight gain, OSA risk approximately doubles. Sleep position: sleeping on the side (lateral position) rather than the back (supine) reduces upper airway collapse — position training, specialised pillows, or positional devices can reinforce side-sleeping in positional OSA. Avoid alcohol (particularly within 3-4 hours of bedtime) and sedative drugs — both dramatically worsen upper airway muscle tone and OSA severity. Treat nasal congestion: optimise allergic rhinitis (intranasal corticosteroids), use saline nasal irrigation, and consider septoplasty for significant nasal obstruction. Regular physical activity — independent of weight loss — improves upper airway muscle tone and modestly reduces OSA severity. Manage comorbidities: treat hypothyroidism (myxoedema worsens upper airway obstruction) and acromegaly (macroglossia-related OSA). Smoking cessation: smoking causes upper airway mucosal inflammation and increases OSA risk. If driving, be aware that untreated excessive daytime sleepiness from OSA is a legal driving impairment — DVLA must be notified (Group 2 licence holders — HGV, bus — cannot drive until AHI is confirmed as below 15 on treatment in the UK).

See a GP if you or your bed partner notice any of: loud habitual snoring, witnessed breathing pauses during sleep, morning headaches, persistent daytime sleepiness despite adequate sleep time, or waking frequently at night choking or gasping. Referral to a sleep clinic or respiratory physician is appropriate for: Epworth Sleepiness Score above 10, STOP-BANG score of 3 or above, oxygen desaturation index above 15 events per hour on overnight oximetry, and suspected OSA with cardiovascular comorbidities. Seek urgent review for: suspected severe OSA with cardiovascular instability, new onset of atrial fibrillation or resistant hypertension (OSA is a contributing factor requiring investigation), and any professional driver with suspected OSA (DVLA notification obligation — cannot drive group 2 vehicles without specialist sleep assessment and treatment confirmation). Parents should seek paediatric assessment for a child who snores loudly, has restless sleep, bedwets, is difficult to wake in the morning, or shows behavioural problems or school difficulties — paediatric OSA is highly treatable.