What is obstructive sleep apnoea?

OSA is a sleep disorder characterised by recurrent partial (hypopnoea) or complete (apnoea) upper airway obstruction during sleep — lasting ≥10 seconds and causing oxygen desaturation, sleep fragmentation and arousal. The throat soft tissue relaxes and collapses → airflow obstruction → O2 falls → partial arousal → breathing resumes → patient returns to sleep (usually unremembered). This cycle repeats many times per hour in severe OSA. Common presentation: loud snoring witnessed by partner; observed apnoeas; unrefreshing sleep; excessive daytime sleepiness; morning headaches; nocturia.

How is OSA diagnosed?

Step 1: Screening — ESS ≥11; STOP-BANG ≥5/8. Step 2: Sleep study. PSG gold standard (in-lab). HSAT acceptable: high pre-test probability, no HF/COPD/hypoventilation. Diagnosis: AHI ≥5 with compatible symptoms OR AHI ≥15 regardless of symptoms. Severity: mild (AHI 5-14.9); moderate (15-29.9); severe (≥30).

What is CPAP and how does it work?

CPAP delivers constant pressurised air through a mask — pneumatically splinting the upper airway open, preventing collapse. Pressure typically 4-20 cmH2O. Completely eliminates apnoeas in most patients. Benefits with adequate adherence: dramatic EDS improvement; improved driving safety; modest BP reduction (2-4 mmHg); improved AF burden; improved QoL. Biggest challenge: adherence (~30-40% inadequate). Proper mask fitting and heated humidification are the two most important adherence factors.

Can OSA be treated without CPAP?

Yes: Weight loss: 10% loss reduces AHI ~26%; bariatric surgery may resolve OSA in some. MAD (mandibular advancement device): effective for mild-moderate or CPAP-intolerant moderate-severe; less effective than CPAP. Positional therapy: ~25-30% of OSA is position-dependent (supine-worse) — position sensor or tennis ball in back pocket prevents supine sleeping. Surgery: UPPP; maxillomandibular advancement (MMA — most effective surgical option); hypoglossal nerve stimulation (Inspire — FDA-approved 2014 for CPAP-intolerant moderate-severe).

How does GMJ News cover OSA?

GMJ News covers 936M global prevalence, 80-90% underdiagnosis, AHI classification, CPAP gold standard and adherence challenges, cardiovascular risk (hypertension, AF, stroke, RTA ×3-7), ESS and STOP-BANG, PSG vs HSAT, OHS, MAD, weight loss, hypoglossal nerve stimulation, driving legal obligations, and paediatric OSA (adenotonsillectomy). Relevant to PHIG's NCD, pulmonology and road safety programme.

Home › Topics › Obstructive Sleep Apnoea

Obstructive Sleep Apnoea

GMJ News knowledge hub · last reviewed August 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Obstructive sleep apnoea (OSA) — recurrent partial or complete upper airway collapse during sleep causing apnoeas (breathing pauses ≥10 seconds), hypopnoeas, oxygen desaturation and sleep fragmentation — is a highly prevalent condition affecting approximately 936 million adults globally (Lancet 2019), with an estimated 80-90% of moderate-to-severe OSA undiagnosed, and carrying a dramatically elevated risk of cardiovascular disease (2-3× higher risk of hypertension, 2× higher risk of atrial fibrillation, 3× higher risk of stroke, 3-7× higher risk of road traffic accidents from excessive daytime sleepiness) (WHO). Continuous positive airway pressure (CPAP) — which pneumatically splints the airway open — remains the gold standard treatment for moderate-to-severe OSA, improving daytime sleepiness, cardiovascular risk markers and quality of life, though its benefits are contingent on adherence (>4 hours/night for ≥70% of nights — achieved in approximately 60-70% of patients with adequate support).

Key messages

936 million adults globally — 80-90% undiagnosed

Lancet 2019 (Benjafield et al.): 936 million adults have mild-to-severe OSA globally. Approximately 80-90% of moderate-to-severe OSA is undiagnosed — a striking gap given the serious cardiovascular and public safety consequences.

AHI — the diagnostic severity index

Apnoea-hypopnoea index (AHI): number of apnoeas (≥10 sec ≥90% airflow reduction) and hypopnoeas (≥10 sec ≥30% airflow reduction + ≥3-4% O2 desaturation or arousal) per hour of sleep. AHI 5-14.9: mild. AHI 15-29.9: moderate. AHI ≥30: severe. Diagnosis: PSG (gold standard) or HSAT (acceptable for high pre-test probability, no significant comorbidities).

CPAP — the gold standard treatment

CPAP pneumatically splints the upper airway open, eliminating apnoeas and hypopnoeas throughout sleep. Gold standard for moderate-severe OSA. Benefits (adequate adherence): dramatic improvement in ESS (Epworth Sleepiness Scale); reduced RTA risk; improved cognitive function; modest BP reduction (2-4 mmHg); improved AF burden. Adherence challenge: ~30-40% of patients do not achieve adequate adherence (>4h/night ≥70% of nights).

OSA — the most common secondary cause of hypertension

OSA causes cardiovascular harm through: chronic intermittent hypoxia → sympathetic activation → hypertension (OSA is the most common secondary cause of hypertension — present in ~50% of OSA patients); oxidative stress → endothelial dysfunction; sleep fragmentation → metabolic dysfunction. Risk ratios: hypertension ×2-3; AF ×2-3; stroke ×3; CAD ×2; road traffic accidents ×3-7 (excessive daytime sleepiness).

Epworth Sleepiness Scale and STOP-BANG screening

ESS: 8-item self-reported questionnaire (max 24). ESS ≥11: excessive daytime sleepiness — investigate. STOP-BANG: Snoring, Tiredness, Observed apnoea, blood Pressure, BMI >35, Age >50, Neck >40cm, Gender (male). ≥5 factors = high OSA risk. ESS is a screening tool only — ~20-30% of significant OSA has normal ESS (do not rely on ESS alone).

Obesity hypoventilation syndrome — beyond simple OSA

OHS (Pickwickian syndrome): obesity (BMI >30) + daytime hypercapnia (PaCO2 >6 kPa) not explained by other conditions. Almost all OHS patients have OSA. Key distinction from simple OSA: daytime CO2 retention; more severe hypoxaemia; pulmonary hypertension; cor pulmonale. Treatment: CPAP treats OSA component but may not correct CO2 → NIV (BiPAP) if CO2 persists. Weight loss is the most effective OHS treatment.

Key statistics

936M

adults globally have OSA (Lancet 2019); 80-90% of moderate-severe undiagnosed

Lancet 2019

AHI ≥30

severe OSA; AHI 15-29.9 moderate; AHI 5-14.9 mild (AASM criteria)

AASM

×3-7

road traffic accident risk from untreated OSA — major public safety issue

AASM/NEJM

50%

of OSA patients have hypertension — OSA is the most common secondary cause

ESC/AHA

ESS ≥11

Epworth Sleepiness Scale threshold for excessive daytime sleepiness

AASM

30-40%

of CPAP patients do not achieve adequate adherence (>4h/night ≥70% of nights)

AASM/ERS

OSA treatment options — effectiveness comparison (AASM/ERS)

Source: AASM/ERS. CPAP gold standard moderate-severe; MAD for mild or CPAP-intolerant; weight loss highly effective in obese.

Glossary of key terms

PSG vs HSAT
Sleep medicinePolysomnography (PSG): full in-lab overnight study — EEG, EOG, EMG, ECG, airflow, SpO2, respiratory effort, body position. Gold standard. Home Sleep Apnoea Test (HSAT): portable device. Appropriate: adults with high pre-test OSA probability, no significant comorbidities (HF, COPD, hypoventilation). HSAT underestimates AHI (no sleep staging — divides events by recording time, not sleep time). Not appropriate: suspected central sleep apnoea; OHS; complex sleep disorders.

CPAP technology and adherence
Sleep medicine/TechnologyAuto-CPAP (APAP): variable pressure responding to airflow limitation — standard first-line. BiPAP/BPAP: separate IPAP and EPAP — for CPAP-intolerant or OHS/hypoventilation. Adherence optimisation: proper mask fitting (most common non-adherence cause); heated humidification; pressure ramp; telemonitoring with early intervention. All modern CPAP devices record: hours used, residual AHI, mask leak.

Mandibular advancement device (MAD)
Dentistry/Sleep medicineCustom-fitted oral appliance — holds mandible forward, increases retroglossal airway, prevents posterior pharyngeal wall collapse. FDA-cleared for mild-moderate OSA and CPAP-intolerant moderate-severe OSA. Effectiveness: reduces AHI ~50-60% (less than CPAP which eliminates >90%); achieves AHI <5 in ~40-50%. Side effects: TMJ discomfort; increased salivation; mild tooth discomfort (usually transient). Requires dental assessment.

OSA and driving — legal obligations
Public safetyUntreated severe OSA increases RTA risk ×3-7. UK DVLA: significant OSA with daytime sleepiness → must inform DVLA + must NOT drive until adequately treated and assessed. CPAP restores driving safety to normal. Commercial licence (HGV, PSV): AHI <15 or demonstrated CPAP compliance required. Clinicians must advise patients of driving safety and legal obligations.

Hypoglossal nerve stimulation (Inspire)
Surgery/OSAInspire (Medtronic) — FDA-approved 2014 for moderate-severe OSA in CPAP-intolerant patients. Implantable device: sensing lead + stimulation lead (hypoglossal nerve) + pulse generator (subcutaneous, right chest). Mechanism: synchronised electrical stimulation of the hypoglossal nerve (tongue protrusion) during inspiration → prevents retroglossal collapse. Criteria: AHI 15-65; BMI <32; no complete concentric palatal collapse on DISE. Efficacy: ~70% responder rate (AHI <15 + >50% reduction). Alternative to surgical UPPP for selected CPAP-intolerant patients.

Paediatric OSA
Paediatrics/SleepMost common cause in children: adenotonsillar hypertrophy (~75%) — unlike adult OSA which is predominantly obesity-driven. Presentation: snoring; witnessed apnoeas; nocturnal enuresis; mouth breathing; hyperactivity/inattentiveness/academic problems (children paradoxically hyperactive, not sleepy). Diagnosis: PSG (not HSAT — different paediatric normative values). Treatment: adenotonsillectomy first-line (highly effective); CPAP for residual OSA; weight management.