Understanding Obstructive Sleep Apnea Hypopnea: Causes, Symptoms, and Treatment
Sleep Medicine • Pulmonology • ENT
Understanding Obstructive Sleep Apnea–Hypopnea (OSA)
OSA is a common sleep‑related breathing disorder caused by repeated upper airway collapse during sleep leading to hypoxaemia, fragmented sleep and daytime consequences. This concise clinician guide covers recognition, investigation and evidence‑based management.
Scope & epidemiology
OSA affects 9–38% of adults depending on definitions and populations; prevalence increases with age, male sex, obesity and craniofacial risk factors. Untreated OSA is linked to hypertension, cardiovascular disease, metabolic dysfunction, daytime sleepiness and impaired quality of life.
Pathophysiology & risk factors
- Intermittent upper airway collapse during sleep — anatomical (neck circumference, mandibular anatomy) and functional (reduced neuromuscular tone) factors.
- Risk factors: obesity, male sex, age, family history, alcohol/sedative use, nasal obstruction, hypothyroidism, and craniofacial abnormalities.
Clinical features
- Loud habitual snoring, witnessed apneas or gasping, unrefreshing sleep, excessive daytime sleepiness, morning headache, nocturia, and cognitive impairment.
- Physical signs: high BMI, large neck circumference (>40 cm), crowded oropharynx, nasal obstruction.
Screening & assessment
- Use validated questionnaires (STOP‑BANG, Epworth Sleepiness Scale) to estimate pretest probability.
- Take a focused sleep history: bed partner observations, daytime function, comorbidities and medication/substance use.
- Examine ENT and airway anatomy; consider awake endoscopy or imaging in complex cases.
Diagnostic testing
- Polysomnography (PSG): gold standard — measures apneas/hypopneas, oxygen desaturation, arousals and sleep architecture. Report AHI (apnea–hypopnea index) and oxygen metrics.
- Home sleep apnea testing (HSAT): acceptable for patients with high pretest probability and no significant cardiopulmonary/neurologic comorbidity; HSAT measures respiratory events and oxygen but not sleep stages.
- Severity classification: AHI 5–14 mild, 15–29 moderate, ≥30 severe (interpret alongside symptoms and oxygenation).
Management — general principles
- Treat clinically relevant OSA (symptomatic or with cardiometabolic risk) — tailor therapy to severity, anatomy, comorbidity and patient preference.
- Combine conservative measures (weight loss, positional therapy, alcohol/sedative avoidance) with device or procedural interventions when indicated.
First‑line therapy: Positive airway pressure
- CPAP: gold standard for moderate–severe OSA — titrated to eliminate apneas/hypopneas and desaturation; improves sleepiness, blood pressure and quality of life when used adherently.
- Auto‑PAP (APAP): useful for home titration; often used when pressure requirements are variable or fixed titration unavailable.
- Adherence support is critical: mask fit, humidification, education, follow‑up and behavioural interventions increase usage.
Oral appliances & positional therapy
- Mandibular advancement devices (MAD): effective for mild–moderate OSA or CPAP intolerance — advance mandible to open airway; custom devices by dental sleep specialists preferred.
- Positional therapy: for positional OSA (worse supine) — devices or behavioural strategies to promote side‑sleeping; combine with other treatments where needed.
Surgical & procedural options
- Uvulopalatopharyngoplasty (UPPP), tonsillectomy (in selected patients), maxillomandibular advancement (MMA), hypoglossal nerve stimulation (implantable), nasal surgery to improve CPAP tolerance — selection depends on anatomy and prior therapy response.
- Hypoglossal nerve stimulation: option for selected CPAP‑intolerant patients with moderate–severe OSA and specific criteria (BMI limits, no complete concentric collapse at palate on DISE).
- Consider multilevel surgical assessment with drug‑induced sleep endoscopy (DISE) for refractory cases.
Adjunctive and lifestyle measures
- Weight reduction (5–10% weight loss reduces OSA severity), exercise, avoidance of alcohol or sedatives before bedtime, and smoking cessation.
- Address nasal obstruction and treat comorbid conditions (hypothyroidism, heart failure) that may worsen OSA.
When to refer / red flags
- Severe daytime sleepiness with high accident risk, significant nocturnal hypoxaemia, resistant hypertension, atrial fibrillation or heart failure—urgent sleep medicine and cardiology referral.
- Failure to tolerate CPAP despite optimal support, complex anatomy, or pediatric OSA—refer to sleep/ENT/dental specialists.
Case vignette
Patient: R., 52, BMI 34, loud snoring, witnessed apneas and daytime sleepiness (ESS 16). HSAT shows AHI 32/h with mean SpO2 nadir 82%. Management: start CPAP with education and mask fitting, refer for weight management programme, review after 4–8 weeks for adherence and symptom response; consider ENT assessment if CPAP intolerance.
தமிழில் — சுருக்கம்
OSA என்பது தூக்கத்தில் வாயுவழி வீக்கம் காரணமாக கலங்கலாக ஏற்படும். நிறுத்தப்பட்ட சுவாசங்கள் தூக்கத்தை கெடுத்துவிடும் மற்றும் நாளிலுள்ள தூக்கமின்மையும் உள்ளடக்கியது. CPAP முதல் வரிசை சிகிச்சை; வாழ்க்கைமுறை மாற்றங்கள் மற்றும் பிற சாதனங்கள் அல்லது அறுவை சிகிச்சைகள் பயன்படும்.
Key takeaways
- Recognise OSA by snoring, witnessed apneas and daytime sleepiness; confirm with PSG or HSAT depending on pretest probability and comorbidities.
- CPAP is first‑line for moderate–severe OSA; individualise care with MAD, positional therapy, weight loss, or surgery when appropriate and support adherence actively.
- Address cardiovascular and metabolic comorbidities and refer early for complex or high‑risk cases.
