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Obstructive Sleep Apnea (OSA)

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Obstructive Sleep Apnea (OSA)

Obstructive sleep apnea (OSA) is a sleep-related breathing disorder characterized by repeated episodes of partial or complete upper airway obstruction during sleep, causing reduced or absent airflow despite continued breathing effort.

Also called

Obstructive sleep apnea syndrome (OSAS)

ICD-10

G47.33

Specialty

Pulmonology

Onset

Chronic

Reviewed

July 2026

On This Page

Overview

During sleep, the upper airway repeatedly narrows or collapses, causing:

  • Reduced airflow (hypopnea)
  • Complete airflow cessation (apnea)
  • Intermittent hypoxemia
  • Repeated sleep disruption

This leads to poor-quality sleep, daytime sleepiness, and cardiovascular complications.

Etiology & Risk Factors

Main Mechanism

Obstructive Sleep Apnea (OSA) occurs when the upper airway becomes too narrow or collapses during sleep.

Major Risk Factors

  • Obesity

  • Increasing age

  • Male sex

  • Large neck circumference

  • Craniofacial abnormalities

  • Enlarged tonsils or adenoids

  • Family history of OSA

Other Risk Factors For Obstructive Sleep Apnea (OSA)

  • Alcohol use

  • Sedative medications

  • Nasal obstruction

  • Smoking

  • Menopause

  • Hypothyroidism

  • Acromegaly

Important Note

Obesity is the most important modifiable risk factor for OSA.

Pathophysiology

Anatomically narrow or collapsible upper airway
⬇
Reduced upper airway muscle tone during sleep
⬇
Partial or complete airway collapse
⬇
Hypopnea or apnea
⬇
Intermittent hypoxemia + Increased CO₂
⬇
Brief arousal from sleep
⬇
Airway reopens
⬇
Repeated cycles throughout the night
⬇
Sleep fragmentation + Sympathetic activation
⬇
Daytime symptoms + Cardiovascular complications

Clinical Presentation

-Nighttime Symptoms

  • Loud habitual snoring

  • Witnessed apneas

  • Choking or gasping during sleep

  • Restless sleep

  • Frequent awakenings

  • Nocturia

-Daytime Symptoms

  • Excessive daytime sleepiness

  • Morning headache

  • Fatigue

  • Poor concentration

  • Memory problems

  • Irritability

  • Reduced work or academic performance

-Signs

    • Obesity

    • Large neck circumference

    • Crowded upper airway

    • Enlarged tonsils

    • Hypertension

History Taking

  • Ask about:

    • Loud snoring?
    • Witnessed breathing pauses?
    • Choking or gasping during sleep?
    • Excessive daytime sleepiness?
    • Morning headaches?
    • Unrefreshing sleep?
    • Poor concentration?
    • Frequent nighttime urination?
    • Falling asleep while driving?
    • Weight gain?
    • Alcohol use?

Physical Examination

-General Examination

Look for:

  • Obesity
  • Increased neck circumference
  • Hypertension

-Upper Airway Examination

Look for:

  • Crowded oropharynx
  • Enlarged tonsils
  • Large tongue
  • Retrognathia
  • Nasal obstruction

-Important Note

A normal physical examination does not exclude OSA.

Investigations

-Polysomnography — Standard Diagnostic Test

An overnight sleep study assesses:

  • Airflow

  • Respiratory effort

  • Oxygen saturation

  • Heart rate

  • Sleep stages

  • Apnea and hypopnea episodes

-Home Sleep Apnea Testing

May be used in selected adults with a high clinical suspicion of uncomplicated OSA.

-Apnea–Hypopnea Index (AHI)

The number of apneas and hypopneas per hour of sleep.

Severity

  • Mild: AHI 5–14 events/hour

  • Moderate: AHI 15–29 events/hour

  • Severe: AHI ≥30 events/hour

-Additional Tests

When indicated:

    • Thyroid function tests

    • Arterial blood gas

    • ECG

    • Echocardiography

Diagnosis

Obstructive Sleep Apnoea (OSA) · Diagnostic Criteria

DIAGNOSIS REQUIRES OBJECTIVE SLEEP STUDY + CLINICAL CORRELATION OSA is defined by repetitive upper airway obstruction during sleep causing apnoeas/hypopnoeas → intermittent hypoxia, sleep fragmentation, and sympathetic activation. Severity is graded by the Apnoea-Hypopnoea Index (AHI) on polysomnography or home sleep testing.
Diagnostic Approach
1
Clinical Suspicion
Snoring, witnessed apnoeas, excessive daytime sleepiness, non-restorative sleep, morning headaches, nocturia, impaired concentration.
History & symptoms
2
Pre-test Screening
STOP-BANG questionnaire or Epworth Sleepiness Scale (ESS) to quantify daytime sleepiness and risk stratify before formal testing.
Questionnaires
3
Sleep Study
Home sleep apnoea test (HSAT/WatchPAT) for uncomplicated suspected OSA. In-lab polysomnography (PSG) if HSAT negative but suspicion remains high, or comorbid sleep disorders suspected.
Confirmatory
4
Grade Severity & Treat
AHI from sleep study defines severity. Combined with symptoms to guide treatment threshold — CPAP, positional therapy, or weight loss/lifestyle.
AHI-based grading
Severity AHI (events/hour) Typical Features Treatment Threshold
Normal <5 events/hour No significant sleep-disordered breathing; snoring may still be present No OSA-specific treatment; general sleep hygiene advice
Mild OSA 5–14 events/hour Mild symptoms; some sleepiness; ESS typically 10–12 CPAP if symptomatic or comorbidities present; positional therapy/mandibular advancement device for positional mild OSA
Moderate OSA 15–29 events/hour More frequent arousals; significant daytime sleepiness; ESS typically 12–15 CPAP recommended; weight loss; optimise sleep position
Severe OSA ≥30 events/hour Severe sleepiness, significant nocturnal hypoxia, increased cardiovascular and metabolic risk; ESS typically >15 CPAP strongly indicated; urgent in drivers, occupational risk; consider BiPAP/ASV if CPAP-intolerant
STOP-BANG Screening Tool
Snoring — do you snore loudly?
Tired — often tired, fatigued, or sleepy during the day?
Observed — has anyone observed you stop breathing during sleep?
Pressure — do you have or are you being treated for high BP?
BMI >35
Age >50 years
Neck circumference >40 cm
Gender — male sex
Score ≥3 = high risk for OSA → refer for sleep study. Score 0–2 = low risk.
Consequences & Comorbidities
Cardiovascular — HTN (treatment-resistant), AF, MI, stroke, pulmonary hypertension
Metabolic — insulin resistance, type 2 diabetes, dyslipidaemia, NAFLD
Neurocognitive — impaired memory/concentration, depression, anxiety
Road traffic accidents — 2–7x increased risk; legal duty to advise cessation of driving until treated
Perioperative risk — increased sensitivity to opioids/sedation; inform anaesthetist; CPAP should be continued perioperatively
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Related Topics

Management

Obstructive Sleep Apnoea (OSA) · Treatment

TREATMENT IS STEPWISE — CPAP IS GOLD STANDARD FOR MODERATE-TO-SEVERE OSA All patients need lifestyle modification regardless of severity. CPAP is first-line for moderate-severe OSA and symptomatic mild OSA. Alternatives (MAD, positional therapy, surgery) are used when CPAP is declined or not tolerated. Treatment relieves symptoms and reduces cardiovascular risk.
Treatment Pillars
1
Lifestyle Modification
Weight loss, positional therapy, alcohol/sedative avoidance, good sleep hygiene. Applies to all patients regardless of severity.
All patients
2
CPAP
Continuous positive airway pressure — pneumatically splints the upper airway open during sleep. Gold standard for moderate-severe OSA and symptomatic mild OSA.
First-line device
3
Mandibular Advancement Device
Oral device that advances the lower jaw, increasing retropharyngeal space. Used in mild-moderate OSA or as CPAP alternative if intolerant.
Alternative/adjunct
4
Surgical / Advanced Options
Bariatric surgery (if obese), upper airway surgery (tonsillectomy, UPPP, Inspire hypoglossal nerve stimulation), or BiPAP/ASV for CPAP-intolerant patients.
Selected cases
Treatment Indication Notes
Lifestyle & Behavioural All patients Weight loss most impactful — 10% weight loss can reduce AHI by 26%. Avoid alcohol and sedatives (worsen muscle relaxation). Avoid supine sleeping. Smoking cessation reduces pharyngeal inflammation.
Positional Therapy Positional OSA (AHI ≥2x worse supine) Positional OSA device or tennis-ball technique to prevent supine sleep. Effective first-line for mild-moderate positional OSA.
CPAP (Continuous Positive Airway Pressure) Moderate OSA (AHI ≥15) or Symptomatic mild OSA Gold standard. Titrated to eliminate apnoeas (usually 5–15 cmH2O). Auto-CPAP (APAP) self-adjusts nightly. Adherence ≥4h/night on ≥70% of nights is benchmark. Reduces sleepiness, BP, cardiovascular risk.
BiPAP (Bilevel PAP) CPAP intolerance or Coexisting hypoventilation Separate inspiratory (IPAP) and expiratory (EPAP) pressures. Useful in obesity hypoventilation, COPD-OSA overlap, or CPAP pressure intolerance.
Mandibular Advancement Device (MAD) Mild-moderate OSA or CPAP refusal/failure Custom-fitted by a dentist. Less effective than CPAP but better tolerated. Contraindicated with severe temporomandibular joint disease or insufficient dentition.
Hypoglossal Nerve Stimulation (Inspire) Moderate-severe OSA + CPAP failure Implantable device stimulates hypoglossal nerve → protrudes tongue during inspiration. AHI 25–65, BMI ≤32, no concentric palatal collapse on DISE. Growing evidence base.
Upper Airway Surgery Anatomical obstruction + CPAP failure Tonsillectomy/adenoidectomy (especially children and adults with tonsillar hypertrophy). UPPP (uvulopalatopharyngoplasty) for selected adults. Variable outcomes — patient selection critical.
Bariatric Surgery BMI ≥35 + OSA Significant weight loss can achieve OSA remission in many patients. Not a guaranteed cure — post-operative sleep study recommended to confirm resolution before stopping CPAP.
Treat Comorbidities All patients Optimise HTN, AF, T2DM, hypothyroidism (worsens OSA). Nasal obstruction treatment (topical steroids, septoplasty) improves CPAP tolerance.
Improving CPAP Adherence
Mask fit — trial multiple mask types (nasal, full-face, nasal pillow); poor fit is the most common reason for dropout
Heated humidification — reduces dryness, mouth breathing, and nasal congestion side effects
Pressure ramp — starts at low pressure, gradually rises during sleep onset to improve comfort
APAP over fixed CPAP — auto-adjusting pressure improves comfort without compromising efficacy
Follow-up & telemonitoring — early review at 4–6 weeks; device data review guides pressure adjustments and identifies leak/AHI residuals
Driving & Special Considerations
Driving ban — patients with excessive daytime sleepiness and OSA must be advised not to drive until adequate treatment (legal and ethical duty)
DVLA/licensing authority — patients must notify relevant authority; commercial vehicle drivers (HGV/bus) have stricter rules and may not drive until confirmed controlled on CPAP
Perioperative — inform anaesthetist; continue CPAP perioperatively; avoid opioids where possible; elevated risk of postoperative respiratory complications
Pregnancy — OSA worsens in pregnancy; associated with pre-eclampsia and gestational diabetes; CPAP is safe and recommended

Complications

  • Systemic hypertension
  • Pulmonary hypertension
  • Coronary artery disease
  • Heart failure
  • Cardiac arrhythmias
  • Stroke
  • Insulin resistance
  • Type 2 diabetes
  • Cognitive impairment
  • Depression
  • Motor vehicle accidents
  • Reduced quality of life

Prognosis

  • OSA is a chronic but treatable condition.
  • Prognosis improves with:
    • Weight loss
    • Effective CPAP use
    • Good treatment adherence
    • Management of cardiovascular risk factors
  • Untreated severe OSA increases the risk of:
    • Cardiovascular disease
    • Stroke
    • Accidents
    • Reduced quality of life
  • Long-term treatment can significantly improve symptoms and outcomes.

Key Points / Clinical Pearls

  • OSA is caused by repeated upper airway collapse during sleep.
  • Obesity is the most important modifiable risk factor.
  • Loud snoring, witnessed apneas, and daytime sleepiness are classic features.
  • Polysomnography is the standard diagnostic test.
  • AHI is used to classify OSA severity.
  • CPAP is the main treatment for many patients with OSA.
  • Weight loss is an important part of management.
  • Untreated OSA increases cardiovascular and accident risk.
  • Falling asleep while driving is a major warning sign.
  • A normal physical examination does not exclude OSA.