Sleep disorder of repetitive upper airway collapse causing reduced or paused breathing (apneas/hypopneas) during sleep; leads to oxygen desaturations and fragmented sleep.
Very common (~25 million US adults) yet underdiagnosed. Untreated OSA increases risk of hypertension (often resistant), arrhythmias (e.g., atrial fibrillation), heart disease, stroke, and diabetes, and causes daytime impairment (accidents, cognitive dysfunction). Recognizing OSA is high-yield because treatment (e.g., CPAP) can greatly improve outcomes.
Classic patient: middle-aged obese man with loud, disruptive snoring, witnessed apneas (partner reports breathing pauses and gasping at night), and excessive daytime sleepiness (dozing off at work or while driving). Often also notes unrefreshing sleep and morning headaches.
Major risk factors: obesity (especially large neck circumference), male sex, older age, and craniofacial anatomy (retrognathia, crowded airway). Risk rises in postmenopausal women and with alcohol or sedative use (relaxes airway tone).
Children can also have OSA, usually due to adenotonsillar hypertrophy. A child with OSA may present with loud snoring plus behavioral problems (irritability, hyperactivity, poor school performance) rather than obvious daytime sleepiness.
Screen high-risk patients using questionnaires like STOP-Bang or the Epworth Sleepiness Scale to identify those likely to have OSA.
Polysomnography (overnight sleep study) is the gold standard diagnostic test, monitoring airflow, oxygen levels, etc., to confirm OSA and quantify severity.
OSA is diagnosed if AHI ≥5 (events/hour) with compatible symptoms (or AHI ≥15 even without symptoms). Severity is classified as mild (5–14), moderate (15–30), or severe (>30) based on the apnea-hypopnea index.
Sleep studies distinguish obstructive vs central apneas: obstructive events show continued respiratory effort (thoracic/abdominal movement) during the apnea, whereas central apneas have no respiratory effort.
Condition
Distinguishing Feature
Central sleep apnea
cessation of respiratory effort (no chest movement); often seen in heart failure (Cheyne-Stokes breathing) or opioid use
Narcolepsy
daytime sleepiness with cataplexy or other REM phenomena; sleep attacks occur despite adequate night sleep (not due to airway obstruction)
Obesity hypoventilation syndrome
obese patient with chronic daytime hypercapnia (elevated CO₂ levels) and hypoxemia; often coexists with OSA (a.k.a. Pickwickian syndrome)
Weight loss (diet, exercise) is recommended for all OSA patients (even a 10% weight reduction can significantly improve OSA severity); avoid alcohol and sedatives, especially before bedtime.
Nightly CPAP (continuous positive airway pressure) is first-line for moderate to severe OSA; it splints the airway open during sleep, resolving apneas and improving daytime alertness and blood pressure.
If CPAP is not tolerated or for mild OSA: consider custom oral appliances (devices that advance the mandible to keep the airway open) or positional therapy (e.g., avoiding supine sleeping, special pillows).
ENT surgical options can be considered in select cases: e.g., uvulopalatopharyngoplasty (UPPP) to remove or reshape airway tissues, jaw advancement surgery, or nasal septum repair. Adenotonsillectomy is first-line in pediatric OSA due to enlarged tonsils/adenoids. A tracheostomy (surgical airway) bypasses the obstruction and is curative but reserved for severe, life-threatening OSA when other treatments fail.
Mnemonic STOP-Bang for OSA risk factors: Snoring, Tiredness (daytime fatigue), Observed apneas, Pressure (high BP); BMI >35, Age >50, Neck >40 cm, Gender male.
Resistant hypertension or difficult-to-control atrial fibrillation should raise suspicion for occult OSA (treating OSA can improve blood pressure and arrhythmias).
Excessive sleepiness leading to motor vehicle accidents or workplace accidents (patients may doze off during driving or operating machinery).
Untreated OSA contributes to resistant hypertension (high BP despite multiple medications) and arrhythmias (like atrial fibrillation); always consider OSA in these scenarios.
Severe OSA can cause abrupt oxygen drops and bradyarrhythmias at night, increasing the risk of sudden cardiac death if left untreated.
Snoring, daytime sleepiness, obesity, or large neck → suspect OSA.
Assess risk with STOP-Bang questionnaire or Epworth Sleepiness Scale; get partner's report of apneas if possible.
If screening is positive or clinical suspicion remains high → confirm diagnosis with overnight polysomnography (sleep study) to measure AHI.
If OSA is confirmed (meets AHI criteria) → counsel lifestyle changes (weight loss, avoid alcohol/sedatives, lateral sleep positioning) and initiate therapy (usually CPAP for moderate-to-severe OSA).
If CPAP is intolerable or OSA is mild → consider alternatives: an oral appliance or refer to ENT for possible surgical intervention. Ensure follow-up to monitor adherence and improvement.
Obese, loud-snoring middle-aged man with daytime sleepiness and resistant hypertension → OSA (obesity-related).
Child with loud snoring, tonsillar hypertrophy, and behavioral problems (inattention, hyperactivity) → OSA (adenotonsillar hypertrophy).
Case 1
A 52‑year‑old obese man with treatment-resistant hypertension is evaluated for loud snoring and daytime sleepiness.
Case 2
A 6‑year‑old boy with nightly snoring and restless sleep is evaluated for hyperactivity and poor school performance.
OSA—upper airway collapse during sleep (illustration).