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Summary Table

Category	Details
Risk Factors	Obesity (BMI > 30), male sex, age > 40, large neck circumference (> 17 in. men / > 16 in. women), craniofacial abnormalities (retrognathia, micrognathia), tonsillar hypertrophy (leading cause in children), hypothyroidism, acromegaly, Down syndrome, alcohol/sedative use, smoking
Etiology	Repetitive partial or complete collapse of the upper airway during sleep due to loss of pharyngeal dilator muscle tone in an anatomically predisposed airway
Patient Presentation	Excessive daytime sleepiness (EDS), loud habitual snoring, witnessed apneic episodes by a bed partner, unrefreshing sleep, morning headaches, nocturia, difficulty concentrating, irritability
Classic Physical Exam	Truncal obesity, increased neck circumference, crowded oropharynx (Mallampati class III or IV), tonsillar hypertrophy, retrognathia, nasal septal deviation, elevated blood pressure
Key Diagnostic Results	Polysomnography (PSG): Apnea-Hypopnea Index (AHI) $\geq$ 5 events/hour with symptoms, or AHI $\geq$ 15 regardless of symptoms. Repetitive oxygen desaturations, arousals from sleep, and increased arousal index
Management	First-line: Continuous Positive Airway Pressure (CPAP). Adjuncts: Weight loss, positional therapy, oral appliances (mandibular advancement devices). Children: Adenotonsillectomy is first-line
Keywords	"Husband snores loudly," "wife noticed he stops breathing at night," "falls asleep at work/while driving," "morning headaches," "unrefreshing sleep," "BMI 35," "neck circumference 18 inches"

1. Pathophysiology

The upper airway is a collapsible muscular tube that lacks rigid cartilaginous or bony support in the pharyngeal segment. During wakefulness, the pharyngeal dilator muscles (most importantly the genioglossus) actively maintain airway patency through tonic and phasic contraction. During sleep, physiological muscle relaxation reduces this neuromuscular drive, narrowing the airway lumen.

In patients with OSA, this normal relaxation becomes pathological because the airway is already anatomically compromised. Factors such as excess adipose tissue surrounding the pharynx, enlarged tonsils or adenoids, retrognathia, or macroglossia reduce the baseline airway caliber. When muscle tone drops during sleep, the narrowed airway reaches a critical closing pressure (Pcrit), and the transmural pressure becomes insufficient to keep it open. The result is either partial collapse (hypopnea) or complete collapse (apnea).

Each obstructive event causes a cascade of consequences. Airflow cessation leads to progressive hypoxemia and hypercapnia, which stimulate peripheral and central chemoreceptors. This triggers a cortical arousal, a brief awakening that restores pharyngeal muscle tone and reopens the airway. The patient resumes breathing, often with a loud snort or gasp, and then falls back to sleep, only for the cycle to repeat. This can occur dozens to hundreds of times per night.

The clinical consequences stem directly from two processes. Sleep fragmentation (repeated arousals preventing deep restorative sleep) causes the hallmark excessive daytime sleepiness, impaired cognition, and morning headaches. Chronic intermittent hypoxia activates the sympathetic nervous system, promotes oxidative stress, systemic inflammation, and endothelial dysfunction. This is why OSA is an independent risk factor for systemic hypertension (particularly resistant hypertension), atrial fibrillation, heart failure, stroke, pulmonary hypertension, and type 2 diabetes. The large negative intrathoracic pressure generated by inspiratory effort against a closed airway (Mueller maneuver) also increases cardiac afterload and promotes atrial stretch, contributing to arrhythmias and cardiac remodeling.

In children, the pathophysiology is dominated by adenotonsillar hypertrophy rather than obesity. The consequences include failure to thrive, behavioral problems (often misdiagnosed as ADHD), enuresis, and poor school performance.

2. Classification and Clinical Manifestation

Severity Classification by AHI

Severity	events/hour	Typical Clinical Picture
Mild	5 to 14	Snoring with mild daytime sleepiness; patient may be unaware of the problem; often detected incidentally or reported by a bed partner
Moderate	15 to 29	Notable daytime sleepiness affecting daily activities; increased accident risk; may have early cardiovascular consequences (borderline or new hypertension)
Severe	$\geq$ 30	Profound sleepiness, falling asleep during conversations or while driving; significant oxygen desaturations (nadir SpO$_2$ often < 80%); strong association with resistant hypertension, arrhythmias, and cardiometabolic disease

Key Definitions

Term	Definition
Apnea	Complete cessation of airflow for $\geq$ 10 seconds
Hypopnea	$\geq$ 30% reduction in airflow for $\geq$ 10 seconds associated with $\geq$ 3% oxygen desaturation or an arousal
AHI	Total apneas + hypopneas per hour of sleep
RDI (Respiratory Disturbance Index)	AHI + respiratory effort-related arousals (RERAs) per hour of sleep

Symptom Domains

Domain	Manifestations
Nocturnal	Loud snoring, witnessed apneas, gasping/choking during sleep, restless sleep, nocturia, dry mouth upon waking
Daytime	Excessive sleepiness (Epworth Sleepiness Scale $\geq$ 10), morning headaches, difficulty concentrating, memory impairment, irritability, decreased libido
Cardiovascular	Resistant hypertension, atrial fibrillation, heart failure exacerbation, nocturnal angina, pulmonary hypertension
Pediatric	Mouth breathing, tonsillar hypertrophy, failure to thrive, behavioral problems, enuresis, poor academic performance

3. Diagnostic Workup

Summary of Diagnostic Tests

Test	Role	Key Findings
Clinical screening (STOP-BANG questionnaire)	Initial risk stratification	Score $\geq$ 3 indicates intermediate-to-high risk; score $\geq$ 5 strongly suggests moderate-to-severe OSA
Epworth Sleepiness Scale (ESS)	Quantifies subjective daytime sleepiness	Score $\geq$ 10 indicates excessive sleepiness (max score 24)
Home Sleep Apnea Test (HSAT)	Best initial diagnostic test for uncomplicated, high-pretest-probability patients	Records airflow, respiratory effort, and oximetry; calculates REI (Respiratory Event Index); useful when PSG is not readily available
In-laboratory Polysomnography (PSG)	Gold standard / most accurate test	Records EEG, EOG, EMG, ECG, airflow, respiratory effort, pulse oximetry, body position, and snoring. Provides AHI, sleep architecture, oxygen nadir, and arousal index
Lateral cephalometry / upper airway imaging	Adjunct for surgical planning	Identifies anatomical obstruction level (retropalatal vs. retrolingual)
Thyroid function tests	Exclude secondary cause	Order when clinical features suggest hypothyroidism as a contributor
Arterial blood gas	Evaluate for obesity hypoventilation syndrome overlap	Daytime hypercapnia (PaCO$_2$ > 45 mmHg) suggests coexisting hypoventilation

The workup for OSA begins with clinical suspicion. A vignette that describes a middle-aged, obese man brought in by his wife because she noticed he stops breathing at night, combined with excessive daytime sleepiness, is the classic setup. The STOP-BANG questionnaire (Snoring, Tiredness, Observed apneas, high blood Pressure, BMI > 35, Age > 50, Neck circumference > 40 cm, male Gender) is a validated screening tool used in primary care and preoperative settings to stratify risk.

The best initial diagnostic test for a patient with a high pretest probability and no comorbidities (no heart failure, no chronic lung disease, no central sleep apnea suspicion) is a Home Sleep Apnea Test (HSAT). This portable device measures airflow, respiratory effort, and oxygen saturation. It is convenient and cost-effective, but it tends to underestimate severity because it cannot measure total sleep time (it uses recording time instead). Therefore, a negative or inconclusive HSAT in a clinically suspicious patient should be followed by a full in-laboratory PSG.

The gold standard and most accurate test is in-laboratory polysomnography (PSG). This is mandatory when HSAT is inconclusive, when comorbid sleep disorders are suspected (e.g., central sleep apnea, periodic limb movements, narcolepsy), or in patients with significant cardiopulmonary disease. PSG simultaneously records brain activity (EEG), eye movements (EOG), muscle activity (EMG), heart rhythm (ECG), airflow (nasal pressure transducer and thermistor), respiratory effort (thoracic and abdominal belts), and oxygen saturation. The AHI derived from PSG is the cornerstone metric for diagnosis and severity grading.

A split-night study is an efficient variant: the first half of the night is diagnostic, and if the AHI exceeds 40 events/hour (or exceeds 20 with clear clinical indication), the second half is used for CPAP titration in the same session.

Always consider checking thyroid function in patients presenting with new fatigue and sleepiness, as hypothyroidism can both mimic and exacerbate OSA. In obese patients with daytime hypercapnia, an arterial blood gas helps distinguish pure OSA from overlap with obesity hypoventilation syndrome (Pickwickian syndrome).

4. Management and Treatment

Intervention	Indication	Details
CPAP (Continuous Positive Airway Pressure)	First-line for moderate-to-severe OSA (AHI $\geq$ 15) and for mild OSA (AHI 5-14) with significant symptoms or cardiovascular comorbidities	Acts as a pneumatic splint to maintain airway patency; optimal pressure determined by titration study (typically 5-20 cm H$_2$O)
Weight loss	All overweight/obese patients	10% weight loss can reduce AHI by approximately 26-50%; may be curative in mild cases
Positional therapy	Positional OSA (events predominantly in supine position)	Devices or techniques to maintain lateral sleep position
Oral appliances (MAD)	Mild-to-moderate OSA, or moderate-to-severe OSA in CPAP-intolerant patients	Mandibular advancement devices reposition the lower jaw forward to enlarge the retrolingual airway
Adenotonsillectomy	First-line in pediatric OSA	Removal of hypertrophied adenoids and tonsils; curative in the majority of children
Uvulopalatopharyngoplasty (UPPP)	Adults who fail CPAP and oral appliances with retropalatal obstruction	Removes redundant oropharyngeal soft tissue; variable success rate (approximately 40-50%)
Maxillomandibular advancement (MMA)	Severe OSA refractory to CPAP with skeletal contribution	Advances both jaws to expand the airway; among the most effective surgical options
Hypoglossal nerve stimulation	Moderate-to-severe OSA, CPAP-intolerant, BMI < 35, no concentric collapse at palate	Upper airway stimulation device (Inspire); stimulates the genioglossus during inspiration
Tracheostomy	Life-threatening OSA refractory to all other treatments	Bypasses the upper airway entirely; considered a last resort and virtually 100% effective
Avoid sedatives/alcohol	All patients	Alcohol and benzodiazepines relax pharyngeal muscles and worsen obstruction

The cornerstone of OSA management is CPAP therapy. CPAP delivers a constant stream of positive pressure through a nasal or oronasal mask, functioning as a pneumatic splint that prevents airway collapse during sleep. The pressure is typically titrated during a PSG or through auto-titrating CPAP (APAP) devices that adjust pressure in real time. CPAP is indicated as first-line therapy for all patients with an AHI $\geq$ 15, and for those with an AHI of 5 to 14 who have symptomatic daytime sleepiness or cardiovascular comorbidities.

The principal challenge with CPAP is adherence. Adequate use is defined as $\geq$ 4 hours per night for $\geq$ 70% of nights. Common barriers include mask discomfort, nasal congestion, claustrophobia, and aerophagia. Interventions to improve compliance include heated humidification, mask fitting optimization, ramp features, and behavioral coaching.

Weight loss is strongly recommended for all overweight patients and should be pursued alongside CPAP. Bariatric surgery may be considered for patients with severe obesity (BMI $\geq$ 40, or $\geq$ 35 with comorbidities) who have failed conventional weight loss. Significant weight reduction can sometimes cure mild OSA entirely and reduce severity in moderate-to-severe cases, though it rarely normalizes AHI in severe disease alone.

For patients who cannot tolerate CPAP, mandibular advancement devices (MADs) are the primary alternative. Custom-fitted by a dentist trained in sleep medicine, these devices pull the mandible and tongue base forward, expanding the retrolingual airway. They are most effective in mild-to-moderate OSA and in patients with retrognathia.

In the pediatric population, adenotonsillectomy is the undisputed first-line treatment. This is a high-yield exam point: when a child presents with snoring, mouth breathing, and behavioral problems, and the exam reveals tonsillar hypertrophy, the next best step is referral for adenotonsillectomy, not CPAP.

Hypoglossal nerve stimulation (upper airway stimulation) is a newer option for adults with moderate-to-severe OSA who are intolerant of CPAP, have a BMI under 35, and do not have concentric palatal collapse on drug-induced sleep endoscopy. The implanted device stimulates the hypoglossal nerve to protrude the tongue during inspiration, preventing retrolingual collapse.

Tracheostomy is the ultimate rescue therapy for life-threatening cases refractory to all other interventions, particularly in patients with severe desaturations and cor pulmonale. It is rarely needed but is essentially 100% effective by completely bypassing the pharyngeal airway.

All patients should be counseled to avoid alcohol and sedative-hypnotics before sleep, as these substances reduce pharyngeal muscle tone and lower the arousal threshold, worsening obstructive events.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Central Sleep Apnea (CSA)	Also presents with excessive daytime sleepiness, witnessed apneas, and sleep fragmentation	PSG shows apneas without respiratory effort (no chest/abdominal wall movement). Associated with heart failure (Cheyne-Stokes respiration), opioid use, or brainstem pathology. In OSA, respiratory effort is present against a closed airway
Narcolepsy	Profound excessive daytime sleepiness, difficulty staying awake	Characterized by cataplexy (sudden loss of muscle tone triggered by emotion), sleep paralysis, and hypnagogic hallucinations. PSG shows sleep-onset REM periods (SOREMPs). No snoring or witnessed apneas as the dominant feature
Obesity Hypoventilation Syndrome (OHS / Pickwickian Syndrome)	Obese patient with daytime sleepiness and hypoxemia	Defined by daytime hypercapnia (PaCO$_2$ > 45 mmHg) in an obese patient (BMI $\geq$ 30) without another cause of hypoventilation. ABG reveals chronic respiratory acidosis with metabolic compensation. 90% of OHS patients also have coexisting OSA, but the distinguishing feature is awake hypercapnia
Hypothyroidism	Fatigue, weight gain, daytime sleepiness, and cognitive slowing	Look for cold intolerance, constipation, dry skin, delayed relaxation of deep tendon reflexes, and elevated TSH. Hypothyroidism can cause or worsen OSA through myxedematous infiltration of the upper airway and reduced ventilatory drive
Major Depressive Disorder	Fatigue, difficulty concentrating, irritability, unrefreshing sleep	Dominant features are depressed mood or anhedonia, sleep disturbance is typically insomnia (not snoring/apneas), and there is no witnessed apnea or oxygen desaturation
Upper Airway Resistance Syndrome (UARS)	Snoring, daytime sleepiness, sleep fragmentation	AHI is normal (< 5), but PSG reveals increased respiratory effort-related arousals (RERAs) without frank apneas or hypopneas. Often seen in younger, non-obese women
Periodic Limb Movement Disorder (PLMD)	Sleep fragmentation and daytime sleepiness	PSG shows repetitive stereotypical limb movements during sleep, not respiratory events. Often coexists with restless legs syndrome (uncomfortable urge to move legs at rest)

6. Traps and High-Yield Pearls

The most common trap on exam questions about OSA involves confusing it with central sleep apnea. Both can present with excessive daytime sleepiness and witnessed apneas, but the critical distinction lies in the presence or absence of respiratory effort. In OSA, the patient is actively trying to breathe against a collapsed airway (paradoxical chest and abdominal movement may be seen). In central sleep apnea, there is no respiratory effort at all. If the vignette mentions heart failure, opioid use, or Cheyne-Stokes breathing, think central. If it mentions obesity, loud snoring, and a large neck, think obstructive.

Another frequent pitfall is choosing the wrong initial management in pediatric OSA. Students often default to CPAP because it is first-line in adults. In children, the answer is almost always adenotonsillectomy when tonsillar hypertrophy is present. CPAP in children is reserved for cases where surgery is not indicated or has failed to resolve the condition.

A third testable trap involves patients with resistant hypertension. When a vignette describes a patient on three or more antihypertensives (including a diuretic) whose blood pressure remains uncontrolled, the question is testing whether you recognize OSA as the most common secondary cause of resistant hypertension. The next best step is screening for OSA, not adding another antihypertensive.

Finally, be aware that HSAT can underestimate severity. If a patient has a clinical picture that strongly suggests moderate-to-severe OSA but the HSAT shows a low or borderline AHI, the correct next step is to proceed with in-laboratory PSG, not to rule out the diagnosis. The exam tests whether you understand the limitations of the screening test and know when to escalate.

The core competency being tested across OSA questions is threefold: (1) pattern recognition of the classic presentation (obese, snoring, witnessed apneas, daytime sleepiness), (2) understanding the hierarchy of diagnostic tests (clinical screening to HSAT to PSG), and (3) selecting the correct first-line treatment based on the patient population (CPAP for adults, adenotonsillectomy for children).

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