OSAS
Obstructive sleep apnea syndrome (OSAS) is a prevalent sleep-related breathing disorder defined by recurrent episodes of partial or complete upper airway collapse during sleep, leading to apneas (complete cessation of airflow for at least 10 seconds) or hypopneas (partial airflow reduction with oxygen desaturation or arousal), often accompanied by excessive daytime sleepiness and other symptoms that impair daily functioning.[1] Globally, OSAS affects an estimated 425 million adults aged 30 to 69 years with moderate-to-severe disease, representing a significant public health concern due to its underdiagnosis and association with comorbidities.[1] In the United States, prevalence is approximately 25-30% among men and 9-17% among women, with higher rates observed in certain ethnic groups such as Hispanics, Blacks, and Asians.[1] Risk factors include obesity (with body mass index strongly correlating to severity), male sex, advancing age, anatomical features like enlarged tonsils or a narrow airway, family history, smoking, nasal congestion, and conditions such as hypertension or diabetes.[1][2] The underlying pathophysiology involves reduced pharyngeal muscle tone during sleep, generating negative intraluminal pressure that promotes airway collapse, exacerbated by factors like alcohol use or sedatives.[1][3] Common symptoms of OSAS include loud snoring, observed breathing pauses or choking episodes during sleep, frequent nocturnal awakenings, morning headaches, dry mouth upon waking, and profound daytime fatigue or drowsiness that interferes with concentration, mood, and libido.[2][3] Diagnosis typically relies on polysomnography, the gold standard sleep study that measures the apnea-hypopnea index (AHI)—with mild OSAS defined as 5-15 events per hour, moderate as 15-30, and severe as over 30—though home sleep apnea testing may suffice for uncomplicated cases.[1] Untreated OSAS heightens risks for cardiovascular complications like hypertension, arrhythmias, heart failure, and stroke; metabolic issues including type 2 diabetes; increased surgical and driving accident risks; and even worsened outcomes in infections such as COVID-19.[1][2] Treatment for OSAS centers on continuous positive airway pressure (CPAP) therapy, which delivers pressurized air via a mask to maintain airway patency and is considered the most effective option for reducing AHI and improving symptoms, though adherence remains a challenge.[1][3] Adjunctive strategies include weight loss for obese patients, oral appliances to advance the jaw, positional therapy to avoid supine sleeping, and surgical interventions such as uvulopalatopharyngoplasty or hypoglossal nerve stimulation for select cases refractory to conservative measures.[1] Lifestyle modifications like smoking cessation, alcohol avoidance, and optimized sleep hygiene are essential for prevention and management.[3] With appropriate treatment, prognosis is generally favorable in the short term, alleviating symptoms and mitigating risks, though long-term outcomes depend on sustained adherence and may still involve reduced life expectancy if cardiovascular comorbidities persist.[1][3]Definition and Classification
Overview and Terminology
Obstructive sleep apnea syndrome (OSAS), commonly abbreviated as OSA, is a prevalent sleep-related breathing disorder defined by recurrent episodes of partial or complete upper airway obstruction during sleep, resulting in apneas (complete cessation of airflow for at least 10 seconds) or hypopneas (partial airflow reduction accompanied by arousal or desaturation), alongside frequent arousals that fragment sleep quality.[1] These events occur despite ongoing respiratory effort, leading to intermittent hypoxemia and hypercapnia.[4] OSAS affects millions worldwide and is linked to significant health risks, including cardiovascular complications, though its core pathology centers on anatomical and neuromuscular factors promoting airway collapsibility.[2] The terminology of OSAS reflects its mechanistic and clinical features: "obstructive" denotes the mechanical blockage or collapse of the pharyngeal airway, distinguishing it from non-mechanical causes of breathing pauses. "Sleep apnea" originates from the Greek term apnoia, meaning "without breath" or "suspension of respiration," combining the prefix a- (absence) with pnoia (breathing).[5] The addition of "syndrome" underscores the constellation of associated symptoms, such as snoring and daytime hypersomnolence, rather than a single isolated event; this suffix derives from the Greek syndromē, signifying "a running together" or concurrence of signs.[6] OSAS differs fundamentally from central sleep apnea (CSA), in which pauses in breathing arise from absent or diminished respiratory effort due to central nervous system dysfunction, without upper airway obstruction.[7] Mixed sleep apnea, by contrast, involves a sequence beginning as central (no effort) and transitioning to obstructive (effort against blockage), often emerging in patients initially diagnosed with OSAS.[8] In OSAS specifically, thoracoabdominal movements persist during obstructive events, highlighting the role of continued ventilatory drive against a compromised airway.[1] In the International Classification of Sleep Disorders, Third Edition (ICSD-3), OSAS is categorized under sleep-related breathing disorders, emphasizing its diagnostic reliance on polysomnographic evidence of obstructive events.[9] This classification framework aids in distinguishing OSAS from other breathing disturbances while noting its variable severity, typically assessed via the apnea-hypopnea index, and common manifestations like excessive daytime sleepiness.[10]Types and Severity Levels
Obstructive sleep apnea syndrome (OSAS) is primarily classified into several types based on clinical presentation and associated conditions. The most common form is primary OSAS, which occurs in both adults and children and is characterized by recurrent upper airway obstruction without an identifiable underlying syndrome.[1] In adults, primary OSAS often stems from multifactorial anatomical and physiological factors leading to isolated airway collapse during sleep.[1] Pediatric primary OSAS, by contrast, frequently involves adenotonsillar hypertrophy as the predominant cause, though it shares the core mechanism of partial or complete airway obstruction.[11] Another variant is positional OSAS, where episodes of apnea and hypopnea predominantly occur in the supine sleeping position due to gravitational effects exacerbating airway collapse, while symptoms are milder or absent in lateral positions.[12] This type accounts for a significant proportion of cases in both adults and children, with prevalence estimates reaching up to 60% in pediatric cohorts undergoing polysomnography.[12] Syndrome-specific forms of OSAS include those linked to obesity hypoventilation syndrome (OHS), where severe obesity (typically BMI >30 kg/m²) combines with chronic hypercapnia and nocturnal hypoventilation, often amplifying OSAS severity through reduced respiratory drive and chest wall mechanics.[13] OHS-associated OSAS is particularly prevalent in adults with morbid obesity and requires integrated management beyond standard OSAS therapy.[13] Severity of OSAS is standardized using the apnea-hypopnea index (AHI), calculated as the total number of apneas and hypopneas per hour of sleep:\text{AHI} = \frac{\text{number of apneas + number of hypopneas}}{\text{total sleep time in hours}}
This metric quantifies the frequency of respiratory events, with apneas defined as ≥90% airflow reduction for ≥10 seconds and hypopneas as ≥30% reduction accompanied by ≥3% oxygen desaturation or arousal.[14] In adults, severity is graded as mild (AHI 5–14.9 events/hour), moderate (15–29.9 events/hour), and severe (≥30 events/hour), thresholds established by the American Academy of Sleep Medicine (AASM) to guide treatment intensity.[1] For children, lower thresholds reflect physiological differences, with mild OSAS defined as AHI 1–4.9 events/hour, moderate as 5–9.9 events/hour, and severe as ≥10 events/hour, emphasizing early intervention to prevent neurocognitive impacts.[11] Pediatric classification often incorporates the respiratory disturbance index (RDI), which extends AHI by including respiratory effort-related arousals (RERAs)—subtle airflow limitations causing EEG arousals without significant desaturation.[15] RDI thus provides a more comprehensive assessment in children, where RERAs contribute substantially to total respiratory disturbances, potentially elevating severity grading beyond AHI alone.[15] Factors such as the oxygen desaturation index (ODI)—the number of ≥3% desaturations per hour—further influence classification, as higher ODI values (>15 events/hour) correlate with increased cardiovascular risk and may prompt reclassification to severe even if AHI is borderline.[1] These metrics collectively ensure severity reflects both event frequency and physiological burden.[1]