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The three major types of sleep-related breathing disorders are obstructive sleep apnea syndrome (OSAS), central sleep apnea syndrome, and sleep-related hypoventilation hypoxemic syndromes. Of these, OSAS is the most common type of sleep-related breathing disorder and is characterized by repetitive episodes of complete apnea or partial hypopnea caused by upper airway obstruction. Episodes last at least 10 seconds, occur during sleep, are usually associated with decreased Sao2%, and are terminated by brief arousals. OSAS is associated not only with neurocognitive dysfunction but also with increased cardiovascular morbidity and mortality.
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OSAS is relatively common, with a prevalence of 4% in men and 2% in women when defined by an apnea-hypopnea index (AHI) ≥5 events/h plus a complaint of excessive daytime sleepiness. Features predisposing to OSAS include male sex, age, obesity, menopausal state, race, craniofacial abnormalities with decreased orohypopharyngeal space, endocrine disorders, and certain congenital disorders (Table 25.1).
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The high male-to-female prevalence ratio for OSAS of 2:1 is attributed to the protective effect of female sex hormones predominant in premenopausal women; the prevalence of OSAS in women triples after menopause and is reduced to premenopausal levels with hormone replacement therapy. Meanwhile, increased body mass index (BMI) is the major risk factor for OSAS in adults (Chap. 12). There appears to be a linear relationship between BMI and OSAS severity: Each 10% increase in body weight results in a 30% increase in AHI. On the other hand, adenotonsillar hypertrophy is the major cause of OSAS in children. For patients who are not overweight or obese, certain craniofacial features (eg, retrognathia, long uvula) can predispose to OSAS. Increased nasal resistance from rhinitis or a deviated nasal septum can worsen airway collapse due to the greater inspiratory effort required to breathe through such nasal passages. Asians may be at a higher risk for OSAS due to crowding of the posterior oropharynx and a steep thyromental plane. Smoking causes nasal and oropharyngeal mucosal edema that can aggravate upper airway obstruction. Hormonal abnormalities may alter craniofacial skeletal and soft tissue structure, thereby promoting oropharyngeal crowding, as seen in the macroglossia of hypothyroidism and acromegaly. Up to 50% of patients with Down syndrome suffer from OSAS due to multiple risk factors. These can include midfacial and mandibular hypoplasia, small upper airways with superficially positioned tonsils and relative tonsillar and adenoidal encroachment, generalized hypotonia, and an increased prevalence of obesity and hypothyroidism.
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Pathophysiology of OSAS
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OSAS occurs due to dynamic upper airway closure or narrowing. These may be secondary to excessive pharyngeal tissue volume from obesity, adenotonsillar hypertrophy, craniofacial anatomy, and can accompany attenuated tone of the pharyngeal dilating muscles during sleep (Fig. 25.1).
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Adverse Health Effects of OSAS
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Left untreated, OSAS is associated with neurocognitive impairment, cardiovascular dysfunction, endocrine abnormalities, and mortality (Table 25.2). In prospective cohort studies, moderate-to-severe OSAS has been associated with an increased incidence in systemic hypertension and diabetes mellitus, as well as an increased risk of overall mortality. The Sleep Heart Health Study, based upon a large cross-sectional population, showed a significant increase in the prevalence of congestive heart failure in middle-aged individuals with moderate-to-severe OSAS. Neurocognitive dysfunction in OSAS is a consequence of poor sleep efficiency and reduced slow wave and rapid eye movement sleep that are caused by frequent nocturnal awakenings from disordered-breathing events. Neurocognitive dysfunction can manifest as hypersomnolence, decreased vigilance, impaired short-term memory, depression, and increased risk of motor vehicle accidents. Meanwhile, the surges in hypoxemia, hypercapnia, and circulating catecholamines associated with OSAS are now implicated in development of both hypertension and increased insulin resistance.
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The diagnosis of OSAS requires the presence of its clinical features (snoring, witnessed apneas, excessive daytime sleepiness, etc), and a polysomnogram showing a respiratory disturbance index (RDI) of ≥5 scoreable respiratory events (obstructive apneas, hypopneas, and respiratory-related arousals) per hour of sleep (Fig. 25.2 and Tables 25.3 and 25.4). In the absence of clinical features or cardiovascular comorbidities, an RDI ≥15 scoreable respiratory events per hour of sleep is required to make the diagnosis. Obstructive apneas correspond to episodes of complete upper airway obstruction (Fig. 25.2), while obstructive hypopneas are episodes of partial upper airway obstruction (Fig. 25.3). Respiratory effort-related arousals (RERAs) are "mini-awakenings," or shifts in electroencephalographic waveforms. These RERAs result from progressively increasing inspiratory efforts (ie, negative intrathoracic pressures) by the patient in an attempt to overcome high upper airway resistance. These arousals are preceded by blunting of the nasal pressure airflow waveform normally associated with increasing respiratory efforts, and are best detected by measuring intrathoracic pressures using esophageal manometry (see Fig. 4.6). RERAs do not meet the criteria for a decrease in Sao2% (of ≥3%-4%) nor the airflow reduction criteria (≥50%) that signify obstructive hypopneas.
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CLINICAL CORRELATION 25.1
The key distinguishing features of OSAS between children and adults can be summarized as tabulated below:
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Therapeutic Approaches to OSAS
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Weight loss for obese patients has been shown to decrease the AHI and improve nocturnal Sao2% in patients with OSAS. Compared to controls, OSA patients have been found to have higher serum [leptin], a peptide hormone which regulates appetite and metabolism. These higher [leptin] levels in OSA patients may indicate resistance to its anorexigenic effect, making weight loss more difficult to achieve.
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Continuous positive airway pressure (CPAP) provides a mechanical air stent to the upper airways and is the mainstay for treating OSAS in adults. CPAP is demonstrated to have multisystemic effects, notably ameliorating the neurocognitive deficits, cardiovascular dysfunction, and endocrinologic abnormalities (Fig. 25.3, Table 25.5). The optimal CPAP level is that pressure (in cm H2O) determined to be effective in abolishing apneas, hypopneas, RERAs, and snoring during a therapeutic CPAP trial.
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Positional obstructive sleep apnea is said to occur in those patients whose supine AHI is twice their lateral decubitus AHI, and in whom the lateral decubitus AHI < 10 events/h. In such patients, relatively simple positional adjustments to promote sleeping in the lateral decubitus position can decrease their overall nightly AHI and respiratory-related arousal index, and ameliorate their excessive daytime sleepiness.
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Oral appliances are dental devices designed to advance the mandible, thereby increasing the orohypopharyngeal space. Oral appliances have been demonstrated to moderately decrease the AHI in patients with mild-to-moderate OSA and, to a lesser extent, their systemic blood pressure if they are hypertensive.
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Tonsillectomy and adenoidectomy is the treatment of choice for children with OSAS and adenotonsillar hypertrophy (Clinical Correlation 25.1). Uvulopalatopharyngoplasty (UPPP) is the most commonly performed surgical procedure for adult patients with OSAS, and involves the surgical removal of the tonsils and redundant soft palate and tonsillar pillars. UPPP has been found to have an overall success rate of 40% when defined as reducing the severity of patients' OSA by at least 50%. Other surgical procedures for OSAS may help correct specific anatomic abnormalities responsible for causing upper airway obstruction (Table 25.6).
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