2.1.1

Snoring

Snoring is a fluttering sound created by the vibrations of pharyngeal tissues during sleep, which is a ubiquitous complaint of bed partners worldwide and leads to many patient requests for treatment recommendations. Most authors support a continuum of snoring from simple snoring through upper airway resistance syndrome (UARS) and to various degrees of OSA. Patients who snore but have an AHI <5 tend to be classified as primary or habitual snorers, but may fall in the category of UARS patients. Although the prevalence of snoring varies between studies because of its highly subjective nature, its prevalence has been reported as 5% to 78% in males and 2% to 59% in females. The gender difference is perhaps not surprising given that being male is one of the risk factors for snoring. This is highlighted in one of the few meta-analyses in the epidemiology of snoring. In addition to gender, sleep positions affect snoring such that supine positions are associated with more snoring and apneas than lateral sleeping positions.

2.1.2

Witnessed Apneas and Nocturnal Choking/Gasping

Witnessed apneas and nocturnal choking are related to apneic events and are the second most common nocturnal symptom reported in OSA. Up to 75% of OSA patients’ bed partners report witnessed apneas. Patients themselves are rarely aware of the apneas. Nocturnal choking or gasping, sometimes described by patients as a sensation of suffocation, has been observed in 18% to 31% of patients with OSA. These episodes typically occur with arousals, are associated with feelings of panic and anxiety, and generally subside within a few seconds. During apneas or hypopneas, greater negative intrathoracic pressures are generated as patients increase their inspiration efforts to overcome the upper airway obstruction. This increases venous return to the heart and thus elevates pulmonary capillary wedge pressure, which produces the sensation of dyspnea. Nocturnal choking or gasping is the more reliable indicator of OSA compared with snoring. However, choking or gasping from OSA must be differentiated from other causes of nocturnal breathlessness such as gastroesophageal reflux (GER) paroxysmal nocturnal dyspnea in patients with left ventricular failure, nocturnal asthma, or Cheyne–Stokes respiration ( Table 2.2 ).

2.1.3

Sleep Bruxism

Sleep bruxism is defined as a stereotyped movement disorder occurring during sleep and is characterized by teeth grinding and clenching, which is also a common finding in OSA patients. There is a positive correlation between the frequency of OSA and sleep bruxism events in OSA patients.

However, sleep bruxism is not directly dependent on apneic episodes but rather seems to be related to sleep disruption and arousal, which is influenced by sympathetic/parasympathetic fluctuations during sleep. It was observed that there is a rise in autonomic sympathetic cardiac activity before bruxism with increasing brain activity, heart rate, suprahyoid muscle tone, amplitude of respiration, and masseter and temporalis muscle activity. The bruxism episodes are followed by activation of the parasympathetic system with bradycardia, hypersalivation, and increased patency of the upper airways. It is also known that due to arousals and hypoxia, the sympathetic nervous system is activated. It is possible that sleep bruxism is part of the arousal process in which respiratory disturbances, leading to sleep fragmentation and arousals, trigger the muscles of the masticatory organ to restore normal breathing. Continuous positive airway pressure (CPAP) alone could eliminate sleep bruxism episodes in OSA patients whose episodes parallel arousal responses. Because the presence of sleep bruxism could represent a contraindication for the use of oral appliances in the treatment of OSA, CPAP treatment may be preferred.

2.1.4

Gastroesophageal Reflux

The prevalence of GER has been reported in 58% to 62% of patients with OSA. However, GER and OSA share several risk factors, which are both confounded by obesity. Apneas may increase respiratory effort, thereby increasing transdiaphragmatic pressure and decreasing intrathoracic pressure, eventually facilitating the retrograde movement of the gastric contents into the esophagus. However, some studies have failed to show a significant relationship between GER and OSA. Although the relationship between the two is not clear, treatment of OSA has been shown to improve GER, and CPAP has been demonstrated to reduce the total 24-hour esophageal acid contact time.

2.1.5

Nocturia

Recent published evidence has identified nocturia as a predictive symptom of OSA. Nocturia is defined by the International Continence Society as “waking once or more at night to urinate.” The sign of nocturia is the number of voids recorded during a night’s sleep: each void is preceded and followed by sleep. The prevalence of nocturia has been reported to be greater in OSA patients than in non-OSA control subjects. Some studies suggest that up to 80% of patients describe nocturia and that the severity of OSA is associated with the number of nocturia episodes.

The causes of nocturia in patients with sleep apnea are not well understood; a putative mechanism causing nocturnal polyuria in patients with OSA is that the increasingly negative intrathoracic pressure caused by partial or full obstruction of the airway stimulates venous return to the right atrium, and atrial natriuretic peptide (ANP) secretion is increased in response to right atrium distension. It has been established that successive CPAP treatment in patients with OSA significantly improves nocturia by eliminating the negative intrathoracic pressure and reducing secretion of ANP, consequently resolving the nocturia.

2.2.1

Excessive Daytime Sleepiness

Excessive daytime sleepiness (EDS) is the most common daytime symptom of OSA. In the general population, the prevalence of EDS is approximately 5% to 10%. In patients with OSA, approximately 23% of women and 16% of men experience EDS. Patients often have a poor perception of EDS severity and underestimate their level of impairment because they may have adapted to this condition over time. EDS in OSA patients is caused by sleep fragmentation leading to frequent arousals and insufficient sleep. It could also be caused by factors independent of OSA, including OSA comorbidities (obesity, depression, and diabetes mellitus), sleep deprivation, or medication side effects. EDS could be subjectively evaluated with various rating scales, including the Stanford Sleepiness Scale (SSS), the Karolinska Sleepiness Scale, and the Epworth Sleepiness Scale (ESS). The SSS assesses various degrees of sleepiness, and the ESS measures sleep propensity. The ESS has been widely used because it is a simple, quick, and inexpensive survey. It is well correlated with the patient’s own perception of sleepiness, but is weakly correlated with objective measures of sleepiness. The gold-standard measures of sleepiness are the Multiple Sleep Latency Test and the Maintenance of Wakefulness Test.

EDS in OSA patients is an important public health concern because it is associated with increased morbidity and mortality from motor vehicle and machinery accidents, poor school or job performance, and relationship discord. Numerous studies have demonstrated that effective CPAP treatment improves EDS.

2.2.2

Morning Headaches

The prevalence of morning headaches has been shown to be 5% to 7% in the general population, whereas in patients with OSA it has been reported at variable levels from 18% to 74%. One study of 563 patients showed that the prevalence of morning headaches was 22% in mild OSA, 36.4% in moderate OSA, and 38.2% in severe OSA. These results show that the prevalence of morning headaches increases with OSA severity.

Hypoxia, hypercapnia, disturbance of cerebral blood flow autoregulation, transient increases in intracranial pressure, and sleep fragmentation have been postulated as the mechanisms by which OSA causes morning headaches. In addition, the characteristics of morning headaches have not been clearly described. Generally, headaches are known to be more common in women. Morning headaches are also shown to be more frequent in female patients with OSA compared with male patients. The effectiveness of CPAP treatment in OSA patients with morning headaches was clearly demonstrated.

2.2.3

Neurocognitive Impairment

Neurocognitive impairment occurs at a high frequency in OSA patients. Cognitive function deficit is a key factor contributing to performance alterations in patients with OSA. However, the exact prevalence of cognitive dysfunction in adult patients with OSA is unknown. A meta-analysis indicated that the processes most affected in OSA appear to be vigilance, executive functioning, and motor coordination, whereas intelligence, verbal, and visual perceptual abilities were not affected.

One proposed mechanism for the increased incidence of cognitive impairment in patients with OSA is the occurrence of hypoxia/reperfusion injury. Recent studies have used functional and structural neuroimaging to delineate the brain areas affected in patients with OSA and neurocognitive dysfunction. A common finding in several of these studies is decreased hippocampal volume. Other affected brain areas include the frontal and parietal lobes of the brain. These changes may only be partially reversed with CPAP treatment, which highlights the importance of early recognition and treatment of OSA.

2.2.4

Psychological Changes and Psychiatric Symptoms

Psychiatric symptoms or disorders associated with OSA include depression, anxiety, delirium, posttraumatic stress disorder, psychosis, and dementia. Depression is the most common mood symptom and is observed in up to 50% of patients with OSA, and anxiety is observed in 11% to 17% in unselected OSA patients. Psychiatric symptoms appear to be more common and more severe in women with OSA than in men. Symptoms of depression and anxiety, although prevalent in OSA, correlate poorly or not at all with OSA severity as assessed using the AHI.

Psychological changes associated with OSA could be secondary to neural injury, consequences of OSA such as excessive sleepiness and impaired quality of life, and conditions associated with OSA such as metabolic syndrome and cardiovascular diseases. Some authors have reported that CPAP may improve psychiatric symptoms in OSA patients, but this has yet to be confirmed.

2.2.5

Sexual Dysfunction

Sexual dysfunction manifested primarily as erectile dysfunction (ED), and decreased libido is associated with OSA. The pathophysiology of sexual dysfunction in OSA is likely affected by several disease-related factors, including obesity, sleep fragmentation, hypoxia and intermittent desaturations, and alteration in vascularity.

Intermittent hypoxic events and sleep fragmentation limit spontaneous nocturnal erections, which have been linked to daytime ED. OSA produces endothelial dysfunction and sympathetic activation, which leads to hypertension and microvascular disease, both of which are established risk factors for ED. Androgen deficiency, which is also commonly identified in patients with untreated OSA, may further contribute to ED in these patients. However, CPAP therapy has been shown to improve both sexual function and satisfaction in the majority of patients.

2.3.1

Anthropometric Measurements

Obesity is one of the greatest sleep apnea risk factors and is assessed based on body mass index (BMI). The prevalence of OSA in obese and severely obese patients is nearly twice that of normal-weight adults. Furthermore, patients with mild OSA who gain 10% of their baseline weight have a sixfold risk increase in OSA progression, and an equivalent weight loss can result in more than 20% improvement in OSA severity. The optimal BMI cutoff point to predict OSA is 30 kg/m ² , and the recommended BMI range for global cardiovascular risk is 25 to 29.9 kg/m ² . However, 18% to 40% of affected patients are less than 20% above ideal body weight, and patients with UARS are typically nonobese.

Increased neck circumference has consistently been shown as a more reliable clinical predictor of OSA in Caucasians. Neck circumference at the superior border of the cricothyroid membrane can be measured to evaluate excessive adiposity in the upper body. Fat deposition in the tissues surrounding the upper airway appears to result in a smaller lumen and increased collapsibility of the upper airway, predisposing patients to apnea. Kushida et al. found that a neck circumference of 40 cm is associated with a sensitivity of 61% and a specificity of 93% for OSA. Thus neck circumference should be routinely measured during physical examination. But neck circumference has been shown to have no predictive value in Thai women.

2.3.2

Craniofacial Structure Evaluation

The craniofacial abnormalities most commonly associated with airway narrowing and SDB are retrognathia and high arched palate. The significance of retrognathia and high arched palate in OSA was supported by Kushida et al., who described four craniofacial parameters indicative of airway narrowing: maxillary intermolar distance, mandibular intermolar distance, palatal height, and dental overjet (a sign of mandibular insufficiency).

Retrognathia, also known as mandibular retroposition, is defined as a retroposition greater than 0.5 cm of the most inferior contour of the chin relative to the plane of the deepest point of the superior aspect of the nasal bone (nasion). Thus retrognathia signifies a narrowed upper airway, particularly in the region of the retroglossal space.

High, narrow arched palates, known as transverse maxilla deficiency, are also associated with upper airway obstruction. A high arched palate was measured after making upper dental impressions; once the model is obtained, it is trimmed until the distal contact point of the first molar appears on the side, and the distance from the deepest point of the palate to a horizontal line traced between the distolingual cusp tips of the first molar is measured. A mean palatal depth of 20 ± 2.2 mm has been measured in one of our groups of 29 asymptomatic subjects (17 women) obtained from the local general population with a mean age of 25 ± 3.7 years. Mouth-breathing individuals are classically described as having a narrow, V -shaped maxillary arch and a high palatal vault. Some studies show a strong relationship between airway resistance and high palatal vault.

Dental overjet is a common sign of underlying mandibular retroposition and refers to the forward extrusion of the upper incisors beyond the lower incisors by more than 2.2 mm. Findings of dental malocclusion and overlapping teeth indicate a restricted oral cavity prone to tongue collapse. Because sleep bruxism is associated with OSA, evidence of teeth grinding or clinching should also be evaluated.

2.3.3

Nasal Cavity, Oral Cavity, and Pharyngeal Examination

Examination of the upper airway, including the nasal cavity, oral cavity, and the pharynx, is an essential component of the clinical evaluation of all patients with suspected OSA to identify potential areas of airway narrowing, as well as to guide future therapies. Nasal cavity, nasopharynx, oropharynx, and tongue base could be examined with the aid of a flexible nasopharyngoscopy in both the upright and supine positions to optimize the detection of anatomic features that predispose to OSA.

Although nasal obstruction is rarely the sole cause of SDB, it appears to occur with higher frequency in SDB and may contribute significantly to increase upper airway resistance and the development of UARS. Examination of the nose should involve the collapsibility of the nasal valves, deviation of the septum, and the size of the inferior turbinates. Identifying nasal obstruction can be particularly important in patients with SDB who have difficulty tolerating nasal CPAP, as nasal surgery can decrease nasal resistance, thereby improving adherence to nasal CPAP.

The oral cavity and oropharynx evaluation, including short lingual frenulum, macroglossia (often associated with lateral lingual scalloping by adjacent teeth), enlargement of the tonsils, redundant soft palate, and elongated uvula, must be inspected to determine whether there is potential risk of soft tissue collapse in decreasing the airway volume during sleep. The upper lip frenulum is much less commonly affected than the lingual frenulum. A “short” lingual frenulum is difficult to determine at this time; in the orthodontic field, the blanching of the lingual frenulum when the tip of the tongue is positioned up against the middle of the hard palate has been considered an indicator of a “short” frenulum. The narrowing of the oropharynx could be further characterized by the Friedman tongue position (intraoral position relative to palatal degree of exposure) or Mallampati score (assessed with the tongue protruded). Both the Mallampati class and tonsil hypertrophy are classified into four categories, with increasing class indicating greater decreasing of airway volume. Using a flexible nasopharyngoscopy with Mueller maneuver allows for a more reliable means of identifying actual static and dynamic obstruction of the retroglossal and retropalatal space and lateral pharyngeal wall collapse.