Signs and symptoms of obstructive sleep apnea and upper airway resistance syndrome

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Chapter 2 Signs and symptoms of obstructive sleep apnea and upper airway resistance syndrome


Obstructive sleep apnea (OSA) and upper airway resistance syndrome (UARS) represent two distinct but related entities in the spectrum of sleep-disordered breathing (SDB). OSA is characterized by repetitive partial or complete collapse of the upper airway during sleep, resulting in disruptions of normal sleep architecture and usually associated with arterial desaturations.1 If these respiratory events occur more than five times per hour of sleep and are associated with symptoms, most commonly snoring, excessive daytime fatigue, and witnessed apneas, the term obstructive sleep apnea/hypopnea syndrome (OSAHS) is applied.2 UARS is a more recent entity and describes patients with symptoms of OSA and polysomnographic evidence of sleep fragmentation but who have minimal obstructive apneas or hypopneas (Respiratory Disturbance Index < 5) and do not exhibit oxyhemoglobin desaturation.

Epidemiologically, OSAHS is estimated to affect 2–5% of the population.3–5 Although it can occur at any age, OSAHS typically presents between the ages of 40 and 60 and increases with age.68 Men are twice as likely to develop OSAHS with an estimated prevalence of 4% vs. 2% in women.8 Other at-risk groups include postmenopausal women911 who have a two to three-fold increase in prevalence of OSAHS, Pacific Islanders, Hispanic-Americans, and blacks.5,1215 Additionally, obesity and weight gain have been shown to be important risk factors in the development and progression of OSAHS inmiddle-aged adults.8,16 UARS epidemiology is less well characterized, and to date, there has been no reliable assessment of its prevalence in the general population. Compared to OSAHS, there appears to be no gender bias,17 and patients with UARS are commonly non-obese (mean Body Mass Index of 25 kg/m2)18,19 and are frequently younger (mean age of 37.5 years).18

OSAHS has been shown to be a gradually progressive disease, even in the absence of weight gain.16,20 Some have attributed this slow progression to upper airway damage characterized by palatal denervation with a localized polyneuropathy and inflammatory cell infiltration of the soft palate thought to be caused by snoring-related vibrations and/or large intraluminal pressure oscillations in the setting of obstruction.21,22 As OSAHS worsens in severity, it has been shown to be associated with the development of significant medical co-morbidities, including hypertension, cardiovascular disease, stroke, obesity, and insulin resistance. Furthermore, the presence of OSAHS has been linked to an increased risk of motor vehicle accidents,2325 impaired daytime performance and quality of life,26,27 and increased mortality independent of co-morbidities.28,29


A thorough history (with participation by the bedpartner if possible) and physical examination are integral to the initial evaluation of patients with suspected SDB. However, studies show that the predictive value of these clinical tools is poor. In an observational study of 594 patients, the sensitivity and specificity of subjective clinical impression in determining the presence of OSAHS were 60% and 63% respectively.30 This study also showed that history, physical examination, and clinician impression were only able to predict OSAHS in about 50% of patients. Furthermore, none of the commonly reported symptoms alone has sufficient predictive value to provide an accurate diagnosis of OSAHS.31 Diagnostic accuracy can be improved by identifying constellations of symptoms, such as snoring and witnessed apneas, which increase the sensitivity and specificity of OSAHS diagnosis to 78% and 67% respectively.32,33 Ultimately, overnight polysomnography remains the gold standard in the initial diagnosis of SDB and the only means of distinguishing OSAHS from UARS. However, as such testing can be expensive, time-consuming, and may not always be readily available, a thorough history and physical examination remain important tools to identify those patients who need further evaluation by polysomnography.



Snoring is the most frequently reported symptom in OSAHS and is found in 70–95% of such patients.34 Typically, the snoring may have been present for many years but has increased with intensity over time and is further exacerbated by nighttime alcohol consumption, weight gain, sedative medications, sleep deprivation, or supine position. Snoring may become so loud as to be greatly disruptive to the bedpartner and is often a source of relationship discord; in one report, 46% of patients slept in a different room from their partners.35 The characteristic snoring pattern associated with OSAHS is one of loud snores or brief gasps alternating with 20- to 30-second periods of silence. Because snoring is so common in the general population (35–45% in men, 15–28% in women8,36), it isa poor predictor of OSAHS; however, only 6% of patients with OSAHS do not report snoring and its absence makes OSAHS unlikely.37 Corroboration with bedpartners is important as approximately 75% of patients who deny snoring are found to snore during objective measurement.38

Witnessed apneas are observed by up to 75% of bedpartners and are the second most common nocturnal symptom reported in OSAHS.30,39 Occasional apneas are normal and do not cause symptoms; however, as the frequency of apneas increases, a certain threshold may be exceeded which results in symptomatic disease. This threshold is variable and unique to each patient such that some patients with a low Respiratory Disturbance Index (RDI) may be profoundly symptomatic while others with frequent respiratory events present with relatively few complaints.40 Particularly in OSAHS of milder severity, the apneic episodes are usually associated with maintenance of respiratory movements and are terminated by loud snorts, gasps, moans, or other vocalizations and sometimes with brief awakenings and body movements. In more severe disease, cyanosis can occur along with the cessation of respiratory movement during the apnea which will often cause considerable distress to the bedpartner. Body movements at the time of arousals in severe OSAHS can be frequent and sometimes violent. Patients themselves are rarely aware of the apneas, vocalizations, frequent arousals, movements, or brief awakenings, although the elderly are particularly sensitive to the frequent nocturnal awakenings and will report insomnia and unrefreshing sleep.1

Nocturnal dyspnea, sometimes described by patients as a sensation of choking or suffocating, has been observed in 18–31% of patients with OSAHS.35,41,42 These episodes typically occur with arousal, 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 inspiratory 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.43,44 Other important causes of paroxysmal nocturnal dyspnea include left heart failure, nocturnal asthma, acute laryngeal stridor, or Cheyne–Stokes respirations; however, these episodes tend to be longer in duration and may also occur during the daytime.39 Further investigation may be warranted to differentiate OSAHS from these other entities although they may also coexist.

Other common symptoms of OSAHS include drooling in about one-third and dry mouth in up to three-quarters of patients.35 In one study of 668 patients with suspected SDB, dry mouth was observed in 31.4% of patients with confirmed OSA as compared to 16.4% in primary snorers and 3.2% in normal subjects.45 Furthermore, there was a linear increase in prevalence of dry mouth as the severity of OSA increased. Sleep bruxism is also a common finding, occurring in 4.4% of the general population, with OSAHS patients being at higher risk (odds ratio 1.8) of reporting sleep bruxism.46 In a small study of 21 patients, 54% of those with mild OSA and 40% of those with moderate disease were diagnosed with bruxism which was not observed to be directly associated with respiratory events but rather seemed to be related to sleep disruption and arousal.4749

In addition to the common complaint of restless sleep and frequent awakenings, up to half of patients with OSAHS report nocturnal sweating that typically occurs in the neck and upper chest area.41,42 This symptom is likely due to the increased work of breathing and respiratory effort in the setting of repetitive airway obstruction,50 but may also be a manifestation of the autonomic instability observed in OSAHS. Similar to dyspnea, nocturnal diaphoresis is a highly non-specific symptom with a broad differential diagnosis, including perimenopausal state, thyroid disease, tuberculosis, lymphoma, and myriad other co-morbid conditions that warrant further investigation.51

Gastroesophageal reflux (GER) also occurs with greater frequency in patients with OSAHS with prevalence rates of 64–73%, but appears to be unrelated to the severity of SDB.52,53 As GER and OSA share several risk factors, the exact relationship between the two entities has been difficult to characterize. However, it has been postulated that OSAHS may contribute to GER via the following mechanism: upper airway obstruction results in increased intraabdominal pressure combined with more negative intrathoracic pressure that produces an increased transdiaphragmatic pressure gradient, thereby promoting reflux of gastric contents into esophagus.50 In a long-term study of 331 patients, treatment of OSAHS with nasal positive pressure resulted in a 48% decrease in the frequency of nocturnal GER symptoms with higher pressures being associated with greater improvement, suggesting that OSAHS may indeed be a causal factor in nocturnal gastroesophageal reflux.54

Nocturia has also been observed with increased frequency in OSAHS with a reported 28% of patients experiencing four to seven episodes nightly.55 The presence and frequency of nocturia have been shown to be related to the severity of OSA,55,56 and the proposed physiologic mechanisms include increased atrial natriuretic peptide secretion with a corresponding increase in total urine output,57 or an increase in intraabdominal pressure. One study of 80 patients showed that although a majority of nocturnal awakenings were actually due to sleep-related phenomena (78.3% of 121 total awakenings), patients voluntarily urinated with each arousal and were only able to identify the correct source of the awakenings in five instances (4.9%).58 These data show that patients mistakenly attributed their arousals to need to urinate when they were in fact due to SDB, suggesting that patient misperception may be a contributing factor to the increased frequency of reported nocturia in OSAHS.


While the nocturnal symptoms of OSAHS are characteristic and tend to be more specific for the disease, the common daytime symptoms are less specific as they can result from abnormal sleep of any cause. Excessive daytime sleepiness (EDS) is the most common daytime complaint in patients with OSAHS;30,35,41 however, as 30–50% of the general population also report moderate to severe sleepiness,8,59 this symptom alone is a poor predictor of OSAHS. EDS is caused by sleep fragmentation leading to frequent arousals and insufficient sleep;40 it is manifested by the inappropriate urge to sleep, particularly during relaxing, sedentary activities (i.e. watching television, reading). As it worsens, the inability to control sleepiness can result in dozing during meetings, active conversations, and at mealtimes. When severe, EDS can be a cause of motor vehicle and machinery accidents, poor school or job performance, and relationship discord.

Establishing the presence and severity of inappropriate daytime sleepiness can be challenging. EDS is often insidious, may be subtle, and is often confused with fatigue or lethargy. Patients themselves often have a poor perception of EDS severity and underestimate their level of impairment.60 Co-morbidities such as chronic insomnia, depression, fibromyalgia, and other organic diseases, as well as medication use or substance abuse, may contribute to the symptom of inappropriate sleepiness. The clinician should focus on the urge to sleep in passive situations, since both physical and mental activity can mask underlying EDS.

The Epworth Sleepiness Scale (ESS) is a simple, self-administered questionnaire that is a quick and inexpensive tool with a high test–retest reliability,2 and is thus a practical means of measuring the general level of daytime sleepiness. Patients are asked to assess their probability of falling asleep in eight situations commonly encountered in daily life, and a numeric score is tabulated. Higher Epworth scores, reflecting increased average sleep propensity, are able to distinguish patients with OSAHS from primary snorers and appear to correlate with severity of OSA as well as sleep latency measured objectively during multiple sleep latency testing.35,61,62 The major disadvantage of the ESS is its reliance on subjective reporting by patients who may underestimate or intentionally underreport severity of daytime sleepiness.39

Morning or nocturnal headaches are reported in about half of patients with OSAHS, are typically dull and generalized, last 1 to 2 hours, and may require analgesics.1,35 However, this symptom is non-specific as morning headaches occur in 5–8% of the general population and have been associated with many other entities, including other sleep disorders as well as depression, anxiety, and various medical conditions.63,64 These headaches have been attributed to nocturnal episodes of oxygen desaturation, hypercapnia, cerebral vasodilatation with resultant increases in intracranial pressure, and impaired sleep quality with corresponding polysomnographic evidence of decreased total sleep time, sleep efficiency, and amount of REM sleep.65,66 It has been observed that treatment of the underlying OSAHS results in disappearance of the morning headaches.

Neurocognitive impairment has also been observed in patients with OSAHS, although there is no practical method of quantifying such deficits in this setting. The processes most affected in OSAHS appear to be vigilance, executive functioning, and motor coordination.67 Decreased vigilance is a result of sleep fragmentation, which can also lead to diminished concentration and memory (short term and long term). However, psychomotor impairment appears to be largely related to hypoxemia with more severe OSAHS potentially resulting in irreversible anoxic brain damage.6870 This hypothesis is supported by the observation that psychomotor deficits in patients with severe OSAHS are only partially reversible with treatment of the underlying sleep disorder with continuous positive airway pressure.68,69

Patients with OSAHS have a tendency to report decrements in their quality of life and often experience concomitant mood and personality changes. Depression is the most common mood symptom, and daytime sleepiness has been identified as a reliable predictor.63,71 Other behavioral manifestations of OSAHS include anxiety, irritability, aggression, and emotional lability.72 Treatment with continuous positive airway pressure has been shown to ameliorate symptoms of depression and thereby improve quality of life in some patients.73,74 Sexual dysfunction, manifested primarily as erectile dysfunction and decreased libido, is also associated with OSAHS, and appears to be fully reversible with treatment of the underlying sleep disorder75,76

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