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Table of Contents

Reviewed
December 15, 2003

Marie M.
Budev, DO, MPH

Department of
Pulmonary and
Critical Care
Medicine

Joseph A.
Golish, MD

Department of
Pulmonary and
Critical Care
Medicine

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Humans spend almost 30% of their lives sleeping. Over the past 30 years, physicians have begun to recognize many of the detrimental consequences of sleep disturbances produced by abnormal breathing patterns termed sleep-disordered breathing (SDB).¹ Sleep apnea and other sleep-related breathing disorders constitute the greatest number of sleep disorders seen by pulmonologists as well as general practitioners in the outpatient setting. Besides being a common disorder, SDB also has been associated with considerable morbidity. Therefore, a basic understanding of this prevalent disease state is essential for the practicing physician.

SDB refers to a wide spectrum of sleep-related breathing abnormalities; those related to increased upper airway resistance include snoring, upper airway resistance syndrome (UARS), and obstructive sleep apnea-hypopnea syndrome (OSAHS).² Many authors regard SDB as a continuum of a spectrum of diseases (Figure 1).³ This concept suggests that an individual who snores may be exhibiting the first manifestation of SDB and that snoring should not be viewed as normal. A patient can move gradually through the continuum, for example, with weight gain and eventual development of Pickwickian syndrome. He or she also can move rapidly through the spectrum through alcohol or sedative use, which can cause an individual who snores to turn into a snorer with obstructive sleep apnea (OSA). Additionally, although continuous positive airway pressure may be effective in the treatment of apnea, the individual may be left with continued residual UARS or snoring.⁴ Therefore, the clinician must recognize the continuum state of this disease entity because patients may continue to suffer from symptoms due to one aspect of SDB while being treated for another aspect of SDB.

     Definition

     Prevalence

     Pathophysiology

     Signs and
     Symptoms

     Diagnosis

     Therapy

     Outcomes

     Definition

     Prevalence

     Pathophysiology

     Signs and
     Symptoms

     Diagnosis

     Treatment

     Outcomes

     Definition

     Prevalence

     Pathophysiology

     Signs and
     Symptoms

     Diagnosis

     Therapy

     Outcomes

Snoring is one of the most common aspects of SDB and has been described throughout history. In the past, snoring generally had been considered a social nuisance without any consequence to the snorer—only to the suffering bed partner. After sleep apnea syndrome was recognized, snoring began being viewed in a new light—as an important clinical symptom. Although it is by far the most common symptom of sleep apnea and is usually the main reason for a patient visit, not all patients who snore have sleep apnea. Many nonapneic snorers present with a constellation of signs and symptoms similar to those found in OSAHS, including daytime somnolence, tiredness, difficulty with concentration, headaches, and reduced work performance. Therefore, separating the effect of primary snoring from apnea is difficult because both conditions are linked closely.

Although the definition of snoring may differ depending on the "ear of the beholder," it is defined by The Random House Dictionary of the English Language as "…breathing during sleep with hoarse or harsh sounds as caused by the vibrating of the soft palate."⁵ The International Classification of Sleep Disorders: Diagnostic and Coding Manual defines primary snoring (ICSD 780.53-1) as "loud upper airway breathing sounds in sleep, without episodes of apnea or hypoventilation."⁶ Phillipson and Remmers⁷ described primary snoring as snoring that does not create disruptions in sleep patterns or problems with insomnia or excessive daytime somnolence. Because the precise definition of snoring is difficult to determine by objective means, it is usually assessed subjectively.

Objective snoring measurement techniques lack standardization and uniformity. In fact, the measurement of snoring is not a routine component of nocturnal polysomnography due to lack of a precise definition of snoring. Although the measurement of snoring can be accomplished easily through use of a microphone to measure sound pressures, the analysis of the signal and the definition of snoring make this measurement more complex and difficult to interpret.

Subjective assessment is the most frequent tool used to study snoring. Patients are asked simple dichotomous questions, such as "Do you snore?" Although questionnaires may ask more detailed questions, lack of response validation limits their usability. Another issue with snoring is that the snorer often is unaware of his or her snoring, and the problem is usually brought to the snorer's attention by the listener. Although some patients report that their snoring wakes them up, this factor has been shown to be inconsistent and should not be used as a marker for significant snoring.

It is clearly recognized that snoring is common in the general population, but estimates vary widely of its prevalence in different populations. These differences mainly are due to subjective perception, depending on who is reporting the snoring (the snorer or the bed partner) and how the question is asked by the clinician. Overall, snoring is reported to affect 19% to 37% of the general population and more than 50% of middle-aged men.⁸ Male predominance has been noted in all snoring epidemiologic studies, possibly due to the differences in perception of snoring by men and women. Other possible reasons for increased male predominance include gender differences in pharyngeal anatomy and function as well as hormonal differences and their effect on upper airway muscles and body fat distribution.

Snoring is produced as a result of the changes in the configuration and properties of the upper airway (from the nasopharynx to the laryngopharynx) that occurs during sleep. This sound can be produced by any membranous portion of the airway that lacks cartilaginous support, including the soft palate, uvula, and the pharyngeal walls (Figure 2). Snoring is a complex phenomenon that depends on the interaction of various upper airway muscles, including the tongue and soft palate, as well as on neural influences, which directly result in changes in the mass and compliance of the airway walls. The vibration of the airway tends to be diffuse rather than localized, making therapy difficult when the vibration is directed toward only one section of the airway.

Snoring is usually an inspiratory sound, but it also may be present in expiration.⁹ Snoring can occur during any stage of sleep but is more common during stages 2, 3, and 4. This is because airway elastance and muscle tone due to sympathetic activity and neural output to the upper airway walls are different during rapid eye movement (REM) and non-REM sleep. Snoring can be heard during nasal breathing, oral breathing, or during combined oronasal breathing. Characteristics of a snore, including the frequency, depend on the segment or segments responsible for production of the sound. But the spectrum of sounds have been found to be dependent on route of breathing, stage of sleep, posture, weight, airway wall mass, and elasticity of the upper airway. Multiple predisposing factors can lead to a snoring abnormality, including age (middle or advanced), regional obesity, body posture, alcohol and muscle relaxant use, retrognathia, nasal blockage, and smoking.¹⁰

A primary snorer is usually asymptomatic and does not suffer from cardiovascular disease. Snoring in this population is usually an annoyance to the bed partner, but the snorer may deny any symptoms of daytime somnolence or difficulty with concentration. In contrast, snoring also may occur in conjunction with a disordered sleep pattern and may be associated with a range of symptoms, including overt OSAHS.

Bedpartners, family members, or friends who may have shared a room with the sleeping patient initially may complain of loud or disruptive noises. The patient may complain of snoring themselves, a feeling of tiredness on waking, excessive sleepiness during the day, poor work performance, and difficulty with concentration.

Although rare, systemic disease may lead to snoring through disruption or dysfunction of the upper airway anatomy; however, signs and symptoms of systemic disease should be carefully sought, including those for hypothyroidism or acromegaly. Some nonapneic snorers may have objective physiologic findings similar to patients with sleep apnea, including high blood pressure, cardiac disease, strokes, and endocrine diseases such as diabetes or impaired insulin resistance. This raises the possibility that, even in the absence of sleep apnea, snoring may be a causative factor in the pathogenesis of these disorders.

A complete history and careful physical examination are paramount in assessing whether sleep apnea is present in a patient with snoring symptoms. The history and examination results also will guide the clinician in deciding whether a nocturnal polysomnogram is necessary and in determining appropriate treatment.

The history should be obtained in the presence of the bed partner, who usually initiates the visit, because the snorer often is unaware of snoring. The clinician also should assess the degree of social disruption caused by the snoring. He or she should ask the bed partner the number of years' duration of the snoring, frequency of snoring (every night or occurring intermittently), postural dependence (lying on side or back), and the association of posture with cessation of breathing.

The patient's risk factors should be assessed, including male gender, increase in weight, ingestion of alcohol, allergies, nasal obstruction, trauma, use of muscle-relaxing medications, and smoking. An assessment of daytime functioning, including concentration levels, work performance, and sleepiness should be documented. The Epworth Sleepiness Scale (Table 1), developed to assess the level of daytime sleepiness, has been used to distinguish primary snoring from OSAHS.¹¹ A history should be sought of previous surgery or trauma to the upper airways (any site between the nose and the larynx) because the compliance of the airways may be affected. A family predisposition to snoring has been described, and many snorers will admit to other family members having a history of snoring if asked.¹²

The physical examination should include documentation of the blood pressure, body mass index (BMI), neck circumference (especially short and fat neck), evidence for vascular disease, and any abnormalities of the upper airway. Upper airway abnormalities of concern include the presence of nasal polyps; septal deviation; previous nasal fractures; crowed pharynx; presence of macroglossia; uvula shape, size, length, and movement during phonation as well as the presence of inflammation of any of the upper airway structures. The uvula, although rarely responsible for snoring, may be red, inflamed, elongated, and unable to lift off the base of the tongue during phonation due to snoring.

Laboratory tests for hypothyroidism or acromegaly are indicated only if clinical signs suggest the presence of these disorders. The decision to order other laboratory investigations should be based on the possible medical consequences of the patient's snoring, the probability of apnea being present, and on factors that may influence successful treatment.

The two main studies usually considered in the evaluation of snoring are nocturnal polysomnography and an airway assessment. In a position statement the American College of Chest Physicians and the Association of Sleep Disorders Centers have expressed that only snorers suspected of having sleep apnea syndrome should undergo polysomnography.¹³ The American Thoracic Society has declared in its position statement that snoring alone is not an indication for a sleep study.¹⁴

In an asymptomatic primary snorer without OSAHS who is losing weight, avoidance of alcohol and sedatives and cessation of smoking may initially treat snoring without the need to obtain a sleep study. Snoring in the absence of OSAHS symptoms provides very low diagnostic accuracy for sleep apnea.¹⁵ However, in a symptomatic primary snorer with no obvious gross anatomic abnormality who is contemplating surgical therapy, a sleep study should be performed. If sleep apnea is demonstrated, noninvasive therapy can be offered. If surgery is still selected by the patient, the sleep study can help identify whether the patient needs optimization of anesthesia and postoperative management. In a primary snorer who is healthy but suffers from an obvious anatomic abnormality, polysomnography or a sleep study is not indicated because it will not alter therapy; however, surgical therapy is necessary. In symptomatic snorers with daytime somnolence, reduced performance, reduced attention, and tiredness, a full noctural polysomnogram is needed to establish a diagnosis of sleep apnea or UARS. Nocturnal polysomnography with a recording of sleep architecture and arousals is necessary.

Polysomnography remains the gold standard for diagnosing SDB. A complete Polysomography is often termed a full sleep study. Sleep is recorded from a number of electrophysiologic signals as well as from breathing and limb movement electrodes. This includes an electroencephalogram (EEG) with two leads, electromyography, electro-oculography, respiratory signals from airflow measurements from nasal pressure, nasal temperature, expired carbon dioxide, ventilation from thoracoabdominal movements or nasal pressure, oxygenation levels, and possible esophageal balloon pressures. Other signals include an electrocardiogram tracing during sleep, pulse rate, position, esophageal pH, and video recording. A detailed airway assessment of upper airway volume and area is not done routinely because it does not predict successful surgical outcomes in a nonapneic snorer. If surgery is being considered, further radiographic imaging may serve to provide an airway assessment and may include cephalometric measurements, computed tomography, or magnetic resonance imaging.

Because snoring and sleep apnea are contained within a spectrum of disease states, the treatment of snoring and sleep apnea may overlap. Treatment of snoring should be directed at improving sleep apnea or UARS. In the snorer without sleep apnea or in the primary snorer, the initiation of treatment may improve quality of life. Lifestyle modification should be addressed in all patients suffering from snoring, including reduction of risk factors such as obesity, alcohol consumption, and muscle relaxant use.

Noninvasive treatments should be recommended initially, including nasal dilators, tongue-retaining devices, and mandibular advancement appliances that can be fixed or adjusted (Figure 3). Used to treat apneic snorers, tongue-retaining devices hold the tongue in a forward position by applying negative pressure. Subsequently, obstruction at the base of the tongue is relieved and nasal breathing is promoted. In 1995, the Task Force for the Standards of Practice Committee of the American Sleep Disorders Association recommended offering oral appliances to all nonapneic snorers.¹⁶

Oral appliances or mandibular devices are usually manufactured by a dentist who has expertise in this area. Oral appliances enlarge the pharyngeal area by preventing tongue and posterior soft palate collapse during sleep. The most common complaints associated with the use of oral appliances include hypersalivation, sore teeth and jaw muscles, and pain in the temporomandibular area. Despite these complaints, patient compliance with oral appliances is about 80%. Several studies have indicated that oral appliances are better tolerated in terms of compliance and side effects than continuous positive airway pressure (CPAP) therapy.¹⁷ In the nonapneic snorer, the use of a popular external noninvasive nasal dilator that is applied to the bridge of the nose may provide some relief from snoring, although no objective measurements exist to support their use.¹⁸

Nonsurgical methods such as treating coexisting allergies and/or nasal congestion, weight reduction, change of sleeping positions, and use of ear plugs have met with limited success. Although many of these modalities have been reported to be successful anecdotally, their efficacy has not been demonstrated in a randomized controlled setting.¹⁹

Patients should be counseled that CPAP carries the greatest guarantee that snoring will be abolished. Application of nasal CPAP via a nasal mask has significantly altered the medical treatment of sleep apnea (Figure 4) because CPAP can almost completely eliminate snoring. Most nonapneic snorers are reluctant to commit to nasal CPAP, and compliance may become an issue that leads to limited efficacy in this population.

Surgical approaches should be discussed with only a limited number of patients—mainly those who suffer from obvious anatomic abnormalities, including nasal or pharyngeal obstruction. Discussions in conjunction with a surgical team should focus on the fact that patients should not expect complete resolution of snoring through surgical techniques but may have improved symptoms. Nasal surgery for the relief of nasal obstruction due to septal deviation or polyps may be associated with improvement in snoring in up to 75% of patients.²⁰ It is thought that nasal surgery alone is unlikely to cure snoring, but it may provide improved breathing, allowing patients to better tolerate therapies such as nasal CPAPs. Uvulopalatopharyngoplasty (UPPP) (Figure 5) and laser-assisted palatal surgery each have reported success rates of greater than 70% for primary snoring.²¹

Laser-assisted uvulopalatoplasty (LAUP) is similar to conventional UPPP but is performed in an outpatient setting under local anesthesia. Less resection of the adjacent palatal tissue and only partial uvulectomy is completed. LAUP is a sequential procedure that usually takes three to four outpatient visits to complete.²²

The best ways to assess snoring treatment outcomes are through the subjective method (by asking the bed partner or the snorer the effects of therapy) and through the objective method, which is also problematic because no standardized measurement techniques and data analysis protocols exist. With these limitations, it is more appropriate to assess treatment outcomes subjectively using a well-designed questionnaire answered by the individual who can best assess the state of snoring before and after the intervention.

A study by Jennum and coworkers²³ did not find increased mortality in snorers but did find that snorers and nonsnorers had the same risk of ischemic heart disease. Another study found that habitual snorers had a higher incidence of falling asleep while driving than nonsnorers; snorers also had a slightly higher rate of traffic accidents due to sleepiness.²⁴

UARS can cause symptoms similar to those found in OSA, yet this syndrome is considerably different due to the lack of oxygen desaturations found during sleep studies. UARS was a term first applied to patients who were found to have excessive daytime sleepiness without a clear cause on a multiple sleep latency test, which was further documented by an overnight polysomnogram. These patients were often labeled as having idiopathic hypersomnia. After many of these individuals were further tested with "invasive polysomnography" (including an esophageal balloon transducer and full pneumotachograph), these patients were found to have increased upper airway resistance. Resistance was indicated by increased negative esophageal inspiratory pressure.²

UARS is characterized by repeated arousals due to upper airway resistance that lead to excessive daytime sleepiness. This disorder often produces a snoring pattern termed crescendo snoring. When the crescendo snoring episode ends, an arousal occurs with rapid decrease in upper airway resistance; the snoring then disappears and stops for a period. UARS events are noted to be typically short—one to three breaths in duration. These events have recently been termed respiratory effort-related arousals (RERAs). In UARS, unlike in OSAHS, there is no evidence of oxygen desaturations.² For the measurement criteria to be classified as a RERA, there must be a pattern of progressively increased negative esophageal pressure that is terminated by a sudden change in the pressure to a less negative level and a sleep arousal. Furthermore, the event must last 10 seconds or longer.

Recognition of UARS has led to a more conservative use of the term snoring. Patients who snore and have no daytime symptoms or excessive daytime sleepiness are called primary snorers. Patients who snore and have daytime sleepiness symptoms may have UARS.

The prevalence of UARS in the general adult population is unknown, yet it has been estimated to be as high as 10% to 15% when the definition is applied to adults that suffer from snoring and excessive daytime sleepiness.²⁵ It has been suggested that UARS occurs in a less obese younger population and more frequently in females than does OSAHS.²

Guilleminault and coworkers²⁶ demonstrated that many nonapneic patients show a reduction in cross-sectional area of the pharynx during sleep. Reduction in airway area is sufficient enough to avoid hypopneas and apnea but enough to increase upper airway resistance. Patients with UARS suffer from increased airway resistance, which generates snoring, then leads to arousal episodes and ultimately to excessive daytime sleepiness. The physiologic basis of arousals is based on the generation of negative intrathoracic pressure as detected by various mechanoreceptors located in the upper airway. After arousal, an immediate reduction in airway resistance is noted, accounting for the cessation of snoring for a period. The American Academy of Sleep Medicine Task Force published a report that notes the key role that RERA plays in the pathophysiology of UARS in the absence of apnea or hypopnea.²⁷

Although patients with UARS share no standard clinical presentation, the cardinal symptom of UARS is excessive daytime sleepiness or fatigue. Patients also may complain of difficulty with concentration, morning headaches, impotence, difficulty sleeping, or restless sleep. They often report having repetitive nightmares, such as choking or being buried alive, which may suggest difficulty with breathing. Abnormal oronasal-maxillomandibular features are noted on visual examination, including deviated nasal septum, enlarged turbinates, crooked teeth, laxity of the temporo-mandibular joint with an audible click, or a narrow face with a high hard palate or enlarged or elongated uvula.²⁸ Bed partners may complain about the cycle of the crescendo snoring pattern, with short arousals and abrupt cessation of snoring only to reoccur later. Again, snoring is not a necessary feature of this syndrome because the upper airway resistance is due to a partial decrease in airway cross-sectional area; therefore, the airway walls do not have to vibrate to produce a snoring sound.³

UARS should not be overdiagnosed. Three essential clinical features consistently have been used by investigators and authors to diagnose UARS:

• excessive daytime somnolence;
• an elevated EEG arousal index, with the arousal related to increased respiratory efforts; and
• a normal respiratory disturbance index (RDI) of less than five events per hour of sleep.²⁹

UARS is present only if there are documented elevations in upper airway resistance, sleep fragmentation, and daytime dysfunction or excessive daytime sleepiness. The clinical complaint of fatigue or daytime sleepiness can be documented by an abnormal increase in the Epworth Sleepiness Scale (Table 1) score to a value greater than 10 or by use of another validated sleep questionnaire. In addition, a low RDI is needed to distinguish UARS from OSAHS. The elevated EEG arousal index related to increased respiratory efforts is the specific measurement that distinguishes UARS from idiopathic hypersomnolence.²⁷ The clinical complaint of snoring (including crescendo snoring), increase in snoring intensity before EEG arousals, and clinical improvement with a short-term trial of nasal CPAP can be regarded as supportive features of UARS.

The diagnosis of UARS requires full polysomnography. Although measurements of upper airway resistance were first used, based on the original definition of UARS, substitute measurements of effort and ventilation may be used as long as no evidence of hypopneas or apneas are present. A normal apnea/hypopnea index (AHI) of less than five events per hour of sleep should be seen on the polysomnograph. Additionally, EEG arousals should occur at a rate of more than 10 per hour of sleep and must be associated with increased respiratory effort (usually made by use of nocturnal esophageal pressure monitoring).

Current literature supports that esophageal pressures greater than -10 cm H₂0 are abnormal. The measurement of esophageal pressure is the gold standard for measuring respiratory effort and is the only consistent measurement reported for the diagnosis of UARS. Substitute measurements can include inductive plethysmography, strain gauges, oronasal temperature measurements, nasal pressures, and the carbon monoxide levels in exhaled gas. Arousals are documented from the EEG tracings and electromyography, although changes in heart rate, ventilation, and other measurements of autonomic activity may play some role in the future.³

CPAP, surgery, oral appliances, and weight loss are possible treatment options for UARS. Ideally, the recommended treatment of UARS should be effective, relieve symptoms, and produce normalized studies posttherapy. These therapies also should be covered by health insurance and have long-term effectiveness. Thus far, however, none of the proposed treatments have fully met these criteria.

Although currently available data supports the use of nasal CPAP as a treatment option for UARS, compliance may be an issue, making this treatment modality less practical. Also, the safety and efficacy of surgical interventions have been poorly documented in the literature. Surgical intervention in the UARS population includes LAUP, which has been shown in small studies to improve sleep quality and daytime somnolence.²⁴ Palatal tissue reduction by radiofrequency ablation and the use of oral appliances may be safer and very effective, although further study of these modalities is needed.²⁴

Another approach to the treatment of UARS is to create a more-negative esophageal pressure and delay arousal times through the application of topical anesthetics to the mechanical receptors responsible for arousals in the upper airway.³⁰

Data in the sleep literature are not yet clear-cut regarding the efficacy, safety, and compliance of UARS treatment modalities, including weight loss, nasal CPAP, oral appliances, and surgery.

OSAHS is not a new clinical entity but is one that has been recognized only recently. Although there have been many accounts of famous apneic individuals throughout history, one of the most classic was by Charles Dickens in the early 1800s in his description of the character "Joe the fat boy." Dickens' ruddy-faced obese character was described as suffering from severe daytime somnolence as well as from "dropsy," or what we now recognize as chronic cor pulmonale, with probable polycythemia due to end-stage sleep apnea.³¹

Evolving from the historical accounts of sleep apnea to the present day, the most significant development in the diagnosis of sleep-disordered breathing is the publication of the American Academy of Sleep Medicine's report on recommendations for syndrome definition and measurement techniques in clinical research. Within this report, the older term obstructive sleep apnea (OSA) was appropriately changed to the newer term obstructive sleep apnea/hypopnea syndrome (OSAHS).²⁷ The complications and potential consequences of OSAHS include increased risk for hypertension and cardiovascular events as well as cerebrovascular events. The clinician must remember that OSAHS not only impacts the health of the sufferer but also impacts the bed partner's sleep state.³²

OSAHS is characterized by recurrent episodes of partial or complete airway obstruction during sleep due to repetitive collapse of the pharynx, necessitating recurrent awakenings or arousals to reestablish airway patency. This airway obstruction or partial obstruction manifests in a reduction in airflow termed hypopnea or in a complete cessation of airflow termed apnea despite ongoing inspiratory effort. Hypopneas are defined in adults as a 10-second event during which there is continued breathing but in which ventilation during sleep is reduced by at least 50% from baseline. Apnea occurs due to total cessation of airflow for at least 10 seconds. Apnea can be obstructive or central. Obstructive apnea is defined as cessation of airflow but with continued respiratory effort, whereas central apnea is a state in which airflow and respiratory effort are both absent. Apnea also can be both central and obstructive, although obstructive apnea is more common. Hypopnea can produce clinical sequelae similar to those of apnea but, in general, apnea may be associated with a greater fall in oxygen saturations.

To be diagnosed with OSAHS, patients must fulfill criterion A or B plus criterion C²:
A) Excessive daytime sleepiness that is not explained by other factors
OR
B) Two or more of the following that are not better explained by other factors:

• Choking or gasping from sleep
• Recurrent awakenings from sleep
• Feeling unrefreshed after sleep
• Daytime fatigue
• Poor concentration

PLUS
C) Overnight monitoring indicates five or more obstructed breathing events per hour during sleep or 30 events per 6 hours of sleep. These events can be a combination of OSA, hypopnea, or respiratory effort-related arousals.

The RDI (or AHI) is the number of apneas plus hypopneas per hour of sleep. This index has now become the standard by which to define and quantify the severity of OSAHS. An RDI greater than 15 events per hour indicates possible OSAHS. Generally, as the RDI increases, the severity of apnea increases.

Most apnea studies have indicated that OSAHS is a relatively common disorder. In a large US epidemiologic study in individuals aged 30 to 60 years, 24% of men and 9% of women had abnormal AHI indices.² Overall, it has been estimated that more than 158 million adults aged 25 and older suffer from sleep apnea and that more than 10 million men and women currently go untreated for the disorder in the United States. Currently, the prevalence of OSAHS is conservatively estimated to be 1% to 2% in middle-aged men and half that, or approximately 0.5% to 1%, in middle-aged women.³³ It is estimated that only 1% of OSAHS patients are receiving appropriate treatment for their disease.³⁴

SDB may be prevalent but difficult to recognize in patients with pulmonary dysfunction, including COPD and chronic bronchitis, or with heart failure. In these patients, the underlying disease may cause nocturnal breathing problems and sleep disruption. Also, patients with central obesity or diabetes may be at risk for SDB. Patients with recent stroke or myocardial infarction may be at higher risk for SDB and apneic activity as well as for the effects of end-organ damage due to hypoxemia and hypoventilation.

OSAHS occurs due to a narrowing of the upper airway during sleep. The site of the narrowing is usually at the level of the pharynx (Figure 6).³⁵ Airway occlusion is noted to be limited to inspiration, which exerts negative pharyngeal pressure and reduces the tone of the genioglossus muscle. This theory remains the cornerstone of understanding OSAHS.

Upper airway size in OSAHS patients is smaller than in normal subjects, as assessed by CT scan and resistance measurements. Patients with OSAHS also have been noted to have a more elliptical upper airway shape than normal subjects, but this may be due to increased body mass as well. The difference in airway size in OSAHS patients is due to fat deposition and facial bone structure. Obese patients with OSAHS have fat deposits lateral to the pharynx. Although this fat deposit may not be substantial, it may predispose patients to OSAHS.³⁶ Retroposition of the maxilla and mandible predisposes patients to OSAHS due to a narrowing of the pharynx caused by posterior displacement of the tongue and palate. These facial traits also are more common in families with OSAHS.³⁷ Patients with OSAHS also have increased palatal muscle bulk, which usually responds to positive pressure.

Arousal in OSAHS patients occurs at a specific level of pleural pressure once an adequate respiratory effort has been stimulated. Arousals may lead to the sequel of sleep disruption, daytime somnolence, and impaired cognitive performance as well as to autonomic changes, including elevations in arterial blood pressure.³⁸

Genetics may play an important role in the pathophysiology of OSAHS. The disorder is more common among family members suffering from OSAHS than in the general population. This relationship seems to be independent of familial obesity tendencies.⁸

The dominant symptoms of OSAHS are sleepiness and daytime somnolence. Other symptoms include difficulty with concentration, fatigue, unrefreshed sleep, nocturnal choking, nocturia, depression, and decreased libido. Bed partners may report snoring, apneas, restless sleep, or irritability. In investigating sleepiness, note whether the patient falls asleep frequently against his or her will or in a dangerous situation, such as when driving.

Although there is no gold standard definition for sleepiness, the Epworth Sleepiness Scale may assist the clinician in documenting this symptom. A score of greater than 12 of 24 points on the Epworth scale is defined as abnormally sleepy (Table 1). Morning headache was initially reported as a feature of OSAHS, but its true association is debatable.³⁹ Patients should also be asked about weight gain and the relationship of developing symptoms to any gain in weight.

Although physical examination has not proved helpful in identifying patients with SDB, BMI and neck circumference (indicators of obesity) appear to be good clinical predictors for OSAHS. BMI (weight in kg/ height in meters) is the most commonly used clinical predictor for OSAHS. Obesity is defined as a BMI greater than 30 kg/m² The neck circumference should be measured at the level of the cricothryoid membrane. Men with a neck circumference of 17 inches or greater and women with a neck circumference of 16 inches or greater are at risk for OSAHS. Upper body obesity also may be associated with a higher risk for OSAHS.

Physical findings of OSAHS may include:

• Obesity
• Increased neck circumference
• Crowding of the upper airway, macroglossia
• Enlarged tonsils
• Nasal obstruction
• Retrognathia
• Hypertension
• Lower limb edema
• Signs of cor pulmonale

Laboratory investigation may include:

• Secondary polycythemia
• Proteinuria
• Respiratory failure
• Nocturnal cardiac arrhythmia
• GERD

Because many of the symptoms of OSA are nonspecific, the index of clinical suspicion for the presence of OSAHS needs to be high to make the diagnosis. The differential diagnosis for OSAHS should include primary snoring, chronic hypoventilation syndrome, and central sleep apnea and Cheyne-Stokes respiration.

Patients suspected of having OSAHS should undergo polysomnography. Because night-to-night variability can occur in mild cases of the disorder, misdiagnosis can occur. Therefore, a negative first night test is insufficient to rule out OSAHS in patients with a high clinical suspicion of the disease.

Many other types of sleep studies are available, with varying settings and parameters measured. A complete level I study is performed in the laboratory; partial and limited studies can be conducted in the home. However, the American Sleep Disorder Association advises that standard polysomnography is the accepted test for diagnosis and determination of the severity and treatment of OSA. The association recommends that portable or unattended recordings are an acceptable alternative only when:

• clinical symptoms are severe and indicative of sleep apnea,
• initiation of treatment is urgent and a standard polysomnography is not readily available,
• the patient cannot be studied in a sleep laboratory, or
• follow-up studies are needed to evaluate therapy response.

Adequate treatment of OSAHS results in improvement of symptoms and may alter morbidity and mortality outcomes. Current therapies in the treatment of sleep apnea are aimed at widening the pharyngeal airway, making it less adept to collapse, or at pneumatically splinting the airway open using CPAP (Figure 4). CPAP is very effective in eliminating pharyngeal collapse, improving overall symptoms, and reducing cardiovascular sequelae, making it the treatment of choice for OSA. In 1981, Sullivan and coworkers⁴⁰ first published a paper on the use of nasal CPAP as an OSA treatment. Effective CPAP settings are determined in the sleep lab by using information from various sleep stages and body positioning during sleep. Patient compliance is the major limitation in the use of CPAP therapy. The use of a well-fitting mask or chin strap to lessen mouth dryness may assist with some of the negative symptoms encountered with the use of CPAP therapy. Also, an initial short course of anxiolytics may help alleviate anxiety and humidified air may relieve symptoms of nasal dryness or congestion that are associated with mask therapy.

Bi-level positive airway pressure (BiPAP) allows the clinician to set different pressures for inspiratory and expiratory breaths. This may be beneficial for patients who occasionally complain of feeling excessive air pressure or of having the sensation of exhaling against positive pressure. The routine use of BiPAP has not been shown to increase compliance, but in patients who have high CPAP requirements, BiPAP may be a more comfortable option.

Oral appliances may enlarge the pharyngeal airway during sleep by moving either the tongue or the mandible anteriorly, partially relieving apneas. Therefore, such appliances are probably more useful in the mild apneic patient than in those with severe apnea.

Upper airway surgery, including radiofrequency ablation of the tongue or soft palate (somnoplasty), LAUP, UPPP, or genioglossal advancement with hypoid myotomy, bimaxillary advancement, or maxillomandibular advancement, aims to enlarge the pharyngeal space and prevent airway collapse. Success rates range from 30% for the less aggressive interventions to 90% for the more aggressive procedures. Common side effects include pain, alteration in taste, and nasal regurgitation.

Patients should be advised to avoid activities or substances that may worsen their disease, including alcohol use before sleep, sedatives, and sleep deprivation. The use of daily decongestants (anticholinergics or steroids) may result in improvement of the nasal pathology associated with OSA. Weight loss also should be encouraged as a long-term strategy to treat sleep apnea. However, although weight loss may improve sleep apnea, it may not totally eliminate it.

The role of pharmacotherapy for sleep apnea remains controversial. Experimental evidence suggests that serotoninergics at certain doses improve sleep efficiency; however, sufficient data is not yet available to support their routine use.

OSAHS outcomes, including feelings of vitality, energy, mental summary scores all improve with treatment. Significant study data has accumulated demonstrating a reduction in cardiovascular morbidity and mortality with CPAP therapy for OSAHS. In fact, health care utilization is significantly reduced when patients adhere to CPAP therapy, resulting in fewer physician claims and hospital stays.

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