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Published: January 2013

Sleep-Disordered Breathing

Puneet S. Garcha

Loutfi S. Aboussouan

Omar Minai

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Humans spend almost 30% of their lives sleeping. Since the 1970s, physicians have begun to recognize many of the detrimental consequences of sleep disturbances produced by abnormal breathing patterns, or sleep-disordered breathing (SDB). Sleep apnea and other sleep-related breathing disorders constitute the greatest number of sleep disorders seen by sleep medicine, pulmonary, and general practitioners in the outpatient setting. SDB has been associated with considerable morbidity.

SDB comprises 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).1 Many clinicians regard SDB as a spectrum of diseases.2 This concept suggests that a person 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 or with alcohol or sedative use, which can cause a person who snores to turn into a snorer with obstructive sleep apnea (OSA). This concept has support from experimental studies showing increasing airway collapsibility during sleep with progression from normal, snoring, UARS, and OSA. Continuous positive airway pressure (CPAP) can effectively treat apnea, but the patient may be left with continued residual UARS or snoring.3 Therefore, the clinician must recognize that this disease entity represents a continuum and that patients can continue to suffer from symptoms caused by one aspect of SDB while being treated for another aspect.

Snoring

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 with no consequences for the snorer, only for the suffering bed partner. After sleep apnea syndrome was recognized, snoring began to be viewed 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, patients by themselves are generally not disturbed by the snoring. Instead it is at the prompting of the bed partner, whose sleep is disrupted due to snoring that the patient sees a physician. Of course, not all patients who snore have sleep apnea.

Definition

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.”4 The International Classification of Sleep Disorders: Diagnostic and Coding Manual defines snoring (ICSD 786.09) as “respiratory sound generated in the upper airway during sleep that typically occurs during inspiration but may also occur in expiration, without episodes of apnea or hypoventilation.”5

Prevalence

It is clearly recognized that snoring is common among the general population, but estimates of its prevalence vary widely among different populations. These differences are mainly due to subjective perception, depending on who is reporting the snoring (the snorer or the bed partner), how the question is asked by the clinician, night-to-night variability of snoring can also make the reporting difficult. Overall, snoring is reported to affect 19% to 37% of the general population and more than 50% of middle-aged men.6 Prevalence of snoring increases with age. Male predominance has been noted in numerous epidemiologic studies of snoring. Possible reasons for male predominance include differences in pharyngeal anatomy and function, hormonal differences and their effects on upper airway muscles, and differences in body fat distribution.

Pathophysiology

Snoring is a result of the changes in the configuration and properties of the upper airway (from the nasopharynx to the laryngopharynx) that occurs during sleep. Any membranous portion of the airway that lacks cartilaginous support, including the soft palate, uvula, and the pharyngeal walls, can produce this sound. Snoring is usually an inspiratory sound, but it can also occur in expiration.7 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. Multiple predisposing factors can lead to a snoring abnormality, including age (middle or advanced), obesity, weight gain, body posture, use of alcohol and muscle relaxants, retrognathia, nasal blockage, development of asthma, and smoking.8

Signs and Symptoms

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, and the snorer might deny any symptoms of daytime somnolence or difficulty with concentration. In contrast, snoring also can occur in conjunction with a disordered sleep pattern and may be associated with a range of symptoms, including overt OSAHS.

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

Diagnosis

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 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 if possible 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 intermittent), positional variation (lying on side or back), and the association of posture with cessation of breathing.

The patient’s risk factors should be assessed, including gender, body weight, alcohol usage, 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), which assesses the level of daytime sleepiness, has been used to distinguish primary snoring from OSAHS.9 A history of surgery or trauma to the upper airways (any site between the nose and the larynx) should be sought because the compliance of the airways may be affected. A family predisposition to snoring has been described, and many snorers admit to other family members of having a history of snoring if asked.10

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 that apnea is present, and factors that can influence successful treatment.

The 2 main studies usually used to evaluate 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 declared that only snorers suspected of having sleep apnea syndrome should undergo polysomnography.11 The American Thoracic Society has declared in its position statement that snoring alone is not an indication for a sleep study.12

In symptomatic snorers with daytime somnolence, reduced performance, reduced attention, drowsy driving and tiredness, a full nocturnal polysomnogram are 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 polysomnography 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 2 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 possibly 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 performed routinely because it does not predict a successful surgical outcome in a nonapneic snorer. If surgery is being considered, further radiographic imaging can provide an airway assessment and may include cephalometric measurements, computed tomography, or magnetic resonance imaging.

Table 1: The Epworth Sleepiness Scale
How likely are you to doze off or fall asleep in the following situations, in contrast to feeling just tired? This refers to your usual way of life in recent times. Even if you have not done some of these things recently, try to work out how they would have affected you. Use the following scale to choose the most appropriate number for each situation:
  • 0 = Would never doze
  • 1 = Slight chance of dozing
  • 2 = Moderate chance of dozing
  • 3 = High chance of dozing
Score

Situation 0 1 2 3
Sitting and reading        
Watching television        
Sitting inactive in a public place (theater, meeting)        
Lying down to rest in the afternoon when circumstances allow        
Sitting and talking to someone        
Sitting quietly after lunch without alcohol        
In a car, while stopped for a few minutes in traffic        
Total score        

© 2012 The Cleveland Clinic Foundation.

Treatment

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

Noninvasive treatments should be recommended initially, including nasal dilators, tongue-retaining devices, and mandibular advancement appliances that can be fixed or adjusted. 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.13

Nonsurgical methods such as treating coexisting allergies or nasal congestion, reducing weight, changing sleeping positions, and using ear plugs have met with limited success. Although many of these modalities are anecdotally successful, their efficacy has not been demonstrated in a randomized controlled setting.14

Patients should be counseled that CPAP carries the greatest likelihood that snoring will be abolished. Application of CPAP via a nasal mask has significantly altered the medical treatment of sleep apnea, because CPAP can nearly eliminate snoring. Most nonapneic snorers are reluctant to com- mit to nasal CPAP, and compliance can become an issue that leads to limited efficacy in this population.

Surgical approaches should be discussed only with patients who suffer from obvious anatomic abnormalities, including nasal or pharyngeal obstruction. Discussions in conjunction with a surgical team should focus on improvement of symptoms. Patients should be counseled to not expect complete resolution of snoring through surgical techniques. 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.15 It is believed that nasal surgery alone is unlikely to cure snoring, but it can improve breathing, allowing patients to better tolerate therapies such as nasal CPAP. Uvulopalatopharyngoplasty (UPPP) (Figure 1) and laser-assisted palatal surgery each have reported success rates of greater than 70% for primary snoring.16

Laser-assisted uvulopalatoplasty (LAUP) is similar to conventional UPPP but is performed in an outpatient setting under local anesthesia. Less adjacent palatal tissue is resected and only partial uvulectomy is performed. LAUP is a sequential procedure that usually takes 3 or 4 outpatient visits to complete.17

Outcomes

The best ways to assess snoring treatment outcomes are through the subjective method (by asking the bed partner or the snorer about 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 person who can best assess the state of snoring before and after the intervention.

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Upper airway resistance syndrome

UARS can cause symptoms similar to those found in OSA, yet this syndrome is considerably different due to the absence of oxygen desaturation found during sleep studies. Upper airway resistance syndrome 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.18 These patients were often said to have idiopathic hypersomnia. After many of these patients were further tested with invasive polysomnography (including an esophageal balloon transducer and full pneumotachograph), they were found to have increased upper airway resistance. Resistance manifested as increased negative esophageal inspiratory pressure.1

Definition

UARS is characterized by repeated arousals, due to resistance to airflow in the upper airway, that lead to excessive daytime sleepiness and fatigue. Snoring has been noted to be present in association with these brief arousals, but snoring is not necessary for identification of UARS. UARS events are noted to be typically short: 1 to 3 breaths in duration. These events have been termed respiratory effort-related arousals (RERAs). In UARS, unlike in OSAHS, there is no evidence of oxygen desaturation.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.

Prevalence

In an epidemiologic study of sleep disorders in more than 1000 volunteers in Brazil, the prevalence of UARS in the general adult population was 15.5%19 UARS occurs in a less-obese, younger individuals and more commonly in women versus men than does OSAHS.1 The natural history of this disorder is not well understood.

Pathophysiology

Guilleminault and coworkers20 demonstrated that many nonapneic patients show a reduction in cross-sectional area of the pharynx during sleep. Reduction in airway area is sufficient to avoid hypopnea and apnea but enough to increase upper airway resistance.21 These patients also have increased airway collapsibility due to abnormal anatomy.22 Patients with UARS suffer from increased airway resistance, which leads to arousal episodes and ultimately to excessive daytime sleepiness. Nasal airway anatomic issues (ie, deviated septum, inferior turbinate hypertrophy, nasal valve collapse, or any combination of these) have been associated with UARS.23

Signs and Symptoms

Clinical presentation of UARS can be varied, the cardinal symptoms of UARS are fatigue and excessive daytime sleepiness. Some patients also complain of difficulty with concentration, morning headaches, impotence, and difficulty with sleep onset and sleep maintenance (insomnia). 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 and the airway walls do not have to vibrate to produce a snoring sound.2 It is now increasingly recognized that the clinical features seen in UARS overlap with functional somatic syndromes such as chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome (IBS), chronic headache, and temporomandibular joint (TMJ) syndrome. Based on the signs and symptoms alone it can be difficult to distinguish the patients with UARS from those with mild OSAHS.

Diagnosis

The diagnosis of UARS requires a high degree of clinical suspicion. Diagnosis of UARS requires symptoms (excessive daytime somnolence, frag- mented sleep, fatigue), anatomic features consistent with upper airway narrowing, and supportive PSG findings.

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. A low respiratory disturbance index (RDI) is also 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.24 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 supporting a diagnosis 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 there is no evidence of hypopnea or apnea. A normal apnea-hypopnea index (AHI) of less than 5 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 nocturnal esophageal pressure monitoring). Studies have shown an association of alpha-delta sleep pattern in the EEG of patients with UARS. Alpha-delta pattern is a nonspecific EEG finding in which there is intrusion of wake alpha pattern into the deep, slow-wave sleep.22 This is also seen in some functional somatic syndromes listed above but is not a feature of OSAHS.

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. Current literature supports that esophageal pressures more negative than 10 cm H20 are abnormal. 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.2

Treatment

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 after therapy. These therapies also should be covered by health insurance and have long-term effectiveness. Thus far, however, none of the proposed treatments has fully met these criteria.

Outcomes

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

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Obstructive sleep apnea-hypopnea syndrome

OSAHS was identified as a distinct entity only in 1999, despite being present for many years. Evolving from the historical accounts of sleep apnea to the present day, the most significant development in the diagnosis of sleep-disordered breathing was the publication of the American Academy of Sleep Medicine (AASM) report on recommendations for syndrome definition and measurement techniques in clinical research. Within this report, the older term obstructive sleep apnea was appropriately changed to the newer term obstructive sleep apneahypopnea syndrome.24 The complications and potential consequences of OSAHS include increased risks of hypertension, insulin resistance and cardiovascular events, as well as cerebrovascular events. OSAHS is also associated with an increase in the rate and severity of motor vehicle accidents, increased healthcare utilization, reduction of work performance, and occupational injuries. OSAHS affects not only the health of the sufferer but also the bed partner’s sleep state.25

Definition

OSAHS is characterized by recurrent episodes of partial or complete airway obstruction during sleep due to repetitive obstruction of the upper airway, necessitating recurrent awakenings or arousals to re-establish airway patency, often with oxygen desaturation. 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 efforts. Hypopnea is 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 is total cessation of airflow for at least 10 seconds. Apnea can be obstructive, central, or mixed. Obstructive apnea is more common and 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. Mixed apnea is recognized by a lack of respiratory effort during initial apnea period followed by gradually increasing effort against an obstructed upper airway. These events are thought to be related pathophysiologically to obstructive apnea. Hypopnea can produce clinical sequelae similar to those of apnea, but in general, apnea is associated with a greater fall in oxygen saturation.

For sleep-disordered breathing to be diagnosed as OSAHS, the patient must have at least 5 obstructed breathing events per hour (or 30 events per 6 hours of sleep) on an overnight polysomnogram. These events can be a combination of obstructive apnea and hypopnea (for the determination of an apnea-hypopnea index or AHI) and additional inclusion of the respiratory effort–related arousals (for the determination of the respiratory disturbance index or RDI). The patient must also have either excessive daytime sleepiness or at least 2 of choking or gasping from sleep, recurrent awakenings from sleep, feeling unrefreshed after sleep, daytime fatigue, or poor concentration. This second group of signs and symptoms must not be better explained by other factors.1

The 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 AHI of more than 5 events per hour indicates possible OSAHS. As the AHI increases, the severity of apnea increases.

Prevalence

OSAHS is a relatively common disorder. The Wisconsin cohort study was a population based study in which 602 working subjects aged 30 to 60 years were enrolled and studied with an overnight polysomnogram. In this cohort, 24% of men and 9% of women had abnormal AHI indices (> 5 events per hour).26 In the United States prevalence of OSAHS is 3% to 7% in adult men and 2% to 5% in adult women.27 Although OSAHS can occur in any age group the prevalence increases with age. Overall, it has been estimated that more than 158 million adults aged 25 years 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. It is estimated that 1% of OSAHS patients are receiving appropriate treatment for their disease.28

Pathophysiology

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.29 Airway occlusion is noted to be limited to inspiration, which exerts negative pharyngeal pressure and reduces the tone of the pharyngeal dilator muscles. This theory remains the cornerstone of understanding OSAHS. During REM sleep there is a further decrease in tone and activity of the pharyngeal dilator muscles causing longer and more distinct apnea and hypopnea events.

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 might not be substantial, it can predispose patients to OSAHS.30  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.31  Patients with OSAHS also have increased palatal muscle bulk, which usually responds to positive pressure.

Genetics might 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 relation seems to be independent of familial obesity tendencies.6 There is an increase in familial susceptibility with an increase in number of affected relatives.32

Signs and Symptoms

The dominant symptom of OSAHS is excessive sleepiness. Other symptoms include daytime somnolence, difficulty with concentration, fatigue, unrefreshing sleep, nocturnal choking, nocturia, night sweats, depression, memory loss, and decreased libido. Bed partners might report snoring, apneas, restless sleep, or personality changes such as irritability, anxiety, and aggressiveness. The symptoms of snoring, apnea, and hypopnea can be exacerbated by alcohol use prior to sleep and with increase in body weight. In investigating sleepiness, it is important to 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 can 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.33 Patients should also be asked about weight gain and the relation 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.. More than 50% of patients with a BMI greater than 50 were a found to have OSAHS in a study conducted by Kripke et al.34 Men with a neck circumference greater than 17 inches and women with neck circumference greater than 16 inches are at a higher risk for OSAHS.35

Physical findings of OSAHS can include obesity, increased neck circumference, crowding of the upper airway, macroglossia, dental malocclusion, uvular edema and erythema, narrow high-arched palate, low-lying and elongated palate, enlarged tonsils, nasal obstruction, septal deviation, inferior turbinate hypertrophy, nasal valve collapse on sniffing, retrognathia, hypertension, lower limb edema, and signs of cor pulmonale. Laboratory investigations, which are non-specific, include secondary polycythemia, proteinuria, respiratory failure, nocturnal cardiac arrhythmia, and gastroesophageal reflux disease.

Diagnosis

Because many of the symptoms of OSA are nonspecific, the clinician needs to have a high index of clinical suspicion to make the diagnosis of OSAHS. The differential diagnosis for OSAHS should include primary snoring, chronic hypoventilation syndrome central sleep apnea, and Cheyne- Stokes respiration. The other causes of sleepiness that need to be distinguished from OSAHS are narcolepsy, idiopathic hypersomnia, insufficient sleep, and periodic limb movement disorder.

Patients suspected to have OSAHS should undergo an overnight polysomnogram. Due to night-to-night variability in mild cases of the disorder, the diagnosis can be missed. Therefore, a negative first-night test is insufficient to rule out OSAHS in a patient in whom there is clinical reason to suspect 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 AASM suggests that standard polysomnography is the accepted test for diagnosing and determining the severity and treatment of OSA.20 The AASM task force recommends that portable monitoring is an acceptable alternative in patients at high risk for OSAHS without a coexisting medical or sleep disorder. Monitoring should be done in conjunction with a comprehensive sleep medicine evaluation. Portable monitoring can be performed in a patient who cannot be safely be transported for laboratory polysomnogram, in whom initiation of treatment is urgent and a standard polysomnography is not readily available, or in whom follow-up studies are needed to evaluate response to therapy.

Treatment

Adequate treatment of OSAHS results in improvement of symptoms and can alter morbidity and mortality outcomes. Current therapies in the treatment of sleep apnea are intended to widen the pharyngeal airway and make it less apt to collapse, or to pneumatically splint the airway open using CPAP. CPAP therapy is very effective in eliminating pharyngeal collapse, improving overall symptoms, and reducing cardiovascular sequelae, making it the treatment of choice for OSAHS. Although CPAP is the mainstay of therapy for OSAHS, there are other types of positive airway pressure therapies available: bilevel positive airway pressure (bilevel PAP), auto-PAP (APAP), and expiratory pressure relief devices. Bilevel PAP 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 bilevel PAP has not been shown to increase compliance, but in patients who have high CPAP requirements, bilevel PAP may be a more comfortable option.

Oral appliances can enlarge the pharyngeal airway during sleep by moving either the tongue or the mandible anteriorly, partially relieving apnea. Such appliances are probably more useful in patients with mild apnea 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, in intended 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 ones. Common side effects include pain, alteration in taste, and nasal regurgitation.

Medical therapy for OSAHS plays a role as an adjunctive rather than a primary treatment option. Weight loss should be recommended via diet, counseling, and exercise. The role of bariatric surgery as a treatment for OSAHS is not clear. In fact, residual OSA may persist despite successful weight loss with either medical therapy or bariatric surgery. Positional therapy can be a successful alternative in patients with predominantly supine-position related symptoms. In patients with OSAHS and coexisting rhinitis, nasal steroid trial may be useful. The U.S. FDA has approved both modafinil and armodafinil for the treatment of residual daytime somnolence in patients with OSAHS despite adequate CPAP therapy.

There is no role for other pharmacologic agents (serotonergics, estrogen replacement, methylxanthine derivatives) in the treatment of sleep apnea.

Outcomes

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

Summary

  • The term sleep-disordered breathing refers to a wide spectrum of sleep-related breathing abnormalities; those related to increased upper airway resistance include snoring, upper airway resistance syndrome, and obstructive sleep apnea-hypopnea syndrome.
  • Polysomnography remains the gold standard for diagnosing sleep-disordered breathing.
  • Lifestyle modifications should be addressed in all patients suffering from snoring, including reduction of risk factors such as obesity, and use of alcohol and muscle relaxants.
  • Patients should be counseled that continuous positive airway pressure is the most effective therapy for abolishing snoring.
  • Surgical approaches should be suggested only to patients who suffer from obvious anatomic abnormalities.

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Suggested Readings

  • American Academy of Sleep Medicine: International Classification of Sleep Disorders, 2nd ed.: Diagnostic and Coding Man- ual. Westchester, IL: American Academy of Sleep Medicine, 2005.
  • Bloom JW, Kaltenborn WT, Quan SF: Risk factors in a general population for snoring. Importance of cigarette smoking and obesity. Chest 1988;93:678-683.
  • Callop N, Cassel DK: Snoring and sleep disordered breathing. In Lee-Chiong T Jr, Sateia M, Carskadon M (eds): Sleep Medicine. Philadelphia: Hanley & Belfus, 2002, pp 349-355.
  • Gavriely N, Jensen O: Theory and measurements of snores. J Appl Physiol 1993;74:2828-2837.
  • Lugaresi E, Cirignotta F, Coccagna G, Piana C: Some epidemiological data on snoring and cardiocirculatory disturbances. Sleep 1980;3:221-224.
  • Lugaresi E, Cirignotta F, Montagna P, et al: Snoring: Pathogenic, clinical, and therapeutic aspects. In Kryger M, Roth T, Dement W (eds): Principles and Practice of Sleep Medicine, 2nd ed. Philadelphia: WB Saunders, 1994, pp 621-629.
  • Phillipson EA, Remmers JE: American Thoracic Society Consensus Conference on indications and standards for cardiopulmonary sleep studies. Am Rev Respir Dis 1989;139:559-568.
  • The Random House Dictionary of the English Language. New York: Random House; 2001.
  • Schwab RJ, Goldberg AN, Pack AJ: Sleep apnea syndromes. In Fishman AP (ed): Fishman’s Pulmonary Diseases and Disorders, 3rd ed. New York: McGraw-Hill, 1998, pp 1617-1646.

References

  1. Callop N, Cassel DK: Snoring and sleep disordered breathing. In Lee-Chiong T Jr, Sateia M, Carskadon M (eds): Sleep Medicine. Philadelphia: Hanley & Belfus, 2002, pp 349-355.
  2. Schwab RJ, Goldberg AN, Pack AJ: Sleep apnea syndromes. In Fishman AP (ed): Fishman’s Pulmonary Diseases and Disorders, 3rd ed. New York: McGraw-Hill, 1998, pp 1617-1646.
  3. Lugaresi E, Cirignotta F, Montagna P, et al: Snoring: Pathogenic, clinical, and therapeutic aspects. In Kryger M, Roth T, Dement W (eds): Principles and Practice of Sleep Medicine, 2nd ed. Philadelphia: WB Saunders, 1994, pp 621-629.
  4. The Random House Dictionary of the English Language. New York: Random House; 2001.
  5. American Academy of Sleep Medicine: International Classification of Sleep Disorders, 2nd ed.: Diagnostic and Coding Manual. Westchester, IL: American Academy of Sleep Medicine, 2005, p 204.
  6. Lugaresi E, Cirignotta F, Coccagna G, Piana C: Some epidemiological data on snoring and cardiocirculatory disturbances. Sleep 1980;3:221-224.
  7. Gavriely N, Jensen O: Theory and measurements of snores. J Appl Physiol 1993;74:2828-2837.
  8. Bloom JW, Kaltenborn WT, Quan SF: Risk factors in a general population for snoring. Importance of cigarette smoking and obe- sity. Chest 1988;93:678-683.
  9. Osman EZ, Osborne J, Hill PD, Lee BW: The Epworth Sleepiness Scale: Can it be used for sleep apnoea screening among snor- ers? Clin Otolaryngol 1999;24:239-241.
  10. Teculescu DB, Mauffret-Stephan E, Gaultier C: Familial predisposition to snoring. [letter]. Thorax 1994;49:95.
  11. Martin RJ, Block AJ, Cohn MA, et al: Indications and standards for cardiopulmonary sleep studies. Sleep 1985;8:371-379.
  12. American Thoracic Society; Medical Section of the American Lung Association: Indications and standards for cardiopulmonary sleep studies. Am Rev Respir Dis 1989;139:559-568.
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