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Clinical polysomnography in the evaluation of snoring and sleep-related breathing disorders
CLINICAL POLYSOMNOGRAPHY IN THE EVALUATION OF SNORING AND SLEEP-RELATED BREATHING DISORDERS GARY K. ZAMMIT, PhD, STEPHEN LUND, MD, JOSEPH GHASSIBI, MD
The advent of laser-assisted uvulopalatoplasty has contributed to a recent increase in the number of patients who are evaluated for snoring and sleep-related breathing disorders. These disorders are often the result of compromised upper airway patency. They are characterized by respiratory disturbance during sleep as well as symptoms occurring during wakefulness. The consequences of sleep-related breathing disorders are significant because they are associated with an increased risk of cardiovascular illness and mortality. The evaluation of snoring and respiration during sleep involves the use of polysomnography, which is required to differentiate simple snoring from more serious sleep-related breathing disorders. Preoperative polysomnography is recommended for all laser-assisted uvulapalatoplasty candidates, and postoperative studies may be indicated to document treatment efficacy and for long-term follow-up.
The a d v e n t of l a s e r - a s s i s t e d u v u l o p a l a t o p l a s t y (LAUP) 1'2 has contributed to a recent increase in the number of patients who undergo sleep laboratory evaluation for snoring and sleep-related breathing disorders. This is because of the need to document the complaint of snoring, as well as to determine the presence and extent of upper airway resistance or obstructive sleep apnea before surgery. Sleep laboratory studies are essential to the development of appropriate treatment plans, especially with respect to the identification of patients who require mechanical or other treatments for sleep-related breathing disorders. This article defines the features of snoring and sleep-related breathing disorders, outlines common clinical and laboratory procedures for evaluating these disorders, and proposes practice guidelines for use by the otolaryngologist.
SNORING Epidemiological studies indicate that snoring is common in the general population. One study of 5,713 individuals has shown that approximately 19% of adults describe themselves as habitual s n o r e r s d This corresponds to 24.1% of the male and 13.8% of the female population. Advanced age is associated with a greater risk of snoring. Up to the age of 30 years, approximately 10% of men and less than 5% of w o m e n are habitual snorers, whereas more than 60% of men and 40% of w o m e n between the ages of 60 and 65 years describe themselves as such. Obesity is a significant factor that contributes to snorFrom the Sleep Disorders Institute, Department of Psychiatry, and the Department of Pulmonary Medicine, St Luke's/Roosevelt Hospital Center, and Columbia University College of Physicians and Surgeons, New York, NY. Address reprint requests to Gary K. Zammit, PhD, Sleep Disorders Institute, St Luke's/Roosevelt Hospital Center, Amsterdam Ave at 114th St, New York, NY, 10025. Copyright 9 1994 by W.B. Saunders Company 1043-1810/94/0504-0001 $05.00/0
ing. 4,s When survey samples are divided between normal-weight individuals and those w h o are >/15% above ideal body weight, only 34% of the normal-weight group report habitual snoring whereas more than 50% of the overweight group report habitual snoring. Snoring may be defined as an audible and typically loud recurrent breath sound during sleep that occurs on inspiration, and that varies in intensity with breath volume and frequency. It is produced by the vibration of soft tissue, including the tonsils, soft palate, uvula, and other structures of the oropharyngeal airway. 6 Snoring is the result of several contributing factors. These include conditions that compromise upper airway patency such as a small or narrow airway, nasal polyps, a deviated septum, or enlarged turbinates. Such conditions produce an increase in airway resistance 7 and negative intraluminal pressure during inspiration, resulting in traction and vibration of tissues in the upper airway. Other functional factors that contribute to snoring include the decrease in upper airway muscle tone that occurs during sleep. It has been shown that the function of the dilator muscles in snorers may be delayed or absent on inspiration, resulting in pharyngeal collapse at lower negative intraluminal pressures than normal, s Snoring never arises spontaneously during wakefulness but may occur immediately on sleep onset. It is possible for snoring to begin during the transition from wakefulness to sleep, at the first signs of stage I sleep, or at subsequent points in the sleep period. Its occurrence may be continuous or intermittent throughout the night, and it seems to be found with equal intensity in all sleep stages. However, some reports have suggested that snoring is w o r s e during n o n - r a p i d - e y e - m o v e m e n t (NREM) sleep. 6 REM sleep, which is associated with a decline in respiratory efficiency, does not seem to be associated with an increase in snoring frequency or volume. Body position during sleep is one important factor in the occurrence of snoring. Snoring is most likely to occur when the patient is in the supine position, and less likely when prone or lateral. 9"1~ The transient improvement in snoring when adopting the latter positions is
OPERATIVE TECHNIQUES IN OTOLARYNGOLOGY--HEAD AND NECK SURGERY, VOL 5, NO 4 (DEC), 1994: pp 221-227
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obvious to s p o u s e s w h o request that the offending sleeper roll over, and has led to the development of devices that can be used in the treatment of snoring (eg, use of a body position monitor/alarm or sewing a tennis ball in the back of pajamas to discourage sleeping in the supine position). I~ Hypothyroidism 6 and tobacco use 4"5 have been found to be associated with snoring, and can contribute to greater long-term risk. Acute and prominent increases in snoring may also result from nasal congestion caused by common colds or allergies, sleep deprivation, and the use of alcohol or sedative-hypnotic agents. 13-15 For many years, snoring was considered an annoying but otherwise benign problem. The International Classification of Sleep Disorders includes a category of primary snoring, which is characterized by loud upper airway breathing sounds in the absence of apnea, hypoventilation, or serious medical sequelae. 16 However, recent data suggest that snoring may be associated with serious health risksJ 7 These risks may be present in snorers i n d e p e n d e n t l y of more severe sleep-related breathing disorders such as sleep apnea. Habitual snoring is known to be associated with hypertension 3'14"18-2~ and heart disease, m and has also been found to be associated with myocardial 22 and brain infarct. 23'24 It has been shown that habitual snorers are as much as 10.3 times more likely to suffer a stroke than those who never or occasionally snore. 21"25 Snoring may also result in significant sleep disruption or fragmentation, 26 which may lead to daytime fatigue, sleepiness, or occupational and safety risks caused by performance impairment.19,27, 28 Perhaps the most significant health risk of snoring is its association with serious sleep-related breathing disorders such as obstructive sleep apnea. Snoring may be the alarm mechanism that alerts the sleeper or bed partner to periods of hypopnea or upper airway resistance, or the termination of apneic events. In fact, it may be the only reported symptom of obstructive sleep apnea or upperairway resistance, and the only symptom that prompts the patient to seek treatment, even when severe obstructive sleep apnea is present.
OBSTRUCTIVE SLEEP APNEA Sleep apnea is a sleep-related breathing disorder that is thought to affect between 1% and 10% of the general population. 29-31 Recent epidemiological data indicate that 2% of w o m e n and 4% of men between the ages of 30 and 60 years meet the minimum diagnostic criteria for sleep apnea syndrome. 32 This is a lower estimate of prevalence than obtained in samples of elderly patients. It seems that the occurrence of the disorder increases with advanced age. 33 In studies of people over the age of 65 years, it has been reported that 24% of people living independently, 33% in acute care inpatient facilities, and 42% in nursing homes have more than five apneic events per hour of sleep, which is the minimum criterion typically used to diagnose sleep apnea in adults. 34 There are several factors that predispose patients to sleep apnea. The disorder is more common in men, with the male:female ratio estimated to be between 3:1 and 20:1. 32"3s Although it may first appear at any age, most cases are identified w h e n patients are between the ages of 40 and 60 years. In women, the disorder is more commonly diagnosed after menopause, 34 possibly be-
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cause of the increased risk associated with aging or hormonal changes. Obesity is a significant risk factor and is thought to contribute significantly to the development of sleep apnea. 36 Recent surveys of patients presenting with the complaint of loud snoring found that obesity is the only clinical variable that has predictive value in identifying patients with sleep apnea, with body weight accounting for 41% of the variance in the sample. Sleep apnea is characterized by multiple respiratory pauses during sleep. These pauses, or apneas, are defined as the complete cessation of airflow measured at the level of the nose and mouth lasting at least 10 seconds. 36 The duration of most apneic events exceeds this minim u m criterion. The average duration of apneic events in an individual with sleep apnea is between 30 and 40 seconds, and there have been documented events lasting as long as 3 minutes. 3s Partial reductions in airflow are known as hypopneas. Hypopneas are defined as the reduction of airflow measured at the level of the nose and mouth lasting at least 10 seconds. They are associated with oxygen desaturation and/or evidence of electroencephalographic (EEG) or e l e c t r o m y o g r a p h i c (EMG) arousal. The mean duration of hypopneic events in an individual with sleep apnea tends to be similar to the duration of apneic events. Obstructive apneas and hypopneas result from similar mechanisms that impede airflow during sleep. Consequently, individuals with sleep apnea often have both apneic and hypopneic events during the sleep period. Another pattern of sleep-disordered breathing that has been recently described is known as upper airway resistance. 39"4~ This disturbance is associated with modest reductions in airflow during sleep that often are not detected by conventional recording methods. Measures of intraesophageal pressure may be required to detect the subtle respiratory characteristics of upper airway resistance. These changes in respiration can result in EEG arousals during sleep that are similar to those seen in sleep apnea. Arousals as short as 3 seconds may be characteristic of upper airway resistance in some cases. Episodes of upper airway resistance may occur in patients with sleep apnea, although the upper airway resistance syndrome has been found to occur independently of sleep apnea. Individuals with sleep apnea experience multiple respiratory events during sleep. These events recur throughout the sleep period, and m a y w o r s e n during REM s l e e p y A minimum of five apneic or hypopneic events per hour of sleep is required to diagnose sleep apnea 16 and, therefore, at least 40 events should be detected during a normal 8-hour sleep recording. However, most people with sleep apnea have many more events. It has been found that the average number of apneic events per hour of non-REM sleep is 65 (range, 48 to 79), and the average number of apneic events per hour of REM slee~ is 42 (range, 17 to 90) in patients with sleep apnea. The recurrence of respiratory events during the sleep period appears to have two main consequences. It results in sleep fragmentation and intermittent transient declines in oxygen saturation. Sleep fragmentation can be so severe that it interferes with sleep architecture and with the occurrence of delta and REM sleep. 42 There seems to be a relationship between sleep fragmentation and the severity of daytime sleepiness associated with sleep apnea. 43-45 Oxygen desaturation may possibly contribute to complaints of daytime sleepiness, but is more likely a contributor to the cognitive deficits seen in some patients with sleep apnea. 46 CLINICAL POLYSOMNOGRAPHY
The diagnosis of sleep apnea syndrome is not made exclusively on the basis of respiratory disturbance during sleep. There are clinical signs and symptoms that define this disorder (see Table 1). Perhaps the two most common signs are snoring and excessive daytime sleepiness. Virtually all patients with obstructive sleep apnea snore, with 94% reporting the development of loud snoring before the age of 21 years. 41 Snoring is frequently loud and interrupted by snorts or other unusual sounds. It is commonly a source of annoyance or embarrassment, and can be quite disturbing to a bed partner. Many individuals with sleep apnea have been evicted from their bedrooms because of loud snoring, and some can relate memorable stories of disturbing others in adjoining rooms or apartments. Excessive daytime sleepiness is considered the primary daytime manifestation of sleep apnea. 47 Subjective complaints of daytime sleepiness are common among individuals with sleep apnea who often report drowsiness, napping, or falling asleep at inappropriate times. When given the opportunity to sleep during the day on the multiple sleep latency test (MSLT), individuals with sleep apnea have been shown to have a mean latency to stage I sleep of 2.6 minutes across four naps, showing that this group of patients is excessively sleepy during the day. 48 It must be kept in mind that there is variability among individuals with respect to the severity of daytime sleepiness and the likelihood that they will report these problems to a physician. Mild symptoms such as fatigue or the tendency to doze in sedentary situations may be the only evidence of daytime sleepiness. These symptoms may not be immediately recognized as problems, 49 and can be easily dismissed if the patient is not questioned carefully. Fatigue-related cognitive impairment may reveal itself as occasional attention or memory lapses, 46 which may be another indicator of daytime sleepiness. Severe symptoms of sleepiness are often characterized by reports of difficulty sustaining alertness in virtually any situation, with some patients reporting that they fall
asleep at work, while socializing, at meal times, or w h e n operating a motor vehicle. The latter has been documented by studies of actual and simulated driving showing that individuals with sleep apnea perform more poorly than normal controls, s~ Severe daytime sleepiness can be debilitating because of its impact on social and occupational functioning, and can result in the risk of accident or injury caused by performance failure. Other common symptoms of sleep apnea are listed in Table 1. Sleep apnea presents a serious health risk. Hypertension is common. Podszus et a152 have reported that the prevalence of systemic h y p e r t e n s i o n averaged 58% among 461 sleep apnea patients evaluated in four studies. 53-56 The occurrence of hypertension correlates with the risk factors commonly associated with sleep apnea, especially age and weight. These findings are complemented by sleep laboratory studies of hypertensive patients with no sleep complaints showing that up to one half meet minimal criteria for the diagnosis of sleep apnea, and one third have apnea indices 920. 57 Approximately 48% of patients with sleep apnea have cardiac arrhythmias. 5s The most c o m m o n types of cardiac events observed are premature ventricular contractions and sinus arrest between 2.5 and 13 seconds in duration. 41 In some patients, transient periods of bradycardia occur during apneic or hypopneic events, followed by tachycardia w h e n respiration resumes. Oxygen desaturation during the night can lead to hypoxemia, and there have been reports of seizures occurring in association with desaturation. 41 The frequent desaturation associated with sleep apnea occasionally results in polycythemia. One evaluation of 1,000 patients found that 7% of those with unexplained polycythemia had sleep apnea. 36 One of the most important health risks associated with sleep apnea is increased mortality. 24"59 In a 9-year longitudinal study of untreated patients with sleep apnea, 6~ it was found that those with 20 or more apneic events per hour of sleep had a high mortality rate, with a cumulative probability of survival of only 0.63, whereas those with fewer than 20 had a cumulative probability of survival of 0.96. These data underscore the need for the early detection and treatment of sleep apnea.
TABLE 1. Symptoms of Obstructive Sleep Apnea Nighttime symptoms Loud, bothersome snoring Witnessed apneas Awakenings secondary to gasping for air/choking Awakenings associated with a sense of dread or anxiety Restless or fitful sleep Nocturnal or morning confusion (sleep drunkenness) Polyuria Daytime symptoms Morning sluggishness, fatigue Excessive daytime sleepiness Dry mouth/sore throat on awakening Early morning headaches Impaired memory Difficulty concentrating Personality changes such as irritability, anxiety, or depression Decreased motivation or "laziness" Diminished libido Associated physical symptoms/findings Cardiac arrhythmia Hypertension Stroke Angina Peripheral edema Polycythemia Hypothyroidism Erectile dysfunction (men)
ZAMMIT ET AL
PREOPERATIVE EVALUATION OF SNORING AND SLEEP-RELATED BREATHING DISORDERS The evaluation of snoring and sleep-related breathing disorders begins with a thorough diagnostic interview. The presence of loud snoring alone is not pathognomonic of sleep apnea or other respiratory disturbance during sleep. However, snoring that occurs in association with obesity or other associated features (see Table 1) may be indicative of a serious sleep-related breathing disorder. It is critically important that a careful inquiry be made during consultation because many patients will deny the presence of clinically significant symptoms. Interview of the patient's spouse or bed partner often yields helpful information regarding nighttime symptoms, daytime symptoms, and associated features. The American Thoracic Society and the American Sleep Disorders Association are currently establishing standards of practice for the evaluation of sleep-related breathing disorders. No guidelines have been released at this time, but the serious health and safety risks associated with sleep apnea syndrome dictate that practitioners exercise caution and thor223
oughness in the evaluation and follow-up of snoring and sleep-related breathing disorders. Snoring, the warning signal that often prompts the patient to seek medical care, may be eliminated by procedures such as LAUP without significant impact on serious breathing disorders such as upper airway resistance or sleep apnea syndrome. The diagnosis of sleep-related breathing disorders is made using standard all-night polysomnography (Level I polysomnography, see Table 2). Polysomnography is usually performed in a sleep laboratory environment, although advances in technology have made it possible to perform this procedure at the patient's home or hospital bedside. The essential feature of polysomnography is the EEG, which is usually obtained from parietal leads placed in the C 3 or C 4 positions, and is used to determine the occurrence of wakefulness and the distinctive patterns of brain electrical activity that are characteristic of sleep. Relaxed wakefulness is characterized by lowvoltage fast EEG activity in the 8- to 13-Hz range. This is usually observed just before sleep onset and during awakenings. There are five stages of sleep. 61 Stage I sleep may be associated with the appearance of slow, rolling eye movements, and is characterized by low voltage EEG activity in the 4- to 7-Hz range. Stage I is a transitional stage of sleep that typically occurs at sleep onset, during sleep stage shifts, and after arousal. This is important because patients with sleep-related breathing disorders often have an elevated percentage of stage I sleep caused by respiratory events. Stage II sleep is characterized by low-voltage mixed EEG activity punctuated by phasic events k n o w n as k-complexes and sleep spindles. A k-complex is a sharp negative wave i>75 p~V that is immediately followed by a sharp positive wave. It is typically about 0.5 seconds in duration. A sleep spindle is a burst of fast EEG activity in the 12- to 15-Hz range that lasts at least 0.5 seconds. Stage II sleep comprises the majority of the night for most healthy adult sleepers. Stages III and IV sleep, otherwise known as slow-wave sleep or delta sleep, are characterized by high amplitude (>75 ~V), low frequency (1 to 3 Hz) waves. Delta sleep usually comprises less than 20% of the sleep period in healthy young adults, but is thought to be associated with deep and restful sleep. REM sleep is characterized by a low-voltage, mixed frequency EEG with occasional sawtooth waves that is accompanied by the appearance of phasic rapid conjugate eye movements and a tonic decrease in muscle tone.
There is an organization to nighttime sleep. Figure 1A shows the sleep architecture of a healthy young adult sleeper. Note that the subject begins the night with a brief episode of stage I sleep, which cascades into stages II, III, and IV sleep. The first REM period, which is brief, occurs approximately 90 minutes after sleep onset. This pattern, k n o w n as a sleep cycle, repeats itself multiple times over the course of the night. As the sleep period continues, the percentages of stages III and IV (delta) sleep normally decline and the percentage of REM sleep increases. The organization of nighttime sleep is critical to the evaluation of snoring and sleep-related breathing disorders because these disorders often disrupt or fragment the normal architecture of sleep. Figure 1B is a representation of sleep architecture in a patient with severe obstructive sleep apnea. Note the frequent shifts into stage I sleep, the low amounts of delta and REM sleep, and the fragmentation of REM sleep during the sleep period. When polysomnography is used clinically to detect sleep-related breathing disorders, multiple variables are measured. Standard measures are those performed in standard level I polysomnography (Table 2). These recordings are sufficient to quantify and characterize sleep stages and architecture as well as the occurrence, nature, and severity of episodes of apnea, hypopnea, and possibly upper airway resistance. The key diagnostic indicators used to determine the presence and severity of a sleep-related breathing disorder include the number of awakenings, n u m b e r of arousals, and sleep efficiency (the percentage of time in bed that is spent asleep). These measures indicate the degree of sleep fragmentation that may be caused by respiratory disturbance. Sleep-stage percentages provide a measure of the disruption of sleep architecture. As the severity of the disorder increases, the percentage of stage I sleep increases, and the percentages of delta and REM sleep tend to decrease. Measures of airflow and respiratory effort are used to detect respiratory events, which are often reported in the apnea/hypopnea index or respiratory disturbance index. These values indicate the average number of apneic and hypopneic events per hour of sleep. Baseline, average, and nadir S a O 2 values during desaturation provide a measure of apnea severity and hypoxemia during sleep. These values are often used to determine the number of times that the SaO 2 decreases below normal, which is considered to be a n S a O 2 level of 90%. Finally, the elec-
TABLE 2. Diagnostic Studies for Snoring and Sleep-Related Breathing Disorders Level I Standard Polysomnography
Level IA Standard Portable Polysomnography
Level II Comprehensive Portable Polysomnography
Level III Modified Portable Sleep Apnea Testing
Parameters
Minimum of seven, including EEG (C4-A1 or C3-A2), EOG, chin EMG, ECG, airflow, respiratory effort, oxygen saturation
Minimum of seven, including EEG (C4-A1 or C3-A2), EOG, chin EMG, ECG, airflow, respiratory effort, oxygen saturation
Minimum of seven, including EEG (C4-A1 or C3-A2) EOG, chin EMG, ECG, airflow, respiratory effort, oxygen saturation
Body position
Documented or objectively measured EMG or motion sensor desirable but optional In constant attendance Possible Laboratory
Documented or objectively measured EMG or motion sensor desirable but optional In constant attendance Possible Laboratory/home/institution
May be objectively measured EMG or motion sensor desirable but optional Not in attendance Not possible Home/institution
Minimum of four, including ventilation (at least two channels of respiratory movement, or respiratory movement and airflow), heart rate or ECG, oxygen satu ration May be objectively measured May be recorded
Leg movement Personnel Interventions Location
Not in attendance Not possible Home/institution
Abbreviations: EOG, electrooculogram; ECG, electrocardiogram. Adapted and reprinted with permission.63
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FIGURE 1. (A) Sleep architecture in a healthy young adult. The night is initiated with a brief period of stage I sleep, followed in orderly succession by stages II, III, IV, and subsequent REM. It is normal for the percentage of delta sleep to decline and the percentage of REM sleep to increase across the night. (B) Sleep architecture in a patient with severe obstructive sleep apnea. There are multiple arousals and brief awakenings secondary to apneas, hypopneas, and upper airway resistance. This results in sleep disruption and dramatic reductions in the percentages of delta and REM sleep. It is not uncommon for REM sleep periods to be fragmented across the night because of worsening respiration often seen in this stage. trocardiogram serves as a measure of cardiac arrhythmias that are commonly observed in patients with sleep apnea. In addition to these measures obtained at night, it is sometimes useful to have data from the MSLT. The MSLT is a test of daytime sleepiness that provides the patient with multiple scheduled opportunities to nap during the day. Latency to sleep onset for each nap period is calculated and an average is obtained. This average is compared with normative data to determine if the patient is pathologically sleepy. Healthy normal subjects have a mean sleep latency of between 10 and 20 minutes, and many subjects will not fall asleep at all. Mean latencies of less than 5 minutes are indicative of a pathological degree of daytime sleepiness. 62 This finding may be crucial in deciding whether to treat mild cases of sleep-related breathing disorders. There are minimal acceptable standards for clinical polysomnography. We believe that standard, level I polysomnography or its equivalent (level IA) must be used for the evaluation of snoring and sleep-related breathing disorders (see Table 2). Unattended portable recording (levels II and III polysomnography) offers conZAMMIT ET AL
venience, accessibility, and may be available at lower cost than standard p o l y s o m n o g r a p h y . H o w e v e r , these types of recording have not been adequately validated, and their potential advantages must be weighed against the possibility of missed or inaccurate diagnoses. 63 This is especially true in patients with mild, moderate, or atypical sleep-related respiratory disturbances that may not be detected by levels II or III p o l y s o m n o g r a p h y . The American Sleep Disorders Association Standards of Practice Committee currently recommends that portable studies not be used for loud snoring or the routine assessment of obstructive sleep apnea. 64 It must be emphasized that snoring and sleep-related breathing disorders also cannot be reliably evaluated using some common alternative techniques. These techniques include daytime nap or abbreviated nighttime studies. Such studies may be useful in detecting some severe cases, but may fail to detect mild to moderate cases. Neither provides a clear indication of the severity of the disorder or its impact on nighttime sleep. Overnight oximetry is not considered a sufficient measure because apneic and hypopneic events commonly occur without desaturation or with minimal (<4%) desaturation, and the diagnosis may be missed. Audio tape cannot be used to discriminate between normal breathing, snoring, and sleep apnea because breath or snoring sounds may persist during periods of hypopnea or upper airway resistance, yielding a false-negative result. It is not clear if any of these measures can be used as part of a screening process before polysomnography. They may yield misleading information that shapes the physician's impression of the patient and leads to a deviation from appropriate diagnostic procedures.
POSTOPERATIVE FOLLOW-UP Postoperative follow-up with polysomnography is an important consideration for patients who have undergone upper airway surgery for snoring or sleep-related breathing disorders. If surgery was performed to treat primary snoring as documented by clinical polysomnography, postoperative follow-up in the sleep laboratory may not be necessary. However, long-term office follow-up is advised to ensure that sleep-related breathing disorders do not develop in the absence of snoring. It is critical to avoid the development of silent sleep apnea, which potentially increases morbidity and mortality without warning the patient. This is especially important to consider as the patient ages or increases in body weight. When upper airway surgery is performed as a treatment for sleep apnea or another sleep-related breathing disorder, follow-up polysomnography is crucial to determine treatment efficacy, as well as the need for adjunctive treatments (e.g., nasal continuous positive airway pressure). All patients who have been treated for a sleep-related breathing disorder should be seen periodically for followup to ensure that daytime symptoms have not returned and that there is no impairment in daytime alertness or functioning.
CONCLUSION The development of new laser-assisted surgical techniques for the treatment of snoring and sleep-related breathing disorders has led to the need for otolaryngolo225
gists to obtain preoperative sleep laboratory evaluation of their patients. Careful evaluation includes history and physical examination, as well as clinical polysomnography. The appropriate use of polysomnography will contribute to the safe and appropriate application of surgical procedures, reliable measures of treatment outcome, and the identification of patients who require mechanical or other treatments for sleep-related breathing disorders.
ACKNOWLEDGMENT The authors thank Sigurd H. Ackerman, MD, for reviewing the manuscript.
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21. Koskenvuo M, Kaprio J, Telakivi T, et al: Snoring as a risk factor for ischaemic heart disease and stroke in men. BMJ 294:16-19, 1987 22. Smirne S, Palazzi S, Zucconi M, et al: Habitual snoring as a risk factor for acute vascular disease. Eur Respir J 6:1357-1361, 1993 23. Palomaki H: Snoring and the risk of ischemic brain infarction. Stroke 22:1021-1025, 1991 24. Spriggs DA, French JM, Murdy JM, et al: Snoring increases the risk of stroke and adversely affects prognosis. Q J Med 83:555-562, 1992 25. Parfinen M, Palomaki H: Snoring and cerebral infarction. Lancet 2:1325-1326, 1985 26. Hoffstein V, Mateika JH, Mateika S: Snoring and sleep architecture. Am Rev Respir Dis 143:92-96, 1991 27. Guflleminault C, Stoohs R, Duncan S: Snoring (I). Daytime sleepiness in regular heavy snorers. Chest 99:40-48, 1991 28. Stradling JR, Crosby JH, Payne CD: Self reported snoring and daytime sleepiness in men aged 35-65 years. Thorax 46:807-810, 1991 29. Kapunuiai LE, Andrew DJ, Crowell DH, et al: Estimated prevalence of sleep apnea in adults based on self report survey apnea scores. Sleep Res 14:175, 1985 30. Lavie P: Incidence of sleep apnea in a presumably healthy working population: A significant relationship with excessive daytime sleepiness. Sleep 6:312-318, 1983 31. Peter JH, Siegrist J, Podszus T, et al: Prevalence of sleep apnea in healthy industrial workers. Klin Wochenschr 63:807, 1985 32. Young T, Palta M, Dempsey J, et al: The occurrence of sleepdisordered breathing among middle-aged adults. N Engl J Med 328: 1230-1235, 1993 33. Coleman RM, Roffwarg HP, Kennedy SJ, et al: Sleep wake disorders based on polysomnographic diagnosis: A national cooperative study. JAMA 247:997-1003, 1982 34. Ancoli-Israel S, Kripke DF, Klauber MR, et al: Sleep disordered breathing in community-dwellingelderly. Sleep 14:486-495, 1991 35. Rubenstein I, Colapinto N, Rotstein LE, et al: Improvement in upper airway function after weight loss in patients with obstructive sleep apnea. Am Rev Respir Dis 138:1192-1195, 1988 36. Guilleminault C: Clinical features and evaluation of obstructive sleep apnea, in Kryger MH, Roth T, Dement WC (eds): Principles and Practice of Sleep Medicine. Philadelphia, PA, Saunders, 1989, pp 552-558. 37. Keidar A, Zammit GK, Krespi YP: The relationship between polysomnographic findings and self-reported symptoms in laser assisted uvulopalatoplasty (LAUP) candidates. Sleep Res 23:271, 1994 38. Krieger J: Obstructive sleep apnea: Clinical manifestations and pathophysiology, in Thorpy MJ (ed): Handbook of Sleep Disorders. New York, NY, Dekker, 1990 39. GuilleminaultC, Stoohs R: The upper airway resistance syndrome. Sleep Res 20:250, 1991 40. Guilleminault C, Stoohs R, Clerk A, et al: A cause of excessive daytime sleepiness: The upper airway resistance syndrome. Chest 104:781-787, 1993 41. Guilleminault C, van den Hoed J, Mitler MM (1978): Clinical overview of the sleep apnea syndromes, in Guilleminault C, Dement WC (eds): Sleep Apnea Syndromes. New York, NY, Liss, 1978, pp 1-12 42. Wittig RM, Romaker A, Zorick FJ, et ah Night-to-night consistency of apneas during sleep. Am Rev Respir Dis 129:244-246, 1984 43. Stepanski E, Lamphere J, Roehrs T, et al: Experimental sleep fragmentation in normal subjects. Int J Neurosci 33:207-214, 1987 44. Stepanski E, Lamphere J, Badia P, et al: Sleep fragmentation and daytime sleepiness. Sleep 7:18-26, 1984 45. Roehrs T, Zorick F, Wittig R, et al: Predictors of objective level of daytime sleepiness in patients with sleep-related breathing disorders. Chest 95:1202-1206, 1989 46. Kribbs NB, Getsy JE, Dinges D (1994): Investigation and management of daytime sleepiness in sleep apnea, in Saunders NA, Sullivan CE, (ed): New York, NY, Dekker, Sleep and Breathing (ed 2). 1994, pp 575-604 47. Guilleminault C, Billiard M, Montplasir J, et al: Altered states of consciousness in disorders of daytime sleepiness. J Neurol SCI 26: 377-393, 1975 48. Roth T, Hartse KM, Zorick F, et al: Multiple naps and the evaluation of daytime sleepiness in patients with upper airway sleep apnea. Sleep 3:425-439, 1980
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49. Westbrook PR: Sleep disorders and upper airway obstruction in adults. Otolaryngol Clin North Am 23:727-743, 1990 50. Findley LJ, Unverzagt ME, Suratt PM: Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis 138: 337-340, 1988 51. Findley LJ, Fabrizio MJ, Knight H, et al: Driving simulator performance in patients with sleep apnea. Am Rev Respir Dis 140:529-530, 1989 52. Podszus T, Greenburg H, Scharf SM: Influence of sleep state and sleep-disordered breathing on cardiovascular function, in Saunders NA, Sullivan CE, (eds): Sleep and Breathing. New York, NY, Dekker, 1994, pp 257-310 53. Burack B, Pollak C, Borowiecki B, et al: The hypersomnia-sleep apnea syndrome (HSA): A reversible major cardiovascular hazard. Circulation 56:111-117, 1977 54. Millman RP, Redline S, Randall C, et al: The relationship between nocturnal sleep events and daytime hypertension in a population of patients with obstructive sleep apnea. Chest 99:861-866, 1991 55. Partinen M, Jamieson A, Guilleminault C: Long-term outcome for obstructive sleep apnea syndrome patients (mortality). Chest 94: 1200-1204, 1988 56. Shepard JW, Jr, Garrison MW, Grither DA, et al: Relationship of
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ventricular ectopy to oxyhemoglobin desaturation in patients with obstructive sleep apnea. Chest 88:335-340, 1985 Scharf SM, Garshick E, Brown R, et ah Screening for subclinical sleep-disordered breathing. Sleep 13:334-353, 1990 Guilleminault C, ConnoUy S, Winkle R: Cardiac arrythmia during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 52:490-494, 1983 Seppala T, Partinen M, Pentilla A, et al: Sudden death and sleeping history among Finnish men. J Intern Med 229:23-28, 1991 He J, Kryger MH, Zorick FJ, et al: Mortality and apnea index in obstructive sleep apnea. Chest 94:9-14, 1988 Rechtschaffen A, Kales A: A Manual of Standardized Terminology, Techniques, and Scoring System for Sleep Stages of Human Sleep Subjects. Washington, DC, US Government Printing Office, 1968 Carskadon MA, Dement WC, Mitler MM, et al: Guidelines for the multiple sleep latency test: A standard measure of sleepiness. Sleep 9:519-524, 1986 Ferber R, Millman R, Coppola M, et al: Portable recording in the assessment of obstructive sleep apnea. Sleep 17:378-392, 1994 American Sleep Disorders Association, Standards of Practice Committee: Practice parameters for the use of portable recording in the assessment of obstructive sleep apnea. Sleep 17:372-377, 1994
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The advent of laser-assisted uvulopalatoplasty has contributed to a recent increase in the number of patients who are evaluated for snoring and sleep-related breathing disorders. These disorders are often the result of compromised upper airway patency. They are characterized by respiratory disturbance during sleep as well as symptoms occurring during wakefulness. The consequences of sleep-related breathing disorders are significant because they are associated with an increased risk of cardiovascular illness and mortality. The evaluation of snoring and respiration during sleep involves the use of polysomnography, which is required to differentiate simple snoring from more serious sleep-related breathing disorders. Preoperative polysomnography is recommended for all laser-assisted uvulapalatoplasty candidates, and postoperative studies may be indicated to document treatment efficacy and for long-term follow-up.
The a d v e n t of l a s e r - a s s i s t e d u v u l o p a l a t o p l a s t y (LAUP) 1'2 has contributed to a recent increase in the number of patients who undergo sleep laboratory evaluation for snoring and sleep-related breathing disorders. This is because of the need to document the complaint of snoring, as well as to determine the presence and extent of upper airway resistance or obstructive sleep apnea before surgery. Sleep laboratory studies are essential to the development of appropriate treatment plans, especially with respect to the identification of patients who require mechanical or other treatments for sleep-related breathing disorders. This article defines the features of snoring and sleep-related breathing disorders, outlines common clinical and laboratory procedures for evaluating these disorders, and proposes practice guidelines for use by the otolaryngologist.
SNORING Epidemiological studies indicate that snoring is common in the general population. One study of 5,713 individuals has shown that approximately 19% of adults describe themselves as habitual s n o r e r s d This corresponds to 24.1% of the male and 13.8% of the female population. Advanced age is associated with a greater risk of snoring. Up to the age of 30 years, approximately 10% of men and less than 5% of w o m e n are habitual snorers, whereas more than 60% of men and 40% of w o m e n between the ages of 60 and 65 years describe themselves as such. Obesity is a significant factor that contributes to snorFrom the Sleep Disorders Institute, Department of Psychiatry, and the Department of Pulmonary Medicine, St Luke's/Roosevelt Hospital Center, and Columbia University College of Physicians and Surgeons, New York, NY. Address reprint requests to Gary K. Zammit, PhD, Sleep Disorders Institute, St Luke's/Roosevelt Hospital Center, Amsterdam Ave at 114th St, New York, NY, 10025. Copyright 9 1994 by W.B. Saunders Company 1043-1810/94/0504-0001 $05.00/0
ing. 4,s When survey samples are divided between normal-weight individuals and those w h o are >/15% above ideal body weight, only 34% of the normal-weight group report habitual snoring whereas more than 50% of the overweight group report habitual snoring. Snoring may be defined as an audible and typically loud recurrent breath sound during sleep that occurs on inspiration, and that varies in intensity with breath volume and frequency. It is produced by the vibration of soft tissue, including the tonsils, soft palate, uvula, and other structures of the oropharyngeal airway. 6 Snoring is the result of several contributing factors. These include conditions that compromise upper airway patency such as a small or narrow airway, nasal polyps, a deviated septum, or enlarged turbinates. Such conditions produce an increase in airway resistance 7 and negative intraluminal pressure during inspiration, resulting in traction and vibration of tissues in the upper airway. Other functional factors that contribute to snoring include the decrease in upper airway muscle tone that occurs during sleep. It has been shown that the function of the dilator muscles in snorers may be delayed or absent on inspiration, resulting in pharyngeal collapse at lower negative intraluminal pressures than normal, s Snoring never arises spontaneously during wakefulness but may occur immediately on sleep onset. It is possible for snoring to begin during the transition from wakefulness to sleep, at the first signs of stage I sleep, or at subsequent points in the sleep period. Its occurrence may be continuous or intermittent throughout the night, and it seems to be found with equal intensity in all sleep stages. However, some reports have suggested that snoring is w o r s e during n o n - r a p i d - e y e - m o v e m e n t (NREM) sleep. 6 REM sleep, which is associated with a decline in respiratory efficiency, does not seem to be associated with an increase in snoring frequency or volume. Body position during sleep is one important factor in the occurrence of snoring. Snoring is most likely to occur when the patient is in the supine position, and less likely when prone or lateral. 9"1~ The transient improvement in snoring when adopting the latter positions is
OPERATIVE TECHNIQUES IN OTOLARYNGOLOGY--HEAD AND NECK SURGERY, VOL 5, NO 4 (DEC), 1994: pp 221-227
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obvious to s p o u s e s w h o request that the offending sleeper roll over, and has led to the development of devices that can be used in the treatment of snoring (eg, use of a body position monitor/alarm or sewing a tennis ball in the back of pajamas to discourage sleeping in the supine position). I~ Hypothyroidism 6 and tobacco use 4"5 have been found to be associated with snoring, and can contribute to greater long-term risk. Acute and prominent increases in snoring may also result from nasal congestion caused by common colds or allergies, sleep deprivation, and the use of alcohol or sedative-hypnotic agents. 13-15 For many years, snoring was considered an annoying but otherwise benign problem. The International Classification of Sleep Disorders includes a category of primary snoring, which is characterized by loud upper airway breathing sounds in the absence of apnea, hypoventilation, or serious medical sequelae. 16 However, recent data suggest that snoring may be associated with serious health risksJ 7 These risks may be present in snorers i n d e p e n d e n t l y of more severe sleep-related breathing disorders such as sleep apnea. Habitual snoring is known to be associated with hypertension 3'14"18-2~ and heart disease, m and has also been found to be associated with myocardial 22 and brain infarct. 23'24 It has been shown that habitual snorers are as much as 10.3 times more likely to suffer a stroke than those who never or occasionally snore. 21"25 Snoring may also result in significant sleep disruption or fragmentation, 26 which may lead to daytime fatigue, sleepiness, or occupational and safety risks caused by performance impairment.19,27, 28 Perhaps the most significant health risk of snoring is its association with serious sleep-related breathing disorders such as obstructive sleep apnea. Snoring may be the alarm mechanism that alerts the sleeper or bed partner to periods of hypopnea or upper airway resistance, or the termination of apneic events. In fact, it may be the only reported symptom of obstructive sleep apnea or upperairway resistance, and the only symptom that prompts the patient to seek treatment, even when severe obstructive sleep apnea is present.
OBSTRUCTIVE SLEEP APNEA Sleep apnea is a sleep-related breathing disorder that is thought to affect between 1% and 10% of the general population. 29-31 Recent epidemiological data indicate that 2% of w o m e n and 4% of men between the ages of 30 and 60 years meet the minimum diagnostic criteria for sleep apnea syndrome. 32 This is a lower estimate of prevalence than obtained in samples of elderly patients. It seems that the occurrence of the disorder increases with advanced age. 33 In studies of people over the age of 65 years, it has been reported that 24% of people living independently, 33% in acute care inpatient facilities, and 42% in nursing homes have more than five apneic events per hour of sleep, which is the minimum criterion typically used to diagnose sleep apnea in adults. 34 There are several factors that predispose patients to sleep apnea. The disorder is more common in men, with the male:female ratio estimated to be between 3:1 and 20:1. 32"3s Although it may first appear at any age, most cases are identified w h e n patients are between the ages of 40 and 60 years. In women, the disorder is more commonly diagnosed after menopause, 34 possibly be-
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cause of the increased risk associated with aging or hormonal changes. Obesity is a significant risk factor and is thought to contribute significantly to the development of sleep apnea. 36 Recent surveys of patients presenting with the complaint of loud snoring found that obesity is the only clinical variable that has predictive value in identifying patients with sleep apnea, with body weight accounting for 41% of the variance in the sample. Sleep apnea is characterized by multiple respiratory pauses during sleep. These pauses, or apneas, are defined as the complete cessation of airflow measured at the level of the nose and mouth lasting at least 10 seconds. 36 The duration of most apneic events exceeds this minim u m criterion. The average duration of apneic events in an individual with sleep apnea is between 30 and 40 seconds, and there have been documented events lasting as long as 3 minutes. 3s Partial reductions in airflow are known as hypopneas. Hypopneas are defined as the reduction of airflow measured at the level of the nose and mouth lasting at least 10 seconds. They are associated with oxygen desaturation and/or evidence of electroencephalographic (EEG) or e l e c t r o m y o g r a p h i c (EMG) arousal. The mean duration of hypopneic events in an individual with sleep apnea tends to be similar to the duration of apneic events. Obstructive apneas and hypopneas result from similar mechanisms that impede airflow during sleep. Consequently, individuals with sleep apnea often have both apneic and hypopneic events during the sleep period. Another pattern of sleep-disordered breathing that has been recently described is known as upper airway resistance. 39"4~ This disturbance is associated with modest reductions in airflow during sleep that often are not detected by conventional recording methods. Measures of intraesophageal pressure may be required to detect the subtle respiratory characteristics of upper airway resistance. These changes in respiration can result in EEG arousals during sleep that are similar to those seen in sleep apnea. Arousals as short as 3 seconds may be characteristic of upper airway resistance in some cases. Episodes of upper airway resistance may occur in patients with sleep apnea, although the upper airway resistance syndrome has been found to occur independently of sleep apnea. Individuals with sleep apnea experience multiple respiratory events during sleep. These events recur throughout the sleep period, and m a y w o r s e n during REM s l e e p y A minimum of five apneic or hypopneic events per hour of sleep is required to diagnose sleep apnea 16 and, therefore, at least 40 events should be detected during a normal 8-hour sleep recording. However, most people with sleep apnea have many more events. It has been found that the average number of apneic events per hour of non-REM sleep is 65 (range, 48 to 79), and the average number of apneic events per hour of REM slee~ is 42 (range, 17 to 90) in patients with sleep apnea. The recurrence of respiratory events during the sleep period appears to have two main consequences. It results in sleep fragmentation and intermittent transient declines in oxygen saturation. Sleep fragmentation can be so severe that it interferes with sleep architecture and with the occurrence of delta and REM sleep. 42 There seems to be a relationship between sleep fragmentation and the severity of daytime sleepiness associated with sleep apnea. 43-45 Oxygen desaturation may possibly contribute to complaints of daytime sleepiness, but is more likely a contributor to the cognitive deficits seen in some patients with sleep apnea. 46 CLINICAL POLYSOMNOGRAPHY
The diagnosis of sleep apnea syndrome is not made exclusively on the basis of respiratory disturbance during sleep. There are clinical signs and symptoms that define this disorder (see Table 1). Perhaps the two most common signs are snoring and excessive daytime sleepiness. Virtually all patients with obstructive sleep apnea snore, with 94% reporting the development of loud snoring before the age of 21 years. 41 Snoring is frequently loud and interrupted by snorts or other unusual sounds. It is commonly a source of annoyance or embarrassment, and can be quite disturbing to a bed partner. Many individuals with sleep apnea have been evicted from their bedrooms because of loud snoring, and some can relate memorable stories of disturbing others in adjoining rooms or apartments. Excessive daytime sleepiness is considered the primary daytime manifestation of sleep apnea. 47 Subjective complaints of daytime sleepiness are common among individuals with sleep apnea who often report drowsiness, napping, or falling asleep at inappropriate times. When given the opportunity to sleep during the day on the multiple sleep latency test (MSLT), individuals with sleep apnea have been shown to have a mean latency to stage I sleep of 2.6 minutes across four naps, showing that this group of patients is excessively sleepy during the day. 48 It must be kept in mind that there is variability among individuals with respect to the severity of daytime sleepiness and the likelihood that they will report these problems to a physician. Mild symptoms such as fatigue or the tendency to doze in sedentary situations may be the only evidence of daytime sleepiness. These symptoms may not be immediately recognized as problems, 49 and can be easily dismissed if the patient is not questioned carefully. Fatigue-related cognitive impairment may reveal itself as occasional attention or memory lapses, 46 which may be another indicator of daytime sleepiness. Severe symptoms of sleepiness are often characterized by reports of difficulty sustaining alertness in virtually any situation, with some patients reporting that they fall
asleep at work, while socializing, at meal times, or w h e n operating a motor vehicle. The latter has been documented by studies of actual and simulated driving showing that individuals with sleep apnea perform more poorly than normal controls, s~ Severe daytime sleepiness can be debilitating because of its impact on social and occupational functioning, and can result in the risk of accident or injury caused by performance failure. Other common symptoms of sleep apnea are listed in Table 1. Sleep apnea presents a serious health risk. Hypertension is common. Podszus et a152 have reported that the prevalence of systemic h y p e r t e n s i o n averaged 58% among 461 sleep apnea patients evaluated in four studies. 53-56 The occurrence of hypertension correlates with the risk factors commonly associated with sleep apnea, especially age and weight. These findings are complemented by sleep laboratory studies of hypertensive patients with no sleep complaints showing that up to one half meet minimal criteria for the diagnosis of sleep apnea, and one third have apnea indices 920. 57 Approximately 48% of patients with sleep apnea have cardiac arrhythmias. 5s The most c o m m o n types of cardiac events observed are premature ventricular contractions and sinus arrest between 2.5 and 13 seconds in duration. 41 In some patients, transient periods of bradycardia occur during apneic or hypopneic events, followed by tachycardia w h e n respiration resumes. Oxygen desaturation during the night can lead to hypoxemia, and there have been reports of seizures occurring in association with desaturation. 41 The frequent desaturation associated with sleep apnea occasionally results in polycythemia. One evaluation of 1,000 patients found that 7% of those with unexplained polycythemia had sleep apnea. 36 One of the most important health risks associated with sleep apnea is increased mortality. 24"59 In a 9-year longitudinal study of untreated patients with sleep apnea, 6~ it was found that those with 20 or more apneic events per hour of sleep had a high mortality rate, with a cumulative probability of survival of only 0.63, whereas those with fewer than 20 had a cumulative probability of survival of 0.96. These data underscore the need for the early detection and treatment of sleep apnea.
TABLE 1. Symptoms of Obstructive Sleep Apnea Nighttime symptoms Loud, bothersome snoring Witnessed apneas Awakenings secondary to gasping for air/choking Awakenings associated with a sense of dread or anxiety Restless or fitful sleep Nocturnal or morning confusion (sleep drunkenness) Polyuria Daytime symptoms Morning sluggishness, fatigue Excessive daytime sleepiness Dry mouth/sore throat on awakening Early morning headaches Impaired memory Difficulty concentrating Personality changes such as irritability, anxiety, or depression Decreased motivation or "laziness" Diminished libido Associated physical symptoms/findings Cardiac arrhythmia Hypertension Stroke Angina Peripheral edema Polycythemia Hypothyroidism Erectile dysfunction (men)
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PREOPERATIVE EVALUATION OF SNORING AND SLEEP-RELATED BREATHING DISORDERS The evaluation of snoring and sleep-related breathing disorders begins with a thorough diagnostic interview. The presence of loud snoring alone is not pathognomonic of sleep apnea or other respiratory disturbance during sleep. However, snoring that occurs in association with obesity or other associated features (see Table 1) may be indicative of a serious sleep-related breathing disorder. It is critically important that a careful inquiry be made during consultation because many patients will deny the presence of clinically significant symptoms. Interview of the patient's spouse or bed partner often yields helpful information regarding nighttime symptoms, daytime symptoms, and associated features. The American Thoracic Society and the American Sleep Disorders Association are currently establishing standards of practice for the evaluation of sleep-related breathing disorders. No guidelines have been released at this time, but the serious health and safety risks associated with sleep apnea syndrome dictate that practitioners exercise caution and thor223
oughness in the evaluation and follow-up of snoring and sleep-related breathing disorders. Snoring, the warning signal that often prompts the patient to seek medical care, may be eliminated by procedures such as LAUP without significant impact on serious breathing disorders such as upper airway resistance or sleep apnea syndrome. The diagnosis of sleep-related breathing disorders is made using standard all-night polysomnography (Level I polysomnography, see Table 2). Polysomnography is usually performed in a sleep laboratory environment, although advances in technology have made it possible to perform this procedure at the patient's home or hospital bedside. The essential feature of polysomnography is the EEG, which is usually obtained from parietal leads placed in the C 3 or C 4 positions, and is used to determine the occurrence of wakefulness and the distinctive patterns of brain electrical activity that are characteristic of sleep. Relaxed wakefulness is characterized by lowvoltage fast EEG activity in the 8- to 13-Hz range. This is usually observed just before sleep onset and during awakenings. There are five stages of sleep. 61 Stage I sleep may be associated with the appearance of slow, rolling eye movements, and is characterized by low voltage EEG activity in the 4- to 7-Hz range. Stage I is a transitional stage of sleep that typically occurs at sleep onset, during sleep stage shifts, and after arousal. This is important because patients with sleep-related breathing disorders often have an elevated percentage of stage I sleep caused by respiratory events. Stage II sleep is characterized by low-voltage mixed EEG activity punctuated by phasic events k n o w n as k-complexes and sleep spindles. A k-complex is a sharp negative wave i>75 p~V that is immediately followed by a sharp positive wave. It is typically about 0.5 seconds in duration. A sleep spindle is a burst of fast EEG activity in the 12- to 15-Hz range that lasts at least 0.5 seconds. Stage II sleep comprises the majority of the night for most healthy adult sleepers. Stages III and IV sleep, otherwise known as slow-wave sleep or delta sleep, are characterized by high amplitude (>75 ~V), low frequency (1 to 3 Hz) waves. Delta sleep usually comprises less than 20% of the sleep period in healthy young adults, but is thought to be associated with deep and restful sleep. REM sleep is characterized by a low-voltage, mixed frequency EEG with occasional sawtooth waves that is accompanied by the appearance of phasic rapid conjugate eye movements and a tonic decrease in muscle tone.
There is an organization to nighttime sleep. Figure 1A shows the sleep architecture of a healthy young adult sleeper. Note that the subject begins the night with a brief episode of stage I sleep, which cascades into stages II, III, and IV sleep. The first REM period, which is brief, occurs approximately 90 minutes after sleep onset. This pattern, k n o w n as a sleep cycle, repeats itself multiple times over the course of the night. As the sleep period continues, the percentages of stages III and IV (delta) sleep normally decline and the percentage of REM sleep increases. The organization of nighttime sleep is critical to the evaluation of snoring and sleep-related breathing disorders because these disorders often disrupt or fragment the normal architecture of sleep. Figure 1B is a representation of sleep architecture in a patient with severe obstructive sleep apnea. Note the frequent shifts into stage I sleep, the low amounts of delta and REM sleep, and the fragmentation of REM sleep during the sleep period. When polysomnography is used clinically to detect sleep-related breathing disorders, multiple variables are measured. Standard measures are those performed in standard level I polysomnography (Table 2). These recordings are sufficient to quantify and characterize sleep stages and architecture as well as the occurrence, nature, and severity of episodes of apnea, hypopnea, and possibly upper airway resistance. The key diagnostic indicators used to determine the presence and severity of a sleep-related breathing disorder include the number of awakenings, n u m b e r of arousals, and sleep efficiency (the percentage of time in bed that is spent asleep). These measures indicate the degree of sleep fragmentation that may be caused by respiratory disturbance. Sleep-stage percentages provide a measure of the disruption of sleep architecture. As the severity of the disorder increases, the percentage of stage I sleep increases, and the percentages of delta and REM sleep tend to decrease. Measures of airflow and respiratory effort are used to detect respiratory events, which are often reported in the apnea/hypopnea index or respiratory disturbance index. These values indicate the average number of apneic and hypopneic events per hour of sleep. Baseline, average, and nadir S a O 2 values during desaturation provide a measure of apnea severity and hypoxemia during sleep. These values are often used to determine the number of times that the SaO 2 decreases below normal, which is considered to be a n S a O 2 level of 90%. Finally, the elec-
TABLE 2. Diagnostic Studies for Snoring and Sleep-Related Breathing Disorders Level I Standard Polysomnography
Level IA Standard Portable Polysomnography
Level II Comprehensive Portable Polysomnography
Level III Modified Portable Sleep Apnea Testing
Parameters
Minimum of seven, including EEG (C4-A1 or C3-A2), EOG, chin EMG, ECG, airflow, respiratory effort, oxygen saturation
Minimum of seven, including EEG (C4-A1 or C3-A2), EOG, chin EMG, ECG, airflow, respiratory effort, oxygen saturation
Minimum of seven, including EEG (C4-A1 or C3-A2) EOG, chin EMG, ECG, airflow, respiratory effort, oxygen saturation
Body position
Documented or objectively measured EMG or motion sensor desirable but optional In constant attendance Possible Laboratory
Documented or objectively measured EMG or motion sensor desirable but optional In constant attendance Possible Laboratory/home/institution
May be objectively measured EMG or motion sensor desirable but optional Not in attendance Not possible Home/institution
Minimum of four, including ventilation (at least two channels of respiratory movement, or respiratory movement and airflow), heart rate or ECG, oxygen satu ration May be objectively measured May be recorded
Leg movement Personnel Interventions Location
Not in attendance Not possible Home/institution
Abbreviations: EOG, electrooculogram; ECG, electrocardiogram. Adapted and reprinted with permission.63
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FIGURE 1. (A) Sleep architecture in a healthy young adult. The night is initiated with a brief period of stage I sleep, followed in orderly succession by stages II, III, IV, and subsequent REM. It is normal for the percentage of delta sleep to decline and the percentage of REM sleep to increase across the night. (B) Sleep architecture in a patient with severe obstructive sleep apnea. There are multiple arousals and brief awakenings secondary to apneas, hypopneas, and upper airway resistance. This results in sleep disruption and dramatic reductions in the percentages of delta and REM sleep. It is not uncommon for REM sleep periods to be fragmented across the night because of worsening respiration often seen in this stage. trocardiogram serves as a measure of cardiac arrhythmias that are commonly observed in patients with sleep apnea. In addition to these measures obtained at night, it is sometimes useful to have data from the MSLT. The MSLT is a test of daytime sleepiness that provides the patient with multiple scheduled opportunities to nap during the day. Latency to sleep onset for each nap period is calculated and an average is obtained. This average is compared with normative data to determine if the patient is pathologically sleepy. Healthy normal subjects have a mean sleep latency of between 10 and 20 minutes, and many subjects will not fall asleep at all. Mean latencies of less than 5 minutes are indicative of a pathological degree of daytime sleepiness. 62 This finding may be crucial in deciding whether to treat mild cases of sleep-related breathing disorders. There are minimal acceptable standards for clinical polysomnography. We believe that standard, level I polysomnography or its equivalent (level IA) must be used for the evaluation of snoring and sleep-related breathing disorders (see Table 2). Unattended portable recording (levels II and III polysomnography) offers conZAMMIT ET AL
venience, accessibility, and may be available at lower cost than standard p o l y s o m n o g r a p h y . H o w e v e r , these types of recording have not been adequately validated, and their potential advantages must be weighed against the possibility of missed or inaccurate diagnoses. 63 This is especially true in patients with mild, moderate, or atypical sleep-related respiratory disturbances that may not be detected by levels II or III p o l y s o m n o g r a p h y . The American Sleep Disorders Association Standards of Practice Committee currently recommends that portable studies not be used for loud snoring or the routine assessment of obstructive sleep apnea. 64 It must be emphasized that snoring and sleep-related breathing disorders also cannot be reliably evaluated using some common alternative techniques. These techniques include daytime nap or abbreviated nighttime studies. Such studies may be useful in detecting some severe cases, but may fail to detect mild to moderate cases. Neither provides a clear indication of the severity of the disorder or its impact on nighttime sleep. Overnight oximetry is not considered a sufficient measure because apneic and hypopneic events commonly occur without desaturation or with minimal (<4%) desaturation, and the diagnosis may be missed. Audio tape cannot be used to discriminate between normal breathing, snoring, and sleep apnea because breath or snoring sounds may persist during periods of hypopnea or upper airway resistance, yielding a false-negative result. It is not clear if any of these measures can be used as part of a screening process before polysomnography. They may yield misleading information that shapes the physician's impression of the patient and leads to a deviation from appropriate diagnostic procedures.
POSTOPERATIVE FOLLOW-UP Postoperative follow-up with polysomnography is an important consideration for patients who have undergone upper airway surgery for snoring or sleep-related breathing disorders. If surgery was performed to treat primary snoring as documented by clinical polysomnography, postoperative follow-up in the sleep laboratory may not be necessary. However, long-term office follow-up is advised to ensure that sleep-related breathing disorders do not develop in the absence of snoring. It is critical to avoid the development of silent sleep apnea, which potentially increases morbidity and mortality without warning the patient. This is especially important to consider as the patient ages or increases in body weight. When upper airway surgery is performed as a treatment for sleep apnea or another sleep-related breathing disorder, follow-up polysomnography is crucial to determine treatment efficacy, as well as the need for adjunctive treatments (e.g., nasal continuous positive airway pressure). All patients who have been treated for a sleep-related breathing disorder should be seen periodically for followup to ensure that daytime symptoms have not returned and that there is no impairment in daytime alertness or functioning.
CONCLUSION The development of new laser-assisted surgical techniques for the treatment of snoring and sleep-related breathing disorders has led to the need for otolaryngolo225
gists to obtain preoperative sleep laboratory evaluation of their patients. Careful evaluation includes history and physical examination, as well as clinical polysomnography. The appropriate use of polysomnography will contribute to the safe and appropriate application of surgical procedures, reliable measures of treatment outcome, and the identification of patients who require mechanical or other treatments for sleep-related breathing disorders.
ACKNOWLEDGMENT The authors thank Sigurd H. Ackerman, MD, for reviewing the manuscript.
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