- Email: [email protected]
The sleep apnea syndrome. Part I: Diagnosis
LABIALPLATEMAJORCONNECTOR
dibulectomy patient. The basic principles of support, retention, and stability should be followed to provide a more rigid design of the prosthesis. The labial plate provides advantages over the labial bar and should be considered a favorable major connector. REFERENCES 1. Girardot RL. History and development of partial denture design. J Am Dent Assoc 1941;28:1399-1408. 2. Roach EF. Mouth survey and design of partial dentures. J Am Dent Assot 1934;21:1166-76.
The sleep apnea syndrome. Jack B. Meyer,
Jr., D.M.D.,*
and Rodney
Part
3. Kelly EK. Full and partial dentures after extensive bone grafts to the mandible. Dent Dig 1950;56:159-64. 4. Smyd ES. Mechanics of dental structures: guide to teaching dental engineering at the undergraduate level. J PROSTNET DENT 1952;2:668-92.
Reprintrequeststo: DR. JACK W. MARTIN UNIVERSITY OF TEXAS SYSTEM CANCER CENTER M. D. ANDEMON HOSPITAL 6723 BERTNER AVE. HOUSTON, TX 77030
I: Diagnosis
C. Knudson,
D.M.D., M.S.**
Wilford Hall U.S. Air Force Medical Center, San Antonio, Tex. Part I of this two-part article presents a review of the symptoms, pathophysiology, and diagnosis of the sleep apnea syndrome. The more common obstructive type is characterized by disturbed sleep and daytime hypersomnolence. Subjective signs and symptoms should be correlated with objective findings by way of polysomnography (sleep study) to confirm the diagnosis and determine the severity of obstructive sleep apnea. Electrocardiographic monitoring during polysomnography has revealed potentially life-threatening arrhythmias during sleep. Differential diagnosis should include central sleep apnea and narcolepsy to avoid inappropriate therapy and worsening of symptoms. (J F'ROSTHET DENT 1989$2:675-B.)
S
leep apnea syndrome is a relatively common and potentially life-threatening disorder. Heightened public awareness, more frequent recognition by health care providers, and sophistication in diagnostic instrumentation, have led to a dramatic increase in the number of diagnosed patients. The increasing demand for noninvasive treatment modalities, including intraoral prostheses, should motivate dentists to become more aware and knowledgeable of this disabling syndrome. In the late 19709, sleep apnea was estimated to affect approximately 50,000 individuals. This figure is now acknowledged as a gross underestimation; the actual figure is projected to be one million or m0re.l This figure includes more than 3% of men from 40 to 60 years of age.2 Even though sleep apnea syndrome tends to be more prevalent in obese men,3 reported cases in men of normal weight and women have increased.
The views expressed herein are those of the authors and do not necessarily reflect the views of the United States Air Force, the United States Army, or the Department of Defense. *Lieutenant Colonel, U.S. Army, DC; Fellow, Maxillofacial Prosthetics. **Lieutenant Colonel, U. S. Air Force, DC; Assistant Chairman for Maxillofacial Prosthetics. 10/l/15824
THEJOURNALOFPROSTAETWDENTISTRY
Much controversy exists over the modality of treatment best suited for patients suffering from this disorder and the ability to predict long-term success. Part I of this article presents a review of the sleep apnea syndrome, its pathophysiology, and the methods of diagnosis. The various options advocated for the treatment of sleep apnea and their complications will be discussed in Part II. Most important, the need for a multidisciplinary approach to the diagnosis and treatment of this syndrome, particularly obstructive sleep apnea (OSA), is needed to obtain timely and effective relief of symptoms. The sleep apnea syndrome, first described by Gastaut,4 is a disorder associated with repetitive cessation of breathing during sleep. Sleep apnea is defined as 30 or more apneic episodes (the cessation of airflow at the mouth and nose for more than 10 seconds) occurring during 7 hours of nocturnal sleep.2*5 In the symptomatic patient, apneic episodes last on average 20 to 60 seconds and may occur as frequently as 200 to 600 times a night. Obstructive, central, and mixed patterns of sleep apnea are possible. The most common form is obstructive sleep apnea, also known as occlusive apnea, which is characterized by cessation of airflow
because of upper airway obstruction
with the
presence of simultaneous respiratory effort. This respiratory effort continues despite obstruction until the individual is aroused
from sleep.
675
MEYER
Central sleep apnea is characterized by simultaneous cessation of both airflow and respiratory effort. Most patients suffering from central apneas also have intermittent obstructive episodes. When more than 55 % of events are central in nature, the form of apnea is defined as central6 Central sleep apnea is most often caused by ‘bulbar poliomyelitis, encephalitis, brainstem neoplasm, brainstem infarction, spinal cord surgery, and cervical cordotomy.7 In mixed apnea, episodes are accompanied by no respiratory effort initially, followed by respiratory muscle movement, and finally, by airflow. This article concentrates mainly on the obstructive type because it is more prevalent and tends to be more responsive to conservative management.
SIGNS
AND
SYMPTOMS
The most common complaints of patients suffering from OSA are hypersomnolence (excessive daytime sleepiness) and disturbed sleep characterized by heavy snoring and frequent arousal. After a night of restless sleep, patients often complain of morning headaches and nausea, which may be a result of nocturnal CO2 retention. Other complaints include intellectual deterioration, tempermental behavior, depression, and severe anxiety. Job performance may be affected as poor judgments at work may lead to occupational accidents. Impotence and nocturnal bed-wetting have been reported in some patients.
PATHOPHYSIOLOGY The suction forces generated during inspiration and gravitational forces (particularly the weight of the tongue and mandible) are normally resisted by residual muscle tone (especially in the genioglossus muscle) and elasticity of the upper airway musculature. When loss of muscle tone occurs, as during sleep, a narrowing of the airway increases resistance. At some point, obstruction is possible as the tongue and soft palate are literally sucked onto the poste-, rior pharyngeal wall. With the upper airway muscles in a relaxed state, partial or complete obstruction of both the oropharynx and nasophaynx occurs. Occlusion of the airway persists because the negative inspiratory pharyngeal pressure is greater than the forces that serve to dilate the airway. During this silent period, which may last from 36 to 90 seconds, uncoordinated abdominal and chest movements are noticeable. Respiratory drive and movement continue against this increased pressure until enough respiratory effort is generated to cause arousal and activate the upper airway muscles to release the obstruction.2p 7 A loud snore typically marks the onset of respiration. Many individuals snore without manifesting the symptoms of obstructive sleep apnea. Normal snoring, however, is more of a nasal phenomenon than the pharyngeal-type snoring typically exhibited by sleep apnea patients. The 676
AND
KNUDSON
pharyngeal type of snoring may precede the development of clinical symptoms by many years. The tone of the genioglossus muscle must be maintained to prevent passive collapse against the palate. Some inves-’ tigators have shown, by way of electromyographic (EMG) studies, that the genioglossus muscle exhibits abnormally low levels of muscle activity during sleep.8 The role of the ’ tongue in the development of OSA has been debated because endoscopy has not always confirmed passive contact of the tongue in pharyngeal closure.g The site of upper airway occlusion may vary. This variance makes treatment selection and predictability difficult. In obese individuals, the loss of airway patency is often attributed to the accumulation of perioropharyngeal fat. Obesity, in itself, seldom causes OSA. Rather, the development of the syndrome seems to be related to lack of control of the oral and pharyngeal musculature. A single mechanism may not apply to all patients. Pathophysiologic changes occuring during OSA include] hypercapnia, hypoxemia, and pulmonary and systemic hypertension. Eventually the hypoxemia triggers an increase in motor activity of the upper airway muscles, which ulti-‘ mately dilates the airway and results in a brief awakening and resumption of ventilation. Patients usually cannot remember the periods of arousal because they quickly fall asleep. Sleep is short, however, because the alternating episodes of apneas and arousals can occur as frequently as every 90 seconds. This sequence represents significant episodes of oxygen desaturation and cardiopulmonary changes potentially accounting for 50 % of a night’s sleep.2 The progressive form of OSA may lead to polycythemia and right-sided heart failure as a result of the severe states of nocturnal hypoxemia and pulmonary hypertension. In addition, various forms of cardiac dysrhythmias including premature ventricular contractions (PVCs), potentially lethal ventricular tachycardias, and atrioventricular (AV) blocks can occur in association with apneic periods.‘O
PHYSICAL
FINDINGS
Many sleep apnea patients are overweight, tending to have a short neck and strong masticatory musculature. This physical profile is not universal, however, because OSA can occur in normal-weight individuals. By definition, obesity is a body weight at least 20 % over ideal for height, age, and sex.ll Morbid obesity represents a body weight greater than 100 pounds over the ideal. It has been reported that approximately 40% of sleep apnea patients are approximately 30% over ideal body weight, and that up to 70% of patients are 20% over ideal weight.3 The morbidly obese, somnolent, hypoventilating “Pickwickian” patient, however, represents only a small percentage (5%) of patients who have obstructive sleep apnea. Although obesity is a common finding, few obese patients actually develop this disorder. Obesity in itself does not mean that redundant tissues are present in the oropharynx.
DECEMBER
1989
VOLUME
62
NUMBER
6
SLEEP
APNEA
SYNDROME.
PART
I
Routine examination may reveal structural abnormalities, including tonsillar hypertrophy, an enlarged uvula, macroglossia from hypothyroidism or acromegaly, a deviated nasal septum, retrognathia and micrognathia, and possible temporomandibular joint derangements. These abnormalities contribute to further narrowing and collapse of the nasopharynx and oropharynx, because of a progressive increase in negative pressure. Another reported finding common to most of these patients is a hyperactive gag ‘reflex.iO
SLEEP
PHYSIOLOGY
The normal sleep cycle consists of two phases, nonrapid eye movement (NREM) and rapid eye movement (REM) sleep.12vl3 The first stage, NREM sleep, is divided into four levels. The first level represents the transition period between wakefulness and sleep when the muscles relax and the pulse slows. During the second level of NREM sleep, ‘the eyes begin to roll from side to side and, if open, the individual is incapable of sight. In the third level, intermediate sleep, the muscles are more relaxed and breathing be’ comes regular. The final level of NREM sleep is the deepest form, which often lasts 20 minutes or more. This “delta” sleep is longer in the first part of the night than toward the morning hours. Levels 3 and 4 of NREM sleep combined are often referred to as slow-wave sleep, because the bodily functions are almost totally under metabolic/spontaneous controls. Deep sleep progressively decreases with an increase in age. The next phase of sleep, REM sleep, is characterized by irregular heartbeats, blood pressure fluctuations, and irregular-rapid breathing. Synchronous eye movements occur as the eyes dart rapidly behind closed lids. During normal REM sleep, the EEG is desynchronized, resembling the state of wakefulness. Skeletal muscles are generally lacking in tone, particularly in the limbs. Because breathing is irregular during REM sleep, apneic episodes of 10 to 20 seconds in adults and up to 10 seconds in children are possible. During a normal 7- to 8-hour sleep period, REM sleep could occupy as much as 1.5 to 2 hours. The first REM period lasts approximately 10 minutes. There is a progressive lengthening of REM periods during normal sleep, with the cycle repeating itself every 90 minutes. As morning approaches, there tends to be less delta sleep and more REM sleep, which can last 30 to 40 minutes. Patients with sleep apnea tend to spend significantly reduced times in slow-wave sleep, particularly during level 4. The most prolonged apneas and most significant oxygen desaturations may occur in REM sleep.
DIAGNOSIS Laboratory
tests
Laboratory tests performed on patients with suspected OSA during waking hours are usually noncontributory to diagnosis. Arterial blood gases, electrocardiograms, and
THE
JOURNAL
OF PROSTHETIC
DENTISTRY
pulmonary function tests are often within normal limits. A complete blood count may reveal an elevated hematocrit, which may be the result of oxygen desaturation during sleep.i4
Polysomnography Measurements of ventilation, gas exchange, and cardiac rhythm must be made during sleep to confirm the diagnosis of sleep apnea. A polysomnogram performed in a sleep laboratory measures the number and length of apneic episodes, measures oxygen saturation, determines sleep stages, and detects arousals. The polysomnogram will also monitor airflow, respiratory effort, and heart rate. Polysomnography is best done at night with at least 4 hours of sleep time recorded. Monitoring daytime naps is not sufficient because the REM stage of sleep, where abnormalities are more likely to occur, may not be recorded. Most sleep studies are conducted on at least two consecutive nights. The first night allows the patient to accommodate to the laboratory environment. A single overnight study may suffice if the patient manifests an extreme form of sleep apnea. Extreme sleep apnea includes oxygen saturations that fall below 60 % , an apneic index greater than 50, prolonged apnea lasting more than 45 seconds, and concurrent cardiac arrhythmias.2s lo Sleep staging is determined by using an electroencephalogram (EEG), right and left electro-oculograms (EOGs), and an EMG of the digastric muscle. Simultaneous EEG, EOG, and EMG tracings are used to distinguish between sleep and wakefulness, to detect arousals, and to correlate respiratory abnormalities with periods of REM and NREM sleep. Air exchange at the mouth and nose is monitored with a temperature-sensitive flow thermistor. The thermistor will reveal the occurrence of apneic episodes. For a diagnosis of sleep apnea, there must be 30 episodes of apnea per night of sleep, each lasting more than 10 seconds. However, it is not unusual for normal individuals to exhibit up to 30 apneic events per night’s sleep. Most patients who manifest the syndrome of sleep apnea may actually demonstrate hundreds of apneic events per night. Respiratory effort is evaluated by using surface intercostal electromyography. Abdominal or thoracic strain gauges provide movement tracings during respiratory efforts. When there is a simultaneous pause of airflow and thoracic or abdominal movement, a central type of sleep apnea has occurred. If airflow ceasesbut respiratory effort continues, sleep apnea of the obstructive type has most likely occurred. Gas exchange can be evaluated with an ear or finger oximeter, which measures changes in arterial oxygen tension or saturation. Mild oxygen desaturation occurs in normal sleep. A 5% decrease in arterial oxygen saturation may occur during significant periods of apnea or hypopnea. In sleep apnea patients, oxygen saturation often falls below the 80% level. In severe forms where apneic periods are prolonged, saturation levels may drop to 60% .2 677
An electrocardiogram is used to monitor possible cardiovascular abnormalities during the sleep cycle. Marked sinus arrhythmias may occur with sleep apnea and are frequently associated with potentially life-threatening tachycardias and bradycardias. Tilkian et all5 used the Holter monitor to evaluate cardiac changes in 15 men with obstructive sleep apnea. Their studies revealed the occurrence of sinus arrhythmias, extreme sinus bradycardias (less than 30 beats per minute), asystole lasting from 3 to 7 minutes, complex ventricular tachycardias, and seconddegree AV blocks. These changes were not evident during waking hours. The most significant electrocardiographic finding for obstructive sleep apnea seems to be an exaggerated sinus arrhythmia. Arrhythmia was recorded in all but one of the subjects examined by Tilkian et all6 Another common finding was a cyclic pattern characterized by a progressive sinus bradycardia during the apnea followed by an abrupt reversal and sinus acceleration when ventilation resumed. The authors postulated these arrhythmias were not caused by sinoatrial (SA) or atrioventricular (AV) nodal disease but were the result of functional and reversible abnormalities precipitated by sleep-related autonomic responses. They suggested that the inspiratory effort against an obstructed airway activated vagal parasympathetic impulses that led to sinus bradycardias. Hypoxia and acidosis may also increase sympathetic tone, thereby giving rise to possible sinus tachycardias, PVCs, and ventricular tachycardias. A study by Tsutomd6 reported electrocardiographic data on six patients suspected of having OSA. All were young obese individuals who had no history of ischemic heart disease. All had significant cardiac arrhythmias during sleep. Atropine administration was ineffective in reversing the parasympathetic response to apneas. This finding was in contrast to those of Tilkian et all5 in which atropine arrested the sinus bradycardia in patients tested.
Differential
diagnosis
Pertinent sleep-related disorders that should be delineated from OSA are central sleep apnea and narcolepsy. A central apneic event differs from the obstructive or mixed apnea by the absence of ventilatory attempts against an occluded airway.6 It is not uncommon for patients demonstrating central apneas to have accompanied obstructive events. The most common event that occurs in the central apnea patient is of the mixed type. This event is characterized by a central respiratory pause, followed by an obstructive ventilatory effort. This sequence suggests the presence of overlapping mechanisms between the various forms of apnea. Clinical characteristics of central sleep apnea consist of complaints of insomnia, frequent awakenings during the night, and depression. Normal body weight is common compared with that of patients with OSA. Daytime hypersomnolence is rare. Other differences from OSA include
678
only mild and intermittent snoring and minimal sexual dysfunction. Finally, central sleep apnea is rare in adults. A common sleep disorder, narcolepsy is often confused, with the sleep apena syndrome because hypersomnolence is a common feature of both disorders. Other significant symptoms of narcolepsy include cataplexy (abrupt loss of muscle tone), hallucinations, and sleep paralysis (total inability to move any muscles when falling asleep or waking up). Narcoleptic patients are generally lethargic and feel exhausted. The narcoleptic patient is often suddenly overwhelmed by the strong urge to sleep. These “sleep attacks” are usually brief, consuming less than 30 minutes when they occur. The patient usually feels refreshed after such naps. OSA patients usually report taking longer naps that fail to refresh. Unlike patients with OSA, narcoleptics usually experience the onset of symptoms as adolescents or young adults. Progressive worsening of symptoms is not characteristic 04 narcolepsy, with maximum severity attained by 30 to 35 years of age. The difficulty in diagnosis stems from the possibility that both disorders can coexist. Fortunately,, sleep apnea in narcoleptics tends to occur in milder forms. A misdiagnosis of narcolepsy and subsequent treatment with stimulants will lead to progressive worsening of ventilatory failure in the sleep apnea patient. The multiple sleep latency test may be helpful in differentiating sleep apnea from narcolepsy. The diagnosis of narcolepsy is made by the finding of a REM period at the beginning of sleep. Narcolepsy is a lifelong illness with no known cure. Antidotal treatment includes the administration of stimulants to lessen daytime hypersomnolence and sleep attacks. Antidepressents are helpful to control cataplexy, sleep paralysis, and hallucinations. Correlation of the clinical course, as described by the patient, with the results of a complete examination, polysomnogram, and multiple sleep latency test will assist in distinguishing between the various sleep-induced disorders. Additional tests. Once a diagnosis of OSA has been established, a complete blood count may reveal secondary polycythemia. Serum electrolytes may also show bicarbonate retention due to carbon dioxide retention. Thyroid function studies may be considered, to rule out hypothyroidism as the etiology. Examination of the upper airway by an otorhinolaryngologist is mandatory to rule out anatomic abnormalities of the nose, pharynx, hypopharynx, and larynx that may either cause the obstruction or contribute to the severity of OSA. A congenitally malformed glottis, hypopharyngeal mass, or lymphomas involving Waldeyer’s tonsillar ring have also been reported in the etiology of hypersomnolence.17 Adults with small retrognathic mandibles and children with micrognathia as seen in the hereditary Pierre Robin syndrome may be predisposed to OSA.lsl lg OSA after par-
DECEMBER
1989
VOLUME
62
NUMBER
6
SLEEPAPNEASYNDROME.PARTI
tial mandibular resections has also been documented.20 Most of these postsurgical patients were found to have obtuse mentocervical angles and retruded tongues. Because the genioglossus muscle is not attached very far anteriorly, the tongue typically assumes a posterior posture. Tongue position often leads to obstruction during sleep.
5. 6. 7. 8. 9.
SUMMARY
10.
Obstructive sleep apnea tends to be a progressive disorder that varies in etiology and severity, making patient selection and treatment predictability difficult to assess. Even though middle-aged obese men have a greater susceptibility to OSA, it has been diagnosed in increased numbers of normal-weight individuals and women. Diagnostic tests including a polysomnogram are needed to establish a diagnosis and determine severity. Misdiagnosis and inappropriate therapy could lead to worsening of symptoms. A multidisciplined approach should be used to reach a diagnosis and establish a plan for appropriate therapy. Part II of this article will review the rationale, v benefits, and potential complications of the treatment modalities advocated for obstructive sleep apnea.
11. 12. 13. 14.
15.
diurnes at noctures due syndrome de Pickwick. Rev Nemo1 (Paris) 1965;112:568-79. Morgan EJ. Sleep apnea syndrome. W V Med J 1979;75:14-8. White DP. Central sleep apnea. Med Clin North Am 1985;69:1205-15. Weaver TE, Millman RP. Broken sleep. Am ,J Nuns 1986;88:146-50. Remmers JE, Degroot WJ, Sauerland EK. Upper airway obstruction during sleep: role of the genioglossus [Abstract]. Clin Res 1976;24:33. Borowicki B. Fibro-optic study of pharyngeal airway during sleep in patients with hypersomnia obstructive sleep apnea syndrome. Laryngoscope 1978;88:1310-3. Clark RW. Sleep apnea. Prim Care 1979;6:658-79. Wittels EW. Obesity and hormonal factors in sleep and sleep apnea. Med Clin North Am 1985;69:1265-77. Sleep: still a scientific mystery. Health Scene 1986;6:6-7. Hiller CF. Medical grand rounds: sleep apnea syndrome. J Arkansas Med Sot 1980;76:391-8. Yasas KM. Sophisticated technology not essential in diagnosis and treatment of sleep apnea. Respir Rev 1986;2:2-4. Tilkian AG. Sleep induced apnea syndrome-prevelance of cardiac arrhythmias and their reversal after tracheostomy. Am J Med 1977;63:348-
57. 16. Tsutomu I. Arrhythmias 17. Zorick F. Intensification
in sleep apnea. Am Heart J 1980;100:513-6. of excessive daytime sleepiness by lymphoma.
Sleep Res 1977;6:199. G, Di Donato G, Verucchi P, Cirignotti F, Mantovani M, Lugaresi E. Hypersomnia with periodic apneas in acquired micrognathia. Arch Neural 1976;33:769-76. and sleep ap19. Imes NK, Orr WC, Smith RO, Rogers RM. Retrognathia nea: a life-threatening condition masquerading as narcolepsy. JAMA 1977;237:1596-7. 20. Panje WR, Homes DK. Mandibuiectomy without reconstruction can cause sleep apnea. Laryngoscope 1984;94:1591-4. 18. Coccsgna
REFERENCES 1. Cartwright RD. The effects of a nonsurgical treatment for obstructive sleep apnea. JAMA 1982;248:705-9. 2. Waidhorn RE. Sleep apnea syndrome. AFP 1985;149:149-62. 3. Vollmer ME. The obstructive sleep apnea syndrome: pathophysiology, diagnosis and treatment. Ind Med 1987;80:1137-77. 4. Gestaut H. Etude polygraphique des manisfestations episodiques
Reprint requests to: DR. JACK B. MEYER, JR. 487 WHEATON FT. SAM HOUSTON,
TX
78234
A mouth splint for severe burns of the head and neck M. Sela, D.M.D.,* Hebrew
and I. Tubiana**
University-Hadassah
School
of Dental
Medicine,
Jerusalem,
Israel
An individual mouth splint device that applies continuous or intermittent pressure to stretch commissures and fibrotic muscles in patients treated for microstomia resulting from facial and neck burns is presented. After an individual lip tray is prepared, the method uses the impression and cast of the region of the lips to construct a pink acrylic resin splint. By using the device, split horixontally and activated with a Ryrx screw, an opening of 14 mm can be obtained within 2 weeks. The device is recommended as being easily constructed, inexpensive, almost painlessly inserted, and progressively activated. (J PROSTHET DENT 1989;62:679-81.)
B
urns of the head and neck region cause skin contractures, which if not prevented result in limitation of opening the mouth (Fig. l), damage to the orbicularis oris
*Senior Lecturer, **Certified Dental
Head, Maxillofacial Technologist.
Prosthetic
10/l/12142
THEJOURNAL
OF PROSTHETIC
DENTISTRY
Unit.
muscle, and inhibition of normal feeding, speech, and dental care.’ Microstomia develops if a preventive prosthesis is not used to stretch the contracted muscles or as a result of reconstructive surgery.2 Treatment may require the use of continuous or intermittent pressure by the splint during healing or therapy periods. The splint may be used in the prevention of early burn contracture of the mouth.3, 4
679
dibulectomy patient. The basic principles of support, retention, and stability should be followed to provide a more rigid design of the prosthesis. The labial plate provides advantages over the labial bar and should be considered a favorable major connector. REFERENCES 1. Girardot RL. History and development of partial denture design. J Am Dent Assoc 1941;28:1399-1408. 2. Roach EF. Mouth survey and design of partial dentures. J Am Dent Assot 1934;21:1166-76.
The sleep apnea syndrome. Jack B. Meyer,
Jr., D.M.D.,*
and Rodney
Part
3. Kelly EK. Full and partial dentures after extensive bone grafts to the mandible. Dent Dig 1950;56:159-64. 4. Smyd ES. Mechanics of dental structures: guide to teaching dental engineering at the undergraduate level. J PROSTNET DENT 1952;2:668-92.
Reprintrequeststo: DR. JACK W. MARTIN UNIVERSITY OF TEXAS SYSTEM CANCER CENTER M. D. ANDEMON HOSPITAL 6723 BERTNER AVE. HOUSTON, TX 77030
I: Diagnosis
C. Knudson,
D.M.D., M.S.**
Wilford Hall U.S. Air Force Medical Center, San Antonio, Tex. Part I of this two-part article presents a review of the symptoms, pathophysiology, and diagnosis of the sleep apnea syndrome. The more common obstructive type is characterized by disturbed sleep and daytime hypersomnolence. Subjective signs and symptoms should be correlated with objective findings by way of polysomnography (sleep study) to confirm the diagnosis and determine the severity of obstructive sleep apnea. Electrocardiographic monitoring during polysomnography has revealed potentially life-threatening arrhythmias during sleep. Differential diagnosis should include central sleep apnea and narcolepsy to avoid inappropriate therapy and worsening of symptoms. (J F'ROSTHET DENT 1989$2:675-B.)
S
leep apnea syndrome is a relatively common and potentially life-threatening disorder. Heightened public awareness, more frequent recognition by health care providers, and sophistication in diagnostic instrumentation, have led to a dramatic increase in the number of diagnosed patients. The increasing demand for noninvasive treatment modalities, including intraoral prostheses, should motivate dentists to become more aware and knowledgeable of this disabling syndrome. In the late 19709, sleep apnea was estimated to affect approximately 50,000 individuals. This figure is now acknowledged as a gross underestimation; the actual figure is projected to be one million or m0re.l This figure includes more than 3% of men from 40 to 60 years of age.2 Even though sleep apnea syndrome tends to be more prevalent in obese men,3 reported cases in men of normal weight and women have increased.
The views expressed herein are those of the authors and do not necessarily reflect the views of the United States Air Force, the United States Army, or the Department of Defense. *Lieutenant Colonel, U.S. Army, DC; Fellow, Maxillofacial Prosthetics. **Lieutenant Colonel, U. S. Air Force, DC; Assistant Chairman for Maxillofacial Prosthetics. 10/l/15824
THEJOURNALOFPROSTAETWDENTISTRY
Much controversy exists over the modality of treatment best suited for patients suffering from this disorder and the ability to predict long-term success. Part I of this article presents a review of the sleep apnea syndrome, its pathophysiology, and the methods of diagnosis. The various options advocated for the treatment of sleep apnea and their complications will be discussed in Part II. Most important, the need for a multidisciplinary approach to the diagnosis and treatment of this syndrome, particularly obstructive sleep apnea (OSA), is needed to obtain timely and effective relief of symptoms. The sleep apnea syndrome, first described by Gastaut,4 is a disorder associated with repetitive cessation of breathing during sleep. Sleep apnea is defined as 30 or more apneic episodes (the cessation of airflow at the mouth and nose for more than 10 seconds) occurring during 7 hours of nocturnal sleep.2*5 In the symptomatic patient, apneic episodes last on average 20 to 60 seconds and may occur as frequently as 200 to 600 times a night. Obstructive, central, and mixed patterns of sleep apnea are possible. The most common form is obstructive sleep apnea, also known as occlusive apnea, which is characterized by cessation of airflow
because of upper airway obstruction
with the
presence of simultaneous respiratory effort. This respiratory effort continues despite obstruction until the individual is aroused
from sleep.
675
MEYER
Central sleep apnea is characterized by simultaneous cessation of both airflow and respiratory effort. Most patients suffering from central apneas also have intermittent obstructive episodes. When more than 55 % of events are central in nature, the form of apnea is defined as central6 Central sleep apnea is most often caused by ‘bulbar poliomyelitis, encephalitis, brainstem neoplasm, brainstem infarction, spinal cord surgery, and cervical cordotomy.7 In mixed apnea, episodes are accompanied by no respiratory effort initially, followed by respiratory muscle movement, and finally, by airflow. This article concentrates mainly on the obstructive type because it is more prevalent and tends to be more responsive to conservative management.
SIGNS
AND
SYMPTOMS
The most common complaints of patients suffering from OSA are hypersomnolence (excessive daytime sleepiness) and disturbed sleep characterized by heavy snoring and frequent arousal. After a night of restless sleep, patients often complain of morning headaches and nausea, which may be a result of nocturnal CO2 retention. Other complaints include intellectual deterioration, tempermental behavior, depression, and severe anxiety. Job performance may be affected as poor judgments at work may lead to occupational accidents. Impotence and nocturnal bed-wetting have been reported in some patients.
PATHOPHYSIOLOGY The suction forces generated during inspiration and gravitational forces (particularly the weight of the tongue and mandible) are normally resisted by residual muscle tone (especially in the genioglossus muscle) and elasticity of the upper airway musculature. When loss of muscle tone occurs, as during sleep, a narrowing of the airway increases resistance. At some point, obstruction is possible as the tongue and soft palate are literally sucked onto the poste-, rior pharyngeal wall. With the upper airway muscles in a relaxed state, partial or complete obstruction of both the oropharynx and nasophaynx occurs. Occlusion of the airway persists because the negative inspiratory pharyngeal pressure is greater than the forces that serve to dilate the airway. During this silent period, which may last from 36 to 90 seconds, uncoordinated abdominal and chest movements are noticeable. Respiratory drive and movement continue against this increased pressure until enough respiratory effort is generated to cause arousal and activate the upper airway muscles to release the obstruction.2p 7 A loud snore typically marks the onset of respiration. Many individuals snore without manifesting the symptoms of obstructive sleep apnea. Normal snoring, however, is more of a nasal phenomenon than the pharyngeal-type snoring typically exhibited by sleep apnea patients. The 676
AND
KNUDSON
pharyngeal type of snoring may precede the development of clinical symptoms by many years. The tone of the genioglossus muscle must be maintained to prevent passive collapse against the palate. Some inves-’ tigators have shown, by way of electromyographic (EMG) studies, that the genioglossus muscle exhibits abnormally low levels of muscle activity during sleep.8 The role of the ’ tongue in the development of OSA has been debated because endoscopy has not always confirmed passive contact of the tongue in pharyngeal closure.g The site of upper airway occlusion may vary. This variance makes treatment selection and predictability difficult. In obese individuals, the loss of airway patency is often attributed to the accumulation of perioropharyngeal fat. Obesity, in itself, seldom causes OSA. Rather, the development of the syndrome seems to be related to lack of control of the oral and pharyngeal musculature. A single mechanism may not apply to all patients. Pathophysiologic changes occuring during OSA include] hypercapnia, hypoxemia, and pulmonary and systemic hypertension. Eventually the hypoxemia triggers an increase in motor activity of the upper airway muscles, which ulti-‘ mately dilates the airway and results in a brief awakening and resumption of ventilation. Patients usually cannot remember the periods of arousal because they quickly fall asleep. Sleep is short, however, because the alternating episodes of apneas and arousals can occur as frequently as every 90 seconds. This sequence represents significant episodes of oxygen desaturation and cardiopulmonary changes potentially accounting for 50 % of a night’s sleep.2 The progressive form of OSA may lead to polycythemia and right-sided heart failure as a result of the severe states of nocturnal hypoxemia and pulmonary hypertension. In addition, various forms of cardiac dysrhythmias including premature ventricular contractions (PVCs), potentially lethal ventricular tachycardias, and atrioventricular (AV) blocks can occur in association with apneic periods.‘O
PHYSICAL
FINDINGS
Many sleep apnea patients are overweight, tending to have a short neck and strong masticatory musculature. This physical profile is not universal, however, because OSA can occur in normal-weight individuals. By definition, obesity is a body weight at least 20 % over ideal for height, age, and sex.ll Morbid obesity represents a body weight greater than 100 pounds over the ideal. It has been reported that approximately 40% of sleep apnea patients are approximately 30% over ideal body weight, and that up to 70% of patients are 20% over ideal weight.3 The morbidly obese, somnolent, hypoventilating “Pickwickian” patient, however, represents only a small percentage (5%) of patients who have obstructive sleep apnea. Although obesity is a common finding, few obese patients actually develop this disorder. Obesity in itself does not mean that redundant tissues are present in the oropharynx.
DECEMBER
1989
VOLUME
62
NUMBER
6
SLEEP
APNEA
SYNDROME.
PART
I
Routine examination may reveal structural abnormalities, including tonsillar hypertrophy, an enlarged uvula, macroglossia from hypothyroidism or acromegaly, a deviated nasal septum, retrognathia and micrognathia, and possible temporomandibular joint derangements. These abnormalities contribute to further narrowing and collapse of the nasopharynx and oropharynx, because of a progressive increase in negative pressure. Another reported finding common to most of these patients is a hyperactive gag ‘reflex.iO
SLEEP
PHYSIOLOGY
The normal sleep cycle consists of two phases, nonrapid eye movement (NREM) and rapid eye movement (REM) sleep.12vl3 The first stage, NREM sleep, is divided into four levels. The first level represents the transition period between wakefulness and sleep when the muscles relax and the pulse slows. During the second level of NREM sleep, ‘the eyes begin to roll from side to side and, if open, the individual is incapable of sight. In the third level, intermediate sleep, the muscles are more relaxed and breathing be’ comes regular. The final level of NREM sleep is the deepest form, which often lasts 20 minutes or more. This “delta” sleep is longer in the first part of the night than toward the morning hours. Levels 3 and 4 of NREM sleep combined are often referred to as slow-wave sleep, because the bodily functions are almost totally under metabolic/spontaneous controls. Deep sleep progressively decreases with an increase in age. The next phase of sleep, REM sleep, is characterized by irregular heartbeats, blood pressure fluctuations, and irregular-rapid breathing. Synchronous eye movements occur as the eyes dart rapidly behind closed lids. During normal REM sleep, the EEG is desynchronized, resembling the state of wakefulness. Skeletal muscles are generally lacking in tone, particularly in the limbs. Because breathing is irregular during REM sleep, apneic episodes of 10 to 20 seconds in adults and up to 10 seconds in children are possible. During a normal 7- to 8-hour sleep period, REM sleep could occupy as much as 1.5 to 2 hours. The first REM period lasts approximately 10 minutes. There is a progressive lengthening of REM periods during normal sleep, with the cycle repeating itself every 90 minutes. As morning approaches, there tends to be less delta sleep and more REM sleep, which can last 30 to 40 minutes. Patients with sleep apnea tend to spend significantly reduced times in slow-wave sleep, particularly during level 4. The most prolonged apneas and most significant oxygen desaturations may occur in REM sleep.
DIAGNOSIS Laboratory
tests
Laboratory tests performed on patients with suspected OSA during waking hours are usually noncontributory to diagnosis. Arterial blood gases, electrocardiograms, and
THE
JOURNAL
OF PROSTHETIC
DENTISTRY
pulmonary function tests are often within normal limits. A complete blood count may reveal an elevated hematocrit, which may be the result of oxygen desaturation during sleep.i4
Polysomnography Measurements of ventilation, gas exchange, and cardiac rhythm must be made during sleep to confirm the diagnosis of sleep apnea. A polysomnogram performed in a sleep laboratory measures the number and length of apneic episodes, measures oxygen saturation, determines sleep stages, and detects arousals. The polysomnogram will also monitor airflow, respiratory effort, and heart rate. Polysomnography is best done at night with at least 4 hours of sleep time recorded. Monitoring daytime naps is not sufficient because the REM stage of sleep, where abnormalities are more likely to occur, may not be recorded. Most sleep studies are conducted on at least two consecutive nights. The first night allows the patient to accommodate to the laboratory environment. A single overnight study may suffice if the patient manifests an extreme form of sleep apnea. Extreme sleep apnea includes oxygen saturations that fall below 60 % , an apneic index greater than 50, prolonged apnea lasting more than 45 seconds, and concurrent cardiac arrhythmias.2s lo Sleep staging is determined by using an electroencephalogram (EEG), right and left electro-oculograms (EOGs), and an EMG of the digastric muscle. Simultaneous EEG, EOG, and EMG tracings are used to distinguish between sleep and wakefulness, to detect arousals, and to correlate respiratory abnormalities with periods of REM and NREM sleep. Air exchange at the mouth and nose is monitored with a temperature-sensitive flow thermistor. The thermistor will reveal the occurrence of apneic episodes. For a diagnosis of sleep apnea, there must be 30 episodes of apnea per night of sleep, each lasting more than 10 seconds. However, it is not unusual for normal individuals to exhibit up to 30 apneic events per night’s sleep. Most patients who manifest the syndrome of sleep apnea may actually demonstrate hundreds of apneic events per night. Respiratory effort is evaluated by using surface intercostal electromyography. Abdominal or thoracic strain gauges provide movement tracings during respiratory efforts. When there is a simultaneous pause of airflow and thoracic or abdominal movement, a central type of sleep apnea has occurred. If airflow ceasesbut respiratory effort continues, sleep apnea of the obstructive type has most likely occurred. Gas exchange can be evaluated with an ear or finger oximeter, which measures changes in arterial oxygen tension or saturation. Mild oxygen desaturation occurs in normal sleep. A 5% decrease in arterial oxygen saturation may occur during significant periods of apnea or hypopnea. In sleep apnea patients, oxygen saturation often falls below the 80% level. In severe forms where apneic periods are prolonged, saturation levels may drop to 60% .2 677
An electrocardiogram is used to monitor possible cardiovascular abnormalities during the sleep cycle. Marked sinus arrhythmias may occur with sleep apnea and are frequently associated with potentially life-threatening tachycardias and bradycardias. Tilkian et all5 used the Holter monitor to evaluate cardiac changes in 15 men with obstructive sleep apnea. Their studies revealed the occurrence of sinus arrhythmias, extreme sinus bradycardias (less than 30 beats per minute), asystole lasting from 3 to 7 minutes, complex ventricular tachycardias, and seconddegree AV blocks. These changes were not evident during waking hours. The most significant electrocardiographic finding for obstructive sleep apnea seems to be an exaggerated sinus arrhythmia. Arrhythmia was recorded in all but one of the subjects examined by Tilkian et all6 Another common finding was a cyclic pattern characterized by a progressive sinus bradycardia during the apnea followed by an abrupt reversal and sinus acceleration when ventilation resumed. The authors postulated these arrhythmias were not caused by sinoatrial (SA) or atrioventricular (AV) nodal disease but were the result of functional and reversible abnormalities precipitated by sleep-related autonomic responses. They suggested that the inspiratory effort against an obstructed airway activated vagal parasympathetic impulses that led to sinus bradycardias. Hypoxia and acidosis may also increase sympathetic tone, thereby giving rise to possible sinus tachycardias, PVCs, and ventricular tachycardias. A study by Tsutomd6 reported electrocardiographic data on six patients suspected of having OSA. All were young obese individuals who had no history of ischemic heart disease. All had significant cardiac arrhythmias during sleep. Atropine administration was ineffective in reversing the parasympathetic response to apneas. This finding was in contrast to those of Tilkian et all5 in which atropine arrested the sinus bradycardia in patients tested.
Differential
diagnosis
Pertinent sleep-related disorders that should be delineated from OSA are central sleep apnea and narcolepsy. A central apneic event differs from the obstructive or mixed apnea by the absence of ventilatory attempts against an occluded airway.6 It is not uncommon for patients demonstrating central apneas to have accompanied obstructive events. The most common event that occurs in the central apnea patient is of the mixed type. This event is characterized by a central respiratory pause, followed by an obstructive ventilatory effort. This sequence suggests the presence of overlapping mechanisms between the various forms of apnea. Clinical characteristics of central sleep apnea consist of complaints of insomnia, frequent awakenings during the night, and depression. Normal body weight is common compared with that of patients with OSA. Daytime hypersomnolence is rare. Other differences from OSA include
678
only mild and intermittent snoring and minimal sexual dysfunction. Finally, central sleep apnea is rare in adults. A common sleep disorder, narcolepsy is often confused, with the sleep apena syndrome because hypersomnolence is a common feature of both disorders. Other significant symptoms of narcolepsy include cataplexy (abrupt loss of muscle tone), hallucinations, and sleep paralysis (total inability to move any muscles when falling asleep or waking up). Narcoleptic patients are generally lethargic and feel exhausted. The narcoleptic patient is often suddenly overwhelmed by the strong urge to sleep. These “sleep attacks” are usually brief, consuming less than 30 minutes when they occur. The patient usually feels refreshed after such naps. OSA patients usually report taking longer naps that fail to refresh. Unlike patients with OSA, narcoleptics usually experience the onset of symptoms as adolescents or young adults. Progressive worsening of symptoms is not characteristic 04 narcolepsy, with maximum severity attained by 30 to 35 years of age. The difficulty in diagnosis stems from the possibility that both disorders can coexist. Fortunately,, sleep apnea in narcoleptics tends to occur in milder forms. A misdiagnosis of narcolepsy and subsequent treatment with stimulants will lead to progressive worsening of ventilatory failure in the sleep apnea patient. The multiple sleep latency test may be helpful in differentiating sleep apnea from narcolepsy. The diagnosis of narcolepsy is made by the finding of a REM period at the beginning of sleep. Narcolepsy is a lifelong illness with no known cure. Antidotal treatment includes the administration of stimulants to lessen daytime hypersomnolence and sleep attacks. Antidepressents are helpful to control cataplexy, sleep paralysis, and hallucinations. Correlation of the clinical course, as described by the patient, with the results of a complete examination, polysomnogram, and multiple sleep latency test will assist in distinguishing between the various sleep-induced disorders. Additional tests. Once a diagnosis of OSA has been established, a complete blood count may reveal secondary polycythemia. Serum electrolytes may also show bicarbonate retention due to carbon dioxide retention. Thyroid function studies may be considered, to rule out hypothyroidism as the etiology. Examination of the upper airway by an otorhinolaryngologist is mandatory to rule out anatomic abnormalities of the nose, pharynx, hypopharynx, and larynx that may either cause the obstruction or contribute to the severity of OSA. A congenitally malformed glottis, hypopharyngeal mass, or lymphomas involving Waldeyer’s tonsillar ring have also been reported in the etiology of hypersomnolence.17 Adults with small retrognathic mandibles and children with micrognathia as seen in the hereditary Pierre Robin syndrome may be predisposed to OSA.lsl lg OSA after par-
DECEMBER
1989
VOLUME
62
NUMBER
6
SLEEPAPNEASYNDROME.PARTI
tial mandibular resections has also been documented.20 Most of these postsurgical patients were found to have obtuse mentocervical angles and retruded tongues. Because the genioglossus muscle is not attached very far anteriorly, the tongue typically assumes a posterior posture. Tongue position often leads to obstruction during sleep.
5. 6. 7. 8. 9.
SUMMARY
10.
Obstructive sleep apnea tends to be a progressive disorder that varies in etiology and severity, making patient selection and treatment predictability difficult to assess. Even though middle-aged obese men have a greater susceptibility to OSA, it has been diagnosed in increased numbers of normal-weight individuals and women. Diagnostic tests including a polysomnogram are needed to establish a diagnosis and determine severity. Misdiagnosis and inappropriate therapy could lead to worsening of symptoms. A multidisciplined approach should be used to reach a diagnosis and establish a plan for appropriate therapy. Part II of this article will review the rationale, v benefits, and potential complications of the treatment modalities advocated for obstructive sleep apnea.
11. 12. 13. 14.
15.
diurnes at noctures due syndrome de Pickwick. Rev Nemo1 (Paris) 1965;112:568-79. Morgan EJ. Sleep apnea syndrome. W V Med J 1979;75:14-8. White DP. Central sleep apnea. Med Clin North Am 1985;69:1205-15. Weaver TE, Millman RP. Broken sleep. Am ,J Nuns 1986;88:146-50. Remmers JE, Degroot WJ, Sauerland EK. Upper airway obstruction during sleep: role of the genioglossus [Abstract]. Clin Res 1976;24:33. Borowicki B. Fibro-optic study of pharyngeal airway during sleep in patients with hypersomnia obstructive sleep apnea syndrome. Laryngoscope 1978;88:1310-3. Clark RW. Sleep apnea. Prim Care 1979;6:658-79. Wittels EW. Obesity and hormonal factors in sleep and sleep apnea. Med Clin North Am 1985;69:1265-77. Sleep: still a scientific mystery. Health Scene 1986;6:6-7. Hiller CF. Medical grand rounds: sleep apnea syndrome. J Arkansas Med Sot 1980;76:391-8. Yasas KM. Sophisticated technology not essential in diagnosis and treatment of sleep apnea. Respir Rev 1986;2:2-4. Tilkian AG. Sleep induced apnea syndrome-prevelance of cardiac arrhythmias and their reversal after tracheostomy. Am J Med 1977;63:348-
57. 16. Tsutomu I. Arrhythmias 17. Zorick F. Intensification
in sleep apnea. Am Heart J 1980;100:513-6. of excessive daytime sleepiness by lymphoma.
Sleep Res 1977;6:199. G, Di Donato G, Verucchi P, Cirignotti F, Mantovani M, Lugaresi E. Hypersomnia with periodic apneas in acquired micrognathia. Arch Neural 1976;33:769-76. and sleep ap19. Imes NK, Orr WC, Smith RO, Rogers RM. Retrognathia nea: a life-threatening condition masquerading as narcolepsy. JAMA 1977;237:1596-7. 20. Panje WR, Homes DK. Mandibuiectomy without reconstruction can cause sleep apnea. Laryngoscope 1984;94:1591-4. 18. Coccsgna
REFERENCES 1. Cartwright RD. The effects of a nonsurgical treatment for obstructive sleep apnea. JAMA 1982;248:705-9. 2. Waidhorn RE. Sleep apnea syndrome. AFP 1985;149:149-62. 3. Vollmer ME. The obstructive sleep apnea syndrome: pathophysiology, diagnosis and treatment. Ind Med 1987;80:1137-77. 4. Gestaut H. Etude polygraphique des manisfestations episodiques
Reprint requests to: DR. JACK B. MEYER, JR. 487 WHEATON FT. SAM HOUSTON,
TX
78234
A mouth splint for severe burns of the head and neck M. Sela, D.M.D.,* Hebrew
and I. Tubiana**
University-Hadassah
School
of Dental
Medicine,
Jerusalem,
Israel
An individual mouth splint device that applies continuous or intermittent pressure to stretch commissures and fibrotic muscles in patients treated for microstomia resulting from facial and neck burns is presented. After an individual lip tray is prepared, the method uses the impression and cast of the region of the lips to construct a pink acrylic resin splint. By using the device, split horixontally and activated with a Ryrx screw, an opening of 14 mm can be obtained within 2 weeks. The device is recommended as being easily constructed, inexpensive, almost painlessly inserted, and progressively activated. (J PROSTHET DENT 1989;62:679-81.)
B
urns of the head and neck region cause skin contractures, which if not prevented result in limitation of opening the mouth (Fig. l), damage to the orbicularis oris
*Senior Lecturer, **Certified Dental
Head, Maxillofacial Technologist.
Prosthetic
10/l/12142
THEJOURNAL
OF PROSTHETIC
DENTISTRY
Unit.
muscle, and inhibition of normal feeding, speech, and dental care.’ Microstomia develops if a preventive prosthesis is not used to stretch the contracted muscles or as a result of reconstructive surgery.2 Treatment may require the use of continuous or intermittent pressure by the splint during healing or therapy periods. The splint may be used in the prevention of early burn contracture of the mouth.3, 4
679