DIAGNOSING AND COMANAGING PATIENTS WITH OBSTRUCTIVE SLEEP APNEA SYNDROME
ARTHUR H. FRIEDLANDER, D.D.S.,
LORI A. WALKER, D.D.S.,
IDA K. FRIEDLANDER, R.N., M.S. and
ALAN L. FELSENFELD, M.A., D.D.S.
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ABSTRACT
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Background. Obstructive sleep apnea syndrome, or OSAS, is a common, but underdiagnosed, disorder that potentially is fatal. It is characterized by repetitive episodes of complete or partial upper airway obstruction leading to absent or diminished airflow into the lungs. These episodes usually last 10 to 30 seconds and result in loud snoring, a decrease in oxygen saturation, and chronic daytime sleepiness and fatigue. The obstruction is caused by the soft palate, base of the tongue or both collapsing against the pharyngeal walls because of decreased muscle tone during sleep. Potentially fatal systemic illnesses frequently associated with this disorder include hypertension, pulmonary hypertension, heart failure, nocturnal cardiac dysrhythmias, myocardial infarction and ischemic stroke.
Clinical Implications. The classic signs and symptoms of OSAS may be recognizable by dental practitioners. Common findings in the medical history include daytime sleepiness, snoring, hypertension and type 2 diabetes mellitus. Common clinical findings include obesity; a thick neck; excessive fat deposition in the palate, tongue (enlarged) and pharynx; a long soft palate; a retrognathic mandible; and calcified carotid artery atheromas on panoramic and lateral cephalometric radiographs.
Conclusions. Dentists cognizant of these signs and symptoms have an opportunity to diagnose patients with occult OSAS. After confirmation of the diagnosis by a physician, dentists can participate in management of the disorder by fabricating mandibular advancement appliances and performing surgical procedures that prevent recurrent airway obstruction.
Obstructive sleep apnea syndrome, or OSAS, is typified by the periodic collapse of the upper airway during sleep and results in absent airflow (apnea) or diminished airflow (hypopnea) into the lungs despite persistent inspiratory effort. These episodes occur most frequently during rapid eye movement sleep when the geniohyoid, genioglossus and tensor veli palatini muscles—all of which usually dilate the upper airway—lose their tone. Obstruction of the airway follows as the negative pressure of inspiration draws the tongue, epiglottis and soft palate posteriorly against the pharyngeal walls (Figures 1
and 2).
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Figure 1. Illustration of an unobstructed upper airway of a person sleeping in the supine (on back) position. The epiglottis (A), base of tongue (B) and soft palate (C) are distant from the posterior pharyngeal wall (D).
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Figure 2. Illustration of an obstructed airway of a person with obstructive sleep apnea syndrome sleeping in the supine (on back) position. Note that the epiglottis and tongue (A), and soft palate (B) are collapsed against the posterior pharyngeal wall (C) and block the air flow.
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An epidemiologic study conducted in the United States estimated that 2 percent of women and 4 percent of men have OSAS.1 The problem is even more common among obese people, with 40 percent of men and 3 percent of women having the disorder.2 Daytime sleepiness resulting from OSAS leads to auto- and work-related accidents, which cost the nation more than $41 billion each year in medical care costs and lost productivity.3,4
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PATHOPHYSIOLOGY
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The periods of compromised airflow usually last 10 to 30 seconds and result in reduced levels of oxygen dissolved in the blood.5 Peripheral chemoreceptors respond to this hypoxemia by increasing sympathetic tone in systemic vascular smooth muscle. This causes vasoconstriction to occur and raises systemic blood pressure approximately 25 percent. Pulmonary hypertension also occurs, as the vasculature in the lungs constricts in response to reduced oxygen levels in the alveolar air sacs. This alveolar hypoxia occurs during episodes of apnea and hypopnea because oxygen continues to be absorbed from the alveolar sacs into the bloodstream but can not be replenished by ventilation because of the obstruction. Bradycardia and a consequent decrease in cardiac output commonly occur. The bradycardia results from hypoxemia—which causes the carotid artery to stimulate the vagus nerve, thus initiating slowing of the heart—systemic vasoconstriction, and progressive negative intrathoracic pressure caused by forceful inspiratory efforts against the occluded airway.6
Eventually, patients mount such vigorous respiratory efforts that they awaken, but it is rare for them to remember the episode. A surge in upper airway muscle dilator tone accompanies the awakening, allowing patients to breathe without obstruction. On opening of the airway, the transient cardiovascular and pulmonary derangements are corrected. Even when the airway is open, partial obstruction frequently occurs and results in loud, irregular snoring sounds caused by air rushing through the narrow passage and stimulating the soft palate, uvula, throat walls and tongue to vibrate. Once the patient is asleep again, however, the obstruction rapidly recurs, and the cycle repeats dozens to hundreds of times a night.7
The brief awakenings often cause excessive daytime sleepiness, fatigue, headache, diminished libido, impotence, impaired memory and concentration, irritability and depression, poor performance in the workplace and traffic accidents.8,9 Recurrent exposure to apnea-induced pathophysiological hemodynamic and hypoxemic events heightens the risk that these people will die of systemic hypertension, pulmonary hypertension, heart failure, nocturnal cardiac dysrhythmias, myocardial infarction or ischemic stroke.10 The cause of these ischemic strokes is uncertain, but it has been attributed to increases in intracranial pressure, decreases in cerebral blood flow, cardiac emboli, and atherosclerosis of either the intracranial or cervical portion of the carotid artery.11 Researchers recently have observed that these patients have exceedingly high prevalence rates of cervical carotid artery atheromas and type 2 diabetes mellitus, both of which are known to be associated with ischemic stroke.12,13
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MEDICAL DIAGNOSTICS
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Oral and maxillofacial surgeons and otolaryngologists employ fiber-optic nasopharyngoscopy to determine the site of airway obstruction. The position of the soft palate and base of tongue relative to the posterior pharyngeal wall are noted in the sitting and supine positions. The patient is asked to perform Müller’s maneuver, which involves inhaling with the nose and mouth closed. This increases intraluminal negative pressure, and the extent of soft palate, base of tongue and lateral pharyngeal wall collapse is evaluated. This, however, is an inexact science because the obstruction usually is at multiple levels, not all of which may be obvious during the examination.
Sleep specialists and pulmonologists confirm the diagnosis of OSAS by documenting impaired airflow. This is accomplished through a laboratory study done overnight during which polysomnography is used to measure electrophysiologic variables such as brain waves (via electroencephalography), eye movements and submental muscle tone; it allows for characterization of sleep quantity and quality, including sleep stages and arousals. Heart rate and heart rhythm are measured with electrocardiography. Respiration measurements include thoracic and abdominal respiratory effort, nasal and oral airflow, and arterial oxyhemoglobin saturation. The number of apneas and hypopneas, their duration, and the degree of hypoxia they cause are quantified. Recently, some institutions have begun to document OSAS through respiratory measurements obtained during overnight unattended sleep monitoring in the home or during attended daytime sleep monitoring.14
The apnea-hypopnea index, or AHI—also known as the respiratory disturbance index—is used by many clinicians to confirm the diagnosis and quantify the illness’ severity. The AHI is calculated by adding the number of times that the airflow is completely blocked for 10 or more seconds (apnea) and the number of times that the airflow is partially impeded (hypopnea) such that there is a 3 percent fall in oxygen saturation or the patient is aroused from sleep. This sum is divided by the number of hours slept. Criteria for the diagnosis of OSAS varies, but a commonly used criterion is an AHI of at least 15 per hour of sleep.15
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DENTAL DIAGNOSTICS
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A dentist may be the first health care provider to identify a person with OSAS because its salient signs and symptoms often are recognizable in the dental office. The majority of people with OSAS are obese men older than 45 years of age.16 They usually have a body mass index greater than 29 kilograms per square meter, a neck circumference that is greater than 17 inches, and a narrowed airway due to excess fat deposition in the palate, tongue (enlarged) and pharynx.17 Also at risk are people with a narrowed posterior airway space resulting from a long soft palate, as evidenced by the uvula lying below the base of the tongue and not being seen during phonation; macroglossia, as evidenced by the tongue lying above the mandibular plane of occlusion; and a small mandible.18 Panoramic dental radiographs taken during the course of routine dental treatment may reveal calcified carotid artery atheromas.
A dentist may be the first health care provider to identify a person with obstructive sleep apnea syndrome because its salient signs and symptoms often are recognizable in the dental office.
Dentists may be consulted by physicians and asked to obtain and evaluate lateral cephalometric radiographs of patients who are suspected of having OSAS. The radiographs of people with OSAS usually show an elongated soft palate, a large tongue, a retropositioned maxilla and mandible, an inferiorly positioned hyoid bone, a narrowed posterior airway space or calcified carotid artery atheromas.19,20
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MEDICAL MANAGEMENT
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Physicians specializing in sleep disorders initially will prescribe the administration of continuous positive airway pressure, or CPAP.21 A high-flow blower delivers a continuous stream of air into a sealed nasal mask that the patient wears while sleeping. The positive pressure pneumatically splints the pharyngeal airway open by preventing the soft palate and tongue from collapsing against the pharyngeal walls. Unfortunately, patient compliance with CPAP is poor because of the noise emanating from the air compressor, a stuffy or runny nose, claustrophobia, having less intimacy with bed partner and facial irritation from the mask.22
Concomitant with CPAP therapy, physicians prescribe a weight-loss regimen to decrease the amount of fat surrounding the airway, thereby allowing it to dilate more fully. They also recommend a reduction in alcohol consumption—because of its propensity to relax the walls of the upper airway permitting collapse—and avoidance of tobacco products, benzodiazepines, narcotics and barbiturates because they tend to worsen apnea.
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DENTAL AND SURGICAL MANAGEMENT
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Dentists caring for these patients can perform restorative procedures that enhance the dentition and enable the patient to properly masticate a high-fiber, high-protein, low-calorie diet that is nutritious and conducive to weight loss. Dentists also can fabricate prosthetic appliances that advance the mandible when worn during sleep and that prevent the tongue and soft palate from collapsing against the pharyngeal walls. These devices historically have been indicated as first-line therapy for patients with mild OSAS as determined by a polysomnogram with an AHI of five to 15 per hour of sleep. They also have been indicated as second-line therapy for patients with mild-to-moderate disease as determined by a polysomnogram with an AHI of 15 to 55 per hour of sleep if they cannot tolerate CPAP therapy and decline surgery, or if these two modalities have failed.23 Recently, some sleep specialists have recommended that these devices be considered first-line therapy for patients with mild-to-moderate disease if, on a postinsertion polysomnograph, they demonstrate efficacy.24
Mandibular advancement appliances are constructed so that the mandible is positioned 2 to 5 millimeters anteriorly (Figure 3). This movement corresponds to between 50 percent and 100 percent of the patient’s maximum protrusive movement and advances the tongue passively because of its attachment to the genial tubercles.25,26 These devices simultaneously move the soft palate anteriorly because of its attachment to the tongue via the palatoglossus muscle.27 These movements enlarge the hypopharyngeal airway and reduce the likelihood that the tongue or soft palate will collapse against the posterior pharyngeal wall when the patient inspires during sleep.
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Figure 3. Nonfixed, two-piece appliance using mounted articulated models with the mandible advanced 5 millimeters (note reference lines on casts).
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Mandibular advancement appliances are fabricated as either a one- or two-piece appliance. A fixed, one-piece appliance positions the mandible anterior to the maxilla and is retained in place by use of clasps made of acrylic or thermoplastic polymer. Anterior breathing holes can be made in the appliance so that oral respiration is permitted for those with restricted nasal air flow. A nonfixed, two-piece appliance—one piece for each arch—positions the mandible anteriorly and is secured to the maxilla by use of thermoplastic buttons, interarch elastics, or a buccal tube and rod (Figure 4). The two-piece appliance affords the patient greater comfort by permitting anterior and lateral mandibular movement.
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Figure 4. Nonfixed, two-piece mandibular advancement appliance in place. The position of the mandible can be modified by changing the length of the lateral bands.
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The effectiveness of these appliances has been demonstrated through research. Dental researchers have shown that these devices decreased AHI to less than 20 per hour of sleep in 12 of 17 patients in whom the untreated AHI ranged from 20 to 60 per hour of sleep; they also have reported that these appliances were able to decrease AHI to less than 10 per hour of sleep in slightly more than one-half of the patients treated.28,29 Other groups of dental scientists have reported that 95 percent of their patients with OSAS experienced a 50 percent or more decrement in AHI when properly fitted with a mandibular advancement appliance, although some patients did not correct to normal levels.30
The long-term ramifications of continually displacing the condyles and stretching retrodiskal tissues and muscle attachments associated with the use of these appliances over a period of 2.5 to four years recently have been determined by questionnaire and clinical examination.31 Of 132 patients responding to the questionnaire, 8 percent said they discontinued use of the device because of intolerable side effects, the most common being temporomandibular joint pain. All other patients reported that their side effects—which included excess salivation (30 percent), temporomandibular joint pain (26 percent), dental pain (26 percent), facial muscle pain (25 percent), xerostomia (23 percent) and occlusal change (12 percent)—were of a minor and temporary nature. A total of 106 of the patients who responded to the questionnaire were examined. An increase in inter-incisal opening was noted in 28 percent of patients (none had a decrease), occlusal changes in 14 percent of patients as manifested by a decrease in overjet of between 1 mm and 3 mm, and an unspecified new sound in one or both temporomandibular joints developed in 8 percent of patients.
People with OSAS may require surgery if they are unable to comply with CPAP or tolerate a prosthetic device, or if 10- to-12 mm movements of the mandible are necessary to reposition the tongue anteriorly and away from the posterior pharyngeal wall. If the respiratory obstruction can be documented as occurring behind the soft palate in the retropalatal area, an otolaryngologist or oral and maxillofacial surgeon can perform uvulopalatopharyngoplasty—excision of portions of the soft palate, uvula, tonsils, and posterior and lateral pharyngeal walls—using a scalpel or laser with the patient under general anesthesia in a hospital operating room.32 Approximately 50 percent of patients with presurgically documented isolated retropalatal obstruction will achieve a 50 percent decrease in AHI, an AHI of less than 20 per hour or both with this procedure. Complications associated with the procedure include difficult intubation, airway obstruction after extubation, postoperative hemorrhage, and velopharyngeal insufficiency resulting in nasal regurgitation of liquids, hypernasal speech and dysphagia.33
If the respiratory obstruction is documented as occurring behind the tongue base in the retrolingual area, an oral and maxillofacial surgeon can advance the entire dental alveolus by performing a bilateral sagittal split mandibular osteotomy. The dental alveolus and the contiguous inferior border of the anterior mandible are advanced along with the attached anterior belly of the digastric muscle and the mylohyoid, genioglossus and geniohyoid muscles. These bone and muscle movements pull the base of the tongue forward and upward, thereby enlarging the posterior airway space (Figures 5 and 6). Moving the dental alveolus forward also creates more anterior space for the repositioned tongue. The bony segments then are fixed rigidly with screws or bone plates to assist in healing and to resist the pull of soft tissues that might cause skeletal relapse. Presurgical orthodontic therapy and simultaneous advancement of the maxilla via a Le Fort I osteotomy frequently are necessary to ensure a functional occlusion and acceptable esthetics.34–38
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Figure 5. Presurgical cephalometric radiograph of a patient with obstructive sleep apnea syndrome and a narrowed posterior airway space (arrows), measuring 6 millimeters.
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Figure 6. Postsurgical cephalometric radiograph of the patient in Figure 5 , showing that surgical advancement of the jaws and chin repositioned the tongue anteriorly, resulting in a 16-millimeter posterior airway (arrows).
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Advancement of the maxilla draws the soft palate to the anterior aspect, enlarging the retropalatal area, and it pulls the palatoglossus muscles forward, increasing tongue support. Additional anterior movement of the tongue and enlargement of the posterior airway space can be obtained by performing a simultaneous genioplasty. Approximately 95 to 100 percent of patients achieve a 50 percent decrease in AHI, an AHI of less than 20 per hour of sleep or both with these procedures. Complications associated with these procedures include difficult intubation, postoperative bleeding and infection, and transient or permanent anesthesia of the inferior alveolar nerve.39–42
Recently, otolaryngological surgeons reported success in treating OSAS by delivering radiofrequency energy to the subsurface of the tongue with needlelike electrodes embedded in the area surrounding the circumvallate papillae.43 After six treatments conducted on an ambulatory basis using local anesthetic and separated by monthly intervals, significant scar tissue developed such that there was a 17 percent reduction in tongue volume, a 55 percent reduction in the AHI, and no adverse effects on speech quality or ability to swallow.
Moving the dental alveolus forward creates more anterior space for the repositioned tongue.
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CONCLUSION
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It must be emphasized that dentistry in concert with medicine has much to offer patients with OSAS. We wrote this article to encourage dentists to diagnose patients with occult OSAS and join with physicians to offer these patients the full range of available treatment options to defeat this often fatal illness.
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FOOTNOTES
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Dr. Walker is the chief, Prosthetic Dentistry, and the director, Dental Education, Veterans Affairs Outpatient Clinic and Nursing Home, Sepulveda, Calif., and an adjunct associate professor, Prosthetic Dentistry, University of California Los Angeles, School of Dentistry.
Ms. Friedlander is a public health nurse, West Valley/Los Angeles County Department of Health, Panorama City, Calif., and a research associate, Veterans Affairs Outpatient Clinic and Nursing Home, Sepulveda, Calif.
Dr. Felsenfeld is an adjunct professor, Oral and Maxillofacial Surgery, University of California Los Angeles, School of Dentistry, and an assistant director, Oral and Maxillofacial Surgery Residency Training Program, UCLA Medical Center.
The authors acknowledge Ann Oliver, program assistant, Office of the Associate Chief of Staff/Education, Veterans Affairs Greater Los Angeles Healthcare System, for her assistance.
Dr. Friedlander is the associate chief of staff, Graduate Medical Education, Veterans Affairs Greater Los Angeles Healthcare System; the director, Quality Assurance, Hospital Dental Service, University of California Los Angeles Medical Center; and a professor, Oral and Maxillofacial Surgery, University of California Los Angeles, School of Dentistry, Los Angeles. Address reprint requests to Dr. Friedlander at Veterans Affairs Greater Los Angeles Healthcare System, 11301 Wilshire Blvd., Los Angeles, Calif. 90073, e-mail "arthur.friedlander{at}med.va.gov".
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A. H. Friedlander
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ABSTRACT
PATHOPHYSIOLOGY
