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Current medical management of sleep-related breathing disorders
Oral Maxillofacial Surg Clin N Am 14 (2002) 297 – 304
Current medical management of sleep-related breathing disorders Kent E. Moore, DDS, MDa,*, Mary Susan Esther, MDb a
Private Practice, Oral and Maxillofacial Surgery, 1718 East Fourth Street, Suite 804, Charlotte, NC 28204, USA b Carolinas Sleep Services, Carolinas Medical Center, Mercy Medical Park, 10724 Park Road, Suite 208, Charlotte, NC 28210, USA
Sleep-disordered breathing, a disorder characterized by repeated apnea (cessation of breathing) and hypopnea (partial cessation of breathing) during sleep, has been shown to be prevalent in the general population. Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a common disorder that can adversely impact longevity and quality of life, and one in which the oral and maxillofacial surgeon possesses a unique ability to assist in managing. Prior to offering surgical therapy, the oral and maxillofacial surgeon must have a working knowledge of medical options these patients may choose to pursue. Medical management of OSAHS requires careful clinical assessment and laboratory evaluation. Sleep-related breathing disturbances were first described polysomnographically in Gustout’s mid-1960s studies of obese patients with hypercapnia [1]. Subsequent research has shown that obstructive sleep apnea can occur in nonobese patients as well. In fact, epidemiological data estimate that 2 – 5% of the population meets the criteria for OSAHS [2]. Community based studies have confirmed that OSAHS is seen in 2% of women and 4% of men between the ages of 30 and 60 years [3]. OSAHS occurs when there are episodes of pharyngeal narrowing and obstruction combined with significant daytime symptoms that result from disrupted sleep. Though the basic processes causing airway narrowing are multifactorial and not completely understood, this disorder is considered to
* Corresponding author. E-mail address: [email protected] (K.E. Moore).
occur over a continuum of severity: the mildest form of upper airway narrowing produces rapid airflow. This rapid airflow imparts kinetic energy to the soft tissues of the upper airway, initially causing stretching of the compliant portions of the soft tissue upper airway (ie, the soft palate and lateral pharyngeal walls), resulting in soft palate elongation and redundancy (ie, secondary elongation), and eventually in snoring. Further airway narrowing results in increased upper airway resistance. This increased airway resistance is sensed by the central nervous system, causing disruption of normal sleep architecture, and forms the basis for the condition of upper airway resistance syndrome (UARS) seen most commonly in young, thin females. Further airway narrowing and frank obstruction are next on the continuum, causing obstructive sleep apnea (OSA). OSA is generally ranked on a scale of severity, based upon the number of times a given patient stops breathing over a given hour of sleep [often called the Respiratory Disturbance Index (RDI), or Apnea-Hypopnea Index (AHI)]. An RDI of 0 – 5 events per hour is considered normal. In most clinics, an RDI of 5 – 20 is considered mild OSA, 20 – 40 or 50 is considered moderately severe OSA, and an RDI >40 – 50 is considered severe OSA. Apnea is defined as a cessation of respiratory flow for at least 10 seconds accompanied by a 2 – 4% drop in oxygen saturation and usually an associated EEG arousal [4]. The syndrome of obstructive breathing requires the combination of daytime symptoms, as well as an apnea-hypopnea index of at least 5 per hour of sleep [5]. Therefore, a careful clinical history, along with the polysomnographic data, is needed. Factors that increase the risk for OSAHS include
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obesity, male gender (2 to 3:1 male-female ratio) as well as family history [6]. Nearly all patents with significant OSAHS snore, though the absence of snoring does not exclude sleep apnea [7]. In addition, apneic episodes are reported by the bed partner in 75% of cases [8]. As snoring can be loud and lead to restlessness during the night, it is not surprising that 46% of patients sleep apart from their partners [9]. Bed partners may report loud snorts or vocalizations, and patients themselves note restlessness, often with associated diaphoresis in neck and upper chest. Nearly 74% of patients complain of morning dry mouth, and 28% report significant nocturia [10]. Daytime sleepiness is, of course, one of the hallmarks of OSAHS. The severity of this symptom can vary from subtle to severe. Untreated sleep apnea puts patients at risk for vehicular accidents [11]. It is common for patients with sleep apnea to report opening car windows, drinking caffeinated beverages, or chewing ice as a help to stay awake. Intellectual impairment has been noted on neuropsychiatric testing, and patients themselves may note decreased concentration and job performance [12]. A recent popular public news telecast nationwide suggested that the neurocognitive deficits of the sleepy driver can be at least as severe (if not more so) than that of the alcohol-impaired driver. Obstructive sleep apnea-hypopnea syndrome has been linked to hypertension. Recent prospective data confirms the association between sleep-disordered breathing and hypertension and its resulting cardiovascular morbidity [13]. Furthermore, there is evidence that OSAHS may place patients at an increased risk for stroke [14]. OSAHS should be looked at as yet another cardiovascular risk factor for susceptible individuals. The decision on when, and how, to treat patents with OSAHS is complex. It must be based on clinical assessment, including physical examination, medical history, and polysomnographic data. The decision must include information about a patient’s sleepiness, snoring, and disruption of the bed partner’s sleep as well as assessment of possible adverse cardiovascular consequences. These factors should all play a role in determining the proper therapeutic option (both surgical and nonsurgical) the oral and maxillofacial surgeon offers to the patient presenting with this disorder.
Effects of medications and associated medical conditions on sleep-disordered breathing Once the diagnosis of OSAHS has been established, treatment options must be explored. First,
however, possible medical conditions, as well as pharmacological agents, that could adversely affect sleep and breathing must be assessed. Even moderate alcohol intoxication can decrease hypercapnic ventilatory response to 50% of baseline [15]. Alcohol can precipitate OSA in vulnerable individuals. Older, obese subjects are more likely to be affected than are young healthy subjects. Patients with mild sleep apnea clearly develop longer and more frequent obstructive breathing events when they consume alcohol, and snorers can develop OSA after alcohol use [16]. Therefore, avoidance of alcohol for obese snorers and patients with obstructive sleep apnea is recommended routinely [17]. Smoking is widely known to impact upper airway physiology detrimentally. The irritation-inflammationedema cycle that occurs with repeated use of an irritant such as smoking is felt to affect a subtle form of mucosal edema of the upper airway, as well as increase upper airway mucosal secretions. The combined effect of these reactive conditions, instead of occurring externally, actually affects closure (or narrowing) of the upper airway. Per Pousille’s equation, small changes (narrowing) in the radius of the upper airway tube can potentially effect an exponential change in airflow and cause a greater chance for obstructive upper airway pathology. Hypnotics can also affect sleep and breathing and are frequently prescribed. Benzodiazepines are mild respiratory depressants [18]. Hypercapneic chronic obstructive pulmonary disease (COPD) patients appear to be particularly vulnerable to the respiratory depressant properties. Benzodiazepines, like alcohol, decrease upper airway muscle tone [19] and in this way may promote the development of OSA in susceptible individuals; therefore, they are best avoided [20]. Newer, non-benzodiazepine agents lack the myorelaxant and respiratory depressant effects of the benzodiazepines [21]. In general, however, it is best to avoid sedative-hypnotic agents in patients with hypercapnia and sleep apnea. Narcotics, too, are powerful respiratory depressants and are best avoided in patients with significant sleep apnea [22]. Hypothyroidism should also be considered in patients with a history of OSAHS. Possible mechanisms for the increase in sleep apnea seen in patients with hypothyroidism include obesity, impaired upper airway muscular function, and macroglossia. Though screening of all patients with OSAHS for hypothyroidism is not cost-effective, careful assessment of clinical symptoms is necessary [23]. In hypothyroid patients, it is important to treat their sleepdisordered breathing during thyroid replacement [24]. It may take considerable time for normalization
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of sleep and breathing, or patients may be suffering from two disorders. Pharmacological treatment of sleep apnea has not proven effective. In the late 1970s, agents such as protriptyline (a tricyclic antidepressant) were shown to reduce the number of apneic events by decreasing the amount of REM sleep and increasing hypoglossal nerve activity [25]. Whereas apneas were reduced in frequency, the total number of sleep and breathing events remained abnormal. Pharmacological agents studied and shown not to be of benefit in treatment include progesterone, tryptophan, and baclofen [26,27].
Use of supplemental oxygen, position restriction, and role of weight loss Other forms of medical treatment for OSAHS that have been studied include supplemental oxygen. Oxygen alone is not sufficiently effective in reducing the frequency of apnea or improving daytime alertness to be a therapeutic option [28]. Oxygen, however, may have a role as an adjunct to positive airway pressure in patients who remain hypoxic after correction of upper airway obstruction. Ongoing studies need to be completed in order to better understand the amount of desaturation that necessitates addition of oxygen. Restriction of sleeping position may offer significant benefit to some patients with OSAHS. Laboratory analysis routinely breaks down the presence of sleep-disordered breathing in both the supine as well as the nonsupine positions. The supine position, with resultant occlusion of upper airway based on effects of gravity on the tongue, can result in apneic or hypopneic events. For the oral surgeon, the effect of positional changes on upper airway volume can most easily be assessed clinically through the use of both acoustic pharyngometry, as well as with fiberoptic nasopharyngoscopy. In many cases, slight cervical extension of the neck while in the supine position may affect volumetric expansion of the upper airway. In this manner, cervical pillows, which allow one to sleep with slight extension of the head (while in the supine position), can be of benefit (one such pillow has shown some merit in minimizing apneic events in patients with mild OSA). But expecting a patient to maintain a substantial degree of uncomfortable cervical extension consistently during supine REM sleep is unrealistic. It is more likely, however, that obese patients will have OSAS regardless of their position during sleep [29]. For some patients, sleep and breathing is satisfactory in the lateral position with main-
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tenance of oxygenation and sleep continuity when lateral. Use of a small ball, such as a tennis ball, pinned to the pajama back may help patients to learn behaviorally to avoid sleeping supine. In addition sleeping with the head and trunk elevated to a 30° angle reduces OSAS as it stabilizes the upper airway [30]. Modification of body position during sleep should be considered in appropriate patients. No discussion of the management of OSAHS is complete without addressing obesity. The effect of obesity on the upper airway appears to be the result of mechanical effects on the upper airway (the pharyngeal dilator muscles are unable to work efficiently with increased load) and increased upper airway resistance. Studies have confirmed that weight reduction can ameliorate sleep-disordered breathing. It appears that the degree of improvement is not linearly related to the amount of weight lost [31]. In fact, it appears that there must be a critical amount of weight lost before there can be seen any significant improvement in sleep-disordered breathing. Obese patients should always be encouraged to lose weight, but obstructive breathing must be treated while the weight loss is underway.
Use of nasal continuous positive airway pressure In part because of the lack of a pharmacological treatment for OSAHS, nasal continuous positive airway pressure (CPAP) is the most established therapy choice. First used in Australia in 1981, its use in America became more widespread in l985 [32]. Nasal CPAP can best be conceptualized as a pneumatic splint that prevents collapse of the pharyngeal airway. CPAP successfully eliminates mixed and obstructive apneas [33]. Titration of the pressure to levels sufficient to eliminate not only the obstruction, but snoring and snore-arousals as well, can be difficult even for veteran sleep technicians. Adjusting to nasal CPAP can be trying, as patients adapt both to the mask and to the pressure cessation, as well as the headgear holding the mask in place. Instructional videos, review of goals of treatment, and time in the laboratory adjusting to the device can ease transition to use. Studies confirm the value of patient education programs to successful CPAP use and improved compliance [34]. Nasal CPAP titration has as its goal the elimination of respiratory related arousals in all sleep stages and positions. Once correct pressure is achieved, the number of arousals triggered by the sleep-disordered breathing should be markedly reduced. This leads to a ‘‘rebound’’ of slow wave and REM sleep [35].
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Snoring should be eliminated because it is a sign of inadequate CPAP pressure. It is apparent that higher CPAP pressures are generally needed when the patient is supine or in REM sleep. Successful titration in REM sleep in the supine position, the most vulnerable combination of stage and position for obstructive breathing, is the goal. Of course, additional factors may have an impact on CPAP pressures. Alcohol, for example, with its known neuromuscular effects, would be expected to result in the need for an increase in CPAP pressure, as would weight gain [36]. If patients have persistent sleepiness after treatment of their sleep-disordered breathing, then review of their sleep history is recommended. Patients may be suffering from a second, primary sleep disorder such as narcolepsy. Hypersomnolence would need to be assessed with a repeat evaluation in the laboratory, with CPAP in place to confirm treatment of sleep-disordered breathing, followed by a Multiple Sleep Latency Test to evaluate daytime fatigue. Problems related to nasal CPAP include mask discomfort, nasal congestion, and social considerations (including bed partner tolerance of the device) and chest discomfort and claustrophobia. The comfort of the CPAP mask is critical, and careful fitting of the mask is crucial to successful treatment. In our laboratory, technicians spend much time helping the patient choose an appropriate mask. Claustrophobic patients, or those who have beards or mustaches are otherwise difficult to fit, are encouraged to come by the laboratory prior to their study to have additional time for choosing an interface system. If a mask does not fit properly, there is an audible leak of air and resultant insufficient pressure and ineffective treatment. The patient may not be tightening the headgear sufficiently at home, whereas in the laboratory the mask was applied properly. If the air is leaking toward the eye, then conjunctivitis may result [37]. If the headband or headgear securing the CPAP is too snug, the increased tension may cause ulceration of the skin around the bridge of the nose. Nasal prongs or pillows alleviate some problems regarding comfort, but these can irritate the nares as well. Patients with claustrophobia may need time in the laboratory for desensitization and graduated exposure in order to be able to tolerate CPAP. Persistent nasal congestion is seen in more than 10% of patients on CPAP even after six months of treatment [38]. It has been found that the relative humidity of air inhaled through CPAP is 20% lower than relative humidity of room air [39]. The postulated causes of nasal congestion include unmasking of allergic rhinitis (particularly in mouth breathers);
vasodilatation of turbinate tissues triggered by mucosal receptors, or septal deviation and fixed obstruction. Efforts to increase nasal patency include the use of topical steroids, humidification, and topical antihistamine sprays. In some patients, correction of septal deviation (via septoplasty), or enlarged turbinates (via either radiofrequency, volumetric tissue reduction, or more traditional surgical turbinectomy) may be necessary before success with CPAP is obtained. Patients with persistent nasal congestion may respond to Passover humidifiers attached to CPAP. A recent study found that among patients with previous uvulopalatopharyngoplasty, those using drying medications, as well as those over age 60, were more likely to develop nasopharyngeal dryness. Heated humidification added to CPAP improved the daily use rate in this group of patients [40]. Nasal CPAP is effective only when the device is used, and used consistently. Studies indicate that even one night off CPAP can lead to the return of pathologic hypersomnolence [41]. But it is also true that patients can achieve some benefit from a partial night’s use. Early studies reporting on patient compliance with nasal CPAP were based purely on subjective patient reporting; these studies suggested a relatively high rate of CPAP compliance. Later studies, done with the use of covert patient monitoring, revealed a much lower compliance rate (these studies are generally felt to be a more accurate reflection of true nasal CPAP compliance). With new CPAP devices allowing for monitoring of patterns of use, more information for further study will soon be forthcoming. Even data on acceptance of CPAP when attempted in a laboratory setting can be confusing. Some studies have reported acceptance rates (agreement to use CPAP at home) of 80%, whereas others are as low as 58% [42,43]. It does appear that patients’ perception of improvement, not the severity of the obstructive breathing itself, is the most predictive measure of compliance [44]. Equally evident is the fact that patients overestimate their CPAP use [45]. It appears that about half of patients will be consistent users of CPAP, and Weaver et al showed that, by as early as day 4 of treatment, nonusers could be separated from nightly users [46]. Follow-up early after starting CPAP is important to help patients adjust to CPAP and to address initial difficulties. Studies do demonstrate that hypersomnolence prior to treatment is predictive of good compliance. Of course, this makes common sense, as the patient’s response to CPAP would be positive reinforcement for continued usage. In fact, one recent study by Barbe et al found that in patients with significant OSAHS but with no subjective sleepiness CPAP
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offered no improvement in cognitive function, quality of life, or arterial blood pressure [47]. This article does not, however, take into account such factors as effect on bed partner’s sleep, nor does it include objective measurement of sleepiness. When, then, should patients be treated? Again, careful clinical assessment is required, taking into account not only hypersomnolence and its associated risk for vehicular or industrial accidents, but also social factors such as unacceptable levels of snoring and potentially reduced cardiovascular risk factors [48]. When CPAP is not tolerated, it is important first to determine the specific cause for the discontinued use. A complete upper airway examination, looking for structural abnormalities, should be performed. Kribb et al have demonstrated that only 46% of patients were able to use CPAP for 4 hours each night at least 70% of the time [49]. Clearly, such objective measures indicate that CPAP compliance is less than optimal [50].
Bilevel positive airway pressure Bilevel positive airway pressure (BiPAP) devices have the capability to allow for a separate pressure for inspiration and expiration. It has been shown that patients with OSA need a lower expiratory pressure than that needed to prevent upper airway occlusion during inspiration [48]. As would be expected, the continuous pressure level of CPAP and the inspiratory pressure of BiPAP for a given patient would be the same. This makes intuitive sense, as identical levels would be needed to maintain inspiratory potency. Sanders et al found that a reduction in expiratory pressure could be achieved, with mean expiratory pressures being 37% lower than inspiratory pressures [51]. BiPAP can be delivered in three ways: (1) through a spontaneous, or patient-triggered mode, (2) through a spontaneous/timed mode, or (3) a timed mode alone. Only the spontaneous mode is usually indicated for OSA; the spontaneous/timed mode can be used in patients with significant neuromuscular disease, whereas the timed mode allows BiPAP to function as a controlled ventilator. BiPAP, because of its increased cost as compared with CPAP, is reserved for those patients who are intolerant of CPAP or who would benefit from lower expiratory pressures. Patients experiencing chest wall discomfort, or those sensing difficulty in exhaling against pressure or a smothering sensation, may benefit from BiPAP [52]. Studies have demonstrated a similar long-term compliance rate for CPAP and BiPAP, though the initial
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acceptance rate of BiPAP is higher [53]. If patients are more likely to accept the treatment initially, use will be increased overall.
Autotitrating CPAP Currently available, and being ever more finetuned, are CPAP devices that detect changes in flow and automatically adjust the pressure. These devices can detect changes in upper airway resistance (such as can be seen after alcohol use) and make the necessary pressure adjustments. Several methodological problems with autotitrating devices have been found, however. The devices appear to be confused by leaks about the cap mask, with resultant over pressure of CPAP as the device tries to compensate [54]. The devices appear to have a median pressure of 70 – 80% of peak ‘‘auto set’’ as compared with manual pressure. For most patients, though changes in position and sleep stage may require minor changes in CPAP pressure, these changes are insignificant and auto PAP offers little advantage. Additionally, auto PAP does not offer an advantage to patients with nasal congestion [54]. Further investigations are underway to establish guidelines on when use of auto PAP may be beneficial.
Alternative interface systems Recent innovations (combining oral appliance technologies with CPAP or BiPAP designs) are intended to minimize the inherent problems associated with nasal CPAP interfaces, troublesome headgear, and patient claustrophobia. CPAP Pro1 is a nasal CPAP interface, which utilizes a maxillary dental mouthpiece to hold a specially designed connector (this connector supports the tubing that attaches to nasal pillows). If properly fitted and oriented, this appliance has the potential to eliminate headgear completely. This appliance is currently being offered with a quick-setting gel polymer (so that the patient can make his or her own maxillary tray), or, as a professional kit, so that a more permanent and durable oral appliance can be fitted and placed by the dentist. This appliance can also be combined with an oral appliance (such as a Klearway1 or Herbst1 appliance) that affects mandibular advancement/ protrusion. The main benefit for their combined use with CPAP Pro is in their ability to maintain closure of the mandible, and to prevent oral leakage of the positive pressure ventilation. It is debatable whether the effect of mandibular
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protrusion will be of dramatic benefit (with this combined appliance) so as to lower the pressures required for elimination of obstructive upper airway pathology because ventilation through the relatively high-resistance nasal airway is still required. Oral Positive Airway Pressure (or OPAP1) has recently received FDA approval as an alternative interface system for patients requiring positive pressure ventilation. This custom-fitted oral appliance is designed to connect directly with the CPAP tubing, permitting oral positive pressure ventilation while bypassing the nasal airway. This one-piece appliance is also designed to permit fixed-position mandibular advancement, thereby potentially affecting expansion of the tongue-base region of the upper airway. In this case, one possible advantage to this design, because of the forward mandibular posturing, is the potential for lower required airway pressures for adequate ventilation and elimination of OSA, as the highresistance nasal airway is bypassed. Potential problems with this system, however, include those patients who have undergone previous uvulopalatopharyngoplasty- with the potential for nasal venting, as well as the drying effect on the oral cavity and pharyngeal airway. With each of the above alternative interfaces (as well as with oral appliances in general), retention of the appliance is critical. Also, as with all oral appliances used in the treatment of OSA, risks of alteration of the existing occlusion, TMJ dysfunction, and damage to existing dental restorations is possible. Compliance data with these newer interface systems is lacking at this time.
Oral appliances Although this topic is covered in detail in another article here, oral appliances have definitely found a place within the medical management of varying levels of upper airway obstructive pathology. The reader is referred to the accompanying article; membership within the Academt of Dental Sleep Medicine (www.dentalsleepmed.org) offers another excellent opportunity for those doctors wishing to learn more about this form of treatment.
Summary Sleep and breathing disorders are common. Assessment by the oral and maxillofacial surgeon should include thorough physical examination and assessment of clinical symptoms both during sleep
and wakefulness, as well as review of polysomnographic data. Treatment then focuses on nasal CPAP as the most widely accepted therapeutic option. CPAP is not always well tolerated, however; suboptimal compliance and complications often lead to its discontinuation. Optimizing CPAP treatment may require changes in the mask style or switching to BiPAP (particularly for patients with hypoventilation or refractory nasal congestion). The interface system may need to be changed entirely, as with OPAP1, in order for a patient to tolerate CPAP. More conservative treatment approaches include weight loss, position restriction, and oral appliances, effective options for patients with largely positional or only mild breathing obstruction. These options must be thoroughly investigated prior to initiating a course of irreversible surgical therapy. Pharmacological options have as yet been of no benefit. Obviously, future investigations must be directed toward better diagnostic tools for assessment of sleep apnea, especially as it relates to distortion of the upper airway when patients are in the supine position during sleep. It is hoped that newer treatments, offering improvement in overall tolerance and compliance, will derive from these efforts.
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[50] Douglas NJ. Systematic review of the efficacy of nasal CPAP. Thorax 1998;53:414 – 5. [51] Sanders MH, Kern N. Obstructive sleep apnea treated by independently adjusted inaspiratory and expiratory positive airway pressures via nasal mask. Chest 1990; 98:317 – 24. [52] Martin T, Sanders M, Atwood CW. Correlation between changes in PaCO2 and CPAP in obstructive sleep apnea (OSA) patients. Am Rev Respir Dis 1993; 147:A681. [53] Reeves-Hoche MK, Hudgel D, Meck R, et al. BiPAP vs. CPAP: Patient compliance in the treatment of obstructive sleep apnea, six month data in a two year study. Am Rev Respir Dis 1993;147:A251. [54] Berthon-Jones M. Feasibility of a self-setting CPAP machine. Sleep 1993;16:s120 – 3.
Current medical management of sleep-related breathing disorders Kent E. Moore, DDS, MDa,*, Mary Susan Esther, MDb a
Private Practice, Oral and Maxillofacial Surgery, 1718 East Fourth Street, Suite 804, Charlotte, NC 28204, USA b Carolinas Sleep Services, Carolinas Medical Center, Mercy Medical Park, 10724 Park Road, Suite 208, Charlotte, NC 28210, USA
Sleep-disordered breathing, a disorder characterized by repeated apnea (cessation of breathing) and hypopnea (partial cessation of breathing) during sleep, has been shown to be prevalent in the general population. Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a common disorder that can adversely impact longevity and quality of life, and one in which the oral and maxillofacial surgeon possesses a unique ability to assist in managing. Prior to offering surgical therapy, the oral and maxillofacial surgeon must have a working knowledge of medical options these patients may choose to pursue. Medical management of OSAHS requires careful clinical assessment and laboratory evaluation. Sleep-related breathing disturbances were first described polysomnographically in Gustout’s mid-1960s studies of obese patients with hypercapnia [1]. Subsequent research has shown that obstructive sleep apnea can occur in nonobese patients as well. In fact, epidemiological data estimate that 2 – 5% of the population meets the criteria for OSAHS [2]. Community based studies have confirmed that OSAHS is seen in 2% of women and 4% of men between the ages of 30 and 60 years [3]. OSAHS occurs when there are episodes of pharyngeal narrowing and obstruction combined with significant daytime symptoms that result from disrupted sleep. Though the basic processes causing airway narrowing are multifactorial and not completely understood, this disorder is considered to
* Corresponding author. E-mail address: [email protected] (K.E. Moore).
occur over a continuum of severity: the mildest form of upper airway narrowing produces rapid airflow. This rapid airflow imparts kinetic energy to the soft tissues of the upper airway, initially causing stretching of the compliant portions of the soft tissue upper airway (ie, the soft palate and lateral pharyngeal walls), resulting in soft palate elongation and redundancy (ie, secondary elongation), and eventually in snoring. Further airway narrowing results in increased upper airway resistance. This increased airway resistance is sensed by the central nervous system, causing disruption of normal sleep architecture, and forms the basis for the condition of upper airway resistance syndrome (UARS) seen most commonly in young, thin females. Further airway narrowing and frank obstruction are next on the continuum, causing obstructive sleep apnea (OSA). OSA is generally ranked on a scale of severity, based upon the number of times a given patient stops breathing over a given hour of sleep [often called the Respiratory Disturbance Index (RDI), or Apnea-Hypopnea Index (AHI)]. An RDI of 0 – 5 events per hour is considered normal. In most clinics, an RDI of 5 – 20 is considered mild OSA, 20 – 40 or 50 is considered moderately severe OSA, and an RDI >40 – 50 is considered severe OSA. Apnea is defined as a cessation of respiratory flow for at least 10 seconds accompanied by a 2 – 4% drop in oxygen saturation and usually an associated EEG arousal [4]. The syndrome of obstructive breathing requires the combination of daytime symptoms, as well as an apnea-hypopnea index of at least 5 per hour of sleep [5]. Therefore, a careful clinical history, along with the polysomnographic data, is needed. Factors that increase the risk for OSAHS include
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obesity, male gender (2 to 3:1 male-female ratio) as well as family history [6]. Nearly all patents with significant OSAHS snore, though the absence of snoring does not exclude sleep apnea [7]. In addition, apneic episodes are reported by the bed partner in 75% of cases [8]. As snoring can be loud and lead to restlessness during the night, it is not surprising that 46% of patients sleep apart from their partners [9]. Bed partners may report loud snorts or vocalizations, and patients themselves note restlessness, often with associated diaphoresis in neck and upper chest. Nearly 74% of patients complain of morning dry mouth, and 28% report significant nocturia [10]. Daytime sleepiness is, of course, one of the hallmarks of OSAHS. The severity of this symptom can vary from subtle to severe. Untreated sleep apnea puts patients at risk for vehicular accidents [11]. It is common for patients with sleep apnea to report opening car windows, drinking caffeinated beverages, or chewing ice as a help to stay awake. Intellectual impairment has been noted on neuropsychiatric testing, and patients themselves may note decreased concentration and job performance [12]. A recent popular public news telecast nationwide suggested that the neurocognitive deficits of the sleepy driver can be at least as severe (if not more so) than that of the alcohol-impaired driver. Obstructive sleep apnea-hypopnea syndrome has been linked to hypertension. Recent prospective data confirms the association between sleep-disordered breathing and hypertension and its resulting cardiovascular morbidity [13]. Furthermore, there is evidence that OSAHS may place patients at an increased risk for stroke [14]. OSAHS should be looked at as yet another cardiovascular risk factor for susceptible individuals. The decision on when, and how, to treat patents with OSAHS is complex. It must be based on clinical assessment, including physical examination, medical history, and polysomnographic data. The decision must include information about a patient’s sleepiness, snoring, and disruption of the bed partner’s sleep as well as assessment of possible adverse cardiovascular consequences. These factors should all play a role in determining the proper therapeutic option (both surgical and nonsurgical) the oral and maxillofacial surgeon offers to the patient presenting with this disorder.
Effects of medications and associated medical conditions on sleep-disordered breathing Once the diagnosis of OSAHS has been established, treatment options must be explored. First,
however, possible medical conditions, as well as pharmacological agents, that could adversely affect sleep and breathing must be assessed. Even moderate alcohol intoxication can decrease hypercapnic ventilatory response to 50% of baseline [15]. Alcohol can precipitate OSA in vulnerable individuals. Older, obese subjects are more likely to be affected than are young healthy subjects. Patients with mild sleep apnea clearly develop longer and more frequent obstructive breathing events when they consume alcohol, and snorers can develop OSA after alcohol use [16]. Therefore, avoidance of alcohol for obese snorers and patients with obstructive sleep apnea is recommended routinely [17]. Smoking is widely known to impact upper airway physiology detrimentally. The irritation-inflammationedema cycle that occurs with repeated use of an irritant such as smoking is felt to affect a subtle form of mucosal edema of the upper airway, as well as increase upper airway mucosal secretions. The combined effect of these reactive conditions, instead of occurring externally, actually affects closure (or narrowing) of the upper airway. Per Pousille’s equation, small changes (narrowing) in the radius of the upper airway tube can potentially effect an exponential change in airflow and cause a greater chance for obstructive upper airway pathology. Hypnotics can also affect sleep and breathing and are frequently prescribed. Benzodiazepines are mild respiratory depressants [18]. Hypercapneic chronic obstructive pulmonary disease (COPD) patients appear to be particularly vulnerable to the respiratory depressant properties. Benzodiazepines, like alcohol, decrease upper airway muscle tone [19] and in this way may promote the development of OSA in susceptible individuals; therefore, they are best avoided [20]. Newer, non-benzodiazepine agents lack the myorelaxant and respiratory depressant effects of the benzodiazepines [21]. In general, however, it is best to avoid sedative-hypnotic agents in patients with hypercapnia and sleep apnea. Narcotics, too, are powerful respiratory depressants and are best avoided in patients with significant sleep apnea [22]. Hypothyroidism should also be considered in patients with a history of OSAHS. Possible mechanisms for the increase in sleep apnea seen in patients with hypothyroidism include obesity, impaired upper airway muscular function, and macroglossia. Though screening of all patients with OSAHS for hypothyroidism is not cost-effective, careful assessment of clinical symptoms is necessary [23]. In hypothyroid patients, it is important to treat their sleepdisordered breathing during thyroid replacement [24]. It may take considerable time for normalization
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of sleep and breathing, or patients may be suffering from two disorders. Pharmacological treatment of sleep apnea has not proven effective. In the late 1970s, agents such as protriptyline (a tricyclic antidepressant) were shown to reduce the number of apneic events by decreasing the amount of REM sleep and increasing hypoglossal nerve activity [25]. Whereas apneas were reduced in frequency, the total number of sleep and breathing events remained abnormal. Pharmacological agents studied and shown not to be of benefit in treatment include progesterone, tryptophan, and baclofen [26,27].
Use of supplemental oxygen, position restriction, and role of weight loss Other forms of medical treatment for OSAHS that have been studied include supplemental oxygen. Oxygen alone is not sufficiently effective in reducing the frequency of apnea or improving daytime alertness to be a therapeutic option [28]. Oxygen, however, may have a role as an adjunct to positive airway pressure in patients who remain hypoxic after correction of upper airway obstruction. Ongoing studies need to be completed in order to better understand the amount of desaturation that necessitates addition of oxygen. Restriction of sleeping position may offer significant benefit to some patients with OSAHS. Laboratory analysis routinely breaks down the presence of sleep-disordered breathing in both the supine as well as the nonsupine positions. The supine position, with resultant occlusion of upper airway based on effects of gravity on the tongue, can result in apneic or hypopneic events. For the oral surgeon, the effect of positional changes on upper airway volume can most easily be assessed clinically through the use of both acoustic pharyngometry, as well as with fiberoptic nasopharyngoscopy. In many cases, slight cervical extension of the neck while in the supine position may affect volumetric expansion of the upper airway. In this manner, cervical pillows, which allow one to sleep with slight extension of the head (while in the supine position), can be of benefit (one such pillow has shown some merit in minimizing apneic events in patients with mild OSA). But expecting a patient to maintain a substantial degree of uncomfortable cervical extension consistently during supine REM sleep is unrealistic. It is more likely, however, that obese patients will have OSAS regardless of their position during sleep [29]. For some patients, sleep and breathing is satisfactory in the lateral position with main-
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tenance of oxygenation and sleep continuity when lateral. Use of a small ball, such as a tennis ball, pinned to the pajama back may help patients to learn behaviorally to avoid sleeping supine. In addition sleeping with the head and trunk elevated to a 30° angle reduces OSAS as it stabilizes the upper airway [30]. Modification of body position during sleep should be considered in appropriate patients. No discussion of the management of OSAHS is complete without addressing obesity. The effect of obesity on the upper airway appears to be the result of mechanical effects on the upper airway (the pharyngeal dilator muscles are unable to work efficiently with increased load) and increased upper airway resistance. Studies have confirmed that weight reduction can ameliorate sleep-disordered breathing. It appears that the degree of improvement is not linearly related to the amount of weight lost [31]. In fact, it appears that there must be a critical amount of weight lost before there can be seen any significant improvement in sleep-disordered breathing. Obese patients should always be encouraged to lose weight, but obstructive breathing must be treated while the weight loss is underway.
Use of nasal continuous positive airway pressure In part because of the lack of a pharmacological treatment for OSAHS, nasal continuous positive airway pressure (CPAP) is the most established therapy choice. First used in Australia in 1981, its use in America became more widespread in l985 [32]. Nasal CPAP can best be conceptualized as a pneumatic splint that prevents collapse of the pharyngeal airway. CPAP successfully eliminates mixed and obstructive apneas [33]. Titration of the pressure to levels sufficient to eliminate not only the obstruction, but snoring and snore-arousals as well, can be difficult even for veteran sleep technicians. Adjusting to nasal CPAP can be trying, as patients adapt both to the mask and to the pressure cessation, as well as the headgear holding the mask in place. Instructional videos, review of goals of treatment, and time in the laboratory adjusting to the device can ease transition to use. Studies confirm the value of patient education programs to successful CPAP use and improved compliance [34]. Nasal CPAP titration has as its goal the elimination of respiratory related arousals in all sleep stages and positions. Once correct pressure is achieved, the number of arousals triggered by the sleep-disordered breathing should be markedly reduced. This leads to a ‘‘rebound’’ of slow wave and REM sleep [35].
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Snoring should be eliminated because it is a sign of inadequate CPAP pressure. It is apparent that higher CPAP pressures are generally needed when the patient is supine or in REM sleep. Successful titration in REM sleep in the supine position, the most vulnerable combination of stage and position for obstructive breathing, is the goal. Of course, additional factors may have an impact on CPAP pressures. Alcohol, for example, with its known neuromuscular effects, would be expected to result in the need for an increase in CPAP pressure, as would weight gain [36]. If patients have persistent sleepiness after treatment of their sleep-disordered breathing, then review of their sleep history is recommended. Patients may be suffering from a second, primary sleep disorder such as narcolepsy. Hypersomnolence would need to be assessed with a repeat evaluation in the laboratory, with CPAP in place to confirm treatment of sleep-disordered breathing, followed by a Multiple Sleep Latency Test to evaluate daytime fatigue. Problems related to nasal CPAP include mask discomfort, nasal congestion, and social considerations (including bed partner tolerance of the device) and chest discomfort and claustrophobia. The comfort of the CPAP mask is critical, and careful fitting of the mask is crucial to successful treatment. In our laboratory, technicians spend much time helping the patient choose an appropriate mask. Claustrophobic patients, or those who have beards or mustaches are otherwise difficult to fit, are encouraged to come by the laboratory prior to their study to have additional time for choosing an interface system. If a mask does not fit properly, there is an audible leak of air and resultant insufficient pressure and ineffective treatment. The patient may not be tightening the headgear sufficiently at home, whereas in the laboratory the mask was applied properly. If the air is leaking toward the eye, then conjunctivitis may result [37]. If the headband or headgear securing the CPAP is too snug, the increased tension may cause ulceration of the skin around the bridge of the nose. Nasal prongs or pillows alleviate some problems regarding comfort, but these can irritate the nares as well. Patients with claustrophobia may need time in the laboratory for desensitization and graduated exposure in order to be able to tolerate CPAP. Persistent nasal congestion is seen in more than 10% of patients on CPAP even after six months of treatment [38]. It has been found that the relative humidity of air inhaled through CPAP is 20% lower than relative humidity of room air [39]. The postulated causes of nasal congestion include unmasking of allergic rhinitis (particularly in mouth breathers);
vasodilatation of turbinate tissues triggered by mucosal receptors, or septal deviation and fixed obstruction. Efforts to increase nasal patency include the use of topical steroids, humidification, and topical antihistamine sprays. In some patients, correction of septal deviation (via septoplasty), or enlarged turbinates (via either radiofrequency, volumetric tissue reduction, or more traditional surgical turbinectomy) may be necessary before success with CPAP is obtained. Patients with persistent nasal congestion may respond to Passover humidifiers attached to CPAP. A recent study found that among patients with previous uvulopalatopharyngoplasty, those using drying medications, as well as those over age 60, were more likely to develop nasopharyngeal dryness. Heated humidification added to CPAP improved the daily use rate in this group of patients [40]. Nasal CPAP is effective only when the device is used, and used consistently. Studies indicate that even one night off CPAP can lead to the return of pathologic hypersomnolence [41]. But it is also true that patients can achieve some benefit from a partial night’s use. Early studies reporting on patient compliance with nasal CPAP were based purely on subjective patient reporting; these studies suggested a relatively high rate of CPAP compliance. Later studies, done with the use of covert patient monitoring, revealed a much lower compliance rate (these studies are generally felt to be a more accurate reflection of true nasal CPAP compliance). With new CPAP devices allowing for monitoring of patterns of use, more information for further study will soon be forthcoming. Even data on acceptance of CPAP when attempted in a laboratory setting can be confusing. Some studies have reported acceptance rates (agreement to use CPAP at home) of 80%, whereas others are as low as 58% [42,43]. It does appear that patients’ perception of improvement, not the severity of the obstructive breathing itself, is the most predictive measure of compliance [44]. Equally evident is the fact that patients overestimate their CPAP use [45]. It appears that about half of patients will be consistent users of CPAP, and Weaver et al showed that, by as early as day 4 of treatment, nonusers could be separated from nightly users [46]. Follow-up early after starting CPAP is important to help patients adjust to CPAP and to address initial difficulties. Studies do demonstrate that hypersomnolence prior to treatment is predictive of good compliance. Of course, this makes common sense, as the patient’s response to CPAP would be positive reinforcement for continued usage. In fact, one recent study by Barbe et al found that in patients with significant OSAHS but with no subjective sleepiness CPAP
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offered no improvement in cognitive function, quality of life, or arterial blood pressure [47]. This article does not, however, take into account such factors as effect on bed partner’s sleep, nor does it include objective measurement of sleepiness. When, then, should patients be treated? Again, careful clinical assessment is required, taking into account not only hypersomnolence and its associated risk for vehicular or industrial accidents, but also social factors such as unacceptable levels of snoring and potentially reduced cardiovascular risk factors [48]. When CPAP is not tolerated, it is important first to determine the specific cause for the discontinued use. A complete upper airway examination, looking for structural abnormalities, should be performed. Kribb et al have demonstrated that only 46% of patients were able to use CPAP for 4 hours each night at least 70% of the time [49]. Clearly, such objective measures indicate that CPAP compliance is less than optimal [50].
Bilevel positive airway pressure Bilevel positive airway pressure (BiPAP) devices have the capability to allow for a separate pressure for inspiration and expiration. It has been shown that patients with OSA need a lower expiratory pressure than that needed to prevent upper airway occlusion during inspiration [48]. As would be expected, the continuous pressure level of CPAP and the inspiratory pressure of BiPAP for a given patient would be the same. This makes intuitive sense, as identical levels would be needed to maintain inspiratory potency. Sanders et al found that a reduction in expiratory pressure could be achieved, with mean expiratory pressures being 37% lower than inspiratory pressures [51]. BiPAP can be delivered in three ways: (1) through a spontaneous, or patient-triggered mode, (2) through a spontaneous/timed mode, or (3) a timed mode alone. Only the spontaneous mode is usually indicated for OSA; the spontaneous/timed mode can be used in patients with significant neuromuscular disease, whereas the timed mode allows BiPAP to function as a controlled ventilator. BiPAP, because of its increased cost as compared with CPAP, is reserved for those patients who are intolerant of CPAP or who would benefit from lower expiratory pressures. Patients experiencing chest wall discomfort, or those sensing difficulty in exhaling against pressure or a smothering sensation, may benefit from BiPAP [52]. Studies have demonstrated a similar long-term compliance rate for CPAP and BiPAP, though the initial
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acceptance rate of BiPAP is higher [53]. If patients are more likely to accept the treatment initially, use will be increased overall.
Autotitrating CPAP Currently available, and being ever more finetuned, are CPAP devices that detect changes in flow and automatically adjust the pressure. These devices can detect changes in upper airway resistance (such as can be seen after alcohol use) and make the necessary pressure adjustments. Several methodological problems with autotitrating devices have been found, however. The devices appear to be confused by leaks about the cap mask, with resultant over pressure of CPAP as the device tries to compensate [54]. The devices appear to have a median pressure of 70 – 80% of peak ‘‘auto set’’ as compared with manual pressure. For most patients, though changes in position and sleep stage may require minor changes in CPAP pressure, these changes are insignificant and auto PAP offers little advantage. Additionally, auto PAP does not offer an advantage to patients with nasal congestion [54]. Further investigations are underway to establish guidelines on when use of auto PAP may be beneficial.
Alternative interface systems Recent innovations (combining oral appliance technologies with CPAP or BiPAP designs) are intended to minimize the inherent problems associated with nasal CPAP interfaces, troublesome headgear, and patient claustrophobia. CPAP Pro1 is a nasal CPAP interface, which utilizes a maxillary dental mouthpiece to hold a specially designed connector (this connector supports the tubing that attaches to nasal pillows). If properly fitted and oriented, this appliance has the potential to eliminate headgear completely. This appliance is currently being offered with a quick-setting gel polymer (so that the patient can make his or her own maxillary tray), or, as a professional kit, so that a more permanent and durable oral appliance can be fitted and placed by the dentist. This appliance can also be combined with an oral appliance (such as a Klearway1 or Herbst1 appliance) that affects mandibular advancement/ protrusion. The main benefit for their combined use with CPAP Pro is in their ability to maintain closure of the mandible, and to prevent oral leakage of the positive pressure ventilation. It is debatable whether the effect of mandibular
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protrusion will be of dramatic benefit (with this combined appliance) so as to lower the pressures required for elimination of obstructive upper airway pathology because ventilation through the relatively high-resistance nasal airway is still required. Oral Positive Airway Pressure (or OPAP1) has recently received FDA approval as an alternative interface system for patients requiring positive pressure ventilation. This custom-fitted oral appliance is designed to connect directly with the CPAP tubing, permitting oral positive pressure ventilation while bypassing the nasal airway. This one-piece appliance is also designed to permit fixed-position mandibular advancement, thereby potentially affecting expansion of the tongue-base region of the upper airway. In this case, one possible advantage to this design, because of the forward mandibular posturing, is the potential for lower required airway pressures for adequate ventilation and elimination of OSA, as the highresistance nasal airway is bypassed. Potential problems with this system, however, include those patients who have undergone previous uvulopalatopharyngoplasty- with the potential for nasal venting, as well as the drying effect on the oral cavity and pharyngeal airway. With each of the above alternative interfaces (as well as with oral appliances in general), retention of the appliance is critical. Also, as with all oral appliances used in the treatment of OSA, risks of alteration of the existing occlusion, TMJ dysfunction, and damage to existing dental restorations is possible. Compliance data with these newer interface systems is lacking at this time.
Oral appliances Although this topic is covered in detail in another article here, oral appliances have definitely found a place within the medical management of varying levels of upper airway obstructive pathology. The reader is referred to the accompanying article; membership within the Academt of Dental Sleep Medicine (www.dentalsleepmed.org) offers another excellent opportunity for those doctors wishing to learn more about this form of treatment.
Summary Sleep and breathing disorders are common. Assessment by the oral and maxillofacial surgeon should include thorough physical examination and assessment of clinical symptoms both during sleep
and wakefulness, as well as review of polysomnographic data. Treatment then focuses on nasal CPAP as the most widely accepted therapeutic option. CPAP is not always well tolerated, however; suboptimal compliance and complications often lead to its discontinuation. Optimizing CPAP treatment may require changes in the mask style or switching to BiPAP (particularly for patients with hypoventilation or refractory nasal congestion). The interface system may need to be changed entirely, as with OPAP1, in order for a patient to tolerate CPAP. More conservative treatment approaches include weight loss, position restriction, and oral appliances, effective options for patients with largely positional or only mild breathing obstruction. These options must be thoroughly investigated prior to initiating a course of irreversible surgical therapy. Pharmacological options have as yet been of no benefit. Obviously, future investigations must be directed toward better diagnostic tools for assessment of sleep apnea, especially as it relates to distortion of the upper airway when patients are in the supine position during sleep. It is hoped that newer treatments, offering improvement in overall tolerance and compliance, will derive from these efforts.
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