Current medical and surgical management of sleep related breathing disorders [1 ed.]

Table of contents :
Preface
History and epidemiology of sleep-related breathing disorders
Pathophysiology of obstructive sleep apnea
Evaluation and diagnosis of sleep-disordered breathing
Current medical management of sleep-related breathing disorders
Principles of oral appliance therapy for the management of sleep disordered breathing
Lasers in the management of snoring and mild sleep apnea
Surgical treatment of snoring and mild obstructive sleep apnea
Surgical evaluation for reconstruction of the upper airway
Radiofrequency thermal ablation therapy for obstructive sleep apnea
Nasal and palatal surgery for obstructive sleep apnea syndrome
Soft tissue hypopharyngeal surgery for obstructive sleep apnea syndrome
Genioglossus muscle advancement techniques for obstructive sleep apnea
Surgical changes of posterior airway space in obstructive sleep apnea
Postoperative management of the obstructive sleep apnea patient
Index

Citation preview

Oral Maxillofacial Surg Clin N Am 14 (2002) xi – xii

Preface

Current medical and surgical management of sleep related breathing disorders

N. Ray Lee, DDS Guest Editor

Since the time of early man, we have gathered information on the endless psychologic and emotional observations of the mysterious state of sleep. Concurrent with the onset of the millennium is a renewed zeal in our quest for increased illumination on the matter of sleep. Thanks to sleep research pioneers such as Dr. William Dement, sleep medicine is now recognized as a specialty by the American Medical Association (1996). Through the avenues of scientific investigation and dramatic advances in technology, our knowledge and understanding of the dynamics of sleep is rapidly increasing. Even so, Americans continue to move in the wrong direction. We have reduced our average sleep time by 30% since Thomas Edison invented the light bulb. We have increased our annual working and commuting time by more than150 hours. Yet, the ideal amount of sleep remains the same: onethird of the average life span or approximately 24 years. Americans are paying a price for insufficient sleep both financially and otherwise. Tens of billions of dollars are expended every year in lost productivity, accidents, and other byproducts of sleep deprivation. Too little sleep delivers a devastating impact on the quality of human life. The immeasurable misery of excessive daytime drowsiness, family dysfunction, loss of life and property, disabilities secondary to psychologic and behavioral malfunction, and cere-

brovascular and gastrointestinal complications is an all too real fact of life in the world of sleep deprivation. The gentle prod to ‘‘sleep tight’’ is obviously not granted automatically. We are simply not biologically prepared to handle interruptions in sleep. So, with increased awareness of the importance of sufficient sleep, more Americans than ever are seeking treatment for sleep disorders. As a surgeon, the gratification of treating patients with sleep-related breathing disorders is incomparable to any other aspect of my practice. To witness the restoration of a patient’s quality of life is a gift to a surgeon; as I listen to a patient’s expression of gratitude I am struck by how significant a role medicine has played in that person’s literal reawakening to the full spectrum of life enjoyment. Thus, the term ‘‘sleep surgeon’’ gives added dimension to a microsubspecialty that is indeed a multidisciplinary culling from numerous surgical specialties. The evolution of the sleep-related breathing disorder surgeon is still in progress. It is clear that future data collection is imperative to continued surgical success. As surgical techniques evolve, it is incumbent upon each surgeon to share and disseminate knowledge to perfect the interdisciplinary expertise that is necessary to advance the field. This publication coalesces a multidisciplinary approach in the treatment of sleep-disordered breathing (SDB). The commitment of the authors to unify their

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Preface / Oral Maxillofacial Surg Clin N Am 14 (2002) xi–xii

diverse expertise brings forth a unified successful treatment of sleep-related breathing disorders. Although there is no universally accepted treatment protocol, site specific surgical reconstruction of the upper airway is generally accepted. Let it be our goal to continue to bring the knowledge of science, experience, and treatment of complications to publication to advance our specialty in the successful treatment of SDB. Working with friends, colleagues, and contributors on this publication has been a valuable and interesting learning experience, and I thank them all for their dedication and contributions to the Oral and Maxillofacial Surgery Clinics of North America. I also thank John Vassallo and the pro-

duction staff of Elsevier Science for making this publication possible. N. Ray Lee, DDS Private Practice, 716 Denbigh Boulevard, Suite C-1 Newport News, VA 23608 Assistant Clinical Professor, Department of Oral and Maxillofacial Surgery, Medical College of Virginia Virginia Commonwealth University 520 North 12th Street, Richmond, VA 23298 Assistant Clinical Professor, Department of Otolaryngology—Head and Neck Surgery Eastern Virginia Medical School P.O. Box 1980 Norfolk, VA 23501 E-mail address: [email protected]

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History and epidemiology of sleep-related breathing disorders Robert D. Vorona, MDa,b,*, J. Catesby Ware, PhDc,d a Division of Sleep Medicine, Department of Internal Medicine, Eastern Virginia Medical School, USA Sleep Disorders Center, Sentara Norfolk General Hospital, 600 Gresham Drive, Norfolk, VA 23507, USA c Departments of Internal Medicine and Psychiatry, and Division of Sleep Medicine, Eastern Virginia Medical School, USA d Sleep Disorders Center, Sentara Norfolk General Hospital, 600 Gresham Drive, Norfolk, VA 23507, USA b

By the late twentieth century, the medical community recognized that snoring and daytime sleepiness were signs of obstructive sleep apnea syndrome (OSAS). Parts of the sleep apnea syndrome complex were, however, known many years earlier by an insightful few. The 1965 polysomnographic study that described obstructive, central, and mixed sleep apnea events during sleep was the beginning of the objective study of what we now recognize as sleep apnea syndrome [1]. Less well known are some earlier descriptions of the problem. Symptoms of heavy snoring and excessive daytime sleepiness were reported in a patient with acromegaly in 1896 [2]. Lavie [3] identified what may have been the first reported case of sleep apnea in a patient who had components of both obstructive and central apnea events [4]. Lavie also described two other 1889 cases with daytime sleepiness and failed respiratory attempts during sleep [5,6]. The description of these patients leaves no doubt that the phenomenon of obstructive sleep apnea, although unnamed and not understood, was recognized well before the advent of polysomnography. C.S. Burwell is often credited with first using the name Pickwickian syndrome when describing an obese patient with respiratory acidosis, heart failure, and sleepiness [7]. The term Pickwickian had actually been used, however, several times earlier to describe sleepy obese patients including the use by

* Corresponding author. E-mail address: [email protected] (R.D. Vorona).

William Osler. In The Principles and Practice of Medicine, Osler wrote in his chapter on obesity, ‘‘A remarkable phenomenon associated with excessive fat in young persons is an uncontrollable tendency to sleep like the fat boy in Pickwick’’ [8]. But because of the lack of understanding of the various conditions that could cause sleepiness and the absence of techniques to study sleep, the term Pickwickian described a heterogeneous group of patients with little regard to specific etiology. After Burwell’s work, the term Pickwickian typically indicated obesity accompanied by somnolence and lethargy, hypoventilation, hypoxia, and secondary polycythemia, but not necessarily repetitive sleep apnea events. By including hypoventilation and polycythemia as part of the syndrome, most of the sleep apnea patients seen in sleep disorder centers today do not have Pickwickian syndrome. The development of basic polysomnographic tools and procedures in the 1950s and 1960s provided a method to study causes of daytime sleepiness. Polysomnography led to the understanding that daytime sleepiness often originated from intrinsic sleep disturbances in the patients’ sleep. Prior to polysomnography, only secondary characteristics of OSAS were recognized and treated.

The growth spurt of the 1970s and 1980s Perhaps the number of publications in the field best reflects the explosion in interest in OSAS. Publications addressing sleep apnea in some form

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increased by nearly tenfold in the 1980s when compared with the 1970s (Fig. 1). At the same time, the reports on Pickwickian syndrome decreased. This decrease in part was from recognition of the heterogeneous population that the term Pickwickian encompassed. An early champion of OSAS in the United States was a young Frenchman, Christian Guilleminault, at Stanford University. Despite a focus on insomnia and narcolepsy by the small community of those studying sleep and sleep disorders in the United States, Guilleminault forged ahead with his interest in sleep apnea, motivated by the idea that differences in the control of vital functions during sleep contributed to a number of medical disorders. Returning to Europe where there was considerable interest in the Pickwickian syndrome, Guilleminault recorded several hundred patients at a sleep medicine clinic at La Salpetriere Hospital in Paris. He realized that breathing irregularities and apnea occurred in a variety of patients, not necessarily obese ones (personal communications, March 2001). Later after his return to Stanford University, Guilleminault and associates helped to demonstrate that OSAS caused excessive daytime sleepiness more often than narcolepsy. They developed an objective definition of OSAS as five

events per hour of sleep lasting at least 10 seconds each [9]. They extended the investigation of apnea to children [10 – 13]. Early on, they also hypothesized that sleep apnea might be related to sudden infant death syndrome [14]. The recognition of children and infants as possible at-risk populations along with his other work considerably increased the interest in and study of sleep apnea. Researchers employed a variety of techniques to better understand what occurs during sleep apnea events. Lateral imaging of the upper airway using Xerography in a small number of severe OSAS patients revealed no specific pathology when awake but a clear collapse of airway space at the base of the tongue during sleep [15]. Compared with controls, fluoroscopy and computed tomography indicated a more narrow section of the airway in patients in the region posterior to the soft palate [16]. Direct observation with fiberoptic endoscopy of the sudden dramatic closure of the airway suggested the possibility of an active process; an alternative explanation was that muscle relaxation and a negative pharyngeal airway pressure accounted for the rapid airway collapse and apnea events [17,18]. In the late 1970s, the recognition that OSAS can occur in families added another dimension to the

Fig. 1. The number of publications listed in PubMed (National Library of Medicine, Rockville Pike, MD) generated by the search terms ‘‘sleep apnea’’ and ‘‘Pickwickian’’ for 5-year blocks, 1965 – 1999.

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problem and further emphasized the complexity without clarifying the etiology [19,20]. For example, the apnea-potentiating trait of a small or retrognathic mandible can have both genetic and environmental contributing factors. Analysis of lateral cephalometric radiographs did help identify those with mandibular deficiencies and a shallow posterior airway space (PAS), although no imaging technique or other test when patients were awake was able to identify all sleep apnea cases [21].

Treatment Surgery The difficulty in treating OSAS patients tempered the excitement of recognizing the problem of OSAS as a primary cause of excessive daytime sleepiness. The standard treatment of tracheostomy was traumatic but successful in relieving OSAS [22,23]. A tracheostomy with its accompanying improvement in areas other than daytime sleepiness gave hints of the complexity of the sleep apnea problem. For example, this surgical procedure not only relieved the apnea events but also reduced cardiac arrhythmias [24] and improved the ventilatory response to CO2 [25]. This helped foster the realization that intermittent obstruction during sleep had pervasive effects on neurological, cardiac, and respiratory functioning. It also helped to emphasize the importance of normal sleep and raised the problematic question of ‘‘How many apnea events during sleep are too many?’’ Even with the threat of a tracheostomy, most obese apnea patients could not lose weight by dieting. Treating OSAS patients with a weight loss prescription, although often beneficial when a patient could lose weight [26], succeeded only in a minority of patients. In addition, there was a high recidivism rate for those who initially lost weight. Therefore, bariatric surgery to induce weight loss and treat obstructive sleep apnea was introduced in the late 1970s [27] and continues to be used successfully in selected cases [28]. Following the recognition that retrognathia could contribute to apnea events, mandibular surgery was used successfully to treat retrognathic OSAS patients [29,30]. In addition, mandibular surgery was successfully used to treat OSAS in an obese patient [31]. The treatment with the greatest impact on OSAS, although unfortunately not the greatest success rate, was that of the uvulopalatopharyngoplasty (UPPP), [32]. The UPPP was a less drastic but less effective procedure than tracheostomy. Because a tracheos-

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tomy was used primarily for end-stage OSAS patients, the development of a surgical technique with the potential of treating less severe cases was welcomed. The UPPP allowed some patients to avoid a tracheostomy. In addition, the UPPP fit well into the conceptualization of the etiology of OSAS. Specific upper airway obstructions, for example, large tonsils and adenoids [33,34], nasal obstruction [35], and supraglottic edema [36], were understood to cause the obstruction and apnea. Evidence suggested, however, that other factors also played a role. A second UPPP benefit was its high failure rate. Because the UPPP was far from 100% successful and was not free of morbidity and mortality, documentation of both the presence and severity of OSAS was necessary before performing an UPPP. Therefore, the availability of the UPPP as a treatment option resulted in the consistent polysomnographic study of a large number of patients with symptoms of OSAS. These clinical studies raised the awareness of the prevalence of OSAS and allowed the development of an appreciation of the range of severities of OSAS (from 0 to 100+ events per hour of sleep). This quantification of the frequency of apnea events also provided a baseline for comparing different techniques for treating OSAS patients. Pre- and postoperative polysomnographic studies of OSAS patients also led to an early awareness that subjective reporting of improvement by the patient often was not congruent with polysomnographic findings [37]. The approximate 50% success of the UPPP [38], recognized early on from those doing postsurgical sleep studies, spurred the search for other treatments. Treatment failures also reinforced the idea that for some OSAS patients, more than a mechanical obstruction of the upper airway was involved. The differences between men and women [39], the effects of aging [40], and the effects of sleep stage on apnea frequency [41] indicated that OSAS involved both physiological and pathophysiological (as well as anatomical) factors. A number of nonanatomical factors may play a role in OSAS. The tone of the pharyngeal dilating muscles, pharyngeal extramural pressure, and pharyngeal compliance all may contribute to OSAS [42], and treatment without regard to the specific etiology is likely to have a significant failure rate. Oral appliances Despite the logic of pulling the mandible forward to open the airway, the sleep community greeted the first reports of using an oral appliance to treat OSAS with considerable skepticism. As is usually the case

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for new procedures, the early reports were not controlled trials [43,44]. But persistence on the part of the dental community, more rigorous studies showing polysomnographic efficacy (rather than self report), and the developing need to treat patients intolerant or nonresponsive to other treatments gained the oral appliances wider use and the opportunity to improve and become an important treatment option. Pharmacological treatment Early pharmacological treatment attempts included use of medroxyprogesterone [45,46] and even strychnine in a ‘‘Don’t do this at home study’’ [47]. The motivation to use strychnine was to correct upper airway hypotonicity. More recently, researchers have attempted to stimulate electrically the upper airway musculature [48]. One of the problems inherent in this technique is the arousal from sleep produced by the electrical stimulation. Thus, it is difficult to separate the specific effects of stimulating the muscle from the more general effects of an arousal from sleep. One of the successful early pharmacological treatments was the use of protriptyline [49,50]. Although protriptyline, an alerting tricyclic antidepressant, may have helped because of improved alertness and mood, it also reduced apnea events possibly by increasing muscle tone. One of the most pronounced effects of protriptyline is the suppression of REM sleep, the sleep stage accompanied by loss of antigravity muscle tone. The stage of REM sleep can have the longest apnea events with the most severe oxygen desaturations. To what degree REM sleep and apnea would return after long-term use is unknown. One study indicated that apnea returns after a year, but patients continued to report feeling better and had slightly higher O2 saturation baseline [51]. Continuous positive airway pressure The technique of using continuous positive airway pressure (CPAP) in the upper airway essentially became the nonsurgical tracheostomy [52] and transformed the field of sleep disorders medicine by providing a low morbidity treatment with a high success rate. If used by the patient, it keeps the upper airway patent. A significant number of patients ( > 30%), however, do not continue to use CPAP over the long term [53]. Practical problems of administering positive air pressure to the upper airway comfortably were difficult to overcome. But FDA approval in the United States in the mid-1980s and product commercialization led to continued refinements in mask fit, material,

and humidification. Once the most common treatments for OSAS was nonsurgical; patients with milder symptoms of OSAS were evaluated and treated. This led to an explosion in the number of sleep disorder facilities and patients studied. This growth also reinforced the need for a credentialing body for clinicians (American Board of Sleep Medicine) and an accreditation body for sleep disorders centers (American Academy of Sleep Medicine). The availability of CPAP allowed for a change in location to nonhospital based centers. Treating less severe patients also opened the possibility for the investigation and use of portable diagnostic equipment and self-titrating CPAP devices. Thus, moving some of the diagnostic and treatment procedures to the home is now under investigation.

Epidemiology of OSAS The problem of OSAS spans all age groups and both sexes and is found throughout the globe. Obesity is often but not always a critical determinant of OSAS. An enlarging body of work reveals the cardiovascular and cerebrovascular links and consequences of OSAS. Classically, OSAS was thought to be a syndrome of the middle-aged. All age groups may have apneic events during sleep, however. In over 1000 healthy full-term infants who ranged in age from 2 to 28 weeks, the absolute numbers of obstructive or mixed apneas in these infants were quite low [54]. Of interest, males between 8 and 11 weeks of age were more apt to have obstructive apneic events and more events per hour than females. The apnea events tended to decline in length with age. Apneas do not always connote disease in infants. Central apneas (apneas without respiratory effort) may occur in normal infants, and even protracted central apneas with desaturation may not be of import [55,56]. Older children are not exempt from OSAS. Redline and associates found 1.6% of their children or teens (2 – 18 years old) had sleep disordered breathing (SDB) as defined by a respiratory disturbance index of greater than or equal to 10 events per hour [57]. Between the ages of 2 and 8 years, children are most apt to have OSAS [58]. The tonsils and adenoids are of great importance in putting these children at risk for sleep disordered breathing events. In contrast with adults in whom tonsillectomy and adenoidectomy are rarely curative for OSAS, in children the same operative procedure is often but not always effective [59]. Frank anatomic abnormalities in children are not, however, the only reason for obstruction of the

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upper airway [58]. Neuromuscular function alteration can also be of import. Cerebral palsy and muscular dystrophy put children at risk for OSAS [60,61]. Skeletal abnormalities also put children at risk for sleep-disordered breathing [59]. Children with OSAS may like their adult counterparts be obese. Redline et al found what they described as a moderate linkage with an odds ratio for obesity and SDB of 4.6 [57]. They also linked respiratory disease of both the upper and lower tract. In contrast with data in adults, they did not, however, find a clear relationship between sex and SDB in children. Work from Spain has investigated sleep disordered breathing in children 12 – 16 years old. This study of 101 teens, buttressed by the use of limited polysomnography, found that 29% snored and 17.8% had a respiratory disturbance index of greater than or equal to 10 [62]. Only 1.9%, however, also had symptoms indicative of the diagnosis of OSAS. The authors noted that this frequency was akin to that found in younger children. Middle school children with poorer performance are more likely to snore [63]. It appears that even medical students who snore are more likely to fail examinations [64]. Potential complications of untreated OSAS in children include failure to thrive, pulmonary hypertension, cor pulmonale, and arterial hypertension [13,59,65]. As OSAS usually has been associated with older patients, the clinician may not be as quick to think of OSAS in the child as in the adult. Nevertheless, the potential complications, though serious, are remediable [59,66] and therefore warrant that clinicians be cognizant of OSAS in children. OSAS, with its complications including daytime sleepiness and difficulties with memory and concentration, obviously can impair school performance. Teens already are at risk for difficulties functioning in the morning because of a tendency to delayed sleep phase (they tend to go to sleep later and wake up later), coupled with high school hours that prod them to start the day early. Concomitant OSAS could only exacerbate this situation and hence deserves consideration. In addition, sleep loss suffered by teens may exacerbate existing sleep apnea [67]. A study at the Chinese University of Hong Kong used a questionnaire to study some 1910 students followed by limited polysomnographic recordings in some [68]. They found by questionnaire that some 25.7% had snoring. In the small subgroup who underwent a limited sleep study, only 2.3% had a respiratory disturbance index of greater than 5. Hence, once again the prevalence of OSAS was relatively low.

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Young et al performed a critical study to assess the impact of sleep disordered breathing in middle-aged adults [69]. In this study of middle-aged Wisconsin state employees aged 30 – 60 years, some 9% of women and 24% of men had a Respiratory Disturbance Index (RDI) of greater than or equal to 5 per hour. When coupled with complaints of excessive daytime sleepiness, 2% of women and 4% of men manifested OSAS. This study is perhaps the best measure of the prevalence of OSAS in the US adult population to date. A study in Spain examining the prevalence of SDB and OSAS in a 50 – 70-year-old population found that 29% of the patients (28% men, 30% women) had an RDI of greater than or equal to 5 per hour. Although there was no sex difference for number of sleep disordered breathing events, only men were symptomatic, and therefore only the men were diagnosed with OSAS as defined both by sleep disordered breathing and symptoms [70]. Another study used oxygen desaturation events of greater than or equal to 4% as a surrogate to screen for OSAS in a 40 – 64-year-old group; the authors projected from their sample that an apnea occurrence of more than or equal to 15 per hour occurred in 20.3% of the men and 7.6% of the women [71]. Some data suggest even higher rates of sleep disordered breathing in the elderly. In one study investigating the frequency of respiratory disturbances in those greater than or equal to 65 years of age, 24% of their sample had greater than or equal to 5 apneas per hour, and 62% had an RDI greater than or equal to 10 per hour [72]. Over the next 8.5 years, however, there was no progression in sleep related respiratory events [73]. The importance of these respiratory events in the elderly is controversial. For example, Ancoli-Israel et al in 1989 showed that elderly women with sleep disordered breathing had an increased mortality [74]. Mant et al [75] in a study of the elderly did not find such increased mortality associated with OSAS as defined by an RDI greater than or equal to 15. Additionally, when Phillips et al. looked at elderly subjects who were ostensibly healthy, those with an RDI over or equal to 5 per hour showed no alteration in daytime performance [76]. Early evidence indicated that OSAS was overwhelmingly a male phenomenon [39]. The more recent information above reveals, however, the male to female ratio more closely approximates 2 – 3: 1. Bixler et al [40] showed that 3.9% of men and 1.2% of women had OSAS. But premenopausal women and postmenopausal women on hormone replacement therapy had much lower prevalences (0.6% and 0.5%,

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respectively) than postmenopausal women (2.7%). They therefore postulated that the premenopausal status and hormone replacement therapy were protective. Those apneic females who were premenopausal or postmenopausal and taking hormones were all obese, thus defining the essential role of obesity in these subgroups. In addition, Pickett et al found that the combination of estrogens and progesterone decreased respiratory events in nine women postovariectomy and hysterectomy [77]. In a large population of Italian women aged 40 – 65 years, 19.7% ‘‘always snored’’ and 10.7% had a respiratory disturbance index from 5 to 9 per hour [78]. Nearly 8% had more severe SDB with a respiratory index between 10 and 19. Interestingly, in contrast with Bixler et al, this study could not correlate menopausal status and sleep disordered breathing. In a study comparing Body Mass Index (BMI) matched men and women presenting to a sleep disorders center, men had significantly more apnea in the young and middle-aged groups but were similar to women in the older age group, presumably when the women were postmenopausal [79]. Sleep disturbances during pregnancy have been frequently noted with snoring and nocturnal choking among the complaints possibly linked to OSAS. Of 127 pregnant women in an outpatient setting, it was determined that 29.8% snored during pregnancy [80]. The majority of these women did not snore prior to pregnancy. By the last quarter of pregnancy, approximately 31% reported awakening choking, a symptom the authors attempted to relate to OSAS. This information achieves greater import when one reviews the data from Franklin et al [81]. In their study of 502 pregnant women, there was a 23% incidence of nightly snoring in the last week of pregnancy. Those who snored were more than two times as likely to develop hypertension during pregnancy and preeclampsia, and to deliver children with growth retardation. A low Apgar score also occurred more frequently in children born to mothers who snored habitually. Treating preeclamptic women with CPAP demonstrated improved upper airway flow mechanics and blood pressure control [82]. Racial differences also occur in OSAS patients. Much of the above information is related to Caucasians from North America and Western Europe. Kripke et al [71] found that 16.3% of the Hispanics and other minority patients had 20 or more events per hour. This was in contrast with only 4.9% of their Caucasian patients. In children, Redline et al [57] showed that African-Americans were at increased risk for OSAS. Elderly African-Americans appear to have twice the risk of severe sleep disordered

breathing when compared with Caucasians [83]. Brachycephaly appears to put Caucasians at risk, whereas soft tissue abnormalities may be of more importance in African Americans [84]. Differences in OSAS between Caucasians and Far East Asians also occur. Ip et al [85] reported that 4.1% of middle-aged Chinese men have OSAS (roughly comparable with Young’s data). Obesity, however, was a less important exacerbating factor for OSAS in Chinese than in Caucasians as found by Young. Caucasian apneics are more obese than Asian apneics [86]. If matched for BMI, the Asians with OSAS had more severe disease than Caucasians with OSAS. The Far East Asians had ‘‘a significantly shorter anterior cranial base and more acute cranial base flexure’’(58). Caucasians and Asians with OSAS also differed on some soft tissue measures (eg, PAS and mandibular plane to hyoid distances). Liu et al compared cephalometrics in Chinese and Caucasians with OSAS and found skeletal differences that they described as ‘‘steeper and shorter anterior cranial bases’’ [87]. Many but not all of the soft tissue structures were similar between Chinese and Caucasians. These differences may have import in planning either treatment approaches with surgery or mandibular repositioning devices. Further, OSAS should not be approached as a monolithic syndrome in these different groups. Although anatomic differences may exist between races with OSAS, obesity is prevalent in its role as a risk factor. Some 60 – 70% of patients with OSAS are obese [88]. Alternatively, more than 50% of obese patients with a BMI of greater than 40 kg/m2 have OSAS [89]. Obesity, although a risk factor for SDB in children and adults, may not be as important in children [57]. Young’s study of the middle-aged noted, ‘‘An increase of 1 SD in any measure of body habitus was related to a threefold increase in the risk of an apnea-hypopnea score of 5 or higher’’ [69]. Grunstein et al showed that increasing central obesity correlated with worsened sleep apnea [90]. As would be expected, weight loss does reduce OSAS. In a study of 690 patients, a 10% weight gain lead to a 32% worsening in RDI and a 10% weight loss lead to a 26% improvement [91]. Of interest, obesity may have differential effects by gender. Upper body obesity worsened OSAS in men more than in women [92]. Although there is controversy, some evidence suggests that BMI may be the best predictor of RDI in women, whereas neck circumference may be the best predictor in men [89]. In addition to the above demographics, the oral surgeon interested in OSAS must appreciate the importance of family history. Pillar and Lavie [93]

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studied the adult children of 45 patients diagnosed with OSAS. Remarkably, 47% of these children had OSAS. They also found that an additional 21.9% of the remaining patients studied had simple snoring. Finally, no discussion of the epidemiology of OSAS would be complete without discussing some of the recent important information concerning mortality and cardiovascular and cerebrovascular complications. He et al [94] noted that an apnea index of greater than 20 per hour was associated with 0.63 eight-year survival. This is compared with 0.96 eightyear survival in those patients with an index less than 20 per hour. As opposed to tracheostomy and CPAP, uvulopalatopharyngoplasty had no impact in decreasing this increased mortality rate. Interestingly, there was a large range in causes of death, a number of which were not obviously related to OSAS. Lavie et al [95] also found an increased death rate in individuals with OSAS. This increased risk of death was in those in the fourth and fifth decades of life. They postulated that the major risk factor for death was hypertension. Recent data clearly associate OSAS and hypertension. The Sleep Heart Health Study evaluated sleep disordered breathing and hypertension in 6132 patients who were either middle-aged or elderly [96]. Despite aggressive attempts at controlling for confounding factors, a moderate relationship occurred between SDB and hypertension. This relationship between SDB and hypertension was dose-dependent (although not linear), thus giving further credence to the relationship. Peppard et al [97] in the Wisconsin Sleep Cohort also discovered a dose-dependent relationship between sleep disordered breathing and blood pressure level four years later. A large study by Ohayon et al [98] comprising 13,057 subjects also linked OSAS and hypertension. An earlier study by Carlson et al linked OSAS and hypertension as well as age and BMI [99]. These associations between OSAS and hypertension are not solely limited to the adult population. Marcus et al [100] have compared blood pressure readings in children with OSAS and children with primary snoring. Diastolic blood pressure was more elevated in the group with OSAS. Conversely, the presence of hypertension in a patient should make the clinician think of OSAS. Worsnop et al [101] found that 34% of untreated and 38% of treated hypertensive patients had OSAS. Hypertension is a major risk factor for coronary heart disease and cerebrovascular disease. OSAS and these two major killers have been investigated. Hung et al [102] used polysomnography to study patients shortly postmyocardial infarction but outside the hospital. OSAS was associated with an increased

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risk of coronary heart disease. The Sleep Heart Health Study revealed what the authors called ‘‘modest to moderate effects of sleep-disordered breathing on heterogeneous manifestations of CVD’’ [103]. They found a more marked relationship for OSAS and congestive heart failure than coronary heart disease. One daunting aspect of the study was that seemingly rather trivial numbers of respiratory disturbances seemed to put one at risk for cardiovascular consequences. A study in Sweden prospectively tracked patients with coronary heart disease and OSAS and found that untreated OSAS was linked with an increased death rate from cardiovascular causes [104]. OSAS and stroke have also been associated in the sleep literature. The Sleep Heart Health Study not only linked OSAS and heart disease but also linked OSAS with stroke. In fact, the association with stroke in this large study was stronger than with coronary heart disease. A study of transient ischemic attack (TIA) and stroke with OSAS found a high frequency of OSAS in both patients with TIA and stroke [105]. The authors pointed out the interesting fact that TIA also was clearly linked to OSAS, making it less likely that the OSAS was a consequence of the cerebral event. A number of reasons have been postulated for the increased risk of cardiovascular and cerebrovascular events. Several investigators have demonstrated increased sympathetic activity in OSAS patients. Somers et al [106] showed that patients with OSAS had increased sympathetic nervous system activity both awake and asleep. In contrast with the norm, these patients showed elevations in blood pressure during sleep. When CPAP was applied to these patients, both sympathetic activity and blood pressure were reduced. Hedner et al [107] interrogated the response of sympathetic activity in OSAS treated by CPAP by measuring norepinephrine, vanilmandelic acid, and metanephrines. They found decreases in catecholamines but change neither in cardiac structure nor in blood pressure.

Directions in the twenty first century In addition to refinements in surgical techniques for treating OSAS, we expect that there will be considerable advances in the understanding of sleepiness and other OSAS symptomatology. Although some details are missing, we now know that repeated disturbances in respiration during sleep play a major role in the typical symptoms of OSAS. In addition, we are beginning to understand how sleep arousals,

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hypoxic and hypercapnic insults, and accompanying autonomic liability contribute to OSAS symptomology. These events may not account, however, for the complete picture. Obesity itself may contribute to the sleepiness [89,108]. The question ‘‘Are obese apnea patients of similar-frequency apnea more sleepy than less heavy patients?’’ is still one that needs to be clearly answered along with the question, ‘‘Why are all sleep apnea patients not sleepy?’’ [109]. Defects in the recently recognized hypocretin neurotransmitter system appear to be the key pathology in narcolepsy [110]. The hypocretin system that also appears to be involved with the regulation of normal sleep-wake behaviors and energy metabolism [111] probably contributes to the symptomatology in OSAS. Learning more about the underlying pathophysiology will allow us to apply our treatment armamentarium better and develop new and improved treatment methods.

[12]

[13]

[14]

[15]

[16]

[17]

Acknowledgments The authors were supported in part by NIH award # HL03652-01A1 to JCW.

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Pathophysiology of obstructive sleep apnea M. Safwan Badr, MD Medical Service, Detroit Veterans Affairs Medical Center, Detroit, MI, USA Division of Pulmonary Critical Care and Sleep Medicine, Department of Medicine, Wayne State University School of Medicine, 3990 John R, Detroit, MI 48201, USA

Obstructive sleep apnea (OSA) is a fairly common disorder with significant adverse health consequences; however, the pathogenetic mechanisms remain incompletely understood. Upper airway (UA) patency is determined by several neuromuscular and nonneuromuscular factors including the following: (1) UA-dilating muscle activity, (2) the collapsing transmural pressure generated during inspiration, (3) changes in caudal traction, (4) vasomotor tone, and (5) mucosal adhesive forces. This article addresses the effect of sleep on UA function and how these factors conspire to cause UA obstruction. The occurrence of UA obstruction during sleep and not wakefulness implicates the removal of the wakefulness stimulus to breathe as a key factor underlying UA obstruction during sleep. Most of the data on sleep effect are derived from studies during nonrapid eye movement (NREM) sleep, given the difficulty in achieving REM during invasive studies in the laboratory environment.

Physiology of sleep The sleep state is classified into two distinct broad states: NREM sleep and REM sleep. Nonrapid eye movement sleep NREM sleep is classified into four stages by increasing depth from 1 through 4. Stage 1 is light sleep, slightly beyond drowsiness; stage 4 represents

E-mail address: [email protected] (M.S. Badr).

deep sleep. The electroencephalogram (EEG) shows decreased frequency and increased amplitude as sleep progresses from stages 1 through 4. Rapid eye movement sleep REM sleep is the stage when most dreaming occurs. While all antigravity muscles are paralyzed; there is increased activity of the central nervous system (CNS), and the EEG is fast with low amplitude waves (resembling an ‘‘awake’’ EEG). Thus, REM sleep is described as ‘‘paradoxical’’ sleep, showing an active CNS and paralyzed periphery. REM sleep occurs in cycles every 90 to 110 minutes. Its duration is often reduced in the laboratory environment, especially if complex instrumentation is used.

Effect of sleep on ventilation Although sleep is viewed as a quiet resting period, judging by the ‘‘passive’’ appearance of a sleeping subject, this is far from true. The sleep state represents a challenge rather than rest period for the ventilatory system. The effects of sleep on ventilation set the stage for the development of sleep apnea and may provide the mechanistic link in susceptible individuals. Loss of the wakefulness stimulus to breathe is the key factor driving changes in breathing during sleep. Thus, ventilation becomes dependent on chemoreceptor and mechanoreceptor stimuli. Consequences of loss of wakefulness include reduced tidal volume, reduced activity and UA dilators, reduced UA caliber and loss of load compensation [1,2] (Fig. 1).

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 3 6 - 5

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Fig. 1. Effects of sleep on ventilation and upper airway mechanics during sleep. VT, tidal volume; VA, alveolar ventilation; PaCO2, arterial CO2 partial pressure.

Reduced tidal volume Reduced ventilatory motor output during sleep is associated with reduced tidal volume, reduced alveolar ventilation, and elevated PaCO2. Increased arterial PCO2 is also caused by increased UA resistance and impaired load compensation (see later). Reduced activity of upper airway dilators UA-dilating muscle activity is reduced during NREM sleep, especially in muscles with tonic activity (independent of the phase of respiration), such as the tensor palatinii muscle, which is reduced at sleep onset [3]. Reduced upper airway caliber UA caliber is reduced during sleep, likely because of decreased UA-dilating muscle activity [4,5]. The mechanical corollary of reduced caliber is increased UA resistance [6,7]. If UA caliber is reduced sufficiently, inspiratory flow limitation develops, manifesting by a plateau in flow despite continued development of negative pressure [8]. Fig. 2 illustrates increased UA resistance and flow limitation during sleep in a normal subject. Loss of load compensation The ability of the ventilatory control system to compensate for changes in resistance is essential for the preservation of alveolar ventilation. Breathing through a resistor during wakefulness (load) leads to increased ventilatory effort to maintain ventilation

and PaCO2. In contrast, loads are not perceived during sleep and immediate compensation to added loads is compromised. Therefore, resistive loading results in decreased tidal volume and minute ventilation, and thus alveolar hypoventilation. The ensuing elevation of arterial PaCO 2 restores ventilation toward normal levels [9,10]. Teleologically, failure to perceive and immediately respond to loads allows for sleep to continue unperturbed. The main consequence of undisturbed sleep is a mild increase in PaCO2. In fact, elevated PaCO2 during sleep is common and is one of few physiologic situations where hypercapnia is tolerated. Snoring, a marker of pharyngeal narrowing Increased UA resistance during sleep is physiologic; however, a substantial increase in resistance may cause ‘‘fluttering’’ of the soft palate because of turbulent flow. This fluttering is responsible for the acoustic phenomenon known as snoring. In addition, individuals who snore demonstrate increased pharyngeal wall compliance during sleep, resulting in inspiratory flow limitation when flow plateaus during inspiration, despite continuous generation of subatmospheric intraluminal pressure(see Fig. 2). If increased resistance and inspiratory flow limitation are severe, increased work of breathing and hypoventilation can lead to frequent arousals from sleep and ensuing excessive daytime sleepiness. Fig. 3 depicts decreased tidal volume, reduced flow with flattening of the flow profile, and increased PCO2 during sleep relative to wakefulness. This has been recently described as a distinct clinical entity called the upper airway resistance syndrome [11].

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Fig. 2. Pressure-flow loops during wakefulness and sleep. Note that flow is less during sleep for a given pressure. Also, note the development of inspiratory flow limitation during sleep evidenced by a plateau in flow despite decreased (more negative) subatmospheric pressure. The arrow indicates the onset of flow limitation.

Chemoresponsiveness and the hypocapnic apneic threshold The loss of the wakefulness stimulus to breathe renders ventilation during NREM sleep critically dependent on chemoreceptor stimuli (PaO2 and PaCO2). Reduced PaCO2 is a powerful inhibitory factor of ventilation. Therefore, central apnea develops when PaCO2 is reduced below a highly reproducible hypocapnic apneic threshold, unmasked by NREM sleep [12] (Fig. 4). Hypocapnia is probably the most important inhibitory factor during NREM sleep. Many cases of central sleep apnea are due to breathing instability leading to hypocapnia.

REM sleep: a special case Most of the studies on sleep effect were in NREM sleep because REM is difficult to achieve under instrumented conditions.REM sleep is associated with muscle atonia affecting many UA dilators

and intercostals; the diaphragm is spared.Despite the muscle atonia, pharyngeal compliance is not increased during REM sleep [4,5]. In fact, the retropalatal airway is less compliant during REM sleep relative to NREM [4]. This finding indicates the significance of non-neuromuscular factors in maintaining UA patency during sleep. REM sleep is a special case because peripheral atonia is accompanied by augmented inspiratory medullary neuronal activity, and the REM sleep EEG shares many features of the awake EEG. Whether hypocapnia inhibits ventilation during REM sleep has not been proved.

Determinants of upper airway patency during sleep Upper airway size and shape There is evidence that the pharyngeal airway is smaller during wakefulness in patients with OSA

288 M.S. Badr / Oral Maxillofacial Surg Clin N Am 14 (2002) 285–292 Fig. 3. A polygraph segment depicting changes in breathing from wakefulness to nonrapid eye movement sleep. Note the augmentation of supraglottic negative pressure (Psg), decreased tidal volume (volume), and increased PET CO2, partial pressure of end-tidal CO2. EEG, electroencephalogram.

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Fig. 4. Induced hypocapnic central apnea. Nasal mechanical ventilation (mech. vent.) was used to decrease PET CO2 below apneic threshold. Termination of mechanical ventilation resulted in a prolonged central apnea. EOG, electro-oculogram; EEG, electroencephalogram; PSG, supraglottic negative pressure; PETCO2, partial pressure of end-tidal CO2; Pmask pressure in the nasal mask.

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compared with that of normal individuals [13,14]. In addition, the pharyngeal airway in patients with sleep apnea has an anterior/posterior configuration unlike the horizontal configuration in normal individuals [13]. The implications of the observed lateral narrowing to the pathogenesis of UA obstruction during sleep are yet to be determined. Transmural pressure A collapsing transmural pressure can be generated either by a negative intraluminal pressure or a collapsing surrounding pressure. The role of negative intraluminal pressure in the pathogenesis of UA obstruction is widely presumed [15]. Accordingly, a subatmospheric intraluminal pressure generated by the thoracic pump muscles causes UA obstruction by ‘‘sucking’’ the hypotonic UA. There are no data showing that subatmospheric intraluminal pressure causes UA obstruction in sleeping humans. In addition, Badr et al [16] have demonstrated that pharyngeal obstruction does not require negative pressure. Using fiberoptic nasopharyngoscopy, they have shown complete UA collapse during central apnea in patients with sleep apnea [16]. The occurrence of complete UA obstruction in the absence of negative intraluminal pressure supports the hypothesis that the UA collapsed by extrinsic pressure. Similarly, Isono et al [17] compared the mechanics of the pharynx in anesthetized, paralyzed normal subjects and patients with obstructive steep apnea. The pharynx was patent at atmospheric intraluminal pressure in normal subjects and required negative intraluminal pressure for closure. In contrast, patients with obstructive sleep apnea had positive closing pressure (ie, the pharynx was closed at atmospheric intraluminal pressure). Thus, the surrounding extraluminal pressure is an important contributor to the collapsing transmural pressure during sleep [18,19]. Pharyngeal compliance The compliance of the pharyngeal wall is an important modulator of the effect of collapsing transmural pressure; a stiff tube is more likely than a compliant tube to remain open, even in the face of a collapsing transmural pressure. The intrinsic stiffness of the pharyngeal wall is caused by neuromuscular and non-neuromuscular factors; however, studies on the effect of UA muscle activity on pharyngeal compliance are inconclusive. For example, patients with OSA demonstrate increased pharyngeal com-

pliance and increased activity of the genioglossus muscle during wakefulness [20] and sleep [21], perhaps to compensate for anatomically reduced caliber. Other studies have shown a dissociation between compliance and reported muscle activity. Rowley et a1 [4,5] showed using nasopharyngoscopy that pharyngeal compliance at the retroglossal level is not increased during REM sleep, relative to NREM sleep (ie, stiffness is unaltered) despite the known inhibitory effects of phasic UA dilators. This finding clearly shows that non-neuromuscular factors play a major role in pharyngeal compliance. Thoracic caudal traction The UA is connected to the thoracic cage and the mediastinum by several structures. Increased lung volume during inspiration is associated with increased UA caliber in awake individuals, likely because of thoracic inspiratory activity providing caudal traction on the UA, independent of UAdilating muscle activity [22]. Caudal traction may transmit subatmospheric pressure through the trachea and ventrolateral cervical structures to the soft tissues surrounding the UA, increasing transmural pressure, and hence dilating the pharyngeal airway. This mechanism has been shown in sleeping subjects who experienced reduced UA resistance and increased retropalatal airway size when end-expiratory lung volume was increased by passive inflation [23]. Caudal traction may either dilate or stiffen the pharyngeal airway. It is likely that patients with OSA are more dependent on the effects of increased lung volume because dilatation and/or stiffening may be more prominent in a highly compliant UA. Vascular and muscular factors Vasoconstriction and vasodilatation cause a decrease and increase in UA resistance, respectively [24]. The effect of changes in vascular blood volume in the neck on UA patency in sleeping individuals remains unknown. Once UA closure occurs, surface mucosal forces— stickiness—may impede subsequent UA opening and promote further narrowing/occlusion. Mucosallining forces may be particularly important in patients with OSA caused by mucosal inflammation from repeated trauma [25]. Data on sleep are limited. A recent study showed that pharyngeal mucosal surface tension is associated with decreased apnea/hypopnea index in sleeping persons [26]. The

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relative contribution of reducing mucosal surface tension to the treatment of sleep apnea has not been determined.

generation of a collapsing transmural pressure, it is unlikely to be the sole mechanism of UA obstruction during sleep.

Upper airway obstruction: putting the pieces together

References

Although many of the determinants of UA patency are known, the pathogenesis of pharyngeal obstruction remains elusive; however, common features can be assembled in plausible proposed mechanisms. The underlying defect is a small pharynx susceptible to collapse. Morrell et al [27] proposed that central breathing instability leading to reduced ventilatory motor output to UA dilators is the critical trigger setting in motion a cascade of events leading to pharyngeal obstruction during sleep. In fact, UA obstruction often occurs during experimentally induced periodic breathing at the nadir of ventilatory motor output [28]. A central breathing instability was found when periodic breathing persisted after tracheostomy in patients with OSA [29]. Accordingly, central ventilatory control instability may be a key mechanism of UA obstruction. The reduction in ventilatory drive leads to reduced pharyngeal stiffness via reduction of neural output to UA-dilating muscles. The ensuing pharyngeal narrowing occurs because of the collapsing transmural pressure, which is caused by collapsing intraluminal and extraluminal forces. The narrowing of the pharyngeal airway leads to increased velocity of flow and subsequently to a further reduction in intraluminal pressure (the Bernoulli principle) and further pharyngeal narrowing. Eventually, complete pharyngeal obstruction occurs. Mucosal adhesive forces and gravity lead to prolonged apnea, asphyxia, and arousal from sleep. The ensuing ventilatory overshooy leads to hyperpnea, hypocapnia, and subsequent reduction of ventilatory motor output when sleep is resumed.This sequence does not explain how the cycle is initiated. In patients with severe sleep apnea, removal of the wakefulness stimulus to breathe may produce a sufficient reduction of ventilatory motor output to cause UA obstruction. Sleep-state instability at sleep onset may be the trigger in others. In conclusion, UA occlusion is a result of an interaction between multiple anatomic and physiologic abnormalities, the common features of which are the development of a collapsing transmural pressure and a small, compliant pharynx. Although subatmospheric intraluminal pressure contributes to the

[1] Henke KG, Badr MS, Skatrud JB, et al. Load compensation and respiratory muscle function during sleep. J Appl Physiol 1992;72:1221 – 34. [2] Skatrud JB, Badr MS, Morgan BJ. Control of breathing during sleep and sleep disordered breathing. In: Altose MD, Kawakami Y, editors. Control of breathing in health and disease. New York: Marcel Dekker; 1999. p. 379 – 422. [3] Tangel DJ, Mezzanotte WS, White DID. Influence of sleep on tensor palatini EMG and upper airway resistance in normal men. J Appl Physiol 1991;70: 2574 – 81. [4] Rowley JA, Zahn BR, Babcock MA, et al. The effect of rapid-eye movement (REM) sleep on upper airway mechanics in normal subjects. J Physiol (Lond) 1998;510:963 – 76. [5] Rowley JA, Zhou X, Vergine I, et al. Influence of gender on upper airway mechanics: upper airway resistance and Pcrit. J Appl Physiol 2001;91:2248 – 54. [6] Hudgel DW, Martin RJ, Johnson B, et al. Mechanics of the respiratory system and breathing pattern during sleep in normal humans. J Appl Physiol 1984;56: 133 – 7. [7] Skatrud JB, Dempsey JA. Airway resistance and respiratory muscle function in snorers during NREM sleep. J Appl Physiol 1985;59:328 – 35. [8] Henke KG, Dempsey JA, Badr MS, et al. Effect of sleep-induced increased in upper airway resistance on respiratory muscle activity. J Appl Physiol 1991;70: 158 – 68. [9] Badr MS, Skatrud JB, Dempsey A, et al. Effect of mechanical loading on expiratory and inspiratory muscle activity during NREM sleep. J Appl Physiol 1990;68:1195 – 202. [10] Wiegand L, Zwillich C, White D. Sleep and the ventilatory response to resistive loading in normal man. J Appl Physiol 1988;64:1186 – 95. [11] Guilleminault C, Stoohs R, Clerk M, et al. A cause of excessive daytime sleepiness: the upper airway resistance syndrome. Chest 1993;104:781 – 7. [12] Skatrud J, Dempsey J. Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation. J Appl Physiol 1983;55:813 – 22. [13] Schwab RJ, Gefter WB, Hoffman EA, et al. Dynamic upper airway imaging during awake respiration in normal subjects and patients with sleep disordered breathing. Am Rev Respir Dis 1993;148:1358 – 400. [14] Morrell MJ, Badr MS. Effects of NREM sleep on dynamic within breath changes in upper airway patency in humans. J Appl Physiol 1998;84:190 – 9. [15] Remmers JE, de Groot WJ, Sauerland EK, et al. Patho-

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M.S. Badr / Oral Maxillofacial Surg Clin N Am 14 (2002) 285–292 genesis of upper airway occlusion during sleep. J Appl Physiol 1978;44:931 – 8. Badr MS, Tbiber F, Skatrud JB, et al. Pharyngeal narrowing/occlusion during central sleep apnea. J Appl Physiol 1995;78:1806 – 15. Isono S, Remmers J, Tanaka A, et al. Anatomy of pharynx in patients with obstructive sleep apnea and in normal subjects. J Appl Physiol 1997;82: 1319 – 26. Wolin AD, Strohl KP, Acree BN, et al. Responses to negative pressure surrounding the neck in anesthetized animals. J Appl Physiol 1990;68:154 – 60. Shelton KE, Woodson H, Gay S, et al. Pharyngeal fat in obstructive sleep apnea. Am Rev Respir Dis 1993; 148:462 – 6. Mezzanotte WS, Tangel DJ, White DP. Waking genioglossal electromyograrn in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism). J Clin Invest 1992;89:1571 – 9. Suraft PM, McTier RF, Wilhoit SC. Upper airway muscle activation is augmented in patients with obstructive sleep apnea compared with that in normal subjects. Am Rev Respir Dis 1988;137:889 – 94.

[22] Van de Graaf WB. Thoracic influence on upper airway patency. J Appl Physiol 1988;65:2124 – 33. [23] Begle RL, Badr MS, Skatrud JB, et al. Effect of lung inflation on pulmonary resistance during NREM sleep. Am Rev Respir Dis 1991;141:854 – 60. [24] Wasicko JJ, Hutt DA, Parisi RA, et al. The role of vascular tone in the control of upper airway collapsibility. Am Rev Respir Dis 1990;141:1569 – 77. [25] Olson LG, Strohl KP. Airway secretions influence upper airway patency in the rabbit. Am Rev Respir Dis 1988;137:1379 – 81. [26] Jokic R, Kilmaszewski A, Mink J, et al. Surface tension forces in sleep apnea: the role of a soft tissue lubricant. Am J Respir Crit Care Med 1998;157:1522 – 5. [27] Morrell M, Arabi Y, Zahn B, et al. Progressive retropalatal narrowing preceding obstructive apnea. Am J Respir Crit Care Med 1998;158:1974 – 81. ¨ nal E, Burrows DL, Hart RH, et al. Induction of peri[28] O odic breathing during sleep causes upper airway obstruction in humans. J Appl Physiol 1986;61:1438 – 43. ¨ nal E, Lopata M. Periodic breathing and the patho[29] O genesis of occlusive sleep apneas. Am Rev Respir Dis 1982;126:676 – 80.

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Evaluation and diagnosis of sleep-disordered breathing Tom Bond, PsyD Sleep Disorders Center for Adults and Children, Williamsburg Community Hospital, 1308 Mount Vernon Avenue, Williamsburg, VA 23185, USA

Sleep-disordered breathing is defined as abnormal breathing patterns that disrupt sleep [1]. There are several types of sleep-disordered breathing patterns including hypopneas, apneas, and respiratory effortrelated arousals. Apnea is defined as a cessation of airflow for 10 or more seconds [2,3]. Partial obstructive events called hypopneas have historically been defined differently by different sleep disorders centers and sleep specialists. Because of a lack of uniformity in definitions, and partly because of difficulties in diagnosing and treating Medicare patients, the American Academy of Sleep Medicine has recently redefined hypopneas as abnormal respiratory events lasting at least 10 seconds, with at least a 30% reduction in airflow or thoracoabdominal movement with at least a 4% oxygen desaturation. The associated arousals historically associated with hypopneas have now been eliminated from the definition. This new definition is based on epidemiological data relating to sleep-related breathing disorders and cardiac disease [2]. The data relating to obstructive sleep apnea syndrome, and to both cardiovascular and cerebrovascular disease, is growing. Another abnormal breathing pattern is termed upper airway resistance syndrome. It is diagnosed in patients who present with daytime sleepiness caused by a narrowing or increased resistance of their upper airway when sleeping without diagnosable apneas or hypopneas. These patients generally have brief electroencephalography (EEG) arousals that may fragment sleep and cause the complaint of daytime sleepiness [4]. Common characteristics of patients who present for an apnea consultation include obesity, sleepiness, snoring, snorting, gasping, choking, and witnessed apneas at night. Hypertension, nocturia, and morning headaches may also be experienced.

Patterns of apnea There are three typical patterns of apnea. Obstructive apnea is the absence of airflow despite respiratory effort [2,3]. Central apnea is an absence of airflow with no respiratory effort. Mixed apnea includes both a central and an obstructive component. The most typical mixed apnea pattern is a central component followed by an obstructive component.

Evaluation Sleep-disordered breathing is best evaluated by a sleep consultation with a board-certified sleep specialist followed by polysomnography if indicated. Screening tests will be discussed later. The consultation should include a full history and physical examination. The history should include, but is not limited to, a thorough discussion of the nature of the patient’s complaint. Often, it is also helpful to interview either the bed partner or an observer. These persons are a rich source of information even though there sometimes may be disagreement between the two individuals. It may be helpful to ask if the observer is a heavy sleeper or not. There is an obvious problem if the patient sleeps alone. If it is not possible to directly interview the observer either in person or by telephone, it is often informative to at least have the bed partner or observer complete a questionnaire regarding the sleep habits and sleep symptoms of the patient. The level of sleepiness should be addressed. This can be done by asking the patient, bed partner, or observer about sleepiness or administering a selfreport measure such as the Epworth Sleepiness Scale. Attention should be directed to driving sleepiness in

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all cases, but especially when the patient is a truck driver or conveys passengers. If significant sleepiness is present, some sleep disorders centers conduct a Multiple Sleep Latency Test or a Maintenance of Wakefulness Test to assess the patient’s level of sleepiness more objectively. These tests are almost always conducted the day following polysomnography and are not central to the topic of this article. Sleep issues should be addressed including bedtime and arising times as well as activities that precede sleep periods. Sleep hygiene issues including caffeine, alcohol, and nicotine should also be addressed. These issues are often crucial to a thorough sleep evaluation. Take the example of a patient who presents with reported snoring and profound sleepiness. On closer questioning, he reveals that he works two jobs and only chronically sleeps 3 – 4 hours in a 24-hour period. Before the ordering of a polysomnogram, the patient should be asked to spend more time in bed for 2 weeks to ascertain if this helps both sleepiness and snoring. As a bonus, snoring may be improved with increased sleep because some patients report dramatically more snoring when fatigued. Symptoms present during sleep should be addressed. These symptoms should include but not necessarily be limited to areas such as morning headaches, frequency and level of snoring, witnessed apnea episodes, dry mouth, drooling, tossing and turning, night sweats, and nocturia. The family sleep and medical history should be taken. Patients often report a generational pattern of snoring and sleepiness, and the family medical history often reveals a strong history of cardiac and cerebrovascular disease. Of course, the medical history of the patient should be reviewed. A limited social history may be relevant, including such factors as work and marital history. If sleep-related breathing problems are severe enough, both of these areas can be affected. Patients will sometimes disclose that they have been terminated from work or are about to be terminated because of their sleepiness. Some patients will report that their marital situation has been affected because of marital conflict brought on by the loudness of their snoring. A general physical examination should be performed with special emphasis on the nasal and oral areas. Cephalometrics may be useful to identify the relationships among the soft tissues and the bony structures of the upper airway. The chief problem of the apnea patient is a small airway. This may be related to fatty deposits, tonsillar hypertrophy, or a small or retroplaced mandible [5]. Despite the continued ordering of thyroid levels on all patients by some sleep experts, there are no data showing that a

thyroid level is an important laboratory value for the overall sleep consultation [6]. Beside weight and height, a measure of neck circumference is important. Men with a neck circumference of 17 inches or higher, and women with a neck circumference of 16 inches or higher, are at increased risk for the presence of obstructive sleep apnea [7]. Blood pressure should also be taken. If standard polysomnography is indicated, some care should be taken to orient the patient to what the test will entail. Most patients are asked to arrive at the sleep disorders center about 2 hours before their customary bedtime. They are typically asked to complete several questionnaires about their various activities during the day. Patients are asked to list their medications and are often given screening psychological tests for depression and/or anxiety or may be given a Minnesota Multiphasic Personality Inventory (MMPI) for a broader psychological profile. Then about 20 sensors are attached to the patient, with most of the sensors going on the head and face, and the remainder on the torso and legs. A pulse oximeter is generally placed on the finger, ear, or toe. Patients should be informed that they will be monitored continuously both by video and audio, and appropriate releases should be obtained. Most patients are concerned about how they will be able to get up to go the bathroom, and the process for this should be explained. No electrodes need to be removed for bathroom breaks but the patient is merely unplugged from the monitoring equipment and can then move about freely. Many patients are concerned about whether or not a person could fall asleep under these circumstances. They should be reassured that the typical patient falls asleep quickly with no pharmacological help. It is also important for patients to be informed about the range of treatment options available and the relative efficacy of each. The positive and negative aspects of each treatment alternative should be reviewed with the patient. If split-night (to be discussed later) studies are used, the criterion and procedures should be carefully explained.

Screening tests Home studies may be generally divided into three areas: unattended portable recordings in the home, attended portable recordings in the home, and home pulse oximetry. The American Academy of Sleep Medicine recommends standard polysomnography as the accepted test for diagnosis of sleep-related breathing disorders. An attended home study that uses

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the same parameters as standard polysomnography is an acceptable way to evaluate sleep-related breathing disorders [8]. The definition of ‘‘attended,’’ however, may vary widely from a technologist actually in the home overnight with the patient to remote monitoring of the patient. This controversy has not been settled. But the patient needs to be observed in real time in order to ensure the quality of the recording and his or her safety. The American Academy of Sleep Medicine generally views unattended portable recordings as an acceptable alternative only in situations such as when there are indications that the breathing disorder may be severe and standard polysomnography is not readily available. Other circumstances include the patient’s inability to be studied in the sleep laboratory or as a follow-up study when diagnosis has been made by standard polysomnography and therapy initiated [8]. The intent here is to verify that the treatment is working. Common therapies that are usually followed in this manner are nasal continuous positive airway pressure (nasal CPAP), a mandibular repositioning appliance (oral appliance), or surgical intervention. Home pulse oximetry has been extensively used as a screening tool. There is only a weak correlation, however, between the results of home pulse oximetry and standard polysomnography. Home pulse oximetry may be useful when there is a long waiting list for standard polysomnogram and strong indications that the sleep-related breathing disorder may be severe [9]. Beside a weak correlation between home pulse oximetry and standard polysomnography, it is often difficult if not impossible to ascertain whether the variations in oxygenation are a result of apnea or the result of changes in body position or leg movements. Furthermore, it is impossible to differentiate REM from non-REM, or even to tell if the patient is asleep at all. If a patient is symptomatic enough to warrant a home pulse oximetry study, what is the referring physician to do if the results are either positive or negative? Generally, the next step would be polysomnography in either case.

Polysomnography Polysomnography is considered the gold standard for the diagnosis of sleep-related breathing disorders. Polysomnography typically involves the measurement of multiple channels of physiologic parameters including, but not limited to, electroencephalography (EEG), electro-oculography (EOG), electromyography (EMG), electrocardiography (ECG), heart rate, respiratory effort, airflow, and oxygen saturation. Additional channels may include a snore-monitoring

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device and anterior tibialis electrodes. These latter electrodes are frequently placed to measure periodic limb movements that occur at night. The electrodes may also be important to ascertain whether changes that appear to be respiratory in nature may be related to body movements secondary to leg jerks. All of these parameters should be measured during an 8-hour attended study by a number of technologists sufficient to monitor their patients effectively as well provide safety for them [3]. This is generally a one-technologist to two-patient ratio. This may vary, however, with circumstances such as more difficult patients including those who are physically, cognitively, or emotionally challenged or pediatric patients.

Split-night polysomnography Polysomnography is referred to as a split-night study when the patient is monitored for half the night for evaluation and diagnosis of a sleep-related breathing disorder, and then in the second half of the night therapy is initiated. This therapy is typically nasal CPAP, but it may also extend to the use of mandibular repositioning devices. There are no conclusive data showing that split-night studies adversely affect a patient’s compliance with treatment [10]. Split-night studies with nasal CPAP in the second half of the night are typically done only if the apnea is severe. This generally means an apnea/hypopnea index of at least 40 during a minimum of 2 hours of diagnostic polysomnography, but different sleep disorders centers may set this figure at different levels. For a splitnight study to be acceptable, there needs to be at least 3 hours of nasal CPAP [3].

Measures of apnea frequency Various measures have been applied to describe the frequency of apneas and/or hypopneas. The apnea index is defined as the number of apnea episodes that occur per hour of sleep. This is also sometimes referred to as the respiratory disturbance index, and there is no difference in these indices. Sleepdisordered breathing is now viewed as comprising apneas, hypopneas, and respiratory effort-related arousals. Using the American Academy of Sleep Medicine’s recent position paper on hypopneas, the recommendation now is that even mild elevations of the apnea/hypopnea index be treated because of the increased risk of cardiovascular disease. Thus, any apnea/hypopnea index greater than or equal to 5 should be treated [2].

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Follow-up After the data is scored by a technologist and thoroughly reviewed by a board-certified sleep specialist, a diagnosis is specified and a treatment plan formulated. The patient is then contacted or a followup appointment is made, and the results of the polysomnogram are discussed between the sleep disorders specialist and the patient. The pertinent treatments are again reviewed and recommendations are made. Some patients will return for a nasal CPAP titration or validation of the efficacy of an oral appliance. Others will seek a surgical solution, and overweight will be encouraged to lose weight. The specifics of various treatments are thoroughly discussed in the following articles.

References [1] American Thoracic Society. Indications and standards for the use of nasal continuous positive airway pressure (CPAP) in sleep apnea syndrome. Am J Respir Med 1994;150:1738 – 45. [2] Meoli AL, Casey KR, Clark RW, et al. Hypopnea in sleep-disordered breathing in adults. Sleep 2001;24(4): 469 – 70.

[3] Standards of Practice Committee of the American Sleep Disorders Association. Practice parameters for the indications for polysomnography and related procedures. Sleep 1997;20(6):406 – 22. [4] Guilleminault C, Stoohs R, Clerk A, et al. A cause of excessive daytime sleepiness. The upper airway resistance syndrome. Chest 1993;104(3):781 – 7. [5] Strohl KP, Redline S. Recognition of obstructive sleep apnea. Am J Respir Crit Care Med 1996;154:279 – 89. [6] Winkelman JW, Goldman H, Piscatelli N, et al. Are thyroid function tests necessary in patients with suspected sleep apnea? Sleep 1996;19(10):790 – 3. [7] Davies RJ, Stradling JR. The relationship between neck circumference, radiographic pharyngeal anatomy, and the obstructive sleep apnoea syndrome. Eur Respir J 1990;3(5):509 – 14. [8] Standards of Practice Committee of the American Sleep Disorders Association. Practice parameters for the use of portable recording in the assessment of obstructive sleep apnea. Sleep 1994;17(4):372 – 7. [9] Golpe R, Jimenez A, Carpizo R, Cifrian JM. Utility of home pulse oximetry as a screening test for patients with moderate to severe symptoms of obstructive sleep apnea. Sleep 1999;22(7):932 – 7. [10] Sanders MH, Constantino JP, Strollo PJ, et al. The impact of split-night polysomnography for diagnosis and positive pressure therapy titration on treatment acceptance and adherence in sleep apnea/hypopnea. Sleep 2000;23(1):17 – 24.

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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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Principles of oral appliance therapy for the management of sleep disordered breathing$ Alan A. Lowe, DMD, PhD Division of Orthodontics, Department of Oral Health Sciences, Faculty of Dentistry, The University of British Columbia, 2199 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3

Dentists have recently become one of the team players in the field of sleep medicine. Oral appliances for the treatment of snoring and obstructive sleep apnea (OSA) fall into two main categories: those that hold the tongue forward and those that reposition the mandible (and the attached tongue) forward during sleep. Before treating either snoring or OSA with any oral appliance, a complete assessment by a knowledgeable physician or sleep disorder specialist is important. Having concluded that treatment with an oral appliance is indicated, the physician provides the dentist/orthodontist/oral surgeon who has skill and experience in oral appliance therapy with a written referral or prescription and a copy of the diagnostic report. Because of the obvious life threatening implications of a number of sleep disorders, it is imperative that oral appliance therapy commences only after a complete medical assessment.

Research undertaken by the author and discussed in this article was supported by grants from the Medical Research Council of Canada, the British Columbia Lung Association, and the National Centres of Excellence, Inspiraplex. Klearway was invented by the author at The University of British Columbia. International patents have been obtained by the University and specific licensees are assigned the rights to manufacture and distribute the appliance world wide. $ This article, with modifications, previously appeared in Lowe AA. Oral appliances for sleep breathing disorders. In Kryger M, Roth T, Dement W, editors. Principles and practice of sleep medicine, 3rd edition. Philadelphia: W.B. Saunders; 2000. p. 929 – 939. E-mail address: [email protected] (A.A. Lowe).

The American Academy of Sleep Medicine reviewed the available literature in 1995 and recommended that oral appliances be used in patients with primary snoring or mild OSA and in patients with moderate to severe OSA who are intolerant of or refuse treatment with nasal continuous positive airway pressure (nCPAP) [1,2]. For some patients, combination therapy with other treatments such as weight loss, surgery and nCPAP may be indicated, and this must be coordinated by the attending sleep physician. Current evidence suggests that the pathogenesis of OSA involves a combination of reduced upper airway size and altered upper airway muscle activity. Features and size of the upper airway have been characterized by cephalometry [3], CT [4,5], and MRI [6]. A high apnea index (AI) was seen in association with a large tongue and soft palate volume, a retrognathic mandible, an anteroposterior discrepancy between the maxilla and mandible and an open bite tendency between the incisors, and obesity [6]. Cephalograms may be useful to estimate the volume of the tongue, nasopharynx, and soft palate but not the oropharynx or hypopharynx [7]. Tongue posture appears to have a substantial effect on upper airway morphology [8]. Tongue cross-sectional area increases and oropharyngeal cross-sectional area decreases when OSA patients change their body position from upright to supine [6]. Oral appliances are believed to have a direct effect on mandibular posture and consequently affect airway size. Three-dimensional analyses have increased our understanding of the mechanisms of different forms of treatment including oral appliances [9,10] and nCPAP [6] and have helped predict the response to upper airway surgery [11]. Tongue and soft palate

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 3 5 - 3

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volumes increase as the body mass index increases [5], which confirms the potential importance of weight loss as an effective treatment for the control of OSA. In response to nCPAP, an increase in pharyngeal volume and a decrease in tongue volume due to the resolution of upper airway edema have been identified [6]. Distinct OSA subgroups may provide some insight on the contribution of obesity to OSA [12], and skeletal subtypes are of considerable importance [13] when selecting which oral appliance to use. Although the control of tongue posture is extremely complex [14,15], an abnormality in genioglossus (GG) timing in OSA subjects has been demonstrated [16]. The duration of the inspiratory GG activity and the total GG activity cycle is shorter in patients with OSA. Oral appliance therapy relates directly to the pathophysiology of OSA, and this article reviews these interactions in light of current knowledge for the most frequently used appliances. This review provides an overview of the seven most frequently used oral appliances and provides guidelines for their use. A detailed titration sequence for one specific adjustable oral appliance is outlined because this clinical procedure is often not well understood by practitioners new to the field.

2. 3. 4.

5.

Clinical protocols for oral appliance therapy 6. A therapy sequence is suggested by the Academy of Dental Sleep Medicine for the management of oral appliances in patients who are being treated for snoring or OSA. 1. Medical assessment is completed by the attending physician or sleep specialist. Before referral to a dentist, the physician should check that the patient has sufficient teeth (at least eight in each of the upper and lower jaws) and that they have no limitations in forward jaw movement (greater than 5 mm) or jaw opening (greater than 25 mm). Full upper and lower dentures may preclude the use of a mandibular repositioner, but some of these patients may have a good treatment response with a tongue retaining device. Partial dentures that replace four or fewer teeth do not preclude oral appliance use. Evidence of a history of temporomandibular joint pathology or chronic joint pain depending on its severity may preclude the use of oral appliances in some patients. Severe occlusal wear (more than 20% of the clinical crown) may indicate severe bruxism and complicate oral appliance therapy. The size of the

7.

8.

mandible is not a reliable predictor of treatment success. Oral appliances do not appear to work as well in the morbidly obese patient although exceptions have been documented. Overnight polysomnogram is done as required by physician or sleep specialist. Written referral or prescription and diagnostic report are sent to dentist or dental specialist. Oral examination is completed and includes Medical/dental histories Soft tissue/intra-oral assessment Periodontal evaluation Temporomandibular joint/occlusal examination Intra-Oral habit assessment Examination of teeth and restorations Initial dental radiographs if not taken in preceding six months Panoramic or full mouth survey Cephalometric radiograph (optional) Diagnostic plaster models as appropriate for the specific oral appliance Appliance determination is made and includes Consideration of mandibular repositioner versus tongue retainer and whether a boil and bite type or a custom made appliance Design, fabrication, fitting, instructions and training Subjective symptom evaluation Refer patient back to attending physician for assessment or repeat overnight sleep study. Complete possible modification, redesign, or remake of appliance as required based on subjective resolution of symptoms, patient compliance and follow-up sleep study. Make dental appointments at least every 6 months for the first 2 years to monitor subjective effectiveness, fit, comfort, temporomandibular joint, and dental status.

Overview of oral appliances Table 1 indicates the oral appliances that received 510k market clearance from the United States Food and Drug Administration (FDA) as of January 7, 1999, for the treatment of snoring, OSA, or both. The FDA has granted 510k market clearance for snoring for 32 different oral appliances. Only 14 oral appliances have received market clearance for both snoring and OSA. Since publication of the AASM position papers [1,2] and other recent reviews [17], two significant advances in this field have occurred. Adjustable appliances that allow titration of the mandibular

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Table 1 Oral appliances 510 k cleared for the treatment of snoring and/or OSA as of 1/7/99 by the Food and Drug Administration Device

Manufacturer

Snoring

OSA

Adjustable PM Positioner Adjustable Soft Palate Lifter Adjustable TheraSnore Dental Anti-snoring Device DESRA Elastic Mandibular Advancement, Titration (EMA-T) Elastic Mandibular Advancement (EMA) Elastomeric Sleep Appliance Equalizer Airway Device Herbst Klearway NAPA OSAP PM Positioner Silencer SILENTNITE Sleep-In Bone Screw System SNOAR Open Airway Appliance Snore-Cure Snore-Ezzer Snorefree Snore Guard Snoremaster Snore Remedy Snore-No-More Snore Peace Snore Tec Snor-X Mouth Guard Snoring Control Device TAP Anti-snoring Device TheraSnore Thornton Oral Appliance Tongue Retaining Device (TRD)

Jonathan A. Parker, DDS Ortho Publications Inc. Distar, Inc. Ortho Publications Inc. D.S.R.A. Inc. Frantz Design, Inc. Frantz Design, Inc. Village Park Orthodontics Sleep Renewal Inc. Orthodontics, State University of NY at Buffalo Great Lakes Orthodontics, Ltd. Great Lakes Orthodontics, Ltd. Snorefree, Inc. Jonathan A. Parker, DDS Silent Knights Ventures, Inc. Glidewell Laboratories Influence Inc. Kent J. Toone, DDS Ortho-Tain, Inc. Snore-Ezzer Scott Feldman, DDS, Norman Shapiro, DDS Snore Guard The Snoremaster Co. Great Lakes Orthodontics, Ltd. Snore Peace Group Marketing Technologies, Inc. Snor-X, Inc. Kenneth Hilsen, DDS Nellcor Puritan Bennett, Inc. Distar, Inc. W. Keith Thornton, DDS Advanced Medical Equipment

B B B B B B B B B B B B B B B B B B B B B B B B B B B B B B B B

B X X X X B B B B B B B B B B X B B X X X X X X X X X X X X B X

(From Lowe AA. Oral appliances for sleep breathing disorders. In: Kryger M, Roth T, Dement W, editors. Principles and practice of sleep medicine, 3rd edition. Philadelphia: W.B. Saunders; 2000. p. 929 – 39; with permission.)

position over time, and the use of materials and designs that significantly improve intraoral retention are major improvements. Of the more than 60 oral appliances currently on the market (not all have received FDA market clearance), only 7 are fully adjustable, and only 3 have undergone any form of controlled or randomized clinical trial. Dentists realized early on that determining the correct jaw position was the most difficult step when using oral appliances successfully. Considerable variations in the initial comfortable range of the anteroposterior movement of the mandible and differences in the speed and the amount of forward jaw position that any given patient could tolerate were found. Single jaw position or nonadjustable appliances often need to be remade if the initial jaw position proves to be inadequate. Gradual titration forward of the mandible without the necessity of making a new appliance each time

became the objective, and adjustable appliances were invented and marketed. A subgroup of patients, particularly those who suffered from sleep bruxism [18], often experience a considerable jaw discomfort in the morning after wearing a rigid hard acrylic single jaw position oral appliance. A need to develop oral appliances that could allow for lateral jaw movement as well as some degree of vertical jaw opening was identified. At the same time, major advances in dental materials significantly improved the flexibility and strength of thermosensitive acrylic resin materials. Appliances made of temperature sensitive material that the patient could heat in hot water before insertion that would cool and harden somewhat intraorally were found to have considerable more retention than traditionally designed cold cure acrylic appliances. The combination of adjustability, lateral and vertical

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Fig. 1. Lateral and superior/inferior views of seven oral appliances used for the treatment of snoring and/or obstructive sleep apnea. (From Lowe AA. Oral appliances for sleep breathing disorders. In: Kryger M, Roth T, Dement W, editors. Principles and practice of sleep medicine, 3rd edition. Philadelphia: W.B. Saunders; 2000. p. 929 – 39; with permission.)

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jaw movement, increased retention, and better defined titration protocols have significantly improved the effectiveness of oral appliances since they were last reviewed. Each of the oral appliances has a primary effect on either the tongue or the tongue and mandible together. Several appliances move the mandible anteriorly, for example, Herbst, Klearway, mandibular repositioner, PM Positioner, Snore Guard, and TheraSnore. The tongue is affected by all the appliances either by direct forward movement of the muscle itself or by changes secondary to an altered mandibular rest position. The TRD is the most commonly used oral appliance that has a direct affect on tongue posture. Herbst Variations of the Herbst appliance (Fig. 1) have been used effectively in orthodontics for many years

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[19 – 21]. HERBST is a registered trademark of Dentaurum, Inc. (Newton, PA). This removable appliance is available from most orthodontic laboratories and is highly effective in advancing the mandible [22]. The plunger mechanism holds the mandible forward in both the open and closed positions [23] and allows for easy adjustments of forward mandibular positions. The Herbst appliance offers the advantages of permitting forward jaw opening and some limited side-toside jaw movements when compared to the other more rigid mandibular repositioning appliances [24]. Clark [25] suggests the use of bilateral interarch elastics to keep the jaw closed during sleep and the incorporation of interproximal ball clasps to increase retention. In 15 subjects who underwent sleep studies before and after appliance insertion, oxygen desaturation levels improved markedly and the respiratory disturbance index (RDI) decreased from a mean of 48.4 to 12.4 4 months after the insertion of a Herbst appliance [25].A

Fig. 2. Cephalometric superimpositions of supine before (solid line) and after (broken line) appliance insertion tracings. A Herbst appliance was used on the left and a tongue retaining device (TRD) on the right. (From Lowe AA. Oral appliances for sleep breathing disorders. In: Kryger M, Roth T, Dement W, editors. Principles and practice of sleep medicine, 3rd edition. Philadelphia: W.B. Saunders; 2000. p. 929 – 39; with permission.)

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39% decrease in stage 1 sleep together with increases in stage 2, 3, 4 and a 50% increase in rapid eye movement (REM) sleep was seen. Some 74% of the subjects were able to use the Herbst appliance successfully at the 18 month follow-up period and no increase in facial pain or jaw dysfunction was seen. The left hand side of Fig. 2 provides a superimposition of supine before (solid) and after (broken) cephalometric tracings of a subject fitted with a Herbst appliance in our laboratory. The RDI decreased from 44.3 to 24.6 and significant increases in the crosssectional areas of the oropharynx (from 386.4 to 739.5 mm2) and the hypopharynx (from 73.7 to 267.6 mm2) were seen. Although great care must be exercised when one uses two-dimensional cephalometric films [26] to evaluate three-dimensional airway size [7], it appears that a forward mandibular position is effective in reducing the severity of the OSA and that the airway tube is significantly altered. Klearway Klearway (see Fig. 1) differs in several ways from other appliances currently available on the market. It works by keeping the teeth together and holding the lower jaw and tongue forward during sleep to open the airway. Klearway possesses retention characteristics designed to keep the appliance in the mouth during all the various complex jaw movements that can occur during sleep. Klearway provides full occlusal coverage of both arches and is designed not to encroach on tongue space. Furthermore, it facilitates the very slow and gradual movement of the mandible by permitting the patient to adjust the appliance according to his or her own comfort level with the guidance of the attending dentist. This fully adjustable oral appliance is much more comfortable to wear than a single jaw position appliance, which often may require time-consuming and expensive remakes to place the mandible in the ideal forward position required to adequately open the airway. Fabricated of thermoactive acrylic, Klearway becomes pliable for easy insertion and confirms securely to the dentition for an excellent fit while significantly decreasing soft tissue and tooth discomfort. A total of 44 forward positions are available in increments of 0.25 mm, which covers a full 11.0 mm range of anteroposterior movement. Such small increments help avoid rapid forward jaw movements that can cause significant patient discomfort. Klearway allows the patient to feel less restricted and thus less claustrophobic, a sensation experienced by a small number of patients during the first few nights of wear. Once warmed under hot water and

inserted, the acrylic resin hardens as it cools to body temperature and firmly affixes itself to both arches. Lateral and vertical jaw movement is permitted, which enables the patent to yawn, swallow, and drink water without dislodging the appliance. Patients with bruxism are also comfortable in this appliance as it does not prevent jaw movements during sleep. In a comparison of 38 patients from three sites [27], RDI was reduced to a clinically acceptable level (less than 15 per hour) in 80% of a group of moderate OSA patients and in 61% of a group of severe OSA patients. Fiberoptic videoendoscopy documented that the airway size was significantly increased at the level of the velopharynx [27]. Covert compliance data measured with a newly developed miniaturized temperature sensitive monitor imbedded in the appliance indicated that it was worn for a mean of 6.8 hours per night [27 – 29]. Patients with mild temporomandibular joint discomfort or bruxism can usually wear Klearway with ease because comfort of the temporomandibular joint and the dentition over the long term is one criteria used to establish the therapeutic jaw position. Totally edentulous patients may not be ideally suited for treatment with mandibular repositioners because they may not have enough intraoral retention to keep the appliance in the mouth during sleep. Patients with edentulous maxillary arches and adequate teeth in the lower arch may respond favorably to Klearway therapy. If the patient wears the appliance every night and is comfortable for 1 month, he or she should be instructed to activate the appliance by turning the screw on the top of the appliance two times per week until the next appointment. Each turn or activation in the direction of the arrow moves the lower jaw gradually forward in 0.25-mm increments, which has a direct effect on the three-dimensional size of the airway. The Klearway appliance has been shown to be particularly effective in increasing the size of the velopharynx [27]. The patient inserts the tip of the key into the hole on the side of the expansion screw at the base of the arrow and turns or pushes the key toward the direction of the arrow imprinted in the metal expansion screw, which shows the correct movement to advance the lower jaw. Once the key is completely turned from one side to the other it is removed, and a new hole appears for the next turn. If the key is removed before a new hole appears after the completed turn, the patient may be unable to fully place the key in the new hole. The key is always removed after turning. Turning the key opposite to the direction of the arrow closes the expansion screw and retracts the mandible. If significant jaw or joint discomfort occurs, advise the patient to stop turning the screw until their next visit.

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Some patients stop snoring and feel more rested shortly after Klearway is inserted, and no further advancement of the mandible is required. Others may require 2 or 3 months of slow and gradual forward repositioning before a significant treatment effect is noted. When the patient or bed partner reports a cessation of snoring and a resolution of symptoms, further advancement of the mandible may not be required and the appliance is considered titrated. The expansion screw should be tied off with stainless steel ligature wire or filled in with cold cure acrylic to prevent any further movement of the screw. The patient should be referred back to his or her physician or sleep specialist for assessment at this time. If the oral appliance has been shown to be effective and the patient is comfortable, recall appointments every 6 month should be scheduled by the attending dentist. At each appointment, the status of the occlusion is checked. Verify that the appliance has not been distorted. Minor cracks in the appliance can be repaired at the chair side with cold cure acrylic. Expansion screws may self-close over time and therefore should always be permanently stabilized for long term Klearway wear. The overall management of the patient’s particular sleep disorder remains the responsibility of the attending physician. In conclusion, the Klearway adjustable mandibular advancement appliance, made from thermoelastic acrylic resin, has a direct effect on airway size, is consistently well worn throughout the night, and significantly improves the sleep quality of OSA patients. Mandibular Repositioner In 1934, Pierre Robin [30] described glossoptosis (tongue obstruction) due to mandibular hypotrophytogether with the design of a monobloc functional appliance to move the mandible forward. Since then, many variations [31] in mandibular repositioning appliances (see Fig. 1) have been used to affect growth, change airway size, and alter the dentition. Meier-Ewert et al [32] were the first to describe a rigid mandibular repositioning appliance to move the mandible 3 to 5 mm forward, which was effective in reducing OSA. In a group of seven subjects, the mean AI was reduced from 38.0 to 12.1 [33]. Using the same appliance in a sample of 44 subjects, an AI reduction from 50.4 to 23.1 was seen [34]. Reports based on single case studies [35 – 37] also documented the use of similar appliances. Ichioka et al [37] found mandibular advancements of 5 to 7 mm reduced the mean AI from 32.2 to 9.9 in a sample of 14 subjects. Bonham [38] evaluated a group of 12 patients who were fitted with a mandibular reposi-

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tioning appliance to the most comfortable protrusive position. The mean AI was reduced from 53.8 to 36.0 after the insertion of the mandibular repositioning appliance. None of the patients complained about temporomandibular joint discomfort during the treatment. The Esmarch Prosthesis advances the mandible forward 3 to 5 mm and has been found to reduce the mean AI from 65.0 to 31.0 in 30 subjects [39] and reduce the mean RDI from 43.3 to 18.2 in 67 subjects [40]. One study [41] advanced the mandible 3 to 5 mm and opened the jaw 4 mm in 12 subjects. A mean AI of 50.4 was reduced to 19.0 after the appliance was inserted and a significant increase in REM sleep was noted. Other recent reports have confirmed the efficacy of mandibular repositioners. Menn et al [42] found that 69% of 23 patients were good responders and Cohen [43] reported a 60% success rate in a group of patients with RDIs greater than 20. Loube et al [44] have also suggested the use of mandibular repositioners for the treatment of upper airway resistance syndrome. A mandibular repositioning appliance for edentulous patients has also been described [45]. Clarke [46] recently reviewed the use of mandibular repositioners and found them to be effective for the treatment of snoring and mild to moderate OSA. A small group of patients discontinued wear because of temporomandibular joint or jaw muscle discomfort and a limited number revealed occlusal changes. Lowe and Schmidt-Nowara [47] reviewed the evidence of effectiveness especially in light of the addition of titratable appliances and concluded that in all large case studies, patients with higher RDIs had a lower proportion of treatment success compared with patients with less severe OSA. Lowe et al [9] reported on the effects of a mandibular repositioning appliance for the treatment of OSA in a subject whose RDI was reduced from 57.3 to 2.3. Fig. 3 provides before (left) and after (right) appliance insertion three-dimensional reconstructions of CT scans from a lateral, superior, and posterior views. The lateral view after appliance insertion on the right reveals a rotated mandible and a more superiorly placed tongue. The threedimensional spatial interactions from a superior view indicate an anteroposterior elongation of the total airway after the insertion of the appliance. In addition, the dorsal aspect of the tongue is narrower and more superior. The posterior view reveals an overall larger airway, which was quantified as a net 27.6% increase in volume from 12.3 to 15.7 mL [7]. This significant increase in airway size especially in the oropharynx could decrease the potential for tissue

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Fig. 3. Before and after appliance insertion 3D reconstructions from a lateral, superior and posterior view. The mandible is shown in white, the tongue in dark gray and the oropharynx in light gray. (From Lowe AA. Oral appliances for sleep breathing disorders. In: Kryger M, Roth T, Dement W, editors. Principles and practice of sleep medicine, 3rd edition. Philadelphia: W.B. Saunders; 2000. p. 929 – 39; with permission.)

collapse during negative inspiratory pressure and thus have a direct effect on the resolution of the OSA. PM Positioner The PM Positioner (see Fig. 1) and the Adjustable PM Positioner have received FDA market clearance for the treatment of snoring and OSA. Formed from a thermoplastic material, the PM Positioner is softened in warm water before insertion into the mouth. The Adjustable PM Positioner [48] can be used to advance the mandible by using a wire instrument to turn the screws located on both sides of the appliance. Initial bite registrations are taken at 65% to 75% of maximum protrusion and the incisors are separated by

approximately 5 mm in the treatment position. Parker [49], based on a study of 15 OSA patients, reported a mean decrease in RDI from 25.8 to 7.3, a mean increase in the lowest oxygen saturation from 78.2% to 83.8%, and an increase in the percentage of REM sleep from 14% to 18.8% with the PM Positioner. Snore Guard The Snore Guard (see Fig. 1) is a boil and bite appliance that is easy to fit and adjust directly on the patient and appears to be well tolerated. The mandible is positioned 3 mm behind maximum protrusion with a 7 mm opening. The appliance covers the anterior teeth only and is lined with a soft polyvinyl for patient

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comfort. The Snore Guard has received FDA market clearance only for the treatment of snoring. SchmidtNowara [49] found that after 7 months of use in 68 patients, 75% of the individuals were using the appliance regularly. Snoring was decreased in all but one subject and eliminated in 29. In 20 OSA subjects, polysomnography revealed a mean RDI decrease from 47.4 to 19.7. In addition, oxygenation and sleep disturbance were improved. Ferguson et al [50] compared the efficacy, side effects, patient compliance, and preference between 4months of Snore Guard and nCPAP therapies in a randomized, prospective, crossover study in patients with mild-to-moderate OSA. The RDI was lower with nCPAP than with the oral appliances. Some 48% of the patients who used the Snore Guard were treatment successes (reduction of RDI to < 10 per hour and relief of symptoms), 24% were compliance failures, and 28% were treatment failures. Four people refused to use nCPAP after using the Snore Guard. Some 62% of the patients who used nCPAP were overall treatment successes, 38% were compliance failures, and there were no treatment failures. Side effects were more common and the patients were less satisfied with nCPAP. Seven patients were treatment successes with both treatments; six of these patients preferred Snore Guard and one preferred nCPAP as a long-term treatment. The Snore Guard is an effective treatment in some patients with mild-to-moderate OSA and is associated with fewer side effects and greater patient satisfaction than nCPAP. The advantages of the Snore Guard are its relatively low cost and reduced clinical time required by the dentist; however, it is nonadjustable, it may apply excessive pressure to the lower anterior teeth in some patients, and retention problems may develop over time. TheraSnore The adjustable TheraSnore (see Fig. 1) is an adjustable boil and bite appliance available on the market and has received FDA market approval only for the treatment of snoring. The appliance consists of upper and lower trays that snap together by means of four locking mechanisms. Both trays are made of a thermoplastic material surrounded by a harder polycarbonate frame. The TheraSnore can be adjusted forward or backward in 1.5-mm increments. The upper tray is designed to fit over the maxilla and the lower tray prevents the tongue and jaw from dropping backward during sleep. The appliance is fitted to the patient’s centric occlusion and the mandible can be advanced by using the position indicators on the appliance. In 13 subjects with OSA,

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Schmidt-Nowara et al [51] documented with MRI an increase in the retropalatal and retroglossal spaces with a Snore Guard or TheraSnore in place. Using the same sample of patients, Schwab et al [52] found that the increase in cross-sectional area was related to a reduction in the thickness of the lateral pharyngeal walls. Miyasaki et al [53] evaluated the TheraSnore in 11 OSA patients and found that 40% of patients had more than a 10% increase in their lowest oxygen saturation level and 70% demonstrated more than a 5% increase. The average RDI decreased from 49.5 to 32.0 and 60% of the patients reported an improvement in subjective symptoms. Tongue Retaining Device (TRD) The TRD is a custom-made appliance (see Fig. 1) with an anterior bulb that by means of negative pressure, holds the tongue forward during sleep [54]. For those patients with blocked nasal passages, a modified TRD with lateral airway tubes to permit mouth breathing is also available. The FDA has granted marketing clearance for the TRD for the treatment of snoring. The TRD appliance is particularly useful in patients who have a large tongue. It is an effective alternate to a mandibular repositioner in patients with a compromised dentition or who are edentulous. The TRD is the only appliance that has been studied in various body positions and in conjunction with other forms of therapy. Cartwright and Samelson [55] evaluated 14 subjects and found a mean AI reduction from 54.4 to 22.7 after insertion of the TRD. In addition, improved sleep and significantly fewer and shorter apneic events were seen. The sleep architecture showed a change toward a more normal pattern with less light sleep and more d-wave and more REM sleep immediately after the treatment began. The results seen were comparable with the rate reported for patients who had been treated either by tracheotomy or uvulopalatopharyngoplasty (UPPP). In a group of 16 male patients [55], individuals with a substantial worsening of the AI while in the supine sleep position were more responsive to the TRD than those who were equally affected in both the lateral and supine position. The AI in untreated subjects was twice as high while supine on their backs as it was in the side position [56]. When obesity, age, and the position ratio were used in a discriminant function analysis, these three variables predicted TRD success (as defined by an AI < 6 or a 50% reduction in AI) correctly for 81% of the patients. In a sample of 30 male patients [57], 65% tried on the TRD alone or in conjunction with other treatments were improved at the 1-year point. Samel-

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son [58] found that the TRD had an effect in 80% of subjects who had used it for 3 years or more. In another TRD report [59], a group of 12 subjects were treated with the TRD alone or in conjunction with some behavioral therapy such as sleep position training [60] or weight loss. A mean RDI reduction from 37.0 to 17.3 was observed in this first group. In another group of with more severe apnea, the TRD was used in conjunction with a submucous resection of the septum or a UPPP. The TRD appears useful either alone or in conjunction with other treatments to improve patients with a wide range of apnea severity provided that the apnea is more severe in the supine position and the patient’s weight is not greater than 50% above the ideal. In another study [61], a sample of 60 adult males with RDI values greater than 12.5 who had two or more times the apnea rate during supine sleep in comparison to their lateral sleep rate were assigned to four treatment groups: TRD only, posture alarm, TRD plus posture alarm [62], and health habit instruction. Some 73% of the TRD group and 80% of the TRD plus posture alarm group improved. The 15 subjects treated with the TRD alone had a reduction in mean RDI from 27.4 to 11.4. Patency of the nasal airway and an initially low side index were the two factors significantly related to successful control of OSA with the TRD. For the 15 subjects in the TRD plus posture alarm group, lower initial obesity and higher weight loss during treatment were the factors associated with best success. A mean RDI reduction from 30.7 to 7.9 was seen for the latter group. The effects of the TRD on baseline tongue muscle activity have been studied. Ono et al [63] found that the TRD has different effects on the awake genioglossus muscle activity in control subjects and OSA patients. In awake OSA patients, the TRD reduces genioglossus muscle activity and corrects the delayed timing of the muscle before an apneic period during sleep [64]. The TRD may counteract fatigue in the tongue muscles and fluctuations in the activity of the genioglossus muscle. In addition, the TRD may provide a pneumatic splint to enlarge the upper airway similar to that seen with nCPAP. The right side of Fig. 2 provides a superimposition of supine before (solid) and after (broken) cephalometric tracings of a subject fitted with a TRD in our laboratory. The mandible and tongue are both positioned forward. A significant reduction of RDI from 17.5 to 0.7 is noted. The cross-sectional area of the oropharynx increases from 289.3 to 343.5 mm2 and the hypopharynx increases from 202.6 to 306.1 mm2.

Overview Oral appliance therapy for snoring, OSA, or both is simple, reversible, quiet, and cost effective and may be indicated in patients who are unable to tolerate nCPAP or who are poor surgical risks. Oral appliances are effective in varying degrees and appear to work because of an increase in airway space, the provision of a stable anterior position of the mandible, advancement of the tongue or soft palate, and possibly by a change in genioglossus muscle activity. The appliances should be used during sleep for life and must be comfortable for the patient. Ideally, they should have full occlusal coverage to prevent vertical changes to the dentition over time. The selection of patients suitable for oral appliance therapy must always be made by the attending physician. The dentist then selects the appropriate oral appliance. Documentation of the obstruction site is useful if such an assessment is available. Although traditional cephalometry can predict with some accuracy the volume of the tongue, soft palate, and nasopharynx, it is not a reliable indicator of oropharynx or hypopharynx size [7]. If a small oropharynx is documented on the basis of CT or MRI evaluations, any appliance that could enlarge the airway by either advancing the tongue alone or advancing the mandible and the tongue together could be useful. If a disproportionately large tongue is seen or if the patient is edentulous or dentally compromised, a TRD could be effective. The TRD is even more effective if it is used in conjunction with behavioral modifications. Mandibular repositioners all are effective in changing the three-dimensional size of the airway tube [63,64]. Oral appliances have an effect on the tongue muscle either by advancing the mandible, holding the tongue forward, or altering the vertical dimension and thus affecting baseline tongue activity [10,11]. Several contraindications for the use of oral appliances have been suggested but not all are applicable to any one appliance. Obviously, they should only be used for the treatment of obstructive not central sleep apnea as quantified by overnight polysomnograms. If oral appliances simply rotate the mandible down and back and a predisposing constriction of the hypopharynx exists, the OSA may worsen. Oral appliances are not well tolerated by patients with arthritis, crepitis, or other significant temporomandibular joint symptoms; however, mild joint problems may be lessened by the forward jaw position. Sufficient healthy teeth to anchor the oral appliance are required for most appliances. Allergic and nasal obstructions may also be contraindications in selected patients. Finally, oral appliances can only be used in cooper-

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ative patients who are motivated to wear the appliance during sleep on a regular basis. Several questions require further study. How can one easily identify the obstruction site in a costeffective way? Which patients are ideally suited for an oral appliance? Which appliance will be most effective in any one patient? What is the long-term compliance with these appliances? Are there any long-term deleterious effects on the temporomandibular joint or dentition? A long-term prospective study of the frequency and amount of occlusal changes is definitely required. Numerous simple solutions exist for the correction of minor tooth position changes, and long-term monitoring of these patients is definitely required. Patients demand alternatives to surgery and nCPAP, and the usefulness of oral appliances for the effective treatment of snoring or OSA is no longer in question. Three comparisons of oral appliances and nCPAP have been completed [50,65,66] and a strong patient preference as well as good efficacy for oral appliances have been demonstrated. In addition, oral appliances have been found to be effective for patients who have not been treated successfully with uvulopalatopharyngoplasty [67]. If the initial assessment is coordinated by the attending physician and good communication is established with the dentist involved, a significant number of subjects with snoring or mild-to-moderate OSA can be treated successfully with oral appliances. References [1] Schmidt-Nowara W, Lowe A, Wiegand L, Cartwright R, Perez-Guerra F, Menn S. Oral appliances for the treatment of snoring and obstructive sleep apnea: a review. Sleep 1995;18:501 – 10. [2] American Sleep Disorders Association Standards of Practice Committee. Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances. Sleep 1995;18:511 – 3. [3] Lowe A, Santamaria J, Fleetham J, Price C. Facial morphology and obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1986;90:484 – 91. [4] Lowe A, Gionhaku N, Takeuchi K, Fleetham J. Threedimensional CT reconstructions of tongue and airway in adult subjects with obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1986;90:364 – 74. [5] Lowe A, Fleetham J, Adachi S, Ryan F. Cephalometric and CT predictors of apnea index severity. Am J Orthod Dentofacial Orthop 1995;107:589 – 95. [6] Ryan C, Lowe A, Li D, Fleetham J. Magnetic resonance imaging of the upper airway in obstructive sleep apnea before and after chronic nCPAP therapy. Am Rev of Resp Dis 1991;144:939 – 44.

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[7] Lowe A, Fleetham J. Two- and three-dimensional analysis of tongue, airway and soft palate size. In: Norton ML, editor. Atlas of the difficult airway. St. Louis: Year Book Medical; 1991; p. 74 – 82. [8] Pae E, Lowe AA, Sasaki K, Price C, Tsuchiya M, Fleetham JA. A cephalometric and electromyographic study of upper airway structures in the upright and supine position. Am J Orthod Dentofacial Orthop 1994;106: 52 – 9. [9] Lowe A, Fleetham J, Ryan F, Matthews B. Effects of a mandibular repositioning appliance used in the treatment of obstructive sleep apnea on tongue muscle activity. In: Issa F, Suratt P, Remmers J, editors. Sleep and respiration. Boston: Wiley-Liss Inc.; 1990. p. 395 – 405. [10] Smith SD. A three-dimensional airway assessment for the treatment of snoring and/or sleep apnea with jaw repositioning intraoral appliances: a case study. J Craniomandib Pract 1996;14:332 – 43. [11] Ryan C, Lowe A, Li D, Fleetham J. Three dimensional upper airway computed tomography in OSA: a prospective study in patients treated by uvulopalstopharyngoplasty. Am Rev Respir Dis 1991;144:428 – 32. [12] Tsuchiya M, Lowe A, Pae E, Fleetham J. Obstructive sleep apnea subtypes by cluster analysis. Am J Orthod Dentofacial Orthop 1992;101:533 – 42. [13] Lowe AA, Ono T, Ferguson KA, Pae E-K, Ryan F, Fleetham JA. Cephalometric comparisons of craniofacial and upper airway structure by skeletal subtype and gender in patients with obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1996;110:653 – 64. [14] Lowe A. Neural control of tongue posture. In: Taylor A, editor. Neurophysiology of the jaws and teeth. London: McMillan Press Ltd.; 1990. p. 322 – 68. [15] Lowe A. The tongue and airway. Otolaryngol Clin North Am 1990;23:677 – 98. [16] Adachi S, Lowe A, Ryan C, Fleetham J. Genioglossus muscle activity and inspiratory timing in obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1993; 104:138 – 45. [17] Lowe AA. Oral appliances for sleep breathing disorders. In: Kryger M, Roth T, Dement W, editors. Principles and practice of sleep medicine. 3rd edition. WB Saunders Co. 2000. p. 929 – 939. [18] Sjo¨holm T, Piha S, Mantyvaara J, Lehtinen I, Polo O, Lowe A. Spectral analysis of circulation in teethgrinders: correlation with masseter activity during sleep. J Dent Res 2002, In press. [19] Herbst E. Dreissigjahrige erfahrungen mit dem retentions-scharnier, zahnartzl. Rundschau 1934; 42:1515 – 24, 1563 – 68, 1611 – 6. [20] Pancherz H. The Herbst appliance – its biologic effects and clinical use. Am J Orthod 1985;87:1 – 20. [21] McNamara J, Howe R. Clinical management of the acrylic splint appliance. Am J Orthodont Dentofacial Orthop 1988;82:142 – 9. [22] Clark G. OSA and dental appliances: the use of dental appliances to treat common sleep disorders has proved to be effective. Calif Dent Assoc J 1988;16:26 – 33.

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[23] Rider E. Removable Herbst appliance for treatment of obstructive sleep apnea. J Clin Ortho 1988;22: 256 – 7. [24] Clark G, Nakano M. Dental appliances for the treatment of obstructive sleep apnea. J Am Dental Assoc 1989;118:611 – 9. [25] Clark GT, Arand D, Chung E, Tong D. Effect of anterior mandibular positioning on obstructive sleep apnea. Am Rev Respir Dis 1993;147:624 – 9. [26] Hoffstein V, Weiser W, Haney R. Roentgenographic dimensions of the upper airway in snoring patients with and without obstructive sleep apnea. Chest 1991;100: 81 – 5. [27] Lowe AA, Sjo¨holm TT, Ryan CF, Fleetham JA, Ferguson K, Remmers J. Treatment, airway and compliance effects of a titratable oral appliance. Sleep 2000; 23(Supp4):172 – 8. ¨ zbek M, Wong M, [28] Lowe AA, Sjo¨holm TT, Low W, O Harrison S. Validity testing of a small intraoral compliance monitor [abstract 1799]. J Dent Res 1997;76:238. ¨ zbek M, Wong M, [29] Lowe AA, Sjo¨holm TT, Low W, O Harrison S. Intraoral compliance monitoring of Klearway appliance wear. Presented at the Inspiraplex Annual Meeting, Montreal, April, 1997. [30] Robin P. Glossoptosis due to atresia and hypotrophy of the mandible. Am J Dis Child 1934;48:541 – 7. [31] Boraz R, Martin H, Michel J. Sleep apnea syndrome: report of case. J Dent Child 1979;46:50 – 2. [32] Meier-Ewert K, Schafer H, Klob W. Treatment of sleep apnea by a mandibular protracting device. Berichtsband 7th Europ Congr Sleep Res Munchen 1984;217. [33] Klob W, Meier-Ewert K, Schafer H. Zur therapie des obstruktiven schlaf-apnoe-syncroms. Fortschr Neurol Psychiat 1986;54:267 – 71. [34] Meier-Ewert K, Brosig B. Treatment of sleep apnea by prosthetic mandibular advancement. In: Peter, Podsrus, von Wichert, editors. Sleep related disorders and internal disease. Berlin: Springer Verlag; 1987. p. 341 – 5. [35] Soll B, George P. Treatment of OSA with a nocturnal airway-patency appliance. N Engl J Med 1985; 313:386. [36] Bernstein A, Reidy R. The effects of mandibular repositioning on obstructive sleep apnea. J Craniomandibular Pract 1988;6:179 – 81. [37] Ichioka M, Tojo N, Yoshizawa M, Chida M, Miyazato I, Taniai S, et al. A dental device for the treatment of obstructive sleep apnea: a preliminary study. Otol Head Neck Surg 1991;104:555 – 8. [38] Bonham P, Currier G, Orr W, Othman J, Nanda R. The effect of a modified functional appliance on obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1988;94: 384 – 92. [39] Mayer G. Efficacy evaluation of Esmarch prosthesis and cephalometric analysis. Sleep Res 1990;19:251. [40] Miyazaki S, Meier-Ewert K. Cephalometric indications for successful prosthetic treatment of sleep apnea. Sleep Res 1990;19:260. [41] Nakazawa Y, Sakamoto T, Yasutake R, Yamaga K, Kotovi T, Miyahara Y, et al. Treatment of sleep apnea

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A.A. Lowe / Oral Maxillofacial Surg Clin N Am 14 (2002) 305–317 [58] Samelson C. A survey of the effectiveness of the tongue retaining device for the control of snoring and/or obstructive sleep apnea. Sleep Res 1989;18:299. [59] Cartwright R, Stefoski D, Caldarelli D, Kravitz H, Knight S, Lloyd S, et al. Toward a treatment logic for sleep apnea: the place of the tongue retaining device. Behav Res Ther 1988;26:121 – 6. [60] Cartwright R, Lloyd S, Lilie J, Kravitz H. Sleep position training as treatment for sleep apnea syndrome: a preliminary study. Sleep 1985;8:87 – 94. [61] Cartwright R, Ristanovic R, Diaz F, Caldarelli D, Alder G. A comparative study of treatments for positional sleep apnea. Sleep 1991;14:546 – 52. [62] Cartwright R, Diaz F, Ristanovic R. Comparing two treatments for positional sleep apnea: TRD and posture alarm. Sleep Res 1990;18. [63] Ono T, Lowe AA, Ferguson KA, Pae E-K, Fleetham JA. The effect of the tongue retaining device on awake genioglossus muscle activity in patients with obstruc-

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Lasers in the management of snoring and mild sleep apnea Robert A. Strauss, DDS, MD Residency Training Program, Department of Oral and Maxillofacial Surgery, Virginia Commonwealth University / Medical College of Virginia, Richmond, VA 23298, USA

In a field that is as complex and confusing as the management of sleep apnea, perhaps no greater controversy has existed over the last few years than the use and efficacy of lasers as a mode of treatment. As with many recent advances in high technology (and especially, when no good low-technology treatment exists), initial enthusiasm and hype, usually propagated by apparent clinical success rather than substantial and objective research, is eventually overtaken by the inevitable complications, lack of the initially seen spectacular results, and the reality that technology is not a replacement for good surgical principles and skill. Eventually, and this is certainly true for the use of lasers in the management of snoring and mild sleep apnea, the practical answer falls somewhere in the middle, indicating that the use of this technology is very much indicated in some cases and contraindicated in others. It is the inherent responsibility of the good practitioner, therefore, to have the data and wisdom to be able to make the clinical judgment differentiating these clinical scenarios. As the pendulum swings back toward its inevitable middle ground based on time and good research, it is becoming more and more evident that lasers have a significant role to play in this disease process, but that role still needs to be better defined. It must be stated at the outset that, in general, the use of lasers in this disease does not represent a new or unique modality of treatment. Rather, the laser is primarily used as a tool to perform procedures that either have been done in the past, or could be done in the present, with other modalities such as scalpels, electrosurgical cautery, or radio-frequency devices. The indication for using the laser is the practical, and

E-mail address: [email protected] (R.A. Strauss).

sometimes theoretical, advantage(s) it represents in any surgical procedure. These include the lack of intraoperative and postoperative bleeding, the ease of access to traditionally difficult areas such as the soft palate and pharynx, the decrease in postoperative pain, and the decrease in scarring. There are currently two commonly performed laser procedures for snoring and mild sleep apnea: laserassisted uvulopalatoplasty (LAUP) and laser-assisted uvulopalatopharyngoplasty (LA-UPPP). Though there is some overlap in their techniques and indications, they are two distinctly different surgeries and will, therefore, be described separately.

History The standard LAUP was originally described by the French surgeon Kamami in 1990 strictly as a means to eradicate simple snoring with a better than 90% success rate, approximately the same as the thencommonplace UPPP [1]. It was adopted in the United States by Krespi in 1992 and rapidly caught on as an office-based alternative to the UPPP [2,3]. The original procedure involved a combination of laser incision within the soft palate and laser vaporization of the uvula. Because the laser used in focused mode as an incision tool is much more effective than the laser used in defocused mode for ablation, the end result was more like a partial uvulectomy than a true palatoplasty. Within a short time, however, the procedure was modified to include laser excision of the uvula and soft palate rather than ablation, thus resulting in a true palatoplasty procedure. The original procedure was described as a multistep surgery because it was felt that performing the surgery in one step would lead to an unacceptably high rate of

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 2 7 - 4

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velopharyngeal insufficiency (VPI) postoperatively. The surgery was done in small increments, usually requiring 3 – 5 operations for completion. Although not a major surgery when used for simple snoring, this nevertheless required the patient to take hours off from work several times and, if sedation was used, several days of work, thus negating one of the major advantages of the LAUP over the then-current one-step procedure for snoring, the UPPP. As the procedure became popular and the comfort level of the surgeons increased, it became evident that this fear was unfounded and that, with moderate care in not overextending the boundaries of the surgical excision, the incidence of VPI was remarkably low. Most surgeons soon adopted the concept of a single-stage surgery, with second-stage procedures done only when a treatment failure occurred and it was felt by the surgeon that there was adequate tissue either superiorly, or more commonly laterally, to warrant a second surgery. In 1994 Kamami published the first article on the use of the LAUP for OSAS [4]. At that time, the procedure performed was identical to the LAUP used for simple snoring. Unfortunately, objective data regarding this procedure was mostly lacking, save for a few early articles [5], and there was justifiable questioning over the use of this surgery [6]. Over the past few years, the procedure has been shown to be safe and effective for socially objectionable snoring, and essentially the same as scalpel UPPP for sleep apnea. Thus, it is fairly effective for mild apnea but is not particularly effective for moderate-severe sleep apnea when used alone, and is therefore only a small part of a much bigger treatment protocol necessary for the treatment of significant sleep apnea. Recently, many surgeons have changed their technique from a LAUP to a LA-UUP, essentially performing a UPPP with a laser instead of a scalpel. This provides similar results but with the bloodless, lower morbidity and more controllable advantages of laser surgery. Most surgeons who use this procedure in the management of sleep apnea do so in combination with other procedures that also are not usually effective by themselves such as genial advancement, hyoid myotomy and suspension, or nasal surgery. In combination with these procedures, the LA-UPPP, like the scalpel UPPP, can be an effective therapeutic tool.

Preoperative evaluation Prior to performing surgery on the airway in any patient, a proven or presumptive diagnosis should be established. It is imperative to differentiate the patient with simple snoring from those with mild sleep apnea,

moderate sleep apnea, and severe sleep apnea. Although these diseases probably represent more of a continuum than separate entities, their management is usually quite different. It is also important to know whether apneic events are obstructive or central in nature, and the severity of any cardiac or hypoxic events. Finally, it is useful to attempt determining the possible anatomical causes of any airway obstruction and rule out pathologic lesions within the airway. For the patient with known or suspected sleep apnea, the workup is relatively straightforward and includes a thorough physical examination with particular emphasis on the upper airway, a cephalometric radiograph, thyroid function studies, and a polysomnogram. Additional targeted laboratory and radiographic studies may be ordered where appropriate. Any patient undergoing surgery of the upper airway for sleep apnea should also have a preoperative nasopharyngoscopy to rule out pathologic entities that may be causing the obstruction as well as to determine the likely sources of the obstruction, thus enabling the surgeon to choose the correct procedure for that patient [7,8]. Diagnostic maneuvers such as Mueller’s manuever can be beneficial in this diagnostic process. The diagnosis and workup of sleep apnea patients is covered extensively elsewhere in this issue and will not be repeated here. More controversial is the appropriate workup for the patient with suspected simple snoring. This is the patient who presents with the singular complaint of snoring, and without associated complaints of daytime somnolence, or cardiac, neurologic, or respiratory signs and symptoms consistent with sleep apnea (or with minimal symptoms consistent with very mild sleep apnea). Though a laboratory polysomnogram would be an ideal method to rule out obstructive sleep apnea, this is an expensive test that requires the patient to be away from home and is often refused by insurance companies as being an unnecessary test in the absence of the signs or symptoms. Nevertheless, it is incumbent on the prudent practitioner to rule out sleep apnea (which requires a different treatment regimen than snoring) in a more objective and reliable way other than just history, which can be incorrect in up to 30% of cases. One reasonable alternative is the use of home polysomnography. A number of commercial, multichannel home recorders are available that enable the patient to take the device home, apply it during sleep, return it to the practitioner who can either read and analyze the information on their own computer, or download the information to a technician remotely who can read the study and relay the information to the practitioner. Another alternative is a home device that measures airway sounds and

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provides interpretive data indicating the presence and severity of sleep apnea. Although these devices fail to provide electroencephalographic data to indicate the stages of sleep, they have been shown in objective studies to correlate well with the final results of full laboratory polysomnograms [9 – 11]. They also have the advantage of their portability, ease of use, and extremely low cost of use. Once the diagnosis has been confirmed, the practitioner can choose the procedure of choice he or she feels appropriate for that particular patient.

Technique Laser-assisted uvulopalatoplasty After appropriate diagnostic workup of the patient indicating simple snoring or mild sleep apnea not requiring other therapeutic measures, the choice of a LAUP may be made as an appropriate procedure. The procedure is most commonly performed in the office environment and may be conducted using local anesthesia only, or light to moderate I.V. sedation. Deep sedation and general anesthesia are rarely necessary and make the procedure more difficult, and in the case of a sleep apneic patient, more dangerous because of potential airway difficulties. It should be remembered that all of these patients have anatomically compromised airways, and intubation is often difficult, leading to a significant rate of morbidity and mortality. After thorough informed consent, the patient is seated in a dental chair in the sitting position. This is the easiest position for the surgeon as it allows the soft palate to drape as far anteriorly as possible, providing the greatest space for the backstop hand piece, keeping the palate off the posterior pharyngeal wall, and minimizing the risk of inadvertent conductive thermal damage. It also decreases the incidence of gagging. Although the surgery can be done in the supine or semisupine position (as would likely be needed for general anesthesia), it is considerably more difficult. Prior to instillation of the local anesthetic or I.V. sedation, the insertion of the levator veli palatini muscle must be identified. This can be accomplished by having the patient phonate while looking for the point of vertical traction of the soft palate. In those rare patients where this is difficult to determine, a cotton swab can be used on the pharyngeal wall to briefly gag the patient. This will exaggerate the insertion and almost always make it easily visible. During surgery, the patient can be asked to repeat this maneuver as needed to confirm its location (another advantage of local anesthesia or light sedation over

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general anesthesia). In all cases where general anesthesia is used, and in some cases where local anesthesia is used, it is helpful to mark this location preoperatively with an indelible marker such as a blue denture-marking stick. It is of utmost importance during the procedure not to violate this insertion, as velopharyngeal insufficiency can result, leading to hypernasal speech and/or nasal regurgitation of fluids after drinking. Although this is not an uncommon temporary annoyance postoperatively (for 1 – 3 weeks), when it occurs long-term it is a major morbidity with significant consequences for the patient. Should I.V. sedation be desired, it is performed in the routine fashion using a benzodiazepine (either diazepam or midazolam) and a short-acting narcotic (eg, fentanyl). Small doses of methohexital or propofol may be used as needed, but it should be remembered that the patient needs to be kept in a light plane of sedation and the dosages adjusted accordingly. The use of supplemental oxygen during the procedure is somewhat controversial. Though no cases have been reported to date of an airway fire during LAUP or LAUPPP, the potential of oxygen to support combustion makes its use during surgery somewhat worrisome at least. There are two techniques that may be used. Of course, the oxygen can be turned off during the actual lasering and replaced only if the pulse oximeter indicates that the patient is getting hypoxic. Alternatively, the oxygen can be given by nasal cannula with the nose draped off from the surgical site. The admixture of the oxygen and room air that reaches the pharynx makes significant combustion unlikely. Keeping the sedation light minimizes the chance of ventilatory depression and the subsequent need for oxygen supplementation. Local anesthesia in this region is remarkably effective and surprisingly uncomplicated. The tongue is retracted with a butterfly tongue retractor. A dental syringe of lidocaine 2% with 1:100K epinephrine and a 1.5 inch, 25 – 27 gauge needle is used to inject in five places: the midline of the soft palate about 1 cm above the base of the uvula, just lateral to the uvula adjacent to the midline injection bilaterally, and above the tonsillar pillars bilaterally. A total of approximately 1.5 – 2.0 cc is injected to limit the amount of fluid in the tissues, prevent distortion of the anatomy, and avert excessive absorption of the CO2 laser and the need for high fluences (the total energy necessary) with resultant lateral thermal spread. If needed or desired, a small additional amount may be comfortably injected after the patient has been anesthetized from the initial dose. Rarely will more than 3 cc be necessary for the entire procedure. Some practitioners prefer to use bupivicaine before or after surgery to

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lessen short-term postoperative discomfort. Finally, some surgeons will inject a small dose of steroids (eg, dexamethasone 4 – 6 mg) directly into the surgical site whereas others provide the dose I.V. to limit swelling and discomfort. It is the experience of the author that the use of systemic steroids does indeed decrease the morbidity of the postoperative course. In order to prevent inadvertent thermal damage to the posterior pharyngeal wall, the use of a backstop hand piece is highly desirable (although a nonbackstop hand piece and a separate protector behind the soft palate will also work). As with all laser procedures, it is imperative for the surgeon to understand completely the physics involved in order to maximize the advantages of the laser while minimizing collateral thermal conductive damage. The basic concept that adjacent tissue damage is primarily related to the time duration of laser exposure is an important tenet in laser surgery. Therefore, it is the goal of the surgeon to perform the surgery with the least time on tissue as possible [12]. That is, the fluence should be applied in the shortest period of time possible (fluence rate) while still being able to maintain control of the laser. This translates into using fairly high power and power densities (generally 15 – 18 watts

with a 0.1 – 0.8 mm spot size depending on the specific laser used) in a series of rapid, short continuous bursts of laser use. This technique also limits heating of the backstop with secondary conduction into the pharyngeal wall. A good rule of thumb is to use the laser continuously for no more than 5 seconds before testing the temperature on a gloved finger. If the backstop is particularly hot to the touch, it should be allowed to cool down before continuing. Patient and operator safety during the procedure is of paramount importance. Because of the large amount of laser plume generated during this procedure, the use of a smoke evacuator with a biologic filter is highly recommended. In addition, specific face masks designed for laser surgery and using a small pore size to capture laser plume particles are commercially available. Everyone in the operatory, including the patient, should have appropriate eye protection as well. Once anesthesia is established, the tongue is retracted again with a butterfly retractor. This can be done by the surgeon, the assistant, or even by the patient. A useful trick to remember is that the patient will often be able to retract further back on the tongue without gagging than if the surgeon or the assistant

Fig. 1. The laser placed just lateral to the uvula for the vertical trenches. The backstop hand piece is used to protect the pharyngeal wall from damage.

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does this. With a small amount of coaching, the patient should be able to use the hand opposite to the side the surgeon is on to enable adequate visualization of the surgical site without interfering with the surgeon’s access and line of vision.The backstop is then placed behind the soft palate, and the procedure begun. Although originally done essentially as a uvulectomy, and performed sequentially in 3 – 5 sessions [1], the procedure has evolved into a much more aggressive resection of the soft palate and tonsillar pillars as well as the uvula, and is done in a single session in most cases. The surgery is essentially comprised of three steps. Initially, the backstop is placed in the junction of the uvula and soft palate on one side and a vertical cut, also called a trench, is made throughand-through the soft palate (Fig. 1). This is done, as mentioned earlier, using high-power density in incisional laser mode (ie, at or near the focal point of the laser). It is extremely beneficial to use a suction tip or bayonet forceps to traction toward the contralateral side during the incision. Vertically, this is taken to approximately 3 – 4 mm below the insertion of the levator veli palatini muscle as described earlier (and which can be found by phonation or via the previ-

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ously made indelible mark). Generally, this translates into a vertical cut of about 1.5 – 2 cm. Great care must be taken not to violate this insertion. This procedure is then performed in an identical fashion on the contralateral side (Fig. 2). The second step is excision of the uvula and soft palate superiorly defined by the two previously made vertical trenches. The backstop is placed at the top of one of the trenches and turned medially. A horizontal cut is then made, in a continuous focused mode, to connect the tops of the trenches (Fig. 3). This can be facilitated by cutting from either side and meeting in the middle, rather than going from one side to the other, and also by again grasping the uvula with a long forceps, as the use of counter traction greatly enhances the cutting ability of the laser. The specimen is then removed and may be submitted for histological examination if desired. Once the central area of the soft palate is removed, one can often find the lateral palate and tonsillar pillars to be still constricting the airway. In the third and final step, the laser can then be used in either a focused or defocused manner to excise or ablate these tissues superiorly to inferiorly (Fig. 4). Generally, this is done

Fig. 2. The bilateral vertical trenches stopping just short of the levator muscle insertion.

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Fig. 3. The backstop is turned sideways to allow for excision of the uvula and soft palate at the top of the vertical trenches. Counter traction is gently applied to the uvula with a forceps or suction.

Fig. 4. The tonsillar pillar tissues can be excised or ablated to increase the airway opening laterally.

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for 3 – 5 mm laterally to minimize postoperative bleeding and pain. Although the surgeon may choose otherwise (some surgeons believe this increases the success of the procedure and decreases postoperative pain), suturing is not necessary for healing. In the unlikely event of mild bleeding, the laser may be used for hemostasis if the vessel is 500 microns or smaller. For vessels that do not respond to the laser but are too small to warrant ligation or the use of an electrocautery, a silver nitrate stick may be very helpful. At the conclusion of the procedure, the patient is asked to phonate and drink a small amount of fluid to verify velopharyngeal competenency, although the anesthetic may make this exam less than realistic. The patient may return to work, school, or home at his or her discretion and predicated on the type of anesthesia used.

Uvulopalatopharyngoplasty: laser-assisted (LA-UPPP) When the diagnosis of sleep apnea (rather than simple snoring) has been made, it is generally accepted that the standard LAUP procedure is not an ideal procedure for cure by itself. Toward this end, the relative efficacies of various laser procedures will be discussed later in this article. One recent alternative, the LA-UPPP, is being used by some surgeons in the management of sleep apnea. Essentially, it is a variation of the traditional UPPP procedure that takes advantage of the strengths of the laser. Because this is a relatively new variation, there is some variability in the manner in which this procedure is performed; however, the basic concept is very similar to that of a standard UPPP in that there is not only removal of the soft palate and uvula, but also excision of both the anterior and posterior tonsillar pillars. In addition, there is some undermining into the lateral pharyngeal tissues, and suturing is done to maximize the airway dilation and prevent relapse. It should be noted that this procedure only works when the patient has either previously undergone tonsillectomy or has small residual tonsils. In this case, the tonsils can be ablated to a depth of a few millimeters as part of the procedure. Large tonsils should either be removed prior to the procedure, or a standard UPPP performed. The LA-UPPP can be done with the same local anesthetic injections used for a standard LAUP. Because many of the patients receiving this surgery are sleep apneics, however, they will often be simultaneously undergoing other surgical procedures, such as genial tubercle advancement and hyoid myotomy

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(GAHM) or nasal surgery. As such, they may require an operating room and general anesthesia. It is also strongly recommended that consideration be given to having these patients admitted for overnight observation because of the greater potential of postoperative airway compromise. In severe cases, or in smaller community hospitals, a monitored bed may be appropriate. The patient is prepped and situated in the same fashion as for a standard LAUP. Once again, the procedure is easier to do in the sitting position, although when done in the OR the supine position may be necessary and is not a problem as long as the levator muscle is marked preoperatively. The initial vertical trenches are the same as in the LAUP, although they are taken as far laterally as can be done comfortably within the soft palate to include some of the anterior and posterior tonsillar pillars. Again, this can be aided by grasping the uvula with a forceps, hemostat, or suction tip, and applying counter traction during the laser incisions. A horizontal incision can then be made across the top of the vertical trenches to remove the uvula, soft palate, and some of the medial aspect of the tonsillar pillars. Additional ablation or excision of the pillars can be carried out until the operator is sure that the airway has been maximized. At this point, the soft palate is grasped with a long forceps, rotated anteriorly so that the long aspect of the palate is facing into the mouth, and a nonbackstop hand piece is used to remove a triangular wedge of tissue from the soft palate between the anterior and posterior palatal mucosa but still leaving 3 – 4 mm to the levator insertion (Fig. 5). This essentially undermines the soft palate and allows for significant thinning. At the conclusion of lasering, there should be an anterior mucosal flap comprised of the oral mucosa of the palate and the anterior tonsillar pillar, and a posterior mucosal flap comprised of the nasal side of the palatal mucosa and the posterior tonsillar pillars. All of the flap edges should, and indeed must be, de-epithelialized. At this point the posterior flap is stretched anteriorly and brought into apposition with the anterior flap, overlapping it for 1 – 2 mm. A series of 4-O polyglactin or polyglycolic sutures are then used to coapt the two flaps (Fig. 6). The resultant suture line is essentially identical to that seen with a standard UPPP (Fig. 7). Advantages of this procedure over standard UPPP include considerably less bleeding and slightly less postoperative discomfort. In addition, the procedure is faster and, when appropriate (for nonapneics), may be performed on an outpatient basis or even in the office. The relative efficacy of these procedures will be discussed later in this article.

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Fig. 5. The soft palate is rotated anteriorly, and a wedge of tissue removed with a nonbackstop hand piece to allow thinning of the soft palate and soft tissue closure.

Postoperative care and instructions

Fig. 6. The posterior tissues are stretched forward and sutured to the anterior tissues. This helps to further open the airway and affect pharyngeal wall tightening.

The postoperative care for both of these procedures is much the same. The patient is instructed to return to work as soon as he or she feels ready after discharge from the office or hospital, usually within 1 – 2 days if sedation or general anesthesia has been used, and immediately postoperatively if local anesthesia has been used. Although the inevitable sore throat lasts 8 – 10 days, patients often do better when back in their normal routine rather than focusing on their pain. Prescriptions are given for short-term systemic steroids (a dosepak is useful but expensive) and a moderate analgesic such as acetominophen elixir with codeine. Stronger analgesics should be avoided as they increase the risk of respiratory depression, apneic events, and airway compromise. If preferred, a longacting local anesthetic such as bupivicaine may be used in place of the lidocaine for initial anesthesia or at the end of the procedure to provide several hours of comfort. The routine use of antibiotics is not necessary because, as with most intraoral surgeries, infections are very rare, and when they do occur they are likely to be candidal. Along with warm saline rinses, topical anesthetic lozenges, sprays, or viscous liquids are very helpful

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Fig. 7. After completion of the LA-UPPP, showing significant opening of the airway.

in controlling the discomfort between the systemic agent doses. A soft, nonthermal diet is also important, as anything excessively hot or cold will cause increased pain. In general, postoperative pain is related primarily to swallowing and when at rest the patient is often nearly pain-free. A bedside humidifier can provide a moist environment at night to prevent drying out of the airway. Sleeping in an upright or semi-Fowlers position is encouraged and the patient should have someone else nearby during sleep for the first 48 hours in the unlikely event of an airway compromise. If the patient was using continuous positive airway pressure (CPAP) before the surgery, it should be continued as soon as it can be worn comfortably after surgery. Usually this is 5 – 7 days postoperatively, but in some cases it can be as long as a few weeks until this can be accomplished.

Complications Although the LAUP and LA-UPPP procedures are usually benign and effective surgeries, there still exists the potential for serious, and occasionally catastrophic, events. Careful diagnosis, treatment planning, and postoperative care can, however, diminish the chances of these complications significantly.

Intraoperatively, the main complication that occurs is bleeding. This usually occurs at the base of the uvula from the small artery that supplies this area. Treatment involves the use of a silver nitrate stick but, if severe enough, may require electrocautery or even a ligature suture. Another intraoperative complication is gagging. This occurs not from action on the soft palate, but rather from depression of the tongue for visibility. This can be limited by minimally retracting the tongue or by having the patient hold down their own tongue, which not only decreases the gagging but also often results in improved retraction. If severe, nitrous oxide can be of benefit, and light I.V. sedation with a small amount of a benzodiazepine will usually eradicate gagging altogether. Postoperative complications include bleeding, velopharyngeal insufficiency, airway compromise, infection, and scarring. Postoperative bleeding may occur when a cut vessel, diminished by the vasoconstrictor, suddenly dilates as the local anesthetic wears off. This is treated in the same manner as bleeding that occurs intraoperatively. Velopharyngeal insufficiency results from inadvertent impingement on the levator palatinus insertion in the soft palate. It is manifested by hypernasal speech and nasal reflux, which may range from mild (eg, nasal reflux when bending over) to complete incompetency [13 – 15].

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Some mild insufficiency is not uncommon after any palatal surgery but usually disappears within a few weeks of the surgery. The incidence of this complication after traditional UPPP ranges from 1 – 13% but should be lower for LAUP and LA-UPPP because they are often performed under local anesthesia and this allows constant visualization and identification of the levator position. Airway compromise is, fortunately, rare after UPPP, LAUP, or LA-UPPP. Nevertheless, case reports of severe bleeding and airway compromise requiring emergency cricothyrotomy or tracheostomy have been reported [13 – 15]. Patients at risk for airway compromise (eg, patients with severe sleep apnea) should be operated on in a controlled environment and should be placed in a monitored hospital bed postoperatively. Patients with simple snoring and mild sleep apnea are commonly operated on quite safely in an office environment and discharged home postoperatively. Even with a standard LAUP for simple snoring, however, studies have shown that in the immediate postoperative period there can be a net decrease in airway size of as much as 4% [16]. Therefore, judicial observation of any patient at perceived risk is warranted. Infections following soft palate surgery are fortunately quite rare, owing to the excellent blood supply of this region. A few cases of oral candidiasis have been reported, undoubtedly caused by the use of antibiotics to prevent bacterial infections [17]. It is the opinion of many surgeons (including this author), that the routine use of antibiotics after surgery is not indicated for this reason. Scarring after laser-assisted palatal surgery can occur either in the soft palate/tonsillar pillar complex or in the pharyngeal wall. Soft palate scarring occurs through the natural process of tissue damage, collagen formation and contraction of the wound. It is usually mild and expected, causing no significant airway constriction or functional problems. Rarely, it can lead to velopharyngeal insufficiency, pain, and some measure of airway diminishment. Scarring of the pharyngeal wall is always caused by inadvertent conducted thermal damage from the backstop hand piece. Although the handpiece is designed to prevent direct laser damage to the pharynx, the backstop itself can be heated by thermal conduction from the lasered tissue, which in turn is then conducted to the pharyngeal wall if touched. It is seen most commonly when the soft palate and pharyngeal wall are in close proximity. This can be easily prevented if the laser is used in short bursts of less than 5 – 10 seconds at a time, if the backstop is kept off the pharyngeal wall, and if the surgeon intermittently checks the backstop

for elevated temperatures. In its worst form, the thermally damaged pharyngeal wall can attach to the denuded surface of the operated soft palate and cause a devastating total or near-total oronasal separation. (Fig. 8). Speech problems following surgery have mostly been related to hypernasal speech secondary to involvement of the levator palatinus muscle. Although it does not seem to be a significant complication, it is at least theoretically possible that normal speech sounds could be affected by any palatal surgery. This would be especially true for patients who speak languages requiring gutteral or trill sounds or who sing a great deal. Because of this it is wise of the surgeon to warn the patient of this possibility prior to surgery and include this in the informed consent process. Finally, many patients who undergo these procedures complain of an abnormal sensation in the back of their throats. It occurs at a rate of approximately 30% of all patients and lasts up to 1 year postoperatively. This sensation, called globus, is not associated with any particular anatomical abnormality and is not a functional problem [18]. It is, however, quite perturbing to a large number of patients. Hence, it is incumbent on the surgeon to warn the patient of this and provide support and reassurance when the patient complains of this after surgery. In summary, it would appear that the LAUP and LA-UPPP, when performed judiciously on selected patients, are relatively safe procedures associated with only rare complications [19]. Mortality is lessened over the standard scalpel UPPP, at least in part, from

Fig. 8. Scarring of the palate to the pharyngeal wall following LAUP. Caused by inadvertent thermal damage to the wall by the backstop with adhesion to the palate.

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the ability to perform these procedures under local anesthesia or I.V. sedation, thereby obviating the need for much higher-risk general anesthesia.

Discussion Despite its detractors, the LAUP procedure, with nearly 10 years of clinical use, is now an accepted method of effectively treating socially unacceptable snoring. Even those surgeons who made the leap to radiofrequency somnoplasty because of its shorter recovery time and decreased postoperative pain are returning to the LAUP for patients with thick palates or those who fail the somnoplasty procedure. Although many of the studies done to demonstrate the LAUP’s effectiveness for simple snoring have been subjective in nature, usually involving patient or sleep partner questionnaires, it is clear that this procedure is clinically effective at diminishing snoring to a socially acceptable level in the majority of patients, approximating the same 90 – 95% success rates seen with scalpel UPPP [20 – 22]. Long-term success rates drop to 50 – 70% caused, no doubt, by some relapse of the soft tissues as well as weight gain and behavioral changes [23,24]. Nevertheless, 92% of our patients questioned at 1 year postoperatively were happy with the results of their surgery and would do the procedure again if the need arose [25]. Several objective studies have also shown that the LAUP does indeed decrease snoring to low and acceptable levels [26 – 28]. Just as importantly, Armstrong et al, in a subjective study, showed that there was a significant improvement in the quality of life after the LAUP in habitually snoring patients and their sleep partners, as measured by marital happiness, physical health, psychological health, and social relationships [29]. When comparing UPPP with LAUP for snoring diminishment, Osman et al showed no significant difference between the two in improvement of snoring index (SI) [28]. Although all of these studies examined the patients after the original standard LAUP, it would seem reasonable to assume that the results after LA-UPPP would be at least as good if not better. In fact, it is the feeling of many surgeons, including this author, that the LAUPPP carries with it the potential for only minimally added morbidity over the LAUP but results in more predictable airway opening and long-term results and should therefore be used routinely in place of the standard LAUP procedure. Further research is needed to prove this hypothesis. The use of the LAUP and LA-UPPP for the management of obstructive sleep apnea is consid-

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erably more controversial, and objective data has only recently been forthcoming. Reda et al have shown that habitual snoring patients have statistically long soft palates, long wide uvulas, and narrowed oropharyngeal isthmuses [30]. Though there are multiple possible anatomical sources for the vibratory etiology of snoring, it would stand to reason that excisional laser procedures of the soft palate, a common source of snoring, would result in shorter and tighter soft palates and diminishment of the snoring. And though Reda et al showed that the LAUP did indeed do this, it also interestingly further reduced the already narrow space between the posterior tonsillar pillars [30]. In fact, one study surprisingly demonstrated a 4% overall decrease in airway volume within the first 72 hours after LAUP. Conversely, other studies have shown an increase in the cross-sectional size of the velopharyngeal area and anteroposterior diameter [31]. Although not an issue for snoring, where subjective improvement is an adequate measure of success, it is the basic concerns over the unpredictable nature of these procedures that have brought the LAUP and LA-UPPP into question as viable and safe treatment alternatives for sleep apnea. A review of the literature reveals a few objective polysomnographic-based studies that bear out this lack of certainty and predictability. Lauretano et al found the LAUP to be effective for snoring yet ineffective for all degrees of sleep apnea. Ryan and Love concluded in their studies that the LAUP is highly variable and unpredictable for sleep apnea, with approximately 36% of patients improving ( > 50% decrease in the Respiratory Disturbance Index or RDI), 34% showing little change, and 30% actually worsened after surgery [27]. Interestingly, they found no change in the SI in these patients either, yet they did find a significant increase in quality of life indicators in all domains, along with a decrease in sleepiness. They concluded from this data that there is little correlation between subjective and objective improvement in sleep apnea following surgery [27]. Conversely, several equally scientific, polysomnographic-based studies showed the LAUP to indeed be both a safe and effective tool in the management of obstructive sleep apnea. Walker and Grigg-Damberger, Walker and Garrity et al, Mickelson and Ahuja, and Pribitkin et al have all published data indicating that the LAUP is at least as good as UPPP for treating obstructive sleep apnea [32 – 35]. Results are generally in the range of 50 – 70% decrease of the RDI in most patients, again approximating the results seen with scalpel UPPP. Some limit this to mild apnea with an RDI of less than 30/hr [33], whereas others

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demonstrated effectiveness even with severe obstructive sleep apnea [35].

Summary The LAUP and the LA-UPPP appear by most measures to be safe and reliable tools in the management of socially unacceptable snoring and mild sleep apnea, although much of the documentation to this effect is subjective. When used for moderate to severe sleep apnea, there are still considerable differences of opinion in the literature as to their effectiveness, although they appear in most of the literature to be more or less equivalent to the scalpel UPPP, with less morbidity. Most surgeons would consider the LAUP and LA-UPPP, just as they would (and should) UPPP, to be one useful facet of a more complicated and complete surgical treatment protocol for moderate to severe sleep apnea.

References [1] Kamami YV. Laser CO2 for snoring: preliminary results. Acta Otorhinolaryngol Belg 1990;44:451 – 6. [2] Krespi YP, Keider A. Laser-assisted Uvulopalatoplasty for the treatment of snoring. Op Tech Otolaryngol Head Neck Surg 1994;5:228 – 34. [3] Krespi YP, Ling EH. Laser-assisted serial tonsillectomy. J Otolaryngol 1994;23:325 – 7. [4] Kamami YV. Ambulatory treatment of sleep apnea syndrome with CO2 laser-a review of 53 cases. J Fr Otorhinolaryngol 1994;43(3):183 – 8. [5] Carenfelt C. Laser uvuloplatoplasty in treatment of habitual snoring. Ann Otol Rhinol Laryngol 1991;100: 451 – 4. [6] Practice parameters for the use of laser-assisted uvulopalatoplasty. Standards of Practice Committee of the American Sleep Disorders Association. Sleep 1994; 17:744 – 8. [7] Crumley RL, Stein M, et al. Determination of obstructive site in obstructive sleep apnea. Laryngoscope 1987;97:301 – 12. [8] Strauss RA. Upper airway examination and nasopharyngoscopy. J Oral Maxillofac Surg 1996;54(8): 12 – 3. [9] Coppola MP, Lawee MS. Management of obstructive sleep apnea syndrome in the home. The role of portable sleep apnea recording. Chest 1993;104:19 – 25. [10] Emsellem HA, Corson WA, et al. Verification of sleep apnea using a portable sleep apnea screening device. So Med J 1990;83(7):748 – 52. [11] Redline S, Tosteson T, et al: Measurement of sleep related breathing disturbances in epidemiologic studies. Chest 1991;100:1281 – 86.

[12] Strauss RA. Lasers in oral and maxillofacial surgery. Dent Clin NA 2000;44(4):851 – 73. [13] Croft CB, Golding-Wood DG. Uses and complications of uvulopalatopharyngoplasty. J Laryngol Otol 1990; 104:871 – 5. [14] Fairbanks DN. Uvulopalatopharyngoplasty complications and avoidance strategies. Otolarygol Head Neck Surg 1990;102:239 – 45. [15] Haavisto L, Suopaa J. Complications of uvulopalatopharyngoplasty. Clin Otolaryngol 1994;18:243 – 7. [16] Terris DJ, Clark AA, et al. Characterization of postoperative edema following laser-assisted uvulopalatoplasty using MRI and polysomnography: implications for the outpatient treatment of obstructive sleep apnea syndrome. Laryngoscope 1996;106:124 – 8. [17] Walker RP, Grigg-Damberger M, et al. Uvulopalatopharyngoplasty versus laser-assisted uvulopalatoplasty for the treatment of obstructive sleep apnea. Laryngoscope 1997;107:76 – 82. [18] Pinczower E. Globus sensation after laser-assisted uvuolpalatoplasty. Am J Otolaryngol 1998;19(2):107 – 8. [19] Remacle M, Betsch C, et al. A new technique for laserassisted uvuolpalatoplasty: decision-tree analysis and results. Laryngoscope 1999;109:763 – 8. [20] Neruntarat C. Laser assisted uvulopalatoplasty:shortterm results and long-term results. Otolaryngol Head Neck Surg 2001;124:90 – 3. [21] Vukovic L, Hutchings J. Patient evaluation of laserassisted uvulopalatolasty. J Otolaryngol 1996;25(6): 404 – 7. [22] Wareing M, Callanan V, et al. Laser-assisted uvulopalatoplasty:six and eighteen month results. J Laryngol Otol 1998;112:639 – 41. [23] Janson C, Gislason T, et al. Long-term follow-up of patient with obstructive sleep apnea treated with uvulopalatoplasty. Arch Otolaryngol Head Neck Surg 1997; 123:257 – 62. [24] Katsantonis GP, Schweitzer PK, et al. Management of obstructive sleep apnea: comparison of various treatment modalities. Laryngoscope 1988;98:304 – 9. [25] Strauss RA. Laser-assisted uvulopalatoplasty and diagnostic nasopharyngoscopy. Data Presented at the International Association of Oral and Maxillofacial Surgeons Biannual Meeting, Budapest Hungary, 1995. [26] Kotecha B, Paun S, et al. Laser-assisted uvulopalatoplasty: an objective evaluation of the technique and results. Clin Otolarygol 1998;23:354 – 9. [27] Lauretano A, Khosla R, et al. Efficacy of laser-assisted uvulopalatoplasty. Lasers Surg Med 1997;21: 109 – 16. [28] Osman EZ, Osborne JE, et al. Uvulopalatopharyngoplasty versus laser-assisted uvulopalatoplasty for the treatment of snoring: an objective randomized clinical trial. Clin Otolaryngol 2000;25:305 – 10. [29] Armstrong MW, Wallace CL, et al. The effect of surgery upon the quality of life in snoring patients and their partners: a between-subjects case-controlled trial. Clin Otolaryngol 1999;24:510 – 22. [30] Reda M, Sims A, et al. Morphological assessment of

R.A. Strauss / Oral Maxillofacial Surg Clin N Am 14 (2002) 319–331 the soft palate in habitual snoring using image analysis. Laryngoscope 1999;109:1655 – 60. [31] Ryan CF, Lowe LL. Unpredictable results of laserassisted uvulopalatoplasty in the treatment of obstructive sleep apnea. Thorax 2000;55:399 – 404. [32] Mickelson SA, Ahuja A. Short-term objective and long-term subjective results of laser-assisted uvulopalatoplasty for obstructive sleep apnea. Laryngoscope 1999;109:362 – 7. [33] Pribitkin EA, Schutte SL, et al. Efficacy of laser-assis-

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ted uvulopalatoplasty in obstructive sleep apnea. Otolaryngol Head Neck Surg 1998;119:643 – 7. [34] Walker RP, Garrity T, et al. Early polysomnographic findings and long-term subjective results in sleep apnea patients treated with laser-assisted uvulopalatoplasty. Laryngoscope 1999;109:1438 – 41. [35] Walker RP, Grigg-Damberger MM, et al. Laser-assisted uvulopalatoplasty for the treatment of mild, moderate, and severe obstructive sleep apnea. Laryngoscope 1999;109:79 – 85.

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Surgical treatment of snoring and mild obstructive sleep apnea Mansoor Madani, MD, DMD* Department of Oral and Maxillofacial Surgery, Capital Health Medical Center, 750 Brunswick Avenue, Trenton, NJ 08638, USA Department of Oral and Maxillofacial Surgery, Temple University, 3401 North Broad Street, Philadelphia, PA 19140, USA Center for Corrective Jaw Surgery, 15 North Presidential Blvd., Suite 301, Bala Cynwyd, PA 19004, USA

Snoring has plagued individuals and societies for centuries. It is just within the past few decades that it was recognized as a sign of a more serious illness of sleep-disordered breathing known as sleep apnea [1 – 7]. Recent understanding of the pathophysiology of snoring, daytime sleepiness, restless sleep, and obstructive sleep apnea has allowed for successful treatment involving both nonsurgical and surgical intervention [8 – 11]. The nonsurgical management of snoring includes exercise, weight loss, decreased alcohol consumption, smoking cessation, altered sleeping position, and dental or nasal appliances [12]. Patient compliance has persistently been the drawback in these types of management. Major studies shows that over half the patients will not follow the conservative treatment for an extended period or patients do not obtain sufficient relief from their snoring with conservative methods and look for surgical modalities to correct their problem. In this article, we look at several surgical modalities to treat snoring and mild obstructive sleep apnea. The surgical goal should be to find a simple, safe, effective, and economical surgical procedure, which benefits the patient and allows a speedy recovery and return to normal daily activities. During the past several decades, a variety of methods have been advocated for treatment of snoring and mild sleep apnea. No single procedure has been proven to have the ideals that justify its sole use over others. In order to choose an appropriate method of treatment, we must first review the pathophysiology of snoring and sleep apnea.

Pathophysiology of snoring and sleep apnea

* Center for Corrective Jaw Surgery, 15 North Presidential Blvd., Suite 301, Bala Cynwyd, PA 19004, USA E-mail address: [email protected] (M. Madani).

One of the most important aspects of surgical treatment is patient selection. Each patient will have a very specific problem, and some may need a combina-

Snoring and obstructive sleep apnea occur in at least eight different sites; nasal (deviated septum, enlarged nasal turbinates), soft palate and uvula (retropalatal) [13], tonsils (obstructive tonsils), tongue base (retrolingual), jaws (retrognathism), lateral pharyngeal walls (pharyngeal muscle hypertrophy), and hyoid and epiglottis (Fig. 1). Turbulent airflow and subsequent progressive vibratory trauma to the soft tissues of the upper airway are important factors contributing to snoring [14 – 16]. Anatomic obstruction leads to greater negative inspiratory pressure, propagating further airway collapse and partial airway obstruction (hypopnea) or complete obstruction (apnea) (Fig. 2). Beside the upper airway anatomy, there are two other factors involved in the development of obstructive sleep apnea, and they are decreased dilating forces of the pharyngeal dilators and negative inspiratory pressure generated by the diaphragm. When surgical procedures are proposed to a patient, all of these factors must be kept in mind, and no guarantee of a cure for sleep apnea should be given based on corrective surgery of only one or two of these factors. The same concept is true for reduction of the snoring sound and not total elimination of the sound, as snoring sound is multifactorial as well.

Clinical evaluation and patient selection criteria

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 2 8 - 6

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Imaging and radiographic studies

Fig. 1. Snoring and obstructive sleep apnea occurs in at least eight different sites. They include nasal septum, nasal turbinate, adenoids, tonsils, base of the tongue, uvula, soft palate, and epiglottis.

tion of procedures, whereas others may not be candidates for surgery at all. History of snoring, daytime sleepiness, gasping for air, and period of witnessed apnea, as reported by the patient and the patients’ bed partner, are important indications for treatment. Most patients with sleep apnea are overweight with short, thick necks. In the head and neck region, the upper airway should be examined for a number of abnormalities (Table 1). Decreased muscle tone during sleep contributes to airway collapse as well. Direct fiberoptic examination or indirect mirror examination may reveal a mass or tumor somewhere in the upper airway, epiglottis enlargement, or vocal cord problems. As we will describe later in this article, the clinical examination of every individual will determine which types of procedures will suit them best. A simple test the author uses to determine the possible origin of the sound of snoring is to ask the patient to imitate the snoring sound with the mouth slightly open. Usually, a loud sound will be detected from the vibration of the soft palate and the uvula. The patient is then asked to make the snoring sound with the lips completely sealed and from the nose. Generally, patients with a nasal problem can make the sound. This is most commonly related to an obstruction in the nasal passage. In our experience, up to 70% of snoring sounds in men come from the vibration of the uvula and the soft palate. Women, in more than 60% of occasions, have a nasal component of snoring.

Two of the most common radiographs taken by oral and maxillofacial surgeons are panoramic and cephalometric radiographs [17]. The values of cephalometric studies are discussed elsewhere in this publication. But, when deciding to choose radioablation treatments, it is a crucial tool for measuring the thickness of the soft palate. A simple panoramic radiograph can show the uvula and the airway, and, in addition, the presence of any cysts or tumors of the maxillary sinus. Some panoramic films show deviated septum and enlarged turbinates. The advantages of these types of radiographs are their simplicity, clarity, and low cost. There are controversies in the literature as to the value of these radiographs, but for surgeons who frequently use them as an adjunct to their clinical examination, it should be a routine matter. MRI studies of the airway, although very precise, are rarely performed [18].

Surgical modalities Several surgical procedures are available to correct each type of snoring (ie, nasal, palatal, tonsillar,

Fig. 2. Anatomic obstruction leads to greater negative inspiratory pressure, propagating further airway collapse and partial airway obstruction (hypopnea) or complete obstruction (apnea).

M. Madani / Oral Maxillofacial Surg Clin N Am 14 (2002) 333–350 Table 1 Upper Airway Abnormalities in Sleep Apnea Enlarged, elongated or edematous uvula Hyperplastic or thick soft palate Constricted oropharynx Macroglossia Enlarged tongue base (noting any posterior collapse)

Prominent oropharyngeal folds Obstructive tonsils Adenoids Deviated septum Enlarged nasal turbinates Presence of nasal polyps or any other obstructive masses

base of the tongue). The retrolingual procedures, such as partial glossectomy and orthognathic surgeries, such as bimaxillary osteotomies, sagittal split osteotomy, and genioglosal advancements with hyoid myotomy, are most effective and discussed elsewhere in this publication [19 – 21]. They are certainly more invasive and complicated than the palatal and nasal procedures, however. Nasal surgeries, such as septoplasty and inferior turbinate resection, rarely provide relief from snoring when used alone. In our experience, they reduce the sound of snoring only up to 25%, and they do not cure sleep apnea to any greater degree. Nasal procedures, however, often improve patient tolerance and response to nasal continuous positive airway pressure (CPAP). They are best used as an adjunct to more definitive surgical procedures. For these reasons, we initially offer most patients who desire surgical treatment a palatal procedure in combination with turbinate radio-ablation procedures. In this article, we review the use of radiofrequency (RF), Harmonic Ultrasound, and laser procedures in the treatment of habitual snoring and mild sleep apnea. Additionally, new techniques will be discussed for treating obstructive tonsils and enlarged nasal turbinates. The advantages as well as disadvantages and potential problems of some of the newer devices will be explored as well. Following FDA clearance of radio-ablation in the United States in 1997, the author has utilized three different RF generator systems, two laser systems (CO2 and Nd Yag laser), and also the latest device used to treat these conditions, the Harmonic Ultrasound. They were all used in a large group of patients for treatment of snoring and sleep apnea. The results were varied and the techniques were modified significantly to achieve the best results. Patient selection, procedural details, and device utilization will be discussed later in this article. But in order to understand the use of radiofrequency, ultrasound, and laser, we should first review the history and physics of these devices.

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Radiofrequency usage in treatment of snoring and mild sleep apnea RF has been used in medicine for over a century in the form of electrosurgery. The French physicist d’Arsonval first used RF energy in 1891. He reported that altering current at frequencies of 2 kHz – 2 MHz could be applied to tissues, causing heat effects without muscle and nerve stimulation [22]. At this point, the development of diathermy and electrosurgery began. In 1928, the physicist, W.T. Bovie, and the neurosurgeon, Harvey Cushing, created the very first electrocautery unit capable of cutting and coagulating tissues [23,24]. RF energy has gained wide usage during this century in many areas of medicine, particularly because of its ability to produce discrete lesions in the central and peripheral nervous systems [25,26]. It has also been used in a variety of dermatological cases as well as for malignancies [27] and for the control of chronic pain syndrome [28]. Collings introduced transurethral electrosurgery for the relief of prostate obstruction in 1932 [29]. In the mid-1980s, RF energy was first used during the experimental treatment of cardiac arrhythmia in animal models by Huang et al, where it safely produced a lesion in the V node, as well as the atrial and ventricular myocardium [30]. RF is also being extensively used now in orthopedic surgery [31 – 35]. The concept of RF tissue ablation or volumetric tissue reduction is not new. Ellis et al presented their preliminary work on stiffening of palatal tissue using the Nd. YAG laser in 1993 [36]. Whinney et al described their approach for stiffening of the soft palate by using 10 – 15 penetration sites on the palatal mucosa using diathermy in 1995 [37]. Powell et al initiated the use of RF for the treatment of snoring and sleep apnea in an animal model in 1996. Investigative animal and human studies by Powell and others showed that using RF energy could safely reduce tongue and soft palate volume in a controlled manner [38]. The author’s studies also showed the effective usage of RF for volumetric reduction of enlarged turbinates and obstructive tonsils [39 – 41].

Physics of radiofrequency The introduction of RF generators to the field of medicine, particularly by William Bovie and Harry Cushing, had an impact on many surgical procedures in the twentieth century. Four types of RF generators are: grounded, isolated, balanced, and returnedelectrode monitoring systems. There are many types

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of RF generators advocated and used in the treatment of snoring and sleep apnea. Advantages of radio-ablation Radiofrequency treatments are certainly less invasive than traditional surgeries. They are designed, when properly used, to reduce patients’ discomfort, tissue damage, mucosal ulceration, and external scar formation. These devices are capable of creating submucosal lesions (also known as ablation) while simultaneously controlling bleeding. The clinical advantages of these procedures are intended to include more precise operative results, reduced surgical time, and rapid recovery. The lesions created by these procedures are naturally resorbed in approximately 8 – 10 weeks, reducing excess tissue volume. Procedures are generally performed in an outpatient setting, and no general anesthesia is required for most of them. The effectiveness of each procedure depends on patient selection, site of the lesions, number of repeated procedures, and the surgeon’s experience. At present, the three most commonly utilized RF devices are SomnoplastyTM, Coblation1, and Ellman/Ellmad1. We will briefly describe each system and then review the relevant procedures. SomnoplastyTM One of the most sophisticated RF systems available to surgeons for the treatment of snoring and sleep apnea is SomnoplastyTM (Somnus Medical Technologies, Inc., Sunnyvale, CA). It is an isolated and monopolar type RF system with floating output and is not designed to cut or cauterize tissues. Its main purpose is to create a submucosal coagulative lesion by heating tissue within a temperature range of 50 – 95° C around the active portion of the electrode. This generator uses a ground pad to complete the electrical circuit. In SomnoplastyTM, a current from the electrode causes electrical arcs to form across the physical gap between the probe and the target tissue. At the contact point of these arcs, rapid tissue heating occurs. Consequently, cellular fluid rapidly vaporizes into steam, causing the release of cellular fragments and producing a layer of necrosis, or dead cells, along the pathway of the probe. As a result of this heating, collateral tissue ablation is produced in regions surrounding the target tissue site. This leads to the creation of vacuolar degeneration in the affected tissue. Over a course of several weeks following the initial treatment, a firmer, fibrous tissue forms, reducing the tissue volume and, thus, resulting in less

vibration. This system consists of a programmable RF generator with temperature and impedance monitoring and a disposable surgical hand piece containing a needle electrode, which delivers RF energy to selected areas. An insulating sleeve at the base of the needle electrode protects the tissue external to the treated area from thermal damage. This prevents tissue sloughing and minimizes patient discomfort. Thermocouples provide monitoring of tissue temperature, providing the surgeon with the ability to protect the mucosa from inadvertent treatment. Coblation1 Coblation1 (Arthrocare Corporation, Sunnyvale, CA) was originally designed for use in orthopedic arthroscopy surgeries, and later modified for use in treatments of snoring and nasal congestion and tonsillar radio-ablation. It is a sophisticated bipolar device that does not require a return pad. The return electrode is within the hand piece and requires saline gel as a conductive medium. It is designed to cut and coagulate as well as ablate the treated tissues on command. The Coblation1 method replaces the extreme heat of laser surgery and standard electrosurgery with a gentle heating of the tissues, causing physical reduction and shrinkage of the affected site. This is achieved by molecular disintegration via a radio-ablation process most closely resembling that of Excimer lasers. Coblation1 occurs when the tip of the probe is merged in a saline gel as a conductive medium and placed over the tissue. Upon applying a sufficiently high-voltage difference between the probe and the tissues, the electrically conducting fluid is converted into an ionized vapor layer, or plasma. As a result of the voltage gradient across the plasma layer, charged particles are accelerated toward the tissue. At sufficiently high-voltage gradients, these particles gain adequate energy to cause dissociation of the molecular bonds within tissue structures. This molecular dissociation produces volumetric removal of tissue. Because of the short range of the accelerated particles within the plasma, however, this dissociative process is confined to the surface layer of the target tissue but produces minimal necrosis of collateral tissue. The advantages of this system are its simplicity, short duration of procedures, and effectiveness of its radio-ablation property. Ellman1, Surgitron1, and Ellmad1 These systems are basic electrocautery devices that have a less sophisticated hand piece and are the

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least studied in the treatment of snoring and sleep apnea. These units are readily available in most surgical practices, easy to use, and are less expensive than the other RF systems. They can also be used to cut, coagulate, and ablate the tissues. The Elman1 unit has an easily adjustable power range to ‘‘dial-in’’ the level of RF energy suitable for any given procedure. The probe temperature rapidly rises and has the potential for mucosal tissue surface damage. As with all other radio-ablation devices, care must be taken to insert the needle directly into the palatal muscle, because superficial placement leads to mucosal sloughing. Also, because the needle is extended into the palate without direct visualization, it might inadvertently be placed through the palate into the nasopharynx.

Procedures There are several procedures that can be performed utilizing any of the above RF devices. For the sake of simplicity, we divide them into four distinct areas: palatal, tonsillar, inferior turbinate, and base-of thetongue radio-ablation. Patient preparation and selection is crucial, as mentioned previously; otherwise, there is the likelihood of treatment failure. In our experience, patients should not be given guarantees that sleep apnea will be totally cured. The procedures may need to be done in repeated sessions, and patients’ compliance is an important factor. The anatomy of the structures treated is also a crucial factor. Patients with excessively long and bulky uvulas, or severely hypertrophic soft palates, will not benefit from palatal radio-ablation for an extended time period. Relapse was noted within 2 years of treatment in 60% of our patient population, and the base-of thetongue procedure in our patient population required an average of five treatments. Because of patients’ tongue movement or weight gain, the lost tongue bulk returned by 70%. On the other hand, inferior nasal turbinates and tonsillar radio-ablation seem to be much more stable even after a single treatment and at 2 years following the surgery. With this in mind, we will review each procedure and advise our readers to use common sense in careful procedure selection as well as patient selection.

General preoperative preparation Prior to the procedure, the patient’s medical history is reviewed, and a careful oral and nasal airway assessment is done. Using nasopharyngoscopy, the

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nasal cavity and nasopharynx are examined. Oral cavity exams include evaluation of the size and position of the uvula, soft palate, tonsils, and tongue. The patient’s occlusion is also recorded. The collar size, body weight, and height are assessed. A snoring questionnaire is given the patient to answer. Patients who utilize any types of anticoagulant including aspirin are asked to stop taking them 5 days prior to surgery, with consent from their primary care physician or cardiologist. Patients at risk of subacute bacterial endocarditis are advised to take the appropriate prophylaxis as recommended by the American Heart Association prior to surgery. Bleeding, infection, prolonged pain, and impaired healing are extremely rare but are the potential complications of these procedures. Generally, pain medications and antibiotic treatment are not required following the procedures with the exception of tonsillar radioablation. Nasal regurgitation following this procedure has not been observed as a complication, but as with any palatal surgery, these are potential complications requiring discussion with patients. In our experience, a second procedure has been generally required 4 months following the initial treatment in severe habitual snorers.

Palatal radio-ablation The patient is brought into an outpatient office setting while blood pressure and other necessary monitors are attached. The best patient position is sitting in a dental or ENT chair. The Coblation1 unit does not require any conductive pad, but the other monopolar RF systems require a conductive pad placed on the lower back area. Topical anesthesia (Benzocaine 20%) is applied to the palate, and the patient is asked to swish that around the mouth for 30 seconds. The topical anesthesia should reduce gagging and also any pain at the injection sites. Then, using a 27 – 30-gauge dental needle, 2.5 – 3.0 ml of Marcaine (or Xylocaine) is injected at the junction of the hard and soft palate, continuing down and on the sides of the soft palate and the base of the uvula. Unlike the CO2 laser, the RF procedures require an adequate amount of local anesthesia to avoid discomfort. It also allows tissue expansion and better conduction of current to the area of the internal ablation. The desired angle of the radiofrequency electrode is 35 – 45°, depending on the anatomy of the hard and soft palate. Placement of the electrode is extremely important. The electrode is entered high in the soft palate so that the end point of the electrodes is just

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The Somnoplasty1 electrode tip has two sections, each one centimeter in length. The very tip of the electrode is not insulated and is the point where the heat is generated around it. It is maintained at a constant temperature of 85° C. The proximal end of the electrode near the hand piece is coated to avoid thermal burning of the palatal mucosa. As the tip temperature approaches body temperature, impedance should be less than 500 ohms. The generator will automatically shut down if the impedance exceeds 500 ohms, an indication that the electrode is improperly placed or is outside of the tissue. Once the electrode is in the proper position, the foot pedal is depressed and the amount of energy (up to 750 joules) is monitored. After the appropriate amount of energy is delivered, the foot pedal is depressed again to stop the procedure; the electrode is fully retracted and removed from the patient’s oral cavity. The lateral electrode placement is generally 10 mm away from the midline on both sides and at the same temper-

Fig. 3. The radiofrequency electrode is entered high in the soft palate so that the end point of the electrodes is just above the uvula but not in the uvula itself.

above the uvula but not in the uvula itself (Fig. 3). In order to assure the proper placement of the electrode, it can be placed over the soft palate to visualize clinically the exact location and position of the electrode entry point prior to insertion. Care must also be taken to deploy fully the active component of the electrode into the patient’s soft palate (Fig. 4). The Coblation1 Reflux wand 55 is used for palatal radio-ablation. It comes prebent and only needs to be dipped in saline gel as its conductive medium. The unit is generally set at # 6 and the probe is kept in place for 10 – 12 seconds. It must not be kept for more than 15 seconds as the surface temperature rises and will cause mucosal erosion and ulceration. The probe temperature reaches approximately 85° C within 10 seconds. The distal end of the probe is the active end, and the proximal end is coated to avoid unwanted mucosal burn. After the single midline lesion is created, two additional sites just lateral to the first lesion are selected, aiming the probe at a 30° angle from the center and toward the side corners of the soft palate (Fig. 5).

Fig. 4. To ensure proper placement of the radiofrequency electrode, it can be placed over the soft palate to visualize clinically the exact location and position of the electrode entry point prior to insertion. Care must also be taken to deploy the active component of the electrode fully into the patient’s soft palate.

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Palatal radio-ablation results

Fig. 5. After the single midline lesion is created, two additional sites just lateral to the first lesion are selected, aiming the probe at a 30° angle from the center and toward the side corners of the soft palate.

ature, but less energy is applied. In our experience, 350 joules is sufficient energy for the lateral lesions. We have experienced even better results by placing two additional far lateral lesions with 300 joules, making a total of five submucosal lesions, 10 – 15 mm apart from other lesions. Similar procedures have been followed using the Ellman unit, but as mentioned earlier, no extensive research has been published on the use of this system to treat snoring and sleep apnea. The patient has to be carefully monitored during the first 24 hours following the radio-ablation procedure. No postoperative antibiotics or narcotic pain medication is needed. Normally, patients experience a feeling of fullness in the back of the throat. Patients must be advised to sleep on a reclining chair or with the head elevated at a 45° angle for the first night after surgery. The soft palate and uvula will become edematous to a variable degree during the first 24 – 48 hours following the procedure. Usually, a minimal sore throat is noted after the procedure and an over-thecounter pain medication will be sufficient for pain management. The palatal stiffening and volumetric reduction process takes 8 – 10 weeks and patients notice a change in the intensity of snoring, but not complete elimination of snoring after the first procedure. A second procedure is usually needed in severe snoring patients 4 months after the initial treatment.

During the past 3 years, 463 patients were treated with radio-ablation using Coblation1 and Somnoplasty1, 271 (58%) male and 192 (42%) female. The men’s average collar size was 16, and the average body weight was 175 lbs. The average RDI (respiratory disturbance index) was less than 15 per hour. Not all patients, however, had a sleep study prior to the procedure. One of the most crucial aspects of this procedure was patient selection. The reduction in snoring following the first treatment averaged 30 – 40%. Improved nasal breathing was reported by 60% of patients. No incidences of major pain, nasal reflux, voice changes, or bleeding were noted. Mucosal blanching was noted in 9% of patients but required no treatment. Patients with three or more lesions had a moderate amount of edema postoperatively; but no treatment was needed. Although patients with the larger number of lesions had more edema immediately after the procedure, they showed much better results in the reduction of snoring and improved breathing 10 weeks following surgery. Patients with a short uvula and floppy soft palate responded the best to this procedure. During a 3-year follow-up period, 234 (50.5%) patients out of the 463 decided to proceed with the laser-assisted uvulopalatopharyngoplasty (UPPP) because of continued loud snoring. These patients experienced less postoperative pain compared with the group that did not have the radio-ablation procedure done. More instant relief of snoring and significant improvement in nasal breathing and sleeping pattern was achieved, however. One of the major reasons for this change in our treatment modality was our limited knowledge of patient selection for these procedures. If a patient has a very large edematous uvula and excessively hypertrophic soft palate, the laser assisted UPPP is the best treatment in our opinion. Now, our success rate has drastically improved as we only perform palatal radio-ablation on habitual snorers with a very thick soft palateand shorter uvula, and on nonsmokers. The success is higher by a ratio of 3:1 in women versus men. This is mostly because of the anatomical differences we have observed in our female population. Subjectively, the snoring intensity reduction in the successful cases was over 68% on average; improved breathing and sleeping was 72%.

Tonsillar radio-ablation Although there has been a significant drop in number of tonsillectomies performed annually in

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Fig. 6. 2 – 3 ml local anesthesia is injected into the base of the tonsil, starting in the lateral part of the soft palate and extending to the area of the lateral wall of the pharynx (tonsillar bed). Four radio-ablation sites demonstrated within the tonsillar mass.

children, there are millions of adults that suffer from chronic irritation of the tonsils. Enlarged tonsils is one of the contributing factors in obstructive sleep apnea [42 – 49]. Many complications have been reported with traditional tonsillectomies, including infection, bleeding, dehydration, angular cheilitis, dysgeusia, pulmonary edema, and loss of time from work or school [50 – 58]. There have been varieties of methods advocated to resect the tonsils, including use of guillotine, electrocautery, laser, and bipolar scissor [59 – 62]. In early 1999, the author introduced tonsillar radio-ablation. Hundreds of patients were treated with a similar procedure as described above for palatal radio-ablation. Patients were seen for the treatment of enlarged tonsils because of chronic inflammation, (multiple) tonsillitis, multiple Strep throat infections requiring frequent antibiotic treatment, obstruction of the airway, and snoring problems. Other considerations were chronic tonsillar hyperplasia, with tonsillar crypt causing further accumulation of food and bacteria leading to infection and halitosis. It must be emphasized to patients that RF procedures primarily reduce the tonsillar size and are not designed to remove the tonsils. The debulking process may require repeat sessions later for further reduction of the tonsils. There are certain precautions that are recommended with this procedure to avoid complications. Starting 2 days prior to the surgery, patients are placed on antibiotic prophylaxis, or IV administration of antibiotics 1 hour prior to surgery for a noninfected and noninflamed tonsil. Chlorhexidine (Peridex1) mouth rinse is given several days prior to surgery,

and patients are asked to continue to use it twice daily for at least 2 months postoperatively. Assurance is made to identify and manage any preexisting infection, fever, and sore throat. The patient is placed in the supine position. Chlorhexidine (Peridex1) mouth rinse is given to the patient to keep in the mouth, gargle, and rinse for 1 minute. Marcaine 0.5% (2 – 3 ml) with 1:200,000 pinephrine is injected into the base of the tonsil starting in the lateral part of the soft palate and extending to the area of the lateral wall of the pharynx (tonsillar bed) (Fig. 6). A plastic doublecheek retractor is placed on the inside of the cheek to give the best visualization and also to protect the patient’s lips. The Coblation1 unit is set to 6, and the Coblation1 Reflex wand 55 is used to deliver the appropriate energy. A conductive saline gel is used and applied to the entire uninsulated portion of the probe and is placed on the most prominent surface of the tonsil (Fig. 7). The foot pedal is used for a short period of time to activate the unit and to insert the probe into the tonsil. Superficial heating of the tonsillar mucosa must be avoided to prevent superficial erosion. This procedure is a submucosal procedure and does not include resection of the tonsils. Once the uninsulated probe is completely inserted in a horizontal direction, the energy is applied for approximately 10 – 15 seconds. The same procedure is repeated two to four additional times on that side. This step is repeated on the other side. Patients are carefully monitored and evaluated for need of additional procedures. The patients are

Fig. 7. Tonsillar channeling, with the direction of the probe parallel to the tonsillar artery and away from the surface.

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infections, and 61% were treated to alleviate the symptoms of obstructive sleep apnea. Patients were followed from 3 months up to 2 years with an average of 15 months. There was no bleeding during or after the procedures. None of the patients treated developed any infection. The discomforts were minimal and, if needed, patients were advised to take over- the-counter pain relievers. All procedures were done in an office setting with average duration of procedures under 6 minutes. All patients treated reported no voice changes or fluid reflux. The day after the procedures, 100% of patients returned to work or school. Fig. 8. When properly done, the tonsil volumetric reduction can be up to 60% 10 weeks after the procedure.

advised that the healing process takes up to 8 weeks postoperatively, and additional treatments may be necessary (Fig. 8). These procedures do not remove the tonsils in their entirety nor do they cure sleep apnea. They will not necessarily prevent a common cold or future Strep infections. The patients are discharged after assurances are made that there is no bleeding and the detailed explanation of the postoperative instructions are given. With the exception of the first day after the procedure, patients can eat anything they can tolerate. Generally, a prophylactic antibiotic, such as Cipro1 (ciprofloxacin hydrochloride, Bayer Corp, West Haven, CT), Keflex1 (cephalexin, Dista Products Co., Indianapolis, IN) or Cleocin1 (clindamycin hydrochloride, Pharmacia & Upjohn, Peapack, NJ), is given to the patient prior to surgery, and patients must continue to take it for a period of 10 days after the procedure. Additionally, they are asked to use a chlorhexidine mouth rinse twice daily for a period of 2 months postoperatively, and a regular mouth wash as often as possible. Pain medication is generally limited to an over-the-counter pain reliever. A sensation of tightness in the back of the throat is normal for the first week after the procedure. Patients are advised to return in 1 week unless there was a need to return earlier and weekly then after.

Nasal radio-ablation Chronic nasal obstruction, or a stuffy nose, is often caused by enlargement of the inferior nasal turbinates. The nasal turbinates, small, shelf-like structures composed of thin bone, covered by mucous membranes (mucosa), protrude into the nasal airway and help to warm, humidify, and cleanse air as it is inhaled and before it reaches the lungs. Chronic enlargement (hypertrophy) of the turbinates and the accompanying symptom of nasal obstruction affect people throughout the day, as well as during sleep. A chronic stuffy

Tonsillar radio-ablation results One-hundred eighty-seven patients, with age range of 13 – 56 years were treated in an office setting with the Coblation1 channeling to reduce tonsillar bulk. The group was comprised of 124 (66%) male and 63 (34%) female patients. Thirty-nine percent of patients were treated because of frequent tonsillar

Fig. 9. The correct placement of the radiofrequency probe (A, B) will ensure satisfactory results and prevent complications of bleeding and mucosal ulceration.

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Fig. 10. For excessively large turbinates, 2 lesions may be required.

nose can impair normal breathing, force patients to breathe through the mouth, and often affects daily activities. Enlarged turbinates and nasal congestion can also contribute to headaches and sleep disorders such as snoring and obstructive sleep apnea, as the nasal airway is the normal breathing route during sleep. Chronic turbinate hypertrophy is often unresponsive to medical treatment such as nasal sprays; thus, surgical treatment is required. It is commonly

Fig. 11. The nasal turbinates are out-fractured to allow bony expansion at the same time as mucosal radio-ablation. The complete healing process takes 10 weeks.

Fig. 12. In uvulopalatopharyngoplasty (UPPP), the incision line must be marked on the soft palate to avoid excessive tissue removal.

associated with rhinitis, the inflammation of the mucous membranes of the nose. When the mucosa becomes inflamed, the blood vessels inside the membrane swell and expand, causing the turbinates to become enlarged and obstructing the flow of air through the nose. Current surgical treatments include nasal septum reconstruction and turbinectomies. They can be associated, however, with lengthy recovery periods, crusting, edema, scab formation, bleeding,

Fig. 13. About 2.5 cc of local anesthesia is infiltrated in the soft palate.

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and significant patient discomfort. Additionally, the nose must be packed for several days with gauze containing an antibiotic ointment. Another method for improving nasal obstruction is outward fracture of the turbinate bone(s), which moves the turbinate away from its obstructive position in the airway. This approach, however, does not address the usual source of obstruction; enlarged submucosal tissue and the fractured turbinate often return to the previous position. Bleeding, which can usually be managed by packing the nose, is the greatest risk for patients undergoing standard turbinate resection. Nasal turbinate radio-ablation is a simple outpatient procedure similar to the other ablation techniques. First, a cotton role soaked with 50% Xylocaine (4%) and 50% with a nasal decongestant is placed in the nasal cavity for a period of 1 minute. Approximately 2 ml of Xylocaine with epinephrine is injected in the inferior turbinate with a 27-gage needle. A reflex wand 45 is used with a setting of 6

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for a period of 10 seconds in each nostril (Fig. 9). For excessively large turbinates, two lesions may be required (Fig. 10). Repeated ablation may lead to scab formation, bleeding, and dryness. At the conclusion of this procedure, the nasal turbinates are out-fractured as well. This technique will allow both bony expansions as well as mucosal ablation. The nasal cavity is then packed with a small cotton role soaked with a nasal decongestant. The packing is removed 2 days later by the patient at home. The complete healing process takes 10 weeks (Fig. 11).

Nasal radio-ablation results The author has treated over 1,450 patients for chronic nasal congestion, using either nasal Coblation1 or Somnoplasty1. One of the greatest advantages of Coblation1 when performing this procedure is that it requires only 10 seconds to do and is least

Fig. 14. The uvula is pulled to one side with a long curved hemostat. The ablation is initiated on the opposite side in the anterior and posterior pillar area.

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annoying for the patients. On the other hand, the Somnoplasty1 probe size is smaller and causes less bleeding, and the hand piece is easier to work. The outcome of this procedure seems to be more promising than palatal radio-ablation. Eighty five percent of patients reported improved nasal breathing, less allergies, reduced postnasal drip, and improved sense of smell. There were no cases of infection, only 5% of patients developed nasal bleeding, and only 2 patients needed electrocautery to stop the bleeding. Bleeding may occur up to 5 weeks postoperatively, particularly if there is scab formation and the nasal cavity is dry, and the patient forcefully blows through the nose. It must be stressed to patients that they remove the nasal packing 48 hours after placement, and it must be completely wet. Holding two pieces of ice cubes on either side will prevent bleeding as well.

Laser-assisted uvulopalatopharyngoplasty (LA-UPPP) vs. ultrasound-assisted uvulopalatopharyngoplasty (UA-UPPP) One of the latest techniques investigated by the author is use of an ultrasonically activated scalpel to perform UPPP. The device we used was the Harmonic Scalpel1 (Ethicon, Endo-surgery, Cincinnati, OH), which cuts and coagulates tissues with ultrasonic vibrations at 55.5 kHz. This device is used in laparoscopic and open abdominal surgeries as well as tonsillectomies. The advantages of this system are that it is smoke-free, causes minimal tissue damage without charring, and is an excellent tool to control bleeding without major thermal damage. It is safe for patients and surgeons. Unlike monopolar electrosurgery, there is no flow of electrical current to or

Fig. 15. The ablation is carried up to an area around 5 – mm above the lower end of the posterior pillar, and the posterior pillar is then released. The ablation is then carried forward to approximately the base of the uvula.

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through the patient. The system is readily available in most operating rooms and can be used as an alternative to electrosurgery or steel blade. The Harmonic Scalpel1 operates in two power modes, variable and full. The blade vibrates longitudinally, like a reciprocating saw blade. The ultrasonic vibration at the blade enhances its cutting ability, whereas the vibrating blade edge coagulates bleeders as tissues are excised. Hemostasis occurs when tissue couples with the blade. The coupling causes collagen molecules within the tissue to vibrate and become denatured, forming a coagulum. The basic technique of performing UPPP with the Harmonic Scalpel1 is very similar to that of laserassisted UPPP surgery. The technique that we use is as follows. First, the oral and nasal cavities are inspected carefully. An excessively elongated and thick uvula, a floppy soft palate, and enlarged tongue as well as swollen tonsils and nasal turbinate hyper-

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plasia are the most common findings in a snoring individual. Lateral pharyngeal walls are also examined for thickness. Seventy-five percent of patients are given mild IV sedation using a combination of Versed1 (midazolam HCL, Roche Laboratories, Inc. Nutley, NJ), 3 mg; fentanyl, 50 micrograms (1 ml); and Propofol, 30 – 40 mg, in a running IV. The patient is placed in the supine position in a dental or ENT chair. Routine monitors are applied, and the patient is prepped and draped in the usually manner. Four mg of IV Decadron1 (Dexamethasone sodium phosphate, Merck & Co. Inc., West Point, PA) is also given. A plastic double-cheek retractor is placed on the inside of the cheek to give the best visualization and also protect the commissures of the lip. The attachment of the levator veli palatini is visualized and marked with a blue marker (Dr. Thompson’s) applicator (Fig. 12). This is done for precision and accuracy of the final excision to avoid excessive

Fig. 16. Laser hand piece has a protective metal shield, preventing the laser from damage collateral tissues. The Harmonic Ultrasound does not have this feature. The surgical technique, however, is the same.

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reduction of the tissues. Marcaine 0.5% with 1: 200,000 epinephrine is injected in a semicircular fashion following the arch of the soft palate. The total amount of injection should be limited to 1.8 – 2.5 cc (Fig. 13). Using a #12 Frazier suction tip, the oral cavity is suctioned and the tip of the uvula is identified, lifted with the suction tip, and grabbed with a long-curved hemostat. As the uvula is pulled to one side, the ablation is initiated on the opposite side in the anterior and posterior pillar area (Fig. 14). The power setting of the unit is put on number 3 in a continuous mode. A gentle touch is sufficient for tissue cutting; a fast side-to-side motion should be avoided because this will cause less effective cutting and more bleeding. As the uvula is held with a curved hemostat, the hand piece is used to start releasing the posterior pillars from the soft palate. The ablation is carried up to an area around 5-mm above the lower end of the posterior pillar, and the posterior pillar is then released. The ablation is then carried forward to

approximately the base of the uvula (Fig. 15). Hence, the hanging part of the uvular is removed, but without total excision of the uvular muscle. Special attention is directed to the anterior and posterior pillars and the soft palate to make sure adequate yet not excessive soft tissue is removed in the fashion similar to the standard laser-assisted UPPP procedure (Fig. 16). If any bleeding is encountered, the flat side of the blade is used to stop the bleeding (Fig. 17). Caution should be taken for the water vapor created by this device. Once the uvula and the desired portion of soft palate are removed, lateral sutures can be placed to expand and secure the soft palate laterally (Fig. 18). There is certainly a learning curve in using this system because, unlike many of the surgical devices used, the extremely fast reciprocating movement of the blade (55,000 rpm) is invisible to the surgeon’s eyes, and contacting the tongue or posterior wall of the pharynx could cause complications. In 50% of patients, sutures are not needed, but by placing lateral

Fig. 17. One of the great features of Harmonic Ultrasound is that, if any bleeding is encountered, the flat side of the blade is used to stop the bleeding.

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success of the operation drastically (Fig. 20). The specimen, including the uvula in its entirety, is sent for histological evaluation. Sleep study is generally recommended prior to and following the completion of the procedure. (In over 5000 of our treated cases, 35% of patients preferred to have a sleep study after the surgery.) The reason for postop study is to make sure there is no residual apnea or to adjust the pressure setting of the CPAP. The patients are advised to follow the instructions of the sleep disorder center for management of any apnea problem. This procedure does not cure the sleep disorder; it helps in reducing snoring by 70% and results in an average reduction of mild sleep apnea by up to 50%. It must be stressed that weight reduction should take place if more effective opening of the airway and increased longevity are desired. Fig. 18. Once the uvula and the desired portion of soft palate are removed, lateral sutures can be placed to expand and secure the soft palate laterally.

sutures and pulling the unprotected edge of the soft palate to the area just above and lateral to the anterior pillar, the airway is expanded even further (Fig. 19). In our experience, this maneuver has increased the

Fig. 19. By placing lateral sutures and pulling the unprotected edge of the soft palate to the area just above and lateral to the anterior pillar, the airway is expanded even further.

Ultrasound-assisted UPPP results Forty-five patients, with age ranging 39 – 54 years, were treated in an office setting with the Harmonic Scalpel1 for snoring and mild obstructive sleep apnea. The procedure was fast and easy, with excellent visualization of the surgical field without smoke or char. If any bleeding were encountered, it was simply coagulated with the side of the harmonic blade. The subjective results were similar to laserassisted UPPP; the snoring sound reduction, on aver-

Fig. 20. Suturing of is of particular value when tonsils are surgically removed with the Harmonic Ultrasound.

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age, was 75%. Patients reported improved breathing and sleeping, remembering vivid dreams, and experiencing less fatigue during the day and restful sleep without gasping for air. One major difference noted when using this device as compared with CO2 laser was that Harmonic Ultrasound UPPP patients had less pain postoperatively as compared with those treated with CO2 laser. The other important issue was the absence of delayed bleeding in ultrasoundtreated patients. Overall, ultrasonic UPPP seems to be an effective alternative to expensive laser systems and can deliver the same or even better results when used properly.

Discussion Every surgeon should customize treatment of snoring and obstructive sleep apnea in accordance with the patient’s anatomy, social and financial concerns, and with his or her own practice parameters. The author’s current clinical practice uses several surgical techniques to varying degrees. Each procedure can have a place in the clinical practice of today’s practitioners. Palatal flutter, obstructive tonsils, and, in some cases, nasal obstructions are the major sources of noise production in individuals who suffer from habitual snoring. Many surgical procedures have been advocated. They include traditional UPPP performed in the hospital under general anesthesia. It has about a 5 – 10% chance of major side effects, such as voice change, bleeding, and nasal reflux. In addition to all its limitations, UPPP is expensive. Costs vary widely among institutions, but the procedure, the anesthesia, and one night of postoperative monitoring in an intensive care unit can cost in excess of $10,600. Laser-assisted uvulopalatoplasty (LAUP) is the staged laser treatment of snoring. There were major drawbacks with LAUP including lack of effectiveness for addressing obstructive sleep apnea [63 – 65]. Patients did not favor this multiple stage technique. Our observation was that because LAUP did not remove the soft palatal tissues on either sides of the uvula, creating a narrow lumen effect and thus making the task of breathing even harder. The modification presented in this article eliminates the hospital visit and is done in an office setting. The author has treated over 5,000 patients by laser-assisted uvulopalatopharyngoplasty (LA-UPPP) without any major complications [66]. This technique is easy, safe, and effective in treating snoring and mild sleep apnea. It has far fewer complications or side effects when compared with traditional UPPP. In our patients

treated by LA-UPPP or UA-UPPP none have developed voice change or food or fluid reflux problems, and overall complications were very rare. The major drawback of these procedures is 2 weeks of intense pain, which are well controlled by pain medications. We routinely have covered our patients with antibiotics, and no one has developed postoperative infections directly related to the surgical site. The use of ultrasound in treating snoring and obstructive sleep apnea is promising; however, further studies are necessary. In search of a painless procedure to treat snoring and mild obstructive sleep apnea, radio-ablation procedures were introduced to this field. The concept is that using the mild heat of radio-ablation devices reduces tissue volume, stiffens the soft palate, and, at the same time, reduces morbidity and mortality. Palatal radio-ablation procedures are safe and easy to perform, but they are only effective in patients with a small uvula and very thick soft palate. Repeated procedures may be needed. Nasal and tonsillar radio-ablations are far easier and less invasive than traditional surgeries. Tongue-based radio-ablation has potential risks for developing abscess and relapse. We have not mentioned every procedure that is used to treat snoring and obstructive sleep apnea. Uvulectomy has been attempted, but its short-term results were poorer than those of other procedures [67]. In addition, other procedures are under investigation, including ones that induce palatal stiffening by injecting sclerosing agents into palatal tissue [68,69]. This procedure and its long-term benefits are highly questionable. Each of these procedures has its own advantages and limitations; and which procedure is the best treatment for excessive snoring and obstructive sleep apnea is a controversial issue. We present our experience with each of these procedures, along with a thorough review of the literature, to help practitioners determine which one is best for their individual patients.

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Surgical evaluation for reconstruction of the upper airway N. Ray Lee, DDS* Private Practice, 716 Denbigh Boulevard, Suite C-1, Newport News, VA 23608, USA Department of Oral and Maxillofacial Surgery, Medical College of Virginia, Virginia Commonwealth University, 520 North 12th Street, Richmond, VA 23298, USA Department of Otolaryngology—Head and Neck Surgery, Eastern Virginia Medical School, P.O. Box 1980 Norfolk, VA 23501, USA

Surgical reconstruction of the upper airway is designed to reduce collapsibility and optimize stability of the airway. A universally accepted protocol for reconstruction of the upper airway does not exist. The philosophy of identifying the anatomic site of airway compromise and surgically correcting it, however, is generally accepted. A successful surgical outcome should be equivalent to successful continuous positive airway pressure (CPAP) treatment. Contributing factors for airway collapse can be complex and involve physiologic, neurogenic, and anatomic findings that demand a comprehensive evaluation before embarking on the reconstructive process. This article discusses evaluation considerations and surgical staging protocols that may be beneficial in achieving a successful surgical outcome.

The consultation Polysomnography identifies the severity of the disease and is usually the first objective data used to assess the patient; however, a detailed history from the patient and bed partner is crucial in identifying behavioral factors contributing to poor sleep architecture and excessive daytime somnolence. Attention to and correction of psychologic dysfunction such as clinical depression only enhances the possibility of a successful surgical outcome [1].

* 716 Denbigh Boulevard, Suite C-1, Newport News, VA 23608, USA. E-mail address: [email protected] (N.R. Lee).

The medical status of the patient is assessed during the initial consultation and determines if the patient is a surgical candidate. The medical considerations for preoperative evaluations are covered in another article in this issue. Preoperative evaluation must include a thorough review of a recent nocturnal polysomnography (NPSG). The apnea hypopnea index (AHI), or the number of apneas and hypopneas per hour of sleep, indexes the severity of the condition. This categorization alone with oxygen desaturation classifies the patient as having mild, moderate, or severe obstructive sleep apnea (OSA). Normal values for the AHI range from 5 to 10 apneas or hypopneas per hour [2,3]. An AHI of 10 to 20 is considered indicative of mild OSA, 20 to 35 apneas or hypopneas per hour is considered moderate OSA, and greater than 40 apneas or hypopneas per hour is considered severe. There is a significant increase in morbidity associated with an AHI greater than 20 per hour [4], and those patients with higher AHI values have been linked to a greater incidence of perioperative airway complications [5]. The SaO2 data as stated previously should be examined to determine the awake base line and mean SaO2 sleep desaturations because lower values are indicative of potential perioperative respiratory compromise [5] Surgical staging consideration is determined by analysis of the preoperative sleep study and the evaluation of the anatomic airway. For example, a surgical candidate with a relatively high AHI classified as moderate to severe OSA may receive recommendations for a bimaxillary advancement as the first stage of surgical reconstruction even in the

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absence of crainofacial abnormality, whereas the patient with a mild to moderate OSA diagnosis may receive recommendation for a uvulopalatopharyngoplasty (UPPP) and anterior mandibular osteotomy with genioglossus muscle advancement as the first stage if the craniofacial anatomy is normal. Surgical staging is discussed in detail later.

Examination of the upper airway Clinical examination of the upper airway is designed to identify compromised anatomic sites that are susceptible to collapse and to identify characteristics that directly contribute to the pathophysiology of OSA [6]. The goals of examination are to (1) identify sites of anatomic upper airway pathology, (2) predict the site and levels of obstruction during sleep, and (3) identify areas where surgery may reduce resistance, increase size, or decrease collapsibility of the upper airway and thereby improve OSA. Staged surgical treatment may then be directed at appropriate segments of the upper airway. [7]. The upper airway performs several physiologic functions including deglutition, vocalization, and respiration. The upper airway is subdivided into three regions on the basis of sagittal imaging nomenclature: (1) nasopharynx (region between the turbinate and hard palate); (2) oropharynx, subdivided into the retropalatal (the level of the hard palate to the caudal margin of the palate) and retroglossal (the caudal margin of the soft palate to the base of the epiglottis) regions; and (3) hypopharynx (region from the base of the tongue to the cervical esophagus) [8 – 10]. The pathogenesis associated with upper airway obstruction is complex, involving muscular, neurologic, anatomic, and developmental anomalies as well as other etiologic factors. This multifactorial picture is impossible to capture with the awake assessment of the upper airway and may not have a direct correlation to obstruction during sleep [11]. Nevertheless, sites of potential collapse and identification of pathologic comprises in the upper airway are useful in directing a definitive surgical plan to improve the stability of the upper airway. The nose The nasal airway is the beginning of the airway conduit, and resistance in nasal airflow can play a major role in snoring and sleep apnea. The greatest increase in resistance occurs at the nasopharyngeal/

retropalatal portion of the upper airway [12]. Therefore, because the upper airway is a collapsible tube, the Starling resistor principle exists. Specifically, proximal resistance determines the critical closure and location of obstruction at distal pharyngeal sites [12]. Therefore, a patent nasal airway with minimal resistance is important to the overall stability of the upper airway. The external examination of the nose can identify compromises in nasal airflow such as a deviated dorsum, constricted nasal width, tip ptosis, and soft tissue asymmetries. Nasal speculum and fiber optic examination is necessary to diagnose rhinitis, septal deviation, hypertrophic turbinates, nasal masses, and polyps. Most nasal pathology can be treated pharmacologically; therefore, medication should be the first line of treatment. The oral cavity The position of the maxilla and mandible relative to the cranial base is manifested by the categorization of the dental occlusion. The skeletal position of the maxilla and mandible is best determined by cephalometric imaging; however, the dental occlusion (class II or class III) may suggest hypoplasia or hyperplasia of the maxilla or mandible and is an important indication of the relative position of soft palate and base of tongue to the posterior pharynx. Maxillary and mandibular hypoplasia is associated with a retropositioning of upper airway soft tissue. The dental health of the periodontium is also important and should be noted in the clinical assessment. The presence of mandibular tori could potentially displace the base of the tongue posteriorly, thus compromising the retrolingual airway space. The oral examination of the palate is significant in determining the overall stability the oropharyngeal airway. The overall length of the soft palate, thickness of the soft palate, and anatomic findings associated with the lateral tonsillar pillars and size of the tonsils if present are important in surgical treatment planning. Relative macroglossia is rare; however, the position of the posterior third of the tongue base relative to the posterior pharyngeal wall and epiglottis should be noted. Again, cephalometric analysis of the posterior airway space is helpful in evaluating the base of tongue relative to the soft palate and posterior pharynx. The circumference of the neck should be measured. Flemmons and colleagues have noted that neck circumference increases are associated with the presence of hypertension, and increased witnessed gasping, therefore, the percentage incidence of OSA increases [13].

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Endoscopic pharyngoscopy Direct visualization of the upper airway aids in the identification of anatomic compromise and potential areas of airway collapse. The accurate determination of the site of obstruction in the upper airway is vital to selecting the appropriate surgical procedure. Most OSA patients have clearly identifiable pathology [14]. Therefore, awake endoscopic pharyngoscopy in the supine position, mouth closed, and at rest obviously is not the same neuromuscular situation as sleep; however, it is a reliable modality to evaluate the anatomic airway. Comparison of endoscopy during pharmacologically induced sleep and physiologic sleep has been controversial and not universally accepted [15]. After the application of a topical anesthetic and a decongestant, nasopharyngoscopy can be performed comfortably. The nasal airway is evaluated for nasal pathology including septal deviation, turbinate hypertrophy, polyps, or nasal masses that may be responsible for partial obstruction of the upper airway. The nasopharynx is then examined to rule out obstruction from adenoids, polyps, masses, or cysts. The nasal aspect of the soft palate is evaluated to determine possible obstruction from tonsillar tissue, base of the uvularis muscle, or a thickened posteriorly positioned palate. The patient is then asked to perform a Muller’s maneuver, which is forced inspiratory effort with the mouth and nose closed, to determine if there is obstruction at the level of the soft palate. A positive Mueller’s maneuver and the degree of obstruction or partial obstruction is quantified subjectively. There is still controversy associated with the clinical significance associated with collapse of the airway during the Mueller’s maneuver. The use of the Mueller’s maneuver and fiber optic endoscopy on the awake patient was first reported by Borowiecki and Sassion [16] and Walsh and Datsantonis [17] who utilized somnofluroscopy to demonstrate that patients with partial collapse at the level of the soft palate only were more likely to benefit from UPPP alone. Sher et al [18] subjectively quantified the degree of collapse at the level of the soft palate as follows: (1) Minimal movement of the components of the circumference of the pharyngeal cross section toward the center. (2) Movement toward the center diminishing cross-sectioned area of the pharynx by 50%. (3) Movement toward the center diminishing cross0sectioned area of the pharynx by 75%. (4) Inward motion obliterating the airway [18]. They concluded that the Mueller’s maneuver provided a simple means of assessing pharyngeal dynamics in relationship to OSA. The endoscopic examination proceeds to the

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level of the oropharynx, and the base of the tongue is evaluated along with the tonsillar tissues. The relationship of the base of tongue to the posterior pharyngeal wall and epiglottis should be noted. Retrolingual positioning is subjective; however, it is identifiable, as is redundant lateral tonsillar tissue. Because most obstruction during sleep occurs at the retropalatal and retroglossal areas [19], this portion of the examination is important to rule out or diagnose multiple sites of airway compromise. The patient is asked to perform another Mueller’s maneuver as the endoscope is passed into the hypopharynx. The position of the base of tongue to the epiglottis and posterior pharyngeal wall is observed to assess a more accurate degree of closure and retropositioning of the base of tongue. The larynx and vocal cords are also evaluated to rule out any supraglottic, glottic, or subglottic pathology. The clinical examination, endoscopic pharyngoscopy, and imaging of the upper airway serve as a guide to select the appropriate surgical procedure or procedures to reconstruct the upper airway adequately without overtreatment. As the level of understanding of the upper airway collapse increases, so too will the sophistication of the diagnostic evaluation. The ultimate goal is to predict success in the selection of the appropriate surgical procedure, which is so elusive today.

Imaging The biomechanics of upper airway collapse in OSA remains complex. Modern imaging techniques have provided much information in assessing the anatomic characteristics of the soft tissue and bony structure of the upper airway. Dynamic and static imaging techniques are useful in evaluating the function of the upper airway in both pretreatment and posttreatment states. Various imaging techniques such as the cephalometric radiograph with and without barium, MRI, CT, and dynamic somnofluroscopy have also promoted understanding of the efficacy of treatment. The cephalometric radiograph, however, is the most inexpensive widely used technique to evaluate the upper airway. This section reviews the efficacy and associated diagnostic capability of each technique. The cephalometric radiograph The cephalometric radiograph is a static twodimensional interpretation of a three- dimensional upper airway. The cephalogram, however, has stand-

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ards that make the interpretation uniform. Each exposure has a standard position and distance of the central beam to the target. One clinician can be responsible for the interpretation, and the exposure is always at end expiration. Radiographs are inexpensive and readily available, which makes this technique attractive for the diagnostic evaluation. DeBerry-Borowiecki et al concluded that cephalometric analysis could be useful in conjunction with the head and neck examination, polysomnographic, and endoscopic studies to evaluate OSA patients and in planning surgical treatment for improvement of upper airway patency. [20] The cephalometric radiograph offers a unique quantification of craniofacial anatomy necessary in the treatment of craniofacial deformities and OSA. The method of interpretation that is most accepted in OSA is the technique of Riley et al, which demonstrates a positive correlation to volumetric analysis of the upper airway by CT [21]. The following cephalometric landmarks are primarily used in interpreting the upper airway in OSA: S: sella; N: nasion; A: subspinale; B: supramental; Pg: pogonion; ANS: anterior nasal spine; PNS: posterior nasal spine: Gn:gnathion; Go: gonion; Mp; mandibular plane; H: hyoid; Ba: basion. The following angles are also primarily used in interpreting the upper airway in OSA patients: SNA; SNB; GoGn-SN; NSBa (cranial base flexure); MP-H; mandibular plane to hyoid) PNS-P (distance from posterior nasal spine to soft palate); PAS (posterior airway space)(Fig. 1).

Fig. 1. Cephalometric analysis screening measurements identify the position of the maxilla and mandible, and the relationship of the PAS. (From Waite PD, Shettar SM. Maxillomandibular advancement surgery: a cure for obstructive sleep apnea syndrome. Oral Maxillofac Surg Clin North Am 1995;7:327 – 36; with permission.)

Jamieson et al demonstrated that OSA patients had the following characteristics: (1) a normally positioned maxilla, (2) a retroposition of the mandible, and (3) different cranial base flexure with a nasion-sellabasion angle smaller than expected (ie, more acute) [22]. The combined effect of a normally positioned maxilla and a retroposition of the mandible reduces the space occupied by soft tissue anchored on the skull and mandible [21]. Barium has been used with the cephalometric radiograph to enhance the soft tissue interpretation. Little additional information, however, is gained with the use of barium and it is not widely used. There are limitations of the cephalogram, and they should be noted. The cephalogram remains a two-dimensional study of three- dimensional anatomy, and thus accurate volumetric analysis of the upper airway is not possible. The effects of tonsillar hypertrophy or other lateral soft tissue on the function of the upper airway cannot be accurately accessed. The cephalogram, however, should be included in the diagnostic armamentarium for evaluating the upper airway anatomy in the OSA patient. CT CT has been used extensively to study the soft tissue and bony structures of the upper airway. CT scanning provides excellent imaging capabilities; however, the soft tissue contrast resolution is not as superior as with MRI. One of the distinct advantages of CT scanning in the supine position is the accurate measurement of upper airway cross-sectional area. Images from CT scanning are only obtained in the axial plane, but volumetric analysis reconstruction of the soft tissue and bony images of the upper airway can be performed [23]. Lowe et al studied a sample of 25 men with OSA using CT volumetric analysis of the upper airway at the base of tongue; volumetric analysis provided an excellent overview of the interaction between these structures [24]. Volumetric analysis can also be accomplished with helical CT scanners, whereas dynamic imaging of the upper airway is possible using electron beam CT scanning. CT scanning does have limitations: it is relatively expensive, there are patient weight limitations, excessive radiation exposure limits repeat studies, and there is poor contrast resolution of upper airway adipose tissue [25]. Despite these relative disadvantages, CT scanning has been and will continue to provide knowledge necessary to understand the impact of soft tissue and bony structures of the upper airway in the pathogenesis of OSA.

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MRI The ideal upper airway imaging modality for patients with OSA should be inexpensive and noninvasive and be performed in the supine position without radiation. In addition, such an imaging technique should provide high-resolution anatomic representation of the airway and surrounding soft tissue structures with the capability of performing dynamic images during wakefulness and sleep. Such an imaging technique does not exist, although MR scanning is an excellent method to access the upper airway. Moreover, MRI maybe the ideal modality for OSA because it provides excellent upper airway soft tissue resolution, accurately determines cross-sectional area and volume, allows imaging in the axial, sagittal, and coronal planes, and can be performed during wakefulness and sleep without radiation [26 – 29]. MR is not without its disadvantages, however. The procedure is expensive and not widely available. Claustrophobia can be a problem and there are patient weight limitations of approximately 300 pounds. Patients with ferromagnetic clips or pacemakers are not candidates for this technique. When indicated MR, however, is an excellent tool to assess the upper airway preoperatively and the technique has been very successful in the understanding of the role of soft tissue and bony anatomy in the pathogenesis of OSA.

Surgical staging Selection of the appropriate surgical procedures and the protocol for reconstruction of the upper airway remains one of the more controversial subjects in the treatment of OSA. Although a universally accepted protocol for reconstruction of the upper airway does not exist, much knowledge has been gained in understanding the pathogenesis of OSA and effectiveness of the advancements in surgical treatment modalities. Surgical treatment of snoring and mild OSA are addressed in another article in this issue. This section discusses surgical staging for adults with moderate and severe OSA. It is universally accepted that the nasal airway must be patent and functional before addressing collapse of the airway at the retropalatal or retrolingual region. Most nasal airway pathology may be treated pharmacologically; however, septoplasty, turbinate reduction, or both may be necessary to achieve airway stability. Kuhlo and colleagues described the earliest surgical method for successful treatment of OSA by bypassing the upper airway with the tracheostomy

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[30]. Later, Fujita et al [31] advocated UPPP, which was a modification of the procedure described by Ikematsu for the treatment of snoring [32]. Further retrospective studies concluded that successful treatment of OSA with UPPP was at best approximately 50% [5]. Riley, Powell, and Guilleminault reviewed UPPP failures and concluded that base of tongue obstruction contributed to airway collapsibility [33,34]. Additional published data established that fact that the soft palate, base of tongue, and pharngeal walls of the hypopharynx contribute to the collapsibility of the airway [35]. Riley and Powell were the first to describe a staged surgical protocol for addressing a site-specific surgical correction to obstruction of the upper airway. For type II obstructions (soft palate and base of tongue) Riley and Powell performed stage I surgery, a UPPP and anterior mandibular osteotomy (AMO) with genioglossus muscle advancement and hyoid suspension (GAHM), which yielded a 97.8% elimination of OSA [34,36]. Whereas Riley and Powell were the first to advocate a two-stage surgical reconstruction of the upper airway, other authors published data on the technique of site specific correction of the upper airway. Johnson and Chinn reported an elimination of OSA (postoperative respiratory disturbance index [RDI] less than 10 and 50% reduction in preoperative RDI) in 77.8% of OSA patients with a UPPP and AMO and genioglossus muscle advancement (GMA) without hyoid suspension [37]. Lee et al [20] reported a review of 35 patients treated with stage I reconstruction, UPPP and AMO/GMA. Most patients responded positively to stage I reconstruction with a postoperative RDI < 20, with oxygen saturation 95 + %). Twenty-four patients (69%) had postoperative RDIs of 20 or less. Of these, 11 patients (31%) had an RDI of 5 or less; 7 patients (20%) had an RDI between 6 and 10, and 6 patients (17%) had an RDI between 10 and 20. The mean preoperative RDI was 53, and the mean postoperative RDI was 19. Of the 3 patients who elected to proceed to stage II reconstruction, all had a postoperative RDI of 10 or less (2 patients [67%] had a RDI of 5 or less, and 1 patient [33%] had an RDI of 6 to 10). This study showed that properly selected patients with OSA syndrome benefit from a staged reconstruction of the upper airway. Other authors have advocated bimaxillary advancement as the first stage of treatment for OSA. Hochban and colleagues [38] reported on a series of 20 patients treated primarily with maxillomandibular advancement (MMA). All patients treated with MMA alone (20) had a postoperative RDI less than 10. One patient required a UPPP to complete reconstruction of the upper airway.

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Waite et al [39] reported on a series of 23 patients treated with MMA alone with a surgical success rate of 65% (RDI less than 10). The failed patients became a surgical success after adjunctive procedures to reconstruct the upper airway. Prinsell [40] reported on a series of 50 patients treated with MMA and a modified anterior inferior mandibular osteotomy for reconstruction of the upper airway. All of these patients had diffusely complex or multiple sites of disproportionate upper airway anatomy. Prinsell reported a 100% surgical success rate (AHI of less than 10) in this group of patients. It is clear that MMA and other adjunctive procedures are effective in the reconstruction of the upper airway; however, the pathogenesis of airway collapse is not as clearly understood. All factors, the AHI, body mass index, length of apneic episodes, neck circumference, oxygen desaturations, presence of craniofacial abnormalities, and sites of disproportionate upper airway anatomy together with consideration of the medical status of the patient are critical in the selection of the surgical procedure to reconstruct the upper airway. Surgical procedures are also selected dependent upon the experience and knowledge of the surgeon performing them. In cases of failed stage I procedures (UPPP, AMO, or GAHM) or in the presence of craniofacial deformities, the decision to proceed with MMA is without question. In addition, in cases of moderate to severe OSA without significant medical compromise, the decision to select MMA as the first procedure for reconstruction of the upper airway is well supported by the literature. Selection of surgical procedures for reconstruction of the upper airway has been an evolutionary process over the past several decades, and MMA has evolved as an effective first line treatment for moderate and severe OSA. After MMA, sitespecific correction of disproportionate anatomy may still be necessary especially if the patient gains weight. The future remains bright for innovative research and acquisition of knowledge to understand better the pathogenesis of airway instability and the biomechanics of successful surgical outcomes. The oral and maxillofacial surgeon is a vital team member and a leader in the discipline of surgical correction of sleep disordered breathing. It is an exciting time for the oral and maxillofacial surgeon as the multidisciplinary approach to the treatment of OSA continues to evolve.

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N.R. Lee / Oral Maxillofacial Surg Clin N Am 14 (2002) 351–357 [21] Riley R, Guilleminault C, Herran J, Powell N. Cephalometric analysis and flow volume loops in obstructive sleep patients. Sleep 1983;6:304 – 17. [22] Jamieson A, Guilleminault C, Partinen M, et al. Obstructive sleep apneic patients have craniomandibular abnormalities. Sleep 1986;9:469 – 477 [23] Ryder CF, Lowe AH, Li D, et al. Three dimensional upper airway computed tomography in obstructive sleep apnea. Am Rev Respir Dis 1984;129:355. [24] Lowe A, et al. Three dimensional CT reconstructions of tongue and airway in adult subjects with obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1986; 90:364 – 74. [25] Esclamado RM, Glenn MG, McCulloch TM, et al. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope 1989;99:1125. [26] Schwab RJ. Upper airway imaging. Clin Chest Med 1998;19:33 – 51. [27] Abbey NC, Block AJ, Green D, et al. Measurement of pharyngeal volume by digitalized magnetic resonance imaging. Am Rev Respir Dis 1989;140:717. [28] Ryan CF, Lowe AA, Li D, et al. Magnetic resonance imaging of the upper airway in obstructive sleep apnea before and after chronic nasal continuous positive airway pressure therapy. Am Rev Respir Dis 1991; 144:939. [29] Soto Y, Matsuo T, Kato T, et al. Evaluation of the pharyngeal airway in patients with sleep apnea: value of ultra fast MR imaging. AJR Am J Roentgenol 1993;160:311. [30] Kuhlo W, Doll E, Frank MD. Erfolgreiche behandlungeines Pickwick-syndromes durch eine dauertrachealkamule. DtSCH Med Worchenschr 1969;94:1286. [31] Fujita S, Conway W, Zorick F, et al. Surgical correction

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Radiofrequency thermal ablation therapy for obstructive sleep apnea Kasey K. Li, MD, DDS, FACS *, Nelson Powell, MD, DDS, FACS, Robert Riley, MD, DDS, FACS Stanford University Sleep Disorders and Research Center, 401 Quarry Road Stanford, CA 94305, USA

Obstructive sleep apnea (OSA) is associated with repetitive nocturnal airway obstruction, which in turn results in daytime sleepiness and cardiovascular derangements [1] It is now known that many patients with OSA have a diffused pattern of airway obstruction including nasal, oropharyngeal, and hypopharyngeal regions. Although the surgical management of OSA has achieved excellent cure rate [2,3], many patients decline conventional surgical treatment because of the associated invasiveness and potential risks. Low wave radiofrequency (RF) energy achieves therapeutic ablation of tissue in a minimally invasiveness fashion. RF thermal tissue ablation has been previously studied in cardiology for ablation of aberrant pathways in Wolfe-Parkinson-White syndrome [4,5], urology for the treatment of benign prostatic hypertrophy [6], neurosurgery for the treatment of trigeminal neuralgia [7], and oncology for the treatment of liver cancer [8]. In 1995, we began the investigation on the use of RF energy to ablate redundant tissue in the upper airway. From a series of clinical trials, we have demonstrated that RF can be safely and effectively applied to the delicate upper airway tissue to improve OSA. This article outlines the current methods of RF thermal ablation therapy for OSA.

Biophysics of RF energy The biophysics of RF thermal tissue ablation result in a predictable tissue injury pattern. RF gen-

* Corresponding author. 750 Welch Road, Suite 317, Palo Alto, CA 94304, USA. E-mail address: [email protected]

erates frictional heating of the tissue around the electrode caused by ionic agitation; thus, the electrode is not heated and the heat actually emanates from the tissue. Because the energy disbursement pattern is proportional to 1/radius4, heat dissipation is limited and excessive tissue injury is minimized. Furthermore, when temperature reaches 90 – 100°C, char formation on the needle electrode leads to an increase in the impedance and results in disruption of current flow, thus serving as a second layer of protection from excessive tissue injury.

Tissue reduction by RF thermal ablation The pattern of the tissue lesion created by RF needle electrode is the shape of an American football (Fig. 1). The length of the lesion is one to two times the length of the active needle portion (eg, 1 cm active needle electrode will create a lesion 1 – 2 cm in length). The diameter of the lesion is approximately two thirds of the length of the active needle portion. The upper airway tissue response to RF energy was first investigated in the porcine tongue [9]. Twentyfour hours after RF treatment on the tongue, there was evidence of cellular injury with mild interstitial edema and focal hemorrhage, with a margin of hyperemic tissue in the periphery. One week after treatment, there was prominent fibroblastic response, with collagen deposition replacing the injured tissue. Three weeks after treatment, there was a well-formed scar occupying the treated area. Assessment of the tongue volume revealed an initial edematous response that promptly tapered at 24 hours with subsequent tissue reduction 10 days after treatment.

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 2 3 - 7

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Fig. 1. The pattern of radiofrequency (RF) lesion.

A continual reduction of tissue volume was evident through 21 days. Because the extent of edema is closely correlated with the amount of energy delivered, RF thermal ablation of the redundant upper tissue was designed to be performed as an outpatient procedure, with sequential application of the RF energy with a healing period of 4 – 6 weeks between treatment session. This approach minimizes excessive postoperative edema and complications. Although increasing the amount of energy delivered during each treatment session can expedite the treatment, the increased risk of airway edema must be anticipated and properly managed.

RF thermal ablation of the soft palate The initial investigation of RF thermal ablation of the soft palate was performed on 22 volunteers in the office setting under local anesthesia [10]. The mean number of treatment sessions was 3.6 per patient. The mean overall total number of joules administered per patient was 2,377 ± 869 J with 688 ± 106 J per treatment session. The mean Epworth Sleepiness Scale (ESS) improved from 8.5 ± 4.5 to 5.2 ± 3.3. The mean snoring scores by visual analog scale (VAS 0 – 10) improved from 8.3 ± 1.8 to 1.9 ± 1.2. There were no major complications such as bleeding, infection, tissue

slough, or speech, taste, and swallowing problems. Soft palate edema occurred in all patients for 1 – 3 days posttreatment, but all resolved without problems. Long-term follow-up All twenty-two patients underwent follow-up evaluation [11]. There was a mean weight increase of 3.1 ± 7.9 kg. The mean follow-up period was 14 months (range 12 – 18 months). There was no adverse effect on speech, swallowing, or taste reported by any of the patients. Thirteen patients (59%) reported continual success without relapse of snoring or daytime sleepiness. Nine patients (41%) reported relapse of snoring (VAS 0 – 10) from 2.1 ± 1.1 to 5.7 ± 2.8. This was accompanied by worsening of ESS from 5.4 ± 3.2 to 7.8 ± 5.3. Twenty-one patients (95%) were satisfied with the procedure and would go through it all over again. One patient felt that there was insufficient response to the treatment and therefore would not have the procedure again. Eight of the 9 patients who relapsed consented for retreatment to control snoring further, and they underwent a total of 10 RF treatments, with 6 patients receiving 1 treatment and 2 patients receiving 2 treatments. The mean RF energy delivered per treatment session was 786 ± 114 J. Each patient received a minimum of one or a maximum of three separate

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RF ablations per treatment session, with each ablation given at a different site of the palate. Mild edema was seen in the first three days, which usually resulted in restless sleep on the first postoperative day. There was no report of alteration in daily activities, and normalization of sleep occurred after three days. No mucosal erosion was encountered in any patient and no adverse effect on speech, taste, or swallowing was reported. The pain score was the highest at 2.7 ± 1.9 posttreatment day 1 and decreased to 0.7 ± 1.1 at one week. Oral analgesic was used by three patients and was limited to one tablet of codeine (30 mg) and either acetaminophen or ibuprofen in low doses. The snoring score fell from 5.8 ± 2.9 to 3.3 ± 3.1, with improved ESS from 7.8 ± 5.6 to 6.3 ± 4.6.

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sheath) is inserted in the midline of the soft palate, with the tip of the needle electrode at the base of the uvula. Typically, 700 – 750 joules are delivered in the midline. Paramedian RF treatment (250 – 350 J on each side) can be performed if desired; increasing edema should be expected, however,. This technique minimizes the risk of ulceration and discomfort. Prescription analgesics are rarely required. But edema usually occurs and may last a few days. Obviously, the extent of edema is directly correlated with the amount of RF energy delivered. The procedure is repeated every 4 – 6 weeks. With proper patient selection, snoring usually can be improved after 3 – 4 sessions.

RF thermal ablation of the tongue RF thermal ablation of the soft palate: current practice RF thermal ablation of the soft palate is reserved for patients with complaints of snoring or mild sleepdisordered breathing. Patients with OSA should be managed with more aggressive treatments such as uvulopalatopharyngoplasty (UPPP). The primary site of treatment is in the mid portion of the soft palate, in the base of the uvula (Fig. 2). Although the paramedian region can be treated, less RF energy should be delivered because of the increased risk of ulceration as the thickness of the soft palate is reduced in this location. The procedure starts with local anesthesia using a 30-gauge needle (2 – 5 ml). A 22-gauge needle electrode (10 mm active length with a 10 mm protective

Tongue base collapse is a major cause of hypopharyngeal airway obstruction. Therefore, reducing the tongue volume can improve OSA. The initial investigation of RF thermal ablation of the tongue base was performed on 18 volunteers in the office setting under local anesthesia [12].; All of the patients have failed at least UPPP. The mean number of treatment sessions was 5.5 per patient. The mean overall total energy administered per patient was 8490 ± 2687 J with 1543 J per treatment session. The mean respiratory disturbance index (RDI) improved from 39.5 ± 32.7 to 17.8 ± 15.6 events per hour. The lowest oxygen saturation improved from 81.9 ± 11.6% to 88.1 ± 5.3%. The mean ESS improved from 10.4 ± 5.6 to 4.1 ± 3.2. Tongue volume was reduced by a mean of 17% based on MRI. Speech and swallowing did not change. Complications

Fig. 2. The soft palate. RF treatment is usually focused on the middle and lower third of the soft palate.

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included one case of persistent tongue pain that gradually resolved, one case of ulceration on the surface of the tongue from improper placement of the needle electrode that spontaneously resolved, and one case of tongue base abscess that required incision and drainage. Long-term follow-up Sixteen of the 18 patients underwent follow-up evaluation. There was minimal weight change. The mean follow-up period was 28 months. There was no significant adverse effect on speech or swallowing. The quality of life (SF-36) remained improved over baseline. The RDI relapsed from 17.8 to 28.7 events per hour, however, and the lowest oxygen saturation worsened from 88.3% to 85.8% [13].

tinuous positive airway pressure (CPAP) or tracheotomy is mandatory in the postoperative period because RF tongue ablation is usually performed on an outpatient basis and postoperative edema is routinely encountered. The procedure starts with local anesthesia delivery using a 25- or 27-gauge needle (5 – 10 ml) in the region of the circumvallate papilla. A 22-gauge needle electrode (10-mm active length with a 10-mm protective sheath) is inserted in the region of the circumvalate papilla (Fig. 3). Typically, 2 – 3 lesions (750 – 1000 J per lesion) are delivered. Prescription analgesics as well as antibiotics are routinely used, and the procedure is repeated every 4 – 6 weeks. Outcomes assessment by polysomnography is usually performed after at least 8000 – 1000 joules have been administered. Further RF treatment is warranted if there is evidence of improvement.

RF thermal ablation of the tongue: current practice

Summary

RF thermal ablation of the tongue base is currently reserved for patients with persistent tongue base obstruction after previous OSA surgery such as UPPP and/or genioglossus advancement. It should be emphasized that most patients with OSA have retropalatal obstruction, and this anatomic region should be adequately addressed (usually be uvulopalatoplasty) before RF thermal ablation of the tongue is considered. Furthermore, airway protection with either nasal con-

Although the data available for RF thermal ablation for the treatment of sleep-disordered breathing is limited, the available data does support the continual investigation of this novel treatment approach. It should be emphasized, however, that despite the minimally invasive nature of this outpatient treatment technique, severe complications such as airway obstruction or infection with abscess formation can occur. The administration of excessive RF energy in

Fig. 3. The tongue base. RF treatment is usually isolated around the circumvallate papilla.

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order to limit the number of total treatments or altered treatment location and technique may increase the risk of complication and adverse effects. Caution is advised.

References [1] Indications and standards for use of nasal continuous positive airway pressure (CPAP) in sleep apnea syndromes. Am J Respir Crit Care Med 1994;150: 1738 – 45. [2] Li KK, Powell NB, Riley RW, Troell, RJ, Guilleminault C. Overview of phase I surgery for obstructive sleep apnea syndrome. ENT J 1999;78:836 – 37, 841 – 45. [3] Li KK, Riley RW, Powell NB, Troell, RJ, Guilleminault C. Overview of phase II surgery for obstructive sleep apnea syndrome. ENT J 1999;78:851, 854 – 57. [4] Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (WolffParkinson-White syndrome) by radiofrequency current. N Eng J Med 1991;324:1605 – 11. [5] Calkins H, Sousa J, El-Atassi R, et al. Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardias during a single electrophysiologic test. N Eng J Med 1991;324: 1612 – 8. [6] Issa M, Oesterling J. Transurethral needle ablation

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(TUNA): an overview of radiofrequency thermal therapy for the treatment of benign prostatic hyperplasia. Curr Opin Urol 1996;6:20 – 7. Sweet W, Wepsic J. Controlled thermocoagulation of trigeminal ganglion and rootlets for differential destruction of pain fibers: I. Trigeminal neuralgia. J Neurosurg 1974;3:143 – 56. LeVeen H, Wapnick S, Piccone V, et al. Tumor eradication by radiofrequency therapy: response in 21 patients. JAMA 1976;253:2198 – 200. Powell NB, Riley RW, Troell RJ, et al. Radiofrequency volumetric reduction of the tongue. a porcine pilot study for the treatment of obstructive sleep apnea syndrome. Chest 1997;111:1348 – 55. Powell NB, Riley RW, Troell RJ, Li KK, Blumen MB, Guilleminault C. Radiofrequency volumetric tissue reduction of the palate in subjects with sleep-disordered breathing. Chest 1998;113:1163 – 74. Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C. Radiofrequency volumetric reduction of the palate: an extended follow-up study. Oto Head Neck Surg 2000;122:410 – 4. Powell NB, Riley RW, Guilleminault C. Radiofrequency tongue base reduction in sleep disordered breathing: A pilot study. Oto Head Neck Surg 1999; 120:656 – 64. Li KK, Powell NB, Riley RW, Troell RJ. Radiofrequency tongue base reduction: long-term outcomes. Oto Head Neck Surg (in press).

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Nasal and palatal surgery for obstructive sleep apnea syndrome B. Tucker Woodson, MD, FACS, ABSM Department of Otolaryngology and Human Communication, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Milwaukee, WI 53226, USA

Sleep disordered breathing is common. In the mildest form, it manifests as snoring which is often considered a cosmetic complaint. Sleep-related breathing disturbances increase in severity to include the upper airway resistance syndrome and obstructive sleep apnea syndrome (OSAS) which result in daytime sleepiness, and have established medical morbidity and mortality risks. Overt OSAS affects an estimated 4% of men and 2% of women [1]. Because of its significant social, functional, and medical morbidity, OSAS frequently presents for treatment. Nasal continuous positive airway pressure (nasal CPAP) has become the preferred initial treatment for most patients; when this or other conservative treatments fail, however, surgery may be offered. Surgery may bypass the upper airway obstruction or may reconstruct the upper airway using either skeletal or soft tissue techniques. It is commonly accepted that airway obstruction in OSAS is complex and, in most patients, multiple levels of the pharynx contribute to collapse, obstruction, and increased airway resistance [2,3]. Surgical goals are to increase airway size, decrease airway collapsibility, decrease airway resistance and the work of breathing, and reduce partial and complete airway obstructions (apnea and hypopnea). Improved ventilation reduces sleep and medical manifestations of OSAS. Nasal and palatal surgeries may contribute to these goals and are part of the surgical treatment armamentarium for OSAS. Although in some patients, nasal and palatal surgeries may be used in isolation,

BTW is a member of the Medical and Scientific Advisory boards for Resmed, Inc., and Somnus, Inc. He has received research support from Somnus, Inc., and Influ-ENT. E-mail address: [email protected] (B.T. Woodson).

for many patients these procedures are only a portion of the treatment. Palatal and nasal surgeries are more often used in isolation for the treatment of snoring of palatal etiology [4]. Primary snoring is a common and significant presenting complaint, and a concern of many patients. This chapter addresses specific surgical procedures that may treat upper pharyngeal and palatal airway obstruction.

Algorithms for treatment A variety of surgical algorithms have been described to treat both snoring and OSAS. Historically, surgery on the nose, upper pharynx, and palate were considered to treat OSAS. Fujita proposed uvulopalatopharyngoplasty (UPPP) as the first specific reconstructive procedure for OSAS [5]. UPPP was a modification of palatopharyngoplasty proposed by Ikamatsu for snoring prior to the recognition of OSAS [6]. Prior to this description, tonsillectomy and nasal surgery were proposed as treatments with limited success in most patients. Uvulopalatoplasty was described by Kamami for the treatment of snoring [7]. Laser-assisted uvula-palatoplasty (LAUP) has multiple modifications and subsequently was applied to the treatment of OSAS [8]. Aggressive UPPP or alternative UPPP techniques have also been described [9]. Two different approaches have been used to improve success of limited pharyngeal surgeries for OSAS. The first approach is to improve patient selection with the goal of eliminating patients at high risk of failure [10]. Patients conceivably at high risk of failure may be those with severe disease, marked obesity, neurologic abnormalities, and sites of obstruction not

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confined to the nose and palate. The second approach has been to combine palatal surgeries with nasal surgery and tongue base surgery to address multiple sites or more severe obstruction better [11]. Both approaches have modestly improved success rates [12]. Although success is not ideal and requires improvement, such an approach often balances the severity of the disorder, improved clinical outcomes, and acceptance by the patient unwilling to proceed with more aggressive and more successful approaches such as maxillo-mandibular surgery or tracheotomy. It is widely accepted that upper airway collapse in OSAS occurs in the soft tissue supra-laryngeal pharynx [13]. The site of obstruction varies both between patients and even in the same patient depending on sleep state and body position. Various methods using endoscopy, manometry, and airway imaging have attempted to define the location of pathology. Nasal obstruction has been associated with complaints of poor sleep, snoring, and OSAS [14 – 16]. Nasal airflow has been shown to stimulate ventilation during sleep [17].

Surgical treatment Nasal Treatment of nasal obstruction varies according to pathology. Septal deviation, inferior turbinate hypertrophy, nasal valve collapse, and nasal polyps are common causes of nasal obstruction. In sleep apnea as well as other disorders with abnormal facial structure, increased nasal resistance may reflect abnormal maxillary morphology [18]. Although nasal airway resistance does not alter static measures of pharyngeal pressure when applying nasal CPAP, nasal obstruction may impair the clinical acceptance of CPAP [19]. Surgical treatment of obstruction may decrease clinically effective nasal CPAP pressures and theoretically improve compliance and acceptance [20]. Treatment of nasal obstruction improves daytime and nighttime subjective quality of life, sleep, and daytime performance. Although successful surgical treatment of the nose may alleviate symptoms, surgery alone offers a low likelihood of definitive OSAS treatment. Nasal surgery, however, may be definitive in selected patients. In a study using lateral cephalometric X rays to define upper airway abnormalities, Series found those patients likely to benefit most had mild OSAS, dramatic obstruction, and no other upper airway pathologies [21]. Nasal procedures may include sepatoplasty, turbinate reduction, nasal valve surgeries, or sinus sur-

gery. Techniques and procedures will vary on the pathology present. Under limited circumstances, nasal surgery may be simultaneously performed with other pharyngeal surgeries. Controversy exists as to the safety of performing simultaneous nasal and other pharyngeal surgeries [22]. Which sleep apnea surgeries are safe to pursue combined with nasal surgery has not been established. Criteria to consider include but are not limited to: (1) mild OSAS, (2) no anticipated requirement of nasal packing that would preclude perioperative nasal CPAP, (3) no major medical comorbidity that will place the patient at risk, and (4) appropriate and skilled postoperative monitoring and observation. Tonsillectomy Tonsil hypertrophy is a common contributor to OSAS in children; however, in adults, it is uncommon. It is commonly accepted that tonsillectomy alone is not definitive for most adults with OSAS. But when tonsilar hypertrophy is present, surgical treatment may be definitive. Verse et al reported an 80 – 100% success rate in adults treated for marked tonsil hypertrophy [23]. Tonsilar hypertrophy treated simultaneously with UPPP also demonstrates higher success rates [24]. Some authors have suggested that, when performed with tonsillectomy, UPPP has higher success rates [25]. Reviews by Sher et al have not been able to confirm this hypothesis [12]. Uvulopalatopharyngoplasty UPPP was initially described by Fujita [5]. For many, the concept of ‘‘surgery for OSA’’ is UPPP. Many have subsequently modified UPPP; all methods have in common a reconstructive operation to enlarge the pharynx for treating OSAS. This is in contrast with other techniques of palatopharyngoplasty that are directed at narrowing or closing the incompetent pharynx such as with cleft palate or velopharyngeal incompetence. Fujita’s initial operation involved partial modification of the uvula, removal of redundant pharyngeal and palatal tissues, and primary closure of the posterior and anterior pillars to enlarge the retropalatal airway. Other modifications have involved complete removal of the uvula and distal soft palate, removal of portion of the palatopharyngeus muscle [26], and an uvulapalatal flap [27]. Historically, UPPP offered the first viable alternative to tracheotomy; however, for many patients UPPP alone was at best partially effective. Although major complications are uncommon, minor complica-

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tions and side effects are not infrequent [28]. Metaanalysis by Sher et al observed that in nonselected patients short-term success was 40.2%. This success decreased to 5% when tongue base obstruction was identified. Multiple authors have attempted to improve UPPP success by improving patient selection. Success has been variable, yet some techniques have been promising. Isono et al using an objective endoscopic method have demonstrated higher success rates [29]. Manometry during sleep has also demonstrated high success rates [30]. Wide applicability is lacking to corroborate these results. UPPP data is difficult to interpret because of incomplete followup, lack of standardized outcomes, and few controlled or randomized studies [31]. Such deficiencies, however, are not unique in the surgical literature as a whole. Important outcomes following surgery include survival, sleepiness, performance, snoring, complications, and long-term results. Overall data with UPPP is consistent with a positive clinical effectiveness. Studies indicate that survival with UPPP is not worse than with nasal CPAP [32]. Sleepiness using multiple sleep latency testing is equal to compliant CPAP patients [33]. Driving performance is improved over both the short and long term [34]. Short-term snoring improvement occurs [35]. Studies have also demonstrated long-term improvement without worsening of OSAS. Concern about UPPP and subsequent CPAP failure has been presented [36]. Increased mouth leaks after palatal shortening is a potential complication, however; its true incidence is unknown. In some patients, removal of pharyngeal redundancy may improve CPAP compliance and effectiveness. Further study is needed. Few prospective randomized studies exist. Studies comparing UPPP with conservative treatments show marked improvements in sleep and quality of life [37]. Final quality of life outcomes were similar to nasal CPAP in compliant patients. Objective respiratory outcomes demonstrated significant improvements, although final outcomes were less than in laboratory success of nasal CPAP. Randomized against oral appliances, UPPP demonstrated better or equivalent outcomes [38]. Laser-Assisted Uvulopalatoplasty LAUP was initially described by Kamami for snoring and subsequently applied to treat OSAS. LAUP results have been controversial with strong proponents and opponents. Limited data exists to determine effectiveness for the treatment of OSAS. Several laser techniques have been described. Initially, LAUP was performed as a serial procedure over many

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sessions. Palatal trenches were created parallel to the uvula into the soft palate. The uvula was then shortened, and the wound allowed to heal by secondary intention. Subsequent modifications involved more aggressive resection of the soft palate and posterior tonsilar pillars [39]. Single stage LAUP has also been described [40]; other modifications include removal of palatal and uvular mucosa and uvula shortening [41]. These palatal stripping procedures have subsequently been described as using electrocautery (cautery assisted palatal stripping) and injection snoreplasty [42]. In the latter procedure, mucosa is ablated using scerotherapy agents injected into the submucosa. Objective evaluation of LAUP is difficult. Few studies use objective respiratory data. Subjective outcomes are often nonstandardized and primarily relate to snoring as a primary outcome. Most studies report a marked improvement in snoring. Short-term success rates of 70% or greater have been reported. Some decrement over time is likely. Effects on OSAS are more controversial. Some reports suggest a 30 – 40% success rate [43]. Other reports raise concern about airway stenosis or potential worsening of OSAS [44,45]. Outcomes may likely differ according to surgical technique used and the surgical patient population. Further objective evaluation is required. Radiofrequency Radiofrequency tissue ablation with or without temperature control has been described for treatment of both snoring and OSAS. These are discussed in other articles. Transpalatal advancement A novel approach to palatopharyngoplasty is the transpalatal advancement approach [46]. This modification increases oropharyngeal size not only by reducing distal pharyngeal redundancy but by palatal advancement. Separating the soft and hard palate and excising distal palatine bone provide advancement. The soft plate is mobilized and advanced into the defect. Compared with UPPP, significant increases in cross-sectional area and decreases in pharyngeal collapsibility are observed [47]. In small series, significant improvement in OSAS is observed.

Summary Significant abnormalities of the nose and upper pharynx contribute to OSAS and primary snoring. Surgical correction may significantly improve these

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disorders. Although when used alone, nasal surgery is only partially successful, it is an important component in the surgical armamentarium. Improvements in methods and surgical selection of palatal surgery are needed. Considering that the upper pharynx is the airway segment most vulnerable to closure, improving the surgical approach to this area likely will increase surgical success.

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References [1] Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328(17):1230 – 5. [2] Katsantonis GP, Moss K, Miyazaki S, et al. Determining the site of airway collapse in obstructive sleep apnea with airway pressure monitoring. Laryngoscope 1993;103(10):1126 – 31. [3] Morrison DL, Launois SH, Isono S, et al. Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea. Am Rev Respir Dis 1993;148: 606 – 11. [4] Liistro G, Stanescu D, Veriter C, et al. Pattern of snoring in obstructive sleep apnea patients and heavy snorers. Sleep 1991;14:517 – 25. [5] Fujita S, Conway W, Zorick F, et al. Surgical correction of anatomic abnormalities of obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981;89:923 – 34. [6] Ikamatsu T. Palatopharyngoplasty and partial uvulectomy method of Ikematsu: a 30 year clinical study of snoring. In: Fairbanks D, Fujita S, Ikematsu T, Simmons FB, editors. Snoring and Sleep Apnea, ed 1. New York: Rivlin Press; 1987. p. 130 – 34. [7] Kamami Y. Outpatient treatment of snoring with CO2 laser: laser-assisted UPPP. J Otolaryngol 1994;23(6): 391 – 4. [8] Krespi Y, Pearlman S, Keidar A. Laser-assisted uvulapalatoplasty for snoring. J Otolaryngol 1994;23(5): 328 – 34. [9] Zohar FY, Strauss M, et al: Surgical treatment of obstructive sleep apnea: comparison of techniques. Arch Otolaryngol Head Neck Surg 1993;119:1023 – 9. [10] Sher AE, Thorpy MJ, Shprintzen RJ, et al. Predictive value of Muller maneuver in selection of patients for uvulopalatopharyngoplasty. Laryngoscope 1985;95: 1483 – 7. [11] Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993;108:117 – 25. [12] Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications for the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996;19:156 – 77. [13] Shepard JW, Thawley SE. Localization of upper air-

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way collapse during sleep in patients with obstructive sleep apnea. Am Rev Respir Dis 1990;141: 1350 – 5. Loth S, Petruson B, Wiren L, Wilhelmsen L. Better quality of life when nasal breathing of snoring men is improved at night. Arch. Otolaryngol. Head Heck Surg. 1999;125:64 – 7. Young T, Finn L, Kim H. Nasal obstruction as a risk factor for sleep-disordered breathing. Allergy Clin Immunol 1997;99:s757 – 62. Lofaso F, Coste A, d’Ortho MP, Zerah-Lancner F, Delclaux C, Gooldenberg F, et al. Nasal obstruction as a risk factor for sleep apnoea syndrome. Eur Respir J 2000;16:639 – 43. McNichols WT, Coffey M, Boyle T. Effects of nasal airflow on breathing during sleep in normal humans. Am Rev Respir Dis 1993;147:620 – 3. Cistulli PA, Sullivan CE. Influence of maxillary morphology on nasal airway resistance in Marfan’s syndrome. Acta Otolaryngol 2000;120:410 – 3. Schechter GL, Ware C, Perlstrom J, McBrayer RH. Nasal patency and the effectiveness of nasal continuous positive air pressure in obstructive sleep apnea. Arch Otolaryrngol Head Neck Surg 1998;118:643 – 7. Friedman M, Tanyeri H, Lim JW, Landsberg R, Vaidyanathan K, Caldarelli D, et al. Effect of improved nasal breathing on obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2000;122:71 – 4. Series F, St Pierre S, Carrier G. Surgical correction of nasal obstruction in the treatment of mild sleep apnoea: importance of cephalometry in predicting outcome. Thorax 1993;48:360 – 3. Fairbanks DNF. Uvulopalatopharyngoplasty complications and avoidance strategies. Arch Otolaryngol Head Neck Surg 1990;102:239 – 45. Verse T, Kroker B, Pirsig W, et al. Tonsillectomy as a treatment of obstructive sleep apnea in adults with tonsilar hypertrophy. Larygoscope 2000;110:1556 – 9. Houghton DJ, Camilleri AE, Stone P. Adult obstructive sleep apnea syndrome and tonsillectomy. J Laryngol Otol 1997;III:829 – 32. McGuirt WF, Johnson JT, Sanders MA. Previous tonsillectomy as prognostic indicator for success of uvulopalatopharyngoplasty. Laryngoscope 1995;105: 1253 – 5. O’Leary MJ, Millman RP. Technical modification of uvulopalatopharyngoplasty: the role of the palatopharyngeus. Laryngoscope 1991;101:1332 – 5. Powell N, Riley R, Guilleminault C, Troell R. A reversible uvulopalatal flap for snoring and sleep apnea syndrome. Sleep 1996;19:593 – 9. Haavisto L, Suonpaa J. Complications of uvulopalatopharyngoplasty. Clin Otolaryngol 1994;19:243 – 7. Isono S, Akiko S, Tanaka A, et al. Efficacy of endoscopic static pressure/area assessment of the passive pharynx in predicting uvulopalatopharyngoplasty outcomes. Laryngoscope 1999;109:769 – 74. Skatvedt O, Akre H, Godtlibsen OB. Continuous pressure measurements in the evaluation of patients for

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laser assisted uvulopalatoplasty. Eur Arch Otorhinolaryngol 1996; 253. Schechtman KB, Sher AE, Piccirillo JF. Methodological and statistical problems in sleep apnea research: the literature on uvulopalatopharyngoplasty. Sleep 1995; 18:659 – 66. Keenan SP, Burt H, Ryan F, Fleetham JA. Long-term survival of patients with obstructive sleep apnea treated by uvulopalatopharyngoplasty or nasal CPAP. Chest 1994;105:155 – 9. Zorick FJ, Roehrs T, Conway W, et al. Response to CPAP and UPPP in apnea. Henry Ford Hosp Med J 1990;38:223 – 6. Haraldsson P, Carenfelt C, Lysdahl M, et al. Long-term effect of uvulopalatopharyngoplasty on driving performance. Arch Otolaryngol Head Neck Surg 1995; 121:90 – 4. Friberg D, Carlsson-Nordlander B, Larsson H, et al. UPPP for habitual snoring: a 5-year follow-up with respiratory sleep recordings. Laryngoscope 1995;105: 519 – 22. Mortimore IL, Bradley PA, Douglas NJ. Uvulopalatopharyngoplasty may compromise nasal CPAP therapy in sleep apnea syndrome. Am J Respir Crit Care Med 1996;154:1759 – 62. Lojander J, Maasilta P, Partinen M, Brander P, Salmi T, Lehtonen H. Nasal-CPAP, surgery, and conservative management for treatment of obstructive sleep apnea syndrome. Chest 1996;110:114 – 9. Wilhelmsson B, Tegelberg A, Walker-Engstrom M, Ringqvist M, Andersson L, Krekmanov L, et al. A prospective randomized study of a dental appliance

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compared with uvulopalatopharyngoplasty in the treatment of obstructive sleep apnea. Acta Otolaryngol 1999;119:503 – 9. Krespi Y, Pearlman S, Keidar A. Laser-assisted uvulapalatoplasty for snoring. J Otolaryngol 1994;23: 328 – 34. Dickson R, Mintz D. One-stage laser-assisted uvulopalatoplasty. J Otolaryngol 1996;25:155 – 61. Clarke R, Yardley M, Davies C, et al. Palatoplasty for snoring: a randomized controlled trial of three surgical methods. Arch Otolaryngol Head Neck Surg 1998; 119: 288 – 92. Brietzke SE, Mair EA. Injection snoreplasty: how to treat snoring without all the pain and expense. Arch Otolaryngol Head Neck Surg 2001;12:503 – 10. Walker R, Grigg-Damberger M, Gopalsami C. Laserassisted uvulopalatoplasty for the treatment of mild, moderate, and severe obstructive sleep apnea. Laryngoscope 1999;109:79 – 85. Finkelstein Y, Shapiro-Feinber M, Stein G, Ophir D. Uvulopalatopharyngoplasty vs laser-assisted uvulopalatoplasty. Arch Otolaryngol Head Neck Surg 1997; 123:265 – 76. Ryan CF, Love LL. Unpredictable results of laser assisted uvulopalatoplasty in the treatment of obstructive sleep apnoea. Thorax 2000;55:399 – 404. Woodson BT, Toohill RJ. Transpalatal advancement pharyngoplasty for obstructive sleep apnea. Laryngoscope 1993;103:269 – 76. Woodson BT. Retropalatal airway characteristics in UPPP compared to transpalatal advancement pharyngoplasty. Laryngoscope 1997.

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Soft tissue hypopharyngeal surgery for obstructive sleep apnea syndrome B. Tucker Woodson, MD, FACS, ABSM Department of Otolaryngology and Human Communication, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Milwaukee, WI 53226, USA

Sleep-disordered breathing is common. In its mildest form, it manifests as snoring which is often considered a cosmetic complaint. Sleep-related breathing disturbances increase in severity to include the upper airway resistance syndrome and obstructive sleep apnea syndrome (OSAS) having established medical morbidity and mortality risks. Overt OSAS affects an estimated 4% of men and 2% of women [1]. Because of its significant social, functional, and medical morbidity, OSAS frequently presents for treatment. Nasal continuous positive airway pressure has been the preferred treatment; however, when this or other conservative treatments fail, surgery may be offered. Surgery may bypass the upper airway obstruction or may reconstruct the upper airway, using either skeletal or soft tissue techniques. It is commonly accepted that airway obstruction in OSA is complex and in most patients multilevel [2]. Surgical goals are to increase airway size, decrease airway collapsibility, decrease airway resistance and the work of breathing, and reduce partial and complete airway obstructions (apnea and hypopnea). Improved ventilation reduces sleep and medical manifestations of OSAS. This article addresses specific surgical procedures to treat lower pharyngeal and tongue-related airway obstruction.

Dr. Woodson is a member of the Medical and Scientific Advisory boards for Resmed, Inc., and Somnus, Inc. He has received research support from Somnus, Inc., and Influ-ENT. E-mail address: [email protected] (B.T. Woodson).

Algorithms for treatment Various surgical algorithms have been described to treat both snoring and OSAS. Most decisions are based on the surgeon’s preference. Multiple procedures exist potentially to treat OSAS and snoring. Outcome data on many procedures is limited [3]. Decisions are based on review of retrospective case series, best available clinical information, community practice, and clinical experience. Factor that may influence surgical treatment selection may be: (1) disease severity, (2) degree of airway pathology, (3) patient comorbidities, (4) risks and morbidity of the procedures, (5) cost and availability of procedures, (6) risk and morbidity of anesthesia, and (7) desired patient outcomes. For example, surgical treatment of snoring often includes treatment of nasal obstruction and palatopharyngoplasty. These choices have been driven by availability, patient acceptance, and lack of tolerable alternatives. Alternatively, more severe sleep apnea is treated by more aggressive and complex protocols. The more severe the disease, the more likely major airway reconstruction will be accepted. The most common of these is the ‘‘Stanford protocol’’ [4]. This algorithm separates procedures into stage I and stage II procedures. Stage I procedures include: palatopharyngoplasty, genioglossus advancement, and nasal and hyoid surgeries. Stage II procedures consist of maxillofacial surgery, and maxillomandibular advancement. Treatment is initiated using stage I procedures. Those patients who fail stage I are offered stage II procedures. Although this protocol has demonstrated effect, it has not found widespread acceptance. Comparative trials of effectiveness are lacking. Technical

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limitations may include patients who are edentulous or with inadequate dentition, poor candidates for osteotomies, those with primary soft tissue abnormalities of the upper airway, or patients who refuse osteotomies. In the Stanford protocol, glossectomy or other soft tissue surgeries are not specifically addressed in either stage I or stage II. An alternative algorithm has been to treat soft tissue abnormalities. Several protocols and other approaches can be gleaned from the literature. Chabolle describes a specific algorithm for patients with soft tissue but without skeletal disproportion [5]. Patients with relative macroglossia, lingual tonsil hypertrophy, or redundant supraglottic tissues may be considered candidates for soft tissue surgeries. Soft tissue surgeries of the lower pharynx or hypopharynx range from several different types of excisional procedures to direct tongue suspension. Many are compatible with simultaneous UPPP. Because these procedures may be performed simultaneously with UPPP or with nasal surgeries, I have arbitrarily classified them as stage I procedures. For patients with severe disease, glossectomy is a major procedure requiring perioperative tracheotomy. These procedures are often staged or performed in conjunction with, or as an alternative to, maxillofacial surgeries, and I would perform them as stage II procedures. Airway evaluation is required for all segmental surgeries for OSAS. It is a critical (yet poorly understood) portion of surgical treatment. Multiple methods are available to evaluate the upper airway. Methods may include routine physical exam, endoscopic exam, cephalometric X rays, MRI or CT scans, and pharyngeal manometry [6 – 9]. Airway assessment both identifies the location and quantifies the degree of lower pharyngeal obstruction. Treatment of the upper airway requires assessment of postoperative airway risk and the possible need of tracheotomy. Hypopharyngeal collapse is often assumed implicit after UPPP failure, but this may not be a correct generalization. Failure occurs at palatal sites after UPPP failure [10,11]. Success with tongue base procedures does not prove this as a primary obstructive segment. Anatomic studies of jaw movement demonstrate that mandibular advancement may address upper (not lower) pharyngeal obstruction [12]. This anatomic linkage of airway segments may result in successful treatment of apnea even when secondary and not primary sites of obstruction are treated. There is no clear consensus to define either the method or degree of hypopharyngeal obstruction. Nasopharyngeal endoscopy and lateral cephalometric X rays are used to determine sites of obstruction. Endoscopy may be performed during wakefulness or

sleep, although the former is more accessible and utilized [13]. The methods of endoscopy even in wakefulness differ. Mueller’s maneuver with collapse during an active inspiratory effort with blocked nostrils and mouth closed (a reverse Valsalva) and passive endoscopic techniques have been described [14]. Methods during sleep are both quantitative and qualitative. Airway obstruction in OSAS is complex and may involve multiple anatomic sites and structures [11]. Following failed uvulopalatopharyngoplasty, obstruction may be complete (apnea) or partial (hypopnea). Sites of persistent obstruction vary both within the same patient as well as among different patients. Primary sites of obstruction following failed UPPP may include the lower pharynx or tongue base. Manometry and endoscopy during sleep have been used to confirm these sites as obstructive. Manometry demonstrates that obstruction is common in both the oropharynx and hypopharynx following failed UPPP. In UPPP failures, 50% may demonstrate hypopharyngeal sites of obstruction [15]. If one assesses airway obstruction as segments of airflow limitation, analysis is more complex. What percentage of individuals demonstrate the hypopharynx to be a site of increased resistance and airflow limitation either before or after UPPP is not known or well understood. Quantitative endoscopic evaluations during sleep identify single segments of narrow obstruction as uncommon. The most common site of isolated obstruction is in the upper pharynx. This is the sole site of blockage in only 20 – 30% of patients [16]. Most patients demonstrated multilevel obstructions involving upper and lower pharyngeal segments. The cause of lower pharyngeal or hypopharyngeal obstruction is variable. Examples include lingual tonsilar hypertrophy and supraglottic tissue redundancy; rarely, tumors, cysts, or lingual thyroid may occur. In most individuals with OSAS, specific pathologic lesions do not occur. Instead, disproportionate anatomy of the tongue base, lateral pharyngeal wall collapse, or other causes of obstruction are observed. This disproportionate anatomy may directly obstruct the airway or may cause increased upper airway resistance. This increased work of breathing may then contribute to the apneic cycle. Often in OSAS, the tongue is not overtly pathologic, but it is obstructive. Macroglossia is related to obstruction of the pharynx and not the oris. The relationship of the size of the tongue and the size of the oral cavity has been shown to be significantly disproportionate. In OSAS patients compared with those without OSAS, oral airway volume is compromised. Tongue and palatal contact on lateral cephalometric X rays is increased [16]. Tongue size is objectively increased, and this has

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been linked to obesity and body mass index [17]. Pathophysiologically, tongue size has been objectively related to airway volume. It is then speculated that decreasing tongue size will increase airway volume. Decreased volume may decrease airway resistance and lessen the likelihood of airway obstruction. Also, the tongue is the anterior wall framework for the lower pharynx and, furthermore, is anatomically linked to the remainder of the pharynx. As the tongue and its position change, so does the pharynx. By reducing soft tissue tongue size, the boundaries of the pharynx may be altered. Although most airway obstruction in adults is assumed to be caused by base of tongue obstruction, proximal hypertrophy and obstruction may occur and may require anterior wedge resections to reduce tongue size. For base of tongue obstruction in OSAS, a wide variety of glossectomy methods have been developed. Specific procedures with published data on OSAS include midline glossectomy, lingualplasty, hyo-epiglottoplasty, and radiofrequency ablation. Tools to perform glossectomy may include traditional surgical steel, CO2 laser, KTP laser, electrosurgery, or radiofrequency [18]. Each has its own advantages and disadvantages. Although conceptually simple, glossectomies may pose several difficulties including exposure for visualization, access to the surgical site to remove tissue and control bleeding, and airway control. With all methods, there is concern about damage to the lingual and hypoglossal neurovascular pedicle. Access to the surgical site may be intraoral (with or without tongue protrusion), endoscopic with laryngoscopes, or transcervical. Tongue protrusion with mouth opening provides limited visualization of tissues posterior to the circumvallate papilla. Contamination of the surgical wound in the oral cavity is a risk for infection. Intraoral approaches do not provide definitive landmarks to identify the neurovascular pedicle. Transcervical approaches allow identification and protection of the neurovascular pedicle. The transcervical approach also allows removal of large volumes of tissues; however, it requires external scars, tracheotomy, and prolonged recovery.

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and performed intraorally without tongue protrusion using a CO2 laser for access [12]. The procedure removes 1.5 – 2.0 cm in width tongue beginning at the circumvallate papillae. The excision is directed in the midline toward the valleculae. By staying in the midline, the lateral neurovascular pedicle is safely avoided. Care must be taken during the procedure to ensure that the midline is correctly identified, and reference maintained. Tissue is removed as aggressively as can be tolerated toward the valleculae. Posterior midline tongue, lingual tonsils, and redundant epiglottis are removed. Fujita observed that 10 out of 11 patients had removal of tracheotomy, but only 25% had clinically definitive reduction in the Respiratory Disturbance Index (RDI). The CO2 laser allows exposure in an often-crowded and anatomically small lower pharynx. It is, however, a cumbersome method to remove large tongue volumes. The laser and endoscope also provide means of accessing the lingual tonsils and redundant supraglottic tissues. Suspension laryngoscopes may remove tissue in the hypopharynx and supraglottic larynx that may not be corrected with maxillofacial or skeletal techniques. This includes anatomic abnormalities of the supraglottis and lingual tonsils. Lingualplasty Woodson and Fujita described lingualplasty [20]. This procedure more aggressively removes tissue and combines midline glossectomy with lateral tongue excisions. The procedure was performed using CO2, KTP, lasers, or electrosurgery. MLG was performed, but, in addition, a lateral wedge of tissue was removed. The remaining posterior tongue was then grasped and sutured anteriorly. In 22 patients, lingualplasty demonstrated a high success rate (70%). This was apparently a higher rate of success than MLG alone. In their series, all patients required perioperative tracheotomy. A more aggressive surgical approach resulted in a higher complication rate with a 25% perioperative complication rate observed. Complications included bleeding, edema, and persistent dysphagia. Other glossectomy

Tongue base procedures Laser midline glossectomy Initially described by Fujita, midline glossectomy (MLG) treated patients with severe OSAS who required tracheotomy [19]. Midline glossectomy is directed at removing a posterior strip of tongue base

Michelson reported MLG in another group of markedly obese patients (Body Mass Index of 38 kg/ M2) with severe OSAS. He used electrosurgery [21]. Routine laryngoscopy, lingual tonsillectomy, or supraglottoplasty was not performed. Glossectomy was successful in 25%. All patients had preexisting or concurrent tracheotomy. Recovery was short with a low complication rate and minimal morbidity.

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Multiple studies have combined glossectomy with other surgical procedures [22 – 24]. Because of widely varying patient populations and multiple concurrent procedures, results are difficult to compare. Significant improvements in OSAS are observed compared with historical controls. Meta analysis by Sher et al [14] reports that patients with Fujita Type II airway anatomy (obstruction at both upper and lower pharyngeal airway sites) UPPP alone would be expected to have a success rate of 5.3%. In Down syndrome glossectomy, palatopharyngoplasty, and maxillofacial surgery have demonstrated improved success over UPPP alone. In adults prospectively classified as Fujita Class II, a protocol with midline glossectomy and UPPP demonstrated higher success [25]. Glossectomy performed with radiofrequency demonstrates significant tongue reduction using a minor surgical procedure [26]. In selected patients, improvements in RDI and sleepiness are observed [27]. A multi-institutional study demonstrates significant clinical improvement in patients undergoing glossectomy with radiofrequency ablation [28]. The definitive treatment – success rate with this method was low, however (20 – 30%).

Several case series have subsequently been presented observing various degrees of clinical improvement. A prospective multi-institutional case series of the tongue suspension suture procedure has been performed [31]. Patients in this study included a wide range of sleep-disordered breathing including both snoring and sleep apnea. Objective improvement in respiratory disturbance was observed in the OSAS group. The improvement was small with changes noted primarily in the hypopnea index and not the apnea index. Objective sleep measures did not change, but symptomatic improvement was observed in both snoring and sleepiness. Most other studies supporting the tongue suspension suture combine patients having multiple procedures such as concurrent UPPP [32]. No study includes control groups. Results are difficult to interpret. Variable outcomes may reflect the widely diverse patient population, different surgical techniques, and the learning curve of surgeons performing the procedure. Advocates suggested that the procedure is more widely accepted by patients than limited osteotomies. Comparative trials are necessary to determine if in patients with multilevel obstruction, the procedure offers benefit over uvulopalatopharyngoplasty alone.

Hyoepiglotoplasty Hyoepiglotoplasty described by Chabolle has a reported 80% success rate when combined with UPPP [5]. This procedure is a transcervical suprahyoid pharyngectomy, glossectomy, and hyoid resuspension. It has the advantage of being able to remove large tissue volumes. Neurovascular structures of the tongue are identified and preserved. The hyoid bone is then resuspended in an anterior and superior location. The position provides increased airway stability. Although Chabolle described 10 patients, patients were prospectively accrued, and no patients were lost to follow-up. Confounding variables such as weight loss were also addressed. Patients demonstrated significant soft tissue disproportion and lack of skeletal abnormalities using head and neck exam, endoscopy, MRI scanning, and lateral cephalometric X rays.

Tongue suspension suture DeRowe described the tongue suspension procedure using a proline suture ‘‘sling’’ into the tongue base [29]. The tongue suspension suture theoretically prevents posterior displacement and passive collapse of the tongue base. Canine studies demonstrated decreases in airway collapse after the procedure [30].

Hyoid suspension Hyoid suspension is often used as part of the treatment for obstructive sleep apnea syndrome. Conceptually, this procedure is most amenable when there is retro-epiglottic airway obstruction. The hyoid bone may be advanced anteriorly to the mandible or alternatively advanced onto the laryngeal cartilage [33,34]. The ideal vector of movement is not known. Moving the hyoid superiorly decreases the mandibular plane to hyoid distance (MPH). This distance is a major cephalometric abnormality observed in OSAS populations. If MPH is the critical distance, hyomandibular movement may be optimal. Other studies demonstrate that anterior and inferior movement of the hyoid apparatus stabilizes the airway to the maximum degree. If anterior inferior movement is best, hyolaryngeal advancement may be preferred. No direct comparisons exist. It is not generally intended that hyoid suspension be performed as an isolated procedure. Most studies review hyoid suspension performed concurrently with other procedures. Riley et al assessed the impact of isolated hyoid suspension in patients who had failed prior UPPP and genioglossus advancement. In eight of fifteen patients, clinically signficant improvement in RDI was observed with hyoid suspension alone.

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Summary Surgical treatment of OSAS continues to evolve. It is appreciated that airway collapse and obstruction is complex and multifactorial. Obstruction likely occurs because of abnormalities in multiple segments in many patients with OSAS. Successful procedures to treat multilevel obstruction and severe OSAS exist. Because of real or perceived morbidity, however, aggressive procedures are not widely accepted by patients or physicians. To improve the low success of site-specific pharyngeal procedures, a variety of adjunctive procedures have been developed or utilized. Sites of obstruction that may be surgically addressed include the nose, palate, lingual tonsils, supraglottis, and tongue base. Conceptually, each of these may help achieve the goal of a larger, more stable upper airway. Comparative studies assessing effectiveness using a scientifically based approach to correcting the upper airway is lacking. Future studies will ultimately better define algorithms using appropriate surgical procedures. At this time, clinical judgment based on a comprehensive evaluation of the upper airway, disease severity, and patient wishes must be used to select these procedures.

References [1] Young T, Palta M, Dempsey J. et.al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328(17):1230 – 5. [2] Katsantonis G, Moss K, Miyazaki S. et.al. Determining the site of airway collapse in obstructive sleep apnea with airway pressure monitoring. Laryngoscope 1993;103:1126 – 31. [3] Schechtman KB, Sher AE, Piccirillo JF. Methodological and statistical problems in sleep apnea research: The literature on uvulopalatopharyngoplasty. Sleep 1995;18:659 – 66. [4] Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a surgical protocol for dynamic upper airway reconstruction. J Oral Maxillofac Surg 1993;51:784 – 9. [5] Chabolle F, Wagner I, Blumen M. et.al. Tongue base reduction with hyoepiglottoplasty: a treatment for severe obstructive sleep apnea. Larynogoscope 1999; 109:1273 – 9. [6] Hudgel DW, Harasick T, Katz RL. et.al. Uvulopalatopharyngoplasty in obstructive apnea: value of preoperative localization of site of upper airway narrowing during sleep. Am Rev Respir Dis 1991;143:942 – 6. [7] Terris D, Clerk A, Norbash A, Troell R. Characterization of postoperative edema following laser-assisted uvulopalatoplasty using MRI and polysomnography: implications for the outpatient treatment of obstruc-

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[10]

[11]

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tive sleep apnea syndrome. Laryngoscope 1996;106: 124 – 8. Woodson BT, Wooten MR. Comparison of upper-airway evaluations during wakefulness and sleep. Laryngoscope 1994;104(7):821 – 8. Riley R, Guilleminault C, Powell N. et.al. Palatopharyngoplasty failure, cephalometric roentgenograms, and obstructive sleep apnea. Otolaryngol Head Neck Surg 1985;93:240 – 4. Shepard JW Jr, Thawley SE. Evaluation of the upper airway by computerized tomography in patients undergoing uvulopalatopharyngoplasty for obstructive sleep apnea. Am Rev Respir Dis 1989;140:7ll – 16. Shepard JW, Thawley SE. Localization of upper airway collapse during sleep in patients with obstructive sleep apnea. Am Rev Respir Dis 1990;141:1350 – 5. Isono S, Tanaka A, Sho Y, Konno A, Nishino T. Advancement of the mandible improves velopharyngeal airway patency. J Appl Physiol 1995;79(6):132 – 8. Pringle MB, Croft CB. A grading system for patients with obstructive sleep apnoea – based on sleep nasendoscopy. Clin Otolaryngol 1993;18:480 – 4. Sher AE, Thorpy MJ, Shprintzen RJ. et.al. Predictive value of Muller maneuver in selection of patients for uvulopalatopharyngoplasty. Laryngoscope 1985;95: 1483 – 7. Woodson BT, Wooten MR. Manometric and endoscopic localization of airway obstruction after uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1994;111(1):38 – 43. Lyberg T, Krogstad O, Djupesland G, Cephalometric analysis in patients with obstructive sleep apnea syndrome: Soft tissue morphology. J Laryngol Otol 1989; 103:293 – 297. Do K, Ferreyra H, Healy J. et.al. Does tongue size differ between patients with and without sleep-disordered breathing? Larynogoscope 2000;110:1552 – 5. Carew J, Ward R, LaBruna A. et.al. Effects of scaplpel, electrocautery and CO2 and KTP lasers on wound healing in rat tongue. Larynogoscope 1998;108: 373 – 80. Fujita S, Woodson BT, Clark J. et.al. Laser midline glossectomy as a treatment for obstructive sleep apnea. Larynogoscope 1991;101:805 – 9. Woodson BT, Fujita S. Clinical experience with lingualplasty as part of the treatment of severe obstructive sleep apnea. Otolaryngol Head Neck Surg 1992;107: 40 – 8. Mickelson S, Rosenthal L. Midline glossectomy and epiglottidectomy for obstructive sleep apnea syndrome. Larynogoscope 1997;107:614 – 9. Lefaivre J, Cohen S, Burstein F. et.al. Down syndrome: identification and surgical management of obstructive sleep apnea. Plast Reconstr Surg 1997;99:629 – 37. Jacobs I, Gray R, Todd NW. Upper airway obstruction in children with Down syndrome. Arch Otolaryngol Head Neck Surg 1996;122:945 – 50. Cohen S, Ross D, Burstein F. et.al. Skeletal expansion combined with soft-tissue reduction in the treat-

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B.T. Woodson / Oral Maxillofacial Surg Clin N Am 14 (2002) 371–376 ment of obstructive sleep apnea in children: Physiologic results. Otolaryngol Head Neck Surg 1998;119: 476 – 85. Elasfour A, Miyazaki S, Itasaka Y. et.al. Evaluation of uvulopalatopharyngoplasty in treatment of obstructive sleep apnea syndrome. Acta Otolaryngol 1998;537: 52 – 6. Powell N, Riley R, Troell R, Blumen M. et.al. Radiofrequency volumetric reduction of the tongue. Chest 1997;111:1348 – 55. Powell N, Riley R, Guilleminault C. Radiofrequency tongue base reduction in sleep-disordered breathing: a pilot study. Otolaryngol Head Neck Surg 1999;120: 656 – 64. Woodson BT, Michelson S, Huntley T, Nelson L. et.al. A multi-institutional study of radiofrequency volumetric tissue reduction for OSAS. Otolaryngol Head Neck Surg 2001;125:303 – 11. DeRowe A, Gunther E, Fibbi A. et.al. Tongue-base suspension with a soft tissue-to-bone anchor for ob-

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structive sleep apnea:preliminary clinical results of a new minimally invasive technique. Otolaryngol Head Neck Surg 2000;122:100 – 3. DeRowe A, Woodson BT. A minimally invasive technique for tongue base stabilization in obstructive sleep apnea. Operative Techniques Otolaryngol 2000;11: 41 – 6. Woodson BT. A tongue suspension suture for obstructive sleep apnea and snorers. Otolaryngol Head Neck Surg 2001;124:297 – 303. Coleman J, Rathfoot C. Oropharyngeal surgery in the management of upper airway obstruction during sleep. Otolaryngol Clin North Am 1999;32:263 – 75. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993;108:117 – 25. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea and the hyoid. A revised surgical procedure. Otolaryngol Head Neck Surg 1994;111:717 – 21.

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Genioglossus muscle advancement techniques for obstructive sleep apnea N. Ray Lee, DDS* Private Practice, 716 Denbigh Boulevard, Suite C-1, Newport News, VA 23608, USA Department of Oral and Maxillofacial Surgery, Medical College of Virginia, Virginia Commonwealth University, 520 North 12th Street, Richmond, VA 23298, USA Department of Otolaryngology – Head and Neck Surgery, Eastern Virginia Medical School, P.O. Box 1980 Norfolk, VA 23501, USA

Genioglossus muscle advancement is a viable adjunctive procedure in the reconstruction of the upper airway. The author has not experienced the complications of osseous segment necrosis, and with appropriate drain placement with the anterior mandibular osteotomy and trephine osteotomy techniques, the risk of infection is low. Neurosensory changes and dental-pulp necrosis may occur, therefore, patients must be informed accordingly. The role of the genioglossus muscle in posterior airway occlusion has been investigated at length [1 – 3]. A study of 10 obstructive sleep apnea (OSA) patients and 4 symptom-free controls found that during subsequent tidal breathing, the timing of the genioglossus onset progressively decreased after the onset of inspiration until the next OSA occurred [4]. This finding suggests that the timing relationship between genioglossus inspiratory activity and inspiratory effort is physiologically important in the pathogenesis of OSA. The rationale for advancement of the genioglossus muscle is as follows: the hypopharyngeal airway is stabilized by the forward movement of the genial tubercle and genioglossus muscle, which places tension on the base of tongue thereby decreas-

* Virginia Commonwealth University, Medical College of Virginia, Department of Oral Maxillofacial Surgery, 716 Denbigh Boulevard, Suite C-1, Newport News, VA 23602. E-mail address: [email protected] (N.R. Lee).

ing the probability it will prolapse into the posterior airway space during sleep [5,6]. The functional genioplasty for surgical reconstruction of the upper airway (UA)was first described by Riley et al [6] as the inferior sagittal osteotomy (ISO). The hyoid was also suspended and fixed to the inferior border of the mandible as an adjunct to the genioglossus advancement. This technique was referred to as genioglossus advancement-hyoid myotomy. In a later study, the hyoid suspension was modified by suturing the hyoid to the thyroid cartilage [7]. The ISO was modified by Powell and Riley [5] because of an increased number of midline mandibular fractures; however, this osteotomy and all future modifications of the technique maintained the same objective: advancement of the genial tubercle and genioglossus muscle. The ISO was then modified and described by Riley et al [5] to retain continuity of the inferior border of the mandible by limiting the osteotomy to a rectangular window, including the genial tubercle. This osteotomy is called an anterior mandibular osteotomy (AMO). Further modification of this procedure was described by Lee and Woodson [8] as a circular osteotomy of the genial tubercle. All procedures have the same objective of ultimate stabilization of the hypopharyngeal airway by advancing the genioglossus muscle. Johnson and Chinn [1] reported a positive response rate of 77.8% in nine patients treated with a combination of UA procedures and genioglossus muscle advancement. Lee et al [2] reported a positive response rate of 69% in 35 patients treated with UA procedures and genioglossus muscle advancement.

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 3 7 - 7

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Fig. 1. (A) The mucusal incision. (B) The dissection of the mental nerves. (C) The full-thickness periosteal incision. (From Lee NR. Genioplasty techniques. Oral Maxillofacial Surg Clin N Am 2000;12:755 – 63; with permission.)

Therefore, when combined with other UA procedures, the genioglossus muscle advancement is a viable surgical treatment for OSA.

Inferior sagittal osteotomy ISO is a technique reserved for the OSA patient with significant anteroposterior deficiencies in the horizontal menton position (microgenia). The inferior border of the mandible is disrupted and advanced with only the dentoalveolar process intact; therefore, a lingual splint is constructed and placed with interdental stainless steel 24-gauge wire. This splint aids

Fig. 2. Inferior sagittal osteotomy to advance the genioglossus musculature for obstructive sleep apnea. (From Lee NR. Genioplasty techniques. Oral Maxillofacial Surg Clin N Am 2000;12:755 – 63; with permission.)

in stress-shielding the forces of mastication and is removed in 6 weeks. All patients who undergo this procedure are requested to restrict their diets to nonchewable foods for 6 weeks following the procedure. The soft tissue approach is the same as for the cosmetic intraoral genioplasty (Fig.1). The osseous midline is scored on the anterior surface of the symphysis. The genial tubercle pedicle is outlined with an oscillating saw in the anterior surface, with emphasis on completion of a full-thickness osseous pedicle that contains the entire genioglossus muscle attachment. The inferior portion of the osteotomy is the same as the

Fig. 3. An anterior mandibular osteotomy showing the advanced and rotated segment, which includes the genial tubercle and genioglossus musculature. (From Lee NR. Genioplasty techniques. Oral Maxillofacial Surg Clin N Am 2000;12:755 – 63; with permission.)

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Fig. 4. System sizing. Select the appropriate trephine system (12 or 14 mm) using the radiograph template and panorex X ray. (From Stryker-Leibinger; with permission.)

horizontal augmentation genioplasty, extending bilaterally and posteriorly toward the gonial notch region. The osseous pedicle is mobilized and advanced anteriorly full thickness. The lingual cortex superior to the genial tubercle is brought to rest on the lateral plate of the dentoalveolar process with attention to coordination of the midline. Stabilization can be achieved by application of two precontoured chin plates at either side of the midline symphysis tubercle process. Soft tissue closure is accomplished in two layers, mentalis muscle and mucosa (Fig. 2).

Anterior mandibular osteotomy The AMO technique is reserved for the OSA patient with a normal, horizontal, soft tissue menton position. The objective is the same as for the ISO— to advance the genial tubercle and genioglossus muscle without disruption of the inferior border of the mandible to improve stability of the hypopharyngeal airway. The soft tissue approach is the same as described for the intraoral genioplasty, except that osseous

Fig. 5. Drilling pilot hole. Drill two superior 1.5-mm holes for guide-plate placement. (From Stryker-Leibinger; with permission.)

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Fig. 6. Guide-plate selection. Choose appropriate guide plate (S, straight; A, angled) depending on tooth root location and genioglossus muscle position. (From Stryker-Leibinger; with permission.)

exposure is significantly reduced posteriorly. Periosteal dissection is accomplished posterior to and just distal to the cuspids bilaterally. The mental nerves do not require exposure and neurosensory deficit is minimal. The patient may experience dental-pulp necrosis of the mandibular anterior dentition, and amputation of the cuspid root tips may occur. This complication is treated by endodontic therapy when the tooth is diagnosed as nonvital. The genioglossus muscle attachment is located by lingual palpation.

The muscle bundle cannot be palpated through the mylohyoid muscle; however, accurate interpretation of the position of the tubercle can be achieved with the anatomic knowledge that the genial tubercle is approximately 5 to 8 mm inferior to the apices of the mandibular incisors. A bicortical 2-mm bone screw is placed at the midpoint of the genial tubercle location. A microsagittal oscillating saw is used to complete a rectangular osteotomy, with the screw serving as a

Fig. 7. Guide-plate fixation. Fixate guide plate to mandible using 2.0-mm-diameter bone screws with sufficient length to accommodate guide-plate profile. Alternate placement of the screws to ensure level guide-plate placement. (From StrykerLeibinger; with permission.)

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Fig. 8. Trephine stop assembly. Place trephine stop at a depth sufficient to osteotomize inferior border completely. Secure trephine stop by tightening the Square-fit set screw. (From Stryker-Leibinger; with permission.)

central guide for a symmetrical segment that contains the genioglossus muscle. Care must be taken not to shorten the lingual plate by excessive angulation of the saw during the osteotomy, with emphasis directed toward parallel walls of the symphysis osteotomy. The bicortical bone screw ensures mobilization of both cortical plates. If the segment does not mobilize, the lingual osteotomy may not be complete and, with force, the lateral cortical plate could fracture with the medullary bone, leaving the lingual plate intact. A bicortical bone screw placement will help prevent this

complication. After mobilization, the segment is transpositioned full thickness anteriorly. The lingual cortical plate is then positioned anterior to the lateral cortical plate and rotated 90°. The medullary bone and lateral cortical plate are osteotomized, which leaves the lingual cortical plate and genioglossus muscle attachment. The segment is then stabilized with one unicortical 2-mm bone screw placed in an inferior position. The soft tissue closure is accomplished in two layers, and a 0.25-inch Penrose drain is placed transmucosally and removed in 24 hours. This

Fig. 9. Guide-rod assembly. Insert guide rod through the back of the minidriver and trephine. Thread guide rod counterclockwise into guide plate. (From Stryker-Leibinger; with permission.)

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Fig. 10. Beginning the osteotomy. Slide the trephine into place over the guide plate onto the bone and start the minidriver. Never release your grip on the guide-rod handle or operate the minidriver in reverse. Complete the osteotomy with short pumping strokes and copious irrigation. (From Stryker-Leibinger; with permission.)

drainage reduces seroma formation. A pressure dressing is then placed on the closure for 48 hours (Fig. 3).

Trephine osteotomy approach The trephine osteotomy (TOA) technique was designed to reduce the risk of amputation of the cuspid root apex and to simplify the osteotomy design for advancing the genioglossus muscle. The soft tissue

dissection is the same as for the AMO technique. The appropriate size template is selected and placed over the lateral aspect of the symphysis at the location for the genial tubercle (Figs.4 and 5) A bicortical hole is drilled and the depth is measured (Fig. 6); the appropriate guide plate is placed and secured with a bicortical screw (Fig. 7). The remaining bicortical screw is then placed to secure the guide plate. The appropriate size trephine is placed with the trephine drill stop placed at the indexed depth of mandible

Fig. 11. Segment mobilization. After completion of the osteotomy, transposition the segment anteriorly by pulling out on the guide-rod handle. (From Stryker-Leibinger; with permission.)

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Fig. 12. Screw placement. Place a 2.0-mm-diameter screw in the center hole. Allow sufficient space below the screw head for screw-holding forceps and fixation-plate placement. (From Stryker-Leibinger; with permission.)

thickness (Fig. 8). The guide rod is inserted through the minidriver and threaded counterclockwise into the guide plate (Fig. 9). Attention is directed to completing the trephine osteotomy. It is important not to operate the minidriver in reverse and not to release the guide-rod handle, either of which can allow the genioglossus muscle to be avulsed (Fig. 10). After completion of the osteotomy, the segment is grasped with bone-holding forceps and the guide rod is removed to free the minidriver. The guide rod is rethreaded and the segment is transpositioned anteriorly full thickness (Fig. 11). The segment-holding forceps are then applied to the lingual cortex, and the bicortical screws and guide plate are removed. The

medullary bone and lateral plate are osteotomized with an oscillating saw. The template is used to drill and then place a central bone screw (Fig. 12). The screw-holding forceps are placed, and the segment is stabilized with the lingual plate resting in a superior position and overlapping the lateral plate of the symphysis (Fig. 13). An elevator placed in an inferior position may be helpful to maintain segment stability and full-thickness augmentation. The rigid fixation plate is placed, engaging the bone screw into the central groove of the plate. The feet of the plate are secured to the symphysis with bicortical screws, and a lateral screw is placed into the face of the plate to secure the segment. The

Fig. 13. Positioning bone segment. Transposition the segment anteriorly by sliding the lingual cortex up to rest on the labial cortex. (From Stryker-Leibinger; with permission.)

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Fig. 14. Plate placement. The gap between the screw-holding forceps and the bone should be sufficient to allow the fixation plate to slide into position. (A) Plate position. Slide the fixation plate up into position so the center screw engages the plate slot. (B) Plate fixation. Place 2.0-mm-diameter fixation screws once bilateral foot-plate holes have been drilled. (Secure bone segment with one lateral segment screw prior to tightening center screw. Do not overtighten center screw.) (From Stryker-Leibinger; with permission.)

central screw is then secured to complete the segment stabilization (Fig. 14). The soft tissue closure is the same as that for the AMO closure, with placement of a transmucosal 0.25-inch Penrose drain. The drain is removed after 24 hours.

[2]

[3]

Summary [4]

Genioglossus muscle advancement has been reported on extensively and remains a viable adjunctive procedure in the reconstruction of the UA. The author has not experienced the complications of osseous segment necrosis, and with appropriate drain placement using the AMO and TOA techniques, the risk of infection is low. Neurosensory changes and dentalpulp necrosis may occur, however, and patients must be informed accordingly.

[5]

[6]

[7]

References [8] [1] Johnson NT. Chinn J. Uvulopharyngoplasty and inferior sagittal mandibular osteotomy with genioglossus ad-

vancement for treatment of obstructive sleep apnea. Chest 1994;105:278 – 83. Lee NR, Wilson J, Given CD Jr, et al. Staged surgical treatment of obstructive sleep apnea syndrome: a review of 35 patients. J Oral Maxillofac Surg 1999;57:382 – 5. Riley RN, Powell NB, Guilleminault C. Maxillary, mandibular, and hyoid advancement for treatment of obstructive sleep apnea: a review of 40 patients. J Oral Maxillofac Surg 1990;48:20 – 6. Adachis, Lowe AA, Tsuchiya M, et al. Genioglossus muscle activity and inspiratory timing in obstructive sleep apnea. Am J Orthod Dentofacial Orthop 104: 139 – 45. Powell NB, Riley RW, Guilleminault C. Maxillofacial surgical techniques for hypopharyngeal obstruction in obstructive sleep apnea. Operative techniques. Otolaryngol Head Neck Surg 1991;2:112 – 9. Riley RN. Powell NB, Guilleminault C. Inferior sagittal osteotomy of the mandible with hyoid suspension: a new procedure for obstructive sleep apnea. Otolaryngol Head Neck Surg 1986;94:589. Riley RW, Powell NB, Guillaminault C. Obstructive sleep apnea and the hyoid: a revised surgical procedure. Otolaryngol Head Neck Surg 1994;111:717 – 21. Lee NR, Woodson T. Genioglossus muscle advancement via a trephine osteotomy approach. Operative techniques. Otolaryngol Head Neck Surg 2000;11:50 – 4.

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Surgical changes of posterior airway space in obstructive sleep apnea Peter D. Waite, MPH, DDS, MD*, Georgios A. Vilos, DDS Department of Oral & Maxillofacial Surgery, University of Alabama School of Dentistry, University of Alabama at Birmingham, 419 School of Dentistry Building, 1530 3rd Avenue South, Birmingham, AL 35294-0007, USA

There are numerous medical and surgical treatment modalities for the management of the sleep apnea patient. Among the medical treatments, weight loss and positive pressure therapy are considered to be the most important. Surgical treatment is directed at increasing the posterior airway space. Among the surgical procedures, tracheostomy, uvulopalatopharyngoplasty (UPPP), and maxillofacial skeletal procedures are the most common. Positive pressure therapy during sleep is considered effective in limiting obstructive events during sleep. Pressure is titrated to the desired value that eliminates upper airway collapse during nocturnal polysomnography; however, despite a reported 65% to 90% compliance rate with positive airway pressure therapy when compliance is assessed by subjective patient reports, long-term compliance is less than optimal when objectively monitored. Kribbs et al [1] used continuous positive airway pressure (CPAP) machines that contained a microprocessor and a monitor that measured actual pressure at the mask for every minute of each 24-hour day for an average of 106 days per patient. Patients were not aware of the monitor inside the CPAP machines. Although 60% of patients claimed to use CPAP nightly, only 16 of 35 (46%) met the criteria for regular use, which was defined as at least 4 hours of CPAP therapy administered on 70% of the days monitored [1]. There is proof that part-time use of CPAP is not satisfactory in controlling obstructive sleep apnea (OSA) [2,3]. Intolerance of CPAP therapy because of poor mask fit, claustrophobia,

* Corresponding author. E-mail address: [email protected](P.D. Waite)

difficulty with exhaling, air temperature (too cold or too warm), or machine noise as well as the cumbersomeness and inconvenience in general may lead to decreased compliance. Acceptance of treatment may be improved with bilevel positive airway pressure (BiPAP), although a study published by ReevesHoche´ and coworkers [4] indicated that in patients who do not accept therapy for home use, compliance is the same for both CPAP and BiPAP systems. Consequently, the option of surgery should be offered to OSA patients who fail to comply with home positive pressure therapy and continue to suffer from heavy snoring, fragmented sleep, excessive daytime somnolence, and cognitive changes.

Primary procedures for the surgical treatment of OSA Tracheostomy Permanent tracheostomy was the first efficacious surgical procedure performed for the treatment of OSA. In the 1970s and 1980s, it was by far the most commonly performed surgical procedure for this problem. Tracheostomy has a success rate of almost 100% in reversing the signs and symptoms of OSA because it bypasses all the potential sites of obstruction in the upper airway. After tracheostomy there is a rapid and striking reduction in daytime somnolence. Additionally, hypoxemia, apnea, pulmonary hypertension, bradycardia, and cardiac dysrhythmias all diminish dramatically with the procedure. The psychologic toll on the patients, however, is sometimes devastating; in addition, there is esthetic disfigure-

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 3 3 - X

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ment and risk for more serious complications such as tracheal stenosis, erosion of vessel walls, and recurrent bronchitis. Therefore, the procedure is used mainly as an interim treatment until surgical reconstruction of the upper airway can be completed. The goal is to decannulate the patient eventually [5]. Simmons et al [6] suggested that tracheostomy should still be the primary treatment for all patients who have life-threatening cardiac dysrhythmias and for those who have frequent oxygen desaturations below 50% during apneic episodes [5,6]. UPPP Ikematsu initially described UPPP in 1964 for the treatment of habitual snoring [6a]. When he investigated habitual snorers, he found that 91% had narrowing of the oropharynx caused by an elongated soft palate and uvula as well as redundant lateral pharyngeal mucosa. Excision of the redundant mucosa in the tonsillar pillars and partial excision of the uvula eliminated snoring in 96% of his patients. With minor modifications Fujita et al first performed the procedure in 1981 for the treatment of OSA [6b]. The procedure was designed to enlarge the potential airspace in the oropharynx by performing a tonsillectomy and adenoidectomy, excising the uvula and redundant lateral pharyngeal wall mucosa, and resecting 8 to 15 mm along the posterior border of the soft palate. UPPP is excellent for the control of snoring; in addition, several reports [5] have shown significant objective improvement in the respiratory distress index (RDI), and hemoglobin desaturation levels on the postoperative polysomnogram range from 41% to 66%. Sher [7] reported in 1996 a success rate of 40% for UPPP alone, which is increased to 60% if the procedure is combined with genioglossus advancement and hyoid myotomy/suspension (GAHM). He also suggested that maxillomandibular advancement should be offered as a primary procedure to nonobese, skeletally deficient patients with moderately severe OSA, whereas obese patients with more severe OSA should receive adjunctive soft tissue procedures such as UPPP [7]. It is now well recognized that although most patients with OSA demonstrate retropalatal narrowing of their airway, this is not the only area of the pharynx that collapses during sleep. Collapse occurs most of the time at multiple sites, and the failure of UPPP to offer a cure to most sleep apnea patients is attributed to the inability of the procedure to control obstruction in other sites of the upper airway besides the retropalatal area [8 – 16]. Suto and coworkers [14] used ultrafast MRI in patients with sleep apnea as well as in healthy control

subjects. The subjects were scanned while awake and during sleep induced with hydroxyzine. The results of this study showed that obstruction occurs most often in the retropalatal area, although frequently there is an additional site of obstruction [14]. Shepard and Thawley [15] studied 18 patients with OSA using overnight polysomnography with simultaneous pressure monitoring in the posterior nasopharynx, oropharynx, hypopharynx, and esophagus. They concluded that the upper airway collapses in the velopharyngeal/retropalatal area in approximately 50% of the cases. In other cases the obstruction can start initially in the glossopharyngeal/retroglossal area. As soon as it appears, the obstruction can extend to involve adjacent segments of the upper airway. This happens more significantly during rapid eye movement (REM) sleep secondary to the pronounced atonia of the upper airway dilator muscles [15]. The results of Morrison et al [16] show that the retropalatal area is the site of primary narrowing in 80% of the patients; however, two or even more sites of narrowing are observed in 82% of the patients. Sher et al [17] showed in 1985 that UPPP is successful when it is performed on patients who obstruct only in the retropalatal section of their oropharynx as evidenced by a preoperative Mueller’s maneuver. Patients were selected for the procedure based on the results of a preoperative Mueller’s maneuver. Of these patients 87%, had > 50% decrease in their RDI [17]. In 1990 Riley et al [18] reported that UPPP most frequently failed in patients with mandibular retrognathia (SellaNasion-B (SNB) point angle < 74°) and morbid obesity (body mass index [BMI] >33 kg/m2]. Ryan et al [19] published the data of a well-designed prospective study that showed an 83% success rate for UPPP for patients selected from preoperative three-dimensional CT reconstructions of their airway to have large tongue volume, decreased upper airway to tongue volume ratio, and decreased upper airway to soft palatal volume ratio. The Stanford protocol for surgical reconstruction of the upper airway In 1986, on the basis of previous surgical experience, Riley, Powell, and Guilleminault [20] first introduced to clinical practice a two-phase protocol for surgical reconstruction of the sleep apneic airway. The protocol entailed a presurgical evaluation that included a physical examination, cephalometric analysis, and fiberoptic pharyngoscopy. The site of obstruction was identified with the help of Mueller’s maneuver, and surgery was directed to the obstructed sites. After the presurgical evaluation each patient was

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classified by the site of obstruction according to Fujita: type I, retropalatal; type II, retropalatal and retroglossal; and type III, only retroglossal. Patients were classified as positive for retropalatal obstruction when fiberoptic examination showed that a redundant soft palate collapsed against the pharyngeal wall with the Mueller maneuver and cephalometric analysis showed elongation of the soft palate. Retroglossal obstruction was positive when the base of the tongue collapsed against the posterior pharyngeal wall and restricted visualization of the larynx during fiberoptic examination or when the cephalometric analysis demonstrated a narrow posterior airway space (PAS). Patients with OSA and mandibular skeletal deficiency (SNB angle < 76°) on cephalometric analysis almost uniformly have a narrow PAS and base of tongue obstruction. In phase I surgery, patients with type I obstruction (soft palate) received UPPP. Patients with type III obstruction (base of tongue) received GAHM. With this procedure the attachments of the genioglossus muscle to the genial tubercles are advanced anteriorly while the body of the hyoid bone is freed from the attachments of the infrahyoid strap muscles and suspended 1 to 1.5 cm anteriorly and superiorly from the inferior border of the mandibular symphysis. Severe dysphagia can be created if the hyoid is suspended more than 1.5 cm [21]. Patients with type II obstruction received during phase I surgery both a UPPP and GAHM. Follow-up polysomnograms were obtained 6 months after phase I surgery, and poor responders were offered phase II surgery, which consisted of surgical advancement of the maxilla and the mandible [2]. In 1993 the same authors [2] reported on the results of this surgical protocol. Criteria for success were considered a postoperative RDI less than 20 per hour with at least a 50% reduction over the preoperative study and lowest hemoglobin oxygen saturation levels (LSAT) equivalent to those seen with nasal CPAP. Most of the 239 patients who entered phase I therapy were type II and, therefore, received a UPPP and a GAHM. The patients who received only a UPPP and were treated successfully in general had long redundant soft palates, no mandibular deficiency (SNB >78), and normal airway space at the base of the tongue (PAS >10 mm). In contrast, the patients with a successful result after an isolated GAHM had mandibular deficiency (SNB < 78), normal palatal tissue without tonsils, and narrow airway space at the base of the tongue (PAS < 6 mm). Overall, 61% of these patients were treated successfully. The majority of the patients who had unsuccessful phase I treatment had severe OSA (mean RDI of 62 per hour) and morbid obesity (mean BMI 32.3 kg/m2). Only 24 of

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the 94 patients who underwent unsuccessful phase I therapy elected phase II therapy, with a success rate of 97% [2]. The same group of authors reported recently on 21 patients with morbid obesity (BMI >40 kg/m2) and severe OSA (RDI >40 per hour) who underwent the same two-phase surgical protocol with a success of 81% [22]. Maxillomandibular advancement (MMA) Isolated reports of using orthognathic surgery for the treatment of OSA first appeared in the literature in the late 1970s and early 1980s [23,24]. Over the next 10 years, combined advancement of the maxilla, mandible, and chin became the surgical procedure of choice for the treatment of OSA. The technique includes a standard Le Fort I osteotomy in combination with bilateral sagittal split ramus osteotomies for the simultaneous advancement of the maxilla and mandible. In many cases, an advancement geniotomy, with or without hyoid myotomy and suspension, is also performed. Waite et al [25] reported on 23 OSA patients treated with MMA along with a high sliding geniotomy without hyoid myotomy and suspension. Originally believed to be indicated only in major skeletal deficiencies after other surgical options failed, MMA now is recommended as a primary surgical option for OSA. MMA is indicated for patients with (1) retroglossal obstruction, (2) severe OSA (RDI >50 per hour), (3) hemoglobin oxygen desaturation lower than 85%, (4) morbid obesity, and (5) failure to respond to other treatment. The procedure is also indicated for maxillomandibular hypoplasias, believed to cause diminished posterior airway space leading to obstruction [26]. A surgical advancement of 10 mm is usually performed. This is an arbitrary value that corresponds to the greatest forward movement that is technically feasible in most cases for the maxilla; however, Paoli et al [27] recently reported on a case of a 44-year-old male patient with severe OSA (preoperative RDI of 88 per hour) whom they treated with mandibular elongation by using intraoral mandibular distraction devices. In this way the amount of mandibular advancement required to eliminate the obstructive events was titrated to effect. The final position of the mandible was 12 mm anteriorly with a postdistraction RDI of 23/hour. This was followed up by a maxillary Le Fort I advancement to the desired dental occlusion. The final polysomnogram revealed an RDI of 7 per hour [27]. The reported success rates of MMA by various authors are summarized in Table 1. Individual reports need to be looked at carefully because most of the time

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Table 1 Reported success rate of maxillomandibular advancement surgery Author

Institution

Patients

a

U.A.B.

23

65%

a

Stanford University

40 (phase II)

97%

a

Stanford University

24 (phase II)

100%

Hochban et al [28] Tiner [5] a Prinsell [29]

Marburg University University of Texas Private practice, GA

21 22 50

95% 95% 100%

a

Stanford University

21 (phase II)

Waite et al [25] Riley et al [18] Riley et al [2]

Li et al [22]

Success

81%

Criteria for success RDI < 10, improvement of symptoms (97% benefited from the procedure) RDI < 20, 50% decrease of RDI, normal or near normal SaO2 RDI < 20, 50% decrease of RDI, LSAT equivalent to nasal CPAP RDI < 10 (no patient with BMI >30 kg/m2 ) RDI < 20, improvement of symptoms RDI < 15, AI < 5, LSAT >80%, >60% decrease in RDI and AIb RDI < 20 (all patients with BMI >40 kg/m2)

Abbreviations: BMI, body mass index; CPAP, continuous positive airway pressure; LSAT, lowest hemoglobin oxygen saturation; RDI, respiratory distress index; SaO2, hemoglobin oxygen saturation; UAB, University of Alabama at Birmingham. a Report on combined surgical procedures (maxillomandibular advancement + uvulopalato-pharyngoplasty +/ geniotomy advancement or genioglossus advancement with hyoid myotomy/suspension). b AI = apnea index (number of apneas per hour of sleep).

MMA is performed on a patient who has already undergone unsuccessful UPPP. Therefore, the reported success rate will be essentially that of a combined procedure and will not represent the true success rate of MMA alone.

Secondary procedures for the surgical treatment of OSA Nasal surgery In patients diagnosed with OSA, nasal procedures aim at decreasing the resistance against the passage of air by increasing the volume of the nasal cavity. Potential reasons for nasal obstruction include a deviated nasal septum and hypertrophic inferior turbinates obliterating the inferior and middle meatuses, which represents the main route followed by the inspired air stream. Septoplasty and inferior turbinectomy may be performed via endonasal approaches or, alternatively, if surgery also includes maxillary advancement, they may be conveniently performed after maxillary downfracture, which greatly facilitates access to these structures. Resection of the deviated portion of the nasal septum may be attempted after careful elevation of the mucoperichondrium that envelops the nasal septum, whereas excision of the bulbous anterior aspect of the inferior turbinate requires a longitudinal incision along the mucoperiosteum of the floor of the nasal cavity. After conclusion of the septoplasty, use of a quilting 4/0 plain gut suture prevents the possibility of a septal hematoma. The longitudinal incisions along the nasal floors may

be closed with running 4/0 chromic gut sutures. This is performed prior to maxillary rigid fixation, whereas after maxillary repositioning, a 2/0 polyglactin suture is required to secure the caudal aspect of the nasal septum to the midline of the premaxilla in the area of the anterior nasal spine, which prevents buckling of the nasal septum laterally, thus restricting the ipsilateral nasal passage. At the conclusion of maxillary orthognathic procedures the nasal musculature usually is reoriented with the help of a sling suture, which has the purpose of preventing potential widening of the alar base. This strategy is generally avoided when the indication of maxillary surgery is OSA. The reason is that a postoperative decrease in the alar width may be beneficial from a cosmetic standpoint; however, it may increase resistance against the passage of air, which for a sleep apnea patient represents a complication. The same concept lies behind performing a piriformplasty. With this procedure the piriform aperture of the nasal cavity is accessed and visualized via a maxillary vestibular incision and widened with the help of rotating instruments. This results in less resistance against the passage of air through the nasal valves. Nasopharyngeal and oropharyngeal soft tissue procedures It is recognized that the presence of hypertrophic adenoids and pharyngeal tonsils is the main cause of OSA in the pediatric population. Even in adult sleep apnea patients, the roof of the nasopharynx should not be missed during the preoperative clinical and radiographic evaluation. A good quality lateral cepha-

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lometric radiograph obtained for evaluation of the maxillofacial skeletal structures sometimes reveals hypertrophic adenoids inferiorly and anteriorly to the sphenoid sinus. CT images of the upper airway, however, are more reliable at visualizing this, especially if sagittal reconstructions are available. Treatment consists of curettage of the hypertrophic lymphoepithelial tissue, which may be performed as an adjunct to other upper airway reconstructive surgical procedures. Obstruction of the upper airway at the retroglossal level occurs in cases of mandibular deficiency. Retroposition is best demonstrated in an infant born with the Pierre-Robin sequence. In these cases it may be beneficial to temporarily suture the tip of the tongue to the chin to avoid the necessity of a tracheostomy. Later, spontaneous mandibular growth or mandibular corrective surgery in the form of mandibular distraction osteogenesis or both can permanently alleviate the problem. A much more common type of retroglossal obstruction is seen in obese individuals whose tongue size and volume have been shown by MRI to be increased compared to non-obese control subjects. In a few selected cases tongue reduction in the form of a midline ‘‘keyhole’’ tongue resection may be advocated for sleep apneic morbidly obese patients. The procedure may be performed as a cold steel excision or thermally with the use of electrocautery or laser to avoid blood loss. The laser excision has the advantage over the electrocautery of provoking considerably less muscle twitching, and thus some surgeons find it more convenient. It is important after the excision to carefully reapproximate the tissues in two layers (muscle and superficial mucosa) with 2/0 or 3/0 polyglactin sutures to avoid postoperative tissue breakdown and a bifid tongue tip. Subjective data suggested that the laser-assisted uvulopalatoplasty (LAUP) was effective as a treatment of snoring [30], which led to a subtle expansion of the indications for LAUP to include OSA treatment. LAUP has the advantage over UPPP in that it is performed on an outpatient clinic basis under local anesthesia supplemented with intravenous sedation. It is less invasive than UPPP because it addresses redundant tissues of the soft palate only. Most commonly it consists of a circumferential excision of an elongated uvula and laser ablation of tissue along the free posterior border of the soft palate. The results are scarification and contracture during the healing process, which decrease the size of the soft palate. The fundamental shortcoming of palatal surgical procedures, such as LAUP and UPPP, is that most OSA patients are inadequately treated on the basis of

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reduction in the RDI postoperatively [31]. The failure of LAUP in the treatment of OSA has been attributed to the limited resection of pharyngeal tissue compared with UPPP. Modification of the LAUP procedure to include a more complete resection of the pharynx was proposed by Mickelson and Ahuja [32], in which only 36 of 59 OSA patients (61%) underwent posttreatment polysomnography. These authors’ conclusion that a more aggressive LAUP procedure is ‘‘an effective treatment for mild, moderate and severe OSA’’ is doubtful in view of the previously reported limited efficacy rate of UPPP and potential selection bias in the current study. The largest trial comparing pretreatment and posttreatment polysomnographic data in 58 LAUP patients showed a worsened posttreatment RDI in mild or moderate OSA patients and the persistence of severe OSA [33]. Somnoplasty is a novel palatal stiffening procedure performed on an outpatient basis. Palatal tissue is not excised or ablated as with UPPP or LAUP, but rather, a needle electrode is inserted near the border of the hard palate and directed toward the uvula. A generator delivers pulses of radiofrequency energy, which cause tissue necrosis and needle tract fibrosis over subsequent weeks to months. In this way a submucosal scar is created along the midline of the soft palate. The study by Powell and colleagues [34] demonstrated no major complications for this application of radiofrequency ablation to the soft palate in 22 patients. The authors also suggest an advantage of somnoplasty over LAUP or UPPP with respect to postoperative pain, which may be a result of the avoidance of mucosal transection; however, repetition of the procedure is usually required before the optimal surgical effect is obtained, which leads to increased cost. The cautery-assisted palatal stiffening operation (CAPSO) is another outpatient mucosal surgery that induces a midline palatal scar to stiffen the floppy palate. Indications for CAPSO are habitual snoring and mild OSA. It has the advantage over radiofrequency ablation and LAUP that it avoids the need for multiple stage operations and does not rely on radiofrequency generators or expensive laser systems and hand pieces. CAPSO eliminates excessive snoring caused by palatal flutter and has success rates that are comparable with those of traditional palatal surgery [35]; however, according to Loube [31], postoperative pain is considerable and could preclude further study of this procedure. Secondary skeletal procedures involving the chin The surgical procedures that involve the chin aim at advancing the genial tubercles, which bear the

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insertions of the genioglossus muscles. These muscles are considered to be upper airway dilators that counteract the action of the pharyngeal constrictors and therefore are responsible for maintaining airway patency in the awakened state. Electromyography, however, has demonstrated marked depression of genioglossus activity, especially during the REM sleep, predisposing to upper airway obstruction in the retroglossal segment of the upper airway. The contribution of upper airway dilator muscle activity to the pathogenesis of OSA is now well recognized. The specifics of the GAHM procedure have already been mentioned. The alternative to the advancement of the genial tubercles is the advancement of the entire inferior border of the mandibular symphysis, which apart from the insertions of the genioglossus muscles also bears the insertions of the geniohyoid and the anterior bellies of the digastric muscles. This procedure is performed in exactly the same manner as a genioplasty, and the advanced segment is rigidly fixed

in position with the help of prebent titanium advancement plates. The procedure has a cosmetic advantage in retrognathic individuals, and because the advanced segment has a bigger vascular pedicle through the lingual muscular insertions, fewer complications in terms of osseous necrosis and wound breakdown are expected with it. Most patients referred for MMA have failed other forms of treatment or have not been compliant with home CPAP therapy and continue to suffer from fragmented sleep and excessive daytime somnolence. They usually have had upper airway reconstructive surgery in the form of UPPP with poor results. As a result, these patients are indicated for MMA surgery because this procedure is considered to be the best alternative to CPAP therapy, especially for obese patients refractory to other forms of treatment. Rarely, a patient presents without prior history of palatal surgery. Often he or she has a normal BMI; however, abnormal craniofacial morphology is demonstrated

Fig. 1. Standard dental models mounted on an articulator are used to fabricate a surgical advancement splint of the mandible (approximately 10 mm). Symmetric left and right movement with proper midlines and buccal overjet is important to reduce rotation.

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clinically and cephalometrically (mandibular or maxillomandibular hypoplasia with narrowed posterior airway space at the level of the base of the tongue). Tracheostomy is performed as a temporary measure in morbidly obese patients when control of the airway with conventional methods is problematic and risky. These patients are decannulated postoperatively when the concern of airway loss secondary to upper airway edema or hematoma ceases to exist. The genial tubercle advancement procedure has come into disfavor because of problems relating to postoperative infection, wound breakdown, or necrosis of the osteotomized and advanced segment. Furthermore, this procedure does not advance the digastric and geniohyoid muscles because their insertions are not included in the osteotomized segment. In our institution geniotomy advancement has replaced genial tubercle advancement as a less morbid and more effective procedure in regard to relieving retroglossal obstruction and suspending the hyoid bone in a more anterior and superior

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position. Midline glossectomy and nasal surgery (septoplasty, turbinectomy) are used as adjunctive procedures in selected patients with macroglossia and nasal obstruction, respectively.

Surgical technique of MMA MMA surgery is performed with the following sequence of procedures: Initially bilateral sagittal split osteotomies mobilize the tooth-bearing portion of the mandible, which is advanced to the desired extent (usually 10 mm) and is temporarily held in this position with the help of a prefabricated advancement splint and maxillomandibular fixation with elastic bands, stainless steel wires, or both. A prefabricated acrylic occlusal splint is made on dental models and simple articulator to symmetrically advance the mandible (10 mm) (Fig.1). In this advanced position the mandibular osteotomies are rigidly fixed using bicor-

Fig. 2. Banked tibial bone is often used as an interpositional bone graft. It is perfectly cut to fit into the maxillary osteotomy and be rigidly fixed so as not to be displaced into the maxillary sinus.

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tical positional screws. Two or three screws are required for rigid internal fixation on each side, and they are introduced in a perpendicular fashion to the bone surface with the help of stab incisions on the cheeks and a transbuccal trocar. The maxillomandibular fixation is then released, the intermediate advancement splint is removed, and the maxillary LeFort I osteotomy is performed. After maxillary downfracture and complete mobilization of the maxilla, the nasal septum and inferior turbinates are addressed. The maxillary segment is then advanced to the appropriate dental occlusion with the mandibular teeth, and in this position 2.0 prebent advancement plates are used for maxillary rigid internal fixation. A bone graft is mortised into the lateral wall of the maxilla and fixated into the advancement plate (Figs.2 – 4). The combination of these fixation plates with allogeneic cortical block grafts (eg, banked tibia) along the maxillary osteotomies is considered necessary to minimize the possibility of postoperative complications such as nonunion of the osteotomized segments or relapse secondary to stretching of the soft tissue drape after such extensive advancements. SurFig. 4. The tibial bone graft is tapered like a wedge so that it will fit tightly into the osteotomy gap and then can be rigidly fixed into the maxillary plates.

gery is concluded with the advancement geniotomy procedure for maximum results.

Changes in upper airway dimensions and configuration after MMA as demonstrated with helical CT scanning

Fig. 3. The bone graft is mortised into the osteotomy gap after initial fixation. Note the bone is resting over the anterior plate and extending behind the maxilla. The two screws have not yet been secured into the graft.

Seven adult OSA patients have undergone surgical treatment by MMA, and the results of preoperative and postoperative polysomnograms and preoperative and postoperative helical CT scans of the upper airway have been evaluated. A retrospective study evaluating the change in upper airway dimensions and configuration resulting from advancement of the maxillomandibular complex has been performed. The polysomnographic evaluation took place at least 2 months after the surgery. All patients had severe sleep apnea expressed as RDIs ranging from 47 events per hour to 134 events per hour (mean, 71.86 per hour). Their preoperative LSATs were recorded in the range of 55% to 88% (mean, 79%). The patients also underwent CT scanning of the upper airway with axial 5 mm cuts from the skull base down to the level of the trachea. All CT scans were obtained in the same

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radiology department of the University of Alabama at Birmingham by using third-generation helical CT scanners. The postoperative scans were obtained at least 2 months after the surgery. For the scans the patients were placed in the gantry with the tragocanthal line perpendicular to the ground. Scanning times with the helical CT scanners were less than 15 seconds. The patients were instructed to breathe normally and to avoid swallowing during the scanning process. Flexible fiberoptic nasopharyngoscopy with Mueller’s maneuver to identify sites of airway collapse with inspiratory effort and lateral cephalometric radiographs to identify abnormal craniofacial and upper airway soft tissue morphology were also included in the preoperative evaluation. The patients were divided into two groups according to their response to MMA by using the postoperative polysomnographic data. In the group of the good responders were included patients who had >50% decrease of their preoperative RDI with the procedure. The patients who did not meet this criterion of success were included in the group of poor

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responders. The purpose was to correlate posterior airway space changes by CT scanning with polysomnogram results. Acquisition of the data was performed with the help of an experienced radiology technician. The raw CT data saved in optical disk were retrieved. The preoperative and postoperative upper airway of each patient was studied starting at the level of the hard palate (level 0) and continuing caudally 10, 20, 30, 40, 50, 60, and 70 mm (levels 1 through 7, respectively) below that level until the body of the hyoid bone was visualized (Fig. 5). A set of three values was obtained at each airway level: (1) Anteroposterior (AP) dimension on the midsagittal plane (Fig.6); (2) maximum lateral dimension (LAT) in an orientation perpendicular to the midsagittal plane (Fig.7); and (3) cross-sectional area of the airway (CSA) (Fig.8). The measurement of the CSA was performed simply by following the perimeter of the airway with the cursor. No tracing or digitizing of the axial images was required (as in older CT studies) because the software available automatically calculated the

Fig. 5. Lateral neck scout view. Examination of the airway starts at the level of the hard palate and continues inferiorly down to the level of the hyoid bone in 5 mm axial cuts.

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Fig. 6. Method for measurement of the AP dimension of the airway.

area contained within the scribbled line. We were also interested in measuring the amount of maxillary advancement. Analysis of the results was performed using descriptive statistics (minimum, maximum, mean, and standard deviation). To calculate statistical significance in upper airway dimensional change resulting from MMA, the means procedure was used, which involved the application of a t-test. No statistical comparisons were attempted between the groups of the good and poor responders because the latter did not include an adequate number of subjects [36]. Demographic, anthropometric, preoperative, and postoperative polysomnographic data of the studied patient group are summarized in Tables 2 and 3. In the group of patients who had a good response to MMA (five out of seven), the mean preoperative RDI was 81 per hour and the mean postoperative RDI was 22 per hour. Overall, the group of the good responders experienced a mean decrease of 57 events per hour of sleep in their RDI. In the group of patients with a poor response to MMA (two out of seven), the mean preoperative RDI

was 53 per hour and the mean postoperative RDI was 45 per hour. One patient in this group experienced significant improvement in the RDI (from 51 per hour to 35 per hour) and an even more significant improvement in the LSAT (from 68% to 83%). The other patient of this group had the same postoperative RDI as preoperatively (55 per hour). Both of the poor responders were obese. The mean preoperative and postoperative CT data of the AP and LAT of the upper airway demonstrated an increase at all levels. The mean airway CSA also increased at all levels after surgery. Statistically significant differences existed for levels at the hard palate and high retropalatal area. This study also looked into the ratio of the LAT dimension to the AP dimension of the upper airway. At all levels the postoperative LAT/AP ratio was less than the preoperative, except for level 3 (high retroglossal area). At this level MMA stretched the airway in a more lateral than in AP fashion; however, the difference was not statistically significant for this level. The quantitative effect of MMA on the LAT/AP dimension ratio at each level of the upper airway was

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395

Fig. 7. Method for measurement of the LAT of the airway.

analyzed. The three patients who demonstrated the best result with a postoperative RDI of less than 20 events per hour appeared to have an airway that was stretched laterally at higher levels (hard palate and retropalatal area). At lower levels (retroglossal area and hypopharynx), their airway was stretched more in an AP fashion. Furthermore, the two patients who experienced >50% decrease in their RDI appeared to have a postoperative airway that demonstrated lateral stretching at more inferior levels compared to the previously mentioned group of patients with the best surgical result.

Discussion and conclusions MMA increases both the AP and the LAT dimensions of the upper airway. The CSA was also increased in all levels. Shepard and Thawley [12] studied the effect of UPPP on the upper airway by using CT. In this study UPPP increased upper airway caliber only at levels 1 and 2 (10 and 20 mm below the level of the hard

palate, respectively) with statistical significance. At level 3 (30 mm below the level of the hard palate), there was a nonsignificant increase in upper airway CSA. In the retroglossal and hypopharyngeal areas (50, 60, and 70 mm below the level of the hard palate), however, the CSA of the airway was significantly smaller postoperatively than preoperatively [12]. MMA increases the CSA along the entire length of the airway by increasing both its AP and LAT dimensions. Skeletal advancement has a significant impact on the volume of the airway when described as a tube. Greater volume results in less resistance against the passage of air. Increase in airway caliber is not followed by proportionate decrease in resistance. The expected decrease in resistance is far greater than that because resistance is inversely proportional to the fourth power of the radius of the airway [26]. According to Prinsell, [29] MMA pulls forward the anterior pharyngeal tissues attached to the maxilla, mandible, and hyoid bone, thereby enlarging the entire velopharynx. The procedure is associated with minimal risks of edema-induced upper airway embarrassment or pharyngeal dysfunction.

396

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Fig. 8. Method for measurement of the CSA of the airway.

There should not be a concern that by advancing the maxillomandibular complex, the airway would be

stretched merely in an AP fashion, bringing the lateral pharyngeal walls closer together toward the midline.

Table 2 Demographic, anthropometric, preoperative, and postoperative polysomnographic data of the patients with good response to maxillomandibular advancement Age, race Patient gender BMI TP PG DC

45 CF 56 CF

Surgical history

55.04 None 16.46 Mandibular setback 48 AAM 45.76 UPPP, septoplasty

GC

57 CM

WB

60 CM

MEAN 53.2

Primary Adjunctive surgical surgical procedure procedure

Date of surgery

MMA MMA

None None

11-Aug-00 134 26-Jul-00 47

88 87

15 5

83 89

11 11

MMA

Geniotomy adv., 12-Jan-00 60 adenoids, turbinates geniotomy adv. 08-Dec-99 100

55

16

79

11

87

47

78

10

Turbinates

88

27

87

7

79.4 81

22

83.2

27.67 Tonsillectomy, MMA nasal Sx 27.65 UPPP, MMA septoplasty 34.52

05-May-99

2

Preop Preop Postop Postop Maxilla RDI LSAT RDI LSAT advance

56

10

Abbreviations: AAM, African-American male; BMI, body mass index (kg/m ); CF, caucasion female; CM, caucasion male; LSAT, lowest hemoglobin oxygen saturation (%); maxilla advance, maxillary advancement (mm); RDI, respiratory distress index (events per hour of sleep).

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397

Table 3 Demographic, anthropometric, preoperative, and postoperative polysomnographic data of the patients with poor response to maxillomandibular advancement Age, race, Patient gender BMI

Surgical history

Primary Adjunctive surgical surgical procedure procedure

SE

38 CM

31.53 UPPP

RJ

38 CM

31.69 UPPP, MMA septoplasty 31.61

MEAN 38

MMA

Date of surgery

Preop Preop Postop Postop Maxilla RDI LSAT RDI LSAT advance

Geniotomy adv., 11-Oct-00 51 septum, turbinates Turbinates 28-Apr-99 55

68

35

83

10

80

55

85

7

53

74

45

84

8.5

Abbreviations: BMI, body mass index (kg/m2); CM, Caucasian male; LSAT, lowest hemoglobin oxygen saturation (%); Maxilla advance, maxillary advancement (mm); RDI, respiratory distress index (events per hour of sleep).

This would place the airway at even greater risk of LAT collapse. Therefore, MMA resembles nasal CPAP, which acts as a pneumatic splint forcing the airway open by its continuous air column [37]. If, however, MMA enlarges the upper airway of sleep apneic patients with less resistance in airflow, then how can failure to respond be explained? A decrease in the postoperative LAT/AP ratio mathematically meant that the AP dimension of the airway increased or the LAT dimension decreased or both. It could also happen if both dimensions decreased; however, the LAT dimension should have decreased more than the AP dimension. The same result could also appear if both dimensions increased postoperatively; however, the AP dimension should have increased more than the LAT dimension. In any case, the net effect on the configuration of the airway would have been an AP stretching. In contrast, using the same logic as before, an increase in the postoperative LAT/AP ratio would result in a lateral stretch of the upper airway postoperatively. In patients in whom a postoperative RDI < 20 events per hour was achieved, the upper airway was stretched with MMA in a LAT orientation in higher levels (hard palate and retropalatal area); however, in lower levels (retroglossal area and hypopharynx), the upper airway was stretched more in an AP fashion. In patients in whom a poorer response to MMA was achieved, judging by a decrease in their RDI of at least 50%, the upper airway demonstrated this LAT stretching in more inferior levels compared to patients with the best result. Finally, the patient who did not respond to MMA at all, judging from equal preoperative and postoperative RDIs, demonstrated AP stretching of the upper airway at all levels, except the very last one in the hypopharyngeal area, where the stretching was evident more in the LAT orientation. It seems that LAT stretching has a high correlation with OSA improvement.

Success of upper airway surgery depends not only on enlargement of the CSA but also on the shape of the airway. Increase in the LAT dimension appeared to be of far greater importance than increase in the AP dimension. This observation is in agreement with conclusions made by Schwab et al [9] and Leiter [38]. Patients with poor response to MMA often have had a UPPP. It is possible that in these patients the failure of the airway to stretch laterally in the crucial retropalatal area may have been caused by scarring, making the tissues of the lateral pharyngeal walls stiffer and thus less responsive to advancement. Experience with cleft palate and UPPP patients shows that full mobilization of the maxilla becomes problematic when the soft palatal pedicle is scarred from previous surgical procedures. It is interesting to note that in this series of patients, the one with the most spectacular response to MMA (preoperative RDI of 134 per hour improving to a postoperative RDI of 15 per hour) did not undergo adjunctive upper airway reconstructive procedures such as UPPP or sliding geniotomy advancement. In addition, this patient was morbidly obese, with the highest BMI (55.04 kg/m2) in the entire group, and the preoperative lateral cephalometric radiograph did not reveal maxillomandibular hypoplasia. CT evaluation did show significant change in posterior airway space. Kato et al [39] used oral appliances to advance the mandible of patients with sleep-disordered breathing in a stepwise fashion (2, 4, and 6 mm). Their study showed that there was a dose-dependent effect of mandibular advancement on pharyngeal mechanics and nocturnal oxygenation. A 20% improvement of the oxygen desaturation index (ODI: number of oxygen drops >4% from the baseline) and of the CT90 (percentage of time spent at arterial oxygen saturation < 90%) could be expected for each 2-mm advancement of the mandible. In their study ODI was significantly associated with the higher PCRIT (airway

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luminal pressure below which airway collapse occurs) values, indicating that improvement of collapsibility of the passive pharynx, mainly at the velopharyngeal level, resulted in improvement of nocturnal oxygenation. When the application of oral devices reduced the PCRIT below atmospheric pressure, ODI decreased to < 10 per hour. By contrast, ODI remained >10 per hour when the PCRIT remained above atmospheric pressure even with oral appliances. The authors [39] concluded that anterior tongue displacement caused by mandibular (genial tubercle) advancement might decrease the external pressure to the soft palate produced by posterior movement of the tongue base (especially in the supine position). Alternatively, anterior tongue displacement might stiffen the velopharynx through the palatoglossal arch, which connects the tongue base to the lateral wall of the soft palate. Mandibular advancement significantly decreased the PCRIT at the retroglossal and the retropalatal (velopharyngeal) area of the oropharynx. The fact that mandibular advancement affects airway anatomy higher up in the airway than expected has also been demonstrated earlier by Isono et al [40]. No attempt has been made yet to study passive pharyngeal mechanics before and after MMA as Isono et al [40] have done for oral appliances. In addition to the relief of anatomic obstruction with mandibular advancement and subsequent forward displacement of the tongue, collapsibility of the pharynx is improved by ‘‘stiffening’’ of the pharyngeal walls through the stretching of the palatoglossus muscle. With MMA, it is not only the tongue that is displaced forward; the soft palate is also advanced, and a second influence on pharyngeal wall mechanics can certainly be hypothesized through the palatopharyngeus muscle. Future Ct or MRI studies are needed to compare the two currently most important surgical approaches for reconstruction of the sleep apneic airway: MMA and UPPP. There is definitively a place for both in our armamentarium; however, it appears that the indications for the former are more frequent than the ones for the latter. It would be very useful but also ambitious to compare the two procedures to nasal CPAP therapy on weight-matched subjects in a prospective randomized fashion.

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sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993;108:117 – 25. Collop NA, Block JA, Hellard D. The effect of nightly nasal CPAP treatment on underlying obstructive sleep apnea and pharyngeal size. Chest 1991;99:855 – 60. 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. Tiner BD. Surgical management of obstructive sleep apnea. J Oral Maxillofac Surg 1996;54:1109 – 14. Simmons FB, Guilleminault C, Silvestri R. Snoring, and some obstructive sleep apnea, can be cured by oropharyngeal surgery. Arch Otolaryngol 1983;109:503. Ikematsu T. Study of Snoring, 4th Report. Therapy (in Japanese) Jpn Oto-Rhino-Laryngol 1964;64:434 – 5. Fugita S, Conway W, Zorick F, et al. Surgical correction of anatomic abnormality in obstructive sleep apnea syndrome: Uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981;89:923 – 34. Sher AE. The role of maxillomandibular surgery for treating obstructive sleep apnea. Sleep 1996;19:S88 – 9. Schwab RJ, Gefter WB, Hoffman EA, et al. Dynamic upper airway imaging during awake respiration in normal subjects and patients with sleep disordered breathing. Am Rev Respir Dis 1993;148:1385 – 400. Schwab RJ, Gupta KB, Gefter WB, et al. Upper airway and soft tissue anatomy in normal subjects and in patients with sleep-disordered breathing: significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995;152:1673 – 89. Ryan CF, Lowe AA, Li D, et al. Three-dimensional upper airway computed tomography in obstructive sleep apnea. Am Rev Respir Dis 1991;144:428. Stein MG, Gamsu G, DeGeer G, et al. Cine CT in obstructive sleep apnea. AJR Am J Roentegnol 1987; 148:1069 – 74. Shepard JW, Thawley SE. Evaluation of the upper airway by computerized tomography in patients undergoing uvulopalatopharyngoplasty for obstructive sleep apnea. Am Rev Respir Dis 1989;140:711 – 6. Launois SH, Feroah WN, Campbell FG, et al. Site of pharyngeal narrowing predicts outcome of surgery for obstructive sleep apnea. Am Rev Respir Dis 1993;147: 182 – 9. Suto Y, Matsuo T, Kato T, et al. Evaluation of the pharyngeal airway in patients with sleep apnea: value of ultrafast MR imaging. AJR Am J Roentgenol 1993;160:311 – 4. Shepard JW, Thawley SE. Localization of upper airway collapse during sleep in patients with obstructive sleep apnea. Am Rev Respir Dis 1990;141:1350 – 5. Morrison DL, Launois SH, Isono S, et al. Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea. Am Rev Respir Dis 1993;148: 606 – 11. Sher AE, Thorpy MJ, Shprintzen RJ, et al. Predictive value of the Mueller maneuver in selection of patients

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for uvulopalatopharyngoplasty. Laryngoscope 1985; 95:1483 – 7. Riley RW, Powell NB, Guilleminault C. Maxillary, mandibular, and hyoid advancement for treatment of obstructive sleep apnea: a review of 40 patients. J Oral Maxillofac Surg 1990;48:20 – 6. Ryan CF, Lowe AA, Li D, et al. Three-dimensional upper airway computed tomography in obstructive sleep apnea. Am Rev Respir Dis 1991;144:428. Riley RW, Powell NB, Guilleminault C. Inferior sagittal osteotomy of the mandible with hyoid myotomysuspension: a new procedure for obstructive sleep apnea. Otolaryngol Head Neck Surg 1986;94:589 – 93. Guyette RF, Waite PD. Adjunctive surgical procedures in obstructive sleep apnea. Oral Maxillofac Surg Clin North Am. 1995;7:301 – 10. Li KK, Powell NB, Riley RW, et al. Morbidly obese patients with severe obstructive sleep apnea: is airway reconstructive surgery a viable treatment option? Laryngoscope 2000;110:982 – 7. Bear SE, Priest JH. Sleep apnea syndrome: correction with surgical advancement of the mandible. J Oral Surg 1980;38:543. Kuo PC, West RA, Bloomquist DS, et al. The effect of mandibular osteotomy in three patients with hypersomnia sleep apnea. Oral Surg Oral Med Oral Pathol 1979;48:385. Waite PD, Wooten V, Lachner J, et al. Maxillomandibular advancement surgery in 23 patients with obstructive sleep apnea syndrome. J Oral Maxillofac Surg 1989;47:1256 – 61. Waite PD, Shettar SM. Maxillomandibular advancement surgery: a cure for obstructive sleep apnea syndrome. Oral Maxillofac Surg Clin North Am. 1995;7: 327 – 36. Paoli JR, Lauwers F, Lacassagne L, et al. Treatment of obstructive sleep apnea syndrome with mandibular elongation using osseous distraction followed by Le Fort I advancement osteotomy: case report. J Oral Maxillofac Surg 2001;59:216 – 9. Hochban W, Brandenburg U, Peter JH. Surgical treat-

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Oral Maxillofacial Surg Clin N Am 14 (2002) 401 – 404

Postoperative management of the obstructive sleep apnea patient Kasey K. Li, MD, DDS*, Nelson Powell, MD, DDS, Robert Riley, MD, DDS Center for Excellence in Sleep Disorders Medicine, Stanford University Medical School, 401 Quarry Road Stanford, CA 94305, USA

It is now well accepted that disproportionate anatomy of the upper airway exists in obstructive sleep apnea (OSA), which leads to obstruction during sleep [1 – 3]. Recognizing that most patients with OSA have more than one site of obstruction in the upper airway, modern surgical approach for the treatment of OSA focuses on multiple sites in the upper airway, including the nose, palate (pharynx), and base of tongue (hypopharynx) [4,5]. Although this treatment approach has achieved a higher cure rate, the risk of postoperative airway compromise may be increased owing to surgically induced edema in multiple regions. In addition to the surgically induced edema, muscle atonia and altered respiration due to general anesthesia and narcotic use further increase the risk in these patients who already have a compromised airway. Indeed, acute airway obstruction after the use of sedatives has been reported in patients with OSA [6,7]. On the basis of a national survey, Fairbanks [8] reported 16 postoperative deaths and 7 near-death incidences after OSA surgery. The most common causes of these catastrophic complications were oversedation and surgical edema. In a retrospective review of 135 patients who had OSA surgery, Esclamando and colleagues [9] identified many complications including death, failed intubation, airway obstruction after extubation, hemorrhage, and arrhythmia. Indeed, patients undergoing OSA surgery often have comorbid issues, especially cardiovascular disease, which

* Corresponding author. 750 Welch Road, Suite 317, Palo Alto, CA, USA. Email-address: [email protected] (K.K. Li).

can complicate treatment. Based on a retrospective review of 182 patients who had OSA surgery, Riley et al [10] identified 31% (56 patients) with hypertension, 5.5% (10 patients) with arrhythmia, and 3.3% (6 patients) with a history of myocardial infarction. Clearly, many factors can complicate the postoperative management of OSA patients. It is imperative for the sleep surgeon to take necessary precautions to minimize complications. To ensure patient safety, a surgical risk-management protocol was developed at our center in 1988, which included ICU monitoring on the first postoperative day, the use of nasal continuous positive airway pressure (CPAP) for airway protection during sleep and after discharge, aggressive hypertension management, and a criterion for the administration of analgesics. In recent years, this protocol has been revised to include preoperative and postoperative fiberoptic airway evaluation.

The Stanford risk management protocol Nasal CPAP The prevention of airway complication is of utmost importance. Therefore, we use nasal CPAP extensively in this protocol for airway protection [11]. Nasal CPAP should be attempted at least 2 weeks before surgery to reverse sleep debt. Nasal CPAP should be readily available at all times during the hospitalization. We routinely place the nasal CPAP immediately after surgery, not only while the patient is asleep but also during wakefulness to minimize edema formation and prevent REM rebound in the postoperative period.

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 3 2 - 8

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All patients are maintained on humidified oxygen (35%) by a fact tent. Oximetry is monitored throughout the hospitalization. In patients who cannot tolerate short-term nasal CPAP use, home oxygen after discharge is often prescribed in those with a respiratory disturbance index (RDI) greater than or equal to 40 and oxygen desaturation of 80% or less.

the use of narcotics, and the different OSA procedures performed through semiannual lectures. Finally, patient-controlled analgesia is not used because of the possibility of oversedation. Upon transfer to the ward on the first postoperative day, intramuscular meperidine HCl and oxycodone elixir are used. Oral hydrocodone is used after discharge.

Tracheotomy Temporary tracheotomy is considered in patients who have a difficult airway, such as with the presence of severe OSA (RDI > 60 and SaO2 < 60), morbid obesity, or significant craniofacial abnormality. Intubation/extubation All patients are induced and intubated with the surgeon present. A fiberoptic intubation with the patient awake is performed if there are any concerns about the airway based on the craniofacial anatomy, body habitus, the severity of OSA, or preoperative fiberoptic airway examination. At the completion of the surgery, wakefulness is confirmed in all patients by the ability to follow commands. All patients are extubated in the operating room. ICU utilization ICU stay is routine in patients with significant comorbid factors such as cardiovascular problems and in patients undergoing multiple procedures such as combining uvulopalatoplasty and genioglossus advancement. This practice maximizes our ability to detect any respiration abnormality, oversedation, or excessive airway edema. Furthermore, hypertension is aggressively treated with intravenous antihypertensive medications to minimize edema development. If necessary, blood pressure monitoring by arterial line is used. On the first postoperative day, all patient are evaluated before transfer to the ward. Obviously, transfer is delayed if there are any concerns of excessive airway edema. Analgesic use Intravenous analgesics such as morphine sulfate or meperidine HCl are used in the ICU. Intravenous medications are administered in graduated doses by the nursing staff (eg, morphine sulfate, 1 to 8 mg every 1 to 2 hours as necessary) while the signs for oversedation are monitored. The nursing and ICU staffs are educated regarding the mechanism of OSA,

Fig. 1. (A) Fiberoptic view prior to UPPP/tonsillectomy/GA. (B) Fiberoptic view at 48 hours after surgery. Note the airway obstruction due to soft palate/pharyngeal edema. (From Li KK, Riley RW, Powell NB, Zonato A. Fiberoptic nasopharyngoscopy for airway monitoring following obstructive sleep apnea surgery. J Oral Maxillofac Surg 2000; 58:1342 – 5; with permission.)

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403

Discharge/fiberoptic examination

Conclusion

The requirements for discharge are adequate oral intake, satisfactory pain control, and stable airway; however, airway compromise remains a concern after discharge, as it can occur 36 hours after surgery [8,12]. Therefore, we now routinely examine the patient’s airway with a fiberoptic scope before discharge [13,14]. Based on a review of 271 patients who had postoperative fiberoptic airway examination during a 24-month period, we have increased our understanding of the postsurgical edema patterns. It was apparent that varying degrees of soft tissue edema involving the soft palate and tongue base occurred in all of the patients who underwent uvulopalatoplasty and genioglossus advancement or hyoid myotomy. Patients who had tonsillectomies combined with uvulopalatopharyngoplasty had a greater soft palate/ pharyngeal wall edema compared to patients without tonsillectomies (Fig.1) [13]. Interestingly, a different edema pattern was noted in the patients after maxillomandibular advancement (MMA), with varying degrees of lateral pharyngeal wall edema identified. Furthermore, hypopharyngeal hematoma involving the pyriform sinus, aryepiglottic fold, arytenoid, and false vocal cord that partially obstructed the airway have been noted (Fig. 2).

The postoperative care of the OSA patient presents a formidable challenge to the sleep surgeon. In addition to all of the comorbid issues that are commonly found, edema is an unavoidable process after surgery, and postoperative airway edema in patients with an already compromised airway presents a major concern. Johnson and Sanders [12] and Burgess and colleagues [15] found that the respiratory disturbance index and the nadir oxygenation saturation may be adversely affected after uvulopalatoplasty in the first and second postoperative day. Fairbanks [8] and Esclamado et al [9] have reported airway complications leading to death shortly after uvulopalatopharyngoplasty and associated procedures. The oral and maxillofacial surgeon who treats OSA patients must have a thorough understanding of the possible consequences and a complication avoidance strategy after surgery. Vigilance must be practiced.

Fig. 2. Unilateral hematoma obscuring the left arytenoid (open arrow). Note the right arytenoid (arrowhead) and the epiglottis (arrow). (From Li KK, Riley RW, Powell NB, Zonato A. Fiberoptic nasopharyngoscopy for airway monitoring following obstructive sleep apnea surgery. J Oral Maxillofac Surg 2000; 58:1342 – 5; with permission.)

References [1] Rojewski TE, Schuller DE, Clark RW, et al. Videoendoscopic determination of the mechanism of obstruction in obstructive sleep apnea. Otolaryngol Head Neck Surg 1984;92:127 – 31. [2] Rivlin J, Hoffstein V, Kalbfleisch J, et al. Upper airway morphology in patients with idiopathic obstructive sleep apnea. Am Rev Respir Dis 1984;129:355 – 60. [3] Remmers JE, DeGrott WJ, Sauerland EK, et al. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978;44:931 – 8. [4] Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C. Overview of phase I surgery for obstructive sleep apnea syndrome. Ear Nose Throat J 1999;78:836 – 45. [5] Li KK, Riley RW, Powell NB, Troell RJ, Guilleminault C. Overview of phase ii surgery for obstructive sleep apnea syndrome. Ear Nose Throat J 1999;78:851 – 7. [6] Simmons FB, Guilleminault C, Dement WC, et al. Surgical management of airway obstruction during sleep. Laryngoscope 1977;87:326 – 38. [7] Hishikawa Y, Furuya E, Wakamatsu H, et al. A polygraphic study of hypersomnia with periodic breathing and primary alveolar hypoventilation. Bull Physiopathol Respir 1970;8:1139 – 42. [8] Fairbanks DNF. Uvulopalatopharyngoplasty complications and avoidance strategies. Otolaryngol Head Neck Surg 1990;102:239 – 45. [9] Esclamando RM, Glenn MG, McCulloch TM, Cummings CW. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope 1989;99:1125 – 9. [10] Riley RW, Powell NB, Guilleminault C, Pelayo R, Troell RJ, Li KK. Obstructive sleep apnea surgery: risk

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management and complications. Otolaryngol Head Neck Surg 1997;117:648 – 52. [11] Powell NB, Riley RW, Guilleminault C. Obstructive sleep apnea, continuous positive pressure, and surgery. Otolaryngol Head Neck Surg 1988;99:362 – 9. [12] Johnson JT, Sanders MH. Breathing during sleep immediately after uvulopalatopharyngoplasty. Laryngoscope 1986;96:1236 – 8. [13] Li KK, Riley RW, Powell NB, Zonato A. Fiberoptic nasopharyngoscopy for airway monitoring following

obstructive sleep apnea surgery. J Oral Maxillofac Surg 2000;58:1342 – 5. [14] Li KK, Powell NB, Riley RW, Zonato A, Troell R, Guilleminault C. Post-operative airway findings after maxillomandibular advancement for obstructive sleep apnea syndrome. Laryngoscope 2000;110:325 – 7. [15] Burgess LPA, Derderian SS, Morin GV, Gonzalez C, Zajtchuk JT. Postoperative risk following uvulopalatopharyngoplasty for obstructive sleep apnea. Otolaryngol Head Neck Surg 1992;106:81 – 6.

Oral Maxillofacial Surg Clin N Am 14 (2002) 405 – 409

Index Note: Page numbers of article titles are in boldface type.

Alcohol intake, and sleep-disordered breathing, 298

Continuous positive airway pressure for obstructive sleep apnea syndrome, 276, 312 – 313, 385 postoperative, 401 – 402 for sleep-disordered breathing, 299 – 301

Anesthesia, in laser therapy, for obstructive sleep apnea syndrome, 321 – 322

Coronary heart disease, obstructive sleep apnea syndrome and, 279

Anterior mandibular osteotomy, for obstructive sleep apnea syndrome, 355, 379 – 381

CPAP PRO system, for sleep-disordered breathing, 301 – 302

A Airway compromise, after laser therapy, for obstructive sleep apnea syndrome, 328

Apnea-hypopnea index, in patient evaluation, for sleep-disordered breathing, 351 B Benzodiazepines, and sleep-disordered breathing, 298 Bilevel positive airway pressure, for sleep-disordered breathing, 301 Bleeding, after laser therapy, for obstructive sleep apnea syndrome, 327 C Carbon dioxide laser therapy, for obstructive sleep apnea syndrome, 373 Cardiovascular disease, obstructive sleep apnea syndrome and, 279 Cautery-assisted palatal stiffening surgery, for obstructive sleep apnea syndrome, 389 Cephalometric radiography, in patient evaluation, for sleep-disordered breathing, 353 – 354 Cerebrovascular disease, obstructive sleep apnea syndrome and, 279 Cigarette smoking, and sleep-disordered breathing, 298 Coblation system, for obstructive sleep apnea syndrome, 336, 338 – 341, 343 – 344 Computed tomography, in patient evaluation, for sleep-disordered breathing, 354

E Electrical stimulation, for obstructive sleep apnea syndrome, 276 Ellmad system, for obstructive sleep apnea syndrome, 336 – 337 Ellman system, for obstructive sleep apnea syndrome, 336 – 337 Endoscopic pharyngoscopy, in patient evaluation, for sleep-disordered breathing, 352 – 353 Esmarch prosthesis, for obstructive sleep apnea syndrome, 311 Extubation, after surgery, for obstructive sleep apnea syndrome, 402 F Fiberoptic examination, after surgery, for obstructive sleep apnea syndrome, 403 G Genioglossus muscle advancement for obstructive sleep apnea syndrome, 377 – 384, 387 anterior mandibular osteotomy in, 355, 379 – 381 historical aspects of, 377 inferior sagittal osteotomy in, 377 – 379 trephine osteotomy in, 381 – 383 for sleep-disordered breathing, 355

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 6 5 - 1

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Index / Oral Maxillofacial Surg Clin N Am 14 (2002) 405–409

Globus, after laser therapy, for obstructive sleep apnea syndrome, 328 Glossectomy, for obstructive sleep apnea syndrome, 373 – 374 H Harmonic Scalpel, for obstructive sleep apnea syndrome, 344 – 348 results of, 347 – 348 technique for, 345 – 347 Herbst oral appliance, for obstructive sleep apnea syndrome, 309 – 310 Hyoepiglottoplasty, for obstructive sleep apnea syndrome, 374 Hyoid suspension for obstructive sleep apnea syndrome, 374, 387 for sleep-disordered breathing, 355 Hypertension obstructive sleep apnea syndrome and, 279 sleep-disordered breathing and, 298 Hypocapnic apneic threshold, in sleep, 287

polysomnography before, 320 – 321 uvulopalatopharyngoplasty, 325, 339, 348 clinical studies of, 329 – 330 complications of, 327 – 329 postoperative care for, 326 – 327 uvulopalatoplasty, 321 – 323, 325, 348, 367, 389 anesthesia in, 321 – 322 clinical studies of, 329 – 330 complications of, 327 – 329 postoperative care for, 326 – 327 safety in, 322 technique for, 322 – 323, 325 Lingualplasty, for obstructive sleep apnea syndrome, 373 Load compensation, loss of, in sleep, 286 M Magnetic resonance imaging, in patient evaluation, for sleep-disordered breathing, 354 – 355 Mandibular repositioners, for obstructive sleep apnea syndrome, 311

Hypopharyngeal surgery, for obstructive sleep apnea syndrome. See Soft tissue hypopharyngeal surgery.

Maxillomandibular advancement for obstructive sleep apnea syndrome, 387 – 388, 390 – 398 for sleep-disordered breathing, 355 – 356

Hypothyroidism, and sleep-disordered breathing, 298 – 299

Muller’s maneuver, in patient evaluation, for sleepdisordered breathing, 353 Muscular factors, in sleep, 290 – 291

I Infections, after laser therapy, for obstructive sleep apnea syndrome, 328 Inferior sagittal osteotomy, for obstructive sleep apnea syndrome, 377 – 379 Intubation, after surgery, for obstructive sleep apnea syndrome, 402 K Klearway oral appliance, for obstructive sleep apnea syndrome, 310 – 311 L Laser midline glossectomy, for obstructive sleep apnea syndrome, 373 Laser therapy, for obstructive sleep apnea syndrome, 319 – 331 evaluation for, 320 – 321 historical aspects of, 319 – 320

N Nasal examination, in patient evaluation, for sleepdisordered breathing, 352 Nasal obstruction, radio-ablation of, 341 – 344 Nasal surgery, for obstructive sleep apnea syndrome, 366, 388 Nasopharyngeal surgery, for obstructive sleep apnea syndrome, 388 – 389 Nonrapid eye movement sleep, in obstructive sleep apnea syndrome, 285 O Obesity and obstructive sleep apnea syndrome, 278 and sleep-disordered breathing, 299 Obstructive sleep apnea syndrome, 273 – 283. See also Sleep-disordered breathing. and cardiovascular disease, 279

Index / Oral Maxillofacial Surg Clin N Am 14 (2002) 405–409

and cerebovascular disease, 279 and coronary heart disease, 279 and hypertension, 279 and stroke, 279 complications of, 279 epidemiology of, 276 – 279 age in, 277 gender in, 277 – 278 obesity in, 278 race in, 278 future directions in, 279 – 280 historical aspects of, 273 – 275 in 1970s and 1980s, 273 – 275 in pregnancy, 278 laser therapy for . See Laser therapy medical treatment of, 275 – 276 oral appliances for . See Oral appliances. pathophysiology of, 285 – 292, 333 REM sleep in, 287 upper airway obstruction in, 291 upper airway patency in, 290 – 291 sleep physiology in, 285 surgical treatment of, 275, 333 – 350, 365 – 369, 385 – 399 algorithms for, 365 – 366 analgesics in, 402 continuous positive airway pressure in, 276, 401 – 402 discharge criteria in, 403 fiberoptic examination in, 403 genioglossus muscle advancement in . See Genioglossus muscle advancement. Harmonic Scalpel in . See Harmonic scalpel. imaging before, 334 intensive care unit in, 402 intubation/extubation in, 402 maxillomandibular advancement in, 387 – 388, 390 – 398 modalities in, 334 – 335 nasal procedures in, 366, 388 nasopharyngeal and oropharyngeal procedures in, 388 – 389 patient selection for, 333 – 334 postoperative care for, 401 – 404 radiofrequency in . See Radiofrequency. skeletal procedures in, 389 – 391 soft tissue hypopharyngeal procedures in . See Soft tissue hypopharyngeal surgery. Stanford protocol in, 371 – 373, 386 – 387, 401 – 403 tonsillectomy in, 366

407

tracheostomy in, 385 – 386 tracheotomy in, 402 transpalatal advancement in, 367 uvulopalatopharyngoplasty in, 275, 348, 366 – 367, 386 ventilation in, effects of sleep on, 285 – 287 Oral appliances for obstructive sleep apnea syndrome, 275 – 276, 305 – 317 advances in, 306 – 309 contraindications to, 314 Herbst appliance, 309 – 310 Klearway appliance, 310 – 311 mandibular repositioners, 311 PM Positioner, 311 – 312 protocols for, 306 selection of, 314 Snore Guard, 312 – 313 TheraSnore, 313 tongue retaining device, 313 – 314 for sleep-disordered breathing, 301 – 302 Oral cavity examination, in patient evaluation, for sleep-disordered breathing, 352 Oropharyngeal surgery, for obstructive sleep apnea syndrome, 388 – 389 Osteotomy for obstructive sleep apnea syndrome . See Genioglossus muscle advancement. for sleep-disordered breathing, 355 Oxygen, for sleep-disordered breathing, 299

P Palatal obstruction, radio-ablation of, 337 – 339 Palatal stiffening surgery, cautery-assisted, for obstructive sleep apnea syndrome, 389 Pharyngeal compliance, in sleep, 290 Pharyngeal narrowing, and snoring, 286 – 287 Pharyngoscopy, in patient evaluation, for sleepdisordered breathing, 352 – 353 Pickwickian syndrome, historical aspects of, 273 PM Positioner, for obstructive sleep apnea syndrome, 311 – 312 Polysomnography before laser therapy, for obstructive sleep apnea syndrome, 320 – 321 of sleep-disordered breathing, 295 Pregnancy, obstructive sleep apnea syndrome in, 278

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Proptriptyline, for obstructive sleep apnea syndrome, 276 R Radiofrequency, for obstructive sleep apnea syndrome, 335 – 344, 359 – 363, 367 advantages of, 336 Coblation system, 336, 338 – 341, 343 – 344 Ellmad system, 336 – 337 Ellman system, 336 – 337 for nasal obstruction, 341 – 344 for palatal obstruction, 337 – 339, 360 – 361 for tonsillar enlargement, 339 – 341 physics of, 335 – 336, 359 preoperative preparation for, 337 procedures for, 337 Somnoplasty system, 336, 338 – 339, 343 – 344, 389 Surgitron system, 336 – 337 tissue reduction by, 359 – 360 tongue base reduction by, 361 – 362 Radiograph, cephalometric, in patient evaluation, for sleep-disordered breathing, 353 – 354 Rapid eye movement sleep, in obstructive sleep apnea syndrome, 285, 287 Respiratory disturbance index, in sleep-disordered breathing, 355 Retroglossal obstruction, in obstructive sleep apnea syndrome, 389 S Scarring, after laser therapy, for obstructive sleep apnea syndrome, 328 Skeletal surgery, for obstructive sleep apnea syndrome, 389 – 391 Sleep-disordered breathing, 293 – 296. See also Obstructive sleep apnea syndrome. apnea frequency in, 295 – 296 diagnosis of, 295 evaluation of, 293 – 294 follow-up of, 296 medical treatment of, 297 – 304 alcohol and, 298 alternative interface systems in, 301 – 302 benzodiazepines and, 298 bilevel positive airway pressure in, 301 continuous positive airway pressure in, 299 – 301 titration of, 301 hypothyroidism and, 298 – 299

oral appliances in, 301 – 302 position restriction in, 299 smoking and, 298 supplemental oxygen in, 299 weight loss in, 299 pattern of apnea in, 293 screening tests for, 294 – 295 upper airway reconstruction for . See Upper airway reconstruction. Smoking, and sleep-disordered breathing, 298 Snore Guard, for obstructive sleep apnea syndrome, 312 – 313 Soft tissue hypopharyngeal surgery, for obstructive sleep apnea syndrome, 371 – 376 algorithms for, 371 – 373 glossectomy in, 373 – 374 hyoepiglottoplasty in, 374 hyoid suspension in, 374 laser midline glossectomy in, 373 lingualplasty in, 373 tongue suspension procedures in, 374 Somnoplasty system, for obstructive sleep apnea syndrome, 336, 338 – 339, 343 – 344, 389 Speech problems, after laser therapy, for obstructive sleep apnea syndrome, 328 Split-night polysomnography, of sleep-disordered breathing, 295 Stanford protocol, in surgery, for obstructive sleep apnea syndrome, 371 – 373, 386 – 387, 401 – 403 Stroke, obstructive sleep apnea syndrome and, 279 Surgitron system, for obstructive sleep apnea syndrome, 336 – 337

T TheraSnore, for obstructive sleep apnea syndrome, 313 Thoracic caudal traction, in sleep, 290 Tidal volume, reduced, in sleep, 286 Tongue base surgery, for obstructive sleep apnea syndrome, 373 – 374 Tongue retaining device, for obstructive sleep apnea syndrome, 313 – 314 Tongue suspension surgery, for obstructive sleep apnea syndrome, 374 Tonsillar enlargement, radio-ablation of, 339 – 341

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Tonsillectomy, for obstructive sleep apnea syndrome, 366 Tracheostomy, for obstructive sleep apnea syndrome, 275, 385 – 386 Tracheotomy, after surgery, for obstructive sleep apnea syndrome, 402 Transmural pressure, of upper airway, in sleep, 290 Transpalatal advancement, for obstructive sleep apnea syndrome, 367 Trephine osteotomy, for obstructive sleep apnea syndrome, 381 – 383 U Ultrasound-assisted uvulopalatopharyngoplasty, for riobstructive sleep apnea syndrome. See Harmonic Scalpel. Upper airway caliber, reduced, in sleep, 286 Upper airway dilators, reduced, in sleep, 286 Upper airway obstruction, in sleep. See Obstructive sleep apnea syndrome: Sleep-disordered breathing. Upper airway patency, in sleep, 290 – 291

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Upper airway reconstruction, for sleep-disordered breathing, 351 – 357 imaging before, 353 – 355 patient evaluation for, 351 – 352 surgical staging in, 355 – 356 upper airway examination in, 352 – 353 Uvulopalatopharyngoplasty for obstructive sleep apnea syndrome, 275, 348, 366 – 367, 386 for sleep-disordered breathing, 355 laser-assisted . See Laser therapy. ultrasound-assisted, for obstructive sleep apnea syndrome . See Harmonic Scalpel. Uvulopalatoplasty, laser-assisted. See Laser therapy. V Vascular factors, in sleep, 290 – 291 Velopharyngeal insufficiency, after laser therapy, for obstructive sleep apnea syndrome, 327 – 328 W Weight loss for obstructive sleep apnea syndrome, 275 for sleep-disordered breathing, 299