2003, Vol.36, Issues 3, Surgery for Sleep Apnea

Preface

Sleep-disordered breathing

David J. Terris, MD, FACSGuest Editor

Many significant advances have been made in the evaluation and treat-ment of sleep-disordered breathing over the past several years. In addition tothe advent of radiofrequency-ablative techniques, progress continues to bemade in electrical stimulation of upper airway dilators. Of equal impor-tance has been the gradual adjudication of the role of various techniquesthat otolaryngologists have at their disposal.

This issue of The Otolaryngologic Clinics of North America emphasizes thislast point, with reassessments of previously described interventions that havefound their place in treatment algorithms. A fresh look at the managementof pediatric sleep apnea is included, as is a comprehensive review of theavailable literature concerning gender differences as they relate to the sever-ity and surgical prognosis of sleep apnea.

Finally, because otolaryngologists continue to maintain a substantialamount of responsibility for the care of patients with sleep disorders, a signifi-cant segment of this issue is devoted to the physiology of sleep-disorderedbreathing and the physiologic impact of sleep apnea syndromes. Further in-sight about the management of sleep disorders will require prospectiverandomized trials (which are beginning to emerge) and thoughtful

Otolaryngol Clin N Am

36 (2003) xi–xii

0030-6665/03/$ - see front matter � 2003, Elsevier Science (USA). All rights reserved.

doi:10.1016/S0030-6665(02)00173-1

failure analysis. Outcome researchers will have an important part to play inthe future development of this field.

David J. Terris, MD, FACSPorubsky Professor and Chairman

Department of Otolaryngology–Head and Neck SurgeryMedical College of Georgia

1120 Fifteenth StreetAugusta, GA 30912-4060, USA

E-mail address: [email protected]

xii D.J. Terris / Otolaryngol Clin N Am 36 (2003) xi–xii

Upper airway physiology and obstructivesleep-disordered breathing

Chris Yang, MD, B. Tucker Woodson, MD*Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin,

9200 West Wisconsin Avenue, Milwaukee, WI 53226, USA

The surgical management of obstructive sleep-disordered breathing(OSDB) is evolving rapidly.With advances in areas of diagnostic and surgicalinstrumentation, the technology available for surgical treatment of obstruc-tive sleep apnea has never been better. Yet our knowledge of anatomic andphysiologic determinants of the upper airway remains inadequate. As a result,our ability to precisely evaluate the airway and our understanding of the effectand mechanisms of pharyngeal surgery remain muddled, inaccurate, andimprecise. The results are too often that surgical outcomes are disappointingfor OSDB [1]. The need for future advances in this field dictates a morethorough understanding of this disease process. This article reviews thecurrent concepts of the pathophysiology of OSDB, with special emphasis onanatomic and physiologic factors that lead to upper airway compromise.

Background

Obstructive sleep-disordered breathing includes obstructive sleep apnea(OSA) and obstructive sleep apnea syndrome (OSAS), which are commondisorders that result from upper airway obstruction during sleep. Ob-structive sleep apnea is defined by a polysomnogram finding that demon-strates obstruction of the upper airway during sleep. Obstructive sleep apneasyndrome is well recognized and requires both OSA with greater than fiveobstructive ventilatory events per hour and presence of clinical symptoms.Increasingly, OSA even without apparent clinical symptoms is consideredpotentially pathologic, but the threshold for determining what constitutes


36 (2003) 409–421

* Corresponding author.

E-mail address: [email protected] (B.T. Woodson).

Dr. Woodson is a member of the Medical Advisory Board for Resmed Inc. He has

received research support from Gyrus ENT and Influ-ENT.


doi:10.1016/S0030-6665(03)00017-3

an abnormal amount of obstructive ventilatory events has not been identi-fied [2]. Current thought considers a respiratory distress index of greaterthan 15 as the minimal threshold of disease when symptoms are absent.But such classifications may prove inadequate, because the scope of thepathophysiology of OSDB involves not only airway obstruction but alsothe consequences arising from arousals, sleep fragmentation, and otherfactors that result in the varied clinical picture of this disease process. Theclinical sequelae of OSDB include hypersomnolence, psychophysiologic dys-function, cardiovascular morbidity, and snoring. In OSDB, however, the de-fining event is airway obstruction during sleep, and therefore it is criticalto enhance our understanding of upper airway collapse such that superiorreconstructive techniques can be developed.

Current evidence supports the axiom that abnormal upper airwaystructure is likely the fundamental abnormality in OSDB [3,4]. In children,this abnormality is most often the result of adenotonsillar hypertrophy. Nosingle structural abnormality has been identified in adults with this disorder,however, and the presence of multiple anatomic and physiologic abnormal-ities is common [5]. Individually, these abnormalities often are considereddisproportionate and not pathologic [6]. Anatomic abnormalities remain thecentral component in the development of OSDB. Additional interactionsbetween abnormal anatomy and normal or pathologic variables, includingventilatory, neurologic, and other factors, contribute to further compromisean inherently vulnerable upper airway [7]. For instance, subjects with OSDBconsistently demonstrate an anatomically small upper airway that is at anincreased risk of collapse when a loss of physiologic muscle tone occursduring sleep. The combination of various other static and dynamic forcesultimately determines ability to maintain an adequate upper airway [8].

Static and dynamic forces

It is easy when conceptualizing the upper airway to oversimplify complexinteractions. Dividing various forces into static and dynamic componentshelps in better conceptualizing various determinants of airway size. Staticdeterminants of airway size can be thought of as the intrinsic pharyngealarea as determined by craniofacial framework and upper airway soft tissuemass. Dynamic forces include phasic neuromuscular tone and dynamicairflow. Each of these forces has additional levels of controls, complexity,physiology, and pathology, some of which are yet to be described adequately.Known abnormal static features that increase risks of obstruction includesmaller maximal upper airway, increased compliance as the airway decreasesin size, more positive closing pressures, and increased airway length [3,9,10].These abnormal static characteristics result in an abnormally collapsibleairway when exposed to conditions of dynamic flow. The mechanics of upperairway collapse may be described using both a static model that evaluates

410 C. Yang, B.T. Woodson / Otolaryngol Clin N Am 36 (2003) 409–421

changes independent of airflow and a dynamic model that includes the effectsof negative inspiratory pressure and airflow [7,11]. Classically, collapse of theupper airway has been thought to occur during inspiration, when negativeinspiratory pressure and airflow predominate; however, collapse is not limitedto inspiration and also occurs during expiration (Fig. 1) [12]. The critical eventactually may occur when passive expiratory collapse or static characteristicspredominate.

Sites of upper airway collapse

Upper airway collapse during sleep is common and universal in humanbeings. The phenomenon of OSDB is almost unheard of in any other species.Humans possess a supralaryngeal and pharyngeal airway that is notcompletely supported by a skeletal or cartilaginous framework. This softtissue supralaryngeal airway presumably is associated with inferior descent ofthe larynx in conjunctionwith the development of speech [13]. Cross-sectionalsize of this soft tissue conduit is determined by a combination of anatomicstructures and by pharyngeal dilator muscle activity (Fig. 2). Variable sites ofnarrowing occur in the upper airway in OSDB and snoring [14]. Maxillaryabnormalities have been implicated increasingly [5,15]. The fact that the

Fig. 1. Phasic fluctuation and cross-sectional airway size are depicted during a single

respiratory cycle. At the onset of inspiration (1), airway size increases with activation of

inspiratory dilator muscles. Dilatation is countered by negative intraluminal pressures during

midinspiration (*). During expiration (2), positive expiratory pressure combined with the effects

of phasic muscular contraction and loss of negative intraluminal pressure results in rapid

dilation of the upper airway. During midexpiration (**), loss of muscle tone predominates and

significant airway collapse occurs. The smallest airway size occurs at end expiration. At this

point, if the airway size is critically small, dynamic inspiratory airway forces may result in

airflow limitation or complete airway collapse.

411C. Yang, B.T. Woodson / Otolaryngol Clin N Am 36 (2003) 409–421

maxilla is amajor contributor toOSDB is no surprise, given the focal role thatmaxillary development plays in facial growth and development. Othercraniofacial abnormalities include decreased mandibular projection, down-ward and posterior rotation of facial development, increased vertical length ofthe upper airway, and increased cervical angulation [16,17]. Soft tissueabnormalities include increased tongue size, excessive palatal length, in-creased lateral wall thickness, enlarged tonsils, increased nasal resistance,rhinitis, and an increased mandibular plane-to-hyoid distance [18–20]. Thefinal common denominator of these structural abnormalities is a smaller andmore collapsible cross-sectional airway size [21].

Upper airway shape

Upper airway shape is critical in determining airflow and in determiningthe function of upper airway muscles. Cross-sectional area is critical indetermining upper airway resistance [22]. Absolute cross-sectional airwaysize has only correlated weakly to apnea severity as measured by respiratorydistress index, however. Part of this discrepancy is explained by shapedifferences among individuals. Individuals with OSA tend to have moreelliptically shaped upper airways than nonapneic individuals [23]. Apneais more severe when airways are elliptically shaped, with the long axis inthe midsagittal plane. The elliptical shape increases the surface area of theairway and frictional resistance compared with a more circular conduit.Additionally, an airway with a long axis in an anterior posterior direction(in the midsagittal plane) is less affected by contraction of major airwaydilators such as the genioglossus muscle.

Body and jaw position

Body position also has major effects on airway size in patients withsnoring and OSA. Several mechanisms, including tissue mass and tracheal

Fig. 2. The observed size of the upper airway at any moment is a function of multiple

interacting variables. The most important variables are structure, muscle tone, airflow, and

intraluminal pressure. If muscle tone, airflow, and pressures are controlled, then the observed

size approximates actual airway structure.


tug, may be involved and may contribute to the changes observed [24].Tissue mass is a major force contributing to collapsing forces to the airway.Because mass and compliance of various structures surrounding the airwaydiffer, it is likely that changing position affects different areas of the airwayin different ways. Studies directed at identifying the effects of gravity innonapneic subjects have demonstrated that the lower pharynx and retro-epiglottic airway are affected more than the upper pharynx [25]. In apneicsubjects, the isolated effects of gravity have not been evaluated. It isspeculated that in apneics with a more unstable upper airway, gravity maycontribute to obstruction in multiple segments, depending on the mass ofthe tissues involved. The upper airway may have marked changes goingfrom the sitting position to the supine position. Similarly, the lateral bodyposition provides a more stable upper airway configuration than the supineposition. The mechanism of this effect has not been demonstrated yet butlikely includes effects of gravity and reflex effects. Reflex effects should notbe dismissed. It is well established that the lateral body position hassignificant effects on the nasal cycle. The idea that body position has reflexeffects on the pharynx is also plausible and may warrant further research.

Nasal pathologic conditions

Evaluation of a patent nasal airway is critical in treatment of OSAS.Nasal pathologic conditions may contribute to OSA and pharyngeal col-lapse in several ways. Nasal obstruction and mouth breathing cause (1)reduction in nasal reflexes, which are important in maintaining musculartone; (2) jaw opening, with backward rotation of the jaw and inferior dis-placement of the hyoid, resulting in worsening of pharyngeal collapse; and(3) increase in ‘‘upstream’’ airflow resistance. Upstream airway resistance in-creases ‘‘downstream’’ collapse. Nasal resistance and obstruction may resultfrom abnormalities of the maxilla and the posterior maxillary airspace[20]. Treatment of nasal obstruction, however, does not alter nasal continu-ous positive airway pressures [26].

Neuromuscular tone

Neuromuscular tone influencing dilation of the upper airway is undercomplex regulation. Physiologic changes in tone occur phasically with therespiratory cycle and sleep-wake state transitions. During expiration, dilat-ing upper airway muscle tone diminishes, which results in partial upper air-way collapse in normal individuals [27]. Yet in nonapneic, anatomically‘‘normal’’ individuals with minimal static collapse, the phasic loss of upperairway muscle tone during expiration and the loss of muscle tone duringsleep are not sufficient to cause significant flow limitation, in contrast toindividuals with severely abnormal upper airway anatomy. In this group,


static collapse is greater. Combined with further loss of phasic muscle toneoccurring during expiration and decreased muscle tone during sleep,abnormal airway anatomy results in complete upper airway obstruction atend expiration [28]. Inspiration then occurs with an already obstructedairway. In individuals with a less abnormal upper airway, static collapse ofthe upper airway in conjunction with loss of muscle tone can result insignificant collapse that exceeds minimal protective threshold at endexpiration. Dynamic collapse during inspiration then results in furtherclosure and obstruction. In both groups with OSDB, obstructive events suchas these episodes do not occur during wakefulness. The primary reason isthat these patients demonstrate augmented motor activity during wakeful-ness that serves a protective function to prevent airflow limitation [29]. Thisincreased activity is presumably to compensate for a structurally smallupper airway. The etiology of this augmented upper muscle activity is yet tobe determined, although evidence suggests that upper airway mechano-receptors (particularly located at the level of the epiglottis) sensitive tonegative airway pressure are involved. Because airway patency requiresaugmented motor activity, greater loss of muscle tone occurs during sleep,resulting in increased ventilatory resistance leading to airflow limitation andincreased work of breathing. The resultant decreased airflow results inasphyxia, whereas increased work of breathing and mechanoreceptorstimulation result in CNS arousal and sleep fragmentation. This increasedmuscle tone activity associated with increases in airway size duringwakefulness explains the lack of differences in airway resistance andcompliance that is measured in subjects with OSA compared with normalsubjects. Part of this increased tonic activity is reflex-mediated.

Other effects of sleep on the upper airway

Both rapid-eye-movement (REM) and non-REM sleep are associatedwith multiple physiologic changes compared with wakefulness. Regardingventilation, the onset of sleep alters the CNS’ response to hypoventilation,leading to both hypoxia and hypercarbia. Hypoxic ventilatory drive isreduced in non-REM and markedly decreased in REM sleep. Hypercapneicdrive also is reduced in non-REM and REM sleep [30]. During non-REMsleep, ventilation is controlled primarily by chemical mechanisms (primarilycarbon dioxide). With the onset of fragmented non-REM sleep and wake-fulness, significant changes in ventilation occur.

The mechanisms are complex and involve oscillations in chemical controlof ventilation during sleep combined with changes in carbon dioxide due toupper airway collapse [31]. Arousals and brief awakenings serve to rapidlyincrease carbon dioxide sensitivity. Ventilatory overshoots occur that thenmay be followed by ventilatory undershoots. Ventilatory undershoots resultin decreased ventilatory drive. The consequence of decreased ventilatory


drive is decreased activity of muscles that are tightly linked to respiratoryneuronal activity, such as the diaphragm. In general, the upper airwaymuscles are less tightly linked to ventilatory drive and thus small changes inventilatory drive may have major effects on their activity. In nonapneicindividuals, the consequence of decreased ventilatory drive may be centralapneas or central hypopneas, but in patients in whom upper airway muscledrive is crucial in maintaining airway size, even a small loss of upper airwaydrive may result in airway obstruction.

Mechanoreceptor-mediated increases in upper airway muscle tone havebeen noted to be critical in maintaining upper airway patency in patientswith OSDB. Mechanoreceptors are known to serve a role in reflex-mediatedcompensatory pharyngeal dilator muscle activity when exposed to collaps-ing negative inspiratory forces [32]. Their importance is greater in patientswith OSDB than in normal patients because they must compensate for theirpoor anatomy. This finding has been demonstrated in laboratory-basedstudies that show both peak and phasic genioglossus electromyographyEMG activity is significantly higher in patients with OSDB compared withnormal control patients during wakefulness. The stimulatory effect ofnegative inspiratory pressure can be ameliorated when continuous positiveairway pressure is applied. And when continuous positive airway pressure isapplied to patients with OSDB during wakefulness, there is a markeddecrease in genioglossus EMG activity, whereas normal subjects displayessentially no change [33]. Waking muscle tone decreases after applicationof topical oropharyngeal anesthesia [34]. The importance of these receptorsduring sleep is demonstrated by the worsening of obstruction in snorers whohave oropharyngeal topical anesthesia during sleep, which suggests thatmechanoreceptor-mediated neuromuscular compensation reflexes may becritical in subjects with OSDB but not necessarily in normal subjects.

Reopening of the upper airway during obstructive events is associatedwith an increase in upper airway muscle tone to levels above baselineactivity. This increase requires arousal, awakenings, and change in sleepstate. As work of breathing increases as a result of increased hypercapneicventilatory drive, increased mechanoreceptor stimulation occurs as apneaprogresses. Increased mechanoreceptor stimulation results in arousal, acti-vation of upper airway muscles, and reopening of the upper airway. Hence,it is mechanoreceptor stimulation that is the primary mediator of corticalarousal and changes in sleep state.

Mechanoreceptors also may work to increase the work of breathing inresponse to ventilatory loads or obstruction. In apneics, ventilatory loaddetection is impaired. The etiology of this impairment is still under debate,but increasingly, abnormalities of the upper airway reflex mediators areimplicated [35]. Some of these abnormalities may be acquired and includeevidence of decreases in pharyngeal sensitivity and evidence of pharyngealnerve damage. These abnormalities are speculated as possibly resultingfrom the vibratory trauma of snoring [36]. Histopathologic studies have


demonstrated evidence of both muscle-bundle hypertrophy and muscle-fiberdegeneration and damage. The cause of these changes may include eccentriccontraction during stretch and from motor neuron damage. Lengthening orstretching during muscular contraction (eccentric contraction) results inmuscle-fiber damage and hypertrophy. Immunohistopathologic changes inmuscle-fiber types are also consistent with muscle denervation and reiner-vation. Electron microscopy and other studies have demonstrated motor-neuron damage in OSA. The ultimate result is both muscle hypertrophy thatmay impinge on airway size and impairment of muscle elastance andstrength of contraction.

Balance of forces and Starling resistor

The multitude of anatomic and physiologic processes so far describedonly begins to touch on the true complexity of the upper airway. Integratingthese and other factors into a manageable concept is difficult. One methodthat allows this integration is the concept of ‘‘balance of forces.’’ Dynamicupper airway collapse may be understood further by applying the conceptsof the ‘‘Starling resistor,’’ which describes flow in collapsible tubes.

Balance-of-forces model

At any instant in time, upper airway size is determined by the combinedcontributions of multiple structural and physiologic variables. The balance-of-forces model allows an accurate description of how multiple variablesalter upper airway size (Fig. 3). Airway size is determined by both dilatingand collapsing forces. Dilating forces include upper airway muscle tone,mechanical force of the airway wall structure, and positive intraluminalairway pressure. Collapsing forces include tissue mass, surface adhesiveforces, and negative intraluminal pressures. The resulting difference in theseforces is the distending force, which acts on the wall of the upper airway.When the distending force increases, the airway size increases; when itdecreases, the airway size decreases.

The distending force of the upper airway is the transmural pressure (Ptm)of the airway. The equation Ptm ¼ Pout � Pin defines transmural pressure,where Pout represents the sum of the dilating upper airway forces andPin represents the sum of the collapsing forces. Another more clinicallyrelevant means to conceive of the forces that act on the upper airway is byconsidering the skeletal airway structure as a constant and describingthe dynamic forces as being either tissue pressures or luminal pressures(Ptm ¼ Ptissue � Pluminal). Tissue pressure includes the forces from tissuemass, tissue elastance, surface tension, and neuromuscular dilating andcollapsing forces. Luminal pressures include the segmental airway pressure(Pairway) and pressures relating to airflow (Pflow). As noted, airway pressuresmay be dilating (if positive, such as with expiration or with the application


of external positive airway pressures) or collapsing (such as during inspira-tion). Studies have been able to replicate a syndrome identical to OSAS innon-OSA subjects by applying negative pressures to the upper airway duringsleep.

Although seemingly esoteric, such a model (Ptm ¼ Pluminal � Ptissue)provides a means of quantifying upper airway collapse. The compliance(dA/dP) of the upper airway represents the tendency of the upper airway tocollapse during respiration. Airway compliance can be calculated, allowingmeasurement of the intrinsic collapsibility of the upper airway. The effectsof airflow on decreasing luminal pressures are determined by its velocityand are described by Bernoulli’s equation. If airflow velocity is zero, then(Pluminal ¼ Pairway þ 0), and if neuromuscular tone is held constant(Ptissue ¼ k), then measured airway pressure represents the distending ortransmural pressure of the upper airway (Ptm ¼ Pairway � k). This measuredpressure, combined with measures of upper airway size, allows calculationof airway compliance (dA/dP) independent of physiologic influences.Airway pressure can be measured and manipulated (such as with nasalcontinuous positive airway pressure) to assess changes in airway size andcompliance.

Starling resistor

The Starling resistor concept describes flow in collapsible tubes, whichserves as an ideal model for the upper airway (Fig. 4). In the human upperairway, the collapsible tube is the supraglottis and pharynx. Upstream

Fig. 3. The balance-of-forces model. Transmural pressure (Ptm) is the force that determines the

size of the airway wall. This force is determined by dilating pressures (Pout) and collapsing

pressures (Pin). Transmural pressure of the airway wall also can be described as the difference

between tissue pressures and intraluminal pressures (see text for details).


pressure is ambient pressure and downstream pressure is pleural pressure.During wakefulness, low negative pleural pressures (ie, 5 cm H2O) combinedwith a large upper airway (the result of multiple balance of forces) resultin unimpeded flow. During sleep, changes occur in the balance of forces,and distinct clinical populations occur. In nonapneic, nonsnoring patients,a structurally larger upper airway remains patent. In snorers and apneicsubjects, a structurally small upper airway results in a cascade of pathologicevents.

The Starling resistor concept builds on Poiseuille’s law, which describesflow in noncollapsible tubes. Poiseuille’s law states V ¼ P1 � P2/R, whereV ¼ flow, P1 ¼ pressure upstream, and P2 ¼ pressure downstream. Theresistance component (R) is determined by length of the tube (L), fluidviscosity (g), and the radius (r) of the tube (R ¼ resistance ¼ 8gL/pr4.Because viscosity and length are constant, changes in resistance are

Fig. 4. Properties of a Starling resistor. Two rigid tubes are separated by a collapsible segment.

The collapsible tube lies within a bucket (baseline). Water can be placed to increase Pout (no

flow). In baseline, Pin is greater than Pout, and the collapsible segment is patent. Unobstructed

flow (flow, lower left) occurs when Pin is greater than Pout and Pus is greater than Pcrit. In no

flow (upper right), water fills the bucket, Pout is greater than Pin (the collapsible tube is

obstructed), Pus is less than Pcrit, and there is no airflow. Increasing Pus dilates the segment;

when this event occurs, flow will resume. In flutter (lower right), Pus is greater than Pcrit, and

flow must occur; however, Pdownstream is increased (as occurs with increased upper airway

resistance during sleep). The orifice (*) is exposed to a negative inspiratory pressure (NIP)

(Pdownstream < Pcrit), and collapse of this segment occurs. With flow cessation, however,

pressure rapidly rises to Pus, and the orifice opens. The orifice now is exposed to Pdownstream

and Bernoulli forces, and collapse occurs. A cycle of rapid opening and closing (flutter) occurs.


primarily related to changes in the area of the tube. Because area isunchanged in a rigid tube, flow in a noncollapsible airway dependssignificantly on pressure across the tube (P1 � P2 ¼ driving pressure). Thistype of flow contrasts to a collapsible, Starling resistor airway in which flowmay be independent of driving pressure. In a Starling resistor, resistance isvariable, and resistance and flow are determined primarily by airway size.Airway size is determined by the surrounding forces that act on the airway.In a simple collapsible tube (ie, a tube with a wall without intrinsic structuralforces that often is modeled with a penrose drain placed between two rigidtubes) the airway size-determinant forces are primarily the upstream anddownstream airway pressures and flow.

Three basic clinical patterns can be observed, which include normalbreathing, snoring, and obstruction. Likewise, three possible conditions offlow across a collapsible upper airway exist and may include unimpededflow, flutter, and obstruction. These three conditions are determined bythe balance of three groups of pressures exerted on the upper airway.These conditions are the downstream pressure (Pds or negative inspiratorypressure), upstream pressure (Pus or ambient pressure), and the transmuralpressure (Ptm). For the condition of unimpeded flow, transmural pressure isgreater than both downstream and upstream pressures (Ptm > Pus > Pds).Because transmural pressure is greater than other pressures, airway collapsedoes not occur, and airway size and resistance are not altered, whichcontrasts with the condition of obstruction in which transmural pressuresare less than both downstream and upstream pressures (Pus > Pds > Ptm).With a negative transmural pressure, airway size is zero and no flow occurs.When transmural pressure is less than upstream pressure but greater thandownstream pressures (Pus > Ptm > Pds), the condition of flutter occurs. Achoke point or narrowing of the airway occurs in the segment of thecollapsible upper airway that is exposed to negative transmural pressure. Inthis segment, airway size decreases (in an ideal Starling resistor, the resultantairway size is zero). When the airway is closed, there is no flow, and thesegment becomes exposed to upstream pressure, which dilates the upperairway. When flow occurs, however, this segment is exposed again to down-stream pressure, which acts to collapse this segment. Repeating this cycleresults in the choke point being exposed to alternating upstream or down-stream pressures, depending on the presence of flow in the airway. The resultis flutter.

Because of these characteristics, flow in a collapsible tube in patients atrisk for OSA is not determined by the difference between upstream anddownstream pressures (driving pressure), but rather by the differencebetween upstream pressures and the pressures surrounding the collapsiblesegment. In a structurally patent airway, the pressure difference across thecollapsible tube wall is of minimal importance; however, in an airway that ismore vulnerable to collapse, these forces may become a major determinateof airway cross-sectional area and therefore resistance to airflow.


Summary

Upper airway competence involves complex interactions between anatomyand physiology. The common final denominator of OSDB is a structurallysmall and abnormally collapsible upper airway. The mechanisms contribut-ing are often an accumulation of many skeletal or soft tissue abnormalitiesand respiratory physiology that individually may or may not be pathologic.So far, simplistic models have hampered progress in this field. Successfulmedical and surgical treatment of OSDB continues to be elusive for too manypatients. Great strides remain to be taken, but the possibility seems withinreach.

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The physiologic impact of sleep apneaon wakefulness

Yau Hong Goh, FRCS, FAMS (ORL)a,*

Kheng Ann Lim, FDSRCS, FAMS (OMS)b

aDepartment of Otolaryngology, Sleep Disorders Unit, Singapore General Hospital,

Outram Road, Singapore 169608bDepartment of Oral Maxillofacial Surgery, National Dental Centre,

5 Second Hospital Avenue, Singapore 168938

Sleep is a transient state of altered consciousness and perceptualdisengagement from one’s environment. Unlike coma, it is an active processinvolving a host of complex interactions among many cortical, brain stem,diencephalic, and forebrain structures. During this ‘‘rest’’ state, the cerebralmetabolism and oxygen consumption within the brain remain significant.Any pathologic condition that interferes with this intriguing cerebral eventduring sleep therefore disrupts the proper execution of this necessary andvital state of existence. Although the function of sleep is controversial andlargely unknown, one observation is evident—that good sleep is critical toa well-functioning awake state.

The phenomenon of sleep is associated with profound physiologicalterations. Under normal circumstances, these physiologic changes in thevarious human systemic functions during sleep occur without any seriousconsequences. In pathologic states, however, changes that ensue in any of thesystemic functions may present serious physiologic risks with consequencesthat affect the qualitative and quantitative aspects of sleep and daytimefunction [1–3].

Of the various sleep disorders, sleep apnea is probably one of the mostimportant and the most common nocturnal problem afflicting human beings.The actual incidence of sleep apnea in the world is unknown, and the numberof clinically unremarkable patients with occult sleep apnea is speculative. Themany patients that the authors frequently encounter in clinical practice who


36 (2003) 423–435


E-mail address: [email protected] (Y.H. Goh).


doi:10.1016/S0030-6665(02)00174-3

were discovered to have significant sleep apnea after having been initiallyinvestigated for cardiovascular or neurologic complaints, for example,suggest that the true incidence of sleep apnea may be mind-boggling. Theproblem of sleep apnea is probably grossly under-recognized and under-diagnosed. Several prevalence studies in adult men have estimated preva-lence rates of 0.4% to 24% [4–8], with estimates tending to increase withincreasing age.

Since the first recognition and description of sleep apnea in 1965 [9,10],crucial clinical and laboratory studies on sleep apnea have added new facetsto the understanding of the physiologic effects of sleep apnea on humans.The effects of sleep apnea on sleep, the daytime consequences that follow,and the clinical impact of this condition on human life may be far moreprofound than currently believed. Patients with this condition may presentwith a variable combination of clinical symptoms affecting both sleep anddaytime function; the former tend to be more specific for sleep apnea,whereas the latter are usually the nonspecific results of abnormal sleep re-gardless of the cause.

To understand the physiologic impact of sleep apnea on wakefulness, it ispertinent to first examine the respiratory physiology during normal sleep,the arousal responses to respiratory alterations during sleep, the effects ofsleep apnea on sleep architecture, and the role of sleep fragmentation onwakefulness.

Respiratory physiology during normal sleep

Breathing during the awake state is regulated by a cluster of complexinter-related factors that includes the following:

1. Voluntary and behavioral factors2. Mechanical signals from lung, airway, and chest receptors3. Chemical factors, such as low oxygen or high carbon dioxide levels and

acidosis

During sleep, however, several important alterations in the physiologicresponses to respiratory stimuli occur.

Hypoventilation during sleep

In the awake state, both cortical activity and voluntary mental concen-tration can influence breathing and bring about an increase in both ventilationand ventilatory responses. The loss of ventilatory drive that is observed duringsleep probably reflects the loss of the ‘‘wakefulness’’ drive to ventilation.

During rapid-eye-movement (REM) sleep, the inhibition of both pre-synaptic and postsynaptic afferent neurons results in an increase in sensoryarousal thresholds to external stimuli and postsynaptic inhibition of motor

424 Y.H. Goh, K.A. Lim / Otolaryngol Clin N Am 36 (2003) 423–435

neurons that produce postural hypotonia characteristic of REM sleep. Thiscombination of decreased sensory and motor function is believed to accountfor the significant impairment of ventilatory responses duringREMsleep. It isthis impaired ventilatory response that permits the development of hypo-ventilation during sleep.

Hypoxic and hypercapnic ventilatory response during sleep

Not only is the voluntary control of respiration seen in the awake statelost with the emergence of sleep but the usual ventilatory responses to bothlow oxygen and high carbon dioxide levels also are blunted [11–14]. Themarked hypoxemia seen during REM sleep in patients with severe lung andchest disease is due to this phenomenon, which is most depressed duringREM sleep. These physiologic responses also may be important in the path-ogenesis of upper airway obstruction during sleep and are responsible fora patient’s failure to arouse rapidly during apneas or hypopneas. The changein ventilatory sensitivity to external stimuli during sleep therefore predisposespatients with airway problems to develop clinically significant hypoxia andhypercapnia before arousal occurs.

Increased airway resistance and ventilatory response during sleep

Besides the blunting of hypoxic and hypercapnic ventilatory responses,sleep also obtunds the ventilatory response to increasing airway resistance.This physiologic phenomenon has been shown to be particularly distinct innon-REM (NREM) sleep [15–18], the phase of sleep when airway resistancetypically reaches the maximum [19,20]. The effect of increased airflow resis-tance on ventilation during REM sleep is not known, however.

Arousal responses to respiratory alterations during sleep

Isocapnic hypoxia

Under normal circumstances, isocapnic hypoxia is a poor stimulus toarousal. Although studies have demonstrated that many subjects are ableto remain asleep with oxygen saturation as low as 70% [11,12,21], nodifference in arousal threshold has been observed between NREM andREM sleep. Patients with sleep apnea, however, have been shown to exhibitreduced arousal sensitivity to hypoxia during periods of asphyxia [22].

Hypercapnia

Although the level of hypercapnia at which arousal is triggered duringsleep is highly variable, laboratory studies have shown that most subjects areawakened before the end-tidal carbon dioxide rises by 15 mm Hg above thelevel in wakefulness [13,23,24]. This response seems to be sensitized by thepresence of coexisting hypoxia.

425Y.H. Goh, K.A. Lim / Otolaryngol Clin N Am 36 (2003) 423–435

Increased airway resistance

Inspiratory resistance [25] and occlusion [26] have been shown to bestrong precipitants of sleep arousals. The arousal frequency during controlsleep periods is most reduced in stage 3 to 4 sleep and remains comparativelylower during slow-wave sleep than in REM sleep with increased inspiratoryresistance [27,28]. Although arousal from REM sleep after airway occlusionis far more rapid than arousal from NREM sleep, patients with obstructivesleep apnea tend to have longer apneas during REM sleep [26,29]. Why thisphenomenon occurs is still unclear.

Whether it is hypoxia, hypercapnia, or increased airway resistance, the finalpathway for arousal from sleep seems to be the level of ventilatory effort [30].Awakening from sleep, whatever the cause, leads to an increase in ventilation,just as sleep onset is associated with a decrease in ventilation. In patients withsleep apnea, this arousal response to the increase in airway resistance has beentermed respiratory effort–related arousals and is an important feature of sleepapnea. Patients with this disorder tend to awaken at relatively reproduciblelevels of pleural pressure, and this arousalmay occurwithout the developmentof either significant hypoxemia or significant hypercapnia.

Effects of sleep apnea on sleep architecture

Sleep apnea [31] is characterized by episodic complete or partial pharyn-geal obstruction during sleep. This multilevel disorder is characterized bynarrowing at a variable number of pharyngeal locations, the soft palatebeing the most common site of collapse and narrowing [32,33].

Whether the decrease in the sleep-related pharyngeal neuromuscularactivity [34] plays a more dominant role compared with the anatomic nar-rowing [35–37] of the pharyngeal space is a controversial issue. The extent towhich each one of these factors contributes to the pathogenesis of sleepapnea is unknown, although the combined action of these two factorsprobably plays a significant role in the development of sleep apnea.Decreasedupper airway dilator muscle activity [38] and reduction in ventilatory re-sponses to hypercapnia and hypoxia [39] have been shown in 24-hour sleep-deprivation studies. Impaired wakefulness therefore depresses arousability tophysiologic challenges. The result is a vicious cycle of a worsening and self-perpetuating breathing disorder during sleep. Depressed physiologic re-sponsiveness due to altered wakefulness is clinically significant for patientswith sleep apnea and other breathing disorders because they are all exacer-bated by sleepiness [38]. Sleep disruption triggered by apnea results in theproduction of more intense and severe pathologic apneas.

The impact of sleep apnea on sleep architecture can be attributed primarilyto tissue vibration during snoring, increase in airway resistance, hypoxia, andhypercapnia. The final outcome of any of these events is arousal (visible or notvisible on the electroencephalogram [EEG]) and an increase in ventilatory


effort. This intrinsic survival mechanism leads to fragmentation of sleep. It isthis sleep fragmentation and the pathophysiologic changes associated withdisrupted breathing that currently are believed to account for the symptomsand complications of sleep apnea.

Other studies have shown that sleep apnea syndromes may be associatedwith suppression of slow-wave sleep or REM sleep. Suppression of slow-wavesleep occurs most commonly in children with sleep apnea, whereas REMsuppression ismore common in adults with sleep apnea syndromes. Successfultreatment of this sleep condition results in slow-wave sleep orREM rebounds.

The role of sleep fragmentation on wakefulness

Increased frequency of arousals causing sleep fragmentation is a commonmanifestation of a number of sleep disorders and medical conditions involv-ing physical pain or discomfort. Sleep apnea, chronic pain from arthritis andneuralgia, and rhinosinusitis, for example, may be associated with sleepthat is punctuated by frequent, brief arousals of 3- to 5-second duration.These arousals are characterized by episodes of EEG speeding or alpha ac-tivity, with transient increase in skeletal muscle tone. This outburst of subtleEEG arousals is especially important in the diagnosis of upper airwayresistance syndrome [40]. Nonvisible sleep fragmentation, defined as an in-crease in heart rate of 4 beats per minute or an increase in blood pressure by4 mm Hg without EEG change in response to sound stimuli, also has beenshown to be associated with increased sleepiness on the multiple sleep latencytest (MSLT) [20,41]. Less well studied are EEG arousals that may beassociated with other subcortical events not seen in the cortical EEG tracing.This abnormalitymay account for the increase in both the absolute amount ofand the proportion of stage 1 sleep, with concomitant reduction of stage 3 to 4sleep seen in patients with sleep apnea. The association of this event withimpaired wakefulness is still not known, however.

Regardless of etiology, sleep arousals generally do not result in shortenedsleep but rather in sleep fragmentation. It is this fragmentation that is believedto be an important factor affecting impaired daytime wakefulness. Studieshave suggested a strong association between sleep fragmentation and daytimesleepiness [42]. Treatment studies also demonstrate a close link between sleepfragmentation and excessive daytime sleepiness. Reduced frequency ofarousals from sleep with resultant reduction in the level of sleepiness is seencommonly in patients who are treated successfully for sleep apnea, whereasthose who do not subjectively benefit from treatment show no decrease inarousals or sleepiness, despite improved sleeping oxygenation. It must bestressed, however, that lack of fragmented sleep does not exempt one fromfeeling sleepy. Partial sleep deprivation may be seen occasionally in patientswho are unable to sustain sleep from repeated sleep disruption. This conditionis seen commonly in patients with anxiety predispositions or superimposedinsomnia.


Wakefulness and sleepiness

The maintenance of wakefulness involves a sophisticated system offeedback mechanisms from the visceral, somatic, and special sensory organsand integration of information in specialized areas within the cerebral cortexand the brain stem. Failure to execute the most minute biochemical pro-cesses that are intrinsic to sleep seems to result in the failure to initiateand facilitate the physiologic events necessary to maintain wakefulness dur-ing the day. Impaired wakefulness is one of the cardinal symptoms of sleepapnea. Sleep that is compromised qualitatively or quantitatively by thisbreathing disorder results in an altered state of wakefulness. In the fieldof sleep medicine, the level of one’s state of wakefulness is never measureddirectly. The degree of wakefulness is instead quantified by measuring one’slevel of sleepiness. It is pertinent to emphasize at this juncture that althoughsleepy patients have impaired levels of wakefulness, not all patients withimpaired wakefulness report sleepiness. The two terms, therefore, shouldnot be regarded as synonymous.

What is sleepiness?

Sleepiness is a basic physiologic need state like hunger or thirst that is vitalto human survival. Deprivation of sleep causes sleepiness, and as eating anddrinking satisfy hunger or thirst, sleeping reverses sleepiness. Under normalcircumstances, severe sleep-deprived states do not occur because normalhomeostatic and behavioral regulation modulates conditions to facilitatesleeping before severe deprivation states develop. The neurologic substratesof sleepiness and the specific nature of this physiologic need state have yet tobe ascertained.

Whether sleepiness is a symptom with varying intensity on a one-dimensional scale or a multidimensional complaint is a philosophical issuethat has generated much discussion. Whether sleepiness and alertness are atopposite ends in a one-dimensional scale is also another debatable issue. It ispossible, however, that sleepiness varies from presence to absence and isdistinct from alertness. Pivik [43], in particular, theorized that sleepinessmay be multidimensional, and REM versus NREM and core versus op-tional sleepiness are among the different types of sleepiness he proposed.

In a typical 24-hour sleep-and-wake biologic time frame, maximum sleep-iness typically occurs in the middle of the night during sleep. When noc-turnal sleep is not permitted to proceed at the time of maximum biologicsleepiness (2:00–6:00 AM), irritability, lethargy, sleepiness, and impairedmental function, such as inability to concentrate and memory lapses, occur.If significant physiologic sleepiness is allowed to intrude into one’s awakerealm during the day, similar symptoms also are experienced.

Essentially, there are two important clinical facets, objective and sub-jective, to sleepiness. Slowing of the alpha rhythm in the EEG seen in MSLT


and performance task tests, particularly those related to vigilance, areobjective evidence of sleepiness, whereas thoughts, sensations, and emotionsthat are associated with sleep deprivation are the subjective components ofsleepiness.

Subjective sleepiness

When examining the nature of subjective sleepiness, three importantissues must be highlighted. First, an intrinsic biphasic pattern of objectivesleep tendency exists in every human being, with two troughs of alertness(one between 2:00–6:00 AM and the other between 2:00–6:00 PM) [44]. Howsleepy one is, therefore, depends on when his or her sleepiness is evaluated.

Second, although sleep-deprived patients may present with increasedtendency to fall asleep at inappropriate times, manymay not report sleepinessat all. These patients often report nonspecific symptoms of decreasedwakeful-ness, such as fatigue, lethargy, irritability, inability to concentrate at work,and a loss of sense of well-being. Also, when sleepiness is most intense, thesepatients may become less aware of the subjective aspects of sleepiness andso may fall asleep without warning. These episodes, called sleep attacks, areexperienced commonly when patients with sleep apnea are driving a car.

Third, the subjective experience of sleepiness and the behavioral indicatorsof sleepiness, such as yawning andheadnodding, frequently can be suppressedunder certain conditions. This sleepy behavior may be reduced or suppressedcompletely in situations of stress and excitement, high motivation, exercise,and competing needs such as hunger and thirst. Behavioral and subjectiveindicators thus do not always precisely reflect physiologic sleepiness. Whenphysiologic sleepiness is most intense, however, the ability to avoid overtbehavior is reduced markedly. Although a physiologically alert person doesnot experience sleepiness or appear sleepy even in a sleep-inducing environ-ment, soporific conditions, such as after heavy meals, lazing in cozy rooms,or sitting through a boring lecture, will unmask physiologic sleepiness.

Several self-assessment analytic scales have been devised to help cliniciansand patients quantify their level of subjective sleepiness. Among the varioustools for the measurement of subjective sleepiness, the Stanford sleepinessscale [45] and the Epworth sleepiness scale [46] are probably the most vali-dated. Although most study subjects show good correlation between sub-jective and objective assessment of sleepiness [47], it also has been shownthat patients’ subjective and objective assessment of sleepiness may not becompletely consistent [48,49]. The highly subjective nature of subjectivesleepiness is indeed a challenging problem for sleep clinicians and researchers.

Objective sleepiness

Most of the performance tasks used to evaluate the effects of sleep lossare rather insensitive. Currently, only long and monotonous tasks are


reliably sensitive in assessing the effects of sleep deprivation, with theexception of the 10-minute visual vigilance task. This test measures task-oriented vigilance lapses (response times �500 msec) and has been shown tocorrelate well with sleep loss [50,51].

Multiple sleep latency testThe MSLT [52] has remained the standard physiologic measure of

sleepiness. This test, which assesses one’s likelihood of falling asleep, hasgained wide acceptance within the field of sleep and sleep disorders as thestandard method of quantifying sleepiness [39]. Besides being a reliableclinical measure of sleepiness, the MSLT has the further advantage of beingable to eliminate a patient’s motivation to stay awake during the test.Although subjects are frequently able, through motivation, to compensatefor impaired performance after sleep deprivation, they are highly unlikely tostay awake for long in a darkened room during the MSLT. The MSLT is animportant clinical tool to identify sleep tendency and the maximum risk forpatients in their daily environment.

Symptoms of impaired wakefulness not related to sleepiness

Apart from reporting sleepiness, patients with sleep apnea may presentwith symptoms of fatigue, mood disturbance, and loss of sense of well-being.Although the association between sleep apnea and daytime sleepiness hasbeen much studied, little is known about the effects of sleep apnea on non–sleepiness-related symptoms. Longitudinal studies of patients with sleep dis-turbances have shown an increased risk of developing major depression,anxiety disorders, and substance abuse and nicotine dependence [53,54].

The antidepressant nature of successful sleep apnea treatment in theauthors’ clinical practice suggests that sleep disturbance from sleep apnea hasprofound effects on patients’ mood and behavior. Recognizing the existenceof these nonspecific symptoms is necessary when treating obese patients withsleep apnea. These patients frequently require prompt treatment becauselingering sleep apnea perpetuates amental and behavioral state that is amajorstumbling block to motivating patients who are attempting weight reduction.More studies are certainly required to evaluate this neuropsychiatric elementof sleep apnea.

Clinical implications

Between the occurrence of pharyngeal closure and the clinical manifes-tation of impaired wakefulness exists a complex series of physiologic eventsinvolving several systemic functions within the human body. The key linkbetween the airway trigger and the eventual alteration in the level of awakestate seems to be the extent of sleep fragmentation from repeated arousals.


Although it is well known that patients with impaired wakefulness do notnecessarily report sleepiness, the relationship between subjective symptomsof disturbed wakefulness and the severity of sleep apnea is less clear.Patients who were deemed to be simple snorers (without symptoms of im-paired wakefulness) on clinical grounds have been shown to have significantobstructive sleep apnea of at least moderate severity during polysomnog-raphy [55,56]. Although few patients with full-blown clinical symptoms ofsleep apnea have minimal apneas or hypopneas, many otherwise asymptom-atic snorers (30%–50%) have significant sleep apnea [57,58].

Patients with altered levels of wakefulness from sleep apnea may notpresent for treatment in sleep centers but may instead report nonspecificsymptoms of lethargy, depression, and cognitive and memory impairment toclinicians in fields such as endocrinology, psychiatry, and neurology. Justhow many of these patients with such nonspecific complaints actually haveunderlying sleep apnea is speculative, but the true incidence of this sleepdisorder is probably grossly underdiagnosed.

One explanation why patients with impaired wakefulness can present insuch a variable manner is that the clinical manifestation of wakefulness isinfluenced by a multitude of factors, such as the extent of sleep architecturedisruption, the patient’s intrinsic factors, and the environmental and externalfactors listed in Table 1. The ability of patients with sleep apnea to overcometheir decreased wakefulness during the awake state by consuming caffeine-laden products or to compensate by sleeping for a longer duration and takingafternoon naps, for example,makes themeasurement of the daytime effects ofsleep apnea extremely difficult and challenging. Factors such as age, gender,and the personality of patients greatly modify the eventual manifestation oftheir altered state of wakefulness.

An important and potentially controversial issue that has been discussedextensively concerns the association of altered wakefulness as a consequenceof sleep apnea with accidents. Although reports of associations of sleep apneawith road traffic accidents abound in the medical literature [25,59,60], directepidemiologic evidence for a causal role of fatigue in car crashes is lacking. Atpresent, there are no well-designed observational epidemiologic studies toestimate the prevalence of impaired wakefulness in the car-driving populationand the level of risk it confers [61]. The recent demonstration that driving aftersleep deprivation presents a risk similar to that of driving under the influenceof alcohol [62,63] has uncovered an entirely new medicolegal aspect to thetreatment of patients with sleep apnea. Although it is logical to hold impairedwakefulness responsible foraccidents (whether traffic, industrial, ordomestic),a direct link between the two is difficult to prove.

The past three decades since the first description of obstructive sleep apneahave seen a rapid increase in understanding of this common sleep condition.Unfortunately, this knowledge still is limited by the constraints of the verytool that have helped in our understanding of sleep apnea and other sleepdisorders, polysomnography. The economics and logistic considerations of


polysomnography are probably the biggest hurdle to holding large-scalestudies for patients with altered levels of wakefulness not typical of sleepapnea (nonsleepy problems). By venturing into newer territories, some dayclinicians may uncover a new, direct association between sleep apnea andproblems related with altered levels of wakefulness, such as depression, thatmay not be sleepiness-related. This knowledgemay change the way we look atneuropsychiatric conditions in the future. Our present understanding of thephysiologic impact of sleep apnea on wakefulness is limited to the effects ofsleep apnea on sleepiness. Future breakthroughs in understanding of the non–sleepiness-related problems of impaired wakefulness brought about by sleepapnea will, without doubt, lead to the earlier diagnosis and treatment of thischallenging condition.

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Table 1

Factors affecting wakefulness in patients with sleep apnea

1. Sleep architecture

Degree of sleep disturbance (arousal index)

Number of sleep arousals (sleep fragmentation)

Duration of arousal-free sleep arousals increases restorative effect of sleep

Nature of stage-related sleep deprivation

The period of disturbance (acute versus chronic)

Recovery/compensatory sleep (length of sleep/naps)

Associated sleep disorders (eg, periodic leg movement, insomnia)

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Personality/psychosocial makeup

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Sex

Associated disease (anxiety, Parkinson’s disease, hypothyroidism, CVA)

3. Daytime environment

Working environment/occupation

Temperature

Light

Noise

4. Other factors

Food/drugs (caffeine, pseudoephedrine, alcohol)

Exercise

Posture


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Nasal obstruction in sleep-disorderedbreathing

Wynne Chen, MD, Clete A. Kushida, MD, PhD*Stanford University Center of Excellence for Sleep Disorders,

401 Quarry Road, Suite 3301, Stanford, CA 94305, USA

The fifth [aberration] is of great interest. . . At the conclusion of the

positive pressure phase [of the nasal pressure curve] there is a period ofapnea [no positive or negative pressure] lasting for only a fraction of asecond or longer. . . It very often occurs in people who have suffered nasalobstruction for a long time and who, we believe, have developed secondary

effects somewhere in the systemic phases of the respiratory act. It is apersisting, most often irreversible finding and is seen even in children andyoung adults. Correction of the causative nasal obstruction does not often

or necessarily change the aberration.—M.H. Cottle [1]

Although several articles have recounted the rich history behind thediscovery of obstructive sleep apnea-hypopnea syndrome (OSAHS) [2–4]and subsequent identification of the clinical syndromes now known as the‘‘sleep-related breathing disorders’’ (SRBDs) [5], it has been generallyunrecognized that reports describing the relationship between nasalbreathing and sleep quality date back to the 1800s. Sleep disturbances wereassociated explicitly with nasal obstruction in 1892 when Carpenter [6]described a patient with ‘‘hypertrophic rhinitis’’ who complained of insomniaand frightening dreams, with impairment of the ‘‘faculties of will, intellect,emotion and memory’’ [7]. Fleiss [8] similarly described 130 cases of what hecalled ‘‘nasal neuroses’’ with the ‘‘incapacity for sustained mental effort, lackof concentrative power, and loss of memory.’’ In 1898, Wells [8] described10 patients with obstructed nasal breathing, eight of whom complained ofexcessive sleepiness that resolved after nasal patency was reestablished. Henoted that patients were often unaware of the connection between theirobstructed nasal breathing and their sleepiness [7] and opined that ‘‘sleephabit’’ should be looked for in mouth breathers. Similar observations also


36 (2003) 437–460


E-mail address: [email protected] (C.A. Kushida).


doi:10.1016/S0030-6665(02)00175-5

were made for children, and in Hill’s paper [9] entitled ‘‘On some causes ofbackwardness and stupidity in children,’’ he noted that the child ‘‘whofrequently suffers from headaches at school, breathes through his mouthinstead of his nose, snores and is restless at night, and wakes up with a drymouth in the morning, is well worthy of the solicitous attention of the schoolmedical officer.’’ He also noted that many children with obstructed airwaysshowed significant improvement in learning abilities after surgical interven-tion [7]. Yetmany of these early observations were largely ignored throughoutmost of the 1900s [4], until otorhinolaryngologist Maurice Cottle calledattention to this relationship in two of his articles published in the 1960s, asdescribed by Lavie [4]. The often marked improvement in sleep quality afternasal surgery and the observed effects of head position on nasal breathing ledhim to suggest that ‘‘nasal valve changes and turbinate excursions areimportant factors in initiating head and bodymovements in sleep, all of whichtogether are greatly responsible for the �rest� the whole body can obtain duringthe sleep period’’ [4]. He later identified apneas or ‘‘mid-cycle rest(s)’’ in hisstudy of uninasal pressure-curve recordings in sleeping adults and commentedthat ‘‘special attention should be paid to the sleeping habits. Sleeping patternsare in great measure dependent on good nasal function.’’

Today it is recognized that the neurocognitive deficits described in theprevious paragraph likely were related to underlying sleep-disorderedbreathing, recurrent arousals with sleep fragmentation, and abnormal sleeparchitecture [10]. The consequences of such arousals are also well establishedand include not only excessive daytime sleepiness, delayed reaction times, andimpaired performance in neuropsychologic testing but also reduced creativity,decreased quality of life, and increased risk of motor vehicle and occupationalaccidents [11]. There is also evidence that the conventional measures of sleepdisturbance (respiratory variables such as apnea-hypopnea index [AHI],respiratory disturbance index [RDI], and ‘‘macrostructural’’ sleep variablessuch as rapid-eye-movement [REM] latency) on which the diagnosis ofOSAHS had first been made are now inadequate in the evaluation of themilder and more subtle forms of sleep-disordered breathing such as upperairway resistance syndrome (UARS). Increasing attention has been placed onthe ‘‘microstructural’’ characteristics of sleep architecture, such as corticalarousals, EEG activation, and the presence of the cyclic alternating pattern(CAP) [12]. An endogenous arousal-related phenomenon consisting ofcharacteristic sequences of electroencephalographic activity, CAP is believedto represent an oscillatory process of unstable sleep [12,13]. An increase in thepercentage of CAP time in non-REMsleep (CAP rate [CAPR]) is found in anystate of internal or external perturbation of sleep (such as increased upperairway resistance), and reduction in the CAPR to more physiologic valuesoccurs with treatment. The eradication of CAPs reflects consolidation andnormalization of sleep structure and autonomic activity [12].

Despite the current recognition that nasal obstruction can interfere withthe titration [14,15] and tolerance [16] of nasal positive airway pressure

438 W. Chen, C.A. Kushida / Otolaryngol Clin N Am 36 (2003) 437–460

therapy in patients with SRBDs and that the relief of such obstruction mayimprove patient compliance with this therapy [10,17], the exact role thatobstructed nasal breathing plays in the pathogenesis of SRBDs remainspresumptive [18–21]. Studies published thus far have been characterized byrelatively small numbers of patients, inconsistent study design, methodol-ogy, and parameters used to measure sleep disturbance. It seems, however,that correction of nasal obstruction may have its greatest impact on milderforms of sleep-disordered breathing, such as UARS [22]. For infants andyoung children, nasal obstruction may have a significant effect on ventila-tion, craniofacial growth, and future risk for SRBD as an adult. The purposeof this article is to review the putative role of nasal obstruction in the pa-thophysiology of sleep-disordered breathing and to examine the clinicalstudies that have attempted to corroborate this theory. The consequences ofnasal obstruction in infants and children are reviewed, as are the variouscauses of nasal obstruction as it pertains to sleep-disordered breathing, andreasonable treatment options are presented.

Pathophysiologic implications of nasal obstruction

in sleep-related breathing disorders

The Starling resistors

Although upper airway obstruction has been shown to occur at morethan one site and to vary among consecutive apneas in the same individual[23], the primary region of obstruction in SRBDs such as OSAHS is believedto be oropharyngeal-hypopharyngeal, defined as the tip of the soft palate tothe level of the vocal cords [24–26]. The nasopharynx, defined as the regionbetween the free edge of the nasal septum and the top of the soft palate, alsohas been implicated [27,28]. The nose, therefore, may play an important partin upper airway resistance, particularly because it primarily functions asa resistor (Fig. 1) [21] and contributes to 50% of upper airway resistance,adding to that provided by the oropharyngeal tissues and the tongue [21,29].Because the nasal cavity has a more rigid frame, its resistance is moreconstant during waking and sleep states when compared with oral breathing.Nasal breathing is more efficient during sleep [30]. As such, the nosefunctions to match the impedance of the remainder of the upper and lowerrespiratory tract, thereby controlling the respiratory rate and length of bothexpiration and inspiration, as well as tidal volume. By prolonging expiration,pulmonary compliance is increased, as are oxygen uptake, alveolar gasexchange, and recovery of water vapor and heat [21]. Conversely, oninspiration, nasal breathing and increased nasal resistance may augment thepressure differential between the atmosphere and intrathoracic space andthus promote upper airway collapse and obstruction [31].

Nasal airflow generally follows a parabolic curve that arches superiorlythrough the nasal valve, which is the major site of nasal resistance [21,32,33].

439W. Chen, C.A. Kushida / Otolaryngol Clin N Am 36 (2003) 437–460


The internal nasal valve is defined as the area between the caudal end of theupper lateral cartilages (ULCs) and the cartilaginous septum; this angle isnormally 10� to 15� in the Caucasian (leptorrhine) nose and is more obtusein African-American and Asian (platyrrhine) noses [34]. The entire nasalvalve complex is bounded superiorly by the reflection between the ULC andthe septum, posteriorly by the head of the inferior turbinate, inferiorly bythe floor of the nose, and laterally by the bony piriform aperture [34].Resistance progressively increases over the first 2 cm of the nose, spreadover a ‘‘flow-limiting segment’’ corresponding to the length of the ULC[35,36]. Electromyographic studies [37] show that the function of the dilatornaris, nasalis muscle, and apices nasi strongly relates to respiration andprobably contributes to nasal valve function [34]. During vigorous inspi-ration, when the negative nasopharyngeal and intranasal pressure increasesto generate more flow, there is a proportional increase in the transmuralpressure gradient (normal atmospheric pressure minus intranasal pressure),until the latter reaches a critical value, leading to collapse of the ULC [32];this ‘‘flow-limiting segment’’ therefore acts like a Starling resistor [35].Partial collapse of the ULC normally occurs at a ventilatory flow of 30L/min, preventing further increases in intranasal pressure from augmentingflow [34].

Nasal resistance also can be affected by the air temperature and humidity,posture, the enlargement or constriction of blood vessels in the nose, andmucosal changes, however [38]. Mucosal changes seem to play a significantrole in the modulation of nasal resistance because apneas and hypopneas

Fig. 1. Similar to the collapsible hypotonic pharyngeal segment described in the ‘‘composite’’

theory [7l] of upper airway obstruction during sleep, the ‘‘flow-limiting segment’’ of the nasal

valve, influenced by nasal reflexes, also can act like a Starling resistor in augmenting nasal

resistance. Accordingly, only two variables influence nasal valve closure—the amount of

negative pressure generated at the nasal valve and the critical transmural pressure gradient;

these variables correspond to static (Stat) and dynamic (Dyn) forms of nasal valve dysfunction

(see text). Mucosal changes related to air temperature and humidity and the effects of posture

on the nasal cycle also may affect resistance at the nose (Rus), however. This increase in

upstream resistance may decrease maximal inspiratory flow (Vmax) by decreasing the upstream

pressure (Pus) in the setting of positive pressure surrounding the collapsible pharyngeal segment

(Pcrit). Narrowing of the pharyngeal airway may contribute to increased pharyngeal

compliance according to the Tube law and increased velocity of airflow within this segment,

with increased inward pressure of the pharyngeal walls (Bernoulli effect). This pharyngeal

narrowing and progressive flow limitation on inspiratory effort culminate in an obstructive

apnea when the upstream nasal pressure (Pus) falls below Pcrit. Underlying genetic sus-

ceptibility for respiratory instability during sleep may affect these interactions. Acute mouth

opening, with or without transition to oral breathing, also may promote pharyngeal collapse by

these mechanisms and promote retrolingual airway obstruction. Chronic mouth breathing in

children may lead to craniomandibular deficiencies and neuromuscular abnormalities that may

increase future susceptibility to upper airway obstruction and sleep-disordered breathing.

GERD ¼ gastroesophageal reflux disease; Patm ¼ atmospheric pressure; PDS ¼ downstream

pressure; V.M.O. ¼ ventilatory motor output; VT ¼ tidal volume. *Poiseuille’s law.

m441W. Chen, C.A. Kushida / Otolaryngol Clin N Am 36 (2003) 437–460

can be induced during sleep from chronic mucosal stimulation with anirritant [39]. Several studies have pointed toward the presence of nonspecificinflammation [40,41], which may work in synergy with these other factors toinfluence nasal resistance [42].

Stimulation of nasal reflexes also may influence upper airway obstruc-tion, because nasal obstruction may disturb reflex mechanisms mediatedthrough the trigeminal or vagal nerves. When afferent input for the nasalsensory receptors is acutely decreased, respiratory rhythm is disturbed,leading to apnea [21,43]. Nasal dilator muscles have been shown to work inconjunction with other dilators of the upper airway during sleep, such as thegenioglossus muscles. In normal subjects, the nasal alae demonstrate in-spiratory bursts of activity, resulting in nasal flaring that precedes diaphrag-matic activity—an event that is referred to as preactivation [21,44,45]. Theinterval between nasal dilator preactivation and initiation of inspirationappears earlier during sleep and hypercapnia [21]. This preactivation isgreatest after an apneic event in men with OSAHS, suggesting thatpreactivation is a compensatory attempt to open the nasal airway before theupper airway pressures are lowered by diaphragmatic contraction, therebypromoting upper airway patency and stability in preparation for the nextattempted breath [21].

Body position also may influence upper airway patency, based on the factthat the nasal mucosa and related resistance exhibit not only diurnal butalso postural variations [18,46]. The cavernous plexuses within the nasalmucosa are responsible for the nasal cycle and are under autonomic control;whereas nasal resistance is maximal at night and in the early morning [46],the nasal mucosa also exhibits an alternating pattern of left-to-rightcongestion and decongestion [18]. It also has been demonstrated that nasalresistance increases in the supine and lateral positions (with higher resistanceon the dependent side) [46,47]. Relatively asymptomatic nasal obstruction,either unilateral or bilateral, may become symptomatic when recumbent[38,47], and ‘‘paradoxical nasal obstruction’’ [38] may occur in the setting ofa fixed unilateral nasal obstruction.

In turn, there are several indirect mechanisms by which nasal obstructionand increased nasal resistance may affect upper airway resistance andsubsequent pharyngeal obstruction [21]. The first involves alterations inupper airway aerodynamics (Fig. 1). Although upper airway obstructionmay begin at end expiration, it is during subsequent inspiration thatpharyngeal flow further decreases and ultimately stops, because the pharynxis normally the major limiting factor in inspiratory flow [21]. As describedby Badr [48], the pharynx may be hypotonic as a consequence of decreasedventilatory motor output associated with postarousal hypocapnia, sleepstage (REM sleep), and genetic predisposition to respiratory instability[21,49]. Because the capacity to sense pressure and airflow in the upperairway may directly affect activity of the respiratory muscles during sleep[21,50], localized polyneuropathy possibly related to vibratory trauma also


may contribute to airway instability and the development of upper airwayobstruction in these patients [21,47,51,52]. Gastroesophageal reflux relatedto excessive diaphragmatic activity may similarly inflame and progressivelyscar the pharyngeal mucosa [52].

Like the nasal valve, the hypotonic pharynx may act as a Starlingresistor, with a collapsible segment that is susceptible to the influences ofthe surrounding pressure (referred to as the critical closing pressure) andsubatmospheric downstream pressure of the thoracic pump muscles,including the diaphragm [48]. Maximal flow through this Starling resistorthen would be determined by the resistance of the upstream segment, ornasal resistance, and the critical closing pressure, which is more positive inpatients with sleep-disordered breathing. The application of negative nasalpressure then would result in progressive flow limitation and obstructiveapnea once nasal pressure is reduced below the critical closing pressure[48]. Narrowing of the pharyngeal airway also would lead to increasedpharyngeal compliance according to the Tube law and owing to increasedvelocity of airflow and increased inward pressure on the pharyngeal walls(Bernoulli effect), promote further pharyngeal narrowing [48].

There also may be a genetic predisposition for sleep-induced respiratoryinstability, as suggested by the finding that nasal occlusion resulted ina significantly higher frequency of apneic episodes in a study of six sons ofpatients with OSAHS when compared with age-matched control subjectswithout familial history of sleep-disordered breathing [49]. It has beensuggested that such individuals may progress to more severe forms ofSRBDs at a faster rate than those without such a neurobiologic pre-disposition [21].

The role of mouth opening in upper airway obstruction

It also should be kept in mind that mouth opening, with or withouttransition to oral breathing (as occurs in complete nasal obstruction), maycontribute further to upper airway flow limitation and collapse, by theinferior movement of the mandible and associated decrease in pharyngealdiameter. This movement of the mandible also is associated with a reductionin the length of the upper airway dilator muscles that lay between themandible and the hyoid bone, which decreases their mechanical efficiency inplacing them at an unfavorable position on their length-tension curve [53].The base of the tongue also may fall backward, resulting in a reduction inthe posterior pharyngeal space [43,47]. With the additional transition to oralbreathing, increased effort is required to overcome the increase in oral air-way resistance related to the relaxation of oral and pharyngeal musculatureduring sleep [30], leading to greater negative pressures in the pharynx andhigher risk for collapse [30]. The loss of nasal reflexes may impair upperairway muscle tone further [54,55].


The clinical association between nasal obstruction

and sleep-related breathing disorders

Early studies and the importance of cephalometrics

Early studies investigating the role of nasal obstruction in sleep-disordered breathing were uncontrolled and limited by small sample sizes.Studies using artificial models such as nasal packing [56,57] showed thatduring periods of acute bilateral (complete) nasal obstruction, healthyvolunteers exhibited more arousals during sleep and experienced lighter(stage 1) sleep; however, the role played by the transition to oral breathingwas not specifically assessed. Lavie et al [58] further examined differencesbetween complete and partial nasal obstruction in 10 healthy adults withoutotolaryngologic lesions. Studied by overnight polysomnography with eitherunilateral or bilateral nasal occlusion with nasal tape, significant increases inapneas per hour were noted. The number of apneas increased from a baselinemean of 1.4 (�1.9) to 3.1 (�3.5) and to 7.9 (�12.2) with unilateral andbilateral occlusion, respectively; the difference seen in the setting of bilateralnasal occlusion was found to be statistically significant (P < 0.03). The mostfrequent findings, however, were periodic breathing of alternating hypopneaand hyperpnea and changes in respiratory rate without noticeable changesin tidal volume, most prominent during light sleep. Two subjects, one maleand one female, showed dramatic increases in the number of bothobstructive and central apneas during one night of bilateral nasal occlusion,suggesting that they may have had anatomic features that may havepredisposed them to more significant upper airway obstruction [59].

This possibility was investigated further by Suratt et al [60], who studiedthe response of 15 healthy men to acute bilateral intranasal occlusion usinggauze impregnated with petrolatum. Overnight polysomnography withesophageal manometry was performed, and oral resistance was measuredusing pulse (inspiratory) flow resistance. They found that intranasal occlusionincreased airway obstruction during sleep, with the minutes of airwayobstruction per hour of sleep significantly increased after nasal occlusion(P < 0.05). Although there was an overall correlation between pulse flowresistance and the number of apneas and hypopneas, this correlation did notreach statistical significance; interestingly, the patientwho developed themostapneas had the highest pulse flow resistance. There was also a trend towardlighter sleep and less slow-wave and REM sleep with nasal occlusion anda statistically significant increase in both sleep latency and REM latency. Theinvestigators hypothesized that subjects with more narrowed oropharyngealairways would have more apneas during nasal obstruction than patients withlarger airways in the setting of pharyngeal muscle atonia during sleep.

Five years later, Series et al [10] revisited this issue in patients with nasalseptal deviation, a natural and more chronic model of nasal obstruction.Their study included 20 generally obese (average body mass index of


34.0 � 1.7 kg/m2), older men and women with obstructive sleep apnea, all ofwhom underwent surgical correction. The subjects also underwent pre-operative and postoperative polysomnography with esophageal manometryand had cephalometric measurements (angle from sella to the nasion tosubspinal point [SNB], posterior airway space [PAS], behind the tongue baseand limited by soft tissues, and distance from mandibular plane to hyoidbone [MP-H]) taken; nasal resistance was measured in 14 subjects whowould allow it. Although nasal surgery was effective in improving nasalairflow, with subjective improvement in all subjects and a reduced diurnalnasal resistance in the subjects in whom it was measured, this decrease innasal resistance did not correlate with respiratory variables; the group asa whole showed no improvement in RDI, total apnea time, or severity ofnocturnal desaturations. Both the PAS and MP-H distances were normal inthe four patients in whom RDIs did return to normal after surgery,however. The mean AHI (16.7) of these four patients was relatively lowwhen compared with the rest of the group. The authors suggested thatoverall, nasal surgery showed limited effectiveness in the treatment of sleepapnea in these adults, but it did benefit all patients who had normal PASand MP-H distances. They believed that this variability in surgical outcomeswas related to the presence of other oropharyngeal abnormalities (which, asthe authors argued, may have been due to chronic nasal obstruction leadingto craniomandibular abnormalities). They sought to verify this hypothesis ina subsequent study [61] examining 14 patients with symptoms suggestive ofsleep-disordered breathing who also had symptomatic fixed nasal obstruc-tion in the form of septal deviation or turbinate hypertrophy with orwithout polyps on examination. All were proven to have mild to moderateOSAHS (AHI, 13.3–25.0) and then were matched by PAS and MP-Hmeasurements into normal and abnormal cephalometry groups. All thepatients also underwent preoperative and postoperative polysomnograms,with eight accepting esophageal manometry and 10 subjects also undergoingnasal resistance measurements. After surgery, each patient felt dramaticimprovement in nasal ventilation, and a similar decrease in nasal resistancewas seen in both groups. Although no significant difference in sleep archi-tecture was seen between the two groups after surgery, sleep fragmentation(as assessed by the number of arousals) was significantly lower in the normalcephalometry group. The frequency of breathing abnormalities (AHI)returned to normal values (<10) in all but one of the subjects in this groupand remained unchanged in all those with abnormal PAS and MP-Hdistances.

Correlation with nasal resistance

An attempt to correlate nasal resistance with nasal obstruction and sleep-disordered breathing was made by DeVito et al [47] in their investigation


into the prevalence of nasal obstruction among 36 of 150 initial subjectsreferred to their otolaryngologic clinic for possible sleep-disorderedbreathing; the subjects ultimately were diagnosed as having OSAHS. Basedon clinical examination and cephalometric measures, these 36 subjects hadevidence of airway obstruction only at the level of the oropharynx, withoutsignificant abnormalities in the tongue, jaw, or hyoid bones. Nasalabnormalities included septal deviation with hypertrophy of the inferiorand middle turbinates, isolated septal deviation, restriction in the valvularregion, and hypertrophy of the inferior turbinates. To account for positionalchanges in nasal resistance, active anterior rhinomanometry was used tomeasure nasal resistance in the seated and supine (awake) positions; sevenpatients had abnormal upright nasal resistance that worsened when supine,nine had normal resistances in a seated position that worsened in a supineposition, and 20 had normal resistances both in a seated and a supineposition. Although there was an upward trend in RDI with increasing nasalresistance from the seated to the supine position, there was no statisticaldifference in the AHI among the three groups.

Using a more accurate measure of nasal resistance (posterior rhinoman-ometry with the use of a mask initially used for CPAP, and tongueprotrusion), however, Lofaso et al [62] were able to correlate nasal resistancewith sleep-disordered breathing in their prospective examination of 541unselected snorers referred for suspected sleep-disordered breathing. Theinvestigators measured nasal resistance in 528 subjects with or withouttopical decongestants. Each subject had anthropometric data collected andunderwent overnight polysomnography, spirometry, and cephalometricanalysis. Two hundred and fifty-nine subjects were found to have OSAHS,based on an AHI of 15 or more (mean, 37.5 � 23.3). Baseline data revealedthat age, sex ratio (men), and body mass index were significantly higherin the OSAHS group than in the non-OSAHS group. Comparisons ofcephalometric measurements showed that the angle from the sella to thenasion to the subspinale (SNA) and PAS were similar in both groups,whereas SNB was lower and the posterior nasal spine to the tip of soft palate(PNS-P) and MP-H were higher in the patients with OSAHS. Nasalresistance was significantly higher in the OSAHS group, and although thehighest unilateral nasal resistance was not significantly different between thetwo groups, basal bilateral nasal resistance did correlate significantly (P <0.0001) with OSAHS severity, and stepwise multiple-regression analysisrevealed nasal resistance to be a contributing factor in OSAHS. Althoughnasal examinations of their subjects were not reported, the investigatorsconcluded that their results supported the hypothesis that nasal obstructionthat is either unresponsive (such as septal deviation) or responsive to nasaldecongestants (such as vasomotor rhinitis) contributes to sleep-disorderedbreathing. They suggested that daytime nasal obstruction, whatever thecause, was a risk factor for OSAHS, but its influence was less than that ofobesity or cephalometric landmarks.


Rhinitis and sleep-related breathing disorders

With allergic and nonallergic rhinitis affecting more than 20% of the USpopulation [63], it is not surprising that this naturally occurring model ofnasal obstruction also has been used to investigate the role of nasal ob-struction in sleep-disordered breathing. Extensively reviewed by Scharf andCohen [31], nasal obstruction does seem to contribute to sleep-disorderedbreathing in predisposed individuals. Most recently, Houser et al [22] retro-spectively examined 50 subjects with seasonal or perennial allergic rhinitisand found significant differences in congestion factors at cross-sectional area 1of the nose (the anterior portion of the inferior turbinate or the nasalvalve) between those withmildOSAHS (meanRDI of 14.5) and thosewithoutsleep apnea (P ¼ 0.03).

Nasal obstruction in infants and children, allergic rhinitis,

and developmental implications

Mouth breathing in infants and children

The issues of rhinitis, nasal obstruction, and attendant mouth breathingare particularly important in infants and children. For infants, the transitionfrom nasal to oral breathing is particularly dangerous because of the closeapproximation of the soft palate, tongue, and epiglottis [64]. The infant’sjaw is also almost horizontal, and its articulation with the skull is unstable,which allows the relatively flexible mandible to displace posteriorly. Thetongue, a mobile muscular mass, sits on the floor of the mouth, anchored tothe mobile mandible and to the hyoid. At birth and usually for the first 5 to6 months of life, the tongue fills the oral cavity unless the infant is crying orgasping, and thus, breathing occurs preferentially through the nasal pas-sages [65]. Nasal obstruction, such as that caused by bilateral choanalatresia, therefore can lead to complete upper airway obstruction [66]. Cycliccyanosis ensues, which is relieved rapidly by crying or mouth opening.

A recent study in young children by McColley et al [67] has shown anincrease in frequency of OSAHS in habitual snorers with allergic sen-sitization. A history of sinus problems (adjusted odds ratio, 5.21; 95% con-fidence interval, 1.66–16.12) also recently was found to be an independentpredictor of sleep-disordered breathing in children and adolescents as part ofa genetic-epidemiology study of sleep-disordered breathing [68].

Tonsillar and adenoidal hypertrophy

Children with allergic rhinitis often become mouth breathers and snore atnight as a result of nasal obstruction and adenoidal hypertrophy [69], withcongestion of the inferior turbinate [70]. This occurrence corresponds withthe peak prevalence of childhood OSAHS, occurring between 2 and 8 years


of age, when the tonsils and adenoids are the largest in relation tounderlying airway size. Increased nasal resistance, as measured by anteriorrhinometry, has been found to correlate with severity of sleep apnea inchildren with adenotonsillar hypertrophy [71]. Because of the difficulties indistinguishing simple snoring from sleep apnea [72], children who snorealways should be evaluated for signs and symptoms of sleep-disorderedbreathing, such as failure to thrive, daytime sleepiness, behavioral problems,and neurocognitive deficits [73–75].

Although several studies have shown that symptoms of sleep-disorderedbreathing in children often completely resolve after adenotonsillectomy[73,76], incomplete resolution of symptoms may occur in the setting of otherdiseases, such as Down’s syndrome, and craniofacial anomalies such as thePierre Robin sequence [76]. Alternatively, OSAHS symptomsmay recur yearslater in some children, particularly in those in whom only a unilateraltonsillectomy is performed [76] or in whommore subtle craniofacial variancesexist [77]. Children successfully treated with adenotonsillectomy for OSAHSshould be followed closely for the recurrence of signs and symptoms of sleep-disordered breathing, particularly in families with bite abnormalities thatmay reach their full manifestation only during puberty [76,78].

Craniofacial and upper airway development

Apart from genetic facial predisposition, chronic nasal obstruction inyoung children may lead to acquired craniofacial abnormalities, which mayfurther compromise the stability of the upper airway [61]. Lowering of themandible to establish the oral airway and requisite posture of the mandibleand lower tongue position may alter the relationship of the dental arches,causing an increased lower facial height and a narrow, high palatal vault[79]. These children exhibit facial changes referred to as the ‘‘adenoid face’’or ‘‘long-face syndrome’’ [80], with a long and narrow facial appearance,retrognathia, micrognathia, and a high, narrowly arched palate [81]. Experi-mental studies of complete nasal obstruction with oral breathing in youngprimates have revealed alterations in the tonic and phasic electromyographicactivity of the upper airway (geniohyoid and genioglossus muscles),mandibular, and facial muscles. Changes in mandibular growth observedin mouth-breathing monkeys (posterior rotation of the mandible with lowerposition of the chin) can be associated with these changes in muscularactivity, and because pharyngeal configuration depends on anatomic bonystructures, chronic nasal airflow obstruction may lead to similar neuromus-cular and craniomandibular abnormalities in humans.

Causes of nasal obstruction

A careful history focusing on nasal symptoms and prior nasal surgery ortrauma should complement the physical examination of the facial muscles,


nasal valve and nasal passages, oral cavity and oropharynx, as well as anassessment of the craniofacial skeleton [30,55,82]. Representative causes ofnasopharyngeal obstruction can be broadly divided into structural, muco-sal, and neuromuscular etiologies (Table 1). Alternatively, they may beseparated into congenital and acquired [83] or congestive versus nonconges-tive etiologies [30]. Among these etiologies, nasal obstruction related to nasalcongestion and pathologic conditions related to the nasal valve deservespecial mention.

Nasal congestion

Nasal congestion involves the cavernous tissues of the turbinates and iscaused most commonly by allergic rhinitis, vasomotor rhinitis, chronicsinusitis, and upper respiratory tract viral infections [30]. As reviewed byCorey et al [30], the most commonly associated structural abnormality isseptal deviation, which can cause the sensation of chronic unilateral nasalcongestion or congestion that fluctuates with the nasal cycle. The inferiorturbinates may exhibit a compensatory hypertrophy on the contralateralside and therefore may lead to bilateral nasal obstruction [30,84] Polyps,nasal or nasopharyngeal, or those associated with cystic fibrosis, asthma, oraspirin sensitivity also may be associated with nasal congestion [30]. Thesymptoms of nonallergic rhinitis with eosinophilia syndrome (NARES) aresimilar to those of perennial allergic rhinitis, and NARES may represent areaction to an unknown agent or an overlap syndrome with vasomotorrhinitis. States of hormonal flux, such as those that occur during pregnancyand puberty, are associated with nasal mucosal engorgement and obstruc-tion; hypothyroidism also can cause rhinitic symptoms [30].

Static and dynamic lesions

Nasal valve dysfunction may contribute to symptoms in 13% of adultsreporting chronic nasal obstruction [34]. The behavior of the nasal valve asa Starling resistor must be kept in mind when discussing its dysfunction, aswell as Poiseuille’s law, which relates airflow to the radius of the nasalpassages, raised to the fourth power (Fig. 1) [34]. Dilator muscles of the nosecan modulate the size of the nasal valve and can decrease the anterior nasalresistance [21], as previously mentioned. Similar to conditions in the pha-ryngeal airway, however, it is important to realize that only two variablesdetermine nasal valve closure—the amount of negative pressure generated atthe nasal valve and the critical transmural pressure gradient, a function ofthe mechanical properties of the cartilage and soft tissues. Nasal valvepathology can cause either static or dynamic dysfunction. Static dysfunctionis caused by fixed obstruction at the level of the nasal valve, requiring morenegative intranasal pressure to generate a given amount of nasal airflow [34];for example, the attempt to maintain nasal airflow in the setting of small


Table

1

Conditionsandrelatedfactors

thatmaycontribute

toincreasednasalresistance

andnasalobstruction

Nature

ofproblem

Structural

Mucosala

Neuromuscular

Location

Softtissue

obstruction

(possibly

reversible)

Bone/cartilage

deform

ity(fixed)

Foreignbody

(reversible)

Nasopharynx

Adenoid

hypertrophy

Tumor

—Posteriornasal

packing

Nasopharyngitis

Infectiousmononucleosis

—

NasopharyngealCA

Hamartoma

Nasalsyphilis

Primary

tuberculosis

Nasopharyngealstenosis

Rhinoscleroma

Tonsillectomy/adenoidectomy

(Klebsiella

rhinoscleromatis)

Pharyngoplastyor

palatopharyngoplasty

Diphtheria

Midfacialgranuloma

Cicatricialbullouspem

phigoid

Wegener’sgranuloma

Syphilis/treatm

ent

Congenital

Congenitalcraniofacialanomalies

Choanalatresia

Antrochoanalpolyps

Polyps

Cystic

fibrosis

Asthma

Aspirin

sensitivity

Amyloidosis

Cysts

Nasalcavity

Septum

Trauma

Polyposis

Septaldeviation

Congenitalcraniofacial

anomalies

Anteriornasal

packing

Trauma

—


Turbinates

Trauma

Polyposis

Conchalhypertrophy


anomalies

Anteriornasal

packing

Allergic

rhinitis

Vasomotorrhinitis

NARES

—

Infectiousrhinitis(viral

orbacterial)

Rhinitismedica

mentosa

Reactionto

BB,ASA,

NSAID

S,andso

forth

Secondary

toDNSor

lesions/polyps

Trauma

Metabolic/endocrine

Pregnancy

Puberty

Hypothyroidism

Nasalvalves

Postrhinoplasty

Trauma

Tip

ptosis

Cicatricialstenosis

Postrhinoplasty

Tip

ptosis

Paradoxic

lateralcrura


anomalies

Anteriornasal

packing

Trauma

Facialparalysis

(zygomaticotemporal

divisionoffacialnerve)

aCongestionmayoccursecondary

toother

causesofnasalobstruction,such

asneoplastic

lesions,idiopathic

polyps,orpolypsrelatedto

cystic

fibrosis,

asthma,aspirin

sensitivity,chronicrhinosinusitis,orallergicrhinitis.A

deviatednasalseptum

maycause

asensationofchronicunilateralnasalcongestionor

congestionthatfluctuateswiththenasalcycleandmaybeassociatedwithcompensatory

hypertrophyofthecontralateralinferiorturbinate.

Abbreviations:

ASA,aspirin;BB,beta-blockers;

DNS,deviated

nasalseptum;NARES,nonallergic

rhinitis

with

eosinophilia

syndrome;

NSAID

S,

nonsteroidalanti-inflammatory

drugs.

Data

from

Refs.

[21,30,34,38,106].


vestibular lesions such as cysts or minor septal deflections can increase thenegative pressure generated at the valve and thus, nasal resistance [21,32].Conversely, dynamic valvular dysfunction is related to flaccid or absentstructural support of the sidewall and results in closure of the nasal valve atlower transmural pressures [34]. Laxity in the soft tissues or cartilage andfacial muscle weakness or paralysis may predispose one to such nasalclosure [21,32,34].

Treatment modalities

Pharmacologic treatment options for rhinitis

Decongestants are appropriate in treating nasal obstruction related torhinitis, and when related to allergies, avoidance of allergens andenvironmental control are also appropriate. In addition, pharmacotherapywith antihistamines, topical intranasal corticosteroids, mast-cell stabilizers,and immunotherapy also may help [30,31]. Later-generation antihistaminesare preferred, because the first-generation (or ‘‘classic’’) antihistamines suchas diphenhydramine, chlorpheniramine, and the phenothiazine prometha-zine are lipophilic and thus sedating; not only may they worsen underlyingsleep-disordered breathing but they also may suppress REM sleep andproduce a marked compensatory rebound above baseline levels afterwithdrawal of these agents [30,31]. This rebound has been associated withan increase in both amount and intensity of REM sleep and thus sleepinstability and fragmentation [31].

Apparatus-related therapy

Nasal dilatation devices directed toward the nasal valve area also havebeen used to reduce nasal resistance. As such, the effectiveness of internal(eg, Nozovent [Prevancure AB; Vastra Frolunda, Sweden]) and external (eg,Breathe Right Nasal Strips [CNS; Bloomington, MN]) dilators has beenstudied, but studies have been limited by relatively small numbers of subjectsand variability in methodology. Several negative studies have beenpublished [85–88]. A study by Kerr et al [89], however, showed that among10 generally obese (body mass index, 25.9–38.9; mean, 32.0 kg/m2) men withmoderate (mean AHI of approximately 20 respiratory events per hour) sleepapnea, six of whom had evidence of chronic nasal obstruction related toseptal deviation, narrowed nasal valves, mucosal swelling, or a combinationof these factors, nasal resistance decreased in all of those who used a topicalnasal vasoconstrictor and internal dilators (vestibular stents). Althoughtreatment was associated with subjective improvement in sleep quality, witha mean drop in nasal resistance (as measured by posterior rhinomanometry)to 73% (P < 0.001), there was no significant improvement in sleeparchitecture or AHI. There was a reduction in the number of arousals


per hour, from 52.4 with placebo to 43.7 with treatment (P < 0.04),however. These findings suggest that there may have been an improvementin upper airway resistance in these patients, because the most importantmechanism of arousal in sleep-disordered breathing may be increasedrespiratory efforts and magnitude of intrapleural pressure swings [90].Alternatively, more significant changes in AHI may have been detected ifthe investigators had accounted for other risk factors for sleep-disorderedbreathing, such as pharyngeal obstruction, body weight, and age [91].

This possibility was addressed by Gosepath et al [91], examined thispossibility by studying the effects of BreatheRight nasal strips onRDI among26 subjects with a history of sleep-disordered breathing and impaired nasalbreathing. The subjects were older (mean age, 52 years), and although all hadanRDI of 10 per hour or higher, the distribution andmeanwere not specified;furthermore, the investigators rather unconventionally defined RDI as thesum of apnea index (AI), hypopnea index (HI), and ‘‘index of obstructivesnoring.’’ Rhinoscopic examination and clinical assessment of pharyngealcollapsibility (Muller’s maneuver) were performed, and each subject wasstudied with overnight polysomnography; most of them also were examinedby anterior rhinomanometry and acoustic rhinometry with and withouttopical decongestion. Although only 19 subjects showed a decrease in RDI, asa group, the average values of both AI and HI did fall significantly (22.8–19.8[P ¼ 0.08] and 8.6-5.8 [P ¼ 0.013], respectively). The four patients in whomthe most dramatic reductions in RDI were seen (to less than 10 per hour) werethose who started with low values (RDIs between 10.3 and 16.7 that fell tobetween 2.2 and 6.3 [58%–81% reductions]), and thus had themildest disease.Similarly, the average RDI of the participants who did show a reductionin RDI with the nasal strips was lower than that of the groups that did not(27.4 per hour versus 43.5 per hour), suggesting that the patients with moresevere sleep-disordered breathing experienced less benefit from the BreatheRight nasal strips.

In an attempt to extend this hypothesis to patients with the mildest SRBD,Bahammam et al [13] studied the effects of Breathe Right nasal strips on 18subjects with the diagnosis of UARS without nasal pathology. However, noesophageal manometry was used, given the risk of sleep disruption andreduction in the nasal cross-sectional area, which could possibly counteractthe effect of the treatment [92]. Therefore, the participants were defined ashaving a ‘‘clinical history of snoring, clinical complaint of excessive daytimesleepiness, and anAHI<15 on original clinical evaluation, andmore than fivearousals per hour associated with snores, snorts, or brief cessations ofbreathing that were shorter than accepted criteria for apnea (<10 sec),’’without specific mention of arousals related to increased respiratory efforts,which is an essential feature of UARS [93]. The subjects� mean RDI was 8.9per hour. Nevertheless, they were given a ‘‘placebo’’ or regular Breathe Rightstrips and studiedwith overnight polysomnography andmultiple sleep latencytesting. Twelve subjects were men, and most were overweight (mean body


mass index of 29�7.4 kg/m2). Significant increases in nasal cross-sectionalarea were seen by acoustic rhinometry, and the percentage of stage 1 sleep,expressed as a percentage of total sleep time, was also significantly loweron the treatment nights (7.1% � 0.7%) compared with placebo nights(8.6% � 0.8%, P ¼ 0.03). Although this finding suggested reduced sleepdisruption, no changes could be detected in the AI or in sleepiness by multiplesleep latency testing.

External nasal dilators may have an effect on more subtle measures ofsleep disruption, such as CAP, however. In a study using Breathe Rightstrips in nine snorers without subjective nasal congestion who may havehad mild sleep-disordered breathing, Scharf et al [94] showed that CAP maybe reduced. Although the subjects studied were described as snorers withAHIs of less than five per hour without ‘‘clinically suspected levels of OSA(to make mild snoring the secondary diagnosis),’’ they may have had upperairway resistance or UARS, because esophageal manometry data were notavailable. As studied for two consecutive nights with or without BreatheRight strips, there was a reduction in CAPR during stage 1 and 2 sleep onthe experimental nights compared with the control nights (28.4% � 15.7%versus 37.9% � 18.4%, P < 0.05).

Positive airway pressure therapy and temperature-controlledradiofrequency reduction of turbinate hypertrophy

In patients who are being treated with either nasal continuous positiveairway pressure (CPAP) or bilevel positive airway pressure (BiPAP) for sleep-disordered breathing, humidification may increase tolerance of positiveairway pressure therapy within the critical first 3 months of therapy. Heatedhumidification may attenuate the mucosal blood flux associated with thecooling and drying effects of such therapy [16] and may be particularlyimportant in patients with allergic rhinitis [95]. Submucosal temperature-controlled radiofrequency reduction of inferior turbinate hypertrophy alsomay improve CPAP tolerance and adherence [17]. Its role as an alternative tonasal CPAP therapy in mild forms of sleep-disordered breathing requiresfurther study, however [96].

Surgical interventions

Although case reports [97,98] have suggested that correction of nasalobstruction such as that due to septal deviation may improve subjectivedaytime complaints of OSAHS, subsequent surgical studies have not beenhelpful in assessing the true effectiveness of nasal surgery in the treatment ofsleep-disordered breathing, mainly because of insufficient data [76]. Studieshave been flawed [10] by the relatively small number of patients studied [99];the fact that nasal surgery often is associated with other surgical procedures,such as tonsillectomy [100]; and the lack of quantification of associated


pharyngeal abnormalities and objective data regarding nasal resistance andrespiratory variables such as AHI or RDI [100,101]. Although the use ofa strict criterion for surgical success, such as improvement in AHI by at least50% with an absolute value below 20 per hour has been recommended[102,103], this goal may be difficult to achieve in mild forms of sleep-disordered breathing. Even when attainable in more severe cases of sleep-disordered breathing, such improvement may not be clinically relevant,because daytime sleepiness and sleep fragmentation still may persist [104]. Ithas been suggested that measures of effectiveness used in assessing othermodes of treatment, such as nasal CPAP, be applied to surgical inter-ventions as well [104]. These measures would include assessment of parame-ters such as microarousals, CAP, and upper airway resistance. Because thereis currently no accepted criteria to predict who will benefit from nasalsurgery, the study by Series et al [61] suggests that at least in mild sleep-disordered breathing, patients with narrowing of the posterior airway spaceand increased distance from the mandible to the hyoid bone may be poorcandidates for such intervention.

Summary

It has been 30 years since Cottle suggested that ‘‘sleeping patterns are ingreat measure dependent on good nasal function’’ [1]. During this time, wehave identified the OSAHS and related forms of sleep-disordered breathingsuch as UARS, and better appreciate the clinical sequelae of recurrentarousals and sleep fragmentation. Yet the exact role that obstructed nasalbreathing plays in the pathogenesis of such sleep disorders remainspresumptive, and robust clinical studies to corroborate this theory remainelusive; however, patients who may benefit most from correction of nasalobstruction as a sole intervention may be those with the mildest forms ofsleep-disordered breathing without other significant predisposing anatomicabnormalities. Clearly, more stringently controlled studies [17,105] areneeded, particularly in these types of patients. Until such time, it is reasonableto address issues of nasal obstruction as an adjunct to surgical and nonsurgicaltreatment in all patients who are diagnosed with a sleep-related breathingdisorder.

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Video sleep nasendoscopy:the Hong Kong experience

V.J. Abdullah, FRCS, FHKAMa,*,Y.K. Wing, MRCPsych, FHKAMb,C.A. van Hasselt, FRCS, FHKAMa

aDivision of Otolaryngology, Department of Surgery, Prince of Wales Hospital,

Chinese University of Hong Kong, Shatin, New Territories, Hong KongbDepartment of Psychiatry, Prince of Wales Hospital,

Chinese University of Hong Kong, Shatin, New Territories, Hong Kong

The study of upper airway dynamics in obstructive sleep apnea syndrome(OSAS) has always posed a challenge to the interested clinician. Until thedynamics of obstructive sleep apnea are well understood, the treatmentoptions cannot be comprehensive. To date, continuous positive airwaypressure (CPAP) remains the most efficacious first-line treatment because itstents open the entire upper airway without a need to know. Many patientsare, nevertheless, not amenable to its lifelong use. They should not bedisregarded, particularly if surgical or nonsurgical options other than CPAPcan alleviate, if not cure, the symptoms caused by their condition. Themuch-disfavored tracheostomy, with its associated problems, always helpsin treating OSAS and has achieved the best long-term survival rate [1,2].This finding confirms the importance of understanding the dynamics of theupper airway above the glottis in OSAS, especially if effective surgery is tobe designed.

From the surgical viewpoint, the clear establishment of the obstructivesites is crucial for the planning of effective treatment, if it is available. TheMuller maneuver, once a popular technique of selecting patients foruvulopalatopharyngoplasty [3], is at best an easy-to-perform estimation oftissue collapse in the upper airway under inspiratory suction. The findingsmay differ quite dramatically from the sleep-breathing situation [4]. Cine CT


36 (2003) 461–471

* Corresponding author. Department of ENT, NTEC Chinese University of Hong Kong,

Alice Ho Miu Ling Nethersole Hospital, 11 Chuen On Road, Tai Po, New Territories, Hong

Kong SAR.



doi:10.1016/S0030-6665(02)00176-7

and cine MRI are ideal but not practicable methods in terms of costs, thedifficulties in the overnight study of a patient with OSAS in a confinedspace, and the problems of irradiation in CT. Through-the-night inspectionof the upper airway of the sleeping patient with the fiberoptic nasopharyn-geal endoscope is an ideal but time- and manpower-consuming technique. Itis seldom well tolerated and often results in significantly disturbing thenormal and abnormal sleep patterns. The surgeon naturally prefers to seethe actual events during sleep-breathing difficulties to guide his or her plansfor the appropriate surgical intervention. Video sleep nasendoscopy (VSE)[5] in the (albeit simulated) sleep-breathing situation is the authors’ pre-ferred technique for assessing surgical candidates. It is probably the mostaccurate assessment of the situation or the most effective in revealing theworst situation that stands to be corrected.

The indications

In the authors’ establishment, VSE is reserved for research protocols,selected snorers, and the OSAS surgical candidates as selected by themultidisciplinary team, which comprises respiratory physicians, psychia-trists, neurologists, otolaryngologists, pediatricians (for the pediatric cases),and physiotherapists for the weight-control program for those who areobese. It is not used for the diagnosis of OSAS, and it is interpreted in thelight of a full night’s polysomnographic (PSG) sleep study. The authors’criteria for surgical intervention in adult patients are as follows: they mustbe PSG-proven snorers; patients with upper airway resistance syndrome;patients with OSAS and a body mass index (BMI) of less than 30; andpatients with correctable craniofacial deficits, such as ‘‘South China chin,’’retrognathia that is common in the Cantonese population in the authors’locality. At the authors’ institution, surgical candidates should be less than60 years of age. All surgical candidates are required to have tried CPAP withthe present-day selection of masks for at least 6 months. The proceduresperformed at the authors’ institution for the different VSE-established sitesof obstruction in patients with OSAS are summarized in Table 1.

Video sleep nasendoscopy is useful only if there is a surgical procedureto treat effectively the diagnosed sites of obstruction. Many medium- andlong-term failures of surgical treatment lie in the fundamental design ofthe surgical procedure. The stiffness or extra room achieved by scarring,tightening, or widening procedures are unable to counter the natural laxityof pharyngeal tissue, which yields to the upper airway negative pressure withtime, resulting in re-obstruction. In obese patients with multiple medicalproblems and multilevel obstruction, the authors’ experience with surgeryhas been disappointing. These patients are not subjected to VSE; they arepatiently counseled and recommended for treatment with CPAP. Bilevelpositive airway pressure (BIPAP) is recommended for patients with obesityhypoventilation who are under the supervision of respiratory physicians, or

462 V.J. Abdullah et al / Otolaryngol Clin N Am 36 (2003) 461–471

a simple tracheostomy can be offered. In the authors’ unit, VSE also hasbeen assessed for the establishment of CPAP level and has proven to be ofgreat promise as an efficient and cost-effective means of CPAP titration.

The procedure of video sleep nasendoscopy

Patients who are surgical candidates are admitted as ‘‘day cases.’’ Anintravenous site is established for access during the procedure. The patient ismonitored for transcutaneous oxygen saturation, electrocardiogram abnor-malities, and blood pressure. At present, simultaneous PSG and electroen-cephalographic monitoring is used for research protocols in the authors’unit. The sleep endoscopy laboratory is equipped with oxygen, suction, aconveniently adjustable BIPAP/CPAP machine, and the standard resusci-tation equipment. The more patent nostril is selected, and 10% xylocainespray is delivered to the nasal cavity and the nasopharynx using a long can-nula. A flexible nasopharyngoscopy with the patient awake is performedto exclude static obstructive lesion. A Muller maneuver is performed forcorrelation. Four milligrams of midazolam are given as an inductionbolus with saline flush. The light is dimmed, and the patient is encour-aged to sleep. The dose is increased 1 mg at a time with saline flush untilthe patient sleeps. A minimal 5-minute wait is recommended after the firstbolus and between increments. Increments are needed only if the patient

Table 1

Surgical procedures performed for different sites of obstructiona

Nasal obstruction

Septoplasty

Turbinoplasty

Functional endoscopic sinus surgery (FESS) for nasal polyposis

Velopharyngeal obstruction

Limited uvulopalatopharyngoplasty (tonsillectomy, uvulectomy, and tonsillar pillar suture)

Tonsillar obstruction

Tonsillectomy

Lateral pharyngeal wall

Tonsillectomy and pillar suture

Tongue base obstruction

Hyoid hitch

Phase I surgery for nonreceding chin

Sliding genioplasty for receding chin

Radiofrequency tongue base reduction (under evaluation)

Distraction osteogenesis under evaluation in children

Phase II surgery not performed to date

Epiglottic flop

One-third–One-half laser epiglottic trim

a All procedures performed at the Prince of Wales Hospital, Chinese University of Hong

Kong.

463V.J. Abdullah et al / Otolaryngol Clin N Am 36 (2003) 461–471

shows no sign of sleep onset. The ceiling dose in the authors’ unit is limitedto 7.5 mg intravenously, after which point the patient is deemed to havefailed sedation. The average dose in the authors’ experience is 0.06 mg/kg inOSAS cases. The dose for snorers is variable, and the authors have appliedthe same ceiling dose of 7.5 mg for this group of patients. Once the patient isasleep, obstructive episodes are observed and the endoscopic examination iscarried out after at least two episodes or cycles of obstruction and arousal.If the oxygen saturation (SaO2) should fall below 70%, the CPAP maskis applied and examination is resumed after 5 minutes of unobstructedbreathing. The endoscopic examination is performed using an Olympus P4(Olympus Optical Co. Ltd., Japan) flexible nasopharyngoscope insertedthrough the anesthetized nostril. In the location of obstructive sites,attention is paid to the following levels:

Soft palateLateral pharyngeal wallTonsilsTongue baseEpiglottisHypopharynx (the pyriform fossae squashing in around the larynx)

Once the level or levels of obstruction are established, the patient isreversed with the slow injection of flumazenil (Anexate) intravenously (300–500 lg). It is important to be aware that the mean elimination half-life offlumazenil, which is 35.5 minutes, is shorter than that of midazolam, whichis 107 minutes. Nevertheless, it helps to shorten the duration of sedation.The patient then is turned on his or her side, and the airway is monitored inthe recovery area and then in the high-dependency area of the ward.

Snorers

Snorers are the most difficult group of patients to sedate optimallyfor viewing asleep because they are usually not hypersomnolent. They areeasy to oversedate. The authors are performing less VSEs in this group ofpatients because most would benefit from any of the present range of softpalate and uvula procedures. When the authors do perform VSE in thisgroup of patients to tailor-make surgical procedures after their PSGs, thepatients are sedated with a protocol similar to that of patients with OSAS,with the midazolam ceiling dose set at 7.5 mg, and no obstructive or desat-uration events should be seen throughout the procedure. Tables 2, 3, and 4summarize the authors’ study of video-captured nasoendoscopic findingsof snore-generation sites in 30 successfully sedated snorers (28 men and 2women; mean age, 41.4 years).

It was interesting that in this study, 75% (n ¼ 9) with single-site snoringhad the snore generated by the soft palate, and 54% (n ¼ 7) of the two-sitesnorers had soft palate plus epiglottic snores. Epiglottic and tonsillar


vibrations seem to feature significantly in snore generation. In the authors’experience with VSE in patients with OSAS, epiglottic flutter commonly isseen as the main source of the loud wake-up snore after the obstructivecycle. These findings also support the concept that the use of palatal-stiffening procedures for snorers is likely to be effective in most patients.

Obstructive sleep apnea syndrome

This group of patients is easy to sedate, and most will sleep with theinitial 4 mg of midazolam with their hypersomnolence. Their respiratoryevents have to be watched carefully throughout the procedure, and CPAPshould be administered to them or their sedation should be reversed withflumazenil if SaO2 levels fall below 70% or if arrhythmic episodes developother than the usual mild cyclical slowing and recovery of heart rate withthe obstructive episodes. The authors recommend that one waits for twoobstructive cycles before viewing the events. In experienced hands, the view-ing usually takes no longer than 15 minutes. With the help of intermit-tent CPAP, sleep stage–correlated events can be recorded when simultaneousPSG is used for study purposes. The authors are in the process of data collec-tion for this group of patients. Between October of 1992 and January of2002, the authors performed 893 sleep nasoendoscopy procedures for dif-ferent research and investigation protocols and did not experience an ad-verse event.

The authors’ data on patients with OSAS indicated that 87% of thepatients had multilevel obstruction. In a recent study the authors conductedon 93 patients with a mean respiratory disturbance index of 48.4

Table 2

Summary of snore-generation sites by VSE recordings in 30 snorers

Snore-generation sites No. of patients Percentage of total

Soft palate 26 87%

Tonsils 12 40%

Tongue base 4 13%

Posterior pharyngeal wall 2 6.5%

Epiglottis 12 40%

Table 3

Summary of single/multiple snore-generation sites by VSE recordings in 30 snorers

No. of snoring sites No. of patients Percentage of total

Single site 12 40%

Two sites 13 44%

Three sites 3 10%

Four sites 1 3%

Five sites 1 3%


(respiratory disturbance index range, 15–89) selected for surgical assess-ment, the levels of obstruction and their different combinations wereanalyzed in detail. Of the 93 patients, four patients (4.3%) failed sedation.The 89 patients analyzed comprised 11 women (mean age, 46.9 years) and 78men (mean age, 39.7 years). The mean BMI of the 89 patients was 27.2; themean BMI for the female patients was 26.7 and that for the male patientswas 27.4. The number and percentages of single/multiple-site obstructionand the mean BMI of each subgroup are presented in Table 5.

As can be seen from the findings, the percentage of patients with single-site obstruction is low, at 14.61%. Despite the observable trend of a higherBMI being associated with four or more sites of obstruction as comparedwith single-site obstruction, no conclusion can be fairly drawn from thisselect group of patients. Many of these potential surgical candidates withlower BMIs would have obvious or subtle facial skeletal deficits as the maincontributor to their OSAS. Aside from one patient with a respiratorydisturbance index of 15 with two-site obstruction adequately treated withphase I surgery, all patients were in the moderate/severe obstructive sleepapnea range. Interestingly, the number of obstructive levels does notnecessarily reflect the severity of OSAS and vice versa. In the selected fewwith single-level tonsillar obstruction, a simple tonsillectomy is curative forsevere OSAS. In the authors’ institution, many of the milder cases are notseen because they are referred for dental devices or CPAP at lower

Table 4

The different combinations of snore-generation sites in 30 patients studied with the use of VSE

recordings

Single site Two sites Three sites Four sites Five sites

SP 9 SP+T 3 SP+T+TB 1 SP+T+TB+E 1 SP+T+TB+PP+E 1

T 3 SP+E 7 SP+T+E 2

T+PP 1

SP+TB 1

SP+E 1

Abbreviations: SP, soft palate; T, tonsils; PP, posterior pharyngeal wall; TB, tongue base;

E, epiglottis.

Table 5

The summary of VSE findings regarding single/multiple-site obstruction in patients with OSAS

selected for surgery

No. of obstructive sites No. of patients Percentages of total Mean BMI

Single site 13 14.61% 23.8

Two obstructive sites 16 17.98% 25.5

Three obstructive sites 17 19.10% 24.4

Four obstructive sites 20 22.47% 28.3

Five obstructive sites 12 13.48% 25.4

Six obstructive sites 11 12.36% 27.2


acceptable pressures, although they may be the best candidates for surgery.The different obstructive sites and their combinations are listed in Table 6.

As is evident from these findings, the three obstructive sites that arefeatured with equal frequency are the soft palate, the lateral pharyngeal wall,and the tongue base. Within the present-day surgical spectrum, the lateralpharyngeal wall at the oropharyngeal level is the least-attended-to site. Thetonsils usually are not the source of the problem. This is the area that is mostdifficult to treat or to treat with any sustained effect. The authors haveobserved side-to-side, concentric, and oblique collapse of this region.

In terms of single-site obstruction, the soft palate is obstructed as oftenas the tongue base. The hypopharynx, interpreted as the pyriform fossasqueezing concentrically around the larynx, interestingly is never featured asa single-site obstruction. This level of collapse is likely to be a secondaryeffect of higher-level obstruction. The authors’ Muller maneuvers correlatedpoorly with the VSE findings.

The different combinations of obstructive sites are challenging to theinterested surgeon. It is the humbling truth that the lasting cure for all theselevels of obstruction is not necessarily in place at this point in time. Thecontinued study of the upper airway dynamics is an important adjunct tothe fine-tuning of present-day surgical procedures and the design of newprocedures for OSAS.

Video sleep nasendoscopy and continuous positive airway pressure titration

Video sleep nasendoscopy can be used to establish the CPAP pressure inpatients with OSAS. This procedure can be conveniently performed at theend of the VSE examination by placing a CPAP mask gently over the noseof the patient, with the flexible endoscope in situ. Despite the presence of theendoscope, a seal can be achieved easily (Fig. 1). The authors have a picture-in-picture oximetric tracing on the video monitor screen to facilitatepressure establishment while watching the changes in the upper airway. Theaim is to achieve unobstructed breathing at the lowest level of CPAPpressure with minimal snoring. It is interesting that a large airway lumen isnot usually necessary to achieve this goal in most of the authors’ patients. Inthe authors’ study of 43 cases (40 men and 3 women), a 67% precisecorrelation of established CPAP pressure values was achieved using theauthors’ technique when compared with those methods established manu-ally overnight in the sleep laboratory. If �1 cm H2O is accepted as theerror margin, a 77% correlation is achieved, and 90% correlation isachieved if �2 cm H2O is the accepted error margin. The technique is simpleand quick. It is still the authors’ preference to titrate CPAP pressuremanually overnight in the sleep laboratory. The authors have found thistechnique to be more reliable than the autotitrators. The VSE technique,nevertheless, can be a cost-effective method of CPAP titration whenperfected, because it takes no longer than 10 minutes to perform.


Table

6

Theobstructivesitesforsurgicalassessm

entandthedifferentsite

combinationsasseen

inVSEfor89patients

Obstructionsitesinvolved

(total,302)

Site

No.

Percentage

IPalate

69

22.8%

IILateralpharynx

64

21.2%

III

Tonsil

41

13.6%

IVTonguebase

62

20.5%

VEpiglottis

37

12.3%

VI

Hypopharynx

29

9.6%

100%

Sitecombinations,number

ofpatients,andpercentages

Site

No.

Percentage

Site

No.

Percentage

Site

No.

Percentage

Site

No.

Percentage

IPalate

44.49%

I+II

44.49%

I+III

0I+

IV5

5.62%

I+V

11.12%

I+II+

III

66.74%

I+III+

IV0

I+IV

+V

11.12%

I+VI

0

I+II+

IV5

5.62%

I+III+

V0

I+IV

+VI

0I+

V+VI

0

I+II+

V1

1.12%

I+III+

VI

0I+

IV+V+

VI

0

I+II+

VI

I+III+

IV+

V0

I+II+

III+

IV7

7.87%

I+III+

IV+

VI

11.12%

I+II+

III+

V2

2.25%

I+III+

V+VI

0

I+II+

III+

VI

22.25%

I+III+

IV+

V+VI

0

I+II+

IV+V

44.49%

I+II+

IV+VI

33.37%

I+II+

V+VI

0

I+II+

III+

IV+V

33.37%

I+II+

III+

IV+VI

44.49%

I+II+

III+

V+VI

I+II+

IV+V+

VI

55.62%

I+II+

III+

IV+V+

VI

11

12.3%


IILateralpharynx

22.25%

II+

III

11.12%

II+

IV0

II+

V0

II+

III+

IV0

II+

IV+

V1

1.12%

II+

VI

0

II+

III+

V0

II+

IV+

VI

22.25%

II+

V+VI

0

II+

III+

VI

0II+

V+

VI

0

II+

III+

IV+

V1

1.12%

II+

IV+

V+

VI

0

II+

III+

IV+

VI

0

III

Tonsil

11.12%

III+

IV1

1.12%

III+

V1

1.12%

III+

IV+

V0

III+

VI

0

III+

IV+

VI

0III+

V+

VI

0

III+

IV+

V+VI

0

IVTonguebase

44.49%

IV+

V3

3.37%

IV+

VI

0

IV+

V+VI

11.12%

VEpiglottis

22.25%

V+

VI

0

VI

Hypopharynx

0


The future of video sleep nasendoscopy

Ever since Croft and Pringle described their technique of sleepnasendoscopy [5], reception has been mixed. Criticisms were generated bythe disappointing results of the once-popular uvulopalatopharyngoplasty[6,7] for which this technique was used to select the appropriate candidatesfor the procedure. The second reason for skepticism is the use of sedationin VSE. Sedation is unnatural sleep and may relax the tongue muscles,thus worsening the pharyngeal collapse. Uvulopalatopharyngoplasty failedbecause of its design—the created scar lies in a region that is massagedconstantly by the act of swallowing. The stiffness could not possibly last forlong. Uvulopalatopharyngoplasty also fell into disrepute because only a fewpatients with OSAS have single-site obstruction at the soft palate, and thisoperation was once performed for all patients with OSAS. Different agentshave been used for sleep endoscopic examination: halothane in children [8],midazolam [5], diazepam [9], and propofol [10]. The Osaka group evaluateddiazepam-induced sleep nasendoscopy under PSG control in 50 patients.The non–rapid-eye-movement parameters were observed to be equal tothose of their nocturnal PSG, and the only difference was in the duration ofrapid-eye-movement sleep [9]. Supporters of VSE for surgical evaluation aremore than a few [11,12]. In the days to come, the optimal sedation for sleependoscopy will require PSG-controlled evaluation. Surface electromyogra-phy would help to clarify the suspected tongue-base relaxation effect. The

Fig. 1. Continuous positive airway pressure mask on the nose and endoscope for VSE-guided

CPAP titration.


authors believe that the small, controlled dose used in the protocol would behypnotic in the hypersomnolent patients with OSAS rather than muscle-relaxing. Polysomnographic data are being collected for midazolam. Theauthors’ 10-year experience with the use of VSE in more than 800 casessupports its safety, if it is performed correctly. At present, however, sleepnasendoscopy should be used only for surgical evaluation, which should beinterpreted in the light of a nocturnal PSG. Through a simulated sleep-breathing situation, sleep nasendoscopy undoubtedly provides qualityinformation on the upper airway dynamics that is closest to reflecting thetrue situation in a cost-effective manner. To the surgeon, this information isinvaluable.

References

[1] Partinen M, Jamieson A, Guilleminault C. Long term outcome for obstructive sleep apnea

syndrome patients: mortality. Chest 1989;96:703–4.

[2] Guilleminault C, Simmons FB, Motta J, Cummiskey J, Rosekind M, Schroeder JS, et al.

Obstructive sleep apnea syndrome and tracheostomy: long-term follow-up experience.

Arch Intern Med 1981;141:985–8.

[3] Sher AE, Thorpy MJ, Spielman AJ, Burack B, Mcgregor PA. Predictive value of Muller

manoeuvre in selection of patients for uvulopalatopharyngoplasty. Laryngoscope 1985;

95:1483–7.

[4] Pringle MB, Croft CB. A comparison of sleep nasendoscopy and the muller manoeuvre.

Clin Otolaryngol 1991;16:559–62.

[5] Croft CB, Pringle M. Sleep nasendoscopy: a technique of assessment in snoring and

obstructive sleep apnoea. Clin Otolaryngol 1991;16:504–9.

[6] Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities in

obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck

Surg 1981;89:923–34.

[7] Fujita S. UPPP for sleep apnoea and snoring. Ear Nose Throat J 1984;63:73–86.

[8] Croft CB, Thomson HG, Samuels MP, Southall DP. Endoscopic evaluation and treatment

of sleep-associated upper airway obstruction in infants and young children. Clin

Otolaryngol 1990;15:209–16.

[9] Sadaoka T, Kakitsuba N, Fujiwara Y, Kanai R, Takahashi H. The value of sleep

nasendoscopy in the evaluation of patients with suspected sleep related breathing disorders.

Clin Otolaryngol 1996;21:485–9.

[10] Roblin G, Williams AR, Whittet H. Target-controlled infusion in sleep endoscopy.


[11] Camilleri AE, Ramamurthy L, Jones PH. Sleep nasendoscopy: what benefit to the manage-

ment of snorers? J Laryngol Otol 1995;109:1163–6.

[12] Takeda K. Sleep nasendoscopy in the selection of surgical treatments for simple snoring

and sleep apnea syndrome. Journal of the Medical Society of Toho University 1998;

45:250–60.


Radiofrequency techniques inthe treatment of sleep-disordered

breathing

Robert J. Troell, MDPlastic Surgery Institute, 653 North Town Center Drive,

Suite 308, Las Vegas, NV 89144, USA

The pathophysiology of sleep-disordered breathing is collapse or ob-struction of the upper airway during sleep. This obstruction may occurat any site along the upper airway passages to include the nasal cavity,nasopharynx, oropharynx, hypopharynx, and larynx. Diagnosis requires anocturnal polysomnogram to document the presence and severity of sleep-disordered breathing. The presurgical evaluation includes a comprehensivehead-and-neck physical examination, fiberoptic nasopharyngoscopy, andlateral cephalometric to determine the site or sites of upper airway obstruc-tion. This analysis is essential in directing surgical therapy in a site-specificapproach. Numerous surgical procedures have been developed to addresseach of these sites of obstruction and have offered the surgeon an arma-mentarium of options, each with its own set of advantages, disadvantages,and success rates.

Radiofrequency (RF) tissue volumetric reduction was developed toreduce tongue-base obstruction by way of an outpatient, minimally invasiveprocedure using local anesthesia and causing minimal discomfort with a lowcomplication rate. The research to bring this technique to fruition dem-onstrated the usefulness of temperature-controlled RF for other areas ofthe upper airway. Radiofrequency may be used to treat nasal obstructionby reducing the size of the inferior turbinate. Soft palatal reduction is analternative treatment for primary snoring, upper airway resistance syn-drome, and mild obstructive sleep apnea syndrome. The current medical in-formation reviewing the use of RF in tissue volumetric reduction in theupper airway for nasal obstruction, primary snoring, and sleep-disorderedbreathing is reviewed.


36 (2003) 473–493



doi:10.1016/S0030-6665(02)00177-9

Background and biophysics of radiofrequency

The RF energy ablation of soft tissues has been applied successfully, inthe past, to humans by specialists in the fields of cardiology, neurology,oncology, and urology [1–4]. Temperature-controlled RF delivers RF at 460kHz by a high-frequency alternating current flow into the tissue, creatingionic agitation. This ionic agitation heats the tissue and as the temperaturerises higher than 47�C, protein coagulation and tissue necrosis ensue. In thefirst study evaluating RF for sleep-disordered breathing, a porcine study [5]evaluated the relationship of lesion size to total RF energy delivery andsubsequent tissue volume reduction. The maximum lesion size is two thirdsthe diameter of the RF electrode or approximately 7 mm, and the maximumlength of the lesion is between 1.5 to 1.75 cm (Fig. 1). Heat is transported byway of conduction to tissue farther away from the electrode and extends thesize of the lesion. The computer algorithm controls the power to maximizethe lesion size, resulting in tissue coagulation with no charring. The healingprocess was analyzed through a serial histologic analysis in the porcinemodel and demonstrated favorable wound healing with a well-defined lesionafter 24 hours, with an acute inflammatory response and edematous re-sponse. Collagen deposition begins approximately 12 days after injury, andat 3 weeks, chronic inflammation, fibrosis, and tissue volume reductionfrom scar contracture occur.

The first human clinical study evaluating the use of RF was in the softpalate for snoring and sleep-disordered breathing, and the investigators

Fig. 1. Biophysical properties of RF.

474 R.J. Troell / Otolaryngol Clin N Am 36 (2003) 473–493

concluded that the technique was safe with minimal complications. Bleed-ing, infection, speech disturbances, and swallowing problems were not ob-served. Results of RF for snoring reduction revealed that the pretreatmentsnoring level was reduced by an overall mean of 77% [6]. The safety andefficacy reported in the previous animal study were confirmed in the humanpalate.

Radiofrequency device

The medical RF device (Gyrus ENT LLC, Memphis, TN) is delivered at460 kHz using an RF generator with custom-fabricated needle electrodes.The essential RF energy parameters of power (watts), temperature limits(Celsius), resistance (Ohms), treatment time (seconds), and total energydelivery in joules (watt � seconds) are controlled by a computer algorithm.The necessary feedback for temperature adjustment is provided by multiplemicrothermocouples embedded along the electrode. The 22-gauge RFelectrodes have a 10-mm active tip. A protective thermal sheath is used onthe proximal portion of the electrode to eliminate surface damage. Themaximum temperature gradient is regulated to less than 90�C, with a targettemperature between 80�C to 85�C. The computer algorithm maximizes theRF lesion size (Fig. 2).

Fig. 2. Radiofrequency factors affecting lesion size.

475R.J. Troell / Otolaryngol Clin N Am 36 (2003) 473–493

Treatment philosophy

A full disclosure to the patient describing the available procedures, thesuccess rates, the potential risks and complications, and the possibility of astaged surgical approach or multiple procedures fathers good medicine anda confident patient-physician relationship. The extent of surgery is medi-ated by the patient’s acceptance, severity of symptoms, severity of objectiveobstruction, level of upper airway collapse, and the severity of the site ofobstruction. The philosophy of ‘‘treatment to cure’’ mandates follow-upon all procedures. The systemic presurgical evaluation in sleep-disorderedbreathing identifies areas of airway collapse or obstruction, logically di-recting surgical treatment to these site-specific areas.

Presurgical evaluation

Although the etiology of sleep-disordered breathing is still poorlyunderstood, it is clear that there exist specific anatomic abnormalities thatobstruct the upper airway during sleep. The three major areas of obstructionare the nose, the palate, and the hypopharynx. Fujita et al [7] described theareas of collapse as retropalatal (type I), retropalatal and retrolingual (typeII), or solely retrolingual (type III). An anatomic obstruction at one or allof these levels may create increased airway resistance and varying degreesof sleep-related obstruction.

It is impossible to direct therapy logically without isolating the area ofobstruction; unfortunately, it is not always possible preoperatively to definethe exact area of obstruction. There are numerous radiologic tests availableto aid in determining the suspected sites of obstruction preoperatively.The author’s presurgical evaluation includes a nocturnal polysomnogra-phy, a comprehensive head-and-neck physical examination, fiberoptic naso-pharyngoscopy with the Muller maneuver, and a lateral cephalometricradiograph.

Classification of disease severity

The understanding of the classification of sleep-disordered breathing isimportant in communicating with other health professionals.

Primary snoring

An apnea-hypopnea index (AHI) of less than five events per hour of sleepwith no oxygen saturation (SaO2) less than 90% during sleep or a peaknegative end-inspiratory esophageal pressure or inspiratory nadir (Pes) ofless negative than �10 cm H2O. These patients do not report excessivedaytime sleepiness.


Upper airway resistance syndrome

An AHI of less than five events per hour of sleep with an SaO2 of greaterthan or equal to 90% during total sleep time and an inspiratory nadir Pesmore negative than �10 cm H2O. Patients without an esophageal pressuremonitor displayed frequent arousals associated with snoring or increaseddiaphragmatic electromyogram activity. Two thirds of these patients snore,and all have an accompanying complaint of excessive daytime sleepiness.

Obstructive sleep apnea syndrome

An AHI of greater than five events per hour of sleep. These patientsusually have accompanying oxyhemoglobin desaturations below 90% andneurobehavioral symptoms, most commonly excessive daytime sleepiness.

Review of nasal obstruction

Nasal obstruction may be the primary complaint or it may be a factor inproducing primary snoring or sleep-disordered breathing. The pathophys-iology of nasal obstruction causing upper airway collapse is an increasednasal resistance, an increased velocity of air flow, an increased negativeintraluminal pressure, and resultant partial obstruction and vibration oftissues of the upper airway predisposed to collapse, including the soft palate,tongue, and lateral pharyngeal walls.

Nasal obstruction may be caused by nasal rim or nasal valve collapse,septal deviation, adenoid hypertrophy, nasal polyps or tumors, and inferiorturbinate hypertrophy. Patients with mild sleep-disordered breathing withan AHI less than 15 may be treated successfully with nasal surgery alone.Nasal surgery may improve the sleep study parameters in patients withobstructive sleep apnea of moderate or severe disease, but it will notsuccessfully treat these patients. If inferior turbinate hypertrophy is thecause of the nasal obstruction, RF is an excellent treatment modality. Thetechnique can be performed on an outpatient basis with local anesthesia,with a minimal risk of post-treatment complications and minimal dis-comfort.

Performing nasal surgery simultaneously with other procedures of theupper airway in patients other than those with mild disease may increasethe risk of airway compromise. The production of significant postopera-tive edema or the use of nasal packing prevents the use of nasal continu-ous positive airway pressure (CPAP), which is used to stent the airwayopen during sleep-induced upper airway collapse. Nasal septal deviation,turbinate hypertrophy, and nasal ala and valve collapse are corrected byseptoplasty, turbinoplasty, and nasal valve cartilage implants, respectively.Adenoid hypertrophy is treated by adenoidectomy.

Nasal obstruction may be addressed in a staged fashion 6 to 8 weekspostoperatively from the first phase of airway reconstruction to allow


adequate healing of the procedures most likely to remedy their disease. Italso may be performed initially to provide a patient with the best possibilityto tolerate nasal CPAP in those with significant nasal obstruction. Inpatients with mild severity of sleep-disordered breathing, nasal surgery maybe combined with soft palatal surgery, but this approach is not recom-mended in those patients with moderate or severe disease, because of therisk of the patient not being able to use nasal CPAP in the immediate post-operative period, when the upper airway swelling is at its height.

The rationale for nasal surgery is to improve nasal patency, whichestablishes physiologic breathing and minimizes oral breathing during sleep.Oral breathing during sleep causes the tongue to be positioned posteriorly,increasing the risk of upper airway obstruction. Also, resolving nasalobstruction reduces nasal resistance and improves the negative intraluminalpressure, which generates upper airway collapse.

Inferior turbinate radiofrequency indications

Nasal obstruction is caused by inferior turbinate enlargement. There arenumerous other methods of turbinate reduction that are available alter-natives, including the following:

Inferior turbinate reduction techniques1. Traditional total turbinectomy2. Traditional partial turbinectomy3. Submucous resection4. Submucous diathermy5. Cryotherapy6. Laser vaporization7. Coblation8. RF

Radiofrequency can be used along the entire length of the inferior tur-binate, depending on the location and magnitude of the turbinate hyper-trophy. This technique has been attempted by the author for the middleturbinate, but because the thickness of the submucosa is much thinner thanthe inferior turbinate, direct surgical excision is the preferred technique fora concha bollosum or middle turbinate hypertrophy.

Surgical technique of inferior turbinate radiofrequency

Radiofrequency of the inferior turbinate can be performed on anoutpatient basis or in the operating room associated with other operativeprocedures, such as a nasal septoplasty. In an outpatient setting, the patientis placed in the sitting position. The anterior nasal cavity is anesthetized witha topical local anesthetic without epinephrine and then cotton pledgets withthe same solution are placed along the anterior and middle aspects of the


inferior turbinate. After approximately 5 minutes, the anterior aspect of theinferior turbinate is injected with between 3 to 5 mL of 1% or 2% lidocainewithout epinephrine. The injection provides anesthesia and enlarges thediameter of the turbinate to prevent mucosal injury while the RF energy isbeing delivered. Between 350 to 550 J of energy are delivered to the anteriorand, if required, middle aspects of the inferior turbinate. After the probe isremoved, a cotton pledget with oxymetazoline (HC 0.05%) is placed alongthe inferior turbinate for hemostasis.

Inferior turbinate radiofrequency results

The initial human study [8] evaluating the efficacy of RF for thetreatment of nasal obstruction caused by inferior turbinate hypertrophy wasa prospective nonrandomized study of 22 adult volunteers (18 men). Themean age was 41.1 years� 10.7. The subjects were diagnosed with nasalobstruction solely from inferior turbinate hypertrophy that had failed torespond to conservative medical management. A mean RF energy deliveryper treatment was 382 J� 102, with a mean temperature of 77�C� 8.4 andmean duration of RF energy of 102.9 minutes� 57. A subjective visualanalog score (VAS) of nasal obstruction was completed 8 weeks aftertreatment, with 21 of 22 patients (95%) having improved nasal symptoms.The patients experienced mild edema for 24 to 48 hours after treatment, and20 of 22 (91%) reported post-treatment discomfort, with a visual analogpain score of 1� 1.8. Three subjects (14%) used analgesics, with a total ofsix 500-mg acetaminophen tablets administered. No bleeding, crusting,dryness, adhesions, or infections were noted.

Additional outcome studies have revealed similar improvement in nasalpatency. Utley et al [9] evaluated 10 patients using a 15-mm RF probe (nolonger available), with two lesions per turbinate. A mean RF energy deliveryon the left turbinate of 492 J� 72 and 429 J� 104 and on the right of 412J� 103 and 465 J� 13 revealed a subjective improvement of 75% on the leftand 68% on the right. Eight of nine patients no longer required allergicmedications, and no narcotics were required postoperatively. Smith et al [10]evaluated 11 patients using a 10-mm RF probe, with one lesion per tur-binate. The mean RF energy delivery on the left of 423 J� 17 and on theright of 428 J� 13 revealed an improvement in subjective nasal obstructionVAS from 7.5 to 3.3. Six of 11 patients reported mild pain during the treat-ment, but only one acetaminophen tablet was administered.

Powell et al [11] evaluated the use of inferior turbinate reduction toimprove compliance with nasal CPAP in patients with nasal obstruction.The double-blinded, prospective study evaluated 22 patients (12 women)with a mean age of 54.3 years, body mass index of 29.3 kg/m2, and a meanAHI of 33.5. A mean of 413 J of RF energy was delivered to each inferiorturbinate. The investigators discovered an overall reduction in size of theinferior turbinate by 27% on a four-point scale (n ¼ 17) compared with the


VAS subjective patient improvement of nasal patency of 48%. Tolerance tonasal CPAP improved by 28.9% (VAS, 4.9–6.3) compared with the placebogroup (n ¼ 5) who decreased CPAP use by 10.4% (VAS, 4.4–3.3).

Inferior turbinate radiofrequency side effects

The post-treatment findings after inferior turbinate RF include nasalswelling for 24 to 72 hours. No wound care or limitation of daily activities isnecessary. Narcotic analgesics are not required, and few patients administeracetaminophen. Bleeding, crusting, dryness, adhesions, and infection arerare complications. Final reduction is complete in 3 to 4 weeks, and re-treatment can be performed if nasal obstruction persists.

Rhee et al [12] evaluated nasal function after RF treatment to the inferiorturbinate. No ciliary dysfunction was appreciated using the saccharin transittime and ciliary beat frequency tests. Butanol threshold testing revealedimproved olfaction, probably from improved nasal patency. Mucous rhe-ologic properties were unchanged. Improved nasal obstruction was com-pared with laser vaporization and revealed an improvement of 81.3% in theRF group and 87.5% in the laser group.

Inferior turbinate radiofrequency: conclusions

Inferior turbinate RF is a technically simple, minimally invasive proce-dure that can be performed as an outpatient procedure under local anesthe-sia with improved nasal obstruction, minimal side effects, and unchangedciliary and mucous properties.

Review of soft palatal obstruction

Primary snoring, upper airway resistance syndrome, obstructive sleepapnea syndrome, and obesity-hypoventilation syndrome encompass a spec-trum of sleep-related upper airway obstruction. Patients with primarysnoring seek treatment because of the social annoyance and disruption ofsleep of a bed partner. The etiology of primary snoring in approximately85% of patients is partial airway obstruction from soft palatal redundancycausing tissue vibration, with resultant sound production [13].

The initial procedure devised to address primary snoring was theuvulopalatopharyngoplasty designed by Ikematsu [13] and modified byFujita et al [7,14] and Simmons et al [15]. Unfortunately, the procedureusually is performed under general anesthesia, produces significant post-operative pain, and has short- and long-term failures for both snoringresolution and persistent obstructive sleep apnea. There have been numer-ous other soft palatal reduction procedures that have been discovered (seefollowing list); unfortunately, each procedure has its limitations and dis-advantages.


Soft palatal reduction procedures1. Uvulopalatopharyngoplasty2. Laser-assisted uvulopalatoplasty3. Uvulopalatal flap4. Cautery-assisted palatal-stiffening operation5. Transpalatal advancement6. Coblation7. Injection snoreplasty8. RF

Alternatively, since the early 1980s, there have been numerous non-prescription, noninvasive medical management options, including nasalCPAP, oral appliances, nasal appliances, and medications. There are morethan 300 patented appliances for snoring and sleep-disordered breathing.These devices have yielded either limited success or are fraught with lowcompliance rates. Minimally invasive procedures, including RF volumetrictissue reduction of the soft palate, injection snoreplasty, and coblation, havegained favor with both patients and surgeons because of the ability to performthem as an outpatient procedure under local anesthesia with minimal post-treatment discomfort, a limited complication rate, and good surgical results.

Soft palatal radiofrequency indications

Most patients with primary snoring and sleep-disordered breathing arecandidates for surgical intervention. Patients must be medically and psycho-logically stable and wish to undergo a surgical procedure. Patients shouldbe informed of the treatment philosophy.

Surgical indications for soft palatal RF include the following: (1) sociallydisruptive snoring; (2) neurobehavioral derangements and excessive daytimesleepiness caused by sleep fragmentation as a result of soft palatal collapsein upper airway resistance syndrome and mild obstructive sleep apneasyndrome—this neurocognitive dysfunction may be confirmed to be due toupper airway collapse with resolution of these symptoms by a nasal CPAPtrial; (3) mild sleep-disordered breathing with an AHI or respiratorydisturbance index less than 20, with mild soft palatal redundancy or tonsillarhypertrophy; and (4) patients with persistent snoring after other soft palatalreduction procedures have been unsuccessful, such as laser assisteduvulopalatoplasty (LAUP), uvulopalatopharyngoplasty, and uvulopalatalflap (UPF).

Soft palatal radiofrequency limitations

Patients with a long, thick uvula most likely will require sharp amputationof part or all of the uvula to treat a redundant soft palate successfully. Patientswith a thin, soft palate, especially the banding between the posterior tonsillarpillar and the uvula, are poor candidates for RF because the mean ablative


lesion diameter is 7 mm. The technique will result in a perforation of the softpalate or lateral scarring and contraction of this band of tissue, narrowing theoropharyngeal introitus. Patients with other than mild sleep-disorderedbreathing most likely will require other surgical procedures, especially thoseaddressing the hypopharynx, to treat their disease severity effectively.

Soft palatal radiofrequency surgical technique

The soft palate is sprayed with 20% benzocaine as a topical anesthetic. Alocal anesthetic as a gel (2% lidocaine) is placed on a cotton-tippedapplicator at the initial soft palatal injection site. A 27- or 30-gauge needle isused to inject 2.0 mL of 0.25% bupivacaine (Marcaine) 1:100,000 withepinephrine at this superior palatal midline site. The local anesthetic diffusesover approximately 5 to 7 minutes caudally, making additional inferior andlateral injections nearly painless. The soft palate from the uvular base to theposterior nasal spine and the paramedian area extending approximately 2cm laterally from the midline is selected for treatment.

The temperature-controlled RF energy delivery maximizes the size ofthe lesion compared with non-temperature-controlled RF delivery systems(Fig. 3). A 22-gauge RF needle electrode (10-mm active length with a 10-mmprotective sheath) in a custom-fabricated device allows placement of theelectrode under the palatal mucosa in the area selected for treatment. Thiselectrode is bent with a crimping tool on an individual patient basis tocontour to the curvature of the soft palate. Radiofrequency energy then is

Fig. 3. Soft palatal lesion size comparison: temperature- and non–temperature-controlled RF.


delivered for 60 to 170 seconds. Four potential sites of treatment duringeach treatment are selected, dependent on the size of the soft palate. Therecommended maximum amount of energy delivered to the superior midlinesoft palate is 750 J; the recommended maximum amount to the uvular baseand the paramedian areas is 350 J. Patients who previously have undergoneother palatal procedures can tolerate higher energy levels laterally, up to550 J, with limited risk of mucosal erosion or perforation. An assessment ofthe thickness of the soft palate should be performed before treatmentto determine the maximal safe dose of RF energy and to limit the risk ofsoft palatal perforation.

In patients with a long uvula, sharp amputation of the uvular tissue up tothe muscle reflection may improve the success rate without any additionalpost-treatment discomfort. If the muscle is cut, then the patient experiencesheightened pain and may require narcotic analgesic administration. Non-steroidal anti-inflammatory medications are an excellent choice for post-operative pain, especially the new generation of Cox-II inhibitors. Thesemedications have the same pain relief as hydrocodone combined with acet-aminophen, with the anti-inflammatory properties to relieve swelling.

Patients who have a prominent gag reflex may benefit from a pretreatment10- to 20-mg oral dose of oral diazepam. Although they are not necessary,oral antibiotics or corticosteroids may be used postoperatively. The authordoes not use antibiotics after soft palatal RF and has not identified any pa-tients with soft palatal cellulitis. A short course of oral methylprednisolone(Medrol), for 3 to 5 days, may be used to limit soft palatal edema, especiallyin those patients with a long uvula or thick soft palate.

Soft palatal radiofrequency results

The initial human soft palatal RF study [6] revealed a reduction ofsnoring by 77%, in 22 subjects with a pretreatment subjective snoring VASmean score of 8.3� 1.8 and a post-treatment mean score of 1.9� 1.2. Themean number of treatment sessions per patient was 3.6� 1.2, with a totalmean of 5� 2 sites and mean RF energy delivered per treatment session of688� 106 J. A follow-up study [16] 12 to 18 months (mean, 14 months) laterreported that subjective snoring scores relapsed by 29% overall. Thirteenpatients (59%) reported continual success without relapse of snoring ordaytime sleepiness. Nine patients (41%) noted relapse of snoring from2.1� 1.1 to 5.7� 2.7. Eight of these patients underwent further RF sessionswith a reduction of snoring from 5.8� 2.9 to 3.3� 3.1. Six patients receivedone treatment session, and two patients received two treatment sessions. Themean RF energy delivered per treatment session was 786� 114 J, and eachpatient received a minimum of one and a maximum of three separate RFablations per treatment session. Overall, 21 of the 22 patients (95%) weresatisfied with the procedure and would repeat it if necessary.


A prospective, nonrandomized multicenter study [17] of 113 patientsvalidated the use of RF applied to the soft palate for snoring reduction. Thesnoring VAS scores went from a mean of 7.8� 2.1 pretreatment to 3.2� 2.3after treatment by delivering a mean of 1977.6� 887 J with a mean of2.4� 1.2 treatment sessions per patient. The average follow-up period aftertreatment was 8 weeks.

Another prospective, nonrandomized study [18] evaluated 43 patientsundergoing soft palatal RF and revealed a 71% reduction of subjectivesnoring. Nineteen patients had a single midline lesion created, with RFdelivering a mean of 698� 52 J per treatment, a total mean of 2165� 1057 Jper patient with a mean of 3.3� 1.6 treatment sessions per patient. Reduc-tion in subjective snoring occurred from 7.8� 1.8 to 2.3� 2.1 (70.5%).Twenty-four patients had three separate lesions, one midline and left andright lateral sites, per treatment session, with RF delivering a mean of1254� 191 J per treatment, a total mean of 2196� 1158 J per patient witha mean of 1.8� 0.9 treatment sessions per patient. Reduction in subjectivesnoring occurred from 8.9� 1.7 to 2.5� 0.8 (71.9%).

Another study comparing single-lesion versus multilesion soft palatal RFin 47 patients [19] revealed a more-than-twice-as-likely cure rate for snoringafter twoRF treatment sessions, with 61%ofmultilesion patients and 25%ofsingle-lesion patients being treated successfully. The authors concluded thatmultilesion RF, using higher energy levels per treatment, is safe and increasedthe efficacy without increasing complications relative to single-lesion therapy.

A study of 12 patients [20] undergoing midline RF to the soft palaterevealed an improvement of subjective snoring from 8.3� 2.1 to a post-treatment snoring level of 2.1� 1.4 or a 75% reduction of snoring. Thesepatients required an average of 2.3 treatment sessions per patient, withbetween 495 and 693 J per treatment session. The mean follow-up periodwas 5.1 weeks after the final RF procedure. The available soft palatal RFstudies reveal a 70% to 77% subjective snoring reduction, with minimalpain and complications.

The author prefers to deliver enough energy per treatment session aspossible without producing mucosal erosions, significant uvular and softpalatal swelling, and post-treatment pain to require narcotic analgesics. Oneor two lesions are created at the initial treatment session, and the amount ofsoft tissue swelling and post-treatment subjective pain is assessed. If thepatient experiences minimal swelling and pain, then high midline palatal,uvular base, and paramedian lesions are created at the second treatmentsession as dictated by the palatal anatomy.

Soft palatal radiofrequency complications

The advantage of the RF technique of the soft palate, which is usedprincipally for primary snoring, is the minimally invasive nature of the


procedure. Most subjects experience restless sleep on the first post-treatmentnight in response to palatal swelling and mild discomfort.

The post-treatment discomfort of RF of the soft palate was comparedwith laser-assisted uvulopalatoplasty and uvulopalatopharyngoplasty [21].The mean number of days with pain after RF, LAUP, and uvulopalato-pharyngoplasty was 2.6, 13.8, and 14.3, respectively. The mean number ofdays requiring narcotic pain medication for RF, LAUP, and uvulopalato-pharyngoplasty was 0.2, 11.8, and 12.4, respectively, whereas the total nar-cotic equivalent was 0.3, 7.4, and 29.6 days, respectively. Soft palatalRF produced significantly less post-treatment pain than either LAUPor uvulopalatopharyngoplasty, making this procedure well tolerated bypatients.

The discomfort experienced with this procedure is related to the numberof lesions, the amount of energy delivered, and the presence of a mucosalinjury. Powell et al’s initial study [6] revealed a mucosal injury rate of 7.6%,with other studies revealing mucosal injury rates as high as 45% [18]. Exceptfor superficial mucosal injuries, when the mucosa is disturbed, patientsexperience increased discomfort. Palatal fistulas or perforations also mayoccur. This complication can be avoided by decreasing the amount of energydelivered in thin soft palates and by refraining from placing the RF probelateral to the uvular and levator veli palatini muscles (Fig. 4).

Uvular slough also may occur, which can lead to increased post-treatment pain. Because the goal of RF therapy is to shrink and tighten thesoft tissue of the soft palate, this incident is not a complication unlesssignificant pain is created. Decreasing the amount of energy delivered to theuvular base and the distance away from the uvular base may aid indiminishing this occurrence.

Most studies evaluating soft palatal RF did not note bleeding, infection,speech disturbances, or swallowing problems. Soft palatal swelling mayproduce a globus sensation, but it usual resolves in 2 to 4 days. Dysphagia,velopalatal insufficiency, and nasopharyngeal stenosis have not been re-ported. Except for some post-treatment mild discomfort, swelling, and a lowincidence of mucosal erosions, complications are minimal.

Overview of hypopharyngeal obstruction

The pathophysiology of sleep-disordered breathing is collapse orobstruction of the upper airway during sleep. This obstruction may bepartly or entirely due to the hypopharynx, and there are preoperative factorsthat may suggest the hypopharyngeal area as a site of collapse (see followinglist) [22].

Factors influencing hypopharyngeal obstruction1. Morbid obesity (body mass index >31 kg/m2)2. Mandibular skeletal deficiency (sella-nasion-supramentale (SNB)<76�)


3. Severe sleep-disordered breathing (AHI >40)4. Minimal soft palatal redundancy5. Retrodisplaced tongue or lateral wall collapse on nasopharyngoscopy6. Narrowed posterior airway space on lateral cephalometric radiograph

(posterior airway space <11 mm)

Once the hypopharynx is suggested to be a site of collapse of the upperairway in sleep-disordered breathing, determining reconstructive procedureis the next step (see following list). Tongue-base RF is an alternativetreatment to decrease the volume of the tongue and to improve the posteriorairway space.

Hypopharyngeal surgical procedures1. Genioglossus advancement2. Hyoid myotomy and suspension3. Partial glossectomy or lingualplasty4. Repose tongue suspension5. Maxillomandibular advancement6. Tongue-base RF

Tongue-base radiofrequency indications

Patients diagnosed with obstructive sleep apnea for whom the pre-operative evaluation suggests tongue-base collapse as the cause of thehypopharyngeal obstruction are candidates for RF. Patients need to be in

Fig. 4. Soft palatal musculature anatomy. PNS – Posterior Nasal Spine.


stable medical condition, understand that the procedure is a multiple-stageprocess, and appreciate the potential complications. Post-treatment airwayconcerns and requirements for monitoring need to be addressed by thesurgeon.

Patients with complaints of dysphagia or dysarthria preoperatively mayundergo a modified barium-swallow or speech-therapy evaluation beforeconsidering these therapeutic options. Those patients with underlyingdiabetes mellitus should be counseled regarding the increased risk of tongueabscess formation. Two treatment approaches exist: (1) performing RFalone and (2) performing RF with other base-of-tongue procedures, such asthe genioglossus advancement or hyoid suspension procedures.

Tongue-base radiofrequency technique

The technique can be performed as an outpatient or an inpatientprocedure in a monitored setting. Depending on the severity of the patient’ssleep-disordered breathing, post-treatment airway protection with nasalCPAP or a tracheotomy should be considered. The oral cavity is preparedwith 0.12% oral chlohexidene (Peridex), and either oral or parenteral cepha-lexin is administered before placing the electrode. If under local anesthe-sia, the tongue is sprayed with 20% benzocaine as a topical anesthetic. Alocal anesthetic as a gel (2% lidocaine) is placed on a sterile, cotton-tippedapplicator at the tongue-injection sites. A 25- or 27-gauge needle is usedto inject 5.0 mL of 0.25% bupivacaine (Marcaine) with 1:100,000 epi-nephrine into each site. A different sterile needle is used at each site of in-jection. Treatment sites should be spaced a minimum of 1.5 cm apart.Lingual nerve blocks may be used but are not necessary. The author doesnot inject saline into the treatment area because there is no study to dateverifying the increased tissue destruction with this method. There is an in-creased risk of infection with each additional injection at the lesion site bybringing potential superficial tongue debris and bacteria into the area to beablated.

A 22-gauge RF needle electrode (10 mm of active length with a 10-mmprotective sheath) in a custom-fabricated device allows placement of theelectrode under the superficial tongue musculature in the area selected fortreatment. This electrode may be additionally bent on an individual patientbasis to contour to the curvature of the tongue. Continual pressure on theelectrode and visualization that the insulation sheath is not retracting outof the tongue tissue reduce the risk of superficial tissue injury. A single-or dual-channel tongue probe may be selected to deliver the RF energy. Ifthe dual-channel probe is selected, the author prefers to bend the probeproximal to the retractable sheath to separate the two RF lesions fartherapart. Potential sites of treatment include the midline, paramedian, andventral tongue areas. As an inpatient procedure, up to 750 J in four sites,with 3000 J total delivery, can be administered safely without significant


tongue swelling, dysphagia, or postoperative pain. Documenting the specifictongue sites of treatment is prudent so that future RF tongue sessions do notplace the RF electrode in previously ablated tongue tissue.

In an outpatient setting, it is prudent to deliver only two sites of RFenergy secondary to the risk of postoperative swelling and airway com-promise in an unmonitored setting at home. Also, too much RF energycan result in dysphagia to the point at which oral intake of fluid is impaired,necessitating a hospital admission for hydration. The recommendedmaximum amount of energy delivered per site is between 750 to 1000 J.The amount of swelling and postoperative discomfort significantly increaseswith RF energy delivered at more than 750 J per treatment site. If tongue-base RF is being performed simultaneously with other base-of-tongueprocedures such as the genioglossus advancement, decreasing the amount ofRF energy may be warranted to prevent severe floor-of-mouth and tongueswelling, which may encroach on the airway. Nonsteroidal anti-inflamma-tory medications are an excellent choice for postoperative pain, especiallythe new generation of Cox- II inhibitors. These medications have the samepain relief as hydrocodone combined with acetaminophen, with the anti-inflammatory properties to relieve swelling. Occasionally, narcotic analgesiais necessary.

Patients with a prominent gag reflex who are undergoing the procedureunder local anesthesia may benefit from a pretreatment 10- to 20-mg dose ofdiazepam. Although they are not necessary, corticosteroids may be usedpostoperatively. The author does not use methylprednisolone because of theconcern of tongue abscess formation. If postoperative swelling and airwaycompromise are of concern, using nasal CPAP, monitoring the patient on aninpatient basis with pulse oximetry, or intensive care monitoring ispreferred.

Tongue-base radiofrequency results

In the first report evaluating RF for sleep-disordered breathing, a porcinestudy [5] evaluated the relationship of lesion size to total RF energy deliveryand subsequent tissue volume reduction. The study showed that tonguemusculature volume could be reduced safely using RF energy in a preciseand controlled manner with minimal risk of mucosal injury or infection.

The first human tongue pilot study [23] investigated the feasibility, safety,and possible efficacy of RF in the treatment of sleep-disordered breathing.Eighteen patients who were treated incompletely for sleep-disorderedbreathing with other upper airway reconstruction procedures enrolled inthe study, and all of them underwent at least a uvulopalatopharyngoplasty.The mean preoperative AHI of 39.6 improved to a mean of 17.8 (55%) aftertreatment, the mean apnea index of 22.1 improved to a mean of 4.1 (80%),and the mean preoperative SaO2 nadir of 81.9% improved to 88.3% (12%)after treatment. The mean energy delivery per treatment session was 1543 J,


for a mean total energy delivery of 8490 J. Tongue volume, as assessed withmagnetic resonance imaging, was reduced by 17%, with an improvement ofthe posterior airway space by 15%. Speech and swallowing, as evaluated byVAS scores, were unchanged. Pain was controlled by oral hydrocodone forup to 4 days. The only complication in 181 treatment sessions was onetongue abscess, which resolved after incision and drainage.

A long-term follow-up study [24] of these same patients revealed that 16patients completed the follow-up at a mean of 28 months after the initialtreatment. Sleep studies were performed using a new nasal cannula by SleepSolutions (Redwood City, CA) that can quantitate airflow. This techniqueis believed to be more accurate in identifying hypopneas. The follow-updata revealed that the apnea index remained the same at 5.4, but the overallAHI relapsed to 28.7 and the SaO2 nadir relapsed to 85.8%. There wereno changes in the quality-of-life scale (SF-36), Epworth sleepiness scale,or speech or swallowing VAS scores. The conclusion was that the successof tongue-base RF may reduce with time with the primary relapse in thehypopnea index. The limitation of the study was the use of different moni-toring devices to document hypopneas.

A prospective, nonrandomized study [25] evaluated 10 sleep apneicpatients who underwent uvulopalatopharyngoplasty and nasal surgery(when indicated), along with tongue-base RF under general anesthesia. Twoadditional RF sessions were performed postoperatively in an outpatientsetting. Nine of the 10 patients received a cumulative dose of approximately12,000 J. The final patient received only the initial 4000 J of RF energy. Fiveof these patients were treated successfully, defined as an AHI less than 20with at least a 50% reduction in AHI. The mean preoperative AHI of29.5� 14.8 improved to a mean AHI of 18.8� 14.6, and the mean apneaindex of 8.7� 6.4 improved to a mean apnea index of 3.7� 4.9.

A multi-institutional study [26] evaluated 73 patients with underlyingobstructive sleep apnea; 56 (76.7%) of these patients completed tongue-baseRF and follow-up polysomnography. Sixty-five (92.9%) had prior pharyn-geal surgery. A mean of 5.4� 1.8 treatment sessions were performed, with amean of 3.1� 0.9 lesions per treatment session and an overall energy deliv-ery of 13,394� 5459 J. The mean AHI of 40.5� 21.5 decreased to a mean of32.8� 22.6 after treatment. The investigators concluded that RF tonguereduction diminishes the severity of obstructive sleep apnea with subjectiveoutcomes comparable to nasal CPAP.

Tongue-base radiofrequency complications

Tongue-base RF is a treatment of tongue-base collapse in patients withsleep-disordered breathing. These patients have inherent postoperativeairway concerns with upper airway reconstructive surgery. To avoid post-operative airway obstruction after tongue-base RF, the surgeon should con-sider in-patient monitoring, nasal CPAP use, and limiting the amount of


RF energy delivery, especially when performed with other upper airwayreconstructive procedures. The potential complications are listed below.

Tongue-base radiofrequency complications1. Superficial ulcer formation2. Infection or cellulitis3. Tongue abscess4. Hypoglossal nerve injury5. Tongue or floor-of-mouth swelling6. Upper airway obstruction

Infection is an uncommon complication, with progression to a tongueabscess in less than 1% of treatment lesions. Some of these suppurativeinfections drain spontaneously, some may be treated by needle aspiration,but definitive treatment usually requires incision and drainage. The symp-toms are a rapid onset of severe tongue pain, usually only mild or moder-ate swelling, and occasional cervical adenopathy or swelling. Diagnosisrequires a high index of suspicion, because the initial physical examina-tion findings may reveal a normal-appearing tongue or only mild swelling.Needle aspiration, ultrasound scanning, or computer tomography scanningmay be required to confirm the diagnosis.

To diminish the risk of infection, the following precautions can be taken:(1) pretreatment with oral antibiotics, usually cephalexin, and a 3-dayprophylactic antibiotic course; (2) instructing the patient to gargle with0.12% oral chlorhexidene (Peridex) for at least 1 minute immediately beforetreatment; (3) use of sterile technique as much as possible; (4) use of a newsterile needle with each injection site; (5) avoidance of steroids, which maylower the immune response; (6) ensuring that the electrode is seatedcompletely into the tongue musculature to prevent a superficial ulceration;(7) checking the curvature of the tongue base to prevent the electrode tipfrom being placed close to the superficial aspect of the tongue; (8) wiping theelectrode tip using sterile technique between treatment lesion sites to removedebris; (9) not delivering greater than 1000 J of energy per treatment site;and (10) considering other treatment alternatives in patients with diabeticmellitus. Following these recommendations limits the incidence of tonguesuperficial ulcerations and infection.

To avoid hypoglossal nerve injury, the surgeon should limit the ablationsites to no more than 2 cm lateral to midline. The neurovascular bundle isapproximately 2 to 3 cm from the surface epithelium and approximately3 cm lateral from midline in a normal-sized tongue (Fig. 5). With decreasedtongue volumes, the RF lesions should not extend beyond 1.5 to 2.0 cmfrom midline to prevent hypoglossal nerve injury. Four studies revealed nohypoglossal nerve injuries, whereas one study had only mild and transienttongue deviations, which resolved completely postoperatively.

Tongue discomfort, odynophagia, and dysphagia may occur for 3 to5 days after treatment. To lower the incidence of significant post-treatment


discomfort, the physician should (1) limit the energy per treatment site to750 J, (2) limit the treatment sites to four per treatment session, (3) usecrushed ice by mouth as much as possible for the first two post-treatmentdays, and (4) follow the treatment techniques to limit the risk of infection. Inthe author’s experience with more than 200 base-of-tongue RF treatmentsfollowing these recommendations, no patient has had a tongue ulcer, infec-tion, abscess, lingual neuralgia, or hypoglossal nerve injury. The incidenceof these complications is largely technique-dependent.

Tongue-base radiofrequency limitations

The specific role of tongue-base RF in sleep-disordered breathing has notbeen established. The efficacy of this procedure when performed simulta-neously with other hypopharyngeal reconstructive procedures has not beenstudied. The effect of saline infiltration into the area to be ablated in alteringthe lesion size has not been delineated. Finally, there are only limited resultson the long-term efficacy and side effects of tongue-base RF.

Tongue-base radiofrequency: conclusions

Tongue-base RF seems to offer promising results in upper airway recon-struction in patients with sleep-disordered breathing. The technique can beperformed as an outpatient or inpatient procedure, under local or general

Fig. 5. Tongue cross-sectional anatomy.


anesthesia, with minimal risks of complications and minimal quality-of-lifechanges.

Upper airway reconstruction surgery follow-up

Three to 4 months after completing upper airway reconstruction, patientsundergo a polysomnogram to determine surgical outcome. Surgical success isdefined as anAHI of less than 20 with at least a 50% reduction compared withthe preoperative study and the lowest oxyhemoglobin saturation levelsequivalent to those seen with nasal CPAP or greater than 90%. In addition toobjective polysomnographic data, patients should experience improvement intheir snoring and sleep hygiene. Elimination of the daytime hypersomnolencecorresponds to reports of better-quality sleep, improved ability to concen-trate, elimination of the necessity of naps, and improved work performance.The surgeon should use the procedures that are the most effective, with thelowest morbidity, and technically reproducible for him or her.

Radiofrequency in upper airway reconstruction: conclusions

Radiofrequency for upper airway reconstructive surgery in sleep-disordered breathing for the nasal inferior turbinate, the soft palate, andthe tongue base offers additional therapeutic options in the surgicalarmamentarium in an area in which there were once limited options. Theprocedures are technically simple and minimally invasive; they are associ-ated with reduced postoperative pain compared with traditional surgicalapproaches; and they can be performed in an outpatient setting underlocal anesthesia with a low complication rate and generally good thera-peutic results. Future studies will aid in delineating the specific role of RFin nasal obstruction and sleep-disordered breathing.

References

[1] Issa M, Oesterling J. Transurethral needle ablation (TUNA): an overview of radio-

frequency thermal therapy for the treatment of benign prostatic hyperplasia. Curr Opin

Urol 1996;6:20–7.

[2] Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular

pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med

1991;324:1605–11.

[3] LeVeen H, Wapnick S, Piccone V, et al. Tumor eradication by radiofrequency therapy:

response in 21 patients. JAMA 1976;253:2198–200.

[4] 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.

[5] 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.

[6] Powell NB, Riley RW, Troell RJ, et al. Radiofrequency volumetric tissue reduction of the

palate in subjects with sleep-disordered breathing. Chest 1998;113:1163–74.


[7] Fujita S, Conway W, Zorick F, et al. Surgical correction of anatomic abnormalities in


Surg 1981;89:923–30.

[8] Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C. Radiofrequency volumetric

tissue reduction of turbinate hypertrophy: a pilot study. Otolaryngol Head Neck Surg

1998;119:569–73.

[9] Utley DS, Goode RL, Hakim I. Radiofrequency energy tissue ablation for the treatment of

nasal obstruction secondary to turbinate hypertrophy. Laryngoscope 1999;109:683–6.

[10] Smith TL, Correa AJ, Kuo T, et al. Radiofrequency tissue ablation of the inferior turbinate

using a thermocouple feedback electrode. Laryngoscope 1999;109:1760–5.

[11] Powell NB, Riley RW, Zonato AI, et al. Radiofrequency treatment of turbinate hyper-

trophy to improve nasal CPAP usage. Presented at the American Academy of

Otolaryngology–Head and Neck Surgery annual meeting, Washington, DC; September

2000.

[12] Rhee CS, Kim DY, Won TB, et al. Changes of nasal function after temperature-controlled

radiofrequency tissue volume reduction for the turbinate. Laryngoscope 2001;111:153–8.

[13] Ikematsu T. Study of snoring: fourth report. Ther J Jpn Otol Rhinol Laryngol Soc 1968;

4:434–5.

[14] Fujita S, Conway WA, Zorick F, et al. Evaluation of the effectiveness of uvulopalato-

pharyngoplasty. Laryngoscope 1985;95:70–4.

[15] Simmons FB, Guilleminault C, Miles L. The palatopharyngoplasty operation for snoring

and sleep apnea: an interim report. Otolaryngol Head Neck Surg 1984;4:375–7.

[16] Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C. Radiofrequency volumetric

reduction of the palate: an extended follow-up study. Otolaryngol Head Neck Surg 2000;

122:410–4.

[17] Sher AE, Flexon PB, Hillman D, et al. Temperature-controlled radiofrequency tissue

volume reduction in the human soft palate. Otolaryngol Head Neck Surg 2001;125:312–8.

[18] Emery BE, Flexon PB. Radiofrequency volumetric tissue reduction of the soft palate: a new

treatment for snoring. Laryngoscope 2000;110:1092–8.

[19] Ferguson M, Smith TL, Zanation AM, et al. Radiofrequency tissue volume reduction:

multilesion vs single-lesion treatments for snoring. Arch Otolaryngol Head Neck Surg

2001;127:1113–8.

[20] Coleman SC, Smith TL. Midline radiofrequency tissue reduction of the palate for both-

ersome snoring and sleep-disordered breathing: a clinical trial. Otolaryngol Head Neck

Surg 2000;122:387–94.

[21] Troell RJ, Powell NB, Riley RW, et al. Comparison of postoperative pain between laser-

assisted uvulopalatoplasty, uvulopalatophayngoplasty, and radiofrequency volumetric tis-

sue reduction of the palate. Otolaryngol Head Neck Surg 2000;122:402–9.

[22] Troell RJ, Powell NB, Riley RW. Hypopharyngeal airway obstruction for obstructive sleep

apnea syndrome. In: Millman RP, editor. Seminars in respiratory and critical care

medicine, vol. 19. New York: Thieme Medical Publishers; 1998. p. 175–184.

[23] Powell NB, Riley RW, Guilleminault C. Radiofrequency tongue base reduction in sleep-

disordered breathing: a pilot study. Otolaryngol Head Neck Surg 1999;120:656–64.

[24] Li KK, Powell NB, Riley RW, et al. Radiofrequency tongue base reduction: long-term

outcomes. Presented at American Academy of Otolaryngology–Head and Neck Surgery

annual meeting, Denver Colorado, September 2001.

[25] Nelson LM. Combined temperature-controlled radiofrequency tongue reduction and

UPPP in apnea surgery. ENT J 2001;80:640–4.

[26] Woodson BT, Nelson L, Mickelson S, et al. A multi-institutional study of radiofrequency

volumetric tissue reduction for OSAS. Otolaryngol Head Neck Surg 2001;125:303–11.


Laser-assisted uvulopalatoplasty revisited

Yosef P. Krespi, MDa,*, Ashutosh Kacker, MDb

aDepartment of Otolaryngology/Head and Neck Surgery, St. Luke’s–Roosevelt Hospital Center,

425 West 59th Street, 10th Floor, New York, NY 10019, USAbDepartment of Otolaryngology and Head and Neck Surgery, New York Presbyterian Hospital,

Weill College of Medicine, York Avenue and 68th Street, New York, NY 10021, USA

Snoring is a social problem and a precursor to the more ominoussyndrome of obstructive sleep apnea (OSA). It affects approximately 50% ofmen and 30% of women. It is estimated that approximately 50% of thoseaffected are habitual snorers (Table 1). Uvulopalatopharyngoplasty (UPPP)was first introduced by Ilkematsu in 1964 and was later modified by Fujitaet al [1] as a surgical treatment for the management of snoring.

The application of office-based laser technology to surgery for snoringand mild OSA led to the introduction of laser-assisted uvulopalatoplasty(LAUP) in the middle to late 1980s. Since then, controversies have arisen,especially with respect to its efficacy. Kamani [2,3], who is credited with theintroduction of LAUP, published data showing remarkable results forits use as treatment for both snoring and OSA. Similar short-term resultswere published by other authors using either a single-stage or multiple-stageLAUP procedure [4–8]. Recently published data tend to contradict earlierresults, with patients showing poorer results or results that worsened withtime [9,10]. Also, because of the indiscriminate use of LAUP, complications(in the form of nasopharyngeal stenosis) were reported. Since then, ourunderstanding of snoring and sleep apnea has improved, which has led tochanges in patient selection and improved results.

Diagnosis

The diagnosis of snoring is determined primarily by history. The char-acter and consistency of the snoring are evaluated to determine its severityand possible associated OSA. The physical examination includes a completeevaluation of the nose, nasopharynx, oral cavity, oropharynx, hypopharynx,


36 (2003) 495–500


E-mail address: [email protected] (Y.P. Krespi).


doi:10.1016/S0030-6665(03)00016-1

and larynx. Flexible fiberoptic examination, as a Muller’s maneuver, helpsin localizing the site of origin of the snoring or OSA.

Use of sleep study to characterize snoring

The authors use the SNAP Laboratories’ (Glenview, IL) sleep-study snor-ing analysis to identify and localize the source of snoring and to detect andquantify sleep apnea [11]. This information is used to select and tailor theprocedure.

Snoring analysis

The sleep study performed by SNAP Laboratories is unique in its abilityto identify and spectrally profile all snoring events into five categories.Clinical correlation studies have shown that these categories help to identifythe likely sites of sound generation and airway compromise. Type 1 and type2 snoring are believed to be predominantly of palatal origin. The incidence(percentage) of each type of snoring and its relative loudness is determined.Another parameter included in the SNAP analysis is the snoring index (fre-quency of snoring and fundamental frequency of snoring). The most usefulparameters for identifying significant velopharyngeal (palatal) snoring, arethe percent and relative loudness of palatal snoring.

The following guidelines (see box) are used to assess the relative velum-like component of overall snoring amplitude and distribution.

Criteria for patient selection

Patients with grade II or III snoring with mild apnea in whom the snoringis localized to the palate on a sleep study are the ideal candidates for LAUP.

Table 1

Grading system of snoring

Grade Snoring Characteristics

Grade I Occasional Overtired, alcohol intake, lying on the back

Grade II Frequent All positions, continues through out night,

heard from one room away

Grade III Always (associated with OSA) Heard throughout the entire home

Types 1 and 2 (%) Amplitude distribution

Minimal <65 <4 dBModerate <85 4–8 dBMajority >85 >8 dB

496 Y.P. Krespi, A. Kacker / Otolaryngol Clin N Am 36 (2003) 495–500

Absolute contraindications for LAUP include severe sleep apnea, uncon-trolled hypertension, severe trismus, cleft palate, velopharyngeal insuffi-ciency, and an uncooperative patient.

Procedure of laser-assisted uvulopalatoplasty

Currently, the senior author (YPK) uses a single-stage, graded, interac-tive procedure in which he performs a stepwise reduction of the uvula andsoft palate. After each step, the patient is asked to snort to re-create thesnoring sound. The procedure is continued until this sound can no longer becreated by snorting.

Anesthesia for laser-assisted uvulopalatoplasty

Laser-assisted uvulopalatoplasty is performed in an upright, sitting posi-tion in an otolaryngology examination chair. The topical anesthetic used is20% benzocaine, which is sprayed in the posterior oral cavity; an injectionof lidocaine 1% with 1:100,000 epinephrine and bupivacaine 0.5% also isgiven.

Surgical procedure

Surgical use of the carbon dioxide laser is commenced after waiting 10minutes for the anesthesia to take effect. A special pharyngeal hand piecewith a backstop is used to incise the soft palate. The power setting is 18 to 20W, continuous mode. The tongue is retracted inferiorly with an ebonizedtongue blade with the integrated smoke-evacuation channel. Through-and-through, full-thickness, vertical trenches measuring 1.0 to 1.5 cm are madeon the free edge of the soft palate on either side of the uvula. These trenchesare created using a focused beam in a continuous mode. The patient isinstructed to take a deep breath, and the laser is activated during slowexhalation to avoid inhalation of the plume.

Shortening and thinning of the uvula are performed with the SwiftLase(Sharplan Lasers, Allendale, NJ) flash scanner attached to the carbondioxide (CO2):laser, using 18 to 20 W. The uvula is reduced to 60% to 90%of its original dimensions by coring it out from the bottom up. Overall, thesurgical goal is to reduce the length and to reshape the soft palate and uvula.Care must be taken not to burn excessively the mucosa overlying the softpalate and uvula. The uvula is shortened by ablating the muscle from within,creating a ‘‘fish-mouth’’ appearance, because the mucosae of the base of theuvula on the nasal and oral surfaces are preserved.

This procedure is performed best with SwiftLase. The advantages ofusing the SwiftLase flash scanner are absence of char, precise layer-by-layersurface ablation, and the ability of the SwiftLase to seal small blood vessels.Excision of the uvula (amputation) at its base using the carbon dioxide laserwith a focus beam may cause undesired bleeding from the uvula and soft

497Y.P. Krespi, A. Kacker / Otolaryngol Clin N Am 36 (2003) 495–500

palate vessels. Light bleeding during surgery occurred in approximately 3%of the patients. This complication is controlled easily by applying silvernitrate. Patients with obstructive sleep apnea syndrome with redundantpharyngeal folds and enlarged tonsils can be helped by the reduction of theupper portion of the pharyngeal folds and the tonsils using the SwiftLase.

Complications

A moderate-to-severe sore throat is the major side effect after LAUP [12].The pain intensity reaches its peak 4 to 5 days postoperatively, with com-plete relief of symptoms approximately 8 to 10 days after surgery. Thepain usually is controlled with hydration, anesthetic gel, and oral analgesics.There was no late or delayed bleeding in the authors’ series. Healing occursby formation of an eschar 3 to 5 days after the procedure. Complete healingtakes place after the slough of the eschar in approximately 10 to 12 days.Vasovagal episodes were encountered in 2% of the patients after injection ofthe local anesthetic. Laser-assisted uvulopalatoplasty was combined withother procedures, such as submucous resection of the septum, laserturbinectomy, laser-assisted serial tonsillectomy, or laser lingual tonsillec-tomy, in approximately 20% of the authors’ patients.

Discussion

Laser-assisted uvulopalatoplasty is an effective method for treatingpatients with loud, habitual snoring. Performed as an office procedure underlocal anesthesia, laser-assisted uvulopalatoplasty has proven to be a safeand reliable method of relieving this sociomedical problem. Because theprocedure is performed under local anesthesia and in stages, patients reportminimal pain, eliminating the need for adults to miss work or to be incapac-itated for several weeks, as is the case after UPPP. In most patients, a reduc-tion in snoring occurs immediately. One major advantage of LAUP overUPPP is the ability of LAUP to titrate tissue removal to achieve optimalbenefit without the danger of overcorrection.

Complications seen in patients undergoing LAUP include postoperativehemorrhage, local infection, temporary palatal incompetence, and tempo-rary loss of taste. More serious complications include hypernasal speech,permanent palatal incompetence, nasopharyngeal stenosis, airway compro-mise, ordeath.Alternateoptions toLAUP includedental obturators, radiofre-quency reduction of the palate, injection snoreplasty, and the conventionalUPPP.

The somnoplasty system uses radiofrequency energy to reduce andtighten excess tissue in the upper airway that is responsible for snoring[13–15]. The reduction of the palate tissues can be performed in a precise,minimally invasive manner. The procedure creates finely controlled zones ofcoagulation at precise locations beneath the tissue in the upper airway.


During a 3- to 8-week period, the treated tissue is resorbed, reducing excesstissue volume and opening the airway. Advantages of somnoplasty includean easy, pain-free procedure and the lack of serious adverse effects. Thedisadvantages include the fact that multiple procedures are required toobtain good results and the cost of the hand piece.

Injection snoreplasty is a new procedure in which sodium tetradecylsulfate 3% (Tromboject 3%) (Omega Labs, Montreal, CA) (a sclerosingagent) is injected into the soft palate to reduce or eliminate palatal-fluttersnoring in habitual snorers [16]. Injection snoreplasty is a simple, safe, andeffective office treatment for primary snoring. Advantages as compared withcurrent snoring procedures include simplicity, low cost, decreased post-treatment pain levels, and minimal or no convalescence. Currently, Sotra-decol is not approved by the Food and Drug Administration for this use.

Summary

When performed correctly in a properly selected patient, LAUP providesgood and lasting results in snoring improvement. A sleep study with snoringanalysis helps in patient selection. Laser-assisted uvulopalatoplasty can beperformed adequately in one sitting.

References



Surg 1981;89:923–34.

[2] Kamami YV. Outpatient treatment of sleep apnea syndrome with CO2 laser: laser-assisted

UPPP. J Otolaryngol 1994;23:395–8.

[3] Kamami YV. Outpatient treatment of snoring with CO2 laser: laser-assisted UPPP. J Oto-

laryngol 1994;23:391–4.

[4] Krespi YP, Pearlman SJ, Keidar A. Laser-assisted uvula-palatoplasty for snoring. J Oto-

laryngol 1994;23:328–34.

[5] Sharp HR, Mitchell DB. Long-term results of laser-assisted uvulopalatoplasty for snoring.

J Laryngol Otol 2001;115:897–900.

[6] Seemann RP, DiToppa JC, Holm MA, Hanson J. Does laser-assisted uvulopalatoplasty

work? An objective analysis using pre- and postoperative polysomnographic studies.

J Otolaryngol 2001;30:212–5.

[7] Neruntarat C. Laser-assisted uvulopalatoplasty: short-term and long-term results. Oto-

laryngol Head Neck Surg 2001;124:90–3.

[8] Osman EZ, Osborne JE, Hill PD, Lee BW, Hammad Z. Uvulopalatopharyngoplasty versus

laser assisted uvulopalatoplasty for the treatment of snoring: an objective randomised

clinical trial. Clin Otolaryngol 2000;25:305–10.

[9] Ryan CF, Love LL. Unpredictable results of laser assisted uvulopalatoplasty in the

treatment of obstructive sleep apnoea. Thorax 2000;55:399–404.

[10] Lauretano AM, Khosla RK, Richardson G, Matheson J, Weiss JW, Graham C, et al.

Efficacy of laser-assisted uvulopalatoplasty. Lasers Surg Med 1997;21:109–16.

[11] Weingarten CZ, Raviv G. Evaluation of criteria for uvulopalatoplasty (UPP) patient

selection using acoustic analysis of oronasal respiration (SNAP testing). J Otolaryngol

1995;24:352–7.

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[12] Walker RP, Gopalsami C. Laser-assisted uvulopalatoplasty: postoperative complications.


[13] Blumen MB, Dahan S, Wagner I, De Dieuleveult T, Chabolle F. Radiofrequency versus

LAUP for the treatment of snoring. Otolaryngol Head Neck Surg 2002;126:67–73.

[14] Troell RJ, Powell NB, Riley RW, Li KK, Guilleminault C. Comparison of postoperative

pain between laser-assisted uvulopalatoplasty, uvulopalatopharyngoplasty, and radiofre-

quency volumetric tissue reduction of the palate. Otolaryngol Head Neck Surg 2000;122:

402–9.

[15] Flexon FB. Somnoplasty: a treatment for snoring. In: Krause JH, Mirante JP, Christmas

DA, editors. Office-based surgery in otolaryngology. Philadelphia: WB Saunders; 1999. p.

79–86.

[16] Brietzke SE, Mair EA. Injection snoreplasty: how to treat snoring without all the pain and

expense. Otolaryngol Head Neck Surg 2001;124:503–10.


Tongue neuromuscular and directhypoglossal nerve stimulation for

obstructive sleep apnea

David W. Eisele, MDa,*, Alan R. Schwartz, MDb,Philip L. Smith, MDb

aDepartment of Otolaryngology–Head and Neck Surgery, University of California, San

Francisco, 400 Parnassus Avenue, Suite A-730, San Francisco, CA 94143-0342, USAbJohns Hopkins Asthma and Allergy Center, Johns Hopkins University

School of Medicine, Bayview Circle, Baltimore, MD 21224, USA

Obstructive sleep apnea (OSA) is caused by recurrent episodes of upperairway obstruction during sleep associated with periodic arousals from sleepand oxyhemoglobin desaturations. Sleep disturbance and abnormal oxygen-ation are believed to cause the primary clinical sequelae of OSA thatinclude daytime hypersomnolence, arterial and pulmonary hypertension,and cardiopulmonary failure. Therapy for OSA is directed toward the reliefof upper airway obstruction so that the clinical manifestations of the disor-der are alleviated or prevented.

Although numerous methods have been used to restore upper airwaypatency during sleep for patients with OSA, no single treatment modalityhas been shown to provide complete reversal of upper airway obstructionduring sleep in all patients with this disorder. The cause of OSA, which isconsidered to be related to diminished genioglossus muscle activity duringsleep, is not addressed by current therapies [1]. To address this problem, theauthors conducted investigations into the effect of neuromuscular stimula-tion of the tongue muscles and direct hypoglossal nerve stimulation onupper airway patency during sleep in patients with OSA. This articlesummarizes the authors’ investigations of selective neuromuscular tongueand direct hypoglossal nerve stimulation on upper airway airflow mechanicsduring sleep in patients with OSA and the feasibility of this interventionfor the treatment of this disorder.


36 (2003) 501–510


E-mail address: [email protected] (D.W. Eisele).


doi:10.1016/S0030-6665(02)00178-0

Neuromuscular stimulation of the tongue

Multiple prior investigations have addressed the concept of electricalstimulation of the tongue in OSA. Approaches have included attempts tostimulate the tongue with surface electrodes placed in the upper neck skin[2,3], sublingual mucosa [4,5], base-of-tongue mucosa [6], and soft palate[7]. Percutaneous wire electrodes, directed near the hypoglossal nerve, alsohave been used [8,9]. The methods used in these studies, however, lackedselectivity in stimulating the genioglossus muscle or hypoglossal nerve andinduced recurrent arousals from sleep. A generalized arousal from sleep re-sulting in pharyngeal muscle activation could have caused the improvementsin pharyngeal airway patency reported in these earlier investigations.

In light of the limitations of these studies, the authors began investi-gations into electrical stimulation of the tongue muscles with three primaryobjectives. First, methods were developed to selectively stimulate the genio-glossus muscle in volunteers and patients with OSA. Second, the effect ofthe selective stimulation of the genioglossus muscle on upper airway airflowdynamics during sleep was determined in patients with OSA. Third, patientswere sought for OSA treatment with an implantable electrical-stimulationsystem. Initially, methods for selective neuromuscular stimulation of thetongue muscles with transorally directed hook-wire electrodes were de-veloped. Tongue motor responses with this method were correlated withtongue motor responses resulting from selective hypoglossal nerve stimu-lation performed during open-neck surgical procedures. This correlationprovided confirmation of proper transoral electrode placement into thegenioglossus muscle based on the motor response observed with stimulation.The observed response to neuromuscular and selective hypoglossal nervestimulation of the genioglossus muscle was tongue protrusion and deviationof the tongue to the contralateral side.

Neuromuscular stimulation of the genioglossus muscle then was exam-ined during sleep in patients with OSA [10]. The level of maximal air-flow before, during, and after stimulation was measured with standardpolysomnographic recording techniques. Arousal from sleep during or afterstimulation was excluded by monitoring electroencephalography, electro-myography, the pattern of respiration, and the heart rate. All patients withOSA studied were morbidly obese with significant apnea-hypopnea indices.Neuromuscular stimulation of the genioglossus muscle resulted in an im-provement in inspiratory airflow of approximately 200 to 250 mL/s (Fig. 1).The improvement in airway patency was limited to the duration of stimu-lation of the genioglossus muscle. Importantly, the results of this study con-firmed that electrical stimulation of the upper airway could be achievedduring sleep in patients with OSA without arousal from sleep. The airway-opening effect produced by stimulation was noted to be directly relatedto genioglossus neuromuscular activation rather than global arousal fromsleep.

502 D.W. Eisele et al / Otolaryngol Clin N Am 36 (2003) 501–510

Selective direct hypoglossal nerve stimulation

Another investigation was undertaken to determine the effect of directhypoglossal nerve stimulation on upper airway patency in patients withOSA during sleep [11]. A tripolar half-cuff electrode (Medtronic 3990; Med-tronic, Minneapolis, MN) was used. This electrode was designed to limitthe electrical current to the nerve and to prevent nerve entrapment. Thehypoglossal nerve was exposed through an upper neck incision in patientswith OSA. Two loci of hypoglossal nerve stimulation, the distal branch tothe genioglossus muscle and the main nerve trunk, were examined. The levelof maximal inspiratory airflow before, during, and after stimulation wasmeasured during sleep with standard polysomnographic techniques. Lack ofarousal from sleep was confirmed by monitoring electroencephalography,electromyography, the respiratory pattern, and the heart rate. Electricalstimulation of the hypoglossal nerve at both stimulation loci resulted ina marked improvement in inspiratory airflow during stimulation, compared

Fig. 1. Mean maximal inspiratory airflow (VI max) levels for eight patients with OSA before,

during, and after neuromuscular stimulation of the genioglossus muscle during sleep. (From

Schwartz AR, Eisele DW, Hari A, et al. Electrical stimulation of the lingual musculature in

obstructive sleep apnea. J Appl Physiol 1996;81:643–52; with permission.)

503D.W. Eisele et al / Otolaryngol Clin N Am 36 (2003) 501–510

with unstimulated breaths, without patient arousal from sleep (Fig. 2). Itwas concluded from this study that airway obstruction in patients with OSAwas alleviated by hypoglossal nerve stimulation, not only when the genioglos-sus muscle was stimulated but also when the tongue retrusor muscles werecoactivated with the genioglossus muscle.

Implantable hypoglossal nerve-stimulation system

After the publication of the above-mentioned studies that confirmed thesuccess of electrical-stimulation methods for opening the airway in patientswith OSA without arousal from sleep and additional animal studies [12],a Food and Drug Administration-approved feasibility study was un-dertaken to investigate the treatment of patients with OSA with a fully

Fig. 2. Mean maximal inspiratory airflow (VI max) in five patients with OSA before, dur-

ing, and after hypoglossal nerve stimulation during sleep. Filled circles indicate stimulation

of the hypoglossal nerve branch to the genioglossus muscle. Open circles indicate main

trunk hypoglossal nerve stimulation. (From Eisele DW, Smith PL, Alam DS, Schwartz AR.

Direct hypoglossal nerve stimulation in obstructive sleep apnea. Arch Otolaryngol Head Neck

Surg 1997;123:57–61; with permission.)


implantable hypoglossal nerve-stimulation system. This system, the Inspire I(Medtronic) (Fig. 3) consists of components that were designed to reliablypredict the onset of the inspiratory phase of respiration and to stimulate thehypoglossal nerve during inspiration. The system components include animplantable pulse generator (IPG), a respiratory pressure sensor, and a tri-polar, half-cuff peripheral nerve-stimulation electrode. The IPG containsa programmable microprocessor. Stimulus frequency, duration, and ampli-tude can be adjusted transcutaneously by the physician programmer. Theperipheral nerve lead and the respiratory pressure sensor interface withthe IPG.

Surgical implantation of the hypoglossal nerve-stimulation system isdescribed in detail elsewhere [13,14]. Briefly, the system is implanted undergeneral anesthesia through three surgical incisions: an upper lateral neckincision, a lower midline neck incision, and an infraclavicular incision. Thehypoglossal nerve is exposed by dissection through an upper neck incision.The stimulation electrode is placed on the peripheral hypoglossal nervebranch to the genioglossus muscle (Fig. 4). Proper placement on the desirednerve is confirmed by stimulation of the nerve with a hand-held pulse gen-erator and observation of tongue protrusion and deviation to the contra-lateral side. Through a midline lower neck incision, the pressure transduceris placed flush with the posterior aspect of the manubrium through a drillhole, and the transducer housing is secured to the manubrium with aminiscrew (Fig. 5). An infraclavicular pocket, superficial to the pectoralismajor muscle fascia, is created by way of an infraclavicular incision (Fig. 6).A tunneling device then is used to tunnel the nerve-electrode lead and thepressure-transducer lead to the IPG pocket. The leads then are connected tothe IPG, and the wounds are closed. The system is checked for functionalintegrity before awakening the patient from anesthesia. Further testing of

Fig. 3. Schematic diagram of Inspire I Hypoglossal Nerve Stimulation System (Medtronic,

Minneapolis, MN).


the system is deferred for 1 month to allow for adequate healing andstabilization of the implanted system.

Therapeutic hypoglossal nerve stimulation in obstructive sleep apnea

Recently, a multi-institutional, prospective trial to investigate the thera-peutic efficacy of the Medtronic Inspire I hypoglossal nerve-stimulationsystem for OSA was completed [14]. Eight middle-aged, moderately over-weight men with moderate to severe OSA during non-rapid-eye-movement(non–REM) and REM sleep underwent implantation of the system. Nightlyunilateral hypoglossal nerve stimulation was initiated at 4 weeks after system

Fig. 4. Half-cuff stimulation electrode placement around distal branch of the hypoglossal nerve

to the genioglossus muscle. (From Eisele DW, Schwartz AR, Smith PL. Electrical stimulation of

the upper airway for obstructive sleep apnea. Op Tech Otolaryngol Head Neck Surg 2000;11:

59–65; with permission.)


implantation. Patients initiated electrical stimulation with a self-controlledprogramming unit. A pre-set delay in system activation allowed patients toinitiate sleep before the start of electrical stimulation.

Sleep and breathing patterns were examined at baseline and at 1, 3, and 6months postoperatively. Results of this clinical trial indicated that unilateralhypoglossal nerve stimulation decreased the severity of the OSA throughoutthe entire study period. Specifically, stimulation reduced the mean apnea-hypopnea indices in non-REM and REM sleep compared with baselinevalues (Fig. 7). The severity of oxyhemoglobin desaturations was reducedsignificantly. All patients were able to tolerate long-term stimulation atnight, and there were no adverse effects related to system implantation ornerve stimulation. Small, consistent increases in stimulus parameters wererequired early in the protocol to maintain therapeutic responses to stimu-lation. After 3 months, however, little further increase in stimulus intensity

Fig. 5. Pressure transducer placement through a drill hole in the manubrium. (From Eisele DW,

Schwartz AR, Smith PL. Electrical stimulation of the upper airway for obstructive sleep apnea.

Op Tech Otolaryngol Head Neck Surg 2000;11:59–65; with permission.)


was required, suggesting that the nerve-electrode interface had stabilizedduring this early postoperative period. The results of this prospective studydemonstrate the feasibility and therapeutic benefit of unilateral hypoglossalstimulation in OSA.

Some system technical issues require resolution before broader applica-tion of a stimulation system for the treatment of OSA. Electrode breakageor respiratory sensor malfunction occurred in some patients, resulting incompromise of long-term stimulation. Patients who remained free fromstimulator malfunction, however, were able to continue to use the device asprimary therapy for OSA.

Fig. 6. Implantable pulse generator placement in an infraclavicular pocket superficial to the

pectoralis major muscle fascia. The nerve-electrode lead and pressure-transducer lead are

tunneled to the IPG pocket and connected to the IPG. (From Eisele DW, Schwartz AR, Smith

PL. Electrical stimulation of the upper airway for obstructive sleep apnea. Op Tech Otolaryngol

Head Neck Surg 2000;11:59–65; with permission.)


Further studies are necessary to optimize patient-selection criteria fortherapeutic hypoglossal nerve stimulation. Patient selection may be basedon baseline differences in upper airway collapsibility or the site of pharyn-geal obstruction. Therapeutic responses may be augmented by the use ofmultisite stimulation, such as bilateral hypoglossal nerve stimulation, orstimulation of other combinations of upper airway and cervical muscles.Most importantly, the effect of electrical stimulation of the upper airway onmeasures of daytime sleepiness, performance, and cardiopulmonary func-tion must be assessed before this treatment modality can be established asa therapeutic option for OSA.

Fig. 7. Non-REM apnea-hypopnea indices for a night without stimulation (baseline) and for

entire-night and continuous periods with hypoglossal nerve stimulation. Patients’ values for the

entire night are the mean of values at 1, 3, and 6 months and last follow-up. (From Schwartz

AR, Bennett ML, Smith PL, et al. Therapeutic electrical stimulation of the hypoglossal nerve

in obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2001;127:1216–23; with

permission.)


Summary

Recent studies have shown that neuromuscular stimulation of thegenioglossus muscle and direct stimulation of the hypoglossal nerve canbe performed selectively and safely. Such stimulation, delivered below thearousal threshold, can modulate airflow during sleep in patients with OSA.The feasibility and potential of upper airway stimulation for the treatmentof OSA have been demonstrated. Further studies and stimulation-systemrefinements are presently underway, with hopes of establishing upper airwaystimulation as a therapeutic option for this challenging disorder.

References

[1] Remmers JE, de Groot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway

occlusion during sleep. J Appl Physiol 1978;44:931–8.

[2] Miki H, Hida W, Chonan T, et al. Effects of submental electrical stimulation during sleep

on upper airway patency in patients with obstructive sleep apnea. Am Rev Respir Dis

1989;140:1285–9.

[3] Edmonds LC, Daniels BK, Stanson AW, et al. The effects of transcutaneous electrical

stimulation during wakefulness and sleep in patients with obstructive sleep apnea. Am Rev

Respir Dis 1992;146:1030–6.

[4] Guilleminault C, Powell N, Bowman B, Stoohs R. The effects of electrical stimulation on

obstructive sleep apnea syndrome. Chest 1995;107:67–73.

[5] Oliven A, Schnall RP, Pillar G, et al. Sublingual electrical stimulation of the tongue during

wakefulness and sleep. Respir Physiol 2001;127:217–26.

[6] Schnall RP, Pillar G, Kelsen SG, Oliven A. Dilatory effects of upper airway muscle

contraction induced by electrical stimulation in awake humans. J Appl Physiol

1995;78:1950–6.

[7] Schwartz RS, Salome NN, Ingmundon PT, Rugh JD. Effects of electrical stimulation to

the soft palate on snoring and obstructive sleep apnea. J Prosthet Dent 1996;76:273–81.

[8] Decker MJ, Haaga J, Arnold JL, et al. Functional electrical stimulation and respiration

during sleep. J Appl Physiol 1993;75:1053–61.

[9] Fairbanks DW, Fairbanks DNF. Neurostimulation for obstructive sleep apnea: investi-

gations. Ear Nose Throat J 1993;72:52–7.

[10] Schwartz AR, Eisele DW, Hari A, et al. Electrical stimulation of the lingual musculature in

obstructive sleep apnea. J Appl Physiol 1996;81:643–52.

[11] Eisele DW, Smith PL, Alam DS, Schwartz AR. Direct hypoglossal nerve stimulation in

obstructive sleep apnea. Arch Otolarygol Head Neck Surg 1997;123:57–61.

[12] Goding GS, Eisele DW, Testerman R, et al. Relief of upper airway obstruction with hypo-

glossal nerve stimulation in the canine. Laryngoscope 1998;108:162–9.

[13] Eisele DW, Schwartz AR, Smith PL. Electrical stimulation of the upper airway for ob-

structive sleep apnea. Op Tech Otolaryngol Head Neck Surg 2000;11:59–65.

[14] Schwartz AR, Bennett ML, Smith PL, et al. Therapeutic electrical stimulation of the hypo-

glossal nerve in obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2001;127:

1216–23.


The limitations of isolated palatal surgeryfor patients with obstructive sleep apnea

Marc G. Dubin, MD, Brent A. Senior, MD*Department of Otolaryngology–Head and Neck Surgery, 610 Burnett-Womack Building,

Campus Box 7070, University of North Carolina, Chapel Hill, NC 27599-7070, USA

The goals of the treatment of obstructive sleep apnea (OSA) should beaimed at alleviating symptoms while decreasing morbidity and mortality ina manner that minimizes side effects. For example, approximately 70% ofpatients with OSA are obese. It has been shown that weight loss improvesand in some cases cures sleep-related breathing disorders and is clearly a low-morbidity treatment modality [1,2]. It also has been shown, however, thatthe improvement in apnea-hypopnea index (AHI) with weight loss, particu-larly in moderate to severe sleep apnea, is only partial [3].

Although other medical treatments for OSA exist, including pharmaco-therapy and dental appliances, the standard treatment for OSA continuesto be continuous positive airway pressure (CPAP). Although highly effectiveat normalizing polysomnographic variables, it is associated with low com-pliance rates (60%–80%) [4–9], and 15% of patients refuse CPAP after asingle night’s use in the laboratory [10,11]. For this sizable group of patientsin whom medical management alone has been of limited value, surgerybecomes essential in the management algorithm.

Many surgical procedures have been described during the past 20 years,but of these procedures, uvulopalatopharyngoplasty (UPPP), first describedin 1981 by Fujita et al [12], continues to be the mainstay. Since its intro-duction, there has been considerable effort expended studying the efficacyof this procedure and the role that it should play in the management ofOSA. Unfortunately, the results of these studies have shown that UPPP asan isolated intervention for the treatment of OSA has met with mediocreresults. This fact is confirmed by evaluating the data of its most ardentsupporters using the best selection criteria available. In an excellent reviewof the literature, Sher et al [13] have shown that UPPP is effective in only


36 (2003) 511–517


E-mail address: [email protected] (B.A. Senior).


doi:10.1016/S0030-6665(02)00179-2

approximately half of the cases of OSA when success is defined as a drop inthe AHI by 50%. When more stringent criteria are used—absolute decline inthe apnea index to less than 10 or an AHI less than 20—the success rate islowered to 40.7% [13]. These data are in marked contrast to the data on theuse of UPPP as part of a multistaged approach to multilevel anatomicobstruction. These series report significantly better results: up to 79%success with phase I (UPPP, genioglossal advancement, hyoid suspension)interventions and 90% to 95% success with phase II (additional maxillary-mandibular advancement) interventions using similar definitions of success[14–16].

The limitations of UPPP as an isolated procedure for the treatment ofOSA center on the challenge of determining the anatomic site of obstructionin an individual with OSA. As is evident by a review of the literature, evenwhen all attempts are made to predict which patients will benefit fromUPPP, successful control of OSA cannot be guaranteed [13]. As with manyprocedures for the treatment of OSA, UPPP has a relatively high morbidityassociated with it, and its complications can be life threatening. In contrast,medical management of OSA with CPAP has a relatively high rate of treat-ment success with few complications, although with mediocre compliance.

Sites of obstruction and their identification

The etiology of anatomic obstruction in OSA is believed to be animbalance between the forces acting to maintain airway patency (the forceof the pharyngeal muscles) and the negative inspiratory forces generated bythe diaphragm [17–19]. This mismatch may be due to a clear anatomicabnormality (ie, micrognathia, macroglossia, or hypertrophy of the tonsilsand adenoids) but more often is subtle. It has been demonstrated thatpatients who have OSA have pharyngeal collapse that is more significantthan in control subjects when the same amount of negative suction pressureis applied [20]. Additionally, patients with sleep apnea have been shown tohave failure of reflex activation of pharyngeal dilators in response to airwayocclusion [18].

In determining the site of obstruction, two problems come to light: Whereis the pharyngeal area of greatest collapse, and how can this area bedetermined accurately? The exact location of pharyngeal collapse is oftendifficult to ascertain with certainty. More confounding is the fact that thearea is often not a single area at all but involves a combination of retro-palatal and retroglossal collapse. Similarly, the collapse may be orientedin an anterior-posterior dimension or in a lateral-medial dimension (or acombination). Emphasizing this point, in one series of 200 patients withOSA, only three were found to have a single anatomic abnormality by rou-tine otolaryngologic examination [21].

Theoretically, accurate identification of the exact sites of collapse shouldaid the surgeon in procedure selection, thereby improving success rates. In

512 M.G. Dubin, B.A. Senior / Otolaryngol Clin N Am 36 (2003) 511–517

most patients, however, it is difficult to identify the anatomic locationsamenable to surgical correction. This challenge in identifying the areas ofanatomic abnormality has led to the development of diagnostic techniques,including fiberoptic airway endoscopy with the Muller maneuver andcephalometrics, among others.

The role of cephalometrics in predicting the site of anatomic obstructionhas led to contradictory data [22–26], which is not surprising given the factthat these static measurements of bony and soft tissue anatomy most likelydo not reflect the dynamic changes in pressure that result in airway collapsi-bility. The role of CT in the assessment of the site of anatomic narrowinghas been similarly unsuccessful. There was clearly no difference in staticcross-sectional area of the pharyngeal lumen in patients who responded toUPPP and those who did not [27,28].

Attempts at predicting the site of collapse using intrapharyngeal pressurerecordings also have been unsuccessful. Various studies have failed tocorrelate palatal collapse by pressure manometry with a successful outcomefrom UPPP [27,29,30]. It has been hypothesized by at least one author thatonly the most proximal site of obstruction can be identified by thesemethods [27]. Methods that would identify distal sites of collapse will aid inpredicting which patients actually will benefit from an isolated surgicalintervention that addresses only the proximal palatal obstruction, or ifadditional surgical modalities may be warranted [27].

Using a related technique, somnofluoroscopy, several authors haveattempted to radiographically localize the site of obstruction during sleep[27,30,31]. In one study, patients who had closure identified at the level ofthe soft palate were more likely than the population as a whole to improveafter UPPP (67% versus 42%) [31]. Unfortunately, despite these limiteddata, this technique is not readily available.

With this in mind, Muller’s maneuver seems to offer the best and easiestanalysis of dynamic airway collapsibility. This maneuver assesses the extentof anterior-posterior collapsibility and lateral collapsibility along variouspoints of the upper aerodigestive tract (ie, retropalatal or retroglossal). Withthis information, the examiner should be able to begin the difficult task ofassessing which areas may be amenable to surgical correction in a multistageprocess. There are several studies that suggest that patients who demon-strate nasopharyngeal collapse on Muller’s maneuvers are more likely toimprove after UPPP [32,33]. Additional data have demonstrated that themaneuver may more accurately identify poor responders to surgical inter-vention with UPPP, although other studies state that the utility of themaneuver as a predictive technique is low [22,26,34,35].

Owing to the difficulty in predicting a single site of obstruction withrelative accuracy, most surgeons currently advocate a multiphase approachin the surgical treatment of OSA, with UPPP playing an integral role.Increased success rates are seen when multiple procedures are used thataddress various sites of obstruction [15,36]. Palatal obstruction is addressed

513M.G. Dubin, B.A. Senior / Otolaryngol Clin N Am 36 (2003) 511–517

with UPPP, and base-of-tongue obstruction frequently is addressed withgenioglossus advancement and hyoid myotomy suspension or base-of-tongue reduction. This procedure then is followed by maxillary-mandibularadvancement for treatment failures [15,36]. The success of these approachesadds support for the argument that the limited success of UPPP when per-formed in isolation is due to its inability to adequately address the multiplesites of obstruction in patients with OSA.

Additional patient-selection criteria

Clearly, the difficulty in precisely determining the anatomic site ofobstruction in patients with OSA leads to challenges in predicting whichpatients will benefit from palatal surgery in isolation. There are numerousother patient factors that have been implicated in contributing to OSA,however, that are measured easily and theoretically could increase the likeli-hood of selecting patients who would benefit from UPPP.

Unfortunately, for all of the data collected during a polysomnograph,none has been correlated consistently with a successful outcome for anisolated UPPP [37,38]. Increasing body mass index or weight of the indi-vidual has been shown to decrease the likelihood of success of a UPPP,however [29,39]. It also has been shown that with more severe OSA (by bothAHI and apnea index), UPPP tends to be less successful [13,39]. In light ofthese data, it was hypothesized that less severe OSA may be more amenableto surgical correction with UPPP. In a study by Senior et al [40], only 40%of patients with mild OSA (AHI >5 and <20) who were treated with UPPPwith or without septoplasty responded (response being defined as a declineof 50% in AHI). Interestingly, in the same series, the patients who did notrespond had an elevation of their AHI from 16.6 � 5 to 26.7 � 18.4 [40].Based on these data, it is concluded that the anatomy of mild OSA is alsocomplex and is not always corrected with isolated UPPP.

Complications

A discussion on the limitations of UPPP in the surgical management ofOSA would be incomplete without mentioning the complications of theprocedure and its associated morbidity. Early reports in the literaturedescribed cases of acute airway obstruction, and in some cases, death afterUPPP in the setting of sedating drugs [41–43]. In one retrospective reviewof 135 patients, cited complications included one death, failed intubation(seven patients), hemorrhage (three patients), and arrhythmia (one patient).In another review of 210 patients, the most frequent complications includedbleeding (four patients), infection (five patients), seroma (three patients),arrhythmia (four patients), and unstable angina (one patient) [44]. In thissame review, significant preoperative comorbidities also were described andincluded hypertension (31%), arrhythmia (5.5%), coronary artery disease


(3.3%), pulmonary disease (7.7%), reflux esophagitis (4.4%), and depres-sion (10%) [44]. In one limited prospective study, it was shown that patientscontinue to demonstrate a significant number of hypopneas and apneas inthe early postoperative period after UPPP when polysomnography wasperformed [45].

Summary

Obstructive sleep apnea is a condition for which palatal surgery inisolation has been shown to have limited success. In comparison, palatalprocedures combined with other surgical approaches that address the mul-tiple sites of obstruction in the upper aerodigestive tract seem to have im-proved success in the carefully selected patient.

References

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MH, Roth T, Dement WC, editors. Principles and practice of sleep medicine. Philadelphia:

WB Saunders; 1994.

[2] Suratt P, McTier R, Findley L, et al. Changes in breathing and the pharynx after weight

loss in obstructive sleep apnea. Chest 1987;92:631–7.

[3] Braver H, Block A, Perri M. Treatment for snoring: combined weight loss, sleeping on side,

and nasal spray. Chest 1995;107:1283–8.

[4] Engleman H, Martin S, Douglas J. Compliance with CPAP therapy in patients with sleep

apnoea/hypopnea syndrome. Thorax 1994;49:263–6.

[5] Kribbs N, Pack A, Kline L, et al. Objective measurement of patterns of nasal CPAP use by


[6] McArdle N, Devereux G, Heidarnejad H, et al. Long-term use of CPAP therapy for sleep

apnea/hypopnea syndrome. Am J Respir Crit Care Med 1999;159:1108–14.

[7] Pepin J, Leger P, Veale D, et al. Side effects of nasal continuous positive airway pressure in

sleep apnea syndrome (a study of 193 patients in two French sleep centers). Sleep 1995;

107:375–81.

[8] Reeves-Hoche M, Meck R, Zwillich C. Nasal CPAP: an objective evaluation of patient

compliance. Am J Respir Crit Care Med 1994;149:149–54.

[9] Pirsig W. Obstructive sleep apnea. In: McCaffrey T, editor. Rhinologic diagnosis and

treatment. Stuttgart: Theime; 1997. p. 229–69.

[10] Krieger J. Long-term compliance with nasal continuous positive airway pressure (CPAP) in

obstructive sleep apnea patients and non-apneic snorers. Sleep 1992;15s:42–6.

[11] Waldhorn R, Herrick T, Nguyen M, et al. Long-term compliance with nasal continuous

positive airway pressure therapy of obstructive sleep apnea. Chest 1990;97:33–8.

[12] Fujita S, Conway W, Zorick F, et al. Surgical correction of anatomic abnormalities in


Surg 1981;89:923–34.

[13] Sher A, Schectman K, Piccirillo J. The efficacy of surgical modifications of the upper

airway in adults with obstructive sleep apnea syndrome. Sleep 1995;19:156–77.

[14] Hochban W, Brandenburg U, Peter J. Surgical treatment of obstructive sleep apnea by

maxillomandibular advancement. Sleep 1994;17:624–9.

[15] Riley R, Powell N, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306

consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993;108:117–25.

[16] Riley R, Powell N, Guilleminault C. Obstructive sleep apnea and the hyoid: a revised

surgical procedure. Otolaryngol Head Neck Surg 1994;111:717–21.


[17] Guilleminault C, Hayes B, Smith L, et al. Palatopharyngoplasty and obstructive sleep

apnea syndrome. Bull Euro Physiopathol Respir 1983;19:595–9.

[18] Hoffstein V. How and why should we stabilize the upper airway? Sleep 1996;19:S57–60.

[19] Simmons F, Guilleminault C, Silvestri R. Snoring and some obstructive sleep apnea can be

cured by oropharyngeal surgery-palopharyngoplasty. Arch Otolaryngol 1983;109:503–7.

[20] Wetmore S, Scrima L, Snyderman N, et al. Postoperative evaluation of sleep apnea after

uvulopalatopharyngoplasty. Laryngoscope 1986;96:738–41.

[21] Rojewski T, Schuller D, Clark R, et al. Videoendoscopic determination of the mechanism

of obstruction in obstructive sleep apnea. Otolaryngol Head Neck Surg 1984;92:127–31.

[22] Doghramji K, Jabourian Z, Pilla M, et al. Predictors for uvulopalatopharyngoplasty.


[23] Gislason T, Lindholm C, Almqvist M. Uvulopalatopharyngoplasty in the sleep apnea

syndrome: predictors of results. Arch Otolaryngol Head Neck Surg 1985;114:45–51.

[24] Riley R, Guilleminault C, Powell N, et al. Palatopharyngoplasty failure: cephalometric

roentgenograms and obstructive sleep apnea. Otolaryngol Head Neck Surg 1985;93:240–4.

[25] Ryan C, Dickson R, Blokmanis A, et al. Upper airway measurements predict response to

uvulopalatopharyngoplasty in obstructive sleep apnea. Laryngoscope 1990;100:248–53.

[26] Yao M, Utley D, Terris D. Cephalometric parameters after multilevel pharyngeal surgery

for patients with obstructive sleep apnea. Laryngscope 1998;108:789–95.

[27] Launois S, Feroah T, Campbell W, et al. Site of pharyngeal narrowing predicts outcome of

surgery for obstructive sleep apnea. Am Rev Respir Dis 1993;147:182–9.

[28] Shepard J, Thawley S. Evaluation of the upper airway by computerized tomography

in patients undergoing uvulopalatopharyngoplasty for obstructive sleep apnea. Am Rev

Respir Dis 1989;140:711–6.

[29] Hudgel D, Horasick T, Katz R, et al. Uvulopalatopharyngoplasty in obstructive apnea:

value of preoperative localization of site of upper airway narrowing during sleep. Am Rev

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[30] Metes A, Hoffstein V, Mateika S, et al. Site of airway obstruction in patients with obstruc-

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uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1986;94:56–60.

[32] DeBerry-Borowiecki B, Kukwa A, Blanks R. Indications for palatopharyngoplasty. Arch

Otolaryngol 1985;111:659–63.

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of patients for uvulopalatopharyngoplasty. Laryngoscope 1985;95:1483–7.

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Treating pediatric patients with obstructivesleep disorders: an update

Anna H. Messner, MD*Division of Otolaryngology/Head and Neck Surgery, Room R135,

Edwards Building, Stanford University, Stanford, CA 94305-5328, USA

It is a truth universally known that a person who sleeps poorly at nightis tired the following day. Although this ‘‘truth’’ may hold for adults, itusually does not hold for young children with obstructive sleep apneasyndrome (OSAS) [1]. Obstructive sleep apnea syndrome is defined as a ‘‘dis-order of breathing during sleep characterized by prolonged partial upperairway obstruction and/or intermittent complete obstruction (obstructiveapnea) that disrupts normal ventilation during sleep and normal sleep pat-terns’’ [2]. Importantly, pediatric patients can show symptoms of obstructivesleep disorder even in the absence of frank apneas (upper airway resistancesyndrome) [3,4]. Obstructive sleep apnea syndrome must be differentiatedfrom primary snoring, which is defined as snoring without obstructiveapnea, frequent arousals from sleep, or gas-exchange abnormalities [5].

One indicator of excessive daytime sleepiness is how quickly children fallasleep during the day. In a study of 54 children diagnosed on polysomnogram(PSG) as having OSAS, only 7 (13%) were found to fall asleep in less than 10minutes when they were evaluated in a sleep laboratory during the day,confirming that daytime sleepiness in children with OSAS is the exception,not the rule [6]. Instead of being sleepy, the child may have nonspecificbehavioral difficulties such as abnormal shyness, hyperactivity, developmen-tal delay, and aggressive behavior. The possibility of a sleep disorder shouldbe considered in any child being evaluated for an attention-deficit disorder.

In an effort to clarify the relationship between poor sleep quality anddaytime functioning, Gozal [7] evaluated a cohort of poorly performingchildren in the first grade. In this prospective study, 297 first graders whowere in the lowest tenth percentile of their class were screened for OSAS


36 (2003) 519–530

* Pediatric Otolaryngology–Head and Neck Surgery, Lucile Packard Children’s Hospital

at Stanford, 725 Welch Road, Palo Alto, CA 94304-5654, USA.



doi:10.1016/S0030-6665(02)00180-9

using a parental questionnaire and a single-night recording of pulse oxi-metry and transcutaneous partial pressure of carbon dioxide. Those whowere found to have abnormalities on the studies (54 of 297) were encouragedto seek medical intervention; 24 of these children underwent tonsillectomyand adenoidectomy (T&A). The performance of the children who under-went T&A was compared to the 30 children who did not undergo T&A,and in second grade the treatment group’s mean grades increased signif-icantly. The author concluded that OSAS is associated with an adverseeffect on learning. Further evidence that OSAS may affect daytime func-tioning is seen in another article by Gozal and Pope [8]. This retrospectivequestionnaire compared snoring in early childhood in matched groups of13- and 14-year-olds who were in the top or bottom quartile of their class.Children with lower academic performance in middle school were found tohave been more likely to have snored during early childhood and to requireT&A for snoring as compared to their better-performing schoolmates. Theauthors concluded that these findings support the idea that a ‘‘learningdebt’’ may develop with sleep-disordered breathing during early childhoodand hamper subsequent school performance.

Nocturnal symptoms of OSAS include snoring, pauses in breathing,gasping for breath, increased respiratory effort (nasal flaring and supra-clavicular, suprasternal, and intercostal retractions), enuresis, and excessivesweating. Frequently, children with OSAS resist going to bed [9]. In adults,sleep apnea is worse when the patient is in the supine position. Conversely,children with OSAS seem to breathe best when they are in the supineposition [10]. Severe OSAS can lead to cor pulmonale.

Etiology of obstructive sleep apnea syndrome in children

It has been theorized that obstructive sleep disorders are familial. Genetictransmission of risk factors such as a high-arched palate, micrognathia, oradenotonsillar hypertrophy may play an etiologic role. A questionnaire-typetelephone survey by Ovchinsky et al [11] showed that 20.4% of first-degreerelatives of 115 index cases with pediatric obstructive sleep apnea hadsymptoms highly suggestive of obstructive sleep apnea. Because the generalincidence of this syndrome is from 3% to 4%, the study supports theconcept that there are genetic mechanisms at work in the development of thedisorder [12]. This study confirmed the familial incidence of 21% of first-degree relatives of index cases with OSAS who were found to have OSAS asreported by Redline et al [13]. In a combined questionnaire-PSG study byDouglas et al [14], a similar (25%) incidence of OSAS was seen again in thefirst-degree relatives of patients with apnea.

Evaluation of the child with symptoms of obstructive sleep apnea syndrome

With the wide range of symptoms, the diagnosis of a significantobstructive sleep disorder in a pediatric patient can be difficult. The most

520 A.H. Messner / Otolaryngol Clin N Am 36 (2003) 519–530

widely recognized and best single laboratory test to support the diagnosis ofobstructive sleep disorder is the nocturnal PSG. A pediatric PSG uses thesame technology to record the same information as is recorded in adults.The recording includes electroencephalography, chin electromylogram,right and left electro-oculogram, electrocardiogram, limb movements, andbreathing measurements. The breathing measurements usually monitoredare airflow, respiratory effort, and pulse oximetry. End-tidal carbon dioxideand esophageal pressure measurements are used in some but not alllaboratories.

Although the PSG unquestionably is the most effective tool available todetermine the presence and severity of an obstructive sleep disorder, somehave questioned the reliability of a single-night study. The possibility of a‘‘first-night’’ effect, that is, a change in a patient’s sleep architecture due tounfamiliar surroundings, has been postulated. It seems that the first-nighteffect is rarely significant. In a study by Katz et al [15], 30 children withsymptoms of sleep-disordered breathing underwent two nocturnal PSGsperformed 7 to 27 days apart. The mean of the respiratory variables, in-cluding apnea index, apnea-hypopnea index, arterial oxygen saturation, andend-tidal partial pressure of carbon dioxide, was not significantly differentfrom night to night. No child changed diagnosis from primary snoring toOSAS (or the reverse) as a result of the second PSG. This finding led to theconclusion that a single PSG night is an adequate measure of OSAS inchildren with symptoms of sleep-disordered breathing.

Currently, the relationships among various parameters of the PSG (apnea-hypopnea index, number of respiratory-related arousals per hour of sleep,minimumoxygen saturation, number of oxygendesaturations<90%per hourof sleep, and the maximum end-tidal carbon dioxide value) and neuro-psychologic parameters (intelligence, memory, attention and impulsivity, andacademic performance) are being studied. Preliminary evidence suggests thatmemory impairment is correlated strongly with the degree of hypoxemiaas indicated by the minimum arterial oxygen saturation value, whereasimpairment in adaptive behavior is correlated with the degree of sleepdisruption as indicated by the respiratory arousal index. Intelligence andacademic achievement are not related to any specific PSG parameter, butinstead are best correlated with a composite of the parameters described [16].

There is controversy concerning the necessity of a PSG in all pediatricpatients with symptoms of OSAS [17]. In April of 2002, the Section onPediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syn-drome of the American Academy of Pediatrics published a clinical prac-tice guideline that addressed the diagnosis and management of childhoodOSAS [18]. Concerning the diagnosis of patients with OSAS, the guidelinerecommends the following: ‘‘(1) all children should be screened for snoring;(2) complex high-risk patients should be referred to a specialist; (3) patientswith cardiorespiratory failure cannot await elective evaluation; and (4)diagnostic evaluation is useful in discriminating between primary snoring

521A.H. Messner / Otolaryngol Clin N Am 36 (2003) 519–530

and OSAS, the gold standard being polysomnography.’’ The guidelineconcludes that history and physical examination are poor at differentiatingprimary snoring from OSAS. Other screening techniques, such as video-taping, nocturnal pulse oximetry, and daytime nap polysomnography wereconsidered helpful if results are positive, but have a poor predictive valueif results are negative [19]. Unfortunately, the lack of pediatric sleeplaboratories makes this guideline difficult to follow.

Tonsillectomy techniques

There is little debate that the primary treatment for most children withOSAS is T&A [18]. Head-and-neck surgeons are constantly searching forbetter ways to perform a tonsillectomy. Although the standard cold(scissors, knife) or hot (electrocautery) techniques are quick, effective, andsafe, the patient invariably experiences significant postoperative pain. Thebest operative technique to minimize postoperative pain has long been andcontinues to be controversial, and thus various techniques are comparedconstantly in the medical literature.

Nunez et al [20] compared electrocautery (hot) versus cold dissectionand snare tonsillectomy prospectively in a group of 54 children. Notsurprisingly, cold dissection resulted in double the intraoperative blood loss(33.7 mL versus 15.1 mL). Recovery in the first 24 hours after surgery wassimilar in both groups. Follow-up of the children, however, revealed asignificantly greater analgesic consumption, longer time to return to eating anormal diet, and more consultations with the family practitioner for throatpain for children in the hot-dissection group.

In an effort to decrease the postoperative pain experience and to decreasethe amount of bleeding intraoperatively, several new techniques have beendescribed recently. A supplemental issue of Laryngoscope was dedicated to‘‘Innovative Techniques for Adenotonsillar Surgery in Children.’’ In it,Koltai et al [21] reviewed their experience with intracapsular tonsillec-tomy—a partial tonsillectomy—using powered instrumentation. The pur-pose of the partial as opposed to the routine tonsillectomy is to preserve thetonsil capsule, thus leaving the pharyngeal muscles covered, and, it ishoped, causing the patient to experience less postoperative pain. A retrospec-tive review of 150 patients who underwent intracapsular tonsillectomy wascompared with 162 children who underwent standard tonsillectomy duringthe same time period. A telephone survey was used to collect data con-cerning the postoperative course. Although the children in the intracapsulargroup had significantly less pain than the total tonsillectomy group, the twogroups were not equivalent; the intracapsular tonsillectomy group wassignificantly younger (mean, 6.0 versus 8.9 years). A prospective, random-ized study by the same group is pending.

The ultrasonic dissector coagulator (Harmonic scalpel [HS]; EthiconEndo-Surger, Cincinnati, OH) is a relatively new surgical tool that uses


ultrasonic technology to cut and coagulate tissues at lower temperaturesthan that used with the electrocautery, thereby minimizing tissue damage(and possibly, postoperative pain). Two studies have compared HS tonsil-lectomy to electrocautery tonsillectomy. The first, a prospective, random-ized study performed by Walker and Syed [22], used a questionnaire tocompare the postoperative course after tonsillectomy with the HS (155patients) with that after electrocautery (161 patients). Intraoperative bloodloss and postoperative hemorrhage were equivalent in the two groups.Patients treated with the HS had a significantly earlier return to normal dietand activity. An upcoming study of 120 children undergoing tonsillectomywho were randomly assigned to the HS (61 patients) and electrocautery(59 patients) also showed equivalent blood loss in the two groups [23].Operating time was significantly longer with the HS, and pain scorestrended lower on postoperative days 2, 3, and 4 but were not statisticallysignificant. Thus far, there does not seem to be enough evidence showingdecreased postoperative pain with the HS, considering its additional costand prolonged operating time, to justify its use during routine tonsillectomy.

A recently published study compared electrocautery tonsillectomy versusplasma-mediated ablation (cold ablation) of the tonsil [24]. Plasma-mediatedablation energizes protons to break molecular bonds between tissues. Thismethod results in less thermal injury, which theoretically may reduce post-operative pain. In this prospective, randomized, blinded study, 34 childrenaged 4 to 7 years underwent tonsillectomy. Postoperative pain scores wererecorded for 10 days, and a histopathologic evaluation of the excised tonsilswas performed.Mean surgical time was increased for the cold-ablation group(23.8 minutes versus 16.2 minutes), whereas estimated blood loss was similar.Histopathologic analysis of the tonsils showed that the mean depth of injurywas significantly greater in the electrocautery group. Two of the childrenundergoing cold-ablation removal of their tonsils required unplanned ad-missions for airway obstruction. Measures of postoperative pain were notsignificantly different between the two groups, leading the authors to concludethat plasma-mediated ablation ‘‘as it is presently delivered should not replacemonopolar electrosurgery for routine tonsillectomy.’’

Pathologic evaluation of the tonsil/adenoid specimen

After the tonsils and adenoids are removed, the circulating nurse in theoperating room typically asks the surgeon if he or she would like thespecimen sent for pathologic evaluation. For the pediatric patient un-dergoing a routine T&A for OSAS, this step seems to be unnecessary. Ina recent study by Younis et al [25], 2438 tonsil-specimen reports werereviewed retrospectively, and none was found to have a histopathologicfinding other than the expected lymphoid hyperplasia. In addition, Stronget al [26] found no occult neoplasms in 1583 specimens reviewed at theirinstitution. They surveyed 4715 members of the American Academy of


Otolaryngology–Head and Neck Surgery and found a significant increase inrespondents ordering ‘‘gross only’’ and ‘‘no pathology.’’

A notable exception to the ‘‘gross-only’’ or ‘‘no-pathology’’ policyconcerns children who have undergone liver transplantation. Lymphoidhypertrophy is common in this group, and an obstructive sleep disorder canresult. On removing the tonsils or adenoids, the specimen always should besent for pathologic review. Post-transplant lymphoproliferative disease canresult in these patients after infection with Epstein-Barr virus. Histologicchanges can range from tonsillar hyperplasia to large-cell lymphoma, neces-sitating changes in the immunosuppressive therapy [27,28].

Postoperative complications

Postoperative hemorrhage has been and continues to be the most im-portant complication after tonsillectomy surgery. A recent retrospectivestudy of 1438 patients found that 51 patients (3.5%) required intervention(termed a significant hemorrhage) for their bleeding [29]. One hundred twelve(7.8%) of all patients in this study had returned for an evaluation when thecaregiver saw blood of any volume. Patients who were younger than the ageof 3 had fewer significant hemorrhages than the older children, with only0.9% (3 of 317) requiring postoperative medical intervention. In the 4-to-11age group, 969 underwent tonsillectomy and 34 (3.5%) required inter-vention. The oldest group (ages 12–20) had the highest significant post-operative hemorrhage rate, with 9.2% (14 of 152) requiring care. The mostcommon time from surgery to initial evaluation for hemorrhage was 6 days.

As stated earlier, children inevitably experience pain after a tonsillectomy.In an effort to objectively measure post-tonsillectomy pain, a standardquestionnaire was developed so that analgesic requirements could be titrated[30]. This questionnaire asked caregivers to report on the child’s drinking,eating, talking, dribbling, crying, activity, and mood, and assigned points toeach response so that higher scores indicate more severe pain. Interestingly,child complaints of pain did not correlate well with the other items in thesurvey, and when this question was removed, the survey had higher internalconsistency. The pain scores also did not correlate with the amount of painmedicine given in the first 24 hours after tonsillectomy surgery.

In an effort to reduce the postoperative pain, a single dose of dexa-methasone can be given intraoperatively to decrease vomiting, improve oralintake, and decrease postoperative pain [31–33]. The doses given in the citedstudies range from 0.15 to 1.0 mg/kg; the optimal dose is not known.Acetaminophen is a standard postoperative medication given to childrenafter tonsillectomy. In a prospective, randomized, double-blind study ofacetaminophen compared to acetaminophen with codeine, the children whoused acetaminophen alone consumed a significantly higher percentage ofa normal diet on the first 6 postoperative days, with no difference in painscores between the treatment groups [34]. Postoperatively, a telephone call


3 to 4 weeks after surgery by an otolaryngology nurse, instead of thetraditional postoperative visit, has been shown to be cost-effective anddesirable to parents [35].

Nonsurgical treatment of pediatric obstructive sleep apnea syndrome

For the patient and family who want to avoid surgery, one option may betopical steroids. In a recent study, 6 weeks of topical fluticasone was found todecrease the apnea-hypopnea index from an average of 10.7 to 5.8 in a smallgroup of subjects (n ¼ 13) [36]. This finding was compared to a similarly sizedcontrol group of subjects who had an increase from 10.9 to 13.1 in their apnea-hypopnea index, although there was no significant change in tonsil size,adenoid size, and symptoms score between the two groups.

Occasionally, patients with obesity, neuromuscular disorders (cerebralpalsy), and craniofacial disorders will have respiratory difficulties in theimmediate postoperative period. Frequently, these patients can be managedin the pediatric intensive care unit with continuous positive airway pressureor bilevel positive airway pressure (BiPAP) [37]. This same group of patients(and occasionally, other children with severe OSAS) frequently have re-sidual OSAS after a T&A is performed. The study by Padman et al [38]supports the use of BiPAP in these patients with persistent OSAS. Theydescribed 10 children (aged 3–18) who underwent pre-BiPAP and post-BiPAP sleep studies. With BiPAP, the apnea index decreased from 19.7 to0.82, the lowest oxygen saturation increased from 75.6% to 89.5%, andbreath length increased from 3.22 to 3.68 seconds. In severe cases of OSASin which BiPAP is not possible, a tracheotomy may be necessary, although itoften can be avoided in the child with craniofacial anomalies who undergoescraniofacial skeletal expansion and soft tissue reduction [39,40].

Patient quality of life before and after tonsillectomy and adenoidectomy

Several recent studies have examined the effect of T&A on patient qualityof life (QOL). Published, validated, reliable QOL surveys relating specif-ically to tonsillectomy include the OSD-6 (Fig. 1) developed by de Serreset al [41] and the OSA-18 (Fig. 2) developed by Franco et al [42]. Bothinstruments survey caregivers on their child’s sleep disturbance, physicalsymptoms, emotional symptoms, daytime activity, and caregiver concerns.The OSD-6 specifically addresses speech or swallowing problems. The OSA-18 was found to correlate with the respiratory disturbance index on nappolysomnography in the 61 children studied.

A before-and-after adenotonsillectomy study using the OSD-6 instru-ment detected large improvements in at least short-term QOL in mostchildren [43]. Specifically, large, moderate, and small improvements in QOLwere seen in 74.5%, 6.1%, and 7.1% of children, respectively. The most


Fig. 1. The OSD-6. (From deSerres LM, Derkay C, Astley S, et al. Measuring quality of life in

children with obstructive sleep disorders. Arch Otolaryngol Head Neck Surg 2000;126:1426;

with permission.)

improved areas were sleep disturbance, caregiver concern, and physicalsuffering. Five percent of children had a poorer QOL after surgery.

Similarly, the OSA-18 instrument was used in addition to the ChildBehavior Checklist (CBCL) by Goldstein et al [44] in a before-and-afteradenotonsillectomy study. A pilot study using the CBCL showed that 10 of36 children (28%) undergoing T&A for chronic upper airway obstructionscored in the abnormal range for behavior. Using both the CBCL andthe OSA-18 to evaluate 64 children who underwent T&A for treatment ofsleep-disordered breathing or recurrent tonsillitis, behavioral and emotionaldifficulties in children with sleep-disordered breathing were found to im-prove after surgery [45]. Again, 25% of children demonstrated behavioraland emotional problems preoperatively on the CBCL. The total problemscores and most domains significantly improved after T&A, and only 8% ofchildren scored in the abnormal range postoperatively.

Fig. 2. The OSA-18. (From Franco RA, Rosenfeld RM, Rao M. Quality of life for children

with obstructive sleep apnea. Otol Head Neck Surgery 2000;123:10; with permission.)


In addition to improved behavior after a T&A, families can be informedpreoperatively that frequently the child will gain weight postoperatively.A recent study confirmed that growth hormone secretion is impaired inchildren with OSAS [46]. After adenotonsillectomy, children with OSASnormalize their growth hormone secretion and gain weight. Further confirm-ing evidence was provided in a retrospective cohort study by Soultan et al[47]. In this retrospective study, 45 children who underwent tonsillectomyand/or adenoidectomy for OSAS an average of 15 months previously (range,6–36 months). Thirty-one children (69%) had substantial weight gainpostoperatively, including 10 of 17 who were obese or morbidly obese at thetime of surgery.

Summary

Obstructive sleep apnea syndrome in children continues to be animportant subject for otolaryngologists because of the high prevalence ofthe disease. The evaluation of a child with OSAS remains controversial,although there is little controversy that T&A is the optimal treatment forthese children. The search for the optimal T&A technique is ongoing,although now either ‘‘cold’’ tonsillectomy or ‘‘hot’’ tonsillectomy is stan-dard. Quality-of-life studies confirm the significant benefit gained after achild undergoes a T&A.

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Surgery for sleep-disordered breathingin female patients

Regina Paloyan Walker, MD*Department of Otolaryngology, Loyola University Medical Center,

2160 South First Avenue, Maywood, IL 60153, USA

The average physician and layperson envision Joe, the fat boy of thePickwick Club, when the medical condition obstructive sleep apnea syn-drome (OSAS) is discussed. Charles Dickens depicted Joe as a morbidlyobese, hypersomnolent boy who snored. Initial research and clinical guide-lines that have been established for the evaluation and treatment of thisdisorder have been based primarily on patients who resemble Joe. Duringthe past 10 years, however, it has become apparent that young and old, maleand female, and obese and nonobese patients may be afflicted with sleep-disordered breathing (SDB). Presenting symptoms may vary depending onthe age and gender of the patient. A child with OSAS may be hyperactive,whereas an adult with the same condition typically has the opposite symptomof hypersomnolence. Clinical response to positive airway pressure and sur-gical treatment varies as well. The astute physician needs to recognize thesedifferences when evaluating and treating patients with sleep disorders.

Epidemiology of sleep-disordered breathing: male versus female

sleep-disordered breathing

Young et al [1] were the first group to perform a large population-basedstudy of sleep apnea that included women. Prior to this publication in 1993,other large population-based studies of OSAS included only male patients[2–4]. In addition to these population-based studies, reports that focused onthe clinical population of patients with OSAS again focused on the malepatients. Review articles from the 1970s and 1980s suggested that the male-to-female ratio for OSAS in a clinical population varied from 10:1 to 60:1


36 (2003) 531–538

* 40 South Clay Street, Suite 135, West Hinsdale, IL 60521, USA.



doi:10.1016/S0030-6665(02)00181-0

[5]. The conclusion that was extrapolated from these articles was that OSASwas a disorder of male patients. The article published by Young et al [1]changed the perception of this disease. This group of investigators studied602 patients (352 men, 250 women) who were from a middle-aged andworking population in Wisconsin. The results of this study revealed that9% of women and 24% of men had SDB. Sleep-disordered breathing wasdefined as an apnea-hypopnea score of five or more. They also estimatedthat 2% of women and 4% of men, in a middle-aged working population,have OSAS. The diagnostic criterion that was used to define a diagnosis ofsleep apnea syndrome was an apnea-hypopnea score of five or more thatwas associated with daytime hypersomnolence. Young et al showed thatapproximately 33% of the sleep apnea population is made up of women. Inanother study, Ohayon et al [6] conducted a telephone-interview survey of4972 people in the United Kingdom that concluded that approximately 30%of patients with OSAS are women.

Clinical population studies examine only the population that presents tophysicians for evaluation of symptoms, whereas population-based studiesfocus on the general population. At this time, population-based studies arereporting that one third of the apnea population is female. Yet in studiespublished in the 1990s that evaluated a clinical population, only 10% to25% of the patients were female [7,8]. Therefore, gender-related differencesare much less pronounced in recent population-based studies than previousclinical studies indicated.

Gender differences in symptoms of obstructive sleep apnea syndrome

In 1996, Young et al [9] addressed the gender bias in the sleep apneapopulation using data from the Wisconsin Sleep Cohort Study. Multiple hy-potheses were evaluated to attempt to explain why sleep apnea is under-diagnosed in women. One hypothesis is that the diagnosis of women withsleep apnea is missed because they have different symptoms than men. Thefindings of Young et al do not support this hypothesis, however. For bothmen and women, the significant predicators of SDB are snoring, breathingpauses, and hypersomnolence. Although these classic symptoms are found inboth men and women, women reported higher rates of morning headaches,depression, and anxiety at presentation in addition to classic symptoms.Morning headaches were reported more commonly in women than in men ina surgical population of apneic patients as well [10]. Morning headaches,depression, and anxiety are not as well recognized as the ‘‘classic symptoms’’of sleep apnea. Another hypothesis that has been proposed is that thereporting of these ‘‘atypical’’ complaints may lead physicians to considerother diagnostic possibilities. For example, if an obese female patient reportsfatigue, typically thyroid function studies are obtained. If an obese malepatient reports fatigue, however, it is muchmore likely that a polysomnogramwill be ordered. The stereotype of ‘‘Joe the fat boy,’’ from Dickens’ Pickwick

532 R.P. Walker / Otolaryngol Clin N Am 36 (2003) 531–538

Papers, is difficult to erase. Physicians need to be educated about the pre-valence of SDB in female patients and the need to take sleep histories inwomen as well.

Preoperative evaluation

Sleep history

Many patients present to an otolaryngologist with the simple complaint ofsnoring. Unless a sleep history is taken, symptoms of sleep apnea often arenot mentioned by the patient. The patient’s focus is usually on the snoringsound he or she produces and the disruption of his or her bed partner’s sleep.Men are ‘‘brought in’’ by their wives to be ‘‘fixed,’’ whereas women oftenpresent without prompting because of their embarrassment about theirsnoring. It is the physician’s responsibility to inquire about the other sleephabits and daytime symptoms before the treatment of snoring can occur,however. In addition, the history should include (1) typical bedtime andarousal time; (2) the use of sleep aids, such as sedatives or alcohol; (3)a history of nocturnal reflux; and (4) daytime stimulant use, for example,caffeine intake. Sleepiness is a subjective complaint that can be evaluatedmore objectively with a standard questionnaire such as the Epworth orStanford Sleepiness Scale. Additional information pertaining to history thatis specific to women includes pregnancy status and the use of hormone-replacement therapy (HRT). Most female patients diagnosed with OSASare postmenopausal [11–15]. The use of HRT may have a protective effectin the postmenopausal woman. The prevalence of sleep apnea is similar inpremenopausal and postmenopausal womenonHRT (0.6%and 0.5%, respec-tively). The prevalence is significantly higher in postmenopausal women whoare not receiving HRT (2.7%), however. With recent research showing thatHRT may not be as useful as once believed, it is plausible that the numberof apneic women will increase as women choose to proceed through meno-pause without HRT. Although a pregnant patient rarely would undergo anykind of elective surgical procedure, it seems that the hormonal changes thattake place during a pregnancy have a protective effect toward SDB [16,17].

Other special cases include women with Turner’s syndrome and polycysticovary syndrome in whom hormonal status is altered. Turner’s syndrome isa common X-linked aneuploidy (XO) characterized by a female phenotype,retarded growth, infertility, and craniofacial abnormalities, in some cases[18]. The upper airway abnormalities and the hormonal status predispose thisgroup of women to SDB. Women with polycystic ovary syndrome are pre-disposed to SDB because of the obesity and androgen excess typically seen inpatients with this disorder [19]. Exogenous administration of testosterone tofemale and male patients has been reported to increase the respiratorydisturbance index (RDI) or to induce sleep apnea in a small group of patients[20,21].

533R.P. Walker / Otolaryngol Clin N Am 36 (2003) 531–538

Physical examination

The physical examination of the patient with SDB should include vitalsigns, height, weight, neck circumference, and a complete head-and-neckexamination. In general, a flexible endoscopic examination is needed toassess the laryngeal airway and hypopharynx. A body mass index (BMI)should be calculated (the weight in kilograms divided by the square of theheight in meters). The neck circumference usually is measured at the cri-cothyroid membrane, although in the obese neck, the laryngeal landmarksare often difficult to discern. Obesity is the most important predisposingfactor in OSAS [1,4,22]. In the author and colleagues’ surgical study of 686patients (111 women and 575 men) diagnosed with OSAS, female patientshad a significantly higher BMI when compared with the male patients atpresentation [10]. The BMI versus RDI was evaluated to determine whethergender modified the effect of BMI on RDI. It was found that for women,there was a weaker correlation between BMI and RDI as compared withmen. Young et al [9] reported similar findings in the Wisconsin Sleep CohortStudy, in which 551 men and 388 women were studied. Women with an RDIof 15 or more had a significantly greater BMI when compared with men.Classically, men have a predominantly android or upper-body fat distri-bution, and women have a gynecoid or lower-body fat distribution [23].Women with a diagnosis of OSAS are typically more obese than their malecounterparts. A patient’s BMI is used to determine his or her weight status(Table 1). Another term often used, morbid obesity, is defined as a BMIgreater than 35 kg/m2. A BMI can be calculated quickly in a clinic settingusing a BMI chart.

Upper-body obesity, seen predominantly in men, may partly explain whymen have OSAS more frequently than women. The overall neck circumfer-ence, commonly much larger in men than women, is correlated with airwayobstruction in men [24]. This upper-body obesity would lead one to predictthat men with OSAS have a smaller pharynx than women with the samedisorder. The opposite is true. Brooks and Strohl [25] found that normal menhave a significantly larger pharynx than women. Men also have been shownto have a larger change in the pharyngeal area with lung-volume change.

Table 1

Weight-classification system

Category BMI (kg/m2)

Underweight Less than 18.5

Healthy weight 18.5–24.9

Overweight 25.0–29.9

Obesity (class 1) 30.0–34.9

Obesity (class 2) 35.0–39.9

Severe obesity (class 3) 40 or more


Normal men may have a greater tendency to collapse their airways, whichmay account for the gender differences in the development of SDB.Mohsenin [26] demonstrated that in middle-aged men and women witha diagnosis of OSAS, women had a smaller pharynx than did men. This studydemonstrated that pharyngeal size was correlated with apnea severity in menbut not in women with OSAS.

The awareness of gender-related differences in the physical examination iscritical when determining a treatment plan for patients with OSAS. Recentresearch has identified the following trends in physical differences betweenmen and women with OSAS:

1. Women have a significantly higher BMI as compared with men.2. Women have lower-body obesity and men have upper-body obesity.3. Men have larger necks than women.4. Women have a smaller pharynx than men.

Polysomnographic findings

Female patients with a diagnosis of OSAS have been noted to have a lowerRDI when compared with men [10]. In a group of 686 patients (111 womenand 575 men) who presented for a surgical evaluation, the mean RDI forwomen was 37, versus 42 in men. This difference was statistically significant.Mohsenin [26] reported polysomnographic findings in 130 patients referredfor evaluation of SDB. The RDI was lower in the female patients (24 versus62 in men). Leech et al [27] noted that among 118 patients with OSAS(77 men and 41 women), women have more hypopneas rather than apneas,and the length of their apneic events was shorter. O’Connor et al [28] catego-rized patients as having one of three main patterns of apnea: (1) obstructivesleep apnea that occurred in the supine position, (2) non–positional-relatedobstructive sleep apnea, and (3) rapid-eye-movement–related apnea. Womenwere found to have rapid-eye-movement–related apnea more often than malepatients (62% versus 24%). In contrast, supine and non-positional apneapatterns were much more common in men. The polysomnographic findingsin women diagnosed with OSAS differ from male patients with the samedisorder. The RDI is lower in women, the proportion of the RDIs made up ofhypopneas is greater, and rapid-eye-movement–related apnea is more com-mon in women.

Surgical treatment

Little information can be obtained from the surgical literature regardingresponse rates of women undergoing various surgical procedures for thetreatment of OSAS. Just as there is no standardization within the medicalcommunity regarding interpretation of a polysomnogram, the analysis ofpostoperative data varies significantly in surgical publications. Another


limitation of studying female patients undergoing surgical treatment is thepaucity of patients. In most surgical series examining uvulopalatophar-yngoplasty or laser assisted uvulopalatoplasty (LAUP), less than 20% of thepatients are women [10,29,30]. Meaningful data on more extensiveprocedures in women, such as genioglossus advancement with hyoidmyotomy-suspension and maxillary-mandibular advancement, are notavailable. In Riley et al’s classic report [31] on 306 surgical patients, only35 were women. Despite all of these limitations and the critical need forfurther investigation, some information is available.

Mickelson and Ahuja [29] reported their results on 36 patients withOSAS who underwent laser-assisted uvulopalatoplasty. In this series, thefemale data were not analyzed specifically, but the individual raw data werepresented. Seven of the 36 patients were female. The author’s group [10] alsostudied patients with OSAS who underwent LAUP treatment. Preoperativeand postoperative data from both series are shown in Table 2. Mickelsonand Ahuja’s series demonstrates a nonsignificant decrease in the RDI(P ¼ 0.2834) and an increase in the lowest oxygen saturation (P ¼ 0.3830)after LAUP treatment for OSAS. In general, a successful surgical outcomeis defined as a postoperative RDI of 10 or less. Of these patients, 43% hadan RDI of 10 or less after treatment. In the author’s series of 16 femalepatients, a significant decrease in the RDI (P ¼ 0.0042) and a nonsignificantincrease in the lowest oxygen saturation (P ¼ 0.1141) were noted. Of these16 patients, 81% had a postoperative RDI of 10 or less.

At this time, only preliminary data are available on the surgical treatmentof female patients. These data only reflect LAUP procedure results; resultsfrom other palatal surgery, specifically uvulopalatopharyngoplasty, are notavailable. Based on these early findings, palatal surgery treatment for femalepatients with OSAS is certainly a viable option. Initial impressions sug-gest that women respond as well as or more favorably to palatal surgerywhen compared with male patients. Further studies are necessary before anyguidelines can be established for female patients.

Table 2

Female patients with OSAS treated with LAUP

Mickelson and Ahuja [29]

(n ¼ 7)

Mean � SD

Walker et al [10]

(n ¼ 16)

Mean � SD

Age 58.1 � 8.6 54.6 � 12.7

BMI 35.2 � 11.8 32.4 � 7.8

Preoperative RDI 26.1 � 13.8 18.7 � 13.9

Postoperative RDI 17.9 � 13.6 6.5 � 7.5

Preoperative LSAT 76.1 � 11.3 84.0 � 4.7

Postoperative LSAT 80.9 � 11.8 86.7 � 4.2

Abbreviations: BMI, body mass index (kg/m2); LSAT, lowest oxygen saturation; RDI,

respiratory distrubance index (events/hour); SD, standard deviation.


Acknowledgments

The author thanks Dr. Chellam Gopalsami and Lisa Harrison for theirassistance in preparing this manuscript.

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Evidence-based medicine in sleepapnea surgery

K. Christopher McMains, MD,David J. Terris, MD, FACS*

Department of Otolaryngology–Head and Neck Surgery, Medical College of Georgia,

1120 Fifteenth Street, Augusta, GA 30912-4060, USA

Historical perspective

Guilleminault et al [1] coined the term obstructive sleep apnea (OSA)to describe patients with disrupted nocturnal breathing. Kuhlo et al [2]performed the first tracheotomy to bypass upper airway obstruction in 1969,which represented the first definitive surgical procedure to treat OSA. Fujitaet al [3] introduced the uvulopalatopharyngoplasty (UPPP) for treatment ofOSA in 1979. Sullivan et al [4] published the first study of continuouspositive airway pressure (CPAP) for nonsurgical treatment of OSA in 1981.As with tracheotomy, CPAP eliminates excessive daytime sleepiness (EDS)and cardiopulmonary sequelae of OSA [5], including normalization of bloodpressure [6]. Only complete compliance was shown to be sufficient to confertreatment benefits from CPAP [7], and incomplete compliance with CPAPproved prevalent [8–10]. Despite increased compliance with autotitratingCPAP, a substantial proportion of patients remained ineffectively treated onCPAP [11]. This finding led to a shift in focus toward surgical treatment ofOSA. In a meta-analysis, Sher et al [12] noted success of UPPP in 41% of allpatients, whereas in patients with tongue base obstruction, success wasachieved in only 6% of cases. This finding is supported further by Isono et al[13], who demonstrated that collapsibility at the level of the retroglossalairway is the most significant determinant of UPPP outcome.

In the wake of objective failure of UPPP in many patients, it became clearthat multiple anatomic sites contribute to obstruction [14–16]. Methods forevaluating levels of obstruction were sought to improve preoperativeassessment and surgical outcomes. The methods the studies used included


36 (2003) 539–561


E-mail address: [email protected] (D.J. Terris).


doi:10.1016/S0030-6665(02)00182-2

the Muller maneuver, cephalometric analysis, CT, and volumetric MRI.The Muller maneuver offers some insight into the level of obstruction anddimensions of obstruction, although it does not accurately predict surgicalsuccess [17]. Cephalometric analysis correlates with three-dimensional CTanalysis [18]. CT provides good airway and bony resolution, although itdoes not provide delineation of the upper airway soft tissue as well as theMRI [19]. Sagittal MRI allows evaluation of the palate and tongue base tothe posterior pharyngeal wall [20]. MRI provides good soft tissue resolutionand supine evaluation in multiple dimensions; however, weight, claustro-phobia, pacemaker placement, and expense can limit its application.

In response to the limitations of UPPP, Riley et al [21] introduced theStanford Protocol (Fig. 1), which involved inferior sagittal osteotomy of themandible andhyoidmyotomyand suspension.Later,Riley et al [22] publishedresults from a two-phase protocol, which involved UPPP for palatal obstruc-tion and genioglossus advancement with hyoid myotomy or suspension fortongue base obstruction in phase I. Thismethod achieved success asmeasuredby polysomnography in 70% to 80% of patients with mild to moderate OSA,although success was obtained in only 42% of patients with severe OSA.Additionally, surgical treatment improved sleep architecture and increasedlowest oxygen-saturation levels to those achieved by CPAP.

For patients with residual OSA as determined by postoperative sleepstudy who were interested in further treatment, phase II involved maxillary-mandibular advancement osteotomy and achieved a 97% success rate [22].Updates on clinical outcomes from the Stanford group continue to reportsimilar outcomes for phase I [23] and phase II [24].

Recent years have seen a proliferation of procedures aimed at a surgicalcure for OSA. Laser-assisted uvuloplasty has been investigated and provedto be an effective treatment for snoring [25], but there are conflicting data onits efficacy in the treatment of OSA [26]. Preliminary studies on tongue-basesuspension sutures demonstrate a modest effect on objective measures [27]and small improvement in functional outcomes, sleepiness, and snoring [28].Radiofrequency energy has been used to decrease the volume of palataltissue [29], turbinate tissue [30,31], and tongue base [32–34], with mixedresults. Bariatric surgery also has been used to affect the degree of obesityand, secondarily, OSA. This tremendous assortment of treatment modalitiesand methods of reporting outcomes raises two fundamental questions: Whatconstitutes failure or success and why do specific interventions succeed orfail by these measures?

Pathologic features of obstructive sleep apnea

To fully understand treatment approaches to OSA, a thorough un-derstanding of the pathologic features of OSA is necessary. Currentunderstanding suggests that obstruction and cessation of ventilation resultfrom anatomic and neurologic factors working to collapse the airway,

540 K.C. McMains, D.J. Terris / Otolaryngol Clin N Am 36 (2003) 539–561

overriding those working to dilate the airway. This effect is known as the‘‘balance-of-forces’’ model [35]. In OSA, these events include apneas,complete cessation of ventilation, hypopneas, significantly reduced ventila-tion secondary to partial obstruction, or respiratory effort–related arousal,which are defined as inspiratory efforts against increased upper airwayresistance that cause transient arousals but do not reach the thresholdfor either apnea or hypopnea [36]. Formerly, it was believed that hyper-somnolence resulted from hypoxemia or hypercapnea associated with

Fig. 1. Staged surgical protocol. From Likk, Powell NB, Riley RW, Troell R, Guilleminault C.

Overview of phase I surgery for obstructive sleep apnea syndrome. Ear Nose Throat J

1999;78:836–45; with permission.

541K.C. McMains, D.J. Terris / Otolaryngol Clin N Am 36 (2003) 539–561

these events. It is now understood that hypersomnolence results from sleepfragmentation [37].

Respiratory drive and tonic control of airway musculature differ inthe sleep and awake states. A ‘‘wakefulness drive,’’ which responds tononmetabolic inputs, modulates changes during the awake state. Whenthis influence is removed during sleep, respiratory drive relies solely onmetabolic inputs to chemoreceptors that allow a higher pCO2 set point.Transition from wakefulness to sleep results in an immediate decreasein respiratory drive. This decrease is followed sequentially by hypoxemia,a brisk respiratory response, arousal, and a large compensatory breath.Therefore, the transition between states represents a time of considerableimportance for the patient with OSA because of the vulnerability of theupper airway [38,39]. Additionally, rapid-eye-movement–phase sleep con-stitutes a higher percentage of sleep during the last third of the night [40] andis associated with decreased muscle tone. The effect of this change in toniccontrol is increased collapsibility during this phase of sleep.

Anatomically, resistance can occur intranasally or at the level of thepalate (type I), at both the palate and the base of the tongue (type II), or atthe base of the tongue alone (type III) [41]. As compared with controlpatients, there is increased pharyngeal resistance during wakefulness inpatients with OSA [42–45]. As compared with the wakeful state, pharyngealairway resistance triples during sleep [42–48]. With arousal and concomitantreturn of the wakefulness drive, dilator muscle activity increases, airwayresistance decreases, and airflow resumes [42–49].

Several specific anatomic differences exist between control patients andpatients with sleep apnea. Smaller upper airways have been observedin patients with OSA [15,47,50]. The cross-sectional area of the pharynxhas been shown to be inversely proportional to the severity of OSA [15].Pharyngeal anterior-posterior axis length greater than lateral axis lengthpredisposes to airway collapse [51]. In contrast to the pharynx in controlpatients, the pharynx in patients with OSA is collapsible to a greaterdegree [52] and collapses under subatmospheric pressure conditions[53]. Lateral walls are the structures most likely to collapse in all subjectgroups. Thickness of the lateral pharyngeal muscular walls is cited asbeing responsible for collapse [54]. The palate of patients with OSA hassignificantly increased muscle and fat mass as compared with controlpatients [55]. Evidence suggests that there is a relationship between OSAand local pharyngeal fat deposits. Additionally, increased fat load in thecollapsible pharyngeal segment has been demonstrated when compared withcontrol patients [47]. These anatomic and physiologic tendencies lead topoor sleep efficiency and downstream physiologic effects. As a result, muchof the available data suggest that OSA negatively affects several measures ofhealth.

Several authors have shown an association between OSA and cardio-vascular disease. The National Commission on Sleep Disorders Research


estimates that there are 38,000 cardiovascular deaths per year in the UnitedStates secondary to OSA [56]. Obstructive sleep apnea is believed to lead topulmonary and systemic hypertension [57,58]. In individuals with an apnea-hypopnea index (AHI) greater than or equal to 15, increased systolic anddiastolic blood pressure was noted during both sleep and wakefulnesswhen compared with individuals with AHIs less than 15 [59]. Hung et al [60]showed increased cardiovascular mortality in patients with apnea indices(AIs) greater than 5.3. Obstructive sleep apnea has been implicated in corpulmonale, arrhythmia, cerebrovascular accident (CVA), and polycythemiaas well [56].

Obstructive sleep apnea has been implicated as a causal factor in motorvehicle accidents. In one study, an AHI greater than 5 yielded a three-foldincrease in motor vehicle accidents, whereas an AHI greater than 15 yieldeda seven-fold increase [33,61]. It is worth noting that an AHI greater than15 falls within the definition of clinical success used by several authors.Reaction times of motorists with OSA were compared with and found to beworse than those of alcohol-impaired drivers [62].

Obstructive sleep apnea has been linked to increased mortality. In middle-aged patients with sleep-disordered breathing (SDB), decreased survival wasdemonstrated, regardless of disease severity [63]. He et al [64] showed in-creased mortality in patients with AIs greater than 20. Despite similarityin overall mortality in the post-uvulopalatopharyngoplasty (UP3) popula-tion, there is a relative risk of three for hypertension and subsequent deathfrom cardiovascular disease (CVD) in patients with OSA as comparedwith control patients [65].

In a review published in 1997, Wright et al [66] contravened conventionalwisdom by questioning the health effects of OSA. They found contradictoryevidence regarding SDB and cardiovascular disease or CVA. They regardedthe evidence linking OSA to EDS as stronger but still inconclusive. Since thattime, much work has been done to further examine the role of OSA incardiovascular andoverall health,most notably through theFraminghamandSleep Heart Health Study. In the Framingham study, SDB was associatedwith increased right ventricular wall thickness, although neither right atrialdimensions, right ventricular dimensions, or right ventricular systolic functionwas affected [67]. Obstructive sleep apnea is associated with overall increasedhealth care use [68]. Nieto et al [69] demonstrated an association betweenhypertension and SDB, as defined by AHI and percent time with oxygensaturation in arterial blood below 90%.Obstructive sleep apnea was shown tohave mild to moderate effects on ‘‘heterogeneous manifestations of CVD’’with even a slight increase in AHI. A stronger association with congestiveheart failure (CHF) and stroke was shown [70]. In a recent review, Young andPeppard [71] wrote of the data: ‘‘collectively they provide evidence that wecannot dismiss the hypothesis that SDB causes CVD.’’ Other authorsargue that correlations among respiratory disturbance index (RDI) and bodymass index (BMI), hypertension diabetes mellitus (HTN, DM), and lipid


levels cloud any conclusions as to whether increased risk of CVD results fromSDB or concomitant risk factors [72]. Despite mounting evidence, debateabout the true effect of OSA on health continues.

Measures of success and failure

Several mechanisms have been used for diagnosing OSA, assessing itsseverity, and assessing the response to treatment. These mechanisms includepurely subjective patient-reported measures, subjective physician-gradedmeasures, and objective monitoring. A brief review of the major modalitiesfollows.

Epworth sleepiness scale

Principal among the symptoms resulting from OSA is EDS. Using EDSin assessment of disordered sleep presents the difficulties of subjectivereporting. Additionally, EDS is not limited to patients with OSA. It wasfound in 21% in patients with RDIs less than 5 versus 35% of patients withRDIs greater than 30 [73]. The Epworth sleepiness scale (ESS), firstdescribed by Johns, is an instrument used to evaluate severity of symptomsfrom OSA in a semiquantitative way [74]. The ESS is a self-administeredsurvey of a patient’s likelihood of dozing during eight activities. For eachactivity, the patient rates his or her chances of falling asleep while engagedin the activity. Scores range from 0 (never dozing in a situation) to 3 (alwaysdozing).

Quality-of-life scales (general and disease-specific)

In early work, global measures of health were used to assess the effect ofOSA. These measures originally were designed to measure aggregate healthcharacteristics and to provide synoptic information regarding a patient’s ownperception of health. The Medical Outcome Survey Short Form (SF-36)includes eight domains tomeasure health andwell-being [75]. Briones et al [76]showed a correlation among the ESS score and vitality, role-emotional, andgeneral health domains, whereas themultiple sleep latency test correlatedwiththe vitality domain. Another study using the SF-36 showed improvement inenergy and vitality and mental and physical functioning domains, althoughanother measure used in the study failed to identify these effects [77]. Mild tomoderate SDBwas associated with a decreased vitality measure on the SF-36,whereas severe SDB was associated with a global decrease in quality of life(QOL) [78]. Oxygen desaturation negatively affects the QOL measured bySF-36 aswell [79]. All dimensions ofQOLwere diminished significantly on theSF-36 in patients with OSA as compared with control patients. Improvementin QOLwas related more to the degree of perceived disability than to the RDIor arousal index [80].


The Nottingham Health Survey demonstrated significant differences inenergy, pain, sleep, social isolation, and physical mobility in patients withOSA as compared with control patients; however, no difference in EDSbetween these groups was noted. No difference in QOL was identified amongpatients with different levels of severity with OSA [81].

Concern about the ability of nonspecific measures to elucidate subtleQOL changes specific to OSA led to development of disease-specific measuresof QOL. The Calgary Sleep Apnea Quality-of-Life Index demonstratedvalidity in assessment of OSA. It also demonstrated a higher responsive-ness index and effect size than did the SF-36 [82]. The Functional OutcomesSleep Questionnaire was designed to assess the effect of sleep-relatedsymptomatology on five daily activities. It demonstrated validity in evalu-ating functional disability as it relates to sleep disturbance and response totreatment [83].

The Obstructive Sleep Apnea Patient-Oriented Severity Index (Table 1)was designed for use in the OSA Treatment Outcome Pilot Study. It involvesresponses to questions regarding five subscales to which importance andmagnitude of effect are assigned. A symptom impact score is generated fromthe product of the importance and the magnitude. The OSA TreatmentOutcome Pilot Study study demonstrated worse QOL in all domains exceptbodily pain [84]. A revised version, the SNORE-25, excluded seven itemsfrom the first and dispensed with symptom-impact scoring, reporting averagemagnitude score instead. This instrument correlates well with the patient’ssubjective response to treatment [85].

Multiple sleep latency test

The multiple sleep latency test (MSLT) evaluates degree of impairment ofdaytime alertness [86]. This test involves recording the time of sleep initia-tion for multiple naps separated by at least 2 hours during a patient’s nor-mal waking period. This instrument can be used to diagnose upper airwayresistance syndrome (UARS) [87] or as an assessment of treatment effect.In the absence of UARS, the MSLT is used to diagnose narcolepsy. It gener-ally is considered the ‘‘gold standard’’ for evaluating daytime somnolenceand sleep latency. Moderate correlation exists between ‘‘irresistible sleepi-ness,’’ which describes the sensation of being overcome by sleep, andMSLT; however, ‘‘irresistible sleepiness’’ failed to identify pathologic MSLTin patients with SDB [88].

Muller maneuver: palate, base of tongue, and lateral walls

The Muller maneuver originated from attempts to evaluate various levelsof upper airway obstruction. The examiner views the upper airway throughthe nasopharyngoscope at rest and with maximal inspiratory effort againstclosed nose and mouth. The base of tongue, lateral pharyngeal walls, and


palate are examined for collapse. The examiner rates collapsibility of eachstructure from 0 (minimal collapse) to 4+ (complete collapse). Mullermaneuver score was shown to be correlated moderately with preoperativeSDB severity, and its reproducibility was verified between examiners [27].Collapse of the palate was correlated highly with RDI, whereas lateral wall

Table 1

Items on the Obstructive Sleep Apnea Patient-Oriented Severity Index

Sleep problems

1. Trouble falling asleep

2. Waking during sleep

3. Loud/excessive snoring

4. Restlessness during sleep

5. Waking ‘‘too early’’ in morning

6. Waking up feeling tired

7. Bed wetting

Awake problems

8. Fatigue or tiredness

9. Frequent yawning

10. Sleepiness while driving

11. Memory and/or concentration problems

12. Productivity limited at certain times of day

13. Often late for meetings or appointments

14. Participation in community, volunteer, religious, or spiritual activities limited

Medical problems

15. Amount of medical care required for OSA

16. Interaction of OSA with other medical problems

17. Travel by automobile to other regions or parts of country limited because of fear of

medical problem

18. Unable to have sexual relations because of medical problem

19. Financial burden as a result of illness

Emotional and personal problems

20. Dread/fear going to bed

21. Nerves are ‘‘right on surface’’

22. Inability to relax, always anxious

23. Marital strain, stress, and tension

24. ‘‘Foul’’ mood

25. Unable to experience closeness with spouse and/or others

26. Lack of desire for sexual relations

27. Feeling that future is hopeless

Occupational impact

28. Competence questioned

29. Reliability questioned

30. Inability or difficulty getting new job

31. Loss of job

32. Modification in job because of excessive sleepiness

From Piccirillo JF, Gates GA, Schectman KB. Obstructive sleep apnea treatment outcomes

pilot study. Otolaryngol Head Neck Surg 1998;118:833–44; with permission.


collapse was correlated moderately, and base-of-tongue collapse was notcorrelated [89].

P close

P close is the pressure at which the upper airway collapses. This value isa significant discriminating feature between normal subjects and patientswith abnormal collapsibility, as is seen in OSA [90]. In apneics, P close tendstoward higher values than in control subjects. Airway collapse can occur atthe level of the palate or tongue base. Positive P close predicted treatmenteffect in patients with OSA. For patients with positive P close, nocturnaloxygenation was normalized after UPPP in 27%, whereas oxygenationcorrected 73% of OSA in patients with negative P close [13]. Trachealtraction [91], UPPP, and palatal advancement result in a decrease in closingpressure [92].

Cephalometrics

Cephalometric radiographs are obtained and evaluated in a standard-ized manner [93]. Relationships of different structures to one another havebeen assessed for predictive value in diagnosing OSA and evaluating sur-gical outcome. Changes in ANB and SNB angles were correlated withpostoperative changes in AHI [94]. Other studies correlated postoperativeoutcomes with increased posterior airway length, increased hyoid-mandib-ular length, and increased posterior airway space (PAS) [95,96]. Li et al [97]report an increase in pharyngeal length and depth of 48% and 53%, re-spectively, after maxillomandibular advancement and report a high successrate for these procedures. Conflicting data were described by Yao et al [89],who found that cephalometric radiographs reflect anatomic changes post-operatively, but these changes did not correlate with efficacy as measuredby improvements in the AHI.

Polysomnogram

The polysomnogram (PSG) was first described in 1974 by Holland et al[98]. Since that time, PSG has become the ‘‘gold standard’’ in diagnosis andfollow-up of sleep apnea because it provides objective data on sleep and re-spiratory status. Originally, the only events evaluated were apnea; however,analysis has expanded to include hypopneas and respiratory event-relatedarousals (RERAs), as described previously. The diagnosis most frequently ismade on the basis of the sum of these events per hour or RDI. In the level Istudy, information gathered includes pulse oximetry, electrocardiography,nasal or oral airflow, respiratory effort, extremity electromyography, sub-mental electromyography, electro-oculogram, positionally dependent sleepchanges, and electroencephalographic evidence of arousal [99]. Despite


collecting information on oxygen desaturation, arousals, limb movements,sleep architecture, and cardiac events, diagnosis most often is made by RDIalone. With the pressures of medical economics, other less costly studieshave been explored that endeavor to adequately diagnose OSA withoutincurring similar costs. These studies range from fully monitored homestudies to overnight oximetry, although each has limitations in the datacollected. In a nap study, the AHI and oxygen desaturation index detectedcorrelates with the severity of OSA as determined by PSG [100]. Data re-ported from portable PSG correlated with those obtained with a laboratory-based control for AHI and diagnosis, although there was reducedconfidence in respiratory scoring secondary to signal quality [101]. Parraet al [102] showed 89% concordance between AHI measured by a homedevice and traditional PSG. Kapur et al [103] reported that unattendedhome sleep studies were acceptable for the evaluation and diagnosis of OSAin 90.6% of cases.

Why surgical procedures fail

The complex interacting factors causing dysfunction in OSA make itdifficult to guarantee effective treatment in an individual patient. The perfecttreatment for OSA would eliminate sleep disturbance, reverse dangerousphysiologic changes, restore restful sleep, eliminate symptoms, and be welltolerated by patients. The principal failure of CPAP is the patient’s inabil-ity to tolerate treatment. Tracheotomy bypasses airway obstruction at alllevels, yielding objective results comparable to CPAP, but it also is poorlytolerated by many patients owing to inconvenience and social stigma.Paradoxically, UPPP may, in some cases, decrease the maximal pressuretolerated by way of CPAP by creating oral air escape and decreasing theeffectiveness of treatment [104]. The importance of patient selection basedon careful examination affects the likelihood of success. In early work, Sheret al [17] showed that selecting patients with pharyngeal changes isolated tothe region of the tonsillar fossae and soft palate increased the success rate ofUPPP. For patients completing phase II surgical treatment, more than 90%have a successful surgical result as measured by RDI; however, manypatients who do not have successful surgery as defined by PSG do not electto complete phase II surgery, limiting the generalizability of results reportedin OSA surgery [105]. Answers to the questions ‘‘What prevents a successfulresult in earlier stages of surgical treatment?’’ and ‘‘How does one maximizethe likelihood of a given patient achieving a cure for his or her disease?’’ maylie in the variability of OSA.

The association of OSA and obesity cannot be disputed. Major weightgain was associated with surgical failures, although there was no negativeeffect from aging and minor weight gain [106]. Failure after UP3 was relatedto preoperative BMI and postoperative weight gain [107]. Bariatric surgery


has been explored in the treatment of OSA, with variable results. Severalauthors report that bariatric surgery provides significant long-term re-duction in weight and OSA severity [108–110], whereas other reports suggesta considerable relapse rate among treated patients [111]. Aggressive weight-reduction programs represent an important component of comprehensiveOSA treatment.

Significant differences in disease presentation and characteristics are seenbetween male and female patients with OSA. Presenting symptoms for menincluded snoring and stoppage of breathing, whereas women reported head-ache on awakening [112]. In another study of SDB, both genders presentedwith similar symptoms of snoring and EDS. This same study showedthat, despite having significantly smaller oropharyngeal airways, women hadmuch milder disease than men. Additionally, upper airway size correlatedwith severity of disease only formen [113]. A higher death rate is noted amongwomen with AHIs greater than five than in similarly affected men [114]. Ina study of obese patients, Vgontzas et al [115] reported OSA in 40% of menand only 3% of women. The association between BMI and RDI is weaker inwomen than in men. Another study of morbidly obese patients showed that77% of men and only 7% of women had OSA [116]. Taken together, theseobservations suggest important gender differences in sleep disorders. Furtherexploration of the nature of these differences may result in a higherpercentage of surgical successes.

Collapse of the lateral pharyngeal wall contributes significantly to ob-struction. Bettega et al [117] wrote, ‘‘No data are available on the effects ofphase I surgical techniques on dilator muscle activity, contraction efficiency,and upper airway collapsibility.’’ This view is disputed by Schwab et al [93],who reported that skeletal advancement surgery increased tension onconstrictors, thereby decreasing lateral wall collapse. Li et al [24] foundthat maxillomandibular osteotomy improves the tension and collapsibilityof the suprahyoid and velopharyngeal musculature. In a later study, Li et al[118] reported that maxillomandibular osteotomy improves retrodisplace-ment of the tongue and more dramatically improves lateral wall stability.Thut et al [119] showed that elongation of the airway had the greatesteffect on collapsibility. Pharyngeal length increases significantly in patientswith OSA as compared with control patients when changing from theupright to the supine position [120]. A distance of less than 21 mm fromthe mandibular plane to the hyoid was associated significantly withUPPP failure [121]. Exploration of airway-lengthening procedures mayexploit the insight gained through Thut’s research to the benefit of patientswith OSA.

Recognition of the influence exerted by other diseases and syndromesmay contribute to the challenge of effective OSA treatment. ‘‘Dispropor-tionate anatomy’’ among the base of the tongue, narrow mandible, andhypoplastic mandible affect upper airway dynamics [16]. This disproportioncan be seen in syndromic patients and in isolation from other abnormalities.


Allergy also may play a role in the pathogenesis of OSA [122]. Allergicresponse not only increases airway resistance intranasally, it may result inedema of pharyngeal segments and predispose to collapse. Hypoventilationsyndrome can occur concomitantly with OSA and cause continued sleepdisturbance despite treatment of obstruction. Recognizing and addressingthese and other comorbidities may affect surgical outcomes positively.

Best current metrics

Despite using RDI as a standard for diagnosis and treatment effective-ness, there is some suggestion that RDI may not completely describe allaspects of the disease. Piccirillo elucidates the principal limitations in theuse of PSG for diagnosis and evaluation of response in OSA [123]:

1. Assignment of severity based on RDI, not oxygen desaturation index (ODI),sleep fragmentation, or patient symptoms. This criticism is supported byKingshott et al [124], who demonstrated that neither apneas nor hypopneasaccount for more than a small percentage of the variation in objective orsubjective sleepiness. Respiratory disturbance index showed poor correlationwith EDS, neuropsychologic functioning, or rates of motor vehicle accidents[61]. Oxygen desaturations negatively affect QOL measured by SF-36 as well[79]. This finding suggests an influence fromdesaturation independent ofRDI;however, ODI has been shown to be specific for OSA diagnosed by PSG [125],whereas ODI coupled with CT90 (percentage of time saturation levels remainbelow 90%) and oximetry is both sensitive and specific for OSA by PSG [126].Sleep fragmentation results from short-alpha electroencephalogram arousalsduring sleep that correlate with increased work of breathing [127]. AlthoughRDI and minimum oxygen saturation in arterial blood were improved ontherapeutic CPAP, no significant difference in sleep architecture was seenbetween therapeutic CPAP and placebo CPAP [128]. Therefore, patients‘‘effectively’’ treated as assessed by RDI alone may not receive the physicalbenefits of restored sleep architecture.

Patient perception of treatmentmaydiffer dramatically fromobjective dataprovided by PSG. The fact that tracheotomy and CPAP can decrease QOLsecondary to inconvenience, discomfort, and social stigma despite effectivebypass or splinting of obstruction highlights the distinction between PSGdataand patient perception [129]. This disparity has been demonstrated for laserassisted uvulopalatoplasty [26], UPPP [130], and dental appliances [131].Epworth sleepiness scale shows correlation with patient-identified sleepinessbut does not correlate withMSLT [132], AHI, or minimum oxygen saturationin arterial blood [133]. In contrast, other studies have found an associationbetween RDI and QOL measures [134]. Li et al [129] showed correlationamong RDI, minimum oxygen saturation in arterial blood, and visual analogscale reporting of symptoms. Most patients report subjective improvement insymptoms afterUP3, although this subjective improvement does not correlatewith AI or sleep architecture for many patients. One suggestion regarding the


difficulty in obtaining postoperative sleep studies is that symptomaticimprovement decreases a patient’s desire to undergo additional testing[130]. In a study of patientswithmildOSA, no additional benefitwas seenwithCPAP treatment compared with placebo on SF-36 or functional outcomes ofsleep questionnaire, suggesting that the placebo effect may obscure subjectivereporting of findings [135]. Additionally, snorers without OSA havedecrements in QOL to almost the same degree as patients who carry thediagnosis of OSA as measured on the Nottingham Health Profile [136].Response bias has been shown to affect medical outcomes survey data [137].Differing data on PSG data and subjective data are competing and cloudconclusions on the relationship among these measures.

2. There is a lack of correlation between AHI and overall health status [81] orQOL [138]. The conflicting data regarding the relationship to OSA defined byPSG and various measures of health are presented in a previous section(‘‘Pathologic features of obstructive sleep apnea’’). Data addressing therelationship between PSG results and QOL also are presented previously inthis section. Although not uniformly disproved, questions about the strengthof each of these relationships persist.

3. Apneas and hypopneas are not reported in a uniform way. Although effortsto standardize definitions of these occurrences have been made [86],considerable variability in definition, evaluation, and reporting continues tocloud comparisons [139]. Various cutoffs are used in individual studies fordiagnosis, benefit, and cure, which further complicate interpretation of PSGdata. Different methods of recording AHI yield dramatically differentdiagnosis and assignment of severity [140]. For example, thermistors havethe potential to be less sensitive to hypopneas than othermethods of recording[116]. Sher [141] states that intraesophageal manometry is the most effectivemethod of distinguishing apnea from hypopnea. In contrast, Skatvedt et al[142] showed no statistical difference between patients undergoing PSG withand without pressure monitoring in any sleep-quality parameter exceptduration of non–rapid-eye-movement sleep with oxygen saturation below90%. The use of different definitions for respiratory disturbance, criteria fordiagnosis, andmeasures of success is perhaps themost significant limitation inevaluating and comparing outcomes from different treatments.

4. Frequency of apneas and hypopneas may vary from night to night. Becausesleep quality may vary from night to night owing to myriad physical and psy-chosocial influences, a one-night studymay be inaccurate [143]. A corollary tothis contention is that monitoring may cause considerable arousal artifactsecondary to mask placement or perception of other monitoring devices. Thiscriticism has been refuted by some studies that show no significant differencebetween first- and second-night sleep studies [144] and reclassification ofdisease or severity in only a few patients based on subsequent night-sleepstudies [145]. Although data conflict on this point as well, attention to thispossibilitymayguide decisions regarding repeating sleep studies or proceedingwith surgical treatment in cases that fall close to diagnostic cutoffs.


Steps have been taken already to incorporate some of these principles indiagnosis and treatment of OSA. The composite clinical-severity index,described by Piccirillo et al [84], includes ESS, BMI, presence of redundantpharyngeal tissue, RDI, and minimum oxygen saturation in assignment ofdisease severity (Figs. 1 and 2). A second generation of this instrument, theSNORE-25, has been developed, and an initial study has been reported [85].Although exploration of this type of multidimensional analysis is in itsinfancy, this approach represents a significant step toward thoroughassignment by considering both objective and subjective measures.

Future strategies

Future strategies for OSA treatment will involve the evolution ofmethods of assessment and treatment. Although related, these areas aredistinct fields of endeavor. Much progress has been made already in the fieldof assessment. Clear definition of respiratory disturbances will help establishuniform reporting and more reliable, valid comparisons among differentstudies. To date, relative contributions of apneas, hypopneas, and RERAshave not been well defined. Research into the relative contributions ofdifferent types of respiratory disturbance to symptomatology and down-stream health effects may provide insight into the true effect of treatment.Despite its utility as an objective measure, traditional PSG reported in termsof RDI alone has limitations. Recognition of these limitations has alreadymotivated the development of instruments that include multiple perti-nent variables. Additionally, continued exploration of the neural inter-face between sleep and awake states may provide new frontiers in OSAtreatment.

Future advances in treatment will likely parallel those made inassessment. On the nonsurgical front, vigorous educational efforts on thepart of the medical community to raise public awareness of OSA will affecthealth behaviors and social stigmata assigned to various treatment modal-ities. Such educational efforts have been reported to increase compliancewith CPAP treatment [146]. Finding new and unique approaches to preventcollapse while decreasing morbidity will likely drive additional treatmentadvances. Continued work on lateral wall collapse offers one area ofpotential improvement. Procedures designed to lengthen the airway mayprovide a breakthrough in prevention of collapse. Early success has beenreported in electrical stimulation of the genioglossus, resulting in decreasedpharyngeal critical pressure [147]. Work will likely continue on applicationof radiofrequency energy in OSA. Other devices also may demonstrateutility in treatment of OSA. Jokic et al [148] reported decreasing surfacetension and, as a result, AHI by applying a topical lubricant to upper airwaytissues. Further work in these areas will likely add to the armamentarium ofOSA treatment.


Fig.2.Creationofclinical-severitystagingsystem

.PanelsA

throughCdem

onstrate

thesequentialconjunctionandconsolidationofkey

physicalexamination

variables,ESS,andPSG

variablesto

ultim

ately

create

theclinicalseverityindex.(A

)PatternofconsolidationofredundantpharyngealtissueandBMIto

form

composite

physical-severityindex.Categories

ofBMIandredundantpharyngealtissueare

conjoined

tocreate

thethree-category

(alpha,beta,and

gamma)physical-severityindex.(B)PatternofconsolidationofESSandphysical-severityindex

toform

composite

functional-severityindex.Categories

of

physical-severityindex

(alpha,beta,andgamma)are

conjoined

withthreecategories

oftheESS(<

9,9–16,>16)to

create

thefunctional-severityindex.(C

)

Patternofconsolidationofminim

um

O2saturationduringapnea

andRDIto

form

thecomposite

PSG-severityindex.Categories

ofthetw

okey

PSG

variables,

minim

um

O2saturationduringapnea

andRDI,

are

conjoined

tocreate

thethree-category

(1,2,and3)PSG-severityindex.(D

)Patternof

consolidationoffunctional-severityindex

andPSG-severityindex

toform

thecomposite

clinical-severityindex.Thethreecategories

(A,B,andC)ofthe

functional-severityindex

andthethreecategories

(1,2,and3)ofthePSG-severityindex

are

conjoined

tocreate

thethree-category

(I,II,andIII)

composite

clinical-severityindex.(From

PiccirilloJF

.Outcomes

researchandobstructivesleepapnea.Laryngoscope2000;110(3

Pt3):16–20;withpermission.)


The complexity of OSA and its variability of expression withinindividuals make identification of one ‘‘best method’’ of assessment andtreatment difficult. As new techniques for treatment continue to evolve,methods of reporting will continue to evolve to more thoroughly illuminatethe complex relationships at work in OSA.

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2003, Vol.36, Issues 3, Surgery for Sleep Apnea