Diagnosis and Management of Childhood Obstructive - Pediatrics

TECHNICAL REPORT

Diagnosis and Management of Childhood ObstructiveSleep Apnea Syndrome

abstractOBJECTIVE: This technical report describes the procedures involved indeveloping recommendations on the management of childhood ob-structive sleep apnea syndrome (OSAS).

METHODS: The literature from 1999 through 2011 was evaluated.

RESULTS AND CONCLUSIONS: A total of 3166 titles were reviewed, ofwhich 350 provided relevant data. Most articles were level II throughIV. The prevalence of OSAS ranged from 0% to 5.7%, with obesity beingan independent risk factor. OSAS was associated with cardiovascular,growth, and neurobehavioral abnormalities and possibly inflamma-tion. Most diagnostic screening tests had low sensitivity and speci-ficity. Treatment of OSAS resulted in improvements in behavior andattention and likely improvement in cognitive abilities. Primary treat-ment is adenotonsillectomy (AT). Data were insufficient to recom-mend specific surgical techniques; however, children undergoingpartial tonsillectomy should be monitored for possible recurrenceof OSAS. Although OSAS improved postoperatively, the proportionof patients who had residual OSAS ranged from 13% to 29% in low-risk populations to 73% when obese children were included andstricter polysomnographic criteria were used. Nevertheless, OSASmay improve after AT even in obese children, thus supporting surgeryas a reasonable initial treatment. A significant number of obesepatients required intubation or continuous positive airway pressure(CPAP) postoperatively, which reinforces the need for inpatient obser-vation. CPAP was effective in the treatment of OSAS, but adherenceis a major barrier. For this reason, CPAP is not recommendedas first-line therapy for OSAS when AT is an option. Intranasalsteroids may ameliorate mild OSAS, but follow-up is needed. Datawere insufficient to recommend rapid maxillary expansion. Pediatrics2012;130:e714–e755

INTRODUCTION

This technical report describes in detail the procedures involvedin developing the recommendations for the updated clinical prac-tice guideline on childhood obstructive sleep apnea syndrome(OSAS).1

The clinical practice guideline is primarily aimed at pediatricians andother primary care clinicians (family physicians, nurse practitioners,

Carole L. Marcus, MBBCh, Lee J. Brooks, MD, SallyDavidson Ward, MD, Kari A. Draper, MD, David Gozal, MD,Ann C. Halbower, MD, Jacqueline Jones, MD, ChristopherLehmann, MD, Michael S. Schechter, MD, MPH, StephenSheldon, MD, Richard N. Shiffman, MD, MCIS, and KarenSpruyt, PhD

KEY WORDSadenotonsillectomy, continuous positive airway pressure, sleep-disordered breathing, snoring

ABBREVIATIONSAAP—American Academy of PediatricsADHD—attention-deficit/hyperactivity disorderAHI—apnea hypopnea indexAT—adenotonsillectomyBP—blood pressureBPAP—bilevel positive airway pressureCBCL—Child Behavior ChecklistCPAP—continuous positive airway pressureCRP—C-reactive proteinECG—electrocardiographyHOMA—homeostatic model assessmentHS—habitual snoringIL—interleukinOSAS—obstructive sleep apnea syndromePAP—positive airway pressurePSG—polysomnographyPT—partial tonsillectomyQoL—quality of lifeRDI—respiratory distress indexSDB—sleep-disordered breathingSES—socioeconomic statusSpO2—oxygen saturationURI—upper respiratory tract infection

(Continued on last page)

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and physician assistants) who treatchildren. The secondary audience forthe guideline includes sleep medi-cine specialists, pediatric pulmonol-ogists, neurologists, otolaryngologists,and developmental/behavioral pedia-tricians.

The primary focus of the committeewas on OSAS in childhood.2 The com-mittee focused on otherwise healthychildren who had adenotonsillar hy-pertrophy or obesity as underlying riskfactors. Complex populations, includ-ing infants <1 year of age and childrenwho had other medical conditions(eg, craniofacial anomalies, geneticor metabolic syndromes, neuromus-cular disease, laryngomalacia, sicklecell disease), were excluded becausethese patients will typically requiresubspecialty referral.

Two professional studies recently pub-lished related guidelines: the AmericanAcademy of Otolaryngology–Head andNeck Surgery3 and the American Acad-emy of Sleep Medicine.4 These guide-lines have similar recommendations tomany of the recommendations in theAmerican Academy of Pediatrics (AAP)guideline.

The recommendations in this state-ment do not indicate an exclusivecourse of treatment. Variations, takinginto account individual circumstances,may be appropriate.

METHODS

Literature Search

A literature search was performedthat included English-language arti-cles, children and adolescents aged 1through 17.9 years, and publicationbetween 1999 and 2008. Animal studies,abstracts, letters, case reports, andreviews were excluded. The MedicalSubject Heading terms that were usedin all fields were snoring, apnea, sleep-disordered breathing (SDB), sleep-related breathing disorders, upper

airway resistance, polysomnography(PSG), sleep study, adenoidectomy,tonsillectomy, continuous positive air-way pressure (CPAP), obesity, adiposity,hypopnea, hypoventilation, cognition,behavior, and neuropsychology. Searchengines used were PubMed, Scopus,Ovid, PsycINFO, EBSCO (including HealthSource [Nursing], Child Developmentand Adolescent Studies), and CINAHL.Articles covering special populations(eg, infants aged <1 year, those withcraniofacial anomalies or syndromes)were excluded during the title andabstract reviews.

Titles and available abstracts of articlesfound by the literature search werereviewed by the committee members inseveral rounds (see Results). In the firstround, duplicates and erroneous hitsfrom the literature search were ex-cluded. In the second round, titles werereviewed for relevancy by 2 committeemembers. Articles with relevant titleswere then reviewed by 2 reviewerseach, on the basis of the abstract. Be-cause of the large number of remainingarticles, text-mining (Statistica, StatSoftversion 9; StatSoft, Inc, Tulsa, OK) wasperformed on the method section of thearticles to reduce the large amount ofarticles for the final step of qualityassessment. Text-mining is the com-bined, automated process of analyz-ing unstructured, natural languagetext to discover information andknowledge that are typically difficult toretrieve.5

Unfortunately, text-mining revealed thatfew articles reported research methods,such as the study design (eg, clinicalcase series, retrospective, observational,clinical experiment), blinding of the as-sessment, and recruitment and/orscoring, that could have been appliedfor further selection. A manual screen-ing of the questionable articles aftertext-mining resulted in a pool of 605articles. The committee decided on a fi-nal round of title selection; that is, each

member was assigned a random batchof articles and selected titles based onrelevance with respect to the guidelinecategories. These remaining articleswere each reviewed and graded bya committee member, as detailed here.Because of the large volume of articlesrequiring detailed evaluation, somecommittee members recruited traineesand colleagues to assist them in theperformance of these reviews, undertheir supervision. Jason Caboot, JuneChan, Mary Currie, Fiona Healy, MaureenJosephson, Sofia Konstantinopoulou,H. Madan Kumar, Roberta Leu, DariusLoghmanee, Rajeev Bhatia, ArgyriPetrocheilou, Harsha Vardhan, and Col-leen Walsh participated. A literaturesearch of more recent articles (2008–2011) was performed by individualcommittee members, per guidelinecategory, and discussed during thecommittee meeting.

As would be expected from any panelof experts in a field, some of thecitations were the work of the panelmembers. For this reason, a variedpanel, including general pediatricians,pulmonologists, otolaryngologists, andsleep medicine physicians, was ar-ranged to provide balance. For initialguideline drafts, committee memberswere assigned sections of the reportthat were not directly in their area ofresearch, and the evidence, searchresults, and conclusions thereof werediscussed by all committee members ata face-to-face meeting. Subsequentdrafts of the guidelines and technicalreport were reviewed by all commit-tee members.

Quality Assessment

The previous literature review form6

was modified to include the evidencegrading system developed by theAmerican Academy of Neurology forthe assessment of clinical utility ofdiagnostic tests (Table 1).7 A specificcustomized software (OSA Taskforce;

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copyright Francesco Rundo and KarenSpruyt) was developed for the litera-ture review form to standardize thispart of the process. Of note, thequality assessment levels were com-parable to the grading levels appliedpreviously.8,9 The quality assessmentapplied involved 4 tiers of evidence,with level I studies being judged tohave a low risk of bias and level IVstudies judged to have a very highlevel of bias. A weaker level of evi-dence indicates the need to integrategreater clinical judgment when apply-ing results to clinical decision-making.The committee’s quality assessment ofdata took into account not only thelevels of evidence in relevant articlesbut also the number of articles iden-tified, the magnitude and direction ofvarious findings, and whether articlesdemonstrated convergent or divergentconclusions.

The evidence-based approach to guide-line development requires that theevidence in support of each key actionstatement be identified, appraised,and summarized and that an explicitlink between evidence and recommen-dations be defined. Evidence-basedrecommendations reflect the qualityof evidence and the balance of benefit

and harm that is anticipated when therecommendation is followed. The AAPpolicy statement “Classifying Recom-mendations for Clinical Practice Guide-lines”10 was followed in designatinglevels of recommendations (Fig 1,Table 2).

RESULTS OF LITERATURE SEARCH

The automated Medical Subject Head-ing search resulted in 3166 hits. Afterduplicates and erroneous hits wereexcluded, 2395 hits fulfilled the criteria.After title review, 1091 articles wereaccepted, with a 0.70 interrater agree-ment between the 2 reviewers. Theseremaining articles were reviewed onthe basis of the abstract, which resultedin 757 articles remaining, with a 0.60agreement rate between reviewers. Afinal decision on those without agree-ment was made by the chairperson ofthe committee. Text-mining, althoughnot helpful in reducing the number ofarticles for further evaluation, illus-trated the spectrum of topics coveredby the articles (Table 3). A manualscreening of the questionable articlesafter text-mining resulted in a pool of605 articles. The final round of titleselection resulted in 397 articles for

detailed review. An additional 47 arti-cles were found to not meet criteriaduring the detailed review. Thus, a totalof 350 articles were included.

On the basis of the final 350 articles,one-third were epidemiologic studies,26% were diagnostic studies, and23% were treatment studies. Table 4lists the type of study design; 34% ofstudies were descriptive and 32% werenonrandomized concurrent cohort se-ries. PSG was the diagnostic methodused for 57% of the articles, whereas45% used questionnaires. The samplesize varied from 9 to 6742 subjects.Figure 2 shows the level of evidenceof the articles; 76% of studies werelevel III or IV. The majority of studiesdid not include a control group,which degraded the studies to levelIII or IV. Few studies applied any formof blinding.

Conclusion

There has been a large increase in thenumber of published studies since theinitial guideline was published. However,there are few randomized, blinded,controlled studies. Most articles evalu-ated were level III or IV, andmany studieswere hampered by the lack of a controlgroup. In most studies, blinding was notpresent or not reported. From a meth-odologic standpoint, a clear need forrandomized clinical trials with blindingis evident.

TERMINOLOGY

OSAS in children is defined as a “disor-der of breathing during sleep char-acterized by prolonged partial upperairway obstruction and/or intermittentcomplete obstruction (obstructive ap-nea) that disrupts normal ventilationduring sleep and normal sleep pat-terns,”2 accompanied by symptoms orsigns as listed in Table 2 of the ac-companying guideline. In this document,the term SDB is used to encompass

TABLE 1 Evidence Grading System7

Level Description

I Evidence provided by a prospective study in a broad spectrum of persons who have thesuspected condition, by using a reference (gold) standard for case definition, in which thetest is applied in a blinded fashion, and enabling the assessment of appropriate test ofdiagnostic accuracy. All persons undergoing the diagnostic test have the presence orabsence of the disease determined. Level I studies are judged to have a low risk of bias.

II Evidence provided by a prospective study of a narrow spectrum of persons who have thesuspected condition, or a well-designed retrospective study of a broad spectrum ofpersons who have an established condition (by gold standard) compared with a broadspectrum of controls, in which the test is applied in a blinded evaluation, and enabling theassessment of appropriate tests of diagnostic accuracy. Level II studies are judged to havea moderate risk of bias.

III Evidence provided by a retrospective study in which either persons who have the establishedcondition or controls are of a narrow spectrum, and in which the reference standard, ifnot objective, is applied by someone other than the person who performed (interpreted)the test. Level III studies are judged to have a moderate to high risk of bias.

IV Any study design where the test is not applied in an independent evaluation or evidence isprovided by expert opinion alone or in descriptive case series without controls. There isno blinding or there may be inadequate blinding. The spectrum of persons tested may bebroad or narrow. Level IV studies are judged to have a very high risk of bias.


both snoring and OSAS when stud-ies did not distinguish between theseentities.

PREVALENCE OF OSAS

The original clinical practice guidelinefound a prevalence of OSAS of 2% (3studies) and a prevalence of habitualsnoring (HS) of 3% to 12% (7 studies).Since publication of the originalguideline, 10 studies (in 12 separatearticles) used the gold standard ofconventional overnight laboratory PSGto diagnose OSAS (Table 5). These

studies were all levels I through IV,depending on the size and character-istics of the sample population, andrepresented many countries and agegroups. They used various criteria, notall of which are standard, to diagnoseOSAS. Many of the studies had a smallsample size and/or studied only a se-lected high-risk sample of the pop-ulation. Despite these limitations, the10 studies found a prevalence of OSASin the general pediatric population of0% to 5.7%. Three studies to notewere those of Bixler et al11 from theUnited States, Li et al12 from China,

and O’Brien et al13 from the UnitedStates. These 3 studies (levels I–II) hadlarge sample sizes from the generalpediatric population and reported OSASprevalence rates of 1.2% to 5.7%. Sixstudies investigated the prevalenceof OSAS by using various ambulatorystudies rather than full, laboratory-based PSG (Table 6). Although thesample sizes were generally larger,home studies are not consideredthe gold standard of diagnosis andwere thus level III. These studiesfound an OSAS prevalence of 0.8% to24%. The 2 outliers (at 12% and24%)14,15 used more liberal criteriato diagnose OSAS. Excluding thosestudies, the OSAS prevalence was0.8% to 2.8%.

Several studies attempted to discernvariables associated with the presenceof OSAS. Three studies found an equalprevalence between males and fe-males,16–18 and 2 studies found anincreased prevalence in males.12,15

Two studies reported an increased riskin children of ethnic minorities,11,19

supporting older data.20 Four stud-ies found an increased risk in obesepatients,12,17,21,22 but 3 studies did

FIGURE 1Evidence quality. Integrating evidence quality appraisal with an assessment of the anticipated balancebetween benefits and harms if a policy is carried out leads to designation of a policy as a strongrecommendation, recommendation, option, or no recommendation. RCT, randomized controlled trial.

TABLE 2 Definitions and Recommendation Implications

Statement Definition Implication

Strong recommendation A strong recommendation in favor of a particular action is madewhen the anticipated benefits of the recommendedintervention clearly exceed the harms (as a strongrecommendation against an action is made when theanticipated harms clearly exceed the benefits) and the qualityof the supporting evidence is excellent. In some clearlyidentified circumstances, strong recommendations may bemade when high-quality evidence is impossible to obtain andthe anticipated benefits strongly outweigh the harms.

Clinicians should follow a strong recommendation unlessa clear and compelling rationale for an alternative approachis present.

Recommendation A recommendation in favor of a particular action is made whenthe anticipated benefits exceed the harms but the quality ofevidence is not as strong. Again, in some clearly identifiedcircumstances, recommendations may be made when high-quality evidence is impossible to obtain but the anticipatedbenefits outweigh the harms.

Clinicians would be prudent to follow a recommendation butshould remain alert to new information and sensitive topatient preferences.

Option Options define courses that may be taken when either thequality of evidence is suspect or carefully performed studieshave shown little clear advantage to 1 approach over another.

Clinicians should consider the option in their decision-making,and patient preference may have a substantial role.

No recommendation No recommendation indicates that there is a lack of pertinentpublished evidence and that the anticipated balance ofbenefits and harms is presently unclear.

Clinicians should be alert to new published evidence thatclarifies the balance of benefit versus harm.




not.15,16,23 Another study reported anincreased risk of OSAS with increasedwaist circumference, a marker forobesity.11 One study found an increasedrisk with nasal abnormalities,11 1 studyfound an increased risk with pre-maturity,19 and 2 studies found in-creased risk with adenotonsillarhypertrophy.12,22

Multiple studies (levels II–IV) in-vestigated the prevalence of HS, whichis one of the most prominent mani-festations of OSAS (Table 7). Thepresence of snoring was based onparental or personal questionnaires.Not all of the questionnaires usedhave been validated, and the data re-lied on subjective responses ratherthan objective clinical evaluations.The reported prevalence of HS var-ied widely, depending on the studyand definition used, from 1.5% to27.6%.

In summary, studies of OSAS and HSshow varied prevalence rates, de-pending on the population studied, themethods used to measure breathingduring sleep, and the definitions usedfor diagnosis. Nevertheless, the pre-ponderance of evidence suggestsa prevalence of OSAS in the range of1% to 5%, making this a relativelycommon disease that would be en-countered by most clinicians in pri-mary practice.

Areas for Future Research

� Population-based studies on thegender and race distribution ofOSAS among different age groups.

SEQUELAE OF OSAS

Neuropsychological and CognitiveProblems Associated With OSAS

Of the 350 articles related to thissearch over the last 10 years, 61articles directly explored the re-lationship between SDB and cognitiveor neuropsychological deficits. In total,29 658 subjects were studied, in-cluding 2 level I studies24,25 with a to-tal of 174 subjects and 5 level IIstudies.26–30 The diagnosis of SDB wasbased on clinical symptoms in 29articles and on PSG in 32 articles.

Cognitive Deficits

All but 1 study (level IV)31 demon-strated deficits in cognition orneuropsychological function in asso-ciation with symptoms, signs, or di-agnosis of SDB. The 1 exceptionexamined children who had mild OSASover a wide age range and did notinclude behavioral assessments. Inthis study, the mean IQ in the OSASpopulation was significantly above thestandard mean. Some32–34 but not allstudies showed a correlation betweenthe severity of obstructive apnea asmeasured on PSG and increasingneuropsychological morbidity. Thereare several reasons why correlationswere not found for all studies. Stan-dard PSG was developed to detectcardiorespiratory variations and maynot be an adequate tool for detectionof sleep changes that affect neuro-psychological function. Another possi-bility is that any degree of SDB isassociated with abnormal neuro-psychological outcomes and might beaffected variably by social, medical,environmental, or socioeconomic fac-tors not measured by using PSG. This

TABLE 3 Results of Text-Mining of theMethods Section of 757 Papers

Term Used for Text-Mining

Percentageof Papers

Snore/snoring 58.3Polysomnography 53.6Diagnosis 53.4Medical management 51.6Survey/questionnaire 38.8Psychological 37.0Surgery/surgical 35.9Treatment 32.1Design 27.8Obese/obesity 25.0BMI 24.6Randomize 20.2Blinding 16.4Sampling 11.7Control group 8.8Actigraphy 2.6Mortality 0.5

TABLE 4 Types of Studies in the LiteratureBased on 350 Articles

Type of Study Percentage

Descriptive study 33.7Nonrandomized concurrent cohortseries

32.0

Descriptive study + other 10.8Nonrandomized historical cohort series 7.8Randomized clinical trial 4.6Retrospective 3.6Case-control study 1.3Prospective consecutive cohort series 1.3Cross-sectional population-basedsurvey

1.0

Nonrandomized historical cohortseries + other

1.0

Randomized + other 1.0Undetermined 1.0Nonrandomized concurrent cohortseries + other

0.7

Experimental study 0.3

FIGURE 2Levels of evidence of articles used for this report.


possibility is confirmed by a recentlevel I study showing that obesity,OSAS, and neurocognitive outcomesare all interdependent.35 Furthermore,most studies were not controlled forsocioeconomic status (SES), which isimportant because SES stronglyaffects the results of neurocognitivetesting and because OSAS is associ-ated with low SES.36 Although somestudies have shown abnormalities insnorers compared with nonsnoringcontrols, in many of these studies,data in snorers still fell within thenormal range.24 In addition, cutoffs forOSAS used in some studies resulted ina blurring of boundaries between theOSAS and snoring groups. For exam-ple, Chervin et al used an obstructiveapnea index cutoff of only ≥0.5/hourto define OSAS, and the mean apneaindex for the OSAS group was 2.9events/hour, indicating that the studygroup had mild OSAS, which was notthat different from the snorers.37,38 Astudy with a wider spectrum of se-verity may have attained differentresults. Finally, most studies have notcontrolled for obesity, which has beenassociated with neurobehavioral andcognitive abnormalities.

Although most studies simply com-pared groups, others have looked atthe correlation between polysomno-graphic indices and neurocognitive/behavioral outcomes and have showna correlation between different poly-somnographic factors and cognitiveoutcomes, behavioral outcomes, andsleepiness.32–34,39

Cognitive deficits associated withpediatric SDB include general intelli-gence level as well as processes mea-sured by using IQ subtests (Table 8).Specific functions objectively measuredby using neuropsychological assess-ments and included in the researchstudies include:

� Learning, memory, and visuospa-tial skillsTA

BLE5

Prevalence

ofOSAS

ontheBasisof

Laboratory

PSG

Source

Year

No.

No.U

ndergoingPSG

Country

Age,y

OSASPrevalence

HSPrevalence

OSAS

Criteria/Comments

Anuntasereeet

al201

2001

1005

8Thailand

6–13

0.69%

8.5%

AHI≥

1Anuntasereeet

al202

2005

755

Unclear,possibly10

1.3%

6.9%

Note:2

studiesused

samecohort

“mostnights”

Beebeet

al21

2007

60obese

All

UnitedStates

10–16.9

0%norm

alAHI>

522

control

13%

obese

↑in

obese

Bixler

etal11

2009

5740

700

UnitedStates

5–12

1.2%

AHI≥

5↑in

↑waist

circum

ference

↑with

nasalabnorm

alities

↑in

minority

race

Brunettiet

al203

2001

895

34homemonitoring

Italy

3–11

1%–1.8%

4.9%

AHI>

3Brunettiet

al23

2010

12PSG

5.4%

Not↑in

obese;Note:2

studiesused

samecohort

“always”

Liet

al172

2010

6447

619

China

5–13

4.8%

7.2%

UsingICSD-IIcriteria4.8%

Liet

al12

2010

“frequently”

↑in

boys

↑in

obese

↑in

↑tonsilsize

Nget

al204

2002

200

16Hong

Kong

6.4±

41%

14.5%

AHI>

1O’Brienet

al13

2003

5728

110

UnitedStates

5–7

5.7%

11.7%

AHI>

5“frequentandloud”

Sogutet

al16

2005

1198

total

28Turkey

3–11

0.9%

–1.3%

3.3%

Used

AHI>3

>3tim

es/week

Boys

=girls

Not↑in

obese

Winget

al17

2003

46obese,

44control

All

China

7–15

2.3%

–4.5%

control;

26%

to32.6%

obese

OAI≥

1or

RDI≥

5Boys

=girls

↑in

obese

Xuet

al22

2008

99obese,

99control

All

China

Elem

entary

school

0ifnotobeseand

noATH

AHI>

5or

OAI>1

↑obese

↑in

ATH

ATH,

adenotonsillarhypertrophy;ICSD,InternationalClassificationof

SleepDisorders;OAI,obstructiveapneaindex.




� Language, verbal fluency, and pho-nological skills

� Concept formation, analytic think-ing, and verbal and nonverbalcomprehension

� School performance and mathe-matical abilities

� Executive functions

Executive functions were measured byusing both objective testing and parent

questionnaires. Executive functions area network of skills and higher orderfunctions that control and regulateother cognitive processes. These skillsrequire mental flexibility, impulse control,

TABLE 6 Prevalence of OSAS on the Basis of Ambulatory Monitoring

Source Year No. No. UndergoingAmbulatoryMonitoring

Country Age, y OSASPrevalence, %

HS Prevalence OSAS Criteria and Comments

Castronovo et al14 2003 595 265 Italy 3–6 12 34.5% OAI ≥5“Often”or “Always”

Goodwin et al15 2005 480 All United States 6–11 24 10.5% RDI ≥1“Frequently” ↑ in male

Not ↑ in obeseHultcrantz and LöfstrandTideström205

2009 393 26 Sweden 12 0.8 6.9% AHI ≥1 and/“Regularly” or OAI ≥1

Rosen et al19 2003 850 All United States 8–11 2.2 AHI ≥5 or OAI ≥1↑ in AA↑ in premature infants

Sánchez-Armengol et al18 2001 101 All Spain 12–16 1.9 14.8% Based on RDI ≥10 and snoring,witnessed apneas, and/orexcessive daytime sleepiness.

“Often” Girls = boysUrschitz et al206 2010 1144 183 Germany 7.3–12.4 2.8 AHI ≥1OAI, obstructive apnea index; AA, African American.

TABLE 7 Prevalence of HS

Source Year No. Country Age, y HS Prevalence, % HS Criteria

Akcay et al207 2006 1784 Turkey 4–17 4.1 “Often”Alexopoulos et al208 2006 1821 Greece 5–14 7.4 >3 times/wkArchbold et al209 2002 1038 United States 2–13.9 17.1 ”More than half of the time”Bidad et al167 2006 2900 Iran 11–17 7.9 ≥3 times/wkChng et al210 2004 11 114 Singapore 4–7 6.0 >3 times/wkCorbo et al166 2001 2209 Italy 10–15 5.6 “Often”Ersu et al211 2004 2147 Turkey 5–13 7.0 “Often”Goodwin et al212 2003 1494 United States 4–11 10.5 “Snoring frequently or almost always”Gottlieb et al213 2003 3019 United States 5 12 ≥3 times/weekJohnson and Roth45 2006 1014 United States 13–16 6 “Every or nearly every night”Kuehni et al214 2008 6811 United Kingdom 1–4 7.9 “Almost always”Liu et al215 2005 517 in China China Grade school 1.5 (China) Snoring loudly 5–7 times/wk

494 in USA United States 9.9 (United States)Liu et al215 2005 5979 China 2–12 5.6 “Frequent”Löfstrand-Tideströmand Hultcrantz216

2007 509 Sweden 4–6 5.3–6.9 “Snoring every night”

Lu et al217 2003 974 Australia 2–5 10.5 ≥4 times/weekMontgomery–Downs et al44 2003 1010 United States Preschool HS and risk

of SDB, 22≥3 times/week

Nelson and Kulnis218 2001 405 United States 6–17 17 “Often”Ng et al219 2005 3047 China 6–12 10.9 6–7 times/wkPerez-Chada et al220 2007 2210 Argentina 9–17 9 “Frequent”Petry et al221 2008 998 Brazil 9–14 27.6 “Frequently” or “always”Sahin et al222 2009 1164 Turkey 7–13 3.5 “Frequently” or “almost every day”Sogut et al16 2005 1030 Turkey 12–17 4.0 “Often” or “always”Tafur et al223 2009 806 Ecuador 6–12 15.1 “Often” or “always”Urschitz et al164 2004 1144 Germany Primary school 9.6 “Always” or “frequently”Zhang et al224 2004 996 Australia 4–12 15.2 >4 times/wk


TABLE 8 Cognitive Deficits Associated With Pediatric SDB

Type of Deficit Source Level No. Findings/Comments

Cognition, general intelligence Beebe et al225 IV 895 Deficits of general intelligence, sensorimotor integration by objectivemeasurement; behavioral abnormalities included as wellBlunden et al226

Kaemingk et al33

Kennedy et al34

Kurnatowski et al227

Carvalho et al228 III 1332 Objective measures of general intelligence, verbal skills affected by SDBMontgomery-Downs et al50

Suratt et al43

Friedman et al26 II 473 General intelligence, executive function, language all affected by SDB andmeasured objectivelyHalbower et al28

O’Brien et al29

Kohler et al30

O’Brien et al24 I 174 General conceptual ability, verbal and nonverbal reasoning, vocabularyaffected by SDB (and time in bed25)Suratt et al25

Poor school performance Chervin et al42 IV 11 110 Academic achievement measured either by parent or school gradesJohnson and Roth45 Additive factors were SES and ethnicity42,45 or BMI,42,45,47 which

contributed to findings of poor school performance in SDBKaemingk et al33

Ng et al219

Perez-Chada et al220

Shin et al47

Urschitz et al229

Montgomery-Downs et al44 III 1010 Snoring associates with ethnicity, school performance in SES-challengedpreschool-aged children

Executive function Beebe et al225 IV 179 Mental flexibility, impulse controlLeBourgeois et al230 Objective testing performedKarpinski et al231

Halbower et al28 II 123 Response preparation, working memory, fluid and quantitativereasoning; objective testing performed by blinded testerKohler et al30

Learning, information processing,memory, visuospatial skills

Goodwin et al212 IV 1838 Objective testing performed in all but Goodwin et al212 (questionnaire)Hamasaki Uema et al232

Kaemingk et al33

Kennedy et al34

Kurnatowski et al227

O’Brien et al233

Spruyt et al234

Giordani et al38

Halbower et al28 II 112 Race28 and BMI may play an additive role in inflammation46 and cognitivedysfunction in SDBTauman et al46

O’Brien et al24 I 118 Primary snoring without gas exchange abnormalities associates withsignificantly lower learning and memory

Language/verbal skills Kurnatowski et al227 IV 3304 Deficits of language or verbal skills in SDBO’Brien et al233 Objective testing performed in all studiesPerez-Chada et al220

Honaker et al235

Lundeborg et al51

Suratt et al43 III 114 Race and time in bed may contribute to abnormal language associatedwith SDBMontgomery-Downs et al50

O’Brien et al24 I 118 Primary snoring without gas exchange abnormalities associatedwith significantly lower verbal skills; deficits of language orverbal skills in SDB

Suratt et al25

Attention Beebe et al225 IV 6411 Objective testing performed for attention except in refs 32,33,213,229,and 236 in which parent or teacher questionnaires were usedChervin et al236

Galland et al237

Gottlieb et al213

Hamasaki Uema et al232

Kaemingk et al33

Li et al238

Mulvaney et al32

Urschitz et al229

Chervin et al37 I 105O’Brien et al24 I 118 Visual and auditory attention




and workingmemory. Executive functionsare required for optimal school perfor-mance and are acquired through ado-lescence in developing children.

Behavioral Abnormalities

The investigations on the cognitiveeffects of SDB in the 61 studies oftenincluded measures of neurobehavioraloutcomes (Table 9). Hyperactivity wasthe most commonly studied and/orreported behavioral abnormality as-sociated with SDB. It was reported asa frequent symptom of SDB in youngerchildren, and in fact, in 1 study, snoringwas found to be strongly predictive ofa future diagnosis of hyperactivityover the long-term (level IV).40 Attention-deficit/hyperactivity disorder (ADHD)or ADHD symptoms, hypersomnolence,somatization, depression, atypicality,aggression, and abnormal socialbehaviors were the other most fre-quently reported behavioral abnormal-ities associated with SDB in children.Most behavioral difficulties were de-fined by using parent or teacher ques-tionnaires in unblinded level IV studies.

Sleepiness

Two studies (levels I–II) have shown arelationship between polysomnographicmeasures and objective measurementof daytime sleepiness on multiple sleeplatency testing.27,39

Exacerbation of NeuropsychologicalDeficits by Other FactorsUnderlying Childhood SDB

Abnormal behavioral alterations as-sociated with SDB might be modifiedor directly caused by other sleepdisorders, such as coexistent periodiclimb movement disorder.41 In childrenwith SDB displaying deficits of cogni-tion, school performance, or behav-ioral functioning, there may beadditive roles played by race,28,42–44

decreased time in bed,25,43 and lowSES,28,42,44,45 at least in part because of

the association between obesity andlow SES.42 Markers of inflammationand increased cardiovascular riskmay point to 1 mechanism related todecreased cognitive function associ-ated with OSAS,46 seen also in childrenwho are obese. BMI correlated withabnormal cognitive function in pedi-atric SDB,42,45,47 although OSAS wasfound to be an independent risk factorfor cognitive deficits. Finally, in 2studies examining brain function,neuronal injury of the brain28 and al-tered cerebral blood flow48 werefound in children who had SDB com-pared with normal controls and wereassociated with behavior and cogni-tive problems. These findings indicatethe possibility of preexisting medicalproblems causing the development ofOSAS or, alternatively, OSAS causingbrain injury. Therefore, studies show-ing improved cognition and behaviorafter treatment of SDB are 1 key in thedetermination of causality (see thefollowing discussion).

Neuropsychological and CognitiveDeficits in Children Who Have SDBImprove After Treatment

In the previous guideline, there werefew before-and-after treatment studiesof pediatric SDB focusing on objec-tively measured cognitive problems. Inthe last 10 years, 19 studies have ex-amined changes in behavior and/orcognition after surgical treatment ofOSAS. The majority of investigationsdemonstrated agreement about post-treatment improvement of behavior,quality of life (QoL), hyperactivity,ADHD, and impulsivity (Table 10). Theexception was 1 study of exercisetreatment (level IV),49 in which snor-ing improved in obese children butbehavior and sleepiness did not. Moststudies used subjective questionnairereports. Excessive daytime sleepinessimproved in 1 study that measuredthis factor, as did depression, sleepquality, and aggressive behavior. Since

publication of the last guideline, 3additional studies have demonstratedimproved cognitive function (by usingobjective measurement) after treat-ment of OSAS, including measures ofgeneral intelligence, attention, mem-ory, and analytic thinking, includinglevel II,26 level III,50 and level IV37

studies (Table 10). Of concern, how-ever, is that some recent articlessuggest that certain deficits of cogni-tion measured by using objectivetesting may not improve to a largeextent after treatment of childhoodOSAS. Language, IQ, and executivefunction did not improve significantlyin a well-designed, controlled study of92 children (level II).30 General in-telligence in at-risk populations im-proved in 1 study (level III),50 butphonologic processes and verbal flu-ency did not improve to normal (levelIII50 and level IV51). QoL increases aftertreatment.37,52–58 Three studies dem-onstrated long-term (≥1 year) behav-ioral or QoL improvements.37,52,53 Themajority of these studies suggest thatin developing children who are de-pendent on executive function, cogni-tion, and behavioral skills for dailyfunction and school performance,treatment of childhood SDB hasbenefits.

Conclusion

In summary, these studies suggestthat, in developing children, early di-agnosis and treatment of pediatricOSAS may improve a child’s long-termcognitive and social potential andschool performance. These findingsimply that the earlier a child is trea-ted for OSAS, the higher the trajec-tory for academic and, therefore,economic success, but research isneeded to support that implication.There is demonstrated benefit interms of behavior, attention, and so-cial interactions, as well as likely im-provement in cognitive abilities with


the treatment of pediatric OSAS.However, more long-term studies areneeded. The risks of treatment dependon the type of treatment but includerisk of surgery, risk of medication,nonadherence to therapy, and cost.

The risks of not treating children whohave OSAS include potentially affectingthe child’s trajectory of developmentalgains dependent on intelligence, exec-utive function, and proper social inter-actions, ultimately lowering lifetime

academic and social achievements.Therefore, the benefit of treatingchildhood OSAS outweighs the riskwhere treatment is feasible.


� Further research is required to de-termine which domains of cogni-tive function will improve withtreatment of OSAS. Reversibility ofcognitive deficits associated withOSAS must be adjusted for the con-founding effects of age, length ofsymptoms, SES, BMI, sleep dura-tion, environment, and race andethnicity.

Cardiovascular Effects of OSAS

A total of 24 studies related to car-diovascular effects of OSAS in child-hood were identified since the lastreview. The levels of evidence were IIIand IV.

In a retrospective, level IV study of 271clinical cases, only 1 child, who hadcongenital heart disease, had signs ofcardiac failure preoperatively, andother cases had no evidence of left orright ventricular hypertrophy.59 How-ever, studies using more sophisti-cated, prospective techniques havefound subclinical evidence of cardiacdysfunction. These studies are de-scribed in Table 11. Although post-operative adenotonsillectomy (AT)cardiac complications are rare (levelIV),59 left and right ventricular hyper-trophy is significantly associated withpostoperative respiratory complica-tions (level III),60 supporting the rec-ommendation in the current and theprevious guidelines that children whohave cardiac abnormalities be moni-tored as inpatients postoperatively.

Blood pressure (BP) has also beenshown to be affected by OSAS in chil-dren. There were 9 recent level III orIV studies, most of which showeda correlation between the presence/

TABLE 9 Behavioral Abnormalities Associated With Pediatric SDB

Type of Deficit Source Level No. Test Conditions

Hyperactivity and/or ADHD Chervin et al236 IV 8101 Hyperactivity generallymeasured by using parentquestionnaire

Chervin et al40

Galland et al237

Golan et al239

Gottlieb et al213

Johnson and Roth45

LeBourgeois et al230

Mitchell and Kelly240

Owens et al189

Roemmich et al191

Urschitz et al229

Montgomery-Downset al44

III 1010 Survey data

Chervin et al37 I 105 ADHD assessed by usingpsychiatric interview andvalidated instrument

Somatization, depression Galland et al237 IV 205Mitchell and Kelly240


Rudnick and Mitchell242

Suratt et al43 III 114O’Brien et al24 I 118

Behavior problems, general Goldstein et al55 IV 1946 Behavior generally measuredby using parent questionnaireGoldstein et al243

Hogan et al48

Li et al238


Mulvaney et al32

Owens et al189

Roemmich et al191

Rosen et al244

Rudnick and Mitchell242

Tran et al58

Wei et al245

Aggression, oppositionaland social problems

Chervin et al246 IV 4407Gottlieb et al213

Galland et al237


Mulvaney et al32

O’Brien et al24 I 118Excessive daytime sleepiness Goodwin et al212 IV 9729 Sleepiness measured

by using questionnairePerez-Chada et al220

Shin et al47

Urschitz et al229

Johnson and Roth45

Gozal et al27 II 92 Sleepiness measuredobjectively by multiple sleeplatency testing on PSG

Chervin et al37 I 105 Sleepiness measured objectivelyby multiple sleep latency testingon PSG

Anxiety O’Brien et al24 I 118




severity of OSAS and indices of ele-vated BP (Table 12).

In a study by Kaditis et al,61 overnightchanges in brain natriuretic peptidelevels were large in children who hadan apnea hypopnea index (AHI) ≥5/hour when compared with thosewith milder OSAS and with controls(level III). This finding suggests thepresence of nocturnal cardiac strainin children who have moderate tosevere OSAS.

Two studies evaluated brain oxygena-tion and cerebral artery blood flow.Khadra et al62 reported that malegender, arousal index, and amount ofnon–rapid eye movement sleep wereassociated with diminished cerebraloxygenation, whereas increasing meanarterial pressure, age, oxygen satu-ration (SpO2), and amount of rapideye movement sleep were associatedwith augmented cerebral oxygena-tion (level III). Hogan et al48 found

a decrease in middle cerebral arteryvelocity postoperatively in patientstreated for OSAS, whereas controlsubjects showed a slight increaseover time (level IV).

Three studies evaluated autonomicvariability in children who have OSAS.Constantin et al63 reported resolutionof tachycardia and diminished pulserate variability after AT in childrenwho had OSAS (diagnosis of OSASbased on oximetry plus questionnairedata) (level IV). Deng et al64 studiedheart rate variability and determinedthat heart rate chaos was modulatedby OSAS as well as by sleep state(level IV). In a study of 28 children whohad OSAS, O’Brien and Gozal65 foundevidence of altered autonomic ner-vous system regulation, as evidencedby increased sympathetic vascularreactivity, during wakefulness in thesechildren (level III). These studies allsuggest that OSAS places stress onthe autonomic system.

In summary, a large number of studies,albeit primarily level III, found thatcardiac changes occur in the presenceof OSAS, with an effect on both theright and left ventricles. OSAS inchildhood also has an effect on bothsystolic and diastolic BP. In addition,several studies suggest that childhoodOSAS can affect autonomic regulation,brain oxygenation, and cerebral bloodflow. These studies suggest thatchildhood OSAS may jeopardize long-term cardiovascular health.66

The association between left ventric-ular remodeling and 24-hour BPhighlighted the role of SDB in in-creasing cardiovascular morbidity.


� How reversible, after treatment,are cardiovascular changes in chil-dren who have OSAS?

� What are the long-term effectsof OSAS on the cardiovascularsystem?

TABLE 10 Cognitive, Behavioral, and QoL Abnormalities Improved After Treatment of PediatricSBD

Deficit Measured Source Level No. Abnormalities ImprovedAfter SDB Treatment

Cognition/IQ Chervin et al37 I 105 Attention measured on continuousperformance test improvedsignificantly after treatment

Montgomery-Downset al50

III 38 General conceptual ability improved(verbal fluency did not improve)

Friedman et al26 II 59 Auditory-visual integration, auditory-motormemory, short-term memory,retention, analytic thinking, IQ/mentalprocessing, attention all improved

Hyperactivity and/orADHD

Galland et al237 IV 247 Hyperactivity and/or diagnosis ofADHD improvedLi et al238



Roemmich et al191

Chervin et al37 I 105 Long-term improvement in hyperactivitySomatization,depression

Galland et al237 IV 153 All showed improvement in depressionand/or somatizationMitchell and Kelly240


Behavior problems,general

Goldstein et al55 IV 450 All showed behavior improvementexcept Davis et al49

Goldstein et al243 Long-term behavior improvement inMitchell et al53Hogan et al48

Li et al238

Roemmich et al191

Tran et al58

Wei et al245

Mitchell et al53

Davis et al49

Aggression, oppositional,and social problems

Galland et al237 IV 113 Improvement in abnormal socialbehavior and aggressionMitchell and Kelly240

Excessive daytimesleepiness

Chervin et al37 I 105 Sleepiness improved by 1 min, asmeasured by using multiple sleeplatency testing on PSG

QoL Colen et al52 IV 787 Includes disease-specific andemotional QoL58

Constantin et al54 Long-term improvements ≥1 y52,53

Goldstein et al55

Sohn et al56

Silva and Leite57

Tran et al58

Chervin et al37 I 105 Long-term improvements at 1 ySleep quality Constantin et al54 IV 590 Improved in both studies

Wei et al245


Growth

The section on obesity contains a de-tailed review of obesity and OSAS,

including the relationship between

OSAS and the metabolic syndrome. The

previous guideline documented many

studies showing a relationship be-tween OSAS and growth, and an in-crease in growth parameters aftertreatment of SDB by AT; this outcomehas been confirmed by a number ofmore recent studies (as discussed inthe recent meta-analysis by Bonucket al67). In a confirmation of previ-ous reports,68,69 Selimo�glu et al70

found a decreased level of seruminsulin-like growth factor-I in chil-dren who have OSAS, which in-creased significantly 6 months afterAT (level III).

Inflammation

Since the publication of the 2002 AAPguideline, there has been growingresearch on the role of OSAS insystemic inflammation. It has beenpostulated that OSAS results in in-termittent hypoxemia, leading to pro-duction of reactive oxygen species. Inaddition, the hypoxemia and arousalsfrom sleep lead to sympathetic activa-tion. These factors may trigger inflam-mation or exacerbate obesity-relatedinflammation. However, the data onOSAS and markers of systemic in-flammation in children are scarceand contradictory.

Eight studies (level II–III) measuredlevels of C-reactive protein (CRP) inchildren who had OSAS. Four studies(including 2 from the same center)showed no relationship between CRPand OSAS,71–74 whereas 4 studies (2from the same center) did show arelationship.46,75–77 Part of the dis-crepancy between studies may beattributable to the varying pro-portions of obese subjects (becauseobesity is associated with high CRPlevels) and varied age of subjects anddefinitions of OSAS in the differentstudies. Some studies controlled forobesity and degree of OSAS, whereasothers did not. The studies showinga positive relationship indicated thatOSAS was associated with elevated

TABLE 11 Structural and Functional Cardiac Abnormalities in Children Who Have OSAS

Source Level No. Findings

Left-sided cardiac dysfunctionAmin et al247 III 28 OSAS Abnormalities of LV geometry in 39% of OSAS vs 15% of PS;

OSAS associated with increased LV mass19 PSAmin et al248 III 48 OSAS Dose-dependent decrease in LV diastolic function with

increased severity of SDB15 PSRight-sided cardiac dysfunctionDuman et al249 III 21 children, ATH;

21 controlsHigher RV myocardial performance index in patient with

adenotonsillar hypertrophy than in controls; thisdecreased significantly after AT, along with symptoms ofOSAS

Ugur et al250 III 29 OSAS Improved RV diastolic function after AT, with postoperativevalues similar to controls26 PS

Biventricular cardiac dysfunctionJames et al59 IV 271 Case review of ECG and chest radiography results found only

1 case of cardiac failure, which occurred in a child whohad congenital heart disease; most other cases showedno abnormalities

Weber et al251 III 30 OSAS Increased RV diameter and area during both systole anddiastole; reduced LV diastolic diameter and ejectionfraction

10 controls

ATH, adenotonsillar hypertrophy; LV, left ventricle; PS, primary snoring; RV, right ventricle.

TABLE 12 BP in Children Who Have OSAS


Kohyama et al175 IV 23 suspected OSAS REM diastolic BP index correlated with AHIAge, BMI, and AHI were significant

predictors of systolic BP index during REMKwok et al66 III 30 PS Children with PS had increased daytime BP and

reduced arterial distensibilityLeung et al252 III 96 suspected OSAS Children with a higher AHI had higher wake

systolic BP and sleep systolic and diastolic BPBMI, age, and desaturation index contributed to

elevation of the diastolic BP during sleep,but only BMI contributed to the wake andsleeping systolic BP

Guilleminault et al253 III Retrospective component:301 suspected OSAS

Some children who have OSAS have orthostatichypotension

Prospective component:78 OSAS

Li et al176 III 306 community sample OSAS was associated with elevated daytimeand nocturnal BP

Amin et al177 III 140 suspected OSAS OSAS associated with an increase in morningBP surge, BP load, and 24-h BP. BPparameters predicted changes in leftventricular wall thickness

Amin et al254 III 39 OSAS OSAS was associated with 24-h BP dysregulation21 PS AHI, SpO2, and arousal contribute to abnormal

BP control independent of obesityEnright et al255 III 239 community sample Obesity, sleep efficiency, and RDI were

independently associated with elevatedsystolic BP

Kaditis et al174 IV 760 communitysample

No difference in morning BP between habitualsnorers and nonhabitual snorers

PS, primary snoring; REM, rapid eye movement.




CRP levels only above a certainthreshold of severity. Thus, the re-lationship between OSAS and CRPseems to be complex and is affectedby obesity and severity of OSAS.

A few level II and III studies haveevaluated other circulating markers ofinflammation in children who haveOSAS. Two studies showed no differ-ence in circulating intercellular ad-hesion molecule-1 between patientswith OSAS and controls.71,73 A singlestudy found elevated p-selectin (ameasure of platelet activation) inchildren who had OSAS comparedwith controls.73 A single study showedelevated levels of interferon-γ in chil-dren who had OSAS.74 One studyshowed increased interleukin (IL)-6and lower IL-10 in those with OSAS,78

whereas another study did not.74 An-other study reported no differencein cytokines IL-1β, IL-2, IL-4, IL-8, IL-12,and granulocyte macrophage colony-stimulating factor levels betweenchildren who had OSAS and controls.74

Data on tumor necrosis factor-α areconflicting,74,79 and differences in lev-els may be related to tumor necrosisfactor-α gene polymorphisms.80

A pathology-based study found in-creased glucocorticoid receptors inadenotonsillar tissue from childrenwho had OSAS compared with tissuefrom children who experienced chronicthroat infections (level III)81; anotherstudy from the same group found ele-vated leukotriene receptors (level IV).82

These findings provide a theoreticalconstruct for the potential utility ofantiinflammatory drugs as treatmentof children who have OSAS, althoughpossibly not for those who have al-ready undergone AT.

In summary, the data on CRP areconflicting, but it may be that CRPlevels increase above a certain thresh-old of severity of OSAS. Further researchinvolving large samples of subjects whohave varying degrees of OSAS severity,

with results controlled for BMI andage, are needed. There are too fewdata on other circulating markers ofsystemic inflammation to enable anyrecommendations.


� Larger studies, stratified for theseverity of OSAS and controlledfor obesity, are required to deter-mine whether OSAS is associatedwith systemic inflammation. If so,what are the long-term sequelae ofthis inflammation? Are inflamma-tory biomarkers potential goodoutcome measurements for OSAStreatment studies? Do they corre-late with clinical outcomes or long-term prognosis?

METHODS OF DIAGNOSIS

The previous guideline discussed thediagnosis of OSAS in great detail. Onthe basis of published evidence at thetime, it was concluded that the posi-tive and predictive value of historyand physical examination for the diag-nosis of OSAS was 65% and 46%,respectively; that is, no better thanchance. It was therefore recom-mended that objective testing be usedfor the diagnosis of OSAS. An evalua-tion of the literature regarding noc-turnal pulse oximetry, video recording,nap PSG, and ambulatory PSG sug-gested that these methods tended tobe helpful if results were positive buthad a poor predictive value if resultswere negative. Thus, children who hadnegative study results should be re-ferred for more comprehensive test-ing. These recommendations werebased on only a few studies, most ofwhich had a low level of evidence.Furthermore, it was recognized thatthese techniques were of limited use inevaluating the severity of OSAS (whichis important in determining manage-ment, such as whether outpatientsurgery can be performed safely). In

addition, the cost efficacy of thesescreening techniques had not beenevaluated and would depend, in part,on how many patients eventually re-quired full PSG. Since the publicationof the initial guideline, there havebeen a number of new studies, butfew are level I or II. Because few of thestudies cited here included data thatwould enable calculation of overallsensitivity and specificity or positiveand negative predictive values, anoverall table could not be provided.For this section, PSG was consideredthe gold standard for diagnosis ofOSAS.

Utility of History Alone for theDiagnosis of OSAS

Several level IV studies evaluated theuse of history alone for the diagnosisof OSAS. Preutthipan et al83 foundoverall poor sensitivity and specificitywhen evaluating various historicalfactors. The Pediatric Sleep Question-naire published by Chervin et al84

performed slightly better than otherpublished questionnaires, with a sen-sitivity of 0.85 and a specificity of 0.87by using a set cutoff. A follow-up studyby the same group showed a sensitiv-ity of 78% and a specificity of 72% forPSG-defined OSAS.85 However, this isstill a relatively low sensitivity andspecificity for clinical purposes. Byusing this instrument, the same groupalso found that negative answers toonly 2 questions on the PediatricSleep Questionnaire were helpful inidentifying patients who had normalPSG results.86 Taken together, theoverall performance of questionnairetools seems to support their use moreas a screening tool than as a di-agnostic tool, such that a negativescore would be unlikely to mislabela child with OSAS as being healthy, buta positive score would be unlikely toaccurately diagnose a particular childwith certainty.


Utility of Clinical Evaluation for theDiagnosis of OSAS

Similar to the data presented in theprevious guideline, most studies foundthat clinical evaluation was not pre-dictive of OSAS on PSG. Godwinet al15 performed a large (N = 480),population-based study of 6- to 11-year-old children. The study included useof a standardized history, someclinical parameters, and ambulatory,full PSG (level II). They concludedthat the sensitivity of any individualor combined clinical symptoms waspoor. Certain parameters, such assnoring, excessive daytime sleepiness,and learning problems, had a highspecificity.

In a level III study, van Someren et al87

compared history and clinical exami-nation by a pediatrician or otolaryn-gologist with abbreviated PSG (videorecording, oximetry, and measure-ment of snoring). Both the sensitivityand specificity of the clinician’s im-pression of moderate/severe OSASwere low (59% and 73%, respectively).In a similar number of cases, theclinicians underestimated (17%) andoverestimated (16%) study results.

In a level III study, it was shown thatwaist circumference z score hada statistically significant but clinicallypoor correlation with symptoms ofOSAS (R = 0.32, P = .006); BMI z scoredid not correlate with symptoms.88

Radiologic Studies

Several studies, all level III or IV,evaluated the utility of radiologicexaminations in addition to clinicalfactors in establishing the diagnosis ofOSAS (Table 13). Overall, these studiesshowed that the presence of airwaynarrowing on a lateral neck radio-graph increased the probability of pre-dicting OSAS on PSG. Cephalometricstudies tended to show a smallmandible in patients who had OSAS

compared with controls, although astudy using an MRI did not confirmthis.89 None of the cephalometric studiesprovided sensitivity and specificity orpositive and negative predictive values.Table 13 simplifies the cephalomet-ric findings for the purpose of pre-sentation. A level I study indicatedthat acoustic pharyngometry may bea useful screening technique forOSAS in older children, but approxi-mately one-half of the children couldnot cooperate well with the testing.90

One uncontrolled study (level IV) showedthat nasal resistance, as measured byusing rhinometry, had a high sensi-tivity and specificity for predictingpolysomnographic OSAS.91 This tech-nique warrants further study andvalidation.

Snoring Evaluation

Two level IV studies found a weak as-sociation between objective snoringcharacteristics and the presence/severity of OSAS that was insufficientto assist in clinical diagnosis.92,93

Cardiovascular Parameters

Studies have evaluated the utility ofscreening tests based on heart rate orother vascular factors in predictingOSAS (Table 14). These studies rangedfrom studies of pulse rate aloneto more sophisticated (and, hence,more expensive or time-consuming)studies, such as analyses of heartrate variability, pulse transit time,and peripheral arterial tonometry.Studies were level II through IV.Overall, the studies found changes incardiovascular variables in childrenwho had OSAS but with varying sen-sitivities and specificities. Thus,some of these measures may poten-tially be useful screening tests inthe future if combined with othermodalities that would increase thesensitivity and specificity but cannot

be recommended for clinical use atthis point.

Nocturnal Oximetry

The previous AAP guideline, on thebasis of a single study by Brouilletteet al,94 indicated that nocturnal pulseoximetry could provide an accuratescreen for OSAS if the result waspositive but that full PSG was neededif the oximetry result was negative. Aneed for further research in this areawas indicated. Four additional studieswere identified for the current report.Two of these did not compare oxime-try versus PSG and therefore will notbe discussed further.95,96

A follow-up study (level II) from thesame group as the previous report byBrouillette et al94 used overnight oxi-metry, primarily obtained in the home,to develop a scoring algorithm.97 Thesubjects’ median age was 4 years. Theoximetry score correlated with the AHIobtained from PSG as well as with thepresence of postoperative complica-tions. However, the positive predictivevalue of oximetry for major post-operative respiratory compromisewas only 13%. Of note, 80% of the 223children had normal, inconclusive, ortechnically unsatisfactory oximetryresults and were therefore referredfor either repeat oximetry or PSG. Incontrast, Kirk et al98 compared over-night home oximetry (by using a sys-tem with an automated oximetryanalysis algorithm that provided adesaturation index) with laboratoryPSG in 58 children aged ≥4 years whohad suspected OSAS (level III). Theyfound poor agreement between thedesaturation index on the basis ofoximetry and the PSG-determined AHI.The sensitivity of oximetry for theidentification of moderate OSAS (AHI>5/hour) was 67%, and specificitywas 60%. The oximetry algorithmtended to overestimate the AHI at lowlevels and underestimate at high




levels. The authors concluded thatoximetry alone was not adequate forthe diagnosis of OSAS. On the basis ofthese limited studies, it seems as ifoximetry alone is insufficient for thediagnosis of OSAS because of the highrate of inconclusive test results andthe poor sensitivity and specificitycompared with PSG, probably, in part,because children may have OSAS thatresults in arousals and sleep frag-mentation but little desaturation. Inaddition, children tend to move a lotduring sleep, which can result inmovement artifact.

Ambulatory PSG

The term “ambulatory PSG” is used forunattended sleep studies conducted

in the home. Frequently, ambulatoryPSG consists of cardiorespiratoryrecordings alone. Although the use ofambulatory PSG is considered appro-priate under certain circumstances inadults,99 there is a paucity of stud-ies evaluating ambulatory PSG inchildren. Zucconi et al100 evaluateda home portable system comprisingmeasurements of airflow (by usingthermistry), snoring, chest and ab-dominal wall movements, electro-cardiography (ECG), position, andoximetry (level II). However, the por-table system was used in the sleeplaboratory for the purpose of thestudy. A small sample of 12 children, 3to 6 years of age, underwent routinePSG and in-laboratory portable testing

on a consecutive night with the por-table system. The portable system hadgood sensitivity for detecting a re-spiratory distress index (RDI) >5/hour(78% with automated scoring; 89%with human scoring) but a specificityof zero. Rosen et al19 reported ona study of 664 children aged 8 to 11years who underwent abbreviatedambulatory study (by using induc-tance plethysmography, oximetry,heart rate, and position) (level III). Ofthese home studies, 94% were con-sidered technically adequate. A sub-sample of 55 children also underwentfull laboratory PSG. Few details weregiven regarding this subsample.However, it was reported that theambulatory studies had a sensitivity

TABLE 13 Relationship Between Airway Measurements and OSAS

Clinical Evaluation Sleep Evaluation Airway Evaluation Source Level No. Findings

Standardizedhistory, clinicalexamination

PSG Lateral neckradiography

Xu et al256 IV 50 Combinations of different predictor variablesresulted in positive and negative predictorvalues ranging from 70% to 80%

Clinical examination PSG Lateral neckradiography

Jain and Sahni257 IV 40 Degree of OSAS correlated with adenoid size onradiography but not with tonsillar size on clinicalexamination

Clinical examination PSG Lateral neckradiography

Li et al258 IV 35 Tonsillar–pharyngeal ratio on radiographycorrelated with AHI but not clinical tonsil size.Clinical tonsil size did not correlate with AHI

For a ratio of 0.479, the sensitivity and specificity inpredicting moderately severe OSAS (AHI >10/h)was 96% and 82%, respectively

NA PSG Cephalometry Kawashima et al259 III 15 OSAS Evidence of retrognathia in OSAS group30 controls

Clinical examination Ambulatoryabbreviatedrecordings

Cephalometry Kawashima et al260 III 38 OSAS OSAS: retrognathia, long facies in those OSASsubjects who had large tonsils31 controls

NA None Cephalometry Kikuchi et al261 IV 29 suspectedOSAS

OSAS: long facies

41 controlsQuestionnaire None Cephalometry Kulnis et al262 IV 28 snorers Snorers: retrognathia, shorter maxilla and cranial

base28 controlsStandardized history Nap PSG Cephalometry Zucconi et al263 III 26 snorers Snorers: retrognathia, decreased nasopharyngeal

space26 controlsNA PSG MRI Schiffman et al89 III 24 OSAS No difference in mandibular size between OSAS and

controls24 controlsClinical assessmentof tonsillar size

Ambulatorycardiorespiratoryrecordings

Acousticpharyngometry

Monahan et al90 I 203 Degree of OSAS correlated with airway size onpharyngometry but not with tonsillar size

Cephalometry Pharyngometric measures also correlated withmandibular length on cephalometry, only 78% of8- to 11-y-old children could produce minimallyacceptable data, and only 54% could producehigh-quality data

Questionnaire, clinicalexamination

PSG Rhinometry Rizzi et al91 IV 73 Nasal resistance of 0.59 Pa/cm3/s had a positivepredictive value of 97% and a negativepredictive value of 86%


of 88% and specificity of 98% in di-agnosing a laboratory PSG–based AHI>5/hour. It is not clear why theresults of this study were so differentfrom that of Zucconi et al but maypossibly be related to the older age ofthe subjects. Goodwin et al101 useda full PSG system, including EEG mea-surements, in the unattended homeenvironment in 157 children aged 5 to12 years (level IV). Adequate data wereobtained from 91% of subjects on thefirst attempt and 97% when the testwas repeated if needed. Data werereported as excellent in 61% of casesand good in 36%. In a small subsampleof 5 subjects, data were similar tothose with laboratory PSG. This studyshows the feasibility of performingunattended full ambulatory PSG inolder children, but results may not bethe same for young children. In sum-mary, ambulatory PSG seems to betechnically feasible in school-agedchildren, although data are not avail-able for younger children. Studies ofdiffering levels, and studying differentage groups, found widely discrepantspecificities for diagnosing moderateOSAS. Clearly, additional studies areneeded.

Nocturnal PSG

Nocturnal, attended, laboratory PSGis considered the gold standard for

diagnosis of OSAS because it providesan objective, quantitative evaluation ofdisturbances in respiratory and sleeppatterns. A recent review describessome of the relationships between PSGand sequelae of OSAS (see “PediatricIssues” section in Redline et al102).PSG allows patients to be stratified interms of severity, which helps de-termine which children are at risk forsequelae (thus alerting pediatriciansto screen for complications of OSAS);which children are at risk for post-operative complications and would,therefore, benefit from inpatient ob-servation postoperatively; and whichchildren are at high risk of persis-tence of OSAS postoperatively, whomay then need postoperative PSG toassess the need for further treatment(eg, CPAP).

Adult patients may sleep poorly thefirst time they are in a sleep laboratorybecause of anxiety, the unfamiliar en-vironment, and the attached sensors.This “first night effect” can lead toaltered sleep architecture and possi-ble underestimation of the severity ofOSAS. Five studies (levels I–IV) evalu-ated the night-to-night variability ofPSG in children101,103–106; in one ofthese articles,101 only a small sub-sample had night-to-night variabilityevaluated (Table 15). The time differ-ence between PSGs varied from 24

hours to 4 weeks. Although some ofthe studies showed minor differencesin respiratory parameters from nightto night, the studies suggest that fewchildren would have been clinicallymisclassified on the basis of a singlenight’s PSG. Thus, 1 night of PSG seemsto be adequate to establish the di-agnosis of OSAS. All studies showedsignificant differences in sleep archi-tecture from night to night. Therefore,research studies evaluating sleep ar-chitecture would require >1 night ofPSG. For consistency, it is recom-mended that PSG be performed andscored by using the pediatric criteriafrom the American Academy of SleepMedicine scoring manual.107

Other Tests

The shape of the maximal flow-volumeloop on pulmonary function testing hasbeen used to attempt to screen forOSAS in adults. Young children can-not perform standard maximal flow-volume loops. One small study of 10subjects evaluated the relationshipbetween tidal breathing flow-volumeloops and PSG (level III).108 The sen-sitivity was 37.5% and specificity was100%, indicating that this methodis of limited utility in screening forOSAS.

Two studies by the same groupevaluated whether urinary/serum

TABLE 14 Utility of Cardiovascular Parameters in Predicting OSAS

Measure Sleep Evaluation Source Level No. Findings

Pulse rate Oximetry Constantin et al63 IV 25 OSAS Pulse rate decreases in children who have OSAS after ATPulse rate Home

cardiorespiratorystudies

Noehren et al264 III 5 OSAS Pulse rate changes poor at detecting differences between respiratoryevents and movements, and between central and obstructive apneas20 controls

Heart rate variability PSG Deng et al64 IV 34 OSAS Heart rate chaos intensity had sensitivity of 72% and specificity of 81% forOSAS18 controls

Pulse transit time PSG Katz et al265 III 24 SDB Depending on the severity of the event, 80%–91% of obstructive respiratoryevents were associated with pulse transit time changes. However, pulsetransit time changes also occurred with spontaneous arousals fromsleep

10 controls

Heart rate, pulsetransit time

PSG Foo et al266 (similardata published inFoo and Lim267)

III 15 suspectedOSAS

Pulse rate had 70% sensitivity and 89% specificity, and pulse transit timehad 75% sensitivity and 92% specificity in identifying obstructive events

Peripheral arterialtonometry

PSG Tauman et al268 II 40 OSAS Peripheral arterial tonometry had sensitivity of 95% and specificity of 35%in identifying EEG arousals20 controls




proteinomic analysis could be used toscreen for the presence of OSAS. Ina level I study of urinary proteinomics,the investigators found that a combi-nation of urinary proteins could pre-dict OSAS with a sensitivity of 95% anda specificity of 100%.109 Similarly, ina level III study from the same group,the investigators found that a differ-ent set of proteins could be used toidentify 15 of 20 children who hadOSAS and 18 of 20 children who weresnorers.110 The authors note that theystudied a highly selected populationmatched for age, gender, ethnicity,BMI, and inflammatory respiratorydisorders, such as allergic rhinitis orasthma. Thus, this technique, althoughpromising, requires further validationin typical clinical cohorts and dupli-cation in another laboratory.

Summary

In summary, few of the screeningtechniques mentioned here havea sensitivity and specificity highenough to be relied on for clinicaldiagnosis. In addition, it should benoted that many of the studies usedan AHI >5/hour when determining

sensitivity and specificity, although anAHI >1.5/hour is considered statisti-cally abnormal in children.111–113 Fewstudies used large study samples, andfew were blinded. As a result, some ofthe studies of screening techniquesresulted in contradictory evidence. Ona pragmatic level, however, it is re-alized that current infrastructure isinadequate to provide PSG for allchildren with suspected OSAS. There-fore, the use of screening tests maybe better than no objective testing atall. However, clinicians using thesetests should familiarize themselveswith the sensitivity and specificity ofthe test used and consider proceed-ing to full PSG if the test result isinconclusive.


� Well-designed, large, controlled,blinded, multicenter, prospectivestudies are required to providemore definitive answers regardingthe utility of screening tests for thediagnosis of OSAS. In particular,additional studies of ambulatoryPSG in children of varying agesare needed.

TREATMENT OF OSAS

AT

Adenotonsillar hypertrophy is themost common cause of OSAS, and ATcontinues to be the primary treatmentfor this issue. Adenoidectomy alonemay not be sufficient for children whohave OSAS because it does not ad-dress oropharyngeal obstruction sec-ondary to tonsillar hyperplasia. Theprevious guideline stated the impor-tance of AT as the primary treatmentfor OSAS in children. No new litera-ture is available to suggest a changeto these recommendations. Table 3 inthe guideline lists relative contra-indications to AT. Note that whereasa submucus cleft palate is a relativecontraindication to adenoidectomy,a partial adenoidectomy may beperformed in such patients. However,postoperative PSG should be per-formed to ensure that OSAS has re-solved.

AT in most children is associated witha low complication rate. Minor com-plications include pain and poor oralintake. More severe complicationsmay include bleeding, infection, an-esthetic complications, respiratorydecompensation, velopharyngeal in-competence, subglottic stenosis, and,rarely, death.

Tarasiuk et al found that health careutilization costs were 226% higher inchildren with OSAS before diagnosiscompared with control children114 andthat health care costs decreased byone-third in children who underwentAT, whereas there was no change inhealth care costs in control childrenor children who had untreated OSAS115

(both studies were level IV).

Partial Tonsillectomy

Several newer techniques for tonsil-lectomy have gained increasing usesince publication of the last guideline.The primary goal of these techniques

TABLE 15 Night-to-Night Variability in Polysomnographic Respiratory Parameters

Time BetweenEvaluations


1–4 wk Katz et al103 I 30 suspectedOSAS

No significant group difference in the AHIbetween nights. Those with the highest AHIhad the most variability. However, no patientwas reclassified as primary snoring versusOSAS on the basis of the second study

7–50 d Goodwin et al101 IV 12 Used unattended home PSG. Studies weresuccessful in 10. No difference in AHI betweennights in this small sample

Consecutivenights

Scholle et al105 III 131 OSAS No difference in AHI between nights

Consecutivenights

Li et al104 III 46 obese AHI was greater on night 244 controls The first night would have correctly identified 11

(85%) of the 13 cases of OSAS if the worstobstructive apnea index over any single nightwas used as the criterion. However, the 2cases that would have been missed by thesingle PSG had only borderline OSAS

Consecutivenights

Verhulst et al 106 I 70 suspectedOSAS

First night classified OSAS correctly in 91% ofsubjects, if the worst AHI over any night wasused as the diagnostic criterion. All but 1 ofthose who were missed had an AHI <5/h


is to decrease the morbidity associ-ated with traditional tonsillectomymethods. One such technique is partialtonsillectomy (PT), in which a portionof tonsil tissue is left to cover themusculature of the tonsillar fossa.Multiple studies, ranging in level fromII to IV, have evaluated recovery timesand adverse effects from PT. However,only a few small, lower-level studieshave specifically looked at the effect ofPT on OSAS. In a level IV study, Tunkelet al116 evaluated 14 children whounderwent PSG before and after PTand found a cure rate (AHI ≤1/hour)of 93% postoperatively. In a retrospec-tive study (level IV), Mangiardi et al117

compared 15 children who underwentPT (of 45 eligible) with 15 childrenwho underwent total tonsillectomy.This study had a number of technicallimitations. A variety of techniques(overnight laboratory PSG, nap sleepstudies, and limited-channel homesleep studies) were performed insubjects preoperatively, and limited-channel home sleep studies wereperformed in all patients post-operatively. These different monitor-ing techniques would be expected toprovide varying results.118,119 In bothsurgical groups, the authors founda higher rate of postoperative OSASthan typically reported in the litera-ture, with a median (range) AHI of 7.5 ±4.3/hour in the PT group and 8.8 ±4.7/hour in the total tonsillectomygroup (not significant).

PT carries an increased risk ofregrowth of the tonsils, which oc-curred in 0.5% to 16% of patients instudies of varied duration. Celenket al120 performed a retrospective re-view of 42 children 1 to 10 years ofage who underwent PT via radio-frequency ablation for symptoms ofOSAS (level IV). Follow-up ranged from6 to 32 months, with a mean follow-upof 14 months. They found tonsillarregrowth on physical examination in 7

(16.6%) patients; 5 of these weresymptomatic and underwent comple-tion tonsillectomy. The time frame foroccurrence of regrowth ranged from1 to 18 months. The authors notedthat some episodes of regrowth oc-curred after episodes of tonsillitis.Zagólski121 evaluated 374 childrenwho underwent PT on the basis ofclinical symptoms of OSAS (level IV).Patients underwent otolaryngologyexaminations annually for 4 years.Twenty-seven (7.2%) children hadtonsillar regrowth; of those, 20 hadclinical symptoms and, therefore, un-derwent completion tonsillectomy.Regrowth of the palatine tonsils wasobserved at a mean period of 3.8years, suggesting the need for long-term follow-up. In a multicenter, ret-rospective case series of 870 childrenwith a mean follow-up of 1.2 years,Solares et al122 found an incidence oftonsillar regrowth of 0.5% (level III).The methods and criteria for assess-ing regrowth were not detailed in thisarticle but may have been a clinicalfollow-up at 1 and 6 months post-operatively. The lower rate of re-growth in this study compared withthe other studies may have been re-lated to the shorter follow-up period.Eviatar et al123 performed a long-term(10–14 years), retrospective, tele-phone survey comparing 33 childrenwho had undergone PT for symptomsof OSAS versus 16 children who un-derwent tonsillectomy; children un-dergoing concomitant adenoidectomywere excluded (level III). They foundsimilar rates of parent-reported snor-ing in the 2 groups (6.1% for PT, 12.5%for total tonsillectomy; not significant)but no cases of OSAS on the basis ofsymptoms.

PT for the treatment of adenotonsillarhypertrophy has shown some successin decreasing immediate postoper-ative pain. Derkay et al124 prospectivelyevaluated 300 children undergoing

either PT or total tonsillectomy foradenotonsillar hypertrophy (level II).They found that children in the PTgroup had an earlier return to normalactivity and were 3 times more likelynot to need pain medication at 3 dayscompared with the total tonsillectomygroup. There was no difference be-tween groups in median return toa normal diet (3.0 vs 3.5 days). In alevel III, retrospective study of 243children undergoing PT versus 107undergoing total tonsillectomy, Koltaiet al125 found less pain and quickerreturn to a normal diet in childrenundergoing PT. In a level II study, Sobolet al126 prospectively evaluated 74children who had adenotonsillar hy-pertrophy scheduled for AT. Theirresults showed a resumption to nor-mal diet 1.7 days earlier in the PTgroup compared with children un-dergoing total tonsillectomy. There wasno significant difference in the resolu-tion of pain or return to normal ac-tivities between the 2 groups, but therewas increased intraoperative bloodloss in the PT group.

In summary, there are no level I studiescomparing PT with total tonsillectomyin the pediatric population. Additionaldata are needed regarding the efficacyof PT for OSAS, by using objectiveoutcome measurements. There ispossibility of tonsillar regrowth afterPT, with studies showing varied ratesof regrowth. These studies are alllimited by lack of blinding, lack ofobjective measures to quantitate ton-sillar regrowth, and lack of poly-somnographic data relating tonsillarregrowth to OSAS. Some studies foundthat patients who undergo PT have lesspain and quicker recovery during thefirst few days compared with childrenundergoing total tonsillectomy. How-ever, PT may be associated withgreater intraoperative blood loss, andthere is a risk of recurrent infectionsin the tonsillar remnants.120,121,123 At




this point, data are insufficient torecommend any particular surgicaltechnique for tonsillectomy over an-other in terms of OSAS. However,children undergoing PT should bemonitored carefully long-term toensure that symptoms of OSAS re-lated to tonsillar regrowth do notoccur, and families should be warnedabout the possibility of recurrence ofOSAS.

Postoperative Management After AT

Tonsillectomy and adenoidectomy canbe safely performed in the vast ma-jority of children on an outpatientbasis. Risk factors that increase therisk of postoperative complicationsinclude age <3 years, severe OSAS,presence of cardiac complications,failure to thrive, obesity, and presenceof upper respiratory tract infection(URI). Although there have beennumerous publications regardingpostoperative complications sincepublication of the last guideline, therehave been no data to suggest a changein the previous recommendations. Chil-dren with medical comorbidities suchas craniofacial anomalies, genetic syn-dromes, and neuromuscular diseaseare also high risk; these special pop-ulations are not covered by thisguideline.

An important advantage of the objec-tive documentation of the severity ofOSAS by using PSG should be the abilityto predict the need for overnighthospital stay after AT on the basis ofa higher risk of postoperative com-plications. Severe OSAS has beenproposed as a criterion for inpatientobservation; the current evidence todefine severe OSAS is derived pri-marily from level III retrospectivestudies. Although considerable physi-ologic information regarding the re-spiratory pattern and gas exchangeduring sleep is available from anovernight PSG, the available studies

have focused primarily on the AHI and,to a lesser degree, the nadir of theSpO2. Relevant studies are listed inTable 16. Studies varied with regard tothe type of patients included (pro-portion of obese patients; patientswho had craniofacial and geneticsyndromes) and severity of OSAS. Al-though the definition of postoperativerespiratory compromise varied, moststudies required that an intervention(eg, supplemental oxygen, nasopha-ryngeal tube, CPAP, intubation) beperformed. Most studies found ahigh rate of postoperative respira-tory complications. Different studiesshowed different PSG predictive fac-tors for postoperative complications,and few studies developed receiveroperating characteristic curves.127

Nevertheless, studies were fairly con-sistent in indicating that an SpO2<80% and an AHI >24/hour werepredictive of postoperative respira-tory compromise. These criteria aremore conservative than the recentlypublished clinical practice guidelinesfrom the American Academy ofOtolaryngology–Head and Neck Sur-gery, which recommend that childrenwho have an AHI ≥10/hour and/or anSpO2 nadir <80% be admitted forovernight observation after AT.3

It is difficult to provide exact PSGcriteria for OSAS severity becausethese criteria will vary depending onthe age of the child; additionalcomorbidities, such as obesity, asthma,or cardiac complications of OSAS; andother PSG criteria that have not beenevaluated in the literature, such asthe level of hypercapnia and the fre-quency of desaturation (comparedwith SpO2 nadir). Therefore, on thebasis of published studies (Table 16),it is recommended that patients whohave an SpO2 nadir <80% (either onpreoperative PSG or during obser-vation in the recovery room post-operatively) or an AHI ≥24/hour be

observed as inpatients postopera-tively because they are at increasedrisk of postoperative respiratory com-promise. In addition, on the basis ofexpert consensus, it is recommendedthat patients with significant hyper-capnia on PSG (peak PCO2 ≥60 mmHg) be admitted postoperatively.Clinicians may decide to admit pa-tients who have less severe PSGabnormalities on the basis of a con-stellation of risk factors (age,comorbidities, and additional PSGfactors) on an individual basis.

Data regarding URIs were based onstudies of children undergoing generalanesthesia for a variety of procedures.The committee could not identify anystudies related specifically to URIs andAT. In a large, level III study, Tait et al128

evaluated 1078 children 1 month to 18years of age who were undergoingan elective surgical procedure. Thepresence of a URI was diagnosed byusing a parental questionnaire. Dataregarding perioperative respiratoryevents were recorded. There were nodifferences between children who hadactive URIs, recent URIs (within 4weeks), and asymptomatic childrenwith respect to the incidences of lar-yngospasm and bronchospasm. How-ever, children who had active andrecent URIs had significantly moreepisodes of breath-holding, desatura-tion <90%, and overall adverse re-spiratory events than children whohad no URIs. Independent risk factorsfor the development of adverse re-spiratory events in children who hadactive URIs included use of an endo-tracheal tube (in those <5 years ofage), preterm birth, history of re-active airway disease, paternalsmoking, surgery involving the airway,the presence of copious secretions,and nasal congestion. In a large levelIII study of 831 children undergoingsurgery with a laryngeal mask air-way, von Ungern-Sternberg et al129


compared children who had a URIwithin 2 weeks of surgery versusthose without a URI; 27% of child-ren had a recent URI. They founda doubling of the incidence oflaryngospasm, bronchospasm, andoxygen desaturation intraoperativelyand in the recovery room in the chil-dren who had recent URIs, althoughthe overall incidence of these eventswas low. The risk was highest inyoung children; those undergoing ear,nose, and throat surgery; and those inwhom multiple attempts were madeto insert the laryngeal mask airway.On the basis of data availableregarding risk with general anesthesia,

the committee concluded that chil-dren who have an acute respira-tory infection on the day of surgery,as documented by fever, cough, and/or wheezing, are at increased riskfor postoperative complications and,therefore, should be rescheduled ormonitored closely postoperatively.Clinicians should decide on an in-dividual basis whether these patientsshould be rescheduled, taking intoconsideration the severity of OSAS inthe particular patient and keeping inmind that many children who haveadenotonsillar hypertrophy exhibitchronic rhinorrhea and nasal congestioneven in the absence of viral infections.

Postoperative Persistence of OSASAfter AT

Although the majority of children havea marked improvement in OSAS afterAT, OSAS may persist postoperatively.OSAS is especially likely to persist inchildren who have underlying illnessessuch as craniofacial anomalies, Downsyndrome, and neuromuscular dis-ease; these special populations are notincluded in this review.

Over the years since the committee’sfirst consensus report, a number ofstudies have been published discus-sing the impact of surgery on child-hood OSAS. Most of these studieswere omitted from consideration for

TABLE 16 Relationship Between PSG Parameters and Postoperative Respiratory Complications

Source Level Type of Study No. Study Group Age, y SpecialPopulationsIncludeda

Findings

Hill et al269 III Retrospective 83 AHI >10 ≤18 Yes Major respiratory complication in 5%; minor in 20%Only age <2 y (P < .01) and AHI >24 (P < .05) significantly

predicted postoperative airway complicationsComplication rate only 4% if special populations were

excludedAHI >24 predicted 63% of complications

Jaryszak et al270 III Retrospective 151 Any child who hada PSG

Not stated Yes Respiratory complication rate was 15%Children with complications had higher AHI (32 vs 14) and

lower SpO2 nadir (72% vs 84%) compared with thosewithout complications

Koomson et al271 III Retrospective 85 AHI >5 Not stated Yes Postoperative desaturation in 28%More likely to desaturate postoperatively if PSG SpO2 nadir

<80%Ma et al272 III Retrospective 86 Any child who had

a PSG1–16 Yes Postoperative desaturation in 7%

No difference in AHI between those with and withoutpostoperative desaturation (11.6 ± 4.5 vs 14.7 ± 16.6)

Sanders et al273 I Prospective 61 61 children who hadOSAS vs 21 who hadtonsillitis

2–16 No Respiratory complication rate was 28%Subjects with RDI ≥30 were more likely to have

laryngospasm and desaturationAt an RDI ≥20, OSAS was more likely to have breath-

holding on inductionSchroeder et al274 III Retrospective 53 Severe OSAS (AHI >25) Not stated Yes 43% required oxygen or PAP

Note: an additional 17 children were electively keptintubated postoperatively

Shine et al196 III Retrospective 26 Obese OSAS 2–17 Obese; othercomorbiditiesnot stated

46% had respiratory complicationsThose requiring intervention for respiratory problems had

a lower SpO2 (68 ± 20% vs 87 ± 18%) but no differencein RDI (27 ± 44 vs 15 ± 28) than those who did notrequire intervention

By using univariate analysis, a preoperative SpO2 <70%was associated with postoperative respiratorycompromise, but no threshold was found for RDI

Ye et al 127 III Retrospective 327 AHI ≥5 4–14 No 11% had respiratory complicationsAn AHI of 26 had 74% sensitivity and 92% specificity for

predicting postoperative respiratory complicationsa Special populations include children with genetic syndromes and craniofacial abnormalities.




this review because of their lack ofpreoperative and postoperative PSGs.Many other studies reported changesin group averages for polysomno-graphic and other measures post-operatively. All published articlesfound that AT leads to significantimprovement in polysomnographicparameters in the majority of patients(although not in all). Studies providingdata that could be interpreted toprovide an estimate of the proportionof patients who were cured of theirOSAS are shown in Table 17. Twentyoriginal articles on the topic havebeen published since 2002, including 2meta-analyses130,131 of other articlesincluded in the review. The lack ofuniform agreement regarding thepolysomnographic criteria for di-agnosis of OSAS complicates thisanalysis of postoperative persistenceof OSAS, as it does other aspects ofthis review, in part because the pre-operative PSG criteria for surgery arenot uniform across the different arti-cles, but more importantly, becausethe postoperative prevalence of OSASis highly dependent on the stringencyof diagnostic criteria. In some cases,articles helpfully provided data onresidual prevalence of OSAS by usingdifferent polysomnographic criteria(eg, AHI >1/hour and AHI >5/hour). Atthis point, it is generally accepted thatAT has a higher success rate thanisolated adenoidectomy or tonsillec-tomy, so although a few of the articlesincluded some patients undergoingonly adenoidectomy, only tonsillec-tomy, or ancillary procedures such asnasal turbinectomy, most focused ex-clusively on the impact of AT.

As shown in Table 17, a total of 11articles were published, describing 10general population cohorts referredeither to a pediatric sleep specialistor otolaryngologist for OSAS, and 1meta-analysis of articles dating backto 1980. Most of these were case

series of patients, with significantmethodologic flaws, including non-blinding and incomplete follow-up fora high proportion of patients, and theseissues were present even in the meth-odologically strongest articles.132–134

The polysomnographic criteria for OSASin each article may or may not havebeen the same as those used as anindication for AT, and these variedfrom an AHI ≥1/hour to AHI ≥5/hourand RDI >2 to 5/hour. Surprisingly, theoverall estimate of postoperative per-sistence of OSAS did not seem to varygreatly by polysomnographic criteriafor surgery. Conversely, the estimatesof residual OSAS were clearly relatedto which polysomnographic criteriafor OSAS were applied to the post-operative PSGs. When using an AHI≥1/hour as the criterion for residualOSAS, estimates of persistence rangedfrom 19%135 to 73%,133 whereas whenusing an AHI ≥5/hour as the criterion,the estimate of persistence of OSASranged from 13%134 to 29%.132 It isimportant to recognize that there areclearly recognizable risk factors forpostoperative persistence of OSAS andthat the prevalence of these risk fac-tors in the populations studied had animportant impact on their estimatesof postoperative persistence of OSAS.For example, >50% of patients in themulticenter study of Bhattacharjeeet al133 were obese, whereas 21% ofthe patients in the series by Ye et al134

were obese, defined as 95th percentilefor the Chinese population. It shouldbe emphasized that although many ofthese studies showed a high pro-portion of patients with residual OSASafter AT, most patients exhibited amarked decrease in AHI postoperatively.

Risk Factors for Postoperative OSAS

1. Obesity

Five studies focused attention on obesepatients (defined as 95th percentilefor weight or BMI for age), and 1

meta-analysis131 combined 4 of thesestudies. The meta-analysis reportedthat 88% of obese patients still had apostoperative AHI ≥1/hour, 75% hada postoperative AHI ≥2/hour, and 51%had a postoperative AHI ≥5/hour.Preoperative obesity was found to bea significant risk factor for post-operative residual OSAS in severalother studies133–135 as well, even whenmultivariable modeling was used tocontrol for other factors such as ageand preoperative AHI. The odds ratiosof persistent OSAS in obese patientsranged in these models from 3.2134 to4.7.136 One study found that the re-lationship of BMI to risk of persistentOSAS was no longer significant whenadjusted for preoperative AHI.137 Incontrast to all of the studies thatlooked at this factor, a study of obeseGreek children found no difference inthe prevalence of residual OSAS inobese versus nonobese children; partof the reason for this finding might bethat this study used a slightly lessstringent criterion for obesity (1.645SDs weight for age, which is the 90thpercentile).138

2. Baseline Severity of OSAS

All studies that evaluated baseline AHIas a potential risk factor for persistentpostoperative OSAS found it to bea significant risk factor, even whenadjusted for other comorbidities suchas obesity.132–134,136,139

3. Age

A series limited to children aged <3years reported a high incidence (65%)of treatment failures in these youngerchildren, but this cohort includeda large proportion of children whohave other risk factors, such as se-vere OSAS and chromosomal andcraniofacial abnormalities.140 In con-trast, 2 studies reported that in-creasing age (especially 7 years andolder) is a risk factor for persistent


TABLE17

StudiesProvidingan

Estim

ateof

theProportionof

PatientsWho

WereCuredof

OSAS

With

Surgery

Source

Year

LevelNo.

Age,y

Population

Polysomnographic

Criterion

for

Surgery

Operation

Follow-up

Period,m

oSubjects

Who

HadOSAS

atFollow-up

Miscellaneous

Generalpopulationstudies

Chervinet

al37

2006

I39

5.0–12.9

AHI≥

1AT

13±

1.4

21%

2articlesdocumentedfindings

inthesamepopulation

Dillonet

al275

Guillem

inault

etal135

2004

III56

1.25–12.5

AHI≥

1or

RDI>

2AT:36(som

eof

whom

also

hadnasal

turbinectomy

and/or

tonsillar

wound

suturing);

A:8;T:11

3AT:19.4%

;A:100%;T:100%

Halfof

ATfailureswerein

obesepatients

Guillem

inault

etal141

2007

III199

1.5–14

AHI≥

1AT

in183;Aor

Tin

19;nasal

turbinectomy

in17.4%

3–5

46.2%

Increasednasalturbinatescore,

presence

ofdeviated

nasalseptum

andincreasedMallampatiscoreof

relationshipof

tongue

touvulaand

retropositionof

themandiblewere

allpredictiveof

higher

failure

rate

Guillem

inault

etal276

2004

IV284

2–12.1

AHI>

1.5

ATin

228;Aor

Tinferior

turbinectomyin

73

3–4

8.8%

ofthosewith

preoperativeAHI<

10andAT;64.7%

ofthose

with

preoperativeAHI

≥10.N

obreakdow

nprovided

regarding

results

ofAT

versus

othersurgery

Anadditional99

childrenhad

RDI>1.5andAHI<

1.5.Of

this

group,100%

hadnorm

alRD

Iafter

ATand9.2%

hadresidual

abnorm

alRD

IafterAor

T.Difficult

tointerpretfindings

becauseof

inconsistent

reportingof

data

Mitchell1

322007

III79

3–14

AHI≥

5AT

1–9.3

16%

(AHI

≥5);29%

(AHI

>1.5)

Severityof

preoperativeAHI

predictedresponse:preoperative

5–10,0%

≥5;preoperative10–20,

postoperative12%

≥5;preoperative

>20,postoperative36%

≥5;13/22

with

postoperativesnoringhad

AHI≥5;0/57

withoutpostoperative

snoringhadAHI≥

5Talet

al277

2003

IV36

1.8–12.6

RDI>

1AT

4.6(1–16)

11.11%

hadRD

I>5

Taum

anet

al137

2006

III110

6.4±

3.9

AHI≥

1AT

1–15

46%

AHI1–5,29%

with

AHI>

5In

logisticregression,AHI

before

surgeryandfamily

historyof

OSAS

weresignificant

predictors

ofAHI>

5postoperative

Walker

etal278

2008

IV34

0.93–5

RDI>

5in

REM

sleep

AT9.8

35%

with

RDI>

5Treatm

entfailureslim

itedto

thosewith

preoperativeRD

Iin

REM

>30

Bhattacharjee

etal133

2010

III578

6.9±

3.8

AHI≥

1AT

1–24

72.8%

with

AHI≥

1;21.6%

>5

Largemulticenterstudy.Age>7y,

increasedBM

I,presence

ofasthma,

andhigh

preoperativeAHIwere

independentpredictors

ofpersistent

postoperativeOSAS




TABLE17

Continued

Source

Year

LevelNo.

Age,y

Population

Polysomnographic

Criterion

for

Surgery

Operation

Follow-up

Period,m

oSubjects

Who

HadOSAS

atFollow-up

Miscellaneous

Brietzke

and

Gallagher

130

2006

III325

4.9

Various

AHI≥1

AT3.3

17.1%

(dependedon

OSAS

criteriaforeach

study)

Meta-analysisof

11case

series

publishedbetween1980

and2004

Yeet

al134

2010

IV84

7.1±

3.2

Chinese

AHI≥5

AT18–23

31%

with

AHI≥

1;13.1%

with

AHI≥

5Obesity

andhigh

preoperativeAHI

weresignificant

independent

predictors

oftreatm

entfailure

Focuson

obesepopulations

Mitchelland

Kelly

279

2004

III30

3.0–17.2

Obese(BMI>

95th

percentile)

AHI>5

AT5.6

54%

Mitchelland

Kelly

139

2007

III72

3–18

Comparisonof

obese(BMI>

95th

percentile)

with

nonobese

AHI≥2:AHI2–5mild,

AHI5–15

moderate

AHI≥

15severe

AT5–6

Obese:76%:(46%

mild;15%

moderate;15%

severe).

Nonobese:28%

:(18%

mild;

10%

moderate).

PreoperativeAHIand

obesity

were

independentrisk

factorsfor

postoperativeOSAS.O

Rfor

persistent

OSAS

inobese,

adjusted

forpreoperativeAHI,

was

3.7(95%

CI:1.3–10.8)

O’Brienet

al1362006

III69

7.1±

4.2

Obese(weight>2SDs

from

meanforage)

RDI≥5

AT20.4±

16.8

Nonobese:22.5%

;Obese:55%

PreoperativeAHIand

obesity

were

independentrisk

factorsfor

postoperativeOSAS.O

Rfor

persistent

OSAS

inobese,

adjusted

forpreoperativeAHI,

was

4.7(95%

CI:1.7–11.2)

Shineet

al194

2006

IV19

6.5±

4.4

Obese(BMI>

95th

percentile)

RDI>5

18AT

(1with

UPPP),1T

2–6

63%

Missing

data

Costaand

Mitchell1

31

2009

III110

7.3–9.3

Obese

Various

AT3–5.7

88%

hadpostoperative

AHI≥

1;75%

had

postoperativeAHI≥

2;51%

hadpostoperative

AHI≥

5

Meta-analysisof

4obesity

studiesincluded

here

Apostolidou

etal138

2008

IV70

6.5±

2.2

Greek;obesedefined

as>1.645SDsfrom

meanweightforage

OAHI

≥1

AT2-14

Overall:75.7%

with

AHI≥

1(77.3%

obese,75%

nonobese).Am

ong

childrenwith

apreoperativeOAHI

≥5:9%

with

AHI≥

5(8%

obese,

10%

nonobese)

Focuson

otherspecialpopulations

Mitchelland

Kelly

140

2005

III20

1.1–3.0

Children<3y

RDI>5

AT4.1–20.4

65%:25%

RDI5–10;25%

RDI10–20;15%

RDI>

20Included

comorbidities(Dow

nsyndrome,cardiacdisease,

cerebral

palsy)

excluded

from

thisguideline.60%

ofpatients

weresevere,w

ithRD

I>20

atbaseline

Mitchelland

Kelly

280

2004

III29

1.4–17

Severe

OSAS

RDI>5;severe:R

DI≥30

AT6

69%

with

postoperative

RDI>

548%

wereobese

A,adenoidectom

y;CI,confidenceinterval;O

AHI,obstructiveAHI;OR,oddsratio;T,tonsillectom

y;REM,rapid

eyemovem

ent;UPPP,uvulopharyngopalatoplasty.


OSAS, even when controlling for obe-sity.132,133

4. Other Potential Risk Factors

Individual studies have noted thatnasal abnormalities or craniofacialdisproportion,141 family history ofOSAS,137 and presence of asthma133

were all predictive of higher failurerate, but these findings were notsubstantiated by other studies. Ofnote, Mitchell132 found that 13 of 22patients in the cohort who had post-operative snoring had an AHI ≥5/hour,whereas none of the 57 patients whodid not exhibit postoperative snoringhad an AHI ≥5/hour. This supports thefindings of older studies reviewed inthe previous technical report thatfound absence of snoring to havea 100% negative predictive value forpostoperative OSAS.6 However, in theChinese cohort, 2 of 11 patients whohave persistent AHI ≥5/hour re-portedly did not snore; it is unclearwhether cultural considerations mighthave affected parental report ofsnoring.134

Summary

AT is the most effective surgicaltherapy for pediatric patients, leadingto an improvement in polysomno-graphic parameters in the vastmajority of patients. Despite thisimprovement, a significant proportionof patients are left with persistentOSAS after AT. The estimate of thisproportion in a relatively low-riskpopulation ranges from a low of 13%to 29% when using an AHI ≥5/hour asthe criterion to a high of 73% whenincluding obese children and adoles-cents and a conservative AHI ≥1/hour.Children at highest risk of persistentOSAS are those who are obese andthose with a high preoperative AHI,especially those with an AHI ≥20/hour,as well as children >7 years of age.Absence of snoring postoperatively is

reassuring but may not be 100%specific; it may therefore be advisableto obtain a postoperative PSG in very-high-risk children even in the absenceof reported persistent snoring.


� What are the risks of persistenceof OSAS and long-term recurrenceof OSAS after PT versus total ton-sillectomy? Large, prospective, ran-domized trials with objectiveoutcome measures including PSGare needed.

� Better delineation of which patientswould benefit from postoperativePSG.

� How well does resolution of OSAScorrelate with resolution of com-plications of OSAS?

� Are some of the newer surgicaltechniques for AT equally effectivein resolving OSAS?

� What are the risks of performingAT in a patient with a URI?

� What are the PSG parameters thatpredict postoperative respiratorycompromise? Future researchshould focus on refining the AHIand SpO2 nadir cutoffs for severeOSAS. In addition, it may be possi-ble to glean other predictive infor-mation from the PSG, such as theextent of hypoventilation, the per-cent sleep time spent with SpO2<90%, the frequency of desatura-tion events, the length of apneasand hypopneas, and the presenceof central apneas, to create formu-lae for risk scores.

CPAP

At the time of the previous report,there were few prospective studies onCPAP use in children, although severalretrospective studies indicated thatCPAP was efficacious in the treatmentof pediatric OSAS. Since that time,there have been at least 7 recent

studies evaluating the use of positiveairway pressure (PAP) in children andadolescents who have OSAS. One ofthese was a randomized trial with lowpower (level II),142 and others werecase series without controls (level IV).A descriptive study examined the useof behavioral intervention in improv-ing CPAP adherence.143 In addition,a level III study described use ofa high-flow nasal cannula as an al-ternative to CPAP.144 In contrast to theprevious guidelines, several of thecurrent studies obtained objectiveevaluation of CPAP adherence by down-loading usage data from the CPAPdevice. In most studies, CPAP ther-apy was instituted for persistentOSAS after AT; in many cases, thepatients had additional risk factorsfor OSAS, such as obesity or cranio-facial anomalies.

A multicenter study (level II) evaluatedPAP in 29 children who were randomlyassigned either CPAP or bilevel positiveairway pressure (BPAP).142 Patientsdemonstrated significant improvementin sleepiness, snoring, AHI, and oxyhe-moglobin saturation while using PAPduring the 6-month follow-up period.However, approximately one-third ofpatients dropped out, and of thosewho used PAP, objective adherencewas 5.3 ± 2.5 hours/night. Parentsoverestimated the hours of PAP usecompared with the devices’ actualobjective recordings of use. Therewas no significant difference in ad-herence between the CPAP and BPAPgroups. A retrospective chart reviewof 46 children started on PAP forOSAS that persisted after AT alsoshowed significant improvement insymptoms of OSAS as well as inpolysomnographic parameters (levelIV).145 Seventy percent of patientswere considered adherent. Parentalreport of adherence was most di-vergent from the machines’ recordingin the least adherent patients. More




than one-half of the children hadcomplicating factors, such as Downsyndrome and Prader-Willi syn-drome.145 Another study of a hetero-geneous group of patients displayedvarying CPAP adherence, with 31 of 79children showing continued CPAP use(level IV).146 A small, nonblinded ret-rospective study (level IV) suggestedthat adherence to CPAP could beimproved with behavioral techniquesif the family accepted the inter-ventions.143

A retrospective review described 9children who successfully used BPAPin the intensive care setting becauseof respiratory compromise after AT.147

Another retrospective review describedthe successful use of CPAP in 9 patientsof a heterogeneous group of 18 chil-dren aged <2 years.148 A nonran-domized, prospective level III studyof 12 children who had OSAS treatedin the sleep laboratory with a high-flow open nasal cannula system asan alternative to formal CPAP dem-onstrated an improvement in oxyhe-moglobin saturation and arousals, butnot AHI, compared with baseline.144

There was a decrease in sleep effi-ciency with the cannula comparedwith baseline. Long-term use anduse in the home situation were notassessed.

In summary, several studies (levels II–IV) have confirmed earlier data dem-onstrating that nasal CPAP is effectivein the treatment of both symptomsand polysomnographic evidence ofOSAS, even in young children. How-ever, adherence can be a major bar-rier to effective CPAP use. For thisreason, CPAP is not recommended asfirst-line therapy for OSAS when AT isan option. However, it is useful inchildren who do not respond ade-quately to surgery or in whom sur-gery is contraindicated. Patient andfamily preference may also be aconsideration (eg, in families with

religious beliefs against surgery orblood transfusions). Objective assess-ment of CPAP adherence is importantbecause parental estimates of useare often inaccurate. If the patient isnonadherent, then attempts should bemade to improve adherence (eg, byaddressing adverse effects, by usingbehavior modification techniques), orthe patient should be treated withalternative methods. A study de-scribed in the previous report notedthat CPAP pressures change over timein children, presumably because ofgrowth and development.149 There-fore, it is recommended that CPAPpressures be periodically reassessedin children.

At this time, data are insufficient tomake a recommendation on the use ofhigh-flow, open nasal cannula systems.


� Efficacy of CPAP use as a first-linetreatment of obese children.

� Determinants of CPAP adherenceand ways to improve adherence.

� Long-term effects of CPAP, particu-larly on the development of theface, jaw, and teeth.

� Changes in CPAP pressure overtime, and the frequency with whichthis needs to be monitored.

� Development of pediatric-specificdevices and interfaces.

Medications

There have been several studiesevaluating the use of corticosteroidsand leukotriene antagonists in thetreatment of OSAS. An older studyshowed no therapeutic effect of sys-temic steroids on OSAS.150 Since then,3 studies (1 level I, 1 level II, and 1level III) have evaluated topical nasalsteroids as treatment of OSAS, 1 levelII study has evaluated montelukast,and 1 level IV study has evaluateda combination thereof. An additional

level I study evaluated the effect ofintranasal steroids on adenoidal sizeand symptoms related to adenoidalhypertrophy but did not include PSGin the evaluation.151

A small, level II, randomized, double-blind trial,152 a level I, randomized,double-blind trial of 62 children,153

and a nonrandomized, open-label levelIII study of intranasal steroids154 allshowed a moderate improvement inpatients who had mild OSAS. However,significant residual OSAS remained in2 of the studies. Berlucchi et al151

reported an improvement in symp-toms of adenoidal hypertrophy, in-cluding snoring and observed apnea,but did not obtain objective evidenceof improvement in OSAS. Two studiesshowed shrinkage of adenoidal tis-sue.151,153 All studies were short term(2–6 weeks), although 1 study showedpersistent improvement 8 weeksafter discontinuation of the steroids(Table 18).153

An open-label, nonrandomized, 16-weeklevel IV study of montelukast in chil-dren who had mild OSAS found a sta-tistically significant but small changein the AHI (AHI decreased from 3.0 ±0.2 to 2.0 ± 0.3; P = .017).82 Anothersmall, open-label, nonrandomized,12-week level IV study of combinedmontelukast and nasal steroids founda mild but statistically significantimprovement in AHI in children whohad mild OSAS (AHI decreasedfrom 3.9 ± 1.2/hour to 0.3 ± 0.3/hour;P < .001).155

In summary, several small level Ithrough IV studies suggest that topicalsteroids may ameliorate mild OSAS.However, the clinical effects are small.On the basis of these studies, in-tranasal steroids may be consideredfor treatment of mild OSAS (defined,for this indication, as an AHI <5/hour,on the basis of studies described inTable 18). Steroids should not be usedas the primary treatment of moderate


or severe OSAS. Because the long-term effects of intranasal steroidsare not known, follow-up evaluation isneeded to ensure that the OSAS doesnot recur and to monitor for adverseeffects. Of note, no studies specificallyevaluated children who had atopyor chronic rhinitis, although 1 studymentioned that similar improvementswere seen in children who hada history of allergic symptoms com-pared with those without.153 Furtherstudy to determine whether childrenwho have atopy are more likely torespond to this therapy is needed.Data are insufficient at this time torecommend treatment of OSAS withmontelukast.


� What is the optimal duration of in-tranasal steroid use? All trialshave been short-term with ashort-term follow-up. Does theOSAS recur on discontinuation oftherapy? How often should objectiveassessment of treatment effects beperformed?

� What is the efficacy of intranasalsteroids in children who havechronic or atopic rhinitis?

� How do the benefits and adverseeffects of long-term nasal steroidscompare with surgery?

� Larger studies, stratified for se-verity of OSAS and controlled forobesity, to determine whetherOSAS is associated with systemicinflammation

� Will these biomarkers be good out-come measurements for treatmentstudies? Do they correlate withclinical outcomes or long-termprognosis?

Rapid Maxillary Expansion

Rapid maxillary expansion has re-cently been used to treat OSAS in selectpediatric populations. It is an ortho-dontic procedure designed to increasethe transverse diameter of the hardpalate by reopening the midpalatalsuture. It does this by means of a fixedappliance with an expansion screwanchored on selected teeth. After 3 to 4months of expansion, a normal min-eralized suture is built up again. Theprocedure is typically used only inchildren with maxillary constrictionand dental malocclusion. Two caseseries without controls (level IV) haveevaluated this procedure as a treat-ment of OSAS in children. One studydescribed 31 patients selected from anorthodontic clinic; 4 months aftersurgery, all patients had normalizedAHI.156 Another screened 260 patientsin a sleep center to find 35 that wereeligible; only 14 were studied.157 Therewas a significant improvement insigns and symptoms of OSAS as wellas polysomnographic parameters. Insummary, rapid maxillary expansionis an orthodontic technique that holdspromise as an alternative treatmentof OSAS in children. However, data areinsufficient to recommend its use atthis time.


� A randomized controlled trial toassess the efficacy of rapid maxil-lary expansion in the treatment ofOSAS in children.

Positional Therapy

Several level IV, retrospective studiesevaluated the effect of body positionduring sleep on OSAS. The studies hadconflicting results. One study foundthat young children had an increasedAHI in the supine position,158 and an-other study found that young childrendid not have a positional change inAHI but older children did.159 Anotherstudy found an increased obstructiveapnea index but not AHI (except in theobese subgroup) in the supine posi-tion,160 whereas a study of obese andnonobese children, which controlledfor sleep stage in each position, foundthat AHI was lowest when childrenwere prone.161 No study evaluatedthe effect of changing body positionsor the feasibility of maintaining achild in a certain position overnight.Therefore, at this point, no recom-mendations can be made with regardto positional therapy for OSAS inchildren.

Other Treatment Options

Specific craniofacial procedures, suchas mandibular distraction osteogen-esis, are appropriate for select chil-dren with craniofacial anomalies.However, a discussion of these chil-dren is beyond the scope of this

TABLE 18 Studies of Antiinflammatory Medications for the Treatment of OSAS

Medication Source Level No. Duration, wk Randomized Placebo-Controlled

BaselineAHI (per h)

AHI on Treatment(per h)

P

Intranasal steroids Brouillette et al152 II 13 OSAS 6 Yes Yes 10.7 ± 9.4 5.8 ± 7.9 .0412 controls

Intranasal steroids Alexopoulos et al154 III 27 OSAS 4 No No 5.2 ± 2.2 3.2 ± 1.5 <.001Intranasal steroids Kheirandish-Gozal

and Gozal153I 62 OSAS 6; crossover Yes Yes 3.7 ± 0.3 1.3 ± 0.2 <.001

Montelukast Goldbart et al82 IV 24 OSAS 16 No No 3.0 ± 0.2 2.0 ± 0.3 .01716 controls

Intranasal steroids +montelukast

Kheirandish et al155 IV 22 OSAS 12 No No 3.9 ± 1.2 0.3 ± 0.3 <.00114 controls




guideline. Minimal experience is avail-able regarding intraoral appliances inchildren.162 A tracheotomy is extremelyeffective at treating OSAS but is as-sociated with much morbidity and istypically a last resort if CPAP andother treatments fail to offer im-provement for a child who has severeOSAS.

OBESITY AND OSAS

This section reviews the evidence re-garding the relationships betweenobesity and SDB (this term is used toencompass both snoring and OSAS,especially in studies that did not dis-tinguish between these entities) in thepediatric population. The prevalence ofchildhood obesity is increasing,163 andmany studies on obesity and OSAShave been published since the lastguideline. Because childhood obesityhas a major impact on OSAS, it isdescribed in detail in this report.Obesity is defined as BMI >95th per-centile for age and gender.

Epidemiology: Obesity as a RiskFactor for Snoring and OSAS

A number of large, cross-sectional,community-based studies includingmore than 21 500 children have ex-amined the risk of SDB conferred byoverweight and obesity (Table 19). Themajority of these studies obtained in-formation regarding potential SDBfrom questionnaires, but some in-cluded objective measurements suchas oximetry or overnight PSG. Simi-larly, many studies based the de-termination of BMI on data fromquestionnaires. The ages ranged from6 to 17 years, consistent with re-cruitment strategies using localschools. Countries from around theworld are represented, includingNorth America, Asia, Europe, and theMiddle East. Taken together, thesestudies indicate that the risk ofsnoring in children is increased

twofold to fourfold with obesity (de-fined as BMI ≥90th or 95th percen-tile). When analyzed, BMI was found tobe an independent risk factor forsnoring.

Several studies based on surveysof thousands of children, in some casessupplemented by use of physical ex-aminations, showed that overweight/obesity was associated with an in-creased prevalence of snoring (Table19).47,164–167 Fewer studies that in-cluded objective measurements toidentify SDB were available. Twopopulation-based studies using PSGdemonstrated a relationship betweenoverweight/obesity and OSAS.11,12 Incontrast to the findings of the major-ity of studies, Brunetti et al23 foundthat although HS was more prevalentin obese children in a sample ofschoolchildren, there was no differ-ence in the incidence of OSAS onPSG among the subset of normal-weight, overweight, and obese chil-dren who have HS who had abnormalovernight oximetry results. Similarto the population-based studies,studies using case series or sub-jects recruited from sleep disordersprograms (some of which use PSGand some of which use surveys)also showed a relationship betweenweight and SDB.168,169

From these studies, it can be con-cluded that obesity is an independentrisk factor for snoring and OSAS. Therange of evidence from individualstudies was II to III (Table 19) and onthe aggregate rise to level I. Thestudies reported on large numbers ofchildren recruited from community-based samples, some of whom hadface-to-face examinations and meas-urements. Data obtained in differentsettings yielded similar results. Theimpact of race, if any, is not yet clear.Population-based studies of Hispanicchildren, a group at high risk of obe-sity and related comorbidities, are not

yet available.163 For the clinician, it isrecommended that particular atten-tion is needed for screening obeseand overweight children for signsand symptoms of OSAS, with a lowthreshold for ordering diagnostictests. Future research should focus onpopulation-based studies, with objec-tive measurements of both measuresof adiposity and PSG, and should in-clude larger numbers of AfricanAmerican and Hispanic youth.

Predictors of Obesity-Related SDB

A number of program-based studiesprovide information regarding thepredictors for SDB in obese chil-dren. Carotenuto et al88 reported viadata gathered from parental ques-tionnaires that in obese subjects re-ferred for obesity evaluation andnonobese controls randomly selectedfrom schools, the waist circumferencez score correlated with symptoms ofSDB (R = 0.37, P < .006) but BMI andsubcutaneous fat did not (level III).Verhulst et al170 examined 91 consec-utive overweight or obese childrenreferred for PSG and found that OSASwas not related to indices of obesity,including bioelectric impedance anal-ysis fat mass (level III). Central apneawas significantly predicted by usingBMI score, waist circumference, waist-to-hip circumference ratio, and per-cent fat mass. Tonsillar size was theonly significant correlate in theirmodel for moderate to severe OSAS. Ina retrospective review of 482 Chinesechildren referred for PSG and evalu-ated by using BMI and a tonsillargrading scale, the group of 111 obesechildren had a significantly highermedian AHI and percentage with AHI>1.5/hour than did the nonobesegroup (level III).171 In a regressionanalysis of log AHI as dependent var-iable, BMI and tonsil grade were pre-dictors, but age and gender were not.In a large study of schoolchildren in


TABLE19

Risk

ofSDBConferredby

OverweightandObesity

Source

Level

Type

ofStudy

No.

Duration

Diagnostic

Technique

OtherFeatures

Findings

PforObesity

asaRisk

Factor

Urschitzet

al164

IICommunity-based

sampleof

thirdgraders

1144

1y

Parental

report

ofsnoring,

BMI,SES,risk

factorsfor

rhinitis,asthma

Habitual

snorersreassessed

at1y,with

49%

continuing

tosnore

BMI≥

90%

conferreda4tim

eshigher

risk

ofHS

versus

aBM

I<75%;25%

ofobesesubjects

hadHS

Corboet

al166

IICommunity-based

sample

of10-to

15-y-old

children

from

10schools

2439

2y

Parental

questionnaire

and

nasalexam

inationandBM

Iby

physician

Snoringincreasedsignificantlywith

BMI

>90%

andwas

>2tim

esforBM

I>95%

vs<75%

.000

Shin

etal47

IVCross-sectionalcommunity-

basedsampleof

high

school

students

3871

NAQuestionnaire

(testedfor

reliability)

completed

bysubject,caretakers,and

sleeppartner

Korean

children;81%

response

rate

tosurvey

Snoringfrequencywas

significantly

associated

with

increasing

BMI

<.001

Bidadet

al167

IICross-sectionalstudyof

11-to

17-y-old

children

3300

NAScripted

face-to-face

interview

andmeasurements

ofBM

Iandtonsilsize

byphysician

7.9%

ofsamplewith

HS(≥

3nights

perweekwhenwell)

>Twofoldrisk

ofsnoringin

overweight

orobesity

Stepanskiet

al168

IIICase

series;

190

NAClinical

interview,P

SG68%

with

SDB(≥5AHI,

<90%

SpO 2,sleep

fragmentation,

ECG

changes)

BMIw

ashigher

intheSDBgroup

<.01

meanage:5.9±

3.7y

Rudnicket

al169

IIIComparedchildrenscheduled

forAT

with

controlgroup

from

sameurbansetting

170SDB

NABM

I,ethnicity

AfricanAm

erican

childrenwho

hadSDB

weremorelikelyto

beobesethan

AfricanAm

erican

childrenwho

did

nothave

SDB

<.02

129controls

Liet

al12


13primaryschools

6447

byquestionnaire

NAQuestionnaire

inallwith

PSG

andexam

inationin

high-risk

groupandlow-risksubset

forcomparison

Hong

Kong

9172

sampled

with

70%

response

rate

Malegender,B

MI,andAT

size

were

independently

associated

with

OSA

410high

risk

and209

lowrisk

with

exam

andPSG

Liet

al172


13primaryschools;same

populationas

previous

study

6349

NAQuestionnaire

Designed

todeterm

ine

prevalence

ofHS

and

associated

symptom

s.

Prevalence

ofHS

was

7.2%

;malegender,

BMI,parental

HS,n

asal

allergies,

asthmawereassociated

with

snoring

<.0001

Brunettiet

al23

IICross-sectional;mean

age7.3y

1207

screened,809

eligible

NAQuestionnaire

inallfollowed

byoximetry

inthe44

who

hadHS;PSG

insubset

who

hadabnorm

aloximetry

results

Southern

Italy

HSmorecommon

intheobesegroup;

nodifferencein

OSAby

PSGacross

weightgroups

.02

Bixler

etal11


grades

K–5

5740

hadquestionnaire

NAQuestionnaire

followed

byPSGin

subset

Prevalence

ofAHI>

51.2%

.Strong

linearrelationship

betweenwaist

circum

ference

andBM

Iwith

SDB

Waistcircum

ferenceassociated

with

all

levelsof

SDB,

also

nasalcomplaints

andminority

race

700random

lyselected

forPSG,

490completed

Urschitzet

al165

IIICross-sectionalcommunity-

basedof

primary

schoolchildren

995

NAOvernightoximetry

Overweight,sm

okeexposure,

respiratoryallergieswere

independentrisk

factorsforsleep

hypoxemia

AT,adenotonsillar;K,kindergarten;

NA,not

available;OSA,obstructivesleepapnea.




Hong Kong, Li et al reported that malegender, BMI score, and tonsillar sizewere independently associated withOSAS (level II).12,172 In 490 US school-children studied by using overnightPSG, Bixler et al11 found waist cir-cumference to be an independent riskfactor for all levels of severity ofOSAS (level II). Urschitz et al165 stud-ied 995 children in a cross-sectional,program-based study in Germany anddivided those with SDB into mild (SpO2nadir 91%–93%), moderate (<90%),and recurrent hypoxemia (>3.9 epi-sodes of desaturation per hour ofsleep) groups (level III). Overweight(BMI >75th percentile) was found tobe an independent risk factor formild, moderate, and recurrent hypox-emia during sleep.

From these studies, it is observed thatthe distribution of body fat may bemore important in predicting SDB thanBMI alone. In addition, tonsillar size isimportant in predicting SDB, even inobese children. The authors of thesearticles comment that SDB is likelymore complicated in obese children,with obesity contributing to gas ex-change and respiratory pattern ab-normalities. Obesity can result indecreased lung volumes, abnormalcentral nervous system ventilatoryresponses, decreased upper airwaycaliber, a potential impact of leptin onventilation, and other factors. Takentogether, the strength of the evidencefor these study findings is level II.Findings are limited by the fact thatcontrols were drawn from differentpopulations than subjects and that thestudies did not all reach the sameconclusions regarding the impor-tance of body fat distribution. Thelatter may have been affected by theuse of different measurement tech-niques. Anthropomorphic measurementthresholds that indicate increased riskfor SDB in children would be of useto clinicians. It is recommended that

clinicians consider fat distribution(eg, waist circumference) and not justBMI in their assessment of the risk ofSDB.

Comorbidities: InteractionsBetween Obesity and SDB

Cardiovascular

Adults who have SDB and are obeseare at increased risk of cardiovasculardisease, including systemic hyperten-sion and blunting of the normal de-crease in BP during sleep (nocturnaldipping). This section deals with theevidence that children and adoles-cents who are obese and have SDBmay be similarly at risk. Six studiesevaluating SDB, obesity, and cardio-vascular complications in children areavailable. Reade et al173 retrospec-tively evaluated 130 patients referredfor PSG and described 56 obese sub-jects (BMI >95th percentile), of whom70% had hypertension and 54% hadOSAS (level IV). Among the 34 non-obese subjects, only 8% (P < .0005)had hypertension and 29% had OSAS(P < .05). The authors concluded thatBMI was a significant determinant ofboth SDB and diastolic BP, with thenumber of hypopneas predictive ofdiastolic BP in both weight categories.In a community-based sample of 760Greek children evaluated by usingmorning BP measurements, BMI, anda questionnaire regarding sleep hab-its, Kaditis et al174 identified 50 chil-dren who had HS (level IV). They foundthat 28% of the children in the HSgroup were obese versus 15% ofnonsnoring children (significance notreported). They reported that HS hadno impact on BP, but that age, gender,and BMI were significant covariatesin predicting systolic BP; inclusionof HS in this analysis did not affectthese relationships. Similar findingswere identified for diastolic BP, withthe exception that age had no effect.This study compared absolute BP

measurements rather than the vari-ance from normal values on the basisof race, age, gender, and body size.Because children from 4 to 14 years ofage were included, this may have af-fected the results and conclusions.Kohyama et al175 examined 32 Asiansubjects referred for PSG and mea-sured overnight BP every 15 minutes.In this study, obstructive apneas andhypopneas were identified indirectlyand, thus, could have been under-estimated or overestimated comparedwith studies with more direct meas-urements of airflow (level IV). Subjectswere divided into low (<10 obstructiveevents per hour; 16 subjects) and highAHI (>10 obstructive events per hour;7 subjects). Of the total, 23 subjectstolerated the BP measurements. Threesubjects were obese. BMI predicted thesystolic BP during rapid eye movementsleep (P < .001) but did not predict anyof the diastolic BP indices. Li et al176

performed a population-based study of306 Asian children 6 to 13 years of agewho had overnight PSG and ambula-tory day and night BP measurements(level III). Children who had primarysnoring were excluded, and those whohad OSAS were divided into normal,mild, and moderate (AHI >5) groups.Multiple linear regression analysisrevealed significant associations forthe severity of hypoxemia and AHI withday and night BP, respectively, in-dependent of obesity. Although BPlevels both awake and asleep in-creased with the severity of OSAS,obesity and waist circumference par-tially accounted for elevations in sleepsystolic BP and sleep mean arterialpressure but not for diastolic BPmeasurements. Amin et al177 studied88 children who had OSAS ranging inseverity from mild to severe and 52controls matched for age and gender.They used PSG, ambulatory BP meas-urements, and actigraphy (level III).The obese SDB group, compared withthe nonobese SDB group, had higher


waking systolic BP (P < .001) andsleeping systolic BP (P = .02) afteradjusting for severity of SDB. Theyconcluded that there was no differ-ence between the effects of SDB andobesity on waking systolic or diastolicBP or sleeping systolic BP but did findthat SDB had a greater contribution tosleeping diastolic BP than did obesity.

In summary, this group of articlesdemonstrates that both obesity andSDB are associated with increased dayand night BP in children, althoughhypertension per se is rare (aggregateevidence level III). It seems that aftercontrolling for obesity, significant in-dependent effects of SDB remain andthat hypoxemia and the frequency ofobstructive events, perhaps via sleepdisruption or intrathoracic fluid shifts,are important. Practitioners should beaware that children and adolescentswho have OSAS are at increased risk ofelevated BP. Future studies wouldbenefit from a treatment arm to de-termine whether BP improves withresolution of sleep apnea, as well aslongitudinal studies to determine theimpact of pediatric obesity related–SDB on adult hypertension.

Metabolic

Obesity is a risk factor for impairedglucose tolerance, liver disease, ab-normal lipid profiles, and other met-abolic derangements. OSAS has beenexplored as a possible contributorto these metabolic abnormalities.Ten articles were reviewed. Verhulstet al178 studied 104 overweight/obesechildren and adolescents with Tannerstaging, overnight PSG, oral glucosetolerance testing, lipid profile, and BPmeasurements (level IV). The subjectswere divided into normal, mild, andmoderate/severe SDB groups. Find-ings consistent with the metabolicsyndrome were present in 37%. Thosewho had a moderate degree of SDBhad a higher BMI z score than the

normal group, and the waist-to-hipcircumference ratio increased acrossthe 3 SDB groups. The severity ofSDB was independently correlatedwith impaired glucose homeostasisand worse lipid profile. Mean SpO2and SpO2 nadir during sleep weresignificant predictors of the meta-bolic syndrome (P = .04 for both). Acommunity-based cohort of 270 ado-lescents was studied by Redlineet al179 using PSG, oral glucose toler-ance testing, homeostatic modelassessment (HOMA [a measure of in-sulin sensitivity]), BMI, waist circum-ference, BP measurements, Tannerstage, sleep diary, SES, and birth his-tory (level II). Metabolic syndrome wasdefined as having at least 3 of thefollowing 5 features: (1) waist cir-cumference >75% of normal; (2)mean BP or diastolic BP >90% ofnormal or receiving current therapyfor hypertension; (3) elevated trigly-cerides; (4) low high-density lipopro-tein; or (5) abnormal oral glucosetolerance or fasting glucose testresults. Twenty-five percent of thesample was overweight, and 19%were deemed to have metabolic syn-drome. The authors found that chil-dren who had metabolic syndromehad more severe hypoxemia and de-creased sleep efficiency and that asAHI severity increased, there wasa progressive increase in the numberof children who had metabolic syn-drome (P < .001). Both overweightchildren and those who had metabolicsyndrome were more prevalent in theSDB group (P < .001) and more weremale. Age, race, birth history, and SESdid not vary with SDB. With adjust-ment for BMI, the SDB group hadhigher BP, fasting insulin, and moreabnormal HOMA and lipid profile. Theyconcluded that adolescents who ex-perience SDB are at a sevenfold in-creased risk of metabolic syndromeand that the relationship is notexplained by gender, race, or SES and,

furthermore, persists with adjustmentfor BMI percentile.

A study by Kaditis et al180 of 110 chil-dren (2–13 years of age) referred forsnoring did not find an impact of SDBon glucose homeostasis in nonobesechildren. The subjects were dividedinto AHI ≥5/h and <5/h; the authorsfound no difference in HOMA, insulin,glucose, or lipid concentrations betweenthe 2 groups (level III). There was norelationship identified between PSGindices and HOMA or fasting insulin.BMI, age, and gender were significantpredictors for fasting insulin andHOMA in multiple linear regressionanalysis. They speculated that OSASmay have more detrimental effects inobese than in nonobese young sub-jects. Similarly, Tauman et al181 stud-ied 116 subjects referred for PSG,one-half of whom were obese, and19 nonsnoring controls. The authorsfound no impact of SDB indices onmetabolic parameters (level III). OnlyBMI and age were important, andthere was no relationship betweenSDB and surrogate measures of in-sulin resistance. They concluded thatobesity was the major determinant ofinsulin resistance and dyslipidemia. Inobese children, data from de la Evaet al182 demonstrated that the severityof OSAS correlated with fasting insulinlevels, independent of BMI (level III). Ofnote, the study by Redline et al179 in-cluded children older than those inthe studies by Kaditis et al180 andTauman et al181; thus, the variation inthe findings may be a function of thelength of time SDB had been presentor perhaps attributable to the stronginfluence puberty has on glucose ho-meostasis. Kelly et al183 compared 37prepubertal and 98 pubertal childrenin a study by using PSG, HOMA, adi-ponectin (an insulin-sensitizing hor-mone secreted by adipose tissue)measurements, as well as urinarycatecholamine metabolites (level III).




Tanner stage was determined by self-attestation. In the prepubertal chil-dren, they found no associationbetween polysomnographic parametersand metabolic measurements aftercorrecting for BMI. Elevated fastinginsulin (≥20 μU/mL) was significantlymore common in the OSAS group (P =.03), even when corrected for BMI.When pubertal obese subjects wereconsidered separately, the risk of el-evated fasting insulin (P = .04) andimpaired HOMA was greater in theOSAS group (P = .05). Pubertal chil-dren who had OSAS also had loweradiponectin and higher urinary cate-cholamine levels, even when con-trolled for BMI. Kelly et al concludedthat OSAS further predisposes obesechildren to metabolic syndrome, likelythrough multiple mechanisms involv-ing adipose tissue and the sympa-thetic nervous system.

In a study that included pretreatmentand posttreatment measurements in62 prepubertal children who hadmoderate to severe OSAS, Gozal et al184

found that although nonobese chil-dren had no change in measures ofglucose homeostasis after treatmentof OSAS, obese children had a signifi-cant improvement even while BMIremained stable (P < .001) (level II).Similar effects were not seen in non-obese children. Treatment (AT) improvedthe lipid profile and inflammatorymarkers in both obese and nonobesechildren.

Other studies have examined differentaspects of altered metabolism inobesity-related OSAS. Kheirandish-Gozal et al185 found elevated alaninetransaminase (a marker for fattyliver) in a large sample of obesechildren who had OSAS (level IV).Verhulst et al186 found elevated serumuric acid (a marker of oxidativestress) in 62 overweight children whohad OSAS, with a significant relation-ship between the severity of OSAS and

serum uric acid independent of ab-dominal adiposity (P = .01) (level IV).Verhulst et al187 demonstrated that, ina group of 95 obese and overweightchildren, total white blood cell andneutrophil counts increased withhypoxemia, and they speculated thatinflammation may contribute to car-diovascular morbidity in obesity-relatedSDB (level IV).

In summary, as expected, this group ofstudies confirms that obesity increa-ses the risk of insulin resistance,dyslipidemia, and other metabolicabnormalities in children. The role thatOSAS plays in altering glucose me-tabolism is still not entirely clear but islikely less important in younger chil-dren and in lean children. Conflict-ing studies exist regarding theindependent effect of OSAS on meta-bolic measures when it coexists withobesity in children. Puberty has animportant role in this relationship.Screening of obese children who haveOSAS for markers of metabolic syn-drome should be considered, espe-cially in the adolescent age group.Individual studies were level II throughIV, with an aggregate level of III.

Neurobehavioral

The neurobehavioral complications ofOSAS are discussed in detail elsewherein this technical report. However, 6studies have explored the potentialcontribution of obesity to behavior andcognition in children with OSAS andwill be discussed in this section. Asubanalysis of the Tucson Children’sAssessment of Sleep Apnea Studyevaluating parent-rated behavioralproblems in overweight children be-fore and after controlling for OSASwas performed by Mulvaney et al(level II).188 They analyzed data from402 subjects, 15% of whom wereoverweight; data were derived fromhome overnight PSG, the Connersscale, and the Child Behavior Checklist

(CBCL). They found that, after con-trolling for OSAS, behaviors such aswithdrawal and social problems werehigher in obese children comparedwith nonobese children. This findingemphasizes the need to control forobesity when designing studies eval-uating neurobehavioral issues inchildren with OSAS. Chervin et al42

evaluated students in the second andfifth grades in 6 elementary schools(level IV). Only 146 of 806 surveys werereturned. Parental survey of health,race, BMI, Pediatric Sleep Question-naire, teacher-rated performance, andSES were collected. SDB was associ-ated with African American race, SES,and poor teacher ratings (P < .01),but only SES was independentlyassociated with school performance.Low SES was not associated with SDBwhen controlled for BMI. The authorsconcluded that future studies evalu-ating the relationship between schoolperformance and SDB should in-corporate direct measurements ofSES and obesity. Owens et al189 ex-amined all children evaluated ata tertiary center for sleep problemsbetween 1999 and 2005; they usedPSG, BMI, the Children’s Sleep HealthQuestionnaire, and a mental healthhistory, including the CBCL (level IV).In this study of 235 participants, 56%had a BMI >85th percentile and werethus considered overweight. Theyfound modest correlations betweenmeasures of SDB and both somaticcomplaints and social problems butnot with other behavioral complaints.Increased BMI was associated withtotal CBCL score, internalizing, so-cial, thought, withdrawn, anxious,somatic, and aggressive behaviordomains in a dose-response fashion(P = .03), thus emphasizing the needto control for obesity in future studies.Short sleep also correlated witha number of subscales on the CBCL(P < .001). Additional sleep dis-orders added to the risk of behavior


problems (P < .001). BMI predictedboth total and internalizing CBCLscores, and sleep duration predictedexternalizing scores. The presence ofan additional sleep diagnosis was thestrongest predictor of all 3 CBCLscores. They concluded that over-weight, insufficient sleep, and othersleep disorders should be consid-ered when evaluating and treatingbehavioral problems associated withSDB. Beebe et al21 studied 60 obesesubjects recruited from a weight-management program compared with22 controls; tools used included BMI;parent- and self-reported validatedsleep, behavior, and mood question-naires; actigraphy; and PSG (level IV).They reported that the obese grouphad later bedtimes (P < .05),shorter (P < .01) and more disrup-ted sleep (P < .05), more symptoms ofOSAS (P < .001), sleepiness (P = .009),parasomnias (P = .007), higher AHI(P < .01), and poorer school per-formance. Another study by Beebeet al190 of 263 overweight subjectsenrolled in a hospital-based weight-management program found a nega-tive relationship between the severityof OSAS and school performance andparent- and teacher-reported behaviorsthat persisted with adjustment forgender, race, SES, sleep duration, andBMI (level IV). Interestingly, Roemmichet al191 found a relationship betweena decrease in motor activity and in-creasing weight in overweight childrenafter surgical treatment of OSAS byusing AT (P = .03) (level IV). They hy-pothesized that a decrease in physicalactivity and “fidgeting” energy expen-diture were responsible for the weightgain. However, because obese controlswithout surgery were not studied, it isunclear whether the degree of weightgain was greater than typically seen inobese children.

In summary, these studies point toobesity as a potential important factor

in childhood performance, mood, andbehavior (aggregate level III). Clini-cians should be aware that childrenwho are obese and have OSAS mightcontinue to have difficulties in thesedomains after treatment of OSAS. It isrecommended that sleep habits andnonrespiratory sleep complaints beincluded in the evaluation and treat-ment of obesity-related OSAS. The re-lationship between SES, obesity, andOSAS is complex and adds furtheremphasis to the premise that studiesof behavior and cognition must becarefully designed and controlled.

QoL

Both obesity and OSAS can affecthealth-related QoL. Two studies haveexamined measures of QoL in childrenwho are obese and have OSAS. Ina study of 151 overweight children byCarno et al192 that used surveys of QoLand SDB and PSG, overweight youthwho have OSAS were found to havelower self- and parent-related QoL(level IV). Neither objective measuresof OSAS by PSG nor BMI correlatedwith QoL, whereas reported symptomsof OSAS did (P < .05). Similarly,Crabtree et al193 compared 85 chil-dren 8 to 12 years of age who hadbeen referred for OSAS and who un-derwent PSG, BMI, QoL ascertainment,and the Children’s Depression In-ventory with a control group withpreviously documented normal PSG(level IV). They found that OSAS did notdiffer between obese and nonobesechildren and that there was no dif-ference in QoL between children whosnore and have OSAS. The referredSDB group had lower QoL scores thanthe control group (P < .001), but theauthors found no difference betweenobese and nonobese SDB subjects orin those with OSAS versus snoring.They concluded that children whosnore have a lower QoL than non-snoring controls, and that this finding

was not related to obesity of the se-verity of SDB.

In summary, QoL is an importantoutcome measure that may be morerelated to perceived symptoms ofOSAS than measured physiologic dis-turbances of sleep and breathing, evenin the obese patient (aggregate levelIV). The impact of obesity on QoL inchildren with SDB is yet to be de-termined by using population-basedstudies and is an important outcomemeasure to be included in longitudinaland treatment studies.

Surgical Treatment of OSAS in theObese Child

Surgical treatment of OSAS in generalis discussed in detail in the technicalreport, but 5 studies have examinedthis area in obesity-related OSAS andare discussed here. Shine et al194

evaluated 19 obese patients treatedwith AT (level IV). Although OSAS im-proved significantly (P < .01), only37% of patients were deemed cured(defined as a postoperative AHI <5/hour), and 10 (53%) subjects neededCPAP postoperatively. A level IV retro-spective review by Spector et al195

included 14 patients who were mor-bidly obese who were electively sentto the ICU after AT (per policy). Onepatient needed intubation, and 2patients required BPAP. Another ret-rospective review of 26 morbidlyobese patients, all of whom were sentto the ICU after AT as per routine,found that 14 patients (54%) had anuncomplicated postoperative course,and 12 (45%) required respiratoryintervention, including 1 requiring in-tubation and 2 requiring BPAP.196

Costa and Mitchell131 evaluated theresponse to AT in a meta-analysis of 4studies that included 110 obese chil-dren who had OSAS (level III). Theyfound that OSAS improved but did notresolve after AT, with 88% of childrenhaving an AHI >1/hour and 51% of




children having an AHI >5/hour post-operatively. Apostolidou et al138 repor-ted on 70 snoring children with a meanage of 5.8 ± 1.8 years who underwentAT; 22 (31%) were obese (level IV). PSGwas performed both preoperativelyand postoperatively. They found nodifference in cure rates betweenobese and nonobese subjects whohad OSAS, by using an AHI <1/hour asthe definition of cure. However, therewas an improvement in AHI in bothgroups, and approximately 90% ofall subjects had an AHI <5/hourpostoperatively.

In summary, few studies have evalu-ated the effects of AT in the obese childwho has OSAS, and studies have beenof a low level of evidence (aggregatelevel IV). Studies suggest that the AHImay improve significantly after AT,even in obese children, supporting theidea that surgery may be a reasonablefirst-line treatment, even in obesepatients. However, better-level studiesare needed to assess the effects of ATin obese children and adolescents,including evaluation of subgroupssuch as adolescents and the morbidlyobese. A significant number of chil-dren required intubation or CPAP post-operatively, which reinforces the needfor inpatient observation in obesechildren postoperatively. Studies havenot been performed to determinewhether children at high risk who areobese and have OSAS, such as thosewith pulmonary or systemic hyper-tension, waking hypoventilation, orpathologic daytime sleepiness, maybenefit from stabilization with BPAPtherapy before undergoing AT to de-crease the risk of postoperativecomplications.

Weight Loss and Other NonsurgicalTreatments

There is a paucity of data regardingthe effects of weight loss on OSAS inchildren and adolescents. Verhulst

et al197 found that weight loss wasa successful treatment of OSAS ina group of 61 adolescents being caredfor in a residential weight loss treat-ment program (level IV). Davis et al49

studied the effects of exercise in 100overweight children by administeringthe Pediatric Sleep Questionnaire be-fore and after enrollment in a no-exercise group, a low-dose aerobicexercise program, or a high-doseaerobic exercise program for 3months (level IV). They found nochange in BMI, but 50% of child-ren who screened positive for SDBimproved to a negative screening re-sult after intervention. They foundtheir results to be consistent witha dose-response effect of exercise onimprovement in SDB (P < .001). Aca-demic achievement did not improve inconcert with changes in the PediatricSleep Questionnaire. Kalra et al198

showed a significant improvement inOSAS after bariatric surgery, in asso-ciation with a mean weight loss of 58 kg(level IV). In summary, along withmany other health-related benefits,achieving weight loss and increasingexercise seem to be beneficial forOSAS and should be recommendedalong with other interventions forOSAS in obese children and adoles-cents (aggregate level IV). However, itshould be noted that the 2 weight lossstudies involved treatment regimensthat are not commonly available to themajority of obese children. The effectsof more modest weight loss regimensrequire further evaluation.

Pulmonary Disease andObesity-Related SDB

Two studies addressed the relationshipbetween obesity-related SDB and pul-monary disease. This has been de-scribed in adults as the “overlapsyndrome,” when chronic obstructivepulmonary disease and OSAS arepresent in the same individual. As part

of the Cleveland Children’s Sleep andHealth Study, Sulit et al199 evaluatedparent-reported wheeze and asthma,history of snoring, and PSG in 788participants (level III). They found thatchildren who experienced wheeze andasthma were more likely to be obese(P = .0097) and concluded that SDBmay partially explain this finding. Theyspeculated that obesity changes air-way mechanics and that SDB may in-crease gastroesophageal reflux, leptinlevels, and cytokines and, thus, in-crease lower airways inflammation.Dubern et al200 studied 54 children whohad BMI z scores >3, 74% of whomwere pubertal, by using history, physi-cal examination, assessment of bodyfat mass, Tanner stage, HOMA, lipidprofile, leptin, pulmonary functiontests, and PSG (level IV). They con-firmed the presence of OSAS, lowerfunctional residual capacity, increasedairways resistance, lower airways ob-struction, and insulin resistance in thisgroup of morbidly obese children.Snoring and AHI correlated with BMI(P = .01) and neck/height ratio (P =.03) (adjusted for age, gender, Tannerstage, and ethnicity). Airways re-sistance correlated with snoring indexand AHI after adjustment. These stud-ies remind us that the upper airway ispart of the respiratory system and thatits function is affected by lung me-chanics. Abnormalities of pulmonarymechanics related to obesity affectOSAS and may add to abnormalities ofgas exchange during sleep. It is sug-gested that evaluation of the child whois obese and has OSAS should includea history and physical examination di-rected at the entire respiratory system,and pulmonary function testing may beindicated.


� What threshold of easily obtainedanthropomorphic measurementspredicts a significant risk of OSAS?


Overweight as well as obese chil-dren should be included in futurestudies.

� Are there additive or multiplicativeeffects of OSAS and obesity on BP?How do these relationships evolveover time, and what is the impactof genetic and racial background?Does treatment of OSAS improvehypertension in obese childrenand adolescents?

� The effect of OSAS on metabolicsyndrome in children and ado-lescents remains controversial.Future research should includetreatment arms with careful mea-surements before and after inter-ventions. Longitudinal studies thattrack changes during puberty andinto adulthood would be of in-terest.

� Further research is needed to clar-ify the effects of AT on OSAS, includ-ing evaluation of subgroups suchas adolescents and morbidlyobese patients. There should alsobe studies evaluating the use ofCPAP or BPAP before surgery inthe obese population, as a wayof stabilizing the cardiopulmonarysystem and reducing operativerisk.

� What is the effect of modestweight loss on OSAS in childrenand adolescents? Research shouldbe directed at identifying strategiesto effectively implement weightloss and exercise programs inthis population.

SUBCOMMITTEE ON OBSTRUCTIVESLEEP APNEA SYNDROME*Carole L. Marcus, MBBCh, Chairperson (sleepmedicine, pediatric pulmonologist; liaison,American Academy of Sleep Medicine; researchsupport from Philips Respironics; affiliatedwith an academic sleep center; published re-search related to OSAS)Lee J. Brooks, MD (sleep medicine, pediatricpulmonologist; liaison, American College ofChest Physicians; no conflicts; affiliated with anacademic sleep center; published researchrelated to OSAS)Sally Davidson Ward, MD (sleep medicine,pediatric pulmonologist; no conflicts; affiliatedwith an academic sleep center; published re-search related to OSAS)Kari A. Draper, MD (general pediatrician; noconflicts)David Gozal, MD (sleep medicine, pediatricpulmonologist; research support from Astra-Zeneca; speaker for Merck Company; affiliatedwith an academic sleep center; published re-search related to OSAS)Ann C. Halbower, MD (sleep medicine, pedi-atric pulmonologist; liaison, American ThoracicSociety; research funding from ResMed; affili-ated with an academic sleep center; publishedresearch related to OSAS)Jacqueline Jones, MD (pediatric otolaryngol-ogist; AAP Section on Otolaryngology–Head and

Neck Surgery; liaison, American Academy ofOtolaryngology–Head and Neck Surgery; noconflicts; affiliated with an academic otolar-yngologic practice)Christopher Lehmann, MD (neonatologist,informatician; no conflicts)Michael S. Schechter, MD, MPH (pediatricpulmonologist; AAP Section on Pediatric Pul-monology; consultant to Genentech, Inc andGilead, Inc, not related to obstructive sleepapnea; research support from Mpex Pharma-ceuticals, Inc, Vertex Pharmaceuticals In-corporated, PTC Therapeutics, and BayerHealthcare, not related to obstructive sleepapnea)Stephen Sheldon, MD (sleep medicine, gen-eral pediatrician; liaison, National Sleep Foun-dation; no conflicts; affiliated with an academicsleep center; published research related toOSAS)Richard N. Shiffman, MD, MCIS (general pe-diatrics, informatician; no conflicts)Karen Spruyt, PhD (clinical psychologist, childneuropsychologist, and biostatistician/epidemiologist;no conflicts; affiliated with an academic sleepcenter)

OVERSIGHT FROM THE STEERINGCOMMITTEE ON QUALITYIMPROVEMENT AND MANAGEMENT,2009--2011

STAFFCaryn Davidson, MA*Areas of expertise are shown in parenthesesafter each name.

ACKNOWLEDGMENTThe Committee thanks ChristopherHickey for administrative assistance.

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ISSN: 1073-0397. 60007. Copyright © 2012 by the American Academy of Pediatrics. All rights reserved. Print the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois,has been published continuously since 1948. Pediatrics is owned, published, and trademarked by Pediatrics is the official journal of the American Academy of Pediatrics. A monthly publication, it


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Diagnosis and Management of Childhood Obstructive - Pediatrics

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