DOI: 10.1542/peds.114.1.33 2004;114;33Pediatrics

Campbell, Andrew C. Goldman, J. Christopher Post and Madu RaoNira A. Goldstein, Vasanthi Pugazhendhi, Sudha M. Rao, Jeremy Weedon, Thomas F.

Clinical Assessment of Pediatric Obstructive Sleep Apnea  

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of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2004 by the American Academy published, and trademarked by the American Academy of Pediatrics, 141 Northwest Pointpublication, it has been published continuously since 1948. PEDIATRICS is owned, PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

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Clinical Assessment of Pediatric Obstructive Sleep Apnea

Nira A. Goldstein, MD*; Vasanthi Pugazhendhi, MD‡; Sudha M. Rao, MD§; Jeremy Weedon, PhD�;Thomas F. Campbell, PhD¶; Andrew C. Goldman, MD*; J. Christopher Post, MD, PhD#; and

Madu Rao, MD‡

ABSTRACT. Objective. To determine whether chil-dren with a clinical assessment suggestive of obstructivesleep apnea (OSA) but with negative polysomnography(PSG) have improvement in their clinical assessmentscore after tonsillectomy and adenoidectomy (T&A) ascompared with similar children who do not undergosurgery.

Methods. In a prospective, randomized, investigator-blinded, controlled trial, 59 otherwise healthy children(mean age: 6.3 years [3.0]; 31 boys, 28 girls) with a clinicaldiagnosis of OSA (clinical assessment score >40) wererecruited from the pediatric otolaryngology and pediatricpulmonary private offices and clinics of a tertiary care,academic medical center. A standardized assessment wasperformed on all patients, including history, physicalexamination, voice recording, tape recording of breathingduring sleep, lateral neck radiograph, echocardiogram,and PSG. A clinical assessment score was assigned. Chil-dren with positive PSG (n � 27) were scheduled for T&A,whereas children with negative PSG (n � 29) were ran-domized to T&A (n � 15) or no surgery (n � 14). Childrenwere reassessed in an identical manner at a planned6-month follow-up.

Results. Follow-up was available for 21 patients withpositive PSG, 11 patients with negative PSG randomizedto T&A, and 9 nonsurgery patients. In the randomizedsubjects, the median reduction in clinical assessmentscore was 49 (range: 32–61) for the T&A patients as com-pared with 8 (range: �9 to 29) for the nonsurgery pa-tients. Nine (82%) of the T&A patients were asymptom-atic (clinical assessment score <20) compared with 2(22%) of the nonsurgery patients.

Conclusion. Children with a positive clinical assess-ment of OSA but negative PSG have significant improve-ment after T&A as compared with observation alone,thus validating the clinician’s role in diagnosing upperairway obstruction. Pediatrics 2004;114:33–43; obstructive

sleep apnea, polysomnography, tonsillectomy, adenoidec-tomy, sleep-disordered breathing, snoring.

ABBREVIATIONS. OSA, obstructive sleep apnea; PSG, polysom-nography; UARS, upper airway resistance syndrome; T&A,tonsillectomy and adenoidectomy; BMI, body mass index; RDI,respiratory disturbance index; ROC, receiver operating character-istic; AI, apnea index.

Obstructive sleep apnea (OSA) was first de-scribed in children in the medical literatureby Guilleminault et al1 in 1975. They and

subsequent investigators described the clinical fea-tures found in children with overnight polysomnog-raphy (PSG) positive for OSA. The prevalence ofpediatric OSA has been estimated to be between 1%and 3% in preschool and school-aged children.2 Ad-ditional work in pediatric sleep disorders has shownthat sleep-disordered breathing is a continuum ofseverity from partial obstruction of the upper air-way, producing snoring, to increased upper airwayresistance syndrome (UARS) to continuous episodesof complete upper airway obstruction or OSA.3 Ton-sillectomy and adenoidectomy (T&A) is successful ineliminating obstruction in 85% to 95% of otherwisenormal children with OSA.4,5

Although the clinical effects of OSA in childrenhave been well described, reports have documentedthe inaccuracy of predicting which children withhistories and physical examinations suggestive ofOSA will have positive PSG. In 7 trials, the accuracyof clinical evaluation of pediatric OSA in predictingpositive sleep studies was poor, ranging from 30% to85%.5–11 On the basis of the published studies andbecause only 20% to 30% of snoring children havepositive PSG, the 1996 American Thoracic SocietyConsensus Committee recommended that PSG beobtained before T&A to differentiate primary snor-ing from OSA.12 Although the published studies sug-gest that clinical evaluation is inaccurate in diagnos-ing OSA in children, most of the studies used adultcriteria for interpretation of the sleep studies, whichare now recognized to be inappropriate for children.In addition, none of the studies considered the diag-nosis of UARS in the evaluations, which requiresesophageal pressure monitoring and is not routine inmost centers. Therefore, it is likely that the number ofchildren with significant sleep-disordered breathingwas underestimated in these studies, as was thevalue of clinical assessment.13

Children with a clinical assessment suggestive of

From the *Division of Pediatric Otolaryngology, State University of NewYork Downstate Medical Center, Brooklyn, New York; ‡Division of Pedi-atric Pulmonology, State University of New York Downstate Medical Cen-ter, Brooklyn, New York; §Division of Pediatric Cardiology, State Univer-sity of New York Downstate Medical Center, Brooklyn, New York;�Scientific Computing Center, State University of New York DownstateMedical Center, Brooklyn, New York; ¶Department of CommunicationScience and Disorders, University of Pittsburgh and the Department ofAudiology and Communication Disorders, Children’s Hospital of Pitts-burgh, Pittsburgh, Pennsylvania; and #Department of Pediatric Otolaryn-gology, Allegheny General Hospital, Pittsburgh, Pennsylvania.Received for publication May 27, 2003; accepted Oct 23, 2003.Dr Pugazhendhi’s current affiliation is the Department of Pediatrics, Med-ical College of Virginia, Richmond, Virginia.Reprint requests to (N.A.G.) Department of Otolaryngology, SUNY Down-state Medical Center, 450 Clarkson Ave, Box 126, Brooklyn, NY 11203.E-mail: ngoldstein@downstate.eduPEDIATRICS (ISSN 0031 4005). Copyright © 2004 by the American Acad-emy of Pediatrics.

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OSA but negative PSG are a treatment dilemma. PSGhas been considered the “gold standard” diagnostictool to determine which children with symptoms ofupper airway obstruction would benefit from T&A,12

yet numerous previous reports have shown thatchildren’s symptoms of upper airway obstructionimprove after T&A regardless of whether apnea isdocumented by PSG.5,14–18 Reports have also docu-mented improvement in children’s behavior andquality of life.19–22

Our objective was to determine whether otherwisehealthy children with a positive clinical assessmentof significant upper airway obstruction but with PSGnegative for OSA have improvement in their clinicalassessment score after T&A as compared with chil-dren who do not undergo surgery. If children with aclinical assessment of pediatric OSA but with nega-tive PSG do not improve with observation alone,then we will validate the clinician’s role in diagnos-ing significant upper airway obstruction.

METHODS

ParticipantsFifty-nine children with a clinical diagnosis of OSA were eval-

uated prospectively by a standardized history, physical examina-tion, voice recording, review of a tape recording of breathingduring sleep, lateral neck radiograph to assess adenoid size, andechocardiogram to evaluate for pulmonary hypertension. A clin-ical assessment score was assigned to each child. PSG was thenused as the gold reference standard to determine the presence orabsence of sleep apnea. Children with a positive PSG (PSG�)underwent T&A. Children with a negative PSG were randomizedto undergo T&A (PSG� T&A) or no surgery (PSG� nonsurgery).It was planned that children would be reassessed in an identicalmanner 6 months later.

Children who were between 2 and 14 years of age and weresuspected of having sleep-disordered breathing were recruitedfrom the pediatric otolaryngology private office and clinic at theUniversity Hospital of Brooklyn, SUNY Downstate Medical Cen-ter, and the otolaryngology and pediatric pulmonary clinics at theKings County Hospital Center in Brooklyn, NY, from March 1999through May 2001. Children were referred to the specialty officesby their primary care physicians for evaluation of snoring andnighttime breathing difficulties. All children were evaluated bythe principal investigator and were required to have a clinical

TABLE 1. Clinical Assessment Scores*

Clinical Feature Frequency or Severity of Symptom, Physical Finding,or Result of Ancillary Study (Score)

Nighttime symptomsSnoring Every night 4 to 6 nights per wk 1 to 3 nights per wk Never

6 4 2 0Pauses Every night 4 to 6 nights per wk 1 to 3 nights per wk Never

6 4 2 0Duration of pauses � 15 s 5 to 15 s � 5 s No pauses

6 4 2 0Chest wall motion associated

with pausesEvery night 4 to 6 nights per wk 1 to 3 nights per wk Never6 4 2 0

Gasping Every night 4 to 6 nights per wk 1 to 3 nights per wk Never6 4 2 0

Choking Every night 4 to 6 nights per wk 1 to 3 nights per wk Never3 2 1 0

Restless sleep Every night 4 to 6 nights per wk 1 to 3 nights per wk Never3 2 1 0

Night sweats Every night 4 to 6 nights per wk 1 to 3 nights per wk Never3 2 1 0

Frequent awakenings Every night 4 to 6 nights per wk 1 to 3 nights per wk Never3 2 1 0

Enuresis (for children �4 y)† Every night 4 to 6 nights per wk 1 to 3 nights per wk Never6 4 2 0

Sleeps with neck extended Every night 4 to 6 nights per wk 1 to 3 nights per wk Never6 4 2 0

Sleeps in fetal position Every night 4 to 6 nights per wk 1 to 3 nights per wk Never3 2 1 0

Daytime symptomsDaytime sleepiness Every day 4 to 6 days per wk 1 to 3 days per wk Never

6 4 2 0Morning headache Every day 4 to 6 days per wk 1 to 3 days per wk Never

3 2 1 0Irritability Every day 4 to 6 days per wk 1 to 3 days per wk Never

3 2 1 0Hyperactivity Every day 4 to 6 days per wk 1 to 3 days per wk Never

3 2 1 0Developmental delay Gross delay‡ �1 activity 1 activity None

3 2 1 0School/daytime performance§ Poor C/D B/C A/B

3 2 1 0Hypertrophy of Waldeyer’s ring

Mouthbreathing Every day 4 to 6 days per wk 1 to 3 days per wk Never6 4 2 0

Chronic rhinorrhea Every day 4 to 6 days per wk 1 to 3 days per wk Never3 2 1 0

Recurrent tonsillitis� 6 to 10/y 4 to 5/y 2 to 3/y 0 to 1/y3 2 1 0

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assessment score �40 to be included in the study (Table 1). Chil-dren with recognized craniofacial syndromes, neuromuscular dis-orders, or known cranial nerve palsies were excluded. The proto-col was approved by the SUNY Downstate Medical CenterInstitutional Review Board, informed consent was obtained fromthe parents, and a consecutive sample was recruited.

InterventionsA standardized history and physical examination were per-

formed. The history evaluated the frequency (every night, 4–6nights per week, 1–3 nights per week, never) of symptoms ofnighttime upper airway obstruction, daytime effects, and symp-toms associated with hypertrophy of Waldeyer’s ring (Table 1).The duration of apneic pauses was recorded as �15 seconds, 5 to15 seconds, �5 seconds, and none. School/daytime performancewas recorded as poor (left back or failed 1 subject), below average(C/D), average (B/C), and above average (A/B). Recurrent ton-sillitis was recorded as 6 to 10 episodes per year, 4 to 5 episodesper year, 2 to 3 episodes per year, and 0 to 1 episode per year. Anepisode of tonsillitis required a physician visit and treatment withan antibiotic.

The physical examination included the patient’s height, weight,blood pressure, presence or absence of mouthbreathing and hy-ponasality, degree of adenoid facies (open mouth, long face, man-dibular hypoplasia scored as severe, mild, absent), tonsil size, andthe ability to fog a mirror with nasal breathing (none, poor, fair,well). Body mass index (BMI) was calculated by dividing thechild’s weight in kilograms by the square of the height in meters.Hyponasality was scored as present or absent by review of a 2- to5-minute audiotape recording of patient conversation by a speechpathologist who was blinded to patient group. Tonsil size wasgraded as the reduction in pharyngeal luminal diameter: 1�, 0%to 25%; 2�, 26% to 50%; 3�, 51% to 75%; and 4�, 76% to 100% asdescribed by Brodsky.23

An audiotape recording of the child’s breathing while asleep(sleep tape) was performed during the PSG by the technician, whowas instructed to record the child’s breathing at its worst. At least20 minutes of the tape was evaluated by the principal investigatorand scored as no apnea, snoring without apneic pauses (pauses inbreathing of at least 5 seconds) or a struggling sound; moderateapnea, snoring with 5- to 10-second apneic pauses or a strugglingsound; or severe apnea, snoring with �10-second apneic pausesand a struggling sound.

The lateral neck radiographs and echocardiograms were ob-tained by standard techniques. The lateral neck radiograph wasgraded according to the degree of adenoid hypertrophy: normaladenoid pad, mild adenoid hypertrophy, moderate adenoid hy-pertrophy, and severe adenoid hypertrophy. The presence or ab-sence of pulmonary hypertension was assessed on the echocardio-gram by estimating the pulmonary artery systolic pressure fromthe tricuspid regurgitation jet using the Bernoulli equation. Thepulmonary artery systolic pressure was considered abnormalwhen it was �30 mm Hg.24 The lateral neck radiographs andechocardiograms were interpreted by clinicians who were blindedto patient group.

Clinical Assessment ScoreEach child was assigned a clinical assessment score (Table 1).

Symptoms highly suggestive of OSA (pauses, gasping, sleepingwith neck extended, daytime sleepiness) contributed more thanthose that were nonspecific (morning headache, poor school per-formance, rhinorrhea). The more frequent the symptom, thehigher the score. Enuresis was scored only for children aged 4 andabove. A score of 2 was given to all children younger than 4.Similarly, height, BMI, and blood pressure were compared withstandard percentiles for age and gender, and those at the extremescontributed more than those closer to the norm.25,26 The moresevere the adenotonsillar hypertrophy seen on physical examina-

TABLE 1. Continued*

Clinical Feature Frequency or Severity of Symptom, Physical Finding,or Result of Ancillary Study (Score)

Physical ExaminationHeight¶ �5th percentile �5th and �10th percentile �10th percentile

6 4 0Body mass index¶ �5th or �95th percentile �5th and �10th or �90th

and �95th percentile�10th or �90th percentile

6 4 0Blood pressure¶,# �95th percentile �90th and �95th percentile �90th percentile

6 4 0Mouthbreathing Present Absent

4 0Hyponasal voice Present Absent

4 0Adenoid facies Severe Mild Absent

6 4 0Tonsil size** 4� 3� 2� 0–1�

6 4 2 0Ability to fog mirror

with nasal breathingNone Poor Fair Well

6 4 2 0Sleep tape Severe apnea (snoring,

struggling sound,� 10 s pauses)

Moderate apnea (snoring,5 to 10 s pauses orstruggling sound)

No apnea (snoring,no pauses orstruggling sound)

12 6 0Lateral neck radiograph Severe adenoid

hypertrophyModerate adenoid

hypertrophyMild adenoid

hypertrophyNormal adenoid

pad6 4 2 0

Echocardiogram Pulmonaryhypertension

No pulmonaryhypertension

12 0

* Total score, sum of all the items; score �20, asymptomatic; score A, sum of items for nighttime symptoms, daytime symptoms,hypertrophy of Waldeyer’s ring, sleep tape, echocardiogram; score B, sum of items for physical examination and lateral neck radiograph.† Item scored as 2 for children � 4 years of age.‡ Gross delay: motor, speech, cognitive.§ Item scored as poor (left back or failed 1 subject), below average (C/D), average (B/C), above average (A/B).� Item scored as episodes/year.¶ Items scored as percentiles for age and gender.# Systolic and diastolic were measured; the higher percentile was scored.** Item scored for the larger of the tonsils.

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tion or demonstrated by the lateral neck radiograph, the higherthe score. A high sleep tape score or an echocardiogram demon-strating pulmonary hypertension contributed heavily to the clin-ical assessment score. In addition to the overall score, each childreceived a separate score for symptoms, sleep tape, and echocar-diogram (score A; Table 1) and physical examination and lateralneck radiograph (score B; Table 1). Surgical removal of the tonsilsand adenoids automatically lowered score B in the surgical pa-tients, whereas improvement in score A reflected only clinicalimprovement.

Although the clinical assessment score has not been previouslyvalidated against PSG, the overall score was developed from theclinical assessment used in the first author’s previous prospectivestudy of the clinical assessment of pediatric OSA.7 Clinical fea-tures were weighted more or less heavily depending on the fac-tor’s association with OSA according to the statistical analysisperformed during the previous data review. The current score alsoincluded an assessment of hyponasality as a measure of adeno-tonsillar hypertrophy27 and an objective measurement of adenoidsize from the lateral neck film. The highest possible score was 164.Children with a score �40 were considered to have OSA, childrenwith a score �20 but �40 were considered to have moderatesymptoms of upper airway obstruction but not apnea, and chil-dren with a score �20 were considered to be asymptomatic. Thesesubdivisions were based on the collective opinion of 2 pediatricotolaryngologists (Dr Goldstein and Dr Post) and a pediatricpulmonologist as well as review of the published studies.

Interobserver ReliabilityClinical assessments were performed by the principal investi-

gator for every child. Additional assessments were performed by1 or 2 independent examiners, a pediatric pulmonary fellow, andan otolaryngology resident for 25 patients. The additional assess-ments were limited to the 25 items scored by the examiningphysician and not independent evaluators (hyponasality, sleeptape, lateral neck radiograph, echocardiogram) or the nursing staff(height, weight, blood pressure). The initial assessments wereperformed before the PSG. The follow-up assessments were per-formed by the investigators who were blinded to whether thechild had had surgery. Evaluation of tonsil size was performed asthe last part of the physical examination after the remainder of theclinical assessment had been recorded. For determining interraterreliability for coding the presence or absence of hyponasality, 20conversational samples were randomly selected and rated by asecond examiner, who was blinded to the treatment status of thechild. Subject-to-subject agreement for the presence or absence ofhyponasality between the 2 raters was .90 (18 of 20).

PSGPSG was performed at the SUNY Downstate Pediatric Pulmo-

nary Function, Exercise, and Sleep Physiology Laboratories andconsisted of respiratory rate, pulse rate, pulse oximetry, inductiveplethysmography of the chest and abdomen and the mathematicalsum of the 2 for respiratory effort, and oronasal airflow from aloose mask or oral and nasal thermistors. Obstructive apnea wasdefined as the cessation of oronasal airflow with continued respi-ratory effort for at least 2.5 times the typical breath interval, andobstructive hypopnea was defined as a decrease in amplitude oforonasal airflow of at least 50% with no decrease in respiratoryeffort for the same duration. PSG was considered positive for OSAwhen the number of obstructive apneas plus hypopneas per hourof sleep (respiratory disturbance index [RDI]) was at least 5 or atleast 10% of the night was spent with oxygen saturation �90%.The 6-month follow-up PSG was analyzed by a pulmonologistwho was blinded to whether the patient had had surgery.

RandomizationRandomization was performed by using a computerized list

generated by the biostatistician in blocks of 2 to ensure equal sizetreatment groups. T&A was performed at the University Hospitalof Brooklyn or the Kings County Hospital Center by a pediatricotolaryngologist who was not 1 of the investigators.

Sample Size EstimationBecause clinical assessment of OSA has been shown to have a

positive predictive value of 50%,7 we predicted that half of the

patients enrolled would have positive PSG. Because T&A relievessymptoms of upper airway obstruction, we expected that 10% ofthe PSG� T&A children would remain symptomatic at the6-month follow-up (overall clinical assessment score �20) and that90% would be asymptomatic (overall clinical assessment score�20). We estimated that 80% of children who had negative PSGand did not undergo surgery would remain symptomatic at the6-month follow-up and that 20% would be asymptomatic. Assum-ing � of .05 and power of .9, we estimated that we would need atotal of 22 children with negative PSG to find a significant differ-ence between the patients who had negative PSG and underwentT&A and those who did not. Of the 22 with negative PSG, 11would be randomized to the surgery group and 11 to the nosurgery group. Therefore, we needed a total of 44 patients for 22to have negative PSG. Assuming that 10 (23%) patients woulddrop out, a total of 54 children were initially recruited. When thedropout rate after the recruitment of the initial 54 children was31%, an additional 5 patients were recruited to help achieve anadequate sample size.

Statistical MethodsThe initial clinical assessment scores and change in clinical

assessment scores were compared between the PSG� T&A andPSG� nonsurgery groups using the Wilcoxon rank sum test; theinitial and final PSG parameters between the PSG� T&A andPSG� nonsurgery groups were also compared using the Wilcoxontest. The proportion of patients with final clinical assessment score�20 and �40 in the PSG� T&A and PSG� nonsurgery groupswere compared using Fisher exact test. Comparisons of age andlength of follow-up between the PSG� T&A and PSG� nonsur-gery groups were performed using the Wilcoxon test; comparisonof the gender and race distributions were compared using Fisherexact test. Interrater agreement for the clinical assessment scorewas measured by intraclass correlations using 2-way randomeffects models. A mixed linear model was used to test for differ-ences among observers in mean clinical assessment scores. Thepositive predictive value of the total clinical assessment score inpredicting a positive PSG was calculated. The sensitivity, specific-ity, and positive and negative predictive values of the sleep tapescore in predicting a positive PSG were calculated, and Fisherexact test was used to determine their significance. A subset ofitems from the clinical assessment score (snoring, pauses, gasping,neck extension, daytime sleepiness, adenoid facies, sleep tape)were analyzed by logistic regression to determine the utility of theitems in predicting a positive PSG. The area under the receiveroperating characteristic (ROC) curve was used as a measure ofpredictive utility for logistic regression analysis. P � .05 wasconsidered statistically significant. SAS (SAS Institute, Cary, NC)software was used for data analysis.

RESULTSThe flow of participants through the study proto-

col is presented in Fig 1. Of the 59 children whoentered the study, 3 would not sleep in the labora-tory, so a PSG could not be obtained. Of the 56children who underwent PSG, 27 (48%) had positivePSG and 29 (52%) had negative PSG. Of the 29 chil-dren with negative PSG, 15 were randomized to T&Aand 14 were randomized to no surgery. The parentsof 3 children in the PSG� group and the parents of 2children in the PSG� T&A group refused surgery. Ahigh rate of attrition occurred during the study pe-riod as 13 (23%) of 56 were lost to follow-up beforethe final study visit. Of the 13, 8 had moved and wereunable to be contacted, and 5 refused to bring thechild back usually stating time constraints. One childin the PSG� group was excluded because his parentsrefused T&A, although he did have follow-up. Onechild in the PSG� nonsurgery group had an ade-noidectomy alone because of parental concern andwas withdrawn from the study.

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Patient demographics are presented in Table 2.The mean age of the children who completed theprotocol was between 5.8 (2.6) and 7.0 (3.6) years,depending on patient group. There were almostequal numbers of boys and girls in the study popu-lation, although more girls with negative PSG wererandomized to surgery and more boys with negativePSG were randomized to no surgery. The patientpopulation was predominantly black, which reflectsthe racial composition of central Brooklyn. Meanfollow-up after initial evaluation and after T&A ispresented in Table 3. There was no significant dif-ference in age, gender distribution, racial distribu-tion, and length of follow-up after initial evaluationbetween the PSG� T&A and PSG� nonsurgerygroups.

PSG results for the 41 children who completed theprotocol and were included in the analysis are pre-sented in Table 3. The median initial RDI was 8.8(range: 5.0–79.7) in the PSG� children, 1.5 (range:0–4.7) in the PSG� T&A children, and 1.3 (range:0–2.6) in the PSG� nonsurgery children. There wasno significant difference between the PSG� T&Achildren and the PSG� nonsurgery children in me-

dian RDI, median apnea index (AI), and medianpercentage of the night spent with oxygen saturation�90% for the initial and final sleep studies. Of thePSG� children, 2 (10%) had positive follow-up PSG.One child is undergoing treatment with nasal bilevelpositive airway pressure and the other has been lostto follow-up. The child who had an initial positivePSG and whose parents refused T&A but returnedfor follow-up evaluation had a normal study at fol-low-up. As expected, no child in the PSG� T&Agroup had a positive PSG at follow-up, although 1(11%) child in the PSG� nonsurgery group did havea positive study. T&A has been recommended.

The intraclass correlations between the principalinvestigator and the 2 independent examiners for theclinical assessment score were .80 and .65. The meantotal score for the principal investigator (50.7 [12.2],n � 60) and the independent examiners (51.9 [15.1],n � 26 and 49.0 [12.8], n � 29) did not differ signif-icantly (P � .194). An additional child who under-went a clinical assessment but was not entered intothe study because his clinical assessment score was�40 was included in these analyses.

The initial and change total clinical assessment

Fig 1. The clinical assessment of pediatric OSA: study profile, 1999–2001.

TABLE 2. Patient Demographics

Characteristic Initial Study Population With PSG(n � 56)

Patients Who Completed Protocol(n � 41)

PSG�(n � 27)

PSG� T&A(n � 15)

PSG� Nonsurgery(n � 14)

PSG�(n � 21)

PSG� T&A(n � 11)

PSG� Nonsurgery(n � 9)

Age (y; mean [SD]) 7.0 (3.6) 5.9 (1.8) 5.8 (2.6) 7.0 (3.6) 6.3 (1.8) 5.8 (2.6)Gender (n [%])

Male 14 (52) 5 (33) 9 (64) 10 (48) 4 (36) 4 (44)Female 13 (48) 10 (67) 5 (36) 11 (52) 7 (64) 5 (56)

Race (n [%])Black 21 (78) 12 (80) 10 (71) 17 (81) 10 (91) 7 (78)Hispanic 6 (22) 2 (13) 2 (14) 4 (19) 0 1 (11)Asian 0 1 (7) 1 (7) 0 1 (9) 0White 0 0 1 (7) 0 0 1 (11)

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score, score A and score B, are presented in Table 4for the 41 children who were included in the finalanalysis. The median initial total score was 77 with arange of 49 to 114 for the PSG� group. The medianinitial total score was 64 with a range of 42 to 77 forthe PSG� T&A group and 50 with a range of 40 to 64for the PSG� nonsurgery group. Although there wasno significant difference in the initial score A be-tween the PSG� T&A and PSG� nonsurgerygroups, the initial total score was significantly lowerin the PSG� nonsurgery group (P � .034) and thedifference in score B approached significance (P �.074). The median total change score (initial totalscore minus final total score) was 59 with a range of26 to 106 for the PSG� children. The total changescore was 49 with a range of 32 to 61 for the PSG�

T&A children and 8 with a range of �9 to 29 for thePSG� nonsurgery children. The total change score,score A change score, and score B change score allwere significantly higher in the PSG� T&A than thePSG� nonsurgery children (P � .001, .002, and .007,respectively).

Initially, no child in any of the groups had a totalclinical assessment score �20 or �40 (Table 5). Thefinal score was �20 for 14 (67%) children in thePSG� group, 9 (82%) children in the PSG� T&Agroup, and 2 (22%) children in the PSG� nonsurgerygroup. The final score was �40 for 19 (90%) childrenin the PSG� group, 11 (100%) children in the PSG�T&A, and 5 (56%) children in the PSG� nonsurgerygroup. The number of children with final scores �20and �40 were significantly lower for the PSG� T&A

TABLE 3. Polysomnography Results for Children Who Completed the Protocol (n � 41)

PSG Parameters Initial Final

PSG� PSG� T&A PSG�Nonsurgery

PSG� PSG� T&A PSG�Nonsurgery

n 21 11 9 21 11 9Follow-up between PSG (mo; mean [SD]) 11.3 (4.9) 8.3 (4.6) 8.8 (2.5)Follow-up after T&A (mo; mean [SD]) 7.9 (3.4) 5.4 (4.3) NARDI

Median 8.8 1.5 1.3 1.8 0.6 1.2Range 5.0–79.7 0–4.7 0–2.6 0–15.9 0–4.2 0–13.0P value* .31 .50

AIMedian 6.2 0.5 0.6 0.9 0.4 0Range 3.4–77.0 0–3.6 0–2.0 0–9.4 0–3.1 0–8.4P value* .97 1.00

% of night with oxygen saturation �90%Median 0.4 0 0 0.4 0 0Range 0–41.7 0–5.6 0–0.7 0–75.6 0–0.5 0–0.5P value* .59 .20

Positive studies (n [%]) 21 (100) 0 0 2 (10) 0 1 (11)

* Wilcoxon rank-sum test of difference between PSG� T&A and PSG� nonsurgery groups.

TABLE 4. Initial and Change Clinical Assessment Scores

Initial Score Change Score (Initial-Final)

PSG�* PSG� T&A PSG�Nonsurgery

PSG� PSG� T&A PSG�Nonsurgery

n 21 11 9 21 11 9Total score

Median 77 64 50 59 49 8Range 49–114 42–77 40–64 26–106 32–61 �9–29P value* .034 .001

Score AMedian 51 42 40 36 31 8Range 36–82 31–59 26–44 18–78 21–53 �9–22P value* .154 .002

Score BMedian 24 20 14 14 16 2Range 8–38 10–30 6–24 4–30 4–24 �2–8P value* .074 .007

* Wilcoxon rank-sum test of difference between PSG� T&A and PSG� nonsurgery groups.

TABLE 5. Initial and Final Clinical Assessment Scores �20 and �40

Initial Score Final Score

PSG� PSG� T&A PSG�Nonsurgery

PSG� PSG� T&A PSG�Nonsurgery

No. of Patients with a score �20, % 0/21 (0) 0/11 (0) 0/9 (0) 14/21 (67) 9/11 (82)* 2/9 (22)*No. of Patients with a score �40, % 0/21 (0) 0/11 (0) 0/9 (0) 19/21 (90) 11/11 (100)† 5/9 (56)†

Fisher exact test of difference between PSG� T&A and PSG� nonsurgery groups: * P � .022, † P � .026.

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group than for the PSG� nonsurgery group (P � .022and P � .026, respectively). The final scores for the 2PSG� children who still had positive studies at fol-low-up were 45 and 23, and the final score for thePSG� nonsurgery patient who had a positive PSG atfollow-up was 71. An intent-to-treat analysis was notperformed because all but 1 of the children who didnot receive their assigned treatment allocation werelost to follow-up.

Initial and final mean and median scores for all ofthe individual items of the clinical assessment scoreare presented in Table 6. On initial evaluation, BMI�95th percentile was found in 14 (34%) children: 9 inthe PSG� group, 3 in the PSG� T&A group, and 2 inthe PSG� nonsurgery group. At follow-up evalua-tion, BMI �95th percentile was found in 17 (41%)children: 11 in the PSG� group, 4 in the PSG� T&Agroup, and 2 in the PSG� nonsurgery group. TheBMI of all 3 children with positive PSG at final eval-uation was �95th percentile. BMI was �5th percen-tile for only 2 (5%) children at both initial and finalevaluations: 1 in the PSG� T&A group and 1 in thePSG� nonsurgery group.

Systemic hypertension was found in a total of 8(20%) children initially: 6 in the PSG� group, 1 in thePSG� T&A group, and 1 in the PSG� nonsurgerygroup. It was �95th percentile in 4 children andbetween the 90th and 95th percentile in 4 children.

Three of these children also had a BMI �95th per-centile. The hypertension had resolved by follow-upevaluation in all children, but 3 (7%) additional chil-dren (all in the initial PSG� group) developed sys-temic hypertension. It was �95th percentile in 1 pa-tient and between the 90th and 95th in the other 2children. All 3 children had negative PSG at finalevaluation, although 2 had a BMI �95th percentile.

Only 1 child had an echocardiogram suggestive ofpulmonary hypertension. The child, in the PSG�group, had a peak velocity of tricuspid regurgitationjet of 24 to 36 mm Hg, estimating right ventricularpressures of 29 to 41 mm Hg on his initial echocar-diogram. The estimated pressure gradient was 19.4mm Hg, estimating normal right ventricular pres-sures on his follow-up echocardiogram, and his fol-low-up sleep study was normal.

The positive predictive value of the initial totalclinical assessment score for predicting a positivePSG was 48% (27 of 56). Of the 27 children withpositive PSG at their initial evaluation, 10 had sleeptapes scored as severe apnea, 13 had sleep tapesscored as moderate apnea, 3 had sleep tapes negativefor apnea, and 1 did not have a sleep tape. Of the 15children in the PSG� T&A group, initial sleep tapeswere scored as severe apnea in 2 children, moderateapnea in 7 children, and negative for apnea in 6children. Of the 14 children in the PSG� nonsurgery

TABLE 6. Initial and Final Item Scores of the Clinical Assessment Score

Clinical Feature Initial Score (Mean [SD], Median) Final Score (Mean [SD], Median)

PSG� PSG� T&A PSG�Nonsurgery

PSG� PSG� T&A PSG�Nonsurgery

n 21 11 9 21 11 9Snoring 6.0 (0), 6 5.3 (1.3), 6 4.9 (1.8), 6 1.0 (1.6), 0 0.18 (0.60), 0 2.9 (2.3), 2Pauses 4.8 (1.9), 6 3.1 (1.6), 2 2.7 (1.4), 2 0.10 (0.44), 0 0 (0), 0 1.1 (1.8), 0Duration of pauses 2.4 (1.2), 2 2.2 (0.60), 2 2.0 (0), 2 0.10 (0.44), 0 0 (0), 0 0.67 (1.0), 0Chest wall motion 3.0 (2.7), 2 1.6 (2.0), 2 1.1 (1.1), 2 0.10 (0.44), 0 0 (0), 0 0.89 (1.1), 0Gasping 3.2 (2.5), 2 1.5 (1.3), 2 1.3 (1.4), 2 0 (0), 0 0 (0), 0 1.3 (2.0), 0Choking 1.5 (1.2), 1 0.64 (0.50), 1 0.33 (0.50), 0 0.05 (0.22), 0 0 (0), 0 0.56 (1.0), 0Restless sleep 2.8 (0.77), 3 2.2 (1.2), 3 2.6 (0.88), 3 1.1 (1.3), 0 1.0 (1.3), 0 1.7 (1.3), 1Night sweats 1.5 (1.4), 1 1.7 (1.3), 2 1.3 (1.3), 1 0.57 (0.93), 0 0.36 (0.50), 0 1.6 (1.1), 1Frequent awakenings 1.3 (1.2), 1 1.5 (1.1), 1 1.2 (1.2), 1 0.71 (0.78), 1 0.64 (0.92), 0 1.1 (1.1), 1Enuresis 1.4 (1.6), 2 1.5 (2.0), 0 0.89 (1.1), 0 0.67 (1.5), 0 1.3 (1.8), 0 1.1 (1.1), 2Neck extension 3.0 (2.3), 2 2.7 (2.7), 2 3.6 (2.2), 4 0.57 (1.4), 0 0 (0), 0 2.2 (2.5), 2Fetal position 1.3 (1.3), 1 0.91 (1.1), 1 0.89 (0.93), 1 0.71 (0.96), 0 0.45 (0.52), 0 0.89 (0.93), 1Daytime sleepiness 2.0 (2.4), 2 1.8 (2.3), 2 1.3 (2.2), 0 0.48 (0.89), 0 0.73 (1.3), 0 1.6 (1.9), 2Morning headache 0.43 (0.75), 0 0.64 (1.2), 0 0.22 (0.44), 0 0.19 (0.40), 0 0.09 (0.30), 0 0.22 (0.44), 0Irritability 0.86 (1.2), 0 1.3 (1.4), 1 1.1 (1.2), 1 0.57 (0.93), 0 0.36 (0.67), 0 0.78 (1.1), 0Hyperactivity 1.5 (1.4), 1 1.5 (1.3), 1 1.2 (1.4), 1 1.4 (1.3), 1 0.82 (1.3), 0 1.3 (1.6), 0Developmental delay 0.52 (1.0), 0 0.09 (0.30), 0 0.22 (0.44), 0 0.19 (0.51), 0 0 (0), 0 0.11 (0.33), 1School/daytime performance 0.62 (0.67), 1 0.91 (0.54), 1 1.1 (0.33), 1 0.57 (0.75), 0 0.55 (0.52), 1 1.1 (0.33), 1Mouthbreathing (history) 5.4 (1.4), 6 4.0 (2.4), 6 3.8 (2.7), 6 0.86 (1.9), 0 0.36 (0.81), 0 3.6 (2.4), 2Chronic rhinorrhea 0.90 (1.1), 1 0.18 (0.40), 0 1.2 (1.4), 1 0.14 (0.65), 0 0.09 (0.30), 0 0.89 (1.4), 0Recurrent tonsillitis 1.1 (1.1), 1 0.91 (1.0), 1 1.2 (0.83), 1 0 (0), 0 0 (0), 0 0.11 (0.33), 0Height 0.19 (0.87), 0 0.55 (1.8), 0 0.44 (1.3), 0 0.19 (0.87), 0 0.55 (1.8), 0 0 (0), 0BMI 2.8 (3.0), 0 2.2 (3.0), 0 2.0 (3.0), 0 3.3 (3.0), 6 3.1 (3.0), 4 2.4 (3.0), 0Blood pressure 1.4 (2.4), 0 0.55 (1.8), 0 0.44 (1.3), 0 0.67 (1.7), 0 0 (0), 0 0 (0), 0Mouthbreathing (physical

examination)3.6 (1.2), 4 2.9 (1.9), 4 2.2 (2.1), 4 0.76 (1.6), 0 0.36 (1.2), 0 1.8 (2.1), 0

Hyponasal voice 2.9 (1.9), 4 2.9 (1.9), 4 1.3 (2.0), 0 0.76 (1.6), 0 0.36 (1.2), 0 1.3 (2.0), 0Adenoid facies 2.5 (2.3), 4 3.5 (1.8), 4 0.89 (1.8), 0 1.0 (2.0), 0 0.73 (1.6), 0 0.44 (1.3), 0Tonsil size 4.3 (1.6), 4 4.2 (1.1), 4 3.8 (1.9), 4 0 (0), 0 0 (0), 0 4.0 (1.0), 4Ability to fog mirror with

nasal breathing1.9 (2.0), 2 1.1 (1.0), 2 0.67 (1.0), 0 0.29 (0.72), 0 0 (0), 0 0.44 (1.3), 0

Sleep tape 8.3 (3.5), 6 5.5 (4.2), 6 2.0 (3.0), 0 0.86 (2.9), 0 0 (0), 0 2.0 (3.0), 0Lateral neck radiograph 4.4 (1.5), 4 2.7 (1.8), 2 2.9 (2.3), 2 0.76 (1.2), 0 0.73 (1.0), 0 2.2 (1.9), 2Echocardiogram 0.57 (2.6), 0 0 (0), 0 0 (0), 0 0 (0), 0 0 (0), 0 0 (0), 0

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group, initial sleep tapes were scored as severe apneain 1 child, moderate apnea in 4 children, and nega-tive for apnea in 9 children. Thus, the sleep tape hada sensitivity of 88% (23 of 26), a specificity of 52% (15of 29), a positive predictive value of 62% (23 of 37),and a negative predictive value of 83% (15 of 18) inpredicting a positive PSG (Phi coefficient � .43, P �.002, Fisher exact test). Of the 3 children with positivePSG at the final evaluation, 1 had a sleep tape scoredas severe apnea (initial PSG� group), 1 had a sleeptape scored as moderate apnea (PSG� nonsurgerygroup), and 1 had a sleep tape negative for apnea(initial PSG� group). Of the 38 patients with nega-tive PSG at final evaluation, 3 had sleep tapes scoredas moderate apnea (all in the PSG� nonsurgerygroup), and 35 had sleep tapes scored as negative forapnea.

Logistic regression using 7 items from the clinicalassessment score (snoring, pauses, gasping, neck ex-tension, daytime sleepiness, adenoid facies, andsleep tape) as predictors was conducted. Only sleeptape was a significant predictor (P � .009); the areaunder the ROC curve was .84. A simpler modelcontaining only the sleep tape predictor was notsignificantly inferior to the full model (likelihoodratio test P � .090); area under the ROC curve for thisreduced model was .75. In other words, although thesleep tape was a moderately useful predictor, theaddition of the other items did not significantly in-crease the predictive utility.

Of the 37 children who underwent T&A, the onlymajor complication was a right thigh burn to 1 childin the initial PSG� group secondary to improperapplication of the grounding of the electrocauteryunit. The wound healed with dressing changes, butthe child was hospitalized for 3 days. Children wereobserved in the hospital for a mean of 21 (12) hoursafter surgery. Children in the PSG� T&A group whowere at least 3 years of age were usually dischargedfrom the hospital 6 hours after surgery, whereas thechildren in the PSG� group were admitted for pulseoximetry observation for 1 night unless the PSG wasconsidered mild enough to warrant a 6-hour stay.Children were observed either on the floor or in amonitored unit at the discretion of the attendingsurgeon. There were no postoperative respiratorycomplications, episodes of postoperative hemor-rhage, or readmissions to the hospital.

DISCUSSIONPSG has been recommended to differentiate chil-

dren with primary snoring from children with OSA.Children with primary snoring do not have othernighttime and daytime symptoms and have normalsleep studies. Primary snoring is considered to be abenign condition that will resolve in 50% of childrenover time.28 Snoring has been shown to progress tomild OSA in only 10% of cases.29 Children withnegative PSG have not been considered to be surgicalcandidates for treatment of upper airway obstructioneven when they have symptoms related to enlargedtonsils and adenoids.

Our results demonstrate that the signs and symp-toms of OSA improve after T&A regardless of

whether OSA is documented by PSG. At follow-up,the children in the PSG� T&A group had significantimprovement in the total clinical assessment score aswell as the subset scores as compared with childrenin the PSG� nonsurgery group. The subset scoreswere designed to separate the items that would au-tomatically be decreased after T&A (tonsil size andadenoid size on the lateral neck radiograph, score B)from the items that would solely reflect clinical im-provement (score A). Eighty-two percent of thePSG� T&A group were asymptomatic at follow-upas compared with 22% of the PSG� nonsurgery pa-tients, resulting in a statistically significant differencebetween the groups. Our findings were close to theassumptions in our sample size estimation, whichpredicted that 90% of the PSG� T&A children and20% of the PSG� nonsurgery children would beasymptomatic at follow-up. There was also a signif-icant difference between the groups in children whowere moderately symptomatic (clinical assessmentscore �20 but �40) at final evaluation. One (11%)child in the PSG� nonsurgery group developed OSAat follow-up, a finding that is comparable to the 10%reported rate of the progression of primary snoringto OSA.

A weakness of our findings is that despite ran-domization at study outset, the PSG� nonsurgerygroup had a significantly lower initial total clinicalassessment score than the PSG� T&A group. Thedifference resulted from findings on the physicalexamination (score B) as opposed to differences insymptoms (score A) and occurred because of thesmall sample size of our patient population. To cor-rect for the differences in initial clinical assessmentscores, we compared changes in clinical assessmentscores between the 2 groups at the final evaluation.

The clinical assessment score may prove to be auseful tool for the office diagnosis of pediatric OSA.Additional study to validate the score against PSGand other external measures such as quality-of-lifeinstruments is needed. Its responsiveness to longitu-dinal change must also be evaluated further. Ourstudy demonstrated a significant difference inchange scores between the PSG� T&A and PSG�nonsurgery groups using a score of �40 as the re-quirement for entry, but there also may be a role fortreatment of children with scores �20 but �40.

Although we demonstrated significant improve-ment in clinical scores, are these changes clinicallyrelevant? Snoring was only 1 of �20 nighttime anddaytime symptoms that brought these children tomedical attention. Entry into the study required aclinical assessment that revealed more than just snor-ing. Symptoms of upper airway obstruction havebeen shown to have a significant impact on chil-dren’s quality of life. De Serres et al19 administeredthe Obstructive Sleep Disorders-6 Survey, a vali-dated health-related quality-of-life instrument, to thecaregivers of 101 children from 7 tertiary care pedi-atric otolaryngology practices across the UnitedStates, before and after T&A performed for treatmentof sleep-disordered breathing. Children’s sleep-dis-ordered breathing was diagnosed on the basis ofclinical assessment as only 8% had preoperative

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sleep studies. Domains of the survey most affected atinitial evaluation were physical suffering, sleep dis-turbance, and caregiver concern. Postoperatively,90% of children had improvement in quality of life,which was considered large in 75% and moderate in6%.

Goldstein et al20 administered another validatedquality-of-life survey, the OSA-18, along with a stan-dardized measure of children’s behavior, the ChildBehavior Checklist, to the caregivers of 64 childrenbefore T&A and 3 months postoperatively. Surgerywas performed for the treatment of upper airwayobstruction in 84% of children, 92% of whom re-ceived a diagnosis on a clinical basis as only 8% hadpreoperative PSG. Postoperatively, a large change inquality of life was found for the OSA-18 domains ofsleep disturbance, caregiver concerns, and physicalsymptoms, and a moderate change was found foremotional symptoms and daytime function. As in thestudy by de Serres et al,19 the change in the impact ofsleep-disordered breathing on quality of life washighly significant after T&A. The study also foundsignificant improvement in behavioral and emo-tional difficulties after T&A as measured by theChild Behavior Checklist Total Problem Score andthe individual scales of Withdrawn, Somatic Com-plaints, Anxious/Depressed, Thought Problems, At-tention Problems, Delinquent Behavior, AggressiveBehavior, Sleep Problems, and Destructive Behavior.

As in the other studies of the accuracy of clinicaldiagnosis in predicting a positive PSG, esophagealpressure monitoring for detecting UARS was notperformed. Children with UARS demonstrate abnor-mally increased upper airway resistance, resulting inincreased respiratory effort and sleep fragmentationwithout apneic or hypopneic episodes or desatura-tion. The clinical effects of UARS are identical to OSAand treatment is the same.30 The children with neg-ative PSG in our study may have been experiencingUARS, with the resulting resolution of signs andsymptoms in those who underwent T&A. Becausethe measurement of UARS is not routine in mostcenters, children with sleep-disordered breathing areoften missed by standard PSG.13 Clinical assessmentremains a valuable tool in assessing upper airwayobstruction and sleep-disordered breathing and de-termining the need for T&A.

Our accuracy of predicting a positive PSG in chil-dren with a clinical assessment suggestive of OSA(48%) when UARS is not evaluated agrees with thefindings of previous studies of pediatric OSA.5–11

Our definition of a positive PSG was an RDI �5.Many sleep laboratories consider an AI �1 to beabnormal, based on studies of normal children.31 Ifwe considered children with an AI �1 to have ab-normal PSG, then 6 of the 15 PSG� T&A childrenand 5 of the 14 PSG� nonsurgery children wouldhave had initial positive sleep studies, increasing ourclinical accuracy to 68%. However, 13 (41%) of the 32children who underwent T&A would have had pos-itive PSG at final evaluation, which is much higherthan the published reports. Because most of the chil-dren were asymptomatic at final evaluation, an AI�1 seems too strict a definition for a positive PSG.

Using the RDI �5 as the definition of a positive PSG,10% of the children with initial PSG positive for OSAhad final PSG still positive for apnea. This findingagrees with previous studies that report that T&A iscurative in 85% to 95% of otherwise healthy chil-dren.4,5

Using a logistic regression model, only sleep tapewas a moderately useful predictor of a positive PSG.The addition of 6 items from the clinical assessmentdid not increase the predictive utility of the model.Previous studies have also demonstrated that scoresthat were based on a subset of items from the clinicalassessment were not sufficiently predictive to deter-mine which children would have a positivePSG.6,7,11,32

The sleep tape had a sensitivity of 88%, a specific-ity of 52%, and a positive predictive value of 62% inpredicting a positive PSG. These results are similar tothose of Lamm et al,33 who found that an audiotapehad a median sensitivity of 71% and median speci-ficity of 80% in predicting a positive PSG in 29 chil-dren who were referred to a sleep laboratory forevaluation of sleep-disordered breathing. Althoughnot specific enough to distinguish children with pos-itive and negative studies, the sleep tape is an inex-pensive, convenient method to confirm the parents’description of the child’s nighttime breathing diffi-culties. Home videotape recording of the child’snighttime breathing has also been shown to be areliable screening method for OSA with a sensitivityof 94% and a specificity of 68% in predicting a pos-itive study.34

In early studies of pediatric OSA, 27% to 69% ofchildren presented with failure to thrive.3 Now thataffected children are identified earlier, failure tothrive is less common. Five percent of the children inour study presented with failure to thrive, whichagrees with more recent reports of a 4% to 13%incidence.6,7 Thirty-four percent of the children inour study presented with obesity (BMI �95th per-centile), which is similar to recent reports of an inci-dence of 26% to 40%.6,7 As demonstrated in previousstudies, substantial weight gain is often found afterT&A even in children who are obese preoperative-ly.35

In adults, hypertension is a common complicationof OSA. Early reports found systemic hypertensionin 10% to 25% of children with OSA, although thesechildren were severely affected.36,37 In a more recentreport, Kunzman et al38 found no increased inci-dence of systemic hypertension in 22 children withOSA as compared with control subjects. Goldstein etal7 found that 18% of children who presented forevaluation of OSA were hypertensive. Marcus et al39

found that 41 children with OSA had a significantlyhigher diastolic blood pressure than 26 children withprimary snoring, although there was no significantdifference in systolic blood pressure between the 2groups. BMI was a significant predictor of elevatedblood pressure. In our study, 20% of the childrenpresented with systemic hypertension, 38% of whomwere obese. It resolved in all children by final eval-uation, although 3 new children were hypertensive, 2of whom were obese. As indicated in previous re-

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ports, systemic hypertension is a complication ofsleep-disordered breathing, especially in obese chil-dren. Early studies reported that between 10% and56% of children with OSA had pulmonary hyperten-sion or cor pulmonale.8,14,36 Now that children re-ceive a diagnosis at a much earlier stage, the inci-dence is much lower. In our study of otherwisehealthy children, only 1 (2%) child presented withmild pulmonary hypertension diagnosed by echo-cardiography.

PSG has been recommended before T&A to iden-tify children who are at risk for postoperative respi-ratory complications. Although the risk of postoper-ative respiratory complications in the generalpediatric population ranges from 0% to 1.3%, rates of16% to 27% have been reported in children withOSA.40–43 Risk factors are age under 3, pulmonaryhypertension or other cardiac abnormalities, cranio-facial syndromes, failure to thrive, hypotonia, acuteairway obstruction, morbid obesity, and severe sleepstudy indices. Anesthetic technique including theuse of opioids has not been shown to influence therate of postoperative respiratory complications.43

The majority of children described in these studieswould have been identified by preoperative clinicalassessment without the need for sleep studies. Inaddition, most postoperative respiratory complica-tions occur within 2 hours after surgery.44,45 As longas appropriate facilities and staff are available fortreatment of these children, including the option forovernight observation, a preoperative sleep study isnot necessarily needed. PSG has been most useful toconfirm the diagnosis of OSA and document its se-verity in the following situations: children who areyounger than 2 years; high-risk patients for whichsurgery is contraindicated; children with craniofacialanomalies, morbid obesity, or cerebral palsy; whenthere is a discrepancy between the history and phys-ical examination; and children who remain symp-tomatic after T&A. PSG is also a prerequisite to treat-ment with nasal continuous or bilevel positiveairway pressure in high-risk children or surgical fail-ures.13,46

CONCLUSIONSOtherwise healthy children with clinical assess-

ments suggestive of OSA benefit from T&A evenwhen PSG is normal. A significant reduction in aclinical assessment score based on the symptoms andsigns of upper airway obstruction occurs in childrenwho undergo T&A as compared with children whodo not undergo surgery. Our results agree with re-ports of improvement in health-related quality of lifeafter T&A performed for treatment of sleep-disor-dered breathing. The current standards for theproper definition of a positive PSG in a child as wellas the appropriate parameters to monitor are cur-rently in evolution. If we had evaluated our studychildren for UARS, then our clinical accuracy forpredicting a positive PSG would have improved.Until a noninvasive, reliable, routinely available testto diagnosis the full spectrum of sleep-disordered

breathing is available, clinical assessment remains avaluable tool in diagnosing upper airway obstruc-tion in children and determining the need for T&A.

ACKNOWLEDGMENTSThis study was supported by research grant 5 R03 HD37386-02

from the National Institute of Child Health and Human Develop-ment, Bethesda, MD (Dr Goldstein).

Presented at the Annual Meeting of the American Society ofPediatric Otolaryngology; May 4, 2003; Nashville, TN.

We thank Alex Sternberg, ScD, for performing the polysomno-grams; Jennifer J. Black for assistance with analysis of the voicetapes; and Kazi Azam, RDCS, FASE, and Denise Lei, RDCS, forperforming the echocardiograms. Ari J. Goldsmith, MD; Jessica W.Lim, MD; and Krishnamurthi Sundaram, MD, along with theSUNY Downstate otolaryngology residents, performed the T&Aprocedures. We thank Ellen M. Mandel, MD, and Jonathan D.Finder, MD, for assistance with study design and Richard M.Rosenfeld, MD, MPH, for critical review of the manuscript. Wethank Tiffany Morgan for administrative support.

REFERENCES1. Guilleminault C, Peraita R, Souquet M, Dement WC. Apneas during

sleep in infants: possible relationship with sudden infant death syn-drome. Science. 1975;190:677–679

2. Ali NJ, Pitson DJ, Stradling JR. Snoring, sleep disturbance, and behav-iour in 4–5 year olds. Arch Dis Child. 1993;68:360–366

3. Greene MG, Carroll JL. Consequences of sleep-disordered breathing inchildhood. Curr Opin Pulm Med. 1997;3:456–463

4. Marcus CL. Management of obstructive sleep apnea in childhood. CurrOpin Pulm Med. 1997;3:464–469

5. Suen JS, Arnold JE, Brooks LJ. Adenotonsillectomy for treatment ofobstructive sleep apnea in children. Arch Otolaryngol Head Neck Surg.1995;121:525–530

6. Carroll JL, McColley SA, Marcus CL, Curtis S, Loughlin GM. Inability ofclinical history to distinguish primary snoring from obstructive sleepapnea syndrome in children. Chest. 1995;108:610–618

7. Goldstein NA, Sculerati N, Walsleben JA, Bhatia N, Friedman DM,Rapoport DM. Clinical diagnosis of pediatric obstructive sleep apneavalidated by polysomnography. Otolaryngol Head Neck Surg. 1994;111:611–617

8. Leach J, Olson J, Hermann J, Manning S. Polysomnographic and clinicalfindings in children with obstructive sleep apnea. Arch Otolaryngol HeadNeck Surg. 1992;118:741–744

9. Nieminen P, Tolonen U, Lopponen H. Snoring and obstructive sleepapnea in children: a 6-month follow-up study. Arch Otolaryngol HeadNeck Surg. 2000;126:481–486

10. Preutthipan A, Suwanjutha S, Chantarojanasiri T. Obstructive sleepapnea syndrome in Thai children diagnosed by polysomnography.Southeast Asian J Trop Med Public Health. 1997;28:62–68

11. Wang RC, Elkins TP, Keech D, Wauquier A, Hubbard D. Accuracy ofclinical evaluation in pediatric obstructive sleep apnea. Otolaryngol HeadNeck Surg. 1998;118:69–73

12. American Thoracic Society. Standards and indications for cardiopulmo-nary sleep studies in children. Am J Respir Crit Care Med. 1996;153:866–878

13. Messner AH. Evaluation of obstructive sleep apnea by polysomnogra-phy prior to pediatric adenotonsillectomy. Arch Otolaryngol Head NeckSurg. 1999;125:353–356

14. Brouillette RT. Fernbach SK, Hunt CE. Obstructive sleep apnea ininfants and children. J Pediatr. 1982;100:31–40

15. Frank Y, Kravath RE, Pollak CP, Weitzman ED. Obstructive sleep apneaand its therapy: clinical and polysomnographic manifestations. Pediat-rics. 1983;71:737–742

16. Guilleminault C, Winkle R, Korobkin R, Simmons B. Children andnocturnal snoring: evaluation of the effects of sleep related respiratoryresistive load and daytime functioning. Eur J Pediatr. 1982;139:165–171

17. Potsic WP, Pasquariello PS, Corso Baranak C, Marsh RR, Miller LM.Relief of upper airway obstruction by adenotonsillectomy. OtolaryngolHead Neck Surg. 1986;94:476–480

18. Rosenfeld RM, Green RP. Tonsillectomy and adenoidectomy: changingtrends. Ann Otol Rhinol Laryngol. 1990;99:187–191

19. de Serres LM, Derkay C, Sie K, et al. Impact of adenotonsillectomy onquality of life in children with obstructive sleep disorders. Arch Otolar-yngol Head Neck Surg. 2002;128:489–496

42 CLINICAL ASSESSMENT OF PEDIATRIC OSA by guest on May 30, 2013pediatrics.aappublications.orgDownloaded from

20. Goldstein NA, Fatima M, Campbell TF, Rosenfeld RM. Child behaviorand quality of life before and after tonsillectomy and adenoidectomy.Arch Otolaryngol Head Neck Surg. 2002;128:770–775

21. Goldstein NA, Post JC, Rosenfeld RM, Campbell TF. Impact of tonsil-lectomy and adenoidectomy on child behavior. Arch Otolaryngol HeadNeck Surg. 2000;126:494–498

22. Gozal D. Sleep-disordered breathing and school performance in chil-dren. Pediatrics. 1998;102:616–620

23. Brodsky L. Modern assessment of tonsil and adenoid. Pediatr Clin NorthAm. 1989;36:1551–1569

24. Bridges ND, Freed MD. Cardiac catheterization. In: Emmanouilides GC,Riemenschneider TA, Allen HD, Gutgesell HP, eds. Moss and AdamsHeart Disease in Infants, Children, and Adolescents Including the Fetus andYoung Adult. 5th ed. Baltimore, MD: Williams & Wilkins; 1995:310–329

25. Ingelfinger JR. Systemic hypertension. In: Adams FH, EmmanouilidesGC, Riemenschneider TA, eds. Moss’ Heart Disease in Infants, Children,and Adolescents. 4th ed. Baltimore, MD: Williams & Wilkins; 1989:1018–1019

26. Hammer LD, Kraemer HC, Wilson DM, Ritter PL, Dornbusch SM.Standardized percentile curves of body-mass index for children andadolescents. Am J Dis Child. 1991;145:259–263

27. Kummer AW, Myer CM III, Smith ME, Shott SR. Changes in nasalresonance secondary to adenotonsillectomy. Am J Otolaryngol. 1993;14:285–290

28. Ali NJ, Pitson D, Stradling JR. Natural history of snoring and relatedbehaviour problems between the ages of 4 and 7 years. Arch Dis Child.1994;71:74–76

29. Marcus CL, Hamer A, Loughlin GM. Natural history of primary snoringin children. Pediatr Pulmonol. 1998;26:6–11

30. Guilleminault C, Pelayo R, Leger D, Clerk A, Bocian RCZ. Recognitionof sleep-disordered breathing in children. Pediatrics. 1996;98:871–882

31. Marcus CL, Omlin KJ, Basinki DJ, et al. Normal polysomnographicvalues for children and adolescents. Am Rev Respir Dis. 1992;146:1235–1239

32. Brouilette R, Hanson D, David R, et al. A diagnostic approach tosuspected obstructive sleep apnea in children. J Pediatr. 1984;105:10–14

33. Lamm C, Mandeli J, Kattan M. Evaluation of home audiotapes as anabbreviated test for obstructive sleep apnea syndrome (OSAS) in chil-dren. Pediatr Pulmonol. 1999;27:267–272

34. Sivan Y, Kornecki A, Schonfeld T. Screening obstructive sleep apnoaesyndrome by home videotape recording in children. Eur Respir J. 1996;9:2127–2131

35. Soultan Z, Wadowski S, Rao M, Kravath RE. Effect of treating obstruc-tive sleep apnea by tonsillectomy and/or adenoidectomy on obesity inchildren. Arch Pediatr Adolesc Med. 1999;153:33–37

36. Guilleminault C, Korobkin R, Winkle R. A review of 50 children withobstructive sleep apnea syndrome. Lung. 1981;159:275–287

37. Richardson MA, Seid AB, Cotton RT, Benton C, Kramer M. Evaluationof tonsils and adenoids in sleep apnea syndrome. Laryngoscope. 1980;90:1106–1110

38. Kunzman LA, Keens TG, Davidson Ward SL. Incidence of systemichypertension in children with obstructive sleep apnea syndrome. AmRev Respir Dis. 1990;141:A808

39. Marcus CL, Greene MG, Carroll JL. Blood pressure in children withobstructive sleep apnea. Am J Respir Crit Care Med. 1998;157:1098–1103

40. McColley SA, April MM, Carroll JL, Naclerio RM, Loughlin GM. Re-spiratory compromise after adenotonsillectomy in children with ob-structive sleep apnea. Arch Otolaryngol Head Neck Surg. 1992;118:940–943

41. Rosen GM, Muckle RP, Mahowald MW, Goding GS, Ullevig C. Post-operative respiratory compromise in children with obstructive sleepapnea syndrome: can it be anticipated? Pediatrics. 1994;93:784–788

42. Ruboyianes JM, Cruz RM. Pediatric adenotonsillectomy for obstructivesleep apnea. Ear Nose Throat J. 1996;75:430–433

43. Wilson K, Lakheeram I, Morielli A, Brouillette R, Brown K. Can assess-ment for obstructive sleep apnea help predict postadenotonsillectomyrespiratory complications? Anesthesiology. 2002;96:313–322

44. Lalakea ML, Marquez-Biggs I, Messner AH. Safety of pediatric short-stay tonsillectomy. Arch Otolaryngol Head Neck Surg. 1999;125:749 –752

45. Postma DS, Folsom F. The case for an outpatient “approach” for allpediatric tonsillectomies and/or adenoidectomies: a 4-year review of1419 cases at a community hospital. Otolaryngol Head Neck Surg. 2002;127:101–108

46. Goldstein NA. Pediatric obstructive sleep apnea. In: Alper CM, MyersEN, Eibling DE, eds. Decision Making in Ear, Nose, and Throat Disorders.Philadelphia, PA: WB Saunders Company; 2001:142–144

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Clinical Assessment of Pediatric Obstructive Sleep Apnea  

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