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ORIGINAL ARTICLE and Obstructive in Children A 6-Month Follow-up Study

Peter Nieminen, MD; Uolevi Tolonen, MD, PhD; Heikki Lo¨ppo¨nen, MD, PhD

Background: Snoring children may present symp- Results: Twenty-seven children had OSAS with an ob- toms suggestive of obstructive syndrome structive apnea/ index greater than 1, while 31 (OSAS). Different and controversial methods to estab- had primary snoring. There were statistical differences lish the diagnosis and to choose the treatment modali- in the symptoms and signs among the 3 study groups. ties have been proposed. Adenotonsillectomy was curative in the 21 children with OSAS who were operated on. Obstructive and hy- Objectives: To study children with symptoms raising popneas in the healthy, nonsnoring children were al- the suspicion of OSAS with overnight polysomnogra- most nonexistent in this study. phy (PSG). To evaluate the efficacy of adenotonsillec- tomy as treatment of pediatric OSAS and to elucidate the Conclusions: Half of the children or fewer with symp- natural history of OSAS and primary snoring. toms suggestive of OSAS actually had the condition. Clini- cal symptoms may raise the suspicion, but it is not pos- Design: A controlled, prospective, nonrandomized clini- sible to establish the diagnosis without PSG. Because cal trial. snoring and obstructive symptoms may resolve over time, a normal PSG finding may help the clinician decide on Setting: Academic medical center. an observation period. Adenotonsillectomy is curative in most cases of pediatric OSAS. Obstructive symptoms may Subjects: Fifty-eight snoring but otherwise healthy chil- continue after adenoidectomy alone. dren aged 3 to 10 years with symptoms suggestive of OSAS underwent PSG twice, 6 months apart. Thirty healthy chil- dren served as controls. Arch Otolaryngol Head Neck Surg. 2000;126:481-486

ORE THAN 10% of This follow-up study was designed to preschool-aged chil- study children with symptoms suggestive dren snore regularly.1 ofOSAS,thepresumptivecauseofthesymp- However, obstructive toms being adenotonsillar hypertrophy. sleep apnea syndrome These were related to (OSAS),M a condition related to snoring with the overnight polysomnographic (PSG) possible serious complications if un- findings. The effect of adenotonsillectomy treated,2,3 is less common. In a recent study, as a treatment of the syndrome was evalu- the prevalence of OSAS was estimated at ated in a repeated study 6 months later in about 3%.4 There is no doubt about the se- the cases with a PSG finding indicative of riousness of pediatric OSAS, but no uni- OSAS.ThechildrenwithPSwhounderwent versally accepted criteria have been de- no therapeutic interventions also received veloped for its diagnosis and treatment. a follow-up examination 6 months later. Much lower apnea indexes and shorter ap- neas than those considered acceptable for RESULTS adults2 have been recognized as indica- tors of OSAS in children.5,6 However, the FIRST VISIT natural history of mild OSAS and pri- mary snoring (PS), ie, snoring with ob- Twenty-seven of the 58 children had patho- From the Departments of structive symptoms but nonpathologic logic OAHIs higher than 1 (OSAS group), (Drs Nieminen and Lo¨ppo¨nen) (PSG) findings, is not while the remaining 31 children had non- 7 and Clinical Neurophysiology well known. The most common cause for pathologic PSG recordings (PS group). The (Dr Tolonen), Oulu University snoring and OSAS in normal children is main general findings for both groups and Hospital, Oulu, Finland. adenotonsillar hypertrophy.3 the control group are given in Table 1.

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 SUBJECTS, METHODS, CLINICAL SYMPTOMS AND MATERIALS The questionnare included 31 questions designed to de- termine the severity of the most typical symptoms of child- hood OSAS. To score the symptoms, we selected those linked We reviewed all referrals from primary health care sites to with a high risk for OSAS,8 and assigned the following nu- the Department of Otorhinolaryngology in the Oulu Uni- meric values to the symptoms of snoring, apneas, night- versity Hospital for adenoidectomy, tonsillectomy, or both, time mouth , and restless sleep: 0, never; 1, oc- for children aged 3 to 10 years from 1994 to 1997. Parents casionally; 2, regularly; and 3, always. Daytime of children with reported snoring, apneas, or difficult night- was assigned the following values: 0, never; 1, occasion- time breathing completed a detailed questionnaire regard- ally; and 2, regularly. Odd sleeping positions were valued ing their child’s nighttime and daytime symptoms. Chil- at 0, no; and 1, yes. The maximum score a child could have dren with known upper airway anomalies, an underlying was thus 15. disease predisposing to upper , , In addition, the (OSA) scor- or perennial allergy were excluded at this point. ing system developed and presented by Brouilette and co- Based on the questionnaire responses, the children with workers9 was applied to our series. According to Brouil- obstructive symptoms underwent an ear, nose, and throat ette et al, an OSA score greater than 0 is predictive of OSAS, evaluation. Where recognized, upper airway anomalies and while a score less than 0 is predictive of normality. A score abnormal facial morphologic characteristics led to exclu- greater than 3.5 should be considered diagnostic of OSAS, sion. After the patient history had been thoroughly up- while a score less than −1.0 indicates absence of OSAS. The dated and the questionnaire responses checked, 78 chil- OSA scores between –1.0 and 3.5 may or may not indicate dren (43 boys; mean age, 5.7 years; range, 2.4-10.5 years) OSAS.9 There is one caveat to our analysis of the OSA scores fulfilled the inclusion criteria (ie, had symptoms sugges- in this study: we used the criterion of laborious breathing tive of OSAS, were regular snorers, and/or had apneas dur- instead of breathing difficulties during sleep as in the origi- ing sleep, the presumable cause for the symptoms being nal formula. adenotonsillar hypertrophy). If a child had a previous ad- enoidectomy, this did not lead to exclusion. CLINICAL SIGNS The children were examined twice, 6 months apart. Fifty-eight children (31 boys; mean age, 5.7 years) partici- Thorough clinical ear, nose, and throat examinations were pated in the entire follow-up study. Fifteen children did done. The palatine tonsils were clinically graded on a scale not participate in the second part of the study; in 4 cases from 1 to 4, slightly modified from the standardized evalu- there was a protocol violation, and in 1 case, technical prob- ation system recommended by Brodsky,10 as follows: grade lems. Thirty nonsnoring, healthy children (17 boys; mean 1 tonsils remain within the tonsillar fossa; grade 2 tonsils age, 7.1 years) were also examined for comparison and to do not reach the midline between the anterior faucial pil- establish normative values for overnight PSG. lar and the uvula; grade 3 tonsils extend medially from the

More children in the OSAS group than in the PS POLYSOMNOGRAPHY and control groups had had a previous adenoidectomy. The average palatine tonsillar size was also greater in the The main polysomnographic results of the OSAS, PS, and OSAS group, with 93% (25/27) having enlarged tonsils, control groups are shown in Table 2. while 68% (20/31) had them in the PS group and only Inclusion of apneas shorter than 10 seconds into the 3% (1/30) in the control group. OAHI would not have changed the categorization. Of all obstructive events lasting longer than 10 seconds, hypop- SYMPTOMS neas accounted for 76.6% in the OSAS and 98.7% in the PS groups. Short obstructive events were much less com- On the symptom scale, the children with OSAS had a me- mon than those lasting longer than 10 seconds in both dian value of 12 (range, 4-14), those with PS, 9 (range, groups. Central apneas did not differ among the 3 groups. 2-14), and the controls, 1 (0-7). The mean OSA score was There were no significant differences in apneic events be- 3.1 for the OSAS group, 2.1 for the PS group (P = .03 for tween the PS group and the control group. Four children, difference from OSAS group), and −3.7 for the control 3 of them in the OSAS group, had 1 central apnea each last- group (PϽ.01 for difference from OSAS group). The con- ing longer than 20 seconds with desaturation below 90%. stancy of snoring and the frequency of nights when the The 4% and 10% desaturation episodes per hour in- parents had detected apneas differed between the OSAS dexes, which indicate events with 4% and 10% drops in and PS groups (Table 1). the oxygen saturation level, were manually checked. Both Nighttime and daytime and odd indexes were higher for the OSAS than PS group (Table sleeping positions were significantly less common in the 2). Both groups had higher 4% indexes than the control control group than in the OSAS and PS groups. Restless group (Table 2). The average width of the saturation dis- sleep was significantly more typical of the OSAS than PS tribution, which shows the variation in oxygen satura- group, 54% vs 22% (P = .03), being nonexistent in the tion between the highest and lowest 10 percentiles, was control group (PϽ.01). Excessive daytime somnolence, greater in the OSAS than the PS group (P = .05), while there the hallmark for OSAS in adults, was rare, and only 6 chil- was no significant difference between the PS and control dren (23%) in the OSAS group suffered from it daily. groups. Periods of cardiac arousals were more frequent in

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 midline; and grade 4 tonsils have a maximum distance of included in this index. Since there was no electroencepha- 4 mm between them. Tonsils graded 3 and 4 were consid- lographic or electro-oculographic tracing, arousals could ered enlarged in this study. not be quantified reliably. To detect periods of increased upper airway respiratory resistance outside of clinically POLYSOMNOGRAPHY significant apneas and , an indirect method was used. The PSG recordings were manually checked for peri- Polygsomnographic monitoring was done in the hospital odic hypopneas with a less than 50% decrease in the oro- under the surveillance of a trained nurse. The children were nasal signal amplitude linked with a pulse increase at the accompanied by a parent through the night. termination of hypopneas. These respiratorily induced A 6-channel computerized PSG was used, developed pulse increases evidently indicate arousals,12 and they may by the Department of Clinical Neurophysiology, with leads be linked to increased upper airway resistance syndrome. for an oronasal thermistor, a thoracoabdominal strain gauge, According to Noda et al,13 these pulse increases are cardiac pulse oximeter, body-position sensor, leg electromyo- arousals. graph, and static charge–sensitive . Although the analy- sis program included a possibility of automatic analysis of TREATMENT PROTOCOL the nighttime events, all recordings were manually checked by the same clinical neurophysiologist (U.T.). The children with OAHIs of 2 or higher underwent ton- In this study, the apneas lasting for 5 to 10 seconds sillectomy (and adenoidectomy, if not previously per- and those lasting longer than 10 seconds were counted sepa- formed) shortly after the first visit. The children with OAHIs rately. An obstructive apneic episode was defined as a to- lower than 2 were followed up without intervention. Two tal cessation of oronasal airflow, as detected by the therm- children with OAHIs above 2 were included in this group istor, in the presence of continuous breathing efforts, as (2.6 and 2.7, respectively) because, owing to ongoing speech revealed by the thoracoabdominal strain gauge or the static therapy, the phoniatrician suggested that surgical therapy charge–sensitive bed, and hypopnea as a reduction of 50% should be avoided. or more in the airflow signal, as proposed by Gould et al.11 A central apnea was defined as a cessation of the airflow in STATISTICAL ANALYSIS the absence of breathing efforts. Central apneas followed by a deep sigh were disregarded. Mixed apneas and hypop- The data were processed using the SPSS for Windows soft- neas starting with a central component and continuing with ware (version 6.1; SPSS Inc, Chicago, Ill). The t test for 2 an obstructive one were classified into the obstructive ap- independent samples and paired samples was applied for nea category. the normally distributed data. The nonparametric Mann- In this study, an obstructive apnea/hypopnea index Whitney U test was applied for the nonnormally distrib- (OAHI) greater than 1, including apneas/hypopneas last- uted data. The Mantel-Haenszel ␹2 test was applied to the ing for 10 seconds or more, was considered abnormal and ordinal variables. The correlation coefficients were counted used as the criterion for OSAS. Central apneas were not with the Pearson 2-tailed test.

the OSAS group (P = .01), while there was also a signifi- to be lighter, however, and he was more alert in the daytime. cant difference between the PS and the control groups Theother4childrencontinuedtosnoreirregularly;1ofthem (PϽ.01). The correlation coefficient between OAHI and reported still having laborious breathing at night. cardiac arousals was 0.61 (P = .01) in the OSAS group. There was a distinct improvement in the PSG re- sults after the operation (Table 3). All indexes except those FOLLOW-UP VISIT for central apneas were significantly improved. The mean Ͻ Surgical Group OAHI dropped from 6.9 to 0.3 (P .01). The remaining obstructive events were also improved, as were all hy- Twenty-one children with OAHI greater than 2 under- popnea indexes. Two children still had pathologic OAHIs went adenotonsillectomy shortly after the first visit. The postoperatively: the boy mentioned above had a score of results are shown in Table 3; 73% of the children op- 5.1 (8.9 at first measurement) and a girl had 1.0 (11.8 at erated on (16/21) had had previous adenoidectomies, first measurement). All the other children had OAHIs of which had not resolved the obstructive symptoms, or the less than 1. The periods of cardiac arousals decreased sig- symptoms had begun after the adenoidectomy. At the op- nificantly, but did not disappear. eration evaluated for this study, the epipharynx was checked, and none of the children appeared to have sub- Conservative Group stantial regrowth of adenoidal tissue. According to the responses to the follow-up questionnaire, Clinically, all children benefited from the operation. 6 children had developed more symptoms, and their mean All the symptoms of 16 children disappeared. Five children (SD; range) OSA scores had risen from 1.2 (2.3, −3.1 to 3.3) continuedtohavesomeminorsymptoms.Nonehadanyneed to 2.4 (2.4, −2.4 to 4.0), though they all had normal PSG find- for additional treatment. On the symptom scale, the median ings(OAHI = 0).Fifteenchildrenhadunchangedsymptoms, score for the children operated on dropped from 12 (range, while 16 reported decreased symptoms. The mean indexes 7-15) to 1 (range, 0-6). The mean OSA score had changed in this group had not changed significantly over the follow- significantly from 3.4 to –3.1 (PϽ.01). The only child with up period (Table 3). Two children had abnormal OAHIs at a postoperative OSA score greater than 0 was a boy, the only the second visit: 1 was a boy with unchanged OAHI 2.6. For one to still snore on most nights. The snoring was thought 1 child, the OAHI increased from 0.5 to 1.0.

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 Table 1. General Findings and Symptoms of the Children in the OSAS, PS, and Control Groups*

Subject Groups

Characteristic OSAS and PS (n = 58) OSAS (n = 27) P † PS(n=31) P ‡ Control (n = 30) P § Age (SD) (range), y 5.8 (1.8) (2.4-10.5) 5.6 (1.9) (2.4-10.5) .36 6.0 (1.8) (3.1-10.0) .02 7.1 (1.8) (4.3-10.9) .03 Sex, M/F 31/27 14/13 .97 17/14 .90 17/13 .92 Earlier adenoidectomy, 52 (31/58) 70 (19/27) .02 39 (12/31) .92 37 (11/30) .02 % (ratio) Grade 3-4 tonsils 78 (45/58) 93 (25/27) .01 68 (20/31) Ͻ.01 3 (1/30) Ͻ.01 OSA score (SD) (range) 2.5 (1.7) (−3.1-4.0) 3.1 (1.4) (−0.3-4.0) .03 2.1 (1.8) (−3.1-4.0) Ͻ.01 −3.7 (1.3) (−3.8-0.4) Ͻ.01 Constant nighttime 75 (43/57) 78 (21/27) .93 73 (22/30) Ͻ.01 7 (2/28) Ͻ.01 mouth breathing Snoring constantly 60 (35/58) 74 (20/27) .08 48 (15/31) Ͻ.01 0 Ͻ.01 Duration of snoring, mo 24 (20) (6-110) 21 (15) (6-60) .42 27 (24) (6-110) Ͻ.01 0 Ͻ.01 Apneas every night 33 (19/56) 59 (16/27) Ͻ.001 10 (3/29) .11 0 Ͻ.01 Odd sleeping positions 67 (39/58) 74 (20/27) .45 61 (19/31) Ͻ.01 10 (3/30) Ͻ.01 Restless sleep 37 (21/57) 54 (14/26) .03 22 (7/31) Ͻ.01 0 Ͻ.01 Regular excessive 10 (6/57) 23 (6/26) .07 0 .01 0 .01 daytime somnolence

*OSAS indicates obstructive sleep apnea syndrome; PS, primary snoring; and OSA, obstructive sleep apnea. Unless otherwise indicated, data are percentage (ratio) of patients. †Between OSAS and PS groups. ‡Between PS and control groups. §Between OSAS and control groups.

Table 2. Polysomnographic Findings of the Children in the OSAS, PS, and Control Groups*

Subject Group

Characteristic OSAS and PS (n = 58) OSAS (n = 27) P † PS(n=31) P ‡ Controls (n = 30) P § Apnea index 3.2 (4.3) (0-16.8) 6.4 (4.4) (1.2-16.8) Ͻ.01 0.4 (0.3) (0-1.0) .20 0.3 (0.30) (0-0.9) Ͻ.01 Obstructive 2.7 (4.0) (0-14.6) 5.7 (4.2) (1.0-14.6) Ͻ.01 0.1 (0.2) (0-0.9) .01 0 Ͻ.01 apnea/hypopnea index Obstructive apnea index 0.5 (1.0) (0-4.2) 1.1 (1.1) (0-4.2) Ͻ.01 0.0 (0.0) (0-0.1) .32 0 Ͻ.01 Obstructive hypopnea 2.2 (3.4) (0-14.5) 4.6 (3.8) (0.4-14.8) Ͻ.01 0.1 (0.2) (0-0.8) .001 0 Ͻ.01 index Central apnea index 0.5 (0.9) (0-5.8) 0.7 (1.2) (0-5.8) .05 0.3 (0.3) (0-0.9) .76 0.3 (0.3) (0-0.9) .05 Short obstructive apnea 0.6 (1.2) (0-5.7) 1.3 (1.5) (0-5.7) Ͻ.01 0.0 (0.1) (0-0.3) .26 0.0 (0.03) (0-0.1) Ͻ.01 index Short central apnea index 1.3 (1.1) (0-6.4) 1.6 (1.1) (0.3-5.0) .10 1.1 (1.1) (0-6.4) .27 0.8 (0.6) (0-2.7) .002 4% Oxygen desaturation 2.3 (5.1) (0-29.6) 4.5 (6.9) (0-29.6) .01 0.4 (0.9) (0-4.1) .05 0.1 (0.2) (0-0.9) Ͻ.01 events per hour (ODI4) 10% Oxygen desaturation 0.1 (0.3) (0-1.4) 0.2 (0.4) (0-1.4) .01 0.0 (0.0) (0-0.1) .34 0 .01 events per hour (ODI10) Mean apnea duration, s 14.4 (3.2) (0-22.1) 15.9 (2.6) (11.6-22.1) .01 13.1 (3.1) (0-20.2) . . . 12.7 (4.9) (0-23.3) .004 Saturation distribution, % 2.9 (1.3) (0.8-10.2) 3.3 (1.8) (0.8-10.2) .05 2.6 (0.7) (1.7-4.5) .24 2.4 (0.7) (0.3-3.7) .02 Increased respiratory 0.9 (0.9) (0-4.6) 1.3 (1.1) (0.2-4.6) .01 0.6 (0.6) (0-2.4) Ͻ.01 0.1 (0.2) (0-1.2)1 Ͻ.01 resistance, min/h Total sleeping time, h 8.8 (0.8) (7.0-10.0) 8.6 (0.8) (7.0-10.0) .45 8.9 (0.7) (7.6-10.0) .45 8.8 (0.7) (7.7-10.0) .45

*OSAS indicates obstructive sleep apnea syndrome; PS, primary snoring; ODI, oxygen desaturation index; and elllipses, not applicable. Unless otherwise indicated, data are index scores (SD) (range). †Difference between OSAS and PS groups. ‡Difference between PS and control groups. §Difference between OSAS and control groups.

COMMENT The natural history of mild OSAS is not well known, though it may be rather uneventful,7 as also suggested As the number of adenoidectomies and tonsillectomies by our results. It is not known, either, how high apnea performed declines because of the increased use of an- indexes and a long duration of OSAS are capable of pro- timicrobial therapy, the risk for obstructive sleep disor- ducing complications. ders may increase in the pediatric population.14 Chil- The pathologic apnea index for children is reported dren who snore and have symptoms suggestive of OSAS to be greater than 15 when real obstructive apneas lasting are frequently encountered in clinical practice. for at least 2 to 3 normal breath cycles are counted into

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 Table 3. Polysomnography Results of the Children Operated On (OAHI Ն2) and Not Operated On*

Subjects Operated On (n = 21) Subjects Not Operated On† (n = 37)

Characteristic Visit 1 P ‡ Visit 2P § Visit 1 Visit 2 Age, y 5.6 (2.1) (2.4-10.5) . . . 6.3 (2.0) (2.9-11.1) . . . 6.0 (1.7) (3.1-10.0) 6.6 (1.7) (3.6-10.6) Earlier adenoidectomy, % (ratio) 76 (16/21) . . . .01 39 (15/37) OSA score 3.4 (1.3) (−0.3-4.0) Ͻ.01 −3.1 (1.3) (−3.8-0.4) .01 (1.8) (−3.1-4.0) 0.5 (2.3) (−3.1-4.0) Apnea index 7.5 (4.4) (2.1-16.8) Ͻ.01 0.7 (1.2) (0-5.3) Ͻ.01 0.8 (1.1) (0-4.9) 0.5 (0.6) (0-2.6) Obstructive apnea/hypopnea 6.9 (4.1) (2.0-14.6) Ͻ.01 0.3 (1.1) (0-5.1) Ͻ.01 0.4 (0.7) (0-2.6) 0.2 (0.5) (0-2.6) index Obstructive apnea index 1.4 (1.2) (0.1-4.2) Ͻ.01 0.0 (0.03) (0-0.1) Ͻ.01 0.05 (0.2) (0-0.7) 0.01 (0.1) (0-0.4) Obstructive hypopnea index 5.5 (3.9) (0.4-14.5) Ͻ.01 0.3 (1.1) (0-5.0) Ͻ.01 0.3 (0.6) (0-2.2) 0.2 (0.5) (0-2.6) Central apnea index 0.7 (1.3) (0-5.8) .08 0.3 (0.4) (0-1.4) .26 0.4 (0.5) (0-2.6) 0.3 (0.3) (0-1.6) Short obstructive apnea index 1.6 (1.6) (0-5.7) .001 0.1 (0.1) (0-0.6) Ͻ.01 0.1 (0.1) (0-0.5) 0.05 (0.2) (0-0.9) Short central apnea index 1.6 (1.1) (0.3-5.0) .23 1.5 (1.0) (0.3-3.9) .15 1.2 (1.1) (0-6.4) 1.1 (1.2) (0-6.9) 4% Oxygen desaturation events 5.0 (7.4) (0-29.6) .04 0.2 (0.6) (0-2.6) .02 0.8 (2.2) (0-12.5) 0.8 (2.7) (0-14.3) per hour (ODI4) 10% Oxygen desaturation 0.2 (0.4) (0-1.4) .02 0 (0.0) (0-0.2) .02 0.01 (0.03) (0-0.1) 0.0 (0.03) (0-0.2) events per hour (ODI10) Saturation distribution, % 3.4 (1.9) (0.8-10.2) .19 2.7 (0.5) (1.7-3.9) .04 2.6 (0.7) (1.7-4.5) 2.6 (0.7) (1.7-6.0) Increased respiratory 1.4 (1.3) (0.2-4.6) .001 0.4 (0.4) (0.0-1.3) .01 0.7 (0.6) (0-2.4) 0.5 (0.5) (0-2.7) resistance, min/h Total sleeping time, h 8.7 (0.8) (7.0-10.0) .21 8.9 (0.7) (7.0-10.0) .21 8.9 (0.8) (7.6-10.0) 8.9 (0.8) (6.9-10.0)

*OAHI indicates obstructive apnea/hypopnea index; ellipses, not applicable; and ODI, oxygen desaturation index. Unless otherwise indicated, data are mean (SD) (range). †Two children with pathologic OAHIs are included in the group not operated on because of contraindications for surgery. ‡Difference before and after surgery. §Difference between those operated on and those not at the first visit.

the index. Obstructive apneas seem to be rare in normal, riodic hypopneas with a less than 50% decrease in orona- nonsnoring children,5 which is confirmed by the results sal signal amplitude linked to pulse increase at the termi- of this study, where only occasional short obstructive hy- nation of the hypopneas were manually checked. These popneas occurred in the control group. Hypopneas ac- respiratorily induced pulse increases evidently indicate counted for most obstructive events in this study. In chil- arousals,12 and may be linked to increased upper airway dren, obstructive events often consist of periods of resistance. Video recording, which helps detect most arous- prolonged instead of clear-cut apneas, als19 was not used on all patients, but the nurse on duty which are rather a culmination of the hypopnea syn- reported in writing both all interventions with reattach- drome.11 In this study, OAHIs higher than 1 were consid- ments of sensors and waking periods. The role of arousals ered abnormal, when obstructive and mixed apneas and in pediatric OSAS remains unclear, and arousals are prob- hypopneas lasting for 10 seconds or more were included ably not an important mechanism in the termination of res- in the index. The criterion of 10 seconds for apneas, which piratory events.15,16,21,22 Hence, electroencephalographic cri- is used for adults, is probably too high for children15,16 be- teria are not essential for determining the clinical severity cause children have a smaller respiratory capacity and of OSA in the pediatric population.23 In our study, none of greater oxygen consumption.6 The separately counted ap- the children with PS showed excessive daytime somno- neas lasting for 5 to 10 seconds should correlate fairly well lence, and only 23% in the OSAS group did so, supporting with the criteria of 2 to 3 missed breaths used by many,5,15 the assumption that interruption of sleep is not a major prob- but the use of shorter apneas as a criterion would not have lem for these children. affected the results of this study. Central apneas were excluded from the index, whether According to our results, PSG is needed to diagnose or not they were accompanied by a desaturation of greater patients with OSAS because some OSAS cases cannot be than 10%. Central apneas occur in children without obstruc- diagnosed on merely clinical grounds. Polysomnography tive symptoms,24 and in this study they were seen equally is the standard method for studying children with sus- often in children with OSAS and PS and in controls. pected obstructive sleep disorders.17 Full-scale PSG, how- That pediatric OSAS is equally common in both sexes16 ever, is quite invasive, may disturb the child’s natural sleep, is supported by the results of this study. The age distri- and is also quite expensive.15,18 Simpler montages suitable bution of the studied children was quite even. All the chil- for home use have been shown to be sensitive and yield dren participating in this study had symptoms of various reliable information of the nighttime events.19,20 The PSG degrees, causing a suspicion of OSAS. The symptom score device used in this study meets most of the minimum re- for OSAS developed by Brouilette and coworkers9 did not quirements of the consensus statement of the American Tho- discriminate very well between the children with OSAS racic Society (1996).17 In this study separate arousals could and those with PS, as has been noted earlier.15 Though only not be quantified owing to a lack of electroencephalo- 1 child in the OSAS group had an OSA score lower than graphic channels, while periods of cardiac arousals were 0.5, children with PS had OSA scores higher than 3.5, which quantified from the PSG recordings. The intervals of pe- are considered by Brouilette et al9 diagnostic for OSAS. The

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 wide range of OSA scores in both groups confirms the dif- this suspicion, but the diagnosis cannot be established ficulty of establishing a diagnosis on a clinical basis,15 and without PSG. A normal PSG finding may help the clini- in many study series, only half or fewer of the children cian decide on an observation period, since snoring and with suspected OSAS are proved to have it by the PSG cri- obstructive symptoms may resolve over time. Adenoton- teria.8,15,18,25 Most of the daytime and nighttime symp- sillectomy is, in most cases, a curative treatment of pe- toms reported as typical for children with OSAS, ie, morn- diatric OSAS, while adenoidectomy alone does not seem ing headaches, bed wetting, profuse sweating, , to be enough. , , concentration difficulties, and fre- quent nighttime awakenings, were quite similar among the Accepted for publication November 16, 1999. OSAS and PS groups, while most of these symptoms were Reprints: Peter Nieminen, MD, Hiirihaukankatu 3, significantly less common in the control group. Only the 65320 Vaasa, Finland (e-mail: [email protected]). habitual snoring, apneas, and restless sleep detected by the parents were significantly more common in the OSAS than REFERENCES the PS group. Tonsillectomy and adenoidectomy are effective in 1. Ali NJ, Pitson D, Strandling JR. Natural history of snoring and related behaviour the treatment of pediatric OSAS, especially when there problems between the ages of 4 and 7 years. Arch Dis Child. 1994;71:74-76. is no underlying predisposition.2,3,26 This fact was con- 2. Guilleminault C, Korobkin R, Winkle RA. Review of 50 children with obstructive firmed by the present results. All children who were op- sleep apnea syndrome. Lung. 1981;159:275-289. 3. Brouilette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and chil- erated on improved in terms of symptoms and PSG re- dren. J Pediatr. 1982;100:31-40. sults. Only 1 boy had clearly pathologic OAHI 4. Gislason T, Benediktsdottir B. Snoring, apneic episodes, and nocturnal hypox- emia among children 6 months to 6 years old: an epidemiological study of lower postoperatively, with some but notably milder obstruc- limit of prevalence. Chest. 1995;107:963-966. tive symptoms. There was also a decline in mild hypopnea- 5. Marcus CL, Omlin KJ, Basinki J, et al. Normal polysomnographic values for chil- induced cardiac arousals, but no total disappearance. dren and adolescents. Am Rev Respir Dis. 1992;146:1235-1239. 6. Carroll JL, Loughlin GM. Diagnostic criteria for obstructive sleep apnea syn- Could this result indicate that these children had a pre- drome in children. Pediatr Pulmonol. 1992;14:71-74. disposition for obstructive sleep disorders? Why do some 7. Marcus CL, Hamer A, Loughlin GM. Natural history of primary snoring in chil- children snore, while some do not, with apparently simi- dren. Pediatr Pulmonol. 1998;26:6-11. 8. Nieminen P, Tolonen U, Lo¨ppo¨nen H, Lo¨ppo¨nen T, Luotonen J, Jokinen K. Snor- lar facial morphologic characteristics and pharyngeal sta- ing children: factors predicting sleep apnea. Acta Otolaryngol (Stockh). 1997; tus? It has been proposed that primary snoring, upper (suppl)529:190-194. 9. Brouilette R, Hanson D, David R, et al. A diagnostic approach to suspected ob- airway resistance syndrome, and OSAS constitute a con- structive sleep apnea syndrome in children. J Pediatr. 1984;105:10-14. 21 tinuum. Most children in the conservative group had 10. Brodsky L. Modern assessment of tonsils and adenoids. Pediatr Clin North Am. periods of obstructed breathing causing cardiac arous- 1989;36:1551-1569. 11. Gould GA, Whyte KF, Rhind GB, et al. The sleep hypopnea syndrome. Am Rev als equally or more often than the children with OSAS Respir Dis. 1988;137:895-898. postoperatively. Is there a similar tendency toward ob- 12. Marcus CL, McColley SA, Carroll JL, Loughlin GM, Smith PL, Schwartz AR. Up- structed breathing in these children, but some differ- per airway collapsibility in children with obstructive sleep apnea. J Appl Physiol. 1994;77:918-924. ence in the upper airway regulatory reflexes? Deficit in 13. Noda A, Okada T, Katsumata K, Yasuma F, Nakashima N, Yokota M. Sup- the central ventilatory drive is probably not a major fac- pressed cardiac and electroencephalographic arousal on apnea/hypopnea ter- 22 mination in elderly patients with cerebral infarctation. J Clin Neurophysiol. tor in the pathogenesis of OSAS. 1997;14:68-72. Normal PSG findings can help the clinician justify 14. Grundfast KM, Witich DJ. Adenotonsillar hypertrophy and upper airway obstruc- an observation period for the snoring child, since the sta- tion in evolutionary perspective. Laryngoscope. 1982:92:650-656. 15. Carroll JL, McColley SA, Marcus CL, Curtis S, Loughlin GM. Inability of clinical bility of the PSG findings in the conservative group seems history to distinguish primary snoring from obstructive sleep apnea syndrome to indicate that, during a short interval, primary snorers in children. Chest. 1995;108:610-618. do not have a tendency to develop OSA, supporting the 16. Ward SL, Marcus CL. Obstructive sleep apnea in infants and young children. 7 J Clin Neurophysiol. 1996;13:198-207. earlier findings. The finding that snoring may be re- 17. American Thoracic Society. Standards and indications for cardiopulmonary sleep stricted to a period of childhood,1 and that almost half studies in children. Am J Respir Crit Care Med. 1996:153;866-878. 18. Leach J, Olson J, Hermann J, Manning S. Polysomnographic and clinical find- of the children in the conservative group showed spon- ings in children with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg. taneous regression of the obstructive symptoms over the 1992;118:741-744. follow-up period, further supports the idea of an obser- 19. Mograss MA, Ducharme FM, Brouilette RT. Movement/arousals: description, clas- sification, and relationship to sleep apnea in children. Am J Respir Crit Care Med. vation period. 1994;150:1690-1696. A history of previous adenoidectomy in snoring chil- 20. Jacob SV, Morielli A, Mograss MA, Ducharme FM, Schloss MD, Brouilette RT. dren has been shown to be a risk factor for OSAS.8 In our Home testing for pediatric obstructive sleep apnea syndrome secondary to ad- enotonsillar hypertrophy. Pediatr Pulmonol. 1995;20:241-252. study, most of the children with OSAS had had earlier 21. Downey R, Perkin RM, MacQuarrie J. Upper airway resistance syndrome: sick, adenoidectomies, which indicates that adenoidectomy symptomatic but underrecognized. Sleep. 1993;16:620-623. 22. Marcus CL, Lutz J, Carroll JL, Bamford O. Arousal and ventilatory responses alone is not always effective in the treatment of pediat- during sleep in children with obstructive sleep apnea. J Appl Physiol. 1998;84: ric OSAS. Nor did adenoidectomy seem to have recon- 1926-1936. stituted nighttime nasal breathing in these children, which 23. McNamara F, Issa FG, Sullivan CE. Arousal pattern following central and ob- structive breathing abnormalities in infants and children. J Appl Physiol. 1996; further indicates that orovelopharyngeal factors are domi- 81:2651-2657. nant in producing obstructive symptoms. 24. Carskadon MA, Harvey K, Dement WC, Guilleminault C, Simmons B, Anders TF. Respiration during sleep in children. West J Med. 1979;128:477-481. 25. Suen JS, Arnold JE, Brooks LJ. Adenotonsillectomy for treatment of obstruc- CONCLUSIONS tive sleep apnea in children. Arch Otolaryngol Head Neck Surg. 1995;121:525- 530. 26. Strandling JR, Thomas G, Warley ARH, Williams P, Freeland A. Effect of adeno- Half or fewer children with symptoms suggestive of OSAS tonsillectomy on nocturnal , sleep disturbance, and symptoms in snor- actually have the syndrome. Clinical symptoms may raise ing children. Lancet. 1990;335:249-253.

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