REVIEW ARTICLE

Concise Indications for Adenoidectomy-

Tonsillectomy in Children with Obstructive Sleep
Apnea Syndrome
Shu-Chi Mu1,2,3, MD, PhD, I Cheng1, MD, Rayleigh Ping-Ying Chiang4, MD, MMS, Tseng-
Chen Sung1*, MD
1
Department of Pediatrics, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
2
Medical College of Fu-Jen University, New Taipei City, Taiwan
3
Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan
4
Department of Otolaryngology, School of Medicine, Taipei Medical University; Department of Otolaryngology–
Head and Neck Surgery, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
Abstract
Few new therapies for pediatric obstructive sleep apnea syndrome (OSAS) have been
validated with randomized controlled trials. Based on the current evidence, it is cruial
to achieve early diagnosis and provide definitive therapy of this condition. This review
provides an update review of epidemiology, clinical features, complications, and treatment
of childhood OSAS and the benefit of tonsillectomy for children who have obstructed
apneas, constant snoring and difficult breathing during sleep. The concise indications for
adeno-tonsillectomy are children over three years of age with OSAS and also those children
who have three or more tonsil infections in one year. (J Pediatr Resp Dis 2013;9:11-21)
Key words: sleep-disordered breathing, tonsillectomy, adenoidectomy,
leukotriene modifier
INTRODUCTION clinical symptoms.3
The patho-physiology and etiology of OSAS in
Sleep-disordered breathing (SDB) may be children are inadequately understood. The complex
considered a disease continuum. It ranges in severity process of airway closure during sleep is a dynamic
from mild obstruction of the upper airway, producing phenomenon not explained by mechanical factors
primary snoring, to increased upper airway resistance alone.
syndrome (UARS), to continuous episodes of complete Children with OSAS encounter a combination of
upper airway obstruction or obstructive sleep apnea oxidative stress, inflammation, autonomic activation,
syndrome (OSAS). There is prominent evidence and disruption of sleep homeostasis. The apnea
implicating OSAS as a risk factor for decreased growth, hypopnea index (AHI) represents the total number of
impaired neuro-cognitive function, and cardiovascular apneic events plus hyperpnoea per hour of sleep. The
morbidity. arousal index describes the number of arousals every
The percentage of individuals younger than 18 hour of sleep. Causes of airway narrowing include soft
years who have been reported with regular heavy tissue hypertrophy, craniofacial abnormalities, and/or
snoring ranged between 8% and 12%.1,2 OSAS was neuromuscular deficits. There appears to be individual
first described in children in 1976. Children with genetic susceptibility and environmental factors that
OSAS may have other abnormal patterns of respiratory influence the expression of OSAS sequelae.4
driving during sleep associated with snoring and Primary snoring is traditionally defined as a benign
Correspondence: Tseng-Chen Sung, MD condition. Recent evidence suggests that snoring may
Department of Pediatrics, Shin-Kong Wu Ho-Su be associated with adverse neurobehavioral outcomes.5,6
Memorial Hospital, No. 95, Wen Chang Road, Shih-Lin The most important risk factors for pediatric
District, Taipei 111, Taiwan. Received: December 20, OSAS include adenotonsillar hypertrophy, adenoid
2012. Accepted: February 18, 2013.
Journal compilation © 2013 Taiwan Society of Pediatric Pulmonology
Mu SC, et al.
hypertrophy, obesity, allergic rhinitis/rhinosinusitis,
gastroesophageal reflux disease, craniofacial
syndromes, neuromuscular diseases and Down
syndrome.7 Adenoids, also known as a pharyngeal
tonsil or nasopharyngeal tonsil, are a mass of lymphoid
tissue situated posterior to the nasal cavity as part of
human defense system. Successful treatment of children
with OSAS is predicated on identifying the origin
of the increased upper airway resistance. In children
with definite OSAS and adenotonsillar hypertrophy,
an adenotonsillectomy is the recommended first-line
therapy.
The multifaceted etiology of OSAS in children
explains why the method-of-choice treatment,
adenotonsillectomy, is not always curative. Persistent
airway obstruction after adenotonsillectomy may be
due to lingual tonsil enlargement. Lingual tonsillectomy
has traditionally been regarded as a difficult procedure
with potentially high morbidity. Should the child’s
tonsil be removed? It is a debatable issue from the
different points of view of otolaryngologists and
general pediatric physicians. The present investigation
of snoring children with symptoms suggestive of
OSAS was designed to increase our knowledge of
this disease and further give guidelines for diagnostics
and treatment of children suffering from OSAS. In
this review, the authors speculate on the adequate and
convincing indications for adeno-tonsillectomy/ lingual
tonsillectomy and aim tocontribute to strengthening
multidisciplinary collaboration, especially between
pediatricians and otolaryngologists, based on evidence-
based medicine.
Epidemiology and Risk Factors
No definitive and few population-based studies
have evaluated the presentations of OSAS in children.
The epidemiology of pediatric OSAS has not been
well-established due to methodological limitations
regarding diagnostic criteria. OSAS occurs in children
from neonates to adolescents, with little evidence
of a systematic variability by age. Habitual snoring
is commonly observed in pediatric OSAS, and the
reliability of a negative clinical history of snoring is
poor, particularly in older children. The prevalence
based on questionnaire phrasing of parent’s prediction
12
for symptomatic children may be unreliable.8 It is
estimated that up to 30% of children snore,9 and of those,
1–3% meet criteria for OSAS.3 The most recognized
risk factor for OSAS is adenotonsillar hypertrophy,
which currently represents a frequent indication for
adeno-tonsillectomy in children.
The prevalence of OSAS is 2.2 to 3.8%.10, 11 There
are seven studies that attempted to establish prevalence
of snoring in childhood.12-18 They came from a variety
of European countries, and all collected data via
parent questionnaires. The prevalence of snoring
in these studies ranged from 3.2% to 12.1%, which
was significantly heterogeneous. 12-18 Three studies
reporting on prevalence of OSAS ranged from 0.7% to
10.3%.12,13,19 The peak prevalence of OSAS with relation
to adenotonsillar hypertrophy is between 2 and 8 years
of age, when tonsils and adenoids are largest in relation
to upper airway size.19 Adenoid hypertrophy can be the
most significant cause of OSAS in children younger
than 24 months of age. Other important risk factors are
obesity, allergic rhinosinusitis, gastroesophageal reflux
disease, male gender, prematurely growing-up children,
Down syndrome, neuromuscular diseases, craniofacial
syndromes, maternal smoking and a positive family
history of OSAS. Ethnicity may be a risk factor in
OSAS. Some orofaciocranial features are found to be
highly suggestive of breathing disorders during sleep
when associated with specific clinical symptoms: a
small chin, a steep mandibular plane, a retro-position
of the mandible, a long face, a high hard palate, and an
elongated soft palate.20 Redline et al.1 have found Afro-
American children to be at higher risk of developing
obstructive sleep disorders. In adults, Far-East-Asian
men seem to have more severe OSAS than white
men, though being usually non-obese, probably due to
craniofacial anatomical differences.21
It is necessary to remember that hypertrophic
tonsils may not be the only factor in a child presenting
with symptoms of OSAS. Excluding and treating
other factors such as above mentioned disorders are
sometimes as important as the surgical procedure itself.
A study of infants between 5 and 12 months of age
documented a significant improvement of the apnea/
hypopnea index (AHI) after adenoidectomy.22
 Adenoidectomy-tonsillectomy in OSAS children

Clinical Symptoms/ Signs has been associated with specific clinical problems
and findings. Snoring is the most common symptom
Abnormal narrowing in the airway from nose, reported by parents of children with OSAS. Snoring is
nasopharynx, oropharynx, to hypopharynx causes very sensitive (most children with OSAS snore) but not
abnormal air exchange during sleep, which in turn leads very specific for OSAS (all snorers do not necessarily
to clinical symptoms. The accompanying symptoms have OSAS).7 The American Academy of Pediatrics
can change with age. Table 1 indicates the parental recommends systematic screening of children for a
complaints concerning children seen at sleep clinics history of snoring. A positive history of snoring should
over time.12,23-30 Abnormal breathing during sleep then lead to further evaluation to rule out or confirm
Table 1. Complaints reported by parents regarding their children1,17-23
Age group and age
Infants, 3-12 mo Toddlers, 1-3 y Preschool-aged children School-aged children
Disturbed nocturnal sleep Noisy breathing or snoring Regular, heavy snoring Regular, heavy snoring
with repetitive crying Agitated sleep or disrupted Mouth breathing Agitated sleep
Poorly established day/ nocturnal sleep Drooling during sleep Abnormal sleeping positions
night cycle Crying spells or sleep terrors Agitated sleep Insomnia
Noisy breathing or snoring Grouchy and/or aggressive Nocturnal awakenings Delayed sleep phase
Nocturnal sweating daytime behavior Confusional arousals syndrome
Poor sucking Daytime fatigue Sleepwalking Confusional arousal
Absence of normal growth Nocturnal sweating Sleep terrors Sleepwalking
pattern or failure to thrive Mouth breathing Nocturnal sweating Sleep talking
Observation of apneic Poor eating or failure to Abnormal sleeping Persistence of bed-wetting
events thrive positions Nocturnal sweating
Report of apparently (?) Repetitive URI Persistence of bed-wetting Hard to wake up in the
life-threatening event Witnessed apneic episodes Abnormal daytime behavior morning
Presence of repetitrive Aggressiveness Mouth breathing
earaches or URI Hyperactivity Drooling
Inattention Morning headache
Daytime fatigue Daytime fatigue
Hard to wake up in the Daytime sleepiness with
morning regular napping
Morning headache Abnormal daytime behaviors
Increased need for napping Pattern of attention-deficit/
compared with peers hyperactivity disorder
Poor eating Aggressiveness
Growth problems Abnormal shyness,
Frequent URI withdrawn and depressive
presentation
Learning difficulties
Abnormal growth patterns
Delayed puberty
Repetitive URI
Dental problems appreciated
by dentist
Crossbite
Malocclusion (class II or III)
Small jaw with overcrowding
of teeth
OSAS:obstructive sleep apnea syndrome; URI, upper respiratory tract infection
13
Mu SC, et al.

Table 2. Comparison of the symptoms and some other features of OSAS in adults and children31
Snoring Often continuous, snorting Loud, alternating with pauses
Predominant respiratory pattern Mixture of obstructive, mixed and Obstructive apneas predominate
central apneas and hypoventilation

Sleep structure Normal macrostructure Sleep pattern disruption

Arousal on apnea termination Usually not Nearly always
Nighttime mouth-breathing Common Common
Restless sleep Common Common
Sweating during sleep Common Common
Odd sleeping positions Common Not common
Excessive daytime sleepiness (EDS) Minority of patients, rather Main presenting symptom
hyperactivity, behavioral changes
Daytime mouth breathing Common Not common
Cognitive impairment May be present, poor school May be present
performance
Obesity Minority of patients Majority of patients
Growth or weight retardation Not rare No
Gender Male-Female 1:1 Male-Female 8-10:1
Enlarged tonsils and adenoids Most common Uncommon
Complication Cardiopulmonary, growth, behavioral, Mainly cardiopulmonary and
developmental complications of EDS
Surgical treatment Adenotonsillectomy curative in most Only in selected cases
cases

the impression of OSAS.14 behavior, personality changes, bed resistance, school

Symptoms of OSAS in children differ in several
ways from those in adults, and may be only nocturnal
(Table 2).31 In spite of troublesome struggle throughout
the night, the children may be quite asymptomatic in the
daytime, at least in the initial stages of the syndrome.
Excessive daytime somnolence, the hallmark of OSAS
in adults, is encountered only in a minority of children
with OSAS.32, 33
The character of pediatric OSAS with prolonged
hypoventilation or hyperpnoea with no necessity of
abundant EEG arousals is probably one explanation for
the relative rarity of excessive daytime sleepiness (EDS)
in pediatric OSAS. Rather than being sleepy, children
may show behavioral deterioration or outbursts, and
increased activity.34 Indeed, externalizing behavior
problems such as hyperactivity, irritability, bizarre
and learning problems and morning headaches are
frequently reported symptoms of OSAS in children and
the reported prevalence of these symptoms is usually
well below 50%.35 Goldstein et al36 reported abnormal
behavior in 28% of children scheduled for adeno-
tonsillectomy due to chronic upper airway obstruction,
with obvious improvement after treatment.
OSAS may lead to serious, even life-threatening
complications in children.37 Evidence exists that even
mild forms of sleep disturbance may have deleterious
effects affecting the daytime functioning of the
child.38 Frank et al39 reported that many children with
OSAS had had symptoms lasting up to five years
without progression in severity or development of
complications, whereas some children developed
severe symptoms and complications in just a few weeks.

14

Table 3. Polysomnographic criteria for children49
AHI >1 or RDI >1.5: in children ages 12 years and below
AHI ≥ 5: IN adolescents, the adult cutoff value is generally used
O2 desaturation nadir <91%
Change in nadir O2 from baseline >9%
Maximal end-tidal CO2 >54 mm Hg
Increased edn-tidal CO2 >50mm Hg for >25% of total sleep time
This pediatric PSG criteria is cited from a clinical guide to pediatric sleep, with modification of the
cutoff value
Cor pulmonale due to chronic upper airway obstruction
in children has been well reported.40, 41 Children with
apparent OSAS suffering from congestive heart-failure
and even pulmonary edema, which resolved after
treatment, have been described.40
Behavioral disorders, which have been reported
in OSAS children, may have negative long-term
consequences for the children if they last for a longer
period. 42, 43
Learning problems may occur at school age.
Aggression, inattention and hyperactivity have been
found to improve after adeno-tonsillectomy in children
with mild sleep disturbance, according to a parent
questionnaire. Surgery also had a positive effect on
vigilance, reflection and impulsivity.38
Diagnosis
Many physicians have to base their diagnosis of
OSAS on the clinical symptoms and signs of the
children. Brouilette et al derived a symptom score
which, according to their research, classified correctly
all controls and 22 out of 23 OSAS patients.44 Observed
apneas, constant snoring and difficulty in breathing
during sleep were found to be fairly predictive of
OSAS. Mahboubi et al stated that the radiologically
assessed adenoidal size would not give much
information about the degree of airway obstruction,
whereas Fernbach et al found hardly any OSAS-
children to have an adenoidal-nasopharyngeal ratio
greater than two standard deviations above the mean
value of normal controls.45,46 But airway obstruction is
a dynamic phenomenon, and lateral neck radiography
does not provide sufficient information on which to
base a decision to perform adeno-tonsillectomy to
relieve airway obstruction during sleep in children .
Adenoidectomy-tonsillectomy in OSAS children
The most accurate and comprehensive method of
diagnosing OSAS is nocturnal polysomnography
(PSG).47 The diagnostic criteria are usually based
on a certain apnea/hyperpnoea index (AHI), but de-
saturation, hypercapnic episodes, and arousals may be
included in the criteria, then often called the respiratory
disturbance index (RDI), either as their own parameters
or in association with apnea or hyperpnoea.48
Consequently, most pediatric sleep specialists
regard an apnea index (AI) of more than 1 or an apnea
hypopnea index (AHI) of 1.5 as abnormal and most
recommend treatment of any child with an AI greater
than 5. Regular PSG parameters such as AI, AHI, RDI
and the nadir of oxygen saturation (SpO2) are helpful
to evaluate the severity of OSAS. (Table 3)49
According to the consensus statement, PSG is
indicated as a diagnostic tool in a variety of situations,
most importantly: 1) for evaluating the child with
disturbed sleep patterns, excessive daytime sleepiness,
cor pulmonale, failure to thrive, or polycythemia
unexplained by other factors or conditions, especially
if the child also snores; 2) in the child who has
clinically significant airway obstruction during sleep
as observed by medical personnel, or documented by
audiovideo recording; 3) Since children with OSAS are
at a higher risk of postoperative complications,50 PSG
is recommended if the surgeon is uncertain whether the
clinical observation of obstructed breathing is sufficient
to warrant surgery.
Videofluoroscopy can provide an information
additional to lateral radiographs and PSG in children
with minor adeno-tonsillar enlargement or with
predisposing factors.46 Virtual endoscopy has proved to
effectively show fixed lesions in the upper airways, but
it is not sensitive enough to detect dynamic movements
leading to obstruction.51 Flexible fiberoscopy has been
15
Mu SC, et al.
shown to identify reliably the site of obstruction in
children with anomalous upper airways with obstructive
symptoms even when awake.52 Sleep nasoendoscopy
combined with rigid laryngo-bronchoscopy has
been suggested to be valuable in detecting the site of
obstruction in children with residual symptoms after
adeno-tonsillectomy.53 Magnetic resonance imaging of
the upper airways may reveal structural abnormalities
in children with OSAS.54
Management of and Concise
Indications for Adenotonsillectomy
The American Academy of Otolaryngology-Head
and Neck Surgery points to a study showing the benefit
of tonsil removal for kids who have had three or more
tonsil infections in a year. However, tonsillectomy and/
or adenoidectomy is recommended if the tonsils are
so large they obstruct breathing or swallowing, or if
the child is diagnosed with obstructive sleep apnea, a
condition where children briefly stop breathing during
sleep and wake up frequently throughout the night.
The predominant cause of adenoidectomy and
tonsillectomy is recurrent infections,55 but there has been
a dramatic increase in OSAS as a significant indication
for surgery.56 Tonsillectomy is reluctantly performed
on children under three years of age, and sleep apnea
seems to be the leading cause for operation in this age
group.57 From the clinical perspective, cephalometrics
is a noninvasive and inexpensive method, and is an
objective technique for evaluation of children with
OSAS and for further treatment planning.58 Even if the
tonsils and/or adenoids are 6 not seemingly enlarged,
adeno-tonsillectomy will provide more airway space.
Different anomalies or concomitant diseases
may predispose to OSAS, and in such cases adeno-
tonsillectomy is not always a curative treatment,
even though the adenoid is enlarged and a supposed
site of obstruction.13 Adeno-tonsillectomy improves
respiratory abnormalities in children with OSAS,
but complete normalization occurs in only 25% of
patients.59 CO2 laser tonsillotomy in combination with
adenoidectomy is highly effective in the treatment
of pediatric OSAS and should be preferred over
tonsillectomy because of less postoperative pain and a
lower risk of postoperative bleeding.60
16
Treatment of OSAS has been shown to improve
dentofacial deformities. Maxillofacial surgery is rare
in children, and obviously applied only in OSAS
cases with upper airway anomalies, where adeno-
tonsillectomy is either insufficient or contraindicated.
The long-term outcome linked the recurrence of
abnormal breathing during sleep to the absence of
dealing with a narrow maxilla and/or mandible at the
time of the initial surgery and the later occurrence of
tongue/mucosal enlargement at the time of puberty,
when 90% of oro-facial adult growth had already
occurred. Adeno-tonsillectomy has been performed
in association with orthodontic treatment.61 Rapid and
slow maxillary distractions are performed between 5
and 11 years of age. Distraction results in widening of
the palate and the nose; thus, this procedure remedies
nasal occlusion related to a deviated septum, for which
little can be done before 14 to 16 years of age.
However, many children, especially the obese, those
with underlying medical conditions such as Down
syndrome or craniofacial anomalies, and those with
more severe OSAS, require further treatment after
this surgery.59,62-64 Continuous positive airway pressure
(CPAP) delivered via a nasal interface is the most
common non-surgical therapy for pediatric OSAS,
especially in cases of congenital malformations,
when in the past, tracheotomy usually had to be
performed if adeno-tonsillectomy failed to relieve
a serious obstruction. Hence, one of the challenges
that pediatric sleep specialists face is finding new
treatments for OSAS, especially as the prevalence of
OSAS is expected to increase along with the current
obesity epidemic.65,66 The current review will focus
on newer treatment modalities for OSAS, including
anti-inflammation, dental treatments, high-flow nasal
cannula, and weight loss. A double-blind, placebo-
controlled study, montelukast effectively reduced
polysomnographic findings, symptoms, and the size of
the adenoidal tissue in children with non-severe OSAS.
The findings support the potential of a leukotriene
modifier as a novel, safe, noninvasive alternative for
children with mild to moderate OSAS.67
Also, the authors have proposed an easy-to-follow
flowchart (Figure 1) regarding the diagnosis and
management of pediatric OSAS for pediatricians.68,69
 Adenoidectomy-tonsillectomy in OSAS children

Children with suspected OSAS

Symptoms/signs
Observation of apnea
Arousal
Habitual snoring Other causes of sleep
Mouth breathing disorders
Daytime fatigue No
Learning difficulties
Abnormal growth
Delayed puberty
Repetitive URI

Yes

Other related diseases Refer to pediatric specialist

Down syndrome Yes for underling diseases
neuromuscular diseases
cerebral palsy craniofacial syndromes

No

Follow-up for any

Polysomnography (PSG) complications
Negative result

Positive result

Management of etiology Repeat PSG if normal then

adenotonsillar hypertrophy ----- adenotonsillectomy follow up for recurrent events
obesity ------ weight loss ( + CPAP for severe case )
allergic rhinosinusitis ---- steroid nasal spray

Figure 1. Diagnosis and management of pediatric OSAS

17
Mu SC, et al.
CONCLUSIONS
Few new therapies for pediatric OSAS have been
validated with randomized controlled trials. Based
on the current evidence, it is reasonable to support
early diagnosis and treatment of this condition. The
purpose of this review has been to provide an update
on the epidemiology, clinical features, complications,
and treatment of childhood OSAS and the benefit of
tonsil removal for kids who have observed apneas,
constant snoring and difficulty in breathing during
sleep. The concise indications for adeno-tonsillectomy
are children over three years of age with OSAS who
have three or more tonsil infections in a year.
Acknowledgement
This project was supported by a grant from Shin-
Kong Wu Ho-Su Memorial Hospital (SKH-8302-101-
DR-19).
REFERENCES
1. Redline S, Tishler PV, Schluchter M, Aylor J, Clark
K, Graham G. Risk factors for sleep-disordered
breathing in children: associations with obesity,
race, and respiratory problems. Am J Respir Crit
Care Med 1999;159:1527-1532.
2. Lumeng JC, Chervin RD. Epidemiology of pediatric
obstructive sleep apnea. Proc Am Thorac Soc
2008; 5:242-252.
3. Guilleminault C, Winkle R, Korobkin R, Simmons
FB. Children and nocturnal snoring: evaluation
of the effects of sleep related respiratory resistive
load and daytime functioning. Eur J Pediatr
1982;139:165-171.
4. Katz ES, D’Ambrosio CM. Pediatric obstructive sleep
apnea syndrome. Clin Chest Med 2010;31:221-
234.
5. Urschitz MS, Guenther A, Eggebrecht E, et al.
Snoring, intermittent hypoxia and academic
performance in primary school children. Am J
Respir Crit Care Med 2003;168:464-468.
6. O’Brien LM, Mervis CB, Holbrook CR, et al.
Neurobehavioral implications of habitual snoring
in children. Pediatrics 2004;114:44-49.
18
7. Sargi Z, Younis RT. Pediatric obstructive sleep apnea:
current management. ORL 2007;69:340-344.
8. Rosen CL. Obstructive sleep apnea syndrome in
children: controversies in diagnosis and treatment.
Pediatr Clin North Am 2004;51:153-167.
9. Schechter MS. Section on Pediatric Pulmonology,
Subcommittee on Obstructive Sleep Apnea
Syndrome: Technical report: diagnosis and
management of childhood obstructive sleep apnea
syndrome. Pediatrics 2002;109:e69.
10. Rosen CL, Larkin EK, Kirchner HL, et al.
Prevalence and risk factors for sleep-disordered
breathing in 8- to 11-year-old children: association
with race and prematurity. J Pediatr 2003;142:383-
389.
11. Schlaud M, Urschitz MS, Urschitz-Duprat PM, et al.
The German study on sleep-disordered breathing
in primary school children: epidemiological
approach, representativeness of study sample, and
preliminary screening results. Paediatr Perinat
Epidemiol 2004; 18:431-440.
12. Ali NJ, Pitson DJ, Stradling JR. Snoring, sleep
disturbance, and behaviour in 4–5 year olds. Arch
Dis Child 1993;68:360-366.
13. Gislason T, Benediktsdottir B. Snoring, apneic
episodes, and nocturnal hypoxemia among children
6 months to 6 years old. An epidemiological study
of lower limit of prevalence. Chest 1995;107:963-
966.
14. Owen GO, Canter RJ, Robinson A. Overnight pulse
oximetry in snoring and non-snoring children. Clin
Otolaryngol 1995;20:402-406.
15. Hultcrantz E, Lofstrand-Tidestrom B, Ahlquist-
Rastad J. The epidemiology of sleep related
breathing disorder in children. Int J Pediatr
Otorhinolaryngol 1995;32:S63-S66.
16. Teculescu DB, Caillier I, Perrin P, Rebstock E,
Rauch A. Snoring in French preschool children.
Pediatr Pulmonol 1992;13:239-244.
17. Corbo GM, Fuciarelli F, Foresi A, De Benedetto
F. Snoring in children: association with
respiratory symptoms and passive smoking. BMJ
1989;299:1491-1494.
18. Ferreira AM, Clemente V, Gozal D, et al. Snoring
in Portuguese primary school children. Pediatrics
2000;106. Available at: http:// www.pediatrics.org/
cgi/content/full/106/5/e64

19. Jeans WD, Fernando DC, Maw AR, Leighton
BC. A longitudinal study of the growth of the
nasopharynx and its contents in normal children.
Br J Radiol 1981;54:117-121.
20. Guilleminault C, Pelayo R, Leger D, Clerk A,
Bocian RC. Recognition of sleepdisordered
breathing in children. Pediatrics 1996;98:871-882.
21. Li KK, Kushida C, Powell NB, Riley RW,
Guilleminault C. Obstructive sleep apnea
syndrome: a comparison between Far-East Asian
and white men. Laryngoscope 2000;110:1689-
1693.
22.Shatz A. Indications and outcomes of adenoidectomy
in infancy. Ann Otol Rhinol Laryngol 2004;113:835-
838.
23. Guilleminault C, Lee JH, Chan A. Pediatric
obstructive sleep apnea syndrome. Arch Pediatr
Adolesc Med 2005;159:775-785.
24. Goodwin JL, Babar SI, Kaemingk KL, et al.
Symptoms related to sleep-disordered breathing in
white and Hispanic children: the Tucson Children’s
Assessment of Sleep Apnea Study. Chest 2003;
124:196-203.
25. Guilleminault C, Khramtsov A. Upper airway
resistance syndrome in children: a clinical review.
Semin Pediatr Neurol 2001;8:207-215.
26. Contencin P, Guilleminault C, Manach Y. Long-
term follow-up and mechanisms of obstructive
sleep apnea (OSA) and related syndromes
through infancy and childhood. Int J Pediatr
Otorhinolaryngol 2003; 67:S119-S123.
27. Marcus CL. Sleep-disordered breathing in children.
Am J Respir Crit Care Med 2001;164:16-30.
28. American Academy of Pediatrics. Clinical practice
guidelines: diagnosis and management of childhood
obstructive sleep apnea syndrome. Pediatrics 2002;
109:704-712.
29. Goldstein NA, Pugazhendhi V, Rao SM, et al.
Clinical assessment of pediatric obstructive sleep
apnea. Pediatrics 2004;114:33-43.
30. Kaynak H, Kaynak D, Ostura I. Does frequency
of nocturnal urination reflect the severity of sleep-
disordered breathing? J Sleep Res 2004;13:173-
176.
31. Nieminen P, Tolonen U, Löppönen H. Snoring and
obstructive sleep apnea in children: a 6-month
follow-up study. Arch Otolaryngol Head Neck
Adenoidectomy-tonsillectomy in OSAS children
Surg 2000;126:481-486.
32. Carroll JL, Loughlin GM. Diagnostic criteria for
obstructive sleep apnea syndrome in children.
Pediatr Pulmonol 1992;14:71-74.
33. Gozal D, Wang M, Pope DW Jr. Objective
sleepiness measures in pediatric obstructive sleep
apnea. Pediatrics 2001;108:693-697.
34. Assessment of sleep disorders in the child. In:
Ferber R & Kryger M eds. Principles and Practice
of Sleep Medicine in the Child, by Ferber R. W.B
Saunders Company,1995:45-53.
35. Laurikainen E, Aitasalo K, Erkinjuntti M, Wanne
O. Sleep apnea syndrome in children - secondary
to adenotonsillar hypertrophy? Acta Otolaryngol
Suppl 1992;492:38-41.
36. Goldstein NA, Post JC, Rosenfeld RM, Campbell
TF. Impact of tonsillectomy and adenoidectomy on
child behavior. Arch Otolaryngol Head Neck Surg
2000;126:494-498.
37. Kravath RE, Pollak CP, Borowiecki B, Weitzman
ED. Obstructive sleep apnea and death associated
with surgical correction of velopharyngeal
incompetence. J Pediatr 1980;96:645-648.
38. Ali NJ, Pitson D, Stradling JR. Sleep disordered
breathing: effects of adenotonsillectomy on
behaviour and psychological functioning. Eur J
Pediatr 1996;155:56-62.
39. Frank Y, Kravath RE, Pollak CP, Weitzman ED.
Obstructive sleep apnea and its therapy: clinical
and polysomnographic manifestations. Pediatrics
1983;71:737-742.
40. Sofer S, Weinhouse E, Tal A, et al. Cor pulmonale
due to adenoidal or tonsillar hypertrophy or both
in children: noninvasive diagnosis and follow-up.
Chest 1988;93:119-122.
41. Wilkinson AR, McCormick MS, Freeland AP,
Pickering D. Electrocardiographic signs of
pulmonary hypertension in children who snore. Br
Med J 1981;282:1579-1581.
42. Owens J, Opipari L, Nobile C, Spirito A. Sleep and
daytime behavior in children with obstructive sleep
apnea and behavioral sleep disorders. Pediatrics
1998;102:1178-1184.
43. Carskadon MA, Acebo C. Parental reports of
seasonal mood and behavior changes in children.
J Am Acad Child Adolesc Psychiatry 1993;32:264-
269.
19
Mu SC, et al.
44. Brouilette R, Hanson D, David R, et al. A diagnostic
approach to suspected obstructive sleep apnea in
children. J Pediatr 1984;105:10-14.
45. Mahboubi S, Marsh RR, Potsic WP, Pasquariello
PS. The lateral neck radiograph in adenotonsillar
hyperplasia. Int J Pediatr Otorhinolaryngol
1985;10:67-73.
46. Fernbach SK, Brouillette RT, Riggs TW, Hunt CE.
Radiologic evaluation of adenoids and tonsils in
children with obstructive sleep apnea: plain films
and fluoroscopy. Pediatr Radiol 1983;13:258-265.
47. ASDA report. Standards and indications for
cardiopulmonary sleep studies in children.
American Thoracic Society. Am J Respir Crit Care
Med 1996;153:866-878.
48. Redline S, Kapur VK, Sanders MH, et al. Effects
of varying approaches for identifying respiratory
disturbances on sleep apnea assessment. Am J
Respir Crit Care Med 2000;161:369-374.
49. Mindell JA, Owens JA. A clinical guide to pediatric
sleep: Diagnosis and management of sleep. 2nd ed.
Philadelphia, PA: Lippincott Williams & Wilkins,
2010.
50. McColley SA, April MM, Carroll JL, Naclerio
RM, Loughlin GM. Respiratory compromise after
adenotonsillectomy in children with obstructive
sleep apnea. Arch Otolaryngol Head Neck Surg
1992;118:940-943.
51. Burke AJ, Vining DJ, McGuirt WF Jr, Postma G,
Browne JD. Evaluation of airway obstruction using
virtual endoscopy. Laryngoscope 2000;110:23-29.
52. Sher AE, Shprintzen RJ, Thorpy MJ. Endoscopic
observations of obstructive sleep apnea in children
with anomalous upper airways: predictive and
therapeutic value. Int J Pediatr Otorhinolaryngol
1986;11:135-146.
53. Myatt HM, Beckenham EJ. The use of diagnostic
sleep nasendoscopy in the management of children
with complex upper airway obstruction. Clin
Otolaryngol 2000;25:200-208.
54. Arens R, McDonough JM, Costarino AT, et al.
Magnetic resonance imaging of the upper airway
structure of children with obstructive sleep
apnea syndrome. Am J Respir Crit Care Med
2001;164:698-703.
55. Paradise JL, Bluestone CD, Bachman RZ, et al.
Efficacy of tonsillectomy for recurrent throat
20
infection in severely affected children:results of
parallel randomized and nonrandomized clinical
trials. N Engl J Med 1984;310:674-683.
56. Rosenfeld RM, Green RP. Tonsillectomy and
adenoidectomy: changing trends. Ann Otol Rhinol
Laryngol 1990;99:187-191.
57. Berkowitz RG, Zalzal GH. Tonsillectomy in
children under 3 years of age. Arch Otolaryngol
Head Neck Surg 1990;116:685-686.
58. Chiang PY, Lin CM, Powell N, Chiang YC, Tsai YJ.
Systematic analysis of cephalometry in obstructive
sleep apnea in Asian children. Larygoscope 2012;
122:1867-1872.
59. Tauman R, Gulliver TE, Krishna J, et al. Persistence
of obstructive sleep apnea syndrome in children
after adenotonsillectomy. J Pediatr 2006;149:803-
8.
60. la Chaux R, Klemens C, Patscheider M.
Tonsillotomy in the treatment of obstructive sleep
apnea syndrome in children: polysomnographic
results. Int J Pediatr Otorhino 2008;72:1411-1417.
61. Pirelli P, Saponara M, Guilleminault C. Rapid
maxillary expansion in children with obstructive
sleep apnea syndrome. Sleep 2004;27:761-766.
62. Suen JS, Arnold JE, Brooks LJ. Adenotonsillectomy
for treatment of obstructive sleep apnea in children.
Arch Otolaryngol Head Neck Surg 1995; 121:525–
530.
63. Bhattacharjee R, Kheirandish-Gozal L, Spruyt K,
et al. Adenotonsillectomy outcomes in treatment of
obstructive sleep apnea in children: a multicenter
retrospective study. Am J Respir Crit Care Med
2010;182:676-683.
64. O’Brien LM, Sitha S, Baur LA, Waters KA.
Obesity increases the risk for persisting obstructive
sleep apnea after treatment in children. Int J Pediatr
Otorhinolaryngol 2006;70:1555-1560.
65. Ogden CL, Carroll MD, Curtin LR, McDowell MA,
Tabak CJ, Flegal KM. Prevalence of overweight
and obesity in the United States, 1999–2004.
JAMA 2006;295:1549-1555.
66. Ogden CL, Flegal KM, Carroll MD, Johnson
CL. Prevalence and trends in overweight among
US children and adolescents, 1999–2000. JAMA
2002;288:1728-1732.
67. Goldbart AD, Sari GD, Tal A. Montelukast for
children with obstructive sleep apnea: a double-
 Adenoidectomy-tonsillectomy in OSAS children

blind, placebo-controlled study. Pediatrics 259.

2012;130:e575-e580. 69. Ray RM, Senders CW. Airway management in the
68. Chun TA, Li AM. Obstructive sleep breathing obese child. Pediatr Clin North Am 2001;48:1055-
disorders. Pediatr Clin North Am 2009;56:243– 1063.

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