Evaluation of Suspected Obstructive Sleep Apnea in Children - UpToDate

4/23/2020 Evaluation of suspected obstructive sleep apnea in children - UpToDate
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Evaluation of suspected obstructive sleep apnea in

children
Author: Shalini Paruthi, MD
Section Editor: Ronald D Chervin, MD, MS
Deputy Editor: Alison G Hoppin, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2020. | This topic last updated: Mar 19, 2020.
INTRODUCTION
Obstructive sleep apnea (OSA) is characterized by episodes of complete or partial upper airway
obstruction during sleep, often resulting in gas exchange abnormalities and disrupted sleep.
Untreated OSA is associated with learning and behavioral problems, cardiovascular complications,
and impaired growth (including failure to thrive [FTT]) [1-6]. Early diagnosis and treatment of OSA
may decrease morbidity. However, diagnosis is frequently delayed [3,7]. (See "Management of
obstructive sleep apnea in children", section on 'Consequences of untreated OSA'.)
The risk factors, clinical manifestations, screening, and diagnostic evaluation of children who are
suspected of having OSA are reviewed here. Pathogenesis, predisposing conditions, and
treatment of pediatric OSA are discussed in other topic reviews:
● (See "Mechanisms and predisposing factors for sleep-related breathing disorders in children".)
● (See "Management of obstructive sleep apnea in children".)
● (See "Adenotonsillectomy for obstructive sleep apnea in children".)
● (See "Cardiovascular consequences of obstructive sleep apnea in children".)
EPIDEMIOLOGY
OSA occurs in 1 to 5 percent of children. It can occur at any age and may be most common in
those between two and six years of age [8,9].
RISK FACTORS
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Adenotonsillar hypertrophy and obesity are the major risk factors for OSA in otherwise healthy
children. The contribution of each of these risk factors varies among individuals and also tends to
vary with age:
Adenotonsillar hypertrophy — Adenotonsillar hypertrophy is a widely recognized risk factor for

OSA in children. The size and location of the tonsils and adenoids are influenced by genetic
factors, infection, and inflammation. Although tonsils that appear large on anterior oral examination
may contribute to a reduction in the airway size, there is not a clear linear correlation of increased
size of tonsils and adenoids with greater severity of OSA. Thus, even "small" tonsils (eg, within the
tonsillar pillars graded as a 1+ (figure 1)) may be clinically significant and cause obstruction in the
airway during sleep. Adenoids are best visualized by nasal endoscopy and can also contribute to
reduction of the airway size [10]. (See "Mechanisms and predisposing factors for sleep-related
breathing disorders in children", section on 'Enlarged tonsils and adenoids'.)
Obesity — Obesity is an important risk factor for OSA at all ages but is particularly prominent
among adolescents. In a prospective study, OSA was diagnosed in 4 percent of adolescents (16 to
19 years of age) and most of them had not had OSA or habitual snoring during mid-childhood [11].
The strongest risk factors for OSA during adolescence were obesity, male sex, and a history of
adenotonsillectomy. The importance of obesity as a predictor of OSA during adolescence is
underscored by a separate study of 37 adolescents with moderate to severe obesity (body mass
index [BMI] >97th percentile), among whom 45 percent had OSA on polysomnogram (defined as
apnea-hypopnea index [AHI] >1.5 in this study) [12]. (See "Mechanisms and predisposing factors
for sleep-related breathing disorders in children", section on 'Obesity'.)
Other — Other risk factors for medical, neurologic, skeletal, or dental conditions that reduce upper
airway size, affect the neural control of the upper airway, or impact the collapsibility of the upper
airway are also risk factors for OSA. Individuals presenting with OSA during infancy are particularly
likely to have an underlying anatomic or genetic anomaly [13]. Examples include the following [14]:
● Cerebral palsy
● Down syndrome
● Craniofacial anomalies (eg, retrognathia, micrognathia, midface hypoplasia)
● History of low birth weight [15,16]
● Muscular dystrophy or other neuromuscular disorders
● Myelomeningocele [17]
● Achondroplasia
● Mucopolysaccharidoses (eg, Hunter syndrome and Hurler syndrome)
● Prader-Willi syndrome
● Orthodontic problems (eg, high narrow hard palate, overlapping incisors, crossbite) [5]
● Family history of OSA [18-20]
● History of prematurity and multiple gestation [21]

Children with any of these conditions should be followed closely for signs and symptoms of OSA.
Objective assessment with polysomnography (PSG) is recommended in children with complex
medical conditions who present with signs and symptoms of OSA [22]. Additional factors that
contribute to the overall risk for sleep-disordered breathing include environmental smoke exposure,
asthma, or allergic rhinitis [23]. These risk factors are discussed in greater detail separately. (See
"Mechanisms and predisposing factors for sleep-related breathing disorders in children", section
on 'Predisposing factors'.)
CLINICAL MANIFESTATIONS
Clinical manifestations of OSA are outlined in the table (table 1). Key features are:
Nocturnal symptoms — Habitual (≥3 nights per week) or loud snoring is present in most children
with OSA [3,5,24-26]. However, a history of snoring is insufficient for the diagnosis because many
children who snore do not have OSA [3,5,24,25]; habitual snoring in the absence of OSA (known
as primary snoring) occurs in 3 to 12 percent of the general pediatric population [8,27-30] and may
still have adverse health consequences. Conversely, the absence of snoring is insufficient to
exclude OSA [31,32].
Other nocturnal symptoms include mouth breathing, noisy breathing, pauses in breathing,
coughing or choking in sleep, restless sleep, and nighttime sweating. Also common but less well-
recognized symptoms are nocturnal enuresis and parasomnias such as sleepwalking and sleep
terrors. (See "Nocturnal enuresis in children: Etiology and evaluation".)
Daytime symptoms — Daytime sleepiness may be less obvious in children than in adults but may
manifest as age-inappropriate daytime napping, complaints of sleepiness, or falling asleep during
school, short car rides, or on the school bus [25,33,34]. Importantly, OSA is associated with
inattention, learning problems, and behavioral problems (eg, hyperactivity, impulsivity,
rebelliousness, and aggression), sometimes leading to a diagnosis of attention deficit hyperactivity
disorder (ADHD) [8,31,35-41]. In some children, treatment of OSA may improve learning and
behavioral problems [8,42-50]. Some children will have irritable mood or difficulty controlling
emotions due to disrupted sleep. (See "Cognitive and behavioral consequences of sleep disorders
in children", section on 'Sleep-related breathing disorders'.)
Mouth breathing or hyponasal speech are common in children with OSA due to the association
with adenoidal hypertrophy. Morning headaches may be present due to disrupted sleep and
repeated arousals from sleep due to respiratory events.
Potential consequences in childhood
● Growth – Severe OSA can be associated with failure to thrive (FTT). The poor growth is due
in part to the increased energy expenditure that is necessary to meet the demands of an

elevated work of breathing during sleep [51]. In addition, nocturnal growth hormone secretion
may be decreased in children with increased upper airway resistance during sleep [4].
Although reported in early literature, FTT is seldom seen now, perhaps because children are
more often diagnosed with OSA before the condition becomes severe enough to cause FTT.
(See "Poor weight gain in children younger than two years in resource-rich countries: Etiology
and evaluation".)
Increased growth and weight gain have been reported after treatment of OSA with
adenotonsillectomy, including in obese children [42,52-57]. (See "Adenotonsillectomy for
obstructive sleep apnea in children", section on 'Weight gain'.)
● Cardiopulmonary – Untreated severe OSA may lead to cardiovascular effects including right
ventricular (RV) and left ventricular (LV) dysfunction, and systemic hypertension [58-61], as
well as endothelial dysfunction [62]. Only limited data exist to suggest an association between
OSA and pulmonary hypertension in children, in contrast with adults, and symptomatic
pulmonary hypertension is rare. The clinical findings and mechanisms for these
cardiopulmonary effects are discussed separately. (See "Cardiovascular consequences of
obstructive sleep apnea in children".)
SCREENING
To screen for OSA, caregivers of all children should be asked about snoring during routine health
care visits and visits when the airway is evaluated (such as upper respiratory illness/sick child
visits), as recommended by the American Academy of Pediatrics (AAP) [63]. Any child who snores
habitually (eg, ≥3 nights per week), has loud snoring, or pauses in breathing should undergo a full
diagnostic evaluation for OSA, as outlined below and in the algorithm (algorithm 1). Other children
may also warrant a diagnostic evaluation if they have risk factors and/or other symptoms that may
be associated with OSA, including attention deficit hyperactivity disorder (ADHD) or related
disruptive behavior (table 1). (See 'Evaluation' below.)
Children with a history of treated OSA should also be followed closely for the possibility of
recurrence or residual OSA symptoms. This is because OSA may recur after treatment (eg,
adenotonsillectomy) and may worsen with age or weight gain [22]. (See "Adenotonsillectomy for
obstructive sleep apnea in children", section on 'Indications for postoperative polysomnography'.)
EVALUATION
Overview and referrals — A complete diagnostic evaluation for OSA consists of the following
steps:
● Focused sleep history

● Physical examination including detailed examination of the oropharynx

● Polysomnography (PSG) and/or referral to a specialist in sleep medicine or otolaryngology
(ear, nose, and throat) for further evaluation and possible treatment [22,63]
Specialty referral and PSG depend on individual patient characteristics including severity of
symptoms. The PSG is needed to make a definitive diagnosis of OSA and can assist with
treatment decisions. (See 'Polysomnography' below.)
Existing literature does not indicate which type of specialty referral serves best. Selection may
depend in part on local resources and practice patterns. The sequence and timing of referral to the
specialist depends on the clinical level of suspicion for OSA (ie, severity of symptoms) and local
resources. In many settings, the most detailed sleep history and PSG are performed by a sleep
medicine clinician. Some sleep medicine clinicians are pediatricians, but the large majority are not.
However, among those who are not pediatricians, many regularly include children in their
practices.
History — The history should specifically evaluate for all of the risk factors for OSA and for
nocturnal and daytime symptoms (table 1), with particular attention to (see 'Clinical manifestations'
above):
● Snoring, especially when frequent or loud

● Labored breathing or observed pauses in breathing during sleep
● Nocturnal enuresis
● Daytime attention, learning difficulties, and behavior problems (eg, attention deficit
hyperactivity disorder [ADHD] or problems with functioning in school)
● Sleepiness
Examination — While most children with OSA have a normal physical examination, several
abnormalities may be observed. These may provide direct or indirect evidence of increased upper
airway resistance [64-66] and provide clues to the cause of the symptoms:
● Growth – The child's height and weight should be plotted on a standard growth chart and
body mass index (BMI) calculated. Obesity is an important risk factor for OSA. Paradoxically,
poor growth can be a sign of chronic severe OSA, particularly in infants and young children
[51,67]. Either of these findings in a child with OSA symptoms warrants a full evaluation. (See
'Obesity' above and 'Potential consequences in childhood' above.)
● Cardiopulmonary – Blood pressure should be measured and every physical examination

should include careful cardiac auscultation for evidence of pulmonary hypertension. (See
"Definition and diagnosis of hypertension in children and adolescents" and "Treatment and
prognosis of pulmonary arterial hypertension in adults (group 1)".)

● Head and nose – Craniofacial anomalies (eg, midface hypoplasia, retrognathia, micrognathia)
suggest abnormal upper airway anatomy. Mouth breathing, long ("adenoidal") facies (figure 2),
decreased nasal airflow, or hyponasal speech are consistent with adenoidal hypertrophy,
which can contribute to OSA. Mucosal or turbinate swelling suggests chronic nasal
congestion, which may be allergic, particularly if it is accompanied by other allergic
manifestations, such as dark circles under the eyes, swollen eyes, or a transverse nasal
crease. Also evaluate for obstructive septal deformity or intranasal mass.
● Mouth – A high-arched and narrow hard palate (picture 1), a crossbite, overlapping incisors,
and a significant overbite suggest a small jaw, which may be due to abnormal
maxillomandibular development [5]. Macroglossia may also reduce flow through the upper
airway. Poor pharyngeal or laryngeal tone raises the possibility of neuromotor disease (eg,
cerebral palsy, muscular dystrophy). The examiner should note tonsil size (figure 1 and picture
2), and Mallampati classification or Friedman score (figure 3) [68,69], to describe the degree
of oropharyngeal crowding. Additionally, the clinician should note information regarding jaw
structure, including overjet, overbite, and molar occlusion classification (if molars have grown
in). There is no linear correlation of tonsil size and severity of OSA. Often, further information
regarding obstruction is obtained during direct laryngoscopy performed by an otolaryngologist
and may inform the choice of treatment. (See 'Adenotonsillar hypertrophy' above and
"Management of obstructive sleep apnea in children", section on 'Choice of therapy'.)
Polysomnography
Indications — Attended in-laboratory nocturnal PSG (overnight PSG) is the gold standard for
diagnosis of OSA [24,64,70-72]. The PSG is the only diagnostic tool that can definitively identify
obstructive events and quantify the severity of OSA, including gas exchange abnormalities and
sleep disruption (arousals associated with respiratory events). Guidelines have been published
regarding indications for PSG [14,63,73]. However, there is considerable variation in practice
regarding the use of PSG to confirm the diagnosis when OSA is clinically suspected. The decision
to order PSG is influenced by several factors, including the evaluating clinician, parent preference,
age of child, child's medical comorbidities, child's tolerance of sensors, availability and accessibility
of testing, etc. We suggest the following approach:
● Standard risk – For children with clinically suspected OSA and without the high-risk
characteristics described below, the child should be offered referral for PSG or referral first to
a sleep medicine clinician or otolaryngologist experienced in evaluation and management of
sleep-disordered breathing in children [22].
● High risk – For children with obesity, Down syndrome, craniofacial abnormalities,
neuromuscular disorders, sickle cell disease, mucopolysaccharidoses, or other underlying
conditions that affect the airway, we recommend referral to a sleep medicine clinician
experienced in pediatric sleep medicine. In these cases, a PSG is also needed to establish a

firm diagnosis of OSA and evaluate its severity before making management decisions and for
postsurgical planning [8,14,73].
In many settings, the PSG is arranged after referral to a specialist in otorhinolaryngology or sleep
medicine (algorithm 1). Alternatively, the primary care clinician may choose to arrange for a PSG if
a facility with experience in pediatric PSG is available. The child should be referred to a sleep
medicine clinician or otolaryngologist if the PSG shows sleep-disordered breathing, or if there are
persistent sleep problems even if the PSG is normal or detects only primary snoring. The sleep
medicine clinician can evaluate and treat several other sleep disorders that may account for sleep
disruption. Moreover, in some cases primary snoring may contribute to sleep disruption and
daytime dysfunction; this issue is the focus of an ongoing study of adenotonsillectomy for children
with primary snoring (NCT02562040). (See "Adenotonsillectomy for obstructive sleep apnea in
children", section on 'Screening and referrals'.)
Technique — The PSG is performed in a sleep laboratory by sleep technologists and

interpreted by clinicians with training in sleep medicine. Sedatives and sleep deprivation prior to
PSG are not recommended, because both may increase upper airway resistance and confound
the assessment of OSA [74,75]. In most cases, children can continue to take their usual
medications. One night of PSG is the gold standard for diagnosis of OSA and is usually sufficient
based on reported night-to-night variability in children [8,76,77]. (See "Overview of
polysomnography in infants and children".)
Multiple sensors are used during PSG to monitor for sleep-disordered breathing, including nasal
and oral airflow sensors, snoring microphone, respiratory impedance plethysmography, pulse
oximetry, electrocardiography, carbon dioxide (CO2) monitoring, electroencephalography (EEG),
and body position monitoring. (See "Overview of polysomnography in infants and children", section
on 'Respiratory monitoring'.)
Measurement of these variables permits detection of events and calculation of summary measures
[78], which contribute to the diagnosis of OSA and severity assessment. (See 'Diagnostic criteria'
below and 'Assessment of severity' below.)
Respiratory events — The following are the most common events documented on PSG
reports; the specific definitions and implications are summarized in the table (table 2). Either adult
or pediatric scoring criteria may be used to score pediatric studies in adolescents between 13 and
18 years of age [78]. However, interpretation of study results and diagnosis of OSA should be
based on the most current version of the International Classification of Sleep Disorders [9]. Fewer
respiratory events are scored if adult criteria versus pediatric criteria for scoring are applied. For
this reason, use of adult criteria for an adolescent may lead to underestimation of the presence or
severity of OSA, underscoring the need for thoughtful interpretation of all of the PSG findings [79].
The adult scoring criteria stipulate that obstructive apneas, hypopneas, and respiratory effort-
related arousals (RERAs) must last at least 10 seconds to be scored, whereas the pediatric

scoring criteria stipulate that they must last for ≥2 breath cycles (which may be shorter than 10
seconds, especially in infants and young children).
● Apneas – ≥90 percent decrease in airflow signal; apneas are further characterized as
obstructive (most common), central, or mixed.
● Hypopneas – ≥30 percent decrease in airflow signal, associated with cortical arousal or
oxygen desaturation of ≥ 3 percent.
● Respiratory effort-related arousal (RERA) – Arousal preceded by evidence of airway

obstruction that is insufficient to qualify as an apnea or hypopnea (eg, increasing thoracic or
abdominal excursion without increased airflow, flattening of the inspiratory portion of the nasal
pressure waveform, or crescendo snoring, or an elevation in the end-tidal CO2). This type of
apneic event is more subtle than apneas and hypopneas, and scoring it is considered
optional.
● Hypoxemia – PSG reports often list the oxyhemoglobin saturation (SpO2) nadir for the entire
study or the percentage of sleep time spent with oxyhemoglobin saturation less than a
specified threshold, such as 90 percent.
● Hypercapnia – End-tidal or transcutaneous CO2 is summarized, as an assessment for sleep-

related hypoventilation.
Summary measures — The following summary measures are generally used for the diagnosis
of OSA and for assessment of severity. (See 'Diagnostic criteria' below and 'Assessment of
severity' below.)
● Apnea-hypopnea index (AHI) – The number of apneas plus hypopneas per hour of sleep.
● Respiratory disturbance index (RDI) – The number of apneas, hypopneas, and RERAs per
hour of sleep.
● Hypoventilation – End-tidal or transcutaneous CO2 >50 mmHg that persists for more than 25
percent of the total sleep time.
Other summary measures that can be calculated from the PSG data include sleep latency, amount
of wake after sleep onset, sleep efficiency (total sleep time x 100 ÷ total recording time), the
arousal index, percentage of sleep time spent in each sleep stage, and AHI in different sleeping
positions or stages of sleep. These events and summary measures are similar to those used in
adults and are described in detail separately. (See "Polysomnography in the evaluation of sleep-
disordered breathing in adults".)
Alternatives to polysomnography — If polysomnography (PSG) is not available, clinicians may

consider referral to an otolaryngologist or alternate diagnostic tests [8]. Diagnostic tests other than
PSG have been evaluated. All of these alternative tests have a low negative predictive value,
indicating that a negative result is not sufficient to exclude OSA, and these tests should not be
used in routine practice [8,63]. However, these tests may be useful in selected cases if PSG is not
available.
● Home sleep apnea tests (HSATs) – HSATs, previously called portable monitoring or out-of-
center sleep testing, are considered acceptable options for diagnosis of OSA in adults under
some circumstances [80]. However, HSATs are not recommended for diagnosis of OSA in
children, as explained in a position paper from the American Academy of Sleep Medicine
(AASM) [81].
After a literature review, the AASM task force found insufficient evidence to support use of
HSATs in children to diagnose OSA. The main concern is that use of HSATs may lead to
underestimation of OSA presence and severity in children, primarily because most HSAT
devices measure fewer physiologic variables than PSG (eg absence of capnography and
identification of arousals). The HSAT is also associated with technical failure (inadequate data
collected) in up to 25 percent of studies, which is substantially higher than attended in-
laboratory PSG [82-84]. Technical failure is often due to loss of pulse oximetry signal and is
most common in younger children. Loss of nasal flow signals is also common in both attended
and unattended studies of children, but it cannot be corrected in the unattended setting [85].
Ambulatory devices that include capnography (end-tidal CO2) are available, but a study of one
such device in pediatric patients with neuromuscular disease reported a sensitivity and
specificity to diagnose OSA of only 68 percent and 67 percent, respectively, compared with
attended in-laboratory PSG (AHI >1 threshold), in part because of high rates of incomplete or
falsely low capnography measurements [86].
An HSAT device has been developed that uses peripheral arterial tonometry to determine the
presence of respiratory events. A small validation study in 38 adolescents showed high
correlations for AHI (r = 0.945, p <0.001 [device versus PSG]) and minimum oxygen saturation
(r = 0.921, p <0.001 [device versus PSG]) [87]. There were several limitations to this study,
including lack of CO2 monitoring, small sample size, and inability to distinguish between
central and obstructive respiratory events. Larger validation studies will be needed to confirm
that this device can accurately diagnose adolescents with OSA. Although this device has been
approved by the US Food and Drug Administration for use in children 13 years and older, it is
not yet a standard of care to perform HSATs in children.
The use of HSATs in adults is discussed separately. (See "Home sleep apnea testing for
obstructive sleep apnea in adults".)
● Nap PSG – Nap PSG is an abbreviated study that records sleep and breathing in the sleep
laboratory during the daytime. This type of study is limited by the short recording time and the
possible absence of rapid eye movement (REM) sleep. Nap PSG has a good positive

predictive value (77 to 100 percent) but a poor negative predictive value (17 to 49 percent) for
identifying OSA in children [88,89]. As a result, a nap study indicating that a child does not
have OSA is insufficient to exclude OSA [14]. This type of testing is often reserved for infants
or younger children who regularly take naps.
● Overnight continuous pulse oximetry – Overnight continuous pulse oximetry that monitors
pulse rate, pulse amplitude, and oxyhemoglobin saturation can identify OSA in some children
by detecting clusters of desaturation events [90,91]. A systematic review reported that
moderate to severe OSA was likely in children with at least three clusters of desaturation
events and at least three desaturation events <90 percent [90]. In one study, pulse oximetry
detected OSA with a positive predictive value of 97 percent and a negative predictive value of
53 percent [92].
● Audiotapes and videotapes – Audiotapes identify OSA with a positive predictive value of 50
to 75 percent and a negative predictive value of 73 to 83 percent [93,94]. Videotapes identify
OSA with a positive predictive value of 83 percent and a negative predictive value of 88
percent [95].
Questionnaires — Several questionnaires have been developed to assess symptoms or signs

associated with OSA. In general, these were designed for use in clinical research. However,
anecdotally they are used for clinical screening or assessment in some settings and especially in
world regions where access to laboratory-based PSG is limited. We favor using a detailed clinical
history and physical examination rather than questionnaires to guide diagnosis for individual
patients and treatment decisions such as adenotonsillectomy or watchful waiting.
One of the best validated questionnaires is the Sleep-Related Breathing Disorder (SRBD) scale
from the Pediatric Sleep Questionnaire (PSQ), which can be obtained and licensed at no charge
[96]. The SRBD scale predicts PSG results to an extent that is useful for clinical research. The
SRBD scale cannot replace PSG in identification of pediatric OSA, but the scale may have utility in
some clinical settings. For example, in contrast with PSG, the SRBD generates a score that
correlates with OSA-related impairment of behavior, quality of life, and sleepiness, and helps to
predict improvement in these morbidities after adenotonsillectomy [97]. The SRBD scale was
originally tested against and validated in two separate groups of children with PSG-confirmed
OSA. The instrument correctly classified 86 and 85 percent of children and had a sensitivity of 0.85
and 0.81, with specificity of 0.87 for both groups [98,99]. Performance characteristics may vary
among children with specific underlying health conditions. The SRBD scale has been validated for
screening for OSA in children with asthma [100] but may have lower sensitivity for children with
underlying neuromuscular disorders and Down syndrome, depending on the targeted
polysomnographic threshold for SRBD [101]. The SRBD scale contains a four-item sleepiness
subscale that has been validated against the Multiple Sleep Latency test (MSLT) [102]. The total
score on the PSQ ranges from 0.0 to 1.0, and a score ≥0.33 suggests high probability for presence
of OSA.
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A questionnaire that elicits key symptoms of OSA in children may be useful as an initial screening
tool in clinical practice. As an example, the eight-item screening tool, I'M SLEEPY, was developed
for primary care clinicians to screen for pediatric OSA and validated in 150 children who underwent
PSG. The parent version of the I'M SLEEPY tool has a sensitivity of 0.82, specificity of 0.5, and
negative predictive value of 0.85 [103]. Thus, this is a reasonable tool to facilitate screening
questions but should not replace a full clinical evaluation.
Among the sleep questionnaires used for research and clinical purposes in adults, only a few are
applicable to children. The Epworth Sleepiness Scale that is commonly used for adults was
modified for use in children [104] and may be helpful to assess sleepiness in disorders such as
OSA or narcolepsy, or to follow response to intervention. The use of the Epworth Sleepiness Scale
in adults is discussed elsewhere. (See "Quantifying sleepiness".)
Other tests — Additional testing may be helpful in selected patients:
● Cardiopulmonary disease – Children with any evidence of underlying cardiopulmonary

disease, such as asthma or signs of pulmonary hypertension, should be evaluated with chest
radiography, electrocardiography, and echocardiography. These tests should also be
considered for children with confirmed severe OSA. The radiographs evaluate for lower airway
disease that might contribute to hypoxemia during sleep, independent of upper airway
obstruction. The cardiac testing evaluates for cardiac function and potential consequences of
OSA, particularly left or right ventricular (LV or RV) hypertrophy. (See 'Assessment of severity'
below.)
● Anatomic abnormalities – Children who have risks for airway abnormalities, such as those
with Down syndrome or craniofacial abnormalities, should be evaluated with airway
radiography, cephalometry (a lateral radiograph of the head and neck), and/or computed
tomography of the upper airway. Some patients may warrant further evaluation with drug-
induced sleep endoscopy (DISE), which is typically performed after referral to a specialist.
These tests can quantify the degree and site of obstruction and help with planning for surgical
procedures, such as adenotonsillectomy, uvulopalatopharyngoplasty, or oral corrective
surgery [105]. These tests are not indicated in the routine diagnostic evaluation of children
with suspected OSA. (See "Adenotonsillectomy for obstructive sleep apnea in children",
section on 'Diagnostic procedures'.)
Any testing that requires sedation or anesthesia should be undertaken with caution since
effects on both upper airway muscle tone and the ventilatory response (to hypoxemia and
hypercapnia) can precipitate respiratory decompensation in children with OSA [106,107].
Laboratory tests are not routinely indicated. Findings such as polycythemia or compensatory
metabolic alkalosis support the diagnosis of OSA but are absent in most children.

Neurocognitive testing may be helpful in planning therapy and appropriate school accommodations
for children with suspected OSA who have behavioral or learning difficulties. (See "Specific
learning disabilities in children: Evaluation", section on 'Psychometric tests' and "Attention deficit
hyperactivity disorder in children and adolescents: Clinical features and diagnosis", section on
'Ancillary evaluation for select patients'.)
DIAGNOSIS
Diagnostic criteria — The following are the diagnostic criteria for pediatric OSA (all children <18
years of age) as defined by the American Academy of Sleep Medicine (AASM) [9]. (See "Clinical
presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnosis'.)
Both clinical and polysomnographic (PSG) criteria should be present for a child to be definitively
diagnosed with OSA.
● Clinical criteria ("A criteria") – The presence of one or more of the following clinical
symptoms:
• Snoring
• Labored, paradoxical, or obstructed breathing during the child's sleep
• Sleepiness, hyperactivity, behavioral problems, or learning problems
● Polysomnographic criteria ("B criteria") – The PSG demonstrates one or both of the
following:
• One or more obstructive apneas, mixed apneas, or hypopneas, per hour of sleep (table 2)
[78].
• A pattern of obstructive hypoventilation, defined as at least 25 percent of total sleep time

with hypercapnia (partial pressure of carbon dioxide [PaCO2] >50 mmHg) in association
with one or more of the following:
- Snoring
- Flattening of the nasal pressure waveform
- Paradoxical thoracoabdominal motion
Upper airway resistance syndrome and obstructive hypoventilation were previously considered
distinct entities but have now been subsumed into the category of OSA [9].
Assessment of severity — The clinical symptoms and the severity of findings on PSG (apneas,
hypopneas, extent of desaturation, sleep disruption) inform treatment decisions. As examples, a
child with mild OSA might be initially managed with watchful waiting or medical therapies for up to
six months, whereas children with severe OSA warrant prompt treatment with adenotonsillectomy

or positive airway pressure. (See "Management of obstructive sleep apnea in children", section on
'Choice of therapy'.)
No clear-cut classification of OSA severity in children has gained uniform acceptance. The PSG
findings should be interpreted by a qualified sleep medicine clinician, using all of the PSG
parameters and in the context of the child's symptoms and any contributing risk factors. The
following simplified classification schemes can be used as a first step in assessing the PSG
findings. These schemes also have been used to define severity groups in research studies.
Preliminary classification using RDI or AHI — PSGs tend to report the respiratory
disturbance index (RDI) or apnea-hypopnea index (AHI) (table 2), and the following categories can
be used as an index of severity:
● Mild OSA – RDI or AHI, 1 to 4.9

● Moderate OSA – RDI or AHI, 5 to 9.9
● Severe OSA – RDI or AHI, >10
These values derive from practice and limited consensus and are not evidence-based [73].
Of note, it is common to observe a small number of central apneas (central apnea index >1 and
<5) in addition to obstructive respiratory events. These central apneas (spontaneous, movement-
related, or sigh-related) usually improve with adenotonsillectomy. A central apnea index >5 is rare
and suggests a need for further evaluation for a cardiac, metabolic, or neurologic disorder [108].
Further interpretation — Some night-to-night variability occurs on sleep studies; as a result, a

patient may have disparate AHI or RDI results on different nights, even when sleep stage and
position are controlled. Nonetheless, the overall severity classification is reasonably consistent. In
one study of 30 children each undergoing PSG on two occasions, RDIs varied between nights, but
the overall severity classification changed in only two of the subjects [76].
Attempts to specify severity of OSA and make treatment decisions solely on the basis of the RDI or
AHI and minimum oxygen saturation may lead to misclassification. Additional variables that can be
informative on sleep studies can include cortical arousals as a measure of sleep fragmentation
(captured by the arousal index, hypopneas, and respiratory effort-related arousals [RERAs]),
number of and nadir of oxygen desaturations, time spent below an oxygen saturation of 90 or 88
percent, capnography, state of sleep (rapid eye movement [REM] versus non-rapid eye movement
[NREM]), and body position during sleep.
Of note, PSG indices are not well correlated with symptoms of daytime functional impairment,
which may include daytime sleepiness (eg, falling asleep at school), headaches, low school grades
due to poor concentration, and several symptoms that can mimic the criteria for attention deficit
hyperactivity disorder (ADHD) [109] (see 'Daytime symptoms' above). Therefore, in practice, a
diagnosis of pediatric OSA should be based on symptoms and signs with confirmatory PSG data.

Whether symptomatic children with negative PSG results still merit treatment for OSA, as
suggested by some reports [50,110], is the subject of a multicenter clinical trial currently in
progress (Pediatric Adenotonsillectomy Trial for Snoring, or PATS).
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around
the world are provided separately. (See "Society guideline links: Sleep-related breathing disorders
including obstructive sleep apnea in children".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Sleep apnea in children (The Basics)")
SUMMARY AND RECOMMENDATIONS
● Obstructive sleep apnea (OSA) is characterized by episodic complete or partial upper airway
obstruction during sleep, usually resulting in gas exchange abnormalities or disrupted sleep.
(See 'Introduction' above.)
● Adenotonsillar hypertrophy and obesity are the major risk factors for OSA. Other conditions
that reduce upper airway size, affect the neural control of the upper airway, or impact the
collapsibility of the upper airway are also risk factors for OSA. (See 'Risk factors' above.)
● Key clinical manifestations of OSA include (table 1):
• Nocturnal symptoms – Habitual or loud snoring is an important clinical feature of OSA.

Most children with OSA habitually snore, while lack of habitual snoring makes OSA less
likely. However, the presence of habitual snoring is insufficient for the diagnosis of OSA

because many children who snore do not have OSA. Other nocturnal symptoms in some
patients include sleepwalking, enuresis, or sweating. (See 'Nocturnal symptoms' above.)
• Daytime symptoms – Inattention, learning problems, and behavioral problems (eg,

hyperactivity, impulsivity, rebelliousness, and aggression) are associated with sleep-
disordered breathing including OSA in children. Daytime sleepiness is also associated
with OSA, but may not be present, especially in young children. The possibility of OSA
should be investigated in children and adolescents presenting with these problems,
particularly if the child also has obesity or other risk factors. (See 'Daytime symptoms'
above.)
● Caregivers should be asked about snoring during all routine health care visits, when
symptoms raise a concern for OSA, and at visits when the airway is examined (upper
respiratory infections, etc). Children who snore on most or all nights, or snore loudly, require a
careful history and physical examination (algorithm 1). Continued concern for OSA should
prompt referral to a clinician with expertise in pediatric OSA. Polysomnography (PSG) is
needed to make a definitive diagnosis of OSA (ie, confirm clinically suspected OSA) and can
assist with treatment decisions. (See 'Screening' above and 'Evaluation' above.)
● Attended in-laboratory nocturnal PSG (sleep study) is the gold standard for diagnosis of OSA.
However, there is considerable variation in practice regarding the use of PSG to confirm the
diagnosis when OSA is clinically suspected. (See 'Indications' above.)
● A definitive diagnosis of OSA requires both clinical and PSG criteria. The PSG criterion is
often an obstructive apnea-hypopnea index (AHI) >1 per hour of sleep (table 2). However, the
AHI must be considered in the context of the child's health, symptoms, and daytime functional
impairment to most accurately assess OSA significance, severity, and impact. Severe OSA is
typically associated with an AHI >10, decreases in oxyhemoglobin saturation, and/or
hypercapnia on PSG. (See 'Diagnosis' above and 'Assessment of severity' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 6363 Version 46.0

GRAPHICS
Standardized grading of tonsil size
Tonsil size is most often described on a scale from 0 to 5:

0 — Tonsils are entirely within the tonsillar pillar, or previously removed by surgery.
1+ — Tonsils occupy less than 25 percent of the lateral dimension of the oropharynx, as
measured between the anterior tonsillar pillars (solid yellow arrow).
2+ — Tonsils occupy 26 to 50 percent of the lateral dimension of the oropharynx.
3+ — Tonsils occupy 51 to 75 percent of the lateral dimension of the oropharynx.
4+ — Tonsils occupy more than 75 percent of the lateral dimension of the oropharynx.
Drawing based on text description in: Brodsky L. Modern assessment of tonsils and adenoids. Pediatr
Clin North Am 1989; 36:1551.
Graphic 103834 Version 2.0

Clinical manifestations of obstructive sleep apnea in children
Nighttime symptoms
Snoring
Labored breathing; paradoxical abdominal movements
Apneas, pauses in breathing, or gasping
Mouth breathing
Restless or agitated sleep
Sleeping in unusual positions (neck extended)
Nighttime sweating, preference for minimal clothing
Nocturnal enuresis or nocturia
Sleepwalking, sleep terrors, or confusional arousals
Daytime symptoms
Mouth breathing, hyponasal speech
Poor school functioning or other behavioral concerns (inattentiveness, difficulty learning, hyperactivity,
impulsivity, irritability, rebelliousness, aggression)
Sleepiness (eg, falls asleep at school or in the car, or excessive napping)
Morning headache
Potential consequences in childhood
A en on deficit hyperac vity disorder (ADHD) or disrup ve behavior disorders

Poor growth (especially in infants and young children)
Hypertension
Altered cardiac morphology (right and left ventricular hypertrophy)
Pulmonary hypertension
Courtesy of Shalini Paruthi, MD.

Overview of evaluation and initial management of obstructive sleep

apnea in children


OSA: obstructive sleep apnea; URI: upper respiratory tract infection; ENT: ears, nose, and throat; PSG:
polysomnography; AHI: apnea-hypopnea index; CPAP: continuous positive airway pressure; RME: rapid
maxillary expansion; ADHD: attention deficit hyperactivity disorder.
* Nocturnal symptoms and signs of OSA may include habitual or loud snoring, mouth-breathing, observed or
witnessed pauses in breathing, sleepwalking, enuresis, or excessive sweating during sleep. Daytime
symptoms include poor school functioning or other behavioral concerns such as ADHD, ADHD-like behavior,
other disruptive behavior, or sleepiness. Risk factors for OSA include obesity, Down syndrome or other
syndrome, craniofacial anomalies, and neuromuscular disorders.
¶ Refer to the UpToDate topic on management of OSA in children regarding selection of patients for intranasal
steroids, leukotriene modifiers, or RME.
Δ For patients with mild to moderate OSA that has been confirmed by PSG, watchful waiting for up to 6
months is a reasonable consideration, as an alternative to adenotonsillectomy or CPAP treatment.
◊ Positional therapy may be considered when a child or adolescent cannot be treated by other means and if
positioning substantially improves the OSA.
§ An adjuvant surgical procedure may be performed as primary therapy for children with multilevel OSA,
typically in those with complex medical conditions such as Down syndrome, craniofacial abnormality,
mucopolysaccharidosis, or a neuromuscular disorder. Adjuvant surgery also may be indicated as a secondary
intervention in children with residual OSA after adenotonsillectomy. Refer to UpToDate content on
adenotonsillectomy for OSA in children.
¥ The approach to reassessment depends on the patient's presenting symptoms and severity of OSA. Patients
with severe OSA (eg, significant symptoms or AHI >10) who undergo adenotonsillectomy usually should be
reevaluated clinically within 1 to 2 months after surgery and with a PSG in 3 to 12 months. Patients with mild
or moderate OSA prior to adenotonsillectomy may be followed clinically if their presenting symptoms have
improved. Reevaluation after treatment is also indicated for patients with progressive obesity. Patients
managed with CPAP should be followed clinically by the prescribing clinician, with follow-up PSG as indicated.
‡ At the time of follow-up, the determination of whether the residual OSA is "clinically significant" depends
upon a global assessment by the specialist, including clinical symptoms and risk factors, and multiple variables
from the PSG. Clinical decisions should not be based upon the AHI result alone. However, most patients with
AHI >10 and some patients with AHI >1 have clinically significant OSA, if this is compatible with other clinical
findings.

Child with allergies
Children with allergic rhinitis may display "allergic shiners" and "adenoid facies," resulting
from longstanding mouth-breathing. The features of adenoid facies include a long, narrow
face; narrow, upturned nose; short upper lip; exposed upper incisors; recessed lower jaw;
and forward head posture.

High arched palate
Palate with a high and narrow maxillary arch in a patient with obstructive sleep
apnea. The tongue cannot fit into the narrow palate. Therefore, the tongue
tends to move backward when the patient is supine, blocking the airway.
Courtesy of Rafael Pelayo, MD.

Large tonsils
Large tonsils often accompany obstructive sleep apnea in children. This

photograph shows tonsils that would be graded as 4+ and could easily cause
airway obstruction during sleep.
Courtesy of Dr. Ron Mitchell.

The modified Mallampati classification for difficult laryngoscopy and

intubation
The modified Mallampati classification [1] is a simple scoring system that relates the amount of
mouth opening to the size of the tongue, and provides an estimate of space available for oral
intubation by direct laryngoscopy. According to the Mallampati scale, class I is present when the soft
palate, uvula, and pillars are visible; class II when the soft palate and the uvula are visible; class III
when only the soft palate and base of the uvula are visible; and class IV when only the hard palate
is visible.
Reference:
1. Samsoon GL, Young JR. Difficult tracheal intubation: a retrospective study. Anaesthesia 1987;
42:487.

Polysomnographic variables in children
Definition Comments
Events
Apnea >90 percent decrease in airflow signal that Apnea is obstructive if there is continued
lasts ≥90 percent of the duration of at least or increased inspiratory effort during the
two normal breaths, as determined from the entire period of decreased airflow.
baseline breathing pattern. Apnea is central if inspiratory effort is
absent during the entire period of airflow
cessation.*
Apnea is mixed if there is absent
respiratory effort during one portion of the
event AND the presence of inspiratory effort
in another portion, regardless of which
portion comes first.
Hypopnea ≥30 percent decrease in airflow signal that Hypopneas may be classified as either
lasts ≥90 percent of the duration of at least obstructive or central, depending on the
two normal breaths, as determined from the presence or absence of snoring, flattening
baseline breathing pattern. The decreased of nasal pressure signal, or paradoxical
airflow is associated with an arousal, or at thoracoabdominal breathing.
least 3 percent oxyhemoglobin desaturation. However, in prac ce, accurate
classifica on of the e ology of
hypopneas is challenging, and usually
not performed. In a pa ent who has
clear obstruc ve sleep apnea,
hypopneas are usually assumed to have
an obstruc ve basis.
Respiratory Respiratory event (increasing respiratory RERAs can be detected with routinely used
effort related effort, flattening of the inspiratory portion of sensors on in-lab PSG or by addition of
arousal (RERA) the nasal pressure waveform, snoring, or an esophageal manometry.
elevation in the end-tidal PCO 2 ), that leads to Upper airway resistance syndrome (UARS)
arousal and does not qualify as an apnea or was previously used to describe presence of
hypopnea. ¶ RERAs in the absence of apneas or
hypopneas. UARS is now subsumed into the
category of OSA.
Sleep-related The end-tidal or transcutaneous CO 2 >50 Some children with breathing disturbance
hypoventilation mmHg for more than 25 percent of the total due to increased upper airway resistance
sleep time. have hypoventilation, but not discrete
apneas or hypopneas.
Obstructive hypoventilation is now
subsumed into the category of OSA.
Additional Arousals, snoring, changes in body position,

events and limb movements.
Summary measures
Apnea The number of apneas plus hypopneas that Concern for clinically significant OSA
hypopnea occur per hour of sleep. generally starts with an AHI >1 or RDI >1.
index (AHI) An AHI ≥1.5 events per hour was
considered abnormal based on a study of a
group of healthy children not suspected of
having sleep-related breathing disorders, in
whom the mean AHI was 0.2 ± 0.6 events
per hour. [1]
Respiratory The number of apneas, hypopneas, and Concern for clinically significant OSA
disturbance RERAs per hour of sleep. generally starts with an AHI >1 or RDI >1.
index (RDI) Some experts have advocated slightly
higher RDI thresholds, such as 1.5, 2, or 3
events per hour.
An RDI >5 events per hour of sleep is often
used to identify an abnormal RDI in adults,
but is insufficiently sensitive for children.
RERA: respiratory effort related arousal; UARS: upper airway resistance syndrome; OSA: obstructive sleep apnea; AI:
apnea index; OAI: obstructive apnea index; RDI: respiratory disturbance index; AHI: apnea hypopnea index; EEG:
electroencephalographic.
* Central apnea also requires one of the following measures of duration: 1) The respiratory event is at least 20 seconds
long; 2) Inspiratory effort is absent for the duration of two respiratory cycles and is followed by a cortical arousal, or
oxygen desaturation ≥3 percent; or 3) The event is associated with a decrease in the heart rate to less than 50 beats per
minute for at least 5 seconds, or less than 60 beats per minute for 15 seconds (infants under one year of age only).
¶ Arousals are determined by electroencephalographic (EEG) criteria.
Reference:
1. Witmans MB, Keens TG, Davidson Ward SL, Marcus CL. Obstructive hypopneas in children and adolescents: normal
values. Am J Respir Crit Care Med 2003; 168:1540.
Data from: Berry RB, Quan SF, Abreu AR, et al for the American Academy of Sleep Medicine. The AASM Manual for the
Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications, Version 2.6, www.aasmnet.org,
American Academy of Sleep Medicine, Darien, IL 2020.

Contributor Disclosures
Shalini Paruthi, MD Nothing to disclose Ronald D Chervin, MD, MS Patent Holder: University of Michigan
[Sleep disorders (Patents and copyrighted material for assessment and treatment of patients with sleep
disorders)]. Other Financial Interests: American Academy of Sleep Medicine [Sleep disorders (Standards,
conferences, services to support physicians and patients)]; International Pediatric Sleep Association [Sleep
disorders (Standards, conferences, services to support physicians and patients)]. Alison G Hoppin,
MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

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Official reprint from UpToDate®

Evaluation of suspected obstructive sleep apnea in

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Adenotonsillar hypertrophy — Adenotonsillar hypertrophy is a widely recognized risk factor for

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Potential consequences in childhood

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● Focused sleep history

● Physical examination including detailed examination of the oropharynx

● Snoring, especially when frequent or loud

● Cardiopulmonary – Blood pressure should be measured and every physical examination

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Technique — The PSG is performed in a sleep laboratory by sleep technologists and

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● Respiratory effort-related arousal (RERA) – Arousal preceded by evidence of airway

● Hypercapnia – End-tidal or transcutaneous CO2 is summarized, as an assessment for sleep-

Alternatives to polysomnography — If polysomnography (PSG) is not available, clinicians may

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Questionnaires — Several questionnaires have been developed to assess symptoms or signs

Other tests — Additional testing may be helpful in selected patients:

● Cardiopulmonary disease – Children with any evidence of underlying cardiopulmonary

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• A pattern of obstructive hypoventilation, defined as at least 25 percent of total sleep time

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● Mild OSA – RDI or AHI, 1 to 4.9

Further interpretation — Some night-to-night variability occurs on sleep studies; as a result, a

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SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

SUMMARY AND RECOMMENDATIONS

● Key clinical manifestations of OSA include (table 1):

• Nocturnal symptoms – Habitual or loud snoring is an important clinical feature of OSA.

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• Daytime symptoms – Inattention, learning problems, and behavioral problems (eg,

Use of UpToDate is subject to the Subscription and License Agreement.

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4. Nieminen P, Löppönen T, Tolonen U, et al. Growth and biochemical markers of growth in

9. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd e

10. Arens R, Marcus CL. Pathophysiology of upper airway obstruction: a developmental

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45. Huang YS, Guilleminault C, Li HY, et al. Attention-deficit/hyperactivity disorder with

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55. Hashemian F, Farahani F, Sanatkar M. Changes in growth pattern after adenotonsillectomy in

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72. Dreher A, de la Chaux R, Klemens C, et al. Correlation between otorhinolaryngologic

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Topic 6363 Version 46.0

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Standardized grading of tonsil size

Tonsil size is most often described on a scale from 0 to 5:

Graphic 103834 Version 2.0

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Clinical manifestations of obstructive sleep apnea in children

Labored breathing; paradoxical abdominal movements

Apneas, pauses in breathing, or gasping

Restless or agitated sleep

Sleeping in unusual positions (neck extended)

Nighttime sweating, preference for minimal clothing

Nocturnal enuresis or nocturia