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Evaluation of suspected obstructive sleep apnea in children
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Evaluation of suspected obstructive sleep apnea in children
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Literature review current through: Jul 2017. | This topic last updated: May 16, 2017.

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".)

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 — 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 exam 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, neurological, 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

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 [17-19]

History of prematurity and multiple gestation [20]

Children with any of these conditions should be followed closely for signs and symptoms of OSA. Objective assessment with polysomnography is recommended in children with complex medical conditions who present with signs and symptoms of OSA [21]. Additional factors that contribute to the overall risk for sleep-disordered breathing include environmental smoke exposure, asthma, or allergic rhinitis [22]. 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 snoring is present in most children with OSA [3,5,23,24]. However, a history of snoring is insufficient for the diagnosis because many children who snore do not have OSA [3,5,23,24]; habitual snoring in the absence of OSA (known as primary snoring) occurs in 3 to 12 percent of the general pediatric population [8,25-28] and may still have adverse health consequences. Conversely, the absence of snoring is insufficient to exclude OSA [29,30].

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 [24,31,32]. 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) [8,29,33-39]. In some children, treatment of OSA may improve learning and behavioral problems [8,40-48]. 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 [49]. 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 "Failure to thrive (undernutrition) in children younger than two years: Etiology and evaluation".)

Increased growth and weight gain have been reported after treatment of OSA with adenotonsillectomy, including in obese children [40,50-55]. (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 [56-59]. In a study of 101 children ages 6 to 13 years with OSA, those with an apnea-hypopnea index (AHI) >5 (compared with those with lower AHI) were found to have lower RV ejection fraction, increased LV diastolic dysfunction and remodeling with larger interventricular septal thickness index on echocardiogram, independent of the effect of obesity [60]. Interestingly, studies show that normal nocturnal blood pressure dipping is preserved in young children with OSA, regardless of its severity [61,62]. In the Childhood Adenotonsillectomy Trial (CHAT), severity of OSA was also positively associated with average heart rate during sleep, though no association was observed with systolic or diastolic blood pressure percentile [63]. In younger, preschool-aged children, a study showed OSA was associated with decreased pulse transit time during rapid eye movement (REM) sleep on overnight polysomnography, suggesting that the association of OSA with increased blood pressure may begin early for some children [64]. Furthermore, a study of 26 children ages 6 to 11 years with OSA (compared with 8 children without OSA) revealed endothelial dysfunction [65]. Children who experienced significant improvement of OSA with treatment also showed significant improvement in cardiac function [60], decrease in average heart rate [63], and improved endothelial function [65]. These findings suggest the cardiovascular consequences associated with OSA may be reversible with treatment.

OSA may lead to pulmonary hypertension or cor pulmonale [57,66]. The overall prevalence is unknown, but the prevalence of symptomatic pulmonary hypertension is low [8,57]. This may be because severe OSA is usually diagnosed and treated before it progresses to symptomatic pulmonary hypertension.

SCREENING — To screen for OSA, caregivers of all children should be asked about snoring during routine health care visits, as recommended by the American Academy of Pediatrics (AAP) [67]. Any child who snores on most or all nights or has other symptoms of OSA (table 1), including attention deficit hyperactivity disorder (ADHD) or other behavioral symptoms, should undergo a diagnostic evaluation, as outlined below. (See 'Evaluation' below.)

Children with a history of treated OSA should also be followed closely for the possibility of recurrence. This is because OSA may recur after treatment (eg, adenotonsillectomy) and may worsen with age or weight gain [21]. (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 [21,67]

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 physician. Some sleep medicine physicians 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)

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 [68-70] 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 [49,71]. 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 "Classification and prognosis of pulmonary hypertension in adults".)

Head and nose – Craniofacial anomalies (eg, midface hypoplasia, retrognathia, micrognathia) suggest abnormal upper airway anatomy. Mouth breathing, long ("adenoidal") facies (picture 1), 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 2), 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 3), and Mallampati classification or Friedman score (figure 2) [72,73], 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 [23,68,74-76]. 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. Guidelines have been published regarding indications for polysomnography [8,14,77]. 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 physician or otolaryngologist experienced in evaluation and management of sleep-disordered breathing in children [21].

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 physician 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 post-surgical planning [8,14,77].

In many settings, the PSG is arranged after referral to a specialist in otorhinolaryngology or sleep medicine. 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 physician 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 physician 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 [78,79]. 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 [8,80,81]. (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 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 [82], 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 [82]. One difference is that the adult scoring criteria stipulate that obstructive apneas, hypopneas, and respiratory effort-related arousals 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.

Respiratory effort-related arousal (RERA) – Arousal preceded by evidence of airway obstruction that is, however, 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 PCO2). 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 PSG — If polysomnography 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 the tests should not be used in routine practice [8,67]. However, these tests may be useful in selected cases if PSG is not available.

Home sleep apnea tests – Home sleep apnea tests (previously called portable monitoring or out-of-center sleep testing) are used increasingly as an option for some adults. However, these tests do not usually record sleep, are not routinely utilized in children, and are not standard of care in this age group. The American Academy of Sleep Medicine (AASM) published clinical guidelines for the use of portable monitoring in adults in December of 2007; no similar guidelines exist for children [83]. However, two studies evaluated comprehensive sleep studies ("type 2" devices with more than seven channels) in school-aged children, with leads applied by a technologist in the home setting; this approach was well-tolerated by the patient and family [84,85]. The largest of these studies included 201 children (recruited from the Caffeine for Apnea of Prematurity Trial) and only measured technical considerations of these sleep studies, which were performed without capnography [85]. Seventeen percent of parents noted a sensor fell off. Study authors noted problems with the nasal pressure signal reliability, with a satisfactory signal for more than 75 percent of recording time in less than two-thirds of the children. The report did not disclose how many children were suspected to have sleep-disordered breathing, or report the mean AHI. Thus, it is premature at this time to apply the findings of this study to use in clinical practice. Other studies were performed with "type 3" devices that have fewer than seven leads and are not attended by technologists. These studies found that the results were unreliable compared with laboratory-based PSG [8,86,87]. This may be in part because of variations in the type of data collected by the portable systems, lack of sensor application by a technologist, or the ages of the subjects. Additionally, cut-off values for data from home sleep apnea tests, used to classify severity of pediatric OSA, remain inadequately studied and defined. (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 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]. 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 exam 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). The SRBD scale can be obtained and licensed at no charge through the following link [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]; it has also been validated in children with asthma [100]. The SRBD scale contains a four-item sleepiness subscale that has been validated against the Multiple Sleep Latency test (MSLT) [101]. 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.  

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 physicians 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 [102]. 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 [103] 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 [104]. 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 [105,106].

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 'Psychometric testing'.)

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) [82].

A pattern of obstructive hypoventilation, defined as at least 25 percent of total sleep time with hypercapnia (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, 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 physician, 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 [77].

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 [107].

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 [80].

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 [RERA]), 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.

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) [108]. (See 'Daytime symptoms' above.)

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".)

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 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 and when symptoms raise a concern for OSA. Children who snore on most or all nights, or snore loudly, require a careful history and physical examination. 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.)

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REFERENCES

  1. Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med 1998; 157:1098.
  2. Enright PL, Goodwin JL, Sherrill DL, et al. Blood pressure elevation associated with sleep-related breathing disorder in a community sample of white and Hispanic children: the Tucson Children's Assessment of Sleep Apnea study. Arch Pediatr Adolesc Med 2003; 157:901.
  3. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and children. J Pediatr 1982; 100:31.
  4. Nieminen P, Löppönen T, Tolonen U, et al. Growth and biochemical markers of growth in children with snoring and obstructive sleep apnea. Pediatrics 2002; 109:e55.
  5. Guilleminault C, Lee JH, Chan A. Pediatric obstructive sleep apnea syndrome. Arch Pediatr Adolesc Med 2005; 159:775.
  6. Beebe DW, Ris MD, Kramer ME, et al. The association between sleep disordered breathing, academic grades, and cognitive and behavioral functioning among overweight subjects during middle to late childhood. Sleep 2010; 33:1447.
  7. Richards W, Ferdman RM. Prolonged morbidity due to delays in the diagnosis and treatment of obstructive sleep apnea in children. Clin Pediatr (Phila) 2000; 39:103.
  8. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2012; 130:e714.
  9. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed, American Academy of Sleep Medicine, Darien 2014.
  10. Arens R, Marcus CL. Pathophysiology of upper airway obstruction: a developmental perspective. Sleep 2004; 27:997.
  11. Spilsbury JC, Storfer-Isser A, Rosen CL, Redline S. Remission and incidence of obstructive sleep apnea from middle childhood to late adolescence. Sleep 2015; 38:23.
  12. Hannon TS, Rofey DL, Ryan CM, et al. Relationships among obstructive sleep apnea, anthropometric measures, and neurocognitive functioning in adolescents with severe obesity. J Pediatr 2012; 160:732.
  13. Qubty WF, Mrelashvili A, Kotagal S, Lloyd RM. Comorbidities in infants with obstructive sleep apnea. J Clin Sleep Med 2014; 10:1213.
  14. Aurora RN, Zak RS, Karippot A, et al. Practice parameters for the respiratory indications for polysomnography in children. Sleep 2011; 34:379.
  15. 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.
  16. Paavonen EJ, Strang-Karlsson S, Räikkönen K, et al. Very low birth weight increases risk for sleep-disordered breathing in young adulthood: the Helsinki Study of Very Low Birth Weight Adults. Pediatrics 2007; 120:778.
  17. Redline S, Tishler PV, Tosteson TD, et al. The familial aggregation of obstructive sleep apnea. Am J Respir Crit Care Med 1995; 151:682.
  18. Buxbaum SG, Elston RC, Tishler PV, Redline S. Genetics of the apnea hypopnea index in Caucasians and African Americans: I. Segregation analysis. Genet Epidemiol 2002; 22:243.
  19. Sundquist J, Li X, Friberg D, et al. Obstructive sleep apnea syndrome in siblings: an 8-year Swedish follow-up study. Sleep 2008; 31:817.
  20. Tapia IE, Shults J, Doyle LW, et al. Perinatal Risk Factors Associated with the Obstructive Sleep Apnea Syndrome in School-Aged Children Born Preterm. Sleep 2016; 39:737.
  21. Kothare SV, Rosen CL, Lloyd RM, et al. Quality measures for the care of pediatric patients with obstructive sleep apnea. J Clin Sleep Med 2015; 11:385.
  22. Weinstock TG, Rosen CL, Marcus CL, et al. Predictors of obstructive sleep apnea severity in adenotonsillectomy candidates. Sleep 2014; 37:261.
  23. Carroll JL, McColley SA, Marcus CL, et al. Inability of clinical history to distinguish primary snoring from obstructive sleep apnea syndrome in children. Chest 1995; 108:610.
  24. Guilleminault C, Korobkin R, Winkle R. A review of 50 children with obstructive sleep apnea syndrome. Lung 1981; 159:275.
  25. Ali NJ, Pitson DJ, Stradling JR. Snoring, sleep disturbance, and behaviour in 4-5 year olds. Arch Dis Child 1993; 68:360.
  26. Gislason T, Benediktsdóttir B. Snoring, apneic episodes, and nocturnal hypoxemia among children 6 months to 6 years old. An epidemiologic study of lower limit of prevalence. Chest 1995; 107:963.
  27. Redline S, Tishler PV, Schluchter M, et al. Risk factors for sleep-disordered breathing in children. Associations with obesity, race, and respiratory problems. Am J Respir Crit Care Med 1999; 159:1527.
  28. Li AM, Au CT, So HK, et al. Prevalence and risk factors of habitual snoring in primary school children. Chest 2010; 138:519.
  29. Rosen CL, Storfer-Isser A, Taylor HG, et al. Increased behavioral morbidity in school-aged children with sleep-disordered breathing. Pediatrics 2004; 114:1640.
  30. Goh DY, Galster P, Marcus CL. Sleep architecture and respiratory disturbances in children with obstructive sleep apnea. Am J Respir Crit Care Med 2000; 162:682.
  31. Frank Y, Kravath RE, Pollak CP, Weitzman ED. Obstructive sleep apnea and its therapy: clinical and polysomnographic manifestations. Pediatrics 1983; 71:737.
  32. Rosen CL. Clinical features of obstructive sleep apnea hypoventilation syndrome in otherwise healthy children. Pediatr Pulmonol 1999; 27:403.
  33. Chervin RD, Archbold KH, Dillon JE, et al. Inattention, hyperactivity, and symptoms of sleep-disordered breathing. Pediatrics 2002; 109:449.
  34. Suratt PM, Barth JT, Diamond R, et al. Reduced time in bed and obstructive sleep-disordered breathing in children are associated with cognitive impairment. Pediatrics 2007; 119:320.
  35. Rudnick EF, Mitchell RB. Behavior and obstructive sleep apnea in children: is obesity a factor? Laryngoscope 2007; 117:1463.
  36. Beebe DW. Neurobehavioral morbidity associated with disordered breathing during sleep in children: a comprehensive review. Sleep 2006; 29:1115.
  37. Beebe DW, Rausch J, Byars KC, et al. Persistent snoring in preschool children: predictors and behavioral and developmental correlates. Pediatrics 2012; 130:382.
  38. Perfect MM, Archbold K, Goodwin JL, et al. Risk of behavioral and adaptive functioning difficulties in youth with previous and current sleep disordered breathing. Sleep 2013; 36:517.
  39. O'Brien LM, Holbrook CR, Mervis CB, et al. Sleep and neurobehavioral characteristics of 5- to 7-year-old children with parentally reported symptoms of attention-deficit/hyperactivity disorder. Pediatrics 2003; 111:554.
  40. Stradling JR, Thomas G, Warley AR, et al. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance, and symptoms in snoring children. Lancet 1990; 335:249.
  41. Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics 1998; 102:616.
  42. Ali NJ, Pitson D, Stradling JR. Natural history of snoring and related behaviour problems between the ages of 4 and 7 years. Arch Dis Child 1994; 71:74.
  43. Huang YS, Guilleminault C, Li HY, et al. Attention-deficit/hyperactivity disorder with obstructive sleep apnea: a treatment outcome study. Sleep Med 2007; 8:18.
  44. Mitchell RB, Kelly J. Child behavior after adenotonsillectomy for obstructive sleep apnea syndrome. Laryngoscope 2005; 115:2051.
  45. Mitchell RB, Kelly J. Behavioral changes in children with mild sleep-disordered breathing or obstructive sleep apnea after adenotonsillectomy. Laryngoscope 2007; 117:1685.
  46. Wei JL, Mayo MS, Smith HJ, et al. Improved behavior and sleep after adenotonsillectomy in children with sleep-disordered breathing. Arch Otolaryngol Head Neck Surg 2007; 133:974.
  47. Garetz SL. Behavior, cognition, and quality of life after adenotonsillectomy for pediatric sleep-disordered breathing: summary of the literature. Otolaryngol Head Neck Surg 2008; 138:S19.
  48. Chervin RD, Ruzicka DL, Giordani BJ, et al. Sleep-disordered breathing, behavior, and cognition in children before and after adenotonsillectomy. Pediatrics 2006; 117:e769.
  49. Marcus CL, Curtis S, Koerner CB, et al. Evaluation of pulmonary function and polysomnography in obese children and adolescents. Pediatr Pulmonol 1996; 21:176.
  50. Williams EF 3rd, Woo P, Miller R, Kellman RM. The effects of adenotonsillectomy on growth in young children. Otolaryngol Head Neck Surg 1991; 104:509.
  51. Katz ES, Moore RH, Rosen CL, et al. Growth after adenotonsillectomy for obstructive sleep apnea: an RCT. Pediatrics 2014; 134:282.
  52. Soultan Z, Wadowski S, Rao M, Kravath RE. Effect of treating obstructive sleep apnea by tonsillectomy and/or adenoidectomy on obesity in children. Arch Pediatr Adolesc Med 1999; 153:33.
  53. Hashemian F, Farahani F, Sanatkar M. Changes in growth pattern after adenotonsillectomy in children under 12 years old. Acta Med Iran 2010; 48:316.
  54. Roemmich JN, Barkley JE, D'Andrea L, et al. Increases in overweight after adenotonsillectomy in overweight children with obstructive sleep-disordered breathing are associated with decreases in motor activity and hyperactivity. Pediatrics 2006; 117:e200.
  55. Lewis TL, Johnson RF, Choi J, Mitchell RB. Weight gain after adenotonsillectomy: a case control study. Otolaryngol Head Neck Surg 2015; 152:734.
  56. Li AM, Au CT, Sung RY, et al. Ambulatory blood pressure in children with obstructive sleep apnoea: a community based study. Thorax 2008; 63:803.
  57. Tal A, Leiberman A, Margulis G, Sofer S. Ventricular dysfunction in children with obstructive sleep apnea: radionuclide assessment. Pediatr Pulmonol 1988; 4:139.
  58. Ross RD, Daniels SR, Loggie JM, et al. Sleep apnea-associated hypertension and reversible left ventricular hypertrophy. J Pediatr 1987; 111:253.
  59. Hodges S, Wailoo MP. Tonsillar enlargement and failure to thrive. Br Med J (Clin Res Ed) 1987; 295:541.
  60. Chan JY, Li AM, Au CT, et al. Cardiac remodelling and dysfunction in children with obstructive sleep apnoea: a community based study. Thorax 2009; 64:233.
  61. Nisbet LC, Nixon GM, Yiallourou SR, et al. Sleep-disordered breathing does not affect nocturnal dipping, as assessed by pulse transit time, in preschool children: evidence for early intervention to prevent adverse cardiovascular effects? Sleep Med 2014; 15:464.
  62. Horne RS, Yang JS, Walter LM, et al. Nocturnal dipping is preserved in children with sleep disordered breathing regardless of its severity. Pediatr Pulmonol 2013; 48:1127.
  63. Quante M, Wang R, Weng J, et al. The Effect of Adenotonsillectomy for Childhood Sleep Apnea on Cardiometabolic Measures. Sleep 2015; 38:1395.
  64. Nisbet LC, Yiallourou SR, Biggs SN, et al. Preschool children with obstructive sleep apnea: the beginnings of elevated blood pressure? Sleep 2013; 36:1219.
  65. Gozal D, Kheirandish-Gozal L, Serpero LD, et al. Obstructive sleep apnea and endothelial function in school-aged nonobese children: effect of adenotonsillectomy. Circulation 2007; 116:2307.
  66. Duman D, Naiboglu B, Esen HS, et al. Impaired right ventricular function in adenotonsillar hypertrophy. Int J Cardiovasc Imaging 2008; 24:261.
  67. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2012; 130:576.
  68. Leach J, Olson J, Hermann J, Manning S. Polysomnographic and clinical findings in children with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1992; 118:741.
  69. Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med 2001; 164:16.
  70. McColley SA, Carroll JL, Curtis S, et al. High prevalence of allergic sensitization in children with habitual snoring and obstructive sleep apnea. Chest 1997; 111:170.
  71. Silvestri JM, Weese-Mayer DE, Bass MT, et al. Polysomnography in obese children with a history of sleep-associated breathing disorders. Pediatr Pulmonol 1993; 16:124.
  72. Friedman M, Tanyeri H, La Rosa M, et al. Clinical predictors of obstructive sleep apnea. Laryngoscope 1999; 109:1901.
  73. Nuckton TJ, Glidden DV, Browner WS, Claman DM. Physical examination: Mallampati score as an independent predictor of obstructive sleep apnea. Sleep 2006; 29:903.
  74. Wang RC, Elkins TP, Keech D, et al. Accuracy of clinical evaluation in pediatric obstructive sleep apnea. Otolaryngol Head Neck Surg 1998; 118:69.
  75. Suen JS, Arnold JE, Brooks LJ. Adenotonsillectomy for treatment of obstructive sleep apnea in children. Arch Otolaryngol Head Neck Surg 1995; 121:525.
  76. Dreher A, de la Chaux R, Klemens C, et al. Correlation between otorhinolaryngologic evaluation and severity of obstructive sleep apnea syndrome in snorers. Arch Otolaryngol Head Neck Surg 2005; 131:95.
  77. Roland PS, Rosenfeld RM, Brooks LJ, et al. Clinical practice guideline: Polysomnography for sleep-disordered breathing prior to tonsillectomy in children. Otolaryngol Head Neck Surg 2011; 145:S1.
  78. Canet E, Gaultier C, D'Allest AM, Dehan M. Effects of sleep deprivation on respiratory events during sleep in healthy infants. J Appl Physiol (1985) 1989; 66:1158.
  79. Hershenson M, Brouillette RT, Olsen E, Hunt CE. The effect of chloral hydrate on genioglossus and diaphragmatic activity. Pediatr Res 1984; 18:516.
  80. Katz ES, Greene MG, Carson KA, et al. Night-to-night variability of polysomnography in children with suspected obstructive sleep apnea. J Pediatr 2002; 140:589.
  81. Verhulst SL, Schrauwen N, De Backer WA, Desager KN. First night effect for polysomnographic data in children and adolescents with suspected sleep disordered breathing. Arch Dis Child 2006; 91:233.
  82. Berry RB, Brooks R, Gamaldo CE, 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 2.4, www.aasmnet.org, American Academy of Sleep Medicine, Darien, IL 2017.
  83. Collop NA, Anderson WM, Boehlecke B, et al. Clinical guidelines for the use of unattended portable monitors in the diagnosis of obstructive sleep apnea in adult patients. Portable Monitoring Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med 2007; 3:737.
  84. Goodwin JL, Enright PL, Kaemingk KL, et al. Feasibility of using unattended polysomnography in children for research--report of the Tucson Children's Assessment of Sleep Apnea study (TuCASA). Sleep 2001; 24:937.
  85. Marcus CL, Traylor J, Biggs SN, et al. Feasibility of comprehensive, unattended ambulatory polysomnography in school-aged children. J Clin Sleep Med 2014; 10:913.
  86. Zucconi M, Calori G, Castronovo V, Ferini-Strambi L. Respiratory monitoring by means of an unattended device in children with suspected uncomplicated obstructive sleep apnea: a validation study. Chest 2003; 124:602.
  87. Poels PJ, Schilder AG, van den Berg S, et al. Evaluation of a new device for home cardiorespiratory recording in children. Arch Otolaryngol Head Neck Surg 2003; 129:1281.
  88. Marcus CL, Keens TG, Ward SL. Comparison of nap and overnight polysomnography in children. Pediatr Pulmonol 1992; 13:16.
  89. Saeed MM, Keens TG, Stabile MW, et al. Should children with suspected obstructive sleep apnea syndrome and normal nap sleep studies have overnight sleep studies? Chest 2000; 118:360.
  90. Kaditis A, Kheirandish-Gozal L, Gozal D. Pediatric OSAS: Oximetry can provide answers when polysomnography is not available. Sleep Med Rev 2016; 27:96.
  91. Garde A, Dehkordi P, Karlen W, et al. Development of a screening tool for sleep disordered breathing in children using the phone Oximeter™. PLoS One 2014; 9:e112959.
  92. Brouillette RT, Morielli A, Leimanis A, et al. Nocturnal pulse oximetry as an abbreviated testing modality for pediatric obstructive sleep apnea. Pediatrics 2000; 105:405.
  93. Lamm C, Mandeli J, Kattan M. Evaluation of home audiotapes as an abbreviated test for obstructive sleep apnea syndrome (OSAS) in children. Pediatr Pulmonol 1999; 27:267.
  94. Goldstein NA, Sculerati N, Walsleben JA, et al. Clinical diagnosis of pediatric obstructive sleep apnea validated by polysomnography. Otolaryngol Head Neck Surg 1994; 111:611.
  95. Sivan Y, Kornecki A, Schonfeld T. Screening obstructive sleep apnoea syndrome by home videotape recording in children. Eur Respir J 1996; 9:2127.
  96. Sleep-Related Breathing Disorder Scale (SRBD Scale), from Pediatric Sleep Questionnaire, to Identify Symptoms of Obstructive Sleep Apnea in Children. Available at: http://inventions.umich.edu/technologies/3773_sleep-related-breathing-disorder-scale-srbd-scale-from-pediatric-sleep-questionnaire-to-identify-symptoms-of-obstructive-sleep-apnea-in-children (Accessed on December 22, 2016).
  97. Rosen CL, Wang R, Taylor HG, et al. Utility of symptoms to predict treatment outcomes in obstructive sleep apnea syndrome. Pediatrics 2015; 135:e662.
  98. Chervin RD, Weatherly RA, Garetz SL, et al. Pediatric sleep questionnaire: prediction of sleep apnea and outcomes. Arch Otolaryngol Head Neck Surg 2007; 133:216.
  99. Chervin RD, Hedger K, Dillon JE, Pituch KJ. Pediatric sleep questionnaire (PSQ): validity and reliability of scales for sleep-disordered breathing, snoring, sleepiness, and behavioral problems. Sleep Med 2000; 1:21.
  100. Ehsan Z, Kercsmar CM, Collins J, Simakajornboon N. Validation of the pediatric sleep questionnaire in children with asthma. Pediatr Pulmonol 2017; 52:382.
  101. Chervin RD, Weatherly RA, Ruzicka DL, et al. Subjective sleepiness and polysomnographic correlates in children scheduled for adenotonsillectomy vs other surgical care. Sleep 2006; 29:495.
  102. Kadmon G, Chung SA, Shapiro CM. I'M SLEEPY: a short pediatric sleep apnea questionnaire. Int J Pediatr Otorhinolaryngol 2014; 78:2116.
  103. Melendres MC, Lutz JM, Rubin ED, Marcus CL. Daytime sleepiness and hyperactivity in children with suspected sleep-disordered breathing. Pediatrics 2004; 114:768.
  104. Slaats MA, Van Hoorenbeeck K, Van Eyck A, et al. Upper airway imaging in pediatric obstructive sleep apnea syndrome. Sleep Med Rev 2015; 21:59.
  105. Francis A, Eltaki K, Bash T, et al. The safety of preoperative sedation in children with sleep-disordered breathing. Int J Pediatr Otorhinolaryngol 2006; 70:1517.
  106. Brown KA, Morin I, Hickey C, et al. Urgent adenotonsillectomy: an analysis of risk factors associated with postoperative respiratory morbidity. Anesthesiology 2003; 99:586.
  107. Boudewyns A, Van de Heyning P, Verhulst S. Central apneas in children with obstructive sleep apnea syndrome: prevalence and effect of upper airway surgery. Sleep Med 2016; 25:93.
  108. Sedky K, Bennett DS, Carvalho KS. Attention deficit hyperactivity disorder and sleep disordered breathing in pediatric populations: a meta-analysis. Sleep Med Rev 2014; 18:349.
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