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 Table of Contents  
Year : 2017  |  Volume : 1  |  Issue : 2  |  Page : 39-45

Pediatric obstructive sleep apnea: A short review of clinical aspects

1 Division of Sleep Medicine, Stanford University, Redwood City, CA, USA
2 Child Psychiatry and Sleep Medicine, Chang Gung Memorial Hospital and Medical College, Linkou, Taiwan, ROC

Date of Web Publication30-Jun-2017

Correspondence Address:
Christian Guilleminault
Division of Sleep Medicine, Stanford University, 450 Broadway Street, MC 5704, Redwood City, CA 94063
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/prcm.prcm_7_17

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This report reviews the historical developments leading to recognition of pediatric obstructive sleep apnea. It briefly summarized the rationale why the upper airway becomes at risk of collapsibility during sleep. It also reviews the complaints that vary with age. It emphasizes points of the examination that must be systematically look for. The report reviews the variables to monitor, to look for, and to be analyzed, and patterns not often looked at but that disturb sleep and lead to complaints and symptoms in sleep polysomnography.

Keywords: Clinical evaluation, complaints, flow limitation, obstructive sleep apnea, pediatrics, polysomnography

How to cite this article:
Guilleminault C, Huang YS. Pediatric obstructive sleep apnea: A short review of clinical aspects. Pediatr Respirol Crit Care Med 2017;1:39-45

How to cite this URL:
Guilleminault C, Huang YS. Pediatric obstructive sleep apnea: A short review of clinical aspects. Pediatr Respirol Crit Care Med [serial online] 2017 [cited 2023 May 31];1:39-45. Available from: https://www.prccm.org/text.asp?2017/1/2/39/209262

  Introduction Top

Sleep-disordered breathing (SDB) involved a decrease in the lumen of the upper airway (UA) during sleep. Historically, this decrease was noted to occur a variable degree overtime, based on the instrument used to investigate this decrease. Initially, respiration during sleep in children was monitored during sleep using nasal and oral prongs or thermistors, thoracic and abdominal strain gauge, calibrated esophageal pressure (Pes), Water ear oximeter, finger plethysmography, thoraco-diaphragmatic electromyography (Dia-EMG), and a neck “microphone” that did not measure decibel but power of UA sounds. In specific research cases, a tightly placed facial mask with a pneumotachograph was used, allowing measurements of tidal volume, expired CO2, proper timing of inspiration time (Ti) expiration time (Te), and variable degree of airflow limitation with or without arterial line placed that allowed continuous monitoring of blood pressure and to intermittently draw arterial blood for blood gases measurements. These respiratory parameters were those used historically for the description of sleep apnea in children. The monitoring of Pes allowed one to accurately describe when there was a decrease in respiratory effort or an increase of such effort. The “dia”-EMG gave a similar indication but was not exactly quantifiable. The nonresearch montage used on all children seen at the Stanford University Sleep-disordered Clinic allows diagnosis of children “apnea”-complete cessation of air exchange at nose and mouth and hypopnea, a partial cessation of air, exchange at nose and mouth. The oximeter indicates a drop of oxygen saturation. The Pes indicated if there was an increase or decrease in effort in association of the abnormal breathing pattern, and based on the recording, an “obstructive” or “diaphragmatic” (called by others “central”) was scored. Simultaneously, sleep/wake markers 3 (electroencephalography [EEG] leads), chin muscle EMG, eye movements (2 leads), and one electrocardiographic leads were monitored, allowing recognition of sleep stages and wakefulness and also changes in autonomic nervous system (ANS) activity using plethysmography and heart rate recordings. These recordings led to the report of “obstructive sleep apnea (OSA) in children” and in infants.[1],[2],[3] The usage of the full face mask with pneumotachograph and Pes indicated that abnormal breathing during sleep was not limited to the above patterns and that there was in some children presence of a limitation of airway flow with increase in effort without evidence of drop in oxygen saturation. This was called “obstructive breathing,” and it was reported to be seen frequently with snoring and disturbance of the sleep EEG.[4] When the pattern was verified by many, the term “Respiratory Related Respiratory Arousal (respiratory event related arousal [RERA])” was applied in the mid-1990s.[5] By that time, efforts were made to replace the thermistors/thermocouples that measured change in temperature but not change in flow by more sophisticated equipment. The laboratory of Rapoport in New York was very much involved in this development. Hosselet et al. in 1998 demonstrated that a nasal cannula/pressure transducer system [6],[7] could provide a noninvasive indicator of flow limitation that can identify periods of elevated UA resistance both in normal participants and those with SDB, and the equipment was recommended as the valid standard for monitoring of nasal breathing in 2000. “Flow Limitation” was calculated as a percentage of total sleep time. Instead of recording nasal cannula, some authors monitored end-tidal CO2 or tried to monitor both signals after 1992, but such double recording was shown to be difficult. With the improvement of transcutaneous CO2 (TcCO2) monitoring, such recording has been common after 2000.

Duration of events monitored during sleep was adjusted to age; abnormal obstructive breathing was scored if events lasted longer than two breaths (i.e., 3 breaths); in neonates, such duration was 3 s, at 12 months 6 s, and older age 10 s.[3]

Most of the descriptions of abnormal breathing are back to these historical descriptions. If Pes is uncommonly monitored today, noninvasive nasal cannula pressure transducer is the norm as it is TcCO2 monitoring. Such montage has eliminated the possibility to score “central hypopnea” as “effort” cannot be monitored with nasal cannula but only with Pes.

  The Upper Airway and Sleep Top

The pharynx is a collapsible tube, unlike lower airways, it has no rigid support, and the skeletal muscles and soft tissues support nonrespiratory functions: sucking, swallowing, vocalization/phonation, etc. However, the physiology during wakefulness is different from sleep; sleep causes fundamental modifications of pharyngeal muscle tone and reflex responses and can lead to narrowing and increased UA resistance in normal individuals. Muscle tone decreases during sleep and its decrease will be different during nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep when it will be more significant. Also there is a greater risk of UA increased resistance at end inspiration during sleep: During wakefulness the decrease in lung inflation and decrease in lower airway size, normally induce a reflex that increases the tonic activation of the UA muscles, but this reflex is decrease during NREM sleep and is inactive during REM sleep.

The UA can be modelled using fluid dynamics physics, Experimentally, normal participants treated with subatmospheric nasal pressure develop OSA. Each individual has a critical pressure (Pcrit) or intrinsic collapsibility and a level of pharyngeal muscle activity that stiffens and enlarges the airway.[8],[9] Experimentally normal participants treated with subatmospheric pressure develop OSA at a variable point: Some subjects have a Pcrit at an atmospheric pressure level and will have a greater of UA collapse if the pressure during expiration goes below their Pcrit as subatmospheric pressure will develop during this phase of the respiratory cycle. Moreover, normally subatmospheric pressure in the UA causes reflex activation of nose and palate dilators (alai nasi, palatoglossus, levator/tensor palatini), oral pharynx/hyoid (genioglossus, geniohyoid, sternohyoid, sternothyroid), and larynx (cricoarytenoid and cricothyroid) – both tonic and respiratory cycled, but this reflex decreases and disappears during sleep, maximum during REM sleep but marked during NREM sleep.

Different factors may play a role in increasing the risk of collapsibility during sleep. Some of these factors involve the neuromuscular control of the UA and the complicated reflex loops involved in this control, and we are lacking information on this aspect particularly during sleep.

There are factors that are “nonsleep” related and that have been studied in the recent time, they are “external factors” that impact on the size of UA, particularly when located retropalatal and retroglossal. These external factors can be influenced by genetic and environmental factors and four factors have been identified: (a) bone structures (oral-facial bones), (b) infiltration of soft tissues - major factor being fat and fat at infiltration of UA is associated with central obesity leading to chest bellows impairment and complex respiratory-ventilatory problem, (c) leukotriene, and (d) inflammation arising from abnormal breathing during sleep.

  Summary of Clinical Evaluation Top

During clinic visits, children must have a pediatric evaluation including body mass index (BMI), vital signs, and neck circumference measurements.[10] The pediatric sleep questionnaire [11] is commonly used.

Complaints will vary with age as follows:


Disturbed nocturnal sleep with repetitive crying, poorly established day/night cycle, noisy breathing or snoring, nocturnal sweating, poor suck, absence of normal growth pattern, or failure to thrive, observation of apneic events, report of apparent life-threatening event, and presence of repetitive earaches or upper respiratory infection (URI).


Noisy breathing or snoring, agitated sleep or disrupted nocturnal sleep, crying spells or sleep terrors, grouchy and/or aggressive daytime behavior, daytime fatigue, nocturnal sweating, mouth breathing, poor eating or failure to thrive, repetitive URI, and witnessed apneic episodes.

Preschool children

Regular, heavy snoring, mouth breathing, drooling during sleep, agitated sleep, nocturnal awakenings, confusional arousals, sleepwalking, sleep terrors, nocturnal sweating, abnormal sleeping positions, and persistence of bedwetting; abnormal daytime behavior and aggressiveness; hyperactivity; inattention, daytime fatigue, and hard to wake up in the morning; and morning headache, increased need for napping, compared with peers, poor eating, growth problems, and frequent URI.

School children

Regular, heavy snoring; agitated sleep; abnormal sleeping positions; insomnia; delayed sleep phase syndrome; confusional arousal; sleepwalking; sleep talking; persistence of bedwetting; nocturnal sweating; hard to wake up in the morning; mouth breathing; drooling; morning headache; daytime fatigue; daytime sleepiness with regular napping; abnormal daytime behaviors/pattern of attention-deficit/hyperactivity disorder; aggressiveness; abnormal shyness, withdrawn and depressive presentation; learning difficulties; abnormal growth patterns; delayed puberty; repetitive URI; and dental problems such as a crossbite, malocclusion (Class II or III), and small jaw with overcrowding.


The suspicion of SDB indicates the need not only for a general pediatric evaluation but also for a thorough evaluation of the UA anatomy.

Starting with the nose, one should look for asymmetry of the nares, a large septal base, collapse of the nasal valves during inspiration, presence of a deviated septum, or enlargement of the inferior nasal turbinates.

Next, the oropharynx should be examined for the position of the uvula in relation to the tongue. Presence of a short lingual frenulum using Kotlow measurement and Queiroz Marchesan scale,[12],[13] much more common than a short nasal frenulum.[14] The scale developed by Mallampati et al. reviewed by Friedman et al.[15] may help evaluating the narrowness of the upper airway. There should be systematic search for missing teeth questioning subject and parents and requesting if necessary help of pediatric dentist with performance of specific X-rays (Panorex).[16] The size of the tonsils should be compared with the size of the airway; application of a standardized scale is useful.[17] The presence of a high and narrow hard palate, overlapping incisors, a crossbite, and an important (>2 mm) overjet (the horizontal distance between the upper and lower teeth) are indicative of a small jaw and/or abnormal maxillomandibular development.[18]

This clinical evaluation provides important details of the UA anatomy and identifies anatomical risk factors that can predispose one to the development of abnormal breathing. The results of this examination must be summarized as the different anatomical narrowings have additive effects. The apparent sizes of tonsils and adenoids are not the only anatomical findings that determine whether or not SDB is present. A change in flow due to an abnormal nose, secondary development of turbulence, and the increased collapsibility at specific vulnerable points in the UA are elements to consider.

  Recording Sleep-disordered Breathing Top

Testing during sleep is the only way to confirm the presence of SDB. Controversy exists concerning the need for and type of test to be performed. Polysomnography (PSG) is described above, and its results are considered as the most accurate. Home study will have less reliability than laboratory studies, but if performed, home studies should have sleep/wake monitoring.

Compared to PSG, nocturnal polygraphy has been performed; it usually involves monitoring of a limited number of the respiratory leads, particularly nasal cannula and oxygen saturation; usually an EEG lead is also monitored. This monitoring device can confirm the presence of abnormal breathing during sleep, but if study is negative, the study cannot affirm the absence of breathing problem during sleep.

An increase in respiratory efforts is associated with changes in ANS settings as measured by nocturnal polygraphic arterial tonometry or pulse transit time (PTT).

These changes will affect the cardiovascular system: In an individual with normal autonomic-nervous-system –ANS-, two types of responses can be seen when an increase in respiratory effort occurs during sleep: activation or arousal with cortical involvement. Activation is related to the recruitment of sensory inputs that will lead to a polysynaptic motor response after relay of sensory input in the brainstem and subcortical structures. An ANS response may be seen with brainstem reflexes leading to full reopening of the UA without EEG cortical arousal, or it may be seen as the consequence of an EEG cortical arousal.

The presence of cortical arousals will be associated with clinical symptoms such as complaints of excessive daytime somnolence, irritability, or unrefreshing sleep. The role of repetitive “activation” is unknown in children. Some ambulatory equipment's recognition of SDB is based on ANS responses, using algorithms, commonly associating results of heart rate, and finger plethysmography analyses. The algorithms are proprietary and undisclosed. Such equipment identifies nocturnal sleep disruption, together with monitoring of oxygen saturation and has been considered to provide information equivalent to those obtained with the limited home recordings.

Recording of variables such as pulse-transit-time-PTT- provided by a device using changes in ANS, cannot be used to recognize abnormal breathing during sleep, but recording of “PTT” may be performed in association with other variables during sleep. As a research tool, it has been used in association with PSG to indicate changes in ANS status with identification of sympathetic activation.

Nocturnal oximetry

This is the simplest type of continuous recording. It does not recognize sleep and wakefulness but may indicate the validity of treatment, particularly positive airway pressure or evidence of abnormal repetitive hypoxemic events during the nocturnal period.

Continuous transcutaneous CO2 monitoring

For a long time, long-term TcCO2 monitoring was considered unreliable, this is not true anymore, but need for change in placement of electrode, need for calibration, and recalibration if sensor is moved are the limitations. This recording may be more helpful in some specific conditions, particularly in children with hypoventilation during sleep related to any cause. If it is not a diagnostic tool in isolation, it may be helpful to follow treated patient at home.

Scoring polysomnography

By 12 months of age, sleep EEG is well developed, and scoring sleep using the Rechtschaffen and Kales criteria and the AASM criteria for short arousal are easy.[19],[20],[21]

Furthermore, respiratory rate (RR) is relatively steady from 2 years on between 16 and 18 breaths/min for Stages 2–4 of NREM sleep 17 and 19 breaths/min during REM sleep.

Defining a respiratory event

Event begins at the start of inspiration of the first abnormal breath. If the start of the inspiration is not detectable (such as incomplete apnea or central apnea), the respiratory event will start at the end of expiration of the last detected breath before the abnormal respiratory event. It ends at the start of inspiration of the breath following the abnormal respiratory event.

Definition used

Apnea [20] is more than 90% fall in airflow at the nose and mouth for longer than 2 breaths, independent of oxygen desaturation, change in EEG, or stages of sleep. It is subdivided in central, mixed and obstructive based on airflow and inspiratory efforts.


An hypopnea [20],[21] is a breathing event lasting at least longer than 2 breaths (i.e., 3 breaths) independent of age of the child (1–18 years). It is scored based on nasal cannula pressure transducer (scoring without esophageal manometry); it is associated with a decrease of the curve by 30% compared to the 3 min prior baseline recording. An hypopnea begins with the drop of the nasal cannula curve to reach a 30% drop during one breath. The hypopneas end when the nasal cannula returns to baseline. The duration of the hypopneas is calculated from the inspiratory movement of the first abnormal breath till the inspiratory movement of the first normal breath.

Stanford adjustment rule

This first breath associated with the arousal may show indication of increased movement amplitude above prior baseline volume and associated with short-lived hyperventilation. If there is more than 1 breath during the arousal period (i.e., at least two successive breaths are required to perform a comparison), the drop in amplitude preceding the arousal may be calculated compared to the breaths associated with the arousal.[22]

Investigation of other respiratory signals should be performed for the breaths involved in the hypopneas: (1) checking presence/absence of increase in inspiratory muscle EMG simultaneously with movement and change in amplitude of the inductive thoracic and/or abdominal belts; such association indicates the presence of obstructive hypopneas. If there is a decrease in all of the above signals during hypopneas, “central hypopneas” as seen in association with phasic events of REM sleep may be suspected but cannot be affirmed without Pes recording.

Obstructive hypopnea

The definition is based on nasal pressure transducer; discernable reduction in the baseline signal amplitude for >2 breaths (3 or more breaths) with persistent respiratory effort associated with an EEG arousal or with oxygen desaturation.

The EEG pattern can be associated with a change of the plethysmographic curve with a visually recognizable descending and short-lived curve pattern indicative of a sympathetic activation. Sympathetic activation cannot per se indicate EEG arousal as “sympathetic activation,” i.e., stimulation at brainstem but stopped by thalamic gate may occur. However, “sympathetic activation may help recognizing EEG arousals.”

Hypopnea with usage of esophageal pressure

Pes makes recognition of hypopnea and other abnormal breathing patterns easier. Pes helps in recognition of hypopnea onset with a change in Pes amplitude compared to prior recorded breaths and allows quantifying (after Pes calibration) the amount of change in inspiratory effort associated with each breath. Patterns such as “Pes crescendos,” “sustain continuous effort,” and “Pes reversal” are systematically looked for. (a) Pes crescendo: sequence of four or more breaths that show increasingly negative peak end inspiratory pressure seen with Pes. (b) Continuous sustained respiratory effort: Definition: repetitive, abnormally negative peak end-inspiratory Pes ending at the same negative inspiratory pressure without a crescendo pattern. It is associated with continuous airflow limitation on nasal cannula pressure transducer signal. Pes allows defining hypopneas with a decreased effort (such as seen in REM sleep).[23],[24],[25]

  Other Patterns of Abnormal Breathing Top

Flow limitation

Evaluation with nasal cannula pressure transducer allows recognition of flow limitation. Definition: flattening of the peak of the nasal cannula pressure transducer wave contour, o r change in the normal round presentation of the peak of the nasal cannula. It is very often but not always associated with changes in Pes recording (and a change in Pes may not be associated with a pattern of flow limitation). It is also often associated with snoring. It may involve one or several breaths. It is not associated with a 3% or 4% SaO2 drop. The “time spent in flow limitation” is the calculated variable. At least four successive breaths must be associated with abnormal wave contour. The duration of flow limitation is calculated from the time of the start of flattening to the time when the wave contour normalizes or returns to baseline. The report indicates the total time of flow limitation from total sleep time and the longest episode of flow limitation (in minute and second).[26],[27] Systematic usage of Pes indicates that flow limitation is associated with systematic increase in inspiratory effort. Flow limitation is associated with abrupt EEG changes that have been described using a different EEG scoring system called the “cyclic alternating pattern” (CAP) scoring system [Figure 1].[28]
Figure 1: Inspiratory flow limitation. Example of a recording of “inspiratory flow limitation” as indicated by the monitoring of nasal airflow through the “nasal cannula-pressure transducer.” No apnea or hypopnea is present in the segment, but the sleep EEGs (4 channels-1-4 from top) indicate the presence of cyclic alternating pattern phase A2, indicative of NREM sleep disturbances. The recording of the nasal cannula measuring airflow exchange is presented on channel 14 from top The figure shows the presence of flow limitation with the presence of an abnormal wave contour: instead of a smooth round wave contour, there is a truncation of the wave contour during inspiration (per convention; up part of the wave), there is no mouth breathing (oral thermistor - channel 15 from top), and chest and abdomen inductive plethysmography bands are indicating breathing efforts. The figure shows a worsening of the flow limitation from left to right with decrease in amplitude of the wave. This worsening is associated with the occurrence of snoring (channel 13 from top). However, with onset of snoring, there is another event occurring: nasal cannula-pressure transducer is an unreliable way to measure expiratory flow, and if an expiratory flow limitation occurs a different variable must be monitored. Normally expiration is mostly “passive” with the absence of involvement of expiratory muscles (monitored on channel 19 from top-bottom channel) as can be seen there is the appearance of “active” contraction of expiratory muscles as seen on the right of the figure. There are simultaneous changes in the inspiratory wave contour with reduction of its amplitude and appearance of expiratory efforts. The oxygen saturation (channel 11 from top) changes somewhat with SaO2going from 94% to 93%, but this 1% change is not a change monitored in any international atlas. Channel 12 monitors the finger photoplethysmography, i.e., the finger vaso-constriction, per convention the curve is presented such as an increase in vasoconstriction indicative of sympathetic activation is associated with a downward displacement of the curve. As can be seen in association with occurrence of snoring and other flow changes, there is a change of the photoplethysmography curve indicative of repetitive stimulation of the sympathetic nerve with snoring, and with swings of the photoplethysmography more pronounced at the right of the figure indicative of a larger stimulation of the sympathetic tone associated with worsening of inspiratory and expiratory flow limitation. None of these changes are taken into consideration in the international scoring manuals looking at abnormal breathing during sleep, despite the fact that many disruptions occur and worsen with snoring.

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Respiratory event-related arousals

Historically, it was defined before flow limitation, and it was related initially to snoring sound and EEG arousal. It is a sequence of breaths ≥10 s characterized by increasing respiratory effort or flattening of the nasal pressure waveform it terminates with an arousal from sleep, and the sequence does not meet criteria for AASM apnea or hypopnea. The major difference with definition of “flow limitation” is that RERAs count only one event at the end of flow limitation period that ends with a 3 s EEG arousal. Studies of “flow limitation”[26],[27] have shown that if “arousal” is scored with a different definition, there are more sleep disturbances - the cause of complaints, signs, and comorbidities - than when just RERAs are scored. However, usage of the CAP [28] that scored an EEG arousal with much shorter EEG changes (i.e., phase A2 of CAP system), or usage of fast Fourier Transform to analyze EEG with a 1 s window have shown that there were more sleep disturbances than when scoring “arousal EEG” lasting 3 s while the cortex react in 300 milliseconds; “flow limitation” may be a better approach but more normative data are needed [Figure 2].
Figure 2: Example of abnormal increased inspiratory effort measured with esophageal manometry [Pes=esophageal pressure].This recording present 15 min of continuous recording. Fourteen channels of the recording have been selected for presentation of the figure from top to bottom. Electroencephalography, Chin electromyography, 2 eye movements, finger photoplethysmography (with sympathetic activation toward the bottom of figure), 2 leg electromyography, pulse oximetry with saturation reading, snore indicated by neck microphone measuring power, nasal cannula-pressure transducer wave contour, chest and abdomen plethysmographic bands, and esophageal manometry recording (bottom). Esophageal pressure has been calibrated before the beginning of recording. The negative peak is per convention placed toward the bottom of the recording. The end of the recording probe is placed in the lower esophagus. This segments of recording show a progressive increase in inspiratory efforts with peak esophageal pressure becoming more and more negative during the following 10 min. There is the presence of inspiratory flow limitation when looking at the nasal cannula wave contour, but no change indicating increase in effort. The electroencephalography analysis indicates the presence of cyclic alternating pattern phase A2, but a clear electroencephalography arousal is only noted at the end of the recording in association with return to normal breathing and important chin electromyography discharge. The investigation of the photoplethysmography indicates that during the entire segment, there are clear indications of several episodes of sympathetic activation that correlate with the cyclic alternating pattern phase A2 bursts, but these short arousals are not sufficient to lead to reopen the airway. A respiratory event- related arousal will be scored at the end of the event in association with the more than 3 s electroencephalography arousal, but the scoring will ignore the long abnormal breathing segment, the calculation of the “flow limitation” gives a better view of the duration and amount of disturbance than calculation of the respiratory -related arousal, moreover “respiratory event related arousals” are not taken into consideration when the apnea-hypopnea index is calculated, the figure indicates the limitations of many scoring systems.

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An increase in RR above that seen during quiet unobstructed breathing: by a minimum of 3 breaths/min in NREM sleep or 4 breaths/min in REM sleep for ≥30 s. After 24 months of age, normal RR is 16–18 breaths/min in NREM sleep and 17–19 breaths/min in REM sleep. No associated changes in oxygen saturation, Pes, or EEG are required. It is based on the definition: Tv × RR = minute ventilation. If the RR increase and oxygen saturation stay stable, this indicates a compensation for decrease in tidal volume and indication of abnormal breathing during sleep.

Mouth breathing

Studies on mouth breathing have shown that normal controls usually spend 4% of total sleep time with mouth breathing, and studies in children showed a maximum amount of mouth breathing of 10% of total sleep time.[29],[30],[31] Mouth opening is associated with a backward and downward displacement of the mandible and the tongue and has been shown to increase the propensity to UA collapse.[32] posterior and inferior movement of the mandible may shorten the UA dilator muscles located between the mandible and hyoid and compromise their contractile force by producing unfavorable length/tension relationships in these muscles. One explanation for this phenomenon is that jaw opening is associated with a posterior movement of the angle of the jaw, which compromises the oropharyngeal airway diameter. Open mouth breathing is associated with an increase in pharyngeal length. The faster airflow generated by the longer and narrower UA may increase the negative intraluminal pressure during inspiration and facilitate collapse of the UA.

  Conclusion Top

We have learned a large amount about SDB over time. We know that certain groups of children are at greater risk of abnormal breathing during sleep; including obese children, when an increase of BMI by 1 kg/m 2 above the upper limit of normal is associated with a 12% increase in risk for OSA, and children born prematurely,[33] and as mentioned above change in oral-facial growth that will begin with birth. this growth change may be related not only to genetic factors (such as those involved in teeth development or oral development) but also to environmental factors, particularly involving functions such as sucking, swallowing, speech development, and nasal breathing.[34],[35] UA allergies with impact on normal breathing and leading to increase in local inflammatory factors have also been considered risk factors. The frequency of SDB related to UA collapse during sleep has oscillated; initially, it was considered as low as 2%–4% of the general population, but with better recognition of the abnormal breathing during sleep, frequency increased; currently, a conservative estimate would be 7%, but some studies go to a frequency as high as 11% of the general children population. Moreover, there is an agreement that certain ethnic groups are at greater risks. more particularly, African-American and their tendency to increase BMI more frequently than Caucasians (and the role of socioeconomic factors have not been well identified) and Far East Asian with the very different orientation of the maxilla at birth compared to Caucasians. However, the main issue is to recognize children with abnormal breathing as early as possible and to know how to give value to indicators seen in testing.

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Conflicts of interest

There are no conflicts of interest.

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