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To know even one life has breathed easier because you lived. This is to have succeeded.

‖ —Ralph Waldo Emerson

OSAS is the most common condition among a group of disorders, known as sleep-disordered breathing, which can affect anyone irrespective of age and sex.3 13 . In 1889 Hill described

snoring and restlessness at night as a cause of “backwardness and stupidity in children”,1 The first study of a series of children with this syndrome was published in 1976 by
Guilleminault et al. (1976). Since then, OSAS in children has been the focus of much attention and research and is now widely accepted as a significant cause of morbidity in childhood.117 The AAP 2012 guideline defines OSAS in children as a ―disorder of breathing during sleep characterized by prolonged partial upper airway obstruction and/or intermittent complete obstruction (obstructive apnea) that disrupts normal ventilation during sleep and normal sleep patterns,‖4 accompanied by symptoms or signs, as listed in Table 120 OSAS needs to be distinguished from primary snoring (PS), which is defined as snoring without obstructive apnea, frequent arousals from sleep, or gas exchange abnormalities.3 Although PS is usually considered benign, this has not been well evaluated, because most studies of snoring children did not discriminate between PS and OSAS.37 Epidemiology OSAS occurs in children of all ages, from neonates to adolescents. It is commonest in the preschool age group, due to adenotonsillar hypertrophy (see below); younger or older children are more likely to have other underlying etiological factors.40 . The prevalence of OSAS is estimated around 2%2,3 in children and about 2.5 to 6% among adolescents. 313 In contrast to adults, where the disease occurs primarily in males, in children it appears to occur equally among the sexes (21). This may be because of the lack of hormonal influences in the prepubertal child. One study suggests that it is more common in African American children, due to either structural differences or socioeconomic factors (21).40 37. There appears to be
some heritability as OSA runs in families. Whether this is due to genetic factors or environmental factors is unclear, but both are likely contributors1 Medical conditions which increase the risk of developing SDB compared to the general population include overweight (including Prader-Willi syndrome), syndromes with midface hypoplasia (e.g., Pierre Robin sequence, Treacher Collins, Crouzon syndrome), large tongue (e.g., Trisomy 21, Beckwith Wiedeman syndrome) and neuromuscular disorders (e.g., cerebral palsy and myotonic dystrophy)14. Children with gastroesophageal reflux (GER) are also at increased risk of developing SDB due to airway oedema causing narrowing. Vice versa, SDB can precipitate or worsen GER due to increased negative intrathoracic pressures.1

1981. and may therefore have preservation of their sleep architecture 31 Differences in characteristics of Obstructive Sleep Apnea syndrome between adults and children are presented in Table 1 (Bower and Gungor. 1992. and adult definitions and criteria are not applicable to children (1. the syndrome is mainly characterized by partial obstruction of the upper airways during sleep (obstructive hypoventilation) and rarely by apneas (Carrol and Loughlin. 2000). children with OSAS often do not have cortical arousals in response to obstructive apneas (3). 1995.10 25 clinic features add table 25 Childhood OSAS is not simply adult OSAS in little people. examined from the pediatric point of view.9 OSA in children is generally considered to be due to enlarged tonsils and adenoids. children with OSA often behave poorly and are misdiagnosed with attention deficit disorder. In contrast.4draw table The syndrome of Obstructive Sleep Apnea.8 In the light of theseunique clinical.12 13 7 the clinical presentation of OSAS in children was found to be quite different from that in adults.9. Bower and Gungor. The recent increased incidence of childhood obesity is considered a secondary cause. 2). As well. Marcus. rather than a junior form of adult OSAS. Boudewyns and Van de Heyning.The soft tissue of the aryepiglottie folds and the epiglottis in young ehildren are more suseeptible to eollapsing into the airway and less resistant to submueosal edema in eomparison with adults. Guilleminault et al. These eharaeteristics are believed to predispose the child towards OSA. has shown differences and special features in comparison to the adult type. 2000).11 Due to poor sleep quality. In children.. First degree relatives (parents and siblings) have a significantly higher likelihood of OSA. 2000.4 . it has been demonstrated that academic performance suffers and then improves once the OSA is managed. Adults with OSAS frequently have fragmented sleep. diagnostic and therapeutic requirements. some authors have recommended that children with OSAS should be regarded as a distinct entity.

18 and imposes a substantial health care burden along with recurrent primary care physician contacts.69. including failure to thrive. Patients with SDB have been shown to have a structurally narrow airway when awake which predisposes them to having increased collapsibility and resistance when asleep19. including the tonsils and adenoids.1. grow more rapidly than the bony structure of the nasopharynx from 3 to 5 years of age. nose.9 pulmonary hypertension and cor pulmonale.10. nasopharynx and oropharynx.Obstructive sleep apnea syndrome in children can result in serious complications.72 Studies using magnetic resonance imaging of the upper airway have shown that children with OSA have larger adenoids and tonsils than control subjects of the same age.14.613 Upper airway soft tissues.25 failure to recognise sleep related breathing disorders can have significant adverse consequences on children’s physical health and on their behaviour and learning. but also on their family.1943 A careful history and detailed physical examination are the first steps in the diagnosis of OSAS. larynx. This leads to reduced or absent airflow resulting in hypopnoeas or apnoeas respectively. dentists may be the first to recognize such disorders and help in their treatment13 pathophysiology The pathophysiology of upper airway obstruction in infants and children is complex and not completely understood.15 and neurobehavioral dysfunction.20. neuromotor tone and inflammation. The size of the pediatric airway is dependent oncraniofacial and soft tissue structures.73 58 Difficulties with nasal breathing.32 As sleep disorders may have devastating effects not only on the child. most .17 Untreated OSAS has also been shown to have a negative effect on health-related quality of life. The two most common symptoms are snoring and difficulty in breathing during sleep. with a consequent decrease in size of the airway during this period.7.16. anatomical structure.71.12 systemic hypertension.25 There are three elements which appear to contribute to the pathophysiology of SDB.13 neurocognitive deficits.7 The available airwayspace may be reduced by abnormalities of oral cavity.

independent of obesity. particularly at the adenotonsillarlevel32.35. possibly because lying supine causes the tongue to maintain a more posterior position23. . the cardinal symptom of OSAS in adults. is uncommon40 Local and systemic inflammation can contribute to the increased resistance.40 McNamara and coworkers (46) found that obstructive apneas were associated with arousal in less than half of the apneas in children.37 P Furthermore. tissue removed surgically for OSA has had oedema and inflammatory cell infiltration. The central nervous system is known to play a crucial role in maintaining upper airway patency. upper airway pressure and flow receptors. Although the overall ventilatory drive appears to be normal in children with OSAS.817 Neuromuscular disease may cause hypotonia of thepharyngeal muscles and reduce airway patency. chemoreceptor afferents. Children with OSAS appear to have a deficit in arousal mechanisms.16 The upper airway neuromotor activation in children is regulated by various factors including central ventilator drive.often due to large adenoids in children. which can also result in narrow nasal passages. thorax and abdomen. which is known to increase CRP levels34. the studies suggest that children not only have increased basal upper airway tone during sleep. suggesting ventilatory drive is an important factor. which may trigger endothelial dysfunction and systemic inflammation36. The mechanism involved is via episodic hypoxia and arousal. increased upper airway neuromotor tone may be one way that patients can compensate for a narrow upper airway. leads to chronic mouth breathing and this can lead to anatomical changes in facial growth. In adults. As a result. which has been shown in adults during wakefulness.3825 Children with SDB have blunted ventilator responses to hypercapnia30 and higher end-tidal CO2 when anaesthetized31. The tendency of the upper airway to collapse is inversely related to the level of activity of the upper airway dilator muscles. narrow dental arches and an anterior crossbite22. pulmonary mechanoreceptors and sleep state. Studies have shown that these patients have elevated arousal thresholds in response to hypercapnia (40) and increased upper airway resistance (43). Children who sleep supine tend to have a smaller maxillary width. This compensatory mechanism was lost during sleep. Obesity increases pharyngeal resistance and may decrease thoracic compliance through mass loading of the pharynx.33At the systemic level. high arched palate and poor maxillary growth. 75). and therefore excessive daytime sleepiness. In children higher levels of cysteinyl leukotrienes have been found in those with SDB32. With chronic mouth breathing. sleep architecture is preserved in children with OSAS (74. and only 18% of apneas in infants. it is possible that central augmentation of upper airway neuromotor function is abnormal.13-15 Therefore. the tongue is unable to mould the palate and this results in a narrow. increased CRP levels have been demonstrated in patients with SDB.

Arousal from sleep has a potent stimulatory effect on the upper airway dilating muscles. This is thought to be due to a reduction in airway muscular activity during sleep. thorax and abdomen. particularly during REM sleep. soft tissue. This is thought to be the predominant factor responsible for spontaneous termination of obstructive apnoeic episodes The leading cause of obstructive sleep apnoea in children is a prominence of lymphoid tissue which increases the upper airway resistive load.26 At sleep onset. Neuromuscular disease may cause hypotonia of the pharyngeal muscles and reduce airway patency. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. and skeleton are of critical importance to the development of OSA. upper airway resistance (airway suction force). ventilatory control. and the contractile force of the airway dilating muscles (airway patency force).25 The pathophysiology of upper airway obstruction in infants and children is complex and not completely understood. Obesity increases pharyngeal resistance and may decrease thoracic compliance through mass loading of the pharynx.16 Narrowing of the aperture of the nasal or pharyngeal airway as seen in various craniofacial syndromes may displace the tongue posteriorly and result in an obstruction. although they do not completely account for the pattern of sleep-disordered breathing. Ventilatory overshoot .38 Neck flexion may also predispose to airway closure. Sleep is the most obvious functional factor that predisposes to airway obstruction. and arousal threshold. This indicates a role for other determinants of airway patency such as neuromuscular activation. Thus. Anatomic measures of the airway lumen.but that the tone can be increased even further in response to a stimulus.8 Pathophysiology Pharyngealairway maintenance thus depends on a dynamic balance between diaphragmatic contractile force. Both functional and anatomical factors may tilt the balance. ventilatory variability increases. airway muscle activity is reduced.25 . pharyngeal muscle activity appears to play a prominent role in preserving upper airway patency in children during sleep. in order to compensate for an anatomically smaller upper airway. and an apneic threshold slightly below eupneic levels is observed in non-REM sleep.

58 Familial Pattern: A familial tendency for sleep apnea has been described.66–68 They may grow downward into the nasopharyngeal lumen. consistent with successful neuromuscular compensation. with a consequent decrease in size of the airway during this period.results in sudden reduction in airway muscle activation.23 Preliminary studies have suggested the familial aggregation of OSAS in children.46 The adenoids. overlapping with the level of oropharyngeal obstruction by the tonsils.69 forward through the posterior choanae.69.70 or inferiorly. in whom the critical pressure at which the upper airway collapses (Pcrit) is positive (mean (SD) 1 (3) cm H2O) compared with a markedly negative Pcrit (−20 (9) cm H2O) in children with primary snoring. obstructive cycling. but relatively few have OSA. grow more rapidly than the bony structure of the nasopharynx from 3 to 5 years of age.74 Many children have adenotonsillar enlargement. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. thus. For most patients.69.71 The tonsils also begin to enlarge in early childhood. Respiratory control mechanisms modulate ventilation and pharyngeal dilator activation. including the tonsils and adenoids. the role of hereditary factors is unknown. Arousal from sleep contributes to ventilatory instability and. contributing to obstruction during non-REM sleep. situated on the roof of the nasopharynx.73 However.21.30 A familial factor may predispose children to develop OSAS by affecting the upper airway resistive loads through craniofacial abnormalities and/or probable ventilatory control . enlarge from infancy through adolescence in normal children and then decrease in size during adult life. Most children with severe OSA will be able to sustain stable breathing during a large portion of sleep.72 Studies using magnetic resonance imaging of the upper airway have shown that children with OSA have larger adenoids and tonsils than control subjects of the same age. Upper airway soft tissues.46 The pathophysiology of OSA in childhood is therefore likely to be a complex interaction between physiological factors such as ventilatory drive and neuromuscular control. collapse may occur. there is not a linear relationship between clinical assessment of adenoid and tonsillar size and severity of OSA.71. in situations of increased upstream resistance such as that caused by enlargement of the upper airway lymphoid tissues in many children with OSA. This may be partly explained by increased upper airway collapsibility in children with OSA. and anatomical factors such as airway structure and adenotonsillar enlargement.26 PATHOPHYSIOLOGY However.73.

23 ETIOLOGY: Obstructive sleep apnea (OSA) occurs when tissues in the upper throat collapse at different times during sleep.30 More studies are needed. there is increase in velocity of air passing through narrow airway which in turn causes vibration of soft tissues especially the soft palate and uvula.'"" sleep disorders among children and infants and how they affect these young patients is well documented in the medical literature. children with obstructive sleep apnea syndrome rarely have cardiac arrhythmias. The airway of a patient with snoring is obstructed due to tongue or hyoid bone andoverlying soft tissues dropping back towards the posterior wall of pharynx when the patient is in supine position. An underlying abnormality of the neurologic control of the upper airway musculature or ventilation during sleep may be present. however. In the adult.23 Complications: In contrast to the adult. In some patients with neurologic disorders. The upper airway is basically a soft tissue tube. thereby blocking the passage of air. airway and anatomical structures9. excessive sleepiness and cardiopulmonary abnormalities are the main complications (see associated features). the patency of which is maintained in part by the activity of muscular groups of which the tensor veli and genioglossus muscles are highly important members. to confirm this familial tendency and any underlying pathophysiological mechanisms25 Pathology: Upper airway narrowing due to either excessive bulk of soft tissues or craniofacial abnormalities predisposes the patient to obstructive sleep apnea syndrome.dysfunctions. a specific lesion affecting the control of pharyngeal muscles can be responsible for the development of obstructive sleep apnea syndrome. . It has complex etiology and consists of multifactorial interplay between the neuromuscular systems . This vibration is the sound of snoring10-1419 Although not well recognized by dentists or physicians.3 . In order to get sufficient oxygen to the lungs .

in a study of ADHD children 6 to 14 years old. 3 Another study's results^' indicated that children with adenotonsillarydiseaseandOSAhadahigherprevalence of right and/or left ventricular enlargement. increased flexure of the cranial base and bony naso pharynx.3 To summarize. shortened mandibular length. 2.'' More recently.3 Sivan et al3° found that infantile OSAdoes occur in infants duetohypertrophicadenoidsandtonsilsandthatthese infants failed to gain weight. Sangal et al'° found neither OSA nor Periodic limb movement disorder (PLMD) to be a common underlying disorder or etiologic factor in patients who met the criteria for ADHD. In a more recent study. as observed during polysomnography testing. In addition to these findings. study'' demonstrated that almost 25% of OSAS children had clinically significant behavioral sleep problems such as sleep walking and nightmares as well as a greater incidence of daytime externalizing behavior problems. 3. almost 26% of children with mild symptoms of attentiondeficit/ hyperactivity disorder (ADHD) also demonstrate OSA. it has been demonstrated that emotionally governed behavior in children may be closely linked to previously diagnosed physiological problems such as OSA and airway obstruction. Rosen et al'^ found a higher prevalence of problem behaviors and hyperactive-type behaviors in children with relatively mild SDB. Aadreou et al^' found that children with sleep disorders and ADHD disorder had a verbal intelligence quotient (IQ) up to 20 points lower than control subjects. Ng et al33 indicated that there is increasing evidence that childhood SDB/OSAis associated with detectable cardiovascular abnormalities. opening ofthegonial angle. .3 Finkelstein et al** reported that significant craniofacial abnormalities were seen in OSA patients and included.

4.4] 18 The American Academy of Sleep Medicine (AASM) rates the average number of obstructive sleep apnea events per hour as respiratory distress index (RDI).18 However. 5. growth-related. The apneahypopnea index measures the frequency of disordered breathing events but does not quantify other processes that may be operative in the pathophysiology of OSA such as the degree of oxygen desaturation.7] An RDI of 0 to 5 is normal. 5 to 20 is mild. . and 6. 9).3 TABLE 1 Symptoms and Signs of OSAS History Frequent snoring (≥3 nights/wk) Labored breathing during sleep Gasps/snorting noises/observed episodes of apnea Sleep enuresis (especially secondary enuresis)a Sleeping in a seated position or with the neck hyperextended Cyanosis Headaches on awakening Daytime sleepiness Attention-deficit/hyperactivity disorder Learning problems Physical examination Underweight or overweight Tonsillar hypertrophy Adenoidal facies Micrognathia/retrognathia High-arched palate Failure to thrive Hypertension a Enuresis after at least 6 mo of continence. 20 to 40 is moderate and over 40 is considered severe. it may result in significant morbidity such as neurobehavioural. if unrecognized and untreated. increased velar thickness. dorsocaudal location of the hyoid. and cardiovascular problems in childhood (5.[3. reduced posterior airway space.[6. 8.20 The severity of the OSA can be assessed using apneahypopnea index and respiratory distress index.

2 Obstructive sleep apnea syndrome (OSAS) is a common condition in childhood and can result in severe complications if left untreated.20 . an appropriate differential diagnosis is necessary to discriminate OSAS in childhood from various types of SRBD.Therefore.