Pediatric Obstructive Sleep Apnea

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1 Special Article Pediatric Obstructive Sleep Apnea Bantu S. Chhangani, Thomas Melgar 1 and Dilip Patel 2 1 Bronson Center for Sleep Studies, Paw, Michigan, USA, Departments of Internal Medicine and Pediatrics and Human Development, 2 Department of Pediatrics and Human Development, Michigan State University/Kalamazoo Center for Medical Studies, Kalamazoo Michigan, USA ABSTRACT For over 100 years obstructive sleep apnea has been recognized as a clinical entity in adults and more recently in children. A comprehensive review of the literature of pediatric obstructive sleep apnea was conducted using a PubMed search for original research articles. Bibliographies of these articles were reviewed for additional relevant articles not identified by the initial PubMed search. This article reviews the epidemiology, pathogenesis and risk factors, clinical features, diagnostic evaluation and treatment of obstructive sleep apnea in children. All physicians who provide care for children should be aware of the unique features of obstructive sleep apnea in children and the appropriate management. [Indian J Pediatr 2010; 77 (1) : 81-85] patel@kcms.msv.edu Key words: Obstructive sleep apnea syndrome; Sleep apnea; Airway obstruction; Polysomnography; Sleep studies Definitions Obstructive sleep apnea (OSA) is defined as a disorder of breathing during sleep characterized by prolonged periods of increased upper airway resistance, and recurrent episodes of partial and/or complete upper airway obstruction that subsequently leads to disruption of normal ventilation and oxygenation during sleep as well as normal sleep patterns. An apnea hypopnea index (AHI) of greater than one helps define OSA on polysomnography in children provided these events are mainly obstructive and not central in nature. 1 Epidemiology It has been estimated that OSA affects 2% - 3% of all children from the newborn age to adolescence. 1-6 It occurs equally in boys and girls, with a peak incidence between the age of 2 and 8 yr. This correlates with the age during which adenotonsillar hypertrophy is most marked. Increasing prevalence has also been noted recently in the middle childhood and adolescent age group due to rising prevalence of obesity in this age group in some parts of the world including the United States. The salient differences between OSA in adults and children are listed in table 1. Correspondence and Reprint requests : Dr Dilip Patel, MD, Department of Pediatrics and Human Development, Michigan State University/ Kalamazoo Center for Medical Studies, Kalamazoo, Michigan, USA. [DOI /s z] [Received January 26, 2009; Accepted April 09, 2009] TABLE 1. Features of Pediatric and Adult OSA Characteristic Pediatric OSA Adult OSA Gender Males = females Males more than females Peak age Preschool (2-8 years) Middle age Etiology Adenotonsillar Obesity hypertrophy Clinical features Snoring Snoring Diagnosis Polysomnography Polysomnography Primary treatment Surgical Medical (CPAP) (adenotonsillectomy) Pathogenesis The pathogenesis of pediatric OSA is complex and still incompletely understood. It involves a complex interplay between functional changes which occur normally during sleep and anatomical factors both normal and abnormal which lead to the narrowing of the upper airway and subsequently to partial or complete obstruction. Children with prominent adenotonsillar hypertrophy alone may not demonstrate obstructive symptoms. 1,4 Children, depending on their age, spend the majority of their sleep time (40-80%) in rapid eye movement (REM) sleep. It is during this stage of sleep that respiration is least stable which makes children even more prone to OSA; while this holds true for the general pediatric population, individual differences in the various parameters of sleep may exist. 7 In order to better understand the pathogenesis of OSA in children, it is important to understand the basic principles which govern airflow. 8,9 Bernoulli stated Indian Journal of Pediatrics, Volume 77 January,

2 Bantu S. Chhangani et al that as a column of air is flowing through a conduit without any narrowing, it has a slower velocity and exerts greater pressure on the lateral walls. However, if there is any narrowing of the conduit, the velocity of the air increases while the pressure being exerted on the lateral walls from within the narrowed lumen decreases. The Venturi effect simply states that there is an acceleration of airflow as it passes through a narrowing. These principles can be applied to the pathophysiology of OSA in children. For instance, during inspiration pressure generated within the airway is slightly lower than atmospheric pressure by the action of the respiratory muscles expanding the lung volume. As long as there is no narrowing in the airway, the air will flow slowly and exert pressure on the pharyngeal walls maintaining a balance. However, if there is an upper airway narrowing, the air will flow faster and exert less pressure on the lateral walls predisposing to collapse of the upper airway. There is a tendency for increase in airway resistance during sleep mainly because of an overall decrease in muscle tone. 8,9 This generalized reduction of muscular tone begins during Stage N1 of NREM and progressively worsens until it is barely perceptible during REM sleep. 8 Normally during inspiration, a relatively low pressure is generated within the airway which can lead to airway collapse. The pharyngeal dilator muscles counteract this negative pressure and maintain airway patency by tonic contractions while awake. However, during sleep, as a result of decreased muscle tone, the pharyngeal dilator muscles relax and are unable to maintain airway patency which contributes to increasing airway resistance. 8 Furthermore, the intercostal muscles are unable to contract and compensate for any increase in airway resistance due to supraspinal inhibition present in REM sleep. 8 There is also a decrease in central chemoreceptor sensitivity to hypoxia and hypercapnia during sleep. Thus, an overall increase in upper airway resistance occurs with a decrease in the compensatory mechanisms which can overcome this resistance. Any anatomic abnormality which can further narrow the airway, it then exacerbates the upper airway resistance predisposing the child to obstruction. The most common anatomic abnormality in children is adenotonsillar hypertrophy while the most common site of obstruction is the retropalatal region. 1,4,10 Once obstruction occurs, impaired ventilation leads to hypoxia and hypercapnia with subsequent increased respiratory effort and finally arousal from sleep in order to re-establish airway patency. This cycle is then repeated several times through the night, resulting in recurrent hypoxia and fragmentation of sleep. Risk factors for OSA in children are listed in table 2. 1,4,3,2,11,12,13,14 TABLE 2. Risk Factors for OSA in Children Anatomic Functional Adenotonsillar hypertrophy Nasal polyps Nasal tumors Allergic rhinitis Anomalies of craniofacial bones Retrognathia Pierre-Robin sequence Micrognathia Pierre-Robin Midface hypoplasia Down syndrome Cleft palate Macroglossia Obesity Generalized hypotonia in neuromuscular diseases e.g., muscular dystrophies Effect of sedative hypnotics Achondroplasia Spina bifida myelomeningocele Mucopolyssacharidosis Prematurity Family history of OSA CLINICAL FEATURES The hallmark of pediatric OSA is snoring and OSA is very unlikely in the absence of habitual snoring. 15 However, not all children who snore actually have OSA. Between 6% and 12% of all children snore at nighttime and only between 10% and 30% of these children have obstructive sleep apnea based on findings on polysomnography. 15 All children should be screened for snoring during their annual health maintenance visit. 1 The symptoms of OSA in children can be classified into nighttime symptoms and daytime symptoms and are listed in table 3. 1,6,15,16,17,18,19,20 TABLE 3. Symptoms of OSA in Children Nighttime symptoms Daytime symptoms Snoring Sleeping in unusual positions Nocturnal sweating Enuresis Daytime somnolence rare in children Aggressiveness Anxiety Hyperactivity Inattentiveness Learning difficulties Deterioration in academic performance Morning headaches Mouth breathing History of recurrent infectious illness Children with OSA may have certain clinical features suggestive of the disorder or may have a completely normal examination. Failure to thrive or the very opposite end of the spectrum, obesity may be 82 Indian Journal of Pediatrics, Volume 77 January, 2010

3 Pediatric Obstructive Sleep Apnea noted. 1,18,19 Adenotonsillar hypertrophy is a frequent examination finding although its presence or absence neither confirms nor excludes the diagnosis. Craniofacial anomalies including retrognathia, midface hypoplasia, and other features associated with specific genetic syndromes may be apparent. Hyponasal voice, nasal polyps, choanal atresia or septal deviation on nasal cavity examination may be noted. Muscle tone should be assessed as patients with neuromuscular disorders have hypotonia. These patients maybe found to have abnormal postures like frog leg position while laying supine, diminished resistance of the joints to passive movement, and an increased range of joint movement. Although the history and physical examination will help delineate likely risk factors and complications associated with obstructive sleep apnea, clinical features are neither specific nor sensitive enough to make the diagnosis or distinguish OSA from primary snoring from OSA. 1 DIAGNOSIS OSA in children, if left untreated can lead to significant cardiovascular, metabolic and neurocognitive sequelae TABLE 4. Complications of OSA in Children Behavioral Cognitive Cardiopulmonary Growth and metabolism Aggression Hyperactivity Anxiety Depressed mood Psychosocial difficulties Nocturnal enuresis Inattentiveness Impaired executive functioning Impaired memory Impaired scholastic function Systemic hypertension Impaired right ventricular function rare Cor pulmonale rare Failure to thrive Delayed physical growth noted in table 4. 1,19-24 A detailed history and thorough physical examination are helpful in screening for patients with OSA, but is of poor diagnostic value. The gold standard and diagnostic test of choice is polysomnography (PSG) which not only confirms the presence of OSA but also categorizes the extent of severity. 1 This overnight test during which several physiologic parameters are simultaneously measured including: sleep stages, eye movements, muscle activity, respiration (PCO2 and SaO2), cardiac activity, and snoring is best performed in a sleep center facility dedicated to pediatrics under conditions which closely resemble the child s sleep environment. Currently an apnea hypopnea index of greater than one per hour is used in order to make the diagnosis of OSA in children provided that the events are mainly obstructive and not central. Due to limitations of diagnostic PSG in the pediatric age group including but not limited to the lack of standardization of analysis and interpretation of data, limited pediatric dedicated sleep centers and personnel, the use of other diagnostic tools have been suggested including: nap polysomnography (during which the PSG is conducted for only one to two hours during daytime), overnight pulse oximetry and audio taping or videotaping of nighttime sleep. These tests have been scientifically evaluated and because of their own limitations are currently used at best for screening purposes only. Negative results still have to be followed with an overnight PSG if there is a high index of suspicion for OSA. 1 MANAGEMENT While the primary treatment for adults is medical management, surgery is the primary treatment for children with OSA. 1,18,23,25,26,27,28,29 Adenotonsillectomy is the treatment of choice for most children with OSA and is curative in 80% of cases. Affected children show resolution of symptoms and normalization of respiratory parameters with subsequent improvement in growth. All patients should undergo clinical evaluation 6 to 8 weeks after surgery and high risk patients may need objective evaluation by doing a post operative PSG looking for residual disease. 1 Other surgical treatments include uvulopalatopharyngoplasty, palatal implants, tongue base reduction and orthognathic surgery as indicated for the individual child. Tracheostomy, which is the definitive treatment for upper airway obstruction should be reserved for severe refractory cases. Continuous positive airway pressure (CPAP) is usually employed in patients with neuromuscular diseases, for patients who either do not desire surgery, or for whom surgery is contraindicated. The presence of residual disease after surgery is another indication for CPAP use. Children with anatomic abnormalities may also benefit from CPAP. 30,31,32,33,34 Continuous positive pressure delivered from a CPAP machine provides a mechanical stent for the airway, maintains its patency, ensuring less collapsibility and thus normalization of breathing and oxygenation. 34 Initially believed to be effective only in adults, studies have demonstrated that OSA in children can be successfully treated with CPAP. 35 An overall improvement in sleep architecture, hypersomnolence, cardiovascular and neurophysiologic systems is noted. 36,37 Compliance though greater than in adults, is still an issue. 33 The use of behavioral Indian Journal of Pediatrics, Volume 77 January,

4 Bantu S. Chhangani et al interventions in order to facilitate increased tolerance and acceptance of the CPAP therapy may be considered for particularly difficult pediatric patients. Once started on CPAP therapy, it is essential that children are monitored frequently as they grow, for mask refitting as well as retitration studies and while CPAP therapy is non invasive and has a relatively benign side effect profile, potential complications of long term use may occur including midface hypoplasia and need to be monitored closely. 38 Other medical measures include weight loss for obese children. Use of nasal steroids has also been postulated but no definite recommendations have been made yet. 39 Contributions: Bantu Chhangani :Contributed to the conception, design, data collection, data organization, data interpretation, manuscript preparation, manuscript revisions, and final manuscript preparation; Thomas Melgar: Contributed to the conception, design, data collection, data organization, data interpretation, manuscript preparation, manuscript revisions, and final manuscript preparation; Dilip R Patel: Contributed to the conception, design, data collection, data organization, data interpretation, manuscript preparation, manuscript revisions, and final manuscript preparation. Conflict of Interest: None. REFERENCES 1. American Academy of Pediatrics. Clinical practice guidelines: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002; 109: Rosen CL, Larkin EK, Kirchner HL et al. Prevalence and risk factors for sleep disordered breathing in 8-11 year old children. Association with race and prematurity. J Pediatr 2003;142: Redline S, Tishler PV, Schluchter M, Aylor J, Clark K, Graham G. Risk factors for sleep disordered breathing in children. Associations with obesity, race, and respiratory symptoms. Am J Respir Crit Care Med 1999;159: Greenfeld M, Tauman R, DeRowe A, Sivan Y. Obstructive sleep apnea syndrome due to tonsillar hypertrophy in infants. Int J Pediatr Otorhinolaryngol 2003;67: Marcus CL, Curtis S, Koerner CB, Joffe A, Serwint JR, Loughlin GM. Evaluation of pulmonary function and polysomnography in obese children and adolescents. Pediatr Pulmonol 1996;21: Gozal D, Pope DW Jr. Snoring during early childhood and academic performance at age 13 and 14 years. Pediatrics 2001;107: Hudgel DW, Gordon EA, Thanakitcharu S, Bruce EN. Instability of ventilatory control in patients with obstructive sleep apnea. Am J Respir Crit Care Med 1998;158: Marcus CL, Katz ES, Lutz J, Black CA, Galster P, Carson KA. Upper airway dynamic responses in children with obstructive sleep apnea syndrome. Pediatr Res 2005;57: Isono S, Shimada A, Utsugi M, Konno A, Nishino T. Comparison of Static Mechanical Properties of the Passive Pharynx between Normal Children and Children with Sleepdisordered Breathing. Am J Respir Crit Care Med 1998;157: Chau KW, Ng DKK, Kwok CKL, Chow PY, Ho JCS. Clinical risk factors for obstructive sleep apnea in children. Singapore Med J 2003;44: McColley SA, Carroll JL, Sampson HA. High prevalence of allergic sensitization in children with habitual snorning and obstructive sleep apnea.. Chest 1997;111: Gozal D, Wang M, Pope DW. Objective sleepiness measures in pediatric obstructive sleep apnea. Pediatrics 2001;108: Marcus CL, Keens TG, Bautista DB, von Pechmann WS, Ward SL. Obstructive sleep apnea in children with Down syndrome. Pediatrics 1991;88: Zucconi M, Weber G, Smirne S. Sleep and upper airway obstruction in children with achondroplasia. J Pediatr 1996;129: Ali NJ, Pitson D, Stradling JR. Snoring, sleep disturbance and behaviour in 4 5 year old children. Arch Dis Child 1993;68: Brooks LJ, Topol HI. Enuresis in children with sleep apnea. J Pediatr 2003;142: Kaditis AG, Alexopoulos EI, Hatzi F et al. Overnight change in brain naturetic peptide in children with sleep disordered breathing. Chest 2006;130: Basha S, Bialowas C, Ende K, Szeremeta W. Effectiveness of adenotonsillectomy in the resolution of nocturnal enuresis secondary to obstructive sleep apnea. Laryngoscope 2005; 115: Gozal D. Sleep disordered breathing and school performance in children. Pediatrics 1998;102: Castronovo V, Zucconi M, Nosetti L et al. Prevalence of habitual snoring and sleep disordered breathing in preschool-aged children in an Italian community. J Pediatr 2003;142: Ng DK, Chan C, Chow AS, Chow P, Kwok K. Childhood sleep disordered breathing and it s implications for cardiac and vascular diseases. J Paediatr Child Health 2005; 41: O Brien LM, Mervis CB, Holbrook CR et al. Neurobehavioral implications of habitual snoring in children. Pediatrics 2004; 114: Stradling JR, Thomas G, Warley ARH, Williams P, Freeland A. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance and symptoms in snoring children. Lancet 1990;335: 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: Ali NJ, Pitson D, Stradling JR. Sleep disordered breathing: effects of adenotonsillectomy on behaviors and psychogical functioning. Eur J Pediatr 1996;155: Friedman BC, Hendeles-Amitai A, Kozminzki E et al. Adenotonsillectomy improves neurocognitive function in children with obstructive sleep apnea syndrome. Sleep 2003;26: Montgomery-Downs HE, Crabtree CR, Gozal D. Cognition, sleep and respiration in at-risk children treated for obstructive sleep apnoea. Eur Repir J 2005;25: Goldstein NA, Post JC, Rosenfeld RM Campbell TF. Impact of tonsillectomy and adenoidectomy on child behavior. Arch Otolaryngol Head Neck Surg 2000;126: Bar A, Tarasiuk A, Segev Y, Phillip M, Tal A. The effect of adenotonsillectomy on serum insulin-like growth factor-i and growth in children with obstructive sleep apnea syndrome. J Pediatr 1999; 135: Marcus CL, Carroll JL, Koerner CB, Hamer A, Lutz J, Loughlin GM. Determinants of growth in children with the obstructive sleep apnea syndrome. J Pediatr 1994;125: Indian Journal of Pediatrics, Volume 77 January, 2010

5 Pediatric Obstructive Sleep Apnea 31. American Thoracic Society. Cardiorespiratory sleep studies in children: establishment of normative data and polysomnographic predictors of morbidity. Am J Crit Care Medicine 1999;160: Cohen SR, Holmes RE, Machado L, Magit A. Surgical strategies in the treatment of complex obstructive sleep apnoea in children. Paediatr Respir Rev 2002;3: Verse T, Pirsig W, Stuck B, Hormann K, Maurer J. Recent developments in the treatment of obstructive sleep apnea. Am J Respir Med 2003; 2: Issa FG, Sullivan CE. The immediate effects of nasal continuous positive airway pressure treatment on sleep pattern in patients with obstructive sleep apnea syndrome. Electroencephalogr Clin Neuropysiol 1986;63: McNamara F, Sullivan CE. Obstructive sleep apnea in infants and it s management with nasal continuous positive airway pressure. Chest 1999;116: Montplaisir J, Bedard MA, Richer F, Roulean I. Neurobehavioral manifestations in obstructive sleep apnea syndrome before and after treatment with continuous positive airway pressure. Sleep 1992;15: Rajagopal KR, Bennett LL, Dillard TA. Overnight nasal CPAP improves hypersomnolence in sleep apnea. Chest 1986; 90: Li KK, Riley RW, Guilleminault C. An unreported risk in the use of home nasal continuous positive airway pressure and home nasal ventilation in children: mid face hypoplasia. Chest 2000; 117: Brouillette RT, Manoukian JJ, Ducharme FM et al. Efficacy of fluticasone nasal spary for pediatric obstructive sleep apnea. J Pediatr 2001; 138: Indian Journal of Pediatrics, Volume 77 January,