177 Epidemiology of childhood OSAS

Abstracts / Sleep Medicine 7 (2006) S1–S127

177 Epidemiology of childhood OSAS Susan Redline * Case Western Reserve University, Division of Clinical Epidemiology, Cleveland, OH, USA Pediatric obstructive sleep apnea syndrome (OSAS) is a disorder characterized by repetitive episodes of upper airway obstruction, intermittent hypoxemia and hypercapnia, and snoring. Increasing data indicate the disorder is common, particularly among vulnerable subgroups, and associated with a wide range of co-morbidities. Limited epidemiological data suggest that the disorder affects 1–4% of children. Childhood OSAS appears to vary among age, gender, and ethnic subgroups. Childhood OSAS prevalence tends to peak at two ages. The first peak occurs in children 2–6 years of age and coincides with the peak age of lymphoid hypertrophy. A second peak occurs during adolescence and appears related to an increase in prevalence of overweight. Gender differences are less than what has been observed in adult populations, with approximately equal distribution of OSAS among pre-adolescent boys and girls. However, a greater prevalence of OSAS has been observed among adolescent boys compared to adolescent girls. Associations between overweight and childhood OSAS also seem stronger among adolescents than among younger children. The most commonly recognized risk factor for childhood OSAS is adeno-tonsillar lymphoid hypertrophy. Several studies, however, suggest that OSAS may persist in 9–30% of children post-tonsillectomy/adenoidectomy. Paradoxically, a history of tonsillectomy is associated with a two- to threefold increased risk of snoring, suggesting that symptoms of OSAS may trigger surgery, but addressing lymphoid tissue may not always resolve intermittent upper airway obstruction. Susceptibility to childhood OSAS may also relate to other factors that influence airway patency, including genetic factors, craniofacial morphology, abnormalities in ventilatory control, as well as overweight, suggesting the complexity of the phenotype. The importance of genetic factors is suggested by ethnic differences in OSAS prevalence, which is two- to fourfold higher in Black children [1,2]; symptoms of OSAS also appear increased in Hispanic children [3]. In addition, recent data suggest that OSAS is also more common in children from poor neighborhoods [4], suggesting that environmental influences associated with chronic irritant/allergen exposures or physical environment stresses which influence airway inflammation or breathing and sleep properties may be of importance. Influences of developmental factors on airway and/or respiratory function are also suggested by increased risk of childhood OSAS among former preterm children. The chronic co-morbidities associated with untreated pediatric OSAS include cognitive deficits, behavioral problems (inattention, hyperactivity, aggression, conduct problems, Attention-Deficit/Hyperactivity

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Disorder), mood impairments, excessive daytime sleepiness, impaired school performance, and poor quality of life [5–8]. Untreated pediatric OSAS also has been associated with adverse cardiovascular and metabolic outcomes. Children with OSAS have higher levels of blood pressure, C-reactive protein (an inflammatory risk factor associated with cardiovascular disease) and increased insulin resistance, as well as left ventricular hypertrophy [9–12] [13], suggesting that childhood OSAS also may increase the risk of developing severe chronic cardiovascular and metabolic conditions. Despite the frequency and severity of OSAS during childhood, there are large knowledge gaps, including scant data that address causal pathways and population vulnerability to the disorder, responses to therapy, and long term influences on health. References [1] 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 problems. Am J Respir Crit Care Med 1999;159:1527–32. [2] Rosen CL, Larkin EK, Kirchner HL, Emancipator JL, Bivins SF, Surovec SA, 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(4):383–9. [3] Goodwin JL, Babar SI, Kaemingk KL, Rosen GM, Morgan WJ, Sherrill DL, et al. Symptoms related to sleep-disordered breathing in White and Hispanic children: the Tucson Children’s Assessment of Sleep Apnea Study 1378/chest.124.1.196. Chest 2003;124(1):196–203. [4] Spilsbury J, Storfer-Isser A, Kirchner HL, Nelson L, Rosen CL, Drotar D et al. Neighborhood disadvantage as a risk factor for pediatric obstructive sleep apnea. J Pediatr 2006 (in press). [5] Rosen CL, Storfer-Isser A, Taylor HG, Kirchner HL, Emancipator JL, Redline S. Increased behavioral morbidity in schoolaged children with sleep-disordered breathing. Pediatrics 2004;114(6):1640–8. [6] Emancipator JL, Storfer-Isser A, Taylor HG, Rosen CL, Kirchner HL, Johnson NL, et al. Variation of cognition and achievement with sleep-disordered breathing in full-term and preterm children. Arch Pediatr Adolesc Med 2006;160(2):203–10. [7] Chervin RD, Dillon JE, Archbold KH, Ruzicka DL. Conduct problems and symptoms of sleep disorders in children. J Am Acad Child Adolesc Psychiatry 2003;42(2):201–8. [8] Crabtree VM, Varni JW, Gozal D. Health-related quality of life and depressive symptoms in children with suspected sleepdisordered breathing. Sleep 2004;27(6):1131–8. [9] Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med 1998;157:1098–103. [10] de la Eva RC, Baur LA, Donaghue KC, Waters KA. Metabolic correlates with obstructive sleep apnea in obese subjects. J Pediatr 2002;140(6):654–9. [11] Amin R. Cardiovascular consequences of sleep apnea in children. In: American Thoracic Conference; 2001; San Franscisco, CA; 2001. [12] Amin RS, Caroll JL, Jeffries JL, Grone CJAB, Chini B, et al. Twenty four hour ambulatory blood pressure in children with sleep-disordered breathing. Am J Respir Crit Care Med 2004;169:950–6. [13] Larkin EK, Rosen CL, Kirchner HL, Storfer-Isser A, Emancipator JL, Johnson NL, et al. Variation of C-reactive protein

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Abstracts / Sleep Medicine 7 (2006) S1–S127 levels in adolescents: association with sleep-disordered breathing and sleep duration. Circulation 2005;111(15):1978–84.

doi:10.1016/j.sleep.2006.07.082

178 Cardiovascular effects of OSA and obesity in children Raouf Amin * Children’s Hospital Medical Center, Pulmonary Medicine, Cincinnati, OH, USA Sleep Disordered Breathing (SDB) is a complex disorder that has a broad range of morbidity. Knowledge about the cardiovascular impact of SDB in the pediatric literature is emerging. The clinical course of the disorder is changing from one that caused cardiovascular morbidity in the pediatric age to one that leads to the development of risk factors for cardiovascular disease in adults. A review of the association between SDB and abnormal vascular structure and function will be presented. The confounding effect of obesity will be discussed. doi:10.1016/j.sleep.2006.07.083

179 Sleep-disordered breathing in patients with Prader– Willi syndrome Gillian Nixon * University of Auckland, Department of Paediatrics, New Zealand Prader–Willi syndrome (PWS) is a genetic disorder with an estimated prevalence of between 1 in 10,000 and 1 in 25,000 live births. Characteristic clinical features vary with age, but most commonly include hypotonia and feeding difficulties in the neonatal period and developmental delay in childhood. During early childhood, most affected children develop marked hyperphagia, with consequent morbid obesity. Patients with PWS appear to have a primary abnormality of the sleep-wake cycle, probably due to hypothalamic dysfunction, and commonly suffer from excessive daytime sleepiness (EDS) from early childhood. Increased nocturnal sleep, EDS and abnormalities of arousal to ventilatory stimuli are all likely to be part of a generalized disorder of arousal. Obesity and cranio-facial features place people with PWS at risk for obstructive sleep apnea, and snoring and breathing difficulty during sleep are commonly reported. Alveolar hypoventilation may also be present during sleep, the incidence and severity of which is related to the degree of obesity. The severity of all types of sleep disordered breathing is accentuated by abnormal ventilatory and arousal responses to hypoxia and hypercapnia. Recent studies have shown beneficial effects of growth hormone treatment in PWS, leading to a decrease in per-

cent body fat and increase in lean muscle mass. Growth hormone may also lead to improvements in resting ventilation and central inspiratory drive, accompanied by an increase in ventilatory response to hypercapnia. However, a link between growth hormone treatment, obstructive sleep apnoea and sudden death has lead to increased vigilance for the presence of OSA in children with PWS, with implication for sleep laboratories. doi:10.1016/j.sleep.2006.07.084

180 Twenty five years of nasal CPAP therapy Colin Sullivan * David Read Laboratory, University of Sydney, Australia The invention of nasal CPAP to treat sleep apnea occurred against a background of experiments in which I was investigating how sleep altered breathing control, while at the same time trying to establish the first clinical facility at Royal Prince Alfred Hospital to manage sleep disorders, where my principal clinical role was to manage patients in respiratory failure. After working with Eliot Philipson in Toronto, I set up his sleeping dog preparations in my animal laboratory within the University of Sydney in 1979. Dogs were prepared with a tracheal stoma that allowed easy intubation of the trachea to measure air flow while the dog slept. Tracheal occlusion in sleep provided a model of airway obstruction to test the differing arousal and ventilatory response in NREM and REM sleep. I wanted to see if there were differences in those responses if the occlusion occurred at the nose (snout), and to do so I made a set of special ‘‘snout’’ masks for the dogs. The arousal and breathing responses at the ‘‘nose’’ were totally different to those at the trachea, observations that led to a series of major publications. Concurrent with these experiments, I had started my first two PhD students on projects in human subjects. Mike Berthon-Jones’ project was to measure the ventilatory and arousal responses to hypercapnia and hypoxia. Faiq Issa’s project was to repeat the ‘‘nasal’’ occlusion studies being done in the dogs in human subjects. Well equipped mechanical and electronics workshops were, and remain, central to my research laboratories, and many hours were spent making devices to undertake the various experiments. In order that we could measure respiratory airflow and manipulate the respired gases, and induce occlusion, it was necessary to make appropriate masks. It was against this background that it occurred to me that it might be possible to reverse upper airway obstruction in sleep by pressurising the entire upper airway. The first all night experiment with nasal CPAP was in June 1980. The patient was a man in his forties with severe sleep apnea who had refused tracheostomy. The circuit use was