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Covariation not proof of cause
- Mats Reimer (2 May 2005)
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Missing area
- Daniel K Ng, Chung-hong Chan, Ka-li Kwok, and Pok-yu Chow (4 May 2005)
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Anaesthetic implications for adenotonsillectomy are important
- David R Ball, Paul Jefferson (6 May 2005)
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Facing changes in the epidemiological trends of childhood obstructive sleep apnoea: potential impact of the obesity epidemic
- Gema Frühbeck (10 May 2005)
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Somnography and the need for Guidelines
- Vivian Singh, Conor Marnane (11 May 2005)
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More On Childhood Obstructive Sleep Apnea
- Suresh Kotagal (15 June 2005)
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Mats Reimer, Community Pediatrician Mölnlycke SWEDEN
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Neuropsychological deficits may be more common among children with obstructive sleep apnoea but that does not prove how much of these deficits are caused by sleep apnoea (OSA). Muscular hypotonia and dyscoordination are common among children with neuropsychiatric disabilities, and can cause snoring and OSA. Dr Kotagal cites a study by O'Brien et al describing "35 children with OSA (mean age 6.7 years) and 35 closely matched controls". This paper by O'Brien does not deal with sleep apnoea, instead it shows that children who only snore a lot (without apnoea) have slightly more problems of different kinds even when the authors beforehand removed all kids with ADHD or hyperactivity from the study. Michael S. Urschitz et al (PEDIATRICS Vol. 114 No. 4 October 2004) found that habitual snoring was significantly associated with hyperactive (OR: 2.4) and inattentive behavior (OR: 4.0). These associations were independent of intermittent hypoxia, which is why I believe that both snoring and OSA are markers for neuropsychological deficits but not necessarily causing the deficits. Competing interests: None declared |
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Daniel K Ng, Consultant Paediatrician 852, Chung-hong Chan, Ka-li Kwok, and Pok-yu Chow
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We would like to point out an important missing area in the editorial "Childhood obstructive sleep apnoea" by Kotagal. [1] Kotagal rightly pointed out the neuropsychological sequalae of childhood obstructive sleep apnea (OSA) without mentioning an as -important effect of OSA, i.e. hypertension. This omission was not uncommon as shown by a similar omission in a report on the global burden of hypertension. [2] Currently, there is good evidence for childhood OSA leading to elevated blood pressure. The reports by Marcus et al, [3] Koyama et al [4] and Tucson group [5] showed that sleep disordered breathing was associated with elevated blood pressure. While a recent study by Amin et al [6] showed that obstructive sleep apnea in children could also have lower blood pressure secondary to BP dysregulation. Our unpublished data on childhood OSA and 24 hour ambulatory BP suggested that 18% of OSA children had nocturnal hypertension only. Other cardiovascular consequences such as left ventricular hypertrophy, [7] altered sympathetic activation. [8] The report from our centre also showed that snoring children without OSA had higher blood pressure but not hypertensive and decreased arterial distensibility when compared with normal controls. [9] The study quoted by Kotagal to support the use of comprehensive clinical assessment to diagnose OSA consisted of a limited sample size of 41. Kotagal overlooked a meta-analysis [10] that demonstrated history and physical assessment alone for the diagnosis of childhood OSA in snoring children gave a combined positive predictive value of 55.8% (95% CI 42.1 to 69.9%), i.e. not significantly better than chance. The comprehensive clinical assessment may be useful in a healthy population without the risk factors of regular snoring, observed apnea, obesity, dysmorphic syndromes or attention deficit, hyperactivity or daytime sleepiness. For those with risk factors, sleep polysomnography should be offered. 1. Kotagal S. Childhood obstructive sleep apnoea. BMJ 2005; 330: 978- 9. 2. Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: analysis of worldwide data. Lancet 2005; 365:217 -23. 3. Marcus CL, Greene MG, Carroll JL, Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med 1998; 152: 1098-103. 4. Kohyama J, Ohinata JS, Hasegawa T. Blood pressure in sleep disordered breathing. Arch Dis Child 2003; 88: 138-42. 5. Enright PL, Goodwin JL, Sherrill DL, Quan JR, Quan SF; Tucson Children’s Assessment of Sleep Apnea Study. 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: 901-4. 6. Amin RS, Carroll JL, Jeffries JL, Grone C, Bean JA, Chini B, et al. Twenty- four-hour ambulatory blood pressure in children with sleep-disordered breathing. Am J Respir Crit Care Med 2004; 15:169:950-6. 7. Amin RS, Kimball TR, Bean JA, Jefferies JL, Wilging JP, Cotton RT, Witt SA, Glascock BJ, Baniels SR. Left ventricular hypertrophy and abnormal ventricular geometry in children and adolescents with obstructive sleep apnea. Am J Respir Crit Care Med 2002; 165: 1395-9. 8. Aljadeff G, Gozal D, Schechtman VL, Burrell B, Harper RM, Ward SL. Heart rate variability in children with obstructive sleep apnea. Sleep 1997; 20:151 -7. 9. Kwok KL, Ng DK, Cheung YF. BP and arterial distensibility in children with primary snoring. Chest 2003; 123:1561-6. 10. Brietze SE, Katz ES, Robertson DW. Can history and physical examination reliably diagnose pediatric obstructive sleep apnea/hyponea syndrome? A systematic review of the literature. Otolaryngol Head Neck Surg 2004; 131: 827–32. Competing interests: None declared |
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David R Ball, Consultant anaesthetist Dumfries and Galloway Royal Infirmary, Dumfries, UK. DG2 9TX, Paul Jefferson
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Kotagal correctly mentions that adenotonsillectomy is performed as a potential treatment for children with obstructive sleep apnoea (OSA) and highlights some of the peri-operative risks. We write to emphasize this, since these children may present important challenges to safe and effective anaesthetic management. Under anaesthesia, children with OSA have impaired ventilatory responses to carbon dioxide compared to controls [1]. This may account, in part, for the increase in respiratory complications recorded in these patients. Children of three years or less,and those with cardiac or neurologic problems are at extra risk of such post-operative complications [2]. On a practical note, administration of atropine at anaesthetic induction has been reported to reduce respiratory complications [3]. For children with "severe" OSA, having their operation in the morning is associated with less post-operative hypoxaemia than those operated in the afternoon [4]. References 1 Strauss SG, Lynn AM, Bratton SL, Nespaca MK. Ventilatory response to CO2 in children with obstructive sleep apnea from adenotonsillar hypertrophy. Anesth Analg 1999;89:328-32. 2 Biavati MJ, Manning SC, Phillips DL. Predictive factors for respiratory complications after tonsillectomy and adenoidectomy in children. Arch Otolaryngol Head Neck Surg 1997;123:517-21. 3 Brown KA, Morin I, Hickey C, Manoukian JJ, Nixon JM, Brouillette RT. Urgent adenotonsillectomy: an analysis of risk factors associated with postoperative respiratory morbidity. Anesthesiology 2003;99:586-95. 4 Koomson A,Morsin I, Brouilette R, Brown KA. Children with severe OSAS who have adenotonsillectomy in the morning are less likely to have postoperative desaturation than those operated in the afternoon. Can J Anaesth 2004;51:62-7. Competing interests: None declared |
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Gema Frühbeck, Clinical Scientist Dept. Endocrinology, Clinica Universitaria, University of Navarra, 31008 Pamplona, Spain
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The interesting editorial by Kotagal (1) draws attention to the relevance of appropriate diagnosis and management of childhood obstructive sleep apnoea (OSA). Classically, the majority of children with OSA have been described as being underweight, daytime hyperactive and with adenotonsillar hypertrophy. Although it needs to be formally studied, it may be suggested that a dramatic change in the epidemiology of the disease has taken place over the past decade. As a consequence of the epidemic proportions reached by paediatric obesity worldwide as well as in the UK (2), waiting rooms are now filled with overweight and obese children, rather than skinny, mouth-breathing kids. Not surprisingly, obesity in childhood is associated to many of the same comorbidities observed in adults such as hypertension, dyslipidaemia, insulin resistance, and sleep- disordered breathing. How common is OSA in obese children and adolescents? In a small study performed almost ten years ago in moderately obese African-American children and adolescents, none of whom had sleep-related symptoms, it was found that 46% had abnormal polysomnograms (3). This finding deserves further consideration even after admitting that the figure is not truly representative of the current obese population given the small sample size, the time lag and the potential confounding influences of race and/or socioeconomic status. Moreover, it has not been elucidated whether childhood OSA related to adenotonsillar hypertrophy is the same disease process observed in obese children, whether the latter more closely resembles the adult disease, and what overlap may exist. Nevertheless, in the face of the studies providing evidence of the presence of metabolic disturbances and cardiovascular alterations in children with OSA (4, 5), general practitioners and paediatricians should be especially alert and active in early identification and treatment of this condition in overweight and obese children. References 1. Kotagal S. Childhood obstructive sleep apnoea. BMJ 2005;330:978-9. 2. Mayor S. Obesity in children in England continues to rise. BMJ 2005;330:1044. 3. 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;21:176-83. 4. de la Eva RC, Baur LA, Donaghue KC, Waters KA. Metabolic correlates with obstructive sleep apnea in obese subjects. J Pediatr 2002;140:654-9. 5. Amin RS, Carroll JL, Jeffries JL, Grone C, Bean JA, Chini B, Bokulic R, Daniels SR. Twenty-four-hour ambulatory blood pressure in children with sleep-disordered breathing. Am J Resp Crit Care Med 2004;169:950-6. Competing interests: None declared |
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Vivian Singh, ENT SpR Bristol Children's Hospital, Conor Marnane
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Suresh Kotagel’s editorial on paediatric Obstructive Sleep Apnoea (OSA) highlights many of the difficulties encountered by those clinicians who evaluate and treat children with this condition. We see and assess many of these of these patients in our paediatric Ear, Nose and Throat clinics and some clear-cut guidance as to the indications for polysomnography, or simple overnight oximetry alone, would be greatly welcomed. In our experience the vast majority of straightforward childhood ‘snorers’ seem to fall into the adenotonsillar hypertrophy subgroup. A thorough history will usually identify those patients with a high likelihood of a diagnosis of OSA {witnessed obstructive apnoea (odds ratio 3.31), parent afraid/wakes child because of breathing (OR 4.41)}. The history and examination should be able to differentiate between a child with simple adenotonsillar hypertrophy and one whose problem lies at the mandibular, tongue-base or laryngeal level. As the management of the former is surgical intervention, even for those who may be apnoeic, the somnography or oximetry assessment in our opinion is often unnecessary and indeed a poor use of resources. In most cases of OSA in childhood, adenotonsillectomy is a highly effective treatment, leading to resolution of abnormal respiration during sleep, and improvements in growth, restless, sleep and daytime behaviour.2,3,4,5,6 One should however remain vigilant in children with Down Syndrome, Pierre- Robin sequence (and other craniofacial syndromes), laryngomalacia, mucopolysaccharoidoses, spina bifida, achondroplasia and cerebral palsy. OSA is particularly prevalent in these conditions and these patients are likely to have other reasons for airway obstruction in addition to adenotonsillar hypertrophy. Clearly a sleep study referral would be highly appropriate in many such cases. As Kotagal points out (pulmonary) oedema can be seen after adenotonsillectomy for OSA, especially in young children and also obese children, so the need for close postoperative monitoring is essential. Whilst in an ‘ideal world’ it would be nice to have access to polysomnography for all patients, this approach is realistically unpractical and in most cases unnecessary. We would therefore suggest that such investigations are reserved for children for whom there is substantial uncertainty about the diagnosis and those for whom surgery or anaesthesia involves an above average risk 1 Stradling JRT; Warley,A.R.H.; Williams,P.; Freeland,A. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance, and symptoms in snoring children. Lancet 1990;335:249-253. 2 Goldstein NA, Fatima M, Campbell TF, Rosenfeld RM. Child behavior and quality of life before and after tonsillectomy and adenoidectomy. Archives of Otolaryngology -- Head & Neck Surgery. 2002;128:770-775. 3 Tarasiuk A, Simon T, Tal A, Reuveni H. Adenotonsillectomy in children with obstructive sleep apnea syndrome reduces health care utilization. Pediatrics. 2004;113:351-356. 4 De Serres LM, Derkay C, Sie Ket al. Impact of adenotonsillectomy on quality of life in children with obstructive sleep disorders. Archives of Otolaryngology -- Head & Neck Surgery. 2002;128:489-496. 5 Mitchell RB, Kelly J, Call E, Yao N. Quality of life after adenotonsillectomy for obstructive sleep apnea in children. Archives of Otolaryngology -- Head & Neck Surgery. 2004;130:190-194. 6 Carroll JL, McColley SA, Marcus CL, Curtis S, Loughlin GM. Inability of clinical history to distinguish primary snoring from obstructive sleep apnea syndrome in children. Chest. 1995;108:610-618. Competing interests: None declared |
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Suresh Kotagal, Consultant in Child Neurology and Pediatric Sleep Disorders Mayo Clinic, Rochester, Minnesota, USA
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Dr. Reimer states that co-variance does not prove causation. I would remind him of the longitudinal, case-controlled study of Dr. David Gozal, in which elementary school children with obstructive sleep apnea (OSA) who underwent adenotonsillectomy showed significantly improved academic performance as compared to those with OSA who did not (1). Dr. Ng questions the value of the clinical assessment, citing the meta-analysis of Brietzke et al (2). It turns out however that 3/12 studies cited in this meta-analysis were questionnaires pertaining to sleep history (#3, 11,12), 3/12 were retrospective (# 4, 6, 9), one actually excluded upper airway anomalies and abnormal facial morphology (#2) and one study (#4) used an invalid polysomnographic scoring criterion for pediatric OSA (apnea length of ten seconds rather than five seconds). I therefore question the authors’ conclusion (4) that clinical assessment is unreliable. The comments of Dr. Vivian Singh also resonate with the need for developing an algorithm based upon history and the clinical examination, as well as updating polysomnographic scoring guidelines. I agree with Dr. David Ball’s comment about the additional peri- operative risk posed by underlying cardiac and neurological disorders during adenotonsillectomy. With regard to Dr. Fruhbeck’s interesting observation about the infrequent observation these days of poor weight gain as a consequence of OSA, one wonders whether this is due to greater awareness of pediatric OSA and it’s more timely diagnosis. REFERENCES 1. Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics 1998; 102: 616-620 2.. Brietze SE, Katz ES, Robertson DW. Can history and physical examination reliably diagnose pediatric obstructive sleep apnea syndrome? A systematic review of the literature. Otolaryngol Head Neck Surg 2004; 131: 827-832 (Word count 274). Competing interests: None declared |
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