Childhood obstructive sleep apnoea
BMJ 2005; 330 doi: https://doi.org/10.1136/bmj.330.7498.978 (Published 28 April 2005) Cite this as: BMJ 2005;330:978
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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
Competing interests: No competing interests
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
Competing interests: No competing interests
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
Competing interests: No competing interests
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
Competing interests: No competing interests
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
Competing interests: No competing interests
More On Childhood Obstructive Sleep Apnea
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
Competing interests: No competing interests