PAEDIATRIC RESPIRATORY REVIEWS (2004) 5, 17–24

doi:10.1016/j.prrv.2003.10.001

MINI SYMPOSIUM: UPPER AIRWAY OBSTRUCTION

Congenital upper airway obstruction

Robert Dinwiddie

Great Ormond Street Hospital for Children, London WC1N 3JH, UK

KEYWORDS Summary Most causes of upper airway obstruction are rare in the neonatal period and
obstructive during infancy. They may, however, cause major respiratory problems either initially or
sleep apnoea; during the first few weeks of life. It is important to recognise these problems at an early
nasopharyngeal airway; stage so that appropriate measures to overcome airway obstruction can be initiated, thus
face mask CPAP avoiding significant hypoxia-related complications. Specific treatment includes the use of
nasal stents, a nasopharyngeal airway or, in severe cases, tracheostomy. Many such infants
have associated feeding problems secondary to the airway obstruction and associated
swallowing difficulties, which can lead to recurrent aspiration. The anomalies seen in
clinical practice are best classified anatomically. Treatment is aimed at overcoming the
mechanical effects of airway obstruction and maximising nutritional input so as to
promote growth of the airway and long-term recovery of normal upper airway function.
ß 2004 Elsevier Ltd. All rights reserved.

INTRODUCTION be about 1 in 8000 live births.1 Bilateral choanal atresia

Congenital upper airway obstruction is a relatively rare but
important cause of major respiratory problems in the
neonatal period. A small number of anomalies can present
with acute respiratory problems either immediately at birth
or within the first few days and weeks of life. Many babies
with congenital upper airway obstruction also suffer from
major problems with feeding secondary to the airway
obstruction and swallowing incoordination. This can lead
to failure to thrive and, not infrequently, recurrent aspira-
tion with the potential for immediate and long-term
damage to the pulmonary tissues.
The anomalies seen are best classified by the level of
major impact on airway function, typically nasal, pharyngeal,
laryngeal or within the extrathoracic part of the trachea.
SPECIFIC PROBLEMS
Choanal atresia and stenosis
One of the most common upper airway anomalies is
choanal atresia or stenosis. The incidence is thought to
Correspondence to: Robert Dinwiddie, Consultant Respiratory
Physician, Great Ormond Street Hospital for Children,
London WCIN 3JH, UK. Tel.: þ44 (0) 207 405 9200;
Fax: þ44 (0) 207 829 8634.; E-mail: R.Dinwiddie@ich.ucl.ac.uk
causes immediate respiratory distress at birth, and these
babies require support with an oral airway until urgent
remedial treatment can be undertaken. Most cases are due
to bony occlusion of the airway, but some 10% are due to
membranous obstruction. Unilateral obstruction also
occurs and is often not detected until later in childhood.
Some children present with feeding difficulties and persis-
tent rhinorrhoea, especially if the patent nostril is partially
blocked because of an infection.1
Sixty to seventy per cent of choanal atresia patients have
other associated congenital anomalies.2 The most common
and most serious of these is the CHARGE association. This
consists of a number of anomalies, including C coloboma of
the eye, H heart disease, A atresia of the choanae, R
retarded growth and development, including the nervous
system, G genital hypoplasia in males, E ear cartilage defor-
mities and deafness. The heart problems vary from minor
abnormalities to those that are life-threatening in the first
weeks of life. These include patent ductus arteriosus, tetral-
ogy of Fallot, double outlet right ventricle, atrioventricular
canal, ventricular septal defect, atrial septal defect, ASD,
right-sided aortic arch and coarctation of the aorta. Many
infants with CHARGE association have major problems with
feeding. These include difficulty in sucking and swallowing
because of the congenital upper airway obstruction, but also
because of neurological abnormalities related to the sucking

1526–0542/$ – see front matter ß 2004 Elsevier Ltd. All rights reserved.
18
reflex secondary to paresis of nerves in the oropharyngeal
region. Gastro-oesophageal reflux is another frequently
associated complication. Although in the past a significant
proportion of such children died because of these
problems, nowadays most survive because they are treated
by Nissen’s fundoplication and gastrostomy.3 A multidisci-
plinary approach to management is essential.4
Congenital anomalies of the choanae can best be imaged
by computed tomography (CT) scan. This can show the
exact site of obstruction and also whether it is bony or
membranous. It is important to ensure that the nasal pas-
sages are as free of secretions as possible at the time of the
investigation, as the presence of excess mucus can give
misleading results.
The emergency treatment of choanal atresia consists of
the insertion of an oral airway and the use of nasogastric
tube feeding. As soon as possible, however, a nasal airway
should be established. This can be achieved by a transnasal
approach using a dilating instrument which minimises the
risk of more posterior damage to the nasal passage or spinal
cord if passed too far.1 When this has been achieved, then
airway stents are passed through the nasal passage to
ensure continued patency for a period of several weeks.
An alternative approach is not to insert such tubes but to
perform choanal dilatation at weekly intervals for a 6-week
period.1 In more severe cases, where the atresia is thicker,
direct drilling of the atretic segment is required.
Nasal mass causing obstruction
A number of conditions result in the presence of a con-
genital mass lesion in the nasal passages. Although rare they
can be of major significance both functionally and patholo-
gically. They vary in severity from simple polyps to ence-
phaloceles, which can communicate directly with the
cerebrospinal fluid. It is therefore very important to carry
out the relevant diagnostic imaging before any corrective
treatment is undertaken. The differential diagnosis of con-
genital obstructive lesions of the nose is set out in Table 1
adapted from Cinnamond.1 These lesions vary from cystic
masses to more solid lesions such as haemangiomas.
Nasal dermoids are solid masses or cystic lesions. They
are of congenital origin, although they may not present until
Table 1 Congenital obstructive lesions of the nose.
Cystic Solid
Meningoencephalocele Haemangioma
Meningocele Neurofibroma
Dermoid cyst Glioma
Epidermoid cyst Lymphangioma
Neuroblastoma
Craniopharyngioma
Rhabdomyosarcoma
Chordoma
R. DINWIDDIE
late childhood in some cases. They can be single or multiple
and usually present with persistent nasal obstruction.5 They
may even be associated with the formation of extra hair
inside the nose.
Other neurologically derived congenital anomalies
within the nasal cavity include nasal meningoencephalo-
celes and gliomas. These are said to account for 1 in 20
congenital nasal swellings.1 They are thought to be due to
abnormal closure of the anterior neural plate within the
upper nasal cavity. Nasal gliomas often cause enlargement
of the bridge of the nose as well as obstructing the nasal
passage. A CT scan should be performed to delineate its
size and position. They may enlarge slowly with time, and
treatment is by surgical excision or laser ablation. Menin-
goencephaloceles usually present as a swelling over the
root of the nose, which increases with crying or as a lesion
seen within the nasal cavity itself.1 CT scanning or magnetic
resonance imaging are vital investigations in order to
delineate the size of the lesion and its local extension.6
Encephaloceles can result in direct connection of the
cerebrospinal space to the nasal mucosa. Apart from the
possibility of cerebrospinal fluid leak, there is the risk of
direct access of potentially pathogenic organisms to the
central nervous system. This situation is one of the causes of
recurrent meningitis in young children. Surgical removal of
the lesion is required either by local excision or by a
craniotomy. It is important to ensure that there is effective
closure of the meninges to prevent subsequent invasion
with pathogenic organisms from the nasal passages.
Another lesion that may obstruct the nasal passage is a
nasal mucocele, which arises in the nasolacrimal duct. This
can be dealt with endoscopically.
Haemangiomas can occur in any part of the upper
respiratory tract. They do occur rarely in the nose, but
can be more pathogenic in the pharyngeal or laryngeal area.
The natural history is one of involution over a period of
time, so unless they cause significant upper airway obstruc-
tion they are best left alone.
Pierre–Robin sequence
One of the most common congenital anomalies of the
upper respiratory tract is the Pierre–Robin sequence. It
consists of micrognathia, glossoptosis and cleft palate,
resulting in a range of upper airway problems from airway
obstruction to feeding difficulties.7 The severity of obstruc-
tion to breathing is variable. In some infants little interven-
tion is required, whereas in others airway support is needed
and, in infants with unrelieved airway obstruction, cor
pulmonale can result from chronic or recurrent severe
hypoxia. As the mandible grows forward with age, parti-
cularly during the first 6 months of life, the problem usually
resolves. In some cases, there is a temporary recurrence of
airway obstruction at the time of the cleft palate repair, and
the nasopharyngeal tube may need to be reintroduced
peri-operatively.
CONGENITAL UPPER AIRWAY OBSTRUCTION
This sequence of anomalies can also be part of a more
extended presentation of congenital malformation such as
Stickler’s syndrome.8 This is an autosomal dominant con-
dition that includes other anomalies affecting the eyes,
including myopia, cataracts and retinal detachment,
together with sensorineural deafness and joint problems,
including severe childhood arthropathy.8
The embryological problem in the Pierre–Robin
sequence is thought to be due to arrested development
of the mandible causing hypoplasia. This results in abnormal
descent of the tongue, thereby preventing closure of the
palatal shelves. This explains the presence of the posterior
cleft of the palate. The incidence is thought to be about 1 in
8000 births.
The clinical outcome is that there is a significant obstruc-
tive airway problem from birth. The micrognathia is obvious
on initial clinical examination. The palatal defect is variable in
severity but can involve up to two-thirds of the hard palate
itself. Cleft lip is not usually an associated anomaly in these
cases. The airway obstruction is most evident in the supine
position, especially during sleep. The short tongue falls back
and is drawn into the pharynx, resulting in major episodes of
obstructed breathing. The resultant hypoxia and hypercarbia
can lead to right heart failure. These infants commonly fail to
thrive because of the increased energy requirements needed
to sustain the extra work of breathing9 often combined with
major feeding difficulties secondary to the difficulty of simul-
taneously co-ordinating sucking, swallowing and breathing.
MANAGEMENT
Infants who have significant airway obstruction, as docu-
mented in sleep studies (Fig. 1) require mechanical relief.
This is best provided by the use of a nasopharyngeal tube
(nasal prong) (Fig. 2).7,10–12 This can result in the abolition
of hypoxic episodes, relief of associated right heart failure,
normalisation of blood gases and improved weight gain
(Fig. 1).10
The exact positioning of the nasopharyngeal tube is
crucial. If it is too short, the prolapsing tongue-related
airway obstruction will continue. If too long, it may irritate
the epiglottis causing recurrent cough and possibly vomiting
during feeds, or it may slip into the oesophagus so failing to
relieve the airway obstruction. Initial tube length can be
estimated from Table 2 (adapted from Heaf et al. 1982).10
The ideal position is just above the epiglottis, and this
should be confirmed by a lateral neck x-ray (Fig. 3). The
function of the tube in relieving the airway obstruction
should be confirmed by overnight sleep studies, which
should document at the very least satisfactory oximetry
and heart rate levels. (Fig. 1).
A small number of these infants may gain relief of the
upper airway obstruction by the use of an individually
moulded dental plate that holds the tongue in a more
forward position and also facilitates the swallowing
mechanism during feeds.
19
Table 2 Crown-heel length vs nasopharyngeal tube length.
Crown-heel Nasopharyngeal
length (cm) tube length (cm)
40 6.5
45 6.8
50 7.4
55 7.9
60 8.3
65 8.8
70 9.3
Feeding problems are very common in these children,
many needing to be partially or totally fed by nasogastric
tube either because of an inadequate oral intake or because
of recurrent aspiration into the lungs.
The airway and feeding problems gradually resolve
during the first few months of life. The median time of
nasopharyngeal tube placement is 6 months.
Dysmorphic syndromes
A number of syndromic craniofacial anomalies can affect
the upper airway, a consequence of which is obstruction to
breathing.13 These can result in acute or chronic hypoxia
and hypercarbia and, in the most severe cases, raised
intracranial pressure.14 If chronic or recurrent hypoxia is
present, then pulmonary hypertension and cor pulmonale
can develop. Examples of these conditions include Crou-
zon, Apert, Pfeiffer, Treacher–Collins, craniofacial micro-
somia and Goldenhar syndromes.
Relief of upper airway obstruction is frequently achieved
by the use of a nasopharyngeal tube, particularly in the
younger child. Face mask continuous positive airway pres-
sure (CPAP) is also particularly helpful,15,16 as definitive
surgery for the craniofacial anomalies may best be carried
out at a later age because of the need to wait for specific
development of cranial, facial and dental tissues.
Crouzon syndrome (craniofacial dysostosis) involves
maxillary hypoplasia, mandibular prognathism and flattening
of the nasal bridge. This combination can lead to significant
upper airway obstruction and sleep disturbance. It is inher-
ited as an autosomal dominant condition, although 50% of
cases are due to new mutations.17
If there is significant airway obstruction, the patient will
present with snoring, sleep apnoea, daytime somnolence
and morning headaches. If sleep studies show significant
hypoxia and a disturbed sleep pattern, then relief of the
obstruction may be achieved by face mask or nasal CPAP
overnight (Fig. 4).14
Apert syndrome (acrocephalosyndactyly) is another
condition inherited as an autosomal dominant disorder
in which there is severe midfacial hypoplasia. The palate
is high and arched, and a cleft palate or bifid uvula occurs in
up to one-third of the children.17 Upper airway obstruction
 20
Figure 1 Oxygen saturation and pulse rates over two 30-min periods in an infant with Pierre–Robin sequence with and without a nasal prong.

R. DINWIDDIE
CONGENITAL UPPER AIRWAY OBSTRUCTION
Figure 2 Nasopharyngeal tube in place to relieve upper airway
obstruction in an infant with Pierre–Robin sequence.
and sleep disturbance is not uncommon and, if severe, will
need treatment by a nasopharyngeal tube in early life or
nasal/facial CPAP in the older child.
Pfeiffer syndrome causes maxillary hypoplasia and nar-
rowing of the nasal passages, which often leads to severe
upper airway obstruction with resultant hypoxia and hyper-
carbia. This can lead to increased intracranial pressure,14
with associated effects such as headache, learning difficul-
ties and potentially impaired intelligence. Relief of upper
airway obstruction is therefore very important.
Treacher–Collins syndrome (mandibulo-facial dysostosis)
is inherited as an autosomal dominant disorder. Half of the
children, however, have new mutations.17 Mandibular hypo-
plasia is associated with narrowing of the nasal passages and a
high arched palate which, in association with the other
dysmorphic facial features of the syndrome, can result in
significant upper airway obstruction. Treatment is with nasal
CPAP if necessary (Fig. 4).
Laryngomalacia
Laryngomalacia is probably the most common congenital
anomaly of the upper airway.18 The condition occurs as a
result of abnormal softening of the laryngeal tissues.18 It is
the most common cause of stridor in infancy. The classical
presenting feature is of inspiratory stridor, usually noted in
the first few days or weeks of life. Its severity may vary
depending on whether the child is quiet, active, crying or
feeding. The stridor worsens with respiratory tract infec-
tions. The symptoms of respiratory distress and inspiratory
21
Figure 3 Lateral neck x-ray to show correct positioning of a
nasopharyngeal tube.
indrawing worsen during the first few months of life, but
thereafter tend to resolve.
To confirm the diagnosis when stridor is persistent, it is
helpful to undertake direct laryngoscopy in all but the mildest
presentations. Such an investigation will also rule out less
common abnormalities, such as laryngeal webs, haemangio-
mas, cysts and sub-glottic stenosis. In laryngomalacia, laryn-
goscopy usually demonstrates that the epiglottis is tall and
tubular in form, slightly involuted, and prolapses backwards
on inspiration. The associated arytenoid cartilages and their
superficial mucosa, which are often large and juicy in appear-
ance, are also sucked in during inspiration. The evaluation of
the larynx, and particularly the vocal cords, requires expert
anaesthesia. The movements of these structures are best
observed as the child wakens and starts to breathe sponta-
neously. Instrumentation of the airway can splint the cords so
that natural movement is not seen properly. The use of
fibreoptic instruments can help to overcome this problem.
Usually, there is a natural resolution of the problem
during the first 1–2 years of life. Where there is significant
difficulty with breathing or feeding then laser excision of
redundant mucosa may be helpful.
Vocal cord paralysis
Vocal cord paralysis can be unilateral or bilateral, congenital
or acquired. Most cases of congenital paralysis present
either in the neonatal period or during the first few months
of life. Bilateral cord paralysis is often symptomatic in early
life, whereas unilateral paralysis may be missed. Infants
present with a weak cry or stridor associated with variable
degrees of large airway obstruction and difficulty in con-
trolling secretions associated with recurrent aspiration and
feeding problems.19 Unilateral cord paralysis is more likely
to lead to a weak cry than a bilateral lesion, which more
commonly presents with clinical evidence of upper airway
obstruction.
 22
Figure 4 Oxygen saturation and pulse rates over two 30-min periods in an infant with a craniofacial malformation with and without face mask continuous positive airway pressure.

R. DINWIDDIE
CONGENITAL UPPER AIRWAY OBSTRUCTION
Because of the difficulty in closing off the larynx during
feeds, control of secretions and difficulties in swallowing are
common presenting features. The infant may have episodes
of cough, choking, spluttering and respiratory difficulty
during feeds. Episodes of wheeze and recurrent lower
respiratory tract infections are very suggestive of aspiration.
A significant proportion of infants who aspirate do so
‘silently’, that is without significant cough at the time.
The reasons for this are not understood, but it may be
due to congenital insensitivity of the cough receptors or
relative insensitivity after recurrent stimulus from repeated
aspiration episodes. A video-swallow to investigate phar-
yngeal and laryngeal muscle co-ordination is therefore an
important investigation.
There are a number of causes for congenital vocal cord
paralysis, including those associated with abnormalities of
the central and peripheral nervous system, such as Arnold–
Chiari malformation, encephalocele, meningomyelocele,
hydrocephalus and myasthenia gravis. Abnormalities of
the base of the skull such as platybasia can also result in
this problem. Cardiovascular anomalies, which result in
cardiomegaly or pressure from great vessels on the nerve
supply to the larynx, can result in laryngeal palsy. Examples
would include ventricular septal defect, tetralogy of Fallot
and vascular ring, such as a double aortic arch. Laryngeal
nerve paralysis is frequently seen in children with more
generalised neuromuscular problems. Specific examples
would include Werdnig–Hoffmann disease and myasthenia
gravis, but any other generalised cause of muscle hypotonia
such as in Down syndrome can result in this problem. Apart
from the hypotonia, the most frequent presenting features
are feeding difficulties and recurrent aspiration. Myasthenia
gravis can present in the neonatal period with swallowing
difficulty, manifested as excessive drooling, poor suck and
aspiration of saliva and milk into the lungs. This neonatal
form of myasthenia is usually associated with maternal
disease. Myasthenia gravis can also present at any other
time throughout childhood. The presenting features are
similar, although more generalised muscle fatigue is seen.
Other conditions that can be associated with laryngeal
nerve palsy include bronchogenic cysts, cleft larynx and
various oesophageal anomalies such as oesophageal atresia.
DIAGNOSIS AND MANAGEMENT
Vocal cord paralysis should be considered in any infant with
a weak or absent cry, significant stridor, feeding and
swallowing difficulties, and evidence of recurrent aspiration.
If there is no other obvious cause for the symptoms then
further investigation is indicated. This will require direct
visualisation of the vocal cords either with a rigid or
preferably a flexible endoscope. It is important to observe
cord movement as the patient lightens from anaesthesia so
that spontaneous movement can occur. When using a rigid
endoscope, it is also important to ensure that the cords are
not splinted by the instrument in any way that could impair
23
their natural movement. It may also be necessary to
stimulate the infant in order to assess the full range of
movement in each case. A full feeding assessment by a
speech and language therapist is also required. Apart from
observation using various liquids and foods of different
textures, a video-swallow should be undertaken. This is an
excellent way of observing swallowing function, including all
the muscles of deglutition, but also of recording evidence of
laryngeal coating (penetration by food and aspiration into
the tracheo-bronchial tree). The results of this test will
determine the safety or otherwise of feeding the infant
orally. In severe cases, nasogastric tube feeding may be
required or even a gastrostomy if the problem is persistent
or severe. Ultrasound of the vocal cords can also be used to
assess movement, but the interpretation is not always easy.
Children with unilateral cord paralysis have a better
prognosis and, as has been stated previously, the milder
problem may be missed initially. Some children can cope
with the disorder using a regimen of thickened feeds and
careful feeding that allows time for adequate swallowing to
occur. More severe cases, especially those involving bilat-
eral lesions, will require extended periods of nasogastric or
gastrostomy feeding. When possible, treatment of any
underlying disorder, such as myasthenia gravis or correc-
tion of any associated oesophageal or cardiac anomaly, will
also increase the chance of improvement with time.
Where the respiratory symptoms are not controlled, a
long-term tracheostomy will be required. A number of
operative procedures have been attempted for the alle-
viation of vocal-cord paralysis, particularly in bilateral cases,
but these have not been undertaken in large numbers. The
long-term outcome is variable depending on the degree
of paralysis and the presence or absence of other con-
genital anomalies. They are best carried out when the child
is fully grown.
PRACTICE POINTS
 Patients with congenital anomalies of the upper
airway frequently present with airway obstruction
from birth.
 Obstructive sleep apnoea continues to be a major
problem in infancy and early childhood.
 Upper airway anomalies causing significant
obstruction frequently lead to major feeding
problems, including swallowing incoordination and
recurrent aspiration of milk into the lungs.
 Cystic lesions in the nose may represent nasal
encephaloceles. These carry the risk of bacterial
spread into the meninges.
 The Pierre–Robin sequence is one of the most
common causes of major airway obstruction in
infancy. The severity of obstruction is best assessed
by sleep studies in patients with significant
breathing problems.
24
 Infants who have the Pierre–Robin sequence of
anomalies should be checked for hereditary
conditions such as Stickler’s syndrome.
 Upper airway obstruction is a major problem for
children with craniofacial anomalies such as
Crouzon, Apert, Pfeiffer, Treacher–Collins,
craniofacial microsomia and Goldenhar
syndromes.
 Videofluoroscopy is the most useful investigation
for infants with feeding problems associated with
upper airway obstruction.
 Some infants have ‘silent aspiration’ episodes with
no obvious cough reflex, despite direct aspiration
of milk into the lower airway.
RESEARCH DIRECTIONS
 Greater understanding of the embryology and
genetic basis of congenital anomalies of the upper
airway.
 Development of sleep study techniques including
measurement of intracranial pressure and
electroencephalogram to evaluate the
physiological effects of upper airway obstruction.
 Studies of the effects of recurrent hypoxia on
school performance.
 Studies of the anatomical effects of early corrective
surgery on the growth and development of the
upper airway.
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