tracheomalacia and bronchomalacia in children: pathophysiology, assessment, treatment and...
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Review article
Tracheomalacia and bronchomalacia in children:pathophysiology, assessment, treatment andanaesthesia management
JAMES AUSTIN F R C A* AND TARIQ ALI F R C A†
*Department of Anaesthesia, Royal Berkshire Hospital, Reading and †Paediatric Intensive Careand Anaesthesia, John Radcliffe Hospital, Oxford, UK
SummaryTracheomalacia and bronchomalacia are becoming increasingly well
recognized. Although pathologically benign conditions, they are
responsible for considerable morbidity, occasional mortality and
significant difficulties in the operating theatre and intensive care unit.
We performed an extensive literature search to identify causal
associations, methods of clinical and investigative assessment, treat-
ment modalities and anaesthetic experience with these conditions.
Keywords: tracheomalacia; bronchomalacia
Introduction
Tracheobronchomalacia is a rare and serious condi-
tion associated with high mortality in children
receiving intensive care (1). It is a condition that is
becoming increasingly recognized and may often
lead to prolonged intubation and ventilation. Anaes-
thetists may be called on to provide anaesthesia for a
range of procedures in children with this condition,
ranging from diagnostic and interventional radiolo-
gical procedures, incidental surgery to surgical
correction. Anaesthesia can be tricky in these
patients and one of the authors has witnessed three
critical incidents in recent years; however, informa-
tion in the anaesthesia literature relating to this
condition is scarce. The intention of this review
article is to provide some background to this condi-
tion and to provide recommendations with regard to
management for Anaesthesia and Intensive Care.
What are tracheomalacia andbronchomalacia?
Malacia means softness and, in the medical context,
is usually used to refer to cartilage or bone. Tracheo-
malacia is therefore a softness of the tracheal
cartilage; and bronchomalacia, softness of the bron-
chial cartilage. The combination of these pathologies
is tracheobronchomalacia, and this may coexist with
laryngomalacia or generalized chondromalacia. In
this review, the term ‘airway malacia’ is used to refer
to any malacia of trachea and/or bronchi, but
excludes laryngomalacia.
What does airway malacia do?
Airway malacia allows the affected portion of the
airway to collapse, under conditions where the
extraluminal pressure exceeds the intraluminal pres-
sure. Most cases of airway malacia are intrathoracic;
hence, during expiration and particularly forcefulCorrespondence to: T. Ali, Department of Anaesthetics, JohnRadcliffe Hospital, Oxford OX3 9 DU, UK.
Paediatric Anaesthesia 2003 13: 3–11
� 2003 Blackwell Publishing Ltd 3
expiration or coughing, intrathoracic pressure is
positive and the affected segment of trachea or
bronchus narrows leading to wheeze.
In the less common case of cervical, extrathoracic
tracheomalacia, the collapse takes place during
inspiration. Negative intrathoracic pressure is trans-
mitted to the upper airway which then narrows
under atmospheric pressure, causing inspiratory
stridor.
What is the scale of the problem?
No population incidence studies are available to tell
us how common airway malacia is. Altman identi-
fied 42 cases of paediatric airway malacia in one
hospital over a 5-year period (2) and Burden et al.recorded 62 cases in Paediatric Intensive Care in the
period 1986–95, although they believe that the
condition is underdiagnosed (1). Although tracheo-
malacia usually presents postneonatally, together
with laryngomalacia, it was the most common
diagnosis (23%) in 132 neonates bronchoscoped for
airway difficulties or tracheo-oesophageal malfor-
mations (3).
Airway malacia is particularly common in three
clinical settings, namely bronchopulmonary dyspla-
sia, tracheo-oesophageal malformations (TOM) and
major aortopulmonary malformations. In these
conditions, malacia complicates management, lead-
ing to extended intensive care unit (ICU) stay and
increased morbidity and mortality. Tracheomalacia
is also a significant cause for the need for long-term
tracheostomy in children. In a series of 44 home
tracheostomies, 14 (32%) were for tracheomalacia
(4). However, modern trends in treatment are likely
to decrease this fraction.
Finally, airway malacia may be an unrecognized
cause of Sudden Infant Death Syndrome (SIDS) (5).
An interesting study in 1983 (6) involved extensive
investigation of 58 ‘near-miss SIDS’, with four
diagnoses of tracheomalacia being made.
Classification and associated conditions
Tracheo- or bronchomalacia may be classified as
congenital (also known as primary) or acquired
(secondary). Although no large classification series
is available, a survey of the literature suggests that
the congenital group is slightly more common.
Congenital airway malacia may be further subdi-
vided into isolated (idiopathic) or part of a recog-
nized condition or association (syndromic). Acquired
airway malacia, on the other hand, is typically due to
either compression or to debilitating conditions of
the lungs or cartilage. Table 1 contains a more
detailed list of conditions causing or associated with
airway malacia, some of which are discussed in
detail below.
Premature infants are particularly prone to
airway malacia as part of the spectrum of
Congenital Acquired
Common Tracheo-oesophageal fistula Compression by great vessels:Brachiocephalic
Oesophageal atresia AortaPulmonary artery
Isolated Vascular slingsBronchopulmonary dysplasia
Rare Chromosomal defects: Pulmonary/mediastinal cystsDown’s syndrome
Trisomy 9 Intrathoracic tumours11p13 deletion (Wilms/aniridia) Large/ectopic thymus22q11 deletion Goitres*18–22 translocation Heart-lung transplantChondrodysplasias Liver failure/transplant
Williams–Campbell syndrome Prolonged intubationDi George syndrome TracheostomyCHARGE association Mucocutaneous LeishmaniasisHunter’s syndrome Tetralogy of FallotHurler’s syndrome
* More common cause of airway malacia in adults.
Table 1Clinical associations of airwaymalacia
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bronchopulmonary dysplasia (BPD), with incidences
in small bronchoscopic series ranging from 25% to
86% (7–9). As Table 1 suggests, the association
between tracheo-oesophageal malformations and
airway malacia is well documented, although the
mechanism is unclear.
In many cases of TOM, the tracheomalacia is
shown to arise from accompanying compression by
large thoracic vessels or by a dilated oesophageal
pouch (10,11).
Whether malacia contributes to adverse outcome
in TOM is debatable. In one series of 240 patients
(12), tracheomalacia was a major contributor in 17
late deaths. However, in another analysis of 223
patients, it was concluded that tracheomalacia had
no influence on outcome in TOM repair (13).
The mechanism of malacia in aortopulmonary
vascular malformations is straightforward: the
abnormal vessel compresses the airway and restricts
cartilage growth. Thus, even when the vasculature is
corrected, dynamic airway collapse can still occur,
again complicating recovery. In one series (14)
following surgery for congenital cardiovascular
malformations, airway malacia was responsible for
six of 22 prolongations of ICU stay.
Tracheomalacia can also result from prolonged
ventilation, due to internal pressure from a tracheal
tube (15) as well as with tracheostomy (16).
In addition to the conditions listed in Table 1, two
conditions deserve additional attention because of
their complex relationship with airway malacia;
namely, gastro-oesophageal reflux (GOR) and
asthma. GOR aggravates and is aggravated by
airway malacia. One series looking at aortopexy as
treatment for tracheomalacia showed good results,
except in concurrent GOR; however, aggressive
treatment of the GOR restored the good results of
aortopexy (17). Airway malacia can often mimic
asthma (18) and is distinguished by its nonrespon-
siveness to bronchodilators. However, a proportion
of patients will have both conditions.
How does airway malacia manifestclinically?
Tracheo- and bronchomalacia are clinically similar,
with a limited repertoire of clinical manifestations.
These manifestations, however, are nonspecific, and
the diagnosis can be difficult to make unless a high
index of suspicion is held. Table 2 lists the reported
clinical presentations of airway malacia.
Broadly speaking, these presentations fall into
two groups: those that present in hospital, compli-
cating management of some other condition, such as
BPD, TOM or thoracic vessel malformations; and
those that present from home, either as an isolated
finding or as a manifestation of a more subtle
abnormality.
Ventilated children with malacic segments lying
distal to the tracheal or tracheostomy tube will
typically start to become distressed as airway
pressures [and particularly positive end expiratory
pressure/continuousairway pressure (PEEP/CPAP)]
are weaned. Positive airway pressure acts to splint
the airway open and, as this is withdrawn and the
patient starts to breathe spontaneously, airway
collapse occurs. On the other hand, those with
malacia proximal to the end of the tube will clearly
be undistressed until extubation (or tracheostomy
decannulation) itself, when they may require rein-
tubation or noninvasive CPAP (19).
Of those that present from home, many are
initially diagnosed as asthma, with wheeze or
recurrent dry cough. Suspicion of airway malacia
should be raised in those who do not respond to
bronchodilators (18).
Intractable cough, usually brassy in nature, may
be a presenting feature in the older child (20). ‘Dying
spells’, or ‘acute life-threatening events’, are a
dramatic presentation of tracheomalacia; initial
distress caused by a malacic collapse leads to
increased respiratory effort, worsening the collapse
in a vicious cycle. Only when the child loses
consciousness due to hypoxia, does respiration relax
allowing relief of the obstruction (21). Sudden death
may be the extreme result of such episodes (22).
Table 2Clinical presentations of airway malacia
Difficult wean from artificial ventilationFailure of extubation or tracheostomy decannulationEpisodic respiratory distressWheezePersistent dry coughRecurrent chest infectionsPectus excavatumDysphagia‘Dying spells’: acute life-threatening eventsSudden death
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Investigation of airway malacia
Investigations can be divided into three main
groups:
(1) Static imaging: plain X-ray, chest computed
tomography (CT), chest magnetic resonance
imaging (MRI) and 3-D reconstruction CT or
MRI.
(2) Dynamic imaging: flexible bronchoscopy; vid-
eofluoroscopy (± contrast); cine-CT.
(3) Spirometry: flow-volume studies.
As airway malacia is a dynamic process, it follows
that dynamic imaging is the modality of choice.
However, other modalities have specific advantages;
in particular, MRI for delineating compressive cau-
ses, and spirometry for giving a continuous measure
of ventilatory response to therapeutic manoeuvres.
Plain X-ray appears to be a remarkably crude
means of investigating airway malacia, but has the
advantage of being routinely and rapidly available
to most children with respiratory symptoms. As
recently as 1999, Walner et al. claimed a 62%
sensitivity for plain airway X-rays in detecting
tracheomalacia (23). A considerably lower sensitivity
for bronchomalacia might be expected.
‘Static’ chest views with MRI or CT may miss the
dynamic airway closure of malacia, but have the
advantage (particularly MRI) of revealing the anat-
omy of compressive structures (24) and may be
useful in planning surgery.
Until recently, flexible bronchoscopy was consid-
ered the investigation of choice in diagnosing airway
malacia. It is preferably performed on spontaneously
breathing patients to reflect near-normal airway
dynamic, although in the artificially ventilated
patient some airway collapse may still be detectable.
Videotaping, with a slow-motion facility enhances
sensitivity further and enables the degree of collapse
to be graded (25). Early bronchoscopy should be
encouraged in ICU children who have difficulties in
weaning from ventilation. In one PICU study,
bronchoscopy revealed unsuspected stenosis or
malacia in nine of 90 children (26). Bronchoscopy
also has the advantage of being used therapeutically,
to place stents; or as an intraoperative adjunct to
pexy or external splinting procedures.
Fluoroscopy with or without contrast is a useful,
relatively noninvasive alternative to bronchoscopy.
Strauss et al. found contrast fluoroscopy to be as
good as (and in eight of 15 patients superior to)
bronchoscopy in patients with combined stenosis
and malacia (27). Another study combined fluoros-
copy findings with duration of ventilation to form a
powerful predictor of PICU mortality, and found
fluoroscopy to be more useful than bronchoscopy in
this regard (1). Fluoroscopy can also be used with
airway manometry to determine best CPAP (Fig 1)
(28). Whilst bronchoscopy and fluoroscopy may
confirm airway collapse, they provide limited infor-
mation as to the cause of compression. Consequently,
high speed Cine-CT and Cine-MRI are being devel-
oped to improve diagnostic accuracy (29).
Spirometry and flow-volume loops present a
completely different ‘take’ on airway malacia,
examining function rather than structure. It provides
a noninvasive and easily repeatable measure of
airway flow and, by derivation, of resistance. This
enables ready assessment of response to medical
manoeuvres.
In summary, bronchoscopy is considered the ‘gold
standard’ in investigating airway malacia but, in
skilled hands, contrast fluoroscopy may provide as
much information or more, less invasively. With
wider availability, cine radiology may supersede
both, giving the advantage of imaging structures
outside the airway. Spirometry has a completely
different role in continuous assessment and optimi-
zation of treatment.
Treatment of airway malacia
There are essentially five modalities of treatment for
airway malacia. In approximate historical order,
they are: (i) long-term ventilation/CPAP; (ii) resec-
tion of the affected segment; (iii) external splinting;
(iv) pexy procedures (tracheopexy, bronchopexy,
aortopexy, pexy of other vessels) and (v) stenting.
Long-term ventilation was originally the treat-
ment of choice for airway malacia, relying on the fact
that weak cartilage strengthened with time if the
original cause was relieved. CPAP, with or without
ventilatory support, was sufficient to hold the
airway open (30,31). This had the advantage of
being technically easy to apply, noninvasive com-
pared with surgery, and relatively successful for any
size airway. Disadvantages were the high consump-
tion of health care resources and the side-effects of
long-term ventilation, including infections, limited
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mobility, delayed speech development and secon-
dary tracheomalacia around the tracheal tube or
tracheostomy site. However, ventilation remains a
slow and complex means of treating airway malacia.
In the search for a more mechanical ‘quick fix’, one
solution (for short-segment malacia) is to resect the
malacic segment and reanastomose the airway (32)
and another is to reinforce the weak cartilage
externally with a splint (Fig 2a). Neither of these
options has become established.
The realization that collapse was not intrinsic, but
depended on positive intrathoracic (and hence
mediastinal) pressure, prompted the introduction
of aortopexy; by lifting the aorta anteriorly in the
mediastinum, it was possible to prevent most of this
pressure being transmitted to the trachea, and hence
prevent (or at least decrease) collapse. This proce-
dure (i.e. the suturing of the aorta anteriorly to the
inner surface of the sternum) seems remarkably
successful even when the aorta is not the obvious
pathological source of the compression (17). It does
not interfere with the later growth of the trachea and
has the advantage of being less invasive than other
intrathoracic procedures, requiring only a small
intercostal window for access (33). In specific cir-
cumstances, the aortopexy principle has been modi-
fied to involve the pulmonary artery (PA-pexy),
ligated patent ductus arteriosus (PDA-pexy) or
innominate (brachiocephalic) artery (34).
The other logical mechanical approach to a malacic
airway is to reinforce it internally, using broncho-
scopically placed stents (Fig 2b). Stents have been
controversial in the past due to their poor results in
early years; however, improvements in material
engineering have overcome most of these problems,
such that stenting is now a competitive mode of
Figure 1(a) Left main bronchomalacia. Fluoroscopy of the respiritory tree showing collapse of the left main bronchus with no PEEP applied.(b) Application of 10 cmH2O PEEP has ’opened’ the left main bronchus. (c) Application of 20 cmH2O PEEP has splinted the left mainbronchus further.
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treatment. Modern expandable reticular stents have
fenestrations allowing ventilation of branching air-
ways, as well as epithelial overgrowth to reestablish
ciliary function. Some stents can be reexpanded at
intervals to allow for growth (35) (Fig 2c).
Complications of stents include displacement
[with one report of a stent being coughed up and
swallowed, with no ill effects (36)], inflammatory
granulomata that may provoke airway obstruction
(37) and fatalities secondary to removal (38). Stents
have the advantage of being easily and rapidly
placed by bronchoscopy, avoiding the resource
outlay and complications of surgery.
Anaesthetic management of patientswith airway malacia
The anaesthetist may be called on to manage airway
malacia in a variety of settings: (i) the patient
undergoing diagnostic (or therapeutic) bronchos-
copy or radiology; (ii) the patient undergoing thor-
acic surgery, with or without correction of the
malacia; and (iii) the patient undergoing surgery
unrelated to the airway malacia.
There is surprisingly little in the literature on
anaesthetic management of airway malacia (39) and
much of it is not available in English. Nevertheless,
Figure 2(a) Splinting of trachea with external plating. (b) Splinting of malacic trachea and left bronchus with expandable internal stents. (c) Ballondilation of internal stents allows for growth.
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sensible recommendations can be made in the
understanding of the underlying pathophysiology.
The two main principles are to prevent airway
collapse and air trapping by the use of PEEP/CPAP
and to minimize coughing.
Diagnostic bronchoscopy or radiology for airway
malacia mandates a spontaneously breathing patient
if it is to be of any use. Thus, in broad terms, there
are three anaesthetic options:
Sedation with topical anaesthesia
In skilled hands, this is perfectly practical in any age
group, and arguably provides the best diagnostic
results in terms of realistic airway dynamics. The
emphasis is on adequate sedation and excellent
topical anaesthesia. Strong opioid premedication
provides sedation and suppresses cough; a concom-
itant anticholinergic suppresses secretions and may
decrease vagal responses to airway irritation. Per-
operative supplementation with midazolam will
decrease the discomfort and psychological trauma
to the child. Local anaesthetic is the key to success,
decreasing coughing and minimizing discomfort.
This method is particularly well suited to flexible
bronchoscopy.
General anaesthesia with inhalationalmaintenance
Gas induction is a logical way to induce anaesthesia
while maintaining spontaneous respiration. For
flexible bronchoscopy, this can be continued via
laryngeal mask airway�, with an attachment port
for the fibrescope or, in the case of rigid bronchos-
copy, the anaesthetic circuit can be attatched to the
side port or an insufflation technique employed.
Again, anticholinergic premedication and topical
local anaesthesia to the airway are recommended to
minimize the risk of coughing and laryngeal spasm.
The main drawback to this technique is that the
severity of collapse may be masked by the effects of
general anaesthesia.
General anaesthesia with intravenousmaintenance
This is ideal in the older child. Careful titration of i.v.
anaesthetic, by bolus or infusion, allows the patient
to maintain spontaneous respiration, while freeing
the airway entirely to the bronchoscopist. Oxygen-
ation can be enhanced by insufflation down the side
port.
General anaesthesia for other procedures, whether
using spontaneous or mechanical ventilation, usu-
ally requires the use of CPAP or PEEP to prevent
intraoperative airway collapse. Collapse leads to air
trapping which, in turn, leads to hyperinflation of
the lungs, with each subsequent breath requiring
greater pressure change to achieve the same volume
change. Eventually, intrathoracic pressure may get
so high as to prevent adequate venous return
resulting in dramatic falls in cardiac output and
pulseless electrical activity until adequate expiration
is established, either by halting ventilation or by
manually compressing the chest in combination with
PEEP. The authors’ have witnessed several of these
crises both in theatre and PICU and they have been
associated with morbidity and mortality (40,41).
While there is no good evidence to support any
particular technique, the avoidance of a tracheal tube
where practical by use of a laryngeal mask airway
(42) may decrease postoperative coughing and the
risk of airway collapse on emergence. ‘Deep’ extu-
bation may allow a smooth recovery.
Much of the detail of managing PICU patients
with airway malacia has already been dealt with, but
a high index of suspicion should be maintained in
patients with associated conditions and in those
patients who have difficulty weaning from ventila-
tion, particularly weaning PEEP or CPAP. Failed
extubation complicated by inspiratory stridor or
expiratory wheeze may be the first signs of the
diagnosis. Ready use of bronchoscopy (or contrast
fluoroscopy) should make the diagnosis promptly.
‘Best’ CPAP/PEEP can be established by using a
manometer in the anaesthetic circuit during contrast
fluoroscopy. Bronchodilators are unhelpful in prin-
ciple, unless there is coexisting reactive airways
disease. Stenting or pexy procedures may provide a
rapid alternative to prolonged weaning with the use
of PEEP/CPAP.
Airway malacia is increasingly widely recognized,
and accounts for a significant expenditure of medical
resources, as well as considerable morbidity and
mortality. Unnoticed, it may cause difficulties dur-
ing anaesthesia or in PICU. These problems can
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largely be minimized by the judicious use of positive
endexpiratory pressure. Anticipation and prompt
diagnosis can save much distress to the patient and
family. While many of the milder cases will resolve
with time, ongoing improvements in therapy allow
the potential of a good outcome even in the most
severely affected child.
References
1 Burden RJ, Shann F, Butt W et al. Tracheobronchial malaciaand stenosis in children in intensive care: bronchograms helpto predict oucome. Thorax 1999; 54: 511–517.
2 Altman KW, Wetmore RF, Marsh RR. Congenital airwayabnormalities in patients requiring hospitalization. ArchOtolaryngol Head Neck Surg 1999; 125: 525–528.
3 Lindahl H, Rintala R, Malinen L et al. Bronchoscopy during thefirst month of life. J Pediatr Surg 1992; 27: 548–550.
4 Duncan BW, Howell LJ, deLorimier AA et al. Tracheostomy inchildren with emphasis on home care. J Pediatr Surg 1992; 27:432–435.
5 Beal SM, Blundell HK. Recurrence incidence of sudden infantdeath syndrome. Arch Dis Child 1988; 63: 924–930.
6 Finder JD. Primary bronchomalacia in infants and children.J Pediatr 1997; 130: 59–66.
7 Miller RW, Woo P, Kellman RK et al. Tracheobronchialabnormalities in infants with bronchopulmonary dysplasia.J Pediatr 1987; 111: 779–782.
8 Greenholz SK, Hall RJ, Lilly JR et al. Surgical implications ofbronchopulmonary dysplasia. J Pediatr Surg 1987; 22:1132–1136.
9 Wheeler WB, Maguire EL, Kurachek SC et al. Chronic respir-atory failure of infancy and childhood: clinical outcomes basedon underlying etiology. Pediatr Pulmonol 1994; 17: 1–5.
10 Guys JM, Triglia JM, Louis C et al. Esophageal atresia,tracheomalacia and arterial compression: role of aortopexy.Eur J Pediatr Surg 1991; 1: 261–265.
11 Davies MRQ, Cywes S. The flaccid trachea and tracheo-oesophageal anomalies. J Paed Surg 1978; 13: 363–367.
12 Choudhury SR, Ashcraft KW, Sharp RJ et al. Survival ofpatients with esophageal atresia: influence of birth weight,cardiac anomaly, and late respiratory complications. J PediatrSurg 1999; 34: 70–74.
13 Rokitansky AM, Kolankaya VA, Seidl S et al. Recent evaluationof prognostic risk factors in esophageal atresia – a multicenterreview of 223 cases. Eur J Pediatr Surg 1993; 3: 196–201.
14 Bandla HP, Hopkins RL, Beckerman RC et al. Pulmonaryrisk factors compromising postoperative recovery aftersurgical repair for congenital heart disease. Chest 1999; 116:740–747.
15 Windsor HM, Shanahan MX, Cherian K et al. Tracheal injuryfollowing prolonged intubation. Aust NZ J Surg 1976; 46: 18–25.
16 Azizkhan RG, Lacey SR, Wood RE. Anterior cricoid suspensionand tracheal stomal closure for children with cricoid collapseand peristomal tracheomalacia following tracheostomy.J Pediatr Surg 1993; 28: 169–171.
17 Malone PS, Kiely EM. Role of aortopexy in the management ofprimary tracheomalacia and tracheobronchomalacia. Arch DisChild 1990; 65: 438–440.
18 Cohn JR. Localized bronchomalacia presenting as worseningasthma. Ann Allergy 1985; 54: 222–223.
19 Wiseman NE, Duncan PG, Cameron CB. Management oftracheobronchomalacia with continuous positive airway pres-sure. J Pediatr Surg 1985; 20: 489–493.
20 Wood RE. Localized tracheomalacia or bronchomalacia inchildren with intractable cough. J Pediatr 1990; 116: 404–406.
21 Cozzi DA, Bonanni M, Cozzi F et al. Recurrent apparent life-threatening event relieved by glossopexy. J Pediatr Surg 1996;31: 1715–1718.
22 Emery JL, Nanayakkara CF, Wailoo MP. Tracheomalacia –lethal factor in a 17-month-old child. Pediatr Pathol 1984; 2:259–265.
23 Walner DL, Ouanounou S, Donnelly LF et al. Utility ofradiographs in the evaluation of pediatric upper airwayobstruction. Ann Otol Rhinol Laryngol 1999; 108: 378–383.
24 Rimell FL, Shapiro AM, Meza MP et al. Magnetic resonanceimaging of the pediatric airway. Arch Otolaryngol Head NeckSurg 1997; 123: 999–1003.
25 Mair EA, Parsons DS. Pediatric tracheobronchomalacia andmajor airways collapse. Ann Otol Rhinol Laryngol 1992; 101:300–309.
26 Downing GJ, Kilbride HW. Evaluation of airway complicationsin high-risk preterm infants: application of flexible fiberopticairway endoscopy. Pediatrics 1995; 95: 567–572.
27 Strauss HJ, Scheel W, Bartel M. Vergleichende kinematograph-ische, endoskopische und funktionsanalytische Untersuchun-gen zur praoperativen Beurteilung des Schweregrades vonTrachealstenosen. [Comparative cinematographic, endoscopicand functional studies of the preoperative estimation of theseverity of tracheal stenoses]. Z Erkr Atmungsorgane 1989; 172:130–142.
28 Little AF, Phelan EM, Boldt DW et al. Paediatric tracheobron-chomalacia and its assessment by tracheobronchography.Austral Radiol 1996; 40: 398–403.
29 Brody AS, Kuhn JP, Seidel FG et al. Airway evaluation inchildren with use of ultrafast CT: pitfalls and recommenda-tions. Radiology 1991; 178: 181–184.
30 Neijens HJ, Kerrebijn KF, Smalhout B. Successful treatmentwith CPAP of two infants with bronchomalacia. Acta PaediatrScand 1978; 67: 293–296.
31 Kanter RK, Pollack MM, Wright WW et al. Treatment of severetracheobronchomalacia with continuous positive airway pres-sure (CPAP). Anesthesiology 1982; 57: 54–56.
32 Masaoka A, Yamakawa Y, Niwa H et al. Pediatric and adulttracheobronchomalacia. Eur J Carthorac Surg 1996; 10: 87–92.
33 Bullard KM, Scott Adzick N, Harrison MR. A mediastinalwindow approach to aortopexy. J Pediatr Surg 1997; 32:680–681.
34 Kamata S, Usui N, Sawai T et al. Pexis of the great vessels forpatients with tracheobronchomalacia in infancy. J Pediatr Surg2000; 35: 454–457.
35 Nesbitt JC, Carrasco H. Expandable stents. Chest Surg ClinNorth Am 1996; 6: 305–328.
36 Mattison LE, Frye MD, Collop NA. Accidental ingestion of atracheal stent. Chest 1995; 108: 875–876.
37 Furman RH, Backer CL, Dunham ME et al. The use of balloon-expandable metallic stents in the treatment of pediatrictracheomalacia and bronchomalacia. Arch Otolaryngol HeadNeck Surg 1999; 125: 203–207.
38 Filler RM, Forte V, Chait P. Tracheobronchial stenting for thetreatment of airway obstruction. J Pediatr Surg 1998; 33: 304–311.
10 J . AUSTIN & T. ALI
� 2003 Blackwell Publishing Ltd, Paediatric Anaesthesia, 13, 3–11
39 Conroy PT, Bennett NR. Management of tracheomalacia inassociation with congenital tracheo-oesophageal fistula. Br JAnaesth 1987; 59: 1313–1317.
40 Katoh H, Saitoh S, Takiguchi M et al. A case of tracheomalaciaduring isoflurane anesthesia. Anesth Analg 1995; 80: 1051–1053.
41 Menichella G, Pierelli L, Dragani A et al. A preliminary surveyof Italian experience on bone marrow harvesting, processingand manipulation. The Italian Cooperative Study Group on
Cell Manipulation in Hematology. Haematologica 1990; 75:39–42.
42 Yamaguchi S, Takanishi T, Matsumoto T et al. Use of alaryngeal mask airway for anesthesia in a patient withbronchomalacia. Masui 1996; 45: 348–351.
Accepted 30 July 2001
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