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Volume 9, Issue 2, Pages 85-94 (June 2008)


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Vascular compression of the airway in children

Clare A. McLaren2Corresponding Author Informationemail address, Martin J. Elliott1, Derek J. Roebuck2

Summary 

Congenital heart disease (CHD) is an important clinical problem. Although survival has improved over recent decades, certain children with CHD remain difficult to treat, usually because of severe co-morbidity or uncorrectable defects. Vascular compression of the airway is one such co-morbidity, occurring in approximately 1–2% of children with CHD. It may be caused by congenital anomalies of the configuration of the great vessels, enlargement of otherwise normal structures or as a result of surgery. The anatomical patterns seen in these children may be complex, and as surgical correction is usually required to relieve the compression, the pre-operative imaging assessment should be as complete as possible. Precise diagnosis and therapy are essential because chronic airway compression in childhood carries a significant morbidity and mortality. Airway stenting is currently reserved for rare occasions when surgical correction is not possible.

Article Outline

Summary

Imaging techniques

Echocardiography

Multidetector computed tomography

Magnetic resonance imaging

Bronchoscopy and bronchography

Interventional radiology

Double aortic arch

Interrupted aortic arch

Right-Sided aortic arch with aberrant left subclavian artery

Absent pulmonary valve syndrome

Other vascular causes of airway compression

Pulmonary artery sling

Innominate artery compression

Left-sided aortic arch with aberrant right subclavian artery

Acquired cardiovascular disease

Conclusion

References

Copyright

Vascular compression of the airway in children is usually caused either by congenital anomalies of the configuration of the great vessels or enlargement of otherwise normal structures (Table 1).1 The most common congenital anomalies associated with airway compression are the vascular rings. The ring may be patent (as in double aortic arch) or alternatively be completed by an atretic arch or ligamentum arteriosum (as in right-sided aortic arch with aberrant left subclavian artery). The aortic arch and its branches and the pulmonary arteries are derived from the embryonic branchial arches. Failure of part of this complex embryological process is uncommon, but is the cause of many of the malformations that result in vascular airway compression.1, 2, 3 An understanding of the embryology of the aortic arch and related structures is helpful for image interpretation.

Table 1.

Causes of vascular compression of the airway in children

• Anomalies of the aorta
○ Double aortic arch
○ Interrupted aortic arch (after surgical repair)
○ Right-sided aortic arch
• With aberrant left subclavian artery
• With mirror-image branching and right ligamentum arteriosum
○ Left-sided aortic arch
• With aberrant right subclavian artery and right ligamentum arteriosum
• Right-sided descending aorta with right ligamentum arteriosum
○ Cervical aortic arch
• Absent pulmonary valve syndrome
• Aberrant left pulmonary artery (’pulmonary artery sling’)
• Acquired cardiovascular disease
○ Dilated cardiomyopathy
○ Aneurysm
• Ascending aorta
○ Ductus arteriosus

Other vascular mechanisms of airway compression exist. The most important of these are seen in children with absent pulmonary valve syndrome, interrupted aortic arch and dilated cardiomyopathy (see below). Less common causes of vascular airway compression include pulmonary artery sling without long segment congenital tracheal stenosis and compression of the trachea by the innominate artery (brachiocephalic trunk).

Symptoms at presentation are variable, ranging from dysphagia, recurrent respiratory infections and stridor to acute respiratory distress or ‘dying spells’.2, 3, 4, 5 Symptoms such as chest discomfort, dyspnoea, wheezing and cough are often misdiagnosed as asthma, which is much more common in older children.6 Affected children may require mechanical ventilation and some may remain ventilator-dependent, even after surgery.

A combination of imaging techniques is usually required for full pre-operative assessment. Precise diagnosis and therapy are essential because chronic airway compression in childhood carries a significant morbidity and mortality.7, 8

Interventional radiology is limited in what it has to offer these children. Stenting is only appropriate when surgical correction is not possible. In our practice the usual indication is a palliative setting as it allows a child to be extubated.

Imaging techniques 

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Different imaging approaches may be appropriate for different causes of vascular compression of the airway. The historical approach was to perform chest radiography and barium swallow (upper gastrointestinal study) to evaluate children with suspected extrinsic compression of the airway. This has now been replaced in most centres by multidetector computed tomography (MDCT) and magnetic resonance imaging (MRI).

The barium swallow is probably acceptably accurate for diagnosis of a vascular ring, but does not delineate the precise anatomy required for surgical planning3 and is usually not helpful for bronchial compression.

The diagnostic imaging pathway in our centre starts with echocardiography and flexible bronchoscopy (combined with bronchography when appropriate). We usually also perform either MDCT or MRI, and occasionally both.7, 9 These are the most useful radiological techniques as they provide information about the tracheobronchial tree, the cardiovascular structures and their relationship to each other. A limitation of MDCT and MRI is that obliterated vascular segments (e.g. the ligamentum arteriosum or an atretic aortic arch) cannot be directly visualized.4

Diagnostic catheter angiography is now obsolescent in this context and has largely been replaced by cross-sectional imaging.3, 10 Chest radiographs may show aortic arch anomalies and dilated pulmonary arteries; however, although airway compression can sometimes be seen,11 a comprehensive assessment is not possible. Radiographs may, however, show hyperinflation, collapse or other lung pathology.

Echocardiography 

This is essential for the evaluation of associated congenital heart disease (CHD) and usually clearly shows abnormal vascular structures. Echocardiography aids the surgeon in understanding complex three-dimensional (3D) relationships. Direct evaluation of airway compression is limited.1

Multidetector computed tomography 

The development of MDCT technology has greatly extended the applications of chest CT in children.12 Scan times for MDCT are much shorter than for MRI and spatial resolution is higher.7 Axial MDCT data are generally sufficient to diagnose the type and severity of airway compression, but multiplanar reconstruction and 3D volume rendered images may provide further useful information.13 Virtual bronchoscopy images can also be generated from MDCT data but rarely add diagnostic information12 and cannot yet be used as a substitute for bronchoscopy. They serve mainly as a method of conveying some information about the airway to clinicians who are familiar with this type of view.

The main disadvantage of MDCT is exposure of the patient to ionizing radiation at the age of greatest sensitivity to its carcinogenic effects. Scan parameters should be modified from adult protocols to reduce the radiation dose. This can be achieved using weight-based protocols13 or tube current modulation techniques. When careful technique is used, the effective dose for a CT study of the chest should be <3mSv, which is comparable to 200 frontal chest radiographs.12

Magnetic resonance imaging 

MRI has excellent intrinsic contrast resolution and multiplanar imaging capabilities.13 Evaluation of cardiac anatomy and physiology with MRI is usually superior to CT. However, most MRI studies for vascular compression will be quite prolonged (>30min), requiring sedation or general anaesthesia in young children. Sedation risks for children with a compromised airway are significant.1, 13 The scan times are often considered to be too long for haemodynamically unstable patients,7 especially given the relative inaccessibility of the MRI scanner.14 In practice, the increase in speed and quality of multiplanar reconstructions provided by MDCT technology means that CT is used more often than MRI in most centres.7, 15

Bronchoscopy and bronchography 

Cross-sectional imaging is probably much better than bronchoscopy at determining the nature of vascular compression of the airway. Current MDCT and MRI techniques do not reliably distinguish between dynamic or static narrowing.14, 15 This is a very important practical point as many children with prolonged airway compression develop secondary malacia. Although improvements in scanning technique are likely to overcome this problem, bronchoscopy and bronchography are currently the best techniques for this purpose. We usually perform these examinations at the same time, injecting isotonic non-ionic contrast (iotrolan [Isovist-240], Schering, Burgess Hill, UK) down the working channel of a flexible bronchoscope or through a separate catheter.16 Malacia should only be assessed when the patient is breathing spontaneously.

Interventional radiology 

The role of metal stents in the airway of children remains controversial. We prefer to restrict their use to two indications: palliation and when all other potential treatments have failed. Stenting with palliative intent may be used to allow a child to be extubated, so he/she can die at home. Our experience has been very favourable in this context, with several children surviving much longer than expected with a good quality of life, e.g. those with acquired cardiomyopathy. In other patients, however, it is sensible to be cautious.

Correct stent selection is important for children with vascular compression of the airway.16 Balloon expandable stents, such as the Palmaz stent (Cordis Europa N.V., Roden, The Netherlands), are rigid and this can lead to erosion through the wall of the airway. Self-expanding stents are much more flexible and less likely to lead to vascular erosion.16 They are also less likely to fracture when there is severe compression, e.g. in dilated cardiomyopathy. The major problems with this type of stent are that they are difficult to remove and cannot easily be post-dilated to allow for future growth.

We usually perform stent insertion under bronchographic control in an angiography suite. The advantage over rigid bronchoscopy is that the whole stent can be visualized on fluoroscopy, ensuring the it does not move during deployment and allowing the operator to position it as close as possible to a bifurcation without covering a bronchial orifice. The procedure is performed under general anaesthesia with muscle relaxation. We usually perform flexible bronchoscopy initially to confirm the diagnosis. Contrast is then injected either through the bronchoscope or through a small angle-tip catheter. When a bronchographic roadmap of the compressed area has been obtained, a guidewire is then passed into a peripheral bronchus. The stent delivery device is passed over the wire and the stent is deployed under fluoroscopic control. The stent can be repositioned during the initial part of deployment, if required. The final stent position can be checked with flexible bronchoscopy if necessary.

Covered, retrievable self-expanding stents are available for use in the airway. These may be easier to deploy than silicone (Dumon) stents, but can be expected to have similar disadvantages such as stent migration and blockage caused by the covering of the stent inhibiting ciliary clearance of secretions from the lungs. It is possible that some form of absorbable stent will be available in the future, in which case the indications for stent insertion may broaden significantly.

Double aortic arch 

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Autopsy studies suggest that 3% of people have a congenital malformation of the aortic arch, but most remain undiagnosed throughout life.3 Double aortic arch (DAA) is the most common cause of vascular compression of the airway in children.3, 4, 9, 17, 18 DAA is defined by the presence of both left- and right-sided aortic arches, which together surround the trachea and oesophagus (Fig. 1). The right arch is usually larger (‘dominant’). The left arch is usually small (‘hypoplastic’) or forms a fibrous cord (‘atretic’ segment) beyond the origin of the left common carotid or subclavian artery.1, 19 The fibrous cord tethers the patent part of the left-sided arch to the descending aorta, completing the ring. A ductal ligament may also be relevant in the creation of a ring at this point, since the ligament often connects the distal left arch to the proximal left pulmonary artery. Schlesinger et al. reviewed the MRI and CT findings of DAA with an atretic left arch.19 They found that the fibrous cord could not be seen on imaging and that the diagnosis was made from the presence of an incomplete left arch.


View full-size image.

Figure 1. Persistent airway compression in a 20-month-old boy following surgery for double aortic arch. (a) 3D CT reconstruction (posterosuperior view) shows the divided left arch and surgical clips (white arrows). The right arch is indicated by a red arrow. (b) Compression is most severe where the descending aorta (arrow) crosses from right to left behind the airway. (c) Frontal bronchography shows a right-sided impression on the trachea from the right aortic arch. (d) Lateral bronchography shows posterior compression by the descending aorta (arrows). (e) 2.2-mm flexible bronchoscopy shows extrinsic compression at the level of the carina.


The descending aorta may be left- or right-sided, or may run in the midline anterior to the vertebral column. When the descending aorta is midline, the structures of the mediastinum are said to be ‘stacked’ abnormally, resulting in compression between the spinal column and the sternum.15

Children with DAA usually present in infancy,1 with symptoms including dysphagia, stridor, wheezing and respiratory distress.10 Surgical correction, usually by transection of the non-dominant arch, is required to relieve the airway compression.9 It is always important to diagnose the arch anatomy before surgery because this determines the operative approach.

About 30% of children have residual symptoms despite surgical treatment of DAA.15 Although Fleck et al. found that residual symptoms may be due to persistent airway compression, some children have severe malacia of the lower trachea (extending to the carina).15 This may develop as a secondary effect of prolonged severe extrinsic compression. In our experience, in most children this problem is self-limiting, and eventually their airway cartilage regains sufficient stiffness for the symptoms to resolve. Although an occasional patient requires tracheostomy during this period, we have never had to insert an airway stent in a child with DAA. Detailed studies of late respiratory function are required in this group.

Interrupted aortic arch 

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Interrupted aortic arch (IAA), in which some part of the lumen of the aortic arch is discontinuous, is found in about 1% of all children with CHD. Children typically present as neonates and, if untreated, usually die by the age of 10 days.20 In type A (30–40%) the arch is interrupted between the origin of the left subclavian artery and the ductus arteriosus. In type B (50–55%) the interruption occurs between the origins of the left common carotid artery and the left subclavian artery. Type C (interruption between the innominate artery and the left common carotid artery) is very uncommon. In all types, deoxygenated blood flows to the lower part of the body through an enlarged ductus arteriosus. Over 95% of children have associated cardiac anomalies.20, 21

Airway compression in IAA is a consequence of surgical repair rather than the malformation itself. Shortening of the arch is inherent in the procedure, in which an end-to-end anastomosis is performed between the ascending and descending aorta, irrespective of the type of IAA. This results in anterior displacement of the descending aorta, posterior displacement of the anterior aorta and consequent compression of the left main bronchus (LMB) between the aorta and the left pulmonary artery (Fig. 2). Surgical correction of this compression is technically challenging22 and further surgery may be required as the child grows. Tracheostomy with pressure support may fail to overcome the LMB compression, and excessive continuous positive airway pressure may even damage the right lung. In some children, therefore, it may be justified to use metal airway stents, despite the risks. As noted above, balloon-expandable and self-expanding designs each have advantages and disadvantages, and the choice of stent will depend on individual clinical factors.16, 23


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Figure 2. A 4-month-old girl with compression of the left main bronchus following surgery for interrupted aortic arch. Axial CT of the thorax showing compression in the midline by the descending aorta (arrow).


Right-Sided aortic arch with aberrant left subclavian artery 

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Right-sided aortic arch (RAA) with an aberrant left subclavian artery and/or a left ligamentum arteriosum is reported in 12–25% of children with vascular rings. Most patients with these anomalies are asymptomatic.24

There are two main patterns of origin of the great arteries to the head and upper limbs in RAA. In ‘mirror-image branching’, a left brachiocephalic trunk (innominate artery) arises first, followed by the right common carotid and the right subclavian arteries. In RAA with aberrant left subclavian artery (Fig. 3) the first branch is the left common carotid, followed by the right common carotid and right subclavian arteries. The aberrant left subclavian artery arises from the descending aorta and passes behind the oesophagus. The vascular ring is completed by the left ligamentum arteriosum, which passes from the origin of the left subclavian artery to the left pulmonary artery.1 The left subclavian artery often originates from an outpouching of the descending aorta, called a Kommerell's diverticulum. Airway compression in RAA is usually due to enlargement of the Kommerell's diverticulum, a short (tight) ligamentum arteriosum or a midline descending aorta.24 Relief of symptoms is usually achieved by transection of the ligamentum arteriosum,24 but it is very important also to excise the diverticulum since this can result in late compression of the oesophagus and/or trachea.


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Figure 3. A 5-year-old boy with a right-sided aortic arch and aberrant left subclavian artery. (a) Axial CT of the thorax showing compression of the trachea by the aberrant artery (arrow). (b) 3D volume rendered image (posterior view) shows the right-sided aortic arch (red arrow) and the aberrant left subclavian artery (white arrow) arising from the descending aorta.


Late diagnosis of this condition does occur, particularly in patients with a Kommerell's diverticulum.

Absent pulmonary valve syndrome 

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Absent pulmonary valve syndrome (APVS) is characterized by the presence of enlarged pulmonary arteries and hypoplastic pulmonary valve cusps. It is most often seen in association with ventricular septal defect (VSD) and right ventricular outflow tract obstruction (RVOTO). APVS occurs in 3–6% of patients with tetralogy of Fallot, but can also be seen in isolation, with an intact ventricular septum and other congenital anomalies.25, 26 There is a strong association with DiGeorge syndrome (chromosome 22q11 deletion).11

The characteristic pattern of compression of the lower trachea, LMB and right main bronchus or bronchus intermedius (Fig. 4) is caused by enlargement of the pulmonary arteries and left atrium.1, 11, 25


View full-size image.

Figure 4. Tetralogy of Fallot and absent pulmonary valve syndrome with airway compression in a 15-month-old boy. (a) CT volume rendered image shows compression of the left main bronchus (arrow). (b) Axial CT of the thorax shows severe compression of the airway between the vertebral body and the grossly enlarged pulmonary arteries. (c) Lateral bronchogram confirms severe anterior compression of the airway caused by the enlarged pulmonary arteries. (d) 2.2-mm flexible bronchoscopy shows canal compression.


The prognosis in APVS depends on the age at presentation and the severity of symptoms. Neonates and infants often present with severe cardiorespiratory compromise.26 Mortality is between 16% and 56% in this group, with an especially poor prognosis in those infants who require mechanical ventilation.11, 25, 26 Children who present later often have milder symptoms, and surgery may be performed on an elective basis, usually simply by repairing the Fallot component of the defect.26

In small babies, there remains some controversy about which surgical technique is best to relieve the tracheobronchial compression. The usual approach involves replacement of the pulmonary artery with conduits or reduction arterioplasty.26, 27 However, the addition of the Lecompte manœuvre (transecting the aorta, allowing the pulmonary arteries to lie anterior to the reconstructed aorta) has proved successful. Any associated cardiac anomalies are corrected at the same operation.25, 26, 27

If possible, airway stenting is avoided in APVS because of the risk of erosion of a pulmonary artery with fatal haemorrhage. This risk can theoretically be minimized by the use of self-expanding stents, but the potential to dilate these stents to allow for future growth is very limited. Stenting is therefore restricted to palliative indications or when all surgical options have been exhausted. Both balloon-expandable28, 29 and self-expanding stents30 have been used.

Other vascular causes of airway compression 

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Pulmonary artery sling 

In this condition the left pulmonary artery has an anomalous course, arising from the posterior aspect of the right pulmonary artery and passing between the lower trachea and the oesophagus to enter the hilum of the left lung. There is a strong association with long segment congenital tracheal stenosis (LSCTS) with complete tracheal cartilage rings. The literature usually states that LSCTS is present in 50% of children with pulmonary artery sling (PAS), but in our experience the proportion is much higher than this, and a diagnosis of airway compression due to PAS without LSCTS should be treated with suspicion.31 Non-invasive imaging is not adequate to evaluate for complete rings and good quality bronchoscopy is mandatory. The distinction is clinically important, because it seems that the prognosis is much better if the LSCTS is repaired at the same time as the left pulmonary artery is re-implanted.31 Slide tracheoplasty is now the treatment of choice for LSCTS.

Innominate artery compression 

Anterior compression of the trachea by the brachiocephalic trunk (innominate artery) is a controversial entity. First, this condition seems to have been over-diagnosed and possibly over-treated in the past. Second, in many patients said to have innominate artery compression (IAC) the main pathophysiological mechanism appears to be tracheomalacia rather than extrinsic compression.32 This is particularly true in children with oesophageal atresia. Third, a large proportion of normal infants have imaging evidence of an anterior impression on the trachea at the level where it is crossed by the innominate artery. In one study, an anterior impression on the tracheal air column was seen on lateral chest radiographs in 30% of children younger than 2 years of age.33This finding is less common in older children.33, 34 Nevertheless, there do appear to be some children in whom arteriopexy,35 re-implantation or even transection of the innominate artery36 is beneficial.

A high (cervical) aortic arch may also compress the trachea, but this is extremely rare.

Left-sided aortic arch with aberrant right subclavian artery 

This relatively common anomaly does not lead to airway compression unless there is a right-sided ligamentum arteriosum.3

Acquired cardiovascular disease 

Dilated cardiomyopathy causes airway obstruction when the left atrium is sufficiently dilated to compress the LMB. This may lead to chronic infection of the left lung and progressive deterioration in the child's clinical condition. If other treatments are unsuccessful, the insertion of a self-expanding stent in the LMB may be effective (Fig. 5).


View full-size image.

Figure 5. A 12-month-old girl, ventilator-dependent, with dilated cardiomyopathy. (a) 2.2-mm flexible bronchoscopy shows compression of the left main bronchus (arrow). (b) On bronchography the left main bronchus is completely occluded with no passage of contrast into the left lung. (c) A self-expanding stent has been deployed. (d) Bronchoscopy shows good position of the stent, with patency of the left main bronchus.


Aneurysm of the aorta or ductus arteriosus is a very rare cause of airway compression in childhood.37

Conclusion 

return to Article Outline

Imaging plays a crucial role in the diagnosis and treatment of vascular compression of the airway in children. In most centres, MDCT and MRI are increasingly used for the evaluation of children with suspected vascular compression, replacing barium swallow studies and catheter angiography. Although we agree with this change in imaging strategy, these techniques still have some limitations. Both MRI and MDCT are at present inadequate to differentiate reliably between dynamic airway obstruction (caused by tracheobronchomalacia) and fixed airway obstruction, as seen in extrinsic vascular compression. This is important as the presence and the severity of tracheobronchomalacia are strongly related to patient outcome. In addition, MDCT and MRI cannot yet identify complete tracheal rings. Stent insertion is only useful in selected patients with airway compression, but it may be appropriate for patients who fail all other forms of treatment.

References 

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1. 1Kussman BD, Geva T, McGowan FX. Cardiovascular causes of airway compression. Paediatr Anaesth. 2004;14:60–74. MEDLINE | CrossRef

2. 2Sebening C, Jakob H, Tochtermann U, et al. Vascular tracheobronchial compression syndromes – experience in surgical treatment and literature review. Thorac Cardiovasc Surg. 2000;48:164–174. MEDLINE | CrossRef

3. 3McLaughlin RB, Wetmore RF, Tavill MA, Gaynor JW, Spray TL. Vascular anomalies causing symptomatic tracheobronchial compression. Laryngoscope. 1999;109:312–319. CrossRef

4. 4Woods RK, Sharp RJ, Holcomb GW, et al. Vascular anomalies and tracheoesophageal compression: a single institution's 25-year experience. Ann Thorac Surg. 2001;72:434–438discussion 438–439. MEDLINE | CrossRef

5. 5Shah RK, Mora BN, Bacha E, et al. The presentation and management of vascular rings: an otolaryngology perspective. Int J Pediatr Otorhinolaryngol. 2007;71:57–62. Abstract | Full Text | Full-Text PDF (390 KB) | CrossRef

6. 6Payne DN, Lincoln C, Bush A. Lesson of the week: right sided aortic arch in children with persistent respiratory symptoms. BMJ. 2000;321:687–688.

7. 7Chen HM, Chiu IS, Chen SJ, Wu SJ, Chan CH. Concomitant management of airway and its adjacent vascular pathology in addition to repair of congenital cardiac defects. Int J Cardiol. 2000;73:181–189. Abstract | Full Text | Full-Text PDF (818 KB) | CrossRef

8. 8Donnelly LF, Strife JL, Bisset GS. The spectrum of extrinsic lower airway compression in children: MR imaging. AJR Am J Roentgenol. 1997;168:59–62.

9. 9ten Berge M, van der Laag J, van der Ent CK, Beek FJ. Clinical, radiological and functional follow-up after surgical decompression of double aortic arch. Pediatr Radiol. 2002;32:561–566. MEDLINE | CrossRef

10. 10Brockes C, Vogt PR, Rothe TB, Arbenz U, Turina J. [Double aortic arch: clinical aspects, diagnosis and therapy in children and adults]. Z Kardiol. 2001;90:127–132. MEDLINE | CrossRef

11. 11Taragin BH, Berdon WE, Printz B. MRI assessment of bronchial compression in absent pulmonary valve syndrome and review of the syndrome. Pediatr Radiol. 2006;36:71–75. MEDLINE | CrossRef

12. 12Papaioannou G, Young C, Owens CM. Multidetector row CT for imaging the paediatric tracheobronchial tree. Pediatr Radiol. 2007;37:515–529. MEDLINE | CrossRef

13. 13Pacharn P, Poe SA, Donnelly LF. Low-tube-current multidetector CT for children with suspected extrinsic airway compression. AJR Am J Roentgenol. 2002;179:1523–1527.

14. 14Cheung YF, Lee SL, Leung MP, Yung TC, Chau AK, Hui HK. Tracheobronchography and angiocardiography of paediatric cardiac patients with airway disorders. J Paediatr Child Health. 2002;38:258–264. MEDLINE | CrossRef

15. 15Fleck RJ, Pacharn P, Fricke BL, Ziegler MA, Cotton RT, Donnelly LF. Imaging findings in pediatric patients with persistent airway symptoms after surgery for double aortic arch. AJR Am J Roentgenol. 2002;178:1275–1279.

16. 16McLaren CA, Elliott MJ, Roebuck DJ. Tracheobronchial intervention in children. Eur J Radiol. 2005;53:22–34. | CrossRef

17. 17Bakker DA, Berger RM, Witsenburg M, Bogers AJ. Vascular rings: a rare cause of common respiratory symptoms. Acta Paediatr. 1999;88:947–952. MEDLINE | CrossRef

18. 18Anand R, Dooley KJ, Williams WH, Vincent RN. Follow-up of surgical correction of vascular anomalies causing tracheobronchial compression. Pediatr Cardiol. 1994;15:58–61. MEDLINE

19. 19Schlesinger AE, Krishnamurthy R, Sena LM, et al. Incomplete double aortic arch with atresia of the distal left arch: distinctive imaging appearance. AJR Am J Roentgenol. 2005;184:1634–1639.

20. 20Reardon MJ, Hallman GL, Cooley DA. Interrupted aortic arch: brief review and summary of an eighteen-year experience. Tex Heart Inst J. 1984;11:250–259. MEDLINE

21. 21Schreiber C, Eicken A, Vogt M, et al. Repair of interrupted aortic arch: results after more than 20 years. Ann Thorac Surg. 2000;70:1896–1899discussion 1899–1900. MEDLINE | CrossRef

22. 22Mitchell MB, Campbell DN, Toews WH, Khan TZ. Autograft aortic arch extension and sleeve resection for bronchial compression after interrupted aortic arch repair. Ann Thorac Surg. 2002;73:1969–1971. MEDLINE | CrossRef

23. 23Kumar P, Bush AP, Ladas GP, Goldstraw P. Tracheobronchial obstruction in children: experience with endoscopic airway stenting. Ann Thorac Surg. 2003;75:1579–1586. MEDLINE | CrossRef

24. 24Donnelly LF, Fleck RJ, Pacharn P, Ziegler MA, Fricke BL, Cotton RT. Aberrant subclavian arteries: cross-sectional imaging findings in infants and children referred for evaluation of extrinsic airway compression. AJR Am J Roentgenol. 2002;178:1269–1274.

25. 25Nolke L, Azakie A, Anagnostopoulos PV, Alphonso N, Karl TR. The Lecompte maneuver for relief of airway compression in absent pulmonary valve syndrome. Ann Thorac Surg. 2006;81:1802–1807. CrossRef

26. 26Brown JW, Ruzmetov M, Vijay P, Rodefeld MD, Turrentine MW. Surgical treatment of absent pulmonary valve syndrome associated with bronchial obstruction. Ann Thorac Surg. 2006;82:2221–2226. CrossRef

27. 27Elliott MJ. Absent pulmonary valve syndrome. In:  Stark JF,  de Leval MR,  Tsang VT editor. Surgery for Congenital Heart Defects. 3rd ed.. London: J Wiley & Sons; 2006;p. 425–434.

28. 28Dodge-Khatami A, Backer CL, Holinger LD, Baden HP, Mavroudis C. Complete repair of tetralogy of Fallot with absent pulmonary valve including the role of airway stenting. J Card Surg. 1999;14:82–91. MEDLINE | CrossRef

29. 29Saygili A, Tiker F, Bagis T, Barutcu O. Absent pulmonary valve syndrome diagnosed by fetal echocardiography. Turk J Pediatr. 2004;46:88–91. MEDLINE

30. 30Kumar P, Roy A, Penny DJ, Ladas G, Goldstraw P. Airway obstruction and ventilator dependency in young children with congenital cardiac defects: a role for self-expanding metal stents. Intensive Care Med. 2002;28:190–195. MEDLINE | CrossRef

31. 31Elliott M, Roebuck D, Noctor C, et al. The management of congenital tracheal stenosis. Int J Pediatr Otorhinolaryngol. 2003;67(Suppl 1):S183–S192. Abstract | Full Text | Full-Text PDF (162 KB) | CrossRef

32. 32Mahboubi S, Gheyi V. MR imaging of airway obstruction in infants and children. Int J Pediatr Otorhinolaryngol. 2001;57:219–227. Abstract | Full Text | Full-Text PDF (485 KB) | CrossRef

33. 33Strife JL, Baumel AS, Dunbar JS. Tracheal compression by the innominate artery in infancy and childhood. Radiology. 1981;139:73–75. MEDLINE

34. 34Swischuk LE. Anterior tracheal indentation in infancy and early childhood: normal or abnormal?. Am J Roentgenol Radium Ther Nucl Med. 1971;112:12–17. MEDLINE

35. 35Shell R, Allen E, Mutabagani K, et al. Compression of the trachea by the innominate artery in a 2-month-old child. Pediatr Pulmonol. 2001;31:80–85. MEDLINE | CrossRef

36. 36Tsugawa C, Ono Y, Nishijima E, Takamizawa S, Satoh S, Muraji T. Transection of the innominate artery for tracheomalacia caused by persistent opisthotonus. Pediatr Surg Int. 2004;20:55–57. MEDLINE | CrossRef

37. 37Hornung TS, Nicholson IA, Nunn GR, Hawker RE. Neonatal ductus arteriosus aneurysm causing nerve palsies and airway compression: surgical treatment by decompression without excision. Pediatr Cardiol. 1999;20:158–160. MEDLINE | CrossRef

1 Department of Cardiothoracic Surgery, The Great Ormond Street Hospital for Children NHS Trust, London, WC1N 3JH, UK

2 Department of Radiology, The Great Ormond Street Hospital for Children NHS Trust, London, WC1N 3JH, UK

Corresponding Author InformationCorresponding author.

PII: S1526-0542(07)00137-6

doi:10.1016/j.prrv.2007.12.008


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