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Ann Thorac Surg 1999;67:1130-1136
© 1999 The Society of Thoracic Surgeons

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Original Articles

Compression of the central airways by a dilated aorta in infants and children with congenital heart disease

^a Divisions of Cardiothoracic Surgery, Pediatric Pulmonology, and Pediatric Cardiology, University of California, San Francisco, San Francisco, California, USA

Accepted for publication September 24, 1998.

Address reprint requests to Dr Reddy, Division of Cardiothoracic Surgery, University of California, San Francisco, 505 Parnassus Ave, M593, San Francisco, CA 94143-0118

	Abstract

Top Footnotes Abstract Introduction Patients and methods Results Comment References

 
Background. Children with congenital heart disease often experience respiratory symptoms in the preoperative and perioperative periods, which can complicate their management. An uncommon but important cause of respiratory insufficiency in such children is external airway compression.

Methods. We operated on 5 patients (median age, 6 months) with significant respiratory distress attributable to compression of the central airways by a dilated ascending aorta before or after repair of concomitant cardiovascular defects. Four of these patients had right aortic arch and 3 had pulmonary atresia with a ventricular septal defect and major aortopulmonary collaterals. In all patients, aortopexy was performed at the time of operation for the cardiovascular defects (n = 3) or after symptoms developed in the postoperative period (n = 2). The 3 patients in whom airway compression produced symptoms preoperatively also underwent reduction ascending aortoplasty.

Results. Symptoms resolved immediately after operation in 3 patients, whereas symptoms persisted in the other 2 patients and tracheostomy was required. At follow-up of 20 months to 5 years, all patients are alive and well, with mild or moderate respiratory symptoms in the 2 patients who required tracheostomy, both of whom were decannulated within 13 months.

Conclusions. External airway compression can cause significant morbidity in patients with congenital heart defects other than vascular rings. In patients with respiratory symptoms in the context of a lesion that involves increased aortic outflow during intrauterine life and consequently, an enlarged ascending aorta, such as tetralogy of Fallot with pulmonary atresia, airway compression should be considered as a cause, especially if a right aortic arch is present or the patient also has pulmonary atresia with a ventricular septal defect and collaterals. Attempts to address this problem surgically may provide substantial relief, but increasing duration of airway compression is likely to lead to tracheal or bronchial malacia and persistent symptoms even after the compression is relieved.

	Introduction

Top Footnotes Abstract Introduction Patients and methods Results Comment References

 
Respiratory symptoms are common in patients with congenital heart disease and may stem from a variety of causes, including the sequelae of increased or decreased pulmonary blood flow, anomalous airways or pulmonary vasculature, infection, and extrinsic airway compression. In children, obstruction of the central airways attributable to external vascular compression most commonly occurs secondary to anomalies of the aortic arch system, which may or may not be accompanied by congenital anomalies of the heart [1, 2]. However, vascular compression of the extraparenchymal upper airway has also been found in association with forms of congenital cardiovascular disease other than rings and slings, including conditions with a left-to-right shunt causing dilatation of the pulmonary arteries [3], truncus arteriosus [4], tetralogy of Fallot with absent pulmonary valve [5], and a malpositioned or dilated aorta [6–10]. Airway compression after operation for congenital heart disease has also been described after procedures such as the arterial switch operation, repair of interrupted aortic arch or truncus arteriosus, and conduit reconstruction of the pulmonary outflow tract [10–12]. Because respiratory symptoms are common in congenital heart disease, airway compression can be difficult to diagnose, and because congenital heart disease and obstructive airway disease can complicate one another, the management of these patients is challenging. We report 5 patients with congenital heart disease who also suffered from respiratory insufficiency attributable to central airway compression by a dilated ascending aorta, along with tracheomalacia and bronchomalacia, either before or after initial repair of their cardiovascular defects.

	Patients and methods

Top Footnotes Abstract Introduction Patients and methods Results Comment References

 
Patients
Between 1993 and 1997, 5 patients with congenital heart disease were diagnosed with significant upper airway compression attributable to a dilated aorta either before or after operation, and underwent surgical therapy for the airway compression concurrently or after operative repair of the congenital cardiovascular defects (Table 1 ). Patients ranged in age from 12 days to 3 years, and 4 were infants. Primary diagnoses were pulmonary atresia with ventricular septal defect and major aortopulmonary collateral arteries (MAPCAs; n = 3), doubly-committed subarterial ventricular septal defect with atrial septal defect and patent ductus arteriosus (n = 1), and cervical arch with coarctation of the aorta (n = 1). All patients had visceroatrial situs solitus, with normal cardiac topology and an enlarged ascending aorta. Four of the 5 had a right-sided aortic arch, with a mirror image branching of the brachiocephalic vessels in 3 and a cervical arch in 1. The patient with a cervical arch had an aberrant left subclavian artery with a left ductal remnant running from the left subclavian artery to the left pulmonary artery, but this was not the cause of airway compression. Aside from this patient there were no brachiocephalic vascular abnormalities. In addition to airway compression, 3 patients had significant esophageal (n = 1) or right pulmonary arterial compression (n = 2). Previous operations had been performed at other institutions in 2 patients, including 1 partial unifocalization and 1 repair of cervical arch with coarctation. Complete repair of the cardiovascular defects was performed at our institution, either concurrently or before diagnosis of the airway obstruction.

Imaging studies
All patients underwent bronchoscopy before intervention for airway symptoms (Fig 1 ). Additional studies performed to evaluate the airways or esophagus included computed tomography (n = 2; Fig 2 ) or magnetic resonance imaging (n = 3) of the chest, contrast tracheography at the time of angiography (n = 2; Fig 3 ), and barium swallow (n = 1). In all patients, the combination of imaging studies led to the diagnosis of external bronchial or tracheal compression caused primarily by a dilated ascending aorta. In all patients, this was compounded by focal or diffuse tracheomalacia or bronchomalacia. In 4 patients, the distal trachea was affected, along with the carina or one or both mainstem bronchi. In all patients, the mainstem bronchus ipsilateral to the aortic arch was obstructed, and in 2 patients with a right arch, the left mainstem bronchus was affected as well (Table 1).

View larger version (148K): [in this window] [in a new window]   Fig 1. Bronchoscopy studies performed in patient 2 (a,b) 16 days postoperatively, and (c,d) after aortopexy. (a) Image from high in the trachea showing anteroposterior flattening of the distal trachea, more pronounced on the right side. (b) Image from low in the trachea showing the carina (open arrow) and origins of both mainstem bronchi, which are clearly compressed in the anteroposterior dimension. (c) Image from high in the trachea demonstrates considerable improvement in the diameter of the distal tracheal lumen, relative to the preaortopexy study shown in (a). (d) At a level similar to that depicted in (b), the substantially more normal (rounded) shape of the orifices of both mainstem bronchi can be appreciated. (A = anterior; P = posterior; R = right.)

View larger version (69K): [in this window] [in a new window]   Fig 2. Noncontrast computed tomography scan performed 13 days after repair in patient 2, with two successive axial slices at 5-mm intervals. In the more proximal slice (top), compression of the carina (arrow) and the origins of both mainstem bronchi can be visualized. The immediately distal slice (bottom) shows diffuse narrowing of the left mainstem bronchus (open arrow).

View larger version (98K): [in this window] [in a new window]   Fig 3. Preoperative (same day) ascending aortogram (A) immediately followed by a contrast bronchogram (B), taken in an anteroposterior plane with mild right oblique angulation, in patient 4. (A) Ascending aortogram shows a right aortic arch with a large ascending aorta and mirror image branching of the head vessels. The right pulmonary artery is narrowed as it passes under the arch through the aortopulmonary window. (B) Contrast bronchogram performed immediately after the aortic root injection. Indentation of the trachea can be appreciated just proximal to the carina (open arrow), and narrowing of the right mainstem bronchus is apparent at the level of the ascending aorta and right pulmonary artery. The catheter tip (arrow) is located in the same position for both frames, and can be used as a reference point for comparison.

	Results

Top Footnotes Abstract Introduction Patients and methods Results Comment References

 
On intraoperative inspection in all patients, it appeared that aortopexy and reduction ascending aortoplasty substantially increased the distance between the ascending and descending aorta, allowing increased space between these structures and the affected mainstem bronchus, and effectively moved the aorta anterolaterally off of the affected airway. Reduction ascending aortoplasty allowed for reduction of the ascending aortic diameter by 15% to 30%. Postoperative magnetic resonance imaging in 2 patients, including the 1 with a right cervical arch, showed significantly increased space between the ascending and descending aorta compared with the preoperative scan.

There were no early postoperative deaths. Two of the patients with preoperative symptoms and 1 patient who developed airway compression after unifocalization were extubated shortly after operation (2 to 6 days) and discharged from the hospital with no further respiratory compromise. The other 2 patients (1 with preoperative symptoms and 1 who developed symptoms after unifocalization) had evidence of decreased airway compression on subsequent bronchoscopy, but could not be extubated and underwent tracheostomy 38 and 43 days after the procedure to relieve airway compression. One of these patients also developed Pseudomonas pneumonia, and both had significant bronchomalacia and mucous plugging of the bronchi on bronchoscopy.

At follow-up ranging from 20 months to 5 years, all patients were alive and well. The patients who required tracheostomy were decannulated 9 and 13 months later, and had mild or moderate respiratory symptoms, most likely related to residual airway malacia. One patient with pulmonary atresia and MAPCAs subsequently underwent closure of the ventricular septal defect. Otherwise, there have been no late reoperations.

	Comment

Top Footnotes Abstract Introduction Patients and methods Results Comment References

 
Respiratory compromise and airway compression in children with congenital heart disease
Respiratory symptoms occur frequently in children with congenital heart disease before operation and in the perioperative period, and can complicate their management. An uncommon but important cause of respiratory insufficiency in children with cardiovascular anomalies is extrinsic airway compression. Most cases of significant airway compression in children result from vascular rings or physiologic changes attributable to cardiovascular anomalies that secondarily cause compression of the airway [1–3]. The most common of such physiologic factors are a hypertensive and dilated pulmonary artery, impingement of the left atrium on the superiorly located bronchi due to volume overload and chamber enlargement, and atelectasis due to compression of the lower lobe of the left lung by an enlarged heart [3, 12]. Similarly, as described in the present report and by other investigators [7–10], a dilated aorta may cause compression of the trachea or bronchi, or both. In congenital heart disease with coexisting airway compression, treatment can be particularly difficult, in large part because these conditions may be mutually exacerbating. In addition, underventilated or atelectatic lung segments are more prone to infection, which is likely to be less well tolerated than in children with normal cardiovascular physiology and may further impair convalescence. Although traditional management approaches may advocate waiting for improvement in symptoms before undertaking a corrective procedure, repair of the congenital heart disease will normalize the cardiovascular physiology and may actually facilitate recovery in such circumstances.

Young patients are particularly susceptible to significant extrinsic airway compression. Because the resistance of an airway correlates inversely with its radius to the fourth power, a slight reduction in the caliber of an already small (that is, infant) bronchus has a relatively large impact on airway resistance. In addition, because central airway conductance in infants is nearly equal to conductance in the peripheral airways (unlike adults, in whom peripheral conductance is five times greater than that of the central airways), the large airways in a young child constitute a significant resistance component [14]. These differences are compounded by the fact that the large airways in infants are more readily compressible than in older individuals, in part because of the greater pliability of their tracheal/bronchial cartilage [3, 14]. Thus, in addition to an increased susceptibility to compression in infants, young airways may lose some of their resiliency and remain prone to malacia even after surgical repair and removal of the compressing structure. In patients with forms of congenital heart disease that predispose to respiratory symptoms, even mild compression may lead to significant functional compromise.

Although most children who undergo repair of vascular anomalies causing airway compression will experience relief soon after operation [1], respiratory symptoms are present at long-term follow-up in a substantial portion of patients [2, 15]. Most premature deaths in these patients, both early and late postoperatively, are attributable to respiratory causes. Morbidity and mortality in patients with congenital heart disease and extrinsic airway compression is understandably higher than in patients who have external airway compression without concomitant cardiac lesions [10, 12]. In such patients as well, respiratory factors are often directly responsible for death or serve as the major source of morbidity. In reported series of patients who have undergone repair of vascular rings/slings, there has been little description of the relationship between intermediate and long-term persistence of symptoms and age at repair or preoperative delay in treatment (ie, duration of symptoms). Intuitively, it seems likely that symptoms will tend to be more persistent after repair in patients with chronic or subchronic preoperative symptoms. If so, prompt diagnosis and operation is imperative to reduce long-term sequelae of external airway compression.

Association with pulmonary outflow tract obstruction and right aortic arch
It is interesting to note that 3 of our patients and 2 of the 4 patients reported by Capitanio and colleagues [7] had pulmonary atresia with ventricular septal defect and MAPCAs. Similarly, 3 of the 4 patients with airway compression by an enlarged aorta in the reports of Fujiwara [8], Gidding [9] , and Robotin [10] and their colleagues had tetralogy of Fallot, albeit without pulmonary atresia. An enlarged ascending aorta is a common finding in both tetralogy of Fallot with and without pulmonary atresia [16], which is most likely due to the fact that increased aortic outflow during intrauterine life in right-sided obstructive lesions leads to greater than normal flow-related growth of the aortic root [17]. In addition, the dextroposition of the aorta, which occurs to varying degrees in these conditions, can alter the anatomic relationship of mediastinal structures. It may also be significant that 9 of the 12 patients with central airway compression by a dilated aorta described in the present series and previous reports [7–10] occurred in patients with a right aortic arch. The relatively high frequency of right aortic arch in tetralogy of Fallot and pulmonary atresia with ventricular septal defect is well documented [16] and is also likely to result from predominance of left ventricular outflow in fetal life [17]. Both patients in this study who did not have pulmonary atresia with MAPCAs had a right aortic arch. In several large studies of right aortic arch, there was no mention of an increased incidence of airway impingement or any intrinsic characteristics of a right-sided arch that would be more likely to compromise the trachea or bronchi than with a left arch [18, 19]. However, the distance between the ascending aorta and descending aorta is shorter in the presence of a right arch than a left arch, attributable in part to the normal location of the ascending aorta to the right of midline. Thus, the association of central airway compression by a dilated aorta with a right aortic arch and no aberrant brachiocephalic vessels is probably a combination of factors: the reduced dimensions of the hilar window in the setting of a right arch are diminished further by dilatation of the ascending aorta, which can often be ascribed to the fetal hemodynamic factors that tend to encourage the predominance of a right arch, such as increased aortic outflow in association with right ventricular outflow tract obstruction, which are also likely to stimulate growth and dilatation of the ascending aorta.

Although the foregoing factors likely contributed to the airway obstruction in our patients and those described in the literature, it is notable that symptoms appeared only after repair in 2 of our patients with pulmonary atresia and MAPCAs (1 patient with a left arch). This suggests that the foregoing features alone are not sufficient explanation for the association of pulmonary atresia and MAPCAs with aortic dilatation and extrinsic airway obstruction in all patients. Another factor that may be important is hypoplasia or anomalous arborization of the intrapulmonary airways in patients with pulmonary atresia and ventricular septal defect. Although such anomalies have not been definitively described in patients with pulmonary atresia and MAPCAs, it has been shown that the intraparenchymal arteries arborize abnormally in some patients with this lesion [20]. Corresponding airways anomalies are a distinct possibility, given that tetralogy of Fallot with absent pulmonary valve syndrome is associated with anomalies of both intrapulmonary arteries and airways [21] and that there is usually a correlation between arborization of the intraparenchymal airways and arteries. If there is indeed an association between anomalous intrapulmonary airways and the manifestation and persistence of symptoms in these patients, it is likely to be that the abnormal anatomy contributes to a decreased functional respiratory reserve and a consequently lower threshold for experiencing respiratory distress. To clarify the issue of whether intrapulmonary airway abnormalities are indeed a contributing factor, further research will be required.

Even if abnormal intraparenchymal airways or arteries are not implicated, decreased respiratory reserve in patients with pulmonary atresia and MAPCAs is likely an important factor in the development of symptomatic postoperative airway compression in these patients. In the acute postoperative state, especially after operation with prolonged periods of cardiopulmonary bypass and interruption of pulmonary arterial perfusion, the airways can become highly stressed. During and after bypass, systemic elaboration of inflammatory cytokines and complement activation increases transudate and soft tissue edema that involves the mucosa and interstitium of the airways [22]. Because nutritive supply to the intraparenchymal upper airways is usually derived from the collateral arteries in patients with MAPCAs [20], ligation of collaterals during cardiopulmonary bypass also effectively interrupts bronchial arterial supply, probably producing more airway ischemia than occurs during cardiopulmonary bypass in patients with normal bronchial blood supply. In addition, during and after operation patients are subjected to endotracheal tube intubation, which often serves to irritate the airways, and can lead to more significant damage if maintained for long periods [23]. Similarly, extensive operative dissection, as is required during a unifocalization procedure for pulmonary atresia with MAPCAs, causes reactive inflammation of the mediastinal soft tissues, which may contribute to crowding and airway compression. Thus, the early postoperative state is conducive to eliciting airway symptoms in patients with mild or asymptomatic compression preoperatively or otherwise abnormal airway status. A patient with MAPCAs and a decreased respiratory reserve who was able to maintain adequate ventilation preoperatively, even when stressed, might experience significant difficulty in the acutely stressed postoperative state and be difficult to extubate. It is important to note that this complication is by no means common in patients with pulmonary atresia, ventricular septal defect, and aortopulmonary collaterals, as we have performed unifocalization procedures in more than 75 such patients and this complication has developed in only 3 patients [13].

Management and outcomes of aortic airway compression with congenital heart disease
The management of suspected external airway compression in patients with congenital heart disease and no vascular rings or slings depends on a number of factors. The first objective in cases of significant obstruction is removal of the source of compression. However, the diagnosis of airway compression in patients with a dilated ascending aorta may be difficult to make. Preoperatively, airway obstruction should be suspected in infants with a large ascending aorta or a right-sided arch and signs of pulmonary overinflation. Various imaging modalities can be used to support this diagnosis, including computed tomography, magnetic resonance imaging, bronchoscopy, and contrast tracheography with angiography. Surgical repair of the cardiac defects along with aortopexy, with or without plication of the ascending aorta, may be adequate to relieve symptoms of obstruction, as in our fourth patient. However, because tracheal/bronchial compression may weaken the already pliable airway cartilage in infants, symptoms may persist postoperatively, or appear in patients with no preoperative symptoms, due to tracheomalacia or bronchomalacia. In such patients, it is important to determine whether a residual compressive component is present before proceeding to other means of management. If residual compression is suspected, prompt bronchoscopy should be performed. This may reveal bronchial mucous plugs of physiologic significance, and is likely to clarify whether residual or recurrent airway compression is present. If compression is likely, immediate surgical intervention may minimize further progression of airway malacia and optimize outcome. One means of helping to avoid postoperative airway compression, especially in patients with extensive operations and cardiopulmonary bypass runs, may be to leave the chest open electively for 2 or 3 days after operation. By decompressing the mediastinum in the critical early postoperative period, this strategy may have a salutary effect.

In 2 of our patients, extubation was unsuccessful even after repeated bronchoscopy, and tracheostomy was performed. Both patients were decannulated within 13 months and are doing well with only minor airway symptoms. A growing literature shows that tracheostomy in infants and children, while not without morbidity and mortality, is a safe and effective approach to airway management in patients with airway compromise [24–26]. As in other forms of airway compression, positive end-expiratory pressure and continuous positive airway pressure may be effective means of ventilatory management, both acutely and chronically.

Alternative approaches to the management of central airway obstruction
There are other potential approaches to the management of this problem, including both surgical and bronchoscopic methods. In recent years, there has been significant improvement in surgical techniques of pediatric airway reconstruction [27]. However, such techniques are significantly more invasive than those that we have used, and nevertheless entail risk of complications. Resection and reconstruction, or simply buttressing of the affected airway with tracheal allograft, may nevertheless be appropriate in patients with persistent airway malacia after relief of the vascular compression [27, 28]. An option that we recommend not be used until exhaustion of conservative medical therapies and surgical relief of the obstruction in children, especially infants and young children, is the use of airway stents. Particularly when the compressive force is not relieved, significant complications can occur with the use of stents to secure tracheal/bronchial patency. For example, Robotin and colleagues [10] described a case of fatal aortobronchial fistula after airway stenting in a patient with extrinsic airway compression and congenital heart disease. Although recent experience with silicone stents has demonstrated less airway inflammation than with the metal type [29], stents can cause significant inflammation and permanent damage to the airways, and remain unproved in a large series of children [28, 30, 31].

	Footnotes

Top Footnotes Abstract Introduction Patients and methods Results Comment References

 
This article has been selected for the open discussion on the STS Web site: http://www.sts.org/section/atsdiscussion/

	References

Top Footnotes Abstract Introduction Patients and methods Results Comment References

 

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