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Anterior Tracheal Suspension

  • Michael E. Mitchell
    Correspondence
    Address reprint requests to: Michael E. Mitchell, MD, 9000 W. Wisconsin Avenue, MS B730, Milwaukee, WI 53226
    Affiliations
    Division of Cardiothoracic Surgery, Department of Surgery, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin
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      Tracheomalacia (TM) is a disorder of the airway consisting of weakness of the anterior tracheal cartilaginous rings and laxity of the posterior membranous trachea, resulting in dynamic airway obstruction. The clinical symptoms range from chronic cough and wheezing to life-threatening apnea with cyanosis and profound airway obstruction (acute life-threatening events). TM in infancy occurs either in isolation or in association with a variety of anatomic conditions, including a wide range of congenital heart lesions, as well as primary tracheal and esophageal disorders. TM is also associated with chromosomal abnormalities, such as 22q11.2 deletion syndrome, and trisomy 21.
      Severe TM is a life-threatening condition with reported mortality rates as high as 80%. Prolonged intubation and chronic positive pressure ventilation is particularly common in affected patients following reparative congenital heart surgery; in the most severe cases, tracheostomy is required. Although often life-saving in these patients, tracheostomy results in a high risk of medical, social, and developmental complications. Patients requiring tracheostomy are technology-bound until their anterior tracheal wall matures and they effectively outgrow their malacia. Most concerning, patients with tracheostomy and persistent severe TM remain at risk of sudden death, recurrent infections, and equipment failure.
      Aortopexy has been accepted as the standard surgical treatment to alleviate TM associated with congenital heart disease and carries a success rate of 85 to 90%. In our experience, innominate artery-pexy coupled with aortopexy has been particularly effective in relieving TM secondary to isolated innominate artery compression. However, it has also been our experience that aortopexy alone has failed to relieve symptoms in a number of cases of more complex TM and tracheobronchial malacia.
      Since March 2008, we have used anterior tracheal suspension for the treatment of severe refractory TM and tracheobronchial malacia in infants and children as an alternative to tracheostomy. The majority of children operated on with this technique had undergone previous surgery to repair congenital heart defects, including division of vascular rings and pulmonary artery slings, repair of atrioventricular canal, tetralogy of Fallot, and ventricular septal defects. Several had undergone slide tracheoplasty for long segment tracheal stenosis, with resultant distal tracheobronchial malacia, or had severe TM following repair of tracheoesophageal fistula. The objective of this operation is to provide direct anterior tracheal support, permitting weaning from positive pressure, and allowing patients to outgrow their malacia without the need for tracheostomy. Additional objectives include safe discharge from the hospital with long-term avoidance of acute life-threatening events.
      We undertake anterior tracheal suspension as a last attempt to avoid the need for tracheostomy. The majority of patients in our series required a prolonged period of intubation following repair of another anatomic defect and had failed several attempts at extubation before consideration of anterior tracheal suspension. Others have described anterior tracheal suspension via a lower neck incision, or posterior tracheopexy via thoracotomy. We have found the anterior approach via a median sternotomy to provide superior exposure to the anterior tracheal wall, permitting more accurate suture positioning. Although the procedure is conceptually simple, several concerning challenges exist. These challenges include accurate suture positioning, precise or correct suture tension to avoid distortion of the airway, and avoidance of long-term risk to the great vessels by encroachment of suspension sutures into the wall of the great vessels. We have found that directly supporting the anterior tracheal wall with precisely placed anterior tracheal suspension sutures provides relief of airway symptoms in the most severe and refractory cases, allowing both reduction in ventilatory time and avoidance of tracheostomy.
      Preoperative evaluation includes bronchoscopy, chest computed tomographic scan with airway series, and intraoperative bronchography. All patients are approached in a collaborative manner by our multidisciplinary tracheal team, which includes ENT specialists, pulmonologists, pediatric surgeons, pediatric cardiothoracic surgeons, anesthesiologists, and pediatric intensivists. All patients are followed longitudinally with clinical protocols that are still in evolution.

      Operative Technique

      Figure 1, Figure 2, Figure 3, Figure 4, Figure 5, Figure 6, Figure 7, Figure 8
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      Figure 1Tracheal anatomy and TM. (A) Normal tracheal anatomy is illustrated, demonstrating supportive anterior cartilaginous rings with posterior membranous trachea. (B) TM consists of weakness of the cartilaginous anterior tracheal wall and is often accompanied by a laxity of the membranous trachea, resulting in apposition of the anterior and posterior tracheal walls. This collapse is dynamic and is particularly pronounced during the expiratory phase of the respiratory cycle. (C) More complex conditions are often encountered, with distal tracheal and proximal right main stem bronchomalacia or tracheobronchial malacia being common variants. (D) Bronchoscopy demonstrates complex tracheobronchial malacia with weakness of the anterior trachea and laxity of the membranous trachea, resulting in near occlusion of the proximal right main stem bronchus.
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      Figure 2The patient is intubated and positioned supine with a roll behind the shoulders. Following positioning, the patient undergoes recorded flexible bronchoscopy and bronchography. These studies serve to both establish baseline anatomy and pinpoint the region of malacia. Without repositioning, the patient undergoes a limited vertical midline incision followed by a full median sternotomy.
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      Figure 3Details of anterior right-sided tracheobronchial suspension. (A) Following median sternotomy, the pericardium is opened in the midline and a pericardial well is fashioned. Dissection begins between the aorta and superior vena cava (SVC). The ascending aorta is retracted leftward, while the SVC is retracted to the right. The right-sided pulmonary artery (PA) is isolated with a vessel loop and retracted inferiorly. The lymph node residing between the SVC and aorta (Ao) is resected. Working in this space, the plane of the anterior wall of the distal trachea and carina is developed. All dissection is anterior to avoid injury to the phrenic or recurrent laryngeal nerves; mobilization of either the lateral or the posterior aspects of the trachea is avoided. Forceps are used to grasp the anterior fascia and elevate while bronchoscopy is performed to define precisely the region of maximal malacia and choose optimal points for suture placement. 5-0 or 6-0 pledgeted Prolene horizontal mattress sutures are placed through the anterior tracheal fascia. In addressing right-sided tracheobronchial malacia, 2 sutures are placed in the distal trachea, 1 in the carina and 1 in the proximal main stem bronchus. Under bronchoscopic guidance, tension is placed, elevating the sutures to demonstrate positive effect and ensure optimal placement. Once the sutures have been adjusted and finalized in position, the sutures are passed through a free pledget and tied, sandwiching the anterior tracheal fascia without narrowing the airway. (B) The sternal retractor is removed and sutures are then sequentially passed through the right sternal plate. The sutures are placed concentrated at the superior aspect of the sternum. Care is taken to ensure that the suspension sutures do not abut the great vessels. In my experience, an acceptable space for these sutures has always been found. PT = pulmonary trunk.
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      Figure 4Details of anterior left-sided tracheobronchial suspension. We have seen several cases of severe left-sided tracheobronchial malacia following division of a vascular ring or double aortic arch through a left thoracotomy. We approach these cases similarly to the method illustrated in . A median sternotomy is performed; the pericardium is opened in the midline, and a pericardial well is fashioned. The ligamentum is divided and dissection begins between the lesser curve of the aortic arch and the superior aspect of the main pulmonary artery. (A) By dividing the ligamentum and retracting inferiorly on the main pulmonary artery, the anterior tracheal wall with carina and proximal left main stem bronchus can be exposed. Forceps are used to grasp the anterior fascia and elevate, while bronchoscopy is performed to define precisely the region of maximal malacia and choose optimal points for suture placement. 5-0 or 6-0 pledgeted Prolene sutures are placed in the adventitia. Tension is applied to the sutures in the precise direction of the anticipated suspension. Under continuous bronchoscopic guidance, suture placement and angle of tension are optimized. Once this has been accomplished, the sutures are passed through an additional pledget and the sutures tied. (B) The sternal retractor is removed and the sutures are then passed directly and sequentially through the left sternal plate, concentrated more toward the central to inferior aspect of the sternum aspect as depicted. Care is taken to avoid impingement on the great vessels: either the aorta or the pulmonary artery. Ao = aorta; PT = pulmonary trunk.
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      Figure 5TM associated with vascular ring or double aortic arch. (A) Double aortic arches and vascular rings are often associated with severe distal tracheal and carinal compression before surgical division. (B) On occasion, following successful division of the double aortic arch or vascular ring via thoracotomy, severe residual TM persists. (C) In cases of residual severe TM in which the patient is unable to be weaned from positive pressure ventilatory support, we perform anterior tracheal suspension as outlined above. Pledgeted 5-0 or in neonates 6-0 Prolene anterior tracheal suspension sutures are used. Ao = aorta; LCCA = left common carotid artery; PT = pulmonary trunk; RCCA = right common carotid artery; RSCA = right subclavian artery.
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      Figure 6TM secondary to innominate artery compression. TM secondary to innominate artery compression is common. (A) Normal relationships among the ascending aorta, aortic arch, head vessels, and trachea are illustrated. (B) Innominate artery compression of the rightward aspect of the anterior trachea with associated superior TM, resulting in upper airway obstruction. (C) This condition is most effectively repaired with anterior innominate artery suspension coupled with distal ascending aortopexy, which in our experience has led to nearly universal success in relieving symptoms. Pledgeted 5-0 or 6-0 Prolene sutures are placed in the anterior adventitia of the vessel and then suspended to the sternum under bronchoscopic guidance. Ao = aorta; IA = innominate artery; LCCA = left common carotid artery; LSCA = left subclavian artery.
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      Figure 7Carinal TM following slide tracheoplasty. (A) Slide tracheoplasty is the technique of choice of many centers for the repair of long-segment tracheal stenosis due to complete tracheal rings, often found in association with a pulmonary artery sling. The surgical approach involves dividing the stenotic segment transversely at the midpoint of the stenosis. (B) Following division, the trachea is filleted longitudinally and anteriorly on one limb, and longitudinally and posteriorly on the other limb, allowing reconstruction of the trachea as an onlay graft. (C) Care is taken during the anastomosis to evert the cut edges to avoid an inverted figure-of-8 deformity of the tracheal lumen. In our experience, successful tracheal reconstruction has often either unmasked or possibly contributed to flattening of the carina with resultant carinal and proximal bronchial malacia. (D) Because we commonly find distal carinal and bronchial malacia following slide tracheoplasty reconstruction, we now routinely place anterior tracheal suspension sutures in the anterior adventitia of the carina to suspend this aspect of the airway following slide tracheoplasty.
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      Figure 8Completion of suspension with chest closure and tying of sutures. (A) After passing suspension sutures through the sternal plate, sutures are gathered in rubber shods. A Blake drain is positioned in the mediastinum. Sternal wires are placed. Bronchoscopy is performed as the sternum is brought together. Once wires are twisted and turned down, tracheal suspension sutures are tied under continuous bronchoscopic guidance. Care is taken to provide adequate anterior suspension without creating distortion. (B) The result is confirmed with bronchoscopy and recorded. Subcutaneous tissue and skin are closed in layers. Postclosure bronchogram is performed to confirm a normal airway without distortion. Postsuspension ventilatory flow loops are recorded.

      Conclusions

      Between March 2008 and January 2011, we performed 16 anterior tracheal suspension procedures. All patients have been successfully weaned from positive pressure ventilatory support and discharged. Our tracheal team follows all patients by a protocol, including follow-up bronchoscopies. One patient with a preexisting tracheostomy was able to be decannulated following the procedure. A second patient with severe long segment TM following tracheoesophageal fistula repair was weaned from ventilatory support following anterior tracheal suspension and discharged, but developed recurrence of tracheoesophageal fistula and was ultimately managed with repair of recurrent tracheoesophageal fistula and tracheostomy. That patient has been successfully decannulated. The traditional and accepted treatment for TM due to vascular compression is aortopexy. We have found a subset of patients who, despite division of vascular ring, and aortopexy, have persistent severe TM and require continued positive pressure ventilatory support. This group of patients has consistently responded to anterior tracheal suspension.
      We have found innominate artery-pexy coupled with distal ascending aortopexy to be an extremely reliable procedure in cases of isolated innominate artery compression, because in these cases aortopexy directly addresses the anatomic problem. However, in general, aortopexy is an indirect approach to TM, as it relies on broad distribution of tension based on the broad fascial attachments between the aorta and trachea, while anterior tracheal suspension provides direct, pinpoint support of the affected region. We have found that direct support of the anterior tracheal wall with anterior tracheal suspension produces an impressive direct effect on the anterior cartilage. We believe this is critical in successfully managing cases of more complex and refractory tracheobronchial malacia. Caution must be taken to avoid distortion of the airway because of excessive tension on the sutures. Careful assessment must be made to ensure safe pathways for the suspension sutures. Currently, we give consideration to this anterior tracheal suspension in all cases of patients with severe TM who are being considered for tracheostomy or chronic ventilatory support, as well as those patients who already have a tracheostomy and suffer from persistent malacia, limiting the ability to wean from ventilatory support.

      Acknowledgments

      I would like to thank the entire Children's Hospital of Wisconsin Tracheal Team for the development of this operation at our institution as well as for the outstanding preoperative, intraoperative, and postoperative care of these challenging patients. Team members include the following: Julie M. Baughn, MD, Richard Berens, MD, David J. Beste, MD, Nicole Braun, RN, Robert H. Chun, MD, Tim Fehrenbacher, PA, Mario G. Gasparri, MD, Nancy Ghanayem, MD, Mary Jean Hubert, RN, Kristina L. Keppel, RN, Joseph E. Kerschner, MD, Tim Martin, MD, Ndidiamaka Musa, MD, Kathleen A. Mussatto, PhD, Daiva Parakininkas, MD, Nisreen Rumman, MD, Aparna Rao, MD, Thomas Sato, MD, William B. Tisol, MD, James S. Tweddell, MD, and Michael R. Uhing, MD.