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Ann Thorac Surg 2000;69:927-929
© 2000 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery, University of Istanbul, Istanbul Medical School, Istanbul, Turkey
Address reprint requests to Dr Toker,
nönü Cad Yildiz Sok STFA B-6 Blok Daire: 13, Kozyata
i,
stanbul 81090, Turkey
e-mail: korkutbostanci{at}superonline.com
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Another very uncommon complication of the procedure is tracheobronchial compression [3, 4]. Worsey and colleagues [3] and Robotin and colleagues [4] reported a total of four cases in which tracheobronchial compression was noticed at 4, 5, 12, and 20 weeks after operation. Our 2 patients presented with these symptoms on the 4th day and in the 3rd month.
We believe that tracheal stenosis in patient 1 aggravated the symptoms and caused early diagnosis of this complication. Nonetheless, we do not believe that the tracheal stenosis was due to the procedure itself or that it was congenital. Probably it was because of early granulation tissue due to intubation. If it had been a congenital stenosis, it would have been impossible to dilate the trachea. Patient 2 presented at week 12, which was similar to other cases in the literature [3, 4]. Symptoms of presentation were the same, eg, severe and sudden onset. Bronchoscopic examination was performed as a first-line diagnostic tool and compression of the left main bronchus was visualized in patient 2. Tracheography in patient 1 helped us to notice the hidden left main bronchial stenosis. Thus we agree with Corno and associates [2] that tracheography is one of the most useful diagnostic methods in congenital heart disease and coexisting airway obstruction. However, the hemodynamic status of the patient must be well enough to tolerate the procedure.
As presented in other reports, airway obstruction is believed to be the result of compression of the left main bronchus between the neoaorta and descending aorta. We performed high transection on the great arteries and Lecompte maneuver in the last 10 TGA cases and did not see this complication. We performed high transection because we believed the root of the neoaorta was preserved and the anastomotic region stayed above the left main bronchus level. In the 2 patients presented here, we had mobilized the pulmonary arteries including their bifurcations and divided the patent ductus arteriosus, but we had not used the high transection and anastomosis technique. The neoaorta anastomotic line stayed in the lower position causing compression of the left main bronchus, and the bronchus was trapped between the neoaorta, descending aorta, and vertebrae (Fig 3). Patient 1 did not have the chance to present with symptoms of bronchial stenosis as she had symptoms of tracheal stenosis. We managed both of her problems simultaneously. The left main bronchus stayed open, which might have been due to increased endobronchial pressure and increased cartilaginous ability to resist the arterial pressure. We did not consider aortopexy and left main bronchus liberalization operation for patient 1 after the tracheal stenosis had been managed, because the tracheobronchogram showed only 30% obstruction of the left main bronchus. As patient 2 did not have additional tracheal stenosis, we planned aortopexy and left main bronchus liberalization operation for him.
In conclusion, left main bronchus compression after arterial switch operation is a complication of the procedure itself. Compression of the bronchus is not only between the ascending and descending aortas but also the vertebrae. Though we do not feel that prolonged mechanical ventilation is the preferred method of treatment, it may be helpful in bronchial stenoses with additional tracheobronchial pathologies. Patients who are believed to have respiratory problems in the postoperative period should be evaluated endobronchially with rigid bronchoscopy for left main bronchus compression.
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