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Ann Thorac Surg 1999;68:1122-1124
© 1999 The Society of Thoracic Surgeons
a Department of Surgery, IRCCS San Matteo, University of Pavia, 27100 Pavia, Italy
To the Editor
We read with interest the article by Massard and associates [1] on postintubation tracheobronchial lacerations and the stimulating discussion that followed on the topic of conservative versus surgical repair [2, 3]. We noticed, however, that no mention was made in either the article or the discussion of the possible role of decompressing tracheostomy in the treatment of this iatrogenic problem.
In the last 3 years, we have successfully treated 3 patients using this sole measure. The patients had large (> 3 cm) longitudinal lacerations of the membranous part of the trachea, caused by standard tracheal tubes during extrathoracic surgical procedures; all 3 were referred to us with mediastinal and subcutaneous emphysema, the iatrogenic lesion having occurred 1, 4, and 6 days before. The diagnosis was confirmed by endoscopy in all cases. A standard tracheostomy cannula (7 mm) was positioned 1 cm below the cricoid under local (one case) or general anesthesia; the tracheostomy tube cuff was removed with scissors before tube insertion in order to prevent its inflation and splitting apart the laceration rims. When necessary, secretion aspiration was carried out using a thin catheter through the tracheostomy tube. All cases healed with this sole procedure within 10 days, at which time, the trachea was reexamined.
Failure of conservative treatment is due to the persistent passage through the laceration of air and tracheobronchial secretions into the mediastinum. This can cause progression of mediastinal and subcutaneous emphysema, impair the patient’s general condition with ventilatory difficulty, and may lead to the onset of pneumothorax, mediastinal abscess, or sepsis, or pseudodiverticular formation at the site of the laceration. Theoretically, tracheo-arterial (innominate artery, pulmonary artery) fistula formation could also occur; however, we have not been able to find any reports of such an occurrence after conservative treatment of postintubation tracheal laceration, probably because of the relative distance between the pars membranacea, where virtually all the iatrogenic lacerations reported in the literature were localized, and the vascular structures. We completely agree with Dr Massard’s opinion that stenotic healing is not a concern in these lesions, which are always located in the membranous trachea, and are usually longitudinally oriented.
Of course, the pressure in the trachea during the respiratory cycle is crucial to the persistence of the passage of air and secretions through the tear into the mediastinum. Thus, cough can increase many fold the very low (1 to 2 cm H2O) physiologic expiratory positive pressure. Moreover, the Valsalva maneuver, sneezing, laughing, or speaking loudly also significantly increase tracheal pressure; this inevitably causes air and secretions to pass through the laceration, and each time splits the fissure margins widely apart, thus frustrating the healing process.
This effect can be fully prevented by tracheostomy, which does not allow the expiratory pressure to increase significantly above the physiologic low expiratory positive pressure, thus providing a permanent high-pressure discharge valve. Even if the modest physiologic expiratory positive pressure of the respiratory cycle may still cause minor displacement of the fissure margins, as can be easily seen during bronchoscopic examination, this is usually not enough to significantly feed mediastinal emphysema; thus, healing can occur regularly and quite quickly.
In our opinion, therefore, if the tracheal tear is not so deep and wide as to have created an open, nonvirtual communication with the pleural space and pneumothorax, tracheostomy decompression is sufficient to keep the laceration "virtual" without further significant air passage, thus allowing tissue healing. In other words, in the absence of pressure peaks caused mainly by cough, sealing of the fissure occurs naturally by the tissue layers sliding in almost all cases, with the same functional result as that of open surgical repair.
We agree with the authors and the correspondents that late repair carries a high risk of failure due to the invariably present inflammation and infection; in our opinion, however, tracheostomy tube decompression may significantly decrease this risk in this particular clinical setting. We added tracheostomy to transthoracic late repair in two cases (10 and 12 days after the lesion), both successfully recovered. In the case illustrated in Figure 1, we thought open surgical repair was necessary because of the evident large pseudodiverticular formation in wide communication with the trachea through the laceration, which had been iatrogenically created by a standard tracheal tube 10 days before during an orthopedic surgical procedure. At the end of the repair (Fig 2), we positioned a minitrach tube, appropriatedly shortened and fenestrated to increase its conductance, to protect the suture line from the cough peak pressure. The suture healed perfectly (Fig 3) and the minitrach tube was removed on the 8th day.
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Although tracheostomy (or minitracheostomy) is still an invasive procedure, it certainly carries lower mortality, morbidity, patient discomfort, and costs than an open surgical repair, either cervical or thoracic.
References
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