Ann Thorac Surg 1996;62:269-272
© 1996 The Society of Thoracic Surgeons
Case Report
Long Tracheobronchial and Esophageal Rupture After Blunt Chest Trauma: Injury by Airway Bursting
Jose L. Martín de Nicolás, MD, PhD,
Antonio P. Gámez, MD,
Felipe Cruz, MD, PhD,
Vicente Díaz-Hellín, MD,
Carmen Marrón, MD,
Jose I. Martínez, MD,
Ramiro Gálvez, MD,
José Toledo, MD, PhD
Departments of Thoracic Surgery and General Surgery, Doce de Octubre Hospital, Madrid, Spain
Accepted for publication January 19, 1996.
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Abstract
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Tracheobronchial rupture can be associated with blunt thoracic trauma. An important factor in the physiopathology of these lesions is reflex closure of the glottis, which can be related to closed chest trauma. We report a case of nonpenetrating thoracic trauma that caused a long membranous tracheal rupture from the subcricoid area to the main carina, extending to both main bronchi. In addition, a complex esophageal rupture occurred due to the great energy liberated by the airway rupture acting as a real tracheal burst. Both lesions were diagnosed by flexible bronchoscopy. The postoperative period was without serious complications.
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Introduction
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Injury to the tracheobronchial tree due to blunt chest trauma is uncommon. However, an increasing number of these thoracic injuries have been reported during recent years; this trend could be attributed to an increase in high-speed traffic accidents, and also to better care of patients suffering trauma. As soon as tracheobronchial tree damage is diagnosed, careful management of the airway is required to avoid procedures that might lead to fatal consequences.
We report a case of a long tracheal disruption that extended to both main bronchi, associated with esophageal rupture, as a result of a nonpenetrating thoracic trauma. We emphasize the mechanisms of traumatic injury, the early diagnosis, the intraoperative incidence, and finally the successful postoperative evolution.
A 14-year-old boy, while lying on the ground, was hit by a basketball basket on the anterior chest area, and brought by ambulance to the Hospital Doce de Octubre Emergency Unit. On admission the patient was conscious, with moderate tachypnea and hemoptysis. A subcutaneous emphysema of both hemithoraces, neck and face presented in progression. The blood pressure was 160/100 mm Hg, and bilateral breath sounds were noticed. Chest roentgenogram showed subcutaneous emphysema and pneumomediastinum, without fractures nor pneumothorax (Fig 1
). Arterial blood gas determination at this time was as follows: pH, 7.31; oxygen tension, 78 mm Hg; and carbon dioxide tension, 45 mm Hg on an inspired oxygen fraction of 0.21. Flexible bronchoscopy showed hemorrhage and disruption of the trachea.
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Fig 1. . Anteroposterior (A) and lateral (B) chest roentgenograms showed subcutaneous emphysema, and pneumomediastinum without fractures or pneumothorax.
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In the operating room the patient was intubated, a nasogastric probe was inserted, and a second flexible bronchoscopy showed a long tracheal rupture with the nasogastric probe visualized in position. A right posterolateral thoracotomy was performed, revealing a large mediastinal emphysema before accessing to the mediastinal pleura. When the main right bronchus was dissected, a 1-cm rupture of the membranous pars of the bronchus was evident. As the dissection proceeded, rupture of the membranous trachea along the whole thoracic length, including the main carina and the onset of the left main bronchus, was found. At this time, selective intubation of the left main bronchus, passing through the injury on the right, was imperative to achieve appropriate ventilation (Fig 2). Rupture of the same length at the esophagus also was confirmed, and esophagectomy performed. Reconstruction of the trachea, carina, and both bronchi was carried out with isolated 3-0 Vicryl (Ethicon, Johnson and Johnson SA, Madrid, Spain) stitches (Fig 3), completed with intercostal muscle flap on the tracheal repair, and reinforced with stitches onto the mediastinal pleura. The thoracic tracheal rupture and its progression to both main bronchi was 8 cm long. A cervical esophagostomy and a feeding gastrostomy were performed after the thoracotomy was closed.
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Fig 2. . (1) Rupture of the thoracic membranous trachea, main carina, and the onset of both main bronchi. (2) End of the orotracheal tube. (3) Main carina. (4) Selective intubation of the left main bronchus with a flexible tube. (5) Distal part of the esophagic rupture. (6) Nasogastric probe. (7) Ligature and section of the azygos vein. (8) Superior vena cava.
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Fig 3. . (1) Reconstruction of the thoracic trachea, (2) main carina, (3) right main bronchus, and (4) left main bronchus. (5) Mediastinal pleura used to cover the suture. (6) Right lung. (7) Superior vena cava.
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Postoperatively, flexible bronchoscopy showed a subcricoid upper tracheal tear; for this reason the cuff of the portex tube was placed under the lesion and conservative management was chosen. The patient's stay in the intensive care unit was complicated by a radiologic infiltrate in the right upper lobe, successfully treated with parenteral antibiotics, and left basal atelectasis, which resolved with flexible bronchoscopic aspiration. The subcutaneous emphysema showed a gradual decrease. On the sixth day postoperatively, disconnection of the ventilator was possible. Additional flexible bronchoscopies showed progressive healing of the cervical tracheal tear. After the patient was transferred to the ward there were no complications. The patient was discharged on the eighteenth postoperative day with nutrition by gastrostomy. Five months later a substernal esophagoileocecocoloplasty was performed to recanalize the digestive lumen. To date, 30 months from discharge, the patient is healthy and presents adequate growth and development.
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Comment
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Rupture of the tracheobronchial tree is an uncommon form of blunt chest trauma [1], and several mechanisms have been proposed to explain it [1–4]. Reflex closure of the glottis together with thoracic compression produces a fast increase of intraluminal pressure, which would be greater in the larger airways, overcoming the elastic tracheobronchial resistance and producing its rupture. A theory states that forceful compression of the thorax pulls each lung apart, with the resulting traction on the trachea and carina producing a tear. Another theory is based on shearing forces on the tracheobronchial tree between the relatively stationary areas of the cricoid cartilage and the main carina with decelerating forces. All these factors probably gather to cause the classic bronchial ruptures, of which more than 80% occur within 2.5 cm of the main carina [[5–7]. Because these injuries are not usually associated with parenchymal or hiliar vascular damage, it has been postulated that extreme violence is not essential; in contrast, the large number of people suffering extreme force to the chest, shown by the incidence of other intrathoracic injuries, rarely sustain tracheobronchial injury, implying that the important factor is not the absolute force but the way in which it is applied to the chest wall [2]. The mechanism of cervical tracheal rupture is probably more simple to understand: the hyperextended neck causes the trachea to be stretched against the cervical spine [2].
In our case, the patient was young, so his chest was flexible enough to resist a greater compression without causing rib fractures. The patient was not moving when he suffered the trauma but lying down, a position that favored forceful compression. Thus we have a patient in a static position suffering a sudden impact on the anterior thoracic area, and we may rule out the possible intervention of deceleration forces in its dynamics. On analyzing the morphology of the tracheobronchial lesion we noticed a longitudinal rupture that extended from some centimeters of the cervical trachea, along the whole length of the thoracic trachea and main carina, to a few centimeters from both main bronchi, too large to be produced by traction forces on the trachea and carina. The location of the rupture, in the most vulnerable part of the airway, "the membranous pars," as well as its form, longitudinal and continuous along the subglotic to hiliar airway, can be explained by the sudden and uniform increase of the intraluminal pressure in the airway produced by a blunt chest trauma in a patient with the glottis closed. Probably under these circumstances the pulmonary parenchyma performs a softening effect on the high pressure in the intrapulmonary airway.
Rupture of the thoracic esophagus from blunt thoracic trauma occurs very rarely [8–10]. We did not include esophagoscopy or esophagography in the diagnostic procedures, but esophageal injury was discovered when we noticed the nasogastric probe through the flexible bronchoscopy in the operating room, before the thoracotomy. This lesion consisted of two longitudinal ruptures, anterior and posterior, of the thoracic esophagus along the same length as the thoracic tracheal injury. This is unlikely to be due to the tension and traction forces because of its muscular consistency, and the volume of air inside the esophagus is too small for the increase in pressure to be able to produce its rupture. We therefore propose the probable cause of esophageal injury to be the impact from the energy released from the burst airway on the esophagus that is located adherent to the tracheal membranous pars and in contact with the thoracic spine; this can also be denominated "intrathoracic bursting injury." Repair of the thoracic esophagus was impossible, so esophagectomy was necessary. The cervical esophagus was intact. We emphasize the importance of the flexible bronchoscopy not only in the early diagnosis but also in the later management of this kind of lesion.
Although some authors [1, 2, 9–15] have reported cases of tracheobronchial ruptures with successful management, some of which were highly complex, we consider this to be a very rare case because it involves a lesion mechanism different from those usually related to these injuries; but with serious consequences causing complex airway injuries and irreparable damage to the esophagus. Moreover, the early diagnosis was fundamental for minimizing morbidity and easing a lifesaving treatment.
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Footnotes
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Address reprint requests to Dr Martín de Nicolás, Department of Thoracic Surgery, Doce de Octubre Hospital, Ctra Andalucía Km 5'400, 28041 Madrid, Spain.
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References
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Abstract
Introduction
