Delayed Bronchial Stenosis After Blunt Chest Trauma

Tracheobronchial rupture is a rare but well recognized complication of blunt chest trauma [1]. This case report describes a patient who experienced blunt thoracic trauma with a resulting bronchial tear that was not initially diagnosed. Bronchoscopic evaluation of the airway was not initially performed because the lungs reexpanded immediately with chest drainage and there was minimal air leak. Subsequent stricture formation resulted in atelectasis, obstructive pulmonary sepsis, and arterial hypoxemia from intrapulmonary shunting. This report describes the consequences of delayed diagnosis of a bronchial rupture after a decelerating chest injury. The anesthetic implications are discussed. Case Report A 21-yr-old male unrestrained driver was involved in a high-speed motor vehicle frontal impact collision. He was admitted to another institution, where he was noted to be alert with a Glasgow Coma Scale score of 15. Documented injuries included bilateral pneumothoraces with subcutaneous emphysema of the upper chest and neck, right-sided second and third rib fractures, and fracture dislocation of his right acetabulum. The patient was initially treated with supplemental oxygen by face mask, and bilateral chest drains were inserted. Chest radiograph confirmed full expansion of both lungs. An investigative bronchoscopy was not performed. A closed reduction of the right hip was undertaken on the second hospital day using a balanced general anesthetic technique and intermittent positive pressure ventilation. The procedure was uneventful. The chest drains were removed within 48 h. The lungs remained fully expanded, and the patient was discharged well on the eighth hospital day. Eight weeks later, the patient presented to our institution with dyspnea on exertion, right-sided chest discomfort and mucopurulent expectoration. Physical examination revealed a temperature of 37.9 degrees C and absent air entry over the right lung. Complete opacification of the right hemithorax was evident on chest radiograph, with apparent blunting of the right mainstem bronchus Figure 1. Arterial blood gas analysis on room air revealed a PaO2 of 57.8 mm Hg, a PaCO2 of 31.5 mm Hg, and a pHa of 7.45. He was treated with antibiotics and supplemental oxygen. Flexible bronchoscopy under local anesthesia demonstrated a circumferential stenosis of the right mainstem bronchus approximately 1 cm distal to the carina and superior to the origin of the right upper lobe bronchus Figure 2. Histology revealed fibrous tissue. Resection of the stricture using a neodymium yttrium aluminum garnet (Nd YAG) laser was undertaken to remove the obstruction, reinflate the lung, and clear the infection. Pulmonary sepsis, hypoxemia, and local inflammatory changes were considered too severe to allow a more definitive surgical resection. An improvement in pulmonary function and patient fitness was sought before definitive repair.Figure 1: Chest radiograph demonstrating total opacification of the right lung field with hyperinflation of the left lung and marked rightward mediastinal shift. There is a linear bronchogram of the right mainstem bronchus (arrow).Figure 2: Bronchoscopy demonstrating the right mainstem bronchus approximately 1 cm distal to the carina and superior to the origin of the right upper lobe bronchus. The medial wall of the bronchus is displaced laterally, and the lumen of the bronchus is reduced (arrow).Standard monitoring for Nd YAG laser resection included pulse oximetry, lead 2 electrocardiogram, and noninvasive blood pressure monitoring. The patient was preoxygenated, and anesthesia was induced with propofol 180 mg. Fentanyl 100 micro gram was given to provide analgesia. Once controlled manual ventilation was established, atracurium 30 mg was administered. A rigid bronchoscope was introduced, and the lungs were ventilated with an oxygen-driven Sanders jet injector. A propofol total intravenous anesthetic technique was used to maintain anesthesia. A stenotic area, approximately 1 cm long, was dissected with the laser. The distal bronchial lumen was normal. At the end of the procedure, the trachea was intubated with a cuffed endotracheal tube for airway toilet, neuromuscular block was reversed, and the lungs were ventilated with 100% oxygen until protective airway reflexes returned. The intraoperative course was uneventful, with arterial oxygen saturation remaining within the normal limits. Postoperative chest radiograph revealed a right-sided pneumothorax that required chest drain insertion. The patient improved and was discharged well. Over the following 6 wk, stricture formation with atelectasis and sepsis recurred and two further Nd YAG laser resections were required. When the patient's respiratory condition was optimized, a definitive surgical resection was scheduled. Standard monitoring plus invasive arterial and central venous pressure monitoring was used. A combined general and regional anesthetic technique was chosen. An epidural catheter was inserted at the T11-12 interspace. After an uneventful test dose of 3 mL of 0.5% bupivacaine, 5 mL of bupivacaine 0.5% plus 25 micro gram fentanyl was given for intraoperative analgesia. After preoxygenation, anesthesia was induced with propofol 180 mg and fentanyl 100 micro gram in a right lateral tilt position. Succinylcholine was given, and a 41 French gauge left-sided double-lumen endobronchial tube was inserted. Controlled ventilation was commenced. Anesthesia was maintained with 1% isoflurane and 66% nitrous oxide in oxygen. Vecuronium was used to maintain neuromuscular block. Oxygen saturation decreased to 92% approximately 5 min after the institution of one-lung ventilation. An inspired oxygen concentration of 1.0 was necessary to maintain an oxygen saturation of 95%. Arterial saturation increased to 97% with the application of 5 cm H2 O continuous positive airway pressure to the nondependent lung. Hemodynamic function was stable intraoperatively. The strictured segment was excised, and an end-to-end right main bronchial anastomosis wrapped in pleura was made. The lung reexpanded fully with ventilation, and the patient made an uneventful postoperative recovery. Eight months later he remains well. Discussion A case of bronchial stenosis in a patient who had previously sustained a decelerating blunt chest injury is described. The case highlighted the failure of bronchial rupture detection after chest injury. Subsequently, the patient developed a bronchial stricture that was complicated by atelectasis, postobstructive pulmonary sepsis, and arterial hypoxemia secondary to intrapulmonary shunting. He posed significant potential anesthetic management difficulties when presenting for bronchial repair. Hypoxemia due to inadequate gas exchange was compounded by intrapulmonary shunting from general anesthesia and one-lung ventilation. Contamination of the contralateral lung could follow relief of the bronchial obstruction. Postobstructive pulmonary sepsis may destroy lung tissue and decrease the possibility of restoring lung function postoperatively. Severe pulmonary sepsis may induce a systemic inflammatory response syndrome with its inherent morbidity. The true incidence of tracheobronchial injuries in blunt chest trauma is difficult to quantify, because many patients sustaining trauma severe enough to cause such injuries die before reaching the hospital. The reported incidence is 5.4% in these patients [2,3]. The reported incidence from clinical series ranges from 0.4% to 1.5% [4]. Most tears are right sided, and more than 80% occur within 2.5 cm of the carina [5,6]. Several mechanisms of injury have been postulated in the literature [3,7,8]. A sudden increase in the transverse thoracic diameter may tear the trachea from the carina after a forceful compression of the thorax. A rapid increase in intrabronchial pressure against a closed glottis may result in a burst injury to the tracheobronchial tree. The production of shear forces at the relatively stationary cricoid and carinal areas after rapid deceleration may cause tearing of these areas. This latter mechanism may have been the mechanism of injury in our case. The manifestations of bronchial rupture include dyspnea (75%), pneumothorax (60%), and subcutaneous emphysema (60%) [9]. After bronchial rupture, air may dissect through the mediastinal planes into the cervical fascial compartment, producing emphysema of the neck and face. Alternatively, when the pleura is torn, a pneumothorax may develop [10]. There may be complete absence of clinical signs in up to 10% of patients, probably because peribronchial connective tissue remains sufficiently intact to permit ventilation in the involved lung. Bronchial obstruction may then develop two to six weeks later when granulation tissue invades the traumatized area. Atelectasis and suppuration develop distal to the obstruction, leading in some cases to abscess formation [11,12]. The diagnosis is suggested by a persisting large air leak through a chest tube, failure to expand the lung with chest drainage, or the presence of pneumomediastinum. If a total tear of a main bronchus occurs, the hilum of the lung may be displaced downward, giving the "fallen lung" sign on chest radiograph [13]. Bronchoscopy is the method of choice for diagnosing a ruptured bronchus and is indicated in all major trauma when bronchial injury is suspected [10,11]. A rigid bronchoscopy may be required if there is a high suspicion of bronchial trauma and flexible bronchoscopy is negative [10]. Occasionally, a bronchogram may be used for objective diagnosis [14]. It must be emphasized that when the peribronchial connective tissue remains intact there may be minimal or no clinical signs. The diagnosis may only become obvious when tension pneumothorax with associated morbidity and/or mortality follows intermittent positive pressure ventilation. The diagnosis may be made retrospectively when bronchial stenosis and its complications develop after chest trauma. A high index of suspicion of this injury is warranted in all patients sustaining severe blunt chest trauma. Routine use of bronchoscopy is advocated for every patient suspected of having this injury. Management of suspected bronchial injuries includes immediate placement of a well-functioning chest drain, even if pneumothorax is not obvious [10]. Institution of positive pressure ventilation in patients with this injury before chest drain insertion may be fatal. Early primary surgical repair with antibiotic cover is the accepted treatment of choice and provides excellent anatomical and functional results [3,5,6,9]. When the diagnosis is delayed, the surgical options include pneumonectomy, lobectomy, and autotransplantation of the remaining lobes or stricture excision and end-to-end anastomosis [15]. Anesthetic management difficulties may be encountered. One-lung ventilation is used to isolate the healthy lung and prevent its contamination. Failure to do so can result in transbronchial spread of blood, tissue, and contents from the bronchial system distal to the stenosis. Transbronchial spread of contents from the diseased side may occur during induction of anesthesia before selective bronchial intubation is performed. This can be avoided by inducing anesthesia with the patient lying head up and tilted toward the diseased lung. Selective bronchial intubation may then be performed readily after administration of succinylcholine. Controlled ventilation should only be commenced after ensuring selective bronchial intubation. A change from two-lung ventilation to one-lung ventilation normally results in impaired oxygenation secondary to continued perfusion of the nonventilated lung, producing intrapulmonary shunting. This may compound an existing inadequate gas exchange if infection with destruction of lung tissue and existing areas of atelectasis are present. If surgical resection is delayed because of pulmonary sepsis or inflammation, as in the case reported, pulmonary function may be improved by opening the stenosis, reinflating the lung, and treating infection [16]. This may be achieved by dilating the stenotic segment or resecting the stenosis with laser therapy. The Nd YAG laser was chosen in this case. Anesthesia for laser therapy presents potential anesthetic problems. Ventilation and oxygenation through a shared airway is difficult [17]. Venturi ventilation, using either 100% oxygen or a 50:50 oxygen-nitrogen mix, with a Sanders jet injector via a rigid bronchoscope, is a well-described technique for laser bronchoscopy [18,19]. Use of a rigid bronchoscope obviates the need for endotracheal tubes with their inherent risk of fire. The technique provides adequate ventilation and has been shown to give lower mean PaCO2 levels compared with conventional ventilation [20]. Venturi ventilation has the advantages of an unobstructed view, a motionless field in conjunction with muscle relaxants, and adequate ventilation, but it carries the risk of pneumothorax and distal embolization of secretions and tissue. Laser resection itself may result in perforation of airway walls, particularly when anatomical landmarks and the direction of the airway is obscured by stenotic fibrosis [21]. The first laser treatment in this case was complicated by ipsilateral pneumothorax, which resulted from one of the above causes. In summary, bronchial rupture is a rare but well-recognized complication of blunt chest trauma. A high index of suspicion for this injury, systematic bronchoscopy, and radiological follow-up are required for early diagnosis. Subsequent stenosis, pulmonary complications, and surgical resection may thereby be avoided. Awareness of the potential associated anesthetic problems may reduce morbidity when diagnosis is delayed.