Trauma

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Larynx

Laryngeal trauma can be caused by external or internal injuries. External injuries are the result of blunt or penetrating trauma. Internal injuries are usually caused by prolonged intubation or chemical or thermal burns.30 Trauma is characterized by mucosal disruption of soft tissues, swelling, and collection of air in the soft tissue structures of the larynx including neck and mediastinum. These soft tissue injuries may be associated with cartilaginous fractures, and dislocations of the arytenoids and epiglottis.31 The blood and edema fluid insinuate along the deep spaces of the larynx, predominantly in the paralaryngeal and epiglottic spaces, followed by a variable degree of airway narrowing. Fractures of the thyroid cartilage may be transverse or vertical, resulting in hemorrhage into the preepiglottic space, with consequent posterior displacement of the epiglottis. Fractures in the cricoid cartilage are often vertical and lead to a variable degree of disruption of the signet ring. Fractures of the cartilaginous structures are associated with a variable degree of displacement and hematoma formation. The arytenoids may be displaced as an isolated incidence or in conjunction with fractures of the cartilaginous structures. They are most often displaced anteriorly and superiorly. Vocal cord motion is usually impaired as a result of hematoma formation, fractures, arytenoid dislocation, fibrosis, or recurrent laryngeal nerve paresis. Disruption of the cricothyroid joint may occur and also lead to dysfunction of the vocal cords. The sequelae of severe laryngeal injuries are variable degrees of stenosis, which may involve the entire larynx or may be localized to the supraglottic, glottic, or subglottic larynx.

CT is the modality of choice for demonstrating the various described findings in laryngeal trauma.32 CT will also demonstrate the extent of soft tissue edema, hematoma formation, the location and extension of fractures, and the deformity of cartilaginous structures after healing (Figure 4-13).

Trachea and Main Bronchi

Tracheobronchial rupture is a rare injury that results from a decelerating injury. The possible mechanisms of injury include compression of the airway between the sternum and the vertebral column, a sudden deceleration of pendulous lung with a fixed trachea creating shearing forces, and forced expiration against a closed glottis raising intrabronchial pressure.

The site of airway rupture and its extent determine the radiographic findings. The tracheal or bronchial tear is usually complete and will lead to subcutaneous emphysema, pneumomediastinum, or pneumo-thorax.33 Tears of the trachea and proximal left main bronchus generally leave the parietal pleura intact and will result in pneumomediastinum (Figure 4-14). Distal left main bronchial tears and right main bronchial tears will generally communicate with the pleural cavity and result in pneumothorax (Figure 4-15). Tears generally occur within 2.5 cm of the carina, and are more commonly seen on the right side. If the central anchoring components of the lung are completely ruptured and the main bronchus disrupted, the lung may collapse peripherally from the hilum, in what has been described as the "fallen lung" sign. In some cases, there may be an incomplete tear and an absence of an air leak when the integrity of the peribronchial or peritracheal connective tissue is maintained, when a cuff occludes the tear, or when fibrin seals the tear. Tears that present in this fashion are often missed initially and have a delayed presentation (Figure 4-16). If healing develops, an rr

figure 4-13 Laryngeal trauma. Axial computed tomography section through the subglottic space of the larynx defines a fracture in the anterior thyroid cartilage (arrow).

figure 4-14 Acute tracheal tear. A, Posteroanterior chest radiograph demonstrates marked diffuse pneumomediastinum extending into the neck. B, Computed tomography scan through the upper chest reveals extensive pneumomediastinum and subcutaneous emphysema. There is a tear of the membranous wall of the trachea.

figure 4-15 Acute left main bronchial rupture. Computed tomography scans through the carina (A) and left main bronchus (B) reveal extensivepneumo-mediastinum, subcutaneous emphysema, and a left-sided pneumothorax. There is marked narrowing of the left main bronchus at the site of laceration (B).

untreated partial laceration will develop a stenosis with a typical hourglass configuration and potentially cause distal collapse of a lung or lobe (Figures 4-17, 4-18). Tracheobronchial trauma is often associated with aortic injury and fractures of the first three ribs or sternum.34-36

Traumatic and Postintubation Stenosis

One of the complications to the larynx and trachea, most commonly seen following intubation, is granuloma formation. Granulomas occur primarily in the posterior supraglottic, glottic, and subglottic larynx, and cervical trachea (Figures 4-19, 4-20). They can attain a large size with subsequent airway obstruction. Late changes secondary to trauma represent laryngeal stenoses causing airway obstruction. These stenoses may occur in the supraglottic, glottic, and subglottic larynx,37 or as a combination of all the sites with extension into the cervical trachea (Figures 4-21,4-22,4-23).38 In severe cases, the entire larynx and/or trachea may become obliterated. Tracheal stenosis is also encountered post-tracheostomy and postintuba-tion.39 They occur primarily at two sites: 1) the tracheostomy opening or stoma, and 2) in the area of the balloon cuff. In a small percentage of cases, both lesions will occur simultaneously.40 With the introduction of compliant, extensible, large-volume latex cuffs, this complication has been prevented to a great degree, and, consequently, the incidence of postcuff stenosis has markedly decreased.

figure 4-16 Subacute right main bronchial tear. A, Anteroposterior chest radiograph reveals complete opacification of the right hemithorax and shift of the trachea and mediastinum to the right, consistent with right lung collapse following contained laceration of the right main bronchus. Computed tomography scans with lung windows at the carina (B) and slightly below the carina (C) demonstrate narrowing of the lacerated right main bronchus. D,E, Soft tissue windows at the same levels reveal a fluid-filled, displaced distal right main bronchus (arrow).

figure 4-16 Subacute right main bronchial tear. A, Anteroposterior chest radiograph reveals complete opacification of the right hemithorax and shift of the trachea and mediastinum to the right, consistent with right lung collapse following contained laceration of the right main bronchus. Computed tomography scans with lung windows at the carina (B) and slightly below the carina (C) demonstrate narrowing of the lacerated right main bronchus. D,E, Soft tissue windows at the same levels reveal a fluid-filled, displaced distal right main bronchus (arrow).

At the stomal site, a large stoma, superimposed infection, or the use of rigid connecting systems increases the incidence of stomal strictures due to pressure erosion.41 The stenosis at the tracheostomy stoma frequently involves the anterior and lateral tracheal wall, and forms a triangularly-shaped area of narrowing (Figure 4-24). Changes in the tracheal wall consist of fibrosis, often associated with granulation tissue. In many instances, a variable amount of calcium and bone that are deposited in the tracheal wall are readily demonstrated on the CT scan. Another complication seen at the tracheostomy site is a formation of an anterior tracheal wall flap from above the stoma, caused by inversion of the anterior tracheal wall into the adjacent lumen. Granulation tissue may form on the flap and increase the severity of the obstruction.

figure 4-17 Post-traumatic tracheal stenosis. A, Computed tomography scan with intravenous contrast material demonstrates a narrowed, misshapen trachea surrounded by soft tissue density, consistent with fibrosis at the site of healed tracheal rupture. B, A lung window through the superior mediastinum reveals marked tracheal stenosis.

figure 4-18 Missed left main bronchial stenosis due to missed bronchial rupture. Posteroanterior chest radiograph (A) and anteroposterior tomogram (B) reveal collapse of the left lung distal to a left main bronchial stenosis.

figure 4-19 Subglottic granuloma. Lateral neck view illustrates a sharply delimited polypoid mass in the anterior subglottic space, consistent with a granuloma (asterisk).

figure 4-20 Tracheal granuloma adjacent to a tracheostomy canula. Oblique spot film demonstrates a granuloma at the tracheostomy tube (arrows).

figure 4-21 Subglottic stenosis. Axial computed tomography scan demonstrates diffuse circumferential thickening of the submucosa in the subglottic space (asterisk). Note the normal cricoid cartilage (arrow).

figure 4-22 Infraglottic and adjacent cervical tracheal stenosis. Lateral view of the neck illustrates slight narrowing of the inferior portion of the subglottic space (asterisk) and adjacent trachea posteriorly. There is thickening of the tracheal wall with some calcification (arrows).

figure 4-23 Subglottic and cervical tracheal stenosis. Lateral neck view shows a long severe subglottic and cervical tracheal stenosis (arrow). Note the tracheostomy tract (asterisk). The inferior margin of the larynx is indicated by a dot.

figure 4-24 Stomal stenosis of the cervical trachea. A, Anteroposterior high-kilovoltage view outlines a localized stenosis in the cervical trachea (arrows). B, Coronal tomogram shows the polypoid configuration of the stenosis. C, Lateral tomogram shows the stenosis chiefly anteriorly and laterally.

When the tracheostomy tube is removed, it may act as a ball-valve mechanism and obstruct the tracheal lumen. These flaps are optimally demonstrated on lateral neck films as a variable and sometimes mass-like soft tissue density above the stomal opening.

A cuff stenosis occurs 1 to 2 cm below the tracheal stoma and is circumferential in configuration. Inflammatory histologic changes are noted within 24 to 48 hours following intubation. The inflammation leads to superficial tracheitis and mucosal ulceration within 1 week. Deeper mucosal ulceration may develop, along with exposure of the underlying cartilage, in 1 to 3 weeks. If the inflammatory process is not halted, cartilage will be exposed and chondritis will ensue, with fragmentation and eventual total destruction of the cartilaginous supporting structures in a period of 2 to 3 weeks following the intubation. Reparative healing will supersede the inflammatory process and lead to fibrotic change and formation of granulation tissue with tracheal narrowing.40 The length and severity of the stenosis are related to the pressure within the cuff, size and shape of the cuff, the number of days of intubation, and the peak inspiratory pressure. The stenosis is usually circumferential and from 1 to 4 cm in length. In its fully developed stage, the lesion at the cuff site may vary in severity, from a circumferential diaphragm of fresh granulation tissue to dense rings of mature fibrous tissue partially covered by metaplastic squamous epithelium, extending over a variable length. A preliminary high-kilovoltage oblique film of the trachea defines the level and length of the stenosis (Figure 4-25). For detailed assessment of the lumen, thickness of the tracheal wall, and presence of mural calcification, CT is currently indicated, whereas in previous years, tomography was performed (Figures 4-26, 4-27).

Tracheomalacia develops, in a small percentage of cases, above the cuff stenosis site or at the stomal site. When the full thickness of the tracheal wall has been damaged, so that cartilages are no longer present in the area of injury, malacia may ensue. In a small number of cases, a malacic segment alone may be found at the cuff site. The malacia can be demonstrated by fluoroscopic examination with observation of the trachea during coughing and maximal inspiration and expiration. There is collapse of the entire tracheal wall, especially the anterior wall. Tracheal stenosis may be associated with other findings and complications, such as vocal cord paralysis, and infraglottic stenosis. Subglottic stenosis is usually secondary to damage of the cricoid cartilage from the cuff of an endotracheal tube, or a high tracheostomy tube with erosion of the

figure 4-25 Cuff stenosis of the cervical trachea. A, Anteroposterior high-kilovoltage view demonstrates narrowing of the trachea (arrow). B, Tomographic image reveals circumferential narrowing of the lumen. Note the asterisk in the subglottic space of the larynx.

cricoid, or from a cricothyroidotomy. In a small number of cases, tracheoesophageal fistula may develop, followed by a sudden increase in profuse secretions plus food aspiration.42 These fistulas are best illustrated with a barium swallow. Different types of foreign bodies may lodge in the trachea, especially in young children, followed by recurrent obstructive pneumonitis, if undetected by either radiographic means or bronchoscopy. Foreign body location in the larynx is uncommon but has occasionally been encountered in adults (Figure 4-28).

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