Traumatic rupture of the aorta alone accounts for 16% of fatalities resulting from motor vehicle crashes, and 85% to 90% of patients with traumatic aortic rupture die before reaching a medical facility (6). In clinical series, 90% of aortic ruptures occur at the aortic isthmus, just distal to the origin of the left subclavian artery (7,8,9,10) (Fig. 8-1). A few aortic injuries (1% to 3%) involve the descending thoracic aorta, typically at the level of the diaphragm (Fig. 8-2). Chest radiographic signs of aortic injury lack sensitivity and specificity. The most sensitive (but not specific) radiographic signs are widening of the mediastinum and loss of definition of the aortic arch (Table 8-1) (11). A normal chest radiograph has a high negative predictive value (98%) but a low positive predictive value for aortic injury.

At many institutions, contrast-enhanced, thin-section CT scanning (3 mm collimation or less with overlapping reconstructions) has replaced conventional aortography in evaluating patients for aortic injury. If mediastinal hemorrhage is present, unless it is minimal and not centered around the aorta (Fig. 8-3), without any direct signs of aortic injury, and if no other explanation for the hemorrhage is shown on CT, the patient is generally referred for conventional angiography. If any direct signs of aortic injury are confirmed on CT, including (a) aortic caliber change at the site of injury (pseudoaneurysm or pseudocoarctation), (b) abnormal or irregular aortic wall or contour, (c) intraluminal irregularities or areas of low attenuation (clot, linear intimal flap), (d) intramural hematoma or dissection, and (e) active extravasation of contrast, the patient may or may not proceed to confirmatory conventional angiography at the discretion of the surgeon (Fig. 8-4). Not only is CT useful for detecting direct signs of aortic injury, but CT can also show other causes of a wide mediastinum, including excessive mediastinal fat (Fig. 8-5), paramediastinal atelectasis or pleural effusion, residual thymic tissue, adjacent lung injury (Fig. 8-6), artifact caused by supine positioning, vascular tortuosity, vascular anomalies, lymphadenopathy, and persistent left-sided superior vena cava (12).

Potential pitfalls in CT interpretation include hemomediastinum caused by sternal or vertebral body fracture, left pleural effusion with left lower lobe subsegmental atelectasis "surrounding" the aorta, pulsation artifacts, atherosclerotic plaques, prominent ductus arteriosus, and pseudointimal flaps secondary to volume averaging of the left brachiocephalic vein
as it crosses in front of the aortic arch. These pitfalls have become less of a problem with the use of multidetector CT and fast scanning techniques.

Occasionally, a chronic pseudoaneurysm can pose diagnostic difficulties. Fewer than 5% of patients will survive long term with an unrepaired pseudoaneurysm (13). Calcification of the wall of the aneurysm and a history of prior thoracic trauma indicate an old aortic injury (Fig. 8-7).

Great vessel injuries (with or without concomitant aortic tear) occur in 1% to 2% of patients with blunt chest trauma (14). A perivascular superior mediastinal or low cervical hematoma, especially in the presence of upper rib fractures or posterior sternoclavicular dislocation, should prompt concern for great vessel injury and injury to other structures in the thoracic inlet (Fig. 8-8).

Abnormal lung parenchymal opacification in trauma patients can result from atelectasis, aspiration, edema, pneumonia, and lung injury (contusion and laceration) and is commonly multifactorial in etiology. Pulmonary contusion ("lung bruise") results in leakage of blood and edema fluid into the interstitial and alveolar spaces. Pulmonary laceration is a more severe injury that causes disruption of the lung architecture.

CT is more sensitive than radiography in demonstrating contusions and lacerations (15,16,17,18,19,20,21,22). On both chest radiography and CT, pulmonary contusions present as areas of airspace opacity, ground-glass opacification, or both, which tend to be peripheral, nonsegmental, and geographic in distribution (Fig. 8-9). Isolated pulmonary contusion in young, healthy patients is not associated with increased mortality (23). Contusions are evident at presentation or within 6 hours after trauma, and they resolve, usually without permanent sequelae, within 5 to 7 days. Pulmonary laceration, on the other hand, may initially be masked by coexistent contusion and other forms of chest injury on the initial radiograph or CT scan, and it generally takes weeks to months to resolve, sometimes with residual scarring (Fig. 8-10). Lung laceration results in tearing of the lung parenchyma and formation of a cavity filled with blood (hematoma), air (pneumatocele), or both. The radiographic or CT diagnosis of lung laceration is based on the presence of a localized air collection within an area of airspace opacity in the setting of acute chest trauma (20) (Fig. 8-11). Both contusions and lacerations tend to occur adjacent to solid structures, such as the ribs and vertebral bodies (Fig. 8-12).

Fat embolization syndrome is characterized by abnormal diffuse lung opacification on chest radiography, dyspnea, mental status changes, and a petechial rash occurring 12 to 72 hours after trauma. Occurring most commonly after long bone fractures, fat embolization syndrome results when fat droplets


from bone marrow are released into the circulation and occlude capillaries. The patient's symptoms are caused by the decrease in perfusion to various organs from capillary occlusion. In the lungs, chemical pneumonitis ensues as a result of lipolysis and release of free fatty acids, which does not occur immediately after trauma and accounts for the 12- to 72-hour delay in clinical signs and symptoms. The chest radiograph initially appears normal but develops patchy opacities and then widespread diffuse opacity within 72 hours of injury. The pulmonary opacity resembles alveolar pulmonary edema from other causes, with perihilar and basilar predominance and sparing of the lung apices (24) (Fig. 8-13). With fat embolization syndrome, the pulmonary opacity does not clear with diuresis. Contusion is generally seen earlier than fat embolization syndrome on the chest radiograph, and it clears more rapidly (5 to 7 days). Pulmonary opacity from fat embolization syndrome can take 7 to 10 days to clear.

The incidence of tracheobronchial injury (TBI) is reported as 0.4% to 1.5% in clinical series of major blunt trauma (25). Blunt trauma must be severe to cause airway rupture, and injury to other structures such as the thoracic cage, lungs, and great vessels is likely. When the intrathoracic trachea or bronchi are injured, the aorta is the most commonly associated injured structure (26). TBI is associated with a 30% overall mortality


rate, mostly from associated injuries (27). Failure to recognize TBI may result in death or allow cicatrization to occur at the site of injury, with airway obstruction arising days or months after initial injury (Fig. 8-14). More than 80% of TBIs occur within 2.5 cm of the carina (28,29).

Rupture of the cervical trachea may occur as a "clothesline injury" when the neck is extended on high-speed contact with ropes, wires, or cables by individuals riding many types of recreational vehicles or running. Tracheal laceration may also occur in a motor vehicle crash when the neck of a driver strikes the top of the steering wheel, compressing the airway against the spine.

Pathologically, tracheal injury most commonly presents as a transverse tear between the tracheal rings or a longitudinal tear in the posterior membranous segment. Complete separation of the trachea may occur, but airway continuity can still be maintained by peritracheobronchial tissue. Injury to the mediastinal trachea or major bronchi produces
pneumomediastinum that rapidly extends into the neck and face, shoulders, and chest wall (Fig. 8-15). Pneumomediastinum is a more specific sign of TBI than is pneumothorax, since pneumothorax is commonly seen with rib fractures. Pneumothorax is seen in 60% to 100% of cases of TBI (30), but it may not be present if the outer adventitial sleeve of the bronchus remains intact and there is no air leak (31). In most cases, pneumothoraces will respond to chest tube placement, so re-expansion of the lung does not exclude tracheobronchial injury. However, a pneumothorax that does not resolve with functioning tube drainage is the sine qua non of mediastinal airway injury (32).

An indication of tracheal tear is elevation of the hyoid bone above the level of C3, as seen on a lateral radiograph of the cervical spine (33). This occurs as a result of injured infrahyoid musculature, causing unopposed elevation of the hyoid bone by suprahyoid musculature. Another sign of tracheal transection is acute overdistension of the endotracheal tube cuff, to the point where it exceeds the normal diameter of the trachea (Fig. 8-16). In tracheal rupture, the balloon may approach the endotracheal tube tip as a result of distal expansion of the balloon in the tear, with partial herniation of the balloon in the tear as the tube moves in the airway or is repositioned (34) (Fig. 8-17).

The "fallen lung sign" (35) is a rarely seen but highly suggestive sign of bronchial tear that can be seen on chest radiographs and CT (Figs. 8-18 and 8-19). This sign refers to the lung falling laterally and posteriorly in supine positioning and falling inferiorly away from the hilum in the upright position. Normally with a pneumothorax, the lung recoils inward toward the hilum.

Acute diaphragmatic rupture occurs in 1% to 7% of patients following major blunt trauma (36,37,38), and the diagnosis is missed on initial presentation in up to 66% of patients (39,40,41,42,43,44,45). Seventy-five percent to 95% of patients with acute diaphragm rupture have abnormal chest radiographs, but only

17% to 40% have highly suggestive radiographic findings (46,47,48). Chest radiographic findings of rupture include a normal appearing diaphragm, pneumothorax, displacement of stomach, liver, spleen, colon, or small bowel into the thorax (Fig. 8-20), superior displacement of an intragastric nasogastric tube (Fig. 8-21), pleural effusion, basilar opacity causing inability to visualize the diaphragm, apparent elevation of the diaphragm, an irregular or lumpy diaphragm contour, fractures of the lower ribs, and contralateral shift of the mediastinum in the absence of a large pleural effusion or pneumothorax (Table 8-2) (49). Rupture of the right hemidiaphragm probably occurs with almost the same frequency as rupture of the left hemidiaphragm, although most clinically recognized diaphragm injuries occur on the left. If diaphragm rupture is not promptly diagnosed, the patient may remain asymptomatic or develop incarceration of herniated abdominal viscera, which can occur at a time remote from the incidence of trauma (Fig. 8-22).

Multidetector CT has been shown to be useful in making the diagnosis of acute diaphragm rupture, and it is superior to conventional CT because volumetric data acquisition provides high-quality sagittal and coronal reconstructions. Acquisition of data during a single breath-hold decreases slice misregistration (50). Individual diagnostic sensitivity for detecting diaphragmatic rupture on CT scanning is 54% to 73%, and specificity is 86% to 90% (51). Most injuries involve the posterolateral aspect of the diaphragm. Direct CT findings associated with acute rupture include diaphragmatic discontinuity (Fig. 8-23), intrathoracic herniation of abdominal contents, and waistlike constriction of bowel ("collar sign") (Fig. 8-24). In addition, Bergin et al (52) have described the "dependent viscera" sign in CT diagnosis of blunt traumatic diaphragmatic rupture. This sign refers to the upper one third of the liver abutting the posterior right ribs or the bowel or stomach lying in contact with the posterior left ribs. Associated CT findings of diaphragm rupture include liver laceration, hemoperitoneum, hemothorax, splenic laceration, renal contusion, lower lobe atelectasis, and lower rib fractures. Although focal discontinuity of the diaphragm is a direct sign of diaphragmatic rupture, it should be noted that there is a normal increase in diaphragmatic defects with age that is not related to trauma (53) (Fig. 8-25).

Injury to ribs, clavicles, scapulae, sternum, and spine can occur as a result of blunt chest trauma. Thoracic spine fractures account for 16% to 30% of all spine fractures and result in complete neurologic deficits in approximately 60% of patients (54,55). A supine chest radiograph provides an opportunity to evaluate the thoracic spine, but optimal evaluation requires dedicated frontal and lateral collimated radiographs or CT. Seventy percent to 90% of spine fractures can be seen on conventional radiographs. Findings include cortical disruption and abnormal vertebral body size, shape, opacity and location. CT and magnetic resonance (MR) imaging may show otherwise occult fractures and are the only ways to directly evaluate the integrity of the spinal cord and the intervertebral ligaments (3). CT and MR are more helpful in distinguishing unstable burst fractures from stable, simple, anterior wedge compression fractures (56).

Fractures to the upper ribs, clavicle, and upper sternum are important in that they may be accompanied by brachial plexus or vascular injury in 3% to 15% of patients (57). Fractures of the lower ribs should increase suspicion of splenic, hepatic, or renal injury, which can be confirmed with CT. Fractured rib ends may lacerate the pleura or lung, with resultant pulmonary hematoma, hemothorax, or pneumothorax. Fracture of five contiguous ribs or segmental fractures of three or more adjacent ribs (a single rib fractured in two or more locations) can result in paradoxic motion of a "flail" segment during the respiratory cycle, which can impair respiratory mechanics and result in atelectasis and pulmonary infection (Fig. 8-26).

Sternal fractures, which occur in 8% of major thoracic trauma admissions (12), may be associated with myocardial contusion and are often clinically silent. These fractures cannot be visualized on frontal chest radiographs and may be relatively inconspicuous on lateral chest radiographs, but they are usually readily identified on CT. Most (58% to 80%) sternal fractures occur in the upper or midbody of the sternum (4) and are often associated with retrosternal hematoma (Figs. 8-27 and 8-28). The presence of a fat plane between the hematoma and the aorta implies that the hematoma is not aortic in origin.

Posterior dislocation of the clavicle can result in injury to the great vessels, superior mediastinal nerves, trachea, and esophagus. Although sternoclavicular dislocations can be demonstrated using angled chest radiographs, they are more easily detected with CT (14) (Fig. 8-29).

Scapular fractures are diagnosed on the initial chest radiograph in only a little more than half of patients (58). When scapular fractures are not seen on the initial chest radiograph,
they are visible in retrospect in 72% of cases, not included on the examination in 19%, and obscured by superimposed structures or artifacts in 9% (58) (Fig. 8-30). CT of the chest, especially if used in combination with conventional radiographs, should demonstrate most scapular fractures. Clavicle fractures are common in injured patients and are usually of minimal clinical consequence.

Pneumothorax is seen on chest radiography in almost 40% of patients with blunt chest trauma and in up to 20% of patients with penetrating chest injuries (59,60). The most common cause in blunt trauma is assumed to be a rib fracture that penetrates the visceral pleura; however, pneumothorax in the absence of rib fractures is occasionally seen in adults and is commonly seen in children. Pleural air will rise to the most nondependent portion of the thorax: at the apex in the upright patient and at the anterior, caudal aspect of the pleural space in the supine patient. Radiographic signs of pneumothorax in the supine patient include (a) the deep sulcus sign, which is a deep, lucent costophrenic sulcus (Figs. 8-31, 8-32, 8-33); (b) a relative increase in lucency at the affected lung base; and (c) the double diaphragm sign, which is created by the interfaces between the ventral and dorsal portions of the pneumothorax with the anterior and posterior aspects of the hemidiaphragm. CT is much more sensitive for diagnosing pneumothorax in the supine patient than is chest radiography (61,62) and identifies pneumothoraces that cannot be seen on conventional supine radiographs in 10% to 50% of patients who have sustained blunt trauma to the chest (61,62,63).

Pneumomediastinum may occur in association with pneumothorax. It can be diagnosed on chest radiographs by the
presence of abnormal lucencies in the mediastinum that highlight the contours of the aorta and pulmonary artery and displace the mediastinal pleura laterally, and by the "continuous diaphragm sign," which is produced by the presence of air between the pericardium and the diaphragm. Pneumomediastinum can be easily identified on chest CT and may signal the presence of an underlying laceration of the pharynx, esophagus, or tracheobronchial airway.

Pleural effusions that develop in the acute posttraumatic setting usually represent hemothorax, and a rapidly expanding pleural effusion is most likely to be caused by arterial bleeding. CT can be helpful in distinguishing hematoma from other pleural collections by showing the high CT attenuation of blood (64) (Fig. 8-34). Rupture of the thoracic duct, which is uncommon, produces chylothorax, with milky fluid recovered through thoracentesis. Rupture of the thoracic duct in the lower thorax produces right-sided chylothorax, whereas rupture above the level where the thoracic duct crosses the midline in the midthorax produces left-sided chylothorax. CT is superior to chest radiography in distinguishing pleural fluid from other causes of radiographic density, such as atelectasis, parenchymal injury, or pneumonia, and it can show loculation of pleural fluid and delineate complex pleuroparenchymal opacities.

The heart and pericardium are fairly well protected from nonpenetrating injury, and documented traumatic injury is uncommon. The chest radiograph plays a relatively minor role in the evaluation of myocardial injury. Its greatest value is in detecting associated injuries, such as rib fractures, sternal fractures, and pulmonary contusion.

Rapid accumulation of blood in the pericardial space can cause cardiac tamponade and severe hemodynamic compromise. Bedside sonographic evaluation of the heart is the method of choice to quickly and noninvasively detect pericardial fluid. CT is also very sensitive for detecting pericardial fluid and may indicate pericardial hemorrhage, as determined by the high CT attenuation of the fluid (Fig. 8-35). A CT density exceeding 35 Hounsfield units differentiates hemopericardium from transudative pericardial effusions. Cardiac tamponade is suggested by CT findings of distension of the vena cavae, hepatic veins, and renal veins and by development of periportal edema within the liver (14).

Interventricular septal rupture and damage to the mitral valve apparatus can result in congestive heart failure. Mitral regurgitation from the latter may cause asymmetric pulmonary edema, classically of the right upper lobe as a result of the direction of the regurgitant jet. Pneumopericardium can occur when air enters through a pericardial disruption in the presence of pneumothorax (Fig. 8-36).

Cardiac contusion may result from blunt chest trauma in 8% to 76% of patients (65,66). The diagnosis is usually made from electrocardiography, nuclear cardiac imaging, or echocardiography. The right ventricle is the most frequently injured, as it comprises almost three times more exposed anterior surface of the heart than does the left ventricle (14). Chest radiography and CT can show sequelae of cardiac contusion, such as congestive heart failure, ventricular aneurysm, or massive cardiac enlargement.

Esophageal tears are more common in patients with penetrating trauma and occur in fewer than 1% of blunt trauma cases (67). Thoracic esophageal tears from trauma are caused almost exclusively by gunshot wounds (16). Esophageal disruption can occur from crushing of the esophagus between the spine and trachea, traction from hyperextension, and direct penetration by cervical spine fracture fragments (68). Most tears occur in the cervical and upper thoracic esophagus, but they also may occur just above the gastroesophageal junction. The thoracic esophagus lies to the left of the trachea at the thoracic inlet but moves to the right as it passes posterior to the aortic arch at the level of the carina. The esophagus crosses back to the left as it enters the stomach. Accordingly, ruptures of the mid- to distal esophagus usually present with a right-sided pleural effusion, and effusions caused by rupture at the gastroesophageal junction occur more commonly on the left.

Chest radiography in patients with esophageal rupture can show persistent severe pneumomediastinum or pneumothorax, pleural effusion, a widened paraspinal line, and retrocardiac lung opacification. CT scans can show similar findings, in addition to leakage of oral contrast from the disrupted esophagus into the mediastinum or pleural space and changes of mediastinitis. The areas of greatest esophageal thickening on CT often
represent the level of perforation. The perforation itself, however, may be obscured by edema, and hemorrhage and is usually not visualized. The diagnosis is confirmed at fluoroscopy using water-soluble contrast material or with endoscopy.

The chest wall has a rich vascular network established by the intercostal and internal mammary arteries. Rib fractures can lacerate intercostal arteries or veins, tear intercostal muscles, or result in bleeding from the raw surface of the bone. In addition, branches of the lateral thoracic artery that supply the pectoral muscles and anastomose with chest wall vessels can be lacerated and bleed. A large amount of blood can collect in the subcutaneous or extrapleural spaces of the chest, especially in the elderly because of skin and subcutaneous tissue laxity. CT scanning can easily distinguish chest wall from parenchymal or mediastinal injury, whereas this differentiation may not be possible with chest radiography. On CT, soft tissue hematomas of the chest wall are readily distinguished from parenchymal injury, and subcutaneous air is distinguished from pneumothorax. CT scanning shows broncho-pleural-cutaneous fistulae, which may not be appreciated on the chest radiograph (Fig. 8-37). Trauma to the breast, which often results in bleeding and hematoma formation, can be produced by a combination of compression and shearing stress produced by a seat belt (Fig. 8-38).

CT scanning is superior to chest radiography in demonstrating pneumothoraces, hemothoraces, pulmonary contusions, and fractures. CT obviates the need for conventional aortography in many patients, and in many institutions CT aortography has become the new gold standard for the diagnosis of acute aortic injury. CT provides a look at the entire chest in addition to the aorta, which is a distinct advantage over conventional aortography. In addition to showing fractures, CT also shows related soft tissue injuries, such as great vessel injury from fracture-dislocation of the clavicle and splenic/liver laceration from adjacent rib fractures. In some cases, CT shows direct signs of tracheobronchial, esophageal, or diaphragmatic injury. Chest CT can be performed quickly on all trauma patients who are referred for abdominal CT as a means of detecting serious chest injuries early.