The manubrium and body of the sternum are united by cartilage at the sternal synchondrosis (the angle of Louis). Blunt trauma to the anterior chest wall can result in dislocation at this site (Fig. 13.28).

Fracture of the sternum usually occurs in its body (Fig. 13.29) but may also involve the manubrium (Fig. 13.30). Clinically, the significance of sternal fracture lies in the mortality rate of 25% to 45%,¹⁸ which results not from the fracture per se but from associated injuries within the chest, such as cardiac injury, ATAI, or tracheobronchial injury. Gibson and colleagues¹⁹ reported a 75% incidence of head trauma associated with sternal fractures caused by motor vehicle accidents. Therefore, the clinician must maintain a high index of suspicion regarding the high association of sternal fractures and head trauma so that a sternal fracture, when present, may serve to alert the clinician to possible associated serious intrathoracic injury. The essential radiograph required to establish the diagnosis of sternal injury is the lateral projection, which may easily be obtained with the horizontal beam with the patient recumbent.

The anterior chest wall hematoma associated with sternal dislocation or fracture may produce the appearance of an ill-defined widening of the mediastinum (Fig. 13.29A) on the supine CXR similar to the appearance of the mediastinal hematoma associated with, but not caused by, ATAT. Some very salient observations regarding the relationship between mediastinal width and ATAT must be stated at this point, although these are amplified in greater depth subsequently in this chapter during the discussion of ATAI. In the first place, and contrary to much surgical and radiologic literature, a mediastinal width greater than 8.0 cm, with or without irregular margins, may be simply the normal appearance of the mediastinum due to recumbency. Second, although it has been established that an indirect relationship does exist between the presence of a mediastinal hematoma and acute aortic tear,^{20, 21, 22, 23} the hematoma is evidenced on the plain CXR by specific signs rather than simply “superior mediastinal widening.” The radiographic signs of mediastinal hematoma are described and illustrated in considerable detail later in this chapter in the discussion of ATAI. The CXR illustrated in Figure 13.39A is insufficiently penetrated for

adequate evaluation of the presence of a mediastinal hematoma. It would be a major diagnostic error, if not an actual injustice, to suggest aortography based on the CXR illustrated in Figure 13.29A. Finally, there is no established relationship between sternal injury and aortic injury.

Rib fractures are usually the result of either compression of the chest or a direct blow to the chest wall. The former type of injury, resulting in a decrease in the arc of the ribs, causes an outward break at the site of greatest compression. This “spring fracture” is rarely associated with puncture of the lung. Direct localized trauma to the chest wall, when of sufficient force, results in fracture at the site of impact. In this circumstance, the fracture ends are more likely to penetrate the chest wall, producing a hemothorax or pneumothorax.

Blunt trauma to the chest may produce incomplete, nondisplaced rib fractures that may not be discernible on the initial CXR. If rib fracture is suspected clinically, or if pain persists, radiographs of the ribs obtained in 10 to 14 days will usually demonstrate callus formation at the fracture site, thereby establishing the diagnosis. Except for a densely calcified first costal cartilage (Fig. 13.31), costal cartilage fractures and costochondral separation are not radiographically visible.

Minimally displaced rib fractures or fractures occurring in the arc of the ribs between the anterior and posterior axillary lines are commonly demonstrated only in oblique projections (Figs. 13.32 and 13.33). On the frontal CXR, minimally displaced rib fractures may be heralded by a focal extrapleural hematoma (Figs. 13.33 and 13.34) or small pneumothorax (Fig. 13.35).

Rib fractures are uncommon in children because of the resiliency of the thoracic cage. However,

with a history of appropriate trauma, the possibility of a rib fracture in a child or any of its possible complications (e.g., pulmonary contusion, pneumothorax, or pleural effusion) must be actively considered during assessment of the radiograph (Fig. 13.36). Similarly, blunt thoracoabdominal trauma to a child may cause pulmonary and/or intraperitoneal injury without causing a rib fracture (Fig. 13.37).

Fractures of the upper ribs are uncommon because the upper ribs are protected by the clavicle, scapula, and large muscle masses of the anterior and posterior chest walls. When present, either alone or in conjunction with fracture of the bones of the shoulder girdle, these fractures indicate simply an injury of considerable force. Contrary to an opinion frequently cited in surgical and radiographic literature, upper (thoracic inlet) rib fractures are not associated with an increased incidence of aortic injury. In fact, Fisher and colleagues,²⁴ in a study of approximately 200 patients, clearly demonstrated that there is no statistically significant difference in the frequency of acute aortic brachiocephalic arterial injury between patients with or without thoracic inlet rib fractures. Lee and colleagues,²⁵ in a comparative analysis of 62 patients with ATAT and 486 without ATAT, found that although fracture of the rib(s) was the most common thoracic skeletal injury associated with ATAT, “the positive predictive value of rib fractures in evaluating ATAT was only 14.7%, a rate similar to the incidence of ATAT at most trauma centers,” and therefore of no value in determining who should have CTA or traditional aortography.

However, because of the magnitude of the causative force, upper rib fractures are commonly associated with pneumothorax or hemothorax, subcutaneous emphysema, pulmonary contusion, and

scapular fractures. All these associated injuries, in addition to the complex normal skeletal anatomy of the thoracic inlet, make the recognition of inlet rib fractures radiographically difficult (Fig. 13.38).

The lower ribs, being less securely attached anteriorly, are more mobile and less susceptible to fracture by blunt trauma. However, these ribs may be fractured by a forceful direct blow and, when such a fracture occurs on the left, splenic and/or renal injury should be automatically considered, and lower rib fractures on the right should prompt an automatic consideration of hepatic and/or renal injury.

Flail chest is defined as segmental fractures of three or more consecutive ribs. Segmental fracture refers to two fracture sites in the same rib, resulting in a separate fragment that is free floating. It is taught that flail chest is clinically diagnosed by recognition of paradoxical movement of the flail segment during respiration due to chest pain. The clinical difficulty with this concept is that the paradoxical movement is very difficult to observe even under optimum conditions and particularly in patients with shallow respirations, in heavily muscled or obese patients, or in women with large breasts. Consequently, the primary responsibility for identification of a flail chest rests with the radiologist. That responsibility is not easily discharged because the diagnosis must almost invariably be made from a single supine CXR. Usually, the patient’s condition precludes obtaining oblique radiographs of the ribs. Additionally, because of the chest trauma, the examination will have been obtained in relative hypoventilation. Pulmonary contusion, pneumothorax, pleural effusion, and subcutaneous emphysema, commonly present, further obscure rib delineation. Therefore, in patients with major blunt thoracic or thoracoabdominal trauma, the presence of multiple rib fractures must prompt a diligent search for segmental rib fractures. Recognition of flail chest is of clinical significance because of its effect on pulmonary physiology, which is usually also adversely affected by pulmonary contusion or hemopneumothorax. Figures 13.39, 13.40 and 13.41
illustrate the difficulty in identifying the segmental fractures of flail chest as well as the evidence of the magnitude and diffusion of the force required to produce flail chest, such as the number of ribs fractured, pulmonary contusion, and the frequently associated clavicular and scapular fractures.

Harris and Harris²⁶ reported that scapular fractures were missed on the initial emergency center CXR in 43% of 100 patients with major blunt thoracic trauma. In 72% of the missed scapular fractures, the scapular fracture was visible on the initial supine CXR but may have been obscured by rib or clavicular fractures, pulmonary contusion, pleural effusion, subcutaneous emphysema, radiograph identification labels, or monitoring leads. Before 1984, when Hardegger and colleagues²⁷ advocated open reduction and internal fixation of fractures of the glenoid fossa or scapular neck as the preferred treatment for these injuries, the failure to diagnose a scapular fracture did not significantly adversely affect patient care. Because it is customary to treat all the orthopedic injuries requiring surgical management at the same time and because open reduction and internal fixation is now the treatment of choice for displaced glenoid fossa and neck fractures, it is very important that scapular fractures be identified on the initial emergency center CXR. Consequently, instead of clavicular and upper rib fractures, pulmonary contusion, and subcutaneous emphysema being offered as excuses for not recognizing scapular fractures, these same injuries should be considered as indicators for a diligent search for scapular fractures.

Lee and colleagues²⁸ reported that although three or more rib fractures in patients 14 years or older carried an increased risk of splenic or hepatic injury, there was no association between the number of rib fractures and aortic injury.

Sternoclavicular dislocation is a rare injury, accounting for less than 1% of all types of dislocations.²⁹ The dislocation is usually posterior and may be caused by indirect trauma applied to the posterolateral aspect of the shoulder by a force that drives the lateral end of the clavicle anteriorly. The
taut costoclavicular ligament, acting as a fulcrum, causes the medial end of the clavicle to be levered posteriorly.³⁰ In our experience, however, the more common mechanism of injury is massive direct trauma to the anterior chest wall, driving the medial end of the clavicle posteriorly or posterolaterally (Fig. 13.42). Posterior dislocation at the left sternoclavicular joint is particularly clinically important because of the proximity of the left subclavian vein. Clinically, patients with sternoclavicular dislocation have a large hematoma and ecchymosis of the upper anterior chest wall and asymmetry of the clavicles to palpation. Radiographically, the dislocation is difficult to diagnose on the AP CXR because displacement is usually minimal (Figs. 13.43 and 13.44), because the normal sternoclavicular anatomy may appear altered simply by rotation of the chest (Fig. 13.43A), and because of superimposed skeletal structures (Fig. 13.44). The dislocation is usually recognizable in a straight supine CXR by lateral displacement of the proximal end of the clavicle (Fig. 13.45) or by asymmetry of the proximal ends of the clavicle (Fig. 13.43A). The quickest and most accurate method to examine the sternoclavicular joint is by CT (Figs. 13.43B and 13.45B).

Blunt chest trauma may cause pulmonary laceration, hematoma, and/or contusion. Of these, pulmonary contusion is the most common, reported to occur in 30% to 75% of blunt chest trauma patients.³¹ In a review of 144 consecutive patients with pulmonary contusion and/or flail chest, isolated flail chest and pulmonary contusion each had a mortality rate of 16%. In combination, the mortality rate increased to 42%.³² Pulmonary contusion may occur without rib fractures,^{31, 33, 34} particularly in children in whom the chest wall is more compliant than in adults.³⁵

Pulmonary contusion is the result of compressive force to the lung parenchyma at the time of impact and of a negative force applied to the lung during recoil after the causative force is dissipated.
Both of these forces result in alveolar and interstitial hemorrhage and edema.^{35, 36, 37} The contusion may be focal and mild (Fig. 13.46) or extensive and severe (Fig. 13.47). Pulmonary contusion is usually mild, usually clears without producing significant respiratory disturbance, and may be clinically masked by other conditions such as flail chest, pneumothorax, or hemothorax. Even when severe, the extent and significance of the lesion, which may not initially be appreciated either clinically or radiographically, is recognized only by arterial PO₂ levels reflecting hypoxia. Therefore, early in the post blunt chest trauma state, alteration of arterial blood gas values is the most sensitive indicator of the presence of pulmonary contusion.

Pathophysiologically, the blast effect of blunt chest trauma, which compresses the lung tissue, results in parenchymal hemorrhage and edema. When the initiating force is released, the lung rebounds, producing an abrupt negative pressure on the already damaged lung tissue. The hemorrhage occurs at the alveolar-capillary level, resulting in both intra-alveolar and interstitial extravasation of blood and edema. The ensuing cellular response to tissue damage combines with the hemorrhage and edema to produce a progressive O₂ diffusion barrier and hypoxemia, which may initially be paradoxical with respect to the clinical and radiographic appearance of the patient and which may become progressively more severe.

The natural history of uncomplicated pulmonary contusion is a dynamic process, with the area of contusion becoming progressively more extensive during the initial 24 hours, followed by a gradual clearing during the 48 to 72 hours after injury. This sequence is reflected radiographically in Figures 13.48 and 13.49. Consequently, the radiographic appearance of pulmonary contusion will vary not only with the magnitude of the causative force but also with the length of time between injury and the initial CXR. Because today’s efficient patient transport systems frequently deliver the traumatized patient to the emergency center within an hour of the time of injury, the initial CXR may be negative for signs of pulmonary contusion. Conversely, the CXR of a patient seen initially several hours following blunt chest trauma will demonstrate well-established changes of pulmonary contusion (Fig. 13.50).

The radiographic signs of pulmonary contusion may not be present immediately but are visible in 70% of cases within 1 or 2 hours after injury.³¹ In the remaining 30%, radiographic evidence of pulmonary contusion may not appear until 6 to 24 hours after injury.^{31, 34} For this reason, serial radiographs of the chest are indicated in patients whose initial chest examinations do not demonstrate changes of pulmonary contusion following significant blunt chest trauma.

In patients with massive blunt chest trauma, the radiographic signs of pulmonary contusion will be positive on the initial supine chest radiograph (Fig. 13.39). The characteristic radiographic appearance of pulmonary contusion consists of patchy, illdefined areas of parenchymal density that may be either solitary and localized (Fig. 13.49), multiple, or diffuse (Fig. 13.51). Multiple foci of contusion in adjacent portions of the lung may coalesce. The area of contusion does not respect anatomic divisions of the lung, and therefore, the changes of pulmonary contusion on CXRs do not coincide with any of the anatomic divisions of the lung.

MDCT accurately reflects the pathophysiology of pulmonary contusion (Fig. 13.46B). On CT, the pulmonary contusion is peripheral and commonly contiguous with the adjacent pleura, involves adjacent segments and/or lobes of the lung without regard for segmental or lobar anatomic divisions, is variable in its degree of involvement, and shows signs of both airway and parenchymal involvement.

Complications of pulmonary contusion include pneumonia, pulmonary hemorrhage (hematoma), and traumatic pulmonary pseudocyst formation. Pneumonia is usually a relatively late complication and is associated with the usual clinical signs of pulmonary infection. Radiographically, postcontusion pneumonia resembles any other bacterial pneumonia except that in this instance, there is a direct radiographic continuum from the initial contusion to the subsequent area of inflammatory consolidation.

Pulmonary hematoma is a collection of blood in an area of pulmonary laceration. The hematoma is probably not a complication of the contusion per se but more likely was present at the time of initial chest trauma but was marked by the more extensive contusion and only became radiographically visible as the contusion cleared (Fig. 13.49). Pulmonary hematoma is usually described as a flame-shaped area (Figs. 13.49 and 13.52) of increased density that persists after the surrounding


contusion clears. The hematoma may be visible on the initial CXR and distinguished from the surrounding contusion as a sharply defined area of homogeneous density within the contusion (Fig. 13.53).

The final complication of pulmonary contusion is the development of single or multiple thin-walled, air-filled spaces within the area of pulmonary contusion referred to as posttraumatic pneumatocele (Fig. 13.54).^{38, 39} Ellis⁴⁰ referred to these lesions as “cysts.” Santos and Mahendra⁴¹ recommend the term “traumatic pulmonary pseudocyst” because the pathologic definition of a cyst requires an epithelial lining, which these evanescent lesions do not have, and because the term pneumatocele has historically been associated with pneumonia. The important aspects of traumatic pseudocysts are that although they usually occur 4 to 5 days after closed chest trauma,⁴² they may rarely be present on the initial CXR. They resolve spontaneously, do not require extensive workup, and do not require surgical intervention.⁴¹

As a reminder that the chest and abdomen must be considered as a single entity in the presence of blunt thoracic or thoracoabdominal trauma, basilar
pulmonary contusion may be the most obvious radiographic finding in patients with lower rib fractures and intra-abdominal injury (Fig. 13.55). It must be apparent that pulmonary contusion may occur without rib fractures in both children (Fig. 13.50) and adults (Fig. 13.56). Finally, pulmonary contusion may resemble aspiration pneumonia in its radiographic appearance. However, the distinction may reasonably be made on the basis that aspiration pneumonia is usually more central, is of greater density medially than peripherally, and is limited to bronchial distribution(e.g., subsegmental or segmental). Pulmonary contusion, on the other hand, is usually more peripheral within the lung, is more dense laterally than medially, and does not respect the segmental or lobar anatomy of the lung (Figs. 13.46, 13.56, and 13.57).

This section is devoted to the pathology and radiographic appearance of air in abnormal spaces within the chest (e.g., pneumothorax,
pneumomediastinum, paramediastinal pneumatocele, pneumopericardium). The radiographic appearance of air within these different spaces is peculiar to each, but within each space, the appearance of the air is the same whether the mechanism of injury is traumatic or nontraumatic. Therefore, the radiographic signs of abnormal air collections caused by both traumatic and nontraumatic etiologies are discussed together.

Air in the pleural space is usually the result of blunt or penetrating trauma that causes a tear in the visceral pleura, allowing air to collect within the pleural space. Pneumothorax secondary to blunt trauma most commonly results from a rib fracture that pierces the visceral pleura, but it may result from an abrupt increase in intra-alveolar pressure against a closed glottis with consequent rupture of a bleb or peripheral bulla. “Spontaneous” (nontraumatic) pneumothorax most commonly results from a rupture of alveolar blebs immediately beneath the visceral pleura. In more than 50% of patients, the etiology of the rupture is unknown. Many diseases may be associated with spontaneous pneumothorax, including such disparate conditions as spasmodic asthma, staphylococcal pneumonia, and pulmonary metastatic disease (Fig. 13.58).

A “closed” pneumothorax occurs when the chest wall is intact. An “open” pneumothorax, also referred to as a “sucking” wound of the chest, indicates direct communication between the ambient air and the pleural space. Pneumothorax may
also be classified based on magnitude of collapse as marginal (Fig. 13.35), moderate, or massive (Fig. 13.59).⁴³

Conventional chest radiography—preferably erect PA and lateral projections, but even supine AP CXR—demonstrates most pneumothoraces and is the initial imaging modality of choice for this purpose. “Occult” pneumothorax is discussed subsequently in this section.

The radiographic diagnosis of pneumothorax depends on demonstration of the very thin, curved linear density of the visceral pleura with the lucency of air in the pleural space interposed between the visceral pleura medially and the parietal pleura and chest wall laterally. Obviously, there will be neither parenchymal nor vascular markings beyond the visceral pleura. When the magnitude of collapse is moderate or massive or when an associated hemopneumothorax or hydropneumothorax produces an air-fluid level within the pleural space (Fig. 13.60), the diagnosis is readily apparent.

The diagnosis of marginal pneumothorax may be exceedingly difficult because of superimposed skeletal shadows or the inherent difficulty in perceiving the faint density of the visceral pleural surface. The pneumothorax may be enhanced in a PA radiograph obtained during forced expiration (Figs. 13.6 and 13.61). The basis of this phenomenon is that the collapsed lung decreases in volume during expiration while the air in the pleural space stays constant. Consequently, the lung “falls away” from the chest wall, rendering the pneumothorax more obvious. Other maneuvers to demonstrate pneumothoraces include placing the supine patient in the semierect (Fig. 13.7), erect (Fig. 13.62), or lateral decubitus position with the suspected side up in which event the pleural air will migrate to the uppermost portion of the pleural space. If the patient cannot be moved from the supine position, a horizontal beam lateral CXR may, and CT will, demonstrate air in the anterior pleural space.

The “deep sulcus” sign (Fig. 13.63) refers to an increase in the depth and width of the costophrenic angle associated with air in the pleural space and is an extremely valuable sign of a pneumothorax that is not visible on a poor quality radiograph. The deep sulcus sign may be the only indicator of pneumothorax on a supine CXR (Fig. 13.64).