There are several causes of traumatic aortic injury, but the common factor is the violence of the shock. Motor vehicle accidents make up 75–80% of the cases, while motorcycle, aircraft, pedestrian accidents, fall from height, and crush injury to chest account for the remainder [5].

Injury to the aortic wall is likely a result of any or a combination of several potential mechanisms include torsion and shearing forces, rapid deceleration, stretching, increased intravascular pressure (water-hammer effect), and compression of the aorta (osseous pinch) [13, 14] (Fig. 9.4). Osseous pinch results from direct compression of the aorta between the vertebral column and the anterior chest wall (sternum, clavicles, and ribs). Torsion indicates rotational forces of the aorta along its longitudinal axis. Shearing forces are caused by differential relative motion at different points of fixation; at the aortic root, the ligamentum arteriosus attachment, and the diaphragmatic crus, the aorta is connected to other tissues, so it’s submitted to increasing regional strain by different deceleration characteristics of the joined tissues. Stretching of the aorta from displacement of vertebrae is the so-called stretch injury. The water-hammer effect, proposed by Lundevall, results when the flow of a non-compressible fluid is occluded dramatically; this condition leads to high-pressure waves being reflected back along the vessel wall, and it could happen after a compression on the abdomen or lower chest. Sudden deceleration is the most common cause of traumatic aortic injury, and it concerns particularly the front seat passenger of a vehicle going at speeds 100 km/h, (sudden deceleration >32 km/h) subjected to frontal or lateral or rear shock [15]. This mechanism causes displacement of the heart, with torsion and shearing forces against the aorta at levels of relative immobility, mainly the ligamentum arteriosus, aortic root, diaphragm, and intercostal arteries.

Direct penetration from fractured ribs, sternum, vertebrae or from gunshot and stab wounds may also occur. Penetrating injuries to the thoracic aorta are uncommon. When present, they are likely to lead to rapid exsanguination, and many of these patients do not survive transport to the hospital.

Depending on the forces in play, the aorta injury site can be the root, ascending aorta, arch, isthmus, descending aorta, or even abdominal aorta (less common). A considerable number of patients have aortic injury at multiple sites.

The isthmus is the commonest location for lesions (approximately 90% of all cases of patients who have been subjected to thoracic trauma) [16]. Its relatively immobile position in the thorax due to its attachment by the ligamentum arteriosus explains the reason for this site being involved in many injuries (Fig. 9.5).

Lesions of the root of the aorta are sometimes associated with damage to the aortic valve. Lesions of the ascending aorta are rare (between 5 and 8% of the cases) [17] and mainly occur close by the brachiocephalic origin. In contrast, injuries infrequently occur at the proximal portion of the ascending aorta [18]. These two types of lesions are sometimes associated with hemopericardium.

Involvement of the aortic arch and its branches is not so common. While involvement of the aortic arch itself is rare (about 2% of the cases) [18], the incidence of aortic arch branch involvement varies considerably in the literature (about 3% have a combined aortic and aortic branch vessel injury, whereas the great vessels alone are injured in about 16%) [19].

At multidetector CT, a careful search for a branch vessel injury should be performed in the presence of mediastinal hematoma when there is no direct sign of aortic injury. The innominate artery accounts for 50% of these injuries and is the second most common injured vessel after the thoracic aorta [20]. The left common carotid and left subclavian artery account for the remaining injuries. Innominate artery and left carotid injuries almost always occur proximally at the vessel origin; anatomically, this is where the vessel is tightly fixed onto the aortic arch, whereas the distal part is more mobile and flexible (Fig. 9.6).

In contrast, blunt subclavian injuries tend to be more distal; these can be explained by adding the direct force of posterior dislocated clavicles [21].

In 1–12% of the cases, there is trauma to the descending thoracic aorta [17]. The distal descending aorta is attached to the adjacent vertebral column by the diaphragm. When there is a shock to the thorax, the resulting shear forces are responsible for lesions at this site. Injuries to this segment of the thoracic aorta can be associated with diaphragm injury in 10% of cases and with adjacent compression fractures of the thoracic spine [22].

In the abdomen, the most common site of injury is the infrarenal abdominal aorta. These injuries are typically related to lap belt compression. There are a number of additional abdominal injuries that are associated with traumatic abdominal aortic injury, including lumbar spine fracture, splenic injury, pelvic fractures, bowel injury, and solid organ injury. Lumbar spine fracture has the highest association with traumatic abdominal aortic injury [23] and if seen should prompt a careful evaluation of the aorta and vice versa.

Clinical signs and symptoms (Table 9.1) are nonspecific and insensitive for the diagnosis and exclusion of BTAI. A majority of patients with BTAI have no clinical signs of aortic injury until the sudden onset of hemodynamic instability [24].

Symptoms of BTAI are thought to be due to stretching of the mediastinal connective tissues by mediastinal blood and include retrosternal pain, referred interscapular pain, dyspnea, and cough [25].

Clinical signs of BTAI are absent in up to one-third of patients but when present include upper limb hypertension and lower limb hypotension with diminished femoral pulses due to “pseudocoarctation syndrome,” systemic hypotension, systolic murmur, external chest wall injuries, fractures (sternal, rib, or vertebral column), and paraplegia [26].

Therefore, the clinical picture of patients with BTAI varies from asymptomatic to profound shock.

The most important factor in preventing a delay in diagnosis is the arousal of clinical suspicion based on mechanism of injury. Patients sustaining massive chest trauma associated with rapid deceleration (motor vehicle accidents or falls) should carry suspicion of thoracic aortic injury.

A number of artifacts can mimic a traumatic injury of the thoracic aorta.

Diagnostic pitfalls (Table 9.6) can be divided into two categories: anatomic and technical [13, 60].

The classic example of technical pitfall is that of the cardiac pulsation artifact, which is particularly present at the root of the aorta and in the ascending aorta that simulates an intimal pseudo-flap (Fig. 9.28). This image continues in the mediastinal fat giving a blurred interface with the hyperdense lumen of the aorta, which can help with diagnosis. Otherwise, these artifacts can be removed by ECG-gated CT in stable patients if there is any doubt. Breathing and patient movement artifacts can also be found. They are revealed by visualizing the thorax in the lung parenchymal window.

Anatomic pitfalls that can be mistaken for BTAI mainly reside around the level of the isthmus, namely a ductus diverticulum, patent ductus arteriosus, and aortic spindle. The ductus diverticulum, found in 9% of the arteriograms in the adult, is a remnant of the closed or partially closed ductus arteriosus which connects the pulmonary artery to the aorta in fetal circulation. Ductal remnants are located at the inferior surface of the aortic arch near the aortic isthmus which leads to confusing them with BTAIs. Ductus diverticulum has typically smooth, obtuse angles with the aortic wall and are often calcified, whereas BTAI usually is more irregular and steeply angled (Fig. 9.29).

A patent ductus arteriosus is a rarity in itself, and it can be recognized as a tubular structure with regular contours, where the differential of active contrast extravasation in BTAI is usually irregular and situated within hematoma.

Aortic spindles are located just distal to the isthmus and are smooth, regular fusiform mild dilatations of the aorta, without periaortic hematoma (Fig. 9.30).

Branch vessel infundibula can also be confused with a small pseudoaneurysm. They can have a similar appearance to a ductal remnant, but are found at the origin of bronchial or intercostal arteries. They are typically cone shaped and smooth walled with a small artery extending from the apex (Fig. 9.31).