The aorta is the largest artery in the body. Each minute, it carries several liters of blood, originating directly from the heart, which subsequently is transported throughout the rest of the body. Aortic rupture is typically the result of a blunt aortic injury in the context of rapid deceleration. After traumatic brain injury, blunt aortic rupture is the second leading cause of death following blunt trauma. Thus, this condition is commonly fatal as blood in the aorta is under great pressure and can quickly escape the vessel through a tear, resulting in rapid hemorrhagic shock, exsanguination, and death. Timely diagnostic evaluation and definitive treatment are critical for survival. Injury mechanism, clinical stability, and associated traumatic injuries all interplay in the timing and method of aortic transection repair.
Traumatic aortic transection or rupture is associated with a sudden and rapid deceleration of the heart and the aorta within the thoracic cavity. Anatomically, the heart and great vessels (superior vena cava, inferior vena cava, pulmonary arteries, pulmonary veins, and aorta) are mobile within the thoracic cavity and not fixed to the chest wall, unlike the descending abdominal aorta. Injury to the aorta during a sudden deceleration commonly originates near the terminal section of the aortic arch, also known as the isthmus. This portion lies just distal to the take-off of the left subclavian artery at the intersection of the mobile and fixed portions of the aorta. As many as 80% of patients with aortic transection die at the scene before reaching a trauma center for treatment. For those individuals who survive the initial injury and reach an emergency department, 30% will succumb to their injury within the first 24 hours. Patients that do survive have sustained either incomplete or non-circumferential lesions to the intima and media. The tunica adventitia, or outermost vessel wall, and mediastinal pleura can prevent free rupture in this clinical scenario. These types of injuries are typically the result of high-energy impacts most commonly following motor vehicle crashes (81%) but also motorcycle and aircraft crashes, automobile versus pedestrian collisions, serious falls (typically 3 meters or more), and crush injuries.
Aortic injuries have traditionally thought to be the result of severe frontal or “head on” vehicle crashes. Recent data on hospital admissions involving motor vehicle accidents demonstrates, however, that side impact collisions also pose a significant risk of aortic injury. Several identifiable crash factors have a strong correlation with aortic injury and rupture. These include a change in vehicle velocity of 20 miles per hour or greater, direct impact on the patient’s side of the automobile, and intrusion of the vehicle wall into the passenger’s compartment of 15 inches or more. This same study found no correlation between the incidence of traumatic rupture and the use of safety restraints such as seatbelts and airbags.
Additionally, aortic rupture can result from penetrating trauma as well as non-traumatic rupture of chronic untreated thoracic or abdominal aortic aneurysms.
In the United States, the annual incidence of traumatic aortic transection is estimated to be between 7500 and 8000 cases. Only 20% of these will make it to a hospital alive. The incidence of aortic transection is reported in less than 1% of patients following motor vehicle accidents; however, aortic transection is responsible for up to 16% of automobile collision deaths. It is reported that approximately 70% of victims are male while 67% of patients are described as overweight or obese.
The isthmus lies at the junction of the relatively mobile ascending aortic arch and the descending thoracic aortic which lies fixed to the posterior chest wall. This transition zone is tethered in place by the ligamentum arteriosum, a vestige of the fetal ductus arteriosus, which increases shearing forces during rapid deceleration. Also, physicians believe that the isthmus may represent a weak point along the aorta, with studies showing decreased tensile strength when subjected to stress. The “water-hammer” effect is another proposed mechanism where occlusion of the aorta at the diaphragm during impact results in a simultaneous increase in intra-aortic pressure and the generation of a high-pressure wave creating severe stress and rupture at the arch. A final theorized mechanism is the “osseous pinch.” This involves entrapment of the aorta between the boney structures of the anterior chest wall and the vertebral column resulting in rupture. However, it is likely that most injuries result from a combination of forces through several of these injury mechanisms.
The time course of aortic rupture occurs in two distinct phases owing to the three histologic layers that compose the vessel wall. Immediately following injury, there is rupture of the inner intima and media layers of the vessel wall. Next, after an indeterminate and unpredictable amount of time disruption of the outermost adventitial layer occurs resulting in rapid clinical decline. Studies have shown the time interval between disruption of the intima-media and adventitial rupture can vary from seconds to years.
Clinically, there are no distinct signs or symptoms of sufficient sensitivity that can accurately diagnose aortic rupture. Thus, aortic rupture may be difficult to detect and is often unnoticed as patients lack specific diagnostic symptoms. Instead, those who present to the emergency department following motor vehicle accidents or other high-impact events should be approached with a high suspicion for an aortic injury. Patients may have nonspecific complaints such as chest pain, sudden onset interscapular pain, dyspnea, or dysphagia. On physical exam chest wall trauma (seat belt or steering wheel lacerations, rib fractures, or flail chest), a left subclavicular hematoma, or a new onset murmur with auscultation may suggest aortic damage or rupture. Pseudo-coarctation presenting with upper extremity hypertension and hypotension in the lower extremities in addition to absent femoral pulses is another physical exam finding that increases suspicion for aortic rupture.
Most cases of aortic rupture occur with other associated injuries that may distract from or complicate diagnosis due to their severity. Associated injuries include closed head injury, multiple rib fractures, flail chest, pulmonary contusion, myocardial contusion, blunt diaphragmatic rupture, splenic or liver damage, small bowel injury, intraabdominal hemorrhage, spinal cord injuries, fractures (pelvic, femoral, tibial), upper extremity injury, and maxillofacial injury.
Prompt identification and diagnosis are critical to obviate patient morbidity and mortality following aortic rupture. The initial diagnostic evaluation for patients with suspected traumatic aortic injury is a chest radiograph. Although it lacks reliable sensitivity, its availability and ease of use make chest radiography a useful diagnostic tool in patients who are too unstable to receive computed tomography. Features on plain chest radiography that suggest aortic injury and can help guide the further use of angiography include; an abnormal aortic arch contour, left apical cap, loss of the aorticopulmonary window, rightward deviation of the trachea, depression of the left main stem bronchus, and a wide left paravertebral pleural stripe. Also, widening of the mediastinum (greater than 8 cm) has a reported sensitivity of 81% to 100% and a specificity of 60%.
A normal chest x-ray, however, does not exclude rupture, as studies have shown patients with blunt aortic injury may present with a normal mediastinum on chest radiography. For this reason, other imagining modalities with greater diagnostic sensitivity are commonly used. Computed tomography angiography (CTA) has replaced traditional angiography and transesophageal echocardiography as the diagnostic test of choice for blunt thoracic aortic injury. This highly sensitive (86% to 100%) and specific (40% to 100%) imaging modality is widely available as well as both time and cost effective. CTA findings indicative of an aortic rupture include active extravasation of intravenous contrast dye from the aorta, pseudo-aneurysm formation, an intimal flap, luminal filling defects, periaortic hematoma formation, as well as aortic contour abnormalities.
Transesophageal echocardiography is another imaging modality used to evaluate and diagnose damage to the aorta. This method is most useful in patients who are hemodynamically unstable since it can be performed quickly at the bedside in the emergency room or the operating theatre by a skilled operator. Other less frequently used options for the identification of aortic transection include intravascular ultrasonography and magnetic resonance imaging.
Following diagnosis, prompt surgical treatment of a ruptured aorta is critical to offer the patient a chance of survival. Repair can be done using either an open or endovascular technique. Open operative repair most commonly occurs through a left fourth intercostal space thoracotomy. After achieving sufficient exposure to the aorta, surgeons are then able to perform either a primary repair (rare) or resection and replacement of the damaged segment utilizing prosthetic graft. Despite technological advancements and surgical modifications, open repair continues to pose a significant surgical risk with high rates of morbidity and mortality.
The most notable progress in the management of aortic rupture has been the widespread adaptation of stent grafting. This method achieves aortic repair through the delivery and placement of endografts through the femoral arteries. These grafts cover the damaged portion of the aorta and prevent further blood loss. Endovascular treatment has become the preferred method for aortic repair based upon improved perioperative morbidity and mortality. Studies have shown a significant reduction in mortality for patients undergoing endovascular repair when compared to open surgery (7.2% versus 23.5%). Further studies have revealed significantly lower postoperative rates of spinal cord ischemia, paraplegia, stroke, and end-stage renal disease in those patients treated endovascularly.
Initial management in the perioperative period involves medical therapy. Therapy requires aggressive blood pressure control to reduce the risk of further transection progression. Intravenous beta blockers (labetalol or esmolol) are the mainstays of therapy during this time. It is necessary to reduce the heart rate to decrease the tension-time effect on the aortic wall. Vasodilators have also demonstrated effectiveness in decreasing shear forces on the aortic wall.
Classification of traumatic aortic injury contains a grading system based on the extent of anatomic aortic wall damage. Imaging allows practitioners to classify a patient’s injury into four distinct grades. These are critical as they effect patient management and treatment strategies.