Epidemiology

Few traumatic injuries are more devastating than great vessel injury (GVI). With an average circulating volume of 5 L and a flow rate of up to 4.8 L/min in the circulatory system, it is easy to see why GVI can result in catastrophic outcomes quickly. The true incidence of traumatic aortic injury may never be known; however, according to the National Trauma Data Bank, blunt thoracic aortic injury occurred in 0.3% of trauma patients admitted to the hospital during a 5-year period.¹ When patients survive an initial injury to their great vessels, rapid diagnosis and treatment are imperative to prevent subsequent exsanguination within the next minutes to hours. This highlights the ever-emphasized “golden hour” of trauma resuscitation.

Several contributing factors are important when evaluating potential GVI (Fig. 90.1). Although the mechanism and specific vessel injured are the most important of these factors, significant attention must be paid to the role of concomitant injuries and comorbid conditions on patients’ morbidity and mortality. Unfortunately, on initial evaluation the emergency physician is often lucky to be privy to one, let alone all, of these factors.

Fig. 90.1 Great vessel injury paradigm of disease, including associated contributing factors, injury spectrum, and variable clinical findings.

The most important branch point for both the likelihood and the type of GVI is a penetrating versus blunt mechanism. Penetrating mechanisms are associated with greater than 90% of great vessel trauma, and any thoracic vascular structure is at risk.² Patients who survive to arrive at the emergency department, particularly if they are not in hemorrhagic shock, have a survival rate that approaches 50%.³

In contrast, blunt traumatic injuries to the great vessels most often affect the aorta, although the innominate artery, pulmonary hilar vessels, and vena cava are also susceptible. Blunt aortic rupture carries an immediate mortality rate of greater than 80% and is responsible for 10% to 15% of motor vehicle accident fatalities.⁴ Because of the high association of blunt ascending aortic injury with fatal cardiac injury, the vast majority of those who survive to hospital evaluation have descending injuries. Of patients who survive until medical evaluation, 30% die within 6 hours and 40% within 24 hours.⁴ Because most of these injuries occur in young healthy males, the overall survival rate is much better than expected given the severity of injury.

Though incompletely understood, it is proposed that blunt aortic injury can result from any combination of shearing forces, rotational forces, increased intraluminal aortic pressure, or a pinching mechanism between the sternum and vertebral column. Given these forces, it is not a surprise that motor vehicle collisions cause the majority of blunt aortic injuries. This association increases with the speed of the accident.^5,⁶ Shearing forces were originally thought to be the highest in frontal-impact accidents, where deceleration forces are the greatest. More recent studies, however, have shown that side-impact accidents are associated with a higher risk for blunt aortic injury. A review of 119 cases of known blunt aortic injury as a result of car accidents in the United Kingdom found that lateral impact direction to the same side was highly associated with aortic injury.⁷ A review of accident data from the United Kingdom and United States in 2004 mirrored these results and found that side impact involving the patient’s side of the vehicle carried a significantly higher risk for aortic injury than did frontal impact.⁸ Although motor vehicle accidents account for the majority of blunt GVI, falls from a height and crushing forces have also been known to cause the disease process.⁵

In part because of difficulty isolating the hilum, injuries to the pulmonary arteries, veins, and thoracic vena cava are associated with mortality rates greater than 60%, regardless of whether they are caused by blunt or penetrating force, although the latter is much more common.⁹

Concomitant injuries clearly play a role in the epidemiology, morbidity, and mortality of GVI. One study on blunt thoracic trauma showed that patient with traumatic aortic injury carried a mean injury severity score (ISS) of 40 whereas patients without vascular injury had a mean ISS of just 16.⁵ Another showed that closed head injury was diagnosed in more than half of patients with GVI, with one quarter having intracranial hemorrhage.³

Comorbid conditions such as underlying vascular disease, cardiopulmonary disease, and renal insufficiency contribute to the morbidity and mortality associated with GVI. Many disease processes affect a patient’s ability to tolerate the initial and delayed physiologic insults accompanying severe GVI.