Thoracic vascular injury

Incidence

Thoracic trauma is responsible for 50% of all trauma deaths. In a large series of thoracic trauma patients, the aorta and great vessels were injured in 4% of cases. More than 90% of the thoracic great vessel injuries are due to penetrating trauma, where all thoracic vessels are potentially susceptible to injury. The anatomic location of the ascending aorta makes it the most at risk from stab wounds, whereas gunshot wounds more commonly involve the descending thoracic aorta. Blunt trauma can potentially cause injury to all thoracic arteries and veins, but the common injuries involve the descending thoracic aorta, the innominate artery origin, the vena cavae, and the pulmonary veins.

Mechanism of injury

A significant number of thoracic great vessel injuries are caused by penetrating or iatrogenic trauma. These injuries can present with external or internal hemorrhage, vascular thrombosis from an intimal flap, or pseudoaneurysm. With the various types of missiles causing penetrating vascular trauma, all thoracic vascular structures are at risk. The bony structures, interestingly, can also provide unique patterns of injuries as they can cause fragmentation of the missile/bone or alter vectors of the original direction of penetration. External bleeding can occur with injuries to vessels at the thoracic outlet, whereas internal hemorrhage commonly occurs with aortic and caval injuries. Intrathoracic great vessel injuries can specifically present with internal bleeding into the mediastinum, pleural space, or pericardial sac. It is important to note that the presence of a normal palpable distal pulse does not rule out a proximal vascular injury. Penetrating vascular injuries can be completely contained by the adventitia of the vessel with blood flow preserved distally.

The absence of a significant amount of bleeding does not rule out vascular injury from penetrating trauma. Vascular injuries from stab wounds can often cause an intimal flap, which may eventually lead to partial or complete thrombosis of injured vessels. Small vascular disruptions may not present initially with bleeding but can present with formation of a pseudoaneurysm. These may later rupture. Blast vascular injuries are often underestimated because intimal disruption sometimes extends beyond external signs of injury. For this reason, meticulous intimal inspection after opening the blood vessel is important during thoracic vascular reconstruction.

Because of the large diameter of thoracic vessels, missiles can enter the vessel and migrate distally ( Fig. 1 ). The diagnosis of bullet embolism is often delayed because the course of the bullet may be unclear. Bullet emboli from thoracic missiles usually lodge in the iliac and femoral vessels but may also embolize to the neck vessels. The site of entry should be controlled for hemorrhage first, followed with attempts at removing the bullet emboli with endovascular intervention or separate arteriotomy.

There are two proposed mechanisms for blunt trauma injuries to thoracic aorta and great vessels. During anteroposterior impact in the thorax, the aorta and its branched vessels may be “pinched” between the sternum and the vertebral column, resulting in vascular disruption. In rapid-deceleration thoracic injuries from either frontal or side impact motor vehicle accidents, the point of attachment of pulmonary veins and vena cava and the relative immobility of the descending aorta at the level of the ligamentum arteriosum and diaphragm increase their susceptibility to rupture. In contrast to patients with aortic medial disease in which the media/adventitia is the restraining barrier, it is the intact parietal pleura that may contain the hematoma and prevent massive hemothorax.