Key Words:
vascular-injury diagnosis , computed tomography , Doppler ultrasound , contrast angiography , pulse deficit , compartment syndrome , multidetector computed tomographic angiography (MDCTA) , ankle-brachial index (ABI) , portable angiography
Introduction
Vascular trauma with vessel disruption presents in a variety of settings and results in findings that range from life-threatening hemorrhage and/or significant ischemia (i.e., hard signs of vascular injury) to less-detectable or soft signs of injury. In some instances, vascular injury may present without any hard or soft physical examination findings and exist as an occult injury. Effective management of vascular trauma is based on early diagnosis and prompt treatment. Isolated vascular injuries are becoming less common at modern urban trauma centers because there is an increasing prevalence of multisystem trauma that includes vascular injury, making early diagnosis more challenging. Successfully identifying vascular injury in a timely manner requires an organized approach with attention to the mechanism of injury, with the presence of hemorrhage at the scene or during transport, and with a thorough physical examination. In many instances, the physical examination must be augmented with Doppler extremity pressure measurements, the multidetector computed tomographic angiography (MDCTA), and/or the selective use of contrast arteriography to diagnose vascular injury. Imaging techniques are discussed at length in subsequent chapters.
Analyses of human error suggest that the following three factors play roles in most major errors: familiarity, distraction, and fatigue. The modern trauma center creates an environment where all three factors are constantly at play and, as such, trauma care is an error-prone process. Avoiding error in the care of the injured patient requires not only an organized approach but also the use of short but effective checklists that assure the application of that organized approach. Unfortunately, most physicians are familiar with long, detailed, and all-inclusive checklists that have not been created by them or by colleagues who provide trauma care. Most physicians do not find these types of checklists useful so they are not often used. The experience of military and civilian aviation communities strongly supports the use of short, practical checklists created by experienced aircrews and thoroughly tested at the point of service until they are effective. The essential history and physical elements that lead to the prompt diagnosis of vascular injury are displayed as a checklist in Box 5-1 .
Review the following questions in the trauma bay:
Consider further evaluation for vascular injury for any positive answer.
- 1.
High-risk mechanism of injury
- •
Significant blunt-force loading and anatomic extent across major vessels?
- •
Penetrating path in area of major vessels (i.e., proximity)?
- •
- 2.
Blood loss at the scene
- •
History of pulsatile bleeding from the wound?
- •
Significant blood at the scene, on clothing, or trail of blood?
- •
Fled the scene and history of significant bleeding from wounds?
- •
- 3.
Bleeding indicators
- •
Prehospital hypotension present and trauma in the area of a major vessel?
- •
Prehospital shock index (HR/SBP) >0.90?
- •
Shock unexplained, with nonbleeding extremity or neck lacerations?
- •
- 4.
Physical Examination
- •
Pulsatile bleeding, copious venous bleeding, or large hematoma?
- •
Absent extremity pulses, absent Doppler signals, ankle-brachial or injured extremity of index <0.9 ?
- •
Bruit or thrill over injury site?
- •
Major deficit in peripheral nerve located in proximity to major vessel?
- •
- 5.
High-risk fractures or joint dislocations?
- •
Cervical spine fracture—vertebral artery injury
- •
Thoracic spine fracture—thoracic aortic injury
- •
Supracondylar humerus fracture—brachial artery injury
- •
Knee dislocation—popliteal artery injury
- •
Tibial plateau fracture—below-knee popliteal artery injury and/or leg compartment syndrome
- •
The Mechanism, Setting, and Patterns of Injury
The evaluation of an injured patient must begin with consideration of the mechanism of injury and the setting in which that injury occurred. This is particularly important in patients injured in high-speed motor-vehicle crashes. The advent of modern automobile passenger-restraint systems has resulted in many occupants surviving what were previously fatal crashes. However, this also resulted in a rising incidence of blunt cerebrovascular and thoracic arterial injuries. These injuries are often asymptomatic, associated with few physical findings on presentation, and occur in the setting of a variety of injury patterns. In most instances, blunt cerebrovascular and thoracic arterial injuries can be found only with further imaging studies. Thus considering both the mechanism and setting of injury will lead to the appropriate diagnostic evaluation. Further consideration of injury patterns will also prompt appropriate early workup and timely recognition and will result in successful management.
Penetrating vascular injuries are rarely occult and usually present with hard signs of hemorrhage, including hematoma, active bleeding, and shock. The nature of bleeding at the scene should always be determined as initial pulsatile flow or large amounts of blood at the scene may be indicative of significant vascular injury. Bleeding during prehospital transport should also be considered a sign of vascular trauma. This information may not be readily available when patients are transported by bystanders or if they flee the scene of the injury. Redirecting attention to apparently nonbleeding wounds in the patient in shock without evidence of chest or abdominal trauma may reveal an underlying extremity vascular injury which has ceased bleeding.
Injury Pattern Recognition
The early diagnosis of vascular injuries requires a high index of suspicion based on both mechanism of injury and injury patterns. The following discussion reviews each anatomic area and the important considerations of both mechanism of injury and injury pattern. Such familiarity will prompt the provider to perform further diagnostic studies to identify vascular injuries in a timely manner. The goal of this review is to generate pattern recognition and decisive action.
Head and Neck Vascular Injuries
The neck and face are areas of relatively superficial major vascular structures. Additionally, the neck is a zone of multiaxis motion with cerebrovascular arterial structures in close proximity to bony prominences. This is a high-risk zone for both blunt and penetrating vascular injuries. Although penetrating injuries are usually obvious because of hemorrhage, blunt injuries are almost always occult. Low-velocity gunshot wounds may cause injuries other than the typical laceration and hemorrhage. As an example, arterial-wall disruption from bullets passing in proximity may cause arterial thrombosis ( Fig. 5-1 ) or pseudoaneurysm formation. Pattern recognition of both blunt-force loading and associated injuries is essential for prompt diagnosis of blunt cerebrovascular injury.
The most common underlying mechanism of significant blunt cerebrovascular injury in the neck and at the skull base is stretching of the vessel, often across a bony prominence, or from direct compression by a fracture fragment. Less likely is focal blunt force with direct compression and partial arterial rupture. There are key anatomic areas where these events occur. At the base of the skull, fracture of the temporal bone in the area of the carotid canal may be associated with internal carotid artery dissection. Hyperextension of the neck may stretch the internal carotid artery across the transverse process of C2 also causing dissection. Hyper-flexion may lead to compression of the internal carotid between the angle of the mandible and the transverse process of C2 with arterial thrombosis. Hyperrotation of C1 on C2 can cause a stretch injury of the vertebral artery resulting in dissection and thrombosis. Any cervical spine fracture that involves transverse processes may cause vertebral artery injury. At the prominent transverse process of C6, direct blunt-force trauma may compress the common carotid artery creating a partial wall disruption and pseudoaneurysm.
Direct trauma to the neck also requires attention to the possibility of vascular injury. Handlebar trauma and other direct blows to the neck may disrupt the carotid artery. Attempted hanging or strangulation may cause blunt carotid disruption. The shoulder harness of an automobile passenger-restraint system may also compress the common carotid artery and cause disruption and thrombosis. External signs of direct neck trauma (e.g., seat-belt sign on the neck) should direct attention to the possibility of carotid injury. Particular attention should be paid to direct lower-neck trauma and hoarseness in the absence of direct laryngeal trauma. The vagus nerve lies adjacent to the common carotid artery, and trauma sufficient to cause injury to the vagus above the takeoff of the recurrent laryngeal trauma may also injure the common carotid artery ( Fig. 5-2 ).
Thoracic Vascular Injuries
Penetrating trauma to the thorax with major vascular injury presents with life-threatening hemorrhage that requires immediate operative intervention to identify the injury and control hemorrhage. In contrast, blunt injuries are often occult, and early diagnosis requires attention to both mechanism and injury pattern. Rapid deceleration or acceleration can create visceral rotation and stretch of the mediastinal structures causing sheer stress at transition points between relatively mobile and fixed vessel segments. The heart and proximal great vessels have been described as moving like a bell clapper in the chest in certain scenarios of high-speed impact. The result of such injuries is that the aorta is partially torn at the isthmus, a transition point between mobile and fixed elements. This type of movement can also stretch and partially tear the branches of the aortic arch. Direct trauma from compression and fracture of the sternum, manubrium, or clavicles can cause vascular injuries. This type of direct compression may injure the aortic arch and its proximal branches or the pulmonary artery at its bifurcation area ( Fig. 5-3 ).
A variety of fracture patterns have been described with blunt thoracic aortic injury. Although first-rib fracture is often described as a harbinger of blunt aortic injury, thoracic spine fracture is the most commonly associated fracture finding. This type of fracture is the result of major force loading on the thorax and indicative of the risk of great vessel injury. Although clavicle fractures are very common, blunt subclavian artery and venous injuries are rarely associated with this finding.
The portable anteroposterior chest radiograph is an important tool in the early recognition of occult mediastinal vascular injury. Despite a wide variety of findings described as being associated with thoracic aortic injury, two are of particular importance. An increased width of the superior mediastinum and the absence of a normal left-side aortic contour are both indications of a mediastinal hematoma and warrant additional CT scan imaging to rule out vascular injury. Finding of rib fractures, thoracic spine fractures, and sternal fractures are less strongly associated with thoracic aorta and great vessel injuries but should also prompt additional imaging with contrast CT.
Abdominal Vascular Injuries
Penetrating abdominal vascular injuries present in a manner similar to thoracic vascular injuries. Hard signs of vascular injury such as intraabdominal hemorrhage and shock require immediate operative intervention both to identify and to control the site of bleeding. Blunt vascular injuries occur in a fashion similar to thoracic injuries. The major difference in the abdomen is the paucity of mobile segments in major arteries due to the retroperitoneal location of the aorta and its proximal branches. The renal hilum is an exception and blunt stretch injuries of the renal arteries are not uncommon. The abdominal aorta and proximal mesenteric arteries may be injured by blunt-force trauma such as lap-belt or passenger-restraint compression of the distal aorta against the sacral promontory in a high-speed motor-vehicle crash. Survivable blunt tears of the celiac and superior mesenteric arteries occur infrequently.
Upper Extremity Vascular Injuries
Penetrating upper extremity vascular injuries typically produce hard signs of vascular injury such as external hemorrhage or acute limb ischemia and are usually obvious in presentation ( Fig. 5-4 ). Blunt injuries, although less obvious, are usually associated with musculoskeletal injuries. Blunt posterior distraction of the shoulder with brachial plexus stretch injury can result in tearing and thrombosis of the axillary artery with absent pulses at the wrist. Proximal fracture of the humerus or humeral head dislocation rarely causes brachial artery occlusion. However, supracondylar humerus fracture is associated with distal brachial artery occlusion and forearm ischemia. Other fractures of the upper arm are infrequently associated with major vascular injuries unless they involve a crush injury.
Lower Extremity Vascular Injuries
Penetrating injuries of the groin and leg resulting in vascular injury most often produce hard signs similar to the upper extremity with either obvious hemorrhage or distal ischemia. Although proximal femur fractures and hip dislocations rarely result in vascular injury, distal femur fracture may be associated with superficial femoral artery injury. The distal superficial femoral artery and proximal popliteal artery are relatively fixed by the transition through the adductor canal. Stretch injury and thrombosis may occur. The most common musculoskeletal injury associated with vascular trauma is posterior knee dislocation. The popliteal artery is fixed proximally by the adductor canal and distally in the upper calf by the trifurcation into the anterior tibial, peroneal, and posterior-tibial arteries. The posterior dislocation of the tibial plateau stretches and disrupts the popliteal artery resulting in thrombosis and distal ischemia. Knee dislocation is associated with as high as a 30% incidence of popliteal vascular injury.
Crush injuries of the lower extremity may cause arterial disruption at any level. Bumper strike trauma in pedestrians struck by a motor vehicle has a particular association with blunt vascular injury in the lower extremity. Compartment syndrome is also a risk in this type of injury. All below-knee fracture of the leg must lead to a suspicion of compartment syndrome. However, tibial plateau fracture is the most commonly associated fracture with calf compartment syndrome. Fractures of the tibia and fibula often involve significant distraction and angulation of fracture segments with ripping of compartment fascial planes. An auto-fasciotomy and decompression of the compartments often result. Tibial plateau fracture usually requires significant force loading but does not result in distraction of fracture segments, and the fascial planes remain intact. Hemorrhage within any of the leg compartments results in a scenario that risks the development of compartment syndrome.
Other High-Risk Injury Patterns
A high index of suspicion for either torso or extremity vascular injury should also attend the evaluation of a variety of other injuries. High-speed side impacts may be particularly high risks for thoracic vascular injuries, as is a fall from a significant height. Aircraft-crash survivors should be evaluated for thoracic aorta and great vessel injuries. Victims of motor-vehicle crash with prolonged entrapment should have careful evaluation for extremity arterial occlusion and compartment syndrome. All crush injuries are similarly at risk and should prompt a careful evaluation for the presence of vascular injury and/or extremity compartment syndrome.
Head and Neck Vascular Injuries
The neck and face are areas of relatively superficial major vascular structures. Additionally, the neck is a zone of multiaxis motion with cerebrovascular arterial structures in close proximity to bony prominences. This is a high-risk zone for both blunt and penetrating vascular injuries. Although penetrating injuries are usually obvious because of hemorrhage, blunt injuries are almost always occult. Low-velocity gunshot wounds may cause injuries other than the typical laceration and hemorrhage. As an example, arterial-wall disruption from bullets passing in proximity may cause arterial thrombosis ( Fig. 5-1 ) or pseudoaneurysm formation. Pattern recognition of both blunt-force loading and associated injuries is essential for prompt diagnosis of blunt cerebrovascular injury.
The most common underlying mechanism of significant blunt cerebrovascular injury in the neck and at the skull base is stretching of the vessel, often across a bony prominence, or from direct compression by a fracture fragment. Less likely is focal blunt force with direct compression and partial arterial rupture. There are key anatomic areas where these events occur. At the base of the skull, fracture of the temporal bone in the area of the carotid canal may be associated with internal carotid artery dissection. Hyperextension of the neck may stretch the internal carotid artery across the transverse process of C2 also causing dissection. Hyper-flexion may lead to compression of the internal carotid between the angle of the mandible and the transverse process of C2 with arterial thrombosis. Hyperrotation of C1 on C2 can cause a stretch injury of the vertebral artery resulting in dissection and thrombosis. Any cervical spine fracture that involves transverse processes may cause vertebral artery injury. At the prominent transverse process of C6, direct blunt-force trauma may compress the common carotid artery creating a partial wall disruption and pseudoaneurysm.
Direct trauma to the neck also requires attention to the possibility of vascular injury. Handlebar trauma and other direct blows to the neck may disrupt the carotid artery. Attempted hanging or strangulation may cause blunt carotid disruption. The shoulder harness of an automobile passenger-restraint system may also compress the common carotid artery and cause disruption and thrombosis. External signs of direct neck trauma (e.g., seat-belt sign on the neck) should direct attention to the possibility of carotid injury. Particular attention should be paid to direct lower-neck trauma and hoarseness in the absence of direct laryngeal trauma. The vagus nerve lies adjacent to the common carotid artery, and trauma sufficient to cause injury to the vagus above the takeoff of the recurrent laryngeal trauma may also injure the common carotid artery ( Fig. 5-2 ).
