Chapter Preview
|
|
|
|
Background
Vertebral artery injury (VAI) secondary to blunt trauma has become an increasingly discussed topic. Initially, these injuries were thought to be extremely rare events with minimal significance. However, studies using rigorous screening protocols demonstrated that VAIs occur with some regularity (the overall incidence in blunt trauma is approximately 0.5%) and can be associated with significant morbidity. Some of these investigators argued that routine anticoagulation is effective and should be considered for patients with these injuries. However, other studies concluded that no compelling evidence exists to recommend treatment of asymptomatic traumatic blunt VAIs (BVIs).
Incidence and Risk Factors
Although the overall incidence of VAI in patients who have sustained blunt trauma is approximately 0.5%, the incidence is certainly higher in certain subsets of patients. Seventy percent of patients with traumatic VAIs have an associated cervical spine fracture. Cervical spine injuries associated with increased VAI include subluxations and dislocations, fractures involving the transverse foramen, and fractures of the upper cervical spine (C1-C3) ( Fig. 20-1 ). Other patients considered at higher risk and potentially requiring screening include those with basilar skull fractures, significant facial fractures, cervical hematomas, neurologic examination findings inconsistent with head computed tomography (CT) scans, or lateralizing neurologic examination findings.
In general, most traumatic BVIs occur after high-energy mechanisms, often with rapid deceleration. Most of these injuries occur after motor vehicle accidents, after falls, or when pedestrians are struck by vehicles. Another rarely cited reason for BVI is chiropractic manipulation. In a large review of published case reports from 1934 to 2003, Ernst found 26 published fatalities associated with chiropractic manipulation. At least 6 of these deaths were believed to have resulted from vertebral artery dissection. The true incidence of such events is difficult to estimate, however. Aside from traumatic BVI, the other major category of traumatic VAI includes penetrating injuries, such as gunshot wounds and lacerations. Traumatic VAIs from lacerations have a high mortality rate related to bleeding.
Relevant Arterial Anatomy
Arteries such as the vertebral artery each have three main layers that comprise the vessel wall. The intima is composed of endothelial cells. The next layer out is the media, which contains the smooth muscle cells that allow contraction of the vessel lumen. The outer layer is the adventitia, which is composed of collagen bundles. The adventitia also contains the vasa vasorum, or vessels to the vessels.
The vertebral artery usually starts from the subclavian artery and then enters the transverse foramen, usually at C6. This first segment, before the artery enters the transverse foramen, is known as V1. V2 is the second segment, as the artery travels superiorly through the transverse foramen at each level, usually from C6 to C1. The third segment is located from the transverse foramen of C1 to where the artery enters the dura. The fourth segment is from the dural entry site to where it joins the basilar artery. Most traumatic injuries to the vertebral arteries occur at the second (V2) or third (V3) segment, often related to cervical injury at these regions. Investigators have demonstrated that the vertebral artery and nerve root are encased in a fibroligamentous band at the level of the intertransverse space, and this band attaches to the lateral side of the uncinate. Perhaps this tethering of the vertebral artery to the bone helps explain why trauma in this region can easily cause arterial injury.
Types and Classification of Vertebral Artery Injuries
Intimal flaps occur when the intima of the vessel has a tear, which can cause a flap to protrude into the vessel lumen. When the intima is injured and bleeding occurs into the vessel wall, dissection can occur. The blood that collects within the vessel wall can cause narrowing of the vessel lumen. When blood is forced through the vessel wall and causes a hematoma, which can cavitate, a pseudoaneurysm may form. Pseudoaneurysms can also effectively narrow the vessel lumen. Occlusions are complete blockages of the artery. Transections are complete arterial divisions ( Box 20-1 ).
- 1.
Intimal flap
- 2.
Dissection
- 3.
Pseudoaneurysm
- 4.
Occlusion
- 5.
Transection
Biffl and colleagues developed a grading scale for injuries that has been used for classification of traumatic VAIs. Grade I includes an irregularity of the vessel wall or an intramural dissection or clot that causes less than 25% stenosis of the vessel. Grade II signifies 25% or more stenosis of the vessel as a result of an intramural clot or dissection, or an intraluminal thrombus or raised intimal flap is seen. Grade III is a pseudoaneurysm. Grade IV includes occlusions of the vessel, and grade V represents a vessel transection ( Table 20-1 ).
Grade I | <25% stenosis of vessel from intramural clot or dissection, or wall irregularity |
Grade II | >25% stenosis of vessel from intramural clot or dissection, or raised flap or intraluminal clot |
Grade III | Pseudoaneurysms |
Grade IV | Occlusions |
Grade V | Transections |
Sequelae of Vertebral Artery Injury
The range of outcomes for traumatic BVIs is wide. Many patients are asymptomatic and have no adverse effects of their injury. Other patients can have visual changes, significant stroke, or death. Neurologic deficit can result from decreased posterior brain circulation (vertebrobasilar insufficiency), clot formation with embolization downstream, obstruction of posterior inferior cerebellar blood flow, and anterior spinal artery compromise that causes subsequent spinal cord ischemia.
Symptoms of dizziness, ataxia, decreased level of consciousness, or visual disturbances can all be evidence of vertebrobasilar insufficiency. More significant ischemia can occur with posterior stroke if collateral flow is not adequate. Collateral flow is extremely important because some patients with bilateral vertebral artery occlusion have no permanent neurologic deficit because they have sufficient collateral flow.