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Introduction
Althought blunt carotid artery injury is uncommon, but it is associated with severe, permanent neurologic deficit. Recent studies have reported blunt carotid artery injury occurred 0.33% and 0.40% of all blunt trauma and 0.67% of all vehicle accident patients.8)13) We report a case of endovascular stent treatment for traumatic common carotid artery dissection with cerebral infarction.
Case Report
A 45-year-old woman presented to emergency department with left hemiplegia and drowsy mentality. Two days before admission she was assaulted by robber at home, producing multiple ecchymosis and stab wound on left face. At the time of admission, the physical examination found severe swelling and ecchymosis on left periorbital area, left lateral neck area and right mid-back area, multiple facial stab wound (Fig. 1). The vital sign was relatively stable except for the coarse and decreased lung sound in the left lower lung field. On neurologic examination, the patient was drowsy and lethargic but could be aroused and follow commands. On examination, the patient displayed central type, left-sided facial weakness, left homonymous hemianopsia and left-sided hemiplegia with no movement to painful stimuli.
The chest X-ray showed right 9, 10th rib fracture and pneumothorax of right thorax. The chest computed tomography (CT) and abdomen CT revealed multiple fractures at right 9, 10, 11, 12th ribs, large amount of air density at anterior aspect of right hemothorax, high density fluid collection and passive atelectasis at right lower lung field, right transverse process fracture of 3th Lumbar spine and subcutaneous emphysema at right back area. The brain CT was performed and showed a right fronto-temporo-parieatal infarct in the area the right anterior and middle cerebral artery distribution and swelling but skull fracture line was not seen. The diffusion magnetic resonance imaging (MRI) revealed acute infarct with cortical hemorrhagic transformation in the area of right middle cerebral artery distribution, especially inferior division (Fig. 2).
The antiplatelet medication was not done because of hemothorax. The patient neurologic state was not aggravated. Three days after admission, patient condition was stable, the angiography was performed.
The angiography revealed the stenosis and dissection in the right distal common carotid artery, associated with the flap at the anterolateral portion (Fig. 3). Because of the favorable anatomic condition in the dissected vessel segment, endovascular stent placement was decided.
Under the local anesthesia, a 8F guiding catheter (Shuttle-SL, Cook) was positioned in right common carotid artery. The dissected segment of the common carotid artery was crossed with 0.014 microwire and 10 mm×4 cm stent (Precise Nitinol stent: Cordis) was advanced over the microwire and positioned in the dissected segment. Then we deployed the stent slowly. The diameter was enlarged to 6 mm in stenotic area and the flap was disappeared (Fig. 4). During and after the procedure, the heparinization was done. Three days later, she was medicated with the antiplatelet and was being rehabilitated.
The patient ultimately recovered with only mild left side weakness and patient’s condition became ambulation was possible. low density lesion in right fronto-temporo-parietal area and hemothoras was disappeared on follow up Brain CT and Chest CT.
Discussion
Incidence
Blunt carotid artery injury occurred with a frequency of 0.08% of all blunt trauma patients, or about one in 1250. More recent studies have cited the somewhat higher rates of 0.33% and 0.40% of all blunt trauma and 0.67% of all motor vehicle accident patients, or up to one in 150.8)13)
Mechanism of injury
Approximately one half of all blunt carotid artery injuries are the result of a direct blow to the neck, often associated with a fracture of the mandible. A second type of injury was an abrupt hyperextension of the neck and rotation of the neck to the opposite side the internal carotid artery (ICA) enters the carotid canal as the petrous segment, where it is firmly fixed within the petrous bone. With extension of the neck, the carotid canal is elevated, stretching and partially fixing the cervical ICA against the lateral masses of the upper cervical spine. Rotation, which largely occurs at the atlantoaxial joint, forces the contra-lateral lateral mass of C1 anteriorly, further stretching the ICA. Because of this relationship, the cervical ICA is the typical site of injury associated with hyperextension-rotation of the head and neck. A third possible mechanism involves intraoral trauma. A final mechanism involves a basal skull fracture, which can damage the petrosal segment of the internal carotid artery. A wide array of sources of seemingly incidental trauma have also been implicated, including violent coughing, dancing, head turning while leading a parade, chiropractic manipulation, carotid compression, yoga exercise, and various other athletic activities.7)10)11)19)
There is an evidence of direct neck injury and lesion is located in the CCA near the bifurcation with anatomic view to see, Our case’s machanism of injury are presumed the result of a direct blow to the neck.
Presentation
Only 6~10% of patients have neurologic signs and symptoms in the first hour, increasing to almost 50%by 10 hours, and 57~73% by 24 hours, leaving only 17~35% of patients to present later than this.6)9)12)18)24)25) The delay in presentation may be due to progression of dissection leading to occlusion. However, it is thought to more commonly result from eventual thrombosis and/or embolus formation at the site of injury.16) The longer delays in presentation are often seen with pseudoaneurysm, in which turbulent flow eventually promotes clot formation and dislodgement.
Screening
Early diagnosis is of utmost importance if permanent neurologic deficit and possibly death due to thrombosis and embolism are to be avoided. Not all patients in motor vehicle accidents can undergo arteriography. Therefore, screening programs are likely the most effective way to identify asymptomatic lesions. Although attempts have been made to detect impaired ICA flow with indirect means such as ocular plethysmography, the current focus for blunt carotid artery injury screening has predominantly narrowed to three modalities. Duplex doppler ultrasonography (US), CT angiography, and magnetic resonance angiography.23)
Radiologic diagnosis
The greater majority occur in the ICA. Only five (6%) of 86 injuries described by Fabian et al8) occurred in the common carotid artery (CCA). Ninety-three percent of injuries in the cases reviewed by Krajewski and Hertzer15) occurred at or distal to the bifurcation. Injury to the petrous and cavernous ICA accounts for a small but clinically important number of cases, usually 5~10% in most large series.5)8)12)15) Blunt injury to the intracranial ICA, the least commonly involved segment, is occasionally reported.14)
Knowledge of the mechanism of injury is useful in predicting the site of injury. Whereas a direct blow to the neck is most likely to result in injury to the CCA near the bifurcation, a hyperextension-rotation injury should provoke careful scrutiny of the upper cervical ICA. Although the classic angiographic finding of blunt carotid artery injury is occlusion of the ICA 1~3 cm distal to the bifurcation, the actual site of injury to the vessel is most commonly the upper cervical ICA near the C1 or C2 level, as would be expected with the most common cause of injury being hyperextension-rotation from motor vehicle accidents.3)17)25) The apparent proximal site of the occlusion is due to proximal extension of the resultant thrombus.2) There are a variety of potential injuries that can be occur at these various sites, including vasospasm, intimal tear, dissection, intramural hematoma, pseudoaneurysm, carotid-carvenous fistula, and complete transection, any of which may be associated with thrombosis and embolism. Intimal tears are thought to be the basic underlying lesion from which many other forms of blunt carotid artery injury arise and represent the most common type of injury.7)8) They may serve as a thrombogenic focus alone or provide a lead point for intramural dissection. Their angiographic appearance ranges from occult or mild contour irregularity to diffuse irregularity and stenosis, depending on the degree of associated spasm. a linear or spiral filling defect may be evident in those approaching classification as dissection. Dissection are usually beginning as an intimal tear, dissections have a variable angiographic appearance depending on the location, extent, patency of the true lumen, and associated pseudoaneurysm formation. The blood may extend subintimally, resulting in compression of the true lumen and giving the narrowed irregular appearance characterized as a scalloped stenosis or “string sign” but pathognomic. Rarely, opacification of both the true and false lumina occurs, resulting in the definitive “double lumen sign” Pseudoaneurysms form when disruption of the vessel wall results in perivascular hemorrhage contained by the tunica adventitia or surrounding fascia. Two largest studies5)8) reporting pseudoaneurysm formation in 13~18% of blunt carotid artery injury. Carotid-cavernous fistulas, accounting for about 5%of blunt carotid artery injuries, generally result when the cavernous portion of the ICA ruptures into the cavernous sinus.5)8) Complete transection is usually not diagnosed radiographically, as these patients tend to present with dense neurologic deficits and shock and usually do not survive long enough to allow procedures. In the study by Cogbill et al,5) complete transection made up 10%of the injuries and had a relatively equal distribution between the CCA and ICA. Thrombosis may result from any of the aforementioned injuries, although the diffuse intimal injuries, related to hyperextension-rotation injury are more likely to result in extensive clotting.18) The tendency to form thrombus is increased substantially by the perivascular edema or hematoma, vasospasm, hypotension, and increased platelet adhesiveness associated with major trauma.4) Propagation of clot or dislodgement of emboli into the intracranial vasculature may result. With the more aggressive management strategies of today, earlier and more widely applied diagnostic evaluation are allowing detection of those injuries that have not yet gone on or would not go on to thrombosis.
Management and outcome
The goal in treating blunt carotid artery injury is to prevent development or worsening of neurologic deficits by preventing thrombosis, propagation of clot, and intracranial embolization. The optimal means of achieving the result has been in question, depending on the location and type of injury, neurologic and cardiovascular status, and the presence of associated injuries. By preventing development or propagation of thrombus, anticoagulation prevents the development of critical occlusion and embolization and gives the intrinsic fibrinolytic system a chance to act. Anticoagulation has also been shown to promote intimal healing, with less smooth muscle proliferation and intimal thickening, and is effective in treating intimal injury as is surgical management. Although many regimens exist, anticoagulation is often achieved with heparin, initially and then maintained with warfarin after 1~3 weeks and continued for up to 6 months.8) The use of antiplatelet medications in lieu of full anticoagulation is an option that many institution choose, as it may allow similar treatment benefits with lower risk of hemorrhagic complications.1) Surgical repair is considered when the lesion is accessible and relatively localized in the CCA or proximal ICA with maintained prograde flow in the absence of severe fixed neurologic deficits, coma, or cardiovascular instability, particularly if symptoms are progressive.12)15)20)21) If indicated, surgical repair should be performed emergently to lessen morbidity and mortality.1) Although surgical repair is contraindicated in patients with severe complete neurologic deficits or CT evidence of infarction. Pseudoaneurysms deserve special consideration for surgery or endovascular inteventions as it has been shown that they rarely resolve with anticoagulation alone and often serve as a source of emboli if not corrected.22)
This case was treated with endovascular stent because that the patient was presented fixed neurological deficit (left hemiplegia and left facial palsy) and anatomically easily accessable lesion by endovascular treatment.
Conclusion
Blunt carotid artery injuries, once considered rare, are being reported with greater frequency and with lesser degrees of severity or progression in recent years, likely due to increasing physician awareness and more aggressive approaches to identifying these injuries in the major trauma centers reporting their experiences, identification of mild injuries is important, as it allows treatment before progression to frank dissection, formation of pseudoaneurysm, or occurrence of thrombosis, thus avoiding permanent neurologic deficits. magnetic resonance angiography, CT angiography, and duplex doppler US are being investigated as screening tools. Angiography remains the reference standard for diagnosis, possibly aided by new techniques such as endovascular US in the near future. Although treatment of some types of injuries is controversial, recent trends favor nonsurgical treatment with systemic anticoagulation or endovascular treatment in the majority.
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