12 Traumatic and Iatrogenic Carotid Artery Injury
Abstract
Carotid injuries have multiple causes and are one of the leading causes of ischemic stroke in the younger population. The majority of these are the result of blunt trauma in the setting of a high-speed motor vehicle collision, but the trauma can also be the result of penetrating injuries. With the increase in endovascular neurosurgical procedures, the incidence of iatrogenic injuries has seen a rise in the past decade. The vast majority of carotid injuries can be managed with medical therapy, but there are indications for both endovascular and open surgical treatment. This chapter will review the causes of carotid injury, the different types of injury, and their clinical and radiological assessment, and will present a therapeutic algorithm for these lesions.
Introduction
Carotid artery injury, whether blunt or penetrating, occurs in 1 to 2% of trauma patients, is one of the leading causes of stroke in the younger population, and is most commonly caused by high-energy motor vehicle collisions. Iatrogenic arterial injury is increasingly common and is secondary to a host of procedures including central venous access, endovascular procedures, and endonasal operations. The overwhelming majority of carotid injuries result in dissections, but other notable sequelae include arteriovenous fistulas, pseudoaneurysms, and lacerations/transections. As troublesome as these injuries might be, it must be remembered that the neurological morbidity associated with symptomatic carotid injury has been reported to be as high as 80%, with a mortality of up to 40%. Nonoperative management with antithrombotic therapy is the first-line therapy for carotid injuries and includes both anticoagulation and antiplatelet regimens. Traditional surgical approaches to carotid injuries have had limited success and have been associated with significant morbidity secondary to either ischemic events or cranial nerve injuries. Endovascular techniques offer the following advantages over open surgery: access to injuries at or near the skull base, preservation of flow within the parent artery, the avoidance of cranial nerve injury, and the ability to readily assess the status of the intracranial circulation. Endovascular therapy offers an attractive option for those patients in whom antithrombotic therapy is either contraindicated or poorly tolerated.
Major controversies in decision making addressed in this chapter include:
The adequate and accurate diagnostic imaging tool.
Whether or not treatment is indicated.
The role of medical management.
Open versus endovascular treatment for carotid artery injury.
Whether to Treat
The management of carotid injuries depends largely on the presence of symptoms in conjunction with radiographic abnormalities. The majority of noniatrogenic carotid injuries are blunt injuries and are initially silent in their presentation and are not associated with obvious signs of cervical trauma. Therefore, one must have a relatively high index of suspicion based on the traumatic mechanism in those patients who present with no neurological symptoms ( 1 in algorithm ). Berne et al found a median time to diagnosis of 12.5 hours for survivors of blunt cerebrovascular injury and 19.5 hours for nonsurvivors, which highlights the necessity to adequately diagnose these injuries. Those patients suspected of having a carotid injury should be evaluated with computed tomography (CT) and CT angiography (CTA) initially. This imaging modality is readily available, and almost every trauma patient undergoes a CT scan as part of their initial trauma protocol ( 1 in algorithm ). The diagnostic accuracy of CTA is directly related to the number of multidetector channels. In centers with eight-channel multidetector CT or less, digital subtraction angiography (DSA) should be considered or the patient transferred to an appropriate trauma center ( 2 in algorithm ). The primary management strategies for carotid injury include observation, antithrombotic regimens, surgical repair, and endovascular therapy. Given the relatively high morbidity and mortality associated with untreated carotid injuries mentioned earlier, observation should be avoided unless there are strong contraindications to other strategies. Aggressive screening to diagnose blunt carotid injury results in early treatment, which leads to improved outcomes and a reduction in stroke rates ( 1 , 2 in algorithm ). Asymptomatic patients with radiographic findings should be considered for medical management with antithrombotic agents ( 3 in algorithm ). Asymptomatic patients with a contraindication to anticoagulation or antiplatelet therapy should be considered for endovascular treatment based on the type of injury and its natural history ( 3, 4 in algorithm ). Those patients with symptoms related to a carotid injury should be considered for immediate treatment. Patients in whom the carotid injury is associated with a dense neurological deficit and a large ischemic insult on imaging derive little benefit from either medical treatment or revascularization, and it is generally felt that these patients be managed in a supportive manner with aggressive intracranial pressure management. There is no level I evidence regarding the treatment of blunt carotid injuries, but the preponderance of evidence in the form of retrospective reviews, case series, and meta-analyses points to intervention as an acceptable and safe form of treatment.
Anatomical Considerations/Pathophysiology
The fundamental mechanisms of blunt carotid injury stem from the anatomical juxtaposition of the relatively mobile cervical carotid artery with the fixed intracranial carotid. The cervical carotid is subject to longitudinal and compression forces such as cervical hyperextension or hyperflexion with rotation that stretches the carotid artery over the lateral masses of the upper cervical vertebrae, direct cervical trauma, intraoral trauma, and basilar skull fractures. High-speed motor vehicle collisions are the most common cause of blunt carotid injury, but other causes include chiropractic manipulation, direct blows to the neck, and any mechanism resulting in rapid deceleration or acceleration accompanied with or without rapid head turning. The resultant injuries have been categorized based on a grading scale proposed by Biffl et al (▶ Table 12.1 ). The most common injury is a dissection, and symptoms include cervical pain, Horner′s syndrome, and signs of either/both ocular and hemispheric ischemia. As the artery is stretched and compressed over the cervical spine, the intima can tear, leading to spectrum of injuries outlined in ▶ Table 12.1 . The portion of the internal carotid between the cricoid cartilage and the angle of the mandible is the most common site of blunt injury as it is the most vulnerable and mobile portion of the artery.
The increasing use of endovascular techniques in the treatment of cerebrovascular diseases has led to a concomitant increase in iatrogenic injuries, and just as with external trauma, dissection is the most common injury. Iatrogenic carotid injuries are associated with an increased morbidity and mortality compared to blunt injuries, and this is likely secondary to the increase in cerebrovascular comorbidity in this particular patient population. Percutaneous deep venous access is associated with a 0.5 to 3.7% risk of arterial puncture, and the incidence is higher when the target vessel is the internal jugular vein compared to the subclavian vein.
Workup
Clinical Evaluation
Absent the presence of such signs as an expanding cervical hematoma, arterial bleeding from the neck, mouth, nose, and ears, Horner′s syndrome, cervical bruit in a patient younger than 50 years, loss of a carotid pulse with a stable or evolving neurological deficit, or hemispheric findings not explained by intracranial injury, predicting the presence of a traumatic carotid injury based on physical exam can prove difficult ( 1 in algorithm ). As mentioned previously, the vast majority of blunt carotid injuries are initially occult and present in a delayed fashion. Therefore, the initial clinical evaluation must entail a high index of suspicion in conjunction with a thorough understanding of the traumatic mechanism and concomitant injuries. Several studies have published risk factors for blunt carotid injury, and these include: an injury mechanism compatible with severe cervical hyperextension with rotation or hyperflexion; Le Fort II or III fractures; basilar skull fracture that involves the carotid canal; closed head injury consistent with diffuse axonal injury with a Glasgow Coma Scale score < 6; cervical spine injury with subluxation or ligamentous injury, any fracture at the level of C1–C3; and external signs of cervical clothesline-type injury. Iatrogenic injury of the carotid during transsphenoidal surgery is readily apparent because of bleeding, and the assessment of neurological function is preempted by the need to control the hemorrhage. Inadvertent puncture of the carotid during central venous access is also usually apparent, and once bleeding has been controlled, a full neurological assessment must be performed. With endovascular iatrogenic injuries, patients may be under general anesthesia or sedated, so using the neurological exam as the initial clinical measure for detection of an injury can be problematic. Iatrogenic dissections usually occur during initial access of the carotid and are commonly identified at the time they occur.
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