The neck has several important anatomical structures which include the carotid arteries bilaterally. While the injury to the carotid artery is not a common event, when it does occur, it is not usually an isolated arterial injury secondary to the proximity of other vital structures. Injury to the artery may be due to either penetrating or blunt trauma. When the trauma is penetrating, exsanguination and hematoma formation can quickly compromise the airway. When the carotid artery is injured bluntly, the sudden trauma usually initiates an intimal dissection and/or a hematoma formation. Carotid artery injuries caused by blunt trauma often cause thrombosis with delayed neurologic deficits and are associated with mortality rates up to 40%.
The common carotid artery is located in zone I of the neck, where other structures at risk include the aortic arch, subclavian vessels, esophagus, trachea, spinal cord, and cervical nerves.
Zone I (the base of the neck) is demarcated by the thoracic inlet, inferiorly, and the cricoid cartilage, superiorly. Injuries in this zone are associated with the highest morbidity and mortality.
Zone II encloses the mid portion of the neck and the region extending from the cricoid cartilage to the angle of the mandible. Most carotid injuries are associated with zone II injuries, and these have the best prognosis secondary to easy accessibility of the vessel or operative repair.
Zone III represents the superior aspect of the neck, bounded by the angle of the mandible and base of the skull. Injuries in this zone are difficult to access surgically.
When a non-penetrating trauma injures the carotid artery, it may be due to excessive hyperextension of the cervical spine or extreme rotation of the neck. These maneuvers result in stretching of the carotid artery that can lead to shearing forces which can ultimately result in dissection and thrombosis. Blunt trauma to the neck typically results from motor vehicle crashes, sports-related injuries, strangulation, direct blows to the neck, and excessive cervical spine manipulation.
In general, neck trauma accounts for 5% to 10% of all severe traumatic injuries and is most commonly seen in young people. Although the reported incidence of blunt carotid injuries ranges between 0.08% and 0.86% of blunt trauma admissions, the exact number of carotid contusion injuries is still unknown as it is usually underdiagnosed or a missed altogether in the setting of asymptomatic injuries.
High-energy, blunt, non-penetrating trauma can result in a disruption in one or more layers of the common or cervical internal carotid artery wall. Direct, blunt trauma to the artery or excessive neck motion may produce intimal tears (varying from localized tears to diffuse intimal injury) exposing subendothelial collagen, resulting in platelet activation and thrombosis with a possible occlusion of the artery. An intimal defect can provide a pathway for blood to enter the layers of the artery wall, causing stenosis or occlusion of the artery. Disruption of the elastic laminae may lead to an expansion of the adventitia, resulting in traumatic aneurysm formation. Furthermore, the trauma-induced hypercoagulable state occurring early after carotid artery injury may result in intracranial ischemic strokes. Spasm of the carotid artery with occlusion has been commonly described as well.
The left and right common carotid arteries supply the head and neck structures with oxygenated blood. The left common carotid originates directly from the aortic arch in the thorax. Hence, it has two components: thoracic and cervical. The right common carotid originates in the neck (cervical portion) from the brachiocephalic trunk. Both arteries follow symmetrical courses, bifurcating into the external and internal carotid arteries each at the upper border of the thyroid cartilage at the level of the fourth cervical vertebra. The average diameter of the common carotids varies from 6.1 mm to 6.5 mm.
The usual evolution of symptoms is slower than might be expected after a major arterial trauma, and the subsequent delay in diagnosis and treatment may unfavorably influence the prognosis. Individuals with carotid artery contusion may have symptoms related to laryngeal and tracheal injuries including dyspnea, dysphonia, hoarseness of voice, dysphagia, stridor, drooling of saliva, subcutaneous emphysema with crepitus, and/or hemoptysis. Other structures at risk in cases of carotid artery injury include the pharynx and the esophagus resulting in dysphagia, bloody saliva, and bloody nasogastric aspirate. Carotid artery contusion may present with neurological deficits. These include weakness, paresthesias, hemiplegia or hemiparesis. Other hard signs of carotid artery injury include an expanding hematoma, pulsatile bleeding, signs of cerebral ischemia, shock unresponsive to fluid resuscitation, or the presence of a new bruit.
Traumatic cerebrovascular injury (TCVI) is a distinct clinical entity which can manifest after blunt trauma to the carotid artery (notably, the cervical portion of the ICA). A significant subset of patients with TCVI-related stroke suffers the ischemic event before admission to the hospital or before initial vascular imaging. Patients diagnosed with TCVI show a variety of symptoms including mild, mono, or hemiplegia to severe neurological deficits and even coma.
Never probe or manipulate a neck wound because it may cause the individual to choke, cough or gag, resulting in dislodgement of the blood clot resulting in severe hemorrhage and exsanguination. A carotid artery contusion is best evaluated with computed tomographic angiography (CTA). This imaging test can be performed rapidly and is associated with few complications. A screening CTA can be done in several minutes and can be included with other CT examinations during initial imaging of poly-trauma patients. CTA scan has the advantage of accurate visualization of various degrees and types of traumatic vascular lesions such as partial or complete occlusion, post-traumatic pseudoaneurysm formation, intimal flaps, dissection and traumatic arteriovenous fistulas. Additionally, CT scans can identify other traumatic lesions involving cervical soft tissues, the aerodigestive tract, and the spinal cord.
Digital subtraction angiography (DSA) has been conventionally considered the gold standard for imaging traumatic carotid injuries. Angiography can detect subtle intimal defects and recognize intraluminal thrombus or aneurysm formation. However, DSA has limitations regarding practicality (time-consuming in poly-trauma patients), invasiveness, expenses, and availability. Angiography is usually reserved for patients with an uncertain diagnosis or those with a clear indication for an endovascular intervention as this imaging modality is therapeutic as well as diagnostic.
Magnetic resonance imaging (MRI) and angiography (MRA) can be a useful adjunct for the detection of post-traumatic carotid ischemic sequelae but does not play a role in the acute workup of a recent carotid injury.
The treatment of carotid artery contusion depends on the patient stability, the presence of symptoms, other organ damage, and comorbidities. Before any specific treatment can take place, the patient must be treated like any trauma patient and stabilized. Undiagnosed or mismanaged cervical injuries secondary to neck trauma can result in a mortality rate of greater than 15%. Furthermore, up to 10% of neck injuries will have associated respiratory compromise. Loss of airway patency may occur, resulting in mortality rates as high as 33%, therefore, securing the airway is the first critical step in management.
The treatment of carotid artery contusion varies from observation to heparinization, to open embolectomy. If the external carotid artery is involved, then conservative measures are adequate.
Conservative management: Multiple studies have demonstrated that systemic anticoagulation improves neurologic outcome in patients sustaining carotid artery contusion and blunt carotid injury-related stroke. Initially, standard heparinization protocols were used. Heparin promotes clot stabilization if present, clot resolution through intrinsic fibrinolytic mechanisms and prevent propagation of thrombosis. Initial studies show that up to 45% of patients with blunt carotid injury-related stroke achieve good neurologic status. Antiplatelet agents have gained a lot of popularity recently due to its ease of administration. Both therapies have equivalent results in prevention of the strokes as well as healing progression rates in carotid trauma patients. Recent studies showed a reduction in stroke rate for carotid artery injury from 64% in untreated patients to 6.8% in treated patients (either anticoagulation or antiplatelet). However, initiation of antithrombotic therapy in multi-injured patients should always be carefully considered due to the risk of bleeding. Antithrombotic therapy is contraindicated in patients with recent traumatic brain injury with or without intracerebral hemorrhage.
Surgical treatment: Simple intimal tears can be repaired by direct suture or via endarterectomy and patch angioplasty. Diffuse intimal tears and transmural damage are repaired via resection and vein graft interposition. Again, open surgical intervention is reserved for patients with acute focal neurologic deficits. Following completion of the arterial repair, a carotid angiogram should be obtained to assess the circulation and to be certain of the patency of the carotid circulation with no residual clots.