Blunt-Trauma Carotid Artery Injury: Mild Symptoms May Disguise Serious Trouble
Sandra Carr, MD; Bryan Troop, MD; Joseph Hurley, MD; Richard Pennell, MDTHE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 2 - FEBRUARY 96
In Brief: Injury to the carotid artery can occur in athletes by direct blow to the neck or by hyperextension of the neck. After such injury, symptoms may be mild or transient. Catastrophic complications such as stroke can occur if the injury is not recognized and treated. Neurologic changes such as transient weakness or transient unilateral blurred vision that occur after a hyperextension injury or a direct blow to the neck may indicate a carotid artery injury. A careful neurologic examination can help identify most carotid artery injuries, but because the symptoms of injury may not appear immediately, follow-up may be necessary. Treatment may consist of anticoagulation therapy or operative repair.
Carotid artery injuries are often associated with major morbidity and mortality, such as stroke or permanent neurologic deficit (1). Furthermore, diagnosis is frequently delayed because of a patient's severe multisystem injury, a physician's failure to suspect an injury caused by minor trauma, or a delay in symptom manifestation (1-3). Fortunately, blunt traumatic carotid injury—the type typical in sports—accounts for only 3% to 15% of all recognized injuries to the carotid artery (2,4,5). The low incidence, however, is part of what makes alertness to the condition important.
Early diagnosis and appropriate treatment of blunt carotid injuries are crucial because they may prevent permanent neurologic deficits (5). Early recognition requires astuteness, because many such injuries result from minor trauma that produces no other injuries (3-5). In addition, clinical manifestations of carotid trauma are often delayed for hours or days after the injury: Only 10% of patients with such injuries have early focal neurologic symptoms that may resemble those produced by closed head injuries (4).
Case 1. A 19-year-old high school hockey goalie was struck in the neck by a puck during a game. His neck was extended when injured, and he was not wearing neck protection. He was stunned for a few minutes but remained conscious. Although the patient wished to continue the game, his friends brought him in for medical assessment.
His neurologic examination in the emergency department was normal. He had a small bruise over his left neck and some swelling of the sternocleidomastoid. A carotid bruit was heard over the bifurcation. A carotid angiogram demonstrated an intimal dissection of the left common carotid artery (figure 1). The patient underwent surgical repair of the dissection and did well postoperatively, eventually returning to competitive hockey.
Case 2. A 31-year-old man was playing unsupervised tackle football when he was struck in the right side of the neck as he attempted to catch a pass. His neck was extended when he was injured. He developed blurred vision in his right eye and experienced a transient weakness of his left arm. He was brought to the emergency room from the field by his friends.
On examination, the patient did not have a carotid bruit. A duplex scan demonstrated a high-grade stenosis of the right internal carotid artery. An angiogram confirmed the injury, which had occurred just below the base of the skull (figure 2). A computed tomography (CT) scan of the brain was normal.
The patient was treated with intravenous heparin and later received warfarin sodium anticoagulation. A magnetic resonance imaging (MRI) scan of his brain was normal 2 days after his admission to the hospital. The patient's symptoms resolved completely within 10 days. MRI angiography several months after the injury confirmed that the patency of the internal carotid artery had been restored. However, a 3-mm pseudoaneurysm had developed, the size of which did not change during 2 years of follow-up via serial MRI angiography. The patient has remained asymptomatic after anticoagulation was stopped.
Causes and Consequences
As do many patients who have sustained blunt carotid injury, the patients described above experienced relatively minor trauma. In 62% of cases in which pathologic factors are known, the initial defect is an intimal tear that results in a thrombus (4). Blunt carotid injury may result from a direct blow, cervical rotation, chiropractic cervical manipulation, or hyperextension, such as during a tennis serve, endoscopy, or endotracheal intubation (3,5,6). The incidence of carotid artery injury in sports is not known.
Approximately 7% of blunt carotid injuries result from a direct blow to the carotid artery, such as in case 1 (2). A direct blow may occur during a fight, but carotid injury is more often associated with motor vehicle accidents, falls, or being tackled in football (4,6-8). The patient described in case 2 sustained a typical hyperextension lesion.
The possible consequences of blunt trauma to the carotid artery include intraluminal stenosis, immediate total occlusion, carotid dissection, chronic pseudoaneurysm, carotid-cavernous fistula formation, and acute hemorrhage (4). Pseudoaneurysms can occur when the media and adventitia are disrupted in addition to the intima (4,5). Carotid-cavernous fistulas might occur with an injury to the cavernous portion of the carotid artery that results in an abnormal communication between the high-pressure arterial system and the low-pressure venous system (4).
Blunt carotid injuries are most common at the internal carotid artery near the base of the skull (figure 3) and can be classified into three types according to the mechanism of injury. Type 1 injuries (stretch, traction, or rotation forces) involve a torn intima, and intramural dissection typically results (1,2,9). Sports in which type 1 injuries may occur include football, soccer, hockey, volleyball, and tennis.
In type 2 injuries, compression of the internal carotid artery occurs between the angle of the mandible and the upper cervical transverse processes. High internal carotid artery injuries result at the junction of the artery and the skull base. The force of impact can displace the brain anteriorly or posteriorly and can stretch and distort the distal internal carotid artery against the anterior clinoid process (5). Motor sport accidents would be most likely to create this scenario.
Type 3 trauma involves transmural crush damage to the artery that may result in secondary injury, thrombosis, and/or distal embolism (5). A direct blow to the neck from a hockey puck, baseball, racquetball, or lacrosse ball could cause such damage.
Diagnosis: Sometimes Delayed
Although many patients with blunt traumatic injuries to the carotid artery become symptomatic within 24 hours, patients may develop symptoms up to 6 months after the injury (3,4,7). Only 10% of patients display immediate symptoms; 55% have symptoms within the first 24 hours, and 35% have no symptoms until 24 hours or more after the injury. Patients with immediate symptoms frequently have a focal neurologic deficit and a normal CT scan (2,4,10). The primary arterial injury usually does not produce symptoms; symptoms typically result from distal thromboembolism.
Some patients may have a neck hematoma on the injured side (4). Other symptoms and signs include hemicrania, Horner's syndrome, paralysis, unilateral facial weakness, hemianesthesia, aphasia, amaurosis fugax (transient, unilateral blindness), or seizure (table 1) (2,4). Symptoms, however, might be minor: The patient in case 1 had minimal neurologic symptoms.
Carotid trauma should be suspected in any alert patient who has posttraumatic hemiparesis, because other insults that can cause hemiparesis are often associated with marked obtundation (3). Carotid trauma should also be suspected in any trauma patient who has a stroke or transient ischemic attack.
Angiographic studies are critical in evaluating patients who have suspected blunt carotid trauma, the clinical signs of which are often subtle (10). Patients with localizing neurologic signs that cannot be explained by known injuries should have carotid angiography. The most common arteriographic findings are those of tapering stenosis and arterial occlusion (6,8). Angiographic studies can be used to identify occlusive or aneurysmal disease and show the degree of collateral circulation. All extracranial vessels should be studied in cases of multiple injuries (2,4,8,10). Visualization of the intracranial circulation should be used to evaluate the patient who has neurologic deficits and to plan an extracranial-to-intracranial bypass (11,12). CT of the brain can be used to evaluate acute intracranial pathologic factors (2).
Conservative vs Operative Treatment
Although some authors advocate routine surgical correction of all carotid lesions, others have shown that such injuries may spontaneously resolve and may be safely managed nonoperatively (1,2,8,10,11). Therapeutic options include observation, use of anticoagulation or antiplatelet medications, surgical repair and/or revascularization, and arterial ligation (5,7). Generally, common carotid artery injuries should be repaired and distal internal carotid artery dissections should be treated with anticoagulants.
Much evidence indicates that nonoperative therapy involving anticoagulation medications yields results equivalent to surgical intervention (1,8). Intimal dissections of the internal carotid artery that extend into the petrous portion are usually treated with anticoagulation because an operative approach is hazardous (1). In patients who have a neurologic deficit, however, there is a slight chance that anticoagulation may convert a nonhemorrhagic infarct into a hemorrhagic infarct—usually with significantly greater morbidity (2).
Many authors have stated that surgical repair is safe and is recommended for patients who have mild neurologic deficits or no symptoms (1,2,4). An intimal tear can cause a thrombotic occlusion or embolus, which surgery can prevent (1,3,5). Injuries to the common carotid artery, as in case 1, are easily accessible and are often treated operatively (1).
Surgical options include thrombectomy with intimal repair, and local excision and grafting procedures (11). Thrombectomy with simple repair is possible in some cases; however, many patients so treated experience diffuse intimal damage (1). This is especially common with hyperextension injuries, as in case 2. In most cases of blunt common carotid injury, resection of the affected area with an interposition graft is recommended (1,4). In patients with injuries to the distal internal carotid artery, extracranial-to-intracranial bypass has been used successfully, but experience with this technique is limited (1).
Arterial ligation is advocated for patients who have severe neurologic deficits that result from blunt trauma. Ligation, however, can be dangerous, because only 20% of the general population has a complete collateral circulation (2). Ligation also may result in propagating a thrombus from the top of an occluded internal carotid artery into a patent middle cerebral artery, which can increase the neurologic deficit and may cause a delayed stroke (1).
Steps for Prevention
Preventing blunt carotid artery injuries should be a major goal of those responsible for the medical care of athletes. Headgear is the most important equipment for preventing carotid injury in hockey and football (12). Mandatory use of face masks in junior hockey has resulted in a substantial decrease in facial and dental injuries (13). Likewise, neck protectors could help prevent carotid artery injuries. Neck protectors should be required in more sports—especially for hockey goalies—to prevent blunt carotid injuries and other sports-related trauma.
Dr Carr is a resident in vascular surgery at Northwestern University Medical School in Chicago. Dr Troop is the director of trauma services in the Department of Surgery at St John's Mercy Medical Center in St Louis and a fellow of the American College of Surgeons. Drs Hurley and Pennell are vascular surgeons at St John's Mercy Medical Center. Address correspondence to Bryan Troop, MD, St John's Mercy Medical Center, 621 S New Ballas Rd, Suite 560A, St Louis, MO 63141.