Blunt traumatic carotid artery dissection still a pitfall? The rationale for aggressive screening

Dissections start with a tear in the intima/media layer of the vessel wall, after which a hematoma develops. Transient ischemic attacks or ischemic strokes after CAD may occur because of thromboembolism, or, in less frequent cases, artery occlusion due to the hematoma in the vessel wall [4, 6, 15]. Dissection can also progress in the subintimal or subadventitial layer, leading to local compression resulting in a loss of function of the adjacent cranial nerves, presenting as Horner syndrome (resulting from periarterial sympathetic plexus disruption), facial nerve palsy, or hypoglossal palsy [1, 14, 15].

Traumatic causes of a CAD are: (1) direct trauma to the artery, (2) hyperextension–rotation, (3) blunt intraoral trauma, (4) skull base and mandible fractures, and (5) combination of head–thorax trauma with overstretching of the carotid artery [4, 16]. A specific risk factor for the occurrence of CAD is therefore a trauma in which there is a serious cervical hyperextension, particularly in combination with complex and dislocated midfacial or mandible fractures, a GCS ≤6, closed head injury, skull base fractures involving the carotid canal or fracture of the petrous bone, Le Fort II or III fracture, or a cervical spine fracture (Table 1) [3‐5, 9, 16, 17]. All of our patients presented with a combination of these CAD risk factors, and all had facial fractures and/or cervical spine fractures.

Typical symptoms of CAD are pain in the ipsilateral face or neck, followed by contralateral weakness or sensory loss. CAD should also be considered when confronted with a hematoma in the neck or a so-called “seatbelt sign,” a cervical bruit in patients younger than 50 years, ptosis and pupillary asymmetry (ipsilateral Horner’s syndrome), a hemorrhage of arterial origin in mouth, nose, or ear, or wounds in the trajectory of the carotid artery [1, 3‐5, 8, 9, 16]. However, multiply injured patients often cannot express pain due to a lower level of consciousness or a distracting injury.

The interval between blunt cervical injury and (neurological) deficits can be periods of hours, days, or even months, like in our five patients [6, 15, 18‐20]. This delay between the moment of dissection and the occurrence of focal neurological symptoms is the critical factor that makes diagnosis a demanding task. Further, it is not at all clear that early detection would have found a treatable lesion after a stroke that is clinically evident hours or days after the injury. Reports of strokes developing after initial negative screening have been made [20]. On the other hand, the time interval between injury and onset of symptoms offers the possibility of screening for CAD and initiating therapy before the neurological symptoms become clear.

The challenge is to identify patients with CAD before the onset of neurological complications. Several authors have proposed that liberal screening for blunt carotid and vertebral artery injuries is justified [10, 11, 16, 21], although not all authors were convinced that early detection by screening would also lead to better outcomes [14, 20]. Cothren et al. [11] showed that a screening programme for traumatic CAD was cost-effective since it reduced ischemic strokes and thus costs due to long-term disability. Furthermore, although intracranial dissections are frequently detected and have relatively poor outcomes, extracranial dissections are detected more frequently and stand to benefit from early detection because they are surgically accessible. If early diagnosis of CAD is essential, then who should undergo imaging for screening? It is definitely not advocated to screen for CAD in every trauma patient because of the increased exposure to radiation and its low cost-effectiveness. The yield of screening is probably greater if screening criteria based on a set of risk factors are used (Table 1) [13, 16, 21]. Aggressive screening using these strict criteria identified CAD in 30% of those screened [17, 26]. The most efficient type of imaging is yet to be determined [13].

Noninvasive imaging, such as CTA, now allows increasingly rapid and safe evaluation of the presence of CAD, although at the cost of some degree of accuracy [8]. The gold standard for diagnosing CAD is still conventional angiography. Besides being expensive and more difficult to obtain, angiography is associated with a complication rate of 1–2% [4]. In the patients reported here, CTA was used. Trauma patients often already have an indication for CT scanning, and CTA can be a part of this modality. Miller et al. [8] found a sensitivity and specificity of 47 and 99%, respectively, for CTA. As stated above, by using the screening protocol (Table 1) for blunt trauma patients, the diagnostic yield can be enhanced, with sixteen-slice multidetector CTA providing the best results so far [8, 22]. However, in our department, as in most trauma centers these days, 128-slice CTA is available, and further upgrades to and development of CT technology will probably provide quicker and more accurate diagnosis. Magnetic resonance angiography (MRA) is not available around the clock in all hospitals, and can be difficult in ventilated patients. Duplex ultrasonography (US) can be used as a quick, noninvasive screening tool, and is easy to implement on the ICU. However, duplex US is not available 24/7 in most hospitals, is less reliable in inexperienced hands, is difficult to interpret if there is a hematoma in the neck, and is less reliable for locating dissections near the skull base [4]. When duplex US leads to suspicion of a dissection, additional CTA, MRA, or angiography should be obtained. In our daily practice, CTA has virtually replaced angiography in CAD diagnosis. Only if the diagnosis remains unclear is angiography performed.

Biffl et al. [25] proposed imaging-based criteria to define high-risk arterial injury patterns for stroke and mortality following CAD, using a five-grade classification system (Table 2). Based on angiographic data, the risk of stroke increased from three percent (grade I) to one hundred percent in grade IV, and mortality accordingly increased from eleven to one hundred percent. This classification system potentially provides an excellent way to classify lesion type, bearing in mind that is was designed for conventional angiography.

Management of CAD due to blunt trauma remains controversial. Treatment options include observation, antithrombotic therapy, and endovascular stenting [2, 7, 21, 23, 24]. It has been suggested that with the help of an angiography-based classification system, it may be possible to provide an individualized therapy [7]. However, the use of a classification system has not yet proven to result in a better outcome [9, 14].

It has also been suggested that early recognition of CAD and initiation of treatment with anticoagulant or antiplatelet therapy reduces the number of cerebral ischemic events and improves outcome [7, 11], but this also remains to be proven. Furthermore, the type (antiplatelet versus anticoagulant agents) and duration of antithrombotic therapy remain controversial [27]. Arthurs et al. reviewed the literature on treatment outcomes for blunt cerebrovascular injury utilizing heparin, antiplatelet agents, and no antithrombotic therapy. They concluded that treatment reduces the neurological morbidity and mortality associated with BCVI. It remains less clear whether patients should be treated with heparin, aspirin, adenosine diphosphate receptor inhibitors, or a combination therapy.

Unfortunately, patients who sustain blunt carotid injuries typically have associated closed head injuries, solid organ injuries, or pelvic fractures that prevent the use of early anticoagulation [27].

Literature on the stenting of traumatic CAD is still limited to small series with relatively short follow-up [7, 23, 24]. A proportion of the dissections occur at the skull base or intracranially, and are therefore inaccessible to surgical or endovascular therapy. However, recent studies of stenting for CAD show excellent early and one-year patency rates and a low major adverse event rate [24]. Further studies are warranted to define the role of this treatment modality in the setting of treatment of blunt carotid injury.

Some authors have stated that screening is not useful because it will not change therapeutical options, leaving antiplatelet therapy as the only therapeutical option [20, 21]. Clearly, if all trauma patients were to receive aspirin, many would be overtreated and incur an increased risk of bleeding. The usefulness of liberal screening could also be questioned based on a recent report demonstrating that nearly one-third of patients with cerebrovascular injuries are probably not candidates for endovascular or antithrombotic therapy due to intracranial lesions or concomitant injuries, as in the third and fourth cases we presented here [20]. However, easily accessible extracranial lesions occur more frequently than intracranial lesions and may benefit from early detection [11, 23].

A limitation of the present report is that we were not informed about the total number of patients in whom a dissection was missed due to a lack of routine CTA screening in our hospital. In the literature, an incidence of CAD of 1% in blunt trauma admissions was suggested. On the other hand, all five patients described above met the criteria for CAD screening mentioned in Table 1 and could possibly have been offered earlier treatment, but it remains uncertain as to whether their outcomes would have been better had a more aggressive screening and treatment policy been adopted. The patients received only medical treatment because of surgically or endovascularly inaccessible lesions, and especially because of delays between trauma and diagnosis. Also, because the cases presented here are major trauma cases, the role that other neurological injuries may have played in these patients’ adverse outcomes is unclear.