Blunt carotid and vertebral artery injuries
Introduction
Blunt cerebrovascular injuries (BCVI) have been sporadically described since 1967 through a number of case series.55 Early case reports described patients with recognised symptoms of cerebral ischaemia, and nearly all were symptomatic at the time of the diagnosis. Presenting symptoms define the laterality of the cerebrovascular injury and isolate it to the respective extracranial arterial supply. Carotid injuries typically present with a contralateral sensory or motor deficit, and vertebral injuries present with ataxia, vertigo, emesis, and possible visual field deficits. A carotid-cavernous fistula may present with orbital pain, proptosis, hyperaemia, cerebral swelling, or seizure. The degree of symptoms is a variable depending on whether the vessel is occluded or whether the resultant injury acts as a nidus for subsequent embolic events. Patients typically have coexisting traumatic brain injuries that may mask signs and symptoms of BCVI.
Three basic mechanisms of injury for BCVI are encountered: (1) extreme hyperextension and rotation, (2) a direct blow to the vessel, and (3) vessel laceration by adjacent bone fractures.21 The most common mechanism causing blunt carotid injury results from hyperextension of the carotid vessels over the lateral articular processes of C1–3 at the base of the skull. There are also scattered case reports of chiropractic manipulation34 and rapid head turning with exercise causing BCVI.53 A direct blow to the artery typically occurs with a misplaced seatbelt across the neck during a motor vehicle crash or in the setting of hanging. This injury pattern typically occurs in the proximal internal carotid artery as opposed to the distal aspect. Injury to the carotid vessels can occur basilar skull fractures involving the petrous or sphenoid portions of the carotid canal. The most common accepted mechanism for vertebral artery injury is injury secondary to fractures of the transverse foramen through which the vessel courses (cervical vertebrae 2–6).19 In addition, the vertebral vessels are relatively fixed throughout the vertebral canal making it susceptible to hyperextension and stretch injuries.
Depending on the nature of the injury, the traumatic event may cause intimal disruption, thrombosis, or rarely transection. Even though the patient may have a small intimal flap at the time of injury, the injury may progress to dissection, near-occlusion, or occlusion. All stages of injury are a nidus for platelet aggregation and a possible embolic source to the cerebral circulation.
Since 1990, there have been two major advances that have altered the care of patients with BCVI:
- (1)
the implementation of standardised screening protocols allowing diagnosis of BCVI prior to the development of neurological ischaemia, and
- (2)
the recognition that antithrombotic therapy essentially eliminates the ischaemic events in asymptomatic patients.
The vast majority of BCVI occur at the base of the skull, within the carotid canal, or within the vertebral canal. Traditional operative repair of these injuries is technically demanding, and if the lesion extends into the base of the skull, technically feasible but not without high surgical morbidity. Antithrombotic therapy has been recommended in the form of early heparinisation; however, many of these patients have coexisting traumatic brain injuries negating the use of heparin. Early anticoagulation has been shown to reduce the incidence of neurological events associated with BCVI, and it appears to impact BCVI related mortality as well. The ensuing review will address the following aspects of BCVI: screening, diagnostic imaging modalities, treatment, outcomes and follow-up.
The overall incidence of BCVI has been universally reported as <1% of all trauma admissions for blunt trauma, but this relatively small population of patients has a stroke rate ranging from 25 to 58% and mortality rates of 31–59%.3, 9, 31 The variability in incidence of BCVI is 0.19–0.67% for unscreened populations as compared to 0.6–1.07% for screened populations.9 Common mechanisms of injury associated with BCVI include motor vehicle crash (41–70%), direct cervical blow (10–20%), automobile versus pedestrian (12–18%), fall from height (5–15%), and hanging (5%).3, 9 Most common associated injuries include closed head injuries (50–65%), facial fractures (60%), and thoracic injuries (40–51%).3, 9 Nearly half of all patients will have cervical spine fractures at the time of diagnosis.
Patients may present to the trauma centre with obvious signs of BCVI; however, significant proportions of patients are initially asymptomatic and subsequently develop symptoms after a latent period. The time from initial injury to the development of symptoms is variable, but several series have reported times from 1 h after injury to several weeks after injury.10, 15, 22, 46 Prior to the initiation of screening protocols, Berne et al. found a median time to diagnosis of 12.5 h for survivors of BCVI and 19.5 h for nonsurvivors suggesting a sufficient window of opportunity for diagnosis and treatment.3 Neither admission GCS nor baseline neurological examination correlated with subsequent development of symptoms. Because a large number of these patients are asymptomatic on arrival to the trauma centre, initial markers are needed to identify patients at greatest risk of injury. In an attempt to identify patients in the asymptomatic latent period, screening protocols were first suggested in the early 1990s.
While there is not consensus on the ideal screening protocol, several authors have found associations with signs, symptoms, and risk factors identified on admission. The first and most comprehensive screening protocol was initiated at the Denver Health Medical Center. These “Denver Criteria” are listed in Table 1.9, 18 With this screening protocol, the authors reported an overall BCVI incidence of 0.86%. Exactly 4.8% of all trauma patients were screened based on defined risk criteria, and 18% of screened patients were found to have an injury. Fifty-two percent of these screened patients were asymptomatic. Neurological morbidity was 16%, and BCVI associated mortality was 15%.9 Using the Memphis criteria (Table 1), they found an incidence of 1.03%, 3.5% of all blunt trauma patients were screened, and 29% of screened patients were found to have an injury.41 Both screening regimens, mandated four-vessel cerebral angiography if the patient met at least one of the screening criteria.
Some authors have suggested a more restricted screening protocol in an effort to limit the number of negative examinations. Rozycki et al. prospectively screened only patients who had a cervical seatbelt sign.9 Their group screened 81 patients for BCVI, and found 4 injuries; however, 2 of the 4 patients died with resultant 50% mortality. Their reported 5% screening yield with a restricted screening protocol is much lower than more conservative series, but this reasoning is largely flawed with Type II error. DiPerna et al. also evaluated the importance of a “seat-belt sign” across the neck and found only 1 patient in a series of 131 patients to have a carotid injury.24 It is important to note that they did not use angiography on all patients and relied on duplex ultrasound for all of their examinations. Even so, relying on just physical signs of blunt injury to the neck fails to identify the majority of occult injuries.
The utility of aggressive screening has been questioned altogether. Mayberry et al. reviewed a 10-year experience and found 17 patients with BCVI.37 Their screening threshold included patients with focal neurological signs and neurological deficits not explained by head CT. Eleven patients developed a stroke and nine patients developed neurological symptoms within two hours of admission. Of the two delayed strokes, only one of the patients would have been identified with a more liberal screening protocol. The study questioned the impact of broad screening on BCVI outcomes. The major limitation of this analysis is that the total number of occult injuries and their resultant outcomes in their population are unknown; therefore, the cost of a missed injury cannot be determined.
All major trauma centres should have predetermined screening criteria for blunt cerebrovascular injury. Using the Denver criteria, an institution can expect a screening yield of 18%, and using the Memphis criteria, a screening yield of 29% can be obtained. Limiting screening criteria further is likely to miss occult injuries with an increased risk of morbidity.
Section snippets
Diagnostic modalities
Selective digital subtraction angiography (DSA) was the initial diagnostic gold standard for screening patients with suspected BCVI. The Denver group designed an angiographic grading system for BCVI (Table 2).8 Most importantly, the grading scale held prognostic value for patients’ future risk of stroke. The stroke risk and mortality (%/%) for each grade are the following: Grade I (3%/11%), Grade II (11%/11%), Grade III (33%/11%), Grade IV (44%/22%), and Grade V(100%/100%).8 The stroke risk
Treatment
While operative intervention has been shown to reduce the mortality and stroke rate associated with these lesions,48 the majority of these lesions have limited embolic potential with early antithrombotic therapy.31 The results of recent series addressing treatment for BCVI are summarised in Table 3. Fabian et al. reported the first large series demonstrating improved neurological outcome associated with early use of antithrombotic therapy.31 Their analysis revealed the benefit of heparin
Conclusions
Over the past two decades, BCVI has been increasingly recognised. Screening protocols have identified patients with injury patterns at greatest risk. Imaging technology continues to improve, and currently, 16-slice CTA is rivalling the accuracy of conventional DSA. Increased awareness and screening protocols have identified a population of patients that are asymptomatic. Recognition and early antithrombotic therapy has reduced the neurological morbidity of this injury, and if the patient is
Conflict of interest
None.
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Cited by (44)
Treatment strategies for patients with concurrent blunt cerebrovascular and traumatic brain injury
2021, Journal of Clinical NeuroscienceCitation Excerpt :Isolated blunt cerebrovascular injury (BCVI) is a relatively rare entity with approximately 1–2% incidence in the setting of trauma [1,2].
Neurovascular trauma: Diagnosis and therapy
2021, Handbook of Clinical NeurologyCitation Excerpt :Blunt injury most commonly affects the extracranial carotid arteries, with an overall incidence of 0.1%–1.6% of trauma victims (Davis et al., 1990; Cogbill et al., 1994; Biffl et al., 1998, 2002a; Rogers, 1999; Berne et al., 2001; Kerwin et al., 2001; Miller et al., 2001). These injuries typically occur in the cervical or petrous segments of the internal carotid artery—which are particularly susceptible to rapid deceleration injuries—and usually spare the carotid bulb (Hart and Easton, 1983; Cothren et al., 2003; Arthurs and Starnes, 2008). Blunt traumatic injury to the intracranial portions of the internal carotid artery, or any other intracranial artery, is uncommon.
Follow-up imaging of traumatic vertebral artery dissections is unnecessary in asymptomatic patients
2019, Journal of Vascular SurgeryLimited Clinical Relevance of Vertebral Artery Injury in Blunt Trauma
2018, Annals of Vascular SurgeryCitation Excerpt :Blunt vertebral artery (VA) injury can be even more difficult to diagnose but can also lead to significant neurologic morbidity and mortality. The improved ability to diagnose BCVI has resulted in the recognition of BCVI in patients while they are still asymptomatic.8–18 BCVI is a potentially devastating injury, carrying a stroke risk up to 50%.19,20
Neurotrauma
2018, Handbook of Clinical NeurologyCitation Excerpt :Typical symptoms include ataxia, vertigo, and nausea. Internal carotid artery injuries secondary to trauma are well described, particularly after hyperextension of the neck (Arthurs and Starnes, 2008). In one study of 67 patients with blunt-force carotid artery injury, 89% were due to road traffic accidents, and 6% to assaults (Fabian et al., 1996).
Epidemiology, pathophysiology, and treatment of traumatic cervical vascular injury
2017, Seminars in Spine SurgeryCitation Excerpt :About 30% of patients are not candidates for antithrombotic therapy due to contraindication from associated injuries.35 Surgical and endovascular interventions exist for the management of vascular injury, including embolization, stent placement, vessel ligation, surgical repair, and revascularization.39 While these interventions may be effective, they present a greater risk for complications.