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Blunt cerebrovascular injury: Treatment and outcomes

Blunt cerebrovascular injury: Treatment and outcomes
Literature review current through: Sep 2023.
This topic last updated: Feb 15, 2022.

INTRODUCTION — Blunt carotid and vertebral artery injuries, collectively termed blunt cerebrovascular injuries, are uncommon but potentially devastating events. The incidence of blunt cerebrovascular injury in patients sustaining blunt trauma is about 1 percent [1,2]. Stroke after blunt carotid injury is associated with mortality rates that range from 23 to 28 percent, with 48 to 58 percent of survivors suffering permanent severe neurologic deficits [3,4].

Given the potential for high morbidity and mortality rates associated with untreated blunt cerebrovascular injury, expectant management is not appropriate unless there are contraindications to treatment. Treatment strategies include antithrombotic therapy, surgical repair, and endovascular intervention. The treatment strategy for a given individual depends upon his/her symptoms, site of injury, severity or grade of injury, associated injuries that may complicate treatment, and local expertise [1].

The treatment and outcomes of blunt cerebrovascular injury are reviewed. The injury mechanisms, screening, and diagnosis of blunt cerebrovascular injury are reviewed elsewhere. (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation".)

Penetrating cerebrovascular injury and spontaneous cerebrovascular dissection are discussed elsewhere. (See "Penetrating neck injuries: Initial evaluation and management" and "Cerebral and cervical artery dissection: Clinical features and diagnosis".)

INJURY GRADING — A grading scale for blunt cerebrovascular injury was created to standardize clinical communication and to guide therapy [5]. This grading scale was developed based on conventional arteriography findings, but it has been validated using computed tomographic angiography [6].

The injury grades given below apply to carotid or vertebral artery lesions.

Grade I: Intimal irregularity or dissection with <25 percent luminal narrowing.

Grade II: Dissection or intramural hematomas with ≥25 percent luminal narrowing, intraluminal clot, or a visible intimal flap.

Grade III: Pseudoaneurysm or hemodynamically insignificant arteriovenous fistula.

Grade IV: Complete occlusion.

Grade V: Transection with active extravasation (hemorrhage) or hemodynamically significant arteriovenous fistula. These injuries are often lethal. Transection injuries mandate immediate attempts to control bleeding. (See 'Other interventions' below.)

For the carotid artery, stroke rates increase with increasing injury grade [5]. Stroke incidence and neurologic outcome for vertebral injury are independent of injury grade. In a study of 171 patients found to have 236 blunt cerebrovascular injuries, the distribution of injury is representative: grade I (58 percent), grade II (22 percent), grade III (14 percent), grade IV (11 percent), and grade V (3 percent) [1,5].

The grading scale has been widely used in its original form, but it has been suggested that within the grade II and III classifications, there may be an incremental increased risk based on a higher degree of luminal narrowing [7].

TREATMENT — Although the incidence of blunt cerebrovascular injury has increased with routine screening, and experience with this problem has grown substantially at busy trauma centers, there are still no controlled trials to help guide management. Treatment is based upon the demonstration of reduced neurologic morbidity and mortality in treated patients compared with those who are untreated (and to historical controls), from indirect evidence derived from the penetrating neck injury literature [8], and from strategies used in the management of nontraumatic cerebrovascular disorders (eg, spontaneous cerebrovascular dissection). Our treatment recommendations are in general agreement with protocols established by major trauma societies (algorithm 1) [9,10].

The mainstay of treatment for surgically inaccessible injuries (>99 percent) is antithrombotic therapy (heparin, warfarin, or antiplatelet therapy), but the optimal regimen is not known with respect to agent, duration of treatment, or endpoint of therapy. Associated injuries often limit antithrombotic therapy. Endovascular intervention is another option, but stents also require antithrombotic therapy. Factors that determine the treatment strategy for a specific individual include symptoms, site of injury, severity or grade of injury, and associated injuries that may contraindicate a specific therapy [5]. The rationale and recommendations for antithrombotic therapy or other intervention, follow-up, and injury grade-specific recommendations are discussed below. (See 'Antithrombotic therapy' below and 'Other interventions' below and 'Follow-up for healing or progression' below and 'Injury grade-specific recommendations' below.)

Antithrombotic therapy — We recommend antithrombotic therapy (heparin or antiplatelet therapy) for all patients with blunt cerebrovascular injury who do not have contraindications (eg, active hemorrhage from the vessel [grade V]). (See 'Associated injuries that may contradict antithrombotic therapy' below.)

The rationale for using antithrombotic therapy for blunt cerebrovascular injury is based on retrospective reviews reporting reduced rates of ischemic neurologic events and better neurologic outcomes among patients treated with heparin or antiplatelet agents compared with untreated patients [1-4,11,12]. Stroke rates in case series from the era prior to screening for these injuries were considerably higher than contemporary series, as injuries were previously not diagnosed until the ischemic neurologic event occurred. In studies that reflect the use of antithrombotic therapies, overall stroke rates for blunt injury (all grades) of the internal carotid artery, common carotid artery, and vertebral injuries are 26 to 41 percent, 11 percent, and 14 to 24 percent, respectively [1,13,14]. Stroke rates increase with increasing injury grade for carotid but not vertebral artery injuries [1,5]. In one study, stroke rates for 114 blunt carotid and 79 blunt vertebral injuries were as follows [1]:

Grade I: Carotid 8 percent; vertebral 6 percent

Grade II: Carotid 14 percent; vertebral 38 percent

Grade III: Carotid 26 percent; vertebral 27 percent

Grade IV: Carotid 50 percent; vertebral 28 percent

Grade V: Carotid 100 percent

Multiple retrospective studies have reported improved neurologic outcomes among symptomatic patients and fewer ischemic neurologic events (stroke) in asymptomatic patients with blunt cerebrovascular injury who are treated compared with those who are not [1,2,4,14-17]. Injury-specific mortality rates are also reduced. However, patients who are not treated are usually more severely injured, with contraindications to treatment, such as head injury, which influences the comparison. The largest of these studies are summarized below.

In a large retrospective review, arteriography was used to screen 727 of 15,767 blunt-trauma patients at high risk for blunt cerebrovascular injury, which was identified in 244 of the patients [16]. Antithrombotic therapy was initiated in 187 asymptomatic patients with heparin (n = 117), low-molecular-weight heparin (n = 11), and antiplatelet agents (n = 59). Asymptomatic patients who were treated with antithrombotic therapy had a lower ischemic neurologic event rate compared with 48 patients who were not able to be anticoagulated (0.5 versus 21 percent).

A retrospective trauma registry review identified 139 blunt cerebrovascular injuries in 96 patients, 75 involving the carotid arteries (14 bilateral), 64 involving the vertebral arteries (14 bilateral), and 15 patients with both [14]. Antithrombotic therapy (heparin, antiplatelet therapy) was used to treat 43 of 75 carotid injuries and 39 of 50 vertebral artery injuries. Stroke rates for treated and untreated patients were 6.8 versus 64 percent for carotid artery injury, and 2.6 versus 54 percent for vertebral artery injury.

Blunt carotid artery injury was identified in 114 patients screened out of 643 patients at risk from 13,280 blunt trauma admissions [15]. None of 73 patients treated with antithrombotic therapy suffered a stroke, whereas 46 percent of the 41 patients who did not receive anticoagulation developed ischemic neurologic events.

Choice of agent — In agreement with major society trauma guidelines (algorithm 1), we suggest initiating antithrombotic therapy in patients with blunt cerebrovascular injury with unfractionated heparin [9,10]. We administer heparin as a weight-based infusion of 15 units/kg per hour (no loading dose), to achieve an activated partial thromboplastin time (aPTT) of 40 to 50 seconds. This is a lower target range compared with other indications and was selected based on its efficacy and attempted minimization of bleeding complications [1,3,4]. (See "Heparin and LMW heparin: Dosing and adverse effects".)

We prefer heparin in the acute setting because it is reversible (many of these patients will require surgery for unrelated injuries) and it may be more effective than antiplatelet drugs [1]. There are no randomized trials directly comparing heparin with antiplatelet therapy in the management of blunt cerebrovascular injury; however, a few small retrospective case series and reports from two large trauma centers suggest that antiplatelet therapy may be at least as effective as systemic heparinization for stroke prevention [1,11,12,18-20]. Key results are summarized below.

A study of 114 patients with blunt cerebrovascular injury reported no significant differences in healing or in progression of injury grade whether the patients were treated with heparin (n = 45) or aspirin (n = 24) [1]. Among the 45 patients who had ischemic neurologic symptoms attributable to the injury, treatment with heparin (n = 31) improved the patient's neurologic status in a greater percentage of patients (71 versus 60 percent) compared with patients treated with aspirin (n = 5), but the difference was not significant.

In a study of 301 patients with blunt cerebrovascular injury (some overlap with the study above), heparin (n = 192), aspirin (n = 67), or aspirin and/or clopidogrel (n = 23) were used to treat 192 asymptomatic patients; 107 patients were untreated [11]. There were no significant differences in injury healing (39, 43, 46 percent) or progression of injury grade (12, 10, 15 percent) between the treatment groups. A single stroke (0.5 percent) occurred among patients who were treated (heparin group) compared with a stroke rate of 21 percent in the untreated group.

A prospective study identified 22 patients with blunt carotid injury over an eight-year follow-up period [20]. Of these, eight patients received no treatment, seven patients were treated with heparin, and seven were treated with antiplatelet therapy. No differences in neurologic outcomes were observed between anticoagulated patients and those receiving antiplatelet therapy. Bleeding complications were higher in patients treated with heparin compared with antiplatelet therapy, with four of the anticoagulated patients suffering major bleeding complications that required cessation of heparin and blood transfusion.

A retrospective study of 677 patients with blunt cerebrovascular injury reported that 23 of 600 (4 percent) treated with aspirin sustained a stroke, compared with 9 of 77 (12 percent) receiving anticoagulation. After adjusting for injury grade, anticoagulation was associated with higher likelihood of stroke (odds ratio [OR] 3.01, 95% CI 1.00-8.21). In the propensity-matched analysis, patients who received anticoagulation had a 15 percent (95% CI 3.7%-26.3%) higher probability of sustaining a stroke compared with those receiving aspirin [21].

For patients who have contraindications to anticoagulation with heparin or if heparin is unavailable, we recommend antiplatelet agents (aspirin 325 mg daily or clopidogrel 75 mg daily). There are currently no data regarding the treatment of blunt cerebrovascular injuries with direct thrombin inhibitors or factor Xa inhibitors. Given the data supporting the safety and efficacy of these medications in other scenarios (eg, stroke prevention with atrial fibrillation, treatment and prevention of venous thromboembolism), they warrant study in this patient population. (See 'Associated injuries that may contradict antithrombotic therapy' below.)

The treatment of patients who suffer stroke after blunt cerebrovascular injury has not been well studied. One group reported significant improvement in neurologic outcomes following heparin therapy [4]. A later trial found that antiplatelet therapy was not inferior to anticoagulation (heparin followed by warfarin) for preventing recurrent stroke after carotid dissection (3 versus 1 percent) [22]. The small advantage offered by antithrombotic therapy was counterbalanced by one major subarachnoid bleed in the anticoagulation group. It should be noted that all of the enrolled patients had suffered a stroke or transient ischemic attack, and that these were not trauma patients, so whether these results can be generalized to patients with blunt cerebrovascular injury is unclear.

Although dual antiplatelet therapy may be indicated for other conditions, we do not use dual antiplatelet therapy in patients with blunt cerebrovascular injury due to an increased risk of bleeding and undemonstrated benefit [23].

For long-term anticoagulation, a transition to warfarin has been used in the past, but antiplatelet therapy may be preferable to warfarin in the long term due to its potential equivalent efficacy (as discussed in the paragraphs above), better safety profile, and lower cost [11,21].

However, this recommendation may change in the future. An analysis of the Nationwide Readmission Database reported that the rate of readmission with new stroke in patients with blunt cerebrovascular injury was 3.8 percent [24]. Patients treated with antiplatelet medications had a higher rate of readmission for stroke compared with those treated with other anticoagulant medications (5.7 versus 1.8 percent). (See 'Follow-up for healing or progression' below and 'Injury grade-specific recommendations' below.)

Monitoring and complications — Patients treated with antithrombotic therapy should be closely monitored for bleeding complications, which can be serious. (See "Heparin and LMW heparin: Dosing and adverse effects", section on 'Other complications' and "Management of warfarin-associated bleeding or supratherapeutic INR", section on 'Mitigating bleeding risk'.)

Preexisting abnormalities in coagulation increase the risk of bleeding in the injured population. Treatment of multiply-injured and brain-injured patients may be compounded by trauma-induced coagulopathy that further increases the risk for hemorrhage. (See "Coagulopathy in trauma patients" and "Management of acute moderate and severe traumatic brain injury", section on 'Management of coagulopathy'.)

Extracranial hemorrhage is a frequent complication of standard anticoagulation in patients with multiple injuries. One study noted that bleeding requiring either transfusion or cessation of heparin occurred in 54 percent of patients treated with heparin when administering a loading dose or titrating to an aPTT goal of 60 to 80 seconds [3]. A more conservative protocol for initiation (no loading dose) and maintenance of heparin infusion (aPTT 40 to 50) should be used in any injured patient at risk for bleeding [1,4]. (See 'Choice of agent' above.)

The presence of new ischemic lesions on magnetic resonance imaging was found in one-half pf patients with blunt cerebrovascular injuries treated with antithrombotic therapy [25]. This deserves further study and may be another means of identifying higher-risk patients or adjusting stroke-preventive treatment.

Associated injuries that may contradict antithrombotic therapy — Some associated injuries (eg, traumatic brain injury) may contraindicate antithrombotic therapy in patients with blunt cerebrovascular injury, at least temporarily. For some other injuries, observational studies have demonstrated that the benefits of early treatment of blunt cerebrovascular injury appear to outweigh any potential harms [26-28]. (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation", section on 'Associated injuries'.)

As an example, in a review of 119 patients with concomitant blunt cerebrovascular injury and traumatic brain injury or solid organ injury, initiation of antithrombotic therapy on median hospital day three did not worsen brain or solid organ injury above baseline [26]. No patient required cessation of antithrombotic therapy, which consisted of heparin infusion in 71 percent and antiplatelet therapy in 29 percent. This has been corroborated by at least two other studies [27,28].

Other interventions — The nature of symptoms, injury location, and specific type (grade) of injury may indicate the need for other interventions in addition to antithrombotic therapy.

Surgery for accessible lesions — For patients without completed hemiplegic deficits, we suggest surgical management for patients with surgically accessible grade II through V blunt cerebrovascular injuries, in agreement with major trauma society guidelines (algorithm 1) [9,10]. However, many blunt cerebrovascular injuries involve the vessel (eg, internal carotid artery) at the base of the skull and are therefore not surgically accessible. In our experience, only 2 of our first 700 patients treated with blunt cerebrovascular injury had a surgically accessible lesion. This experience is shared by others. Thus, inaccessibility precludes direct surgical repair in most patients with blunt cerebrovascular injury.

Indirect evidence of benefit for this approach comes from observational studies of patients with penetrating cerebrovascular injury, which have found lower rates of neurologic morbidity and mortality for patients undergoing neck exploration and vascular repair compared with nonoperative management [8,29,30]. In retrospective studies that compared carotid artery repair with carotid artery ligation, patients with minimal neurologic deficits did much better with repair [13,31,32]. However, these results may not necessarily extrapolate to all patients with blunt cerebrovascular injury.

Similar to penetrating injury, a number of studies performed prior to the more frequent use of anticoagulation and endovascular techniques found that patients with blunt cerebrovascular injury who had minimal or no symptoms and an accessible carotid lesion did well with operative intervention (debridement, repair) [13,33-35]. As an example, one study reported a mortality of 8 percent for patients undergoing repair compared with 50 percent for those undergoing ligation, and patients who did not have a deficit before surgery were not likely to develop a deficit if the vessel was repaired [31]. However, patients with profound neurologic deficits on presentation are not likely to have any improvement.

Extracranial-intracranial bypass has been successfully employed in selected patients, but the use of this procedure for this indication is controversial [36].

Endovascular therapy for inaccessible lesions — Given that most blunt cerebrovascular injuries are surgically inaccessible, endovascular therapy may provide a treatment option for such injuries [1,5,9,10,12,37]. Our recommendations for endovascular treatment include placing stents only for severe flow-limiting stenoses, arteriovenous fistulae, or enlarging pseudoaneurysms greater than 1.0 to 1.5 cm in diameter. As a life-saving maneuver, endovascular embolization is recommended for vascular lacerations/transections (grade V injuries). Embolization has also been promoted in the setting of grade IV injuries to prevent distal embolization in the event of that the artery recanalizes; however, this approach has not been studied in any controlled manner in this subset of patients, and the risks must be considered in light of the data indicating that patients do well with antithrombotic therapy alone [38].

Many small series and case reports describe successful endovascular interventions for various types of blunt cerebrovascular injury, but there have been no controlled trials, and clear indications for endovascular therapy have yet to be developed [29,39-43]. Some groups have reported a good safety profile and patency with endovascular stenting [12,44-46]; however, the risks of endovascular treatment may exceed the benefits [47,48]. One study reported a 17 percent incidence of stent-related complications and a 45 percent occlusion rate [48]. The carotid artery occlusion rate was higher in patients who underwent stenting compared with patients who were treated with antithrombotic agents alone (21 versus 5 percent). One retrospective review reported a decrease in stent usage over time, which may possibly have been a response to adverse outcomes data. From 2011 to 2012, endovascular stenting was used to treat blunt cerebrovascular injuries in 34 percent, but from 2013 to 2016, stenting was used in only 9 percent [49]. Given that the stroke rate was no different, the authors concluded that anticoagulation alone was sufficient for the majority of blunt cerebrovascular injuries.

It is clear that caution is needed when endovascular therapy is chosen to avoid dislodging debris during stent deployment, and post-stent antithrombotic therapy is mandatory. (See "Overview of carotid artery stenting", section on 'Dual antiplatelet therapy'.)

Lytic therapy for patients with ischemic neurologic symptoms — The management of patients with blunt cerebrovascular injury who have a persistent neurologic deficit is similar to that of other stroke etiologies. Patients with ischemic neurologic symptoms within the hyperacute period may be eligible for thrombolytic therapy, provided there are no significant associated injuries to contraindicate its use, and appropriate expertise is available. (See "Management of acute moderate and severe traumatic brain injury" and "Cerebral and cervical artery dissection: Treatment and prognosis", section on 'Reperfusion therapy for eligible patients'.)

However, for the majority of patients with stroke due to blunt cerebrovascular injury, coexistent injuries will contraindicate lytic therapy and, for some, antithrombotic therapy as well.

Transcatheter embolectomy may be an option for some, but this also requires specialized expertise.

FOLLOW-UP FOR HEALING OR PROGRESSION — There are no good long-term outcome data to guide the duration of antithrombotic therapy. Because a significant number of injuries evolve in a manner that alters therapy, we perform a follow-up imaging study 7 to 10 days after the injury has been identified (inpatient or outpatient), or for any change in neurologic status (image 1). If complete healing has been demonstrated by follow-up imaging, antithrombotic therapy can be discontinued. For those with grade IV injuries, early repeat imaging may not be needed since few (<10 percent) of these resolve [50]. Although digital subtraction angiography is considered the standard for vascular imaging of the cerebral arteries, most literature on blunt cerebrovascular injury focuses on imaging using multidetector row computed tomographic (CT) angiography (≥16 slice) because of its less invasive nature. Magnetic resonance angiography is an alternative but is less well studied for evaluation of blunt cerebrovascular injury. The advantages and disadvantages of the various imaging modalities for the evaluation of blunt cerebrovascular injury are reviewed separately. (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation", section on 'Imaging evaluation'.)

The dynamic nature of blunt cerebrovascular injury is illustrated in the following studies:

In a study of 114 patients with blunt cerebrovascular injury, follow-up arteriography was performed within 10 days in all patients [1]. Grade I and grade II injuries frequently changed, with 57 percent of grade I and 8 percent of grade II injuries healing completely, allowing cessation of treatment. Progression to pseudoaneurysm formation was seen in 8 percent of grade I and 43 percent of grade II lesions, prompting interventional treatment. Higher-grade injuries changed very little, with 93 percent of grade III and 82 percent of grade IV injuries remaining unchanged.

A review of consecutive patients treated and followed over 10 years found 133 blunt cerebrovascular injuries [12]. Of the surviving patients, no patient experienced cerebral infarction after discharge. Angiographic follow-up was available for 50 patients representing 67 injuries at a mean of six months. Seventy-two percent of grade I injuries were healed at follow-up. Of the grade II lesions, 40 percent worsened while 30 percent improved. Most grade III lesions remained the same or enlarged, prompting treatment with endovascular stents.

In a retrospective review, 1204 patients with 1604 vessel injuries treated at a level I trauma center were followed for progression or resolution [51].

High-grade (III-V) injuries were less likely to resolve compared with low grade (I, II) injuries.

High-grade injuries were more likely to progress than low-grade injuries.

Among injuries that improved or resolved, most (76 percent) did so within 30 days of the initial injury; the remainder did so between 30 and 90 days.

Among injuries that progressed, most (87 percent) changed within 90 days.

Beyond 90 days, no improvement or resolution occurred, and only 1.4 percent progressed.

If the lesion remains, the patient should be maintained on antithrombotic therapy, but the optimal drug and duration of therapy have not been studied [1,2]. In an analysis of the Nationwide Readmission Database, patients with blunt cerebrovascular injury had a 3.8 percent rate of readmission with new stroke [24]. Those treated with antiplatelet medications had a higher rate of readmission for stroke compared with those treated with other anticoagulant medications (5.7 versus 1.8 percent). However, details of the treatment regimens were not provided in the database and further study is warranted.

For those who do continue antithrombotic therapy, we obtain a CT angiography at three months following the injury to determine whether antithrombotic therapy can be discontinued, and whether another treatment (eg, stenting) is needed. In the absence of documented healing of the vessel, it is reasonable to provide ongoing treatment, since delayed stroke can occur and has been reported as long as 14 years after injury [52]. We continue antiplatelet therapy (typically aspirin, 325 mg daily) indefinitely for patients who do not demonstrate documented healing (ie, persistent flap, dissection) of the vessel on follow-up imaging (digital subtraction arteriography or CT angiography). However, for some patients, risks associated with the imaging examination may be greater than simply continuing antithrombotic therapy.

INJURY GRADE-SPECIFIC RECOMMENDATIONS — Factors that determine the strategy for treatment and follow-up include symptoms, site of injury, severity or grade of injury, and the presence of associated injuries.

Grade I — Intimal flap injuries have a low stroke risk and high rate of resolution with antithrombotic therapy. In one study, one-half of those that were not even treated were healed at follow-up [1,5]. Initial treatment with either heparin or antiplatelet therapy is appropriate for grade I injuries, as there are no data demonstrating superiority of one over the other. We generally administer heparin in hospitalized patients who may be undergoing surgical procedures, because the effects can be quickly reversed. However, once the risk for bleeding is reduced, we transition to antiplatelet therapy given its low cost and simplicity of administration. We recommend antiplatelet therapy until the lesion is healed.

Because these lesions do not have flow-limiting potential, additional treatment (surgical or endovascular) is not necessary [1]. We suggest follow-up imaging 7 to 10 days following the injury, or for any change in neurologic status. If the intimal flap has healed, antithrombotic therapy can be discontinued. Some patients with stable low-grade lesions may elect to continue antiplatelet therapy given the relatively low risk of daily aspirin and forego numerous follow-up imaging studies.

Grade II — Arterial dissections often progress in spite of treatment [1,5]. We recommend initiating antithrombotic therapy using heparin for these patients, reserving antiplatelet therapy for those who have contraindications to heparin. We suggest follow-up imaging 7 to 10 days following the injury, or for any change in neurologic status. Long-term treatment with antiplatelet therapy appears to be adequate for stroke prevention for patients with stable lesions. Endovascular stenting may be indicated if carotid injury progresses to the point of near-occlusion. Stenting may be preferred since the distal extent of the injury often precludes adequate surgical control of the vessel.

Grade III — Arterial pseudoaneurysm injuries are less likely to heal compared with lower-grade injuries [1,12]. We recommend initiating antithrombotic therapy with heparin for these patients, reserving antiplatelet therapy for those who have contraindications to heparin. In one study, over one-half of pseudoaneurysms remained the same size or enlarged at a mean of six months. Intervention is generally warranted once a pseudoaneurysm reaches a size of 1.0 to 1.5 cm or is symptomatic. Surgically accessible carotid artery pseudoaneurysm can be treated with resection and repair (patch or interposition graft). Alternatively, arterial pseudoaneurysms (carotid or vertebral) can be treated using endovascular techniques such as stenting or coil embolization (image 2) [53,54]. (See "Extracranial carotid artery aneurysm".)

Grade IV — Injuries with complete arterial thrombosis are associated with high mortality, particularly when the injury is in the carotid artery, and the neurologic outcome is proportional to the degree of neurologic impairment on presentation [34]. When initially asymptomatic patients with arterial occlusion are treated with antithrombotic therapy, stroke rates are lower than with no treatment. We recommend initiating antithrombotic therapy using heparin, reserving antiplatelet therapy for those with contraindications to heparin. In one study, 82 percent of grade IV injuries remaining unchanged [1]. Over time, a small number of occlusions may recanalize. It has been hypothesized that this may lead to stroke, and that angioembolization may be preventative [55]. There are no data demonstrating any additional benefit for endovascular therapy (compared with antithrombotic therapy) or to guide long-term management in asymptomatic patients. Since the early follow-up examination is unlikely to change in a manner that will alter treatment, we suggest not obtaining a routine follow-up study at 7 to 10 days, unless there is a change in clinical status that raises concern for ischemic neurologic event [50]. We generally suggest lifelong antiplatelet therapy for patients with occlusions.

Grade V — Transection injuries of the carotid artery are associated with high rates of stroke and high mortality. Hemorrhage from the neck as evidenced by an expanding hematoma (zone II) should be controlled by direct pressure until surgical control, if accessible, or endovascular control can be achieved. Hemorrhage from the mouth or ears is often indicative of a lesion that will require angioembolization for control.

Surgically accessible carotid artery transections can be managed by exposing and controlling the vessel through a neck incision and performing a primary repair, if length permits, and if not, by using an interposition graft. Ligation of the vessel, at times, may be necessary.

Inaccessible lesions often require embolization of the vessel to manage the hemorrhage. Angioembolization may be the best means of vascular control depending upon the site of the injury. Once the bleeding is under control, the clinician should evaluate the risks versus benefits of antithrombotic therapy following stent placement or angioembolization. There are no data to guide this decision, other than that extrapolated from grade III or IV injuries. Follow-up imaging is recommended per recommendations for grade III or IV injuries.

STROKE AND MORTALITY — Stroke after blunt cerebrovascular injury is historically associated with mortality rates ranging from 23 to 28 percent, with 48 to 58 percent of survivors having permanent severe neurologic deficits [3]. Internal carotid artery injuries result in mortality and stroke rates ranging from 13 to 21 percent and 26 to 41 percent, respectively [1,13,14]. Mortality and stroke rates for common carotid injuries appear to be lower at 11 percent each [13]. For vertebral injuries, the incidence of posterior circulation stroke is 14 to 24 percent, and the associated mortality is 4 to 8 percent [14,56,57].

In the carotid artery, stroke rates increase with increasing injury grade [5]. By contrast, stroke incidence and neurologic outcomes are independent of blunt vertebral injury grade [14,58]. (See 'Injury grading' above.)

Injuries with complete arterial thrombosis are associated with high mortality and poor neurologic outcome proportional to the degree of neurologic impairment on presentation [34]. In a multicenter study, 37 percent of patients with stroke had clinical evidence at the time of initial presentation [59]. Among the remainder, a diagnosis of stroke was made at a median of 48 hours after presentation. Of note, 15 percent of the stroke victims had grade I injuries, and six patients suffered stroke as a result of an interventional procedure.

As more asymptomatic injuries have been identified and early treatment is initiated, the absolute rate of stroke has decreased over time even though outcomes related to stroke remain poor. The use of antithrombotic therapy is associated with lower rates of stroke. The Parkland Carotid and Vertebral Artery Injury Survey has published a series of papers reporting that stroke rates are much lower in the era of aggressive screening and prophylactic antithrombotic therapy [60-63]. Though, in a multicenter study, 22 percent of patients were receiving antithrombotic therapy at the time of stroke [59]. In addition, there is concern that more ischemic lesions may occur than are being recognized clinically. In a series of consecutive patients with blunt cerebrovascular injury who were asymptomatic and treated with antiplatelet agents, new ischemic lesions were identified on diffusion-weighted magnetic resonance imaging in 43 percent of the territories of the injured artery [25].

FUNCTIONAL OUTCOMES — Although there are no data looking specifically at functional outcomes of patients with blunt cerebrovascular injury compared with other etiologies of stroke, outcomes may be worse for blunt cerebrovascular injury given the high incidence of associated brain injury. (See "Overview of ischemic stroke prognosis in adults".)

A prospective study followed 133 consecutive patients with blunt carotid injuries over a 10-year period [12]. Clinical follow-up was available in 55 of 81 patients who survived to discharge. The same or improved Glasgow outcome scale was found in 95 percent of the patients at a mean follow-up of 34 months. No patient experienced cerebral infarction or died following discharge from the hospital. On the other hand, an analysis of the Nationwide Readmission Database reported that patients with blunt cerebrovascular injury had a 3.8 percent rate of readmission with new stroke [24].

For blunt vertebral injury, a review of the National Trauma Database found 574 patients with blunt vertebral injury among the 761,385 blunt trauma admissions (0.08 percent incidence) [57]. Overall mortality was 8 percent, and stroke was diagnosed in 12 percent of patients who had no associated blunt carotid injury. Functional outcomes measures were available for 261 patients, and about one-half the patients demonstrated functional independence upon discharge.

A later series reported functional outcomes among 68 patients with blunt cerebrovascular injuries who were assessed an average of 35 months after discharge [64]. Not surprisingly, functional independence scores were significantly worse in those who had a stroke compared with those who did not. Functional deficiencies among those who did not sustain stroke were likely related to other injuries.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Blunt cerebrovascular injury".)

SUMMARY AND RECOMMENDATIONS

Blunt carotid and vertebral artery injury are collectively termed blunt cerebrovascular injury; they are rare but potentially morbid injuries. The overall incidence for these injuries is about 1 percent of blunt trauma admissions. (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation", section on 'Introduction'.)

For the carotid artery, stroke rates increase with increasing injury grade. Stroke incidence and neurologic outcome for vertebral injury are independent of injury grade. Injury grades for blunt cerebrovascular injury are as follows (see 'Injury grading' above and 'Stroke and mortality' above):

Grade I: Intimal irregularity or dissection with <25 percent luminal narrowing

Grade II: Dissection or intramural hematomas with ≥25 percent luminal narrowing, intraluminal clot, or a visible intimal flap

Grade III: Pseudoaneurysm or hemodynamically insignificant arteriovenous fistula

Grade IV: Complete occlusion

Grade V: Transection with active extravasation, or hemodynamically significant arteriovenous fistula

For patients with blunt cerebrovascular injury who do not have a persistent neurologic deficit in the territory of the injured artery and who do not have contraindications, we recommend antithrombotic therapy (unfractionated heparin, antiplatelet agents) over no such therapy (Grade 1B). Neurologic outcomes are improved in symptomatic patients, and fewer ischemic neurologic events (stroke) occur in asymptomatic patients who are treated with antithrombotic therapy. (See 'Treatment' above.)

For most patients suspected of having blunt cerebrovascular injury, we suggest initiating unfractionated heparin rather than antiplatelet therapy provided there are no contraindications to heparin or heparin is not available (Grade 2C). Antiplatelet therapy is an alternative depending upon the nature and extent of associated injuries. The duration of therapy is unknown; however, we continue antiplatelet therapy, typically aspirin (325 mg daily), indefinitely for patients who do not demonstrate documented healing of the vessel on follow-up imaging (digital subtraction arteriography or computed tomographic [CT] angiography). (See 'Choice of agent' above.)

We suggest exploration and repair of surgically accessible grade II through grade V injuries to the cervical carotid artery, rather than endovascular repair or no repair (Grade 2C). However, the majority of blunt cerebrovascular injuries involve the carotid artery at the base of the skull, and these are not surgically accessible. No studies are available directly comparing surgical versus endovascular management of surgically accessible blunt cerebrovascular lesions. (See 'Surgery for accessible lesions' above.)

Endovascular techniques can be used, but are rarely needed, to manage surgically inaccessible blunt cerebrovascular injuries with a flow-limiting stenosis (grade II), pseudoaneurysm formation (grade III), or transection (grade V). (See 'Endovascular therapy for inaccessible lesions' above.)

We obtain follow-up imaging 7 to 10 days following identification of the cerebrovascular injury using CT angiography. For those with grade IV injuries, repeat imaging may not be needed since few (<10 percent) of these resolve. For most patients who remain on antithrombotic therapy, the decision to perform additional delayed imaging should be individualized. The lesions are unlikely to change significantly, so the decision is based on the risk of long-term antiplatelet or antithrombotic therapy. Further imaging in patients who have undergone definitive repair (surgical or endovascular) is guided by the nature of the intervention. (See 'Follow-up for healing or progression' above and 'Injury grade-specific recommendations' above.)

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Topic 16136 Version 20.0

References

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