Blunt Cerebrovascular Injury - Treatment and Outcomes - UpToDate

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Blunt cerebrovascular injury: Treatment and outcomes

Authors: Walter L Biffl, MD, Clay Cothren Burlew, MD, Ernest E Moore, MD
Section Editors: Eileen M Bulger, MD, FACS, John F Eidt, MD, Joseph L Mills, Sr, MD
Deputy Editor: Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2020. | This topic last updated: Sep 05, 2019.
INTRODUCTION
Blunt carotid and vertebral artery injuries, collectively termed blunt cerebrovascular injury, are uncommon but potentially
devastating events. The incidence of blunt cerebrovascular injury in patients sustaining blunt trauma is about 1 percent
[1,2]. Untreated 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 "Spontaneous 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]. 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].
The injury grades given below apply to carotid or vertebral artery lesions.
● Grade I: Intimal irregularity or dissection with <25 percent luminal narrowing.
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● 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.)
TREATMENT
Because the incidence of blunt cerebrovascular injury is very low and experience with this problem is limited, even in busy
trauma centers, no controlled trials are available to help guide management. Treatment is based upon the demonstration
of reduced neurologic and other 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 [6], and from strategies used
in the management of non-traumatic cerebrovascular disorders (eg, spontaneous cerebrovascular dissection). Our
treatment recommendations are in general agreement with protocols established by major trauma societies (algorithm 1)
[7,8].
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 [grade V]) from the vessel. (See
'Associated injuries that may contradict antithrombotic therapy' below.)
The rationale for using antithrombotic therapy for blunt cerebrovascular injury is based upon reduced rates of neurologic
morbidity and mortality identified in retrospective reviews of anticoagulated patients or those treated with antiplatelet
agents compared with untreated patients with treatment contraindications or historic, untreated controls, for whom stroke
rates are typically 50 percent or greater [1-4,9,10]. Stroke rates in case series from the era prior to screening were
considerably higher than contemporary series, as injuries were not diagnosed until the ischemic neurologic event. 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 [1,11,12]. 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 found improved neurologic outcomes among symptomatic patients and fewer ischemic
neurologic events (stroke) in asymptomatic patients with blunt cerebrovascular injury who are heparinized compared with
those who are not [1,2,4,12-15]. 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 [14]. 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 [12].
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 [13]. 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 [7,8]. We administer
heparin as a weight-based infusion of 15 units/kg per hour (no bolus), to achieve an activated partial thromboplastin time
(aPTT) of 40 to 50 seconds (lower target range compared with other indications). (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 may be more effective than antiplatelet drugs. 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 [1,9,10,16-18]. Key results are summarized below.
● A study of 114 patients with blunt cerebrovascular injury found 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 [9]. 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 [18]. Of these,
eight patients received no treatment, seven patients were treated with heparin, and seven 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.
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). (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) [19]. 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 [20].
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 above), better safety profile,
and lower cost [9]. (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 "Acute coagulopathy associated with trauma" 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 bolus dose or titrating to a standard activated partial thromboplastin time (aPTT) goal
of 60 to 80 seconds [3]. A more conservative protocol for initiation (no bolus) and maintenance of heparin infusion (aPTT
40-50) should be used in any injured patient at risk for bleeding [1,4]. (See 'Choice of agent' above.)
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 [21-23]. (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 3 did not worsen brain or solid organ above
baseline [21]. 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 [22,23].
Microemboli burden, as assessed by transcranial Doppler, is associated with higher risk of stroke due to internal carotid
(but not vertebral) artery injuries [24]. Such testing may prove to be a useful tool in the risk/benefit assessment for
anticoagulation in the setting of associated injuries.
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 [7,8]. 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 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 [6,25,26]. In retrospective studies that
compared carotid artery repair to carotid artery ligation, patients with minimal neurologic deficits did much better with
repair [11,27,28]. 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) [11,29-31]. 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 [27].
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 [32].
Endovascular therapy for inaccessible lesions — Given that most blunt cerebrovascular injuries are surgically
inaccessible, endovascular therapy may provide a treatment option for certain injuries, in addition to antithrombotic
therapy [1,5,7,8,10,33]. 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 [25,34-38].
Some groups have reported a good safety and patency with endovascular intervention [10,39-41]; however, the risks of
endovascular treatment may exceed the benefits [42,43]. One study found a 17 percent incidence of stent-related
complications and a 45 percent occlusion rate [43]. 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 revealed a difference in stent usage. Endovascular intervention was performed in 9 percent of
237 patients with blunt cerebrovascular injuries identified from 2013 to 2016, whereas among 128 patients identified from
2011 to 2012, stents were used in 34 percent [44]. Given that the stroke rate was no different, the authors concluded that
anticoagulation alone is 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 "Carotid artery stenting and its complications", section on '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. (See "Management of acute moderate and severe traumatic
brain injury" and "Spontaneous cerebral and cervical artery dissection: Treatment and prognosis", section on
'Thrombolysis'.)
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.
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 study 7 to 10 days after the injury has been
identified (inpatient or outpatient), or for any change in neurologic status (image 1). For those with grade IV injuries,
repeat imaging may not be needed since few (<10 percent) of these resolve [45]. If complete healing has been
demonstrated by follow-up imaging, antithrombotic therapy can be discontinued.
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 [10]. 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. The majority of
grade III lesions remained the same or enlarged, prompting treatment with endovascular stents.
If the lesion remains, the patients should be maintained on antithrombotic therapy, but the optimal drug and duration of
therapy have not been studied [1,2]. For those who do continue antithrombotic therapy, we obtain a study at three months
following the injury to determine whether antithrombotic therapy can be discontinued, and if 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 [46]. We continue antiplatelet
therapy (typically aspirin, 81 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 computed tomographic [CT]
angiography). However, for some patients, the risk of the imaging examination may be greater than simply continuing
antithrombotic therapy.
Studies identifying progression or healing of the vascular lesion have typically used conventional arteriography, but we
prefer to use CT angiography (≥16 slice) because of its noninvasive nature. Magnetic resonance (MR) angiography is an
alternative (image 2A-C). The advantages and disadvantages of the various imaging modalities for the evaluation of blunt
cerebrovascular injury are discussed elsewhere. (See "Blunt cerebrovascular injury: Mechanisms, screening, and
diagnostic evaluation", section on 'Imaging evaluation'.)
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 [1,10]. 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 (stent or coil embolization) (image 3) [47,48]. (See "Extracranial carotid artery aneurysm".)
Grade IV — Injuries with complete arterial thrombosis are associated with high mortality, and the neurologic outcome is
proportional to the degree of neurologic impairment on presentation [30]. 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 [49]. There are no
data demonstrating any benefit for endovascular therapy or to guide long-term management. Since the follow-up
examination is unlikely to change in a manner that will alter treatment, we suggest not obtaining a routine follow-up study
[45]. 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].
In the carotid artery, stroke rates have been found to increase with increasing injury grade [5]. Injuries with complete
arterial thrombosis are associated with high mortality and poor neurologic outcome proportional to the degree of
neurologic impairment on presentation [30]. Internal carotid artery injuries result in mortality and stroke rates of 13 to 21
percent and 26 to 41 percent, respectively [1,11,12]. Mortality and stroke rates for common carotid injuries appear to be
lower at 11 percent each [11]. (See 'Injury grading' above.)
For vertebral injuries, the incidence of posterior circulation stroke is 14 to 24 percent, and the associated mortality is 4 to 8
percent [12,50,51]. Stroke incidence and neurologic outcomes are independent of blunt vertebral injury grade [12,52].
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 [53-56]. (See 'Antithrombotic therapy' above.)
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 "Ischemic stroke prognosis in adults".)
A prospective study followed 133 consecutive patients with blunt carotid injuries over a 10-year period [10]. 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.
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) [51]. 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 [57]. 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.
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, we routinely schedule CT angiography at three months to
determine if long-term antithrombotic therapy is needed. Progression of the injury under certain circumstances may
indicate the need for intervention. 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.)
REFERENCES
1. Biffl WL, Ray CE Jr, Moore EE, et al. Treatment-related outcomes from blunt cerebrovascular injuries: importance of
routine follow-up arteriography. Ann Surg 2002; 235:699.
2. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: analysis of
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Topic 16136 Version 12.0
GRAPHICS
Algorithm for diagnosis and management of blunt cerebrovascular injury
BCVI: blunt cerebrovascular injury; TIA: transient ischemic attack; CT: computed tomography; MRI: magnetic
resonance imaging; TBI: traumatic brain injury; GCS: Glasgow coma scale; MS: mental status; CTA: computed
tomographic angiography; PTT: partial thromboplastin time; DSA: digital subtraction angiography.
* CTA with multidetector-row CT; 64-channel is optimal. If fewer than 16 channels, interpret CT angiogram with
caution; DSA is the gold standard.
¶ Patient has not suffered completed stroke.
Δ If signs/symptoms or high clinical suspicion and negative CTA, consider DSA.
◊ For positive arteriogram (DSA), follow treatment algorithm per multislice CTA results.
§ Heparin is preferred in the acute setting as it is reversible and may be more effective than antiplatelet agents.
Anticoagulation may be contraindicated due to other injuries. Antiplatelet therapy is typically aspirin 325 mg
daily.
¥ Stenting should be performed with caution and appropriate antithrombotic therapy administered concurrently.
‡ If symptomatic common carotid fistula, consider arteriography and endovascular therapy. If asymptomatic
common carotid fistula, reimage with CTA at three to four weeks.
† Aspirin alone (325 mg daily) is adequate and should be considered lifelong as its risk profile is superior to
warfarin.
Adapted from: Burlew CC, Biffl WL, Moore E, et al. Blunt cerebrovascular injuries: Redefining screening criteria
in the era of noninvasive diagnosis. J Trauma Acute Care Surg 2012; 72:330. DOI:
10.1097/TA.0b013e31823de8a0. Copyright © 2012 American Association for the Surgery of Trauma.
Reproduced with permission from Lippincott Williams & Wilkins. Unauthorized reproduction of this material is
prohibited.
Graphic 78174 Version 13.0
Grade III internal carotid artery injury on CTA
Four months after sustaining blunt trauma related to a motor vehicle collision, this 30-year-old male presented with headache
and left-sided weakness. Coronal (A, B) and axial (C) contrast enhanced CT angiographic images demonstrate multiple
pseudoaneurysms (arrows) involving both internal carotid arteries.
CTA: computed tomographic angiography.
Courtesy of Joe Farnam, MD.
Grade II traumatic injury of the carotid on MRI
A 48-year-old male presents with several weeks of left-sided, retro orbital headache. He sustained blunt trauma
two months prior to this presentation. Axial (A) and 3D reconstructed (B) MR angiographic images demonstrate a
short segment stenosis (arrow) at the distal cervical segment left internal carotid artery with approximately 40
percent luminal narrowing. Axial fat-suppressed T1-weighted image (C) demonstrates T1 hyperintensity at the
vessel wall (arrow), consistent with dissection.
MRI: magnetic resonance imaging.
Grade III internal carotid artery injury on MRA
MR imaging six months following initial diagnosis. Contrast-enhanced coronal MR angiography (A) redemonstrates multiple
bilateral internal carotid pseudoaneurysms (arrows). Fat-saturated axial T1 images (B, C) demonstrate T1 hyperintensity
(arrowheads) consistent with hematoma at the location of these pseudoaneurysms.
MRA: magnetic resonance angiography; MR: magnetic resonance.
Courtesy of Joseph Farnam, MD.
Grade III carotid injury two-year follow-up on MRA
Follow-up imaging performed at 18 months following initial diagnosis. Contrast-enhanced

coronal MR angiography demonstrates persistent right-sided internal carotid
pseudoaneurysms (arrows) with interval resolution of the left internal carotid
pseudoaneurysm.
MRA: magnetic resonance angiography.
Pseudoaneurysm of the internal carotid artery with subsequent stent placement
An internal carotid angiogram (A) shows a focal dissection (arrow) in the cervical portion of the carotid artery. An angiogram performed two years
later (B) shows a pseudoaneurysm at the previous site of dissection (arrow). Image C shows stent placement (arrowheads) across the mouth of
the pseudoaneurysm. Six months later (D), an angiogram shows resolution of the pseudoaneurysm (arrowhead).
Courtesy of Thanh Nguyen, MD.
Contributor Disclosures
Walter L Biffl, MD Nothing to disclose Clay Cothren Burlew, MD Nothing to disclose Ernest E Moore, MD Grant/Research/Clinical
Trial Support: Haemonetics [Coagulopathy (Thromboelastography); Instrumentation Laboratory [Coagulopathy (Rotational
thromboelastometry)]; Prytime [REBOA (REBOA catheter)]; Humacyte [Hemodialysis (Vascular graft)]. Patent Holder: Haemonetics
[Coagulopathy (Thromboelastography)]. Equity Ownership/Stock Options: Thrombo Therapeutics [Coagulopathy]. Eileen M Bulger,
MD, FACS Grant/Research/Clinical Trial Support: Atox Bio [Necrotizing soft tissue infections (AB103)]; Potrero Medical [Critical care
(Advanced urine output monitor)]. Consultant/Advisory Boards: Opticyte [Shock (Direct cellular oximeter)]. Equity Ownership/Stock
Options: Opticyte [Shock (Direct cellular oximeter)]. John F Eidt, MD Nothing to disclose Joseph L Mills, Sr,
MD Grant/Research/Clinical Trial Support: Voyager Trial [Peripheral artery disease (Rivoxaraban)]. Consultant/Advisory Boards:
Innomed [Peripheral artery disease (Femoral artery stent)]. Equity Ownership/Stock Options: NangioTx [Peripheral artery disease (Self-
assembling nanotubules)]. Other Financial Interest: Elsevier; Rutherford [Vascular surgery (Rutherford and Comprehensive Vascular
and Endovascular Surgery textbooks)]. Kathryn A Collins, MD, PhD, FACS Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through
a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced
content is required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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Blunt cerebrovascular injury: Treatment and outcomes

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

● Grade III: Pseudoaneurysm or hemodynamically insignificant arteriovenous fistula.

● Grade IV: Complete occlusion.

● Grade I: Carotid 8 percent; vertebral 6 percent

antithrombotic therapy' below.)

FOLLOW-UP FOR HEALING OR PROGRESSION

INJURY GRADE-SPECIFIC RECOMMENDATIONS

STROKE AND MORTALITY

SUMMARY AND RECOMMENDATIONS

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

• Grade III: Pseudoaneurysm or hemodynamically insignificant arteriovenous fistula

• Grade IV: Complete occlusion

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

Topic 16136 Version 12.0

Algorithm for diagnosis and management of blunt cerebrovascular injury

Graphic 78174 Version 13.0

Grade III internal carotid artery injury on CTA

CTA: computed tomographic angiography.

Courtesy of Joe Farnam, MD.

Graphic 96260 Version 1.0

Grade II traumatic injury of the carotid on MRI

MRI: magnetic resonance imaging.

Courtesy of Joe Farnam, MD.

Graphic 95681 Version 1.0

Grade III internal carotid artery injury on MRA

MRA: magnetic resonance angiography; MR: magnetic resonance.

Courtesy of Joseph Farnam, MD.

Graphic 96261 Version 2.0

Grade III carotid injury two-year follow-up on MRA

Follow-up imaging performed at 18 months following initial diagnosis. Contrast-enhanced

MRA: magnetic resonance angiography.

Courtesy of Joe Farnam, MD.

Graphic 96262 Version 1.0

Pseudoaneurysm of the internal carotid artery with subsequent stent placement

Courtesy of Thanh Nguyen, MD.

Graphic 101592 Version 1.0

Conflict of interest policy

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