Blunt cerebrovascular injuries in severe traumatic brain injury: incidence, risk factors, and evolution

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OBJECTIVE

Blunt cerebrovascular injuries (BCVIs) affect approximately 1% of patients with blunt trauma. An antithrombotic or anticoagulation therapy is recommended to prevent the occurrence or recurrence of neurovascular events. This treatment has to be carefully considered after severe traumatic brain injury (TBI), due to the risk of intracranial hemorrhage expansion. Thus, the physician in charge of the patient is confronted with a hemorrhagic and ischemic risk. The main objective of this study was to determine the incidence of BCVI after severe TBI.

METHODS

The authors conducted a prospective, observational, single-center study including all patients with severe TBI admitted in the trauma center. Diagnosis of BCVI was performed using a 64-channel multidetector CT. Characteristics of the patients, CT scan results, and outcomes were collected. A multivariate logistic regression model was developed to determine the risk factors of BCVI. Patients in whom BCVI was diagnosed were treated with systemic anticoagulation.

RESULTS

In total, 228 patients with severe TBI who were treated over a period of 7 years were included. The incidence of BCVI was 9.2%. The main risk factors were as follows: motorcycle crash (OR 8.2, 95% CI 1.9–34.8), fracture involving the carotid canal (OR 11.7, 95% CI 1.7–80.9), cervical spine injury (OR 13.5, 95% CI 3.1–59.4), thoracic trauma (OR 7.3, 95% CI 1.1–51.2), and hepatic lesion (OR 13.3, 95% CI 2.1–84.5). Among survivors, 82% of patients with BCVI received systemic anticoagulation therapy, beginning at a median of Day 1.5. The overall stroke rate was 19%. One patient had an intracranial hemorrhagic complication.

CONCLUSIONS

Blunt cerebrovascular injuries are frequent after severe TBI (incidence 9.2%). The main risk factors are high-velocity lesions and injuries near cervical arteries.

ABBREVIATIONS BCVI = blunt cerebrovascular injury; CAI = carotid artery injury; CTA = CT angiography; DSA = digital subtraction angiography; GCS = Glasgow Coma Scale; GOS = Glasgow Outcome Scale; ICH = intracranial hemorrhage; ICP = intracranial pressure; IQR = interquartile range; ISS = Injury Severity Score; LMWH = low-molecular-weight heparin; ROC = receiver operating characteristic; TBI = traumatic brain injury; VAI = vertebral artery injury.

Abstract

OBJECTIVE

Blunt cerebrovascular injuries (BCVIs) affect approximately 1% of patients with blunt trauma. An antithrombotic or anticoagulation therapy is recommended to prevent the occurrence or recurrence of neurovascular events. This treatment has to be carefully considered after severe traumatic brain injury (TBI), due to the risk of intracranial hemorrhage expansion. Thus, the physician in charge of the patient is confronted with a hemorrhagic and ischemic risk. The main objective of this study was to determine the incidence of BCVI after severe TBI.

METHODS

The authors conducted a prospective, observational, single-center study including all patients with severe TBI admitted in the trauma center. Diagnosis of BCVI was performed using a 64-channel multidetector CT. Characteristics of the patients, CT scan results, and outcomes were collected. A multivariate logistic regression model was developed to determine the risk factors of BCVI. Patients in whom BCVI was diagnosed were treated with systemic anticoagulation.

RESULTS

In total, 228 patients with severe TBI who were treated over a period of 7 years were included. The incidence of BCVI was 9.2%. The main risk factors were as follows: motorcycle crash (OR 8.2, 95% CI 1.9–34.8), fracture involving the carotid canal (OR 11.7, 95% CI 1.7–80.9), cervical spine injury (OR 13.5, 95% CI 3.1–59.4), thoracic trauma (OR 7.3, 95% CI 1.1–51.2), and hepatic lesion (OR 13.3, 95% CI 2.1–84.5). Among survivors, 82% of patients with BCVI received systemic anticoagulation therapy, beginning at a median of Day 1.5. The overall stroke rate was 19%. One patient had an intracranial hemorrhagic complication.

CONCLUSIONS

Blunt cerebrovascular injuries are frequent after severe TBI (incidence 9.2%). The main risk factors are high-velocity lesions and injuries near cervical arteries.

Blunt cerebrovascular injuries (BCVIs) are caused by penetration of circulating blood into the arterial wall. Intramural hematoma creates a false lumen that leads to stenosis, occlusion, or pseudoaneurysm of the affected artery.2 In the past decade BCVIs have been increasingly recognized due to initiation of different screening protocols, with an incidence of approximately 1% in patients with blunt trauma.15,24,25 These lesions are rare but potentially devastating because they can lead to neurovascular events.5,6

Mechanisms of these events are dual: usually embolic, from intraluminal thrombi forming at the site of the intimal tear, or hemodynamic, by arterial stenosis or vessel occlusion that may lead to low-flow infarcts.21 It is now recognized that a latent, asymptomatic period between injury and development of stroke frequently exists.17,20 An antithrombotic or anticoagulation therapy established during this period may improve neurological outcome and mortality rates.8,19,23 However, systemic anticoagulation carries a significant risk of hemorrhage in patients who suffer a trauma. Especially after traumatic brain injury (TBI), anticoagulation should not be given within 3 days of injury for moderate- or high-risk intracranial hemorrhage (ICH), because the administration of heparin, even at a prophylactic dose, may cause ICH expansion.1

Thus, in case of BCVI associated with TBI, the physician treating the patient is challenged by a hemorrhagic and an ischemic risk, both with potentially devastating neurological consequences. However, this association is poorly studied in the medical literature. The only available data showed a BCVI incidence of 3.9% in a subgroup of head-injured patients (isolated cranial fractures with or without intracranial hematoma).24 The main objective of this study was to describe the incidence and characteristics of BCVI in patients with severe TBI.

Methods

Study Design and Patient Selection

We conducted a 7-year prospective, observational, single-center study at the Sainte Anne Military Hospital of Toulon, France. Between January 2007 and December 2013, all intubated patients with TBI admitted to the ICU were eligible. Inclusion criteria were as follows: patients older than 18 years who had severe TBI, defined as a minimum Glasgow Coma Scale (GCS) score of ≤ 8 after resuscitation. Patients suffering from penetrating trauma and those in whom no CT scan was obtained within the first 24 hours were excluded from the study.

All patients were sedated, intubated, and received mechanical ventilation in accordance with the international guidelines and with the following objectives: head elevation 30°, PaO2 > 85 mm Hg, PaCO2 between 35 and 45 mm Hg, natremia between 140 and 145 mEq/L, targeted temperature < 37.5°C, intracranial pressure (ICP) < 20 mm Hg, and cerebral perfusion pressure > 60 mm Hg. If ICP increased, the protocol included moderate hypocapnia (PaCO2 between 30 and 35 mm Hg), increase of sedation with propofol, muscle paralysis with cisatracurium, and moderate hypothermia (34°C–35°C). Third-line therapy included barbiturate infusion and/or unilateral craniectomy.9–14

The institutional review board approved the study and waived the requirement for informed consent from the patient or patient's next of kin, given the observational nature of the study.

Data Collected and Diagnostic Modalities

Patient characteristics, mechanisms of injury, initial GCS score, results of whole-body CT scan, location and grade of BCVI, timing and type of initial therapy, followup imagery, evolution of the disease, in-hospital mortality, and outcome according to the Glasgow Outcome Scale (GOS) at 6 months and 1 year were collected. A thoracic trauma included all chest lesions except for thoracic vertebral fractures.

Primary screening of BCVI was done using a 64-channel CT scanner with CT angiography (CTA) (General Electric Medical Systems). Patients were positioned with their arms down to the side and underwent head and cervical spine studies without contrast. Scout images were obtained and the carotid vessels identified. Radiopaque iodinated contrast dye injection at 4 ml/sec was given (Omnipaque 65 ml). When a contrast blush was noted at the origin of the carotid arteries, the CTA head/neck scan was initiated from the clavicles and continued to the apex of the calvaria. Images were acquired at 0.625-mm-thick slices and 0.625-mm intervals. If necessary, patient whole-body imaging was completed. Digital reconstruction was performed immediately after the completion of CT scans. Sagittal and coronal images were reconstructed at 2-mm by 2-mm intervals, whereas axial images were at 1-mm by 1-mm intervals.

In the situations indicated by the institutional protocol, digital subtraction angiography (DSA) (Philips Healthcare) was performed by an experienced neuroradiologist. Selective single-plane DSA of the aortic arch and each of the subclavian arteries, and biplanar 4-vessel DSA of the cerebrovascular arteries were performed. The attending neuroradiologist's interpretations of CTA and/or DSA were used to determine BCVI location and grade according to the Biffl et al. grading scale.7 Grade I injuries were defined as irregularity of the vessel wall or a dissection ≤ 25% luminal stenosis. Grade II injuries included an intraluminal thrombus, intimal flap, or dissections or intramural hematomas with > 25% luminal stenosis. Grade III injuries were pseudoaneurysms. Grade IV injuries were vessel occlusions. Grade V injuries were complete vessel transection with free contrast extravasation or arteriovenous fistulas.

Treatment Methods

Patients in whom BCVI was diagnosed were treated with systemic anticoagulation (unfractionated heparin or low-molecular-weight heparin [LMWH]). The beginning point and type of systemic anticoagulation were chosen at the discretion of the treating physician, while respecting the benefit-risk ratio. In the case of unfractionated heparin, partial thromboplastin time was maintained at 45–60 seconds. In case of LMWH, anti–factor Xa activity was maintained at 0.4–0.6 IU/ml. A small number of patients received no systemic treatment due to endovascular treatment, major bleeding risk, or withdrawal of care.

Study End Points

The primary end point of this study was to determine the incidence of BCVI after severe TBI. Secondary end points were to determine risk factors of BCVI in this population and to describe the evolution of the disease in patients with BCVI.

Statistical Analysis

Statistical analysis was performed with XLSTAT version 2015.3.01 (Addinsoft). Continuous data were reported as the mean ± SD, or the median with the interquartile range (IQR) (25th–75th percentile) when data were not normally distributed. Nominal variables are reported as numbers and proportions (%).

For this observational study with consecutive sampling, α = 0.05, β = 0.2, and an estimated incidence of 4% for BCVI after severe TBI, we planned to include at least 191 patients to yield an expected incidence rate of 5%.24

A univariate analysis was conducted using the chi-square test or Fisher's exact test to compare categorical variables, and the Mann-Whitney test or Student t-test to compare groups for continuous variables (for comparison of medians and comparison of means, respectively). Independent factors associated with BCVI were identified using a logistic regression model. All parameters with p value < 0.05 on univariate analysis and clinical relevance were included in the multivariate regression model. The Hosmer-Lemeshow goodness-of-fit test and the area under the receiver operating characteristic (ROC) curve were used to evaluate the overall fit of the final model. The final model expressed the odds ratio and 95% confidence intervals. For all tests, p < 0.05 was considered statistically significant.

Results

Patient Population

During the study period, 243 intubated patients with TBI were admitted to the ICU. Fifteen patients were excluded: 10 due to mild or moderate TBI (minimum GCS score of > 8 after resuscitation); 4 due to penetrating trauma; and 1 due to the absence of a CTA study obtained within the first 24 hours. The remaining 228 were included. The most common mechanism of injury was motorcycle crash (30.1%) (Fig. 1). The median age of the population was 37 years (IQR 23–55 years), the median Injury Severity Score (ISS) was 24 (IQR 16–34), and the median initial GCS score was 6 (IQR 4–8). There were 179 male (78.5%) and 49 female (21.5%) patients.

FIG. 1.
FIG. 1.

Pie chart showing the mechanism of injury of enrolled patients.

Blunt Cerebrovascular Injuries

A BCVI was detected in 21 patients. These included 15 patients (71%) with carotid artery injury (CAI), 5 (24%) with vertebral artery injury (VAI), and 1 (5%) with injury to both of them. The incidence of BCVI was 9.2% of all admissions for severe TBI. A CAI occurred in 19 vessels (7 left, 6 right, and 3 with bilateral lesions). A VAI occurred in 6 arteries (2 left, 4 right). The majority of injuries were dissections (Grade I or II injuries): 17 vessels (68%). Table 1 provides the location and grade of detected injuries.

TABLE 1.

Grade and location of BCVIs

VesselGrade IGrade IIGrade IIIGrade IVGrade VTotal (%)
Rt CAI242019 (36)
Lt CAI2501210 (40)
Rt VAI110204 (16)
Lt VAI200002 (8)
Total (%)7 (28)10 (40)2 (8)3 (12)3 (12)25 (100)

Comparisons of patients with and without BCVI are displayed in Table 2. Notably, patients with BCVI were more severely injured, with a median ISS of 41 (IQR 29–50) versus 22 (IQR 16–32) (p < 0.0001) for those without BCVI. Patients with BCVI also had initial hemodynamic shock and/or hypoxia (SpO2 < 90% during > 5 minutes) more frequently: 12 of 21 (57%) versus 44 of 207 (21%) (p = 0.0002), and 9 (43%) versus 29 (14%) (p = 0.001), respectively. The number and type of intracranial lesions were comparable between the groups. However, associated lesions were more frequent in patients with BCVI (90% vs 66%, p = 0.02). Patients with BCVI had more thoracic trauma (90% vs 45%, p < 0.0001), cervical spine injuries (43% vs 8%, p < 0.0001), and hepatic lesions (24% vs 3%, p < 0.0001). Initial GCS scores were lower in patients with BCVI: median 4 (IQR 3–6) versus 7 (IQR 4–9) (p = 0.005). The predominant mechanism of injury in the BCVI group was motorcycle crash (57% vs 28%, p = 0.005).

TABLE 2.

Characteristics of patients according to the presence of BCVI*

VariablePatients w/o BCVI, n = 207Patients w/BCVI, n = 21p Value
Age in yrs38 [23–58]31 [21–46]0.18
Male sex159 (77)20 (95)0.05
SAPS II42 [33–53]45 [36–61]0.36
ISS22 [16–32]41 [29–50]<0.0001
Brain injury
  EDH35 (17)2 (10)0.38
  SDH110 (53)8 (38)0.19
  IPH28 (14)2 (10)0.61
  SAH99 (48)10 (48)0.99
  Contusion60 (29)2 (10)0.06
  Petechial85 (41)11 (52)0.32
  IVH29 (14)2 (10)0.57
  Shift60 (29)3 (14)0.15
  Brain swelling60 (29)4 (19)0.33
  Marshall category2 [2–5]2 [2–3]0.11
Associated lesions136 (66)19 (90)0.02
Facial trauma91 (44)12 (57)0.25
  Upper lesions34 (16)3 (14)0.8
  Middle lesions63 (30)8 (38)0.47
  Lower lesions14 (7)1 (5)0.72
  Basilar skull fracture39 (19)9 (43)0.01
  Involving carotid canal12 (6)6 (29)0.0002
Spine injury38 (18)11 (52)0.0002
  Cervical spine16 (8)9 (43)<0.0001
  Thoracic spine17 (8)4 (19)0.1
  Lumbar spine17 (8)3 (14)0.35
Thoracic injury94 (45)19 (90)<0.0001
  Pulmonary contusions72 (35)16 (76)0.0002
  Hemothorax23 (11)3 (14)0.66
  Pneumothorax43 (21)5 (24)0.75
  Rib fractures48 (23)10 (48)0.01
Abdominal trauma31 (15)6 (29)0.11
  Hepatic lesion7 (3)5 (24)<0.0001
  Splanchnic lesion10 (5)1 (5)0.99
Pelvic trauma32 (15)4 (19)0.67
Orthopedic lesions71 (34)12 (57)0.04
Neurological symptoms
  Minimum GCS score6 [4–8]4 [3–6]0.04
  Lateralizing deficit114 (55)8 (38)0.14
  Anisocoria74 (36)4 (19)0.12
  Bilat mydriasis20 (10)3 (14)0.5
Initial hemoglobin in g/dl12.7 [11.2–14.2]12.3 [8.9–14.2]0.5

EDH = epidural hematoma; IPH = intraparenchymal hematoma; IVH = intraventricular hemorrhage; SAH = subarachnoid hemorrhage; SAPS II = Simplified Acute Physiology Score; SDH = subdural hematoma.

Data are presented as the number (%) or the median [IQR: 25th–75th percentile].

Risk Factors for BCVI

After multivariate logistic regression analysis, major significant predictors of BCVI were as follows: motorcycle crash (OR 8.2; 95% CI 1.9–34.8, p = 0.004); fracture involving the carotid canal (OR 11.7; 95% CI 1.7–80.9, p = 0.01); cervical spine injury (OR 13.5; 95% CI 3.1–59.4, p = 0.001); thoracic trauma (OR 7.3; 95% CI 1.1–51.2, p = 0.04); and hepatic lesion (OR 13.3; 95% CI 2.1–84.5, p = 0.006). Other variables included in the model are shown in Table 3. The accuracy of the model was excellent, with an area under the ROC curve of 0.94. The Hosmer-Lemeshow test demonstrated a good model fit (χ2 = 3.3, df = 8, p = 0.92).

TABLE 3.

Multivariate logistic regression model for risk factors of BCVI*

VariableOR95% CIp Value
ISS1.041.01–1.080.02
Initial GCS score0.820.63–1.070.14
Motorcycle crash8.171.92–34.780.004
Basilar skull fracture2.180.46–10.270.32
Fracture involving the carotid canal11.651.68–80.860.01
Cervical spine injury13.553.09–59.360.001
Thoracic lesion7.351.06–51.190.04
Hepatic lesion13.262.08–84.540.006

Area under the ROC curve: 0.94; Hosmer-Lemeshow test: χ2 = 3.3, df = 8, p = 0.92.

Treatment, Stroke Rate, and Hemorrhagic Complications

Four of the 21 patients with BCVI died prematurely before definitive treatment; these individuals had significant associated injuries. Among the 17 survivors, 14 patients (82%) had medical treatment with systemic anticoagulation therapy. Four patients received unfractionated heparin and 10 had LMWH. The beginning of systemic anticoagulation was at a median of Day 1.5 (IQR Day 1–4). Seven patients (41%) were treated with systemic anticoagulation within the first 24 hours after admission. Two patients (12%) had endovascular interventions with coils (for treatment of Grade III right CAI and Grade V bilateral CAI, respectively). One patient (6%) had just chemoprophylaxis for deep vein thrombosis started at Day 5 (Grade I right VAI with severe ICH). Four patients with BCVI suffered an ischemic stroke, for an overall stroke rate of 19%. One stroke was present on arrival (Grade IV left CAI), 1 developed before introduction of systemic anticoagulation therapy (Grade II right CAI), and 2 developed despite early anticoagulation therapy (2 patients with Grade II left CAI). One patient (6%) had an ICH complication due to systemic anticoagulation. This patient developed a surgically evacuated epidural hematoma at Day 5 following the insertion of an ICP monitoring device.

Posttreatment Outcomes

Clinical follow-up was not different between patients with and those without BCVI, in terms of intracranial hypertension episodes, use of barbiturate or therapeutic hypothermia, or number of decompressive craniectomies (Table 4). The mortality rate was comparable between the groups: 33% in patients with versus 26% in patients without BCVI (p = 0.48). The incidence of poor outcome (defined as a GOS score between 1 and 3) was not different at 6 months and 1 year between patients with or without BCVI: 50% versus 45% (p = 0.66) and 47% versus 43% (p = 0.7), respectively.

TABLE 4.

Clinical follow-up and outcomes according to the presence of BCVI*

VariablePatients w/o BCVIPatients w/BCVIp Value
Barbiturate therapy51 (25)2 (10)0.12
Therapeutic hypothermia67 (32)5 (24)0.42
Decompressive craniectomy44 (21)4 (19)0.81
Intracranial hypertension frequency91 (44)13 (62)0.12
Day of sedation interruption3 [1–8]4 [3–10]0.4
Duration of MV in days7 [2–13]9 [3–16]0.38
Tracheostomy75 (36)8 (38)0.87
Early-onset pneumonia89 (43)9 (43)0.99
ICU length of stay in days9 [3–17]11 [3–20]0.69
Hospital length of stay in days17 [7–31]22 [5–39]0.77
In-hospital mortality54 (26)7 (33)0.48
GOS Score 1–3 at 6 mos92/205 (45)10/20 (50)0.66
GOS Score 1–3 at 1 yr80/187 (43)9/19 (47)0.7

MV = mechanical ventilation.

Data are presented as the number (%) or the median [IQR: 25th–75th percentile].

Some patients were lost to follow-up (often foreign patients on holiday in our region): 3 patients at 6 months (1 in the BCVI group and 2 in the non-BCVI group); and 22 patients at 1 year (2 in the BCVI group and 20 in the non-BCVI group).

Discussion

To our knowledge, this article is the first to focus on BCVI in patients with severe TBI. Our results highlight a rate of 9.2% for BCVI in this particular population. BCVI is increasingly recognized, due to advancements in screening and imaging technology. In the recent literature, the incidence of BCVI in all patients with blunt trauma has increased from 0.1% to 1.7%.4,8,15,24,25,27,31,35 It is now recognized that patients with facial fractures, cervical spine injury, or thoracic lesions have an increased risk of BCVI.4,25,32

Our study strongly suggests that patients with severe TBI are a very high-risk population for BCVI. This is probably due to common physiological mechanisms. Indeed, the main mechanisms of BCVI are the following: hyperextension with contralateral rotation of the head, laceration of the artery by adjacent fractures, direct blow to the neck, and direct intraoral trauma with a hard object.7,16,17,26,34 These mechanisms generally result from a high-speed deceleration crash with cervical hyperextension or hyperflexion, or direct blunt trauma to the neck, face, head, or upper chest. For TBI, similar mechanisms of injury exist: impact—in which the immediate force makes contact with the skull and leads to injury; and impulse—in which a force causes head movement without directly acting upon the head.3 Moreover, in our study, patients with severe TBI frequently had injuries to the upper body: facial fractures (103/228; 45%), cervical spine injuries (25/228; 11%), and thoracic lesions (113/228; 50%). All of these can explain the very high incidence of BCVI found in this population.

The main risk factors of BCVI after severe TBI are fracture involving the carotid canal, cervical spine injury, and thoracic trauma. This is consistent with the literature.4,25,27,30 In fact, Franz et al. demonstrated that cervical spine and thoracic injuries are significantly associated with BCVI in all blunt trauma admissions (OR 5.45 and 1.98, respectively).25 We also found new significant predictors of BCVI: ISS and, surprisingly, hepatic lesions. This is certainly reflecting the violence of the crash. This hypothesis is confirmed by the fact that a motorcycle crash is also an independent risk factor for BCVI. However, 2 well-established predictors of BCVI were not retrieved: basilar skull fracture and initial GCS score.4,27 This is probably due to the particular population of the study. Indeed, only patients with severe TBI (GCS score of ≤ 8) were included. This limits the power of the study to recognize GCS score as an independent risk factor. Concerning basilar skull fractures, they are too frequent in our population (21%) to find a significant difference in multivariate analysis.

Untreated vascular injuries could have an overall stroke rate approaching 40%–60%, with a stroke-related mortality as high as 50%.4,18,22,35 It is now well established that medical therapy (with anticoagulation or antiplatelet agents) that is started before the onset of neurological symptoms could reduce the occurrence of neurological events by a factor of 6.28,35 The stroke rate could be as low as 4% in treated patients.28,35 Consistent with other studies, our overall stroke rate was 19%, despite the frequent and early use of anticoagulation therapy. Some could have doubts concerning the safety of this therapy in patients with severe TBI. Recently, Callcut et al. examined the safety and efficacy of early pharmacological treatment for patients with both BCVI and traumatic neurological injury, including TBI and/or spinal cord injury.18 They found that early medical therapy significantly reduces the stroke rate (from 57% to 4%), without increasing the risk of ICH expansion (from 5% to 6%). However, pharmacological treatment was only initiated at a median of Day 3, and their patient population was different, including individuals with mild or moderate TBI.

In our study, anticoagulation therapy was started sooner, at Day 1.5, and 41% of patients were treated on arrival in the ICU. We chose to perform this therapy early because the latent period between injury and ischemia was observed mostly within 10–72 hours.8,29 Despite this very early therapy, only 1 ICH was reported following an ICP monitoring. There was no hemorrhagic deterioration of initial lesions due to pharmacological exposure. The literature demonstrated no difference in the efficacy of anti-platelet and anticoagulation therapies at preventing stroke in patients suffering from BCVI.28 In our institution, systemic anticoagulation is preferred for 2 reasons: 1) its effects can be easily monitored (by partial thromboplastin time or anti–factor Xa activity); and 2) in case of hemorrhagic complication or emergency surgery, this therapy can be quickly counteracted by the administration of protamine sulfate.

Study Limitations

Our study had several limitations. First, the relatively small number of patients with BCVI limits the power of the multivariate analysis. Second, our results cannot be transposed to all ICUs or trauma centers, due to the single-center recruitment. Finally, CTA by 64-channel multidetector scanner was used for diagnosing or excluding BCVI. A previous study using 32-channel CTA showed an inadequate sensitivity of 51% compared with DSA.22 However, compared with the 32-channel CT scanner, Paulus et al. recently highlighted that 64-channel CTA demonstrated a significantly improved sensitivity of 68%.33 Specificity and negative predictive value were 92% and 97%, respectively. Despite better results with the 64-channel CTA, we could have missed a certain number of patients with true BCVI in our study population, and therefore the true incidence may be higher. However, Paulus and colleagues found that 62% of the false-negative findings involved low-grade injury (Grade I).33 These low-grade injuries probably have a lower impact in patients and are rarely complicated by neurovascular events. Indeed, Biffl et al. highlighted their finding that two-thirds of mild intimal injuries (Grade I) healed at Day 7, regardless of therapy.7 Thus, our results seem to stay relevant in daily practice.

Conclusions

Despite these limitations, the present work is, to our knowledge, the first designed to evaluate the incidence of BCVI in patients with severe TBI. In this particular population, the incidence of BCVI was very high, approximately 9%. The main risk factors reflected high-velocity injuries like those sustained in motorcycle crashes or leading to hepatic lesions; or were related to cervical artery proximity injuries such as fractures involving the carotid canal or cervical spine injuries. In addition, our study demonstrates that early administration of medical therapy could be safe. However, prospective randomized multicenter studies are mandatory to confirm this last point.

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

Conception and design: Esnault, Cardinale, Boret. Acquisition of data: Esnault, Cardinale, Boret, D'Aranda, Montcriol, Bordes. Analysis and interpretation of data: Esnault, Boret, Prunet, Joubert. Drafting the article: Esnault, Boret, Dagain, Goutorbe, Kaiser, Meaudre. Critically revising the article: Boret, Dagain, Goutorbe, Kaiser, Meaudre. Reviewed submitted version of manuscript: Esnault. Approved the final version of the manuscript on behalf of all authors: Esnault.

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    Burlew CCBiffl WL: Imaging for blunt carotid and vertebral artery injuries. Surg Clin North Am 91:2172312011

  • 18

    Callcut RAHanseman DJSolan PDKadon KSIngalls NKFortuna GR: Early treatment of blunt cerebrovascular injury with concomitant hemorrhagic neurologic injury is safe and effective. J Trauma Acute Care Surg 72:3383462012

  • 19

    Cothren CCBiffl WLMoore EEKashuk JLJohnson JL: Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg 144:6856902009

  • 20

    Cothren CCMoore EEBiffl WLCiesla DJRay CE JrJohnson JL: Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg 139:5405462004

  • 21

    Debette SLeys D: Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurol 8:6686782009

  • 22

    DiCocco JMEmmett KPFabian TCZarzaur BLWilliams JSCroce MA: Blunt cerebrovascular injury screening with 32-channel multidetector computed tomography: more slices still don't cut it. Ann Surg 253:4444502011

  • 23

    Fabian TCPatton JH JrCroce MAMinard GKudsk KAPritchard FE: Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Ann Surg 223:5135251996

  • 24

    Fleck SKLangner SBaldauf JKirsch MKohlmann TSchroeder HWS: Incidence of blunt craniocervical artery injuries: use of whole-body computed tomography trauma imaging with adapted computed tomography angiography. Neurosurgery 69:6156242011

  • 25

    Franz RWWillette PAWood MJWright MLHartman JF: A systematic review and meta-analysis of diagnostic screening criteria for blunt cerebrovascular injuries. J Am Coll Surg 214:3133272012

  • 26

    Fusco MRHarrigan MR: Cerebrovascular dissections: a review. Part II: blunt cerebrovascular injury. Neurosurgery 68:5175302011

  • 27

    Jacobson LEZiemba-Davis MHerrera AJ: The limitations of using risk factors to screen for blunt cerebrovascular injuries: the harder you look, the more you find. World J Emerg Surg 10:462015

  • 28

    Markus HSHayter ELevi CFeldman AVenables GNorris J: Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol 14:3613672015

  • 29

    Mayberry JCBrown CVMullins RJVelmahos GC: Blunt carotid artery injury: the futility of aggressive screening and diagnosis. Arch Surg 139:6096132004

  • 30

    McKinney AOtt FShort JMcKinney ZTruwit C: Angiographic frequency of blunt cerebrovascular injury in patients with carotid canal or vertebral foramen fractures on multidetector CT. Eur J Radiol 62:3853932007

  • 31

    Miller PRFabian TCCroce MACagiannos CWilliams JSVang M: Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg 236:3863952002

  • 32

    Mundinger GSDorafshar AHGilson MMMithani SKManson PNRodriguez ED: Blunt-mechanism facial fracture patterns associated with internal carotid artery injuries: recommendations for additional screening criteria based on analysis of 4,398 patients. J Oral Maxillofac Surg 71:209221002013

  • 33

    Paulus EMFabian TCSavage SAZarzaur BLBotta VDutton W: Blunt cerebrovascular injury screening with 64-channel multidetector computed tomography: more slices finally cut it. J Trauma Acute Care Surg 76:2792852014

  • 34

    Sliker CW: Blunt cerebrovascular injuries: imaging with multidetector CT angiography. Radiographics 28:168917102008

  • 35

    Stein DMBoswell SSliker CWLui FYScalea TM: Blunt cerebrovascular injuries: does treatment always matter?. J Trauma 66:1321442009

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Article Information

Correspondence Pierre Esnault, Service de Réanimation—Brûlés, Hôpital d'Instruction des Armées Sainte Anne, Blvd. Sainte Anne, Toulon 83000, France. email: pierre.esnault@gmail.com.

INCLUDE WHEN CITING Published online July 29, 2016; DOI: 10.3171/2016.4.JNS152600.

Disclosures The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

© AANS, except where prohibited by US copyright law.

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Figures

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    Pie chart showing the mechanism of injury of enrolled patients.

References

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Bratton SLChestnut RMGhajar JMcConnell Hammond FFHarris OAHartl R: Guidelines for the management of severe traumatic brain injury. X. Brain oxygen monitoring and thresholds. J Neurotrauma 24:Suppl 1S65S702007. (Erratum in J Neurotrauma 25:276–278 2008).

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Bratton SLChestnut RMGhajar JMcConnell Hammond FFHarris OAHartl R: Guidelines for the management of severe traumatic brain injury. XIV. Hyperventilation. J Neurotrauma 24:Suppl 1S87S902007. (Erratum in J Neurotrauma 25:276–278 2008)

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Bromberg WJCollier BCDiebel LNDwyer KMHolevar MRJacobs DG: Blunt cerebrovascular injury practice management guidelines: the Eastern Association for the Surgery of Trauma. J Trauma 68:4714772010

16

Burlew CCBiffl WL: Blunt cerebrovascular trauma. Curr Opin Crit Care 16:5875952010

17

Burlew CCBiffl WL: Imaging for blunt carotid and vertebral artery injuries. Surg Clin North Am 91:2172312011

18

Callcut RAHanseman DJSolan PDKadon KSIngalls NKFortuna GR: Early treatment of blunt cerebrovascular injury with concomitant hemorrhagic neurologic injury is safe and effective. J Trauma Acute Care Surg 72:3383462012

19

Cothren CCBiffl WLMoore EEKashuk JLJohnson JL: Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg 144:6856902009

20

Cothren CCMoore EEBiffl WLCiesla DJRay CE JrJohnson JL: Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg 139:5405462004

21

Debette SLeys D: Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurol 8:6686782009

22

DiCocco JMEmmett KPFabian TCZarzaur BLWilliams JSCroce MA: Blunt cerebrovascular injury screening with 32-channel multidetector computed tomography: more slices still don't cut it. Ann Surg 253:4444502011

23

Fabian TCPatton JH JrCroce MAMinard GKudsk KAPritchard FE: Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Ann Surg 223:5135251996

24

Fleck SKLangner SBaldauf JKirsch MKohlmann TSchroeder HWS: Incidence of blunt craniocervical artery injuries: use of whole-body computed tomography trauma imaging with adapted computed tomography angiography. Neurosurgery 69:6156242011

25

Franz RWWillette PAWood MJWright MLHartman JF: A systematic review and meta-analysis of diagnostic screening criteria for blunt cerebrovascular injuries. J Am Coll Surg 214:3133272012

26

Fusco MRHarrigan MR: Cerebrovascular dissections: a review. Part II: blunt cerebrovascular injury. Neurosurgery 68:5175302011

27

Jacobson LEZiemba-Davis MHerrera AJ: The limitations of using risk factors to screen for blunt cerebrovascular injuries: the harder you look, the more you find. World J Emerg Surg 10:462015

28

Markus HSHayter ELevi CFeldman AVenables GNorris J: Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol 14:3613672015

29

Mayberry JCBrown CVMullins RJVelmahos GC: Blunt carotid artery injury: the futility of aggressive screening and diagnosis. Arch Surg 139:6096132004

30

McKinney AOtt FShort JMcKinney ZTruwit C: Angiographic frequency of blunt cerebrovascular injury in patients with carotid canal or vertebral foramen fractures on multidetector CT. Eur J Radiol 62:3853932007

31

Miller PRFabian TCCroce MACagiannos CWilliams JSVang M: Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg 236:3863952002

32

Mundinger GSDorafshar AHGilson MMMithani SKManson PNRodriguez ED: Blunt-mechanism facial fracture patterns associated with internal carotid artery injuries: recommendations for additional screening criteria based on analysis of 4,398 patients. J Oral Maxillofac Surg 71:209221002013

33

Paulus EMFabian TCSavage SAZarzaur BLBotta VDutton W: Blunt cerebrovascular injury screening with 64-channel multidetector computed tomography: more slices finally cut it. J Trauma Acute Care Surg 76:2792852014

34

Sliker CW: Blunt cerebrovascular injuries: imaging with multidetector CT angiography. Radiographics 28:168917102008

35

Stein DMBoswell SSliker CWLui FYScalea TM: Blunt cerebrovascular injuries: does treatment always matter?. J Trauma 66:1321442009

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