Optimizing Screening for Blunt

Cerebrovascular Injuries
Walter L. Biffl, MD, Ernest E. Moore, MD, Patrick J. Offner, MD, Kerry E. Brega, MD,
Reginald J. Franciose, MD, J. Paul Elliott, MD, Jon M. Burch, MD, Denver, Colorado

BACKGROUND: The recognition that early diagnosis

and intervention, prior to ischemic neurologic
injury, has the potential to improve outcome following blunt cerebrovascular injuries (BCVI), led
to a policy of aggressive screening for these injuries. The resultant epidemic of BCVI has created a dilemma, as widespread screening is impractical. We sought to identify independent
predictors of BCVI, to focus resources.
METHODS: Cerebral arteriography was performed
based on signs or symptoms of BCVI, or in
asymptomatic patients with high-risk mechanisms (hyperextension, hyperflexion, direct blow)
or injury patterns. Logistic regression analysis
identified independent predictors.
RESULTS: A total of 249 patients underwent arteriography; 85 (34%) had injuries. Independent
predictors of carotid arterial injury were Glasgow
coma score 6, petrous bone fracture, diffuse
axonal brain injury, and LeFort II or III fracture.
Having one of these factors in the setting of a
high-risk mechanism was associated with 41%
risk of injury. Of patients with cervical spine fracture, 39% had vertebral arterial injury.
CONCLUSIONS: Patients sustaining high-risk injury
mechanisms or patterns should be screened for
BCVI. In the face of limited resources, screening
efforts should be focused on those with high-risk
predictors. Am J Surg. 1999;178:517522.
1999 by Excerpta Medica, Inc.

lunt cerebrovascular injuries (BCVI) have the potential for devastating complications. Historically,
the vast majority have been diagnosed only after the
appearance of neurologic deficits.1 8 Based on a multicenter review of blunt carotid injuries (BCI),6 we proposed
that these injuries were often unrecognized or masked by
brain injury. To test this hypothesis, we began a prospective analysis of screening at our center in November 1994.9
In this phase, all patients undergoing arteriography to rule
out traumatic aortic injuries were additionally evaluated

From the Departments of Surgery (WLB, EEM, PJO, RJF, JMB)

and Neurosurgery (KEB, JPE), Denver Health Medical Center and
University of Colorado Health Sciences Center, Denver, Colorado.
Requests for reprints should be addressed to Walter L. Biffl,
MD, Department of Surgery, Box 0206, Denver Health Medical
Center, 777 Bannock Street, Denver, Colorado 80204-4507.
Presented at the 51st Annual Meeting of the Southwestern
Surgical Congress, Coronado, California, April 18 21, 1999.

1999 by Excerpta Medica, Inc.

All rights reserved.

with selective cerebral arteriography. The incidence of BCI

in this select group was 3.5%; notably, there was no clinical
suspicion of BCI prior to angiography in 3 of the 6 injured
patients. Recognizing further that the majority of BCI have
a latent period prior to the appearance of clinical symptoms,2,3,8,10,11 and with evidence from Memphis8 that neurologic outcome could be improved with anticoagulation, a
more aggressive policy of screening was subsequently
adopted at our center. Indeed, this policy has uncovered an
epidemic of BCI.12
Unfortunately, a clinical dilemma has emerged. Although our data12 suggest that early diagnosis and therapy before the appearance of neurologic deficits contribute to improved neurologic outcome following BCI, a
liberal screening approach is logistically impractical in
most centers. Moreover, currently only cerebral arteriography and magnetic resonance angiography (MRA) are reliable screening tests.13 Thus, in remote facilities, patients
may need to be transferred to other institutions to exclude
BCVI. Our screening criteria, based on anatomic and
mechanistic considerations, might be considered too inclusive. We hypothesized that a subgroup at high risk for
BCVI could be identified, who warrant screening evaluation. Specifically, the purpose of this study was to determine the association between various injury mechanisms
and patterns and BCVI.

METHODS
Patients
Denver Health Medical Center is a certified urban level
I trauma center with pediatric commitment, and serves as
the Rocky Mountain regional trauma center for Colorado
and adjoining regions. The number of trauma admissions
during the study period (January 1990 through September
1998) has been stable at 3000 to 3200 patients per year,
and 86% of admissions have resulted from blunt injury.
Our trauma registry records patients at the time of their
hospitalization, and was employed to identify patients
screened and diagnosed with BCVI prior to August 1996.
Subsequently, patients undergoing cerebral arteriography
to exclude BCVI have been identified, and specific data
collected prospectively.
Diagnosis
The diagnosis of BCVI is confirmed by four-vessel cerebral arteriography in all cases. Digital subtraction techniques are used, and all studies include the aortic arch and
cerebral vessel origins. Trauma patients undergo emergent
arteriography if any of the following signs or symptoms
suggestive of cerebrovascular injury are present: (a) hemorrhagefrom mouth, nose, ears or wounds of potential
arterial origin; (b) expanding cervical hematoma; (c) cer0002-9610/99/$see front matter
PII S0002-9610(99)00245-7

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SCREENING FOR BLUNT CEREBROVASCULAR INJURIES/BIFFL ET AL

RESULTS

TABLE I
Screening Criteria for Blunt Cerebrovascular Injury
Injury mechanism
Severe cervical hyperextension/rotation or hyperflexion,
particularly if associated with
Displaced midface or complex mandibular fracture
Closed head injury consistent with diffuse axonal injury
Near-hanging resulting in anoxic brain injury
Physical signs
Seat belt abrasion or other soft tissue injury of the anterior
neck resulting in significant swelling or altered mental status
Fracture in proximity to internal carotid or vertebral artery
Basilar skull fracture involving the carotid canal
Cervical vertebral body fracture

vical bruit in a patient 50 years old; (d) evidence of

cerebral infarction on CT scan; or (e) unexplained or
incongruous central or lateralizing neurologic deficit, transient ischemic attack (TIA), amaurosis fugax, or Horners
syndrome. In August 1996 we began to screen at-risk
asymptomatic patients (ie, no suggestive signs or symptoms) for BCVI. The criteria for screening arteriography
are listed in Table I. Follow-up arteriography is performed
within 7 to 10 days when possible, to evaluate efficacy of
the initial therapy.
Data Analysis
All patients undergoing cerebral arteriography to exclude
BCVI were studied. Demographic information, injury
mechanisms and associated injuries were analyzed to identify risk factors for BCVI. Statistical analysis was performed
on an IBM compatible personal computer using StatMost
32 for Windows 95 (DataMost Corp., Sandy, Utah) and
SPSS 9.0 for Windows (SPSS, Inc., Chicago, Illinois).
Means of continuous data were compared using Students t
test. Categorical data were compared using Fishers exact
test or the chi-square test, where appropriate. Risk factors
for BCI or blunt vertebral artery injuries (BVI) were evaluated in univariate logistic regression analyses. Craniocervical risk factors that were associated with BCI or BVI with
a P value 0.20 were entered into multiple logistic regression analysis. This cutoff was chosen to exclude variables of
questionable importance, but to include variables of potential clinical relevance. In the multiple logistic regression
analysis, significance was evaluated at the 0.05 level. Adjusted odds ratios and 95% confidence intervals were calculated for each of the independent predictors. The conditional probability of having a BCI or BVI was calculated
as follows: if four risk factors were identified (X1, X2, X3,
X4), then five coefficients (a, B1, B2, B3, B4) were derived
from the analysis, and the conditional probability (CP) of
having BCVI is:

Patients
From January 1990 through September 1998, cerebral
arteriography was performed in 249 patients to exclude
BCVI; 85 (34%) were diagnosed with injuries. Sixty-five
patients had carotid injuries, 10 had vertebral injuries, and
10 had both carotid and vertebral injuries. Carotid injuries
were bilateral in 32 patients, and vertebral injuries bilateral
in 5. Forty patients initially presented with signs or symptoms of BCVI; 28 (70%) had injuries. Among 209 asymptomatic patients, we diagnosed injuries in 57 (27%). The
mean age of the 249 total patients was 37.9 1.1 years
(range 5 to 83). Those with BCVI were younger (35.3
1.6 years) than those without BCVI (39.2 1.4; P
0.05). Males comprised 79% of the total group (196
patients). Sixty-four of 196 (33%) males had injuries, compared with 21 of 53 (40%) females (P 0.05).
Mechanism of injury was motor vehicle crash in 113
(45%), pedestrian struck in 30 (12%), motorcycle crash in
28 (11%), fall in 25 (10%), assault in 15 (6%), skier versus
tree in 12 (5%), and other mechanisms (bicycle crash,
near-hanging, strangulation, construction accidents, and
miscellaneous) in 26 (10%) patients. There was no difference in mechanism between the groups with and without
injuries. Of those involved in motor vehicle crashes, 25%
of the BCVI group were using passive restraints, compared
with 29% of the group without BCVI (P 0.05).
Risk Factors
Risk factors for BCVI are listed in Table II, which separately compares the groups with and without BCI and
BVI, and lists the P value for each factor according to
univariate analysis. In this analysis, significant risk factors
for BCI were younger age, lower Glasgow Coma Score
(GCS), GCS 6, diffuse axonal brain injury (DAI), presence of any head injury, petrous bone fracture, LeFort II or
III fracture, associated chest injury, and associated abdominal injury. Significant risk factors for BVI were cervical
spine fracture, any spine fracture, and associated abdominal
injury.
Multiple logistic regression analysis included all categorical variables with a P value 0.20 by univariate analysis.
However, because of their questionable clinical relevance,
the following factors were excluded despite low P values:
associated chest injury, associated abdominal injury, and
any head injury. Independent predictors of BCI by this
analysis were GCS 6, petrous bone fracture, DAI, and
LeFort II or III fracture (Table III). The only independent
predictor of BVI was cervical spine fracture. Table IV lists
the conditional probability of BCI and BVI in the presence
of various risk factors; probability ranges reflect individual
risk factors and combinations thereof.

COMMENTS
CP 1/(1 ez), where z
a B1(X1) B2 (X2) B3(X3) B4(X4)
The risk factors X1, X2, X3, and X4 were assigned a value
of 1 if present and 0 if absent. Continuous data are
expressed as mean the standard error of the mean.
518

Blunt cerebrovascular injuries (BCVI) have the potential

for devastating complications. Early reports collectively
established mortality rates of BCI to be 28%, with 58% of
survivors suffering severe neurologic sequelae.13 Subsequent multicenter reviews corroborated these disconcerting morbidity and mortality figures, and identified the
incidence of BCI to be 0.08% to 0.17% among patients

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SCREENING FOR BLUNT CEREBROVASCULAR INJURIES/BIFFL ET AL

TABLE II
Results of Univariate Logistic Regression Analyses of Risk Factors for Blunt Carotid (BCI) and Vertebral Artery (BVI) Injury
Factor
Mean age
Mean GCS
GCS 6
Diffuse axonal injury
Subdural hematoma
Epidural hematoma
Subarachnoid hemorrhage
Brain contusion
Skull fracture
Any head injury
Sphenoid fracture
Petrous fracture
Any basilar skull fracture
Nasal fracture
Mandible fracture
Any midface fracture
Mandible plus any midface fracture
LeFort II or III fracture
Tripod fracture
Any facial fracture
Cervical spine fracture
Any spine fracture
Chest injury
Abdomen injury
Pelvis fracture
Extremity fracture

BCI (n 75)

No BCI (n 174)

P Value

BVI (n 20)

No BVI (n 229)

P Value

34.6 1.7*
8.7 0.6*
36 (48%)*
11 (15%)*
12 (16%)
9 (12%)
23 (31%)
21 (28%)
11 (15%)
45 (60%)*
10 (13%)
14 (19%)*
20 (27%)
9 (12%)
10 (13%)
20 (27%)
9 (12%)
8 (11%)*
6 (8%)
25 (33%)
10 (13%)
20 (27%)
34 (45%)*
20 (27%)*
12 (16%)
22 (29%)

39.3 1.3
11.2 0.4
45 (26%)
8 (5%)
17 (10%)
15 (9%)
40 (23%)
46 (26%)
23 (13%)
73 (42%)
20 (11%)
13 (7%)
39 (22%)
25 (14%)
19 (11%)
48 (28%)
10 (6%)
5 (3%)
16 (9%)
61 (35%)
21 (12%)
40 (23%)
52 (30%)
22 (13%)
20 (11%)
50 (29%)

0.001
0.001
0.001
0.009
0.164
0.409
0.203
0.799
0.760
0.010
0.683
0.012
0.470
0.618
0.587
0.881
0.095
0.018
0.761
0.793
0.508
0.500
0.020
0.008
0.332
0.924

39.0 3.1
10.8 1.2
4 (20%)
3 (15%)
2 (10%)
1 (5%)
6 (30%)
4 (20%)
1 (5%)
10 (50%)
1 (5%)
0 (0%)
2 (10%)
4 (20%)
1 (5%)
3 (15%)
1 (5%)
0 (0%)
0 (0%)
4 (20%)
12 (60%)*
13 (65%)*
9 (45%)
7 (35%)*
2 (10%)
7 (35%)

37.8 1.1
10.4 0.3
75 (33%)
16 (7%)
27 (12%)
23 (10%)
57 (25%)
63 (28%)
33 (14%)
108 (47%)
29 (13%)
27 (12%)
57 (25%)
30 (13%)
28 (12%)
65 (28%)
18 (8%)
13 (6%)
22 (10%)
82 (36%)
19 (8%)
46 (20%)
77 (34%)
35 (15%)
30 (13%)
65 (28%)

0.363
0.383
0.801
0.208
0.811
0.475
0.615
0.471
0.265
0.808
0.332
0.719
0.151
0.393
0.352
0.208
0.648
0.728
0.747
0.163
0.001
0.001
0.309
0.030
0.693
0.533

* P 0.05.
GCS Glasgow Coma Score.

TABLE III
Predictive Model for Blunt Cerebrovascular Injuries Based
on Multiple Logistic Regression Analysis
Predictor

Estimate

P
Value

Carotid artery injury

Constant
1.39 0.20

GCS 6
0.68 0.31 0.029
Petrous fracture
0.97 0.43 0.025
Diffuse axonal injury 1.13 0.52 0.030
LeFort II or III
fracture
1.31 0.61 0.033
Vertebral artery injury
Constant
3.37 0.38

Cervical spine
fracture
2.67 0.51 0.001

Odds Ratio
(95% CI)

1.98 (1.073.65)
2.64 (1.136.19)
3.09 (1.128.57)
3.70 (1.1212.29)

14.50 (5.3039.63)

CI confidence interval; GCS Glasgow Coma Score.

admitted to trauma centers following blunt injury.4 7

Based on our involvement in one such review,6 we hypothesized that these injuries were often unrecognized or
masked by brain injury. Consequently, we began a prospective analysis of screening for BCI in 1994.9 By imaging the
cervical vessels in patients undergoing postinjury thoracic
aortography, we found BCI in 3.5%. Only one half of these
patients had the injury suspected prior to the diagnostic
test.
Around the time our pilot screening study9 was coming to

a close, Fabian and colleagues8 published a large singleinstitution series of BCI. Their reported incidence of BCI
was 0.33%, nearly triple that of previous reviews, confirming that a higher index of suspicion would lead to the more
frequent diagnosis of these injuries. Despite the high index
of suspicion among the Memphis group, however, 93% of
their patients already had neurologic symptoms at the time
of diagnosis; furthermore, while they demonstrated improved neurologic outcome when patients were fully anticoagulated with heparin, the ultimate outcome included a
mortality of 31% and neurologic morbidity of 37%. Given
these data, we pursued the potential to further improve
neurologic outcomes by identifying and treating BCVI
prior to the occurrence of cerebral ischemia. In fact, the
characteristic latent period between the time of injury and
the occurrence of cerebral ischemia makes screening a
tenable concept. Krajewski and Hertzer,2 in their literature
review of 96 patients with BCI, noted that 58% of patients
first manifested symptoms 10 or more hours after the injury,
and 36% became symptomatic 24 hours or more postinjury.
Perry and colleagues3 similarly reported that 23% of patients first had symptoms more than 24 hours after injury.
Mokri and colleagues10 had 9 of 18 BCI patients develop
symptoms more than 3 days postinjury, with one injury
manifesting 14 years later! Fabian and colleagues11 in 1990
reported 33% of their patients had a neurologic change
12 hours postinjury.
These data collectively formed the basis for an aggressive

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TABLE IV
Conditional Probability of Blunt Cerebrovascular Injuries
Based on Multiple Logistic Regression Analysis
Carotid artery injury
No risk factors
Any one risk factor
Any two risk factors
Any three risk factors
All four risk factors
Vertebral artery injury
No cervical spine fracture
Cervical spine fracture

20%
33% to 48%
56% to 74%
80% to 88%
93%
3%
33%

Risk factors were GCS 6, petrous fracture, diffuse axonal brain injury, or
LeFort II or III fracture.
GCS Glasgow Coma Score.

policy of screening at our institution, which led to the

discovery of an epidemic of BCI.12 Unfortunately, the
documentation of a relatively high incidence of asymptomatic BCI, as well as BVI, has created a clinical dilemma.
Although our data12 suggest that early diagnosis and therapy before the appearance of neurologic deficitsmay
contribute to improved neurologic outcome, we recognize
that a liberal screening approach is impractical in most
centers. A major reason for this is the absence of a reliable
noninvasive screening test. Duplex ultrasonography, considered by many to be the modality of choice for imaging
the carotid arteries, had just an 86% sensitivity for BCI in
a multicenter review.6 Duplex requires significant stenosis
to detect flow disturbances, and does not clearly image the
arteries at or above the skull base. Computed tomographic
angiography (CTA) is attractive in that most multisystem
trauma patients have indications for CT scanning.14 However, our experience has shown that it has a sensitivity
similar to duplex ultrasonography.15 To image the cerebral
vessels in their entirety with a slice thickness and pitch
adequate for sufficiently sensitive reconstruction is not
practical; in addition, there is bony artifact in the carotid
canal, obscuring injuries in that segment of the artery. A
reliable alternative to arteriography appears to be MRA,13
but a major impediment to its widespread application is the
lack of availability at many institutions, as well as incompatibility with many orthopedic fixation devices and ventilatory equipment. Until MRA has been rigorously evaluated, cerebral arteriography remains the predominant
screening modality, and therein lies the dilemma. There is
an understandable reluctance to subject patients to an
expensive, labor-intensive, invasive examination for
screening purposes alone. Many physicians believe that
strokes as a result of BCVI are rare events, and therefore
have difficulty accepting the concept of aggressive screening. Moreover, although our data12 are supportive, there
are no prospective, controlled studies demonstrating an
outcome benefit related to early diagnosis and intervention.
The concept of screening is not unique to our institution,
and has typically been based on injury patterns.
Eachempati and colleagues16 reported 8 patients diagnosed
with BCI in whom the diagnosis was pursued because of
basilar skull fracture through the carotid canal. Rogers and
colleagues14 similarly screened asymptomatic patients with
520

specific injury patterns, including basilar skull and mandibular fractures. The recognized association between cervical
spine fractures and vertebral artery injuries has similarly
prompted screening. Following mid-cervical spine fracture
or subluxationincluding locked or perched facet, facet
destruction with instability, or fracture involving the foramen transversariumWillis and colleagues17 demonstrated a 46% incidence of vertebral artery injuries. Woodring and colleagues18 performed arteriography in 8 patients
in whom transverse process fractures of the cervical vertebrae extended into the foramen transversarium; 7 (88%)
had vertebral artery injuries.
Our screening criteria are based on the presumed pathophysiology of BCVI, and include injury mechanisms in
addition to associated high-risk fracture patterns (Table I).
The most common mechanism whereby the internal carotid artery (ICA) is injured is hyperextension and contralateral rotation of the head and neck. This may be
explained by anatomical relationships unique to the upper
cervical region. The lateral articular processes and pedicles
of the upper three cervical vertebrae project more anteriorly than do those of the lower four cervical vertebrae.
Thus, the overlying distal cervical ICA is prone to stretch
injury during cervical hyperextension.19 Rotation at the
atlantoaxial joint may result in anterior movement of the
contralateral C1 lateral mass, further exacerbating the
stretch injury. In instances of acute cervical hyperflexion,
as seen in motor vehicle crashes or falls, the artery may be
compressed between the mandible and vertebral prominences.19 Seat belt injuries, strangulation injuries, and
near-hangings may injure the common or ICA by a direct
blow mechanism. Our screening criteria have taken these
factors into account, and considered associated injury patterns as indicators of force vectors.
In our series, the incidence of arteriographically demonstrable BCVI was 70% in the presence of suggestive signs or
symptoms of cerebrovascular injury. Based on our screening
criteria, 27% of selected asymptomatic patients were diagnosed with BCVI. This is a relatively high yield, particularly for an injury with such potentially devastating consequences. However, we acknowledge the seeming
inclusive nature of the screening criteria and the impracticality of implementing such a screening protocol at many
institutions. Therefore, we sought to identify markers for
high risk to help focus diagnostic resources. While the
dangers of BCI have been well documented, the neurologic
morbidity and mortality associated with BVI are less clear.
We tend to treat BVI less aggressively than BCI, generally
instituting anticoagulation only in the setting of highgrade, bilateral, or symptomatic lesions. Therefore, for purposes of generating predictive models, we separated the
analyses of risk factors for BCI and BVI. Multiple logistic
regression analysis identified four individual factors that are
independently associated with the existence of BCI. It is
important to keep in mind that these factors must be in the
context of a mechanism of injury with cervical hyperextension/rotation, hyperflexion, or a direct blow. In this
setting, a GCS 6, DAI, petrous bone fracture, or LeFort
II or III fracture identify the patient at particularly high risk
for BCI. Petrous bone fractures represent a risk to the ICA
in the carotid canal. Diffuse axonal injury is thought to be

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related to traumatic head rotation or abrupt deceleration,

also important in the pathogenesis of BCI. LeFort fractures
are associated with significant frontal impact, again consistent with hyperextension or hyperflexion mechanisms.
The significance of a GCS 6 lies in the fact that BCI
have probably been historically underrecognized because of
the presence of severe brain injury, masking neurologic
changes. The severe brain injury reflects a significant blow
to the head, which can result in cervical hyperextension or
hyperflexion. Regardless of symptoms, in the presence of
any one of the four risk factors, the incidence of BCI was
41%. The conditional probability of BCI of 20% with no
risk factors (Table IV) reflects the fact that 20% of our
patients with BCI had no significant associated injuries.20
The only independent predictor for BVI we identified was
the presence of a cervical spine fracture, present in 65% of
patients with BVI. If a patient presented with cervical
spine fracture, there was a 39% chance of finding a BVI on
arteriography. Further experience will clarify the high-risk
cervical fracture levels and types.
An analysis of the sensitivity and specificity of each
screening criterion was impossible for a number of reasons.
First, symptoms that in retrospect were attributed to BCVI
were sometimes ascribed to head injury at the time of
presentation, confusing the issue of whether the patient
was considered truly symptomatic; second, patients with
severe associated injuries may have fit the screening criteria
but did not undergo arteriography because of cardiopulmonary instability or early demise; third, there are some patients who underwent arteriography who did not clearly
meet the criteria, and some who arguably met the criteria
but were not studied.
In sum, we have identified markers of high risk for BCVI
in patients sustaining trauma with cervical hyperextension/
rotation, hyperflexion, or direct blow mechanisms. Given
the number of patients we have treated who sustained
BCVI as a result of trivial trauma, or who had no associated injuries, these high-risk markers will fail to identify
some injuries. However, they represent a basis for more
aggressive screening at facilities that lack the specific resources for widespread definitive diagnostic testing. The
question of optimal criteria will ultimately require a multicenter collaborative effort. Perhaps most importantly,
accumulating data will help to determine whether this
approach will improve patient outcomes.

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David V. Feliciano, MD (Atlanta, Georgia): Drs. Biffl
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209 asymptomatic patients subsequently undergoing arteriography based on the new criteria presented today since
1996.
In summary, 85 patients over a period of 7 or 8 years, an
extraordinary number, were found to have injury to the
cerebrovascular vessels at one hospital. As stated, they
then used univariate logistic regression analysis based on
incidences, followed by multiple logistic regression analysis
using the most significant categorical variables and univariate analysis. The authors concluded that independent

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521