Diagnostics

Blunt Trauma to the Carotid Arteries
ANTHONY G. SANZONE, MD,* HERNANDO TORRES, MD,*
STEPHEN H. DOUNDOULAKIS, MD'I"
Carotid artery dissection is a rare occurrence in the trauma patient. Two
cases of blunt trauma resulting in carotid artery dissection are reported.
Initial recognition by clinicians is often difficult because of the diverse
clinical manifestations, the delay in presentation, and the associated
multi-organ system injuries that accompany carotid artery dissection.
Because the diagnosis of carotid injury is rarely suspected in patients
with neurological deficits, the first diagnostic test performed is usually
computed tomography (CT) of the head. Angiographyshould he strongly
considered when the following occur: (a) Neurologic deficits are incompatible with CT findings; (b) there is monoparesis or hemiparesis with a
normal mental status examination; (c) there is severe cervical trauma
with an abnormal neurological exam; or (d) a basilar skull fracture is
present in a patient with an abnormal mental status exam. Once diagnosed, the management of carotid artery dissection is complex and no
generalized guidelines have been established. (Am J Emerg Med 1995;
13:327-330. Copyright © 1995 by W.B. Saunders Company)
Carotid artery dissection secondary to blunt t r a u m a is often not recognized at the time of admission and its diagnosis
offers the clinician a challenge. The recognition of this injury
is often delayed because of the following factors: (1) frequent
association with other severe multisystem injuries, particularly a closed head injury1"5; (2) failure to suspect this injury
after m i n o r head and neck traumaS'6; and (3) frequent delay
in the appearance of clinical symptoms. 5"8 If the carotid artery injury can be diagnosed early and subsequently treated
aggressively, p e r m a n e n t neurological deficit and perhaps
mortality might be avoided. 9 The following report of two
cases and review of the literature highlight the importance of
early detection and aggressive treatment in carotid artery
injury secondary to blunt trauma.

CASE REPORTS
Case 1
A 39-year-old man, intoxicated with ethanol, presented to the
emergency department (ED) after being struck multiple times on the
head and neck with a lead pipe. Paramedics reported a loss of con-

From the *Department of Neurosurgery and 1"Department of
Neuroradiology, University of Health Sciences, The Chicago
Medical School, Mt Sinai Hospital Medical Center, Chicago, IL.
Manuscript received May 24, 1994; revision accepted July 1,
1994.
Address reprint requests to Dr Torres, Department of Neurosurgery, University of Health Sciences, The Chicago Medical
School, Mt. Sinai Hospital Medical Center, 2755 West 15th St,
Chicago, IL 60608.
Key Words: Carotid artery, dissection, trauma, angiography.
Copyright © 1995 by W.B. Saunders Company
0735-6757/95/1303-001955.00/0

sciousness, but at the time of admission the patient could be
aroused, and had a Glasgow Coma Scale score of 10 and a trauma
score of 11. On physical examination, the patient had severe periorbital edema, multiple facial lacerations, a floating mid-face on
palpation of the maxilla, and multiple missing teeth. Pupils were
equal and sluggishly reactive bilaterally. The cervical spine was uninjured and the soft tissue of the neck had no ecchymosis or edema.
On neurological examination, no motor or sensory deficits were
found, and reflexes were symmetric bilaterally. Facial roentgenograms and computed tomography (CT) of the facial bones showed a
LeForte IlI fracture. CT of the head demonstrated a questionable
infarct in the left frontal region and a comminuted fracture through
both left frontal sinus walls. Approximately 18 hours after admission, the patient developed right hemiplegia and a fixed dilated left
pupil. CT of the head (Figure 1) was immediately performed and
showed a developing infarction in the left frontal area and a slightly
dilated superior opthalmic vein on the right side suspicious for a
carotid cavernous fistula. A cerebral angiogram was performed (Figure 2) and showed a 10-cm segment Of progressive distal tapering of
the left internal carotid artery beginning approximately 2 cm distal to
its origin. The patient was immediately heparinized and no further
neurological deficits developed. On the tenth day of his hospitalization, the patient underwent repair of the LeForte fracture, tracheostomy, and feeding tube placement. Repeat CT showed left middle
cerebral artery infarcts and anterior communicating artery infarcts.
The patient's subsequent hospital course was uncomplicated and he
was transferred to a rehabilitation center with mild right-sided weakness. On 2-month follow-up examination, no neurological deficits
were present.

Case 2
A 27-year-old man was assaulted in the mouth with a lead pipe,
producing soft palate lacerations and cracked teeth requiring emergent operative repair. On awakening the next morning, he was unable to get out of bed and noticed weakness of his left side. CT was
performed and showed a right parietal infarct in the area of the right
middle cerebral artery distribution. The patient was subsequently
transferred to our institution for a cerebral angiogram. Initial physical examination found a lethargic 27-year-old man who could be
aroused and was able to follow commands. On examination, the
patient displayed left-sided facial weakness, left homonymous hemianopsia, and left-sided hemiplegia with some movement to painful
stimuli. An angiogram was performed (Figure 3) and showed complete occlusion of the right internal carotid artery approximately 2
cm distal to its origin and tapering as the artery moved distally,
suggestive of extrinsic compression or dissection. The patient was
heparinized. During his hospital course, his left facial weakness and
left lower extremity weakness improved. He was transferred to a
rehabilitation center 2 weeks after admission on oral anticoagulants
and with persistent left upper extremity weakness. On four-month
follow-up, little improvement was noted in his left upper extremity
weakness.

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FIGURE 1. Dilation of the right superior opthalmic vein consistent with engorgement. This is suspicious for a carotid-cavernous
sinus fistula or external-to-internal carotid artery fistulization.

DISCUSSION
Blunt trauma causing carotid artery dissection occurs infrequently and comprises only 3% to 10% of all carotid injuries. 4's-12 In a review of 140 cases extending from 1975 to
1983, the mean age was 45 with a slightly higher male predominance. 13,14 Injuries resulting in permanent neurological
deficits range from 40% to 80% and mortality rates range
from 20% to 40%. 3'4'6'8"11'15'16 Predilection for one side has
thus far not yet been elucidated. 13
Injuries to the internal carotid artery are most commonly
secondary to motor vehicle accidents. 9"13"17 Other mechanisms of injury include fist fights, falls, blows to the head and
neck with various objects, hanging by the neck, carotid artery compression, and local surgical procedures. 14'17 Blunt
intraoral trauma has also been reported to cause carotid artery injury via the foreign body striking the peritonsillar region. This is occasionally encountered when a child falls
with a foreign object in his or her mouth. 17q9 Additionally,
carotid injuries have been reported after apparently less
traumatic activities such as coughing, nose blowing, yoga
exercises, chiropractic manipulation, sports activities, and
even neck turning while leading a parade. 13'a°'21 Predisposing conditions that can contribute to carotid artery dissection
include fibromuscular dysplasia (which has been noted in
approximately 15% of cases in 2 reports), syphilis, Marfans
syndrome, atherosclerosis, and hypertension-induced intireal thickeningJ 3
The spectrum of injuries that may occur as a result of blunt
trauma to the internal carotid artery include spasm, intimal
disruption, dissection, pseudoaneurysm formation with possible emboli, and complete transection. Crissey and Burnstein 7 described four distinct mechanisms believed to produce carotid artery injury. Type 1 injuries are caused by a

FIGURE 2. Subtraction angiography of the left common carotid
demonstrates a tapered proximal internal carotid artery to the petrous portion of the left internal carotid artery with total occlusion
distally. There is no evidence of fistulization.

FIGURE 3. Subtraction angiography of the right common carotid
demonstrates a tapered proximal internal carotid artery with total
occlusion.

SANZONE ET AL • BLUNT TRAUMA TO THE CAROTID ARTERIES

direct blow to the neck; type 2 injuries result from a blow to
the head or face that subsequently causes rotation and hyperextension of the head or neck; type 3 carotid injuries are
secondary to intraoral trauma; and type 4 injuries damage
the intrapetrous portion of the internal carotid artery. 4'7
A thorough comprehension of the anatomic relationship
between the internal carotid artery and its surrounding structures is essential in understanding the clinical symptomatology of carotid artery injury. As the carotid artery ascends
from its origin to the base of the skull, it lies anterior to the
longissimus capitus muscle and the transverse processes of
the cervical vertebrae. The axis differs from the inferior cervical vertebrae in that its lateral articular process and pedicle
lie more anterior. When blunt trauma causes extended hyperextension and contralateral rotation, the carotid artery is
stretched over these bony prominences, which can result in
(1) arterial stretching without intimal damage, (2) an intimal
tear leading to thrombus formation with possible distal emboli, or (3) transmural disruption leading to an internal carotid artery pseudoaneurysm with possible distal emboli. 5
Another reported mechanism of extracranial carotid artery dissection includes a traumatic event initiating hemorrhage into the medial layer of the artery. The consequence of
the hemorrhage includes (1) dissection subintimally causing
stenosis, (2) dissection into the subadvential plane producing
a sac-like dilation of the vessel wall, or (3) rupture through
the intima forming a false lumen communicating with the
true lumen in each end. The latter two pathological mechanisms subsequently cause intimal damage and may lead to
platelet aggregation with possible embolization. 13
Intracranially, the internal carotid artery traverses the inferior portion of the petrous temporal bone and takes an
inverted L-shaped course to the apex of the petrous bone. It
then enters the cranial cavity via the foramen lacerum and
takes an S-shaped course to the cavernous sinus. From the
sinus the internal carotid artery exits through the dura at the
medial edge of the anterior clinoid process. In this area the
intracranial internal carotid artery is most susceptible to injury, which means that any trauma displacing the brain anteriorly or posteriorly can stretch the internal carotid artery
against the anterior clinoid process. A carotid-cavernous fistula may occur if the artery is damaged within the confines of
the low-pressure c a v e r n o u s sinus. 5"22
Finally, the intracranial internal carotid artery may be injured superior to the cavernous sinus. This would create a
pseudoaneurysm that has the potential to cause pressure on
surrounding areas, erode into the sphenoid sinus, or rupture
into the subarachnoid or intraventricular space. 5"23
Patients who sustain blunt trauma to the carotid arteries
frequently have multiple organ systems injuries, thereby
making the initial diagnosis difficult for the clinician. 1-5 Furthermore, the interval between the traumatic event and the
onset of signs and symptoms has been reported to range
from minutes to years, further complicating diagnosis. 1'4"6'7-9'11'13 The spectrum of neurological findings include the following: headache, vertigo, visual changes, global aphasia, expressive aphasia, seizures, retrograde amnesia,
dysgeusia, syncope, ipsilateral tongue paresis, and incomplete ipsilateral Homer's syndrome. Other presentations include a lucid interval followed by a focal neurological defect,
or a progressive limb paresis in an otherwise alert and ori-

329

ented patient. Associated findings can include scalp tenderness, skin lacerations, neck pain, lateral neck hematoma formation, bruits, a pulsatile mass below the angle of the jaw,
and a fracture of the m a n d i b l e . 1'4'5'1°'11'13'14'24'25
A carotid-cavernous fistula resulting from intracranial internal carotid artery injury classically presents with an audible bruit, exopthalmos, pulsation of the orbit, chenosis,
diplopia, visual disturbances, headache, and paresthesias to
the face and scalp. All of these manifestations are attributable to the new onset of high pressure in the cavernous sinus
resulting in compression of surrounding structures and dilation of the previous low-pressure venous system. 5'26 One
final clinical manifestation of intracranial internal carotid artery injury is massive epistaxis, which may occur as a result
of the injured artery eroding into the sphenoid sinus. 5'23
Because the diagnosis of carotid injury is rarely suspected
in patients with abnormal neurological findings, CT of the
head is usually the first diagnostic test performed. If no abnormalities are seen on the CT scan, a cerebral angiogram
should be performed immediately. The gold standard for the
diagnosis of blunt carotid artery injury is angiography. 27-34
Blunt trauma to the head and neck most commonly cause
only single vessel injury; however, multiple artery injuries
have been reported and, therefore, all four extracranial vessels should be studied. 4"18"35Angiography should be strongly
considered in the following scenarios: (1) Neurological findings are incompatible with CT of the head; (2) monoparesis
or hemiparesis occur with normal mental status; (3) there are
signs or a history of severe cervical trauma with an abnormal
neurological exam; and (4) there is a basilar skull fracture in
a patient with altered status.I° If the diagnosis is considered
but the clinician is reluctant to subject the patient to the
potential morbidity of an arteriogram, a carotid duplex scan
can aid in the diagnosis. Davis et al29 reported that carotid
duplex enabled the appropriate diagnosis of carotid injury in
4 out of 5 patients and was a useful screening test in patients
at risk of carotid artery injury. MRI has recently been
proven to be an effective modality in the diagnosis of carotid
artery dissection. This modality allows the visualization of
the arterial wall noninvasively and without contrast. 36
Generalized guidelines have not been established for the
management of traumatic injuries to the internal carotid artery. Factors of importance to consider before treatment include (1) the anatomic location of the injury, (2) the type of
injury, and (3) associated injuries. 11 Therapeutic options include observation, anticoagulation, ligation of the carotid
artery with or without extracranial/intracranial bypass, and
arterial reconstruction. In patients with major fixed neurological deficits, cardiac instability, or coma, surgical treatment is contraindicated. 11 The decision to begin anticoagulant therapy in patients with multiple system injuries is often
difficult and must be made on a case-by-case basis. Patients
with an injury to the distal internal carotid artery are best
treated conservatively with anticoagulant therapy. These lesions are difficult to expose, thereby making a surgical procedure technically demanding. Surgically accessible lesions
may be repaired via ligation, bypass, or reconstruction if the
patient is clinically asymptomatic or has only mild neurological deficit. Kestenberg recently reported that patients with
intimal injuries treated by anticoagulation therapy did as well
as patients treated surgically. 37 Furthermore, Sawchuk et

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a138 studied the natural history of intimal flaps in a canine
model and reported that these injuries are not hemodynamically significant and may not require surgical repair. In addition, Clowes and Clowes 39 and Majesky et aP ° reported
that anticoagulant therapy aids intimal healing, decreasing
smooth muscle cell proliferation and decreasing intimal
thickening. Finally, in all patients with a carotid artery injury, a follow-up angiogram is recommended a few months
after the event to reevaluate the previously injured artery.
In summary, blunt trauma causing carotid artery injury
occurs infrequently and its diagnosis is frequently delayed.
After diagnosis, the clinician must treat the injury aggressively to prevent subsequent neurological injury and possibly death.
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