1979, British Journal of Radiology, 52, 704-708

Bilateral extracranial internal carotid artery injury due to
non-penetrating trauma—report of three cases
By T. M. H. Chakera, M.R.C.P., F.R.C.R., M.R.A.C.R.
Department of Diagnostic Radiology, Royal Perth Hospital, Perth, Western Australia
{Received December 1978 and in revisedform April 1979)

ABSTRACT

Angiographic features of three patients with bilateral
internal carotid artery injury (spasm/dissection/thrombosis)
due to non-penetrating trauma are reported. All three
patients were involved in motor vehicle accidents. Focallocalizing neurological signs were present and the patients
were suspected of having extracerebral haematomas. The
diagnosis of traumatic spasm/dissection/thrombosis of the
cervical portion of the internal carotid arteries was made
following angiography. The need to include views of the
cervical carotid arteries in cases of traumatic hemiparesis is
stressed and possible effect of cranial CT scanning in these
patients on diagnosis of carotid artery injury discussed.
Spasm and thrombosis (with or without complete
occlusion) of the extracranial internal carotid
artery resulting from blunt trauma has been
reported not infrequently in medical literature.
However, to date there has only been one report of
bilateral internal carotid thrombosis associated
with non-penetrating trauma (Ojemann and Moser,
1964). All three patients described here with
bilateral carotid artery injury were suspected of
having an epi- or subdural haematoma and the
diagnosis was not made until carotid angiography
was carried out.
CASE REPORTS

Casei
A forty-four-year-old woman, who was the driver of a
car involved in a head-on collision, was admitted to another
hospital complaining of left hip pain. She was wearing a
seat belt and was not displaced from her seat. There was no
evidence of trauma to the head and neck. Radiographs of
the pelvis and left hip did not reveal any fracture. Twoand-a-half hours following admission she had a grand-mal
fit and was transferred to Royal Perth Hospital where a
neurological examination revealed a left hemiparesis.
Again, no external evidence of head and neck injury was
detected. Skull and cervical spine radiographs showed no
abnormality. Clinical diagnosis of acute right subdural
haematoma was made and a bilateral carotid angiogram
was carried out. This showed severe, remarkably symmetrical, luminal narrowing and irregularity of both the
internal carotid arteries (Figs. 1 and 2). Angiographic
interpretation was that the patient had suffered a nonpenetrating injury to the cervical portion of the two internal
carotid arteries resulting in intimal tears associated with
severe spasm and thrombosis. There was no intracranial
space occupying lesion and left hemiparesis was thought to
be due to distal embolization. The patient was anticoagulated and despite extensive rehabilitation, has made
no neurological recovery.
704

FIG.1.

Right carotid angiogram.

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1979

Bilateral extracranial internal carotid artery injury due to non-penetrating trauma

FIG. 2.
Left carotid angiogram. Oblique views showing, as on the
right, severe luminal irregularity and narrowing of the
internal carotid artery.

Case 2
A twenty-two-year-old girl (front seat passenger) was
thrown out of the car which was involved in an accident.
When seen in casualty, she was stuporose and had a
left hemiparesis. There was no evidence of trauma to the
neck. Radiographs revealed a linear fracture of the right
parietal bone. Cervical spine radiographs showed no
abnormality. A clinical diagnosis of right-sided epidural
haematoma was made. Angiography revealed intimal
dissection with incomplete thrombosis of the right internal
carotid artery extending from 2.5 cm beyond the bifurcation to the base of the skull, with poor perfusion of the
middle cerebral artery (Fig. 3). The left internal carotid
artery showed extensive smooth narrowing due to traumatic
spasm (Fig. 4). Both the anterior cerebral arteries opacified
from the left side. The patient was treated with Dexamethasone and Rheomacrodex. Follow-up 18 months later shows
good neurological recovery with minimal residual weakness
of the left leg.
Case 3
A twenty-year-old girl was the front seat passenger in a
car which was involved in a head-on collision. She was
wearing a seat belt and was restrained in her seat. On
admission, she was noted to have a right hemiplegia.

FIG. 3.
Right carotid angiogram showing intimal dissection and
narrowing of the lumen of internal carotid artery.

There was no evidence of injury to the neck and the
admitting casualty officer remarked that the carotid artery
pulsations were present and normal. Skull and cervical
spine radiographs were normal. Clinically she was suspected of having an acute left-sided subdural haematoma.
Angiography revealed complete occlusion of the left
internal carotid artery, secondary to traumatic thrombosis
extending from 3.0 cm above the bifurcation up to the
intracavernous portion of the carotid artery (Fig. 5). The
right internal carotid artery showed spasm of a 3.5 cm length
of the carotid artery just below the base of the skull (Fig. 6).
There was no intracranial space effect. At operation, the
presence of traumatic intimal dissection and thrombosis of the
left internal carotid artery was confirmed and an endarterectomy was carried out. The adventitia was noted to be
intact. Post-operatively she deteriorated and died. Postmortem examination revealed re-thrombosis of the left
internal carotid artery. The right carotid artery was intact and
of normal calibre along its entire length, confirming that the
segmental narrowing seen on angiography was due to
spasm without underlying intimal damage.

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T. M. H. Chakera

FIG. 5.
Left carotid angiogram showing complete traumatic
thrombosis of the internal carotid artery from 3.0 cm above
the bifurcation. Note the retrograde filling of the terminal
carotid artery.
FIG. 4.
Left carotid angiogram showing extensive spasm and
"straightening" of the internal carotid artery.

DISCUSSION

In the last three years, we have documented
seven cases of internal carotid artery injury following
non-penetrating trauma to the neck. Of these,
the three cases presented here showed bilateral
carotid artery lesions. It is accepted that contusion
or stretching of a major artery can damage the
intima and media of that vessel (Gurdjian et al.,
1971), to cause its occlusion by spasm or thrombosis (Houck et ah, 1964). Intimal lacerations may
lead to stripping of the intima where the dissected
lining forms a plug and occludes the vessel or the
intimal tear becomes the site of thrombus formation.
Injury to the intima and media may also lead to
aneurysm formation (Sullivan et ah, 1973). It is of

interest to note that in two of the cases reported
here (Nos. 2 and 3) the site of the arterial spasm
corresponds to the anatomical explanation put
forward by New and Momose (1969). They noted
that the distal portion of the cervical carotid artery
lies anterior to the lateral articular mass of the atlas.
Extension of the head and neck stretches and
partly fixes the carotid artery at this level, and
contralateral rotation of the head occurring at the
atlanto-axial joint further stretches the artery.
These two movements carried out suddenly and to
the extreme are likely to cause focal compression of
the internal carotid artery.
None of the three cases reported here was
suspected of having carotid artery injury. Yamada,
in a study of 52 cases of injury to the internal
carotid artery due to acute non-penetrating trauma,
found that only three of the 52 cases were admitted
with the diagnosis of carotid artery insufficiency

706

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1979

Bilateral extracranial internal carotid artery injury due to non-penetrating trauma

FIG. 6.
Right carotid angiogram showing spasm of the internal
carotid artery below the skull base.

due to trauma (Yamada et al., 1967). Diagnosis of
carotid artery occlusions in non-penetrating injuries
is very difficult as the clinical picture resembles
that of the more common epi- or subdural haematoma. That the pulsation of vessels in the neck is
of poor diagnostic value has been amply confirmed
by our third case (Schneider and Lammens 1952).
It has been said in the past and this article concurs,
that apart from an autopsy, angiography is the only
accurate method of diagnosing traumatic lesions of
the carotid artery (Gurdjian et al., 1963). Development of neurological signs may be delayed up to
24 hours. The latent period probably represents the
time necessary for the formation of thrombus and
subsequent occlusion of the vessel or distal embolization. Case 1 reported in this paper had no
neurological symptoms or signs when first seen;

left hemiparesis was noted following a grand-mal
seizure two-and-a-half hours after admission.
Cranial CT scanning, rightly, is now the first
investigation in patients involved in motor vehicle
accidents who are suspected of having intra- or
extra-cerebral haematoma. However, one should be
aware that the patients with a negative cranial CT
scan, who have definite neurological signs, may
have carotid artery injury even though there may
not be any external manifestation of trauma to the
neck. Already CT scanning has led to a great
reduction in angiograms carried out in most
neurosurgical centres. This decrease in the number
of carotid angiograms in patients with suspected
head trauma may, in fact, lead to a "false" reduction
in the number of diagnosed carotid artery injuries
from non-penetrating trauma. When carotid angiography is carried out in patients suspected of
having epi- or subdural haematoma, it is imperative
that the views of the cervical portion of the carotid
arteries are included. If this is not done, then
patients who are suffering from spasm/dissection/
thrombosis of the extracranial portion of the
internal carotid artery will be missed (Zilkha, 1970).
Also, as indicated in this report, it is not unusual to
see bilateral lesions. It is the policy of the Department of Diagnostic Radiology to carry out bilateral
carotid angiography in all trauma cases suspected of
having epi- or subdural haematoma. We feel that
the high detection rate (three out of seven) of
bilateral carotid artery lesions in our experience is
the result of this policy. At Royal Perth Hospital,
most of the cerebral angiography is performed by
transfemoral catheterization. This approach, we
feel, minimizes the risks of iatrogenic damage to the
carotid arteries and allows bilateral carotid angiography to be carried out without much difficulty.
In all three of our cases, post-traumatic hemiplegia
was the reason for angiography. If the angiographic
study had been limited to the appropriate side,
bilaterality of lesions would not have been recognized. We would like to suggest that bilateral
internal carotid artery injury is not uncommon in
patients with non-penetrating trauma to the neck.
A limited angiographic study advocated in the past
(Murray, 1957) would account for the lack of
previous reports indicating the bilaterality of
lesions.
ACKNOWLEDGMENTS

I thank all members of the Department of Diagnostic
Radiology for their encouragement and also thank the staff
of the Department of Neurosurgery for allowing me to
study these patients. My thanks also to Miss Alison Swales
for typing this manuscript.

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T. M. H. Chakera
dissection of the internal carotid artery at the atlantoaxial
level secondary to non-penetrating injury. Radiology, 93,
41-49.

REFERENCES
GURDJIAN, E. S., ANDET, B., SIBAYAN, R. W., and THOMAS,

L. M., 1971. Spasm of the extracranial internal carotid
artery resulting from blunt trauma demonstrated by
angiography. Journal of Neurosurgery, 35, 742-747.

OJEMANN, R. G., and MOSER, H. W., 1964. Acute bilateral

internal carotid artery occlusion. Report of case following
a parachute jump. Neurology, 14, 565-568.

GURDJIAN, E. S., HARDY, W. G., LINDNER, D. W., and

THOMAS, L. M., 1963. Closed cervical cranial trauma
associated with involvement of carotid and vertebral

SCHNEIDER, R. C , and LEMMEN, L. J., 1952. Traumatic

internal carotid artery thrombosis secondary to nonpenetrating injuries to the neck. Journal of Neurosurgery,
9, 495-507.

arteries. Journal of Neurosurgery, 20, 418—427.
HOUCK, W. S., JACKSON, J. R., ODOM, G. L., and YOUNG,

W. G., 1964. Occlusion of the internal carotid artery in
the neck secondary to closed trauma to the head and neck.
Annals of Surgery, 159, 219-221.

SULLIVAN, H. G., VINES, F. S., BECKER, D. P., 1973.

MURRAY, D. S., 1957. Post-traumatic thrombosis of the

YAMADA, S., KINDT, G. W., and YOUMANS, J. R., 1967.

internal carotid and vertebral arteries after non-penetrating injuries of the neck. British Journal of Surgery 44,
556-561.

Carotid artery occlusion due to non-penetrating injury.
The Journal of Trauma, 7, 333-342.
ZILKHA, A., 1970. Traumatic occlusion of the internal
carotid artery. Radiology, 97, 543-548.

NEW,

P. F. J., and MOMOSE, K. J., 1969. Traumatic

Sequelae of indirect internal carotid injury. Radiology,
709,91-98.

Book review
Corcadeus' Gynaecologic Cancer (Fith Edition). Edited by
S. B. Gusberg and H. C. Frick II, pp. xii+494, 1978 (The
Williams and Wilkins Company, Baltimore), $49.50.
ISBN 0-683-03854-0.
In the preface, the authors reflect that the 1940's were
notable for the increasing sophistication of surgical and
radiotherapeutic techniques, the 50's saw the trend towards methods of earlier diagnosis, the 60's heralded
developments in cell physiology and kinetics for chemotherapy, radiation physics, tumour immunology and
epidemiological studies to select high risk patients. The
1970's may be known as the "decade of therapeutic translation" when the insights derived can be applied.
The introduction covers the statistics of incidence, site,
stage at presentation and the factors which influence the
outcome. Known aetiological factors and the principles of
diagnosis including cytology, histology and radiological
methods are discussed. This section is well illustrated
with photomicrographs and contains much useful information based on personal experience.
The principles of radiation therapy are covered in a
broad way dealing with intracavitary and external radiation
techniques. This is a short, factual chapter summarizing
the art, providing the pros and cons of various treatments,
giving dosages but avoiding detailed physics and radiotherapy techniques. I did not find any reference to afterloading techniques which can be so useful in reducing the
exposure to staff and which in this country are becoming
increasingly popular.
There is a chapter dealing with the principles of chemotherapy which, in addition to basic principles, includes
reference to the dosages which are most often used in
gynaecological malignancy. These are classified in the
usual way based on their chemistry but there is also reference
to the phases of action in relation to cell cycle theory.
There is a particularly useful table of the characteristics
and properties of the various stages of the cell cycle which
makes a convenient summary of our present understanding.
Chapters then follow dealing in full detail with the

common gynaecological cancers. These cover the usual
aspects such as incidence, aetiology, investigation, staging,
histology, management and the results of various forms of
treatment. All these chapters are very well illustrated and
the views expressed are very representative of current
practice. This will be of considerable value to those studying
for higher examinations in radiotherapy as well as gynaecological surgery.
In addition to the more common neoplasms, the authors
deal with sarcomas and various gestational trophoblastic
neoplasms. The chapter about the latter covers hydatidiform
mole and chorio-carcinoma in a way which offers sound
guidance to the clinician. It is very good to see a section on
pain included in the book. This discusses the neurological
pathways involved as well as the various theories of pain,
before giving details of the different analgesics, antidepressants and surgical operations for control of pain.
As well as a useful account of menopausal problems
there is a section on the endocrinological aspects of gynaecological cancer. This includes the physiological processes
involved and also the production of hormones in certain
pathological states, for example by tumours. Current
views on the metabolism of hormones in target tissues and
the present theory of the roles of receptor sites in breast
cancer are included for completion. Breast cancer is usually
not included in works on gynaecological cancer and understandably is not covered in this volume.
There is a particularly interesting chapter on basic
clinical immunology for the gynaecologist. This covers this
very complex topic in a concise and readable way. It was
thoughtful to include a glossary of immunological terms
which will be greatly appreciated.
The volume closes with chapters on epidemiology and
biostatistics. It is an extremely well prepared work covering
the subject and a great many more related problems, in a
concise and informative way. It is well illustrated throughout and fully indexed. It can be highly recommended to
radiotherapists and gynaecologists.

708

B. HALE.