Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2012;18 (4):347-350

Case Report

Olgu Sunumu
doi: 10.5505/tjtes.2012.66900

Cerebral infarction caused by traumatic carotid artery dissection
Travmatik karotid arter diseksiyonuna bağlı serebral enfarktüs
Ayşegül BAYIR,1 Demet AYDOĞDU KIREŞİ,2 Ali SÖYLEMEZ,3 Osman DEMİRCİ4

Traumatic carotid artery dissection, if not diagnosed and
treated early, is a serious problem with permanent neurological deficit and a high mortality rate of up to 40%. We present
a case with delayed diagnosis of traumatic carotid artery dissection in a 21-year-old female. While there were no ischemic infarct findings on the admission cerebral computerized
tomography (CT), such findings were observed on two cerebral CTs taken because of the left hemiplegia noticed seven
days later when the patient regained consciousness. The patient was referred to our emergency service, and definitive diagnosis was achieved with arterial Doppler ultrasonography,
cerebral magnetic resonance imaging (MRI), diffusion MRI,
and MR angiography. We did not consider invasive treatment
since the neurological damage was permanent and dissection grade was IV according to angiography findings. The
case was discharged within a week and physiotherapy was
advised. Despite the advances in diagnostic methods, diagnosis of traumatic carotid artery dissection is still missed or delayed, as in the case presented here. Early diagnosis can ameliorate permanent neurological damage or even prevent it.
However, the vital factors for early diagnosis are the obtained
anamnesis leading to appropriate radiological examinations,
detailed physical examination and high clinical suspicion.

Travmatik karotid arter diseksiyonu eğer erken tanı konulup tedavi edilmezse kalıcı nörolojik defisit ve %40’lara
varan ölüm oranı yaratabilen ciddi bir sorundur. Bu yazıda,
travmatik karotid arter diseksiyonu tanısı geç dönemde konan 21 yaşında kadın hasta sunuldu. Kabulde çekilen beyin
bilgisayarlı tomografisinde (BT) iskemik enfarkt bulguları
yok iken, bilinci açıldıktan sonra yedinci gün sol hemiplejisi fark edildiğinde çekilen ikinci beyin BT’sinde enfarktüs bulguları saptandı. Hasta acil servise kabul edildi. Kesin tanı, arteriyel Doppler ultrasonografi, serebral manyetik rezonans görüntüleme (MRG), difüzyon MRG ve MR
anjiyografi ile konuldu. Hastada kalıcı nörolojik hasar geliştiği ve anjiyografi bulgularına göre evre IV olduğu için
invaziv tedavi düşünülmedi. Hasta fizyoterapi tavsiye edilerek bir hafta içinde taburcu edildi. Tanısal yöntemlerdeki gelişmelere rağmen travmatik karotid arter diseksiyonunun tanısı bu olguda olduğu gibi halen atlanmakta veya
gecikmektedir. Erken tanı kalıcı nörolojik hasarı önleyebilir ya da hafifletebilir. Bununla birlikte erken tanı için en
önemli faktörler uygun radyolojik incelemeyi yönlendirecek anamnez, ayrıntılı fiziksel inceleme ve yüksek klinik
şüphedir.

Key Words: Doppler ultrasonography; internal carotid artery;
magnetic resonance angiography; traumatic dissection.

Anahtar Sözcükler: Doppler ultrasonografi; internal karotid arter; manyetik rezonans anjiyografi; travmatik diseksiyon.

The incidence of internal carotid artery dissection
(ICAD) caused by blunt trauma is unknown, since the
onset of symptoms and signs are frequently delayed,[1]
but it has been reported to be 0.08%.[2] Traumatic
ICAD is often accompanied by thrombosis, resulting

in permanent neurological deficits and carrying a mortality rate of up to 40%.[3,4] In this case report, we present a patient whose ICAD was diagnosed one week
after being involved in a motorcycle accident and hospitalized at an outlying hospital.

1
Department of Emergency Medicine, Selcuk University
Selcuklu Faculty of Medicine, Konya; 2Department of Radiology,
Selcuk University Meram Faculty of Medicine, Konya; 3Department of
Neurology, Suleyman Demirel University Faculty of Medicine, Isparta;
4
Department of Emergency Medicine, Siirt State Hospital, Siirt, Turkey.

Selçuk Üniversitesi Selçuklu Tıp Fakültesi, Acil Tıp Anabilim Dalı,
Konya; 2Selçuk Üniversitesi Meram Tıp Fakültesi, Radyoloji
Anabilim Dalı, Konya; 3Süleyman Demirel Üniversitesi Tıp Fakültesi,
Nöroloji Anabilim Dalı, Isparta; 4Siirt Devlet Hastanesi Acil Servisi,
Siirt.
1

Correspondence (İletişim): Ayşegül Bayır, M.D. Selçuk Üniversitesi Selçuklu Tıp Fakültesi, Acil Tıp Anabilim Dalı, Konya, Turkey.
Tel: +90 - 332 - 241 50 00 e-mail (e-posta): aysegulbayir@hotmail.com

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CASE REPORT
A 21-year-old female motorcycle passenger was involved in a motor vehicle accident and was brought to
the emergency service of a rural government hospital.
She was comatose on presentation, and was found to
have left radius-ulna fractures on plain films and cerebral edema on non-contrast head computerized tomography (CT) scan. In the neurosurgical intensive care
unit (ICU), as she regained consciousness over the
next few days, weakness of her left arm and leg was
noted. A repeat head CT showed a hypodense infarct
in the right frontoparietal and basal ganglion areas
(Fig. 1a). With a diagnosis of ‘acute embolic stroke’,
she was transferred to our tertiary care university hospital emergency department.
Upon arrival, she was conscious and cooperative
with complaints of left hemiparesis. Her vital signs
were blood pressure (BP) 120/70 mmHg, pulse rate 72/
min, respiratory rate 18/min and temperature 36.8°C.
Her pupillary exam was normal and her Glasgow
Coma Score was 13. Motor strength was 1/5 in the left
upper extremity and 1/5 in the lower extremity. Her
left Babinski reflex was positive. Given her clinical
picture of posttraumatic stroke, carotid artery injury
was suspected.
Diffusion magnetic resonance imaging (MRI)
of the brain demonstrated decreased diffusion in the
ADC map area, compatible with a large acute infarct
and mainly diffusion in the frontal-temporal and parietal zone of the right cerebral hemisphere (Fig. 1b).
On T2 axial MR images, loss of flow in the right ICA
was observed at the level of the cavernous sinus on the
right. Signal alterations consistent with acute infarct
were seen in the right frontal, temporal and parietal
lobes, including the basal ganglia. The right carotid
superior was filled to the Circle of Willis, and subacute
hematoma and right ICAD at the level of the inferior
pars petrosa were seen (Figs. 1c, d). On MR angiography, no flow of contrast was seen in the right ICA
and carotid bulbus superior, or in the middle portion
of the right ICA (Figs. 1e, f). Carotid Doppler ultrasonography showed dissection of the right ICA and a
thrombus causing total occlusion beginning at the bifurcation (Figs. 1g, h).
The patient was hospitalized for treatment and
follow-up. Since permanent neurological damage had
developed and the infarct area was large, anticoagulation was not performed due to concerns that such treatment might trigger hemorrhage in the ischemic infarct
area. The patient was discharged with follow-up in
the neurology and physical medicine and rehabilitation clinics. The patient’s neurological symptoms and
signs (permanent left hemiplegia) were unchanged
during three months of follow-up.
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DISCUSSION
Traumatic ICAD is a rare and serious cause of
embolic stroke in the younger age group. The basic
pathophysiological mechanism is stretching of the
artery through rotation-hyperextension or distractionflexion.[5] While only 10% of cases have an immediate
onset of symptoms, in most patients, clinical signs of
the dissection occur within the first 24 hours following
the traumatic event. No symptoms occur within the
first 24 hours after trauma in 35% of cases. In patients
with traumatic ICAD who exhibit neurologic deficits,
brain CT performed within the first 24 hours is usually
non-diagnostic.[6]
Traumatic ICAD is usually suspected and diagnosed when a neurological deficit develops unexpectedly after trauma, evolving clinically into a ‘stroke’ in
80% of the cases during the first week after symptom
onset.[1] In addition to a detailed history and careful
physical examination, duplex carotid ultrasound, CT,
CT angiography, MRI, MR angiography, and conventional angiography are imaging studies that can be
performed to diagnose traumatic ICAD.[7,8]
The present case was referred to us with a diagnosis of acute embolic stroke although she had no signs
of ischemia on her CT performed at the first hospital.
A comprehensive neurologic exam could not be performed secondary to her depressed level of consciousness. In light of the patient’s young age and history
of trauma, we suspected traumatic ICAD when we
viewed her CT and found corresponding neurologic
deficits. To make the definitive diagnosis in our patient, we performed brain MRI, diffusion MRI, carotid
Doppler ultrasound, and MR angiography.
Traumatic CAD is divided into five grades according to angiographic findings, and therapy is undertaken accordingly: Grade I: with ≤25% narrowing of
the lumen, luminal disruption or dissection; Grade II:
>25% narrowing of the lumen, together with dissection or intramural hematoma, intraluminal thrombus
or split flap, Grade III: pseudoaneurysm, Grade IV:
complete occlusion, and Grade V: signs of transection
with contrast extravasation.[9] Grade I traumatic ICAD
is treated conservatively with anticoagulants, as only
7% will progress to a higher grade. However, 70% of
Grade II dissections rapidly progress to pseudoaneurysm formation and occlusion, and thus require aggressive surgical treatment.[5]
With the latest improvements in endovascular stenting, successful results have been obtained in Grade I
and Grade II ICADs.[10] Grade IV dissections are usually complicated by cerebral embolism and stroke. Recanalization procedures in Grade IV traumatic ICAD
are associated with a high rate of complications, thus
observation and/or anticoagulation is advised. Grade
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Cerebral infarction caused by traumatic carotid artery dissection

V ICAD requires urgent surgical ligation and hemorrhage control.[5]

that the dissected superior carotid artery was filled
with Willis Polygon.

Our patient had a Grade IV ICAD, as diagnosed by
MR angiography. The delay in diagnosis at the outlying hospital may have led to the development of permanent neurologic deficits. MR angiography revealed

Traumatic ICAD is a rare occurrence and its diagnosis can easily be missed or delayed despite advances in imaging procedures. Obtaining a detailed
history and performing a comprehensive examination

(a)

(b)

(c)

(d)

(e)

(f)

Fig. 1. (a) Non-contrast CT performed at 7 days in our 23-yearold motorcycle accident victim.
A hypodense lesion in the right
frontoparietal and basal ganglion area, suggestive of ischemia,
can be seen. (b, c) Diffusionweighted MRI in the right frontotemporal and parietal lobes,
suggesting an acute infarct in the
ADC map. (d) T2 contrast MRI
showing loss of the flow of the
(h)
(g)
internal carotid artery at the level of the cavernous sinus on the right. (e, f) Contrast MR angiogram showing cut-off of flow in the internal carotid artery at
the level of the carotid bulb. Flow is also absent in the right middle cerebral artery. Longitudinal (g) and transverse (h) Doppler ultrasound images of the right internal carotid artery just superior to the carotid bulb showing a linear echogenic band (white arrow) in the lumen, compatible with dissection.
Cilt - Vol. 18 Sayı - No. 4

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Ulus Travma Acil Cerrahi Derg

will lead the clinician to suspect ICAD in the setting
of post-traumatic unilateral neurologic abnormalities
with a normal or near-normal non-contrast CT. Carotid
Doppler is an easily performed study that can rule out
the presence of ICAD in suspicious cases. Advances
in CT and MR angiography techniques and machines
have made it possible to establish a rapid and accurate
diagnosis. After an accurate diagnosis has been made,
immediate treatment to reduce complications and optimize outcome should be performed.

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