Tveita et al. Journal of Medical Case Reports (2017) 11:148
DOI 10.1186/s13256-017-1316-1

CASE REPORT

Open Access

Dissection of the internal carotid artery and
stroke after mandibular fractures: a case
report and review of the literature
Ingrid Aune Tveita1* , Martin Ragnar Skjerve Madsen2 and Erik Waage Nielsen3,4,5

Abstract
Background: We present a report of a patient with blunt trauma and mandibular fractures who developed a
significant cerebral infarction due to an initially unrecognized injury of her left internal carotid artery. We believe
that increased knowledge of this association will facilitate early recognition and hence prevention of a devastating
outcome.
Case presentation: A 41-year-old ethnic Norwegian woman presented to our Emergency Room after a bicycle
accident that had caused a direct blow to her chin. At admittance, her Glasgow Coma Scale was 15. Initial trauma
computed tomography showed triple fractures of her mandible, but no further pathology. She was placed in our
Intensive Care Unit awaiting open reduction of her mandibular fractures. During the following 9 hours, she showed
recurrent episodes of confusion and a progressive right-sided hemiparesis. Repeated cerebral computed tomography
revealed no further pathology compared to the initial scan. She had magnetic resonance angiography 17 hours after
admittance, which showed dissection and thrombus formation in her left internal carotid artery, total occlusion of her
left medial cerebral artery, and left middle cerebral artery infarction was detected.
Conclusions: Carotid artery dissection is a rare but life-threatening condition that can develop after trauma to the
head and neck. There should be a high index of suspicion in patients with a mechanism of injury that places the
internal carotid artery at risk because blunt vascular injury may show delayed onset with no initial symptoms of
vascular damage. By implementing an algorithm for early detection and treatment of these injuries, serious brain
damage may be avoided.
Keywords: Blunt cerebrovascular injury, Mandibular fracture, Carotid artery dissection, Facial trauma, Blunt
vascular injury

Background
The case presented illustrates the link between facial
fractures and blunt cerebrovascular injury (BCI) that,
falsely, has long been considered a curiosity. In order to
identify these patients at an early stage this case report
emphasizes the need for implementation of appropriate
screening protocols in the Emergency Room (ER). This
was not the case at our hospital at the time the actual
patient was admitted, and hence diagnosis was delayed
with consequences for patient outcome.

* Correspondence: ingrid.aune.tveita@nordlandssykehuset.no
1
Department of Ear Nose and Throat Surgery, Nordland Hospital, Bodø,
Norway
Full list of author information is available at the end of the article

BCI has long been considered a curiosity, and may
explain why clinically recognizable neurological symptoms
often occur before diagnosis is made [1]. Early reports suggest mortality rates of 28%, and subsequent multicenter
reviews have confirmed these rates, with 48 to 58% of survivors having permanent severe neurological deficits [2].
The incidence of BCI among all patients experiencing
blunt trauma in the United States of America (USA) is
estimated at approximately 0.1%, rising to 1.6% with initiation of screening [2–4].
Early antithrombotic intervention has the potential to
improve neurologic outcome, given that BCI is confirmed
and that no contraindications for this treatment exist (for
example, bleeding pelvic fracture) [5–7].

© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Tveita et al. Journal of Medical Case Reports (2017) 11:148

Case presentation
A healthy, non-tobacco smoking, 41-year-old ethnic
Norwegian woman presented to our ER 10 minutes
after a bicycle accident. On arrival, she was conscious
and complained of jaw pain. She explained that she,
after rapid deceleration, had fallen over the handlebars
and landed on her face. She was wearing a helmet. A
trauma assessment was initiated: her Airway, Breathing,
Circulation, Disability, Exposure assessment and Glasgow
Coma Scale (GCS) were normal. A physical examination
revealed blood pressure 130/60 mmHg, respiratory rate
20 breaths per minute, and normal auscultatory findings
of her heart and lungs. Her blood tests showed normal
complete blood count (CBC), bleeding status, and coagulation status, as well as liver and renal function.
A trauma computed tomography (CT) scan reported
normal brain status, but fractures of the mandible

Page 2 of 6

were found in both condylar necks and the left paramedian corpus (Fig. 1).
She was taken to our Intensive Care Unit (ICU) and,
due to stable fractures, the surgery was planned for the
next morning. She became confused and had several
bouts of tachycardia 1.5 hours after admittance. She
responded to verbal contact but was unable to follow
instructions. After a few minutes she seemed more alert
and took instructions more actively.
A quick neurological examination was made, with the
only concern being a slightly impaired finger-nose test
on the right side.
The evening passed with a few more episodes of brief
confusion.
A repeated neurological examination gave suspicion of
brain stem involvement with a decline in GCS to 7 (M 5,
V 1, E 1). A repeated CT scan, 10 hours after admission,

Fig. 1 a, b Computed tomography scan at admittance shows fractures of the mandible (bilateral condylar neck and left corpus paramedian)

Tveita et al. Journal of Medical Case Reports (2017) 11:148

showed no recent changes. Unfortunately, no further immediate radiologic assessment was initiated.
Her vital parameters were stable; magnetic resonance
imaging (MRI) was planned for the next morning.
The following morning she presented with palsy in her
right extremities and acquired anisocoria with a larger
right pupil. She had a GCS of 6 (M 4, V 1, E 1). She was
intubated and an MRI and magnetic resonance angiography (MRA) of her head and neck were conducted
17 hours after admission. An extensive left middle cerebral artery infarction was detected, with cessation of diffusion in the supply area of her left middle cerebral artery
(MCA). Further, an occluded left internal carotid artery
(ICA) was diagnosed, approximately 1 cm above the bifurcation, in addition to occlusion of her left MCA (Fig. 2).
She was given 300 mg acetylsalicylic acid intravenously
to reduce risk for progressive thrombosis, and immediately
transferred to a level 1 trauma center where she received
neurointensive care and a pressure-releasing hemicraniectomy. Postoperatively, CT angiography and ultrasound of
her carotid arteries were made and confirmed dissection of
her left ICA with total occlusion of the vessel. In addition,
dissection and a moderate-grade to high-grade stenosis of
40% of her right ICA was found.
She was treated with dual platelet inhibition, and fixation of her mandibular fractures was postponed. After
4 days, she was extubated and transferred to our neurological department for rehabilitation. The mandibular
fractures were fixated 8 days after the initial trauma. She
still has aphasia and a right-sided hemiplegia 2 months
after the bicycle injury.
The mechanisms of vessel injury in this case are probably a combination of linear and torsional forces due to
hyperextension. Direct pressure from her dislocated mandibular bone may have contributed. Bouts of tachycardia
could stem from a disturbed carotid body or from cerebral
ischemic insults.

Discussion
In the case presented, a healthy woman presented with
clinical signs of rapid deterioration in neurological status
10 hours after admission to our hospital due to a blunt
trauma to her chin. In retrospect, the repeat CT scan
showing no recent changes was insufficient to rule out
cerebrovascular damage, and should have prompted
follow-up angiographic imaging. Unfortunately, this was
delayed and 17 hours after admission cerebral MRI and
MRA detected an extensive left middle cerebral artery infarction caused by a thrombus occluding her left MCA.
Due to the late diagnosis of a BCI, antithrombotic intervention was delayed until 20 hours after admittance.
It is not known whether earlier diagnostic screening
and intervention would have altered our patient’s outcome, but the literature covering BCI indicates that early

Page 3 of 6

recognition and treatment of this condition have the potential to reduce fatal outcome. Antithrombotic therapy
is usually the only treatment option as surgical repair is
not possible due to the location of the thrombus. Thus,
early antithrombotic treatment of our patient might have
halted progression of thrombosis, and thus possibly reduced the chance of development of serious focal neurological deficit.
Searching for case reports on the subject, there are few
records of cases with patients presenting clear symptoms
of cerebrovascular injury at hospital admittance. Insight of
the mechanisms of trauma associated with BCI is thus
crucial for all health care providers working with trauma
care. This knowledge will raise awareness and ensure recognition of patients at risk for BCI, and prompt early and
appropriate diagnostic screening allowing early institution
of treatment.
To facilitate our awareness and recognition of this
condition, we present a synopsis of a literature search
on BCI emphasizing pathophysiology, screening options,
and treatment.
Pathophysiology

High impact trauma to the neck or face is a potential
risk for BCI. An increased awareness of this relationship
is crucial to facilitate early recognition of the injury and
to initiate early intervention to prevent further complications [8].
Four characteristic mechanisms of blunt carotidal injury
are listed in Table 1 [9].
The pathophysiological cascade is believed to be an
intimal tear of the artery created by a force that twists or
stretches the vessel, or the vessel is impinged against the
underlying bone. This forms a thrombogenic surface,
platelet aggregation, and the formation of a thrombus
that is partial, complete, or with secondary embolization.
Over time the intimal tear may cause subintimal dissection of the vessel [2].
Pseudoaneurysms are less common and occur as a
result of partial transection of the artery. Free rupture is
also reported.
The latency period between the injury and the development of cerebrovascular symptoms is a characteristic
feature of BCI, and considered an opportunity for initiation
of preventive therapy. Approximately 80% of patients with
BCI show no obvious neurologic manifestations at
presentation [5]. Studies suggest that 25 to 50% of
patients develop symptoms of BCI as late as 12 hours
after the trauma [6, 10–13].
Screening

There seems to be a lack of consensus regarding the optimal diagnostic strategy for detection of BCI, with controversy about the cost-effectiveness of aggressive screening

Tveita et al. Journal of Medical Case Reports (2017) 11:148

Page 4 of 6

Fig. 2 a Head magnetic resonance imaging taken 17 hours after admittance (top); Shows an extensive left middle cerebral artery infarction. b
Magnetic resonance angiography taken 17 hours after admittance (bottom); Shows an occluded internal carotid artery on the left side
approximately 1 cm above the bifurcation, in addition there is occlusion of the left middle cerebral artery

[14]. With the use of well-compiled screening criteria,
patients at risk may be identified early, and preventive
treatment initiated.
How to recognize patients at risk? During the years
1990 to 1998 Biffl et al. performed linear regression
analysis of a liberally screened population (n = 249),
and defined four independent risk factors for BCI. In

1996 they initiated a screening of at-risk asymptomatic
patients using arteriography based on these criteria [1].
Using this approach, 85 patients (34%) were diagnosed
as having vascular injuries: 65 patients had carotid injuries,
10 had vertebral injuries, and 10 had both carotid and vertebral injuries. Carotid injuries were bilateral in 32 patients.
Among 209 asymptomatic patients, cerebrovascular injuries

Tveita et al. Journal of Medical Case Reports (2017) 11:148

Table 1 Characteristic mechanisms of blunt carotidal injury [9]
Type

Mechanism

1

Direct application of force to the neck (seatbelt, strangulation,
near-hanging)

2

Hyperextension and contralateral rotation of the head and neck

3

Intraoral trauma that affects the internal carotid artery at the
angle of the jaw

4

Laceration of the artery resulting from basilar skull fracture

were diagnosed in 57 (27%). This shows a relatively high
yield, considering the potentially devastating outcome of
these injuries [1].
In 2010 the Eastern Association for the Surgery of
Trauma set out to perform a review of all relevant literature concerning management of BCI, and to develop
guidelines for screening, diagnosis, and treatment [15].
Screening has clearly increased the number of BCI
injuries diagnosed [5–7], and many trauma centers have
implemented screening protocols. The optimal screening
criteria remain a topic of debate.
In regard of cost-effectiveness, studies have shown
screening to be beneficial [14]. The 2016 recommendation of Biffl et al. involves an algorithm based on
clinical signs and symptoms that prompt immediate
diagnostic evaluation and neurovascular imaging [16].
In the absence of prospective, randomized clinical trials,
the current recommendations are based on published
observational studies only.
CT angiography is believed to be the most reliable
noninvasive screening modality. Sensitivity depends on
the number of imaging slices, with 16 slices or more
needed for consistent correlation with the results of
digital subtraction arteriography (DSA) [17].
DSA remains the gold standard of diagnosis, and is
indicated when the level of suspicion is high, despite
negative initial imaging results. However, arteriography
is an invasive procedure and associated with complications
[5]. Another aspect is cost and availability. Arteriography
should be reserved for cases where it is required for a
definite diagnosis or when an appropriately sensitive
CT scanner is not available. MRA has poor specificity
(67%) and sensitivity (50 to 75%) compared to DSA and
is not recommended [6].

Page 5 of 6

of stroke in asymptomatic patients with BCI receiving antithrombotic therapy compared with those not
treated [5, 11, 14, 18].
Heparin is preferred in the acute setting due to its
reversibility. There are, however, no randomized trials
comparing clinical outcome of different antithrombotic
treatment regimens.
For most patients with BCI, inaccessibility of the site
of injury precludes direct surgical repair, as the involved
vessel is often located at the base of the skull. According
to the grading scale for BCI created in 1999 [20], the
recommendation is surgical management for patients
with accessible Grade II to V BCI; this in agreement
with the guidelines of major trauma societies [15, 21].
Follow-up imaging using CT angiography is recommended 7 to 10 days after identification of the cerebrovascular injury, with repeat imaging after 3 months
to determine whether long-term antithrombotic therapy is
needed.

Conclusions
BCI, once considered a rare occurrence, has been recognized with increasing frequency in recent years. With
the institution of new screening protocols, BCI is now
more commonly observed. Early diagnosis and prompt
anticoagulation therapy have reduced the occurrence of
ischemic neurologic events and disability.
Adequate management requires a high index of suspicion in victims of trauma where the mechanism of injury
places the ICA at risk. As illustrated by the case presented
here, high-impact trauma resulting in facial fractures represents a risk for BCI. In order to identify these patients at
an early stage we emphasize the need for implementation
of appropriate screening protocols in the ER [16].
Abbreviations
BCI: Blunt cerebrovascular injury; CBC: Complete blood count; CT: Computed
tomography; DSA: Digital subtraction arteriography; ER: Emergency Room;
GCS: Glasgow Coma Scale; ICA: Internal carotid artery; ICU: Intensive Care
Unit; MCA: Middle cerebral artery; MRA: Magnetic resonance angiography;
MRI: Magnetic resonance imaging
Acknowledgements
None.
Funding
Not applicable.

Treatment

Symptoms, site of injury, severity grade of injury, and
associated injuries impact the choice of treatment and
follow-up strategy. In the absence of contraindication,
such as active hemorrhage, an injury grade-specific
recommendation for antithrombotic therapy is given
[18, 19]. Several retrospective studies have reported
convincing improvement in neurologic outcome among
symptomatic patients, with a reduction in the occurrence

Availability of data and materials
Not applicable.
Authors’ contributions
All authors contributed in the diagnosis and treatment of the patient and in
preparing the final manuscript. All authors read and approved the final
manuscript.
Competing interests
The authors declare that they have no competing interests.

Tveita et al. Journal of Medical Case Reports (2017) 11:148

Consent for publication
Written informed consent for the publication of this case report and any
accompanying images was obtained from the patient’s husband. A copy of the
written consent form is available for review by the Editor-in-Chief of this journal.
Ethics approval and consent to participate
Not applicable.

Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in
published maps and institutional affiliations.
Author details
1
Department of Ear Nose and Throat Surgery, Nordland Hospital, Bodø,
Norway. 2Department of Oral and Maxillofacial Surgery, Nordland Hospital,
Bodø, Norway. 3Department of Anesthesiology and Intensive Care, Nordland
Hospital, Bodø, Norway. 4Institute of Clinical Medicine, University of Tromsø,
Tromsø, Norway. 5Faculty of Professional Studies, Nord University, Bodø,
Norway.
Received: 11 January 2017 Accepted: 9 May 2017

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