Neurol Med Chir (Tokyo) 49, 590¿593, 2009

Unstable Stenosis of the Internal Carotid Artery
Caused by a Craniofacial Nail-Gun Injury
—Case Report—
Tetsuya HIRAISHI*,**, Tadashi KAWAGUCHI*, Tsutomu KOBAYASHI*,
Masaru TOMIKAWA*, Yasushi ITO**, and Yukihiko FUJII**
*Department of Neurosurgery, Nagaoka Red Cross Hospital, Nagaoka, Niigata;
**Department of Neurosurgery, Brain Research Institute, University of Niigata, Niigata

Abstract
A 30-year-old carpenter suffered accidental piercing of his jaw by a 3-inch nail from a nail gun. No neurological deficits were found on admission. Computed tomography showed that the tip of the nail had
reached the foramen lacerum. Cerebral angiography revealed severe stenosis at the C4 portion of the left
internal carotid artery (ICA) and marked decrease in the flow of the distal ICA. He had developed right
hemiparesis and sensory aphasia by the following morning. T2-weighted and fluid-attenuated inversion
recovery magnetic resonance imaging showed a focal hyperintense signal in the left central region indicating cerebral infarction. Repeat angiography demonstrated that the antegrade blood flow from the
occluded point on the admission day had partially resumed, and endovascular trapping of the ICA was
successfully carried out. The nail was then removed safely without problematic bleeding. The patient
suffered no additional deficit, and his sensory aphasia and right hemiparesis gradually improved. The
fluctuating blood flow through the unstable stenosis of the ICA related to nail movement possibly
caused the delayed cerebral infarction. To avoid the occurrence of such events, rapid treatment after
necessary investigations is recommended in patients with craniofacial penetrating injuries that affect
the ICA.
Key words:

nail,

endovascular trapping,

internal carotid artery,

Introduction

January 20, 2009;

Accepted

cerebral infarction

terioration.

Case Report

Penetrating craniofacial injuries resulting from nail-gun
use are increasingly reported around the world. The nail
gun is a common tool in the workplace and even the home
because of its simplicity and availability. The Centers for
Disease Control and Prevention in the United States indicated that an average of 37,000 patients with injuries related to nail-gun use were treated annually in emergency
departments during the 5-year period spanning 2001–
2005.6) The most common cause of nail-gun injury is workrelated accidents, but self-harm or suicide in psychiatric
patients is also known.9) Various types of such craniofacial
injuries may be associated with obstruction of the internal
carotid artery (ICA). However, the therapeutic strategy
will depend on various individual factors, such as the type
and degree of the ICA injury, the dynamics of the cerebral
blood flow, and the patient's condition. Endovascular
techniques may be useful to treat the injured ICA.1,10,15)
We treated a patient presenting with delayed cerebral
ischemia caused by unstable stenosis of the ICA in the
acute phase after a craniofacial nail-gun injury, using endovascular trapping to avoid further cerebrovascular deReceived

trauma,

A 30-year-old carpenter suffered accidental piercing of the
left side of his jaw by a 3-inch nail from a nail gun while
working. He was ambulatory when admitted to our
hospital. His Glasgow Coma Scale score was 15. He
presented with restricted opening of the mouth and dysphagia due to pain, but no neurological deficits.
Craniography showed the nail embedded within the soft
tissue of the face (Fig. 1A). Multiplanar reconstructed
computed tomography images revealed that the nail had
reached the foramen lacerum (Fig. 1B–D). Cerebral digital
subtraction angiography (DSA) on the day of admission
revealed severe stenosis at the C4 potion of the left ICA
and marked decrease in the flow of the distal ICA (Fig. 2).
DSA revealed no extravasation from the ICA and no evidence of vascular wall dissection or formation of a pseudoaneurysm. The crossflow through the anterior communicating artery (AcomA) and the backflow through the
posterior communicating artery (PcomA) were satisfactory. We performed tracheostomy on the day of admission to
avoid difficulty in breathing if laryngeal edema occurred.
He had developed slight right hemiparesis and sensory

April 28, 2009

590

Unstable ICA Stenosis Caused by a Nail-Gun Injury

Fig. 1 A: Lateral craniogram showing a nail embedded in the
face. B–D: Multiplanar reconstructed computed tomography
images showing the exact location of the nail, with the tip of the
nail reaching into the foramen lacerum as confirmed on the axial (B), coronal (C), and sagittal (D) views.

Fig. 2 Anteroposterior (A) and lateral (B) left internal carotid
arteriograms showing the left internal carotid artery is severely
stenotic at the C4 portion due to compression by the nail, and
the distal flow is markedly decreased. The anterior and middle
cerebral arteries are not shown. There is no evidence of extravasation.

Neurol Med Chir (Tokyo) 49, December, 2009

591

Fig. 3 A: Axial fluid-attenuated inversion recovery (FLAIR)
magnetic resonance images showing a hyperintense signal indicating cerebral infarction in the left central region. B: Single photon emission computed tomography scans with technetium-99m hexamethylpropyleneamine oxime revealing
decreased perfusion only in the focal region corresponding to
the hyperintense signal on the FLAIR images.

aphasia by the following morning, and could not react to
any vocal or gestural orders. T2-weighted and fluid-attenuated inversion recovery (FLAIR) magnetic resonance
imaging showed hyperintense areas in the cortico-subcortical region of the left frontoparietal lobe (Fig. 3A). Single
photon emission computed tomography (SPECT) with
technetium-99m
hexamethylpropyleneamine
oxime
showed an obvious decrease in perfusion in the areas appearing hyperintense on FLAIR images (Fig. 3B). We
promptly initiated anticoagulation with administration of
15,000 units/day of heparin and 60 mg/day of edaravone to
prevent further cerebral infarctions.
On the third day after admission, we planned to repeat
cerebral DSA and prepared to perform indicated endovascular treatment. DSA clearly demonstrated partial antegrade blood flow in the ICA from the point of occlusion on
the day of admission, and also partially visualized the distal middle cerebral artery. We repeatedly attempted to perform endovascular trapping for the ICA around the injured portion. We finally accomplished complete obliteration of the left ICA (Fig. 4).
Immediately after endovascular intervention, the
patient was transferred to the operation room. Under
general anesthesia, the nail was safely removed without
problematic bleeding (Fig. 5) by a team including an
otolaryngological surgeon and an oral and maxillofacial

T. Hiraishi et al.

592

Fig. 4 Pre- (A) and post-embolization (B) anteroposterior left
internal carotid arteriograms showing the antegrade flow to the
top of the internal carotid artery (ICA) from the occluded point
is clearly recanalized, and the middle cerebral artery can also
be identified (A). Coil embolization of the ICA around the
stenotic portion was performed to obliterate the blood flow (B).

Fig. 5 Photographs showing the nail pulled out from under the
tongue (A). This nail was 9 cm in length (B).

surgeon. Throughout this course of treatment, the patient
suffered no additional deficit, and his sensory aphasia and
right hemiparesis gradually improved.

Discussion
In the present case, the nail that was accidentally driven
into the lower jaw unfortunately reached the foramen
lacerum, but without perforating the ICA, and caused unstable stenosis of the ICA resulting in delayed cerebral infarction. Endovascular trapping of the ICA allowed us to
remove the nail safely and also prevented further progression of the cerebrovascular events related to the injured

ICA. There is no clear consensus regarding the timing and
method to treat such traumatic ICA injuries because of
variations in their status and injury pattern, and the individual dynamics of cerebral circulation. We performed
various evaluations to assess the injury and the patient's
status as exactly as possible on admission. However, the
cerebral infarction of the left frontoparietal lobe occurred
on the day after admission. We speculate that the mechanism underlying this event was an artery-to-artery embolism originating from the stenotic portion. The thrombus was presumably formed distal to the angiographically
occluded site of the ICA. Resumption of distal blood flow
after revascularization due to movement of the nail accompanying movement of the lower jaw carried the
thrombus to the distal vessels. Similar repeated cerebral
infarctions were observed in a patient with a craniofacial
screw injury.3) Considering the occurrence of such
delayed events, if the patient has any traumatic obstruction to the ICA resulting from a craniofacial penetrating
injury, we recommend that the obstruction be treated rapidly after necessary investigations are performed. The timing of anticoagulant administration for such patients is
controversial. We observed the patient's status without anticoagulants on the first day because of the risk of hemorrhagic events caused by the carotid injury. However, anticoagulant administration may be the optimum choice after initial diagnosis to prevent subsequent events.
Complications of ICA injuries, such as perforation of
the ICA, pseudoaneurysm formation, dural arteriovenous
fistula, carotid-cavernous fistula, fatal epistaxis,
subarachnoid hemorrhage, and intracerebral hemorrhage,
are well known to lead to posttraumatic neurological
deficits.2,4,5,7,9,13,15) Pseudoaneurysms that rupture after
head injuries are associated with particularly high rates of
mortality of 32–54%.5,9) In the present case, we performed
endovascular trapping of the ICA to remove the nail safely
and also to prevent fatal bleeding and other complications
such as pseudoaneurysm formation and traumatic carotidcavernous fistula. We planned to remove the nail after coil
embolization of the ICA from the distal to proximal sites of
the obstructed portion. Cerebral aneurysm formation or
growth may occur after trapping of the ICA.8) Our patient
will require careful long-term observation.
From the technical aspect, the proximal occlusion balloon catheter was used to control the blood flow in case of
unexpected bleeding from the ICA during the procedure.
The absence of neurological deficits on admission, when
the ICA was almost occluded on DSA, the apparently adequate collateral circulation by cross flows through the
AcomA and PcomA on DSA, and the limited focal
decrease in perfusion at the region corresponding to obvious infarction on SPECT were considered to be favorable
indicators of the patient's tolerance for ICA trapping. If
poor collateral circulation is suspected, acetazolamide
SPECT should be performed to confirm the residual
capacity for cerebrovascular perfusion, and then ICA trapping may be performed after the appropriate bypass surgery. Although catheterization through the severely
stenotic potion was possible in the present case, we generally manipulate the microcatheter and microguidewire via

Neurol Med Chir (Tokyo) 49, December, 2009

Unstable ICA Stenosis Caused by a Nail-Gun Injury
the AcomA or PcomA into the distal ICA in more difficult
cases.
Direct surgical trapping of the ICA or endovascular
treatment with a covered stent11,12,14,16) are other proposed
treatment options. Surgical trapping of the ICA is the most
successful method to occlude the ICA, but would have
been extremely invasive in the present patient. Surgical
trapping necessitates double ligation of the ICA at the
cervical portion and at the proximal portion to the
ophthalmic artery using permanent clipping via left
pterional craniotomy. Recently, repair or reinforcement
of the injured ICA with a covered stent has been attempted
for lesions in the skull base and in the intracranial vasculature,14) following the first report of autologous veincovered stent repair of a cervical ICA pseudoaneurysm.11)
Although this new technique would result in adequate
restoration of the circulation in the ipsilateral ICA, embolic side effects may occur inside the stent. Therefore, this
treatment is suitable for blunt injury of the ICA, but not
penetrating injury. This distinction was obscure in the
present case. Acute injury of the ICA should possibly not
be manipulated within 48 to 72 hours of the event and endovascular stents placed in traumatized arteries require
full systemic anticoagulation.5)
The treatment strategy for craniofacial penetrating injury involving the ICA should be determined for each
patient based on the advantages and disadvantages of individual therapies, but we suggest that the wait and watch
strategy is not ideal in the acute phase.

5)

6)

7)

8)

9)
10)

11)

12)

13)

14)

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Address reprint requests to: Tetsuya Hiraishi, M.D., Department
of Neurosurgery, Brain Research Institute, University of
Niigata, 1–757 Asahimachidori, Chuou–ku, Niigata, Niigata
951–8585, Japan.
e-mail: tetsuya_hiraishi＠me.com