Chapter 211: Carotid Endarterectomy with Shunt
muscle. The vertebral arteries originate
from the proximal subclavian arteries in
the neck taking an ascending course,
usu-ally opposite the internal mammary
artery, which takes a descending course
into the chest.
Common Carotid, Internal Carotid,
and External Carotid Arteries
The CCAs have different anatomy proxi-
mally, but then have similar distal anatomy.
The right CCA originates from the brachio-
cephalic trunk and the left CCA originates
from the aorta as the second branch in the
aortic arch. The CCAs then ascend in the
neck anterior to the anterior scalene mus-cle,
longus coli muscles, and the sympa-thetic
chain. The CCA is contained in a fas-cial
sheath that includes the internal jugular vein
and the vagus nerve. The internal jugu-lar
vein is lateral to the CCA, and the vagus
nerve typically runs posteriorly and between
the CCA and internal jugular vein. The ansa
cervical nerve typically runs anterior to the
CCA after originating from the hypoglossal
nerve. The hypoglossal nerve, in turn, runs
anterior to the internal carotid artery (ICA)
and posterior to the occipital branch of the
external carotid artery (ECA).
The CCA bifurcates into the ICA and
the ECA at approximately the level of C2
to C3. There can be considerable variation
in the level of the bifurcation. The CCA
and the ICA remain within the carotid
sheath throughout the cervical course. The
ECA runs anterior and medial to the ICA.
It sup-plies branches to the face, scalp,
orophar-ynx, and skull. There are eight
main branches of the ECA: the superior
thyroid, lingual, facial, occipital, posterior
auricu-lar, ascending pharyngeal, internal
maxil-lary, and superficial temporal. These
vessels act as important collaterals to the
intracra-nial circulation in the setting of
severe stenosis or total occlusion of the
ICA or ver-tebral arteries.
The ICA originates at the carotid bulb,
which is a dilation of its most proximal seg-
ment. It then ascends in its cervical portion in
which there are no significant branches. The
vessel enters the skull base at the ca-rotid
canal, where it passes through the pe-trous
portion of the temporal bone just lat-eral to
the middle ear. It then continues in the
cavernous segment where it takes a gen-tle S-
shape. It is in this segment that the next
branch of clinical significance, the ophthal-
mic artery, originates. The ophthalmic ar-tery
is the first major branch of the ICA. The ICA
then branches into the middle cerebral artery
(MCA) and the anterior cerebral ar-tery
(ACA).
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Vertebral Arteries
The vertebral arteries are the first branches
of the subclavian arteries. They ascend ini-
tially in a straight manner, entering the
transverse foramina of C6, and then con-
tinuing to run within the transverse pro-
cesses through C1. The vessel then turns to
enter the cranium via the foramen mag-
num, after which the vertebral arteries
course medially to join in the midline as
the basilar artery. The vertebral arteries are
of-ten of disparate size (as opposed to the
more uniform carotid arteries). The left is
dominant in 50% and right in 25%, and
they are equal in 25%. There are numerous
con-nections between small vertebral
branches and the occipital or ascending
pharyngeal branches of the carotid arteries.
CLINICAL PRESENTATION
Carotid stenosis is often first diagnosed as an
asymptomatic finding. This is often be-cause
a duplex scan or other imaging stud-ies such
as magnetic resonance arteriogra-phy (MRA)
or computerized tomographic arteriography
(CTA) is performed for vague neurologic
symptoms that usually are not directly
attributable to carotid artery dis-ease or for
evaluation of a cervical bruit detected on
physical examination. Numer-ous studies
have demonstrated a poor cor-relation
between a cervical bruit and the severity of
carotid stenosis, although the presence of a
bruit is usually indicative of the presence of
carotid stenosis and war-rants further
investigation with a duplex scan.
Additionally, a carotid duplex scan might be
performed as a “screening” test in patients
with other symptoms of or risk factors for
atherosclerosis. Symptomatic presentation
can take several forms, which usually reflects
atheroembolic disease originating from
plaque in the carotid ar-tery, or rarely more
global ischemic changes from overall
diminished cerebral blood flow.
Transient ischemic attacks (TIAs) or an
ischemic stroke may be the presenting
symptom. Clinically, an ischemic stroke is
determined to have occurred if the neuro-
logic deficit is present for over 24 hours.
Complete resolution of a neurologic deficit in
less than 24 hours is considered to be a TIA,
regardless of the severity of the tran-sient
deficit. From a practical point of view, most
TIAs last only several minutes. Some
patients with a clinical presentation of TIA
may have evidence of acute or chronic cere-
bral infarction on neuroimaging by comput-
erized tomographic (CT) scan or magnetic
resonance imaging (MRI) of the brain.
When an ischemic stroke or a TIA oc-
curs, an assessment must be performed that
will identify the location of the lesion in
the brain and the mechanism of the deficit.
This includes a thorough history and
physical examination, including a de-tailed
Vascular Surgery
neurologic examination. In the set-ting of
an acute stroke, decisions about initiating
urgent thrombolysis will require
consideration.
Embolic sources of strokes include not
only the ICA, but also the heart, the aortic
arch, and the great vessels. A history of atrial
fibrillation or intracardiac thrombus may
point to a cardiac source, and plaque in the
aortic arch and brachiocephalic or CCAs may
provide evidence of these ana-tomic areas as
sources of atherosclerotic emboli. The
distribution of the deficit can be determined
clinically and radiologically. This can often
be broken down into pat-terns associated
with specific large intrac-ranial vessels, or
more punctuate lesions associated with
smaller vessels within the brain cortex.
Large, named intracranial ves-sels include
the MCA, the ACA, the poste-rior cerebral
artery (PCA), the basilar ar-tery, and
vertebral arteries. The MCA, ACA, or PCA
distributions can cause weakness in the face,
extremities, and/or aphasia. The motor
deficits typically occur in the side of the body
opposite the hemisphere of the neurologic
deficit. Classic cerebral hemi-spheric TIAs
related to disease in the right carotid artery
include left upper and/or lower extremity
weakness, numbness, or paralysis. Classic
hemispheric TIAs related to disease in the
left carotid artery include aphasia or other
speech difficulties in addi-tion to right upper
and/or lower extremity weakness, numbness,
or paralysis. Athero-emboli to the ophthalmic
artery, a branch of the ICA as it travels
intracranially, can present with visual loss or
with the classic symptom of amaurosis fugax.
Amaurosis fu-gax is temporary monocular
blindness ipsi-lateral to the diseased carotid
artery, and is often described by the patient as
a window shade coming down over the visual
field and subsequently resolving. In addition
to clinical amaurosis fugax, Hollenhorst
plaques, which represent evidence of athe-
roemboli to branches of the retinal arteries,
can sometimes be seen on ophthalmologic
examination.
The severity of neurologic deficits can
range from severe hemiplegia to minor fine
motor deficits or cognitive and behavioral
disturbances. Symptoms of ataxia, dizziness,
vertigo, diplopia, or circumoral numbness
may be caused by vertebral basilar TIAs.
Syn-cope, light-headedness, or seizures are
rarely caused by carotid or vertebral disease.