1.

2Carotid Artery

a.
b.
c.
d.
e.
f.

g.

i. The hypoglossal nerve or the recurrent laryngeal nerve is most commonly

injured.
 1. The glossopharyngeal nerve is among the least frequently injured,
but permanent damage is associated with severe impairment due to
swallowing difficulties.
h.

i. The superior and inferior laryngeal branches of the vagus supply the
muscles of the larynx, and varying degrees of dysphonia result when they
are injured. The superior laryngeal nerve accompanies the artery of
the same name from its origin high in the neck and is at direct risk
from mobilization of the artery.
ii. Injury to the Superior Laryngeal Nerve will result in voice fatigue
i.

j. The recurrent laryngeal nerve, arising low in the neck, is at indirect risk from
injury to the main vagal trunk in the midneck. In rare cases, a nonrecurrent
laryngeal nerve may branch directly from the vagus at the level of the carotid
bifurcation and course medially behind the carotid bulb to reach the larynx. This
anomaly is usually seen on the right side, associated with an aberrant right
subclavian artery
i. Injury to the recurrent laryngeal nerve results in hoarseness, impaired
phonation, and an ineffective cough.
k.

i. The glossopharyngeal nerve gives sensory and motor fibers to the tongue
and pharynx which may result in aspiration in the rare instances when it is
injured due to inability to elevate larynx/pharynx
1.
2.

3.
 a. The stylopharyngeus is above the digastric and can be
divided to get higher on the carotid
4. Division of the stylopharyngeus and styloglossus muscles and the
stylomandibular ligament, and removal of the styloid process, can
be beneficial.
5. The glossopharyngeal nerve should remain medial. Periadventitial
dissection of the distal cervical portion of the internal carotid artery
can help prevent injury to this structure.
6.

a. The carotid sinus nerve (Nerve of Herring) arises from the

glossopharyngeal nerve and descends to the carotid sinus
receptors in the dilated bulb and proximal internal carotid
artery. In its course, it anastomoses with the vagus, superior
cervical sympathetic ganglion, and carotid body. Its distal
segment is entwined with the plexus of nerves associated
with the carotid body.
b. The hypoglossal nerve is tethered by the
sternocleidomastoid branch of the occipital artery
c. The superior thyroid artery requires isolation when it
branches directly from the common carotid artery
 i. The omyhyoid can to be cut to obtain more
proximal control
d. The superior laryngeal nerve courses behind the external
carotid artery and is avoided by encircling the artery at its
most proximal point.
e. Post-auricular extension of the carotid endarterectomy
incision decreases risk of injury to the marginal mandibular
branch of the facial nerve
7.

a. In isolating the internal carotid artery, care should be taken

to identify and ligate small crossing branches of the jugular
vein. The lower edge of the parotid gland is retracted
anteriorly during this maneuver. Division of the posterior
belly of the digastric muscle allows exposure of the internal
carotid artery within 2 cm of the skull base
b. The occipital artery and its accompanying vein course near
the lower margin of the posterior belly of the digastric
muscle and should be ligated at the time of muscle division.
Higher exposure of the internal carotid artery is obtainable
by dividing the stylohyoid ligament and stylohyoid,
stylopharyngeus, and styloglossus muscles to permit
removal of the styloid process. The glossopharyngeal nerve
is at risk for injury during these maneuvers.
l. Carotid-Carotid Bypass:
 i. The carotid sheath is opened and the common carotid artery is dissected
free bilaterally.
1. The pharynx is identified medially, and blunt dissection is used to
create a tunnel posterior to the pharynx/esophagus and anterior to
the prevertebral fascia.
2. This retropharyngeal tunnel, eliminates the risk of skin erosion,
enables transposition of the carotid artery, and places any graft
safely away from possible future tracheostomy

3.
m. Structures in Carotid Sheath:
i. Vagus Nerve: Injury can result in unilateral adductor vocal paralysis
(hoarseness), and cricopharyngeal dysfunction (dysphagia)
ii. Cervical Sympathetic
1. Embedded in the most posterior fibers of carotid sheath
iii. Ansa Cervicalis
1. Found in anterior fibers of the sheath
2. Innervation to the strap muscles (sternohyoid, sternothyroid,
thyrohyoid, omohyoid)
n. NASCET:
i. Randomized patients with symptomatic carotid stenosis > 70% into a
medical treatment (aspirin, blood pressure control) arm and a surgical
(carotid endarterectomy) arm. The risk for ipsilateral stroke at 2 years with
medical management was 26% and the risk for any stroke or death was
32%. For carotid endarterectomy, the risk for ipsilateral stroke was 9% at
2 years.
1. The benefit became apparent at 3 months and persisted for 8 years
ii. Risk of stroke in 2 years (NASCET) = 26%, reduced to 9% after CEA
iii. In 1991, NASCET demonstrated that for patients with Symptomatic carotid
stenosis 70–99%, the two year risk of ipsilateral stroke was 26% with medical
therapy vs. 9% with carotid endarterectomy.
1. In 1998, NASCET demonstrated that for patients with Symptomatic
carotid stenosis 50–69%, the five year risk of ipsilateral stroke was 22.2%
with medical therapy vs. 15.7% with carotid endarterectomy (p<.05).
 2. NASCET showed strong benefit of carotid endarterectomy over best
medical therapy for symptomatic patients with 50–99% stenosis. 
a. However, best medical therapy at the time did not include statins
and generally included aspirin as the only antiplatelet. 
3. Echogenic plaque is calcium rich and is thought to be more stable.
4. Echolucent plaque is more consistent with lipid rich or hemorrhagic
plaque that is more likely to be unstable
iv. NASCET: In those patients with less than 50% stenosis, there was a risk
of stroke in the medical group of 18.7% and in the surgical group of
14.9% (not significant). The results of this trial support performing carotid
endarterectomy in symptomatic patients with ipsilateral carotid stenosis
greater than 50%. 
o. ACAS:
i. Risk of stroke in 5 years (ACAS) = 11%, 5% after surgery. 3.9% if you
exclude the risks of carotid angiograms during the ACAS trial.
ii. 1600 Patients with a > 60% asymptomatic carotid stenosis into a surgical
(carotid endarterectomy) arm and a medical management arm (mainly
aspirin therapy). After a mean of 2.7 years of follow up, the 5-year
Kaplan-Meier projected risk for any stroke or death with medical
management alone was 11% compared to a 5.1% risk in those who
underwent carotid endarterectomy.
1. Also demonstrated that Carotid Angiogram has
Morbidity/Mortality of 1.2%, thus showed that duplex is favored
for initial diagnostics
iii. Asymptomatic Carotid Atherosclerosis Study (ACAS) and the
Asymptomatic Carotid Surgery Trial (ACST): The consensus
interpretation for the benefit of prophylactic carotid endarterectomy
compared to best medical therapy is that the relative stroke risk reduction
at 5 years was 50%, which is based on an absolute risk from 12% with
medical therapy to 6% with carotid endarterectomy. Therefore, absolute
annualized stroke risk reduction is approximately 1% to 2% for surgical
patients compared to patients managed with best medical therapy ({12%-
6%}/5 years).
iv. With respect to stroke/death, by Kaplan-Meier analysis, there was not a
statistically significant difference favoring CEA until 5 years. Similarly,
rates of stroke were not statistically significantly different until 5 years.
Closer inspection of the curves show that the KM curves do not cross until
approximately 3 years. Hence, in patients with abbreviated lifespans of 3
years or less, carotid endarterectomy cannot lower the risk of stroke
compared to best medical therapy. 
p. The Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST)
initially evaluated 4-year outcomes and found that stroke was statistically
significantly higher within the CAS arm compared to the CEA arm (4.1% vs 2.3%
respectively, p = 0.01).
 i. In the 4-year CREST trial, patients undergoing CEA had higher rates of
MI (defined as troponin elevation plus either symptoms or EKG changes).
1. Patients undergoing CAS had higher rates of minor and major
stroke.
a. However, the primary composite endpoint of MI, stroke,
and Death was not significantly different between groups.
b. Of note, even though most strokes were minor, there was a
greater decrease in quality of life for patients with stroke
compared to MI in both CEA/CAS groups
ii. In 2016, however, the CREST investigators published the 10-year follow-
up results. Their primary long-term endpoint was post-procedural
ipsilateral stroke. There was no statistically significant difference found
between stroke/MI rates between the CAS and CEA arms at 10 years
(6.9% vs 5.6%, p = 0.96).
1. However, the composite endpoint of stroke/death showed that
there was an increased risk of stroke/death in the CAS arm (HR
1.37; 95% CI 1.01-1.86)
q. Multiple randomized controlled trials have supported the safety and efficacy of
intravenous alteplase (0.9 mg/kg; maximum dose of 90 mg) for confirmed
ischemic strokes of less than 3 hours duration.
i. IV alteplase treatment in the 3- to 4.5-h time window is recommended for
those patients ≤80 y of age, without a history of both diabetes mellitus and
prior stroke
ii. Concurrent intravenous abciximab administration is a contraindication to
alteplase administration.
iii. Other contraindications include a blood pressure of 185/110 mm Hg or
higher; intracranial hemorrhage on CTA; a history of stroke, severe head
trauma, or intracerebral or intraspinal surgery within 3 months;
gastrointestinal bleeding within 21 days; and concurrent usage of low-
molecular weight heparin/thrombin or factor Xa inhibitors.
r. There are no studies to suggest endovascular intervention of asymptomatic carotid
in-stent restenosis improves patency or decreases long-term stroke rates.
s. The stroke prevention by aggressive reduction in cholesterol levels (SPARCL)
randomly assigned nearly 5,000 patients who had stroke or TIA within 1 to 6
months of enrollment to high dose (80 mg) atorvastatin per day or placebo.
i. With a 5-year follow up, the overall mortality rates were similar between
the groups; however, there was a reduction in the overall incidence of
strokes and cardiovascular events with a small increase in hemorrhagic
stroke.
1. Mortality was similar, however there were less overall events in
the treatment group. A small increase in hemorrhagic stroke was
noted in the treatment group.
t. Major trials have defined “recent” as within the past 6 months. In general, remote
events are not considered when determining whether a current lesion is
symptomatic carotid lesion.
u. Staged carotid endarterectomy (CEA) followed by CABG were associated with
the lowest stroke/death rates, with the highest stroke rates noted in those
undergoing CABG then CEA. 
i. Rates of complications are comparable if carotid artery stenting is
substituted for CEA in staged or synchronous CABG. The largest
systematic review shows that mortality is highest among patients
undergoing synchronous CEA and CABG.
v. In HD patients, carotid revascularization (either CAS or CEA) is associated with
an increased perioperative stroke risk. 
i. Overall, the data most consistently show an increased risk of stroke in
nonrevascularized patients with ESRD and high-grade asymptomatic
carotid artery stenoses; therefore decision to treat must be made on a case-
by-case basis
w. Both carotid endarterectomy (CEA) and carotid artery stenting (CAS) have been
studied in patients who have prior cervical radiation therapy.
i. Regardless of symptom status, periprocedural stroke and death rates are
nearly equivalent for CEA and CAS in this cohort. 
ii. Increased nerve damage risk in redo-CEA
x. The standard therapy for arterial injury from a 7 Fr (or greater) catheter on the
right side of the neck is open repair by either a cervical approach or a combination
of supraclavicular approach with partial median sternotomy if there is an injury to
the innominate artery or aorta.
i. If there is involvement of the aorta, the left side of the neck may require a
posterolateral thoracotomy or even possibly a trapdoor procedure,
depending on the location of the catheterization
y. Acute Stroke Post-CEA:
i. If the patient exhibits signs of an ipsilateral stroke after awakening from
anesthesia, the artery should be evaluated for thrombosis with ultrasound.
1. If thrombus is present at the endarterectomy site, the
endarterectomy site should be explored to ensure no technical
defect.
2. If a distal embolus is suspected, percutaneous methods of
retrieving the embolus may be undertaken.
3. Systemic tPA is not recommended due to risk of bleeding.
ii. Thrombosis after post-op CEA: If no technical defect is identified on re-
exploration, the presumed etiology of the thrombosed CEA site is platelet
and fibrin aggregation, with adherence to the freshly endarterectomized
surface. If this is not replaced, there is a high chance of re-thrombosis.
Thus, it must be replaced with saphenous vein interposition
iii. Treatment:
1. Immediate:
 a. re-exploration (for immediate, 1 hr delayed)
b. cerebral angiography with intra-arterial
thrombolysis (intra-cranial emboli, patent
endarterectomy site)
c. Open the wound in the OR under local
anesthesia. Why local: no hypotension on
induction.
d. Then perform intraoperative duplex. If the
duplex shows a technical defect or clot,
heparinize and open the carotid.
i. If it doesn’t, then get an angiogram
ii. If angiogram is negative, get a head CT
to look for bleed.
e. Risk of hemorrhagic conversion is high.
2. Delayed:
a. Deficit 1-2 days after CEA is usually secondary to cerebral
hemorrhage and/or edema secondary to hyperperfusion.
b. The syndrome is HTN/Headache/seizures
c. Tx = BP control and anti-seizure medications, in addition
to minimizing anticoagulation.
z. Special considerations apply to blood pressure (BP) control in patients with acute
ischemic stroke who are candidates for intravenous thrombolytic therapy.
i. Before thrombolytic therapy is started, treatment is recommended to keep
systolic BP at or below 185 mmHg and diastolic blood pressure at or
below 110 mmHg.
ii. BP should be maintained at or below 180/105 mmHg for at least 24 hours
after thrombolysis.
iii. For patients with acute ischemic stroke who are not treated with
thrombolytic therapy, a BP should not be treated acutely unless systolic
BP exceeds 220 mmHg or diastolic BP exceeds 120 mmHg, or the patient
has active ischemic coronary disease, heart failure, aortic dissection, or
hypertensive encephalopathy.
1. It is appropriate to start or resume antihypertensive medications
during hospitalization for patients with BP greater than
140/90 mmHg who are neurologically stable.
2. For patients with extracranial or intracranial large artery stenosis, a
slower reduction in BP (i.e., over 7 to 14 days after ischemic
stroke) is recommended in an effort to maintain cerebral blood
flow to ischemic brain regions.
aa. Contralateral carotid artery occlusion will result in compensatory increases in
flow velocities and thus could cause overestimation of the degree of stenosis.
bb. CHF, Excessive Calcification, Proximal CCA Disease, or Distal ICA Disease, can
result in falsely low flow velocities.
cc. Asymptomatic Hollenhorst plaques on fundoscopic exam are not considered symptomatic
carotid stenosis
dd. Carotid Endarterectomy is MODERATE cardiac risk surgery.
ee. Plaque Features:
 i. Homogeneity suggests stable plaque
ii. Ulceration, Intraplaque hemorrhage, Lipid Rich Necrotic Core, Irregular
Surface and Heterogeneity suggest higher risk of rupture
iii. Echogenic plaque is calcium rich and is thought to be more stable.
iv. Echolucent plaque is more consistent with lipid rich or hemorrhagic plaque that is
more likely to be unstable
ff. Incidental asymptomatic cerebral aneurysms should be treated if >8mm
i. If smaller size, then asymptomatic ICA disease can be treated first.
gg. Patients with a Hollenhorst plaque should undergo evaluation; however, the
decision to treat a carotid stenosis can be made independent of the ocular finding.
i. They are age-indeterminate micro-atheroembolus from any proximal
cardiovascular structure. Thus, they are not specifically associated with
severe carotid disease, and have negligible stroke risk.
hh. Measurement of the degree of carotid stenosis can be performed by using one of the two
methods described in the North American Symptomatic Carotid Endarterectomy Trial
(NASCET *Normal Distal ICA) and the European Carotid Surgery Trial (ECST
*Estimate at location). 
i. Both methods use the ratio of greatest stenosis to an approximate of normal, with
NASCET using the normal internal carotid artery distal to the bulb and ECST
using an estimate of the original width of the artery at the stenosis.
ii. CT angiography is that dense calcifications can obscure intraluminal contrast and lead to
overestimation of the degree of carotid stenosis.
i. MR angiography is not limited by calcification and should be used when
calcification limits CT angiography or duplex.

jj.
kk. Cerebral Hyperperfusion:
i. High mortality, 38%
ii. This syndrome is believed to be due to loss of vascular autoregulation at
the arteriolar level, resulting in cerebral edema and potentially progressing
to intracranial hemorrhage.
iii. Usually within 1-2 weeks, median 3 days
 iv. The condition is not believed to be related to ongoing microembolization
or postoperative hypovolemia.
v. Elevated mean velocities in the middle cerebral artery may be observed
with transcranial Doppler
vi. Work-up:
1. Non-contrast CT
2. MRI (FLAIR) – Cerebral Edema, T2
vii. Treatment:
1. Aggressive BP Control
2. EEG, for subclinical seizure
3. Consider Stopping Antiplatelet/Antithrombotic
ll. Preoperative balloon occlusion testing combined with Xenon-enhanced SPECT
imaging has demonstrated safety with carotid sacrifice.
i. A study is considered low risk for postoperative ischemia if there are NO
neurological deficits and normal diffusion on SPECT.
ii. A balloon occlusion test is recommended to be performed for 30 minutes
of ipsilateral occlusion and is considered clinically positive if any
neurologic deficits present, with or without hypotensive challenge.
iii. The ratio of radioactivity in the ipsilateral versus the control hemisphere
with Xenon enhanced SPECT imaging has been added to the clinical test
to improves sensitivity.
1. A ratio of 0.9 and greater is considered a normal test and the
likelihood of stroke increases in a linear fashion as the ratio drops
below 0.9.
mm. For those performing selective shunts under general anesthesia, various
cerebral monitoring techniques have been used to direct shunt placement during
CEA, the most common of which is slowing and decreased amplitude of alpha
and beta waves on EEG.
i. Carotid stump pressures > 40 mm Hg do not require shunting.
ii. A > 15% decrease from baseline value in either hemisphere in cerebral
oximetry is the threshold for shunt placement.
iii. Severe slowing in the middle cerebral artery on transcranial Doppler
(TCD) examination correlates to postoperative stroke and may benefit
from shunt placement.
nn.
oo. For Acute thrombosis of the ICA during carotid stenting most appropriate first
step in this patient who is acutely neurologically decompensated is to attempt to
disaggregate the platelet plug and thrombus with administration of intra-arterial
abciximab and thrombolytic therapy directly into the ipsilateral carotid artery.
i. Endovascular salvage attempts may ensue, including suction
thrombectomy, repeat stenting, and balloon angioplasty.
ii. While conversion to CEA may ultimately be required, immediate
conversion may also be too time-consuming and physiologically stressful
for the patient
pp. Carotid Aneurysm, similar to popliteal artery aneurysms, the primary risk of
carotid aneurysms is associated with distal thromboembolism or atheroembolism
from intraluminal thrombus, instead of aneurysm rupture.
i. No studies have been performed to evaluate the efficacy of anticoagulation
for ipsilateral stroke risk reduction; therefore, currently invasive
reconstruction is recommended provided the patient is an appropriate
surgical candidate.
ii. Unlike carotid stenosis related to atherosclerotic disease, the degree of
intraluminal stenosis is not the primary determining factor to recommend
repair in the setting of a carotid artery aneurysm. There is no stenosis
threshold for repair, as any stenosis is likely the result of aneurysm sac
intramural thrombus, thus predisposing the patient to future ipsilateral
stroke.
qq. Carotid Dissection:
i. Stretch injury at C2-C3 level.
ii. Patient have triad of unilateral headache/face pain, stroke, Horner’s or are
asymptomatic
iii. Physiology of sympathetic nerve disruption along the carotid artery as a
cause of partial Horner’s syndrome (oculosympathetic syndrome),
including miosis and ptosis, but excluding anhidrosis. 
iv. Generally not associated with hoarse voice since no mass-effect
v. Most are managed with anticoagulation
vi. CTA would show Intramural Hematoma with Crescent Sign
rr. FMD:
i. FMD most commonly affects carotid/renal arteries which are medium
sized vessels
ii. A nonatheromatous, noninflammatory, proliferative process
iii. Predominantly in women between 15 and 50 years of age
1. Accounts for less than 10% of cases of renovascular hypertension
iv. Its principal pathologic form involves primarily the media; it affects long,
unbranched segments of medium-sized conduit arteries such as the renal
artery and the internal carotid artery but has been observed in almost every
artery in the body
1. FMD occurs most frequently (>90%) in women between 20 and 60
years
 v. FMD is the second most frequent cause of renal artery stenosis after
atherosclerosis and the most common cause of renal hypertension in
young individuals.
vi. Because FMD is a noninflammatory process, it is not associated with
anemia, thrombocytopenia, or the increased acutephase reactants that often
occur in patients with vasculitis.
vii. The histopathologic scheme classified FMD into three categories related
to the pathologic layer of the arterial wall affected— fibroplasia of the
intima, media, or adventitia (periarterial fibroplasia)
1.

viii. About 12.9% of patients with FMD (renal or carotid) had at least one
intracranial aneurysm.
1. The location of the extracranial FMD did not influence the
incidence of intracranial aneurysms, so all patients with FMD
require imaging for an intracranial aneurysm.
2. Although there are no formal guidelines mandating brain imaging
in patients with FMD, it would seem prudent based on the 12.9%
prevalence of intracranial aneurysms.
ix. Carotid FMD:
1. Can present as stroke in young woman
2. Locations are not same as typical atherosclerotic (branch points)
3. Registry show the extracranial carotid and vertebral arteries to be
nearly as often involved as the renal arteries, primarily in middle-
aged women.
a. Carotid FMD is associated with cerebral aneurysms and
FMD involving the renal arteries.
4. Among the four types of FMD, the internal carotid artery is most
often affected by medial fibroplasia, which results in an
arteriographic appearance resembling a string of beads seen in
80% to 95% of the lesions.
a. The arterial segments involved tend to be more distal than
in the case of arteriosclerosis; they are located in the middle
 and distal segments of the extracranial internal carotid
artery
5. Vertebral artery disease is usually located at the level of the C2
vertebral body and does not extend intracranially
6. Intracranial aneurysms and occlusive disease. This is found in at
least 10% of patients with FMD in general and as many as 51% of
patients with internal carotid FMD in particular.
a. Solitary intracranial aneurysms are present in 80% of these
patients, but multiple aneurysms occur in the remaining
20%.
b. These aneurysms tend to be on the same side as the
extracranial carotid FMD.
c. They pose an independent threat of rupture and
hemorrhage, and their natural history has the potential to be
worsened by relief of a proximal stenosis
7. FMD is classified based on the layers of the wall that are affected
a. Medial FIBROplasia: Associated with the classic String of
Beads
i. #1
b. Perimedial Dysplasia:
i. Commonly affects renal arteries and is associated
with microaneurysms
ii. #2
c. Medial Hyperplasia:
i. Appears as a single, concentric stenosis or long
tapering stenosis
ii. #3
d. Intimal Fibroplasia:
i. Appears as a single, concentric stenosis or long
tapering stenosis
e. Adventitial Hyperplasia:
i. Very rare and is usually seen in localized stenosis
f.  The presentation of FMD in the cerebrovascular
circulation is varied.
i. While both transient ischemic attacks and
cerebrovascular accidents have been reported, more
patients are asymptomatic and present with
incidental findings of FMD.
ii. Other benign presentations include pulsatile
tinnitus, a "whooshing" sound in the ear, and
headaches.
iii. Stroke is also a presentation
g. The treatment for asymptomatic carotid fibromuscular
dysplasia is antiplatelet therapy with aspirin.
i. In symptomatic patients, transluminal balloon
angioplasty can be considered.
 1. Stents should be avoided, only used with
dissections or aneurysms
2. **Angioplasty is also preferred if there is
fibrodysplasia in peripheral vasculature
h. Patients who have FMD and present with a vertebral
dissection acutely started on anticoagulation therapy with
heparin and transition to NOAC, and treated if
symptomatic. Same as a regular vertebral dissection.
i. Those associated with FMD are typically proximal
and occur bilaterally.
i. Given the generally benign behavior of asymptomatic
disease, patients with asymptomatic carotid FMD should be
monitored and treated medically, with antiplatelet therapy
for primary stroke prevention.
i. There is no evidence to suggest a role for lipid-
lowering therapy in patients with isolated FMD,
although it should be considered as part of a
primary prevention strategy
j. Although asymptomatic lesions seem to have a generally
benign course, such may not be the case in a patient who
suffered a stroke on the contralateral side from the same
pathology
i. Patients with carotid FMD often have nonfocal
symptoms, some of which may be due to global
ischemia
k. Because of the relative safety and effectiveness of
mechanical intervention dilation of the artery is appropriate
for lesions causing focal ischemic events (hemispheric or
ocular) or episodes of cerebral hypoperfusion.
l. A lesion causing a focal cerebral ischemic event should be
considered for treatment because it remains a significant
threat.
m. Hypoperfusion is rare but can occur in the setting of
critical bilateral carotid FMD or even unilateral disease
when there is a significant defect in the circle of Willis.
n. Percutaneous transluminal angioplasty (PTA) has been
successful in the treatment of renal artery FMD, and carotid
angioplasty with stenting has a growing role in the
management of carotid disease; however, the results and
durability of balloon angioplasty for carotid FMD with or
without stent placement are not known.
o. It is not clear whether carotid balloon angioplasty should be
accompanied by stent placement in FMD. Stent placement
is not usually required after PTA in renal artery FMD
because the results are excellent without stents and the
 patients are usually otherwise young and healthy with good
life expectancies.
i. In light of this paucity of cases, more time will be
required to determine the role of PTA with or
without stenting in the treatment of patients with
carotid FMD.
p. Patients with asymptomatic carotid stenosis secondary to
FMD should be started on a regimen of antiplatelet agents
q. Carotid FMD should be monitored at intervals of 6 months
with a noninvasive study
r. Chiropractic manipulation of the neck should be avoided,
as should sports that are likely to produce whiplash-type
neck injuries.
s. The main disadvantage of open surgical dilation is that it is
performed without imaging of the luminal surface. The
length of the arterial segment to undergo treatment must be
estimated. Kinks and coils must be managed by “feel”
without direct guidance
i. PTA has become the preferred approach for more
proximal internal carotid artery FMD.
 t.

x. Renal FMD:
1. Unlike atherosclerotic renal artery stenosis, the origin of the renal
artery is often spared
2. Luminal narrowing leads to renal parenchymal damage and
ischemic nephropathy in patients with FMD.
a. However, this seems to be less important in patients with
FMD than in those with atherosclerotic RAS
b. In addition, renal perfusion correlates inversely with the
degree of stenosis in FMD but not in atherosclerotic RAS,
further emphasizing that FMD hypertension is more truly
renin-dependent than hypertension due to atherosclerosis
3.

4. A renal-to-aortic pressure ratio less than 0.90 has been correlated

with increased renin levels in the renal vein, suggesting a
physiologically relevant stenosis.
a. A mean pressure gradient across the stenosis of more than
10 mm Hg predicts a favorable response to dilation.
5. FMD most commonly involves the distal main renal artery and its
branches.
a. Patients with FMD do demonstrate a significant decrease in
mean cortical thickness and reduced renal length compared
to comparable patients with essential hypertension.
i. However, the incidence of renal failure remains
remarkably low.
ii. A successful endovascular treatment outcome
appears to be associated with an age < 50 years, the
absence of associated coronary and carotid stenosis,
and duration of hypertension less than 8 years.
6. Renal FMD is classified based on the layers of the wall that are
affected
a. Medial FIBROplasia: Associated with the classic String of
Beads
i. #1
b. Perimedial Dysplasia:
i. Commonly affects renal arteries and is associated
with microaneurysms
ii. #2
c. Medial Hyperplasia:
i. Appears as a single, concentric stenosis or long
tapering stenosis
ii. #3
d. Intimal Fibroplasia:
 i. Appears as a single, concentric stenosis or long
tapering stenosis
e. Adventitial Hyperplasia:
i. Very rare and is usually seen in localized stenosis
f. Ostial lesions are normally seen in atherosclerotic disease;
the technique for the operative repair of these lesions
i. In patients with FMD requiring open surgery,
lesions are most commonly located in the distal
portion of the main artery, often combined with
branch artery stenosis, and are normally repaired
with in situ techniques.
ii. Graft material for the reconstruction may be either
saphenous vein or arterial homograft. In the
treatment of FMD, autologous vein grafts are
usually preferred for reconstructions in adults, and
autologous hypogastric artery grafts are favored for
bypass in children.
1. The hypogastric artery may also be used in
adults, especially if several branches must
be reconstructed.
2. Dacron or expanded polytetrafluoroethylene
grafts can be used in renal artery lesions but
are not the first choice
g. A large proportion of patients with FMD exhibit the string
of-beads appearance, with small aneurysmal areas
interspaced by webs in the renal artery
h. Most renal artery aneurysms have a low risk of rupture and
only a few ruptured FMD lesions have been reported. How
FMD-related aneurysms measuring 1 to 2 cm should be
handled is uncertain. Conservative treatment may be
successful
i. If additional risk factors are present, treatment may
be justified. Aneurysms larger than 2 cm should
probably be excluded
i. In hypertensive patients with FMD in whom an aneurysm
constitutes part of the indication for surgery, suturing of the
aneurysm (aneurysmorrhaphy) is normally not adequate. A
saphenous vein graft interposition is usually required.
j. Endovascular Tx in Children:
i. Because children have a greater tendency than
adults for vasospasm during endovascular
procedures, many centers give small doses of
nitroglycerin at every exchange of catheters or
wires to minimize this problem.
ii. The string-of-beads type of lesion is not frequent in
children. After ballooning of a stenosis, the
 frequency of recoil is high. If this persists after
more prolonged dilation, oversized or cutting
balloons should not be used until it has been
determined whether the artery is dysplastic or
hypoplastic. Patients with a suspected hypoplastic
renal artery or a complex stenosis should be
considered for open surgical repair.
iii. Because series are small, centralization of treatment
is recommended.
1. Treatment of very young children to achieve
a moderate improvement may allow open
surgery to be delayed until they are older,
when the procedure can be performed with
better long-term results.
ss. Tandem Carotid Lesion:
i. In symptomatic carotid lesion, teat the bulb disease first and then medical
management for the intracranial lesion
1. Only treat intracranial lesion if symptomatic after CEA and
medical management
tt. When doing retrograde CCA stent with CEA, do the CEA first to prevent long
time stagnant flow in the CCA stent
uu. The main benefit of local anesthesia for CEA is better neuro-monitoring
vv. Eversion Endartectomy is best for kinked/coiled carotids
ww. Carotid to carotid bypass 
i. Standard carotid exposure is performed bilaterally, and blunt dissection is
used to create a tunnel POSTERIOR to the pharynx and anterior to the
prevertebral fascia.
ii. This eliminates the risk of skin erosion, enables transposition of the
carotid artery, and avoids the risk of injury to the graft in the case of a
tracheostomy. 
xx. Subclavian transposition 
i. Higher long-term patency rates compared with bypass.
yy. Carotid-Subclavian Bypass, Prior to TEVAR
i. Indications:
1. LIMA CABG
2. LUE AVF/AVG
3. L VA Terminates in the PICA
4. Dominant Vertebral
ii. The subclavian is ligated proximally so that the flow in the bypass does
not contribute to a retrograde type II endoleak.
iii. The tunnel is Retro-Jugular
zz. Treatment for inflammatory diseases:
i. For stenosis of an arch vessel that is severe enough to cause symptoms, the
inflammatory disease process must have been active for some time. In
most cases, treatment with anti-inflammatory medications is aimed at
 reducing the inflammatory state and not at decreasing the amount of
stenosis in the vessel.
ii. Because revascularization procedures in these disease states are hampered
by cell overgrowth and neointimal hyperplasia, it is important to ensure
that the patient’s disease is quiescent before vascular reconstruction by
any route. This should include normalization of inflammatory serum
markers and improvement in systemic symptoms such as fevers and
malaise.
iii. Nevertheless, occasionally cerebral ischemic symptoms develop that
mandate acute attention to revascularization, even with an active
inflammatory state. In this setting, reconstruction ideally with autogenous
material carries the lowest risk of recurrence.
1. Endovascular intervention in the setting of acute inflammation can
be achieved, although immediate and long-term success rates
appear lower than those achieved in patients with atherosclerotic
disease, and recurrence rates are related to the degree of ongoing
inflammation.
2. There is a suggestion that covered stents may be of some benefit
in treating lesions in this scenario.
a. Once the inflammatory state has diminished, the residual
lesion in question should be assessed. Improved
endovascular outcomes are obtained with the treatment of
short focal stenoses.
b. Stent placement appears to have a distinct advantage over
angioplasty alone. For complex lesions, especially long
occlusions, it appears that autogenous reconstruction via
arch vessel transposition offers recurrence rates that are
about half those of endovascular therapy.
aaa. Takayasu:
i. Granulomatous Pan arteritis of all three vessel layers with a skip pattern
ii. Takayasu’s arteritis is a common vascular condition mainly involving the
aorta and its branches. Upper extremity ischemia may occur with disease
within the subclavian arteries.
iii. Large Vessels
1. Aorta and Primary Branches
2. Pulmonary artery, the coronary arteries, and the heart valves can be
affected; but the subclavian and carotid arteries are most
commonly affected.
iv. Lesions tend to be symmetric, in paired arteries, and contiguous in the
aorta
v. Takayasu’s arteritis would usually present in younger patients with
involvement of the origins of aortic branches in particular.
vi. Younger patients (10-40)
vii. Skip Lesions
viii. Subacute constitutional onset of symptoms
 ix. Shortness of breath and cardiac symptoms may be present if the
pulmonary arteries are involved.
x. Female predominance (8:1) in child-bearing age with Asian predominance
xi. Elevated ESR is predictive of response
xii. Affects all Three Layers
xiii. Primary treatment with immunosuppression (traditionally with
corticosteroids) will limit or prevent subsequent occlusive disease.
1. During the quiescent or occlusive phase of the disease,
symptomatic arterial occlusions are traditionally treated with open
surgical reconstruction.
xiv. Classification system
1. Type I- Arch and great vessels
2. Type II- Middle aortic syndrome. Distal thoracic and
visceral abdominal aorta
3. Type III- Aortic arch and abdominal aorta
4. Type IV – Pulmonary arteries
xv. The operative approach for the lesions associated with Takayasu’s disease
is different than that for atherosclerotic lesions.
1. Inflow of a bypass should originate for a disease-free segment. For
mid-aortic syndrome, this should often be the distal thoracic aorta.
a. Bypass of diseased renal arteries is indicated to treat
renovascular hypertension in this young patient. The donor
artery for the renal artery bypass should be uninvolved
aorta or the aortic bypass graft since other aortic branches
(such as the celiac artery) can develop stenoses from
Takayasu’s arteries in the future, making splenorenal
bypass or ilio-renal bypass unfavorable options.
bbb. Giant Cell
i. Giant cell arteritis mainly involves the walls of medium and large arteries.
1. The temporal artery is the most commonly involved; however,
upper extremity arteries are occasionally affected
ii. GCA has a predilection for the cranial arteries, including the temporal
arteries, but a disease variant (large-vessel GCA) can also impact the aorta
and its major branches, especially in the upper extremities.
1. Large Vessel GCA:
a. Distal Arterial Segments, commonly the axillary artery
iii. GCA is characterized by a subacute onset of symptoms that are usually
first constitutional, making diagnosis challenging. Low-grade fever,
fatigue, weight loss, headache, and myalgia may be present. In the case of
large-vessel GCA, arm claudication may be present. Jaw claudication,
transient vision loss, and permanent visual loss are also possible features
of GCA.
iv. Affects all Three Layers
v. The clinical history usually begins with a constitutional symptoms, such as
fever and myalgia, followed by symptoms referable to the affected
arteries.
 vi. Symptomatic subclavian-axillary occlusion often presents with symptoms
of headache, malaise, anorexia, weight loss, and jaw claudication.
1. Pain may also occur overlying the temporal artery. Unilateral
blindness occurs in up to 17% of patients with GCA, followed by
contralateral, usually permanent, blindness in one third of these
patients within 1 week. 
2. Amaurosis fugax is an important warning sign that precedes visual
loss in 44% of patients.
vii. In addition, patients with GCA have increased risk of thoracic aortic and
abdominal aortic aneurysms.
viii. Classic arteriographic findings of GCA include smooth, tapering stenoses
of subclavian, axillary, and brachial arteries.
ix. GCA almost never occurs in persons younger than age 50. Its incidence
rises steadily thereafter, peaking between the ages of 70 and 79.
x. Caucasian (specifically Scandinavian) populations are the most commonly
affected.
xi. Equal Male/Female predominance
xii. Primary treatment with immunosuppression (traditionally with
corticosteroids) will limit or prevent subsequent occlusive disease. During
the quiescent or occlusive phase of the disease, symptomatic arterial
occlusions are traditionally treated with open surgical reconstruction.
xiii. Giant cell arteritis has a variable presentation and a significant portion of
patients may not have the classic symptoms of headache and jaw
claudication associated with involvement of the temporal artery. 
1. Vascular symptoms do not comprise the most common
presentations of GCA. Although definitive diagnosis of GCA
requires a biopsy, temporal artery biopsy is associated with false
negatives and other large vessel involvement may not be amenable
to tissue sampling.
2. Therefore, most clinicians treat patients with high suspicion with
empiric corticosteroids. Serial testing for inflammatory markers
and serial imaging is required to follow the course of the disease
while being treated.
3. Surgical intervention for complications of GCA are not the
mainstay of therapy for GCA. 
a. Rather, surgery is typically reserved for those failing
medical therapy.
b. In some cases, there may be aneurysmal degeneration of
the involved arteries, which would be an indication for
surgical intervention, especially in a patient who is
symptomatic (Abdominal pain) from a vascular standpoint.
i. Whether open or endovascular repair is preferred is
unknown because of the rarity of the disease.
 ii. Endovascular repair is appealing because of the
peri-aortic inflammatory changes that are
encountered during open surgery, but the tolerance
of the aorta to endovascular manipulation and
ballooning is not known.
ccc. Polyarteritis Nodosa:
i. Focal, segmental, necrotizing vasculitis affecting medium-sized arteries
with multiple aneurysms
ii. Polyarteritis nodosa (PAN) is a disseminated disease characterized by
focal necrotizing lesions involving primarily medium-size muscular
arteries.
1. This is a rare disorder with peak incidence in the 40s. The clinical
manifestations of PAN are varied.
2. It can involve only one organ or multiple organs simultaneously or
sequentially over time.
3. The hallmark of PAN is the formation of multiple saccular
aneurysms associated with inflammatory destruction of the media,
with the most frequently involved organs being the kidney, heart,
liver, and gastrointestinal tract. 
4. The most frequent manifestations of PAN include a characteristic
crescent-forming glomerulonephritis, polyarteritis, polymyositis,
and abdominal pain.
iii. Regress with vigorous steroid and cyclophosphamide therapy should be
recommended for all asymptomatic visceral aneurysm
iv. P-ANCA
v. PAN may be idiopathic or secondary to hepatitis B infection.
ddd. Clopidogrel Resistance:
i. Associated with CYP2C19 P450 Gene
ii. PPIs can decrease the effect of clopidogrel
eee. Awake neurologic monitoring is the most reliable.
1. Agitation should be interpreted as neurologic compromise and an
indication for shunting
ii. EEG monitoring has higher rate of false positives
iii. If stump pressure are used <40 mmHg is concerning
fff. Eversion Endarterectomy:
i. The ICA is transected at the bifurcation
ii. A shunt can still be used, however it is more difficult
iii. Similar rates of perioperative stroke/death/neck hematoma and a carotid
occlusion
iv. Advantages of the eversion technique are that it does not require a patch,
closure is often faster, and redundancies can be corrected within the ICA
ggg. Carotid after Stroke:
i. Crescendo transient ischemic attacks (TIAs) represents an unstable plaque
and calls for an emergent carotid endarterectomy.
 ii. After a severe stroke, there is usually an interval of recovery before
endarterectomy should be considered
iii. Transient ischemic attacks with a carotid stenosis should be treated
aggressively whether it is associated with an intracranial stenosis or not,
but this is not considered an indication for emergent surgery, it is urgent.
hhh. Carotid Aneurysm:
i. Can present as TIA (Most Common), Amaurosis, Mass Effect, Dysphasia
ii. Treatment:
1. Resection with interposition bypass (Vein)
iii. High Exposure
1. Nasotracheal intubation
2. Division of posterior belly of digastric muscle
a. When you divide, Glossopharyngeal Nerve (9), this nerve
is involved in sour taste at the back of tongue, and gag
reflex
3. MEDIAL Mobilization of Hypoglossal
4. Mandible Subluxation
5. Mobilize Parotid Gland
6. Divide occipital branches around the hypoglossal
7. Divide stylopharyngeus, styloglossus, stylohyoid.
8. Use a balloon for distal control
iv. Can be ligated, if >60-70 mmHg
1. EC-IC bypass if not sufficient
2. If patient passes balloon occlusion test, otherwise need EC-IC
3. Results in thrombosis of the artery up to the ophthalmic, thus
patient should be anticoagulated
v. Treat if > 2cm or symptomatic
iii. Carotid Body Tumor:
i. Carotid body tumors develop within the adventitia of the medial aspect of
the carotid bifurcation.
ii. The carotid body originates in the neural crest and is responsible for acute
adaptation to fluctuating concentrations of oxygen, carbon dioxide, and
pH. Most are sporadic but familial type (10-50%) is more common in
younger patients.
iii. The rare hyperplastic form is seen primarily in patients who have chronic
obstructive pulmonary disease (COPD) or cyanotic heart disease.
iv. Carotid body tumors are slow growing and present most commonly as an
asymptomatic palpable neck mass in the anterior triangle of the neck.
v. The carotid body is highly vascularized by branches of the ascending
pharyngeal artery, itself a branch of the external carotid artery.
vi. Carotid body tumors are treated with either surgery or radiotherapy
depending on the presence or absence of other paragangliomas and the
patient's age and health status.
1. If catacholamine levels are elevated, an evaluation for adrenal
pheochromocytomas should also be performed.
 a. If detected these other tumors should be removed prior to
the carotid surgery.
vii. Presents as mass, hoarseness, tinnitus
viii. Mean age of diagnosis is 55 years
ix. There is female predominance
x. Fontanes Sign: Laterally Mobile, but Vertically Fixed
xi. Splayed our Bifurcation on Angiogram
xii. Risk factors include conditions that lead to chronic hypoxemia, which
include living at high altitudes, smoking, and chronic obstructive
pulmonary disease. CBTs can occur sporadically but are also seen as part
of syndromes.
xiii. Malignancy is not determined on a histologic basis—it is diagnosed
according to clinical behavior of the tumor: local invasion, recurrence, or
evidence of metastasis. These are rare findings that occur in less than 5%
of cases.
xiv. Carotid body tumors (CBT) are sporadic in 75% of cases; however, 25%
are associated with familial history and/or underlying germline mutations.
1. Genetic testing is recommended in all patients with multi-focal
tumors, CBT associated with paraganglioma, CBT associated with
pheochromocytoma and or a positive family history.
2. The succinate dehydrogenase complex subunit D (SDHD) gene is
the most common gene associated with familial paraganglioma.
a. This autosomal dominant, affects a component of the Kreb
cycle metabolic pathway. These hypoxia-related pathways
can be activated by chronic hypoxia (e.g., living at high
altitude), leading to increased neural crest call proliferation
with decreased apoptosis.
b. Patients with familial CBT tend to be younger (mean age
35 years), have bilateral involvement, and may have
associated pheochromocytoma and/or other paraganglioma.
3. Class I tumors are localized and are generally resected with a very
low probability of carotid artery reconstruction or nerve injury.
Class II tumors are adherent to or partially circumscribe the carotid
artery. Class III tumors encase the common, external, or internal
carotid artery. Resections of large Class II tumors and Class III
tumors have a higher probability of necessitating carotid resection
and reconstruction and are associated with a higher probability of
cranial nerve injury. Preoperative embolization of large Class II
and Class III tumors should be considered, but is not mandatory.
Proponents of preoperative embolization of carotid body tumors
cite a lower blood loss after embolization. The idea that
embolization may reduce the risk of cranial nerve injury has not be
supported in multiple studies. If preoperative embolization is
performed, surgical resection should ensure within 24-36 hours
 after embolization to minimize the peri-tumor inflammation that
ensues after embolization.
xv. Shamblin Classification:

1.
2. Obtain Vein Map, Catecholamines, Plasma Metanephrines (since
5% are pheochromocytoma)
3. Have malignant potential, low via the Lymphatics
4. Family members should be screened
jjj. Carotid Trauma:
i. Classified as Penetrating vs. Blunt, followed by Symptomatic vs.
Asymptomatic

ii.
iii. Treatment:
1. Exploration:
a. Penetrating with Zone-2
2. Carotid Stent:
a. Pseudoaneurysm
3. Anticoagulation: 3-6 months
a. Blunt Dissection or Thrombosis
kkk. Stump Syndrome:
i. Occurs as symptomatic carotid with occluded ICA
ii. Confirm with CTA/Angiogram since there may be a string-sign which was
not seen in a duplex
iii. A vault at the origin of the occluded ICA syndrome acts as a reservoir for
the fresh thrombus that can embolize of the ECA and into the brain via
retrograde flow through the supra/infra-orbital vessels
iv. Treatment:
 1. E-CEA w/ Patch + Ligation of the ICA
2. Best results in patient with Amaurosis Fugax
lll. Radiation induced carotid disease occurs in area not typical of carotid disease
mmm. Carotid Restenosis:
i. Early: May Regress, rare progression to occlusion
1. Early restenosis is usually secondary to the development of intimal
hyperplasia, and lesions that develop after several years are most
frequently due to disease progression or the development of new
atherosclerotic disease.
2. Myointimal Hyperplasia
3. Less prone to embolization
ii. Late: Recurrent Extrinsic Atherosclerosis, Stroke Risk
iii. Overall incidence of restenosis is reported to occur between 5-14%. Very
few of these patients were symptomatic.
iv. Specifically, early (0-3 months) restenosis events are usually related to
incomplete endarterectomy and/or clamp site injury while restenosis
occurring outside the perioperative period out to 3 years postoperatively
most often are due to neointimal hyperplasia.
a. Neointimal hyperplastic lesions result from platelet
aggregation along the endarterectomized surface of the
vessel which leads to recruitment of inflammatory cells
which activate vascular smooth muscle cells.
b. The vascular smooth muscle cells migrate and proliferate
and contribute to interaction with fibroblasts leading to
collagen deposition. These lesions are smooth and regular
in appearance which is different than de novo
atherosclerotic disease which is often more focal, irregular
and characterized by heterogeneous plaque features.
c. For restenosis events after 3 years, frequently development
of metachronous atherosclerotic disease is frequently
implicated.
nnn. For stent ultrasound the presence of indwelling stents may falsely elevate
measured velocities, thereby causing a false-positive result at the time of
screening.
2. Vertebral Artery:
i. Branches of the external carotid artery also serve as important collateral
pathways to the vertebral artery.
1. The V3 segment of the vertebral artery receives anastomotic branches
from the occipital artery (most commonly) and the cervical ascending
artery.
2. Persistent fetal communications may also serve as important anastomic
bridges between the carotid and vertebral systems. These fetal
connections include the trigeminal, hypoglossal, proatlantal, and otic
arteries. When these bridges exist, the vertebral or basilar artery are
usually hypoplastic or incomplete.
ii.

1. Vertebral arteries enter the transverse process at C6 as it dips under the

longus colli muscle, the Vertebral Artery proximal to this segment is
termed V1
2. Supraclavicular approach affords excellent exposure of the vertebral
artery at its origin, the exposure is relatively limited and requires
transection of the sternocleidomastoid muscle. The anterior cervical
approach does not require muscular transection, and it permits rapid
extension of the incision for vascular control of more distal vertebral
artery segments, thus is used for traumas.
iii. Supraclavicular Approach:
1.
2.

3. The external jugular vein is divided at the lateral border of the

sternocleidomastoid muscle. Division of the clavicular head of the
sternocleidomastoid muscle and retraction of the sternal head exposes
the underlying carotid sheath. The sheath is mobilized by vertical
dissection along the lateral border of the internal jugular vein. and the
omohyoid muscle is divided. When operating on the left side, the
thoracic duct should be ligated and divided near its termination of the
junction of the left internal jugular and subclavian veins
a.

b. The medial margin of the scalene fat pad is next mobilized, and
the fat pad is retracted laterally.
c. Mobilization of the fat pad exposes the underlying anterior
scalene muscle. The phrenic nerve is located on the ventral
surface of the anterior scalene muscle and is usually found
coursing near the muscle's medial border
d. The vertebral artery is located in the center of the angle formed
by the anterior scalene and longus colli muscles. The artery is
most easily identified and isolated by retracting the anterior
scalene laterally.
 e.
f. The inferior thyroid branch of the thyrocervical trunk and
vertebral vein should be ligated
4. Anterior Cervical Approach:
a.

b. The superior belly of the omohyoid muscle may be divided at

this point to achieve adequate expose me in the inferior aspect of
the wound.
c.

d. The carotid sheath and its contents are carefully freed by vertical
dissection along the lateral border of the internal jugular vein.
e. Avoid injury to the vagus nerve and sympathetic chain, which
course in the posterolateral aspect of the carotid sheath. Once
freed from surrounding tissue, the carotid sheath and its contents
are retracted medially
f. V2:
 i.

ii. The superior incision should be curved posteriorly at its

uppermost margin, such that it passes just inferior to the
lobe of the ear.
iii. The carotid sheath, pharynx, and larynx are next freed
from the prevertebral fascia by clearing attachments
between the visceral and prevertebral fasciae in the
retropharyngeal space
iv. This leaves the sympathetic ganglia lying on the
prevertebral muscles just medial to the bulge of the
transverse processes.
v.

vi. The anterior longitudinal ligament is exposed deep in the

medial wound . It is incised vertically over the vertebral
column for the length of the incision. A periosteal
elevator is used to separate the prevertebral fascia, longus
colli, and longus capitis muscles away from the vertebral
bodies and transverse processes. Avoid extending the
dissection beyond the lateral border of the transverse
processes to prevent injury to the cervical nerve roots
 vii.

viii. The artery is most conveniently controlled within the

bony canal rather than between the transverse processes
because of the multiple venous tributaries that surround
the artery in the latter.
ix. Because the V2 segment is located within the cervical
transverse processes, diseases of the V2 segment most
often require distal bypass to the V3 segment. The most
common pathology in the V2 segment is compression
from osteophytes, but it is also the most common location
for extracranial aneurysmal degeneration of the vertebral
arteries. It is also a frequent site of traumatic or
spontaneous AV fistulas.
g. V3: Artery in the space between transverse process of C1/C2
 i.

ii. Partial or complete detachment of the

sternocleidomastoid origin greatly enhances exposure.
Important to identify the spinal accessory nerve, which
usually enters the sternocleidomastoid 2 to 3 cm below
the mastoid The nerve should be mobilized and gently
retracted anteriorly.
iii. The tip of the transverse process of the atlas ( C1) should
be palpated in the superior wound deep to the digastric
muscle. It should be noted that the tip of the transverse
process of the atlas is anterior to the transverse process of
the axis (C2) due to head rotation. The prevertebral fascia
is next incised posteriorly from the transverse process of
C1 along a line parallel to the spinal accessory nerve.
 iv.

v. Once the spinal accessory nerve is retracted anteriorly,

the levator scapulae and underlying splenius cervicis
muscles are readily identified in the posterior wound.
These muscles cover the Cl and C2 interspace in which
the vertebral artery is most accessible.
vi. The anterior ramus of the C2 nerve root emerges from
under the anterior border of the levator scapulae and
serves as an important landmark in the safe division of
the covering muscles. A small retractor should be inserted
between the C2 nerve ramus and the muscles. The
retractor serves as a guide as the levator scapulae and
splenius cervicis muscles are divided as close to the
transverse process of Cl as possible. Excision of these
muscles over the Cl and C2 interspace will expose the
vertebral artery.
vii. The C2 nerve ramus will be noted to emerge behind the
artery and will require protection during arterial
manipulation. Many small venous tributaries enter the
vertebral vein posterior to the artery.
viii. Perform anastomosis to the VA first, and bring the vein
graft behind the jugular vein near the common carotid
artery.
h. V4: Between C1 and the base of the skull
 i.

ii. Prone positioning in the Park-Bench Position

iii. Incision from Mastoid Process to Midline of the Occipital
Protuberance
iv.

v.

vi. Trapezius, splenius capitis, semispinalis capitis, and

longissimus capitis muscles are divided. The greater
occipital nerve (dorsal ramus of C2) courses upward over
 the semispinalis capitis muscle and may require division
as it is encountered approximately lateral to the posterior
midline.
vii.

viii. The sternocleidomastoid muscle should be divided at its

mastoid insertion and reflected inferiorly. This will
expose the internal jugular vein and the accessory nerve
in the lateral wound.
ix. Palpate the Transverse process of C1 to identify the
obliquus capitis superior muscle, which attaches to the
superior margin of the bony prominence. The large
condyloid emissary vein should be ligated and divided
near the muscle's medial border.
1. Partial division of the rectus capitis posterior
major muscle lying in the medial wound will
expose a large venous plexus which overlies the
vertebral artery.
x.
 xi.

xii. Meticulous ligation and division of bridging vein

segments will allow the plexus to be dissected away from
the arterial adventitia. Branches of the suboccipital nerve
should be divided as they cross the vessels at this level.
xiii. Avoid injury to the ventral ramus of the C1 root, which
courses below the vertebral artery in this location.
 xiv.

xv. Distal internal carotid artery can be isolated in the lateral

wound for use as inflow.
1. The artery can be exposed in the plane medial to
the sternocleidomastoid muscle and isolated
between the hypoglossal and vagus nerves
i. The vertebrobasilar system is formed from the fusion of 2 sets of
vascular plexuses. Thus, there is considerable asymmetry of the
vertebral arteries.
j. The left vertebral artery is frequently larger and dominant.
k. The most common origin aberrancy of the left vertebral artery is
the separate aortic origin of the left vertebral artery. 
l. Hypoplasia of the vertebral artery, which occurs in 7-12% of
individuals, results in termination of the vessel in the posterior
inferior cerebellar artery or occipital artery.
m. Bifid vertebral arteries are associated with aneurysmal formation
and dissection.
n. The most common right vertebral anomaly is the origin from the
aortic arch.
i. It can arise from the right common carotid less commonly
and is usually accompanied by the right subclavian artery
retroesophageal aberrancy.
o. Bowhunter Syndrome: Dynamic compromise of the dominant
vertebral artery
i. Typically caused by vessel compression with next
extension by hypertrophic osteophyte, cervical
spondylosis, fibrous band or thickened alantoaxial
membrane
 i. Diagnose by angiogram with neck extension
ii. Treatment options:
1. Cervical fixation
2. Osseous or fibrous band decompression
3. Distal vertebral bypass if also concomitant arterial
disease
a. Use venous conduit
p. Ostial V1 segment stenosis:
i. Stenosis in the V1 segment of the vertebral artery
(origin) is usually atherosclerotic in nature.
ii. Patients who are symptomatic from microembolism
are candidates for repair.
iii. Options include transposition of the vertebral artery
to the adjacent carotid artery, a bypass using
saphenous vein or PTFE from the carotid or
subclavian artery to the vertebral artery, and rarely a
subclavian-vertebral artery endarterectomy.
1. Endovascular stents may be an option, but
large studies comparing open to
endovascular therapy are lacking.
Additionally, longer term durability of
stenting may be an issue with higher rates of
restenosis or stent-facture. At present, these
procedures should be reserved for select
patients.
q. The most commonly reported complication of proximal
vertebral artery reconstruction is a Horner’s syndrome
(ptosis and miosis) from disruption of the sympathetic
chain. This is often transient and occurs in up to 20% of
cases. 
i. Horner’s is more common than lymphocele
r. Vertebral Artery Dissection:
i. Most common cause of lateral medullary syndrome
in young adults
ii. Clinical presentation can be as benign as an
occipital headache and/or neck pain, as well as
posterior circulation ischemia
iii. Dissection typically occurs in the distal one third of
the vessel where mechanical traction and stretch is
maximal and often precipitated by trauma.
iv. The dissection can progress to intraluminal
thrombosis due to compression of the true lumen.
v. The dissection can also extend distally and obstruct
flow, compress cranial nerves, and result in
subarachnoid hemorrhage.
 vi. Atraumatic or spontaneous dissections can occur as
a result of hypertension or fibromuscular dysplasia
(FMD).
1. Those associated with FMD are typically
proximal and occur bilaterally.
vii. Patient should be started on anticoagulation therapy
with heparin and transition to NOAC.
1. This treatment is continued for 3-6 months
to permit healing of the dissection and
prevent propagation of potential thrombus.
2. However, in patients who are refractory to
anticoagulation and continue to have
symptoms, percutaneous stent therapy may
be of benefit.