Carotid endarterectomy

Carotid endarterectomy
Dr Dheeraj sharma
M.Ch CTVS 2nd yr. resident

Outline
• Anatomy of carotid arteries
• Basic pathology
• Epidemiology
• Indications and contraindications
• Investigations
• Treatment options
• Complications

THE INTERNL CAROTID ARTERY:
• The internal carotid artery is located within the carotid
triangle, under and deep to the stylohyoid muscle and the
posterior belly of the digastric muscle.
• The internal carotid arteries are direct continuations of the
common carotids superior to the origin of the external carotid
artery, at the level of the superior border of the thyroid
cartilage.
• The internal carotid does not give origin to any branches in
the neck, since its supply is limited to intracranial structures. It
is crossed laterally by the hypoglossal nerve.

THE EXTERNAL CAROTID ARTERY:
• The external carotid artery begins at the bifurcation of the
common carotid artery at C4. It continues upward to a point
posterior to the neck of the mandible (approximately 1.5 cm
below the zygomatic arch) where it bifurcates to form the
maxillary and superficial temporal arteries.
• The 8 variable branch arteries of the external carotid are:
maxillary, superficial temporal, superior thyroid, lingual, facial,
ascending pharyngeal, occipital, and posterior auricular
arteries.

CLINICAL CORRELATIONS
• The common carotid may bifurcate high at the level of the
hyoid bone, or lower at the level of the cricoid cartilage.
• Despite abundant collateral circulation of the common carotid
artery, unilateral ligation of the artery should never be done
unless it is absolutely necessary. Ligation of the common
carotid artery has been said to reduce the blood flow of the
internal carotid artery and, therefore, the supply to the brain
by approximately 50%.
• Ligation of the internal carotid artery should be absolutely
avoided. According to Dandy there was a death rate of 4%
following ligation of the internal carotid .

Etiology and basic pathology
• By far the most common causes of carotid artery obstruction
are:
1. atherosclerosis(most common)
2. fibromuscular dysplasia
3. intimal hyperplasia
4. radiation injury
• The CEA is indicated most commonly in patients with
atherosclerotic obstructive disease.

introduction
• Definition :
Atherosclerosis (art
eriosclerotic
vascular disease) is
a condition in which
an artery wall
thickens as a result
of the accumulation
of fatty materials.
• In
Greek, athere means
gruel, and skleros
means hard.

Epidemiology- ubiquitous among most developed
nations...’’lifestyle and diet disease’’
MAJOR RISKS LESSER OR UNCERTAIN RISKS
Nonmodifiable Obesity
•Increasing age Physical inactivity
•Male gender Stress (type A personality)
•Family History Postmenopausal estrogen def.
•Genetic Abnormalities High Carbohydrate intake
Potentially Controllable Lipoprotein (a)
•Hyperlipidemia Hardened (trans) unsaturated
fat intake
•Hypertension Chlamydia pneumoniae
infection
•Cigarette smoking
•Diabetes
Multiplicative
effect:
•2 risk factors
increase risk
fourfold
•3 risk factors
increase the rate
of MI seven
times!

Pathogenesis
• Response-to-injury hypothesis- 4 main stages
to atherogenesis:
1. Chronic endothelial injury
2. Accumulation of lipoproteins
3. Resultant Inflammation & Factor release
4. Smooth muscle cell recruitment, proliferation
and ECM production

Response-to-injury hypothesis
1) CHRONIC
ENDOTHELIAL INJURY :
– Hyperlipidemia
– Hypertension
– Smoking
– Homocysteine
– Hemodynamic factors
– Toxins
– Viruses
– Immune Reactions

2) Accumulation of Lipoprotein
in vessel wall
• Dyslipoproteinemia
• Other underlying disorder
that affects the circulating
levels of lipids :
• nephrotic syndrome,
alcoholism,
hypothyroidism, or
diabetes mellitus
• (1) increased LDL
cholesterol levels,
• (2) decreased HDL
cholesterol levels, and
• (3) increased levels of the
abnormal Lp(a)

4) Smc proliferation and
ecm production
 Intimal SMC proliferation and ECM
deposition convert a fatty streak to
a mature atheroma.
 Intimal SMC-proliferative, synthetic
phenotype
 Growth factors:
1. PDGF (platelets,
macrophages, ECs, and
SMCs)
2. FGF
3. TGF α.
 SMCs synthesize ECM (notably
collagen), which stabilizes
atherosclerotic plaques.
 Inflammatory cells in atheromas
can cause intimal SMC apoptosis,
and they also increase ECM
catabolism, resulting in unstable
plaques.

Mechanisms of Stroke
• There are two mechanisms by which strokes arise from atherosclerosis and
superimposed thrombotic occlusion of the internal carotid artery.
– Occlusion of the carotid may give rise to an embolus that passes distally in the
territory of its tributary vessels, downstream from the internal carotid artery
(middle and anterior cerebral arteries and their branches). This has been
termed artery-to-artery embolism.
– Occlusion of the carotid artery may lead to ischemia in the distal field
(watershed or border zone) in the region of lowest perfusion between its
major branch vessels. (less often)

Atherogenesis and Stroke
Development of fatty streaks, small subendothelial deposits of lipid.
Plaque consisting of a central lipid core bounded on its lumen side by an endothelialized fibrous cap
containing vascular smooth muscle cells (VSMC), and connective tissue
As the plaque grows, due to the process of positive remodelling, the vessel may expand, so that initially lumen
diameter is not compromised (large volume atherosclerotic plaques may coexist without significant luminal
stenosis and not be readily apparent on purely angiographic imaging modalities)
Clinical events are caused by rupture of the fibrous cap and by exposure of the highly thrombogenic lipid core to
the circulation, resulting in the rapid formation of thrombus
Vessel expansion when the plaque grows
Vessel stenosis
Rupture of fibrous cap and Thrombus formation
Plaque neovascularization, intraluminal hemorrhage
Fibrous cap Formation

Sites of Stenosis
• The region of the common carotid bifurcation and proximal
internal carotid artery is by far the most common site of
involvement.
• At this location, stenosis greater than 50 per cent is about two
to three times more common than complete arterial
occlusion.
• The common carotid can be occluded by an atheromatous
plaque at its origin, more often on the left side.
• Intracranial arterial stenosis or occlusion is uncommon.
Individually, the basilar, intracranial carotid, and proximal
circle of Willis arteries are each involved in 1 to 4 per cent of
patients.

Common Clinical Features of Carotid
Stenosis
• Symptoms:
– Transient ischaemic attack.
– Amaurosis fugax.
– Cerebral infarction.
• Signs:
– Carotid bruit: 40- 80%.
– Upper motor neuron lesions following cerebral infarction.
– Retinal infarctions/cholesterol emboli.

Classification
• carotid stenosis is generally classified as
– severe (70 to 90 per cent)
– moderate (50 to 69 per cent)
– mild (less than 50 per cent).
• Markedly severe stenosis causes slowing of internal carotid blood flow,
resulting in delayed filling of intracranial branches as compared with
extracranial ones

Radiological investigations
• Duplex ultrasound.
• CTA
• Magnetic resonance angiography (MRA).

Doppler ultrasound
• Doppler ultrasound is a major diagnostic technique for
evaluation of carotid stenosis.
• It is noninvasive, rapid and relatively low cost and is
reasonably sensitive and accurate in the evaluation of the
degree of carotid bifurcation stenosis.
• However, the technique does not provide anatomical detail of
the vessels within the neck.
Ultrasound image of the carotid artery bifurcation with
the ultrasound probe located in the proximal internal
carotid artery.

Doppler ultrasound
• It may be analyzed for pulsatility of the flow with periodical
increases and decreases in velocity and for the turbulence of
the flow, which shows red blood cells accelerating and
decelerating when an obstruction is encountered.
• The Doppler signal then spreads out—a process described as
"filling in the window beneath the curve"
• Turbulent currents are seen at obstructions within the vessel,
such as at an atherosclerotic plaque.

Doppler ultrasound
• It has a limited area of coverage and thus cannot see tandem
lesions or even isolated lesions within the distal internal
carotid artery near the skull base.
• Thus, while Doppler ultrasound is valuable in screening
patients with carotid vessel disease, its limitations require
complementary studies to provide information in instances
where Doppler ultrasound has major limitations.

Color Flow Duplex Scanning
• Flow direction through an individual pixel may be displayed as
a color.
• Typically, red is used to depict blood flow towards the brain
and blue is used to depict blood flow away from the brain.
• White usually denotes very high blood velocity at a stenosis.
• Increasing velocity may be displayed by a variation in colors.
• With this combination of Doppler and ultrasound techniques,
real-time noninvasive depiction of flowing blood within a
vessel is possible
Color flow duplex study of a high-grade stenosis with
white signal intravascularly denoting high velocity of flow
at the stenosis .

Indication For Ultrasound Doppler
1. A screening test for a carotid artery flow stenosis in a patient presenting
with
• an ipsilateral transient ischemic attack or completed stroke.
• the potential of multiple causes for these events.
2. In the postoperative follow-up of patients to detect evidence of
subclinical restenosis of an operative vessel.
3. Identify different components within atherosclerotic plaque.
– Low echogenicity may be seen in areas of thrombus or excessive
deposition of lipid.
– Calcium is particularly reflective. Small amounts of calcium within a
plaque are seen as a bright signal return.
4. The intraoperative assessment of carotid endarterectomy patients.
– Confirmation of resumption of flow after unclamping of the carotid
artery and the search for lumen irregularities or intimal flaps before
wound closure.

CTA
• In most cases, a diagnostic evaluation for
cerebral vascular disease can be performed by
using either MRA or CTA.
• CTA requires iodinated contrast agents to be
injected at a relatively high flow rate.
• Patients with renal disease may not tolerate
intravenous contrast agents.
• Motion artifacts remain a problem if the
examination is performed by using older CT
equipment

MR Angiography
• Magnetic resonance angiography (MRA) is a medical imaging
modality used to reveal the shape of vessels for diagnosis and
therapeutic purposes.
• It is non-invasive and provides three-dimensional (3D) data
sets as opposed to the planar or two-dimensional (2D)
projections of conventional x-ray digital subtraction
angiography (DSA)
• Contrast-enhanced MRA (CE MRA) uses contrast agents to
enhance the vascular lumen.

CE MRA
• In order to obtain high quality images with arterial- phase CE MRA the
timing of the contrast bolus and the rate of injection is crucial. The period
of preferential carotid enhancement is typically brief (e.g. as short as 5
seconds).
• Imaging too late can result in significant jugular venous contamination of
the images and poor carotid visualization.
• The optimal rate of contrast media injection has been shown to be
approximately 2 mL per second
• Injection of this 18-20 mL bolus of Gd-chelate contrast agent is followed
immediately by a 20 mL bolus of normal saline injected at the same rate (2
mL/sec) in order to flush the contrast agent rapidly through the arm veins
and superior vena cava.
• This helps to ensure that the full dose of contrast reaches the cervical
vessels in a uniform bolus.

Volume Rendering
• VR is a technique that displays all of the 3D data at once
• It reveals internal structures that would normally be hidden or omitted when using
surface rendering techniques.
• Frequently, 3D VR image displays of vascular anatomy provides excellent anatomic
information for surgical planning.
Volume rendered view of the aortic arch and branches

Virtual Intraluminal Endoscopy
• Virtual intraluminal endoscopy (VIE) is a recently developed technique for
assessing the inside of the vascular wall
• It combines the features of endoscopic viewing and cross-sectional volumetric
imaging and involves the generation of a sequence of perspective views calculated
from points (flight path) located within the vascular lumen.
Virtual endoscopy of the abdominal aorta guided by the vessel centerline (red line)

MRA - Pitfall
• The major discrepancy is that of overestimation of vessel
stenosis, increasing possibility of miscategorizing the lesion.
• Miscategorizing a lesion due to overestimation could result in
a patient undergoing invasive endarterectomy when in
actuality the degree of stenosis was somewhat less than 70%
if evaluated by catheter angiography
• In patients with severe high grade stenosis that result in a
flow void on the MRA that is misdiagnosed as total vessel
occlusion when in reality the vessel is patent
• MRA is contraindicated in patients who have cardiac
pacemakers or cerebral aneurysm clips or in those who have
undergone certain other medical procedures.
• In addition, MRA is highly motion sensitive. Many patients
require sedation.

MRA Vs catheter angiography
• Catheter angiography provides the reference gold standard
• Catheter angiography is an invasive procedure there are
measurable risks and complications associated with it.
– Clinical series have shown that reversible complications
occur in 1 – 14% of catheter angiograms and that
significant and often irreversible complications with severe
morbidity or mortality occur in between 0.5 and 1% of
cases

MRA vs CTA
MRA CTA
Lumen stenosis Accurate quantitation of vessel
lumen stenosis
Dense calcium deposits are present
within an atherosclerotic plaque at the
carotid bifurcation this may limit accurate
quantitation of vessel lumen stenosis
Post-traumatic
vessel injury or
dissection
MRA has the advantage of being
more specific for traumatic vessel
dissection since it detects the
presence of intramural hematoma.
Unable to detect the presence of
intramural hematoma.
Satefy in Trauma Since many trauma patients may be
unable to give a proper history, MR
safety considerations may preclude
use of MRA in the acute situation.
There are not the critical safety concerns
with CTA.
Availability Less rapidly available More rapidly available in many
emergency

RECOMMENDATIONS
• If CDU suggests carotid stenosis, then MRA is the best non invasive confirmatory
test, whereas CTA should be used when CDU detects carotid occlusion.
• Iodine contrast may limit CTA in patients with renal insufficiency or cardiac failure.
• Conventional angiography remains the gold standard, although most centres will
recommend surgery on the basis of duplex ultrasound findings alone.
• The argument against the routine use of angiography is the low but recognized
complication rate. In patients with asymptomatic stenosis, the risk is
approximately 1%.
• Doppler carotid ultrasound has very rarely reported to cause stroke, presumably
because of dislodgement of plaque by the transducer.
• A practical approach to assess the degree of carotid stenosis would be CDU
combined with either CTA or MRA.
• Rather than using catheter or conventional angiography as the first test, it could be
used to resolve equivocal findings, especially to resolve occlusion versus near-
occlusion.

ASSESSMENT OF DEGREE OF STENOSIS BY
VARIOUS METHODS
• NASCET and ECST used conventional cerebral angiography, whereas the
Asymptomatic Carotid Atherosclerosis Study (ACAS) and the Asymptomatic Carotid
Surgery Trial (ACST) used carotid duplex ultrasound.
• The results of meta-analyses of computerized tomographic angiography (CTA),
magnetic resonance angiography (MRA) and colour duplex ultrasound (CDU) are
shown

Descision making of carotid artery
disease in different subgroups

In Asymptomatic Patients
• Asymptomatic can refer to absence of symptoms in the
carotid hemisphere ipsilateral to the carotid disease, the
anterior circulation, or any brain/brainstem origin.
• Two trials:
1. Asymptomatic Carotid Atherosclerosis Study (ACAS)
2. European Asymptomatic Carotid Surgery Trial (ACST)

• Carotid Endarterectomy Trial Outcomes:
• Both the ACAS and the ACST demonstrated a benefit of CEA
with medical therapy (aspirin and atherosclerotic risk factor
reduction) over medical therapy alone for patients with
carotid stenosis in the 60% to 99% range.
• The relatively benign natural history of asymptomatic carotid
stenosis is an important take-home message from ACAS and
ACST. The overall stroke risk in patients managed with medical
therapy alone is on the order of 2%/yr. This means that
although CEA was shown to be of benefit, the benefit is
relatively small and dependent on patient selection.

Study Degree
of
Stenosis
(%)
Number
of
Patients
Endpoin
t
Medical
Event
Rate (%
Surgical
Event
Rate (%)
Absolute
Risk
Reductio
n (5
Year) (%
Relative
Risk
Reductio
n (5
Year) (%)
ACAS 60-99 1662 IPSILATE
RAL
STROKE
11.0 5.1 6.1 53
ACST 60-99 3120 ANY
STROKE
11.8 6.4 5.4 46

• RECOMMENDATION FOR CEA :
• Patients should be at low risk for perioperative adverse events
and have a reasonable life expectancy (at least 5 years or
longer).
• If perioperative combined event rates are higher than 3% or if
patients with limited life expectancy undergo intervention (or
both), it is likely that more strokes could be caused than
prevented by intervention.

In Symptomatic Patients
• patients with recent ipsilateral carotid territory symptoms.
• Trials:
1. NASCET(The North American Symptomatic Carotid
Endarterectomy Trial Collaboration (NASCET) (1991) )
2. ECST(European Carotid Surgery Trialists Collaborative Group
1991)

NASCET TRIAL
• symptomatic patients have a fourfold higher risk for
perioperative stroke or death than do asymptomatic patients
(6.5% versus 1.5%).
• In NASCET, the medically treated group with 70% to 99%
stenosis had a 26% risk for ipsilateral stroke within 2 years.
The 17% absolute stroke risk reduction at 2 years achieved by
CEA in symptomatic patients with greater than 70% stenosis
• there was a significant benefit for patients with stenosis in the
50% to 69% range, but the benefit was less than that for those
with higher degrees of stenosis.Patients with less than 50%
stenosis did not benefit from CEA

RESULTS
Study Degree
of
Stenosis
(%)
Number
of
Patients
Endpoin
t (Time
and
Event)
Medical
Event
Rate (%)
Surgical
Event
Rate (%)
Absolute
Risk
Reductio
n (%)
Relative
Risk
Reductio
n (%)
NASCET 70-99 659 2 YR
IPSILATE
RAL
STROKE
26 9.0 17 65
ECST 80-99 576 3 YR
IPSILATE
RAL
STROKE
20.2 6.8 13.8 67
NASCET 50-69 858 5 YR
IPSILATE
RAL
STROKE
22.6 15.7 6.5 29

Recommendations Of NASCET, ECST:
1. CEA is indicated for symptomatic patients with stenosis of 70-
99%, this is valid only for centres with a perioperative
complication rate (all strokes and death) less <6% (level I).
2. CEA may be indicated for some patients with stenosis of 50-
69% without a severe neurologic deficit; this is valid only for
centres with a perioperative complication rate (all strokes and
death) less <6%; males with recent hemispheric symptoms are
the subgroup of patients most likely to benefit from surgery
(level I).
3. CEA is not recommended for patients with stenosis less <50%
(level I).
4. CEA should not be performed in centres not exhibiting equally
low complication rates like NASCET or ECST.
European Stroke Initiative
Recommendations for Stroke Management, 2002

Patient Characteristics and Outcome
for Intervention Decision Making
Characteristic Outcome*
Female gender Lower risk for stroke with medical therapy
Higher risk for stroke or death with CEA
Age >75 Higher risk for stroke with medical
therapy in symptomatic patients
Increasing degree of stenosis over 50% Higher risk for stroke with medical
therapy in symptomatic patients
Contralateral carotid occlusion Higher risk for stroke or death with CEA
Increasing time from TIA/stroke Lower risk for stroke with medical therapy
Ocular symptoms only Lower risk for stroke with medical therapy
Lower risk for stroke with CEA

Timing of Intervention
• It has been suggested that a much more aggressive approach
(i.e., within 48 hours) is necessary for symptomatic patients.
• the risk for a new or recurrent stroke may approach 7% in 2
days and 10% within 7 days of the initial event.
• Operative risk is probably elevated with very early
intervention.
• In patients who are medically stable and have relatively small
or no infarcts seen on imaging studies, it seems reasonable to
perform early intervention (i.e., within 48 hours) after a
stroke.

TREATMENT OPTIONS
• MEDICAL
• SURGICAL: CEA / CAS

MEDICAL MANAGEMENT
• Antiplatelet Therapy
1. Meta-analyses of antiplatelet therapy trials published by the
U.K. Antithrombotic Trialist Group in 1994 and 2002
concluded that antiplatelet therapy significantly reduces the
incidence of stroke in high-risk patients, with a resultant 25%
reduction in strokes overall.
2. The risk for perioperative stroke and death was 1.8% in
patients taking 650 to 1300 mg ASA daily versus 6.9% in
patients taking 0 to 325 mg daily.

• Heparin
1. Heparin has been administered as therapy for acute stroke or
crescendo TIAs to patients before undergoing CEA. The
International Stroke Trial did not find any benefit of routine
heparin administration for acute stroke because of increased
numbers of hemorrhagic stroke and fatal extracranial
bleeding.
2. Unfractionated heparin is routinely used intraoperatively to
prevent carotid thrombosis despite a lack of level I evidence
to support this practice. The combination of aspirin and
intraoperative heparin administration appears to be
especially effective in preventing thrombosis.

• Protamine Administration:
1. This trial demonstrated significantly reduced wound drainage
with protamine but a trend toward an increased rate of
stroke and death from carotid thrombosis.
2. In a recent publication of observations of protamine use
during the GALA trial (General Anesthesia versus Local
Anesthesia for carotid surgery), protamine was not found to
be associated with stroke

• Dextran:
1. Dextran is a polysaccharide that inhibits platelet
aggregation. It has been used to control embolic episodes
both preoperatively and postoperatively.
2. In a follow-up study they found that a 3-hour infusion
was just as effective as a 6-hour infusion.

• Statins:
1. A reduction in cholesterol levels with statins may be
associated with plaque regression .
2. statin medications to be highly effective in primary and
secondary stroke prevention.
3. statins are associated with a reduced rate of perioperative
cardiac morbidity and overall mortality in patients
undergoing major vascular surgical procedures.
4. In a series of nearly 1600 patients undergoing CEA, statins
were associated with a reduced 30-day incidence of stroke
(1.2% versus 4.5%, P < .01), TIA (1.5% versus 3.6%, P < .01),
and mortality (0.3% versus 2.1%, P < .01).

SURGICAL TREATMENT
• INDICATIONS:
• CEA should be attempted in any patient with carotid stenosis in whom
surgery will improve the natural history of disease to a degree more than
that by medical treatment.
IN SYMPTOMATIC PATIENTS:
1. One or more TIA’s in past 6 months and carotid artery stenosis exceeding
50%.
2. Ipsilateral carotid artery stenosis more than 70% combined with CABG.
3. Progressive stroke and carotid artery stenosis more than 70%.
IN ASYMPTOMATIC good risk patients treated by surgeon with surgical
mortality and morbidity of less than 3% the proven indication for CEA is
stenosis more than 60%.

• CONTRAINDICATIONS:
CEA is contraindicated if patients general condition includes a
serious illness that will substantially increase perioperative
risk and shorten the life span.
Also contraindicated in patients presenting with acute major
stroke with minimal recovery and altered sensorium. In acute
stage the the ischemic infarct may be converted to
haemorrhagic infact leading to death.

Grading of patients undergoing carotid
endarterectomy

Factors associated with increased risk of
perioperative death and stroke
• Most authorities accept that contralateral carotid occlusion
and age >75 years increase the risk of perioperative stroke.
• In NASCET, medical complications such as myocardial
infarction, arrhythmia, congestive heart failure and sudden
death were 1.5 times more likely in patients with a history of
myocardial infarction, angina or hypertension (P < 0.05)

Surgical Technique
• Anesthetic Considerations And Positioning
• Operative Procedure
• Intraoperative Monitoring And Shunt Use
• Patch Angioplasty
• Postoperative Care
• Complications Of Endarterectomy

ANESTHETIC CONSIDERATIONS AND
POSITIONING
• Most surgeons perform carotid endarterectomy with
the patient under general anesthesia
• The principal goals of anesthetic management are to
maintain adequate cerebral and myocardial
perfusion.

Positioning
The patient is placed in the supine position with the head turned
away from the side of the operation with a small roll beneath the
shoulder
Atherosklerotic Chatper 25,Ruherford’s
Vascular Surgery,7th ed

Skin incision
• Two types of skin incision were used:
1. A standard longitudinal incision : parallel to
medial border of SCM.
2. A transverse skin crease incision usually 1-2
cm inferior to angle of jaw. Associated with
excellent cosmetic result. But is difficult to
extend caudally and cranially.

Outline of the procedure
• Vertical incision at the medial border of the sternocleidomastoid.
• Common, internal and external carotid arteries are dissected free and taped.
• Carotid sinus is blocked with lignocaine.
• Arteries above and below the diseased segment are clamped.
• Arteriotomy is made through the diseased segment into the normal vessel above
and below.
• Intraluminal Javid shunt is then inserted into the common carotid vessel and
internal carotid artery through the arteriotomy, to allow cerebral circulation to
continue
• Plane between the plaque and arterial wall is developed.
• Full extent of the plaque is removed.
• Distal intima is tacked down.
• Clamps are reapplied and the shunt removed.
• Arteriotomy is closed with a patch.

OPERATIVE PROCEDURE
• The patient is placed in the supine
position with a small roll beneath the
shoulder and the head turned away
from the side of the operation.
• The incision runs along the anterior
border of the sternocleidomastoid
muscle and curves posteriorly 1 cm
below the angle of the mandible to
avoid injury to the facial nerve.
• The platysma is incised, and the
dissection is carried along the medial
border of the sternocleidomastoid
muscle.
• Keep the medial blade of self-retaining
retractors in the superficial layers of the
wound (deeper placement can cause
injury to the recurrent laryngeal or
superior laryngeal nerve.)
•Beneath the sternocleidomastoid muscle,
the internal jugular vein is encountered.

Zollinger RM Jr,Zolinger RM Sr: Zollinger’s
atlas of surgical Operations *th edition

• The vagus nerve> vocal cord
paralysis.
• The hypoglossal nerve > deviation
of the tongue and dysphagia.
• The ansa hypoglossi branches
from the hypoglossal nerve >
sacrificed without significant
consequence
• The carotid body > hypotension
and bradycardia, cardiovascular
effects that can be blocked
effectively by injecting the carotid
body with 1% lidocaine.
• The facial nerve is at the most
cephalad extent of the incision
and should be well out of the
field anteriorly.

• The common facial branch of this vein,
which courses medially, is doubly
ligated and divided, and the vein is
gently retracted laterally
• The carotid artery can be gently
palpated, and the carotid sheath is
visible.
• The carotid sheath is opened inferiorly
along the anterior surface of the artery
to the level of the omohyoid muscle.
• The superior thyroid artery, the first
branch of the external carotid, was
next isolated.
• Dissection is then completed around
the external carotid artery and
superior thyroid artery, which are
isolated with vessel loops.

• Proximal control of the common carotid artery
is obtained by careful dissection of the
posterior wall from the underlying vagus nerve
and passage of a vessel loop
• A Rumel tourniquet is fashioned by
placing the umbilical tapes on the internal
carotid and common carotid arteries
through a segment of rubber tubing.
• The hypoglossal nerve was located by following
the ansa hypoglossi upward across the carotid
bifurcation
• The hypoglossal nerve crosses the distal
internal carotid artery.
• It can be mobilized and gently retracted
medially for better distal exposure.
• All vessels were isolated and encircled with
vessel loops.
• The area between internal and external carotid
artery was not dissected, leaving the carotid
sinus nerve intact.

• Before manipulation of the carotid artery in
the region of the bifurcation, lidocaine (2
per cent Xylocaine) without epinephrine is
instilled into the carotid sinus and along the
course of the nerve of Hering to minimize
bradycardia and hypotension resulting from
stimulation of these structures.
• The patient was anticoagulated with IV
heparin, 100 units/kg .
• The blood pressure is maintained at or
slightly above awake baseline, and the
electroencephalography results are
examined
• The shunt tubing is filled with heparinized
saline and clamped to ensure that there are
no intraluminal bubbles, and it is compared
with the internal carotid artery to ensure
proper sizing.
• The internal carotid artery is clamped first
to prevent any embolic episode. Artery is
clamped distal to plaque and it is of bluish
colour in plaqued region.
• The common carotid artery is then clamped
and the external carotid artery and superior
thyroid artery are clamped.

The clamp test:
• If LA or intraoperative EEG is used for selective shunting then
a clamp test distal to ICA has to be applied for at least 3
minutes to check for changes in neurologic examination and
EEG pattern.
• If such changes occurs then the artery should be unclamped
to allow reperfusion before reclamping and opening carotid
artery to place a shunt as shunt placement take 2-3 min and
cannot be done on already ischemic brain.

• An arteriotomy is started about 1 cm
proximal to the bifurcation in the midline of
the common carotid artery using a #11 blade
• The electroencephalogram is again examined
to determine whether shunt placement is
necessary
• If no changes have occurred, dissection is
carried distally along the plaque is completed
with an angled Pott’s scissors (along the
anterior midline of the internal carotid artery
)
• Dissection must be carried to at least 1 cm
distal to the end of the plaque to allow for
posterior wall extension and placement of a
shunt, if necessary
• The incision is carried through the arterial
wall until plaque is encountered, and a
smooth plane is developed between plaque
and artery wall.

• The shunt was inserted into the distal internal carotid
artery, taking care not to cause a dissection of the
intima or embolization of debris distally.
• The proximal end of the shunt was placed in the
common carotid artery and distal blood flow was
reestablished.

• carefully separate the plaque from the media, starting
proximally with circumferential dissection of the
plaque.
• A curved clamp is placed between plaque and artery
wall, and the plaque is sharply incised with a scalpel.
• Care must be taken to ensure that the remaining
plaque in the common carotid artery has a smooth
edge
• The plaque is then dissected free from the arterial
wall with the Penfield dissector to the bifurcation and
into the external carotid artery.
• It is often helpful to have the assistant temporarily
release the external carotid artery clamp as dissection
proceeds up that artery and the plaque is gently torn
free from its distal attachment.
• The line of cleavage is within the media, leaving the
adventitia and media externa for closure.

• Division of the proximal plaque was completed from
the lateral side.
• The plaque was separated from the vessel wall up to
the bifurcation
• A critical part of the dissection involves the distal
attachment of the plaque to normal intima of the
internal carotid artery.

• The plaque was dissected distally to normal intima.
• Note the manipulation of the shunt to allow clear
visualization.
• By gentle dissection and proximal traction on the
plaque (eversion endarterectomy), it will usually tear
away from its distal attachment.
• The orifice of the vessel was probed with a small
probe to remove any remaining plaque.
• If the intima at this site is not adherent, it should be
further resected or, less commonly, tacked to the
arterial wall with a 7-0 Prolene suture.
• The vessel is shown after removal of the plaque.

• tacking sutures to prevent
subintimal dissection. Double
armed 7-0 polypropylene sutures
were used to tack the distal
intima to the media and prevent
distal dissection
Zollinger RM Jr,Zolinger RM Sr:
Zollinger’s atlas of surgical
Operations 8th edition

• The surface of the exposed media was carefully washed
with heparinized saline and inspected under 3.5X
magnification to wash away debris and ensure that there
were no wisps of loose material.
• A collagen impregnated dacron patch was sutured with
6-0 polypropylene to the edges of the arteriotomy
starting at the distal corner.
• Suturing of the medial wall of the patch was completed.
• The lateral wall was closed, leaving a 4 mm gap through
which the shunt could be extracted.
• Note the stabilization of the vessel wall in preparation for
removal.

• The distal end of the shunt was removed first.
• Just before final suturing at the proximal end of the
arteriotomy, the internal carotid artery clamp is briefly
released
• The resulting backflow of blood ensures that the artery is
patent and flushes any residual debris from the lumen.
• The lateral suture line was completed.
• The superior thyroid artery clamp is removed as the final
suture is placed in order to have continuous backflow of
blood.
• The clamps are then removed in the following order:
– external carotid artery
– common carotid artery
– internal carotid artery
• This sequence ensures that any potential embolic material
is flushed into the external artery circulation.

• Thrombin-soaked cellulose foam was applied to the
vessel to seal any residual needle puncture sites, and
gentle pressure is applied to the wound with a sponge
for about 1 minute.
• Meticulous hemostasis is maintained during closure;
occasionally, a small drain is placed in the superficial
wound.
• The vagus nerve is seen posteriorly between the carotid
and internal jugular vein.

• Ultrasound was standing by for intraoperative
assessment of the repair.
• The sterily wrapped ultrasound head was applied to the
distal internal carotid artery.
• Duplex scanning showed a good caliber vessel with good
flow, normal velocity and no intimal flaps.
• A closed suction drain was placed for 24 hours.
• The closed incision is shown.

Eversion endarterectomy
• Two different versions of eversion endarterectomy are
performed.
• DeBakey originally described eversion endarterectomy with
partial transection of the anterior portion of the carotid
bifurcation.
• Etheredge improved on DeBakey’s technique with complete
transection of the bifurcation,which allowed the origins of
both the ICA and ECA to be everted for a longer distance.

• The endarterectomy is performed by mobilizing the entire
circumference of the carotid adventitia off the plaque
(described as a “circumcision” by Etheredge) and then
everting the adventitia and mobilizing it upward while gentle
caudad traction is applied to the plaque.
• This maneuver is performed distally into the orifices of
the ICA and ECA and then proximally into the CCA.
• Once the endarterectomy is complete, the divided
bifurcation is reunited with a simple end-to-end
anastomosis.

• Advantages of this technique are that the anastomosis can be
performed rapidly and it is not prone to restenosis, and
therefore patching is not required.
• Disadvantages:
1. more extensive dissection is sometimes necessary to
mobilize the vessels during the eversion,
2. the procedure does not lend itself readily to shunting
(although shunting is not precluded by this technique).
3. it can be difficult to visualize the endpoint in the ICA after
the plaque has been removed; the artery tends to retract as
soon as the plaque pulls away from the adventitia.

• Kieney’s modification:
1. A modification of eversion endarterectomy in which the
origin of the ICA is excised obliquely off the carotid
bifurcation, the ICA is inverted on its own, and
endarterectomy of the CCA and ECA is performed through
an arteriotomy in the side of the carotid bifurcation.
2. This technique allows rapid plaque extraction, the
anastomosis is not prone to restenosis, and no prosthetic
material is required. This technique is particularly
effective for dealing with redundant, coiled, or kinked
ICAs.

Comparison of Conventional and
Eversion Carotid Endarterectomy
• EVEREST (EVERsioncarotid Endarterectomy versus Standard Trial
study), a randomized prospective multicenter study performed in
Italy that was published in 1997.
• There were no statistically significant differences in outcomes
between the two techniques, although a slightly higher incidence of
perioperative complications was noted with eversion CEA and a
slightly higher incidence of restenosis with standard CEA.
• EVEREST trial demonstrated that patients who underwent eversion
CEA had a lower incidence of restenosis than standard CEA (patch
and primary closure), but standard CEA with patch angioplasty had
the lowest incidence of neurologic complications and the lowest
rate of restenosis—1.5% —versus 2.8% for eversion CEA and 7.9%
for standard CEA with primary closure.

Exposure for High Lesions
• The carotid bifurcation can be located anywhere between the
second and seventh cervical vertebrae.
• a bifurcation located high in the neck poses technical
challenges that can increase perioperative risk for stroke and
cranial nerve injury.
• Ideally, one will recognize a high bifurcation on the
preoperative imaging study. This is a potential advantage of
CTA, in which bony anatomy is always included in the images.

Methods for exposure of high lesions
1. Nasotracheal Intubation:
With the patient’s mouth closed, the vertical ramus of the
mandible is displaced anteriorly 1 to 2 cm relative to its position
when the mouth is open with an oral endotracheal tube.
2. Division of the Digastric Muscle:
The next step to enhance distal exposure is to divide the posterior
belly of the digastric muscle.
Nerves that can be injured high in the neck are the spinal
accessory nerve, which enters the tendinous portion of the
sternocleidomastoid muscle, usually in the upper third of the
muscle, and the glossopharyngeal nerve and hypoglossal nerve,
which lies deep to the digastric muscle.

• Resection of the Styloid Process:
This maneuver alone permitted exposure of the ICA all the
way to the skull base. The insertions of the muscles on the
styloid process are excised and the styloid process is carefully
resected .
• Anterior Subluxation of the Mandible:
Anterior subluxation of the mandible requires placing the
mandible in temporary intermaxillary fixation.

Cerebral Protection and Monitoring
1. SHUNTING
2. CEREBRAL MONITORING
3. STUMP PRESSURE MEASUREMENT
4. AWAKE ENDARTERECTOMY UNDER RA/LA.

Shunting
• It is long standing debated issue regarding the use of
intravascular shunts: routine nonuse of shunts, selective use
of shunts, and routine use of shunts.
• Routine nonuse of shunts: small incidence of stoke, and the
etiology of the stroke is intraoperative cerebral ischemia
during carotid artery clamping.
• Routine use of shunts: incidence of stroke was attributed to
technical problems related to use of the shunt.
• Selective use of shunts: is to use shunts selectively in patients
who would be at high risk for ischemic stroke if a shunt were
not used.

• Techniques to identify candidates for selective shunting:
1. intraoperative measurement of carotid “stump
pressure” after the CCA and ECA have been clamped.
2. intraoperative neurologic monitoring of the patient’s
electroencephalogram or somatosensory evoked
potentials (SSEP), measurement of MCA flow by TCD.
3. monitoring with cerebral oximetry.

• The etiology of intraoperative stroke may be ischemic or
embolic.
• Placing a shunt has the capacity only to prevent ischemic
stroke, and it could actually increase the risk for embolic
stroke if performed poorly.
• This should translate into prevention of stroke in these
patients if embolic complications related to shunt placement
are minimized. In fact, there is evidence that the benefits of
shunting outweigh the risks in these patients.

Cerebral Monitoring
• The majority of CEAs are performed today under GA, and
strategies to assess cerebral ischemia include stump pressure
measurement; EEG, TCD, and SSEP monitoring; and
measurement of regional blood and cerebral oxygen
saturation.
• By using these criteria, shunt use can be minimized.

Stump Pressure
• Measurement of carotid stump pressure was the first method
used to predict intraoperative ischemia.
• In patients with measured stump pressures lower than 50
mm Hg, Hays and colleagues noted a 50% neurologic event
rate in those who were not shunted versus a 10% rate in
those who were.
• Harada and associates found that a stump pressure lower
than 50 mm Hg had a positive predictive value of only 36%.
• even in the setting of what appears to be a satisfactorily high
stump pressure, there may still be regions of the brain that
are relatively hypoperfused.

Electroencephalographic and Somatosensory
Evoked Potential Monitoring
• Intraoperative EEG monitoring is the most widely used
method of intraoperative cerebral monitoring.
• It can be performed by using 8, 12, or 16 leads, with the 16-
lead configuration being standard.
• Standard criteria for intraoperative ischemia are at least a 50%
decrease in fast background activity, increase in delta wave
activity, or complete loss of EEG signals.
• electroencephalography is overly sensitive—positive in 10%
to 40% of patients with unilateral carotid disease and positive
in as many as 69% with bilateral carotid disease,thereby
overestimating the number of people who require shunts.

• several series have documented neurologic events that
occurred in the absence of EEG abnormality when shunting
was not used.
• Tempelhoff and associates found that 5 of 6 patients with
postoperative deficits in a series of 103 patients showed EEG
changes only late in the operation, when shunting was no
longer feasible.
• In a meta-analysis of 15 studies, Wober and colleagues found
that SSEP monitoring is not a reliable means of detecting
ischemia and predicting neurologic outcome.

Transcranial Doppler
• Transcranial Doppler was introduced by Schneider and
coworkers in 1988.
• Normal TCD findings one could safely avoid shunting in a
third of patients but that abnormal findings on TCD predicted
ischemia by EEG criteria only 60% of the time.
• TCD has the unique advantage of detecting microemboli
intraoperatively.
• Belardi and associates also reported that TCD (as well as
stump pressure) was not accurate in predicting cerebral
ischemia.

Awake Carotid Endarterectomy with Regional
or Local Anesthesia
• Performing CEA under RA is the most reliable method of
predicting the need for selective shunting.
• the decision to shunt is based solely on the development of
hemispheric or global neurologic symptoms after the carotid
artery is clamped.
• This criterion is considered the gold standard for selective
shunting.
• Shunt rates are consistently lower than with other modalities,
on the order of 5% to 15%.

• ADVANTAGES:
1. a lower rate of myocardial infarction.
2. significant decrease in the neurologic event rate.
3. decreased length of stay.
4. cost-effectiveness
• DISADVANTAGES:
1. Unfamiliarity with technique as cervical block is a advance
technique.
2. Poor tolerance by patients.
3. risk of seizure or cardiac arrhythmia with inadvertent
administration of local anesthetic into the carotid artery or jugular
vein.

Arteriotomy Closure
• Simple primary closure
• Patch closure or patch angioplasty.

Primary closure
• primary closure of a longitudinal arteriotomy can result in
significant stenosis of the vessel, yet this is the simplest and
most efficient way to close an arteriotomy

PATCH ANGIOPLASTY
• The routine use of vein or synthetic patch angioplasty in
carotid endarterectomy has been advocated.
• Angioplasty provides theoretical advantage compared with
direct closure by maintaining a larger lumen and improving
flow patterns at the distal end of the arteriotomy, thus
limiting acute occlusion or restenosis at this site
• Patch angioplasties require additional cross-clamping time
and are susceptible to aneurysmal dilatation and rupture,
especially patches from smaller veins.
• Types of patch used:
1. Vein patch
2. Synthetic patches: PTFE, woven polyester (Dacron), and
bovine pericardium

Vein Patches
• the surgeon’s choices for patch material included saphenous
vein or external jugular vein.
• Imparato used vein patching routinely as early as 1965
• Saphenous vein patching has been used extensively with good
results, but problems specific to saphenous vein patching
include wound complications at the harvest site, potential
compromise of a valuable conduit for later bypass procedures,
and the devastating complication of patch rupture, which has
been reported to occur in 0.5% to 4% of cases.
• Lord and coworkers also noted that aneurysmal expansion of
saphenous vein patches can occur in up to 17% patients.

• Archie found that by using a GSV with a distended vein
diameter of greater than 3.5 mm and maintaining a carotid
bulb diameter of less than 13 mm, patch rupture was
completely avoided.

Comparative Analyses
• The British Joint Vascular Research Group RCT compared 104
patients undergoing primary closure with 109 patients treated
by patch closure with either autologous vein or Dacron.
• Six strokes occurred in the primary closure group and two in
the patch group, and six perioperative thromboses were
noted in the primary closure group versus none in the
patched group. At 1 year there were 17 occlusions of greater
than 50% stenosis in the primary closure group versus 6 in the
patch group.
• AbuRahma and colleagues found a significantly higher
perioperative stroke rate for primary closure than for patching
(4% versus 0%).

• Rockman and coworkers reviewed outcomes with primary
closure versus patch angioplasty or eversion endarterectomy.
• Perioperative stroke was significantly more common with
primary closure than with eversion or patching (5.6% versus
2.2%, no difference between eversion and patching), as well
as higher perioperative stroke rates and death with primary
closure than with eversion or patching (6% versus 2.5%).
There were no differences in any outcomes between eversion
and patching.

Optimal Patch Material
• Grego and colleagues compared the results of patching with
external jugular vein and PTFE and reported no difference in
stroke-free survival at 12, 30, and 60 months and no
difference in recurrent stenosis rates, but a trend toward
improved results with vein patch.
• Marien and associates performed an RCT in which bovine
pericardium was compared with Dacron patch and observed
significantly less suture line bleeding with bovine pericardium
than with Dacron (4% versus 30%) and no difference in
neurologic outcomes.

• AbuRahma and colleagues examined the outcomes of primary
closure versus patching with GSV, jugular vein, and PTFE.
• They found that perioperative neurologic event rates were
significantly higher with primary closure than with all patch
methods
• . Event rates were slightly higher with jugular vein patches,
and recurrent stenosis was also higher in this group than in
the GSV or Dacron patch group and similar to primary closure.
• In a follow-up study 2 years later, they reported that primary
closure had a higher incidence of restenosis and need for
reoperation, especially in women who had smaller carotid
arteries.

• AbuRahma and associates found a higher stroke rate with
Dacron that was largely due to perioperative thrombosis.
• As a result of this trial the manufacturer of the Dacron patch
re-engineered it.

Completion Studies
• To minimize the risk of thromboembolism or carotid artery
thrombosis resulting from technical imperfections in repair of
the carotid artery, intraoperative completion studies have
been used.
• Including continuous wave Doppler, duplex ultrasound, and
intraoperative angiography.
• Intraoperative angiography has been considered the gold
standard of completion studies.
• options for angiography include “single-shot” exposure on a
flat plate of x-ray film performed through a needle in the CCA
or fluoroscopic studies with a portable C-arm or even a fixed
fluoroscopy unit.

Perioperative Stroke Management
• Mechanisms can be grouped in decreasing order of frequency
as postoperative arterial thrombosis and embolization,
cerebral ischemia during carotid clamping, and intracerebral
hemorrhage.
• Perioperative carotid arterial thrombosis most often results
from technical imperfection in performance of the operation,
such as disruption of the intima during placement of the
intraluminal shunt, residual intimal flaps or atheromatous
disease, or residual luminal thrombus.

Intraoperative management
• A patient undergoing CEA under GA should be awakened in the operating room
immediately after wound closure, and a neurologic examination performed.
• new focal central neurologic deficit is identified, the artery should be immediately
re-evaluated. The incision is opened, and the ICA is checked for a pulse and flow
with Doppler
• If flow appears to be present, the surgeon should perform duplex ultrasonography
or arteriography to identify a potential correctable etiology.
• if the ICA does not have flow or if duplex/arteriography identifies a local defect,
the endarterectomy must be re-explored.
• Intracranial imaging should be included if no cause is found at the endarterectomy
site because a distal embolus is potentially treatable by thrombolysis or
extractable via microcatheter techniques.

• If acute thrombosis of the endarterectomy site is identified,
meticulous search for a technical defect, such as a distal
intimal ledge, should be performed after careful
thromboembolectomy.
• If there is a local flap, platelet accumulation, or other problem
within the endarterectomy, it should be corrected. Correction
may involve extending the endarterectomy, performing a
patch angioplasty if not initially carried out, or resecting the
vessel and replacing it with a bypass graft.

Postoperative stroke management
• If the patient awakens neurologically intact in the operating room and
then a new deficit develops in the recovery room or later postoperatively.
• Initially, the patient should undergo Duplex ultrasound if it can be
performed rapidly. If this testing indicates occlusion of the vessel or
abnormal flow velocities suggestive of an intimal flap or other anatomic
deficit, the patient should be immediately taken to the operating room for
re-exploration.
• If the noninvasive studies are negative and thus suggest a patent vessel,
head computed tomography (CT) should be performed immediately to
rule out a cerebral hemorrhage. If negative, carotid angiography should be
performed to identify any technical defect requiring revision at the
operative site or a possible intracerebral embolus.

• The availability of intracerebral catheter-directed
thrombolysis has provided another tool for neurologic salvage
in a patient who experiences an embolic event associated
with CEA.
• catheter-directed administration of 500,000 units of urokinase
is associated with complete neurologic recovery.
• Timing is crucial because most neurologic deficits are
significantly reversible if flow is restored within 1 to 2 hours
after vessel thrombosis.

Postoperative Care
• All patients should be observed in an intensive care unit for 24 to 48 hours after
the procedure with sequential neurological examinations by nursing staff.
• Blood pressure should be rigidly controlled in the approximate preoperative range
with continuous monitoring by arterial catheter; hemodynamic parameters are
similarly monitored by Swan-Ganz catheter in selected patients.
• Intravenous fluids, pressors, inotropes, and antihypertensive agents are routinely
administered to optimize these indices.
• Postoperative electrocardiography and chest radiography should be performed for
all patients.
• Urine output and serum electrolytes are monitored during the period of intensive
care.
• The cervical wound is repeatedly examined for enlargement or superficial
bleeding.
• Aspirin therapy is initiated immediately after surgery, and stable patients are
usually discharged to home within 3 to 5 days.

Complications
1. Cardiac complications
2. Cranial nerve injuries
3. Hemodynamic instability
4. Cerebral hyperperusion syndrome
5. Wound infection
6. Bleeding
7. Recurrent carotid stenosis

Cardiac complications
• Myocardial infarction is responsible for 25% to 50% of all
perioperative deaths after CEA. At least 40% to 50% of
patients who undergo CEA have symptomatic CAD.
• The 30-day incidence of myocardial infarction was 1.5%.

Cranial Nerve Injury
• Cranial nerve dysfunction is the most common neurologic
complication of CEA.
• The incidence of postoperative dysfunction of cranial nerves
ranges from 5% to 20%.
• Approximately a third of the patients with documented
deficits were asymptomatic and would have been missed by
cursory clinical examination.
• the risk for permanent nerve injury was 0.5%.

• Incidence of Cranial Nerve Dysfunction after CEA.
NERVE INCIDENCE OF DYSFUNCTION
HYPOGLOSSAL 4.4 - 17.5 %
RECURRENT LARYNGEAL 1.5 – 15 %
SUPERIOR LARYNGEAL 1.8 – 4.5 %
FACIAL (marginal
mandibular branch)
1.1 -3.1 %
GLOSSOPHARYNGEAL 0.2 – 1.5 %
SPINAL ACCESSORY < 1.0 %

• Most deficits are due to direct blunt injury during dissection,
stretch trauma from excessive retraction, electrocoagulation
damage, inexact placement of ligatures, or pressure injury
secondary to postoperative hematoma formation.
• Cranial nerve injury is much more likely during reoperative
surgery because of excessive scar formation.

Hypoglossal Nerve
• Manifested by ipsilateral tongue weakness and deviation to
the affected side with protrusion and difficulty masticating.
• Is the most frequent cranial nerve deficit documented in most
reports.
• if a patient has an unusually high carotid bifurcation or if
atheromatous plaque extends well past the origin of the ICA,
cephalad extension of incision is usually required for
adequate operative exposure causing nerve injury.
• Unilateral injury is rarely serious but bilateral injury causes
serious articulation deficiency and severe upper respiratory
obstruction requiring tracheostomy.

Vagus nerve
• Injured when lie anteriorly in carotid sheath.
• Injury to recurrent laryngeal nerve leads to paralysis of
ipsilateral vocal cord in paramedian position and menifest as
hoarseness of voice and loss of effective cough.
• In case of bilateral injury severe airway obstruction ensues.

Superior laryngeal nerve
• Lies posterior to ICA and ECA, thus get injured during
injudicious clamping of ICA and ECA.
• It has 2 branches : internal and external branch.
• Injury to internal branch leads to reduced sensation in
laryngeal inlet .
• Injury to external branch leads to loss of tensioning of
ipsilateral vocal cord menifested by easy fatigability of voice
and loss pitched voice.

Glossopharyngeal nerve and spinal
accessory nerve
• Injury to these structures are rare as they lie in upper limit of
incision. They get injured while cephalic extension of incision
we divide the digastric muscle.
• Glossopharyngeal nerve provides sensory and motor
innervation to larynx and injury to this nerve poses risk of
recurrent aspiration.
• Injury to spinal accessory nerve leads to drooping of shoulder
and pain, difficulty in abducting shoulder – trapezius muscle
weakness.

Facial nerve
• Injury to marginal mandibular branch of facial nerve leads to
drooping of ipsilateral lower lip.
• It may be injured while the face is turned to opposite side and
chine is extended for exposure of carotid bifurcation. Injury is
due to excessive stretching by retractor in transverse incision.

Cutaneous sensory nerves
• Greater auricular and transverse cutaneous nerve get injured.
• Greater auricular nerve lies in upper part of incision and
injury causes sensory loss in region of ipsilateral ear lobe and
angle of mandible.
• Transeverse cutaneous nerve lies in lower part of incision and
injury causes sensory loss in anterior skin.

Hemodynamic instability
• Carotid sinus baroreceptors located in outer muscle layer of
artery at carotid bifurcation transmit impulse to carotid sinus
nerve to vasomotor center in medulla.
• Stimulation of carotid sinus leads to inhibition of central
nervous system sympathetic discharge thus hypotension and
bradycardia.
• The hypotension and bradycardia immidiately or 2 hour after
CEA is due to baroreceptor dysfunction.
• It is supported by fact that injection of carotid sinus with local
anaesthetic reduces this complication.
• In some cases hypovolemia may be the underlying cause.

• Postoperative hypertension is closely correlated to
preperative hypertension especially uncontrolled, but exact
mechanism is still unknown.
• Other mechanism may include elevated cerebral
norepinephrine and elevated renin production.
• In 80% of patients this hypertensive response get normalised
in 24 hours and in 60% In 16 hours.

• Treatment of hypotension:
Infusion of colloids to achieve normovolemia
If hypotension persists give norepinephrine to treat baroreceptor
mediated hypotension.
• Treatment of hypertension:
Give SNP, as it has shorter duration of action and is direct arterial
dilator.
NTG is given when associated with CAD.

Cerebral hyperperfusion syndrome
• Cerebral hyperperfusion syndrome usually occurs several
days after CEA and is often associated with severe
hypertension and acute neurologic deficite frequently
preceded by severe headache.
• Intracerebral haemorrhage is most devastating complication
of this syndrome.
• Reported incidence ranges from 0.4 – 7.7% after CEA.
• Presentation includes migrain like headache proceeding to
siezures and intracerebral haemorrhagic stroke.
• Mortality ranges from 75 -100%.

• Mechanism : increased cerebral blood flow secondary to
disordered intracerebral autoregulation after relief of high
grade carotid stenosis in setting of severe contralateral
stenosis.
• Risk factors:
• 1. preoperative hypertension
• 2. CEA within 3 months of contralateral CEA.
• 3. use of anticoagulants and antiplatelet agents.

Recurrent carotid stenosis
• After CEA it occurs in about 5-22% cases.
• According to MEDLINE database the incidence of recurrent
carotid stenosis was 10% with in first year, 3% in second and
2% in third year after CEA.
• Causes:
1. Intimal hyperplasia : with in first 36 months
2. Residual atherosclerotic disease
3. New atherosclerotic lesions: present after many years.

• Risk factors:
1. Female sex
2. Smoking
3. Hypercholestrolemia
4. Diabetes
5. Hypertension
6. Primary closure of arteriotomy.

• Results:
According to EVEREST trial the cumulative risk of restenosis
at 4 years after eversion, patch closure and primary closure
were 3.5 %, 1.7% , 12.6 % respectively.
Treatment :
1. repeat CEA
2. Carotid artery stenting(CAS).

CAS – Carotid Artery Stenting
• Endovascular stent placement via stab wound
in the groin
• For plaque stabilization to reduce the risk of
future stroke

CAS - Advantages
• If patient has contraindication for a CEA
(already had a CEA, multiple diseases and a
high surgical risk)
• Stabilizes the plaque to minimize risk of
embolization
• Avoids the risk of cranial nerve damage
• Does not require general anesthesia
• Option for patients

CAS - Disadvantages
• Potential for embolization resulting in stroke
• Not all patients are suitable for stenting:
1.Severe aortic arch and supra-aortic vessel
tortuosity
2.Patients with very long & severe lesions
3.Heavy all around calcification of the artery

Endovascular versus Open Surgical
Decision Making for Carotid Bifurcation
Disease
CLINICAL SCENARIO RECOMMENDED APPROACH
Asymptomatic or nonspecific symptoms in
a patient with high medical risk or limited
life expectancy
Medical therapy
a patient with low or typical medical risk
Medical therapy or CEA
a patient with high anatomic risk* and low
or typical medical risk
Medical therapy or CAS
Younger symptomatic patient with high
medical risk
CAS or CEA under local/regional
anesthesia
Older symptomatic patient with high
medical risk
CEA under local/regional anesthesia
Symptomatic patient with high anatomic
risk
CAS

Results
• One of the perceived advantages of CAS over CEA in patients
who have increased medical risk for surgery.
• In the Stenting and Angioplasty with Protection in Patients at
High Risk for Endarterectomy (SAPPHIRE) trial, the rate of
myocardial infarction was significantly higher in the CEA group
(6.6%) than in the CAS group (1.9%).

Overall risk of CVA or death
0.00%
2.00%
4.00%
6.00%
8.00%
10.00%
12.00%
day 0 3 months 6 months
CEA
Stenting

Conclusion
• The choice of CEA versus CAS is limited by a lack of adequate
evidence. CEA is a much more mature procedure with an
established record.
• CAS is still an evolving procedure, and there are limited data
with respect to results.
• There are no good data regarding the adverse event rate of
CAS appropriately stratified by patient symptom status for the
typical patients who have been undergoing CEA.
• The published trials of CAS versus CEA have not yet
established CAS as an equivalent procedure to CEA with
respect to the risk for periprocedural stroke.

Special considerations
• Combined carotid and coronary artery disease
• External carotid endarterectomy

Combined carotid and coronary
artery disease
• Significant carotid disease occurs in approximately 3% to 14%
of patients undergoing cardiac surgery.
• Carotid occlusions in particular are associated with increased
perioperative events, and the extent of disease in the
contralateral artery correlates directly with the risk for
perioperative mortality; the presence of a high-grade (>60%)
stenosis contralateral to a carotid occlusion may be associated
with perioperative stroke rates as high as 25%.

• The risk for stroke after coronary artery bypass grafting
(CABG) was 2% overall—less than 2% in patients without
carotid disease, 3% in asymptomatic patients with unilateral
50% to 99% stenosis, 5% in those with bilateral 50% to 99%
stenosis, and 7% to 11% in patients with carotid occlusion.

Risk factors for perioperative stroke in
coronary bypass patients
Demographic factor preoperative intraoperative
• age > 65 years • hypertension
•Diabetes mallitus
•Carotid bruit
•Prior CVA
•CVD
•Tobacco use
•LMCA > 50 %
• cardiopulmonary bypass
time
•Use of IABP
• use of membrane
oxygenators

Mechanism of stroke in CABG patients
Mechanism of stoke % in CABG patients
embolic 62.1
Hypoperfusion / ischemic 8.1
lacunar 1
thrombotic 1
Multiple etiologies 10.1
unclassified 13.9

Risk factors for carotid disease in CABG
patients
Highly significant significant
Prior CVA Tobacco use
Prior CVD LMCA > 50%
Peripheral vascular disease Previous CEA
Carotid bruit hypertension
Age> 65 years

Decision Making for Combined
Coronary and Carotid Disease
Clinical scenario recommendation
Symptomatic carotid stenosis with
indications for elective CABG
CEA preceding or concurrent with CABG
Asymptomatic patient with unilateral
carotid high-grade stenosis and
indications for elective CABG
CABG followed by CEA
Asymptomatic patient with bilateral high-
grade carotid stenosis/contralateral
occlusion and indications for elective
CABG
CEA preceding or concurrent with CABG
Symptomatic carotid stenosis with a
patent drug-eluting coronary stent placed
within 1 year previously
CAS

Surgical treatment
• Staged CEA
• Reverse staged CEA
• Combined CEA-CABG

Staged CEA
• Carotid lesion is addressed first by CEA followed by CABG.
• Rationale is to reduce incidence of perioperative stroke.
• Appropriate for symptomatic carotid artery disease.
• Inappropriate for severe coronary artery disease or multiple
vessel disease due to risk of MI.
• Risk of MI and incidence of stroke is around 5%.

Reverse staged CEA
• Here we do CABG first followed by CEA.
• Apropriate for more critical coronary artery disease.
• Rationale is to reduce the incidence of MI.
• Stroke rates are higher than preoperative MI.

Concommitant CEA-CABG
• Various techniques are:
1. CEA before opening thorax
2. CEA after opening thorax but before canulation
3. CEA while patient is on CPB.

RESULTS
Meta analysis year combined staged
str
oke
MI deat
h
str
ok
e
MI deat
h
Moore et al 1995 6.2 4.7 5.6 5.
3
11.5 9.4
Borger et al 1999 6 - 4.7 3.
2
- 2.9
Das et al 2000 3.9 - 4.5 1.
5
- 5.9
Naylor et al 2003 4.6 3.6 4.6 2.
7
6.5 3.9

Results
• Reverse staged procedures (CABG-CEA) were associated with
the highest risk for ipsilateral stroke (5.8%) and any stroke
(6.3%). Perioperative myocardial infarction was lowest after
the reverse staged procedure (0.9%) and highest in patients
undergoing staged CEA-CABG (6.5%).

External Carotid Endarterectomy
• In the setting of ICA occlusion, atherosclerotic disease of the
ipsilateral ECA can result in embolic stroke through the
various collateral pathways.
• In a review of 195 ECA endarterectomies and 23 ECA
bypasses, resolution of symptoms was seen in 83% of
patients, with another 7% showing marked improvement. The
perioperative mortality rate was 3%, mostly secondary to
stroke, and the overall neurologic complication rate was 5%.
• There is no evidence that ECA endarterectomy should be
performed prophylactically for asymptomatic disease.

Carotid endarterectomy

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