Carotid endarterectomy

Dr Dheeraj sharmaM.Ch CTVS 2nd yr. resident

Outline

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

ANATOMY OF CAROTID ARTERIES

ICA

Triangles of neck

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 (arteriosclerotic 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 intakePotentially 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 injury2. Accumulation of lipoproteins3. Resultant Inflammation & Factor release4. 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 StrokeDevelopment 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

Endpoint

Medical Event Rate (%

Surgical Event Rate (%)

Absolute Risk Reduction (5 Year) (%

Relative Risk Reduction (5 Year) (%)

ACAS 60-99 1662 IPSILATERAL 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

RESULTSStudy Degree

of Stenosis (%)

Number of Patients

Endpoint (Time and Event)

Medical Event Rate (%)

Surgical Event Rate (%)

Absolute Risk Reduction (%)

Relative Risk Reduction (%)

NASCET 70-99 659 2 YR IPSILATERAL STROKE

26 9.0 17 65

ECST 80-99 576 3 YR IPSILATERAL STROKE

20.2 6.8 13.8 67

NASCET 50-69 858 5 YR IPSILATERAL 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 InitiativeRecommendations for Stroke Management, 2002

Patient Characteristics and Outcome for Intervention Decision Making

Characteristic Outcome*

Female gender Lower risk for stroke with medical therapyHigher 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 therapyLower 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.

RECOMMENDATIONS

TREATMENT OPTIONS

• MEDICAL• SURGICAL: CEA / CAS

TREATMENT PROTOCOL

MEDICAL MANAGEMENT

• Antiplatelet Therapy1. 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.

• Heparin1. 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.

Atherosklerotic Chatper 25,Ruherford’s Vascular Surgery,7th ed

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

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. SHUNTING2. CEREBRAL MONITORING3. STUMP PRESSURE MEASUREMENT4. 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 patch2. 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 complications2. Cranial nerve injuries3. Hemodynamic instability4. Cerebral hyperperusion syndrome5. Wound infection6. Bleeding7. 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 months2. Residual atherosclerotic disease3. New atherosclerotic lesions: present after many years.

• Risk factors:1. Female sex2. Smoking3. Hypercholestrolemia4. Diabetes 5. Hypertension6. 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

tortuosity2.Patients with very long & severe lesions3.Heavy all around calcification of the artery

Endovascular versus Open Surgical Decision Making for Carotid Bifurcation

DiseaseCLINICAL SCENARIO RECOMMENDED APPROACH

Asymptomatic or nonspecific symptoms in a patient with high medical risk or limited life expectancy

Medical therapy

Asymptomatic or nonspecific symptoms in a patient with low or typical medical risk

Medical therapy or CEA

Asymptomatic or nonspecific symptoms in 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

CEAStenting

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 thorax2. CEA after opening thorax but before canulation3. CEA while patient is on CPB.

RESULTSMeta analysis year combined staged

stroke

MI death

stroke

MI death

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.