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Carotid artery surgery (endarterectomy) is a vascular surgical procedure that removes atherosclerotic plaque from the internal carotid artery to restore normal blood flow to the brain and significantly reduce the risk of ischaemic stroke. The carotid arteries, running bilaterally along the neck, supply approximately 80% of the brain's blood flow. Atherosclerotic narrowing (stenosis) of the internal carotid artery, particularly at the carotid bifurcation, is one of the most important preventable causes of ischaemic stroke and transient ischaemic attack (TIA).

The procedure involves a longitudinal incision along the anterior border of the sternocleidomastoid muscle in the neck, surgical exposure of the common, internal, and external carotid arteries, temporary clamping of the vessels to arrest flow, and a longitudinal arteriotomy through which the atheromatous plaque core and associated intima are meticulously extracted (endarterectomy). A temporary bypass shunt may be inserted during carotid clamping to maintain cerebral perfusion while the arteriotomy is open, especially in patients with impaired contralateral carotid flow. The arteriotomy is closed primarily or with a patch (Dacron or bovine pericardium) to prevent restenosis, and blood flow is restored to the brain.

The entire procedure takes approximately 1.5 to 2.5 hours under general or locoregional (cervical plexus block) anaesthesia. CEA is the most evidence-based surgical procedure for stroke prevention in symptomatic carotid disease, with randomised evidence from NASCET and ECST trials establishing its superiority over medical therapy alone in patients with 50% or greater symptomatic stenosis.

The primary indication for carotid endarterectomy is symptomatic internal carotid artery stenosis of 50% or greater — defined as stenosis causing ipsilateral TIA, amaurosis fugax (transient monocular blindness), or ischaemic stroke within the preceding six months. The absolute risk reduction from CEA in symptomatic 70 to 99% stenosis is approximately 16% for stroke or death at five years (NASCET), making it one of the most effective preventive surgical interventions in medicine. For symptomatic 50 to 69% stenosis, CEA provides a more modest but still meaningful absolute risk reduction of 7.8% at five years, with greater benefit in men, older patients, and those with recent symptoms.

Asymptomatic carotid artery stenosis of 60 to 99% (detected incidentally by ultrasound or during evaluation for contralateral disease) is a secondary indication, with CEA providing a 5 to 11% absolute risk reduction compared to optimal medical therapy in carefully selected patients under 75 years old with low surgical risk. Current guidelines recommend shared decision-making for asymptomatic disease, given improving outcomes with contemporary medical therapy (dual antiplatelet, high-intensity statins, aggressive risk factor control). CEA is also indicated for carotid ulceration and complex plaque morphology associated with high embolic risk identified on imaging.

The ideal candidate for CEA is a patient with recently symptomatic (within six months) moderate-to-severe internal carotid artery stenosis confirmed by duplex ultrasound and CT or MR angiography, with acceptable perioperative risk. ACC/AHA and ESVS guidelines recommend CEA within two weeks of TIA or minor stroke for symptomatic high-grade stenosis, as the risk of recurrent stroke is highest in the first two to four weeks after the index event. Patients should have a perioperative stroke and death risk below 6% to derive net benefit from CEA for symptomatic disease.

Contraindications include complete internal carotid occlusion (which CEA cannot reverse), distal stenosis beyond surgical reach (above C2 vertebra), prohibitive comorbidities such as severe cardiac or pulmonary disease making general anaesthesia unsafe, contralateral hemisphere stroke causing fixed neurological deficit (where ipsilateral surgery offers no further protection), and active carotid dissection unless presenting with threatened stroke. Life expectancy of less than five years diminishes the long-term benefit of CEA and should weigh in clinical decision-making. Carotid artery stenting (CAS) is an alternative for patients considered high surgical risk for CEA due to hostile neck anatomy, contralateral laryngeal nerve palsy, or prior neck radiation.

Standard carotid endarterectomy (conventional CEA) employs a longitudinal arteriotomy, plaque removal under direct vision, and patch angioplasty closure. Patch closure with prosthetic or vein patch significantly reduces restenosis risk compared to primary closure and is recommended by the Cochrane meta-analysis for most patients. Eversion carotid endarterectomy is an alternative technique in which the internal carotid artery is transected at its origin, everted upon itself for plaque removal, then reimplanted — avoiding a patch and maintaining the natural vessel architecture; it carries equivalent stroke risk and lower restenosis rates in experienced hands.

Cerebral monitoring during carotid clamping — using electroencephalography (EEG), transcranial Doppler (TCD), somatosensory evoked potentials, or regional anaesthesia with awake patient monitoring — identifies the need for shunt insertion during the vulnerable ischaemic period. Locoregional cervical plexus block anaesthesia with the patient awake allows continuous neurological monitoring without EEG and avoids general anaesthesia risks in high-risk patients. Carotid artery stenting (CAS) with embolic protection devices is a catheter-based alternative to CEA for anatomically or medically high-risk surgical candidates, with equivalent outcomes to CEA in asymptomatic patients but somewhat higher 30-day stroke risk in symptomatic disease per CREST and ICSS trial data. The treating surgeon individualises the chosen technique based on patient anatomy, the extent and nature of the underlying condition, available equipment, and the balance of procedural benefit against risk — a decision made in consultation with the patient following a thorough informed consent discussion covering all available options.

CEA for symptomatic high-grade stenosis reduces the absolute five-year risk of ipsilateral stroke by 15 to 17% compared to optimal medical therapy alone (NASCET trial), translating to a number needed to treat of approximately six to seven patients to prevent one stroke. Benefit is greatest when surgery is performed within two weeks of the index TIA or minor stroke, with early CEA reducing the 90-day stroke risk from 10 to 20% with medical therapy alone to below 3%. Long-term carotid patency after patch endarterectomy exceeds 95% at five years, with restenosis rates below 5%.

Beyond stroke prevention, successful CEA eliminates embolic risk from the plaque source, resolves carotid bruit, and in selected patients with cerebral hypoperfusion, may improve cognitive function and resolve haemodynamic TIAs. Perioperative stroke and death rates at high-volume vascular surgery centres are 1 to 2% for elective CEA — well below the risk threshold above which benefit is negated — demonstrating the safety and durability of the procedure in skilled hands.

The most consequential perioperative complication of CEA is stroke, occurring in 1 to 2% of patients at specialised centres. Stroke may result from intraoperative embolisation during plaque manipulation, carotid thrombosis, or haemodynamic ischaemia during carotid clamping. Myocardial infarction occurs in 0.5 to 1% of patients, reflecting the frequent concomitant coronary artery disease in this population. Cranial nerve injury — most commonly of the hypoglossal nerve (tongue deviation), marginal mandibular nerve (lip asymmetry), and superior laryngeal nerve (hoarseness) — occurs in 5 to 8% of cases, with the majority transient.

Wound haematoma requiring surgical evacuation occurs in 2 to 3% of cases and can cause tracheal compression if unrecognised. Carotid restenosis from intimal hyperplasia occurs in 5 to 10% of patients within two years but rarely causes symptoms and is managed by re-intervention only if symptomatic. Hyperperfusion syndrome — sudden increase in cerebral blood flow following restoration of flow through a previously stenotic vessel — presents with ipsilateral headache, seizure, and haemorrhagic stroke in 0.3 to 1% of cases and is managed by aggressive blood pressure control in the postoperative period.

Most patients are observed in a high-dependency unit for 12 to 24 hours post-CEA to monitor for neurological changes, blood pressure instability (carotid baroreflex disruption can cause labile pressure), and wound haematoma. Hospital discharge occurs on day one to two post-surgery. The neck wound heals within two weeks; suture removal or Steri-Strips are used at the outpatient follow-up visit at ten to fourteen days. Antiplatelet therapy (aspirin 75 to 100 mg daily) is commenced preoperatively and continued indefinitely. High-intensity statin therapy and rigorous vascular risk factor management are mandatory.

Duplex ultrasound surveillance at one month and twelve months post-CEA detects early restenosis. Subsequent annual surveillance is guided by symptoms and stenosis severity at the one-year scan. Return to driving is typically permitted after two to four weeks once wound healing is confirmed and blood pressure is stable. Aerobic exercise and cardiovascular rehabilitation improve long-term vascular outcomes. The contralateral carotid artery should be assessed periodically, as bilateral disease progression occurs in a meaningful proportion of patients.

Carotid endarterectomy in the United States costs USD 15,000 to USD 35,000 including hospitalisation, anaesthesia, and surgical fees. Emergency CEA within 48 hours of TIA — increasingly the standard of care — incurs additional costs for urgent vascular imaging and expedited theatre access. In the UK, private CEA costs GBP 6,000 to GBP 12,000, and the NHS typically performs the procedure urgently for symptomatic disease.

For patients exploring medical tourism for elective CEA, India offers the procedure at USD 2,500 to USD 5,000 at JCI-accredited vascular surgery centres in Delhi, Mumbai, and Chennai. Thailand provides CEA for USD 5,000 to USD 9,000. Patients must confirm that international centres have a dedicated vascular surgery team, intraoperative neurological monitoring capability, and 24-hour postoperative neuromonitoring in a high-dependency setting to ensure safety equivalence with Western standards.

Carotid artery stenting (CAS) with embolic protection devices is the primary endovascular alternative to CEA. CAS avoids a surgical incision and is preferred for patients with technically hostile CEA anatomy (high bifurcation, prior neck radiation, contralateral nerve palsy) or high surgical risk from cardiac or pulmonary comorbidities. Meta-analyses of CREST, ICSS, EVA-3S, and SPACE trials demonstrate that CAS carries a somewhat higher periprocedural stroke risk than CEA in symptomatic disease (approximately 5% versus 3.5%), particularly in older patients above 70 years, though MI risk is lower with CAS.

Optimal medical therapy (OMT) alone — high-intensity statin, dual antiplatelet therapy with aspirin and clopidogrel for 30 days post-TIA, ACE inhibitor, and aggressive cardiovascular risk factor management — is appropriate for asymptomatic patients with low-grade stenosis below 60%, patients with prohibitive surgical risk, and those with complete carotid occlusion. Contemporary OMT has improved substantially, and ongoing trials (CREST-2) are evaluating whether modern medical therapy may be equivalent to revascularisation for asymptomatic stenosis.