17:I[462708,["/_next/static/chunks/3yo3kiro3bmlp.js","/_next/static/chunks/3vr2wvd8f2efb.js","/_next/static/chunks/2vtmb68_vu-9t.js","/_next/static/chunks/2s8mt6_8wrpfo.js","/_next/static/chunks/3vkulz2i3l61y.js","/_next/static/chunks/1cqw2i1silz0i.js","/_next/static/chunks/14dbm3lm_t629.js","/_next/static/chunks/335_v2mb569ld.js","/_next/static/chunks/3ykn5ops9bft5.js","/_next/static/chunks/3cmavum774kjt.js","/_next/static/chunks/3th-0-a2xf9qs.js","/_next/static/chunks/0p0xpwde6kzmv.js","/_next/static/chunks/401-sxxnzbtf_.js","/_next/static/chunks/0wywtv698a1v0.js","/_next/static/chunks/2botzqwpnrzyj.js"],"ArticleReader"] 18:T6178,## Summary Atherosclerotic extracranial internal carotid artery stenosis causes retinal and cerebral ischemia primarily through plaque disruption and artery-to-artery embolism. The decisive distinction is **symptomatic versus asymptomatic disease**. A recent ipsilateral retinal ischemic event, transient ischemic attack (TIA), or ischemic stroke attributable to the stenotic carotid artery defines symptomatic disease and confers a high early recurrence risk.[1-4] - **Symptomatic 70–99% stenosis:** carotid endarterectomy (CEA) is recommended for most suitable patients when expected procedural stroke/death risk is acceptably low.[1-4] - **Symptomatic 50–69% stenosis:** CEA provides smaller benefit and is appropriate for selected patients after considering age, sex, event type, comorbidity, anatomy, timing, and center outcomes.[1-4] - **Symptomatic <50% stenosis:** CEA is not indicated for prevention based on the carotid lesion alone.[3] - When CEA is indicated after a nondisabling event, benefit is greatest when performed early, generally **within 14 days**, but routine CEA **within the first 48 hours after acute ischemic stroke is not beneficial** and can increase perioperative harm; wait until neurologic and imaging stability supports intervention.[1,3,5] - **Asymptomatic high-grade stenosis:** intensive medical management is foundational. The 2026 CREST-2 trials found a 4-year primary-outcome rate of 6.0% with medical therapy versus 2.8% with stenting (P=0.02), and 5.3% versus 3.7% with CEA (P=0.24). The findings support selective, anatomy- and operator-dependent revascularization rather than automatic procedures based only on stenosis percentage.[6] - Do not screen the general adult population for asymptomatic carotid stenosis.[1,7] - Revascularization never substitutes for antithrombotic therapy when indicated, intensive lipid lowering, blood-pressure control, smoking cessation, diabetes management, and other vascular-risk reduction.[2,4] > **Caution:** A severe carotid stenosis discovered during stroke work-up is not automatically the stroke mechanism. Confirm that the event is ipsilateral and compatible with carotid-territory embolism, and assess competing causes such as atrial fibrillation, intracranial atherosclerosis, small-vessel disease, dissection, and aortic disease. ## Definitions ### Symptomatic carotid stenosis A lesion is symptomatic when it has caused a recent **ipsilateral** retinal or cerebral ischemic event. Qualifying events include: - transient monocular visual loss attributable to retinal ischemia; - retinal artery occlusion; - hemispheric TIA with contralateral motor or sensory deficit, aphasia, or another compatible cortical syndrome; - nondisabling ischemic stroke in the ipsilateral carotid territory. Most trials and guidelines use a symptom window of approximately 6 months, although the clinical urgency is greatest in the first days and weeks after the event.[3,4] Nonspecific dizziness, isolated syncope, generalized weakness, chronic imbalance, or bilateral visual blurring do not by themselves make a stenosis symptomatic. ### Asymptomatic carotid stenosis Asymptomatic stenosis is a carotid lesion without a recent ipsilateral retinal or cerebral ischemic event attributable to that artery. Its absolute stroke risk depends on stenosis severity, plaque biology, progression, contralateral disease, patient risk factors, and quality of medical therapy. ### NASCET measurement The North American Symptomatic Carotid Endarterectomy Trial (NASCET) method calculates stenosis relative to the normal distal internal carotid artery. Reports should specify method because alternative historical methods yield different percentages. | NASCET category | Clinical implication | |---|---| | <50% | No CEA benefit for symptomatic stenosis based on the lesion alone | | 50–69% | Moderate stenosis; CEA benefit is selective in symptomatic patients | | 70–99% | Severe stenosis; urgent revascularization assessment if symptomatic and otherwise suitable | | Near-occlusion | Distal internal carotid caliber reduction/collapse; routine CEA benefit is uncertain and specialist imaging review is required | | Complete occlusion | Routine CEA/stenting is not used to reopen a chronic occlusion for stroke prevention | ## Epidemiology and vascular risk Carotid atherosclerosis shares the major determinants of systemic atherosclerotic cardiovascular disease: - older age; - smoking; - hypertension; - dyslipidemia; - diabetes mellitus; - chronic kidney disease; - coronary or peripheral artery disease; - family history of premature atherosclerotic disease. The carotid lesion is a marker of systemic risk. Myocardial infarction and cardiovascular death remain important competing outcomes even after technically successful revascularization. ## Pathophysiology and plaque risk Stroke from carotid atherosclerosis is usually embolic. Plaque rupture or erosion, intraplaque hemorrhage, ulceration, and superimposed thrombus release embolic material into the retinal or intracranial circulation. Severe stenosis can also compromise perfusion when collateral reserve is poor. Risk is not determined by percentage stenosis alone. Features associated with higher risk in observational studies include: - rapid progression; - silent ipsilateral infarction; - plaque ulceration; - intraplaque hemorrhage on MRI; - microembolic signals on transcranial Doppler; - contralateral TIA/stroke or occlusion in selected settings; - impaired cerebrovascular reserve.[4] These features can inform asymptomatic decision-making but do not replace trial-based procedural thresholds. ## Clinical presentation ### Retinal ischemia Transient monocular visual loss is usually abrupt, painless, and negative rather than positive visual phenomena. Persistent retinal artery occlusion causes sustained loss. Ipsilateral retinal ischemia is a symptomatic carotid event and requires the same urgent vascular pathway as cerebral TIA. ### Hemispheric TIA Typical manifestations are abrupt contralateral weakness or numbness, aphasia, or other focal cortical deficits. Symptoms may resolve completely while diffusion MRI shows a small infarct. ### Ischemic stroke Persistent focal deficit requires an acute stroke pathway. Carotid surgery is not the first intervention when reperfusion therapy may be indicated. > **Caution:** Do not delay IV thrombolysis or mechanical thrombectomy assessment to pursue carotid revascularization. Acute reperfusion eligibility and later carotid prevention are separate decisions.[5] ## Initial pathway after a carotid-territory event 1. Establish time last known well and neurologic severity. 2. Obtain urgent brain imaging to exclude hemorrhage and define infarct burden. 3. Obtain head/neck arterial imaging when large-artery disease is suspected. 4. Treat eligible acute stroke with reperfusion therapy according to current stroke guidance. 5. Begin antithrombotic and vascular-risk treatment when safe. 6. If ipsilateral 50–99% stenosis is present, involve stroke and vascular specialists promptly so an indicated intervention is not delayed beyond the period of greatest benefit.[1-5] 7. Determine whether infarct size, hemorrhagic transformation, neurologic instability, or medical instability requires delay. Related references: [Acute Ischemic Stroke](../neurology/acute-ischemic-stroke.md) and [Transient Ischemic Attack in Adults](../neurology/transient-ischemic-attack-in-adults.md). ## Diagnostic imaging ### Duplex ultrasonography Duplex ultrasound is the usual first-line test for extracranial carotid stenosis and the standard surveillance modality. It integrates B-mode plaque imaging with Doppler velocities. Interpretation should use laboratory-validated criteria. Peak systolic velocity, end-diastolic velocity, internal-to-common carotid ratio, plaque appearance, and distal waveform all contribute. Results can be distorted by: - contralateral occlusion; - low cardiac output; - tandem lesions; - severe vessel tortuosity; - heavy calcification; - operator/technical limitations. A clinically important or unexpected duplex result should generally be confirmed with cross-sectional angiography before a procedure.[1,4] ### CT angiography CTA is rapid and widely available. It shows lumen narrowing, plaque calcification, arch anatomy, tandem disease, intracranial vessels, and procedural anatomy. Limitations include iodinated contrast, radiation, and calcification blooming that can overestimate severe stenosis. ### MR angiography MRA is useful when iodinated contrast is undesirable or brain MRI is already planned. Noncontrast time-of-flight MRA can overestimate stenosis from flow-related signal loss; contrast-enhanced MRA can improve lumen definition when appropriate. ### Catheter angiography Digital subtraction angiography offers high spatial resolution but carries embolic and access-site risk. Reserve it for discordant noninvasive studies, complex anatomy, or endovascular treatment planning rather than routine screening. ## Differential diagnosis of a carotid-territory event | Alternative mechanism | Clues | Next step | |---|---|---| | Atrial fibrillation/cardioembolism | Multiple territories, atrial arrhythmia, cardiac thrombus | ECG/telemetry, extended rhythm monitoring when indicated, echocardiography | | Intracranial atherosclerosis | Intracranial stenosis in the symptomatic territory | Intracranial vascular imaging and disease-specific medical therapy | | Carotid dissection | Neck/head pain, trauma, younger patient, tapered stenosis | CTA/MRA with vessel-wall assessment as needed | | Small-vessel disease | Lacunar syndrome with deep small infarct | Treat vascular risk; do not assume incidental carotid stenosis caused event | | Aortic embolic source | Complex arch atheroma or aortic pathology | Aortic/cardiac evaluation when clinically indicated | | Vasculitis/other arteriopathy | Multifocal stenosis, inflammatory/systemic clues | Targeted laboratory and vascular work-up | ## Intensive medical management ### Antithrombotic therapy For noncardioembolic TIA or ischemic stroke, use antiplatelet therapy according to secondary-prevention guidance.[2] Short-course dual antiplatelet therapy is appropriate in selected high-risk TIA or minor stroke pathways, but long-term dual therapy is not routine because bleeding increases. Carotid stenting requires peri-procedural dual antiplatelet therapy. CEA antiplatelet management follows the surgical protocol, commonly continuing aspirin. Anticoagulation is not a treatment for carotid atherosclerosis itself. Use anticoagulation for a separate indication such as atrial fibrillation, and avoid unnecessary addition of antiplatelet therapy when bleeding risk outweighs incremental benefit. ### Lipid lowering Use high-intensity statin therapy unless contraindicated. Add nonstatin therapy when necessary to reach the applicable secondary-prevention target. Modern carotid care assumes aggressive LDL lowering rather than procedural treatment alone.[2,4] ### Blood pressure, diabetes, and lifestyle - Treat chronic hypertension after the acute stroke period; avoid unindicated rapid reduction during acute ischemia. - Optimize diabetes therapy and avoid severe hypoglycemia. - Stop tobacco exposure. - Use a cardioprotective dietary pattern and regular physical activity appropriate to neurologic status. - Address obesity, sleep apnea, and adherence when relevant. ## Symptomatic stenosis: revascularization decisions ### 70–99% stenosis CEA is the preferred revascularization strategy for most standard-risk patients with recent ipsilateral TIA or nondisabling stroke when procedural stroke/death risk is low.[1-4] The benefit is largest when treatment is performed promptly after the qualifying event. ### 50–69% stenosis CEA benefit is more modest. Favor intervention when the event is convincingly carotid-related, procedural risk is low, life expectancy is reasonable, and patient factors predict meaningful benefit. Delay reduces benefit. ### <50% stenosis Do not perform CEA for stroke prevention based on the stenosis alone.[3] ### Near-occlusion Near-occlusion requires specialist image review because the distal artery may be collapsed and conventional percent-stenosis measurements become misleading. Routine intervention is not supported as strongly as for ordinary severe stenosis. Recurrent symptoms despite optimal therapy may justify individualized consideration.[4] ## Timing after TIA or ischemic stroke ### Within 14 days When CEA is indicated, guidelines generally recommend intervention as early as safely feasible and preferably within **14 days**.[1,3,4] Early benefit reflects the high recurrence risk soon after the index event. ### First 48 hours The 2026 AHA/ASA acute ischemic stroke guideline specifically states that, in acute ischemic stroke or unstable neurologic status from high-grade carotid disease without an intracranial occlusion, **emergency CEA within 48 hours is not beneficial** for improving functional outcome.[5] The guideline cites a large meta-analysis in which CEA within 2 days, compared with days 3–14, was associated with higher 30-day stroke (OR 1.57) and death (OR 5.19).[5] This recommendation applies to acute ischemic stroke. A patient with recurrent TIA and no substantial infarct may require individualized urgent management by an experienced team. ### Delay revascularization when - there is a large territorial infarct, edema, or mass effect; - hemorrhagic transformation is present or likely; - neurologic status is unstable; - stroke is severely disabling with limited preventive benefit; - severe uncontrolled hypertension or another medical instability persists; - the relationship between stenosis and symptoms is uncertain. ## CEA versus carotid stenting ### CEA CEA remains the reference procedure for most symptomatic standard-surgical-risk disease.[1-4] Important complications: - perioperative ischemic stroke; - myocardial infarction; - cervical hematoma/airway compromise; - cranial nerve injury; - hyperperfusion syndrome or intracranial hemorrhage; - restenosis. ### Transfemoral carotid artery stenting Stenting is useful when CEA risk or neck anatomy is unfavorable and endovascular anatomy is suitable. Relative disadvantages include embolic risk from arch/lesion traversal and the need for dual antiplatelet therapy. Advanced age, heavy calcification, severe tortuosity, and complex arch disease may increase risk.[3,4] ### Transcarotid artery revascularization Flow-reversal transcarotid techniques are increasingly used for selected anatomy and surgical-risk profiles. Evidence is largely observational/registry-based compared with the randomized evidence supporting CEA and the transfemoral strategy used in major trials. Do not extrapolate CREST-2 stenting results automatically to every stent platform or access route.[6] ## Asymptomatic stenosis ### Do not screen the general population The U.S. Preventive Services Task Force recommends against screening asymptomatic adults because procedural harms and false-positive pathways outweigh proven benefit at the population level.[7] The Society for Vascular Surgery similarly advises against general population screening, while allowing selective screening of higher-risk patients only when a positive result would lead to a realistic intervention discussion.[1] ### Guideline framework before CREST-2 The 2022 Society for Vascular Surgery guideline recommends CEA for selected low-surgical-risk patients with **70–99%** asymptomatic stenosis if the center's perioperative stroke/death rate is **<3%**.[1] The 2023 European Society for Vascular Surgery guideline recommends considering CEA for selected **60–99%** asymptomatic stenosis when clinical/imaging features indicate higher late-stroke risk despite best medical therapy, expected 30-day stroke/death risk is ≤3%, and life expectancy is generally more than 5 years.[4] ### 2026 CREST-2 results CREST-2 enrolled patients with **≥70% asymptomatic carotid stenosis** into two parallel randomized trials: intensive medical management alone versus the same medical management plus carotid stenting, and medical management alone versus medical management plus CEA.[6] | Trial | Intensive medical therapy | Revascularization + intensive therapy | 4-year primary outcome | |---|---:|---:|---| | Stenting trial | 6.0% | 2.8% | Significant absolute reduction; P=0.02 | | CEA trial | 5.3% | 3.7% | Difference not statistically significant; P=0.24 | The primary outcome included peri-procedural stroke/death and subsequent ipsilateral stroke. Early procedural events occurred in both revascularization groups, so benefit depends on excellent operator/center performance.[6] > **Current practice:** CREST-2 strengthens the rationale for discussing stenting in carefully selected patients with severe asymptomatic disease, but it does not justify routine stenting for every ≥70% lesion. Anatomy, age, antiplatelet tolerance, center results, life expectancy, competing morbidity, patient preference, and plaque-risk features remain central.[6] ### Practical asymptomatic decision pathway **High-grade asymptomatic stenosis confirmed** → Start/optimize intensive medical management → Confirm imaging severity and anatomy with a second modality when intervention is contemplated → Estimate life expectancy and competing cardiovascular/cancer risk → Review plaque-risk features and progression → Verify audited local peri-procedural outcomes → Discuss medical therapy alone versus revascularization with explicit procedural risk Do not perform a procedure merely because a numerical stenosis threshold is met. ## Procedural selection table | Clinical factor | Often favors CEA | Often favors stenting / alternative approach | |---|---|---| | Typical symptomatic standard-risk patient | Yes | Only when specific advantages exist | | Older age with unfavorable arch anatomy | Yes | Transfemoral stenting less attractive | | Prior neck radiation or hostile neck | May increase surgical risk | Stenting may be preferable | | High cervical lesion | Surgical access may be difficult | Endovascular option may be preferable | | Severe calcification/tortuosity | Can still favor CEA | Can increase stenting risk | | Need to avoid dual antiplatelet therapy | Favors CEA | Stenting requires dual therapy | | Severe cardiopulmonary surgical risk | Individualize | Endovascular strategy may reduce some surgical hazards | | Asymptomatic ≥70% disease after CREST-2 | CEA benefit was not statistically significant in trial | Stenting showed benefit in trial, but only with expert selection/performance | ## Perioperative and postprocedural monitoring ### After CEA Monitor for: - new focal neurologic deficit; - neck swelling, hematoma, stridor, or airway compromise; - hypo- or hypertension; - myocardial ischemia; - cranial nerve dysfunction; - hyperperfusion syndrome: severe ipsilateral headache, seizures, neurologic deficit, or intracranial hemorrhage. Tight but safe blood-pressure control is important after revascularization. ### After stenting Monitor for: - stroke/TIA; - access-site complications; - bradycardia/hypotension from carotid sinus stimulation; - contrast-associated kidney injury in at-risk patients; - adherence and bleeding on dual antiplatelet therapy. ## Surveillance After CEA or stenting, use duplex surveillance according to local vascular protocol, particularly when restenosis risk would change management. After nonprocedural management, repeat imaging is reasonable when progression would alter an intervention decision. Surveillance frequency should reflect baseline severity, progression rate, contralateral disease, and candidacy for treatment rather than an automatic schedule for all patients.[1,4] ## Special situations ### Contralateral carotid occlusion Contralateral occlusion can increase operative complexity and may alter duplex velocities and cerebral perfusion reserve. It does not by itself mandate stenting. Choose procedure through multidisciplinary assessment of anatomy and center outcomes.[4] ### Prior radiation or neck surgery A hostile neck can increase CEA technical risk and cranial nerve/wound complications, making an endovascular strategy more attractive when anatomy is favorable. ### Chronic kidney disease Minimize unnecessary iodinated contrast and optimize renal protection. Duplex ultrasound and noncontrast MRA may be useful, but procedure choice must also account for overall cardiovascular risk and life expectancy. ### Older adults and frailty The preventive value of asymptomatic revascularization diminishes when life expectancy is limited or competing mortality is high. Frailty, cognition, cancer, severe heart/lung disease, and patient goals should be part of the decision. ## Complications ### Untreated carotid disease - retinal ischemia; - TIA; - ischemic stroke; - recurrent embolic events; - progression to severe stenosis or occlusion. ### Revascularization-related - stroke or death; - myocardial infarction; - cranial nerve injury after CEA; - access complications after stenting; - cervical hematoma after CEA; - hyperperfusion syndrome; - restenosis; - bleeding related to antiplatelet treatment. ## Bedside checklist **Recent ipsilateral retinal/cerebral event + carotid stenosis** - Confirm event is truly carotid-territory. - Treat as urgent stroke/TIA and initiate medical therapy. - Confirm stenosis severity with high-quality vascular imaging. - 70–99%: urgent CEA assessment in most suitable patients. - 50–69%: individualized CEA decision. - <50%: no CEA for lesion alone. - Avoid routine CEA in the first 48 hours after acute ischemic stroke; proceed once stable, aiming for treatment within 14 days when indicated.[1,5] **Asymptomatic severe stenosis** - Do not stop at the percentage stenosis. - Optimize medical therapy. - Confirm severity/anatomy. - Estimate procedural risk, life expectancy, and plaque-related risk. - Incorporate CREST-2 evidence into shared decision-making.[6] ## Recent guideline and evidence changes The 2026 AHA/ASA acute ischemic stroke guideline clarified that emergency CEA within 48 hours for acute ischemic stroke or unstable neurologic status caused by high-grade carotid stenosis/occlusion without intracranial occlusion provides no functional benefit and should not be routine.[5] CREST-2 materially changed the asymptomatic evidence base. In contemporary patients with ≥70% asymptomatic stenosis receiving intensive medical therapy, stenting reduced the 4-year composite outcome compared with medical therapy alone, whereas the CEA comparison did not reach statistical significance.[6] Existing 2022–2023 procedural guidelines were written before these primary results and therefore need to be interpreted in that context.[1,4] ## References 1. AbuRahma AF, Avgerinos ED, Chang RW, et al. Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovascular disease. *J Vasc Surg*. 2022;75(1S):4S-22S. DOI: 10.1016/j.jvs.2021.04.073. PMID: 34153348. https://pubmed.ncbi.nlm.nih.gov/34153348/ 2. Kleindorfer DO, Towfighi A, Chaturvedi S, et al. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack. *Stroke*. 2021;52:e364-e467. DOI: 10.1161/STR.0000000000000375. https://www.ahajournals.org/doi/10.1161/STR.0000000000000375 3. Bonati LH, Kakkos S, Berkefeld J, et al. European Stroke Organisation guideline on endarterectomy and stenting for carotid artery stenosis. *Eur Stroke J*. 2021;6(2):I-XLVII. DOI: 10.1177/23969873211012121. PMID: 34414302. https://pubmed.ncbi.nlm.nih.gov/34414302/ 4. Naylor R, Rantner B, Ancetti S, et al. European Society for Vascular Surgery 2023 Clinical Practice Guidelines on the Management of Atherosclerotic Carotid and Vertebral Artery Disease. *Eur J Vasc Endovasc Surg*. 2023;65(1):7-111. DOI: 10.1016/j.ejvs.2022.04.011. PMID: 35598721. https://pubmed.ncbi.nlm.nih.gov/35598721/ 5. American Heart Association/American Stroke Association. 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke. *Stroke*. 2026;57:e316-e436. DOI: 10.1161/STR.0000000000000513. https://www.ahajournals.org/doi/10.1161/STR.0000000000000513 6. Brott TG, Howard G, Lal BK, Voeks JH, et al. Medical Management and Revascularization for Asymptomatic Carotid Stenosis. *N Engl J Med*. 2026;394(3):219-231. DOI: 10.1056/NEJMoa2508800. PMID: 41269206. https://pubmed.ncbi.nlm.nih.gov/41269206/ 7. U.S. Preventive Services Task Force. Screening for Asymptomatic Carotid Artery Stenosis: Recommendation Statement. *JAMA*. 2021;325(5):476-481. DOI: 10.1001/jama.2020.26988. PMID: 33528542. https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/carotid-artery-stenosis-screening19:T61ba,## Summary Atherosclerotic extracranial internal carotid artery stenosis causes retinal and cerebral ischemia primarily through plaque disruption and artery-to-artery embolism. The decisive distinction is **symptomatic versus asymptomatic disease**. A recent ipsilateral retinal ischemic event, transient ischemic attack (TIA), or ischemic stroke attributable to the stenotic carotid artery defines symptomatic disease and confers a high early recurrence risk.[1-4] - **Symptomatic 70–99% stenosis:** carotid endarterectomy (CEA) is recommended for most suitable patients when expected procedural stroke/death risk is acceptably low.[1-4] - **Symptomatic 50–69% stenosis:** CEA provides smaller benefit and is appropriate for selected patients after considering age, sex, event type, comorbidity, anatomy, timing, and center outcomes.[1-4] - **Symptomatic <50% stenosis:** CEA is not indicated for prevention based on the carotid lesion alone.[3] - When CEA is indicated after a nondisabling event, benefit is greatest when performed early, generally **within 14 days**, but routine CEA **within the first 48 hours after [acute ischemic stroke](/library/acute-ischemic-stroke) is not beneficial** and can increase perioperative harm; wait until neurologic and imaging stability supports intervention.[1,3,5] - **Asymptomatic high-grade stenosis:** intensive medical management is foundational. The 2026 CREST-2 trials found a 4-year primary-outcome rate of 6.0% with medical therapy versus 2.8% with stenting (P=0.02), and 5.3% versus 3.7% with CEA (P=0.24). The findings support selective, anatomy- and operator-dependent revascularization rather than automatic procedures based only on stenosis percentage.[6] - Do not screen the general adult population for asymptomatic carotid stenosis.[1,7] - Revascularization never substitutes for antithrombotic therapy when indicated, intensive lipid lowering, blood-pressure control, smoking cessation, diabetes management, and other vascular-risk reduction.[2,4] > **Caution:** A severe carotid stenosis discovered during stroke work-up is not automatically the stroke mechanism. Confirm that the event is ipsilateral and compatible with carotid-territory embolism, and assess competing causes such as [atrial fibrillation](/library/atrial-fibrillation), intracranial atherosclerosis, small-vessel disease, dissection, and aortic disease. ## Definitions ### Symptomatic carotid stenosis A lesion is symptomatic when it has caused a recent **ipsilateral** retinal or cerebral ischemic event. Qualifying events include: - transient monocular visual loss attributable to retinal ischemia; - retinal artery occlusion; - hemispheric TIA with contralateral motor or sensory deficit, aphasia, or another compatible cortical syndrome; - nondisabling ischemic stroke in the ipsilateral carotid territory. Most trials and guidelines use a symptom window of approximately 6 months, although the clinical urgency is greatest in the first days and weeks after the event.[3,4] Nonspecific dizziness, isolated syncope, generalized weakness, chronic imbalance, or bilateral visual blurring do not by themselves make a stenosis symptomatic. ### Asymptomatic carotid stenosis Asymptomatic stenosis is a carotid lesion without a recent ipsilateral retinal or cerebral ischemic event attributable to that artery. Its absolute stroke risk depends on stenosis severity, plaque biology, progression, contralateral disease, patient risk factors, and quality of medical therapy. ### NASCET measurement The North American Symptomatic Carotid Endarterectomy Trial (NASCET) method calculates stenosis relative to the normal distal internal carotid artery. Reports should specify method because alternative historical methods yield different percentages. | NASCET category | Clinical implication | |---|---| | <50% | No CEA benefit for symptomatic stenosis based on the lesion alone | | 50–69% | Moderate stenosis; CEA benefit is selective in symptomatic patients | | 70–99% | Severe stenosis; urgent revascularization assessment if symptomatic and otherwise suitable | | Near-occlusion | Distal internal carotid caliber reduction/collapse; routine CEA benefit is uncertain and specialist imaging review is required | | Complete occlusion | Routine CEA/stenting is not used to reopen a chronic occlusion for stroke prevention | ## Epidemiology and vascular risk Carotid atherosclerosis shares the major determinants of systemic atherosclerotic cardiovascular disease: - older age; - smoking; - hypertension; - dyslipidemia; - diabetes mellitus; - chronic kidney disease; - coronary or peripheral artery disease; - family history of premature atherosclerotic disease. The carotid lesion is a marker of systemic risk. Myocardial infarction and cardiovascular death remain important competing outcomes even after technically successful revascularization. ## Pathophysiology and plaque risk Stroke from carotid atherosclerosis is usually embolic. Plaque rupture or erosion, intraplaque hemorrhage, ulceration, and superimposed thrombus release embolic material into the retinal or intracranial circulation. Severe stenosis can also compromise perfusion when collateral reserve is poor. Risk is not determined by percentage stenosis alone. Features associated with higher risk in observational studies include: - rapid progression; - silent ipsilateral infarction; - plaque ulceration; - intraplaque hemorrhage on MRI; - microembolic signals on transcranial Doppler; - contralateral TIA/stroke or occlusion in selected settings; - impaired cerebrovascular reserve.[4] These features can inform asymptomatic decision-making but do not replace trial-based procedural thresholds. ## Clinical presentation ### Retinal ischemia Transient monocular visual loss is usually abrupt, painless, and negative rather than positive visual phenomena. Persistent retinal artery occlusion causes sustained loss. Ipsilateral retinal ischemia is a symptomatic carotid event and requires the same urgent vascular pathway as cerebral TIA. ### Hemispheric TIA Typical manifestations are abrupt contralateral weakness or numbness, aphasia, or other focal cortical deficits. Symptoms may resolve completely while diffusion MRI shows a small infarct. ### Ischemic stroke Persistent focal deficit requires an acute stroke pathway. Carotid surgery is not the first intervention when reperfusion therapy may be indicated. > **Caution:** Do not delay IV thrombolysis or mechanical thrombectomy assessment to pursue carotid revascularization. Acute reperfusion eligibility and later carotid prevention are separate decisions.[5] ## Initial pathway after a carotid-territory event 1. Establish time last known well and neurologic severity. 2. Obtain urgent brain imaging to exclude hemorrhage and define infarct burden. 3. Obtain head/neck arterial imaging when large-artery disease is suspected. 4. Treat eligible acute stroke with reperfusion therapy according to current stroke guidance. 5. Begin antithrombotic and vascular-risk treatment when safe. 6. If ipsilateral 50–99% stenosis is present, involve stroke and vascular specialists promptly so an indicated intervention is not delayed beyond the period of greatest benefit.[1-5] 7. Determine whether infarct size, hemorrhagic transformation, neurologic instability, or medical instability requires delay. Related references: [Acute Ischemic Stroke](../neurology/acute-ischemic-stroke.md) and [Transient Ischemic Attack in Adults](../neurology/transient-ischemic-attack-in-adults.md). ## Diagnostic imaging ### Duplex ultrasonography Duplex ultrasound is the usual first-line test for extracranial carotid stenosis and the standard surveillance modality. It integrates B-mode plaque imaging with Doppler velocities. Interpretation should use laboratory-validated criteria. Peak systolic velocity, end-diastolic velocity, internal-to-common carotid ratio, plaque appearance, and distal waveform all contribute. Results can be distorted by: - contralateral occlusion; - low cardiac output; - tandem lesions; - severe vessel tortuosity; - heavy calcification; - operator/technical limitations. A clinically important or unexpected duplex result should generally be confirmed with cross-sectional angiography before a procedure.[1,4] ### CT angiography CTA is rapid and widely available. It shows lumen narrowing, plaque calcification, arch anatomy, tandem disease, intracranial vessels, and procedural anatomy. Limitations include iodinated contrast, radiation, and calcification blooming that can overestimate severe stenosis. ### MR angiography MRA is useful when iodinated contrast is undesirable or brain MRI is already planned. Noncontrast time-of-flight MRA can overestimate stenosis from flow-related signal loss; contrast-enhanced MRA can improve lumen definition when appropriate. ### Catheter angiography Digital subtraction angiography offers high spatial resolution but carries embolic and access-site risk. Reserve it for discordant noninvasive studies, complex anatomy, or endovascular treatment planning rather than routine screening. ## Differential diagnosis of a carotid-territory event | Alternative mechanism | Clues | Next step | |---|---|---| | Atrial fibrillation/cardioembolism | Multiple territories, atrial arrhythmia, cardiac thrombus | ECG/telemetry, extended rhythm monitoring when indicated, echocardiography | | Intracranial atherosclerosis | Intracranial stenosis in the symptomatic territory | Intracranial vascular imaging and disease-specific medical therapy | | Carotid dissection | Neck/head pain, trauma, younger patient, tapered stenosis | CTA/MRA with vessel-wall assessment as needed | | Small-vessel disease | Lacunar syndrome with deep small infarct | Treat vascular risk; do not assume incidental carotid stenosis caused event | | Aortic embolic source | Complex arch atheroma or aortic pathology | Aortic/cardiac evaluation when clinically indicated | | Vasculitis/other arteriopathy | Multifocal stenosis, inflammatory/systemic clues | Targeted laboratory and vascular work-up | ## Intensive medical management ### Antithrombotic therapy For noncardioembolic TIA or ischemic stroke, use antiplatelet therapy according to secondary-prevention guidance.[2] Short-course dual antiplatelet therapy is appropriate in selected high-risk TIA or minor stroke pathways, but long-term dual therapy is not routine because bleeding increases. Carotid stenting requires peri-procedural dual antiplatelet therapy. CEA antiplatelet management follows the surgical protocol, commonly continuing aspirin. Anticoagulation is not a treatment for carotid atherosclerosis itself. Use anticoagulation for a separate indication such as atrial fibrillation, and avoid unnecessary addition of antiplatelet therapy when bleeding risk outweighs incremental benefit. ### Lipid lowering Use high-intensity statin therapy unless contraindicated. Add nonstatin therapy when necessary to reach the applicable secondary-prevention target. Modern carotid care assumes aggressive LDL lowering rather than procedural treatment alone.[2,4] ### Blood pressure, diabetes, and lifestyle - Treat chronic hypertension after the acute stroke period; avoid unindicated rapid reduction during acute ischemia. - Optimize diabetes therapy and avoid severe hypoglycemia. - Stop tobacco exposure. - Use a cardioprotective dietary pattern and regular physical activity appropriate to neurologic status. - Address obesity, sleep apnea, and adherence when relevant. ## Symptomatic stenosis: revascularization decisions ### 70–99% stenosis CEA is the preferred revascularization strategy for most standard-risk patients with recent ipsilateral TIA or nondisabling stroke when procedural stroke/death risk is low.[1-4] The benefit is largest when treatment is performed promptly after the qualifying event. ### 50–69% stenosis CEA benefit is more modest. Favor intervention when the event is convincingly carotid-related, procedural risk is low, life expectancy is reasonable, and patient factors predict meaningful benefit. Delay reduces benefit. ### <50% stenosis Do not perform CEA for stroke prevention based on the stenosis alone.[3] ### Near-occlusion Near-occlusion requires specialist image review because the distal artery may be collapsed and conventional percent-stenosis measurements become misleading. Routine intervention is not supported as strongly as for ordinary severe stenosis. Recurrent symptoms despite optimal therapy may justify individualized consideration.[4] ## Timing after TIA or ischemic stroke ### Within 14 days When CEA is indicated, guidelines generally recommend intervention as early as safely feasible and preferably within **14 days**.[1,3,4] Early benefit reflects the high recurrence risk soon after the index event. ### First 48 hours The 2026 AHA/ASA acute ischemic stroke guideline specifically states that, in acute ischemic stroke or unstable neurologic status from high-grade carotid disease without an intracranial occlusion, **emergency CEA within 48 hours is not beneficial** for improving functional outcome.[5] The guideline cites a large meta-analysis in which CEA within 2 days, compared with days 3–14, was associated with higher 30-day stroke (OR 1.57) and death (OR 5.19).[5] This recommendation applies to acute ischemic stroke. A patient with recurrent TIA and no substantial infarct may require individualized urgent management by an experienced team. ### Delay revascularization when - there is a large territorial infarct, edema, or mass effect; - hemorrhagic transformation is present or likely; - neurologic status is unstable; - stroke is severely disabling with limited preventive benefit; - severe uncontrolled hypertension or another medical instability persists; - the relationship between stenosis and symptoms is uncertain. ## CEA versus carotid stenting ### CEA CEA remains the reference procedure for most symptomatic standard-surgical-risk disease.[1-4] Important complications: - perioperative ischemic stroke; - myocardial infarction; - cervical hematoma/airway compromise; - cranial nerve injury; - hyperperfusion syndrome or intracranial hemorrhage; - restenosis. ### Transfemoral carotid artery stenting Stenting is useful when CEA risk or neck anatomy is unfavorable and endovascular anatomy is suitable. Relative disadvantages include embolic risk from arch/lesion traversal and the need for dual antiplatelet therapy. Advanced age, heavy calcification, severe tortuosity, and complex arch disease may increase risk.[3,4] ### Transcarotid artery revascularization Flow-reversal transcarotid techniques are increasingly used for selected anatomy and surgical-risk profiles. Evidence is largely observational/registry-based compared with the randomized evidence supporting CEA and the transfemoral strategy used in major trials. Do not extrapolate CREST-2 stenting results automatically to every stent platform or access route.[6] ## Asymptomatic stenosis ### Do not screen the general population The U.S. Preventive Services Task Force recommends against screening asymptomatic adults because procedural harms and false-positive pathways outweigh proven benefit at the population level.[7] The Society for Vascular Surgery similarly advises against general population screening, while allowing selective screening of higher-risk patients only when a positive result would lead to a realistic intervention discussion.[1] ### Guideline framework before CREST-2 The 2022 Society for Vascular Surgery guideline recommends CEA for selected low-surgical-risk patients with **70–99%** asymptomatic stenosis if the center's perioperative stroke/death rate is **<3%**.[1] The 2023 European Society for Vascular Surgery guideline recommends considering CEA for selected **60–99%** asymptomatic stenosis when clinical/imaging features indicate higher late-stroke risk despite best medical therapy, expected 30-day stroke/death risk is ≤3%, and life expectancy is generally more than 5 years.[4] ### 2026 CREST-2 results CREST-2 enrolled patients with **≥70% asymptomatic carotid stenosis** into two parallel randomized trials: intensive medical management alone versus the same medical management plus carotid stenting, and medical management alone versus medical management plus CEA.[6] | Trial | Intensive medical therapy | Revascularization + intensive therapy | 4-year primary outcome | |---|---:|---:|---| | Stenting trial | 6.0% | 2.8% | Significant absolute reduction; P=0.02 | | CEA trial | 5.3% | 3.7% | Difference not statistically significant; P=0.24 | The primary outcome included peri-procedural stroke/death and subsequent ipsilateral stroke. Early procedural events occurred in both revascularization groups, so benefit depends on excellent operator/center performance.[6] > **Current practice:** CREST-2 strengthens the rationale for discussing stenting in carefully selected patients with severe asymptomatic disease, but it does not justify routine stenting for every ≥70% lesion. Anatomy, age, antiplatelet tolerance, center results, life expectancy, competing morbidity, patient preference, and plaque-risk features remain central.[6] ### Practical asymptomatic decision pathway **High-grade asymptomatic stenosis confirmed** → Start/optimize intensive medical management → Confirm imaging severity and anatomy with a second modality when intervention is contemplated → Estimate life expectancy and competing cardiovascular/cancer risk → Review plaque-risk features and progression → Verify audited local peri-procedural outcomes → Discuss medical therapy alone versus revascularization with explicit procedural risk Do not perform a procedure merely because a numerical stenosis threshold is met. ## Procedural selection table | Clinical factor | Often favors CEA | Often favors stenting / alternative approach | |---|---|---| | Typical symptomatic standard-risk patient | Yes | Only when specific advantages exist | | Older age with unfavorable arch anatomy | Yes | Transfemoral stenting less attractive | | Prior neck radiation or hostile neck | May increase surgical risk | Stenting may be preferable | | High cervical lesion | Surgical access may be difficult | Endovascular option may be preferable | | Severe calcification/tortuosity | Can still favor CEA | Can increase stenting risk | | Need to avoid dual antiplatelet therapy | Favors CEA | Stenting requires dual therapy | | Severe cardiopulmonary surgical risk | Individualize | Endovascular strategy may reduce some surgical hazards | | Asymptomatic ≥70% disease after CREST-2 | CEA benefit was not statistically significant in trial | Stenting showed benefit in trial, but only with expert selection/performance | ## Perioperative and postprocedural monitoring ### After CEA Monitor for: - new focal neurologic deficit; - neck swelling, hematoma, stridor, or airway compromise; - hypo- or hypertension; - myocardial ischemia; - cranial nerve dysfunction; - hyperperfusion syndrome: severe ipsilateral headache, seizures, neurologic deficit, or intracranial hemorrhage. Tight but safe blood-pressure control is important after revascularization. ### After stenting Monitor for: - stroke/TIA; - access-site complications; - bradycardia/hypotension from carotid sinus stimulation; - contrast-associated kidney injury in at-risk patients; - adherence and bleeding on dual antiplatelet therapy. ## Surveillance After CEA or stenting, use duplex surveillance according to local vascular protocol, particularly when restenosis risk would change management. After nonprocedural management, repeat imaging is reasonable when progression would alter an intervention decision. Surveillance frequency should reflect baseline severity, progression rate, contralateral disease, and candidacy for treatment rather than an automatic schedule for all patients.[1,4] ## Special situations ### Contralateral carotid occlusion Contralateral occlusion can increase operative complexity and may alter duplex velocities and cerebral perfusion reserve. It does not by itself mandate stenting. Choose procedure through multidisciplinary assessment of anatomy and center outcomes.[4] ### Prior radiation or neck surgery A hostile neck can increase CEA technical risk and cranial nerve/wound complications, making an endovascular strategy more attractive when anatomy is favorable. ### Chronic kidney disease Minimize unnecessary iodinated contrast and optimize renal protection. Duplex ultrasound and noncontrast MRA may be useful, but procedure choice must also account for overall cardiovascular risk and life expectancy. ### Older adults and frailty The preventive value of asymptomatic revascularization diminishes when life expectancy is limited or competing mortality is high. Frailty, cognition, cancer, severe heart/lung disease, and patient goals should be part of the decision. ## Complications ### Untreated carotid disease - retinal ischemia; - TIA; - ischemic stroke; - recurrent embolic events; - progression to severe stenosis or occlusion. ### Revascularization-related - stroke or death; - myocardial infarction; - cranial nerve injury after CEA; - access complications after stenting; - cervical hematoma after CEA; - hyperperfusion syndrome; - restenosis; - bleeding related to antiplatelet treatment. ## Bedside checklist **Recent ipsilateral retinal/cerebral event + carotid stenosis** - Confirm event is truly carotid-territory. - Treat as urgent stroke/TIA and initiate medical therapy. - Confirm stenosis severity with high-quality vascular imaging. - 70–99%: urgent CEA assessment in most suitable patients. - 50–69%: individualized CEA decision. - <50%: no CEA for lesion alone. - Avoid routine CEA in the first 48 hours after acute ischemic stroke; proceed once stable, aiming for treatment within 14 days when indicated.[1,5] **Asymptomatic severe stenosis** - Do not stop at the percentage stenosis. - Optimize medical therapy. - Confirm severity/anatomy. - Estimate procedural risk, life expectancy, and plaque-related risk. - Incorporate CREST-2 evidence into shared decision-making.[6] ## Recent guideline and evidence changes The 2026 AHA/ASA acute ischemic stroke guideline clarified that emergency CEA within 48 hours for acute ischemic stroke or unstable neurologic status caused by high-grade carotid stenosis/occlusion without intracranial occlusion provides no functional benefit and should not be routine.[5] CREST-2 materially changed the asymptomatic evidence base. In contemporary patients with ≥70% asymptomatic stenosis receiving intensive medical therapy, stenting reduced the 4-year composite outcome compared with medical therapy alone, whereas the CEA comparison did not reach statistical significance.[6] Existing 2022–2023 procedural guidelines were written before these primary results and therefore need to be interpreted in that context.[1,4] ## References 1. AbuRahma AF, Avgerinos ED, Chang RW, et al. Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovascular disease. *J Vasc Surg*. 2022;75(1S):4S-22S. DOI: 10.1016/j.jvs.2021.04.073. PMID: 34153348. https://pubmed.ncbi.nlm.nih.gov/34153348/ 2. Kleindorfer DO, Towfighi A, Chaturvedi S, et al. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack. *Stroke*. 2021;52:e364-e467. DOI: 10.1161/STR.0000000000000375. https://www.ahajournals.org/doi/10.1161/STR.0000000000000375 3. Bonati LH, Kakkos S, Berkefeld J, et al. European Stroke Organisation guideline on endarterectomy and stenting for carotid artery stenosis. *Eur Stroke J*. 2021;6(2):I-XLVII. DOI: 10.1177/23969873211012121. PMID: 34414302. https://pubmed.ncbi.nlm.nih.gov/34414302/ 4. Naylor R, Rantner B, Ancetti S, et al. European Society for Vascular Surgery 2023 Clinical Practice Guidelines on the Management of Atherosclerotic Carotid and Vertebral Artery Disease. *Eur J Vasc Endovasc Surg*. 2023;65(1):7-111. DOI: 10.1016/j.ejvs.2022.04.011. PMID: 35598721. https://pubmed.ncbi.nlm.nih.gov/35598721/ 5. American Heart Association/American Stroke Association. 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke. *Stroke*. 2026;57:e316-e436. DOI: 10.1161/STR.0000000000000513. https://www.ahajournals.org/doi/10.1161/STR.0000000000000513 6. Brott TG, Howard G, Lal BK, Voeks JH, et al. Medical Management and Revascularization for Asymptomatic Carotid Stenosis. *N Engl J Med*. 2026;394(3):219-231. DOI: 10.1056/NEJMoa2508800. PMID: 41269206. https://pubmed.ncbi.nlm.nih.gov/41269206/ 7. U.S. Preventive Services Task Force. Screening for Asymptomatic Carotid Artery Stenosis: Recommendation Statement. *JAMA*. 2021;325(5):476-481. DOI: 10.1001/jama.2020.26988. PMID: 33528542. https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/carotid-artery-stenosis-screening7:["$","$L17",null,{"article":{"id":"medical-carotid-artery-stenosis-in-adults","title":"Carotid Artery Stenosis in Adults","slug":"carotid-artery-stenosis-in-adults","description":"Atherosclerotic extracranial internal carotid artery stenosis causes retinal and cerebral ischemia primarily through plaque disruption and artery-to-artery embolism. The decisive distinction is symptomatic versus asym…","aliases":[],"category":"Vascular Medicine","tags":["Vascular Medicine"],"updatedAt":"$undefined","body":"$18","headings":[{"id":"summary","text":"Summary","level":2},{"id":"definitions","text":"Definitions","level":2},{"id":"symptomatic-carotid-stenosis","text":"Symptomatic carotid stenosis","level":3},{"id":"asymptomatic-carotid-stenosis","text":"Asymptomatic carotid stenosis","level":3},{"id":"nascet-measurement","text":"NASCET measurement","level":3},{"id":"epidemiology-and-vascular-risk","text":"Epidemiology and vascular risk","level":2},{"id":"pathophysiology-and-plaque-risk","text":"Pathophysiology and plaque risk","level":2},{"id":"clinical-presentation","text":"Clinical presentation","level":2},{"id":"retinal-ischemia","text":"Retinal ischemia","level":3},{"id":"hemispheric-tia","text":"Hemispheric TIA","level":3},{"id":"ischemic-stroke","text":"Ischemic stroke","level":3},{"id":"initial-pathway-after-a-carotid-territory-event","text":"Initial pathway after a carotid-territory event","level":2},{"id":"diagnostic-imaging","text":"Diagnostic imaging","level":2},{"id":"duplex-ultrasonography","text":"Duplex ultrasonography","level":3},{"id":"ct-angiography","text":"CT angiography","level":3},{"id":"mr-angiography","text":"MR angiography","level":3},{"id":"catheter-angiography","text":"Catheter angiography","level":3},{"id":"differential-diagnosis-of-a-carotid-territory-event","text":"Differential diagnosis of a carotid-territory event","level":2},{"id":"intensive-medical-management","text":"Intensive medical management","level":2},{"id":"antithrombotic-therapy","text":"Antithrombotic therapy","level":3},{"id":"lipid-lowering","text":"Lipid lowering","level":3},{"id":"blood-pressure-diabetes-and-lifestyle","text":"Blood pressure, diabetes, and lifestyle","level":3},{"id":"symptomatic-stenosis-revascularization-decisions","text":"Symptomatic stenosis: revascularization decisions","level":2},{"id":"7099-stenosis","text":"70–99% stenosis","level":3},{"id":"5069-stenosis","text":"50–69% stenosis","level":3},{"id":"50-stenosis","text":"<50% stenosis","level":3},{"id":"near-occlusion","text":"Near-occlusion","level":3},{"id":"timing-after-tia-or-ischemic-stroke","text":"Timing after TIA or ischemic stroke","level":2},{"id":"within-14-days","text":"Within 14 days","level":3},{"id":"first-48-hours","text":"First 48 hours","level":3},{"id":"delay-revascularization-when","text":"Delay revascularization when","level":3},{"id":"cea-versus-carotid-stenting","text":"CEA versus carotid stenting","level":2},{"id":"cea","text":"CEA","level":3},{"id":"transfemoral-carotid-artery-stenting","text":"Transfemoral carotid artery stenting","level":3},{"id":"transcarotid-artery-revascularization","text":"Transcarotid artery revascularization","level":3},{"id":"asymptomatic-stenosis","text":"Asymptomatic stenosis","level":2},{"id":"do-not-screen-the-general-population","text":"Do not screen the general population","level":3},{"id":"guideline-framework-before-crest-2","text":"Guideline framework before CREST-2","level":3},{"id":"2026-crest-2-results","text":"2026 CREST-2 results","level":3},{"id":"practical-asymptomatic-decision-pathway","text":"Practical asymptomatic decision pathway","level":3},{"id":"procedural-selection-table","text":"Procedural selection table","level":2},{"id":"perioperative-and-postprocedural-monitoring","text":"Perioperative and postprocedural monitoring","level":2},{"id":"after-cea","text":"After CEA","level":3},{"id":"after-stenting","text":"After stenting","level":3},{"id":"surveillance","text":"Surveillance","level":2},{"id":"special-situations","text":"Special situations","level":2},{"id":"contralateral-carotid-occlusion","text":"Contralateral carotid occlusion","level":3},{"id":"prior-radiation-or-neck-surgery","text":"Prior radiation or neck surgery","level":3},{"id":"chronic-kidney-disease","text":"Chronic kidney disease","level":3},{"id":"older-adults-and-frailty","text":"Older adults and frailty","level":3},{"id":"complications","text":"Complications","level":2},{"id":"untreated-carotid-disease","text":"Untreated carotid disease","level":3},{"id":"revascularization-related","text":"Revascularization-related","level":3},{"id":"bedside-checklist","text":"Bedside checklist","level":2},{"id":"recent-guideline-and-evidence-changes","text":"Recent guideline and evidence changes","level":2},{"id":"references","text":"References","level":2}],"readingMinutes":15},"linkedMarkdown":"$19","backlinks":[],"related":[],"previewBySlug":{"abcde-approach":{"title":"ABCDE Approach","description":"The ABCDE approach is a structured method for the immediate assessment and treatment of a deteriorating or critically ill patient: Airway, Breathing, Circulation, Disability, Exposure. 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