ANZCA Final
Vascular Surgery
Interventional Neuroradiology
Neuroanaesthesia
High Evidence

Anaesthesia for Carotid Artery Stenting (CAS)

Carotid artery stenting (CAS) is a minimally invasive alternative to carotid endarterectomy (CEA) for carotid stenosis. Indications : High surgical risk (medical comorbidities, hostile neck, previous CEA/restenosis),...

Updated 3 Feb 2026
30 min read
Citations
98 cited sources
Quality score
56 (gold)

Clinical board

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Urgent signals

Safety-critical features pulled from the topic metadata.

  • Acute stroke during procedure (new focal deficit)
  • Acute carotid occlusion (loss of flow)
  • Severe bradycardia/asystole (baroreflex)
  • Hyperperfusion syndrome (severe headache, seizure)

Exam focus

Current exam surfaces linked to this topic.

  • ANZCA Final Written
  • ANZCA Final Clinical Viva

Editorial and exam context

ANZCA Final Written
ANZCA Final Clinical Viva
Clinical reference article

Quick Answer

Carotid artery stenting (CAS) is a minimally invasive alternative to carotid endarterectomy (CEA) for carotid stenosis. Indications: High surgical risk (medical comorbidities, hostile neck, previous CEA/restenosis), anatomically difficult CEA (high bifurcation, above C2), radiation-induced stenosis. Cerebral protection: Distal embolic protection devices (filter wires, balloon occlusion) or proximal flow reversal systems reduce stroke risk. Key complications: Periprocedural stroke (2-4%), bradycardia/hypotension from carotid baroreflex activation, hyperperfusion syndrome (1-3%), carotid dissection. Anaesthetic considerations: Most procedures performed under local anaesthesia with sedation (allows neurological monitoring), GA occasionally required (patient factors, complex cases). Perioperative management: Antiplatelet therapy mandatory (aspirin + clopidogrel), blood pressure control, contrast minimization. [1-15]

Pathophysiology

Carotid Stenosis and Stroke Risk

Pathophysiology:

  • Atherosclerotic plaque: Carotid bifurcation predilection (flow disturbance)
  • Stroke mechanisms:
    1. Artery-to-artery embolism: Plaque embolization to cerebral circulation (most common)
    2. Hemodynamic: Severe stenosis → hypoperfusion (rare, requires >90% stenosis or bilateral disease)
    3. Thrombosis: Acute occlusion (uncommon)

Symptomatic vs. Asymptomatic:

  • Symptomatic: Recent TIA, stroke, amaurosis fugax
    • High early stroke risk (10-20% at 2 weeks with >70% stenosis)
    • Greatest benefit from revascularization
  • Asymptomatic: No recent neurological symptoms
    • Lower stroke risk (~2% per year)
    • Benefit of revascularization less clear (selective approach)

Carotid Artery Stenting vs. Endarterectomy

CEA Advantages:

  • Lower periprocedural stroke rates (lower risk in symptomatic patients)
  • Established durability (>95% patency at 5 years)
  • No radiation exposure
  • Lower restenosis risk (1-2% vs. 5-10% for CAS)

CEA Disadvantages:

  • Surgical risks: Cranial nerve injury (5-10%), neck hematoma (5%), MI (1-2%), wound complications
  • Access issues: High bifurcation (above C2), previous neck surgery/radiation, unstable coronary disease
  • Not suitable for: High-risk surgical candidates

CAS Advantages:

  • Minimally invasive (local anaesthesia, no neck incision)
  • Lower MI and cranial nerve injury rates
  • Suitable for: High surgical risk, hostile neck, high bifurcation, previous CEA with restenosis, radiation stenosis
  • Shorter hospital stay (often day case or overnight)
  • No general anaesthesia risks (if performed awake)

CAS Disadvantages:

  • Higher periprocedural stroke risk than CEA in symptomatic patients (especially elderly >70 years)
  • Requires dual antiplatelet therapy (bleeding risk if emergency surgery needed)
  • Radiation exposure
  • Contrast nephropathy risk
  • Technical failure (tortuous anatomy, severe calcification)
  • Cost (expensive devices)

Evidence:

  • CREST trial: No difference in composite outcome (stroke, MI, death) between CAS and CEA; CAS higher stroke, CEA higher MI
  • ICSS (International Carotid Stenting Study): CAS had higher stroke/death rate than CEA in symptomatic patients
  • SPACE trial: No difference between CAS and CEA
  • ACT-1: CAS non-inferior to CEA in asymptomatic standard-risk patients
  • Age effect: CAS outcomes worse in patients >70 years (vessel tortuosity, aortic arch disease)

Current Indications for CAS:

  • High surgical risk: Severe cardiac/pulmonary/renal disease
  • Anatomically unfavourable for CEA: High bifurcation (above C2), deep cervical carotid, tandem intracranial stenosis
  • Hostile neck: Previous radical neck dissection, tracheostomy, radiation therapy (fibrosis)
  • Previous CEA with restenosis: Surgery more difficult, higher cranial nerve injury
  • Bilateral stenosis: Staged CAS may reduce cranial nerve injury risk
  • Concurrent cardiac disease: Patient requiring CABG (staged or combined)

Embolic Protection Devices (EPD)

Rationale:

  • Carotid manipulation (guide catheter, stent deployment, angioplasty) causes microembolization
  • Without protection: 10-20% silent embolic events on DWI MRI
  • EPD reduces periprocedural stroke risk (evidence supports routine use)

Types:

1. Distal Filter Devices (Most Common):

  • Mechanism: Filter wire placed distal to lesion, captures emboli while maintaining flow
  • Deployment: Filter opened distal to stenosis before stent deployment
  • Advantages: Maintains antegrade flow, ipsilateral cerebral perfusion
  • Limitations: Cannot be placed if lesion extends to skull base, crossing lesion may embolize, filter may fill/occlude
  • Examples: SpiderFX, Angioguard, Emboshield

2. Distal Balloon Occlusion:

  • Mechanism: Balloon distal to lesion inflates, stopping flow; aspirated blood with debris discarded
  • Procedure: Occlude → intervene → aspirate → deflate
  • Advantages: Complete embolic protection
  • Disadvantages: Cerebral ischemia during occlusion (tolerance 3-5 minutes), requires landing zone
  • Example: PercuSurge GuardWire

3. Proximal Flow Reversal:

  • Mechanism: Balloon in common carotid + external carotid balloon or flow reversal via sheath; creates reverse flow, debris goes to external carotid or aspiration
  • Procedure: Occlude CCA + ECA → flow reversal → intervene → aspirate → deflation
  • Advantages: Protection before crossing lesion (theoretical benefit), no need to cross lesion
  • Disadvantages: Incomplete flow reversal in some patients, requires large sheath (9-11 Fr), intolerance in some (ECA collateral dependence)
  • Examples: MO.MA, GORE Flow Reversal

Protection Device Selection:

  • Distal filter: Default choice (adequate landing zone, no ECA disease)
  • Proximal reversal: Severe tortuous anatomy, lesion extends to skull base, ulcerated plaque
  • No protection: Only if absolutely contraindicated (significantly increases stroke risk)

Evidence:

  • SAPPHIRE: EPD reduces stroke in high-risk patients
  • Multiple meta-analyses: EPD reduces periprocedural stroke (number needed to treat ~20)
  • Sentinel device (TAVR): Transcranial Doppler shows dramatic embolic reduction with protection

Carotid Baroreflex Physiology

Anatomy:

  • Baroreceptors: Located in carotid sinus at bifurcation
  • Afferent: Glossopharyngeal nerve (CN IX) → nucleus tractus solitarius
  • Efferent: Vagus nerve → cardiac slowing, vasodilation

Stenting Effect:

  • Mechanism: Balloon angioplasty and stent deployment stretch carotid sinus → activate baroreceptors
  • Response: Bradycardia, hypotension, AV block, asystole (rare)
  • Incidence: 20-40% significant bradycardia, 5-10% hypotension, <1% asystole
  • Risk factors: Calcified plaques (stiffer, more baroreceptor stretch), previous contralateral CEA (denervation → hypersensitivity), recent MI (vagal sensitivity)

Management:

  • Prevention: Atropine 0.5-1 mg IV pre-angioplasty (reduces but doesn't eliminate)
  • Monitoring: Continuous ECG, arterial line (beat-to-beat BP)
  • Treatment: Atropine 0.5-1 mg IV (repeat), glycopyrrolate, volume loading, vasopressors
  • Pacing: External pacing pads (rarely needed), temporary transvenous pacing (rare)
  • Balloon deflation: Immediate deflation if severe bradycardia/asystole

Hyperperfusion Syndrome

Pathophysiology:

  • Chronic hypoperfusion: Severe stenosis → maximal cerebral vasodilation (loss of autoregulation reserve)
  • Acute restoration: Stenting restores flow → high perfusion pressure → breakthrough hyperemia
  • Impaired autoregulation: Cannot constrict vessels to compensate
  • Blood-brain barrier disruption: Leads to edema, hemorrhage

Risk Factors:

  • Severe stenosis (>90%)
  • Contralateral carotid occlusion (no collateral reserve)
  • Recent stroke (impaired autoregulation in ischemic territory)
  • Hypertension (drives perfusion pressure)
  • Diabetes (microvascular disease)

Clinical Features:

  • Timing: Usually 24-72 hours post-procedure (can be immediate or delayed up to 7 days)
  • Headache: Ipsilateral, severe, throbbing
  • Seizures: Focal or generalized
  • Focal deficits: Transient (Todd's paralysis) or permanent (hemorrhage)
  • Intracerebral hemorrhage: Catastrophic, 0.5-1% incidence, 50% mortality

Prevention:

  • Blood pressure control: Strict normotension pre/during/post-procedure
    • Target SBP 100-140 mmHg (some centres <120 mmHg in high-risk)
    • Avoid hypertension at all costs
  • Gradual flow restoration: Consider staged angioplasty (rarely practiced)
  • Monitoring: Neurological assessment every 15-30 minutes post-procedure

Treatment:

  • BP control: IV agents (labetalol, hydralazine, nicardipine, clevidipine)
  • Seizure management: Benzodiazepines, antiepileptics
  • ICU admission: Close neurological monitoring
  • CT brain: If severe headache or neurological change (exclude hemorrhage)
  • Mannitol: If edema (rarely needed)

Differentiation from Contrast Encephalopathy:

  • Hyperperfusion: Focal, ipsilateral to stented artery, delayed 24-72 hours
  • Contrast encephalopathy: Bilateral, transient cortical blindness, seizure, occurs during/immediately post-procedure

Clinical Presentation

Preprocedural Assessment

History:

  • Neurological: TIA/stroke timing and symptoms, baseline deficits
  • Risk factors: Hypertension, diabetes, smoking, hyperlipidemia, family history
  • Cardiac: CAD, previous MI, arrhythmia, heart failure (risk of periprocedural MI, baroreflex sensitivity)
  • Previous CEA: Restenosis pattern, cranial nerve injury
  • Neck anatomy: Previous surgery, radiation, tracheostomy
  • Medications: Antiplatelets, anticoagulants, antihypertensives
  • Allergies: Iodinated contrast (anaphylaxis, nephropathy)

Physical Examination:

  • Cardiovascular: BP in both arms, cardiac murmurs, rhythm
  • Neurological: Complete exam (baseline for comparison), cranial nerve function
  • Airway: Assessment (if GA required)
  • Vascular: Peripheral pulses (femoral access), carotid bruits

Investigations:

Imaging:

  • Carotid duplex: Stenosis severity, plaque characteristics (echolucent = higher risk)
  • CTA/MRA: Arch anatomy (tortuosity, type III arch increases CAS difficulty), intracranial circulation, tandem lesions
  • CT brain: Baseline (prior infarcts, hemorrhage)

Cardiac:

  • ECG: Ischemia, arrhythmia
  • Echocardiography: LV function, wall motion, valve disease
  • Stress test: If active symptoms (high-risk for periprocedural MI)

Laboratory:

  • FBC, coagulation: Baseline
  • Creatinine: Renal function (contrast nephropathy risk)
  • Electrolytes: Baseline
  • Glucose: Diabetes control

Risk Stratification:

Medical Risk (High-risk for CEA):

  • Severe CAD (unstable angina, recent MI, EF <30%, severe valvular disease)
  • Severe COPD (FEV₁ <30%, home oxygen)
  • Severe renal disease (CrCl <30 mL/min)
  • Age >80 years
  • Contralateral carotid occlusion
  • Previous ipsilateral CEA
  • High cervical/internal carotid lesion (above C2)
  • Prior neck radiation or radical surgery

Anatomical Risk (Technical difficulty):

  • Severe aortic arch atheroma (embolization risk)
  • Type III aortic arch (acute angle, difficult catheterization)
  • Severe carotid tortuosity (sheath/filter delivery difficulty)
  • Long, ulcerated lesion
  • Severe circumferential calcification (stent expansion difficulty, baroreflex activation)
  • Near-occlusion ("string sign")

CAS vs CEA Decision Algorithm

Symptomatic Patients:

  • Standard surgical risk: CEA preferred (lower stroke rate, especially >70 years)
  • High surgical risk: Consider CAS (but recognize stroke risk higher than CEA)
  • Anatomically unfavourable for CEA: CAS
  • Recent MI/unstable angina: CAS preferred (lower MI risk), or medical therapy until cardiac stabilized

Asymptomatic Patients:

  • Standard risk: CEA if appropriate (better long-term durability)
  • High risk: CAS can be considered (ACT-1 showed non-inferiority)
  • Age >70: CEA preferred (CAS stroke risk higher in elderly)

Emerging Role:

  • TCAR (TransCarotid Artery Revascularization): Hybrid approach (surgical CCA exposure + flow reversal protection + stenting)
    • Combines surgical safety of CCA access with cerebral protection
    • Avoids aortic arch manipulation
    • Promising early results, may become preferred for many high-risk patients

Management

Patient Selection and Preparation

Antiplatelet Therapy (Mandatory):

  • Aspirin: 75-325 mg daily (continue through procedure)
  • Clopidogrel: 75 mg daily for 5-7 days pre-procedure (or 300-600 mg loading if urgent)
  • Dual therapy: Reduces periprocedural stroke (evidence-based requirement)
  • Prasugrel/ticagrelor: Alternatives (faster onset, more potent bleeding risk)
  • Post-procedure: Continue dual antiplatelet for 1-3 months, then single agent lifelong

Statins:

  • Continue: Statin therapy (periprocedural protection)
  • High-intensity: Atorvastatin 40-80 mg or rosuvastatin 20-40 mg (if not already)

Prehydration:

  • Contrast nephropathy prevention: IV fluids (isotonic saline 1 mL/kg/hour for 6-12 hours pre-procedure if time permits)
  • N-acetylcysteine: Controversial benefit (may give 600-1200 mg BD pre/post)
  • Minimize contrast: Use lowest amount necessary (biplane angiography, roadmap)

Anaesthetic Technique

Local Anaesthesia with Sedation (Preferred):

Rationale:

  • Allows continuous neurological monitoring (speech, motor function)
  • Detects ischemia/embolization immediately
  • Earlier intervention if stroke occurs (thrombolysis, aspiration)
  • No GA-related hemodynamic lability
  • Shorter recovery, day-case possible

Technique:

  • Local anaesthetic: Lidocaine 1-2% infiltration at femoral puncture site (± conscious sedation)
  • Conscious sedation: Dexmedetomidine 0.2-0.5 μg/kg/hour or midazolam 1-2 mg + fentanyl 25-50 μg (light, arousable)
  • Monitoring: Standard + arterial line (essential for beat-to-beat BP, baroreflex response detection)
  • Neurological monitoring: Continuous patient interaction (counting, hand squeezing, awareness)

Advantages:

  • Immediate detection of neurological changes
  • Patient can report symptoms (visual changes, headache)
  • Avoids GA risks
  • Evidence suggests better outcomes in some studies (neurological monitoring benefit)

Disadvantages:

  • Patient discomfort, anxiety
  • Movement risk (must remain still during stent deployment)
  • Cannot control ventilation (contrast-induced laryngospasm rare)
  • Conversion to GA if patient intolerant (stroke, anxiety, airway compromise)

General Anaesthesia (Selected Cases):

Indications:

  • Patient refusal of awake procedure
  • Severe anxiety/claustrophobia
  • Movement disorder (Parkinson's, tremor)
  • Airway compromise risk (unable to protect airway)
  • Expected long/complex procedure
  • Patient factors (language barrier, cognitive impairment)

Technique:

  • Monitoring: Arterial line essential
  • Induction: Hemodynamically stable (propofol cautiously, etomidate, ketamine)
  • Airway: LMA or ETT (if prolonged/complex)
  • Maintenance: TIVA or low-dose volatile
  • Cerebral monitoring: EEG not routine (different from CEA)
  • Emergence: Rapid wake-up for neurological assessment

Disadvantages:

  • Cannot do continuous neurological monitoring
  • Hemodynamic lability (induction, emergence)
  • Delayed neurological assessment (until awake)
  • May mask hyperperfusion symptoms (headache)

Hemodynamic Management

Blood Pressure Goals:

  • Pre-procedure: Controlled (SBP 100-140 mmHg)
  • During procedure:
    • Baseline to slight elevation (maintain cerebral perfusion)
    • Avoid hypotension (ischemia risk during balloon inflation)
  • Post-procedure: Strict control (SBP 100-120 mmHg in high-risk patients)
    • Prevent hyperperfusion
    • Prevent neck hematoma (if closure device fails)

Bradycardia/Hypotension Management:

  • Prophylaxis: Atropine 0.5-1 mg IV 5 minutes before angioplasty/stent deployment
  • Monitoring: Continuous ECG, arterial line
  • Response:
    • Mild (HR 50-60, BP >90): Atropine, observation
    • Moderate (HR 40-50, BP <90): Atropine 1 mg, volume, phenylephrine
    • Severe (HR <40, BP <70, asystole): Atropine, CPR if needed, balloon deflation
  • Vasopressors: Phenylephrine (α-agonist, maintains coronary perfusion), noradrenaline if refractory
  • Pacing: External pacing pads on all patients; temporary wire rarely needed

Post-procedure Hypertension:

  • Cause: Previously hypertensive patients, loss of baroreflex after stenting (dysfunction), pain
  • Treatment: IV agents (labetalol 5-20 mg, hydralazine 5-20 mg, GTN infusion)
  • Goal: SBP <140 mmHg (ideally <120 in hyperperfusion risk)

Procedural Technique and Protection

Vascular Access:

  • Femoral: Standard (6-8 Fr sheath)
  • Radial/brachial: Alternative (rare)
  • TCAR: Surgical cutdown on CCA (direct access)

Sheath Selection:

  • Guide catheter: 6-8 Fr, positioned in common carotid
  • Long sheath: 90 cm (for tortuous anatomy)

Embolic Protection:

  • Selection based on anatomy (see above)
  • Deployment: Distal filter placed distal to lesion before any intervention
  • Monitoring: Contrast injection to confirm filter position, flow

Stent Selection:

  • Self-expanding nitinol: Standard (conforms to vessel, flexible)
  • Balloon-expandable: Rare (rigid, used for heavily calcified)
  • Closed-cell vs open-cell: Closed-cell theoretically captures more emboli (controversial benefit)
  • Tapered vs straight: Tapered for ICA (smaller distal)

Predilation:

  • Indication: Severe stenosis (cannot pass stent delivery system)
  • Technique: Small balloon (2-3 mm), brief inflation
  • Risk: Highest embolization risk period

Stent Deployment:

  • Position: Cover lesion with adequate landing zones
  • Post-dilation: Often performed (optimize apposition)
  • Risk period: Highest baroreflex activation

Completion Angiography:

  • Assess stent position, residual stenosis, branch patency
  • Look for complications (dissection, perforation, distal emboli)

Complication Management

Periprocedural Stroke:

  • Detection: Awake (neurological change), Asleep (angiographic filling defect, delayed awakening)
  • Immediate action:
    • Confirm EPD position (not occluded)
    • Angiography (identify lesion)
    • Aspiration thrombectomy if possible
    • IV thrombolysis (if within window, no contraindications)
    • Emergency neuroimaging (CT head)
    • Transfer to stroke unit/intervention
  • Prognosis: Major stroke 0.5-2%, minor stroke 1-3%

Carotid Dissection:

  • Cause: Wire/sheath manipulation, aggressive predilation
  • Detection: Angiographic intimal flap, double lumen
  • Management: Prolonged stent (cover dissection), rarely surgery

Carotid Perforation:

  • Rare but serious: Guide catheter, wire perforation
  • Detection: Contrast extravasation, sudden hypotension
  • Management: Reverse heparin, covered stent, surgery if uncontrollable

Contrast Reactions:

  • Mild: Urticaria (antihistamines)
  • Severe: Bronchospasm, anaphylaxis (adrenaline, ICU)
  • Contrast encephalopathy: Cortical blindness, seizure (supportive, usually reversible)

Access Site Complications:

  • Hematoma: Manual compression, reversal of anticoagulation if severe
  • Pseudoaneurysm: Ultrasound-guided thrombin injection
  • Retroperitoneal bleed: High femoral puncture, resuscitation, surgery

Post-procedure Care

Monitoring:

  • Neurological: Hourly for 24 hours (detect hyperperfusion, delayed stroke)
  • Blood pressure: Aggressive control (prevents hyperperfusion)
  • Access site: Groin checks (hematoma, pseudoaneurysm)
  • Renal function: Creatinine at 24-48 hours (contrast nephropathy)

Medications:

  • Antiplatelet: Continue dual therapy (aspirin + clopidogrel) for 1-3 months minimum
  • Statin: Continue high-intensity
  • Antihypertensives: Optimize regimen

Discharge:

  • Timing: Day case possible (selected patients), usually overnight observation
  • Follow-up: Carotid duplex at 1 month, then annually (restenosis surveillance)
  • Lifestyle: Smoking cessation, BP/diabetes control, exercise

Restenosis Surveillance:

  • Incidence: 5-10% at 5 years (higher than CEA 1-2%)
  • Pattern: Intimal hyperplasia (early) vs. recurrent atherosclerosis (late)
  • Management: Re-intervention if symptomatic or severe (>70-80%)

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Patients

Higher Cardiovascular Risk:

  • Earlier onset: Cerebrovascular disease 10-15 years younger than non-Indigenous
  • Higher prevalence: Hypertension, diabetes, smoking, renal disease
  • Risk factors: Clustering of metabolic syndrome components

Access and Equity:

  • Geographic barriers: Remote communities require transfer to metropolitan interventional centres
  • Delayed presentation: May present with completed stroke rather than TIA
  • Revascularization rates: Lower rates of CEA/CAS compared to non-Indigenous (access, comorbidity, presentation patterns)

Cultural Considerations:

  • Informed consent: Clear explanation of CAS vs CEA options, risks/benefits
  • Family involvement: Extended family may need to be present for decision-making
  • Communication: Use interpreters if needed, plain language
  • Cultural support: Aboriginal Liaison Officers involvement
  • Post-procedure: Coordination with remote primary care for medication management, follow-up

Secondary Prevention:

  • Medication adherence: Complex dual antiplatelet regimens challenging without support
  • Lifestyle modification: Smoking cessation programs, culturally appropriate
  • Cardiac rehabilitation: Often unavailable in remote areas

Māori Health Considerations

Health Inequities:

  • Cardiovascular disease: Higher rates of stroke, TIA
  • Risk factors: Higher diabetes, smoking, hypertension prevalence
  • Mortality: Higher cardiovascular mortality

Access Issues:

  • Rural populations: South Island rural Māori may need transfer to Auckland/Wellington
  • Interventional services: Limited to major centres
  • Presentation: May present later in disease course

Cultural Safety:

  • Whānau involvement: Family conferences for treatment planning
  • Communication: Risk/benefit discussion with cultural sensitivity
  • Kaupapa Māori services: Māori health workers involvement
  • Discharge planning: Coordination with primary care, community services

Shared Decision-Making:

  • CAS vs CEA: Consider patient preferences, cultural factors
  • Medical therapy: In high-risk surgical patients, optimal medical therapy may be culturally acceptable alternative
  • Follow-up: Ensure accessible surveillance for restenosis

Data:

  • New Zealand data shows Māori have 1.5-2× higher stroke rates
  • Revascularization disparities exist (lower rates for Māori compared to non-Māori)
  • Addressing barriers to care essential for equity

ANZCA Final Exam Focus

SAQ Patterns

Common Questions:

  • "Compare carotid artery stenting (CAS) with carotid endarterectomy (CEA)."
  • "What are the indications for CAS over CEA?"
  • "Describe the pathophysiology and management of carotid baroreflex activation during CAS."
  • "What is hyperperfusion syndrome and how is it prevented/managed?"
  • "Discuss cerebral embolic protection devices used in CAS."

Marking Scheme Priorities:

  • CAS vs CEA evidence (CREST, ICSS, SPACE trials)
  • Indications for CAS (high surgical risk, hostile neck, high bifurcation)
  • Baroreflex physiology and management (atropine, arterial line, vasopressors)
  • Hyperperfusion syndrome (risk factors, BP control, timing)
  • Embolic protection types and selection
  • Periprocedural stroke management

Viva Scenarios

Scenario 1: Bradycardia During Stent Deployment

  • HR drops to 35 bpm, BP 70/40 during balloon angioplasty
  • Immediate: Atropine 1 mg, balloon deflation
  • Prevention: Pre-treatment with atropine
  • Post-procedure: Monitor for recurrent episodes

Scenario 2: Post-procedure Hyperperfusion

  • Severe headache, confusion, mild left hemiparesis 36 hours post-CAS
  • BP 190/110 mmHg
  • Management: Urgent CT head (exclude hemorrhage), aggressive BP control (labetalol, nicardipine), ICU admission

Scenario 3: CAS vs CEA Decision

  • Symptomatic 80% stenosis, high surgical risk (EF 25%, severe COPD)
  • Discussion: CAS appropriate but higher stroke risk; TCAR alternative; optimal medical therapy if both high risk
  • Evidence: CREST showed equivalence in composite outcome but CAS higher stroke, CEA higher MI

Scenario 4: Embolic Protection

  • Complex anatomy, ulcerated plaque, lesion extends to skull base
  • Discuss: Proximal flow reversal (MO.MA) vs. distal filter; crossing lesion risk; TCAR option

Key Points for Examination Success

  1. CAS vs CEA: CREST trial equivalence in composite; CAS higher stroke, CEA higher MI; elderly >70 CEA preferred
  2. CAS indications: High surgical risk, hostile neck, high bifurcation, radiation stenosis, restenosis post-CEA
  3. Embolic protection: Distal filter default; proximal reversal for complex anatomy; reduces stroke (use routinely)
  4. Baroreflex: 20-40% bradycardia, atropine 0.5-1 mg pre-angioplasty, arterial line essential
  5. Hyperperfusion: 1-3% incidence, risk factors (severe stenosis, contralateral occlusion, recent stroke), BP control critical
  6. Antiplatelet therapy: Dual mandatory (aspirin + clopidogrel), continue 1-3 months post-procedure
  7. Anaesthesia: Local with sedation preferred (neurological monitoring); GA for selected cases
  8. Periprocedural stroke: 2-4% major/minor combined; detection and immediate management essential
  9. TCAR: Emerging hybrid option (surgical CCA access + flow reversal + stenting)
  10. Post-procedure care: BP control, neurological monitoring (hyperperfusion 24-72 hours), restenosis surveillance

Assessment Content

SAQ 1: CAS vs CEA and Embolic Protection (20 marks)

Question: A 75-year-old man with symptomatic 80% right internal carotid artery stenosis presents for revascularization. He has severe coronary artery disease (EF 30%, triple vessel disease not revascularized), severe COPD (FEV₁ 0.8 L), and chronic kidney disease (eGFR 35 mL/min).

a) Discuss the advantages and disadvantages of carotid artery stenting (CAS) compared to carotid endarterectomy (CEA) in this patient. (8 marks) b) What types of embolic protection devices are available for CAS? Compare their advantages and limitations. (6 marks) c) Outline the anaesthetic management for this patient undergoing CAS under local anaesthesia with sedation. (6 marks)

Model Answer:

a) CAS vs CEA advantages/disadvantages (8 marks):

CAS Advantages:

  • No surgical neck incision (avoids cranial nerve injury risk) (1 mark)
  • Lower myocardial infarction risk (critical in this patient with severe CAD) (1.5 marks)
  • No general anaesthesia required (lower risk with severe COPD) (1 mark)
  • Shorter recovery, possible day case (1 mark)

CAS Disadvantages:

  • Higher periprocedural stroke risk than CEA (especially age >70) (1.5 marks)
  • Contrast nephropathy risk (significant with CKD stage 3b) (1 mark)
  • Dual antiplatelet therapy required (bleeding risk if urgent cardiac surgery needed) (0.5 marks)
  • Restenosis higher (5-10% vs 1-2% for CEA)

Patient-specific consideration:

  • High surgical risk makes CAS reasonable option despite age; consider TCAR as alternative (0.5 marks)

b) Embolic protection devices (6 marks):

Distal filter devices:

  • Mechanism: Filter wire distal to lesion captures emboli while maintaining flow (1 mark)
  • Advantages: Maintains antegrade cerebral perfusion, familiar technique (1 mark)
  • Limitations: Must cross lesion (embolization risk), requires landing zone, may occlude if filled (1 mark)

Proximal flow reversal:

  • Mechanism: Balloons in CCA and ECA create reverse flow; debris to external carotid (1 mark)
  • Advantages: Protection before crossing lesion, no landing zone needed (1 mark)
  • Limitations: Large sheath (9-11 Fr), requires ECA balloon/tolerance, incomplete reversal in some (1 mark)

c) Anaesthetic management (6 marks):

  • Pre-procedure: Continue aspirin, clopidogrel loading; prehydration for renal protection; strict BP control (1.5 marks)
  • Monitoring: Arterial line essential (beat-to-beat BP, baroreflex detection); continuous ECG (1.5 marks)
  • Sedation: Light sedation (dexmedetomidine 0.2-0.5 μg/kg/hour) allowing neurological monitoring (1 mark)
  • Bradycardia prophylaxis: Atropine 0.5-1 mg IV 5 min before angioplasty (1 mark)
  • Contrast minimization: Use lowest amount possible; consider iso-osmolar contrast (iodixanol) for renal protection (1 mark)

SAQ 2: Complications of CAS (20 marks)

Question: A 68-year-old woman undergoes successful left carotid artery stenting for symptomatic 90% stenosis. The procedure was performed under local anaesthesia with sedation. Thirty-six hours post-procedure, she develops severe headache, nausea, and confusion. Her blood pressure is 185/105 mmHg.

a) What is the most likely diagnosis? What features support this? (4 marks) b) What are the risk factors for this complication? (4 marks) c) Outline the immediate and ongoing management. (8 marks) d) How might this complication have been prevented? (4 marks)

Model Answer:

a) Diagnosis (4 marks):

  • Hyperperfusion syndrome (2 marks)
  • Supporting features: Severe ipsilateral headache, neurological symptoms (confusion), timing 24-72 hours post-procedure (1 mark), severe hypertension (drives syndrome), high-grade stenosis (>90%) (1 mark)

b) Risk factors (4 marks):

  • Severe stenosis (>90%) with chronic hypoperfusion (1 mark)
  • Contralateral carotid occlusion (loss of collateral reserve) - check if present (1 mark)
  • Recent stroke/ischemic event (impaired autoregulation) (1 mark)
  • Hypertension (drives perfusion pressure) (0.5 marks)
  • Diabetes mellitus (microvascular disease) (0.5 marks)

c) Management (8 marks):

Immediate:

  • Urgent CT head: Exclude intracerebral hemorrhage (catastrophic complication) (2 marks)
  • Aggressive BP control: IV agents to reduce SBP to <140 mmHg (ideally <120) (1.5 marks)
    • Labetalol 5-20 mg IV, nicardipine/clevidipine infusion, hydralazine
  • ICU admission: Close neurological and hemodynamic monitoring (1 mark)
  • Seizure prophylaxis: If seizure occurs (lorazepam, antiepileptics) (0.5 marks)

Ongoing:

  • Neurological monitoring: Hourly GCS, focal deficits (1 mark)
  • Maintain normotension: Avoid both hypotension (ischemia) and hypertension (worsening hyperperfusion) (1 mark)
  • Mannitol: If cerebral edema (rarely needed) (0.5 marks)
  • Neurosurgical consultation: If hemorrhage or refractory edema (0.5 marks)

d) Prevention (4 marks):

  • Strict perioperative BP control: Target SBP 100-140 mmHg throughout (1.5 marks)
  • Post-procedure monitoring: Frequent neurological assessments to detect early (1 mark)
  • Gradual flow restoration: Consider staged angioplasty in very high-risk patients (0.5 marks)
  • Patient selection: Recognize high-risk patients (severe stenosis, contralateral occlusion) and optimize BP pre-procedure (1 mark)

Viva Scenario: Intra-procedural Bradycardia

Examiner: "You are anaesthetising a patient for carotid artery stenting under local anaesthesia with sedation. During balloon angioplasty, the patient's heart rate drops to 30 bpm and blood pressure falls to 65/40 mmHg."

Candidate: "This is likely carotid baroreflex activation from stretching the baroreceptors in the carotid sinus during balloon inflation. This is a common complication of CAS, occurring in 20-40% of cases. My immediate actions would be to ask the interventionalist to deflate the balloon immediately, as this is the most effective treatment. I would administer atropine 1 mg IV rapidly, and have vasopressors ready - phenylephrine or noradrenaline to support blood pressure."

Examiner: "The heart rate recovers to 50 bpm and BP to 90/60 after balloon deflation and atropine. The procedure needs to continue. How do you prevent recurrence?"

Candidate: "For the next balloon inflation, I would pre-treat with atropine 0.5-1 mg 5 minutes before. I would ensure adequate volume status and have phenylephrine boluses ready. The patient should have continuous arterial line monitoring for beat-to-beat feedback. If recurrent severe bradycardia occurs, we might consider temporary transvenous pacing, though this is rarely needed. Some operators use glycopyrrolate as an alternative to atropine."

Examiner: "What predisposes to severe baroreflex response?"

Candidate: "Risk factors include severely calcified plaques which are stiff and create more baroreceptor stretch, recent myocardial infarction which increases vagal sensitivity, and previous contralateral carotid endarterectomy which may cause baroreceptor hypersensitivity due to unilateral denervation. The location of the stenosis matters too - lesions at the carotid bifurcation involve the sinus more directly."

Examiner: "The procedure completes successfully. What are your post-procedure concerns?"

Candidate: "Post-procedure, I'm concerned about hyperperfusion syndrome, particularly in this patient with severe stenosis who likely had chronic hypoperfusion. I would maintain strict blood pressure control, targeting SBP 100-140 mmHg. I'd do frequent neurological assessments every hour for the first 24 hours, watching for severe headache, seizures, or focal deficits which would suggest hyperperfusion or hemorrhage. I would also monitor the access site for hematoma, ensure renal function is checked at 24 hours given contrast exposure, and confirm antiplatelet therapy is continued."

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