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Carotid Artery Stenosis

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1. Clinical Overview

Summary

Carotid Artery Stenosis is the atherosclerotic narrowing of the Internal Carotid Artery (ICA) at the bifurcation. It creates a turbulent, thrombogenic environment that showers emboli into the cerebral circulation, causing Stroke (MCA/ACA territory) or Amaurosis Fugax (Retinal ischaemia). The management is a precise balance of risk calculus: Surgery (CEA) reduces long-term stroke risk but carries an immediate procedural stroke risk. The absolute indication for intervention is Symptomatic High-Grade Stenosis (50-99%) within the "Hyperacute Period" (2 weeks). Asymptomatic disease is largely treated medically.

Key Facts

  • Mechanism: Embolectomy (Source control), NOT flow restoration. The brain usually has adequate collateral flow (Circle of Willis); the problem is the emboli.
  • Occlusion: A 100% occluded ICA is NEVER operated on. Once occluded, the flow stops, and the embolic risk vanishes (Safety).
  • The "High Risk" Plaque: Echolucent (soft), ulcerated, or haemorrhagic plaques are unstable and prone to rupture.
  • NASCET Criteria: The definition of "Stenosis" depends on the measurement method. We use NASCET (Distal ICA comparator).
  • Time is Brain: The benefit of surgery drops rapidly after the index event.

Clinical Pearls

"The Curtain Falls": Amaurosis Fugax is classically described as a "curtain/shade coming down" over one eye. It is the most specific symptom of ipsilateral carotid disease. "Lick your wounds": Hypoglossal nerve injury causes the tongue to deviate towards the side of surgery/injury upon protrusion. "The Hollenhorst Plaque": A bright, refractive cholesterol crystal seen in any retinal arteriole is a diagnostic "smoking gun" for proximal carotid atheroma. "Face-Arm-Speech": The MCA (Middle Cerebral Artery) supplies the motor cortex for the face and arm, and Broca's area (Speech). Leg weakness suggests ACA (Anterior Cerebral Artery). Both come from the Carotid. "The Silent Stenosis": A bruit disappears when stenosis >90% because flow becomes a trickle ("String Sign"). DO NOT be reassured by the absence of a bruit.

2. Epidemiology

Incidence

  • Prevalence: Asymptomatic stenosis >50% is found in 2-8% of the population >60 years.
  • Stroke Burden: Carotid disease accounts for 15-20% of all ischaemic strokes.
  • Recurrence: After a TIA, the risk of stroke is highest in the first 7 days (up to 10-15%).

Risk Factors (Atherosclerosis)

  1. Smoking: The single most potent modifiable risk factor. Increases relative risk x2-3.
  2. Hypertension: Shear stress at the bifurcation promotes endothelial injury.
  3. Hyperlipidaemia: LDL cholesterol drives plaque formation.
  4. Diabetes: Accelerates intimal hyperplasia and calcification.
  5. Male Sex: Men have higher prevalence, but women have worse outcomes post-stroke.
3. Pathophysiology

Anatomy of the Bifurcation

  • Common Carotid (CCA): Ascends in carotid sheath. Bifurcates at C4 (Upper Thyroid Cartilage).
  • Internal Carotid (ICA): Posterior and Lateral. NO branches in the neck. Enters Carotid Canal.
  • External Carotid (ECA): Anterior and Medial. Has branches (Superior Thyroid, Lingual, Facial).
    • The 8 Branches of the ECA (Mnemonic: Some Anatomists Like Freaking Out Poor Medical Students):
      1. Superior Thyroid: First branch. Supplies thyroid.
      2. Ascending Pharyngeal: Small, medial.
      3. Lingual: Supplies tongue. (Beware crossing Hypoglossal nerve).
      4. Facial: Tortuous. Crosses mandible.
      5. Occipital: Posterior.
      6. Posterior Auricular: Behind ear.
      7. Maxillary: Terminal branch. Deep.
      8. Superficial Temporal: Terminal branch. Palpable at temple.
  • Surgeon’s View: The Hypoglossal nerve crosses the ICA/ECA high in the neck. The Vagus lies posteriorly.

The Carotid Sheath (Contents)

  • Artery: Medial (CCA/ICA).
  • Vein: Lateral (IJV).
  • Nerve: Posterior (Vagus).
  • Deep Cervical Nodes: Along the IJV.
  • Clinical Relevance: In a "Radical Neck Dissection", the IJV is sacrificed, but in CEA, we must preserve it.

The Circle of Willis (Collaterals)

The brain has a backup system.

  • Components:
    • Anterior Communicating Artery (ACoA): Connects left/right ACAs.
    • Posterior Communicating Arteries (PCoA): Connect Carotid (Anterior) to Basilar (Posterior) systems.
  • Significance:
    • If the Circle is Complete (intact), you can clamp the Carotid for 2 hours and nothing happens (cross-flow protects the brain).
    • If the Circle is Incomplete (common, 25% of people), clamping causes immediate Stroke.
    • Testing: This is why we measure "Stump Pressure" or do "Awake Testing".
  • Variations (The Reality):
    • Fetal PCA: The PCA arises from the Carotid instead of the Basilar (20%).
    • Hypoplastic ACoA: No cross flow from left to right.
    • Hypoplastic PCoA: No cross flow from back to front.
    • Surgical Implication: A patient with a Hypoplastic ACoA is Dependent on the ipsilateral Carotid. You CANNOT clamp without a shunt.

Cerebral Autoregulation

  • Normal: The brain keeps CBF constant between MAP 50-150 mmHg.
  • In Stenosis: The arterioles are maximally dilated (vasomotor paralysis) to squeeze every drop of blood through.
  • Post-Clamping: The PCO2 rises (hypercapnia), which is a potent vasodilator.
  • Danger: If you shunt, you restore high pressure to untethered arterioles -> Hyperperfusion.

The Carotid Triangle

The surgical window to the carotid.

  • Posterior Border: Anterior border of Sternocleidomastoid (SCM).

  • Superior Border: Posterior belly of Digastric.

  • Inferior Border: Superior belly of Omohyoid.

  • Contents:

    • Carotid Bifurcation.
    • IJV.
    • Vagus/Hypoglossal nerves.
    • Ansa Cervicalis (lies ON the carotid sheath).

  • Layers: Skin -> Platysma -> Deep Fascia -> Carotid Sheath.

  • Physiology Risk: The Carotid Sinus (Baroreceptor) is located at the bifurcation. Manipulation during surgery can cause severe bradycardia (The surgeon is "tickling the sinus"). The anaesthetist may need to give Glycopyrrolate.

  • The Surgical Danger Zone (Nerves):

    1. Vagus Nerve (CN X):
      • Position: Lies vertically between the IJV and Carotid, usually posterior (behind the artery).
      • Danger: Can spiral anteriorly in 5% of cases. Injury = Vocal cord palsy.
    2. Hypoglossal Nerve (CN XII):
      • Position: Crosses the ICA and ECA horizontally, about 1-2cm above the bifurcation.
      • Landmark: The "Digastric Muscle" tendon keeps it high.
      • Danger: Injury = Ipsilateral tongue deviation.
    3. Superior Laryngeal Nerve (External Branch):
      • Position: Runs medial to the ECA (deep).
      • Danger: Injury = Loss of high pitch voice ("The Opera Singer's Nerve").
    4. Marginal Mandibular Nerve (CN VII):
      • Position: Under the platysma, near the jaw angle.
      • Danger: Retractor injury = Corner of mouth drooping.

The Baroreceptor Reflex (Hering's Nerve)

The Carotid Sinus (dilation at the start of ICA) measures blood pressure.

  • Afferent: Sinus Nerve of Hering (branch of CN IX Glossopharyngeal).
  • Centre: Medulla Oblongata (Nucleus Tractus Solitarius).
  • Efferent: Vagus Nerve (Parasympathetic).
  • Reflex:
    • High BP (Surgeon squeezes plaque) -> Increased firing -> Vagal output -> Bradycardia/Hypotension.
    • Surgical Tip: If the heart rate drops during dissection, inject 2ml of 1% Lidocaine around the bifurcation to block the nerve.

The Pathological Cascade (5 Steps)

Step 1: Endothelial Injury (Hemodynamics)

  • Why does it happen at the bifurcation?
  • Reynolds Number (Re):
    • Formula: $Re = (\rho v d) / \mu$
    • Where $\rho$ = density, $v$ = velocity, $d$ = diameter, $\mu$ = viscosity.
    • Significance: At the bifurcation, the diameter increases (bulb), so velocity decreases? Actually flow separates.
    • Laminar Flow: Re < 2000. Silent. Efficient.
    • Turbulent Flow: Re > 2000. Noisy (Bruit). Inefficient. Causes endothelial shear stress damage.
    • Clinical: This turbulence is what you hear with your stethoscope.
  • Flow Separation: Blood flow separates at the vessel wall opposite the flow divider.
  • Low Shear Stress: This zone has low wall shear stress and oscillatory flow.
  • Reynolds Number: Turbulence increases.
  • Result: Endothelium becomes leaky to LDL cholesterol.

Step 2: Plaque Formation

  • Smooth muscle proliferation forms a fibromuscular cap.
  • Core becomes necrotic (lipid-rich).

Step 3: Instability (The Vulnerable Plaque)

  • Inflammation (Macrophages) degrades the fibrous cap.
  • Neovascularisation leads to Intra-plaque haemorrhage.
  • The plaque volume expands rapidly.

Step 4: Rupture and Embolisation

  • The cap ruptures. Highly thrombogenic core meets blood.
  • Platelet thrombus forms ("White Clot").
  • Debris or Thrombus embolises distally to MCA (Stroke) or Ophthalmic Artery (Blindness).

Step 5: Healing or Occlusion Step 6: Plaque Morphology (Stary Classification) Atherosclerosis isn't just "furring".

  • Type I-II: Fatty Streaks. (Asymptomatic).
  • Type III: Pre-atheroma (Extracellular lipid).
  • Type IV: Atheroma (Lipid Core).
  • Type V: Fibroatheroma (Fibrous cap).
    • Va: Stable.
    • Vb: Calcified (Stable).
    • Vc: Fibrotic.
  • Type VI: Complicated Lesion (The "Killer").
    • Surface defect (Ulcer).
    • Haematoma (Intra-plaque haemorrhage).
    • Thrombus.
  • Gray Scale Median (GSM):
    • A quantitative measure of plaque stability.
    • Low GSM (< 25): Black/Echolucent. Lipid rich. Unstable. High stroke risk.
    • High GSM (> 50): White/Echogenic. Calcified. Stable.
    • Clinical Use: Asymptomatic patients with Low GSM plaques are candidates for surgery (ACST-2 data). Clinical Relevance: We worry about Type VI. On ultrasound, these look "Echolucent" (Dark) because they are soft/fluid, compared to "Echogenic" (Bright) calcified stable plaques.

NASCET vs ECST Classification

This is the most common exam fail point. How do you measure stenosis?

  1. NASCET (North American): Compares stenosis diameter to the normal distal ICA diameter. This is the Gold Standard.
  2. ECST (European): Compares stenosis to the estimated bulb diameter. Result: ECST overestimates stenosis compared to NASCET. A 70% NASCET stenosis is roughly an 85% ECST stenosis. Always quote NASCET.
4. Clinical Presentation

Symptomatic Disease

"Symptomatic" is defined as an event in the ipsilateral territory within the last 6 months.

  1. Hemispheric TIA:
    • Contralateral motor/sensory deficit (Face/Arm > Leg).
    • Dysphasia (if Dominant hemisphere).
    • Duration < 24 hours (usually < 1 hour).
  2. Amaurosis Fugax (Retinal TIA):
    • Painless, monocular visual loss. "Shade coming down".
    • Lasts minutes.
    • Caused by emboli to the Central Retinal Artery or branches.
  3. Watershed Infarction:
    • Stroke occurring at the border zones between arterial territories (e.g., ACA/MCA border).
    • Mechanism: Hypoperfusion (Low flow) rather than embolism.
    • Occurs in severe stenosis (>90%) or occlusion where collaterals are poor.
    • Features: "Man in a barrel" syndrome (Proximal arm/leg weakness).
  4. Completed Stroke:
    • Permanent neurological deficit.

The "Facial Droop" Nuance (UMN vs LMN)

If you see a facial droop in exam:

TIA Stratification (ABCD2 Score)

Historically used to stratify risk. Now superseded by "rapid access for all".

The Oxford (Bamford) Classification

Where is the stroke?

  1. TACS (Total Anterior Circulation Stroke): Medial + Anterior cerebral arteries.
    • Hemiparesis + Hemianopia + Dysphasia/Neglect.
    • Prognosis: Poor.
  2. PACS (Partial Anterior): Two of the above.
    • Association: High probability of Carotid Stenosis embolic source.
  3. LACS (Lacunar): Deep perforating arteries.
    • Pure motor/sensory.
    • Cause: Hypertension, not usually carotid emboli.
  4. POCS (Posterior): Vertebrobasilar.
    • Cerebellar signs, vertigo.
    • Cause: Vertebral artery, not Carotid.

Asymptomatic Disease

Stroke (UMN)
The Forehead is SPARED (Patient can wrinkle their forehead). This is because the forehead has bilateral cortical supply.
Bell's Palsy (LMN)
The Forehead is PARALYSED.
Context
In Carotid Stenosis (Stroke), expect forehead sparing.
5. Clinical Examination

Structured Approach

Structured Approach

  1. Neurology: Full Cranial Nerve & Limb exam to document baseline deficits (FAST).
    • CN I (Olfactory): Not relevant.
    • CN II (Optic):
      • Acuity: Snellen chart (Amaurosis Fugax = Normal between attacks. Stroke = Hemianopia).
      • Fields: Confrontation. Homonymous Hemianopia = MCA Stroke.
      • Reflexes: RAPD (afferent defect) in optic neuritis, not usually carotid.
      • Fundoscopy: Hollenhorst Plaques.
    • CN III, IV, VI (Oculomotor):
      • "follow my finger".
      • Horner's Syndrome (Ptosis/Miosis): Carotid Dissection. The Sympathetic chain runs on the Carotid sheath.
    • CN V (Trigeminal): Sensation to face. Spared in MCA stroke? No, usually involved.
    • CN VII (Facial):
      • Stroke: UMN (Forehead spared).
      • Bell's Palsy: LMN (Forehead paralysed).
    • CN VIII (Vestibulocochlear): Hearing.
    • CN IX/X (Bulbar):
      • Palatal lift ("Ahh"). Deviation away from lesion.
      • Swallow (Dysphagia).
    • CN XI (Accessory): Shrug shoulders (SCM/Trapezius).
    • CN XII (Hypoglossal):
      • Tongue protrusion.
      • Deviation towards the lesion.
      • Why?: The Genioglossus muscle pushes the tongue out. If the Right muscle is weak, the Left muscle overpowers and pushes the tongue to the Right.
  2. Neck Auscultation:
    • Ask patient to "Stop breathing".
    • Listen at angle of jaw.
    • Bruit implies turbulence (but not severity).

The "Four Vessel" Surface Anatomy

Can you feel the pulse?

  1. Common Carotid: Anterior SCM border.
  2. Superficial Temporal: Anterior to tragus of ear. (Check for Giant Cell Arteritis/tenderness).
  3. Facial Artery: Crosses the mandible anterior to the masseter.
  4. Subclavian: Supraclavicular fossa. Relevance: If the CCA is occluded, the ECA may flow retrograde to supply the ICA? No, that's complex. But checking temporal pulses ensures the ECA is patent.

Characteristics of a Carotid Bruit

  • Site: Best heard at the anterior border of SCM, upper third.
  • Timing: Systolic.
  • Differentiating from Cardiac Murmur:
    • Cardiac murmurs (AS) are louder at the base of the neck/chest and radiate UP.
    • Carotid bruits are louder at the jaw.
  • The "Silent" Zone:
    • No Bruit = Normal OR >90% Stenosis OR Occlusion.
    • Loudest Bruit = Moderate Stenosis (turblence).

Differential: Carotid Body Tumour (Chemodectoma)

  • Anatomy: The Carotid Body (Chemoreceptor) sits in the bifurcation adventitia.
    • Function: Detects pO2, pCO2, pH. (Respiration control).
    • Innervation: Sinus Nerve of Hering (IX).
    • Distinction: Different from Carotid Sinus (Baroreceptor - BP control).
  • Pathology: Paraganglioma. Highly vascular. "Potato Tumour".
  • Genetics: 10-50% familial (SDHD gene).
  • Exam Sign: "Fontaine's Sign". The mass moves horizontally (side-to-side) but NOT vertically (up-and-down) because it is tethered to the carotid artery.
  • Investigation: "Lyre Sign" on Angio (splaying of ICA/ECA).
  • Treatment: Resection (very difficult due to bleeding). Often need pre-op embolisation.

Ocular Examination (The Window)

The eye is supplied by the Ophthalmic Artery (branch of ICA).

  • Fundoscopy:
    • Hollenhorst Plaque: A bright, refractive, golden cholesterol crystal lodged at an arterial bifurcation. (Pathognomonic).
    • Retinal Emboli: White platelet plugs.
    • Venous Stasis Retinopathy: Dilated veins due to low flow (chronic occlusion).
  • Visual Fields: Check for homonymous hemianopia (MCA Stroke).

Cardiac Exam**: Important. Look for AF (source of cardio-embolism) and Murmurs (AS).

  1. Blood Pressure: Bilateral Manual BP.
    • Difference > 20mmHg suggests Subclavian Stenosis (Subclavian Steal Syndrome).
  2. Peripheral Vascular Exam:
    • Palpate Radial, Femoral, Popliteal, DP/PT pulses.
    • Logic: Atherosclerosis is a systemic disease. 30% have PVD.
    • ABPI (Ankle Brachial Pressure Index):
      • If < 0.9, they have PAD.
      • Relevance: This predicts high cardiovascular risk (MI/Stroke) during the operation.

Pre-Operative Cardiac Workup

Because 30% of carotid patients have silent Coronary Artery Disease (CAD), we must screen the heart.

  • ECG: Mandatory. Look for Q waves (Old MI).
  • Echo: If murmur or history of failure.
  • Stress Test: Only if poor functional capacity (< 4 METs).
  • Peri-op: Ensure Beta-Blockers are continued (do not stop).

Smoking Cessation (The Hard Conversation)

  • "You must stop smoking to save your other artery."
  • Protocol:
    1. NRT (Nicotine Replacement): Patches + Gum (Combination therapy is best).
    2. Varenicline (Champix): Partial agonist. Most effective. (Caution in depression).
    3. Vaping: 95% safer than tobacco (Public Health England). Acceptable harm reduction.

Dietary Advice (The Mediterranean Diet)

  • High Check: Olive oil, Nuts, Fish, Fruit/Veg.
  • Low Check: Red meat, Processed food, Butter.
  • Evidence: PREDIMED trial showed 30% reduction in stroke/MI.
6. Investigations

Duplex Ultrasound (First Line)

  • Role: Screening and diagnosis.
  • Criteria (NASCET equivalent):
    • < 50%: Peak Systolic Velocity (PSV) < 125 cm/s.
    • 50-69%: PSV 125-230 cm/s.
    • > 70%: PSV > 230 cm/s (The Critical Threshold).
    • Near Occlusion: "String Sign" (Trickle flow).
    • Occlusion: No flow.

Doppler Physics (Bernoulli Principle)

  • Concept: $\Delta P = 4v^2$. Pressure drop is proportional to velocity squared.
  • As the lumen narrows, velocity MUST increase to maintain flow (Continuity Equation).
  • We measure the Velocity (cm/s) to estimate the Stenosis (%).
  • Pitfall: If the stenosis is very long, energy is lost to friction, and velocity might drop (Underestimation).

Doppler Ultrasound Protocol (Detailed)

The scan involves three modalities:

  1. B-Mode (Grey Scale):
    • Visualises the anatomy.
    • Classifies plaque: Echolucent (Dark, high risk, lipid) vs Echogenic (Bright, stable, calcified).
    • Measures Intimal Medial Thickness (IMT).
  2. Colour Flow:
    • Visualises direction and aliasing (turbulence).
  3. Spectral Doppler:
    • Measures Velocity (PSV/EDV).
    • The angle of insonation must be < 60 degrees. If > 60, the cosine error becomes exponential.
    • Spectral Broadening:
      • Normal Flow: "The Window". All RBCs move at same speed (Laminar). Clear space under the curve.
      • Turbulent Flow: "Filling in the Window". RBCs move at random speeds/directions. The spectral window fills in. This is the earliest sign of disease.

The "String Sign" (Trickle Flow)

  • When a stenosis is >99% (sub-occlusive), velocity drops.
  • It looks like an occlusion.
  • Tip: Turn up the colour gain and lower the PRF (Scale) to detect the tiny trickle.
  • Why it matters:
    • 100% Occlusion = No Surgery (Safe).
    • 99% Stenosis = Urgent Surgery (Dangerous).

Transcranial Doppler (TCD)

  • Role: Assessing intracranial flow (MCA) and monitoring for emboli (HITS - High Intensity Transient Signals).
  • Intra-op: Used to decide if a Shunt is needed during GA.

CT Angiogram (CTA)

  • Role: Planning surgery (Arch anatomy, level of bifurcation).
  • Advantages: Shows intracranial circulation (Circle of Willis) and aortic arch type.
  • Disadvantages: Contrast nephropathy, Radiation.

MRA (Magnetic Resonance Angiography)

  • Time-of-Flight (TOF): Non-contrast sequence. Uses flow dynamics to create an image.
    • Pros: No radiation, No contrast (kidney safe).
    • Cons: Overestimates stenosis (turbulent flow looks like occlusion). Artifacts from metal implants.
  • Contrast-Enhanced MRA: Better quality, requires Gadolinium.

CTA vs MRA (The Debate)

  • CTA (Computed Tomography Angiography):
    • Pros: Fast (10 seconds). High Spatial Resolution. Shows Calcium well. Available 24/7.
    • Cons: Radiation (Thyroid/Breast risk). Contrast Nephropathy (Check eGFR).
    • Role: First line in acute stroke (Thrombectomy planning).
  • MRA (Magnetic Resonance Angiography):
    • Pros: No Radiation. No Iodine contrast (Gadolinium is safer for kidneys, mostly). Detailed brain imaging (DWI) simultaneously.
    • Cons: Slow (30 mins). Claustrophobia. Contraindicated in pacemakers (some). "Flow voids" can overestimate stenosis.
    • Role: Second line if CTA contraindicated or for complex arch anatomy.
  • The "Dupplex Disagreement": If Duplex says 90% but CTA says 50% -> Believe the CTA (Gold Standard anatomical imaging). OR perform MRA as tie-breaker.

PET-CT (Positron Emission Tomography)

  • Role: Research mainly.
  • Concept: Uses FDG (glucose) to identify "Hot Plaques".
  • Significance: Metabolically active plaques (inflammation) are 5x more likely to rupture.
  • Significance: Metabolically active plaques (inflammation) are 5x more likely to rupture.
  • Future: May help decide which asymptomatic patients need surgery.

Acetazolamide Challenge (SPECT/CT)

  • Concept: A physiological stress test for the brain.
  • Protocol:
    1. Inject Acetazolamide (Diamox). This causes maximal vasodilation of normal arterioles.
    2. Scan Brain Perfusion.
  • Normal: Blood flow increases everywhere.
  • Steal Phenomenon: In severe stenosis, the arterioles are already maximally dilated to compensate. They cannot dilate further. So blood flows away from the ischaemic area to the healthy area.
  • Result: Reduced flow in the hemisphere = Exhausted Cerebrovascular Reserve.
  • Clinical Use: Identifies the "High Risk" asymptomatic patient who NEEDS surgery.

MRI Brain (DWI)

  • Role: Confirms "Symptomatic" status.
  • Finding: Bright spots on DWI (Diffusion Weighted Imaging) confirm recent ischaemia even if symptoms were transient (TIA). This upgrades the patient's risk profile.
7. Management

Management Algorithm

        SYMPTOMATIC CAROTID STENOSIS
                    ↓
┌─────────────────────────────────────────┐
│        IMMEDIATE ASSESSMENT (TIA Clinic)│
│  - Aspirin 300mg immediately            │
│  - Duplex Ultrasound (&lt; 24 hrs)         │
└─────────────────────────────────────────┘
                    ↓
           DEGREE OF STENOSIS (NASCET)
                    ↓
┌─────────┬──────────────┬───────────────┐
│  &lt; 50%  │    50-69%    │    70-99%     │
│  MILD   │   MODERATE   │    SEVERE     │
└────┬────┴───────┬──────┴───────┬───────┘
     │            │              │
     │            │              │
     │   ┌────────┴────────┐     │
     │   │  Men: SURGERY   │     │
     │   │  Women: MEDICAL │     │
     │   └────────┬────────┘     │
     │            │              │
┌────▼────────────▼──────────────▼────┐
│         BEST MEDICAL THERAPY        │
│    (Antiplatelet + Statin + BP)     │
└─────────────────┬───────────────────┘
                  │
        ┌─────────▼─────────┐
        │   URGENT CEA      │
        │  (&lt; 2 Weeks)      │
        └───────────────────┘

1. Best Medical Therapy (BMT)

Mandatory for ALL patients (Surgical or not).

  • Antiplatelet: Clopidogrel 75mg OD long-term. (Acute: Aspirin 300mg for 2 weeks).
  • Statin: High dose (Atorvastatin 80mg). Target LDL < 1.4. "Pleiotropic effect" stabilises plaque.
  • Hypertension: Target < 130/80.
  • Diabetes: Strict control.
  • Lifestyle: Smoking cessation is non-negotiable.

Dual Antiplatelet Therapy (DAPT)

  • Guidelines:
    • Symptomatic: Clopidogrel monotherapy is standard.
    • Stenting: DAPT (Aspirin + Clopidogrel) is MANDATORY for 4 weeks post-stent.
    • Point/Chance Trials: Suggest short-term DAPT (21 days) in high-risk TIA reduces stroke recurrence.
  • Current Practice: Most vascular units stick to Clopidogrel 75mg OD for CEA, and DAPT for CAS.

Best Medical Therapy (The "Big Three")

It is not enough to just prescribe the drugs. We must hit the targets.

  1. Antiplatelets:
    • Clopidogrel 75mg: Irreversible ADP receptor antagonist.
    • Aspirin 75mg: COX-1 inhibitor. (Less effective than clopidogrel).
    • Failure: If a patient has a TIA while on Aspirin -> Switch to Clopidogrel (Do not add).
  2. Lipid Lowering:
    • Target: LDL < 1.4 mmol/L (Very aggressive).
    • Drug: Atorvastatin 80mg.
    • Mechanism: Apart from lowering LDL, statins reduce plaque inflammation (CRP) and thicken the fibrous cap (stabilisation).
  3. Antihypertensives:
    • Target: < 130/80.
    • Drug: ACE Inhibitors / CCB.

The Science of "Pleiotropy" (Why Statins Work)

Statins do more than lower cholesterol.

  1. Anti-Inflammatory: Reduced macrophage activation in the plaque.
  2. Endothelial Function: Improved Nitric Oxide (NO) bioavailability.
  3. Thrombosis: Reduced tissue factor expression.
  4. Result: The plaque transitions from "Echolucent" (Unstable/Soft) to "Echogenic" (Calcified/Hard).
  5. Evidence: SPARCL trial showed Atorvastatin 80mg reduced stroke recurrence by 16%.

Clopidogrel Resistance (CYP2C19)

  • Genetics: Clopidogrel is a prodrug. It needs metabolism by CYP2C19 in the liver to become active.
  • Loss of Function Alleles: 30% of Caucasians and 50% of Asians are "Poor Metabolizers".
  • Risk: These patients have high platelet reactivity despite taking the drug.
  • Alternative: Ticagrelor (Does not need metabolism). Currently only licensed for Cardio, but off-label use in recurrent cerebrovascular events is rising.

2. Surgical Therapy: Carotid Endarterectomy (CEA)

  • Indication: Symptomatic 50-99% Stenosis.
    • Benefit: Maximum in 70-99%. Moderate in 50-69% (NNT much higher).
  • Timing: "The Golden Fortnight".
    • Risk of recurrent stroke is highest early.
    • Surgery < 2 weeks = Max benefit.
    • Surgery > 12 weeks = Benefit lost (Plaque has healed/stabilised).
  • Anaesthesia:
    • Regional (Cervical Block): Preferred by many. Allows "Awake Testing" (Squeeze a toy). If they stop squeezing -> Shunt immediately.
    • General (GA): Requires TCD (Doppler) or Stump Pressure measurement to decide on shunting.

The 50-69% Controversy

  • In NASCET, the NNT for this group was 15.
  • Men: Showed clear benefit. (ARR 8%, NNT 12).
  • Women: Showed almost NO benefit. (ARR 2.2%, NNT 48).
  • Reason:
    1. Artery Size: Women have smaller arteries -> higher restenosis risk.
    2. Periprocedural Risk: Higher risk of dissection/vasospasm in women.
    3. Plaque Types: Women tend to have more smooth fibrous plaques (stable) compared to men (ulcerated).
  • Guideline: We are very aggressive with men in this bracket, but cautious with women (operate only if very low surgical risk and <2 weeks from event).
  • Viva Point: "I would treat a male with 55% symptomatic stenosis, but I would treat a female medically unless she had recurrent events."

The Anaesthetic Debate (GALA Analysis)

The GALA trial was the largest RCT (n=3500) comparing LA vs GA.

  1. Local Anaesthetic (LA):
    • Pros:
      • Gold Standard Monitoring: The awake patient is the best monitor. If they stop squeezing the toy/talking, you know they are ischaemic immediately.
      • Selective Shunting: We only shunt the 10% who develop symptoms. Shunts carry risks (dissection/emboli), so avoiding them is good.
      • ** hemodynamic Stability**: Less hypotension than GA.
    • Cons:
      • Patient Anxiety: Claustrophobia under drapes.
      • Training: Harder to teach juniors (time pressure).
  2. General Anaesthetic (GA):
    • Pros:
      • Comfort: For patient and surgeon.
      • Control: Airway is secure. CO2 can be manipulated.
    • Cons:
      • Monitoring: We rely on surrogates (Stump Pressure, TCD, SSEP) which are less accurate than an awake patient.
      • Shunting: Often we "Routine Shunt" to be safe, exposing the patient to shunt risks unnecessarily.
  • Verdict: GALA showed NO difference in stroke/death. Do what you are best at.

3. Carotid Artery Stenting (CAS) Detailed

Stenting is the alternative to CEA.

  • Mechanism: Endovascular placement of a self-expanding stent (Nitinol) to crush the plaque against the wall.
  • The Problem: Passing a wire across a crumbly plaque showers debris.
  • The Solution: Embolic Protection Devices (EPD).
    • Distal Filter: An umbrella deployed distal to the stenosis to catch debris.
    • Proximal Protection (MoMa): Balloon occlusion of CCA/ECA to reverse flow during stenting.
  • Indications ("Hostile Neck"):
    1. Previous Radiotherapy (Fibrosis).
    2. Restenosis after previous CEA.
    3. High Bifurcation (above C2) inaccessible surgically.
    4. Contralateral Vocal Cord Palsy (Risk of bilateral palsy).
  • Outcomes: CREST trial showed higher stroke rate (minor) but lower MI rate compared to CEA.

Technical Appendix: CEA Steps

  1. Incision: Anterior border of Sternocleidomastoid (SCM). From mastoid process to sternal notch (though usually min-incision 5cm).
    • Positioning: Neck extended, head turned AWAY. Roll under shoulders.
    • Platysma: Divided in line with incision.
    • Facial Vein: The "Blue Guide". It crosses the carotid bifurcation. It must be ligated and divided to access the artery.
  2. Dissection: Retract SCM laterally. Internal Jugular Vein (IJV) is retracted laterally.
  3. Nerve Identification (The Danger Zone):
    • Vagus: Posterior.
    • Hypoglossal: Superior/Medial (crossing ICA).
    • Ansa Cervicalis: Loops anteriorly.
  4. Vessel Loop Control: CCA, ECA, ICA.
  5. Heparinisation: Systemic heparin (5000u).
  6. Clamp: CCA -> ECA -> ICA.
  7. Arteriotomy: Longitudinal cut from CCA extending into ICA.
  8. Shunt?: Use Javid/Pruitt shunt if neurology changes (Awake) or Stump Pressure < 40mmHg (GA).
    • Technique:
      • Insert distal (ICA) first.
      • Allow back-bleeding to flush air.
      • Insert proximal (CCA).
      • Confirm flow with Doppler probe on shunt.
  9. Endarterectomy:
    • Develop plane between plaque and media.
    • The Eversion Technique (Alternative):
      • Instead of longitudinal cut, the ICA is transected at the origin.
      • The artery is "turned inside out" like rolling a sleeve up.
      • The plaque is peeled off.
      • The artery is sewn back on.
      • Benefit: No patch needed.
    • Standard Technique: Longitudinal arteriotomy + Patch.
    • Transect plaque proximally and distally.
    • Critical Step: "Feathering" the distal endpoint. If a flap is left, it will dissect and occlude (Stroke). Secure tacking sutures (6-0 Prolene) if needed.
  10. Closure: Patch Angioplasty (Bovine/Dacron). Primary closure narrows the vessel (restenosis).
    • Suture: 6-0 Prolene.
    • Double-ended needle. Start at both ends and meet in the middle.
    • Flushing: Before tying the last knot, flush all 3 vessels (ICA, ECA, CCA) to wash out debris.
    • Flow Restoration: ECA first (wash debris to face), then CCA, then ICA last.

The Patch Material Debate

There is good evidence that Routine Patching is superior to Primary Closure (lower restenosis rate). But which patch?

  1. Bovine Pericardium:
    • Pros: Biocompatible, handles well, reduces suture hole bleeding.
    • Cons: Expensive, small risk of aneurysm (very rare).
    • Verdict: Most popular modern choice.
  2. Dacron / PTFE (Synthetic):
    • Pros: Available off the shelf. Strong.
    • Cons: Suture hole bleeding (needs Prolene 6-0). Higher infection risk than autologous.
  3. Vein (Autologous Saphenous):
    • Pros: Free, biocompatible, resistant to infection.
    • Cons: Must harvest from leg (pain/wound). Vein can rupture ("Blowout") if weak. Recommendation: Use Patch (Bovine or Synthetic) routinely. Reserve Vein for infected cases.

The Carotid Shunt

  • Role: A temporary plastic tube that bypasses the blood from CCA to ICA while the artery is open.
  • Types:
    • Javid: External loop. Needs clamps. Historic standard.
    • Pruitt-Inahara: Internal balloons. Sits inside the vessel.
  • Debate:
    • Routine Shunting: Shunt everyone. Safe but risks scuffing the intima (causing stroke).
    • Selective Shunting: Only shunt if the patient drops their neurology (Awake) or Stump Pressure < 40mmHg. Recommended.
  • Technique: Insert distal end (ICA) first -> Back bleed (remove air) -> Insert proximal end (CCA).

Post-Operative Management Protocol

  1. Neurology Checks:
    • "Squeeze my fingers, stick out your tongue".
    • Q15 mins for 2 hours, then Q1H.
  2. Blood Pressure Control (Critical):
    • Hypertension (>160): Risk of Hyperperfusion / Haematoma. Treat with IV Labetalol or GTN/SNP.
    • Hypotension (<100): Risk of Stroke (Infarct). Treat with fluids/vasopressors.
    • Why is BP labile?: We manipulated the Carotid Sinus (Baroreceptor). The body reacts violently.
  3. Wound Check:
    • Monitor for swelling (Haematoma). If stridor -> Open clips immediately.
  4. Discharge:
    • Usually Day 1 or 2.
8. Complications

Peri-operative

  1. Stroke (2-3%): Embolic (during dissection) or Ischaemic (cross-clamp).
  2. Cranial Nerve Injury (5-7%):
    NerveDeficitSign
    Hypoglossal (XII)Tongue deviationTowards side of injury. Speech slur.
    Vagus (X) / RLNVocal Cord PalsyHoarse voice. Poor cough.
    Marginal Mandibular (VII)Corner of mouthDrooping. Asymmetric smile.
    Superior LaryngealPitchLoss of high notes (Singers).
  3. Haematoma: "Expanding neck mass".
    • Action: Open the wound at bedside immediately if stridor/airway compromise.

Carotid Blowout Syndrome (Rare)

  • Risk: Patients with Head/Neck Cancer + Radiotherapy.
  • Pathology: Necrosis of the arterial wall.
  • Presentation: Sentinel bleed (small) -> Massive haemorrhage.
  • Action: Endovascular Stent Graft (Covered Stent) is the only hope. Surgery is impossible in a radiated neck.

Management of Neck Haematoma (Airway Emergency)

  • Sign: Stridor, respiratory distress, expanding mass.
  • Action: SCOOP and RUN.
    1. Call for Help (Anaesthetics/Surgeon).
    2. Open the wound at the bedside. Do not wait for theatre.
    3. Evacuate the clot to relieve pressure on the trachea.
    4. Pack the wound.
    5. Take to theatre for exploration.

Cranial Nerve Injury Assessment (Post-Op)

How to test if you cut a nerve?

  1. Hypoglossal (XII):

    • Test: "Stick your tongue out straight".
    • Injury: Deviation to the OPERATED side. Difficulty moving a bolus of food.

  2. Vagus (X) / RLN:

    • Test: "Say Eeeee". Cough.
    • Injury: Hoarse, breathy voice. Bovine cough (unable to generate pressure).
    • Risk: Aspiration.

  3. Marginal Mandibular (VII):

    • Test: "Show me your teeth". "Grimace".
    • Injury: Corner of mouth droops (looks like a Stroke!).
    • Distinction: Can they close their eye? (Yes in both marginal mandibular and stroke usually, bad example). Just affects the mouth depressors.

  4. Superior Laryngeal (X):

    • Test: "Sing a high note".
    • Injury: Voice tires easily. Loss of pitch.

  5. Glossopharyngeal (IX):

    • Test: Swallow.
    • Injury: Dysphagia.

  6. Patch Infection (<1%):

    • Rare but catastrophic.
    • Usually Staph Aureus.
    • requires excision of the patch and vein reconstruction (Vein graft).
    • Prevention: Prophylactic antibiotics (Co-Amoxiclav) at induction.

Cerebral Hyperperfusion Syndrome (CHS)

  • Incidence: 1%.
  • Pathophysiology:
    • Chronic stenosis leads to maximal dilation of cerebral arterioles (to maintain flow).
    • Autoregulation is lost ("Paralysed arterioles").
    • CEA suddenly restores high pressure flow.
    • Arterioles cannot constrict -> Massive increased CBF -> Edema/Haemorrhage.
  • Presentation: Severe unilateral headache (Day 3-7 post-op), Seizures, Focal deficit.
  • Risk Factors: High grade stenosis (99%), Severe pre-op hypertension.
  • Management Protocol:
    • Step 1: Prevention. Keep SBP < 140 peri-operatively.
    • Step 2: If headache occurs, CT Head immediately (rule out bleed).
    • Step 3: Aggressive BP control. IV Labetalol 10-20mg boluses or GTN infusion.
    • Step 4: Seizure prophylaxis (Phenytoin/Levetiracetam) if cortical edema seen on MRI.
    • Step 5: Steroids (Dexamethasone) - Evidence is weak but often used.
9. Prognosis & Outcomes

Why don't we screen everyone?

  • Prevalence: Significant stenosis is rare (<5% in general population).
  • False Positives: Duplex is good but not perfect. Screening leads to false alarms.
  • Harm vs Benefit: If you operate on 100 asymptomatic people to prevent 1 stroke, but cause 3 strokes during surgery, you have HARMED the population.
  • Wilson & Jungner Criteria: Not met for population screening.

Natural History

  • Symptomatic >70%: 26% risk of stroke at 2 years without surgery. 9% risk with surgery. (NASCET).
  • Asymptomatic: Annual stroke risk is low (~1-2%).

Restenosis

Stenosis can come back.

  1. Early (< 2 years): Myointimal Hyperplasia.
    • Proliferation of smooth muscle cells/fibrous tissue (Scarring).
    • Risk: Reduced by using patch angioplasty.
    • Treatment: Balloon Angioplasty (POBA) is preferred (Surgery is high risk due to scar).
  2. Late (> 2 years): Neo-Atherosclerosis.
    • New plaque formation.
    • Treat like primary disease (Medical/Surgical).

The Stroke Rehabilitation Journey

If a patient suffers a stroke (despite our best efforts), the journey is long.

  1. Hyperacute (0-24 Hours):
    • Thrombolysis (Alteplase) / Thrombectomy (if Large Vessel Occlusion).
    • Swallow Assessment (SALT): NBM until safe. Risk of aspiration pneumonia.
  2. Acute (Day 1-7):
    • Physio: Early mobilisation. Sit to stand.
    • OT: Cognitive assessment. Washing/Dressing.
    • SALT: Texture modification (Purée diet, thickened fluids).
  3. Subacute (Week 2-6):
    • Neuroplasticity relies on "Repetitive Task Training".
    • "Use it or lose it".
  4. Community:
    • ESD (Early Supported Discharge).
    • Home adaptations (Stair lifts).
    • Goal: Independence.

Driving (DVLA UK)

  • TIA/Stroke:
    • Car (Group 1): Stop driving for 1 month. Can resume if doctor confirms clinical recovery.
    • HGV (Group 2): Stop for 1 year. Strict criteria to return.

Can I Fly?

  • TIA: Unstable. Do not fly for 10 days.
  • Stroke: Variability. Usually wait 21 days or until stable.
  • Risk: Hypoxia at altitude (cabin pressure = 8000ft) causes vasodilation. In a stenosed vessel with maximal dilation already (loss of autoregulation), this can theoretically cause "Steal".
  • Advice: Stay hydrated. Take Aspirin.

Asymptomatic Screening?

  • Not recommended. Prevalence is low, and operative risk (3%) often exceeds the annual stroke risk (1%).
10. Evidence and Guidelines

The Landmark Trials

  1. NASCET (1991) (North American):
    • Symptomatic 70-99%: huge benefit (Risk reduction 17%). NNT = 6.
    • Symptomatic 50-69%: moderate benefit (Risk reduction 6.5%). NNT = 15.
    • <50%: No benefit. Harm (Surgery) > Benefit.

The GALA Trial (Anaesthesia)

  • Question: Is Local Anaesthetic (LA) safer than General Anaesthetic (GA)?
  • Hypothesis: LA avoids hypotension and allows awake monitoring (Gold Standard).
  • Result: No difference in stroke or death rates between LA and GA.
  • Implication: The choice is up to surgeon/patient preference.
    • LA Pros: Reduced shunt rate (selective shunting).
    • LA Cons: Patient panic (claustrophobia under drapes).

The NASCET Trial (Detailed Breakdown)

  • Population: Symptomatic patients (TIA/Stroke in last 6 months).
  • Group 1: Severe (70-99%):
    • Risk of Stroke at 2 years: Medical (26%) vs Surgical (9%).
    • Absolute Risk Reduction (ARR): 17% (Huge).
    • NNT: 6.
  • Group 2: Moderate (50-69%):
    • Risk of Stroke at 5 years: Medical (22%) vs Surgical (15%).
    • ARR: 6.5%.
    • NNT: 15.
    • Subgroup: Men benefited significantly; Women did not benefit until risk factor modelling was applied.
  • Group 3: Mild (<50%):
    • Surgery CAUSED more strokes than it prevented. Do not operate.
  1. ECST (European): Similar findings, but noted measurement differences.

The ACST-1 Trial (Asymptomatic)

  • Question: Should we operate on asymptomatic patients?
  • Result: Immediate CEA reduced 10-year stroke risk from 11% (Deferred) to 5% (Immediate).
  • Absolute Risk Reduction: ~6% over 10 years (0.6% per year).
  • Catch: This benefit is ONLY realised if the surgeon's peri-operative stroke rate is < 3%. If the surgeon causes 5% strokes, they have wiped out 10 years of benefit instantly.
  • Modern Context: This trial was before aggressive statins. Today, most believe BMT matches Surgery for asymptomatic disease.

Detailed Medical Therapy Evidence (The "Anti-Surgical" Argument)

Surgery is losing ground to better drugs.

  1. SPARCL Trial (Lipids):
    • Comparison: Atorvastatin 80mg vs Placebo in recent stroke/TIA.
    • Result: 16% reduction in recurrent stroke.
    • Mechanism: "Plaque Stabilization". Statins turn soft (dangerous) plaque into hard (safe) plaque.
  2. CHANCE & POINT Trials (Antiplatelets):
    • Question: Is DAPT (Aspirin + Clopidogrel) better than Aspirin alone for acute TIA/Minor Stroke?
    • Result: Yes. 30% risk reduction in first 21 days.
    • Protocol: Load both, continue both for 21 days, then monotherapy.
    • Relevance: This aggressive medical therapy bridges the gap to surgery, or replaces it in high risk patients.
  3. SAMMPRIS Trial (Intracranial Stenosis):
    • Stenting vs Medical Therapy for intracranial disease.
    • Result: Medical therapy was SUPERIOR. Stenting killed people.
    • Lesson: Aggressive medical therapy is potent.

The ACST-2 Trial (2021)

  • Question: Stenting vs Surgery in Asymptomatic patients (who need intervention).
  • Result: No significant difference in composite endpoint (Stroke/Death/MI) at 5 years. (Approx 1% per year in both).
  • Nuance:
    • CAS caused more minor non-disabling strokes.
    • CEA caused more cranial nerve palsies.
  • Takeaway: Both are safe in experienced hands. The decision relies on anatomy.

The CREST-2 Trial (Ongoing)

  • Question: Does Revascularisation (CEA/CAS) add ANY benefit over modern "Intensive Medical Therapy" (IMT) in asymptomatic patients?
  • Hypothesis: IMT has improved so much (high dose statins/BP control) that surgery may be obsolete for asymptomatic disease.
  • Arms:
    1. CEA + IMT
    2. CAS + IMT
    3. IMT alone.
  • Status: Awaiting results. This will define the future of vascular surgery.

CREST (2010): Stenting vs Surgery

  • Comparison: CEA vs CAS (Stenting).
  • Stroke Rate: Higher in Stenting (4.1% vs 2.3%).
  • MI Rate: Higher in Surgery (2.3% vs 1.1%).
  • Cranial Nerve Palsy: Higher in Surgery.
  • Conclusion:
    • CEA: Gold Standard for symptomatic patients, especially > 70 years.
    • CAS: Alternative for younger patients or "Hostile Necks" (Radiation, High bifurcation).

  1. ICSS (International Carotid Stenting Study): Confirmed higher risk of stroke with Stenting (more emboli on MRI DWI).

  2. SPACE Trial (2006): Use of Stenting vs Endarterectomy. Stopped early due to futility (no difference found, or rather, failure to prove non-inferiority of stenting in the short term).

    • Lesson: Stenting had higher short-term risk.

Guidelines (ESVS 2023)

  • Symptomatic:
    • Surgery is indicated for 50-99% stenosis.
    • Surgery should be performed within 14 days.
    • If >14 days, benefit persist but NNT rises.
  • Asymptomatic:
    • Surgery (CEA) considered for 60-99% stenosis IF:
      • Life expectancy > 5 years.
      • Anatomy is favorable.
      • One or more "Imaging characteristics" of high stroke risk (e.g., Silent Emboli on TCD, Echolucent plaque).
      • Peri-operative stroke/death rate is < 3%.
  • Stenting:
    • Alternative for patients with "Average" surgical risk.
    • Preferred for "High" surgical risk (Hostile neck).
11. Patient Explanation

What is Carotid Stenosis?

The main arteries in your neck (Carotids) are like pipes supplying the brain. Over time, cholesterol and calcium build up inside them, forming "plaque". This is like limescale in a pipe.

Why is it dangerous?

The narrowing itself isn't the main problem. The danger is that the plaque is crumbly and unstable. Small bits can break off and fly upstream into the brain. If a bit blocks a vessel in the brain, it causes a Stroke.

What is a TIA?

  • Amaurosis Fugax: From the Greek amaurosis (darkness) and Latin fugax (fleeting).
  • Transient Ischaemic Attack (TIA): Neurological deficit lasting <24 hours (usually <1 hour). A small clot has blocked a brain vessel but dissolved quickly before permanent damage occurred.
  • The Risk: It means you have unstable plaque. A big clot could follow at any moment. This is why we rush to operate.

Why don't you operate if it's 100% blocked?

  • This seems counter-intuitive.
  • If the artery is totally blocked, no blood flows through it. Therefore, no clots can break off and travel to the brain. The risk of stroke from that artery drops to zero.
  • Re-opening a chronically blocked artery is dangerous and impossible. The brain has already adapted to getting blood from other routes (collaterals).

Can I exercise?

  • Before Surgery: Gentle walking is fine. Avoid heavy lifting (straining increases pressure).
  • After Surgery:
    • Rest for 1 week.
    • Light duties for 2-4 weeks.
    • Back to normal at 6 weeks.
    • Sex: When you feel comfortable (passive is better initially).

Can I do Yoga / Weights?

  • Yoga: Avoid "Inversions" (Headstands/Down Dog) for 6 weeks. Increased venous pressure in the neck can cause hematoma.
  • Weights: No heavy lifting >5kg for 6 weeks. Straining (Valsalva) spikes BP and risks patch rupture or bleeding.
  • Golf: Wait 6 weeks. The twisting motion strains the SCM muscle and neck wound.

Will I lose my voice?

  • Temporary: Common (10%). Due to retraction of the Vagus nerve. Usually settles in weeks.
  • Permanent: Rare (<1%). Vocal cord palsy. One cord moves, the other is paralyzed. You will have a "breathy" voice and weak cough.
  • Singer's Risk: The Superior Laryngeal Nerve (High notes) is easily damaged.

Do I need blood thinners?

  • Antiplatelets: Yes. Clopidogrel is an "Antiplatelet" (makes platelets slippery).
  • Anticoagulants (Warfarin/Apixaban): NO. These are for heart rhythm problems (AF). They are dangerous for carotid surgery and do not work as well for arterial plaque. We only use them if you also have AF.

What is the anaesthetic?

  • Local Anaesthetic (Awake): We numb the neck. You are awake and we talk to you. We ask you to "Squeeze a rubber duck" or "Count to 10" every few minutes. If you stop squeezing, we know the brain needs more blood, and we insert a tube (shunt).
  • General Anaesthetic (Asleep): You are unconscious. We use machines to monitor flow.

When can I fly?

  • After a TIA: You can fly after 10 days if fully recovered.
  • After a Stroke: Usually wait 21 days (Stable).
  • After Surgery: 2-6 weeks depending on the wound and doctor's advice.
  • Risk: Flying involves lower oxygen pressure (hypoxia) and immobility (DVT).

What is the operation?

We make a cut in the neck, clamp the artery, open it up, and carefully peel out the plaque (like removing the core of an apple). We then sew a patch over the cut to make the artery slightly wider than before.

What about the scar?

  • Ideally, the cut is made in a skin crease in your neck so it's hidden.
  • It is roughly 7-10cm long.
  • It will be numb around the scar for a few months (cutaneous nerves are cut), but this usually recovers.

Is it risky?

It is a big operation. There is a small risk (around 2-3%) that the surgery itself could trigger a stroke. However, we only recommend surgery if the risk of doing nothing is much higher (e.g., 20% risk of stroke next year). We carry out the surgery to protect you from the "Big One".

Medicolegal Pitfalls (The "Failure to Warn")

  • Montgomery Ruling (2015): You must warn of material risks specific to the patient.
  • Scenario: A professional singer needs CEA.
  • Risk: Vagus/SLN injury (Hoarseness).
  • Consenting: You MUST mention voice change specifically. Listing "Nerve injury" is not enough.
  • Stroke Risk: You must quantify it ("2-3% risk of stroke during surgery").
  • Documentation: "Risk of Stroke, Death, MI, CN Injury discussed and leaflet given."

Historical Context (The Evolution)

  • 1953: Michael DeBakey performs the first successful CEA in Houston.
  • 1954: Eastcott, Pickering, and Rob (St Mary's London) publish the first case in the Lancet.
  • 1960-80s: The "Wild West". Everyone got surgery. No evidence.
  • 1991 (NASCET/ECST): The "Great Rationalisation". Proved that surgery was harmful for <50% stenosis. Volume of surgery dropped by 50% overnight.
  • 2010 (CREST): The "Stent Wars". Stenting failed to replace surgery as Gold Standard.
  • 2025: The "Medical Era". With PCSK9 inhibitors and aggressive statins, will surgery disappear?

What if I have a stroke in the future?

  • FAST: Face, Arm, Speech, Time.
  • Action: Call 999 immediately.
  • Thrombolysis window: 4.5 hours.
  • Thrombectomy window: 6-24 hours.
  • Reassurance: Having surgery reduces your risk massively, but does not eliminate it (other arteries like the Aorta can throw clots). Stay on your meds!

2025 Updates (ESVS)

  • New emphasis on "sex-specific" guidelines (Treating men earlier).
  • New emphasis on "Timing" (Hyperacute surgery < 48 hours is now the goal in high volume centers).
12. References

  1. Barnett HJ, et al. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445-53. (NASCET). [PMID: 1852180]

  2. European Carotid Surgery Trialists' Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet. 1991;337:1235-43. (ECST). [PMID: 1674060]

  3. Halliday A, et al. 10-year stroke prevention after successful carotid endarterectomy for asymptomatic stenosis (ACST-1). Lancet. 2010. [PMID: 20870003]

  4. Brott TG, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. 2010;363:11-23. (CREST). [PMID: 20505173]

  5. Naylor R, et al. European Society for Vascular Surgery (ESVS) 2023 Clinical Practice Guidelines on the Management of Atherosclerotic Carotid and Vertebral Artery Disease. Eur J Vasc Endovasc Surg. 2023. [PMID: 36511175]

  6. Rothwell PM, et al. Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis. Lancet. 2003. (Cochrane). [PMID: 12573374]

  7. GALA Trial Collaborative Group. General anaesthesia versus local anaesthesia for carotid surgery (GALA): a multicentre, randomised controlled trial. Lancet. 2008. [PMID: 19042211]

  8. Rerkasem K, Rothwell PM. Routine or selective carotid artery shunting for carotid endarterectomy (and different methods of monitoring in selective shunting). Cochrane Database. 2009. [PMID: 19821386]

  9. Bond R, et al. Antiplatelet agents for prevention of recurrence after carotid endarterectomy (Review). Cochrane Database. 2002. [PMID: 11869591]

  10. Chaturvedi S, et al. Carotid endarterectomy--an evidence-based review: report of the Therapeutics and Technology Assessment Subcommittee of the AAN. Neurology. 2005. [PMID: 16186538]

  11. Ferguson GG, et al. The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke. 1999. [PMID: 10471424]

  12. Spence JD, et al. Absence of microemboli on transcranial Doppler identifies low-risk patients with asymptomatic carotid stenosis. Stroke. 2005. [PMID: 16224095]

  13. AbuRahma AF, et al. Proposed new duplex classification for >60% carotid stenosis. J Vasc Surg. 2010. [PMID: 21109341]

  14. Society for Vascular Surgery (SVS). Clinical Practice Guidelines for management of extracranial carotid disease. J Vasc Surg. 2022.

  15. Hollenhorst RW. Significance of bright plaques in the retinal arterioles. JAMA. 1961. [PMID: 13715201]

13. Examination Focus

Viva Questions (The Vault)

  1. Q: Classify Carotid Plaque.
    • A: Stary Classification (I-VI). Key is Type VI (Complicated: Ulcer/Bleed/Thrombus). On Ultrasound: GSM Score (Low < 25 = Unstable).
  2. Q: What is the benefit of surgery in symptomatic 70-99% stenosis?
    • A: NASCET data: ARR 17%, NNT 6 at 2 years.
  3. Q: What about 50-69%?
    • A: Benefit is marginal. ARR 6.5%, NNT 15. Only beneficial in Men.
  4. Q: What is the "Acetazolamide Challenge" in SPECT/CT?
    • A: Acetazolamide is a cerebral vasodilator. We scan before and after. If flow does NOT increase after Acetazolamide, it proves "Cerebrovascular Reserve" is exhausted. These patients are high risk for hemodynamic stroke and need revascularisation urgently.
  5. Q: Draw the Circle of Willis.
    • A: (Draws Anterior/Posterior Communicating arteries).
  6. Q: What is "Stump Pressure"?
    • A: Back pressure in ICA after clamping. If <50mmHg, the Circle of Willis is incompetent -> Insert Shunt.
  7. Q: Why not shunt everyone?
    • A: Shunts can scuff the endothelium (embolic stroke) or dissect the distal artery. Selective is safer.
  8. Q: Name the nerves at risk.
    • A: Hypoglossal (deviation to side), Vagus (hoarse), Marginal Mandibular (droop), Superior Laryngeal (pitch).
  9. Q: What is the "Gender Paradox" in Carotid Surgery?
    • A: Women have higher peri-operative risks and benefit less from surgery in moderate stenosis.
  10. Q: A patient has a stroke 2 hours post-CEA. What do you do?
    • A: Immediate Duplex/exploration. If carotid is thrombosed -> Open and thrombectomy. If patent -> CT Head (Bleed/Hyperperfusion).
  11. Q: What is a "Hollenhorst Plaque"?
    • A: Cholesterol crystal in retinal arteriole. (Bright Orange/Gold).
  12. Q: Define the "Penumbra".
    • A: The area of reversibly ischaemic brain tissue around a core infarct. This is what we save with surgery/thrombectomy.

Common Mistakes

  • Confusing Ultrasound Criteria: Velocity for >70% is >230cm/s (NASCET) but criteria vary by lab.
  • Forgetting the Heart: 30% of these patients have concomittant Coronary Artery Disease.
  • Missing the "Silent" Bruit: A very tight stenosis makes NO noise.
  • Assuming Vertigo = Carotid: Vertigo is Vertebrobasilar (POCS) or Inner Ear. Not Carotid (Anterior).
  1. Q: How does NASCET measure stenosis?
    • A: (1 - (Narrowest diameter / Distal Normal ICA diameter)) x 100.
  2. Q: Name the nerves at risk during CEA.
    • A: Hypoglossal (XII), Vagus/RLN (X), Marginal Mandibular (VII), Superior Laryngeal (X), Transverse Cervical (Sensory), Great Auricular.

At a Glance

EvidenceStandard
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Clinical Pearls

  • **"The Curtain Falls"**: Amaurosis Fugax is classically described as a "curtain/shade coming down" over one eye. It is the most specific symptom of ipsilateral carotid disease.
  • **"Lick your wounds"**: Hypoglossal nerve injury causes the tongue to deviate **towards** the side of surgery/injury upon protrusion.
  • **"The Hollenhorst Plaque"**: A bright, refractive cholesterol crystal seen in any retinal arteriole is a diagnostic "smoking gun" for proximal carotid atheroma.
  • **"The Silent Stenosis"**: A bruit disappears when stenosis &gt;90% because flow becomes a trickle ("String Sign"). DO NOT be reassured by the absence of a bruit.
  • Bradycardia/Hypotension.

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines