Vascular Sonography 2: Extracerebral Arterial Exam Study Guide
1. Extracerebral Arterial Exam Overview
Definition of "Extracerebral": Examination of arteries outside of the head, specifically neck vessels.
Case Study Introduction:
Patient Profile: A 68-year-old male presenting for an assessment of carotid arteries.
Clinical Indication: Requisition states "? TIA’s."
Transient Ischemic Attack (TIA): A "mini stroke" where symptoms resolve within hours.
Signs to Assess: Slurred/wrong speech, weakness/drooping, and bilateral blood pressure (BP).
2. Risk Factors for Vascular Disease
Hypertension: Injures the vessel wall.
Diabetes: Vascular atherosclerosis at an early age; leads to "hard vessels."
Smoking: Causes persistent irritation of the endothelial lining.
Obesity and Diet: High-fat and high-cholesterol diets.
Dyslipidemia: Abnormal plasma lipid levels initiate plaque formation.
Hypercholesterolemia: Genetic defect in LDL receptors.
Sex: Male predominance below age 50; risk equalizes after age 50 due to estrogen.
Age: Risk increases with cumulative plaque buildup.
Patent Foramen Ovale (PFO): Clots can travel to the brain.
Physical Inactivity.
Genetic Predisposition/Family History: Increases risk for stroke, cardiac disease, or diabetes.
Homocystinaemia: Elevated homocysteine levels lead to increased stroke risk.
Cardiac Disease.
Previous TIA or Stroke.
Screening: Performed before major cardiac procedures.
3. Physical Examination and Indirect Assessment
Auscultation for Bruits:
Turbulent blood flow creating a bruit.
May not be detected in severe stenosis.
A "thrill" is a palpable bruit.
Bilateral Blood Pressures:
A difference of > 20 \, mmHg indicates a possible subclavian steal.
4. Signs and Symptoms of Cerebrovascular Compromise
4.1 Anterior Circulation (Hemispheric/Lateralizing)
Supplied by Internal Carotid Arteries (ICAs).
Contralateral Rule: Left ICA disease causes right body symptoms.
Visual Exception: Visual symptoms are typically unilateral and ipsilateral.
Specific Conditions:
Amaurosis Fugax: "Black curtain" over one eye.
Aphasia/Dysphasia: Language comprehension or production issues.
Dysphagia: Difficulty swallowing.
Dysarthria: Impaired speech articulation.
Hemiparesis/Hemiplegia: Weakness or paralysis on one side.
Homonymous Hemianopsia: Visual field loss in half of vision.
Paresthesia: Tingling or numbness.
4.2 Posterior Circulation (Vertebrobasilar/Non-lateralizing)
Supplied by vertebral arteries to cerebellum and posterior hemispheres.
Specific Conditions:
Ataxia: Lack of coordination.
Binocular Blindness: Loss of vision in both eyes.
Diplopia: Double vision.
Dizziness.
Drop Attacks: Sudden falls while walking.
Syncope: Transient loss of consciousness.
Vertigo: Sensation of spinning.
4.3 Miscellaneous/Visual Notes
Headache, Neck Pain, Confusion: General neurological symptoms.
Visual Distribution: Unilateral disturbances are typically ipsilateral and anterior; bilateral disturbances can be anterior or posterior.
5. Questions & Discussion: Case Study Follow-Up
Patient Status: Normal BP, non-smoker, no family history, vision problems for a month.
Follow-Up Questions: Ask about one or both eyes, precise sensation description.
Scenarios: If loss of vision in the left eye, focus on left ICA (Amaurosis Fugax). If diplopia, focus on posterior circulation.
6. Classification of Neurologic Deficits
Asymptomatic: Bruit found without symptoms.
Transient Ischemic Attack (TIA): Neurologic deficit lasting < hours.
Resolving Ischemic Neurologic Deficit (RIND): Lasts > hours but resolves within weeks with no permanent damage.
Cerebrovascular Accident (CVA/Stroke): Causes permanent brain damage.
Vertebrobasilar Insufficiency (VBI): Causes posterior circulation symptoms.
7. Mechanisms of Disease
Cardiac Causes: Emboli from atrial fibrillation or perfusion cessation.
Carotid Origin: Atherosclerotic stenosis leading to thrombosis or emboli.
Cerebral Artery Rupture: Aneurysm or vasospasm.
Miscellaneous: Sickle cell anemia or congenital AVM.
8. Plaque Formation and Morphology
Arteriosclerosis: General hardening of arteries, loss of elasticity.
Atherosclerosis: Arterial disease involving hard and soft plaque.
8.1 Pathogenesis Stages
Stage 1: Injury to endothelial lining.
Stage 2: Lipids enter, inflammation, fatty streak forms.
Stage 3: Platelet deposition and scar tissue formation.
Stage 4: Hemorrhage causes ischemia, unstable plaque can release emboli.
9. Ultrasound Characterization of Plaque
9.1 Surface Characteristics
Smooth: Continuous surface.
Irregular: Discontinuous; increased embolization risk.
Ulceration: Hard to confirm, often reported as irregular.
9.2 Echogenicity
Anechoic: Indicates soft, dangerous plaque.
Hypoechoic: Fibrofatty plaque.
Hyperechoic: Fibrous tissue.
Calcified: Presence of calcium often non-obstructive if flow is normal.
9.3 Echotexture
Homogenous: Consistent echogenicity.
Heterogeneous: Contains various elements.
10. Quantitative Stenosis Measurement
10.1 NASCET
Normal: ICA PSV <125\,cm/s.
50–69% Stenosis: ICA PSV .
>70% Stenosis: Variable; visible plaque; non-detectable flow in occlusion.
10.2 Formulas
Diameter Reduction (NASCET):
Area Reduction:
11. Doppler Principles in Carotid Assessment
Color Doppler: Locates stenosis.
Spectral Doppler: Most accurate for stenosis extent.
PSV: Highest velocity; key parameter.
EDV: Remains normal if stenosis is mild.
12. Treatments for Carotid Artery Disease
Medical: Risk factors modification; TPA within hours of ischemic stroke; anticoagulants.
Surgical:
Carotid Endarterectomy: Plaque removal.
Angioplasty and Stenting: Opening of stenosis with a mesh tube.
13. Post-Intervention Duplex Evaluation
Endarterectomy Follow-up: First exam within days.
Stent Complications: Deployment issues, neointimal hyperplasia, progressive atherosclerosis.
14. Other Carotid Pathologies
Carotid Artery Dissection: Tear causing a false lumen; stroke/TIA risk.
Fibromuscular Dysplasia (FMD): Non-atherosclerotic disease affecting mainly women.
Carotid Body Tumor (CBT): Highly vascular, benign tumor.
Aneurysms and Pseudoaneurysms: True ballooning vs. walled-off blood leak.
Arteritis (Vasculitis): Inflammation affecting arteries.
15. Other Imaging Modalities
Cerebral Arteriography (Angiography): Invasive, high risk.
Computed Tomography (CT): Spiral imaging.
MRA/MRI: Detailed, lower risk imaging.
16. Questions & Discussion: General Notes
Tardus Parvus Diagnosis: Check proximally for stenosis source.
Innominate Artery: Stenosis here affects flow.
High/Low Velocities Bilaterally: Consider cardiac output as a cause.