Carotid Disease


Background: Stroke

  • 1.

    Fourth most common cause of death in the United States

  • 2.

    One million hospital admissions/year

  • 3.

    Significant neurologic morbidity

  • 4.

    Risk factors for stroke

    • a.

      Nonmodifiable

      • (1)

        Sex (male)

      • (2)

        Age (>55 years)

      • (3)

        Race (African American)

      • (4)

        Family history

    • b.

      Modifiable

      • (1)

        Hypertension—preeminent risk factor

      • (2)

        Smoking

      • (3)

        Obesity

      • (4)

        Physical inactivity

      • (5)

        Diet

      • (6)

        Diabetes

      • (7)

        Hypercholesterolemia

      • (8)

        Alcohol

      • (9)

        Renal insufficiency

  • 5.

    Etiologies of stroke

    • a.

      Ischemic—insufficient blood supply

      • (1)

        Embolic (two-thirds of ischemic strokes)—clot or plaque formation outside of the cerebral vasculature

        • (a)

          Carotid embolization —cholesterol or fibrin/platelet matter

        • (b)

          Cardiogenic embolization—valvular disease, atrial fibrillation

        • (c)

          Hematologic causes—hypercoagulability disorders

      • (2)

        Thrombotic

        • (a)

          Local in situ occlusion of cerebral vessels, or

        • (b)

          Carotid thrombosis

          • (i)

            Circle of Willis collateralizes in response.

          • (ii)

            Chronicity and extent of thrombosis may determine symptoms.

          • (iii)

            Acute flow impairment may occur (e.g., a hypotensive event).

    • b.

      Hemorrhagic—10%–15% of strokes

      • (1)

        Intracranial hemorrhage caused by trauma, among other factors

      • (2)

        Rupture of cerebral aneurysm

  • 6.

    Definition of transient ischemic attack

    • a.

      Commonly referred to as mini-stroke

      • (1)

        Strokelike symptoms lasting less than 24 hours

    • b.

      Warning signs for stroke

      • (1)

        A total of 30% of patients with a transient ischemic attack (TIA) will go on to develop an ischemic stroke in 5 years.

      • (2)

        Although often lasting much less than 24 hours, infarction may have occurred.

Diagnosis

History

  • 1.

    Characteristics of neurologic symptoms—can localize a circulatory impairment (see Table 56.1 for a more complete review)

    • a.

      Onset—left leg weakness and speech difficulty

    • b.

      Provoking factors—none, onset is sudden and unexplained

    • c.

      Palliative factors—none, resolves with time

    • d.

      Timing differentiates between TIA and stroke—majority of TIAs last less then 6 hours.

    • e.

      Associated symptoms

    • f.

      Pertinent negatives—denies nausea, vomiting, fevers, chest pain, or chest palpitation

    TABLE 56.1
    Relation of Neurologic Impairment with Vascular Lesion
    Symptoms Vascular Distribution Neurologic Distribution
    Transient monocular blindness (amaurosis fugax)
    Visual field disturbances Retinal artery Limited to the ipsilateral retina/eye
    Altered mental status
    Impaired judgment
    Contralateral motor weakness Anterior cerebral artery Cerebral hemisphere
    Loss of sensation
    Speech/language deficits
    Visual field deficits Middle cerebral artery Cerebral hemisphere
    Hemianopsia
    Impaired memory Posterior cerebral artery Cerebral hemisphere
    Dysarthria, dysphagia, diplopia
    Limb or gait ataxia
    Simultaneous motor, sensory, and visual loss Vertebrobasilar Brainstem, cerebellum, cerebrum

  • 2.

    Medical history—risk factor assessment including hypertension, diabetes, and coronary disease

  • 3.

    Surgical history

    • a.

      Three-vessel coronary artery bypass grafting 2 years ago

    • b.

      Guidelines recommend carotid evaluation in the preoperative work-up of selected high-risk potential coronary bypass patients.

  • 4.

    Allergies/medications—no known drug allergies; currently taking atenolol, metformin, lisinopril, and aspirin

  • 5.

    Social history—nonsmoker, quit 10 years ago; drinks alcohol socially; no recent travel

Physical Examination

  • 1.

    HEENT (head, eyes—presence of Hollenhorst plaque does not increase the risk of TIA or stroke, ears, nose, and throat)

    • a.

      There are no carotid bruits bilaterally.

    • b.

      The presence of a carotid bruit has low sensitivity for detecting more than 70% stenosis.

    Amaurosis fugax alone is associated with the same stroke risk as a TIA.

  • 2.

    Cardiovascular

    • a.

      Rate and rhythm are regular, with no murmurs.

    • b.

      Evaluate pulse and murmurs for possible cardiac sources of emboli.

  • 3.

    Pulmonary—clear bilaterally

  • 4.

    Abdomen—no palpable masses or audible periumbilical bruits

  • 5.

    Vascular

    • a.

      Two plus carotid, radial, femoral, popliteal, and dorsalis pedis pulses bilaterally

    • b.

      A full vascular examination is important to diagnose other possible pathologic conditions, including aneurysms.

  • 6.

    Neurologic

    • a.

      Cranial nerves II–XII intact. 5 of 5 strength in all upper and lower extremity muscle groups. No evidence of hyperreflexia

    • b.

      A full neurologic examination may help to identify symptoms in active stroke and localize a lesion.

Imaging

  • 1.

    Carotid duplex ultrasound ( Fig. 56.1 )

    • a.

      Advantages

      • (1)

        Noninvasive

      • (2)

        Can give information on velocities, anatomy, and plaque morphology

      • (3)

        Can achieve high sensitivity (>75%) and specificity (>95%) if combinations of parameters are measured ( Table 56.2 ).

        • Contralateral stenosis/occlusion can falsely elevate velocities; low cardiac output can influence velocities

        TABLE 56.2
        Carotid Stenosis Velocity Criteria by Carotid Duplex Ultrasound
        Degree of Stenosis of the Internal Carotid Artery Peak Systolic Velocity End-Diastolic Velocity Internal Carotid Artery/Common Carotid Artery Ratio
        Normal <50% <125 <40 <2.0
        Between 50%–70% 125–230 40–100 2.0–4.0
        >70% >230 >100 >4.0
        Occluded Undetectable N/A N/A

    • b.

      Disadvantages: Ultrasound is limited by the following factors:

      • (1)

        Operator dependence

      • (2)

        Tortuous vessels

      • (3)

        Visualizations of proximal common carotid or intracranial branches

      • (4)

        Arterial calcification

    FIG. 56.1, Report of carotid duplex ultrasound.

  • 2.

    Computed tomographic angiography

    • a.

      Advantages

      • (1)

        Anatomy of the arch—important planning for carotid stenting

      • (2)

        Demonstrates relative position of calcifications and stenosis near the carotid bifurcation

      • (3)

        Provides an estimate of the residual lumen and less likely to overestimate stenosis

    • b.

      Disadvantage—requires a contrast bolus comparable to that of angiography

  • 3.

    Magnetic resonance angiography

    • a.

      Advantages

      • (1)

        Avoids nephrotoxic contrast agents

      • (2)

        May allow characterization of plaque morphology

    • b.

      Disadvantages

      • (1)

        Can overestimate stenosis

      • (2)

        Incompatible with implanted metallic devices

      • (3)

        Claustrophobia

  • 4.

    Angiography—no longer the gold standard

    • a.

      Advantages

      • (1)

        Used mostly in the case of conflicting results between two other imaging techniques

      • (2)

        Evaluation of entire carotid system including collaterals and the aortic arch

      • (3)

        Necessary for patients undergoing carotid artery stenting (CAS)

    • b.

      Disadvantages

      • (1)

        Invasiveness and cost

      • (2)

        Neurologic and vascular morbidity (risk of stroke or TIA can be as high as 1.3%)

      • (3)

        Limited views

Differential Diagnosis of Stroke/Transient Ischemic Attacks

Atherosclerotic Disease

  • 1.

    Comprises 90% of carotid occlusive disease cases

  • 2.

    Anatomy influences hemodynamics—formation of plaque on lateral walls

  • 3.

    Pathophysiology

    • a.

      Hyperlipidemia, hypertension, diabetes, and so on, lead to endothelial injury.

    • b.

      Monocytes driven by more low-density lipoproteins adhere to and invade the damaged endothelium.

    • c.

      Plaque size increases.

    • d.

      Increased platelet activity furthers endothelial damage.

    • e.

      Platelets stimulate intimal smooth muscle cells to secrete extracellular matrix.

    • f.

      Muscle cells accumulate lipids, and the plaque center becomes necrotic.

    • g.

      Plaque ulceration and rupture are similar to acute coronary syndrome.

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