Cerebrovascular DiseaseRiyaz Kamadoli MSIII

Stroke Epidemiology3rd Leading cause of death in the United statesMore prominent in Elderly, Men, African AmericansLong term survivors 48%-hemiparesis, 22%-cannot walk, 24-53% are dependant for normal daily activities

Risk FactorsHypertension ( 4x for >160/95mmHG )Cigarette smokingSickle cell diseaseTransient Ischemic Attack (TIA)Cardiac Diseases (atrial fibrillation, Infective endocarditis)

Anatomy

PathologyAtherosclerosis of arteries supplying the brain, the leading cause of ischemic strokeMost commonly at the carotid bifurcations, 3 main mechanisms a) Embolization of atherosclerotic or thrombotic material b)thrombotic occlusion c) hypoperfusion from advanced stenoses

Pathology

The atheroma contains intrinsic vascular wall cells (endothelium and smooth muscle cells) and unwelcome visitors, the inflammatory leukocytes (monocytes/macrophages and T-lymphocytes)

In the early phase of atherogenesis, the first event that occurs in response to hypercholesterolemia is an attachment of leukocytes to the intact endothelium.

Specific leukocyte adhesion molecules expressed by the endothelium, usually in response to inflammatory mediators such as cytokines, govern these adhesive interactions between white cells and the endothelium.

Once adherent, leukocytes respond to chemotactic stimuli by penetrating from the endothelial surface into the arterial intima

Once resident in the arterial intima, the mononuclear phagocyte undergoes activation. It expresses scavenger receptors that can internalize modified low-density lipoprotein. This promotes foam cell formation,

After the leukocytes have accumulated in the lesion, they often undergo death, sometimes by apoptosis, which can lead to a lipid core covered by a fibrous cap.

Reasons for Plaque RuptureWhen the force acting on the plaque and its fibrous cap exceeds the tensile strength of these structures.Along with plaque rupture with dissection of blood into its interior can lead to dramatic growth of the plaqueOnce cap has ulcer Surface lining ulcer is highly thrombogenic Stim platelet aggregation +blood coagulationPlatelet thrombogenesis at rupture site emboliztion into the internal carotid causing TIA, Amaurosis Fugax.

Clinical PresentationSymptomatic pts TIAs, Amaurosis Fugax, or StrokeTIA- Brief episodes of focal loss of brain function due to ischemia, localized to that portion of the brain supplied by one vascular system. Lasting less than 24 hrs. (2-15 min). Leaves no persistent deficit.Amaurosis Fugax is a transient monocular visual disturbance. Usually shorter than TIAs. Curtain shade descending to the horizontal mid-visual field and then ascending.DX is based on historyWARNING SYMPTOMS OF MAJOR STROKE

Pathology

Complications of Artery Occlusion

Occlusion of Internal Carotid Artery

Work UpRule out carotid artery occlusive disease with Duplex Ultrasonography.If advanced carotid stenosis is present ipsilateral to the symptoms, Carotid endarterectomy is generally indicated.Contrast arteriography is generally helpful for lesser degrees of stenosis B/C Ultrasonography tends to be inaccurate when the occlusion is between 40-59 %

Indications for Carotid EndarterectomySymptomatic PatientAge >70Gender (Male)Systolic Hypertension (>160mmHG)Diastolic Hypertension (>90mmHG)Most recent onset of symptoms (80 %)HX of smoking, MI, CHF,DM, elevated blood lipid levels.

Contraindications for SurgeryUncontrolled CHFRecent MIUnstable anginaAdvanced MalignancyUncertain Diagnosis

Preoperative EvaluationMI is the leading cause of death after carotid endarterectomyDetailed cardiac hx and electrocardiogram.Aspirin therapy started at the time of dx of TIAs, Amaurosis fugax or stroke. 80-325mg/day. Or plavix 75/day.Pts continue to have TIAs despite antiplatelet therapy IV Heparin therapy (Partial thromboplastin time at 1.5X control is Rec.

Surgical Intervention

Surgical PrinciplesOblique incision along the anterior border of the SCM.Begins at the mastoid and extends anteriorly along the anteriomedial border of the SCM muscle up until 1-2 finger tips above the sternal notch.Location of the carotid bifurcation can be determined preoperatively via duplex ultrasonography or arteriography.

Surgical Principles ContdSection the platysmal muscle in the line of the incision, the plane of dissection is anteromedial to the SCM beginning inferiorly and proceeding superiorly.Upper mid portion of the incision, Transverse Cervical nerveCarotid Sheath- formed by deep cervical fascia and prevertebral fascia. Carotid artery, int jugular vein, Vague nerve.

Surgical Principles ContdTo expose the carotid sheath the medial and inner borders of the SCM are dissected and retracted posteriorlyAfter the internal jugular vein is identified, the carotid sheath is opened along the anterior and medial borders of this vein. Branches coursing anteriorly are ligated.Important to keep the dissection along the anterior border of this vein to avoid injury to the spinal accessory nerve.

EndarterectomyBegins in the proximal common carotid artery, extending into the internal carotid artery.Important to extend the arteriotomy above and below the gross intimal damage.Once the vessel is cleaned it is closed with a prosthetic patch. This minimizes postoperative occlusion and ischemic events, and renstenosis.

Endarterectomy ContdAfter closure the external and common carotid arteries are first opened and then the internal carotid artery is opened. This minimizes chance of air or particle emboli into the internal carotid artery system.Arterial wall is palpated to determine presence of a thrill.If detected an arteriogram should be performed. Clot or debris the vessel must be reopened.

Timing of operation after stroke4-6 Weeks in patients dx with acute stroke. Because of possible conversion of a bland infarct into a hemorrhagic one.

Postoperative ComplicationsNeurologic deficits within the first 12 hrs thromboembolic events stemming from the endarterectomy site or damaged internal, common, or external carotid arteries. TX: Immediate heparinization and exploration w/o need for an arteriography.Neurologic deficits beyond 12-24 hrs are usually due to postoperative hypoperfusion or intracerebral hematoma. These conditions are worsened by immediate heparinization. Therefore deficits occurring during this period should be promptly investigated via CT or arteriography.

Hyperfusion Syndrome and Intracerebral HematomaIncidence between 0.3-1.0%Secondary to paralysis of autoregulation from chronic ischemia.Pathologic changes include cerebral edema, petechial hemorrhages, to frank intercerbral hemorrhage.Ipsilateral frontal headache within 1st week after enarterectomy.

Risk Factors for Hyperfusion Syndrome>70% stenosisPoor collateral hemispheric flowContralateral carotid occlusionHypertensionPre-existing ipsilateral cerebral infarction.Seizures from Hyperfusion syndrome treated with phenytoin.

Postoperative ComplicationsPostoperative instability of blood pressure is caused by carotid sinus malfunctionPatients with atherosclerosis of the carotid body often loose effective baroreceptor activityFollowing enarterectomy, the carotid bulb can again distend carotid sinus reflex can over-respond postoperative hypotension cerebral ischemia

Operative Damage to NervesTransverse cervical nerve and greater auricular nerve frequently injured during surgery. Resulting in ipsilateral numbness of upper face, lower neck, lower ear.Recurrent laryngeal nerve is 5-7%Hypoglossal nerve 4-6%Spinal accessory nerve 0.5-1%Superior laryngeal nerve 1-3%

Endarterectomy vs. Carotid StentingMore studies are needed to determine which is better for patients.