Cerebrovascular Occlusive Disease

I)Epidemiology

A) Stroke 3rd most common cause of death in US

 extracranial carotid disease most common cause (60%)

hemorrhagic and cardiac embolic are each 15%

 500K strokes/year with 200K deaths

2/3 of survivors are disabled

tremendous health cost

II)Anatomy

A) Paired internal carotid arteries supply 80 – 90% of cerebral blood flow

 paired vertebral arteries supply 10 – 20%

 often anastomose with each other in Circle of Willis

very variable, with 35% having no anastomoses between either anterior and posterior circulations or right and left circulations

B) Clinically significant collateral pathways

most important is internal carotid—ophthalmic artery—external carotid collateral system

 left to right external carotids by way of facial arteries

external carotid to vertebral artery via muscle branches in the neck

III)Pathophysiology

A) fibromuscular dysplasia: mostly women between 30 and 50 y/o; associated

with Berry aneurysms and multiple arteries affected

B) vasculitides such as Takayasu’s arteritis

C) spontaneous dissections, aneurysms and arterial kinks

D) atherosclerosis: mostly at sites of turbulent flow (i.e. carotid and common

femoral artery bifurcations)

i) plaques tend along outer wall of bifurcation & proximal-most external carotid artery

ii) plaque thickest @ bifurcation and extends 2cm into proximal internal

iii) plaque occupies media and intima

iv) plaque ruptures and causes embolization and/or thrombosis

v)on duplex, mature plaques are calcified (highly echogenic) and less likely to be symptomatic, while soft plaques (anechoic) are complicated and more likely to be symptomatic

vi) usual risk factors for carotid plaque genesis, but strong correlation between homocysteine levels and carotid plaques

IV)Clinical Presentation

A) TIA or hemispheric stroke

i) TIA: symptoms resolve completely by 24 hours

ii) stroke: last beyond 24 hours and are often permanent

B) Common symptoms: amaurosis fugax, motor/sensory deficits, visual field deficits, ataxia, vertigo, nystagmus, drop attacks, aphasia, vertigo, dysphasia, dysarthria

V)Diagnosis

A) H&P: evaluate for HTN, risk factors, cardiac arrhythmias

B) Carotid duplex scanning: localize disease anatomically, determine significance of occlusion by velocity of blood flow

C) Transcranial Doppler: mostly for vasospasm s/p SAH

D) Angiography: considered gold standard but has inherent risks

E) CT angio and MRA: noninvasive but not perfect in determining degree of stenosis; complements carotid duplex in distinguishing anatomy

VI)Natural History of Carotid Artery Occlusive Disease-

A) Symptomatic Disease

i)risk for stroke 3 years s/p TIA is ~ 15%

ii) 10 – 20% the first year and ~ 6%/year x 5 years

iii) cumulative risk over 5 years was ~40%

iv) high risk for death from coronary disease—1/3 died by 5 years

v) initial stroke mortality rate ~ 25%, recurrent stroke risk is 5 to 40% and 1/3 are lethal

B) Asymptomatic Disease

i) only 10% of patients with stroke had a prior TIA

ii) carotid bruits are not diagnostic of stenosis

 can be radiation of cardiac murmurs or calcified vessels

 5% of pts > 50 y/o have bruits

  • 23% of pts with bruit have carotid stenosis > 50%

iii) overall prevalence of stenosis is 30%

 only 3.7% of stenoses are > 50%

 only 0.9% of stenoses are > 80%

iv) peri-operative stroke risk for CABG is elevated when B/L high grade stenosis exists, but not if unilateral

 simultaneous and staged repairs offer similar risk

VII)Management-

A) Medical treatment-

i) prevention via lifestyle modification if caught early

ii) no clear benefit of anticoagulation or ASA in preventing strokes

 plavix decreases relative risk by 7% compared to ASA alone in pts with prior stroke

B) Surgical management-

i)CEA- indications are stroke with minimal residual deficits, TIA or asymptomatic disease with high grade stenosis

ii) closely monitor patients post-op for 12 to 24 hours for hemodynamic instability and mental status changes

VIII)Complications of Carotid Endarterectomy-

A)Neurologic complications

i) stroke: from inadequate blood flow intra-op, embolization during dissection or after endarterectomy

 if within 24 hours, re-exploration warranted to evaluate cause

 if POD 2 or 3, think of intracerebral hemorrhage: CT head

ii) cranial nerve dysfunction in up to 39%

 only 60% with clinical symptoms: hoarseness, difficulty swallowing, change in speech

 most commonly affected: recurrent laryngeal, hypoglossal, superior laryngeal

=> rare injuries to marginal mandibular (nasolabial fold droop), greater auricular, spinal accessory, and glossopharyngeal

 most resolve by 6 months post-op

B) Non-neurologic complications-

i) significant hemorrhage in 1 - 5%, higher if on ASA

ii) labile BP

 hypotension and bradycardia form dissection of plaque off baroreceptor: treat with 1% lidocaine injection to area

 HTN from interruption of carotid sinus nerve

iii) MI: most common cause of death post-op

iv) re-stenosis: common, occurring in up to 30%, but less than 3% are symptomatic

 if within 6 months, intimal hyperplasia is cause

 if after 2 years, atherosclerotic plaque is cause

IX) Efficacy of CEA in Prevention of Stroke-

A) Studies:

i) NASCET showed that stroke rate was 9% s/p CEA while 26% with medical therapy only and that advantage seen early; VACSP confirmed

ii) ACAS showed 4.8% stroke rate s/p CEA while medical therapy had a 10.6% rate

X) Endovascular Therapy-

A) minimally invasive, more patients could undergo repair, but complications by embolization and plaque dislodging are frightening

B) Studies are not consistent in proving efficacy & safety over CEA