1 / 34

Carotid, Subclavian, and Vertebrobasilar Disease

Carotid, Subclavian, and Vertebrobasilar Disease. Kelley Hodgkiss-Harlow 9/30/2009. Carotid Disease: History. 1875—Gowers case report of R hemiplegia/L blindness 1914—Hunt recognizes syndrome of TIAs as prodrome to stroke 1937—Moniz: Arteriography used to diagnose carotid artery occlusion

gaius
Download Presentation

Carotid, Subclavian, and Vertebrobasilar Disease

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

  2. Carotid Disease: History • 1875—Gowers case report of R hemiplegia/L blindness • 1914—Hunt recognizes syndrome of TIAs as prodrome to stroke • 1937—Moniz: Arteriography used to diagnose carotid artery occlusion • 1954—Eastcott publishes first report of successful CEA

  3. Pathology • Atherosclerosis: 90% • Deposition fat intimafatty plaque with intermittent hemorrhage/ulceration • Bifurcation predominance-secondary to arterial geometry, velocity profile, and wall shear stress • Other 10%: • FMD • Mechanical • Inflammatory • Radiation

  4. Stroke • 3rd leading cause of death in USA • Age is risk factor: • Male:female ratio about 1.5:1 • >65 y/o incidence 150-200/100,000 • High rate of recurrence if no intervention: • 10-20% within one year, 20-42% within 5 years • Roughly accepted 10%/yr recurrence risk • Majority recur within one year • High mortality rate with recurrence • 35-65%

  5. Stroke distribution • MCA: contralateral sensory/motor loss, head and eye deviation toward infarcted side • left—aphasia/neuropsych symptoms • ACA: rare, contralateral lower extremity weakness/sensory, urinary incont, apathy, mutism, gait apraxia • PCA: mesencephalon, thalamus, occiptal and temporal lobes—homonymous visual field deficit, alexia, prosopagnosia, amnesia, hallucinations • Watershed areas: ACA/MCA and MCA/PCA borders • Lacunar (brain stem, basal ganglia): pure motor, pure sensory, ataxis hemiparesis, and dysarthria.

  6. TIA • Definition: Transient focal neurologic deficit of either anterior or posterior circulation • Rochester study: TIAs followed for five yr • Incidence stroke 36% • 51% of these occurred within first year • Lit review: annual stroke incidence in pts with TIAs ranges from 5.3-8.6%/yr for first 5 years • Approx 1/3 pts with TIA will suffer stroke within 5 years

  7. TIA II • Embolic theory of transient cerebral ischemia (versus mechanical flow reduction) • Atheromatous debris, thrombus, or plt aggregates • Ischemic attacks stop after occlusion • TIA vs small stroke? Cerebral infarction and atrophy is correlated with percent stenosis and h/o TIAs • 2% e/o stroke on CT with pts with ‘mild’ stenoses • 58% in pts with asymptomatic high-grade stenoses • Therefore, important to identify asymptomatic lesions BEFORE TIA occurs

  8. Timing of CEA • Historically: weeks to months delay after TIA or stroke • ipsilateral hemorrhage and extension of the infarct supported in several series • Old data prior to current imaging studies • No RCT addressing the question • Large meta-analysis 2003: • No diff between rates of stroke or death for pts with stable stroke symptoms when CEA performed early (<3-6 weeks) or delayed (>3-6 weeks) • Pooled analysis of NASCET and ESCT data • Greatest benefit from surgery in group randomized within 2 wks of surgery and this benefit decreased with further delay from symptom onset

  9. Imaging Studies • CT scan—90% cortical ischemic infarctions are detectable with a clinical neurologic event after 24h • Hypodensities, mass effects, loss of distinction between cortical gray and subcortical white matter • Hemorrhagic areas of reperfusion • Only dx ~50% brainstem infarcts • CTA vs. Angiography: Overal accuracy for correct stenosis 90-96%, risks of complications avoided • MRA: Sensitivity 83-97% and specificity 92-98% for detecting flow voids, tends to overestimate when compared to angiography

  10. Symptomatic Disease • NASCET:2226 pts randomized to medical care or CEA. • Patients had either a transient ischemic attack or stroke within 4 months of enrollment and a 30-99% internal carotid artery stenosis. • For patients with a >=70% stenosis, carotid endarterectomy reduced the risk of any ipsilateral stroke from 26% to 9% at 2 years (P<0.001). • Conclusion: CEA better if symptomatic with stenosis >70%

  11. Asymptomatic disease • Natural history studies: 30-50% pts who have suffered a stroke did NOT have TIA prior • 20% pts with bruit will have hemodynamically significant stenosis of the carotid bulb • ACAS trial (1995): Called off after 2.7 yrs f/u • 5 yr risk for ipsi stroke, any periop stroke, and death was 5.1% surgical group c/w 11% medical group. • Absolute risk reduction of 5.9% and relative risk reduction of 53% in favor of CEA. • Combined neurologic morbidity and mortality 1.52% for surgery.

  12. Asymptomatic Disease II • Conclusion: CEA better if can offer with morbidity/mortality <1.5%, recc if >60% stenosis • Corresponds to 80% stenosis when using standardized duplex criteria • ASCT (2004): 5 yr trial results confirm and extend ACAS results. • 5 yr risk for ipsi stroke, any periop stroke, and death was 6.4% surgical group c/w 11.8% medical group. • Benefit in pts >60% stenosis • Most benefit in pts >75 y/o

  13. Duplex Criteria • Individualized to each vascular laboratory with a program of internal quality control.

  14. Pre-Op Medications • Antiplatelet Therapy • Cochrane meta-analysis: ASA 81mg statistically significant benefit in reducing rate of stroke from any cause, but not death or cardiac events • 81mg as effective as 325mg with less bleeding complications/risks • Statin • Reduction in in-hospital mortality, perioperative stroke and death rates, but not in-hospital cardiac events • Multivariate analysis: 3-fold reduction in stroke, 5-fold reduction in death

  15. CEA: Techniques • Vertical vs. Horizontal Incision • Identification and Mobilization: • Cervical lymph nodes • Hypoglossal nerve • Gaining distal ICA exposure: • Digastric muscle division • Mandibular subluxation • Endarterectomy—Eversion vs. Patch • No difference in rate of stroke/death • Advantage—faster, less exposure, no suture line on ICA • Disadvantage—tech challenging, mobilization of bulb, less visualization of endpoint, shunting cumbersome • Shunting—”snow plowing the intima”

  16. Selective Shunting • Local/Regional Anesthesia (0-1.1% permanent deficit) • 10% all procedures done • Lesser fluctuations in blood pressure • EEG Monitoring (1.5-3.5%) • Wide threshold between EEG monitoring becoming abnormal vs. infarction • ?sensitivity/specificity • Stump pressure measurements (0.8-2%) • 50mmHg based on correlations with EEG monitoring, status of contralateral artery, and reported outcomes

  17. To Shunt or Not To Shunt • Clamping ischemia is uncommon cause of perioperative stroke • 93-96% pts tolerate carotid clamping without shunt under local/regional anesthesia • Embolization or thrombosis usually due to technical difficulties • Shunt does not protect or contribute to stroke risk—no superiority in either technique between selective shunting vs. routine shunting. (Cochrane stroke group)

  18. Intraoperative Assessment • Operative Arteriography • If routinely performed, a reduction in mortality, stroke rate, and fatal strokes has been noted in several studies • Angioscopy • Direct visualization of the luminal surface • Increases cross-clamp time, no info on patterns of blood flow • Duplex Ultrasonography • Detection and correction of turbulent blood flow and anatomic defects lead to decreased occlusions and restenosis

  19. CEA vs. CAS • Randomized clinical trials to gain evidence on which to base clinical decisions. • CAS vs. CEAneed to enhance our understanding of their roles. • CAVATAS—angioplasty alone vs. surgery, horrible results both arms, of historical interest only

  20. SAPPHIRE (Stenting and Angioplasty with Protection in Pts at High Risk for Endarterectomy) • Initially, data showed results for stenting statistically significantly superior to those of CEA….but • Primary endpoint was amalgam of short and intermediate term results (periprocedural stroke, MI, or death, and one year ipsilateral stroke or death) • No statistically significant difference in outcome in any individual endpoint (death, stroke, or MI). • Majority of MI’s were non Q-wave and of doubtful significance. • <30% high-risk pts had symptomatic dz, treatment groups are not equal in terms of comorbidities/age • No medical management arm

  21. Symptomatic Trials • EVA-3S: >60% symptomatic stenosis equally eligible pts • 30 day: Stroke/death rates 3.9% (CEA) vs. 9.6% (CAS) • 6 months: 6.1% vs. 11.7% • But…less experienced surgeons, no CPD • SPACE: symptomatic pts randomized CEA vs. CAS, failed to prove “non-inferiority” • CPD in only 27%

  22. CREST • 2500 pts equally eligible for CEA vs. CAS, enrolled based on NASCET/ACAS guidelines (50%/70%) • Lead-in results suggest that older pts suffer worse outcomes (P=0.0006)

  23. Conclusions: CAS vs. CEA • The low morbidity and mortality rates in both nonrandomized and randomized series studying CEA for both asymptomatic and symptomatic pts must be equaled for CAS. • 30d stroke and stroke/mortality rates for CAS appear to be marginally statistically significantly higher than those associated with CEA (1.3%) • Accepted indications: • Surgically inaccessible lesion • Hostile Neck • Restenosis • Medical high risk (hard to define) • Participation in RCT

  24. Vertebrobasilar Ischemia • Symptoms: Commonly manifested as vertigo, visual disturbances, progressive neuro deficit • Mechanisms: • Microembolization: from heart or more proximal arteries. Less common. • innominate, prox subclavian, and vertebrals • Low-flow: lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid. • More frequent • Stenosis/occlusion of vert, also extrinsic compression • Orthostatic hypotension, antihypertensive meds, arrythmias, CHF, pacemaker malfunction, anemia

  25. Evaluation of Patients • Dizziness, vertebral artery stenosis are common complaints/findings • Imaging brain to r/o tumor, investigate for infarctions • Check bilateral arm BP’s to r/o subclavian steal syndrome • Document reversal of flow by duplex • Extrinsic compression by osteophytes • Turning head side to side, slowly, then briskly to differentiate from BPV • Confirm with angiogram

  26. Global ischemia • “Drop attacks” comprise roughly 30% of presentations • One or both internal carotid arteries occluded or with severe siphon stenosis. • Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded. • Minimal anatomic req to justify vert reconstruction is >60% stenosis in dominant if contra is hypoplastic, or >60% in both.

  27. Angiography • Most common athersclerotic lesion is stenosis of its origin • Presence of post-stenotic dilation proximally is suggestive of hidden stenosis • Extrinsic compression seen at V2—multiple views/manipulation necessary • V2-V3 segments: site of traumatic injury from periosteum/adventitia fixation • V3 usually area of reconstitution secondary to collaterals from occipital artery

  28. Angiography

  29. Treatment • Anticoagulation • Trial of medical therapy prior to pursuing any surgical intervention • Most effective for lesions that cause symptoms through embolization or thrombosis of small arteries • If definite clinical syndrome, MRI documenting absence of alternate pathology, arteriography with structural lesion, and persistent symptoms on anticoagulationsurgery

  30. Surgical Options • Transposition of Vertebral Artery into the Common Carotid Artery • Origin stenosis • Supraclavicular at level of C6 • Patency 90-97%, stroke risk 2%, mortality risk <1% • Complications: Horner’s, lymphocele • Distal Vertebral Artery Reconstruction • GSV • Level of C2 • Endovascular interventions?

  31. Subclavian Disease • Atherosclerotic disease left>right • Asymptomatic lesions even with asymptomatic stealtreatment deferred • Subclavian steal: • Retrograde blood flow associated with proximal subclavian stenosis or occlusion • Upper extremity ischemia (71%), VBI (44%), Hemispheric TIA (29%)

  32. Subclavian Steal Syndrome • Physical exam • Blood pressure differential >=20mmHg • 2-3x more common on the left • Embolic phenoma to hands • Duplex ultrasonography • Reversal blood flow within vertebral • Monophasic waveforms in subclavian a. • High-frequency blood flow pattern • Arch aortography with selected views

  33. Treatment • Treat ICA lesion first! • If symptoms persist • Transposition of subclavian artery onto the common carotid • Approx 100% patency rate at followup • Carotid-Subclavian bypass • Approx 94% patency at 10 years • Axilloaxillary bypass • Setting of previous extensive neck surgery or radiation • Long-term durability inferior • Subclavian artery stenting/angioplasty

  34. Any Questions?

More Related