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CT Angiography & CT Perfusion in Management of Acute Stroke 



CT Angiography & CT Perfusion in Management of Acute Stroke

 

 
 
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Published:  January 09, 2010
 
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Slide 1: Stroke – past CT Angiography and CT Perfusion in the Management of Acute Stroke Stroke – present good outcome with IV tPA(mRS 0-1): 39% vs. 26% 1 most patients arrive too late (>3 hrs for NINDS) currently, only 0.6-1.8% of strokes get IV tPA 2,3 0.6- Stroke – present IV tPA exclusions / contraindications 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. > 3 hrs from stroke onset 80 > age > 18 pregnancy (up to 10 days postpartum) “symptoms suggestive of SAH” – despite negative CT “rapidly improving or minor symptoms” “seizure at onset of stroke” ever: → history of intracranial hemorrhage within 3 mo: → stroke, serious head trauma, intracranial surgery within 21d: → GI/urinary/pulmonary hemorrhage within 14d: → major surgery within 7d: → arterial puncture at a non-compressible site SBP > 185 mmHg or DBP > 110 mmHg aggressive treatment required to reduce BP to specified limits current use of anticoagulants (or recent, with PT > 15s) use of heparin within 48hrs and elevated PTT platelets < 100,000 glucose < 50 or > 400 mg per deciliter brain tumour, abscess, aneurysm, AVM bacterial endocarditis known bleeding diathesis – includes renal, hepatic insufficiency etc… Odds Ratio for Favorable Outcome NINDS NEJM 19951, Katzan JAMA 20002, Qureshi NRS 20053 Stroke – present IV tPA is less effective for severe strokes 1 NIHSS ≥ 10: 75% decreased chance of good outcome NIHSS > 20: only 8% will attain NIHSS=1 after IV tPA “Time is brain” typical supratentorial large vessel stroke: ~54ml brain is lost over ~10 hrs per hour: 830 billion synapses, 120 million neurons, 447 miles of myelinated fibre lost each hour, brain effectively ages 3.6 years hour, IV tPA is less effective for large vessel occlusions 2,3 ICA recanalization rate is 1/3 that of MCA tandem ICA/MCA has poor recanalization & bad prognosis IV tPA is relatively slow-acting 4,5 slowTCD over 6hrs → 30% recan (of which ¾ are within 1hr tpa) tpa) angio 1hr after tPA → 1/10 ICA/proximal MCA, 1/3 distal MCA 1: NINDS Stroke 1997; 28:2119–2125 2: LInfante Stroke 2002; 33:2066-2071 33:20663: Rubiera Stroke 2006; 37:2301-2305 37:23014: Christou Stroke 2000; 31:1812-1816 31:18125: Lee Stroke 2007; 38:192-3 Saver, Stroke 2006; 37:263 1
Slide 2: Stroke – future? now. Treatment of Acute MI 1987 IV tPA 1993 PTCA 2000 Stent 2003 Cypher Stroke – new tools Thrombolytics: GIIb/IIIa inhibitors: Mechanical disruption: Clot retrieval: Ultrasound Catheter: Angioplasty / Stenting → Alteplase, Retavase → Reopro, Integrilin → microwire / snare → MERCI, Penumbra → EKOS → Gateway / Wingspan Treatment of Acute Stroke 1996 IV tPA today 2004 ??? 1999 PROACT II MERCI Retriever Multimodal Revascularization CT: early left caudate head, basal ganglia infarct Case example: 45 yo male acute LMCA stroke R paretic, R hemianopic, R facial droop, dysphasic, dysarthric. NIHSS = 15 CTP: ↑↑MTT, ↓CBF, ↑CBV Flow Interpretation: small caudate and frontopolar infarcts, surrounded by large (but salvageable) ischemic penumbra… Volume Transit Time 2
Slide 3: CTA: LM1 occlusion (w/distal collateral) CTA: LCCA/inominate stenosis AP: Sag: LCCA origin severe stenosis, 5F sim2 finally pops in but is occlusive (static dye column) T-occlusion equivalent: proximal LA1, LM1 occluded, poor collateralization All-star 0.014 wire maintains access to LCCA, pigtail arch run shows severe origin stenosis Cross LM1 occlusion with MERIC 18L microcatheter over transend AP 1. Aviator 6x30mm over All-star wire, LCCA origin angioplastied 2. Sim2 back over Allstar wire into distal LECA 3. All-star wire then exchanged for 0.035 stiff exchange glidewire 4. Sim2 swapped out for 7F concentric balloon guide over stiff exchange wire, parked in LCCA 5. Concentric guide catheter taken to distal cervical LICA 6. LMCA occlusion crossed with 18L Concentric microcatheter over Transend microwire… Lateral 3
Slide 4: Deploy MERCI L5 retriever Clot retreived, flow restored AP Lateral AP Lateral Pre AP AP Lateral Post Post – Arch MRA: LCCA stenosis better, inominate as before, will need tx later IA Thrombolysis: New Tools Thrombolytics: Alteplase, Retavase GIIb/IIIa inhibitors: Reopro, Integrilin Reopro, Mechanical disruption: microwire/snare Clot retrieval: MERCI (X6, L5, variants) Ultrasound assisted Catheter: EKOS Balloon Angioplasty Primary Stenting 4
Slide 5: Imaging for stroke intervention GOAL: To select out patients with viable brain tissue at risk that can be treated with the optimal tool for revascularisation New-generation CTA/CTP = anatomy+physiology 1. faster: <5 min total acquisition time 2. less motion artifact 3. less dye (CTA+CTP <120ml) → <50ml with 320-slice! 4. CTA (arch to vertex) : • lesion presence/absence/location • lesion accessibility • a priori knowledge = no guessing! 5. CTP: • absolute numbers for CBF, CBV • 4-8 slices, + post-fossa coverage → full coverage with 320-slice! • CBF ≈ penumbra+core; CBV ≈ collateral supply • CBF/CBV mismatch = salvageable penumbra! HOW? FLOW VOLUME 37.3±5.01 25.0±3.82 13.3±3.75 1.78±0.30 2.15±0.43 1.12±0.37 CBFxCBV sensitivity=97.0% specificity=97.2% accuracy=97.1% for CBFxCBV and subsequent stroke threshold=31.3 Murphy, B. D. et al. Radiology 2008;247:818-825 Murphy, B. D. et al. Radiology 2008;247:818-825 5
Slide 6: Figure 3: Scatterplot shows mean CBV versus mean CBF in penumbra and infarct regions in patients with acute stroke and confirmed recanalization at 24 hours (dashed line represents CBF×CBV = 8.14) - 40 patients, median NIHSS=16, 19 received iv-tpa - compared initial CTP/CTA and day #3 postop MRI/MRP - reperfusion defined as normalization of ≥80% area with increased MTT Murphy, B. D. et al. Radiology 2008;247:818-825 CTP parameters can predict hemorrhage rCBF prediction of symptomatic ICH following IA treatment for MCA occlusion Regions with infarction (based upon DWI+ADC) at day #3 compared with CBV maps on initial CTP → in hypoperfused areas ( ↓↓CBF, ↑↑MTT), does CBV predict eventual infarction? CBV With reperfusion Low 97% (go on to infarct) Normal 41% (go on to infarct) High ~ 13 ml per 100g/min 3% (go on to infarct) No reperfusion 94% (go on to infarct) 63% (go on to infarct) 94% (go on to infarct) Gupta 2006 Stroke 37:2526 ~ 1/3 MCA territory Stroke Algorithm CTP in posterior circulation! Acute Stroke CTA / CTP 0-3 hr >3 hr CBF CBV MTT DWI large vessel occl. (ICA, M1/M2, A1, VA/BA) large ischemic penumbra > infarct large stroke (NIHSS≥10) yes no large vessel occl. (ICA, M1/M2, A1,VA/BA) large ischemic penumbra > infarct large stroke (NIHSS≥10) yes no IA Tx ± bridging IV tPA IV tPA IA Tx no acute thrombolysis, later medical or surgical stroke prophylaxis 6
Slide 7: SUMMARY CTP is available and powerful: Transit time = very sensitive (but not specific) Flow = penumbra plus core Volume = penumbra vs core (collateral supply) preserved → penumbra (still salvageable) decreased → core (dead) CBF/CBV = crude “risk/reward” ratio onset often unclear → CT perfusion = more accurate physiological data perfusion beats onset POD#1 DWI: frontopolar, caudate, basal ganglia infarcts (predicted by CTP), but large LMCA territory salvaged POD#1 FLAIR: small caudate head, basal ganglia, frontopolar infarcts POD#2 CT Case example: 83 yo male acute right hemisphere stroke left plegic, R gaze preference, L facial droop, dysarthric NIHSS > 10 last normal > 14hrs ago past medical history = paroxysmal atrial fibrillation (discovered on this admission) 7
Slide 8: Emergency CT perfusion: Low CBF but preserved CBV → stroke is still salvageable. thrombectomy and lytics → inferior division open, residual clot in superior division balloon angioplasty → superior division now also open preop CBF preop CBV residual clot Pre Post preop CBF preop CBV INITIAL CTP: Case example: 33 yo female acute right carotid stroke left hemiplegia, facial droop, dysarthria, hemianopia, neglect, decreased left body sensation, drowsy, fixed gaze deviation to right. NIHSS = 16 onset > 4 hrs past medical history = smoker, oral contraceptive pills -Very low blood flow -Very slow blood flow -Preserved blood volume -BUT: > 4hrs onset CBF TTP CBV 8
Slide 9: Complete right internal carotid artery occlusion → no intracranial blood flow microcatheter run shows distal blood vessels remains patent MERCI thrombectomy opens distal carotid and proximal middle cerebral artery, balloon angioplasty opens distal middle cerebral artery MRI few days later… Mid-BA occlusion Case example: 76 year old female Found 2:30 am at outside institution with stroke, onset unknown Rapidly transferred to tertiary-care institution. When seen, unable to move anything except eyes rapidly loosing consciousness → crash intubated in ED NIHSS = 30 9
Slide 10: Access is going to be tough!!! Big Problem… ar m ar m Bigger Problem…? Pooled NASCET, ECST, VA309 results Lancet 2003,361(9352):107 Case example #1: 70 yo male acute LMCA stroke driving → swerved off road → min. responsive on scene right plegic, aphasic, fixed gaze to left in ED NIHSS = 22 onset <1.5 hrs PMH = HTN, NIDDM, dyslipidemia, atrial flutter, on ASA hyperdense sign 10
Slide 11: CBV reduction matches reduction in CBF → no collateral reserve, no penumbra, infarct already well established. CBF CBV TTP 13.6 x 0.9 = 12.2 Case example #5: 70 yo male acute RMCA stroke initial NIHSS=12 in ED, worsened to > 18 → intubated onset > 6 hrs PMH = MI, CABG, PVD, HTN, NIDDM, previous L parietal subcortical stroke CT (pre) CTP (pre) CBF CBV TTP 11
Slide 12: Treatment: Angio = RMCA bifurcation occlusion, ant. temporal open Retavase 2mg M1 Retavase 1mg M2inf wire both M2’s Merci M2sup x2 Pre Post CT (POD#1) Outcome: TIMI-3 M1/M2’s distal branch of inferior M2 remained occluded R basal ganglia ICH, R parietal infarct rest of MCA territory spared discharged 17 days later to rehab, NIHSS=16 return w/urosepsis one month later → no sig improvement CT 44 days later…NIHSS still 16. CTP keypoints: 1. TTP/MTT is very sensitive – but not specific 2. CBV distinguishes infarction vs. ischemic penumbra (dead vs. salvageable brain) 3. Areas at risk for hemorrhage post-thrombolysis can be predicted 4. Crude risk/benefit ratio = CBV / CBF deficit Bottom line = physiological imaging is real and powerful…CTP does not lie! 12
Slide 13: SUMMARY CTP is available and powerful: Transit time = very sensitive (but not specific) Flow = penumbra plus core Volume = penumbra vs core (collateral supply) preserved → penumbra (still salvageable) decreased → core (dead) CBF/CBV = crude “risk/reward” ratio onset often unclear → CT perfusion = more accurate physiological data perfusion beats onset 13

   
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