3 Course ECNR Antalya
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Lernkarten
Wie behandelt man intrakranielle stenosen
Intracranial stenosis ≥50% should be treated with aspirin monotherapy and risk factor modification especially focusing on hyperlipidemia and blood pressure management
Evtl zusätzlich plavix
stenting nur noch
- Symptomatic stenosis > 70 % with failure 2 antiplatelet
- Hemodynamic stenosis with no reserve after Diamox!
Hyperacute ischemia
Understand cerebral autoregulation. • Consider heterogenity of cerebral ischemia due to perfusion pressure, site of arterial occlusion, and collateral capacity. • 20ml/100gxmin is the threshold for functional impairment • 10ml/100gxmin is the threshold for ischemic damage (tolerated for 20 min only). • No infarction within the first 6 hours of arterial occlusion. • Net uptake of water predicts infarction
Keypoint HEmorrhagic Transformation
HT is a common phenomenon of severely injured ischemic brain tissue
• HT is a marker of tissue reperfusion
• HT is per se irrelevant for the clinical course if not extended and causing mass effect
• the risk for dense HT (Parenchym Hematoma) is associated with the extend of ischemic injury and the time to reperfusion
Summary drug antiplatet
Aspirin Generally the first choice anIplatelet agent Clopidogrel Second most common used anIplatelet, either as monotherapy, or combinaIon to aspirin Prasugrel, Icagrelor Should be considered in paIents with resistance to clopidogrel Ticlopidine A cheaper alternaIve for clopidogrel resistant paIents, usage hindered by agranulocytosis risk GP-IIb-IIIa inhibitors Adjuvant therapy in endovascular operaIons; usage in acute stroke not established
Summary anticoagulans
Warfarin Most commonly used oral anIcoagulant, issues with narrow therapeuIc index NOACs New alternaIves on the rise, low risk of intracerebral hemorrhage, no INR monitoring Heparin and lmwh First choice parenteral anIcoagulants, risk of HIT Heparinoids Reserved for paIents with HIT
Trigger for agregating platlets
Trigger: Exposure to collagen, von Willebrand factor, fibronecAn, laminin
Pathway of platlet agregation and drug anti it
Thromboxane pathway: – Aspirin, triflusal • ADP pathway:– Clopidogrel, Iclopidine, Icagrelor, prasugrel, ... • GPIIb-IIIa pathway: – Tirofiban, abciximab, epIfibaIde
Wann ist Aspirin erwiesen als therapie
Nach Myokardinfarkt
akuter Myokardinfarkt
nach stroke oder TIA
Nachteil ticlopidin
Agranulocytosis
Welchen Faktor betreffen Low moleculare herparin fast nicht im Gegensatz zu heparin
Faktor II A
nur X
Qualitäten Low molekular heparin
Better bio-availability • Longer half-life • Less binding to platelets and PF-4 • Caution in paIents with renal failure • Antagonist: protamine
Risk for aneurysma
Smoking, Kokain , alcohol
neoplastic,
disectimg
Auftreten aneurysma
1-7 %
zweites aneurysma 20-30 %
Aneursymagroessen
Small < 4 mm
medium bis 10
gross bin's 2.5 cm
giant > 2.5 cm
Risk of ruptured aneurysma vorderer circualtion
posteiot
Anterior 0.05% ( <7 mm)
basilar (> 10 mm) 0.5 %
Risk of bleeding avm per Year
2-4 Prozent
Over 10 Year 50% when <3 cm
Risk of bleeding dural Fistulae
2% per Year
Unterschied avm and dural Fistula
In dural fistula an Arterie Show direkt Flow in vein without network of arteries
Risk of bleeding cavernoma
0.5 % per Year
Capillara teleangiektasie
Venous Channel in normal parenchyma
Growth Risk of unruptered aneurysma
2-7 % per Year
Followup of ruptured aneurysma
New
growth
Risk of de Novo aneurysma
0.5 % per Year
What is a recamalistion of an Treatments aneurysma
More the. 10 % filling
Recanalisation Faktors
Demographic - Hypertonie, Age, Diabetes
ameursymal Factor - Size, Location necksize
therapeutic - coiling,
Risk of rerupture aneurysma treated
Stable 0.9%
when rekan 3%
Follooww up coiling ?
Mri tof or ce-mra
Follow up coiling Montreal scale
Occlusion
neckr emnant
aneurysma remnant
Follow up stent or Flow diverter
Tof oder ce-mra
Artefakts in lumen
DSA is best
aneurysmasize T2 Flair oder T1 km
Devolepment aneurysma Flow diverser
30 % disapear
50 % shinkage
Follow up clipped aneurysma
MRA - Artefakt
CTA
DSA
Timing of folloup stenting
4-6 mt
1year
Therapie of dissction
OAK
agressiv: occlusion or stenting Even think of Bypass
Danger of ruptured dissektion aneurysma
Rebleed in First month
occlusion parent
coiling, Flow diverter
Incidence SVT
3 per Million
Increased incidence of SVT
Neonates, children
pregnant
Isolated cortical vein thromososis
Coronar
t2, T1 , ffe
In SVT is vasogenic and cytotoxic oedema
Yes both
How many Patient does detoriet with heparin
13% -> thrombolysis
Mortalität 4%
DEf DVA
Pathologie Connection of dural arterijes with durals Sinus and veins
