AVM Flashcards
What is AVM
Dysplastic blood vessels artery drain to vein w/o capillary, 🚫 brain 🧠 pranchyma in the nidus
Flow in AVM
Medium to high pressure
High flow
%%Risk of hemorrhage
1st time 1%/y
Recurrent 5%/y
Risk factor for ⬆️ AVM rupture ⭐️
Female , Age
Deep venous drainage
Feeding artery anurysum
Small AVM
Previous hemorrhage
%risk of seizure
1st time unrupture AVM 8%
5-y risk of epilepsy and recurrent seizure 60%
Source of AVM bleeding
Anurysum
SRS sterotactic surgery obligation rate
70-80%
Indication of SRS
Deep lesion
< 3 cm
Embolization indication
High grade S-M
High flow
Classification or type of AVM
1- parenchyma AVM. ( pial, subcortical,paraventricuLr,, combined)
2- dural AVM
3- mix prannchyma+dural AVM
MMC age of AVM
Young 30 vs 🔛 anurysum 40s
Syndrome asso w/ AVM ⭐️
Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia)
Klippel-Trénaunay-Weber syndrome,
Parkes Weber syndrome,
Sturge Weber syndrome.
MCC presentation AVM
Hemorrhage [ pure IVh 🔜 paraventriculrAVM , SAH
Smallest AVM bleed more than large ⏩️ high flow and pressure ) ,)
2nd seizure
Mass effect ,
Bruit if dural
HC in ped 🔜 VOM
The strongest prognosticator for future hemorrhage
Previous hemorrhage
RF seizure
Young
Temporal
Cortical
Idus > 3
Hemorrhage
DX
CT to r/ o hemorrhage , calcification within the nidus
CTA high sensitivity and specificity
MRI ; T1, T2 GRE, SWi ( flow viod,feeding and draining hemosidrine)
🔘 edema ➡️ tumors , hemosidren ⭕️ SVM
MRA ➖ limited to detect small BV < 1 Mm , small nidus < 10 mm , anurysum
DSA ( tangle , draining and feeeding )
Spetzler-Martin (S-M) grade of AV
Estimate risk of surgical resection
Requiring DSA or cross section image CT,MRI
Grade 6 untreatable
Mc grade present at stage III S-M
⭐️ Class A (S-M Grade I & II): surgical resection
● Class B (S-M Grade III): multimodality treatment
Class C (S-M Grade IV & V): f/ angiogram every 5 year if ➡️ new deficit ,steal sx,anurysum migh treat
AVM mature at
At age 18 becom more compact
Lawton-Young supplementary grading scale for AVMs
Better than S- M
Predict post operative surgical outcome using mRS
Use only inoperative AVM
When can resection AVM after hemorrhage evacuation
2-6 week to allow ⬇️ edema and better AVM evaluation
Mangment of rupture AVM
If low S- M with low L-Y , or high S- M with low L-Y
High S-M with fixed neurological deficit unlikely to affect after surgery
Tx un rupture AVM according to ARUBA = medical > medical + intervention
Surgical resection indication , cons , pron
Indication S-M 1 or 2
Cons eliminate risk of rebleeeidng and seizure controls
Cons invasive , cost 💲
SE of SRS
Delay Se
Radarion necrosis🔘
🧠 edema , cystic formation
Pregnancy neurological changes
SRS prons vs cons
Pron+ outpatient , non invasive , no recovery preriod , gradual reeducation , seizure control
- latency period take 1-3 y to respond
Risk of bleeding same during latency
Endovascular AVM
Should done ✅ before 24-48 hr before resection
Pros +facilitate surgery if size
Cons- no permanent olitration , multiple procedures
E,bolization prior SRS rate
W/ embolization 47%
W/o 70%
Things had to take in consideration when tx AVM
associated aneurysms: on feeding vessels, draining veins, or intranidal
- flow: high or low
- age of patient
- history of previous hemorrhage
- size and compactness of nidus
- availability of interventional neuroradiologist
- general medical condition of the patient
Surgical techniques
Wide exposure
Isolate and clip A then ▶️ vein
Working sulci and fissure
Delay complication
NBPB normal pressure breakthrough ➡️ post op hemorrhage
Strok ➡️ occlusive hypermia
Rebleedin
Seizure
Follow up 🔝
If complete ✅ resection ⏩️ post op DSA or MRI then ⏩️ 1 &5 y CTA or MRA
After SRS ☢️⏩️ a 6 m MRA, MRI oIF ❌🚫 CTA
If obliterate bu SRS ☢️ post op DSA ( latency period )
📍 MCC location for AVM
parietal➡️ insula, frontal, and temporal lobe
📍 apex of AVM
Preiventricular
📍 AVM base
Cortex
factors AVM ➡️ spontaneous occlusion
single draining vein
single feeding artery
Small nidus (<3 cm
Factor increase ⬆️ AVM bleeding 🩸
Anatomical factor ; aneurysm , nidus( diffuse morphology ) , location ( deep preiventricular, intraventricualr, infratentorium) , impaired venous drainage ( deep venous drainage, venous stenosis, single draining vein, and venous reflux into a sinus or a deep vein), small size AVM
Hemodynamic➡️ high feeding artery pressure
Patient factor ➡️ increasing age, pediatric patients, pregnancy, HTN
Others residual nidus
S-M 4 -5
Factor ⬇️ AVM bleeding
Arterial stenosis
- Arterial angioectasia
- Arterial border zone location of brain AVMs
- Venous recruitment
Theory of seizure in AVM
Low CBF ➡️ ischmic insult brain
Gliosis around nidus might cause seizure
ARUBA inclusion and exclusion criteria ⭐️
Inclusion Criteria:
Patient must have unruptured BAVM diagnosed by MRI/MRA, CTA and/or angiogram
Patient must be 18 years of age or older
Patient must have signed Informed Consent, Release of Medical Information, and Health Insurance Portability and Accountability Act (HIPAA/U.S. only) Forms
Exclusion Criteria:
Patient has BAVM presenting with evidence of recent or prior hemorrhage
Patient has received prior BAVM therapy (endovascular, surgical, radiotherapy)
Patient has BAVM deemed untreatable by local team, or has concomitant vascular or brain disease that interferes with/or contraindicates any interventional therapy type (stenosis/occlusion of neck artery, prior brain surgery/radiation for other reasons)
Patient has baseline Rankin ≥2
Patient has concomitant disease reducing life expectancy to less than 10 years
Patient has thrombocytopenia (< 100,000/μL),
Patient has uncorrectable coagulopathy (INR>1.5)
Patient is pregnant or lactating
Patient has known allergy against iodine contrast agents
Patient has multiple-foci BAVMs
Patient has any form of arteriovenous or spinal fistulas
Previous diagnosis of any of the following -
Patient has a diagnosed Vein of Galen type malformation
Patient has a diagnosed cavernous malformation
Patient has a diagnosed dural arteriovenous fistula
Patient has a diagnosed venous malformation
Patient has a diagnosed neurocutaneous syndrome such as cerebro-retinal angiomatosis (von Hippel-Lindau), encephalo-trigeminal syndrome (Sturge-Weber), or Wyburn-Mason syndrome
Patient has diagnosed BAVMs in context of moya-moya-type changes
Patient has diagnosed hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber)
