ENDOVASCULAR TREATMENT OF AVMS Rohan Chitale, PGY III Department of Neurosurgery, TJUH Grand Rounds April 2, 2010
Arteriovenous Malformations
Congenital abnormal collection of blood vessels wherein blood flows from arterial circulation directly into venous circulation, bypassing capillary beds Incidence/Prevalence not definitively studied, but estimated incidence is 1.1/100,000 in populationbased studies Slight male preponderance Average age diagnosed ~33 years old
Arteriovenous Malformations
Presentation/Clinical Features
Hemorrhage (50%)
Intracerebral, subarachnoid, intraventricular
Seizures (20-25%) Headache (15%) Mass effect - direct compression/swelling of adjacent structures Ischemia - preferential flow through the AVM due to decreased resistance, causing hypoperfusion of surrounding brain parenchyma
Why Treat AVMs
2-4% annual risk of rupture
Independent risk factors for rupture: Associated aneurysm (feeding artery, intranidal) Previous rupture Small AVM size Deep venous drainage
Goal is to determine risk of conservative treatment vs risk of intervention
ARUBA trial – A Randomized Trial of Unruptured Brain AVMs
Spetzler-Martin Classification
Size Small (< 3cm) Medium (3-6 cm) Large (> 6 cm)
1
2 3
Eloquence of adjacent brain Non-eloquent Eloquent
0
1
Pattern of venous drainage Superficial only Deep
0 1
Pretherapeutic Evaluation
Noninvasive Techniques CT/CTA MRI/MRA fMRI
Local increase in cerebral blood flow and volume after stimulation of eloquent cortex
Diffusion-Tensor Imaging
Visualization of white matter pathways and their relationship to AVM
Imaging
Imaging
Pretherapeutic Evaluation
Invasive Techniques
Provocative Injection Testing(Wada’s Test)
Amobarbital sodium injection of selective feeding vessels to predict/avoid post-embolization deficits
Pretherapeutic Evaluation
Angiography Arterial feeders, size of AVM, nidus characteristics, drainage pattern Other anatomical characteristics
deep location, deep venous drainage pattern, presence of a single draining vein, venous stenosis, eloquent location and diameter of AVM
Associated aneursyms(feeding artery, intranidal, circle of Willis, venous) Pseudoaneurysms AVM-associated AV Fistulas
Pretherapeutic Evaluation
Angiography Angiogram following hemorrhage can result in false negative secondary to nidus compression Gold standard is follow-up angiogram 3 months after hemorrhage for detection of AVM
Perioperative/Anesthetic Considerations
Continuous arterial transductions Deliberate systemic hypotension General anesthesia adenosine-induced cardiac pause – slow flow through AVM for controlled deposition of embolic material
Pulse Oximeter Ipsilateral to femoral sheath
Vessel obstruction, thromboemboli, over-compression following sheath removal
Foley catheter- fluid management (Supplemental O2 // Nasopharyngeal airways for those under sedative-hypnotic agent)
Anatomy-Based Management
Neuroanatomy to understand at-risk territories Done under general anesthesia Patient comfort Ensures motionless patient
Theoretically, because AVM has no functional intervening tissue, embolization of appropriate vessels should not cause functional deficit Neurophysiologic monitoring
SSEP/EEG
Physiology-Based Management
Evaluation of functional anatomy during procedure Requires intravenous anesthesia with short-acting agents(propofol, midazolam) Wide variability and cortical reorganization described in AVM patients
Endovascular Technique
Preoperative discussion Vascular access with No. 7 Fr gauge sheath into femoral artery via Seldinger technique Anticoagulation algorithms to prevent thromboembolic complications
JHN-continuous heparinized flush, no bolus
No. 6 Fr gauge guiding catheter introduced into ICA or verterbral artery Flow-directed/flow-assisted microcatheters to reach intranidal target
Variability in flexibility, torque, maneuverability, and responsiveness.
Identification of Embolization Point
Tip of catheter directly into nidus Tip of catheter into feeder that does not share supply with adjacent normal brain
If normal brain at risk, pretherapeutic/intraoperative functional evaluation can be performed to avoid neurologic deficit from embolization
Injection of Embolic Material
Polyvinyl alcohol n-butyl cyanoacrylate Onyx Ethibloc Silk Microcoils Combination
Polyvinyl Alcohol (PVA)
Available in different sizes based on size of target vessels Slower occlusion than liquid embolic agents Occlude low-pressure shunts first
High recanalization rates
Results in increase in intranidal vessel pressureÆhemorrhage risk prior to nidal obliteration Development of collateral feeders secondary to proximal occlusion of AVM with large size particles may contribute to this high rate
Used with success preoperatively to reduce flow prior to open or radiosurgical treatment
n-BCA
Liquid monomer that permanently polymerizes to a solid compound after contact with anions Occlusion by initiation of inflammatory endothelial response Combined with Ethiodal (iodine-based oil) to make lesion opaque on X-rays
Tantalum powder added to increase opacity(currently less common)
n-BCA
Viscosity and Polymerization time
Increasing Ethiodal concentration increases viscosity and delays polymerization Delayed polymerization helpful in lesions that exhibit slow flow Increased viscosity delays transit within lesion
Temperature, homogeneity of mixture, and changes in pH of solution also influence polymerization time
n-BCA
Acetic acid and glaciar acid to decrease pH
Delays polymerization without compromising viscosity
Dextrose 5%
Delays polymerization time by delaying contact of blood with n-BCA
n-BCA
Factors that influence choice of viscosity and polymerization time: Distance between microcatheter and nidus Tortuosity of vessels Intranidal flow
n-BCA
1:1 dilution(nBCA:oil) used when flow is very fast and catheter is close to nidus
n-BCA
“Flow Control” – Microcatheter occludes distal blood flow as it reaches smaller vessels, thus preventing blood from contacting glue, allowing for distal penetration Injection stops when glue reaches venous system through nidus or there is backflow towards the catheter Remove catheter quickly to prevent catheter retention
Onyx
Ethylene-vinyl alcohol copolymer(EVOH) mixed in dimethyl-sulfoxide(DMSO) solvent Tantalum for radiopacity Lower concentrations of EVOH Æ decreased viscosity Soft and nonadhesive mass that does not fragment Increased embolization from single catheter position Allows for angiography between injections
NonabsorbableÆpermanent occlusion
Onyx
Pitfalls
Angiotoxicity related to DMSO
swine rete mirabilis embolization model report risk of mild transient acute vasospasm
Separation of tantalum from Onyx
Increases difficulty of viewing smaller feeding pedicles
Treatment Objectives
Embolization for definitive cure Embolization as a precursor for definitive operative resection Embolization as a precursor for radiosurgery Embolization as palliative treatment for progressive debilitating symptoms Target embolization of high risk lesions
Treatment Objectives
Embolization for definitive cure
N-BCA complete obliteration rates(~10%) Deruty, et al – 5% but primarily used in high-grade AVM Vinuela, et al – 9.9% in small to medium AVM with less than 4 pedicles(405 pts) Lundqvist, et al – 13% Valavanis and Yasargil – 40% in 387 consecutive patients Gobin – 11.2% in patients after embolization prior to radiosurgery (125 pts who were poor surgical candidates)
Treatment Objectives
Embolization for definitive cure
Onyx complete obliteration rates
Perez-Higueras, et al – 22% in series of 45 patients Pierot, et al – 4.2% in series of 48 patients Leonardi, et al – 5.9% among 34 pts SM III-IV van Rooij, et al – 15.9% among 44 pts SM I-II Weber, et al – 20% among 93 patients Mounayer, et al – 27.7% among 94 patients treated with Onyx, n-BCA, or combination Panagiotopoulos – 24.4% among 82 pts
Reconstitution of flow to AVM nidus can occur through dilation of preexistent collateralization
Rare cases reported for n-BCA Recent reports of reperfusion for Onyx(Perez-Higuera, Weber, Panagiotopoulos)
Treatment Objectives
Anatomic features predictive of angiographic cure with n-BCA (Valavanis and Christoforidis) Direct or dominant feeding arteries Monocompartmental nidus Dominant fistulous component of nidus without perinidal angiogenesis
Anatomic features predictive of angiographic cure with Onyx Supratentorial and cortical location Compact and plexiform nidus Small number of supplying(direct) feeders 1 superficial draining vein
Case 1
26 yo female PMH migraines who presented with a seizure two years ago. Imaging revealed R temporoparietal AVM fed by MCA and PCA branches, with superficial drainage veins
Case 1
Patient underwent staged embolization with n-BCA over three sessions to achieve angiographic obliteration of AVM
Treatement Objectives
Embolization as a precursor for definitive operative resection
Goals: Reduction of size of nidus Occlusion of deep arterial feeding vessels which may be surgically inaccessible Treatment of intranidal aneurysms and high-flow fistulas to promote progressive nidus thrombosis Reduce blood loss, improve operative time, convert high Spetzler-Martin AVMs to lower grade lesionsÆreduce morbidity and mortality
Treatment Objectives
Embolization as a precursor for definitive operative resection
Avoid embolizing draining veins
Restricting venous outflow increases hemorrhage risk
Proximal embolizationÆcollateral developmentÆtreacherous open surgical resection
Case 2
32 yo male with no PMH presented with seizure. Imaging revealed R temporal AVM being fed by the MCA with superficial drainage.
Embolization of M4 pedicle and Anterior Temporal pedicle resulted in 95% treatment of AVM.
Craniotomy for complete excision of remaining AVM was performed. Intraoperatively, lesions embolized with n-BCA exhibit a harder, less compliant mass in contrast to lesions embolized with Onyx, which is a softer agent
Treatment Objectives
Embolization as a precursor for radiosurgery
Goals:
Decrease target size of AVM
Reduce weakness in AVM angioarchitecture by eliminating intranidal/venous aneursyms
Allows higher dose of radiation to smaller volume
Reduces hemorrhage risk in latency period
Flow reduction alone without reduction in AVM volume does not improve radiosurgical success
Case 3
40 x 40 mm L parietal AVM fed by L MCA and PCA
Staged embolization over four sessions with n-BCA enabled reduction of AVM volume prior to radiosurgery. Patient now undergoing LINAC treatmetn for residual AVM.
Note residual AVM with diffuse pattern and persistence of early venous drainage
Treatment Objectives
Embolization as palliation for progressive debilitating symptoms
Target embolization of high-risk lesions
Alternative for large, non-resectable AVMs Progressive neurologic deficits secondary to arterial steal Medically intractible seizures Venous hypertension causing HA or local mass effect from engorged veins
Associated aneursyms Increased pressure in veins that have outflow restriction
Rapidly forming collaterals reduces long-term effectiveness
Complications
Hemorrhage/Edema Arterial perforation, intranidal aneurysm rupture, draining vein occlusion Occlusive Hyperemia—passive engorgement of vessels and arterial stagnation in adjacent brain following obliteration of AVM resulting in edema/hemorrhage Normal Perfusion Pressure Breakthrough Theory—loss of autoregulation in surrounding ischemic tissue following embolization, resulting in disruption of capillary beds Mural necrosis induced by embolic material
Complications
Treatment of Hemorrhage
Protamine for reversal of anticoagulation
Treatment of Edema
Steroids
Complications
Ischemia Inadvertent embolization of normal blood vessels Thrombotic emboli Retention of microcatheter
Treatment Deliberate hypertension Platelet glycoprotein IIb/IIIa inhibitors
Morbidity and Mortality
10% morbidity regarding temporary neurological deficit 8% morbidity regarding permanent deficit ~1% mortality Complications tend to occur in higher grade AVMs
Risk of Embolization by SM Grade— Kim, et al Neurosurgery 2006
Retrospective review of 153 patients, 508 vessels, 203 sessions Age, sex, AVM grade, location of lesion, number and location of embolized arteries, and number of embolization sessions reviewed with respect to neurologic/vascular complications Number of branches embolized was only variable related to neurologic deficit (p=0.017)
Risk of Embolization—Kim, et al Neurosurgery 2006
Immediate/Long term neurologic deficit
(selection bias-most ii-iii not usually embolized; represent more challenging subset of lesions requiring multimodality tx)
Number of avm per grade was too small for meaningful analysis
Spetzler-Martin Grade
Immediate neurologic deficit (p=0.103)
Follow-up neurologic deficit
I
0%
0%
II
8%
5%
III
12 %
7%
IV
15 %
10%
V
18 %
18%
Conclusion
Pre-operative evaluation Noninvasive/Invasive Imaging Anesthetic/Perioperative Considerations Endovascular Technique Embolization Materials Treatment Objectives of Endovascular Approach Outcomes/Complications Future
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