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Cardiology
Embolization for Fistulas and Arteriovenous Malformations Brain Arteriovenous Malformations
Built from Cardiovascular Catheterization and Intervention: A Textbook of Coronary, Peripheral, and Structural Heart Disease
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6 sections · 124 slides
Brain arteriovenous malformations
- Abnormal artery-to-vein shunt with a nidus Nidus replaces the normal capillary bed Among the most complex neurovascular lesions Often congenital, but not invariably so Carries cumulative lifetime hemorrhage risk Ruptured vs unruptured management still debated
- Rupture: intraparenchymal, subarachnoid or IVH Outcomes after rupture can be devastating Seizures from cortical irritation Progressive deficits from shunting and steal Compromised flow to adjacent brain tissue
- Most AVMs are sporadic Some occur in hereditary hemorrhagic telangiectasia KRAS mutations implicated in pathogenesis KRAS is a key regulator of angiogenesis Mutation drives RAS/RAF/MEK/ERK signalling Somatic KRAS linked to aggressive AVM behaviour
- Pathogenesis of the AVM nidus
- Applies to incidental and symptomatic lesions Weigh treatment risk against natural history Patient age and comorbidities Rupture status and AVM grade Operator and neurosurgical expertise Patient preference carries real weight
- Vascular neurologists Neuroradiologists Neurosurgeons Neurointerventionalists Patient preferences built into the decision Collaboration yields the best outcomes
- Annual hemorrhage risk about 2%-4% Other series suggest 1%-3% Smaller AVMs carry higher rupture risk Hemorrhage is first presentation in about half Intraparenchymal hemorrhage is the usual pattern
- Young or otherwise healthy patient Spontaneous intracerebral hemorrhage Lobar or cortical location No history of hypertension Prompts dedicated vascular imaging
- Formula: 1 - (risk of no hemorrhage) to the power n n is the remaining life expectancy in years Simpler approximation: 105 minus age in years Gives a rough overall lifetime estimate Younger patients accumulate more risk-years
- Seizures common with cortical temporal or parietal AVMs Patients under 20 years more often hemorrhage Patients over 60 years more often hemorrhage Intermediate ages more often present with seizures Headache without rupture in about 15%
- Steal: shunt diverts flow from adjacent brain Produces regional ischemia and deficits Mechanism is less well established Deficits may also follow direct mass effect Both occur without any hemorrhage
- Compact nidus: organised malformed capillary bed Compact nidus displaces normal parenchyma Diffuse nidus: loosely organised channels Diffuse nidus has sparse abnormal AV channels Normal brain co-exists within a diffuse nidus
- Nidus architecture
- Introduced in 1986 by Spetzler and Martin Assesses risk of surgical intervention Points for nidus size Points for eloquence of adjacent brain Points for pattern of venous drainage Best validated of the AVM grading systems
- Spetzler-Martin grading scale
- Devised by Lawton and colleagues Adds age at presentation Adds prior hemorrhage or unruptured status Adds whether the nidus is angiographically diffuse Used alongside the Spetzler-Martin score
- Flow far exceeds that in normal brain tissue Produces considerable hemodynamic shear stress Feeding arteries dilate and become tortuous High flow may produce feeding artery aneurysms Draining veins face raised intraluminal pressure Veins dilate, thicken and become tortuous
- Feeding artery aneurysms Venous outflow stenosis Deep lesion location Small nidus size All amplify high-pressure, high-flow conditions Shear stress on vessel walls increases
- High flow enlarges the feeding arteries Enlarged vessels become aneurysm-prone Aneurysm walls have weakened endothelium Vulnerable to rupture under sustained high pressure Rupture may be catastrophic
- Shunted blood bypasses the capillary bed Draining vein pressure rises Veins become dilated and tortuous Stenosis impedes outflow further Nidal pressure rises as a result
- Basal ganglia and thalamic AVMs are deep Deep location carries higher rupture risk Surgical access is difficult Treatment planning is correspondingly complex
- Smaller AVMs may paradoxically rupture more MATCH registry: higher rupture rate under 3 cm Independent factors: small nidus, venous stenosis Altered flow parameters also independent Newer models weight hemodynamics over size
- Manifestations depend on nidus size and location Hemorrhage: focal deficit, nausea, vomiting Seizures in about 30% at diagnosis Headaches in about 14% of cases Annual rupture risk 2%-4% untreated Risk rises with prior bleed or intranidal aneurysm
Management of brain AVMs
- Historically the established treatment modality Advances in microsurgical technique improved outcomes May follow preoperative endovascular embolization Success depends on careful patient selection Classification systems guide that selection
- Grades I and II: new deficit in under 2% Grade V: new deficit in 31% Scale predicts postoperative morbidity Validated as a surgical risk instrument Not a predictor of untreated natural history
- Grade III lesions are heterogeneous in risk Small nidus, eloquent, deep drainage behaves lower grade Nidus 3-6 cm with superficial drainage behaves higher grade Refinement guides which grade III to operate
- Arterial perforator feeders Diffuseness of the nidus Advanced patient age Deep venous drainage, to a lesser degree Eloquence, to a lesser degree All outweigh nidus size itself
- Gradual de-arterialization of the nidus Minimise damage to surrounding brain Preserve venous drainage until the end Sharp resection along the gliotic plane
- Advances in microcatheter technology Balloon catheters and improved embolic agents Better angiographic visualisation Dual-lumen balloons and transvenous embolization Paradigm shifting from surgery alone
- AVM location and size Angioarchitecture of feeders and nidus Rupture status and presenting symptoms Patient medical history and preference Endovascular-specific grading aids stratification
- Predicts complications of endovascular AVM treatment Number of arterial pedicles Diameter of arterial pedicles Eloquent location of the AVM nidus
- Roles of endovascular treatment
- Reduces intraoperative blood loss Allows a safer and shorter operation Reduces vascular supply to the nidus Better delineates nidus margins EVOH cast helps define the resection plane
- Reduces the radiosurgical target volume Lowers risk of recanalization Lowers risk of regional remodelling Treats high-risk feeding artery aneurysms early Radiosurgery has a 2-3 year lag to efficacy
- Complete occlusion often achievable in small AVMs Favourable: single feeder, single draining vein SNIS 2022: role of primary curative embolization uncertain Adjunctive embolization better supported Amenable angioarchitecture has broadened over time
- Pressure cooker technique Transvenous embolization Transvenous pacing and proximal flow arrest Reverse pressure cooker technique Multiplug technique Pioneered across centres globally
- Targets high-flow shunts Relieves symptoms of intracranial steal Relieves venous hypertension Treats high-risk feeding artery aneurysms Aim is symptom control and lower bleed risk
- Randomised unruptured brain AVM management Compared medical management with intervention Suggested superiority of medical management Criticisms of design and applicability persist Timing of embolization remains debated
- Limitations of the ARUBA trial
- Follow acute spontaneous ICH guidelines first CT angiography of the head MRI brain Catheter angiography for high-risk features Immediate EVT to prevent further bleeding Or delayed treatment after hematoma resolves
- Workup after AVM rupture
- n-butyl-2-cyanoacrylate (n-BCA) predominantly used Ethylene vinyl alcohol copolymer (EVOH) also standard Choice reflects properties and catheter compatibility EVOH gives better complete embolization rates EVOH has lower recurrence than n-BCA EVOH carries slightly higher complication rates
- Single or dual microcatheter technique Double-lumen balloon catheters as an option Choice reflects anatomy, hemodynamics, operator Aim: adequate nidal penetration Avoid non-target embolization Avoid premature venous outflow occlusion
- Catheter entrapment in the embolic cast Reflux of embolic material along the catheter Non-target embolization of normal territory Premature occlusion of venous outflow Vessel perforation with hemorrhage
- Manage in a dedicated neurointensive care unit Maintain normocapnia Seizure prevention and early detection Strict normotension is the rule Occasionally induced mild hypotension Prevents normal perfusion pressure breakthrough
- Non-invasive alternative to open surgery Suited to smaller AVMs with a compact nidus Also an option across grades and locations Useful where surgery or embolization is high-risk Aims to obliterate the nidus Latency to effect of 2-3 years
- Mechanism of radiosurgical obliteration
- AVMs in eloquent cortex: motor strip, speech areas Basal ganglia and thalamic lesions Deeply located AVMs generally Patients unfit for general anaesthesia Where surgery or embolization would be high-risk
- Embolization can reduce nidus size before radiation May offer protection against hemorrhage Risk of AVM rupture during treatment Risk of incomplete obliteration Results mixed against radiosurgery alone
- Gliotic change after radiation aids dissection May reduce the risk of new deficits Residual AVM in eloquent areas may get further radiosurgery
- Large nidus treated in separate Gamma Knife sessions Different nidus portions targeted over time Obliteration rate of 65% reported Shrinkage in a further 35%
- Accurate delineation of the nidus is critical DSA with fiducial markers gives high spatial resolution DSA may lack three-dimensional detail CT or MR angiography used alongside DSA
- Neurological examination plus MRI every 6 months Six-monthly imaging for the first 2 years Annual assessment thereafter Loss of flow voids on MRI suggests obliteration Confirm with cerebral angiogram or MRA Retreat if not obliterated by 3-4 years
- Three treatment modalities compared
Illustrative AVM cases
- 47-year-old woman with subarachnoid hemorrhage Ruptured left PCA feeding artery aneurysm Treated by primary coiling Left frontal convexity AVM, middle and inferior frontal gyri Spetzler-Martin grade III Size 2, drainage 0, eloquence 1
- Left internal carotid injection, AP view
- Lateral view showing pericallosal feeders
- Lateral view after staged Onyx embolization
- AP view confirming complete obliteration
- 38-year-old man presenting with seizures Cingulate gyrus AVM, Spetzler-Martin grade III Stage one: transarterial balloon-assisted Onyx Stage two: transvenous embolization Followed by neurosurgical resection
- Selective anterior cerebral artery angiogram
- Dual microcatheter transvenous access
- Reverse pressure cooker technique with coil plug
- Control run after staged embolization
Dural cranial arteriovenous fistula
- Abnormal connection within the dura mater Between dural arteries and venous sinuses or cortical veins Bypasses the normal capillary network No nidus, unlike a brain AVM 10%-15% of intracranial AV connections
- Primarily affects middle-aged adults Typically acquired, not congenital Rare in children and more complex when present Linked to venous sinus thrombosis Linked to hypercoagulable states Trauma, surgery and radiation also implicated
- Occipital artery Middle meningeal artery Ascending pharyngeal artery Usual source of DAVF arterial supply Multiple feeders are the rule
- Ethmoidal branches of the ophthalmic artery Meningohypophyseal trunk Artery of Bernasconi and Cassinari Lateral tentorial artery Artery of Davidoff and Schechter, from the PCA Artery of Wollschlaeger, from the superior cerebellar artery
- Range from incidental to hemorrhage Deficits from venous congestion Arterial steal causing vascular insufficiency Pulsatile tinnitus, headache, visual deficits Hemiparesis, aphasia, cranial nerve deficits Seizures, cognitive decline, ataxia, myelopathy
- Bruit or pulsatile tinnitus is common Associated with transverse and sigmoid sinus fistulas Turbulent flow transmitted to the middle ear May be the only symptom of a benign lesion
- CT head or MRI brain first, by presentation Detect hemorrhage and parenchymal edema CT or MR angiography next Look for prominent cortical vessels DSA remains the diagnostic gold standard DSA shows feeders, fistula and drainage pattern
- Bilateral selective internal carotid injections Bilateral selective external carotid injections Bilateral vertebral artery injections Incomplete study misses additional feeders Essential before any treatment decision
- Exact cause in adults remains unclear Associated with venous sinus thrombosis Hypercoagulable states implicated Thrombosis releases angiogenic factors VEGF and basic fibroblast growth factor named Closed head injury, surgery and radiation reported
- Theories of dural AV fistula formation
- Previous hemorrhage Pattern of venous drainage Borden classification assesses risk Cognard classification assesses risk Drainage pattern matters more than feeders
- Type I: drains directly into a dural venous sinus Type II: drains into sinus with cortical venous reflux Type III: drains directly into cortical veins Based on presence of cortical venous drainage
- Type I: sinus drainage with normal antegrade flow Type IIa: sinus drainage with retrograde sinus flow Type IIb: sinus drainage with cortical venous reflux Type III: cortical venous drainage without ectasia Type IV: cortical venous drainage with ectasia Type V: cortical and spinal perimedullary drainage
- Classification schemes for dural arteriovenous fistulae
- Type A: direct shunt from internal carotid artery Type B: indirect, from internal carotid meningeal branches Type C: indirect, from external carotid meningeal branches Type D: from both internal and external carotid branches
- Ectatic vein larger than 5 mm Or more than three times normal diameter Defines type IV rather than type III Marks a higher-risk lesion
- Cortical venous drainage: 7.5% annual risk Nonaggressive DAVFs: 1.5% annual risk Aggressive lesions have symptomatic drainage Retrograde flow opposes normal cortical outflow Raises venous pressure and hemorrhage risk
- Aggressive: symptomatic cortical venous drainage Produces hemorrhage, seizures, headache, deficits Disrupted outflow causes ischemia Raised intracranial pressure follows Nonaggressive: no symptomatic cortical drainage Nonaggressive lesions less likely to cause harm
- Borden type I has a benign prognosis May stay asymptomatic or nearly so Occasionally causes disabling tinnitus Types II and III more concerning Type III: direct cortical drainage, high-flow shunt Higher rates of hemorrhage and deficits
- Requires detailed knowledge of cerebrovascular anatomy Angioarchitecture must be fully understood Surgical ligation is one option Endovascular embolization is the other Multidisciplinary team management Interventional neuroradiology plus neurosurgery
- Less aggressive approach is acceptable Serial imaging, typically MRI and MRA Monitor for development of cortical drainage Treat if tinnitus worsens Treat if quality of life is significantly affected
- Reduction or cessation of pulsatile tinnitus Prompts cerebral angiography May indicate altered venous outflow Can change the urgency of treatment
- Angiographic cure is necessary Applies with or without prior hemorrhage Embolize the fistula point into the foot of the vein Or surgically ligate the proximal draining vein Ligation performed adjacent to the fistula point
- Simple, surgically accessible fistula Partial embolization has made surgery feasible Arterial supply involves critical branches Embolization would risk cranial nerve injury Ophthalmic artery supply, as in anterior fossa fistulas
- Deliver embolic to penetrate the fistulous connection Occlude the foot of the draining vein Occlude the venous pouch of the fistula Penetration of the fistula point is paramount Coils reserved for the transvenous route
- Marketed as Trufill in the United States Commonly used embolic agent for DAVFs Rapid polymerisation seals abnormal vessels Immediate sealing suits selected cases Risk of reflux and non-target embolization
- Ethylene vinyl alcohol copolymer Dissolved in dimethyl sulfoxide (DMSO) Tantalum powder added for fluoroscopic visibility Often preferred for cranial DAVFs Better long-term outcomes than n-BCA in studies Microcatheters must be DMSO-compatible
- Forms a vascular plug at the catheter tip Plug prevents reflux of subsequent injection Ensures antegrade penetration into target vessels Dual-lumen balloon microcatheter may be added Balloon aids control in high-flow lesions May improve long-term occlusion rates
- Precise hydrophobic injectable liquid Available in Europe Superior visualisation under fluoroscopy Minimal streak artefact, no tattoo effect Hydrophobic nature may reduce reflux Newer and less studied than Onyx
- Accesses the fistulous connection and venous pouch Often allows complete disconnection Used when the sinus is occluded Used with proximal arterial occlusion Used when transarterial access is difficult Coils may occlude a non-functional sinus
- Combining transvenous with transarterial improves outcomes Particularly for deep or difficult lesions Dual-lumen or balloon microcatheters used Double microcatheters with reverse pressure cooker Facilitates retrograde embolization Used when standard methods fail
- Partial or incomplete obliteration Embolization of cranial nerve blood supply Non-target parenchymal embolization: ischemic stroke Vessel perforation causing hemorrhage Incomplete treatment recruits new feeders Recruitment makes later cure harder
- Reflux of embolic material into the sinus Pulmonary embolism can result Venous sinus thrombosis Venous infarction Argues for controlled, plugged injection
- Ascending pharyngeal neuromeningeal branch Supplies cranial nerves IX, X and XI Jugular foramen lesions carry higher risk External to internal carotid anastomoses exist External carotid to vertebral anastomoses exist Must be identified before injection
- Recurrence after presumed cure remains a concern Risk factor: tentorial location Risk factor: cortical venous drainage Risk factor: deep cerebral venous drainage Multimodal treatment may be needed Delayed angiography at least 1 year after cure
Illustrative fistula cases
- 32-year-old woman with developmental delay Months of left pulsatile tinnitus and headache Dizziness and gait unsteadiness Prominent flow voids on imaging Left petrotentorial DAVF, Borden type III Cognard IV: reflux into ectatic cerebellar veins
- Internal carotid supply to a tentorial fistula
- External carotid feeders and the fistula point
- Onyx cast after balloon-assisted embolization
- Control angiogram after fistula obliteration
- 59-year-old man with pulsatile tinnitus and TIA Left ethmoidal dural arteriovenous fistula Borden type III, Cognard IV Coexisting carotid stenosis treated by stenting First treated transarterially with n-BCA
- Ophthalmic artery supply to an ethmoidal fistula
- Recruitment of external carotid ethmoidal branches
- Transvenous balloon-assisted Onyx embolization
- Final common carotid control run
Summary
- Artery-to-vein shunt with a nidus, no capillary bed Annual hemorrhage risk about 2%-4% Small nidus, venous stenosis raise rupture risk Spetzler-Martin predicts surgical, not natural, risk Embolization best supported as an adjunct Radiosurgery has a 2-3 year latency
- Dural shunt without a nidus; usually acquired Risk set by venous drainage, not by feeders Cortical venous drainage: 7.5% annual hemorrhage risk No cortical drainage: 1.5% annual risk Cure means closing the fistula point Delayed angiography at 1 year for high-risk lesions
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- Cardiovascular Catheterization and Intervention: A Textbook of Coronary, Peripheral, and Structural Heart Disease
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