Brain AVM Embolization

Although cerebral vascular malformations had long been known in the literature, William McCormick is credited with developing the first comprehensive pathological classification method for these lesions in the 1960s. Capillary telangiectasia, developmental venous abnormality, cavernous malformation, and arteriovenous malformation are all named after him in modern literature. Arteriovenous fistulae and mixed vascular malformations are also included in certain schemes for completeness. 

Cerebral AVMs are complicated lesions made up of a network of aberrant arteries and veins with no intervening capillary bed, leading to high AV shunting. AVMs are congenital and most typically occur sporadically, despite the fact that familial cases have been reported. Various investigations have discovered a link between inherited hemorrhagic telangiectasia, Sturge-Weber syndrome, and Wyburn-Mason syndrome. Intracranial bleeding is a common symptom of AVMs, but seizures, headaches, and localized neurological impairments can also occur. A yearly hemorrhage risk of 3% to 4% is frequently reported, with a 6 to 25 percent chance of death and a 10 to 50 percent risk of neurological impairment. The Spetzler-Martin grading system, which provides points for AVM size, position, and venous drainage pattern, was originally designed as a surgical risk assessment tool. It is now routinely used to define AVMs in the clinical environment.

Microsurgical resection, endovascular embolization, and stereotactic radiosurgery are some of the current therapy options for cerebral AVMs. While any of these modalities can be utilized on its own, a combination is frequently required to achieve the optimum therapy results. It might be difficult to decide what form of intervention to provide or whether intervention should be provided at all. Finally, a risk-benefit assessment should be undertaken, taking into account the AVM's natural history as well as the hazards associated with the planned therapies. Recent data imply that medical care may be better than interventional therapy for unruptured AVMs, at least in the near term, emphasizing the need for such research. For properly managing AVMs, establishing a multidisciplinary team with competence in medical, surgical, endovascular, and radiation treatment is crucial.

The interdisciplinary management of all AVMs should include endovascular expertise. Even if conservative care is anticipated, all AVMs should be defined by a catheter cerebral angiography, with rare exceptions. The presence of concomitant aneurysms or venous outflow blockage, as well as the number and location of supplying vessels and draining veins, are all important factors to consider when making a selection. Pre-microsurgical embolization, pre-radiosurgical embolization, curative embolization, and palliative embolization are all options if endovascular intervention is chosen.

 

Epidemiology

Epidemiology

It's been difficult to assess the frequency and prevalence of brain AVMs, resulting in a number of erroneous estimates being circulated in the literature. Population-based studies have found rates of brain AVM detection ranging from 0.9 to 1.3 instances per 100,000 person. Variable prevalence estimates of less than 0.03 percent to 0.2 percent have also been recorded.  The highly referenced New York Islands AVM research found an annual AVM detection rate of 1.3 instances per 100,000 person-years and concluded that due to the disease's rarity, congenital nature, and extended silent development, a true prevalence may never be determined.

Despite recent advances toward a more frequent diagnosis of unruptured lesions, intracranial bleeding remains the most prevalent presentation for individuals with AVMs. According to a survey of ten large AVM series, 45 to 73 percent of AVM patients have bleeding. Ondra et al. estimated a 4 percent yearly risk of bleeding, a 1.8 percent annual risk of morbidity, and a 1 percent annual death risk in 165 unoperated symptomatic brain AVM patients monitored for an average of 24 years.  ApSimon and colleagues found that the vast majority of cerebral AVMs will become symptomatic during a patient's lifetime, with bleeding accounting for the bulk of cases.

AVM-related hemorrhage can have a severe economic effect. In a population-based cohort, van Beijnum et al. reported a 41% incidence of death or dependence one year following an AVM-related intracerebral hemorrhage. In 114 patients, Hartmann et al. identified a 16 percent risk of at least moderately debilitating impairment and no mortality following an episode of AVM hemorrhage.  Bendok et al. evaluated the risk of death after an AVM-associated hemorrhage to be between 12% and 15% based on their review of the literature, while total morbidity and mortality was estimated to be 17% per episode of bleeding.

 

Brain AVM Pathophysiology

Brain AVM Pathophysiology

One or more feeding arteries, a nidus, and one or more drainage veins make up an AVM. There are frequently little pial and perforating subcortical feeders that are not evident on angiography. Because there is no intervening capillary bed, high-flow AV shunting is possible. AVMs are dynamic lesions with active angiogenesis, inflammatory reactions, and adaptive structural changes over time. The feeding artery dilates and the draining vein arterializes as a result of AV shunting. The artery elastic and muscle layers are changed histologically. The internal elastic lamina can be reduplicated or interrupted, and the media can be thickened and thinned in different ways. Aneurysms of the feeding artery can form in areas of thinning media, while leiomyoma-like nodules can form in areas of thickening. There is also collagen deposition and luminal thrombosis, which leads to draining vein thickening. Gliotic brain parenchyma stained with hemosiderin frequently surrounds and infiltrates the nidus. Vascular steal has also been linked to neuronal damage in the surrounding brain parenchyma.

 

Brain AVM Embolization Indications

Brain AVM Embolization Indications

Although surgical removal represents the gold standard for eradicating most brain AVMs, when used as an adjuvant therapy before microsurgery, endovascular embolization has the potential to improve AVM treatment safety and effectiveness. Preoperative AVM embolization has been found to shorten operation time and intraoperative blood loss while having no effect on postoperative complications or long-term neurological prognosis. When compared to patients who just had surgery, Pasqualin et al. found that patients who received embolization before surgery had fewer postoperative neurological impairments and fatalities, as well as a lower frequency of postoperative epilepsy. Embolization can also convert high-grade Spetzler-Martin lesions to lower-grade lesions, potentially turning inoperable lesions into operable ones. Embolization improves surgical results by removing deep feeding arteries like the anterior perforating vessels, choroidal vessels, and posterior cerebral vessels, shrinking the active nidus, and removing the feeding pedicle or nidal aneurysms that have bled or are at risk of rupturing. Presurgical embolization lowers the risk of postoperative hemorrhage induced by changes in hemodynamics in the normal brain, and it can also serve as a surgical roadmap because embolized veins are easily visible. When compared to surgery alone, preoperative embolization in combination with surgery has also been found to be cost-effective.

 

Brain AVM Embolic Agents

Brain AVM Embolic Agents

To embolize AVMs, a variety of agents have been employed. Silastic spheres, gelfoam, silk stitch, dehydrated ethanol, balloons, blood clots, muscle, and a variety of other agents are all historically interesting. Currently, embolizing AVMs is done with n-butyl cyanoacrylate, ethylene-vinyl alcohol copolymer, platinum coils, and polyvinyl alcohol particles.

 

N-Butyl Cyanoacrylate

N-butyl cyanoacrylate (NBCA) is a liquid embolic agent that was produced to substitute isobutyl cyanoacrylate, which was thought to be carcinogenic. When this substance comes into contact with ionic fluid, it polymerizes almost instantly, increasing the risk of microcatheter sticking within the embolized artery. To adjust the rate of polymerization, NBCA is combined with different volumes of ethiodized oil or glacial acetic acid. To boost radiopacity, tantalum or tungsten powder can be added to the mixture. By washing the delivery microcatheter with a dextrose solution, premature polymerization is avoided. Recanalization may occur despite the fact that NBCA is a persistent embolic agent that causes a strong vascular inflammatory response. When NBCA is accumulated in the proximal feeding artery without nidus penetration, the likelihood of recanalization is very significant.

 

Ethylene-Vinyl Alcohol Copolymer

Onyx (ethylene-vinyl alcohol copolymer) is a more recently discovered liquid embolic agent that is also utilized to embolize cerebral AVMs. It's made up of an ethylene-vinyl alcohol copolymer and tantalum dissolved in dimethyl sulfoxide (DMSO) and comes in three pre-mixed viscosity levels. Because it hardens slowly as the DMSO solvent diffuses, onyx is regarded to be a more controllable agent than NBCA, minimizing the danger of microcatheter trapping. Longer and more frequent Onyx administrations within the same AVM pedicle are achievable, allowing it to be pushed farther away from the nidus. Onyx, like NBCA, is regarded as a persistent embolic agent, albeit recanalization is probable.

 

Platinum Coils and Polyvinyl Alcohol Particles

Solid embolic agents such as platinum coils and polyvinyl alcohol particles (PVA) are employed far less commonly to embolize AVMs. Coils aren't usually utilized to obstruct AVM feeders, but they can be effective for reducing the flow within specific compartments such that a liquid embolic agent can be used later. PVA particles range in size from 60 to 1000 micrometers. Because vessel recanalization is likely following PVA embolization, prompt surgical excision of the AVM is required.

 

What to Expect from AVM Embolization?

Endovascular AVM embolization is a one- or two-hour catheter-based surgery. A short, flexible tube (catheter) is inserted into a blood vessel, commonly in the groin, by neurointerventional neurosurgeon. Throughout the surgery, they will use X-rays to view and guide the catheter through the vessels to the AVM site. Then a glue-like material or a coil will be administered into the vessels to obstruct blood flow to the AVM and block the vessel. During the procedure, you will be given a sedative to keep you relaxed yet conscious.

Before considering endovascular embolization, neurovascular specialists will carefully weigh the risks. Most cases are treated in high-quality centers. Patients benefit from this level of competence by having shorter procedures with fewer problems and faster recovery times, especially if the procedure is elective.

 

Premicrosurgical AVM Embolization

Premicrosurgical AVM Embolization

In the comprehensive multimodality care of cerebral AVMs, pre-microsurgical embolization is the most typical application for endovascular therapy. Pre-microsurgical embolization entails removing deep artery pedicles that are first found in the later stages of surgical removal and securing AVM-related aneurysms, especially if they are far away from the resection site. Aneurysms that are not hemodynamically related can be treated conservatively. Some endovascular specialists try to embolize all accessible artery pedicles, although this is a controversial and sometimes risky method.

Despite the fact that low Spetzler-Martin grade AVMs should generally not be embolized preoperatively, it is important to examine the diagnostic angiography in each case and make an informed decision. We believe that a phased approach, with each round separated by a week or more, is the safest for patients who require embolization of several pedicles. This allows for the progressive normalization of local and regional hemodynamics, potentially preventing life-threatening post-procedure hemorrhages caused by fast and widespread arterial and venous thrombosis. Although this method has been verified in the literature, there is still debate, with some practitioners preferring single-staged embolization.

 

Preradiosurgical AVM Embolization

Pre-radiosurgical embolization has two goals: to eliminate high-risk angiographic features that predispose to hemorrhage during the latency period after radio-surgical treatment and to reduce AVM volume to a level that can be treated with radiosurgery.

It is necessary to treat aneurysms that are hemodynamically related to an AVM. This comprises both proximal and pedicular aneurysms, as well as intranidal aneurysms, which have an 8 to 10 percent annual risk of bleeding. It is unlikely that pre-radiosurgical embolization should be used to address other angio-architectural abnormalities such as venous aneurysms or merely to reduce flow.

On giant AVMs, pre-radiosurgical embolization has been used to reduce their volume to 10 cc or fewer. For lesions that do not surpass this volume criterion, obliteration rates of over 82% have been recorded after two years. In a study of 124 patients, Gobin et al. found that pre-radiosurgical embolization decreased average AVM sizes by more than 32% and allowed for a 64 percent likelihood of AVM cure in patients who were deemed suitable for radiosurgery following embolization. Other organizations have reported obliteration rates ranging from 65 to 80 percent. It's worth noting that a number of studies have found a link between effective AVM radiosurgical obliteration and prior embolization. As a result, using a pre-radiosurgical embolization technique to reduce AVM volume is a good idea.

 

Curative AVM Embolization

Only a small percentage of AVMs can be treated with embolization alone. All nidal filling and early venous drainage must be minimized to establish such an endovascular cure. If undetected feeders keep filling a partially embolized nidus, patients with angiographically cured AVMs may still be at risk for severe bleeding. It's still up for debate whether permanent curative AVM embolization is viable, given the possibility of recanalization through collateral routes. Frizzle and colleagues reported a 7% cure rate for AVMs managed by embolization after a comprehensive review of the literature spanning 35 years and 1,245 patients. Patients who are specifically chosen for curative embolization have the highest percentages of endovascular AVM cure. Small AVMs with few feeding pedicles, noncompartmental fistulous niduses, and no perinidal angiogenesis are common in these patients. Furthermore, Onyx has been linked to a higher incidence of AVM cure by embolization than previously found with other embolic treatments.

 

Palliative AVM Embolization

Palliative AVM Embolization

Patients who have little hope of being cured by multimodality therapy but who might benefit from targeted embolization of specific angioarchitectural features may benefit from palliative AVM embolization. It has already been noted how important it is to treat aneurysms that are hemodynamically related to an AVM. It may also be advantageous to use embolization to remove specific shunts that cause vascular steal syndromes. Apart from these cases, partial AVM embolization is not recommended because the results appear to be worse than natural history.

 

AVM Embolization Risks

AVM Embolization Risks

AVM embolization can result in significant treatment-related morbidity and mortality. Complication rates associated with AVM embolization have been observed to range from 6% to 15%. According to a recent meta-analysis by van Beijnum et al., complications after AVM embolization resulted in irreversible neurological impairments or death in 6.5 percent of patients. In their cohort of 202 patients who underwent preoperative embolization, Taylor et al. found a 9.5% rate of lifelong neurological impairments and a 3% probability of death as a result of embolization. In a similar study, Hartmann et al. looked at 234 patients who had AVM embolization with the goal of endovascular or multimodality cure. There was a 15% risk of treatment-related neurological abnormalities, a 3% rate of chronic debilitating deficits, and a 1.2% chance of death, according to the researchers. After 845 embolization in 407 individuals, Baharvahdat et al. observed a 10 percent procedural complication rate. After embolization, 7.5% and 1.5 percent of patients, respectively, experienced persistent, new impairment and mortality due to hemorrhage.

 

Recovery After AVM Embolization

After AVM embolization, you will spend nearly one night in the hospital. If your AVM has ruptured, you will spend a few days in the intensive care center. The length of your recuperation and when you can resume daily normal activities will be determined by the condition of your AVM (ruptured or unruptured). In difficult cases, full recovery can take up to five months. Following the AVM embolization, you will have follow-up sessions to ensure a smooth recovery. Additional medical imaging may be required to study the embolization site and determine further therapy, which may include AVM surgery to remove the AVM.

 

New Trends in Embolization Techniques

New Trends in Embolization Techniques

Balloon-assisted Embolization

While the balloon is expanded within the feeding artery, DMSO compatible double-lumen balloon microcatheters allow injection of Ethanol/water or NBCA. This provides a wedge-like configuration for the microcatheter or forms a temporary plug to improve liquid embolic penetration with minimum or no reflux. This should ideally reduce fluoroscopy time and radiation dose while also making microcatheter removal easier after administration. This method is particularly effective in AVMs with large-caliber feeders that are fistulous. In flow arrest situations, balloon expansion prevents reflux and allows for a more controlled administration. In order to avoid the feeder from rupturing, more care must be taken during inflation. Uninflated balloons should be changed if there is difficulty with balloon inflation, as they may increase the likelihood of catheter trapping. If there is reflux along the inflated balloon, additional light inflation will typically stop it. To avoid over-inflation and rupture, extreme attention should be used when inflating the balloon within the arterial feeders.

 

Transvenous Embolization

Despite the fact that transvenous embolization evokes venous outflow obstruction, one of the most terrifying scenarios for a neuroendovascular specialist during AVM embolization, it is becoming more common in limited situations. Transarterial embolization may be impossible for hemorrhagic AVMs with small twisty feeders or en passage feeders because of their complicated structure. Theoretically, transvenous embolization has the advantages of deeper penetration of the AVM nidus, reduced risk of ischemic events due to arterial obstruction, and easier navigation through larger and typically straighter veins. In the literature, total obliteration rates ranging from 85 to 100 percent have been documented.

For effective and reliable transvenous embolization, a triaxial system with a strong guiding system with an 8F sheath and distal access catheter is required. A 6F transjugular access catheter with a 6F distal access catheter can also be used. In feasible anatomy, removable tip microcatheters or balloon microcatheters may be used to prevent reflux and venous blockage. After prolonged injection, some centers purposefully allow a 2.5 cm reflux and keep the microcatheter inside the system after severing the microcatheter shaft at the skin insertion site.

 

Pressure Cooker Technique

The pressure cooker technique, first reported by Chapot et al., uses a coil-and-glue plug instead of the traditional ETOH plug used in the plug-and-push method. To construct a plug, coils are deployed and NBCA is administered. A microcatheter for ETOH injection is inserted into the feeding artery and a second microcatheter is inserted between the tip of the first microcatheter and the separation site. The placement of the first microcatheter, frequently makes the navigation of the second security microcatheter easier. 

In small diameter vessels, a 1.2F Magic microcatheter is utilized, whereas, in larger size arterial feeders, an Echelon 10 microcatheter is used as a second microcatheter. Injectable flow coils are utilized since removable coils are not compatible with the Magic 1.2F microcatheter. Injectable coils may flow accidentally toward the tip of the initial microcatheter in larger caliber arteries with high flow arteriovenous shunts. Removable coils are deployed using a standard 1.7F like the Echelon 10 for precise coil and adhesive plug placement. This type of plug is more resistant to ETOH reflux and allows for a stronger and more consistent ETOH infusion. It forms a wedge-like posture, similar to what happens when ETOH is injected into balloon microcatheters. Better navigability of flow-directed microcatheters and avoidance of vascular perforation during balloon inflation are possible advantages over balloon-assisted embolization.

 

Conclusion

It is crucial that a patient comprehend both the natural history and the treatment-related risks and benefits before beginning therapy for a cerebral AVM. A skilled multidisciplinary team must coordinate the safe and final treatment of these complicated and threatening lesions. Living with an uncorrected brain AVM causes anxiety and uncertainty, which is a significant and widespread burden for both patients and their families. For many patients who want permanent AVM ablation, a significant upfront operative risk may be worth it. Embolization is an important part of the multimodality treatment of AVMs in the brain. Many AVMs, it is recognized, cannot be safely healed without the use of this method.