Endovascular Neurosurgery

Published on 13/03/2015 by admin

Filed under Neurosurgery

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 3629 times

Chapter 17 Endovascular Neurosurgery

Clinical Pearls

Endovascular neurosurgery has undergone tremendous expansion in the past two decades and is becoming a mainstay of treatment of cerebrovascular disease and other vascular disease of the head and neck as a primary or alternative treatment to open microvascular treatment.

Endovascular techniques are used to treat a wide variety of cerebrovascular conditions that include severe symptomatic vasospasm after subarachnoid hemorrhage (SAH), arteriovenous malformation (AVM) and tumor embolization, cerebral aneurysm occlusion, and temporary or permanent balloon occlusion during parent vessel sacrifice.

Endovascular therapy is expanding the time-window after stroke symptom onset for revascularization in patients with acute ischemic stroke. Clinical trials have established a benefit of intra-arterial thrombolysis (IAT) up to 6 hours after stroke symptom onset, with an increase in recanalization rates. The mechanical device trials show effectiveness of mechanical revascularization therapy up to 8 hours after stroke symptom onset.

Endovascular treatment of intracranial aneurysms has undergone and continues to undergo improvements since the introduction of Guglielmi detachable coils for endosaccular occlusion of cerebral aneurysms in 1994. Current adjunctive techniques include balloon-assisted and stent-assisted coiling to improve the success rate of long-term occlusion of the aneurysm. Flow diversion for giant aneurysms may be a promising technology.

Preoperative endovascular embolization of feeding arteries has rendered many previously difficult AVMs much easier to remove surgically. Only a minority of AVMs can be cured by endovascular embolization despite the significant advances in embolic material such as Onyx. Most intracranial tumor embolization procedures have been performed on neoplasms with robust vascular pedicles in order to decrease the blood loss during resection.

Endovascular therapy is evolving and adds a plethora of tools and opens up multiple options with which to treat complex vascular lesions, in addition to microsurgical approaches. Currently, neurosurgeons who desire to be trained in treating the entire spectrum of cerebrovascular disease may pursue both microsurgery and endovascular neurosurgery training.

Introduction (Box 17.1)

The treatment of neurovascular diseases has been completely revolutionized with the introduction and growth of endovascular neurosurgery. Endovascular neurosurgery is becoming a primary treatment alternative to conventional open surgery for multiple neurovascular pathological conditions, including carotid and vertebral atherosclerotic stenosis, cervical vessel dissections, acute and chronic cerebral ischemia, intracranial aneurysms, arteriovenous malformations (AVMs), and dural arteriovenous fistulas (dAVFs). Endovascular revascularization has resulted in recanalization rates as high as 70% to 100% for acute large vessel occlusions responsible for ischemic stroke in patients in whom intravenous (IV) tissue plasminogen activator (t-PA) therapy has failed or was contraindicated. Endovascular techniques are used to treat severe symptomatic vasospasm after subarachnoid hemorrhage (SAH), for tumor embolization, and for temporary or permanent balloon occlusion during parent vessel sacrifice. Neuroendovascular surgery is being increasingly integrated into the neurosurgical training curriculum. It is essential for future neurosurgeons to have a basic understanding of endovascular techniques and tools and have them as an option for treating cerebrovascular pathological conditions. In this chapter, we discuss the basics of arterial access, catheters for supra-aortic and intracranial access, access site management, and the rationale and techniques for the treatment of various cerebrovascular diseases.

BOX 17.1 Abbreviations Used

ACAS, Asymptomatic Carotid Atherosclerosis Study

ACST, Asymptomatic Carotid Surgery Trial

AVM, arteriovenous malformation

CAS, carotid angioplasty with stenting

CCA, common carotid artery

CE, Conformité Européenne

CEA, carotid endarterectomy

COCOA, Complete Occlusion of Coilable Intracranial Aneurysms Study

CT, computed tomography

DAC, distal access catheter(s)

dAVF, dural arteriovenous fistula

DMSO, dimethyl sulfoxide

DSMB, Data and Safety Monitoring Board

ECA, external carotid artery

ECST, European Carotid Surgery Trial

EVIDENCE, Endovascular Treatment of Intracranial Aneurysms with Pipeline versus Coils with or without Stents

FDA, Food and Drug Administration

F, French

GESICA Groupe d’Etude des Sténoses Intra-Crâniennes Athéromateuses symptomatiques

HR, hazard ratio

IA, intra-arterial

IAT, intra-arterial thrombolysis

ICA, internal carotid artery

ICH, intracranial hemorrhage

IDE, Investigational Device Exemption

ISR, in-stent restenosis

IV, intravenous

IVT, intravenous thrombolysis

MCA, middle cerebral artery

MERCI, Mechanical Embolus Removal in Cerebral Ischemia

MR, magnetic resonance

mRS, modified Rankin scale

NASCET, North American Symptomatic Carotid Endarterectomy Trial

NIH, National Institutes of Health

NIHSS, National Institutes of Health Stroke Scale

NINDS, National Institute of Neurological Disorders and Stroke

PED, Pipeline Embolization Device

PGLA, polyglycolic-polylactic acid

PITA, Pipeline Embolization Device in the Intracranial Treatment of Aneurysms

PROACT, Prolyse in Acute Cerebral Thromboembolism

PUFS, Pipeline for Uncoilable or Failed Aneurysms Study

PVA, polyvinyl alcohol

SAH, subarachnoid hemorrhage

SAMMPRIS, Stenting vs. Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis

SAPPHIRE, Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy

SARIS, Stent-Assisted Recanalization in Acute Ischemic Stroke

SES, self-expanding stent

SWIFT, Solitaire FR with the Intention for Thrombectomy

TIA, transient ischemic attack

TIMI, Thrombolysis in Myocardial Infarction

TLR, target lesion revascularization

t-PA, tissue plasminogen activator

VA, vertebral artery

WASID, Warfarin vs. Aspirin for Symptomatic Intracranial Disease

General Principles

Femoral Artery Puncture

The groin is prepared and draped in the usual sterile fashion. The femoral pulse is palpated at the inguinal crease, and local anesthesia is administered via infiltration of 2% lidocaine (5-10 mL) at the site of the planned groin incision. A 5-mm incision is made parallel to the inguinal crease. A Potts needle with the bevel facing upward is advanced at a 45-degree angle to the skin, pointing to the patient’s opposite shoulder. On posteroanterior fluoroscopy, the femoral artery is located approximately 1 cm medial to the center of the femoral head. A single-wall puncture technique is performed by looking into the hollow of the needle for blood return; the needle is advanced 1 to 2 mm after blood is seen to maneuver the stylet into the vessel. A J-wire is gently advanced through the needle for 8 to 10 cm. For diagnostic angiography, the needle is exchanged for a regular 5-French (F) 10-cm sheath that is secured with a silk stitch. Sheaths are available in sizes of 4F and larger. The size refers to the inner diameter. The outer diameter is 1.5 to 2.0F larger than the stated inner diameter size. We are increasingly using a micropuncture technique for femoral puncture. In this technique, a 21-gauge needle is inserted in the same fashion as a Potts needle. A 0.018-inch microwire is inserted into the needle. The 21-gauge needle is exchanged for the dilator, and the dilator is exchanged for the sheath. The puncture hole is smaller with this technique and the technique gives a better “feel” of the vessel and needle entry.

For interventional procedures, a 6F sheath is used. Sheaths are also available in various lengths, most commonly 10 or 25 cm. The 25-cm version has the advantage that it bypasses any tortuosity in the iliac arteries. Having the distal end of the sheath in the aorta prevents any danger of injuring the iliac artery during catheter introduction through the sheath. Sheaths that are 90 cm in length, such as the Shuttle (Cook Inc., Bloomington, IN), can reach the carotid artery and can be used as a large-lumen guiding catheter or for added stabilization for a standard guiding catheter.

Radial or brachial artery access can be attempted if femoral artery access is not feasible.

Intracranial Access

Intracranial access and intervention require a stable microwire-microcatheter system. Biplane or three-dimensional roadmapping is essential for safe and expeditious navigation. A wide variety of microwires are available, with differing properties such as size, softness, visibility on fluoroscopy, shapeability, steerability, trackability, and torque control. All microwires suitable for neuroendovascular procedures are hydrophilically coated to reduce friction. Wires can have a shapeable distal tip or may come preshaped. Microwires range from 0.008 inch for the Mirage (ev3, Irvine, CA), to a variety of 0.10-inch and 0.014-inch wires, up to the 0.016-inch Headliner (Terumo Medical Corporation, Somerset, NJ). The Transend EX 0.014-inch Platinum (Boston Scientific) and the Synchro-14 0.014 inch (Boston Scientific) are our main microwires for intracranial manipulations.

Microcatheters are of three types: over the wire (commonest), flow-directed, and steerable. With over-the wire microcatheters, a curved microwire is manipulated toward the target position and the microcatheter is passively advanced over the wire until it reaches the proper position. If Onyx (ev3) is contemplated as an embolic agent, a microcatheter that is compatible with dimethyl sulfoxide (DMSO) must be used. Flow-directed catheters (e.g., Magic microcatheter, A.I.T.-Balt, Miami, FL) are so flexible distally that the catheter tip is pulled along by blood flow, making this a good choice for high-flow lesions, such as AVMs. Steerable catheters are over-the wire microcatheters (Enzo, Boston Scientific) with a steerable tip to allow access to difficult angulated branches. In our experience, these catheters are very rigid and we use them rarely. Two-marker, over-the-wire microcatheters, rather than single-marker catheters, are necessary for the use of detachable coils. The two markers in microcatheters used in detachable coils are 3 cm apart to determine that the coil is properly deployed.

Ischemic Stroke Intervention

Stroke remains the third most common cause of death in industrialized nations and the single most common reason for permanent adult disability.1 Each year, approximately 795,000 Americans experience a new or recurrent stroke.2 The estimated direct and indirect cost of stroke for 2010 is $73.7 billion.2 The incidence of new or recurrent strokes per year is projected to rise to 1.2 million per year by 2025.3

The only medical therapy approved by the Food and Drug Administration (FDA) for acute ischemic stroke treatment until recently was IV recombinant t-PA (rt-PA) administered within 3 hours of symptom onset to patients eligible for thrombolysis.4,5 The American Heart Association/American Stroke Association guidelines6 recommend evaluating patients for consideration of IV t-PA therapy 3 to 4.5 hours after stroke symptom onset (on the basis of data from the European Cooperative Acute Stroke Study III).7 Unfortunately, less than 1% of acute ischemic stroke patients in the United States receive t-PA, primarily because of a delay in presentation for treatment.8 Early reocclusion following thrombolysis has been demonstrated by transcranial Doppler imaging to occur in 34% of patients receiving IV t-PA and may result in neurological worsening in many of these patients.911 Recanalization rates after IV t-PA therapy for proximal, large vessel arterial occlusions are poor and range from only 10% for ICA occlusion to 30% for middle cerebral artery (MCA) occlusion.12 IV thrombolysis (IVT) is not as effective in thromboembolic obstruction of these large, proximal vessels, as compared with more distal smaller vessels.13 The outcome after large intracranial vessel thromboembolic occlusion currently remains dismal and is associated with high rates of morbidity and mortality.1417 Patients who do not meet the eligibility criteria for thrombolytic therapy, who fail to improve neurologically after thrombolytic therapy, or who improve and then worsen (patients with reocclusion) are currently candidates for endovascular revascularization therapies.

Endovascular Stroke Revascularization Techniques

Techniques for stroke revascularization can be classified as mechanical and pharmacological. Mechanical methods include microwire manipulation; snare; the current FDA-approved embolectomy devices, namely, the Penumbra (Penumbra Inc., Alameda, CA) and the Merci retriever (Concentric Medical Inc., Mountain View, CA); and stent-assisted or stent-platform-based stroke thrombectomy devices.

Time Window for Endovascular Stroke Therapy

Endovascular therapy is expanding the time window after stroke symptom onset for revascularization in patients with acute ischemic stroke The Prolyse in Acute Cerebral Thromboembolism (PROACT) trials18,19 established a benefit of intra-arterial thrombolysis (IAT) up to 6 hours after stroke symptom onset, with an increase in recanalization rates. Flow is reestablished faster with mechanical revascularization strategies than with thrombolytics; thus, such strategies may increase the benefit of treatment, even when there is a delay in presentation for treatment. The Mechanical Embolus Removal in Cerebral Ischemia (MERCI),20,21 Multi-MERCI,22 and Penumbra23 trials show effectiveness of mechanical revascularization therapy up to 8 hours after stroke symptom onset. There is increasing evidence that identification of potentially salvageable brain tissue with advanced magnetic resonance (MR) and computed tomography (CT) imaging may allow the selection of patients who can be effectively and safely treated more than 8 hours post ictus.7,2429

Higher Recanalization Rate and Improved Outcome after Stroke Intervention

In MERCI,20,21 Multi-MERCI,22 and the combined analysis of data from the Interventional Management of Stroke I and II studies,30 functional outcome (measured by modified Rankin Scale [mRS] score of ≤2 at 3 months) was significantly better and the 3-month mortality rate was significantly lower in patients who had thrombolysis in myocardial infarction (TIMI) scores 2 or 3 recanalization than in patients in whom vessels failed to recanalize after endovascular therapy. In a review of 53 studies that included 2066 patients, good functional outcome (mRS score ≤2) at 3 months was identified more frequently in patients with vessel recanalization than without vessel recanalization.31 The 3-month mortality rate was reduced in patients in whom vessels were recanalized. Higher rates of recanalization were achieved with endovascular methods, particularly mechanical therapies, and consequently were associated with better outcomes.

Stent-Assisted Thrombolysis

Self-expanding stents (SES) designed specifically for the cerebrovasculature are available. These stents can be delivered to intracranial target areas with a greater than 95% technical success rate with an increased safety profile because they are deployed at significantly lower pressures than balloon-mounted coronary stents.33 With the stent-for-stroke technique (using Wingspan [Boston Scientific] and Enterprise [Codman Neurovascular] SES), vessel recanalization is instantaneous, and the chance of early reocclusion after treatment is decreased. Reocclusion after IVT (34%) and pharmacological IAT (17%) has been shown and is associated with poor outcome.34

For stent-assisted thrombolysis, standard femoral access is obtained, and a 6F (or larger) guide catheter is placed in the target vessel proximal to the occlusion. To minimize the release of distal emboli, the occlusion is crossed in a fashion similar to that used for the Merci clot retriever. First, a .014-inch steerable wire is softly advanced through the clot. A low-profile catheter is then advanced over the wire distal to the occlusion. Following microangiographic confirmation that the microcatheter is distal to the occlusion, an exchange wire is brought through the microcatheter and anchored distal to the occlusion. The microcatheter is removed, and the stent delivery catheter is delivered over the exchange wire. To minimize the release of debris, the stent is deployed first distal to the occlusion (thus trapping any debris that may be later released between the stent and the vessel wall), then through the occlusion, and finally just proximal to the occlusion.

Several retrospective case series reported successful use of SES for acute stroke treatment, with higher rates of recanalization than other recanalization modalities.3537 Presently, SES are used only off-label under a humanitarian device exemption as a salvage therapy when current FDA-approved thrombectomy devices fail. On the basis of these preliminary data, we received FDA approval for a pilot study, Stent-Assisted Recanalization in Acute Ischemic Stroke (SARIS),38 to evaluate the Wingspan stent for revascularization in patients who did not improve after IVT or had a contraindication to IVT. Average presenting NIHSS score was 14. Seventeen patients presented with a TIMI score of 0 and three patients with a TIMI score of 1. Intracranial SES were placed in 19 of 20 enrolled patients. One patient experienced recanalization of the occluded vessel during positioning of the Wingspan stent delivery system, prior to stent deployment. In two patients, the tortuous vessel did not allow tracking of the Wingspan stent. The more navigable Enterprise stent was used in both these cases. Twelve patients had other adjunctive therapies. TIMI 2 or 3 recanalization was achieved in 100% of patients; 65% of patients improved more than 4 points in NIHSS score after treatment. One patient (5%) had symptomatic ICH, and two had asymptomatic ICH. At the time of the 1-month follow-up evaluation, 12 of 20 (60%) patients had mRS scores of 2 or less and nine (45%) had mRS scores of 1 or less. Mortality rate at 1 month was 25%. None of these patients died because of stent-placement-related causes; all deaths were due to the severity of the initial stroke and associated comorbid conditions.

Stent-Platform-Based Thrombectomy Devices (Stentrievers)

The Solitaire FR Revascularization Device (ev3) (Figs. 17.3 and 17.4) and Trevo device (Concentric Medical Inc.) are recoverable self-expanding thrombectomy devices that are being tested clinically in the United States and Europe, respectively, for acute ischemic stroke revascularization. The advantage of these devices is that they are fully recoverable, SES-platform-based devices that can be used for both temporary endovascular bypass and thrombectomy. The devices restore flow immediately and avoid the placement of a permanent stent, thus obviating the need for antithrombotic therapy and the risk of in-stent stenosis. The Solitaire can be electrolytically detached like a coil in case a permanent stent is necessary, such as in the setting of an atherothrombotic lesion. The Solitaire FR With the Intention for Thrombectomy (SWIFT) trial is an ongoing multicenter randomized controlled trial that is testing the ability of the Solitaire FR device versus the Merci device to achieve TIMI 2 or 3 recanalization without symptomatic ICH. Two small preliminary studies with this device have shown promising results.39,40

image

FIGURE 17.4 A, Solitaire FR device with retrieved clot (actual size). B, Solitaire FR.

(A from Natarajan SK, Siddiqui AH, Hopkins LN, Levy EI. Retrievable, detachable stent-platform-based clot-retrieval device (Solitaire FR) for acute stroke revascularization: first demonstration of feasibility in a canine stroke model. Vasc Dis Management 2010;7:E120-E125; B courtesy of ev3, Irvine, CA.)

Perfusion Imaging for Complication Avoidance and Patient Selection

Endovascular revascularization is an invasive procedure and is associated with acceptable complications in light of the morbidity and mortality risks associated with a major stroke if recanalization is not achieved. Despite aggressive revascularization with mechanical therapies, only up to 45% of patients recover to an mRS score of 0 to 2 at 3 months, and there is approximately an 8% to 10% procedure-related risk of symptomatic ICH, a potentially detrimental complication.1923,32,38 CT and MR perfusion imaging are utilized in attempts to differentiate the three zones of postischemia brain tissue that are critical for patient selection and complication avoidance, and thus the ability to discriminate among them with these modalities is envisioned to lead to an improvement in outcomes after endovascular stroke therapy in the future. The three zones are core (tissue that is dead), penumbra (tissue at risk of death if not revascularized/reperfused), and benign oligemia (tissue that will tolerate the reduced blood flow and will survive even without reperfusion, mainly dependent on collaterals). Currently, no imaging modality is capable of differentiating between penumbra and benign oligemia. MR-diffusion-weighted imaging and cerebral blood flow maps obtained with CT perfusion imaging are able to identify core tissue with acceptable false positive and false negative rates. At our center, we have found that core tissue in the basal ganglia region or a core occupying more than 30% of occluded territory presages a higher risk of symptomatic ICH after endovascular stroke intervention. Sophisticated and precise imaging is needed to identify these three territories after cerebral ischemia.

Intracranial Atherosclerosis Treatment

Approximately 8% to 10% of ischemic strokes are attributable to intracranial atherosclerosis.41,42 An estimated 40,000 to 60,000 new strokes per year in the United States are due to intracranial atherosclerosis.43 In a study of patients with intracranial stenosis undergoing repeat angiography at an average interval of 26.7 months, 40% of lesions had stabilized, 20% had regressed, and 40% had progressed.44 Stenosis progression, as detected by transcranial Doppler imaging, was an independent predictor of stroke recurrence.45

Need for Treatment

The most definitive study of symptomatic intracranial stenosis thus far is the prospective Warfarin versus Aspirin for Symptomatic Intracranial Disease (WASID) trial, which found an 11% to 12% first-year risk of ischemic stroke in territory attributable to the patient symptoms.46 The majority of strokes (73%) in WASID patients were in the territory of the stenotic artery.47 Patients in the Extracranial-Intracranial Bypass Study with MCA stenosis who were randomized to medical therapy had an annual ipsilateral ischemic stroke rate of 7.8%.48,49 In the prospective, nonrandomized Groupe d’Etude des Sténoses Intra-Crâniennes Athéromateuses symptomatiques (GESICA), 102 patients with more than 50% symptomatic intracranial stenosis had “optimal” medical therapy, with a follow-up period of 23.4 months.50 Among these patients, ipsilateral transient ischemic attack (TIA) occurred in 12.6% and ipsilateral stroke in 7.0%.

Endovascular Tools and Technique

The Wingspan Stent System with the Gateway percutaneous transluminal angioplasty balloon catheter was designed for the treatment of intracranial atherosclerotic stenosis and received FDA approval for this indication under the humanitarian exemption device provision in August 2005. Prestent dilation of the stenotic lesion is done with the angioplasty balloon and the stent, a self-expanding nitinol device, is then deployed (Fig. 17.5 and Video 17.3).

Essential devices for the angioplasty portion of the procedure include an exchange-length microwire, a microcatheter, and a balloon. Microwire properties that are most important for intracranial angioplasty are “beefiness,” trackability, and torque control. A relatively soft distal tip is helpful as well to minimize the chances of vasospasm or perforation of distal vessels. We prefer to use the 0.014-inch, 300-cm Transend FloppyTip microwire (Boston Scientific) because it has superior torque control compared with other microwires. The 0.014-inch, 300-cm X-Celerator microwire (ev3) is another option; it has a soft tip, relatively supportive body, and is very lubricious. A low-profile, straight microcatheter, usually of any kind, is sufficient. The 1.7-F Echelon-10 microcatheter (ev3) can be pushed through tortuous and stenotic vessels better than other microcatheters.

The Gateway balloon is a modified version of the Maverick 2 Balloon Catheter (Boston Scientific) with silicone coating on the balloon and hydrophilic coating on the catheter to facilitate access. Radiopaque markers on the balloon permit visualization of the proximal and distal ends of the balloon during fluoroscopic imaging. With roadmap guidance, the balloon is advanced until the balloon markers are across the lesion. A guide catheter angiogram is performed with the balloon in position to confirm proper positioning. The balloon is slowly inflated to nominal pressure, at a rate of approximately 1 atm every 10 seconds, under fluoroscopy. When the balloon is fully inflated, it is left inflated for another 10 to 20 seconds and then deflated. A guide catheter angiogram is obtained prior to removal of the balloon.

The Wingspan is a 3.5F, nitinol, over-the-wire SES. The design of this stent is very similar to that of the Neuroform 2 stent (Boston Scientific), which will be described later. The Wingspan has four platinum markers at each end for visualization and is deployed from the delivery microcatheter (called the “outer body”) with the “inner body”; the inner body is analogous to the “stabilizer” device that is used to deploy Neuroform stents. The rotating hemostatic valve is tightened on the inner body to prevent its migration, and the outer body of the Wingspan system is advanced over the exchange-length microwire. The inner body is advanced just proximal to the stent using the marker bands to identify the position of the stent. The outer body is pulled back to bring the outer body tip into position just past the region of stenosis. Holding the inner body in a stable position with the right hand, while slowly withdrawing the outer body with the left hand, results in deployment of the stent. The goal of therapy in these cases is to open the vessel to only 80% of its normal diameter.

Wingspan Studies

U.S. Wingspan Registry

In the U.S. Wingspan registry,5153 treatment with the stent system was attempted in 158 patients with 168 intracranial atheromatous lesions. Of these, 161 lesions were successfully treated (96.0%) during the first treatment session. Of the 168 lesions in which treatment was attempted, there were 9 (5.4%) major periprocedural neurological complications, 4 of which ultimately led to the death of the patient within 30 days of the procedure. The total periprocedural event rate was 12.5% (21 of 168 cases). Most postprocedure events (18 of 21) were related to definable (and potentially controllable) issues: early antiplatelet interruption (n = 6) and in-stent restenosis (ISR) (n = 13). Imaging follow-up was available for 129 treated lesions (75 anterior circulation, 54 posterior circulation). Thirty-six of 129 (27.9%) patients with imaging follow-up of treated lesions experienced ISR. Of these 36, 29 (80.6%) underwent target lesion revascularization (TLR) with angioplasty alone (n = 26) or angioplasty with restenting (n = 3). Post-Wingspan ISR was more common in patients younger than 55 years old (odds ratio = 2.6). This increased risk can be accounted for by a high prevalence of anterior circulation lesions in this population, specifically those affecting the supraclinoid segment. When patients of all ages were considered, much higher rates of both ISR (66.6% vs. 24.4%) and symptomatic ISR (40% vs. 3.9%) were associated with supraclinoid segment lesions, by comparison with all other locations. Of the 29 patients undergoing primary TLR, 9 required one intervention for recurrent ISR, for a total of 42 TLR interventions. Only one major complication, a postprocedural reperfusion hemorrhage, was encountered during TLR (complication rates: 2.4% per procedure; 3.5% per patient). Angiographic follow-up was available for 22 of 29 patients after primary TLR. Eleven of 22 (50%) patients demonstrated recurrent ISR at follow-up angiography. Subsequently, 9 of these patients have undergone multiple re-treatments (6 patients had two re-treatments each, 2 had three re-treatments each, and 1 had four re-treatments) for recurrent ISR.

The 12-month follow-up results were recently published.54 The average follow-up duration was 14.2 months with 110 patients having at least 12 months of follow-up. The cumulative rate of the primary endpoint (stroke or death within 30 days or ipsilateral stroke after 30 days) was 15.7% for all patients and 13.9% for patients with high-grade stenosis (70-99%). Thirteen ipsilateral strokes occurred after 30 days, and 3 of these patients died. Ten of 13 (76.9%) strokes occurred within the first 6 months of the stenting procedure, and no events occurred after 12 months. An additional 9 patients had ipsilateral TIA after 30 days. Most postprocedure events (86%) were related to in-stent restenosis (n = 12), interruption of antiplatelet therapy (n = 6), or both (n = 1).

Wingspan NIH Registry

In the Wingspan National Institutes of Health (NIH) registry,37 129 patients with symptomatic 70% to 99% intracranial stenosis were enrolled from 16 medical centers. The rate of technical success (stent placement across the target lesion with <50% residual stenosis) was 97%. The rate of any stroke, ICH, or death within 30 days or ipsilateral stroke beyond 30 days was 14% at 6 months. The rate of 50% or greater restenosis on follow-up angiography was 25% among 52 patients with follow-up. The NIH registry investigators published a posthoc analysis report of 158 of 160 patients who had successful placement for intracranial atherosclerotic lesions with 50% to 99% stenosis.55 The primary endpoint (any stroke or death within 30 days or stroke in the territory of the stented artery beyond 30 days and up to 6 months) occurred in 13.9%. In multivariable analysis, the primary endpoint was associated with posterior circulation stenosis (vs. anterior circulation) (hazard ratio [HR] 3.4, p = 0.018), stenting at low enrollment sites (<10 patients each) (vs. high enrollment site) (HR 2.8, p = 0.038), 10 or fewer days from qualifying event to stenting (vs. ≥10 days) (HR 2.7, p = 0.058), and stroke as a qualifying event (vs. TIA or other cerebral ischemic event, such as vertebrobasilar insufficiency) (HR 3.2, p = 0.064).

SAMMPRIS Study

In 2007, the NIH approved funding for the multicenter, prospective, randomized Stenting vs. Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) study.56 The hypothesis of the study is that “Compared with intensive medical therapy alone, intracranial angioplasty and stenting combined with intensive medical therapy will decrease the risk of the primary endpoint by 35% over a mean follow-up of 2 years in high-risk patients (patients with 70-99% intracranial stenosis who had a TIA or stroke within 30 days prior to enrollment) with symptomatic stenosis of a major intracranial artery.” A total of 764 patients will be recruited within 30 days of TIA or stroke due to 70% to 99% stenosis of a major intracranial artery. The patients will be randomized to either stent treatment with the Wingspan intracranial stent and Gateway balloon system plus intensive medical therapy with management of blood pressure, lipids, and other risk factors for vascular events or to this intensive medical therapy alone. Each patient will be followed for a minimum of 1 year and a maximum of 4 years after randomization. On April 11, 2011, the National Institute of Neurological Disorders and Stroke (NINDS) issued an alert57 to the SAMMPRIS investigators to stop enrollment in this trial because the last data and safety monitoring board (DSMB) review found that 14% of patients treated with angioplasty combined with stenting experienced a stroke or died within the first 30 days after enrollment compared with 5.8% of patients treated with medical therapy alone, a highly significant difference. The 30-day rate of stroke or death in the intensive medical treatment arm was substantially lower than the estimated rate of 10.7% based on historical control subjects, most of whom received standard medical care. In addition, the 30-day rate in the stent group was substantially higher than the estimated rate of 5.2% to 9.6%, based on registry data. The SAMMPRIS Executive Committee was in agreement with NINDS and the DSMB that enrollment in the study should be stopped and that the trial data currently available indicate that aggressive medical management alone is superior to angioplasty combined with stenting in patients with recent symptoms and high-grade intracranial arterial stenosis. Follow-up of currently enrolled patients and a comprehensive analysis of the total trial dataset will be important in the final interpretation of this study.

Carotid Angioplasty and Stenting

Atherosclerotic disease in the carotid arteries is thought to be the cause in up to 30% of ischemic strokes.41 The North American Symptomatic Carotid Endarterectomy Trial (NASCET),58,59 Asymptomatic Carotid Atherosclerosis Study (ACAS),60 Asymptomatic Carotid Surgery Trial (ACST),61 and the European Carotid Surgery Trial (ECST)62,63 established carotid endarterectomy (CEA) as an effective means of future stroke prevention in at-risk populations with significant carotid artery disease. Carotid angioplasty with stenting (CAS) was introduced as a less-invasive alternative to conventional CEA. With the subsequent development of distal embolic protection devices and stents for the carotid system, CAS became a promising and viable option for patients who were poor candidates for CEA.6466

The major impetus for the advancement of CAS came with the publication of the results of the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial,67 which demonstrated effectively that patients considered high risk for CEA were less likely to have complications if treated with CAS. This resulted in the approval of CAS by the FDA, Centers for Medicare & Medicaid Services, and Medicare as a viable option for such patients. More recently, an entirely new method of embolic protection achieved through flow reversal from the ICA into the arterial guide sheath, classified as proximal embolic protection, is being tested.68

Technique (Video 17.4) and Tools

An aortic arch angiogram is initially performed to define the atherosclerotic burden as well as the anatomical configuration of the great vessels, which allows the operator to predict the feasibility of carotid cannulation and select the devices needed for the procedure. Selective carotid angiography is then performed, and the severity of the stenosis is defined. The diameters of the CCA and ICA are measured with attention paid to determining a landing zone for the embolic protection device. Intracranial angiography is also essential before the intervention because the presence of tandem lesions should be considered in the management strategy as well as for comparison of pre- and post-intracranial angiograms to confirm the absence of any vessel dropout suggestive of embolism.

After completion of the diagnostic angiogram and positioning of the catheter in the CCA, roadmapping of the cervical carotid artery is performed. An exchange-length 0.035-inch wire is positioned in the ECA. The diagnostic catheter is exchanged over the wire for a 90-cm, 6F to 10F sheath that is then advanced into the CCA below the bifurcation. For patients who have undergone complete diagnostic cerebral angiography before the stenting procedure, a combination of a 6F, 90-cm shuttle over a 6.5F Headhunter 125-cm slip-catheter (Cook) or a 5F, 125-cm Vitek catheter (Cook) can be used. In these cases, the shuttle is introduced primarily in the femoral artery over a 0.35-inch wire and is parked in the descending aorta. The inner obturator and wire are removed. The 125-cm catheter is then advanced into the shuttle, and the target vessel is catheterized. The shuttle is brought over the wire and the catheter in the CCA. The size of the shuttle is usually dictated by the profile of the embolic protection device and compatibility with the stent system. An optimal angiographic view that maximizes the opening of the bifurcation and facilitates crossing of the stenosis should be sought. The lesion is crossed with the protection device. Predilation of the stenotic vessel segment is performed at the operator’s discretion. We avoid predilation of the lesion whenever possible; however, if predilation is necessary, we prefer to undersize the balloon to simply facilitate crossing of the stent, usually using a 2- to 3-mm-diameter balloon. A 3- to 4-mm coaxial angioplasty balloon is advanced to the lesion over the 0.014-inch wire holding the protection device. On rare occasions, predilation needs to be performed before the introduction of an embolic protection device.

The diameter of the stent should be sized to the caliber of the largest segment of the carotid artery to be covered (usually 1-2 mm more than the normal caliber of the CCA). Oversizing of the stent in the ICA does not usually result in adverse events, but a tapered stent can better conform to the vessel wall. Particular attention should be paid to the selection of a stent that is long enough to cover the entire lesion.

After removing the stent system, poststent dilation is performed using a balloon with a diameter matching that of the ICA distal to the stent. A coaxial balloon is usually preferred for this purpose. The embolic protection device is then removed, using its retrieval catheter. (When a balloon occlusion catheter is used for cerebral protection, the embolic debris is aspirated before deflation and retrieval of the balloon.)

Embolic Protection Devices

All embolic protection systems currently on the market can be classified under three main groups, each with its own working principle: (1) distal occlusion balloons, (2) distal filters, and (3) proximal occlusion devices. With the distal occlusion devices, a balloon is inflated in the ICA between the lesion and the brain to block the blood flow toward the cerebrum. Consequently, debris cannot enter the cerebral vasculature during the procedure. The debris is aspirated and flushed, forcing it either into the ECA or out of the body, through a sheath in the CCA. Filtration systems function in the manner of an umbrella- or windsock-like filter hose, which are opened in between the carotid lesion and the brain to capture all debris during the CAS procedure. Together with the distal filter, the debris is removed at the end of the procedure. A distal filter can be mounted on a guidewire, on which it is directly brought in place and retrieved, or alternatively, can come with its own specific delivery and retrieval system. Proximal occlusion systems (Fig. 17.6) are characterized by two compliant balloons to be inflated, one in the proximal CCA and one in the ECA. This double-balloon inflation creates either a no-flow or a reversed-flow pattern within the ICA, thereby preventing embolization of debris in the cerebral circulation. Proximal occlusion devices are especially attractive because complete cerebral protection is established before the device is passed across the lesion. The concerns associated with proximal protection devices are their large size (currently requiring 9F access to the femoral artery) and the concurrent delivery of a 9F system into tortuous CCAs.

Intracranial Aneurysm Treatment

The overall prevalence of unruptured intracranial aneurysms in the general population is between 0.8% and 6%. The incidence of aneurysmal subarachnoid hemorrhage (SAH) is between 10 and 15 per 100,000 people per year. Endovascular treatment of intracranial aneurysms has undergone multiple changes since the introduction of Guglielmi detachable coils (Boston Scientific/Target, Fremont, CA) for endosaccular occlusion of these aneurysms in 1994. When there was a high recurrence rate for wide-necked aneurysms after simple coiling, adjunctive techniques including balloon-assisted and stent-assisted coiling were introduced. Onyx liquid embolic agent is being tested for aneurysm occlusion. The concept of flow diversion and parent vessel reconstruction without endosaccular occlusion of the aneurysm has gained momentum and has been useful in complex aneurysms that could not be adequately treated with previously available endovascular techniques. Flow-diversion devices are being widely tested for the safety and efficacy of aneurysm exclusion.

Aneurysm Coils

A coil consists of a fine platinum thread tightly looped around a thicker platinum wire. The coil is connected to a “pusher wire”; the attachment site is the location of the detachment mechanism, which may be electrolytic, thermal, or hydraulic in design. The coil and pusher wire come from the manufacturer in a slim plastic delivery sheath; the sheath is placed within the hub of the rotating hemostatic valve, and the coil and pusher wire are threaded together into the microcatheter.

The coil is designed to assume one of a number of shapes as it is pushed out of the microcatheter. Framing coils are three-dimensional coils designed to “frame” the aneurysm; that is, these coils are meant to “sphericize” the aneurysm with gentle outward radial force to permit packing with two-dimensional coils. Filling coils are intended to occupy space within the aneurysm after framing. These coils usually have a helical shape and are of intermediate stiffness. Finishing coils are the softest coils and are designed for final packing of the aneurysm and “finishing off” of the neck.

Observations of aneurysm recanalization after treatment with bare platinum coils led to the introduction of coils containing materials meant to enhance fibrosis within the aneurysm and decrease the chance of recanalization. Several “bioactive” coil systems are on the market currently; some contain polyglycolic-polylactic acid (PGLA) while others contain hydrogel. The PGLA polymer degrades by hydrolysis to glycolic acid and lactic acid, which promote fibrocellular proliferation. Matrix 2 (Boston Scientific) coils are platinum coils covered with PGLA. Cerecyte (Micrus Endovascular, Sunnyvale, CA) and Nexus (ev3) coils also incorporate PGLA. The HydroCoil® system (MicroVention, Inc., Aliso Viejo, CA) consists of platinum coils coated with an expandable hydrogel. The hydrogel provides a greater filling volume than bare platinum coils by filling the interstices of the coil mass. No firm scientific data yet exist to support one coil type over another.

Balloon-Assisted Coil Embolization (Fig. 17.7)

The use of balloons to occlude the aneurysm neck during coiling of wide-necked aneurysms was first described in 1994 by Moret and associates.69 A 6F or larger guide catheter is required to accommodate both a balloon catheter and a microcatheter. A microcatheter is placed into the aneurysm fundus, and a balloon catheter is centered over the neck of the aneurysm. The balloon is subsequently inflated during placement of a coil and then deflated intermittently in between coils to allow antegrade flow. Sequential inflations and deflations are performed as additional coils are placed until the aneurysm is completely coiled, at which point the balloon is removed. The rationale behind this technique is that the presence of the balloon prevents distal embolization and conforms the coil mass to the shape of the balloon and that the coil mass shape becomes stable, thereby protecting the parent artery as the individual coils interlock. During the initial insertion of a coil, one should be careful to form a loop that directs the distal end of the coil away from the aneurysm fundus in order to limit the risk of aneurysm perforation during balloon inflation.

At our center, balloon assistance is used for cases of ruptured wide-necked giant aneurysms in which the use of antiplatelet agents is contraindicated and in which the deployment of a stent is not feasible. The number of patients in the second category is decreasing as more deliverable intracranial SES become available. We currently use the HyperGlide and HyperForm balloons (Micro Therapeutics, Irvine, CA) in such cases.

Balloon-Assisted Onyx Embolization (Fig. 17.8)

Onyx embolization for the treatment of intracranial aneurysms is an investigational procedure. Onyx is composed of an ethylene vinyl alcohol copolymer dissolved in DMSO and suspended in micronized tantalum powder (for visualization under fluoroscopy). The ethylene vinyl alcohol copolymer is infused through a microcatheter into an aqueous environment; the DMSO diffuses outward into the surrounding tissue, allowing the material to precipitate into a spongy, space-occupying cast. Onyx embolization of aneurysms requires a balloon-assisted technique to permit infusion of the material into the aneurysm without embolization into the distal circulation. DMSO-compatible devices must be used.

Patients are administered a loading dose of aspirin and clopidogrel prior to the procedure as described in stent-assisted coiling. A deflated compliant, DMSO-compatible balloon (Hyperglide, ev3) is placed in the parent vessel adjacent to the aneurysm. A DMSO-compatible microcatheter (Rebar, ev3) is navigated into the aneurysm. The balloon is inflated, and contrast material is gently injected through the microcatheter as a test to confirm that the balloon has made an adequate seal over the aneurysm neck. After the microcatheter is primed with DMSO, a Cadence Precision Injector syringe (ev3) is filled with Onyx and attached to the hub of the microcatheter. Onyx is injected under fluoroscopic observation at a rate of approximately 0.1 mL/minute or slower. The injection is continued and paused after each incremental volume of approximately 0.2 to 0.3 mL to allow the material to polymerize and to allow temporary balloon deflation. Several sequential reinflations and injections may be necessary.

At the completion of the embolization process, with the balloon deflated, the microcatheter syringe is decompressed by the aspiration of 0.2 mL of Onyx left in the microcatheter, which prevents dribbling of Onyx material during removal of the microcatheter. An interval of 10 minutes is allowed to elapse prior to microcatheter removal, in order to permit the Onyx material to set within the aneurysm. As the microcatheter is withdrawn, the balloon is inflated a final time to stabilize the Onyx mass. The patient should be kept on an antiplatelet regimen for 1 month after the procedure.

In a multicenter investigation of cerebral aneurysm treatment with Onyx, the rate of permanent neurological morbidity was 8.3% (8/97 patients), and there were two procedural deaths.70 The procedures for large and giant aneurysms were lengthy (up to 6 hours). Delayed occlusion of the carotid artery occurred in 9 (9%) of 100 patients. At the 12-month follow-up evaluation of 53 patients, 38 (72%) large and giant aneurysms were completely occluded. Re-treatment was performed in 9 (11%) of 79. Although some single-center studies show slightly better results,71 in our opinion, the relatively high complication rate and high rate of delayed carotid artery occlusion do not justify this treatment in patients with unruptured aneurysms who cannot tolerate carotid artery occlusion. Currently, short-term results of Onyx occlusion for large aneurysms are not better than for selective coil occlusion, and the immediate and delayed complication rates are probably higher.

Self-Expanding Intracranial Microstents

Presently, there are two intracranial SES designed specifically for stent-assisted coiling of wide-necked intracranial aneurysms available in the United States: the Neuroform 3 stent (Boston Scientific) and the Enterprise Vascular Reconstruction Device and Delivery System (Codman Neurovascular). Both devices consist of a self-expanding nitinol stent that is deployed in the parent vessel adjacent to the aneurysm neck; the stent then acts as a scaffold to hold coils in place inside the aneurysm. Both devices are extremely navigable (compared to delivery of balloon-mounted coronary stents), and the Enterprise stent presents several benefits over the Neuroform stent, including reconstrainability, a lower profile delivery system, and a technically less complicated deployment mechanism.

Recently, SES have begun to be viewed not only as adjunctive devices to support coiling but also as tools that could potentially support the long-term durability of coil embolization, particularly in difficult cases in which the aneurysm is prone to recurrence. This is because stents have several possible effects on the physiology and biology of the aneurysm–parent vessel complex: altering the parent vessel configuration and thus possibly altering intra-aneurysmal flow dynamics; disruption of the inflow jets; reduction in the vorticity and wall shear stress on the aneurysm wall and reduction of the water-hammer effect of the pulsatile blood flow that causes coil compaction by the tines of the stents; and providing a scaffolding and stimulus for the overgrowth of endothelial and neointimal tissue across the neck of the aneurysm, creating a matrix for “biological remodeling” in the region of the aneurysm neck.

Neuroform Stent (Fig. 17.9)

The Neuroform stent comes from the manufacturer preloaded in a 3F microdelivery catheter. A “stabilizer” catheter (also preloaded in the delivery microcatheter) is then used to stabilize and deploy the stent as the microdelivery catheter is withdrawn. The stent consists of a fine wire mesh that cannot be seen on standard fluoroscopy; however, the four platinum marker bands at each end can be seen. The devices come in sizes ranging between 2.5 and 4.5 mm in diameter and 10 and 30 mm in length. The recommended diameter for placement is 0.5 mm greater than the largest diameter of the parent artery to be stented. The length is chosen such that the stent extends for at least 5 mm proximal and distal to the aneurysm neck. The struts composing the stent measure approximately 60 µm in thickness. The interstices of the fully expanded stent are large enough to accommodate a microcatheter tip size of 2.5F or less (realistically, <2.0F) for coiling.

A microcatheter and microwire (0.010 or 0.014 inch) are navigated past the aneurysm, using roadmap guidance. The microwire is removed and replaced with an exchange-length 0.014-inch microwire with a soft, J-shaped distal curve. The microdelivery catheter containing the Neuroform stent is threaded onto the exchange-length wire and advanced across the neck of the aneurysm. The stabilizer catheter is then held firmly in place as the microdelivery catheter is pulled back over the stabilizer and microwire, such that the stent is unsheathed. As the stent expands, the marker bands can be seen to spread. The microdelivery catheter and stabilizer are removed over the exchange-length wire. A standard-length microcatheter is advanced over the microwire until it is past the stent. The exchange-length microwire is removed and replaced with a standard-length microwire. The microwire and microcatheter are then guided through the stent and into the aneurysm for coiling.

Enterprise Stent (Fig. 17.10 and Video 17.6)

The Enterprise stent comes from the manufacturer within a plastic sheath (the “dispenser loop”). A delivery wire is preloaded within the stent, and both the stent and delivery wire come from the manufacturer in the dispenser loop. The delivery wire has three radiopaque zones: the proximal wire, the “stent positioning marker” (which indicates where the undeployed stent is loaded, and runs the length of the stent), and the distal tip. The Enterprise measures 4.5 mm in diameter when unconstrained and as such is indicated for use only in vessels measuring between 2.5 and 4 mm in diameter. The device comes in lengths of 14, 22, 28, and 37 mm. The struts of the Enterprise, like those of the Neuroform, are approximately 60 µm thick. The stent struts cannot be seen on standard fluoroscopy; each end of the four platinum marker bands can be seen, but these are considerably more difficult to visualize than the markers on the Neuroform stent. The interstices of the fully expanded Enterprise stent are large enough to accommodate a microcatheter tip with an outer diameter size less than or equal to 2.3F for coiling.

The Enterprise is a closed-cell stent; this design makes it reconstrainable. A Prowler Select Plus microcatheter (a 2.9F/2.3F proximal/distal outer diameter; 0.021-inch inner diameter; Codman Neurovascular) and microwire (0.010 or 0.014 inch) are navigated past the aneurysm using a roadmap. The tip is positioned at least 12 mm distal to the neck of the aneurysm. The microwire is removed, and the Enterprise stent is inserted into the Prowler Select Plus microcatheter by placing the tip of the dispenser loop in the rotating hemostatic valve and advancing the delivery wire. The delivery wire can be advanced without fluoroscopy until the marker on the wire is at the rotating hemostatic valve. The marker on the delivery wire is 150 cm from the distal tip. The delivery wire and stent are then navigated into position across the aneurysm neck. The stent is deployed by holding the delivery wire firmly in place while carefully retracting the microcatheter. If the stent position is unsatisfactory, advancing the microcatheter may allow recapture of the stent. Stent recapture may be done provided that less than 80% of the stent has been deployed. If the proximal end of the stent-positioning marker is still within the microcatheter, the stent can be recaptured. The stent should be recaptured only once. If further repositioning is needed, the stent should be removed and a new one used. When the operator is satisfied with the position of the stent, the microwire and microcatheter are guided through the stent and into the aneurysm for coiling.

Indications for Self-Expanding Intracranial Microstents

The current indications for self-expanding intracranial microstents include stent-assisted coil embolization, rescue during embolization, and balloon-assisted coiling followed by stenting.

Advanced Self-Expanding Intracranial Microstent Techniques Used in Complex Aneurysms

Balloon Anchor Technique for Difficult Distal Vessel Access (Fig. 17.11 and Video 17.7)

This technique is used in wide-necked aneurysms with a dominant flow jet that constantly directs any device used for distal vessel access into the aneurysm. This, coupled with the inability to achieve stable distal purchase of the access after it is obtained, often leads to abortion of the procedure. Distal parent vessel access was obtained by allowing the microwire to follow the local hemodynamics into a giant internal carotid artery aneurysm and around its dome into the distal vessel. An over-the-wire balloon inflated in the distal vessel followed by gentle retraction of the balloon catheter and microwire allowed only a wire bridge across the aneurysm neck, thereby allowing the stent catheter to be brought up in a standard fashion.

image

FIGURE 17.11 The balloon anchor technique. A, A fusiform aneurysm with different inlet and outlet flow directions. This makes directing the microwire into the distal parent vessel difficult. B, The microwire is allowed to follow the inlet flow and curve around in the aneurysm to exit at the outlet. C, A balloon is inflated in the distal parent vessel to serve as an anchor, and the wire is slowly pulled to bridge the neck of the aneurysm. D, A stent is placed across the aneurysm neck. E, Stent-assisted coiling of the aneurysm.

(From Snyder KV, Natarajan SK, Hauck EF, et al. The balloon anchor technique: a novel technique for distal access through a giant aneurysm. J NeuroInterventional Surg 2010;2:363-367, and Levi EI, Siddiqui AH, Crumlish A, et al. First Food and Drug Administration-approved prospective trial of primary intracranial stenting for acute stroke; SARIS [Stent-Assisted Recanalization in acute Ischemic Stroke). Stroke 2009;40:3552-3556.)

Waffle-Cone Technique (Fig. 17.13)

In cases in which a Y-stent is not feasible, a stent may be deployed from the parent artery directly into the aneurysm (i.e., “intra-extra” aneurysmal stent placement or waffle-cone technique) to achieve parent artery protection. Using this technique, a single stent can be used to stabilize an intra-aneurysmal coil mass.78 However, the final construct sets up a vector of flow redirection directly into the terminal aneurysm sac and actually disrupts flow into the bifurcation branches. One might expect that such a construct could lead to high rates of recanalization. In addition, if this technique fails or leads to recanalization, other available means of treatment (surgical clipping, endovascular therapy with balloon remodeling or Y-stent reconstruction) are made considerably more difficult, if not impossible.

image

FIGURE 17.13 Waffle-cone technique. A, Catheter over wire. B, Neuroform stent (Boston Scientific, Natick, MA) being deployed in aneurysm. C, Stent deployed in aneurysm with microwire within the aneurysm. D, Microcatheter in aneurysm with coil being deployed. E, Coiled aneurysm with waffle-cone configuration.

(From Horowitz M, Levy E, Savageau E, et al. Intra/extra-aneurysmal stent placement for management of complex and wide-necked bifurcation aneurysms: eight cases using the waffle cone technique. Neurosurgery 2006;58(4 Suppl 2):ONS-26.)

Flow-Diverting Devices

The concept of parent vessel reconstruction is quickly advancing with the recent development of dedicated flow-diverting endovascular constructs designed for intracranial use. These devices primarily target parent vessel reconstruction, rather than endosaccular occlusion, as the means by which to achieve definitive aneurysm treatment. The current flow-diverting devices are high-metal surface area coverage, stent-like constructs that are designed to provide enough flow redirection, and endovascular remodeling to induce aneurysm thrombosis without the use of additional endosaccular occlusive devices (i.e., coils). At the same time, the pore size of the constructs is large enough to allow for the continued perfusion of branch vessels and perforators arising from the reconstructed segment of the parent vessel.80 Large or giant size or the presence of intra-aneurysmal thrombus, which are both factors typically associated with coil compaction and aneurysm recurrence, are not an issue with the flow-diverting devices, because no endosaccular coils are placed. In addition, as a purely “extrasaccular” treatment strategy, no direct catheterization or manipulation of the aneurysm sac is required with the flow-diverting devices, possibly reducing the likelihood of procedural rupture and potentially improving the safety of endovascular aneurysm treatment. The Pipeline Embolization Device (PED) (ev3) represents the first flow-diversion device used in humans. We have recently used the SILK flow-diverting device (BALT, Montmorency, France) in a patient (on a compassionate basis). Multiple other flow-diverting devices are currently in development and testing.

Pipeline Embolization Device (Fig. 17.14 and Video 17.9)

The PED is a cylindrical, stent-like construct composed of 48 braided strands of cobalt, chromium, and platinum. The device is packaged within an introducer sheath collapsed upon a delivery wire. The device is loaded into and delivered via the hub of a 0.027-inch internal diameter microcatheter that has been positioned across the neck of the aneurysm. Initially collapsed within the delivery sheath or microcatheter, the device is elongated approximately 2.5 times its deployed length when expanded to nominal diameter. As it is deployed, the device foreshortens toward its nominal length (which it achieves only if allowed to expand fully to its nominal diameter). Currently, the available devices range from 2.5 to 5 mm in diameter (in 0.25-mm increments) and 10 to 20 mm in length (in 2-mm increments). The deployed device is very flexible and conforms to the normal parent vessel anatomy, even in very tortuous vascular anatomy.

When fully expanded, the PED provides approximately 30% metal surface area coverage. When deployed in a parent artery smaller than the nominal diameter of the device, the PED cannot fully expand, and as such, it deploys longer than its nominal length and yields a lesser metal surface area coverage. To augment surface area coverage, several devices can be overlapped, or an individual device can be deployed with forward pressure on the microcatheter. To achieve coverage of vessel defects measuring longer than 20 mm, multiple devices can be telescoped to reconstruct longer segments of the cerebrovascular anatomy. The tremendous versatility of the device essentially allows the operator to achieve reconstructions of most any segment of the cerebrovascular anatomy and allows some control of the metal surface coverage of different regions of the conglomerate construct. This control over the length, shape, and porosity of the final reconstructed vessel allows the operator to build a “customized” implant for each patient treated.

By August 2010, 1178 aneurysms had been treated with the PED.81 The Pipeline Embolization Device in the Intracranial Treatment of Aneurysms (PITA) trial was an industry-sponsored safety trial for the Conformité Européenne (CE) mark of approval. The trial comprised a prospective four-center, single-arm study with core laboratory image analysis. Thirty-one patients with unruptured wide-necked intracranial aneurysms in whom treatment with coil embolization had failed were enrolled. The mean aneurysm neck diameter was 5.8 mm, and the mean aneurysm diameter was 11.5 mm. The PED was used alone in 48% of patients and with coils in 52% of patients. Six-month imaging follow-up was conducted in 96% of patients. Complete occlusion at 6 months was achieved in 93.3% of patients. At 6 months, the mortality and permanent morbidity rates were 0% and 6.5%, respectively.82 This unprecedented rate of complete angiographic occlusion at follow-up surpasses any of the reported occlusion rates for aneurysms after endovascular therapy and far exceeds those rates reported for large or wide-necked lesions.

The Budapest single-center study, which was a continuation of the PITA study, confirmed the findings of that study.83 A total of 19 large or giant wide-necked aneurysms were treated in 18 patients. Angiography at 6 months demonstrated complete occlusion in 17 aneurysms. Four neurological complications resulted in one patient (5.5%) with permanent morbidity and one (5.5%) death. Of the 17 ophthalmic arteries that were covered by a PED, one (5.9%) was occluded acutely, with visual deficit, and two (11.8%) were occluded in a delayed fashion, with no clinically detectable deficit. No other side branch occlusions were documented.

The Buenos Aires study,84 a prospective single-center registry that comprised 53 patients with 63 intracranial aneurysms, also expanded on the PITA study and confirmed the findings of the aforementioned two studies. Thirty-three (52.4%) aneurysms in the Buenos Aires study were small wide-necked aneurysms. Complete angiographic occlusion was achieved in 56%, 93%, and 95% of aneurysms at 3 months (n = 42), 6 months (n = 28), and 12 months (n = 18), respectively. There were no deaths; three patients (5%) with giant aneurysms experienced transient exacerbation of preexisting cranial neuropathies or headache. Five patients developed hematomas at the femoral puncture site.

The experience of the group at Hacettepe University (Ankara, Turkey) with the PED was presented recently.85 The study comprised 129 patients with intracranial aneurysms treated with the PED. The 12-month occlusion rate was 95%. There was one (0.8%) symptomatic parent artery stenosis, four (3.2%) permanent morbidities, and one (0.8%) death. Again, the outcomes were similar to the other three reported studies.

The PED has also been used to successfully treat nonsaccular (fusiform or circumferential) aneurysms. Three such cases have been performed in North America under an FDA exemption.86 All three lesions, which were judged to be untreatable with existing endovascular or open surgical technologies, were angiographically cured with PED treatment, without technical or neurological complications. In two cases, eloquent perforator or side-branch vessels were covered by the PED construct; and in both cases, vessels remained patent at angiographic follow-up. Two of these patients now have more than 1 year of clinical and angiographic follow-up and remain angiographically cured of their lesions and are without neurological symptoms.85

The Pipeline for Uncoilable or Failed Aneurysms Study (PUFS) was a U.S. investigational device exemption (IDE), nonrandomized, single-arm, multicenter premarket approval study using a historical control group.87 PUFS enrolled 120 patients with large or giant (paraclinoid or cavernous) ICA aneurysms and 6-month data were available in 107 (89%) patients. After reviewing these data, the FDA on April 6, 2011, approved the PED “for the endovascular treatment of adults (22 years of age or older) with large or giant wide-necked intracranial aneurysms in the ICA from the petrous to the superior hypophyseal segments.”88,89

The Complete Occlusion of Coilable intracranial Aneurysms (COCOA) study is an ongoing, randomized, multicenter U.S. IDE study comparing coiling to the PED for the treatment of small paraclinoid aneurysms (aneurysm diameter <10 mm and neck diameter <4 mm). The safety endpoint is death and ipsilateral stroke, and the effectiveness endpoint will be assessed on the basis of complete aneurysm occlusion at 6 months.

A multicenter randomized clinical trial has been planned to compare coiling and PED. This trial is the U.S. government-sponsored endovascular treatment of intracranial aneurysms with Pipeline versus coils with or without stents (EVIDENCE) trial. The aim is to recruit patients with intracranial aneurysms between 7 mm and 15 mm. The study protocol details have not yet been published.

SILK Flow-Diverting Device

The SILK device is similar to the PED and has 48 braided wires (44 nitinol and 4 platinum). It is available in 2.0- to 5.5-mm diameters (0.5-mm increments) and 15- to 40-mm lengths (5-mm increments). The SILK device shortens by at least 50% when deployed. It comes prepackaged with a delivery system comprising a delivery wire and an introducer and a reinforced microcatheter for placement (Vasco + 21 2.4F for devices 2-4.5 mm in diameter and 3F for devices 5-5.5 mm in diameter; preshaped with a multipurpose distal curve). The SILK device is preloaded on the delivery wire inside the introducer. After microcatheter access to the aneurysm has been obtained, working projections and vessel measurements are taken for device sizing. The SILK device is transferred from the introducer into the hub of the microcatheter using a Y-connector and by gently advancing the delivery wire. The device is positioned past the aneurysm neck at least 1.5 times the diameter of the parent vessel. The delivery wire is gently pushed until the distal radiopaque end is out of the distal marker on the microcatheter. Withdrawing the microcatheter to deploy the SILK device to approximately 1 cm creates a fix-point on the delivery wire. This manipulation ensures that SILK does not move distally, which can result in the wire struts of the SILK damaging the vessel wall. Once the SILK is deployed by approximately 1 cm, the distal tip is positioned by simultaneously pulling on the catheter and delivery wire. The SILK device may be moved by pulling the delivery wire, as long as the distal ring of the catheter does not superimpose the marker on the delivery wire. If repositioning of the device is required, the catheter is gently advanced over the deployed SILK, the system is repositioned, and the device is re-deployed in the new location. The SILK is fully deployed when the marker of the delivery wire lines up with the distal ring of the catheter. It is then impossible to resheath the SILK. The delivery wire is pushed until its marker passes the catheter’s marker by a minimum of 2 mm. The microcatheter is positioned distal to the stent to maintain access through the stent before removal of the delivery wire. The main advantages of the SILK device over the PED are the better translatability of the one-to-one movement of the microcatheter and the delivery system and the ability to recapture and reposition the system even up to 90% deployment. In our experience, the ability to recapture a flow-diverting device in our experience is very important. These devices frequently require repositioning because they foreshorten during deployment, and we often realize the final position of the stent only after it has been partially deployed.

The main limitations of flow-diverting devices when compared to intracranial SES are the efficacy and safety of their use in bifurcation aneurysms, as there is a potential for jailing of one limb of the bifurcation, and the lack of data regarding the safety of these devices in vessels rich with eloquent perforators. Available data in experimental animal models and in humans, especially with the PED, suggest that coverage with a single device is safe.

Parent Vessel Sacrifice

Parent vessel sacrifice is still used as a last resort in giant aneurysms that are high risk for open surgical methods and cannot be safely excluded by currently available endovascular reconstructive techniques. Balloon test occlusion is performed concurrently if permanent vessel occlusion (endovascular or surgical) is considered as a treatment option or as a bail-out maneuver. Currently, deconstructive strategies without a bypass are used only as a bail-out when other treatment options are not available because all the temporary occlusion tests for the presence of collateral supply have false negative results; and there is a 16% to 20% chance of developing an ischemic event after carotid sacrifice even if balloon occlusion tests were negative.90,91 If surgical bypass is planned, endovascular sacrifice should be performed promptly after the surgical procedure to minimize the risk of graft thrombosis due to low flow.

The key step in the sacrifice of a large vessel, such as the ICA or the VA, is temporary proximal flow arrest to prevent inadvertent embolization into the cerebral vasculature during the procedure. In general, the parent vessel should be occluded either at or immediately proximal to the lesion. Occlusion of the vessel can be accomplished with detachable coils or detachable balloons. Although detachable balloons are not commercially available in the United States at the present time, they are available in Europe and Japan.

Detachable Balloon Embolization

The Goldvalve detachable balloon (Acta Vascular/Nfocus Neuromedical Inc., Santa Clara, CA) is available in most of the world outside the United States, and the vendor is working on obtaining approval for the North American market. Complete stasis of flow can be achieved more rapidly with balloons than with coils, but balloons require more preparation prior to use. Occlusion of an artery with detachable balloons should always be undertaken with two balloons placed end to end, with the proximal balloon functioning as a “safety” balloon to minimize the chance of distal migration of the balloons.

A large guide catheter is required, often 7F or 8F (alternatively, a 6F or 7F, 90-cm sheath may be used). A balloon is chosen that is slightly larger than the diameter of the vessel to be occluded. The balloons are attached to their recommended delivery catheters. If the guide catheter is large enough, it is preferable to advance the two balloons simultaneously through the guide catheter and into the vessel in order to limit the risk of premature detachment. Ideally, the balloons should be positioned in a relatively straight segment of the vessel. When the balloons are in proper position, they are inflated with contrast material. If they are properly sized, they will flatten out and elongate as they are inflated. When the position and stability of the balloon appear to be satisfactory, the distal balloon is detached by slowly, gently pulling back on the balloon catheter. The proximal balloon is for flow arrest and is deflated and removed after the distal balloon is deployed.

Intracranial Arteriovenous Malformation Embolization

The prevalence of AVMs is estimated at approximately 0.01% of the general population, but reported rates range from 0.001% to 0.52%. Cerebral AVMs are detected at a rate of 1 per 1 million person-years and account for 2% of all hemorrhagic strokes. Given the relatively high rate of hemorrhage associated with AVMs without treatment and the prospect of cure with treatment, obliteration of these lesions is usually desirable. Surgical resection is favored for patients in good medical condition with a good life expectancy who harbor small to medium-sized AVMs in anatomically accessible locations within the brain. Both radiosurgery and endovascular embolization have important roles in AVM management. The former is a viable alternative to surgical resection when small lesions (<3 cm) are either deep or in eloquent areas. The latter is a useful adjunct in facilitating microsurgical or radiosurgical therapy and less often a primary cure.

Endovascular Embolization

Only a minority of AVMs can be cured by endovascular embolization. The ability to obliterate AVMs via the endovascular route has increased in conjunction with the use of Onyx for embolization. At our center, most AVMs are resected after endovascular embolization unless they are in deep, inaccessible, or eloquent locations, or unless we are convinced that the embolization is complete and that we will be able to evaluate the patient for follow-up on a regular basis. As a stand-alone therapy, endovascular embolization is not commonly a definitive treatment.

Preoperative endovascular embolization of feeding arteries has rendered many previously difficult AVMs much easier to remove surgically. In general, endovascular embolization is most useful for Spetzler-Martin grade III AVMs.92 If endovascular access to the feeding vessels can be achieved without placing normal vessels at substantial risk, it can be used for lower grade AVMs as well.

The goal of preoperative embolization is to facilitate surgical resection. Preoperative embolization can facilitate surgery by (1) decreasing intraoperative bleeding and operating time; (2) embolizing surgically difficult areas, such as deep regions of AVM near the ventricles and areas of the AVM nidus bordering eloquent regions; and (3) delimiting very small AVMs that would be very difficult to identify in the parenchyma. The risks of embolization increase as the number of embolized pedicles increases and as the percentage of the AVM embolized increases. We traditionally embolize 30% to 50% of the AVM during a single sitting and bring the patient back for additional sittings, if necessary, 4 to 6 weeks apart. It is important to tailor the endovascular procedure only to facilitate surgical resection and not to embolize the entire AVM nidus unless that is the original plan or there is evidence during the procedure that venous outflow has been compromised and therefore the patient will need emergent surgery immediately after embolization. During embolization, it is very important not to overshoot 50% of the AVM nidus at a sitting. Most important, it is critical to remain mindful of the venous outflow and its character and timing because any increase in delay or any changes in venous outflow can presage a hemorrhage. Because a decision to operate on an AVM on an emergency basis can be made during or after the intervention, we try to perform our embolization procedures during the initial half of the day so that surgical intervention, if necessary, may be done using routine daytime operating room personnel.

Technique of Embolization

At our center, most AVM embolizations are performed under conscious sedation to allow neurological examinations to be performed throughout the procedure. In addition, we routinely perform Wada testing in the arterial pedicle to be embolized to determine whether the AVM is located in an eloquent region or there is en passant supply from the selected pedicle. We most commonly use Onyx as the embolic agent during embolization procedures. After microcatheterization, often with a flow-directed microcatheter, we initially perform microruns to study the angioarchitecture in detail. The endovascular neurosurgeon must be aware of en passant feeders and critical feeders taking off proximal to the point of injection in order to judge the safest distance for allowable reflux of the embolic agent (Fig. 17.15A). We initially use Onyx-34 to create a plug around the microcatheter (Fig. 17.15B), and this facilitates the forward injection of Onyx-18. Oblique views are obtained to see the tip of the catheter clearly, so that the any reflux of the Onyx can be appreciated readily.

image

FIGURE 17.15 A, Preferably, the direct feeder with the longest possible reflux distance should be chosen for Onyx (ev3, Irvine, CA) injection. B, Position of the microcatheter for Onyx embolization. Notice the reflux of Onyx around the tip of the microcatheter to form a plug.

(From Natarajan SK, Ghodke B, Britz GW, et al. Multimodality treatment of brain arteriovenous malformations with microsurgery after embolization with Onyx: single-center experience and technical nuances. Neurosurgery 2008;62:1213-1226.)

Once the microcatheter tip is in the desired position, the injection of the Onyx is carried out as follows: the microcatheter is flushed with 10 mL of normal saline; 0.23 mL DMSO is injected into a Marathon flow-directed microcatheter (ev3) to fill the dead space. DMSO is also used to wash the hub of the syringe to avoid the polymerization of Onyx (when it comes in contact with water). Onyx is aspirated into a 1-mL syringe. Meniscus-to-meniscus connection is made between the Onyx (in the syringe) and the DMSO (in the catheter hub). Onyx is then injected slowly at a flow rate of 0.1 mL/second to fill the microcatheter and replace the DMSO in the dead space. The embolic agent is released at the tip of the microcatheter under free-flow conditions and fills the nidus compartment directly in an antegrade fashion, with subsequent reflux into the feeding artery beyond the tip of the microcatheter (first penetration). The goal is to form a cast of Onyx around the tip of the microcatheter over a short distance, so that when the Onyx is injected, it flows forward into the AVM and not retrogradely into the feeding vessel. The injection procedure is then interrupted for up to 1 minute to allow the cast to form, and small volumes of the Onyx are injected per cycle until there is enough reflux to form an attenuated cast for a second penetration of the nidus. The maximum safe distance of reflux is usually approximately 2 cm or at least 1 cm distal to a cortical branch of the feeding artery. Careful repeated subtraction roadmaps allow better visualization of the regions of the AVM that are being embolized. We are currently using a triple coaxial guide system containing an Outreach DAC or a Neuron (Penumbra Inc.) catheter to allow more distal placement in order to perform better selective angiography and further selective MCA, posterior cerebral artery, or anterior cerebral artery catheterization to evaluate further details of the AVM with the remainder of the circulation subtracted. Further, in our experience, the use of a triple coaxial guide system greatly facilitates removal of the microcatheter from the Onyx plug after completion of the embolization procedure.

Intracranial Dural Arteriovenous Fistula Embolization

dAVFs account for 10% to 15% of all intracranial AVMs.93 The venous drainage pattern is the most important predictor of the clinical behavior, and dAVFs with cortical venous reflux exhibit a much higher incidence of ICH or venous infarction. The annual mortality rate for dAVFs with cortical venous reflux may be as high as 10.4%, whereas the annual risk for hemorrhage or nonhemorrhagic neurological deficits during follow-up of nontreated lesions are 8.1% and 6.9%, respectively, resulting in an annual event rate of 15%.94 Recent studies demonstrate evidence that the risk of bleeding for a dAVF with cortical venous reflux is less when the patient does not present with a hemorrhage or a nonhemorrhagic neurological deficit.95,96 Strom and colleagues96 report that asymptomatic versus symptomatic dAVFs (in patients presenting with hemorrhage or neurological deficit) have annual hemorrhage rates of 1.4% versus 19%, respectively. Although small, these studies make the important point that the natural history may depend on the type of presentation.

With the advent of Onyx (ev3), most intracranial dAVFs can be successfully managed with endovascular techniques. Onyx is more often used for transarterial access when the ECA branches supplying a dAVF can be safely embolized. dAVF location close to dural venous sinuses also facilitates access and transvenous occlusion through the sinus, mainly with coils. The combination of transarterial and transvenous embolization results in higher obliteration rates than previously reported in series with only transvenous embolization.

Endovascular Therapy for Vasospasm

Symptomatic cerebral vasospasm (also known as clinical vasospasm or delayed ischemic neurological deficit) is the leading cause of death and disability in patients with SAH. Symptomatic vasospasm occurs in some 20% to 25% of patients.97,98 Balloon angioplasty is an option for symptomatic vasospasm affecting intracranial arteries larger than 1.5 mm in diameter, such as the intracranial ICA, the M1, A1, and the VA and basilar arteries and P1 segments. The internal elastic lamina and smooth muscle cells are stretched and thinned during angioplasty. Dilation of the vessel segments is essentially “permanent” for the duration of the clinical vasospasm; vasospasm generally does not recur after angioplasty. Reversal of neurological deficits with angioplasty has been reported in 30% to 70% of patients who fail hypervolemic, hypertensive, and hemodilution (triple H) therapy.99101 Clinical improvement appears to be strongly dependent on the timing of the procedure, with significantly better results reported with angioplasty done within 24 hours99 and within 2 hours102 of the neurological change. An IA infusion of antispasmodic medications (verapamil, nimodipine, or nicardipine) can supplement angioplasty and can be used for the endovascular treatment of spasm of vessels distal to the circle of Willis that are too small for balloon angioplasty.

The balloons used for angioplasty are either compliant balloons, such as the HyperGlide (ev3) or HyperForm (ev3), or noncompliant balloons, such as the Maverick 2. Because noncompliant balloons are difficult to navigate into small distal vessels, angioplasty is usually limited to larger proximal vessels, where one is less likely to face problems. For most cases, the HyperGlide 4 × 10-mm balloon is most suitable. At our center, we use the Maverick 2 balloon as it has fixed size, and we undersize it to prevent complications. The microwire and balloon are advanced into the target vessel under roadmap fluoroscopy. The balloon is carefully and gently inflated under fluoroscopic visualization. In cases of severe spasm and constriction of the target vessel, pretreatment with an IA injection of nitroglycerin (20 µg) may allow passage of the balloon. The drug is slowly infused through a microcatheter positioned in the proximal portion of the vessel.

Tumor Embolization

Most intracranial tumor embolization procedures have been done for neoplasms with robust vascular pedicles, such as meningiomas, hemangiopericytomas, and paragangliomas. Tumor embolization was primarily used for the reduction of blood loss during subsequent surgery. More recently, IA therapies for recurrent and malignant brain neoplasms have been reported. Although the results of these studies show promise, especially in that chemotherapeutic agents can be delivered to tumor beds while sparing patients from many of the systemic toxicities associated with the treatment, larger studies are needed. Controversy remains regarding preoperative embolization of meningiomas. Although there may be a role for preoperative embolization in cases in which large tumor vessels and significant vascular blushing are appreciated on angiography, many meningiomas may not be sufficiently vascular to warrant the risk and expense of preoperative embolization.

Embolic Agents

Several agents are currently used for tumor embolization and include polyvinyl alcohol (PVA), Gelfoam (Pfizer, New York, NY), coils, alcohol, and trisacryl gelatin microspheres. The goal of embolization is to saturate the tumor vascular bed with these agents and not simply to occlude large feeding arteries. Thus, the choice and order of embolic agents used are important when attempting to first saturate the fine network of vessels that supply the deepest regions of the tumor bed. Gelfoam powder, microspheres, and polyvinyl alcohol are available in particle sizes as small as 50 µm and as large as 1 mm. Smaller particles should be used during the initial stages of pedicle embolization as these can penetrate and occlude the fine, distal vasculature supplying the tumor bed. As these vessels become saturated with particles, larger particles can then be used to embolize more proximal, and therefore larger, vessels supplying the tumor. We caution that smaller particles have an increased risk of penetrating distal branches of normal parenchyma should reflux occur, as compared to larger particle that cannot penetrate the tumor bed beyond the more proximal vessels. Some interventionists advocate the use of microspheres during the later stages of tumor embolization as microspheres are less likely to occlude the catheter during slow injections because of their uniform nature. Although liquid embolic agents such as alcohol have been used for tumor embolization, this technique is typically reserved for embolization of distal vessels unreachable by microcatheters. Typically, a balloon is inflated proximal to the microcatheter tip to prevent reflux of the alcohol. Usually, less than 5 mL is needed to attain the desired effect of intimal disruption, inflammation, and tumor necrosis.

Epistaxis

Epistaxis is a common condition that can be managed conservatively in most cases. When these measures, including anterior and posterior packing of the nasal cavity, are unsuccessful at controlling the bleeding (in 5% of cases), interruption of the blood supply to the sinonasal area can be performed, either by surgical ligation or by transarterial embolization.

Embolization should be preceded by thorough diagnostic angiography. Aside from aiding with subsequent selective catheterization and embolization, such angiography may reveal significant anatomical anomalies, anastomoses, or an unsuspected cause of epistaxis. Taking these findings into account, the interventionist may decide to refrain from embolization or adjust the technique to minimize the risk of adverse events, which are mostly related to inadvertent embolization of the ICA or ophthalmic artery.

Endovascular treatment for nosebleeds usually consists of superselective catheterization with particle embolization of the nasal vessels, usually the sphenopalatine arteries. Complications can be minimized by careful attention to angiographic anatomy and awareness of dangerous anastomoses. Provocative testing with amobarbital and lidocaine prior to embolization is an added safety factor. The contralateral sphenopalatine artery is checked during the angiogram, even if the bleeding is obviously unilateral, because there can be side-to-side collaterals. Ethmoidal branches from the ophthalmic may be the cause of treatment failure after embolization of the internal maxillary artery. Embolization of the branches of the ophthalmic artery is not recommended because of the risk to vision and the availability of a fairly easy and safe surgical procedure to ligate these vessels. Accessory meningeal arteries may also rarely be a source of bleeding in epistaxis and can be embolized.

Materials frequently used for embolization include pledgets of gelatin sponge (Gelfoam); Gelfoam powder (Pfizer); PVA particles, ranging in size from 50 to 700 µm; platinum coils; or a combination of materials. Smaller particles (50-150 µm) are discouraged, because they are more likely to enter dangerous anastomoses. PVA particles, usually between 150 and 500 µm, with or without the subsequent addition of Gelfoam sponge pledgets or platinum coils, are the main embolic agents used.

References

1. Report of the WHO Task Force on Stroke and Other Cerebrovascular Disorders, 1989. Recommendations on stroke prevention, diagnosis, and therapy. Stroke. 1989;20:1407-1431.

2. Lloyd-Jones D., Adams R.J., Brown T.M., et al. Heart disease and stroke statistics—2010 update: a report from the American Heart Association. Circulation. 2010;121:e46-e215.

3. Broderick J.P., William M. Feinberg Lecture: stroke therapy in the year 2025: burden, breakthroughs, and barriers to progress. Stroke. 2004;35:205-211.

4. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995;333:1581-1587.

5. Adams H.P.Jr., del Zoppo G., Alberts M.J., et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Circulation. 2007;115:e478-e534.

6. del Zoppo G.J., Saver J.L., Jauch E.C., et al. Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen activator. A science advisory from the American Heart Association/American Stroke Association. Stroke. 2009;40:2945-2948.

7. Hacke W., Kaste M., Bluhmki E., et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008;359:1317-1329.

8. Barber P.A., Zhang J., Demchuk A.M., et al. Why are stroke patients excluded from TPA therapy? An analysis of patient eligibility. Neurology. 2001;56:1015-1020.

9. Alexandrov A.V., Grotta J.C. Arterial reocclusion in stroke patients treated with intravenous tissue plasminogen activator. Neurology. 2002;59:862-867.

10. Janjua N., Alkawi A., Suri M.F., et al. Impact of arterial reocclusion and distal fragmentation during thrombolysis among patients with acute ischemic stroke. AJNR Am J Neuroradiol. 2008;29:253-258.

11. Saqqur M., Molina C.A., Salam A., et al. Clinical deterioration after intravenous recombinant tissue plasminogen activator treatment: a multicenter transcranial Doppler study. Stroke. 2007;38:69-74.

12. Wolpert S.M., Bruckmann H., Greenlee R., et al. Neuroradiologic evaluation of patients with acute stroke treated with recombinant tissue plasminogen activator. The rt-PA Acute Stroke Study Group. AJNR Am J Neuroradiol. 1993;14:3-13.

13. Saqqur M., Uchino K., Demchuk A.M., et al. Site of arterial occlusion identified by transcranial Doppler predicts the response to intravenous thrombolysis for stroke. Stroke. 2007;38:948-954.

14. Arnold M., Nedeltchev K., Mattle H.P., et al. Intra-arterial thrombolysis in 24 consecutive patients with internal carotid artery T occlusions. J Neurol Neurosurg Psychiatry. 2003;74:739-742.

15. Jansen O., von Kummer R., Forsting M., et al. Thrombolytic therapy in acute occlusion of the intracranial internal carotid artery bifurcation. AJNR Am J Neuroradiol. 1995;16:1977-1986.

16. Zaidat O.O., Suarez J.I., Santillan C., et al. Response to intra-arterial and combined intravenous and intra-arterial thrombolytic therapy in patients with distal internal carotid artery occlusion. Stroke. 2002;33:1821-1826.

17. Sorimachi T., Fujii Y., Tsuchiya N., et al. Recanalization by mechanical embolus disruption during intra-arterial thrombolysis in the carotid territory. AJNR Am J Neuroradiol. 2004;25:1391-1402.

18. del Zoppo G.J., Higashida R.T., Furlan A.J., et al. PROACT: a phase II randomized trial of recombinant pro-urokinase by direct arterial delivery in acute middle cerebral artery stroke. PROACT Investigators. Prolyse in acute cerebral thromboembolism. Stroke. 1998;29:4-11.

19. Furlan A., Higashida R., Wechsler L., et al. Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in acute cerebral thromboembolism. JAMA. 1999;282:2003-2011.

20. Gobin Y.P., Starkman S., Duckwiler G.R., et al. MERCI 1: a phase 1 study of mechanical embolus removal in cerebral ischemia. Stroke. 2004;35:2848-2854.

21. Smith W.S., Sung G., Starkman S., et al. Safety and efficacy of mechanical embolectomy in acute ischemic stroke: results of the MERCI trial. Stroke. 2005;36:1432-1438.

22. Smith W.S., Sung G., Saver J., et al. Mechanical thrombectomy for acute ischemic stroke: final results of the Multi MERCI trial. Stroke. 2008;39:1205-1212.

23. Bose A., Henkes H., Alfke K., et al. The Penumbra System: a mechanical device for the treatment of acute stroke due to thromboembolism. AJNR Am J Neuroradiol. 2008;29:1409-1413.

24. Hacke W., Albers G., Al-Rawi Y., et al. The desmoteplase in acute ischemic stroke trial (DIAS): a phase II MRI-based 9-hour window acute stroke thrombolysis trial with intravenous desmoteplase. Stroke. 2005;36:66-73.

25. Furlan A.J., Eyding D., Albers G.W., et al. Dose escalation of desmoteplase for acute ischemic stroke (DEDAS): evidence of safety and efficacy 3 to 9 hours after stroke onset. Stroke. 2006;37:1227-1231.

26. Thomalla G., Schwark C., Sobesky J., et al. Outcome and symptomatic bleeding complications of intravenous thrombolysis within 6 hours in MRI-selected stroke patients: comparison of a German multicenter study with the pooled data of ATLANTIS, ECASS, and NINDS tPA trials. Stroke. 2006;37:852-858.

27. Kohrmann M., Juttler E., Fiebach J.B., et al. MRI versus CT-based thrombolysis treatment within and beyond the 3 h time window after stroke onset: a cohort study. Lancet Neurol. 2006;5:661-667.

28. Davis S.M., Donnan G.A., Parsons M.W., et al. Effects of alteplase beyond 3 h after stroke in the echoplanar imaging thrombolytic evaluation trial (EPITHET): a placebo-controlled randomised trial. Lancet Neurol. 2008;7:299-309.

29. Hacke W., Furlan A.J., Al-Rawi Y., et al. Intravenous desmoteplase in patients with acute ischaemic stroke selected by MRI perfusion-diffusion weighted imaging or perfusion CT (DIAS-2): a prospective, randomised, double-blind, placebo-controlled study. Lancet Neurol. 2009;8:141-150.

30. Tomsick T., Broderick J., Carrozella J., et al. Revascularization results in the interventional management of stroke II trial. AJNR Am J Neuroradiol. 2008;29:582-587.

31. Rha J.H., Saver J.L. The impact of recanalization on ischemic stroke outcome: a meta-analysis. Stroke. 2007;38:967-973.

32. Penumbra Pivotal Stroke Trial Investigators. The Penumbra Pivotal Stroke Trial: Safety and effectiveness of a new generation of mechanical devices for clot removal in intracranial large vessel occlusive disease. Stroke. 2009;40:2761-2768.

33. Henkes H., Miloslavski E., Lowens S., et al. Treatment of intracranial atherosclerotic stenoses with balloon dilatation and self-expanding stent deployment (WingSpan). Neuroradiology. 2005;47:222-228.

34. Qureshi A.I., Siddiqui A.M., Kim S.H., et al. Reocclusion of recanalized arteries during intra-arterial thrombolysis for acute ischemic stroke. AJNR Am J Neuroradiol. 2004;25:322-328.

35. Brekenfeld C., Schroth G., Mattle H.P., et al. Stent placement in acute cerebral artery occlusion: use of a self-expandable intracranial stent for acute stroke treatment. Stroke. 2009;40:847-852.

36. Levy E.I., Mehta R., Gupta R., et al. Self-expanding stents for recanalization of acute cerebrovascular occlusions. AJNR Am J Neuroradiol. 2007;28:816-822.

37. Zaidat O.O., Klucznik R., Alexander M.J., et al. The NIH registry on use of the Wingspan stent for symptomatic 70-99% intracranial arterial stenosis. Neurology. 2008;70:1518-1524.

38. Levy E.I., Siddiqui A.H., Crumlish A., et al. First Food and Drug Administration-approved prospective trial of primary intracranial stenting for acute stroke: SARIS (Stent-Assisted Recanalization in acute Ischemic Stroke). Stroke. 2009;40:3552-3556.

39. Cohen J.E., Gomori J.M., Leker R.R., et al. Preliminary experience with the use of self-expanding stent as a thrombectomy device in ischemic stroke. Neurol Res. 2011;33:439-443.

40. Miteff F., Faulder K.C., Goh A.C., et al. Mechanical thrombectomy with a self-expanding retrievable intracranial stent (Solitaire AB): experience in 26 patients with acute cerebral artery occlusion. AJNR Am J Neuroradiol. 2011;32(6):1078-1081. (epub April 14, 2011)

41. Sacco R.L., Roberts J.K., Boden-Albala B., et al. Race-ethnicity and determinants of carotid atherosclerosis in a multiethnic population. The Northern Manhattan Stroke Study. Stroke. 1997;28:929-935.

42. Wityk R.J., Lehman D., Klag M., et al. Race and sex differences in the distribution of cerebral atherosclerosis. Stroke. 1996;27:1974-1980.

43. Higashida R.T., Meyers P.M., Connors J.J.3rd, et al. Intracranial angioplasty and stenting for cerebral atherosclerosis: a position statement of the American Society of Interventional and Therapeutic Neuroradiology, Society of Interventional Radiology, and the American Society of Neuroradiology. AJNR Am J Neuroradiol. 2005;26:2323-2327.

44. Akins P.T., Pilgram T.K., Cross D.T.3rd, et al. Natural history of stenosis from intracranial atherosclerosis by serial angiography. Stroke. 1998;29:433-438.

45. Arenillas J.F., Molina C.A., Montaner J., et al. Progression and clinical recurrence of symptomatic middle cerebral artery stenosis: a long-term follow-up transcranial Doppler ultrasound study. Stroke. 2001;32:2898-2904.

46. Chimowitz M.I., Lynn M.J., Howlett-Smith H., et al. Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med. 2005;352:1305-1316.

47. Kasner S.E., Chimowitz M.I., Lynn M.J., et al. Predictors of ischemic stroke in the territory of a symptomatic intracranial arterial stenosis. Circulation. 2006;113:555-563.

48. EC/IC Bypass Study Group. Failure of extracranial-intracranial arterial bypass to reduce the risk of ischemic stroke. Results of an international randomized trial. N Engl J Med. 1985;313:1191-1200.

49. Bogousslavsky J., Barnett H.J., Fox A.J., et al. Atherosclerotic disease of the middle cerebral artery. Stroke. 1986;17:1112-1120.

50. Mazighi M., Tanasescu R., Ducrocq X., et al. Prospective study of symptomatic atherothrombotic intracranial stenoses: the GESICA study. Neurology. 2006;66:1187-1191.

51. Albuquerque F.C., Levy E.I., Turk A.S., et al. Angiographic patterns of Wingspan in-stent restenosis. Neurosurgery. 2008;63:23-28.

52. Fiorella D.J., Levy E.I., Turk A.S., et al. Target lesion revascularization after Wingspan: assessment of safety and durability. Stroke. 2009;40:106-110.

53. Turk A.S., Levy E.I., Albuquerque F.C., et al. Influence of patient age and stenosis location on wingspan in-stent restenosis. AJNR Am J Neuroradiol. 2008;29:23-27.

54. Fiorella D.J., Turk A.S., Levy E.I., et al. US Wingspan registry: 12-month follow-up results. Stroke. 2011;42(7):1976-1981. (epub June 2, 2011)

55. Nahab F., Lynn M.J., Kasner S.E., et al. Risk factors associated with major cerebrovascular complications after intracranial stenting. Neurology. 2009;72:2014-2019.

56. Derdeyn C.P., Chimowitz M.I. Angioplasty and stenting for atherosclerotic intracranial stenosis: rationale for a randomized clinical trial. Neuroimaging Clin North Am. 2007;17:355-363. viii-ix

57. National Institute of Neurological Disorders and Stroke (NINDS). Alert issued. April 11, 2011. Available at http://www.heart.org/idc/groups/ahamah-public/@wcm/@sop/@scon/documents/downloadable/ucm_425679.pdf

58. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445-453.

59. Barnett H.J., Taylor D.W., Eliasziw M., et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med. 1998;339:1415-1425.

60. Asymptomatic Carotid Atherosclerosis Study Group. Study design for randomized prospective trial of carotid endarterectomy for asymptomatic atherosclerosis. Stroke. 1989;20:844-849.

61. Halliday A., Mansfield A., Marro J., et al. Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet. 2004;363:1491-1502.

62. European Carotid Surgery Trialists’ Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet. 1991;337:1235-1243.

63. European Carotid Surgery Trialists’ Collaborative Group. Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet. 1998;351:1379-1387.

64. Diethrich E.B., Ndiaye M., Reid D.B. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg. 1996;3:42-62.

65. Jordan W.D.Jr., Voellinger D.C., Fisher W.S., et al. A comparison of carotid angioplasty with stenting versus endarterectomy with regional anesthesia. J Vasc Surg. 1998;28:397-403.

66. Theron J., Courtheoux P., Alachkar F., et al. Intravascular technics of cerebral revascularization. J Mal Vasc. 1990;15:245-256.

67. Yadav J.S., Wholey M.H., Kuntz R.E., et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med. 2004;351:1493-1501.

68. Ansel G.M., Hopkins L.N., Jaff M.R., et al. Investigators for the ARMOUR Pivotal Trial. Safety and effectiveness of the INVATEC MO.MA(R) proximal cerebral protection device during carotid artery stenting: results from the ARMOUR pivotal trial. Catheter Cardiovasc Interv. 2010;76:1-8.

69. Moret J., Pierot L., Boulin A., et al. Remodeling of the arterial wall of the parent vessel in the endovascular treatment of intracranial aneurysms (abstr S83). Proceedings of the 20th Congress of the European Society of Neuroradiology. Neuroradiology. 1994;36(Suppl 1):S83.

70. Molyneux A.J., Cekirge S., Saatci I., et al. Cerebral Aneurysm Multicenter European Onyx (CAMEO) trial: results of a prospective observational study in 20 European centers. AJNR Am J Neuroradiol. 2004;25:39-51.

71. Weber W., Siekmann R., Kis B., et al. Treatment and follow-up of 22 unruptured wide-necked intracranial aneurysms of the internal carotid artery with Onyx HD 500. AJNR Am J Neuroradiol. 2005;26:1909-1915.

72. Hanel R.A., Boulos A.S., Sauvageau E.G., et al. Stent placement for the treatment of nonsaccular aneurysms of the vertebrobasilar system. Neurosurg Focus. 2005;18:E8.

73. Fiorella D., Albuquerque F.C., Han P., et al. Preliminary experience using the Neuroform stent for the treatment of cerebral aneurysms. Neurosurgery. 2004;54:6-17.

74. Lavine S.D., Larsen D.W., Giannotta S.L., et al. Parent vessel Guglielmi detachable coil herniation during wide-necked aneurysm embolization: treatment with intracranial stent placement: two technical case reports. Neurosurgery. 2000;46:1013-1017.

75. Chow M.M., Woo H.H., Masaryk T.J., et al. A novel endovascular treatment of a wide-necked basilar apex aneurysm by using a Y-configuration, double-stent technique. AJNR Am J Neuroradiol. 2004;25:509-512.

76. Sani S., Lopes D.K. Treatment of a middle cerebral artery bifurcation aneurysm using a double Neuroform stent “Y” configuration and coil embolization: technical case report. Neurosurgery. 2005;57:E209.

77. Thorell W.E., Chow M.M., Woo H.H., et al. Y-configured dual intracranial stent-assisted coil embolization for the treatment of wide-necked basilar tip aneurysms. Neurosurgery. 2005;56:1035-1040.

78. Horowitz M., Levy E., Sauvageau E., et al. Intra/extra-aneurysmal stent placement for management of complex and wide-necked bifurcation aneurysms: eight cases using the waffle cone technique. Neurosurgery. 58, 2006. ONS-258–262

79. Kelly M.E., Turner R., Gonugunta V., et al. Stent reconstruction of wide-necked aneurysms across the circle of Willis. Neurosurgery. 2007;61:249-255.

80. Kallmes D.F., Ding Y.H., Dai D., et al. A new endoluminal, flow-disrupting device for treatment of saccular aneurysms. Stroke. 2007;38:2346-2352.

81. Wong G.K., Kwan M.C., Ng R.Y., et al. Flow diverters for treatment of intracranial aneurysms: current status and ongoing clinical trials. J Clin Neurosci. 2011;18:737-740.

82. Nelson P.K., Lylyk P., Szikora I., et al. The Pipeline embolization device for the intracranial treatment of aneurysms trial. AJNR Am J Neuroradiol. 2011;32:34-40.

83. Szikora I., Berentei Z., Kulcsar Z., et al. Treatment of intracranial aneurysms by functional reconstruction of the parent artery: the Budapest experience with the pipeline embolization device. AJNR Am J Neuroradiol. 2010;31:1139-1147.

84. Lylyk P., Miranda C., Ceratto R., et al. Curative endovascular reconstruction of cerebral aneurysms with the Pipeline embolization device: the Buenos Aires experience. Neurosurgery. 2009;64:632-643.

85. Cekirge S. FD or “homemade” FD with multiple stents? Presented at the 2nd European Society of Minimally Invasive Neurological Therapy (ESMINT) Congress, Nice, France, Sept. 10, 2010.

86. Fiorella D., Woo H.H., Albuquerque F.C., et al. Definitive reconstruction of circumferential, fusiform intracranial aneurysms with the Pipeline embolization device. Neurosurgery. 2008;62:1115-1121.

87. Szikora I. Results using flow diverter devices: ongoing or reported studies. Presented at the 2nd European Society of Minimally Invasive Neurological Therapy (ESMINT) Congress, Nice, France, Sept. 10, 2010.

88. U.S. Food and Drug Administration. Instructions for use (IFU) Pipeline embolization device. Available at http://www.accessdata.fda.gov/cdrh_docs/pdf10/P100018c.pdf. Accessed May 18, 2011.

89. U.S. Food and Drug Administration. Pipeline embolization device—P100018. Available at http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cftopic/pma/pma.cfm?num=p100018 Accessed May 18, 2011

90. Larson J.J., Tew J.M.Jr., Tomsick T.A., et al. Treatment of aneurysms of the internal carotid artery by intravascular balloon occlusion: long-term follow-up of 58 patients. Neurosurgery. 1995;36:26-30.

91. Origitano T.C., al-Mefty O., Leonetti J.P., et al. Vascular considerations and complications in cranial base surgery. Neurosurgery. 1994;35:351-363.

92. Lawton M.T. Spetzler-Martin grade III arteriovenous malformations: surgical results and a modification of the grading scale. Neurosurgery. 2003;52:740-749.

93. Newton T.H., Cronqvist S. Involvement of dural arteries in intracranial arteriovenous malformations. Radiology. 1969;93:1071-1078.

94. van Dijk J.M., terBrugge K.G., Willinsky R.A., et al. Clinical course of cranial dural arteriovenous fistulas with long-term persistent cortical venous reflux. Stroke. 2002;33:1233-1236.

95. Soderman M., Pavic L., Edner G., et al. Natural history of dural arteriovenous shunts. Stroke. 2008;39:1735-1739.

96. Strom R.G., Botros J.A., Refai D., et al. Cranial dural arteriovenous fistulae: asymptomatic cortical venous drainage portends less aggressive clinical course. Neurosurgery. 2009;64:241-248.

97. Charpentier C., Audibert G., Guillemin F., et al. Multivariate analysis of predictors of cerebral vasospasm occurrence after aneurysmal subarachnoid hemorrhage. Stroke. 1999;30:1402-1408.

98. Murayama Y., Malisch T., Guglielmi G., et al. Incidence of cerebral vasospasm after endovascular treatment of acutely ruptured aneurysms: report on 69 cases. J Neurosurg. 1997;87:830-835.

99. Bejjani G.K., Bank W.O., Olan W.J., et al. The efficacy and safety of angioplasty for cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery. 1998;42:979-987.

100. Fujii Y., Takahashi A., Yoshimoto T. Effect of balloon angioplasty on high grade symptomatic vasospasm after subarachnoid hemorrhage. Neurosurg Rev. 1995;18:7-13.

101. Haque R., Kellner C.P., Komotar R.J., et al. Mechanical treatment of vasospasm. Neurol Res. 2009;31:638-643.

102. Rosenwasser R.H., Armonda R.A., Thomas J.E., et al. Therapeutic modalities for the management of cerebral vasospasm: timing of endovascular options. Neurosurgery. 1999;44:975-980.