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6. ENDOV ASCULAR Badih Daou and Pascal Jabbour ndovascular neurosurgery has evolved dramati cally since the first description of aneurysm coil ing in 1991 and is now employed as a primary treatment strategy for managing a multitude of cerebro vascular pathologies, including aneurysms, arteriovenous malformations (AVMs), and management of acute ische mic stroke. Endovascular treatment of cerebral aneurysms has frequently replaced craniotomy for clipping in a large population of aneurysms since the publication of the International Subarachnoid Aneurysm T rial (ISA T), which showed better outcomes for endovascular coil occlusion of ruptured aneurysms compared with surgi cal clipping in selected cases. The endovascular approach offers an attractive, minimally invasive alternative for aneurysm treatment with low procedure- related morbid ity and mortality. The durability and long- term efficacy of endovascular interventions is continuously evolving, especially with the introduction of newer coils, stents, and flow- diversion techniques. With the development of catheter and guidewire tech nology and novel embolic materials, endovascular man agement of AVMs has gained significant popularity and has become common practice. Endovascular management of AVMs can be used for presurgical embolization, prera diosurgical intervention, or palliative embolization or as a primary treatment for curative embolization, depending on the characteristics of the lesion. Over the past few decades, the management of stroke has progressed exponentially, beginning with US Food and Drug Administration (FDA) approval of intrave nous recombinant tissue plasminogen activator (r- tPA). Advances in endovascular management of acute stroke have further increased the therapeutic window of r- tPA administration using the intraarterial route and led to the introduction of new devices for clot removal and vessel recanalization. CASE 1 HISTORY AND PHYSICAL EXAMINA TION A 58- year- old woman with a history of migraines presented to the emergency department with the worst headache of her life, accompanied by nausea, vomiting, and dizziness. On physical examination, the patient was lethargic but oriented ×3. She had corneal, gag, and cough reflexes. Pupils were equal and reactive to light. Extraocular muscles were intact. Face was symmetrical. All other cranial nerves were intact. She was moving all extremities with 5/ 5 strength. IMAGING STUDIES Brain computed tomography (CT) demonstrates exten sive subarachnoid hemorrhage (SAH) bilaterally, mainly in the region of the anterior aspect of the corpus callosum/ cingulate gyrus (Figure 6.1). No hydrocephalus or evidence of large territorial infarction is noted. An angiogram is performed and shows a 2– × 1.5- mm anterior communicating artery aneurysm (Figure 6.2). ANALYSIS OF CASE AND SURGICAL PLAN In patients with suspected SAH, a non– contrast- enhanced head CT should be obtained. If CT is nondiagnostic but suspicion is high, a lumbar puncture can be performed. Digital subtraction angiography (DSA) with threedimensional rotational angiography is indicated to confirm the presence of an aneurysm and to devise a treatment plan. A multidisciplinary team is required to determine the best treatment strategy depending on patient and aneurysm characteristics. For ruptured aneurysms amenable to both microsurgical clipping and endovascular coiling, careful consideration of each treatment option should be given.

eurysm and to devise a treatment plan. A multidisciplinary team is required to determine the best treatment strategy depending on patient and aneurysm characteristics. For ruptured aneurysms amenable to both microsurgical clipping and endovascular coiling, careful consideration of each treatment option should be given. Endovascular management of the ruptured aneurysm

eurysm and to devise a treatment plan. A multidisciplinary team is required to determine the best treatment strategy depending on patient and aneurysm characteristics. For ruptured aneurysms amenable to both microsurgical clipping and endovascular coiling, careful consideration of each treatment option should be given. Endovascular management of the ruptured aneurysm 48 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW should be performed early, within 24 to 72 hours aiming at complete obliteration of the aneurysm to reduce the rate of rebleeding after aneurysmal SAH. Aneurysm rebleeding is associated with very high mortality and poor prognosis for functional recovery. The risk for rebleeding is maximum in the first 2 to 12 hours, occurring at a rate of 3% to 4% within the first 24 hours. The ISA T showed a reduction in death and disability from 31% in patients treated with microsurgery to 24% in the endovascular group (relative risk reduction, 24%). The risk for epilepsy and significant cognitive decline was also decreased in the endovascular treatment arm. However, the rate of late rebleeding (2.9% after endovascular repair versus 0.9% after open surgery) was higher with endovas cular treatment, and the rate of complete aneurysm oblit eration was lower in coiled aneurysms (58% versus 81% of clipped aneurysms). In patients with ruptured intracranial aneurysms, endovascular coiling may be favored in older patients (>65 years of age), patients with poor- grade SAH, patients with concomitant vasospasm, and those with pos terior circulation aneurysms (e.g., basilar apex aneurysms). Patients with ruptured middle cerebral artery (MCA) aneurysms, wide- necked aneurysms, aneurysms with one or more branches incorporated into the neck or dome of the aneurysm, and large intraparenchymal hematomas should be considered for microsurgical clipping instead of coiling. Arterial access for endovascular treatment is usually obtained by inserting a sheath through the common femo ral artery and connected to a heparinized flush. A guiding catheter is advanced over a guidewire into the aortic arch. Multiple runs in multiple views are obtained to identify the aneurysm, and then a microcatheter is advanced over a microguidewire into the aneurysm. Coils are available in Figure 6.1 Brain computed tomographic scan demonstrating extensive subarachnoid hemorrhage bilaterally, mainly in the region of the anterior aspect of the corpus callosum/ cingulate gyrus. No hydrocephalus or evidence of large territorial infarction are seen. Figure 6.2 A: Cerebral angiogram showing a 2- × 1.5- mm anterior communicating artery aneurysm. B: Three- dimensional reconstruction showing the aneurysm.

aterally, mainly in the region of the anterior aspect of the corpus callosum/ cingulate gyrus. No hydrocephalus or evidence of large territorial infarction are seen. Figure 6.2 A: Cerebral angiogram showing a 2- × 1.5- mm anterior communicating artery aneurysm. B: Three- dimensional reconstruction showing the aneurysm. E NDO v ASCULAR • 49 many lengths, diameters, and shapes, and some coils have bioactive coatings or volume expanding gels. Coils are designed to be stretch resistant during manipulation or retrieval. The platinum coil wire is delivered through the microcatheter. When coils are inserted into the lumen of the aneurysm, a local thrombus forms that leads to oblit eration of the aneurysmal sac. Endovascular coiling is usu ally performed under general anesthesia for appropriate hemodynamic management and to obtain high- quality images. Neurophysiologic monitoring, including somato sensory evoked potential, electroencephalography, and brainstem auditory evoked potential monitoring, is often used. Patients with high- grade SAH should have intracra nial pressure monitoring with a ventriculostomy and hemodynamic monitoring with a Swan- Ganz catheter and radial arterial line. Between the time of SAH onset and aneurysm obliteration, blood pressure should be controlled with a titratable agent (decrease in systolic blood pressure to <160 mm Hg) to control the risk for stroke, rebleeding, and maintenance of cerebral perfusion pressure. Patients are managed in the intensive care unit after aneurysm therapy with continu ous hemodynamic and neurological monitoring. Imaging follow- up should be performed at 6 months and 1 year and at later time intervals depending on the occlusion status of the aneurysm. If magnetic resonance angiography (MRA) or computed tomographic angiography (CT A) shows evi dence of recurrence, an angiogram should be performed. Long- term aneurysm recurrence after coiling occurs in about one fifth of all coiled cerebral aneurysms, and 10% of coiled aneurysms require another intervention. Cerebral vasospasm affects approximately 60% to 70% of patients after SAH, resulting in symptomatic ischemia in approximately half of these patients. V asospasm occurs most frequently 7 to 10 days after aneurysm rupture. T ranscranial Doppler can be used to monitor for the development of arterial vasospasm. Oral nimodipine should be admin istered to all patients with aneurysmal SAH. Initial man agement of vasospasm consists of hyperdynamic therapy including hypervolemia, hemodilution, and induced hypertension. In patients who are refractory to medical therapy, cerebral angioplasty or intraarterial vasodilator therapy in the affected territory may be beneficial in improving angiographic and clinical outcome, if performed in a timely manner. Patients who develop acute hydrocephalus are usually managed by external ventricular drainage (EVD) or lumbar drainage. The patient had placement of a ventriculostomy cath eter and was emergently taken to the interventional neu roradiology suite for an angiogram, which showed an anterior communicating artery aneurysm. The decision was made to coil the aneurysm. With a Seldinger tech nique, the right- sided femoral artery was catheterized with a 7- French sheath hooked to continuous heparinized flush. A guidewire and a catheter were introduced into the descending aorta up to the arch. Selectively, the left inter nal carotid artery (ICA) was catheterized. Superselectively, the aneurysm was catheterized, then embolization with coils was performed. A  16- month follow- up angiogram in this case shows complete occlusion of the aneurysm (Figure 6.3). COMPLICA TIONS Complications related to endovascular treatment of intra cranial aneurysms can arise during different phases of treatment.

vely, the aneurysm was catheterized, then embolization with coils was performed. A  16- month follow- up angiogram in this case shows complete occlusion of the aneurysm (Figure 6.3). COMPLICA TIONS Complications related to endovascular treatment of intra cranial aneurysms can arise during different phases of treatment. Complication rates depend on patient characteristics (e.g., vascular tortuosity, atherosclerotic disease, and resis tance to antiplatelet therapy), on aneurysm- related factors (e.g., size, shape, and location), and on operator experience. The main complications related to endovascular treatment include thromboembolic complications, intraprocedural aneurysm rupture, and access- related complications. Thromboembolic complications with resultant ischemic symptoms occur at a rate of about 5% and depend highly on the use of antiplatelet treatment before intervention and on the concurrent use of balloon- or stent- assisted techniques. If thromboembolic complications are detected during the Figure 6.3 A 16- month follow- up angiogram showing complete occlusion of the aneurysm.

toms occur at a rate of about 5% and depend highly on the use of antiplatelet treatment before intervention and on the concurrent use of balloon- or stent- assisted techniques. If thromboembolic complications are detected during the Figure 6.3 A 16- month follow- up angiogram showing complete occlusion of the aneurysm. 50 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW procedure, adequate heparinization should be confirmed by activated clotting time (ACT) measurements. If the patient is adequately heparinized and a branch occlusion is seen, pharmacologic thrombolysis using tPA or intraarterial antiplatelet agents (glycoprotein IIb/ IIIa receptor antagonists) can be used, or mechanical thrombolysis can be performed in the case of significant branch occlusions. The aneurysm should be well coiled before thrombolytic treatment to avoid aneurysm rerupture. Intraprocedural aneurysm rupture has been reported to occur in 1% to 5% of coil embolization procedures. Risk factors for intraprocedural rupture include ruptured aneurysm status, lower initial Hunt and Hess Stroke Scale grade, small aneurysm size, and low operator experience. Intraprocedural aneurysm rupture is associated with a significant risk for permanent neurological disability and death (38% for ruptured aneurysms and 29% for unrup tured aneurysms). It may be accompanied by a sudden and massive rise in blood pressure with or without bradycardia attributable to an elevation in intracranial pressure. When intraoperative aneurysm rupture is encountered, protamine should be given if the patient is heparinized. For perfora tions at the aneurysm dome, rapid packing with coils can be performed, and a balloon can be inflated for temporary parent artery occlusion. For aneurysms perforated at the neck or parent vessel, parent vessel occlusion or a salvage technique using a balloon and liquid embolic agents can be considered. Intracranial pressure should be aggressively controlled after securing the aneurysm with ventricular drainage and medical management (e.g., hyperventilation and osmotic diuresis). A CT scan should be performed to rule out a large intraparenchymal hemorrhage that may require evacuation. Finally, if antiplatelet agents were administered, the patient should receive platelet transfu sions when indicated. Aneurysm rerupture and rehemorrhage following endovascular coiling is strongly related to the degree of aneurysm occlusion. Long- term follow- up is necessary to monitor for that risk. CASE 2 HISTORY AND PHYSICAL EXAMINA TION A 68- year- old woman presented to the clinic with persis tent headaches of several months’ duration and two recent episodes of diplopia. The patient has a family history of aneurysmal SAH. On physical examination, the patient was neurologically intact. IMAGING STUDIES A head CT does not show any evidence of acute intracra nial hemorrhage (Figure 6.4). CT angiography shows the presence of a 10- mm, wide- necked aneurysm arising from the right cavernous ICA and projecting anteromedially (Figure 6.5). It is lobulated in appearance. An angiogram is performed and shows the right cavernous ICA aneurysm (Figure 6.6). ANALYSIS OF CASE AND SURGICAL PLAN Unruptured intracranial aneurysms (UIAs) are found in about 3.2% of the adult population. They are being found with an increasing frequency because of the wide spread use of magnetic resonance imaging (MRI). UIAs may also be discovered when patients present with cranial nerve deficits (most commonly a third nerve palsy), sei zures, mass effect, or motor and sensory deficits. Initial imaging should provide a complete evaluation of the anatomy of the aneurysm with accurate measurement of the neck size, neck- to- dome ratio, and relationship to the surrounding vessels.

esent with cranial nerve deficits (most commonly a third nerve palsy), sei zures, mass effect, or motor and sensory deficits. Initial imaging should provide a complete evaluation of the anatomy of the aneurysm with accurate measurement of the neck size, neck- to- dome ratio, and relationship to the surrounding vessels. The techniques of aneurysm imaging have expanded greatly, with MRA, CT A, and DSA being performed with high sensitivity and specificity. CT A is Figure 6.4 Non– contrast- enhanced brain computed tomography showing no acute intracranial hemorrhage and no abnormal extraaxial fluid collection. E NDO v ASCULAR • 51 frequently added to the non– contrast- enhanced head CT to assist diagnosis. DSA remains the “gold standard” of aneurysm diagnosis. Overall, the annual rupture rate of UIAs is about 1%. Risk factors for rupture include patient characteristics that consist of increasing patient age, female sex, cigarette smoking, hypertension, prior personal history of SAH from a different aneurysm, and family history of SAH. Risk fac tors related to aneurysm features include larger aneurysm size; aneurysm morphology (increased rupture risk with aneurysms that have daughter sacs); documented aneu rysmal growth during follow- up; aneurysm location in the posterior circulation, posterior communicating artery, or anterior communicating artery; and symptomatic sta tus of the UIA. All of these factors should be considered in selecting the optimal management of UIAs. The treat ment strategies for UIA include conservative management, endovascular intervention, and surgical treatment. Given that the patient in our case had a positive family history of SAH, a symptomatic aneurysm, and an aneurysm at least 10  mm in size, she was strongly considered to undergo aneurysm treatment. For patients with small aneurysms (<10  mm) without a family or personal history of SAH, with small asymptomatic UIAs, and with low hemorrhage Figure 6.5 Computed tomographic angiogram showing the presence of A: A 10- mm wide- necked aneurysm arising from the right cavernous internal carotid artery and B: Projecting anteromedially. It is lobulated in appearance. A B Figure 6.6 A: Cerebral angiogram, right internal carotid artery injection showing a 10- mm right cavernous carotid artery aneurysm. B: Threedimensional reconstruction showing the 10- mm aneurysm.

rising from the right cavernous internal carotid artery and B: Projecting anteromedially. It is lobulated in appearance. A B Figure 6.6 A: Cerebral angiogram, right internal carotid artery injection showing a 10- mm right cavernous carotid artery aneurysm. B: Threedimensional reconstruction showing the 10- mm aneurysm. 52 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW risk by location, size, and morphology, observation with periodic follow- up imaging can be performed. If changes in aneurysm size or morphology are documented, treatment should be strongly considered. Although surgical clipping is an effective treatment for UIAs, treatment strategies of UIAs have shifted dramatically toward endovascular ther apy. Patients with UIAs who are considered for treatment should be fully informed about the risks and benefits of both strategies. Patient age, presence of medical comorbidities, and aneurysm characteristics should be carefully taken into consideration because these are strong predictors of perioperative morbidity and rupture risk. In older patients (in this case, a 68- year- old patient), the benefit of endo vascular treatment compared with surgery appears to be greater, especially because the rate of surgical complications is higher in this age group. Endovascular management is associated with a reduction in procedural morbidity, length of hospital stay, and mortality compared with surgical clipping in selected cases; however, endovascular treatment has an overall higher risk for recurrence than microsurgical treatment, and the latter confers more durable protection against aneurysm regrowth. Coiling represents the most commonly employed endovascular strategy. However, large, giant and widenecked aneurysms tend to have higher recurrence and retreatment rates after coiling. Several technologies are available to target these lesions, including stent placement, stent- assisted coiling, and flow diversion. Recanalization and retreatment rates are lower with these techniques. The Pipeline Embolization Device (PED) was used in this case because of the size and wide neck of the aneurysm. The PED is FDA approved for the treatment of large and giant wide- neck aneurysms in the ICA, from the petrous to the superior hypophyseal segments. The PED belongs to a family of devices known as flow diverters, which work by acting as a scaffold for endothelial overgrowth of the aneurysm neck and cause parent vessel remodeling. The main structural differences from previous stents are the higher metal surface area coverage and the low poros ity, which allows more flow reduction into the aneurysm neck. The PED has gained popularity because it pro vides a more physiologic and durable treatment strategy compared with other endovascular interventions, and studies have confirmed its high success rate in achieving aneurysm occlusion and low aneurysm recurrence and retreatment rates. For endovascularly treated aneurysms, follow- up imaging with DSA or noninvasive methods is usually performed 6 months to 1 year after treatment. Later follow- up imaging can be obtained depending on the occlusion status of the aneurysm because residual aneurysms can still present with late hemorrhages and aneurysm recurrences. This patient’s UIA was treated using the PED. She was started on 75 mg/ day of clopidogrel and 81 mg/ day of aspirin 10  days before the intervention. Preoperative P2Y12 reaction unit values were checked to assess platelet inhi bition in response to clopidogrel, with a target therapeu tic range between 60 and 240. During the procedure, the patient received a bolus of intravenous heparin to main tain an activated clotting time that was 2 to 3 times her baseline. T reatment was performed under general anesthesia.

checked to assess platelet inhi bition in response to clopidogrel, with a target therapeu tic range between 60 and 240. During the procedure, the patient received a bolus of intravenous heparin to main tain an activated clotting time that was 2 to 3 times her baseline. T reatment was performed under general anesthesia. Her motor evoked potentials, somatosensory evoked potentials, and brainstem evoked potentials were moni tored, and they were stable throughout the procedure. An angiographic evaluation was obtained to assess the dimen sions of the aneurysms. An 8- French femoral sheath was used for access. A  6- French shuttle sheath was placed in the carotid bulb, and a catheter was placed at the level of the petrocavernous carotid junction. A  microcatheter was then introduced distally to the M1- M2 junction. The PED was sized according to the width of the inflow vessel to avoid any endoleak. The PED was introduced through the microcatheter. After embolization was accomplished, a control angiogram was obtained. Heparin was stopped at the end of the procedure. After conclusion of the proce dure, the catheters and sheaths were removed, and manual compression was applied for 20 minutes to achieve hemo stasis. The site was checked for further bleeding, and the leg was immobilized. After discharge, the patient was scheduled for clinical follow- up and a follow- up angio gram. A  follow- up angiogram performed at 6  months in this case showed complete obliteration of the aneurysm (Figure 6.7). COMPLICA TIONS Risks common to all procedures with endovascular access include vascular injury, vessel dissection, and perforation or aneurysm rupture. Patients with access- related complications (groin complications), including groin hematomas, retroperitoneal hematomas, fistulas, and pseudoaneurysms, may present with severe pain at the puncture site with or without hemodynamic instability. Management consists of manual compression, abdominal and pelvic CT to check for hemorrhage, volume expansion with intravenous fluids, transfusion if needed, and reversal of antithrombotic treatment if necessary. The main complications related to treatment with the PED and other stents can be grouped into thromboembolic and hemorrhagic complications. Because the PED consists

pelvic CT to check for hemorrhage, volume expansion with intravenous fluids, transfusion if needed, and reversal of antithrombotic treatment if necessary. The main complications related to treatment with the PED and other stents can be grouped into thromboembolic and hemorrhagic complications. Because the PED consists E NDO v ASCULAR • 53 of a bare metal stent that aids in neointimal tissue forma tion, platelet activation can result in local thrombosis with cerebral infarction or distal embolization. For this reason, patients who are scheduled to undergo stent placement require a preoperative administration of a dual antiplatelet therapy including clopidogrel and Aspirin for about 10 days before the intervention to prevent stent thrombosis. This, however, may facilitate the occurrence of hemorrhagic complications, mainly intraparenchymal hemorrhage. CASE 3 HISTORY AND PHYSICAL EXAMINA TION A 21- year- old man presented after having a new- onset secondary generalized tonic- clonic seizure accompanied by 30 minutes of postictal confusion. On presentation, the patient was awake, alert, and oriented ×3. He was neuro logically intact on physical examination. IMAGING STUDIES A head CT shows a focal hyperdensity in the left temporal lobe which has a tubular configuration and may represent an arteriovenous malformation (Figure 6.8). An angiogram is performed and shows a left temporal lobe arteriovenous malformation, 2.4 × 2 × 2.3  cm with superficial venous drainage (Figure 6.9). ANALYSIS OF CASE AND SURGICAL PLAN Patients with brain AVM most commonly present with hemorrhage, with intraparenchymal hemorrhage being the most common followed by SAH and intraventricular hemorrhage. The second most common presentation is seizures. Less common presentations include headache, focal neurological deficit, and as an incidental finding. The risks of treating unruptured brain AVM must be weighed against the natural history of the lesion. The annual risk of first hemorrhage has been reported to be 2% to 4%. The features most consistently associated with an increased risk for hemorrhage include deep venous drain age, a single draining vein, high feeder mean arterial pres sure, small nidus size, associated aneurysms, and deep or posterior fossa locations. ARUBA (A Randomized T rial of Unruptured Brain Arteriovenous Malformations), however, concluded that medical management alone is superior to combined medical and interventional treatment for the prevention of death or stroke in unruptured brain AVMs followed for 33 months. Longer follow- up is still required to confirm these findings. Complete angiographic evaluation should be per formed to assess the arterial supply of the AVM, the char acteristics of the nidus, and identification of the venous drainage for planning the treatment strategy. AVMs dem onstrate arteriovenous shunting on angiography, resulting in early opacification of the draining veins and a decrease in the arteriovenous transit time. Figure 6.7 Lateral (A) and anterior (B) views on a 6- month follow- up angiogram with right internal carotid artery injection showing complete occlusion of the aneurysm with no in- stent stenosis.

ng on angiography, resulting in early opacification of the draining veins and a decrease in the arteriovenous transit time. Figure 6.7 Lateral (A) and anterior (B) views on a 6- month follow- up angiogram with right internal carotid artery injection showing complete occlusion of the aneurysm with no in- stent stenosis. 54 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW The Spetzler- Martin grading system is the most widely used for grading AVMs to predict operative morbidity and mortality. The system employs three criteria: brain AVM size, the venous drainage pattern, and the eloquence of adjacent brain parenchyma. The lesion in this case is a Spetzler- Martin grade 2 AVM (<3 cm, in an eloquent location with superficial venous drainage). Figure 6.8 Non– contrast- enhanced brain computed tomographic scan showing focal hyperdensity in the left temporal lobe that has a tubular configuration. Both on A: Above windows and B: Below windows. Figure 6.9 Lateral (A) and anterior (B) views on a cerebral angiogram with left internal carotid artery injection showing a 2.4- × 2- × 2.3- cm anterior pole arteriovenous malformation with superficial venous drainage and arterial feeders from the distal M3 and M4 branches.

oth on A: Above windows and B: Below windows. Figure 6.9 Lateral (A) and anterior (B) views on a cerebral angiogram with left internal carotid artery injection showing a 2.4- × 2- × 2.3- cm anterior pole arteriovenous malformation with superficial venous drainage and arterial feeders from the distal M3 and M4 branches. E NDO v ASCULAR • 55 Definitive treatment of a brain AVM requires its com plete obliteration to prevent subsequent hemorrhage. Therapeutic options include endovascular embolization, surgery, stereotactic radiosurgery, or combined therapies. Although surgical resection remains the standard for the definitive treatment of most intracranial AVMs, endovascular management can be used for presurgical embolization to improve the safety and efficacy of the procedure. Presurgical embolization can be used for large or giant cortical AVMs to reduce the blood flow within the nidus, to embolize deep and surgically inaccessible arterial feeders, or to occlude associated intranidal aneurysms. This can be achieved with low morbidity and mortality. Preoperative embolization of AVMs can reduce operative time and intraoperative blood loss, makes surgical resection easier, results in less postop erative neurological deficits and postoperative epilepsy compared with surgical treatment alone, and does not present with significantly more complications than surgery alone. Presurgical embolization can also convert inoperable Spetzler- Martin high- grade lesions to lower grade AVMs that can be amenable to surgical treatment. Endovascular management can be used for emboliza tion of AVMs before radiosurgical treatment to reduce the nidus size. Smaller lesions (<3 cm in diameter) have a higher cure rate and a lower morbidity rate after radiosurgery. Preradiosurgical embolization may also be used to occlude arterial feeder or intranidal aneurysms to reduce the risk for hemorrhage and to target large high- flow AVMs, which are less sensitive to radiosurgery. Endovascular embolization can also be used to treat residual lesions that persist after radiosurgery. Endovascular treatment can be employed for palliative embolization in patients with progressive or refractory neurological deficits secondary to high flow or venous hyper tension and seizures. However, palliative embolization does not eliminate the risk for bleeding. Partial AVM emboli zation is not recommended as the only strategy for AVM management; however, it can be used as part of a treatment plan aimed at staged AVM obliteration. Endovascular embolization can be used as the primary treatment for some AVMs for curative embolization. There are several factors that determine the efficacy of emboliza tion for curative purposes. Smaller AVMs and AVMs with a low number of arterial feeders are more likely to achieve complete cure following endovascular embolization. Superficial AVMs, lesions in noneloquent locations, and those with an overall lower Spetzler- Martin grade are more likely to be cured as well. Embolic agents used in brain AVM management con sist of solid agents (e.g., coils, silk threads, balloons, and particulates such as polyvinyl alcohol) and liquids agents (e.g., cyanoacrylates, Onyx, and ethanol). The most com monly used agents are the liquid agents n- butyl cyano acrylate (NBCA) and Onyx, which is a premixed, liquid embolic agent that consists of ethylene- vinyl alcohol copolymer and tantalum powder for radiopacity, dissolved in dimethyl sulfoxide.

) and liquids agents (e.g., cyanoacrylates, Onyx, and ethanol). The most com monly used agents are the liquid agents n- butyl cyano acrylate (NBCA) and Onyx, which is a premixed, liquid embolic agent that consists of ethylene- vinyl alcohol copolymer and tantalum powder for radiopacity, dissolved in dimethyl sulfoxide. Onyx was preferred in this case for multiple reasons: it has a lower thrombogenicity and causes less inflammation than NBCA; it has a nonadhesive nature that decreases the risk for adherence of the catheter to the ves sel wall; it allows for longer, slower, and more controlled injections with better penetration into the AVM; it offers better handling during later surgical intervention; and recent studies have demonstrated that embolization using Onyx results in complete occlusion in 50% of appropriately selected cases. Patients are observed in the neurointensive care unit following AVM embolization. Mild hypotension may be induced for 24 hours after embolization of a large, highflow AVM. In patients for whom the treatment plan includes other sessions, additional embolization procedures are staged every 3 to 4 weeks. Follow- up imaging is crucial for any incompletely obliterated lesion. In the present case, initial endovascular emboliza tion was performed for management of seizures. Because the AVM had accessible arterial feeders from the distal M3 and M4 branches, endovascular management was attempted. T wo embolization sessions using Onyx resulted in angiographic cure of the AVM (Figure 6.10). For both procedures, general anesthesia was induced. The right common femoral artery was catheterized with a 7- French sheath, hooked to continuous heparinized flush. With a 6- French catheter and a guidewire, the aorta was ascended up the arch. Selectively, the left ICA was catheterized. At that point, superselectively, the M3 and M4 pedicles were microcatheterized followed by embolization using Onyx. The microcatheter was then removed. A  control cerebral angiogram showed a significant decrease in the size of the AVM after the first intervention and angiographic cure after the second treatment session. Manual compression was held for 20 minutes in the right groin. The patient was neurologically intact. COMPLICA TIONS Most complications related to AVM embolization are related to hemorrhagic and ischemic events. The combined major morbidity and mortality rates from embolization with ethylene- vinyl alcohol copolymer are quoted to be 10%. Complication rates that have been reported depend

tient was neurologically intact. COMPLICA TIONS Most complications related to AVM embolization are related to hemorrhagic and ischemic events. The combined major morbidity and mortality rates from embolization with ethylene- vinyl alcohol copolymer are quoted to be 10%. Complication rates that have been reported depend 56 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW on patient selection, AVM characteristics, and agents used. Intracerebral hemorrhage can be the result of techni cal factors, including arterial dissection or perforation by the microwire or microcatheter, rupture of an associated aneurysm, and vascular injuries during catheter retrieval. Hemorrhage may also be the result of hemodynamic changes related to the embolization procedure, which may result in a reduction of flow through the fistulous nidus with stagnation in the draining veins. This can lead to venous outflow thrombosis and a delayed hemorrhage or a venous infarct. Embolization of large, high- flow AVMs can result in normal perfusion pressure breakthrough and hemorrhage. This is due to a sudden elevation in arterial pressure and a decrease in venous pressure, decreasing cerebral per fusion pressure in patients with impaired autoregulation. The resulting parenchymal hyperperfusion can cause cere bral edema or hemorrhage. If a hematoma is encountered, immediate intubation, hyperventilation, osmotic diuresis, barbiturate anesthesia, and emergent surgical evacuation are indicated. Ischemic stroke may result from arterial dissection related to microcatheter or guidewire manipulation, occlusion of normal arterial branches by the embolic agent, reflux of the embolic material into normal cere bral vasculature, and showering of glue droplets during retrieval of the microcatheter. Brain AVM embolization requires advancing a suitable microcatheter into the dis tal aspect of the arterial feeder to the nidus. Neurological deficits may be caused by embolization of branches aris ing from feeders that supply normal brain parenchyma. Provocative testing (the superselective W ada test) can be performed to determine the safety of embolization. Intraarterial injection of amobarbital through the micro catheter placed at the site of planned embolization is performed, and appropriate neurological and neurophysi ologic testing is carried out. Pulmonary emboli are uncommon but have occurred with the use of embolic agents. Complications such as groin hematoma or dissection and other complications related to endovascular intervention such as contrast allergy, infec tion, and nephrotoxicity may occur as well. CASE 4 HISTORY AND PHYSICAL EXAMINA TION A 77- year- old man with a history of hypertension and hyperlipidemia presents with a right- sided hemiplegia and aphasia. The patient was last seen normal 5 hours ago. On Figure 6.10 Lateral (A) and anterior (B) views on a postembolization cerebral angiogram with left internal carotid artery injection showing no evidence of an arteriovenous malformation, no clear nidus, no shunting, and no abnormal venous drainage.

hemiplegia and aphasia. The patient was last seen normal 5 hours ago. On Figure 6.10 Lateral (A) and anterior (B) views on a postembolization cerebral angiogram with left internal carotid artery injection showing no evidence of an arteriovenous malformation, no clear nidus, no shunting, and no abnormal venous drainage. E NDO v ASCULAR • 57 neurologic examination, the patient has global aphasia and is not following commands. Cranial nerves are notable for left gaze preference and right facial weakness. Motor strength was notable for antigravity spontaneously in the left upper and lower extremity, 3/ 5 in the right upper and 2/ 5 in the right lower extremity. The National Institutes of Health Stroke Scale score was 22. IMAGING STUDIES Non– contrast- enhanced head CT shows loss of graywhite differentiation within the left insular ribbon con sistent with early left MCA territory infarct, without evidence of hemorrhage (Figure 6.11). CT A shows focal tapering cutoff of the left ICA just distal to the bifurca tion (Figure 6.12). The left ICA reconstitutes intracrani ally at the level of the left posterior communicating artery. Focal cutoff of the left MCA at the proximal M1 segment, with no significant opacification of distal MCA branches, is seen. CT perfusion shows increased mean transit time (Figure 6.13) and decreased cerebral blood flow (Figure 6.14) involving nearly the entire left MCA territory, with a smaller area of decreased cerebral blood volume (Figure 6.15). ANALYSIS OF CASE AND SURGICAL PLAN Given the narrow therapeutic window for treatment of acute ischemic stroke, timely evaluation and diagnosis are vital. The initial evaluation of a potential stroke patient begins with immediate stabilization of the airway, breathing, and circulation. This is quickly followed by an assessment of neurological deficits and possible comorbidities. Emergency non– contrast- enhanced head CT is recommended before initiating any specific therapy to treat acute ischemic stroke to exclude intracerebral hemorrhage. Laboratory tests to consider in all patients include blood glucose, electrolytes with renal function studies, complete blood count with platelet count, cardiac markers, prothrombin time, inter national normalized ratio, and activated partial thrombo plastin time. Intravenous fibrinolytic therapy with r- tPA (0.9 mg/ kg, maximal dose 90 mg) is recommended in patients presenting within 4.5 hours of onset of ischemic stroke and should not be delayed while awaiting coagula tion studies unless a coagulopathy is suspected. Timely brain imaging and interpretation are critical. A  noninvasive intracranial vascular study (CT A, MRA) should be performed during initial imaging if either intra arterial fibrinolysis or mechanical thrombectomy is being considered to evaluate the size, location, and vascular dis tribution of the infarction and document the presence of large- vessel occlusion. CT perfusion and MRI perfusion and diffusion imaging provide measures of infarct core and penumbra size to evaluate the degree of reversibility of ischemic injury. They play an important role in the selection of patients with “salvageable” tissue for acute reperfusion therapy. A  scan consistent with a mismatch between cerebral blood volume and cerebral blood flow or mean transient time is a favorable patient selection criterion. Stroke imag ing should not delay intravenous r- tPA therapy. Mechanical thrombectomy devices seek to salvage ischemic, but not yet fully infracted, brain tissue by restoring perfusion through the occluded artery. It can be used as a primary reperfusion strategy or in conjunction with phar macologic fibrinolysis. It is most effective when performed as early as possible.

therapy. Mechanical thrombectomy devices seek to salvage ischemic, but not yet fully infracted, brain tissue by restoring perfusion through the occluded artery. It can be used as a primary reperfusion strategy or in conjunction with phar macologic fibrinolysis. It is most effective when performed as early as possible. The initial goal of mechanical thrombectomy is to achieve recanalization, defined by a Thrombolysis in Cerebral Infarction (TICI) grade of 2b (complete filling of all of the expected vascular territory is visualized but the filling is slower than normal) or 3 (complete perfusion). Mechanical thrombectomy should be considered in patients with neuroimaging excluding hemorrhage, with a small infarct core (patients with large territorial infarcts on CT scan are at a higher risk for hemorrhagic conversion following treatment) and large artery occlusion in the proxi mal anterior circulation, as demonstrated on CT A, MRA, Figure 6.11 Non– contrast- enhanced head computed tomography shows loss of gray- white differentiation within the left insular ribbon consistent and early left middle cerebral artery territory infarct, without hemorrhage.

t) and large artery occlusion in the proxi mal anterior circulation, as demonstrated on CT A, MRA, Figure 6.11 Non– contrast- enhanced head computed tomography shows loss of gray- white differentiation within the left insular ribbon consistent and early left middle cerebral artery territory infarct, without hemorrhage. 58 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW or DSA. Mechanical thrombectomy should not prevent the initiation of intravenous thrombolysis when indicated. If intravenous thrombolysis is contraindicated, mechanical thrombectomy should be considered as first- line treatment if the patient is eligible. Mechanical thrombectomy should be performed as soon as possible and within 8 hours of stroke symptom onset when indicated. The decision to proceed with mechanical thrombectomy should be made by a multidisciplinary team and performed by an experienced neurointerventionalist in centers providing comprehensive stroke care. There are currently four mechanical thrombectomy devices that are approved for clot removal in selected patients. The Merci Retrieval System is a coil retrieval device that is composed of a memory- shaped nitinol wire. The Penumbra System is an aspiration device that employs vacuum aspiration to remove the thrombus from the occluded vessel. The Solitaire Flow Restoration Device and the T revo device are stent- retriever devices that employ a self- expanding stent deployed within the thrombus, push ing it aside and incorporating it within the stent’s struts followed by extraction of the thrombus. Intraarterial treatment with mechanical thrombectomy reduces disability and improves outcomes and functional independence and is superior to intravenous thrombolysis alone in eli gible patients with proximal large artery occlusions in the Figure 6.12 A: Computed tomographic angiogram shows focal tapering cutoff of the left internal carotid artery (ICA) just distal to the bifurcation (Arrow). The left ICA reconstitutes intracranially at the level of the left posterior communicating artery. B: Focal cutoff of the left middle cerebral artery (MCA) at the proximal M1 segment (Arrow), with no significant opacification of distal MCA branches. Figure 6.13 There is increased mean transit time involving nearly the entire left middle cerebral artery territory, with sparing of a small portion of the left basal ganglia. Figure 6.14 There is decreased cerebral blood flow involving nearly the entire left middle cerebral artery territory, with sparing of a small portion of the left basal ganglia.

mean transit time involving nearly the entire left middle cerebral artery territory, with sparing of a small portion of the left basal ganglia. Figure 6.14 There is decreased cerebral blood flow involving nearly the entire left middle cerebral artery territory, with sparing of a small portion of the left basal ganglia. E NDO v ASCULAR • 59 anterior circulation. Second- generation stent- retriever devices seem to have the best safety and efficacy profiles. For this reason, the Solitaire flow- restoration device was used in the present case. Acute interventions are most commonly performed under general anesthesia to improve procedural safety and efficacy. Femoral access is established in the symp tomatic lower extremity, if possible. An angiogram is performed for a detailed examination of the cerebro vascular anatomy and to note any proximal stenosis or occlusion. Proximal vessel disease may require immediate treatment with balloon angioplasty or stenting, or both, to allow access to the intracranial pathology. Patients are admitted to the neurointensive care or stroke unit after treatment with monitoring of hemodynamic and neuro logical status. This patient was treated using the Solitaire device. Bilateral groins were prepared and draped in a sterile fashion. With a Seldinger technique, the right femoral artery was catheterized with a 6- French sheath hooked to a continuous heparinized flush. A  guidewire and a cath eter were introduced into the descending aorta up to the arch. Selectively, the left ICA was catheterized showing an M1 occlusion. Superselectively, the M2 was catheterized. Mechanical thrombectomy with Solitaire was then per formed. TICI grade 3 recanalization was achieved after two passes (Figure 6.16— before mechanical thrombectomy; Figure 6.17— after thrombectomy). The patient had an excellent recovery and had a modified Rankin scale score of 2 at the 3- month follow- up. Figure 6.15 There is a much smaller area of decreased cerebral blood volume involving a portion of the left basal ganglia, left corona radiata, and insular cortex, extending into the left anterior temporal lobe. In the more peripheral left middle cerebral artery territory, there is normal to increased cerebral blood volume. Figure 6.16 Cerebral angiogram with left internal carotid artery injection shows an M1 occlusion. Figure 6.17 Cerebral angiogram with left internal carotid artery injection after mechanical thrombectomy with the Solitaire device shows resolution of the occlusion with a Thrombolysis in Cerebral Infarction grade 3 recanalization.

16 Cerebral angiogram with left internal carotid artery injection shows an M1 occlusion. Figure 6.17 Cerebral angiogram with left internal carotid artery injection after mechanical thrombectomy with the Solitaire device shows resolution of the occlusion with a Thrombolysis in Cerebral Infarction grade 3 recanalization. 60 • G OODMAN ’S N EUROSURGERY O RAL B OARD R E v IEW COMPLICA TIONS Mechanical thrombectomy for acute ischemic stroke is associated with several risks. Symptomatic intracerebral hemorrhage occurs in 10% of patients with first- generation Merci and Penumbra devices but is substantially lower with stent- retriever devices (2% to 6%). A head CT can be obtained after the endovascular procedure. In patients with asymptomatic and small hemorrhages, conservative treat ment is warranted (heparin reversal, fresh frozen plasma and platelet transfusion, tight blood pressure control). In patients with symptomatic and significant hemorrhage, medical measures, intubation, mannitol, ventriculostomy (in the case of symptomatic hydrocephalus), and craniot omy for clot evacuation should be considered. T rauma to the vessel wall can arise from endovascular manipulation resulting in permanent vascular injury, vessel rupture, and SAH. This is especially of concern in old, fri able vessels. Fragmentation of the target thrombus during clot removal may result in embolization of dislodged clot material to the distal circulation, resulting in additional ischemic threats. BIBLIOGRAPHY 1. Berkhemer OA, Fransen PS, Beumer D, et  al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med . 2015;372(1):11– 20. 2. Connolly ESJr, Rabinstein AA, Carhuapoma JR, et  al. Guidelines for the management of aneurysmal subarachnoid hemor rhage: A guideline for healthcare professionals from the American Heart Association/ American Stroke Association. Stroke. 2012;43(6):1711– 1737. 3. Molyneux AJ, Kerr RS, Y u LM, et  al. International subarachnoid aneurysm trial (ISA T) of neurosurgical clipping versus endovas cular coiling in 2143 patients with ruptured intracranial aneu rysms: A randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. 2005;366(9488):809– 817. 4. Morgan MK, Davidson AS, Koustais S, Simons M, Ritson EA. The failure of preoperative ethylene- vinyl alcohol copolymer emboliza tion to improve outcomes in arteriovenous malformation manage ment: case series. J Neurosurg. 2013;118(5):969– 977. 5. UCAS Japan Investigators, Morita A, Kirino T, et  al. The natural course of unruptured cerebral aneurysms in a Japanese cohort. N Engl J Med. 2012;366(26):2474– 2482. 6. Ogilvy CS, Stieg PE, Awad I, et  al. Recommendations for the management of intracranial arteriovenous malformations:  A  state ment for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association. Circulation. 2001;103(21):2644– 2657. 7. Saver JL, Jahan R, Levy EI, et  al. Solitaire flow restoration device versus the Merci Retriever in patients with acute ischaemic stroke (SWIFT):  A  randomised, parallel- group, non- inferiority trial. Lancet. 2012;380(9849):1241– 1249. 8. Starke RM, Komotar RJ, Otten ML, et al. Adjuvant embolization with N- butyl cyanoacrylate in the treatment of cerebral arteriove nous malformations:  outcomes, complications, and predictors of neurologic deficits. Stroke. 2009;40(8):2783– 2790. 9. Thompson BG, Brown RDJr, Amin- Hanjani S, et  al. Guidelines for the management of patients with unruptured intracranial aneurysms:  A  guideline for healthcare professionals from the American Heart Association/ American Stroke Association. Stroke. 2015;46(8):2368– 2400. 10. Wiebers DO, Whisnant JP, Huston J 3rd, et al.

hompson BG, Brown RDJr, Amin- Hanjani S, et  al. Guidelines for the management of patients with unruptured intracranial aneurysms:  A  guideline for healthcare professionals from the American Heart Association/ American Stroke Association. Stroke. 2015;46(8):2368– 2400. 10. Wiebers DO, Whisnant JP, Huston J 3rd, et al. Unruptured intracranial aneurysms: Natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet. 2003;362(9378):103– 110.