Embolization Therapy: Principles and Clinical Applications, 1 Ed.

Vascular Tumors

Robert F. James • Lacey B. Martin • John R. Gaughen, Jr • William J. Mack

Highly vascular tumors of the head and neck often pose significant surgical challenges. Bleeding can result in decreased operative visibility and inadvertent injury to adjacent vital structures. Significant blood loss and volume depletion can lead to major morbidities. Embolization of vascular head and neck tumors before surgical resection may help to minimize blood loss, reduce operative time, and facilitate surgical resection. However, the additional endovascular procedure is not without risk to the patient. Multiple anastomotic connections exist between the arteries of the head and neck. Aberrant embolization through these channels can lead to neurologic injuries such as visual loss, paralysis, or ischemic injury to the cranial nerves. It is imperative that the interventionalist and the operating surgeon discuss the goals of embolization and the overall treatment plan before the endovascular procedure. The most common vascular tumors of the head and neck region suitable for preoperative embolization include meningiomas, paragangliomas, juvenile nasopharyngeal angiofibromas, hemangiopericytomas, and hemangioblastomas. Here we will discuss the relevant procedure-related devices and materials, techniques, clinical applications, and potential complications. Most discussion focuses on meningiomas as they are the most frequently encountered of the vascular head and neck tumors. Subsections are devoted to specific concerns for the other tumor types. Table 16.1 details important dangerous anastomoses with the cranial nerve blood supply.

DEVICE/MATERIAL DESCRIPTION

Catheters

A coaxial system of an outer guide catheter and an inner microcatheter is usually employed for transarterial endovascular embolization. We typically use guide catheters with a 0.053-in or 0.070-in inner diameter. The 6-Fr 070 Neuron guide catheter (0.070-in inner diameter; Penumbra, Inc., Alameda, California) can be used for the internal carotid artery (ICA) access, the 053 Neuron guide catheter for the external carotid artery (ECA) (0.053-in inner diameter), and either the 053 or 070 Neuron guide catheter for the vertebral artery (VA), depending on vessel diameter.

There are various-sized microcatheters with multiple features that are beyond the scope of this chapter. The Echelon-10 and Marathon (Covidien, Irvine, California) microcatheters can be used for routine embolizations. The Scepter C balloon catheter (MicroVention, Inc., Tustin, California) enables a new balloon-augmented embolization technique through a single microcatheter.1,2 Typically, 0.014-in diameter guidewires are used to help navigate the microcatheter because of their superior steering and trackability. However, smaller guidewires such as the 0.008-in Mirage (Covidien, Irvine, California) may be safer in small, distal cerebral vasculature (Note: the 0.008-in guidewires are essentially unsteerable and navigating bifurcations is often an exercise in persistence of the trial and error technique and/or uncanny tip reshaping proficiency). The size and angioarchitecture of the feeding vessel may require altering or modifying the microcatheter, often necessitating very small and “floppy” catheters for difficult-to-reach anatomy. In these situations, the Marathon flow-directed microcatheter could be advantageous. Unfortunately, guidewires 0.012 in or smaller are necessary when using the Marathon microcatheter due to its 0.013-in distal lumen diameter. However, the catheter is surprisingly compatible with the 0.014-in Traxcess guidewire (MicroVention, Inc., Tustin, California), as both the catheter and wire taper in a similar fashion. Preference is given to use the 0.014-in Traxcess guidewire when the Marathon microcatheter is required, as the Traxcess wire has superior steerability and provides a more rigid tracking platform compared to the other compatible guidewires.

Particles

The most common agent used for embolization of meningiomas and other head and neck tumors is a suspension of particles mixed with a contrast agent. Particles are small substrates that aggregate to obstruct the vessel. The choices of particle material and size impact results and potential complications associated with embolization. As differences in the granulometric distribution of particles exist, they may not match exactly with their advertised size range. Compressibility, elastic recovery, aggregation, and visualization of particles can all affect performance.

Polyvinyl alcohol (PVA) particles are nonspherical and are available in preparations of varying size ranges. Limitations with PVA embolization include difficulty with aggregation and microcatheter obstruction, leading to premature termination of the embolization or microcatheter exchange. Injection under increased pressure to clear the catheter should never be performed. This maneuver increases the risk of forcing particles into undesired territories once they are released.

Smaller particles allow deeper penetration into the tumor bed for more complete devascularization and increased tumor necrosis; however, they have a higher likelihood of reaching potentially dangerous or disabling arteries.3Larger particles are safer but may not fully penetrate and devascularize the tumor bed and, therefore, may be less efficient at reducing surgical blood loss. Maintaining particle size greater than 150 µm is thought to reduce the risk of damaging the vasa nervorum of the cranial nerves.4,5 A large study of 201 embolized meningiomas found small particle size (45 to 150 µm) to be the sole risk factor for complications, hemorrhagic or otherwise.5 In high-flow situations, increasing particle size to greater than 500 µm may be beneficial, or an alternate class of embolic agent can be considered. Size selection of the PVA particles is a balance between desired tumor penetration and unwanted target embolization. In most situations, selecting particles with a diameter between 150 and 350 µm will provide optimal results.6

Trisacryl Microspheres

Calibrated spherical particles made of trisacryl and cellulose porous beads were developed to address the disadvantages of PVA particles, specifically their irregular size and nonspherical nature. Trisacryl microspheres are partially compressible and, as a result, allow for easier transit through the delivery catheter.7,8 Microspheres are thought to redistribute after initial clumping and delayed control angiography is therefore warranted. A study of 60 patients comparing trisacryl particles to nonspherical PVA particles found lower surgical blood loss with trisacryl embolization.9

Gelfoam

Gelfoam should be delivered via the transarterial embolization approach. For head and neck tumors, powder and sponge forms can be used.10 Gelfoam persists for 3 to 6 weeks before recanalization begins.

Liquid Embolics

The two most common liquid embolic agents are N-butyl cyanoacrylate (NBCA: Trufill; Codman & Shurtleff, Inc., Raynham, Massachusetts) and ethylene vinyl alcohol (Onyx; Covidien, Irvine, California). The choice of liquid embolic is a matter of preference, with each having advantages and disadvantages. Onyx offers a decreased theoretical risk of catheter retention, whereas NBCA has more versatility by altering the rate of polymerization with dilution strategies.

Advantages of liquid embolic agents include decreased peritumoral edema and the prevention of delayed recanalization (sometimes seen after particle embolization). They can be used with transarterial or direct puncture embolization techniques. Potential disadvantages include an inability to select the size of vessels that the liquid embolic will enter (compared to particle embolization). There is risk that the liquid embolic agent will occlude vessels prematurely without deep penetration into the tumor.11 Further, liquid embolics are more expensive than particles.

NBCA is a liquid embolic that is injected as a mixture with Ethiodol. The safety of tumor embolization with NBCA has been studied. Kim et al.12 examined 35 consecutive tumor patients embolized with NBCA (17% meningiomas). The authors suggest that NBCA had better fluoroscopic visibility than PVA particles, enabling precise identification of embolized vessels and tumor mass. Disadvantages include quicker polymerization and risk of catheter retention. Proper embolization with NBCA requires greater technical skill than PVA administration. NBCA is also considered more permanent than PVA particles. When dangerous anastomoses are encountered, coils can be used to obstruct their origins and prevent distal embolization of the liquid embolic agent into unwanted territories.12

Onyx is an effective embolic agent that can penetrate into tumor capillaries. A small case series reported no increased postembolization tumor edema and no hemorrhagic complications following Onyx embolization.11 The Onyx mixture is radiopaque and highly visible during angiography.13 Care must be taken to create a meniscus between the dimethyl sulfoxide (DMSO) and the Onyx. Mixing of Onyx and DMSO in the catheter hub can dilute the Onyx, rendering it less radiopaque and more difficult to visualize. This can increase the risk of embolization to unwanted vascular territories. Onyx can be injected over a longer time frame than NBCA, which makes it more controllable and therefore may result in more uniform lesion penetration.14

Coils

Coils are shaped (curled) pieces of metal, usually platinum, that are released into a vessel for occlusion. Detachable and pushable coils can serve as an alternative to particle and liquid embolization methods. Some debate exists regarding the appropriateness and use of coils in the setting of head and neck tumors. Coils may be suitable for masses with large feeding vessels, greater than 1.5 mm in diameter.15However, some argue that proximal coil occlusion may not only create collaterals but may also prevent repeat access in case of tumor recurrences.16 Coils can be an excellent adjunct to liquid embolization, preventing penetration of the liquid embolic into unwanted territories without causing ischemia.

Other Embolic Agents

Additional agents that have been used in embolization of vascular head and neck tumors include fibrin glue, ethyl alcohol (ETOH), hydroxyapatite ceramics, phenytoin, hyperosmolar mannitol, and Lipiodol.1722

TECHNIQUE

Preembolization Workup and Considerations

A complete medical history and physical examination is required before any embolization procedure. A review of noninvasive imaging is critical; findings on computed tomography (CT) and magnetic resonance imaging (MRI) studies can help guide the treatment. A complete angiographic evaluation of the tumor is recommended. For intracranial meningiomas, a comprehensive study includes a six-vessel intracranial and extracranial angiogram (bilateral ECA, ICA, and VA). Large vessel sacrifice may be warranted when paragangliomas encase the carotid artery. In these cases, angiography can be combined with balloon test occlusion to assess the feasibility of vessel sacrifice.23

Subsequently, superselective angiography of individual arterial pedicles, with specific attention to dangerous anastomoses and the at-risk blood supply of cranial nerves, is necessary to plan the embolization procedure (Table 16.1).24 Blood supply to most meningiomas is derived from the dural arterial vasculature (middle meningeal artery, posterior meningeal artery, tentorial artery of Bernasconi and Cassinari, etc.), arising from the ECA, VA, or ICA. A typical finding on superselective angiography is an intense vascular tumor blush from the arterial phase through the late venous phase, often with a “sunburst” type pattern.25 Tumors located in specific anatomical locations such as the orbital, parasellar, petroclival, and cervicomedullary regions will have associated, and predictable, patterns of these dangerous anastomoses or at-risk cranial nerve blood supply relative to their location.24 Careful study of the superselective angiographic images with a strong understanding of the usual dangerous anatomy is imperative for the avoidance of complications.

Procedural Considerations

Timing and Adjunctive Medications

Preoperative embolization is typically performed within several days of surgical resection. Delaying surgical resection at least 24 hours after embolization may be beneficial.26 One study suggests the optimal latency for meningioma resection following embolization may be 7 to 9 days, allowing for maximal tumor softening, decreased operative times, and lower Simpson grades.27 However, in tumors that have been embolized with excellent tumor bed penetration (especially with smaller particle size such as 60 to 150 µm), delay of surgical resection may lead to significant increases in peritumoral edema and mass effect.6 Most interventionalists advocate high-dose intravenous steroids during and after meningioma embolization procedures where the tumor is large or there is already a significant amount of edema present.5,6 Provocative testing with injection of Amytal and/or lidocaine with simultaneous neuromonitoring or immediate neurologic examination can help predict the risk of embolization to dangerous territories.28 ECA vasospasm may occur during the embolization procedure. Prophylactic application of a transdermal nitroglycerin patch or sublingual calcium channel antagonists may reduce the occurrence of vasospasm. Administration of papaverine (30 to 60 mg), nitroglycerin (100 to 300 µg), or verapamil (5 to 20 mg) through the catheter system may reduce vasospasm and allow more predictable results.

Endovascular Technique

Embolization should be performed by a well-trained neurointerventionalist in a biplane digital subtraction fluoroscopy suite. Intravenous sedation, monitored anesthesia care (MAC), or general endotracheal anesthesia should be provided according to the specific goals and challenges of the procedure. Arterial endovascular access is obtained most often by puncture of the common femoral artery and insertion of a 5-Fr or 6-Fr short sheath using the modified Seldinger technique. Alternatively, embolization may be performed using a direct puncture technique (DPT).

The patient should be given a bolus of intravenous heparin with a goal of 2 to 2.5 times the baseline activated clotting time (ACT) to help prevent thromboembolic complications. If not performed previously, a detailed angiographic study of the tumor blood supply is then performed via superselective angiography using microcatheters.

After the decision to proceed with embolization is made, a suitable guide catheter is selected to allow for a working platform within the major artery supplying the tumor. The ICA, ECA, or the distal V4 segment of the VA may be accessed by a 90-cm guide catheter in most patients. However, vessel tortuosity or patient height may dictate the use of a longer guide catheter. The outer diameter of the guide catheter is usually 5-Fr or 6-Fr, and the inner diameter should easily accommodate the desired microcatheter(s).

After the microcatheter is in position within the target arterial pedicle and the interventionalist is confident that safe embolization can be performed, the embolic material is selected and prepared. The embolic material is injected slowly with simultaneous biplane fluoroscopy to identify flow into the feeding artery and tumor bed. Reduction of tumor blush by 80% or more following embolization should be the goal, as reaching this threshold may be necessary to impart a beneficial effect.23 Injection should stop when the embolic agent no longer reaches the tumor or, in the case of particle embolization, when there is contrast stagnation of the feeding artery (Fig. 16.1). If there is any identification of embolic material tracking into undesired territories, or reflux along the microcatheter, the injection should cease immediately. Deep penetration of embolic agent into the tumor bed may result in complete devascularization of the tumor, often without embolization of all of the feeding arteries. In other circumstances, selection of additional pedicles may be necessary to obtain adequate embolization results. This typically requires obtaining a fresh microcatheter. After completion of the embolization, a thorough neurologic examination is performed to assess for ischemic or hemorrhagic complications. Close clinical surveillance is indicated over the following hours as delayed complications such as intratumoral hemorrhage, increased edema, and mass effect may develop. These complications can usually be quickly and reliably treated if recognized in a timely manner.4,5

Route of Embolization

The approach to head and neck tumor embolization varies based on different factors including, but not limited to, the material chosen, the location of the tumor, and the comfort level of the operator. The traditional transarterial route has been used in most meningioma embolization procedures. Rarely, vascular anatomy prevents appropriate endovascular access to the tumor and, therefore, prevents intra-arterial treatment. In these situations, a percutaneous (or transmucosal) DPT may be the only available route for embolization.23 Occasionally, a previous craniotomy can allow DPT access for the embolization of intracranial meningiomas (Fig. 16.2). Typically, liquid agents with 18- to 20-gauge needles are employed for DPT alone or in combination with the transarterial approach. Although DPT may yield increased tumor penetration,14 systematic comparisons of transarterial and DPT embolizations have not been performed. DPT does eliminate the issue of catheter obstruction. DPT is not without risk of major complications.29 Care must be taken during DPT as the embolic material is driven by pressure and it may be pushed through physiologic collaterals into undesired territories because of the pressure gradient that is created.30 Pain from tumor necrosis may occur during the DPT procedure. The patient should be aware of this possibility and may require general anesthesia.31

CLINICAL APPLICATIONS

Meningiomas

Meningiomas represent approximately 20% of all intracranial tumors.11,25,28 They usually display benign histopathology and are typically extra-axial or intraventricular in location. Despite their typical benign pathology, they may cause seizures and/or neurologic deterioration as a result of their space-occupying nature. Tumors that are small and asymptomatic can be followed with periodic imaging monitoring for enlargement or development of neurologic dysfunction.32,33 Symptomatic tumors often require surgical resection, which is typically curative and results in resolution of symptoms.28

Angiographic evaluation of meningiomas should be performed with catheterization of the bilateral external carotid, internal carotid, and vertebral arteries before embolization. Blood supply to meningiomas can be bilateral and may be derived from the intracerebral vessels (ICA and VA). On angiography, meningiomas typically appear as circumscribed areas of contrast staining that persists well into the venous phase. Large feeders may show the classic “sunburst” pattern.15

Surgical resection of meningiomas can result in significant morbidity and mortality. Chan and Thompson34 reported on the surgical morbidity and mortality of meningioma resection in a series of 257 patients. The authors noted a surgical morbidity and a mortality of 30% and 4%, respectively.34 Advanced age appears to be a significant surgical risk factor. A series of meningioma resections in an elderly patient population documented a 6.6% mortality rate and a 48% rate of surgical morbidity.35

Embolization of arteries supplying the tumor that are not anatomically accessible during surgery may help to reduce surgical morbidity and mortality by minimizing intraoperative bleeding or softening of the tumor.26,28 A nonrandomized prospective study compared 30 patients who underwent preoperative embolization in one center with 30 patients in a second center who were not embolized. Those patients with greater than 90% tumor embolization had decreased blood loss but no other identified benefit. No differences in surgical morbidity and mortality were demonstrated between the two groups.36 This study is limited by inherent selection bias and potential systematic differences in administration of care between the two centers. Other studies comparing patients who had preoperative embolization to those who did not undergo embolization have similar limitations. Macpherson37 describes a personal series of 52 meningioma patients of whom 28 patients were embolized and 24 patients were not. The study reported decreases in surgical difficulty with bleeding, blood transfusions, surgical complications, and poor outcomes for the patients who were embolized. This study is influenced by the subjective scoring methods employed for determination of surgical bleeding difficulties. The operating surgeon generated scores by comparing the technical difficulty of each surgery to previous experiences of resecting tumors of comparable size situated in similar anatomic locations.37 Similarly, in a retrospective matched-pair analysis of 18 meningioma patients treated with embolization and 18 patients without embolization, embolized patients had significant decreases in estimated blood loss and transfusions. This study is limited by a lack of sufficient detail reported for the methods of determining estimated blood loss and extent of devascularization achieved.38

Evidence of postembolization tumor necrosis can be documented via diminished perfusion on proton spectroscopy, contrast-enhanced CT, and contrast-enhanced MRI studies.3941 Embolization of meningiomas without subsequent surgical resection has been shown to be beneficial as palliative therapy in several cases.39,42

Decisions regarding preoperative meningioma embolization should be made on a case-by-case basis, considering both the risks and benefits associated with the procedure. Tumor location, size, overall vascularity, and specific angiographic features are key factors. Large convexity meningiomas are often ideal for presurgical embolization. In such cases, significant blood loss can result during the initial craniotomy before surgical control of the tumor. The convexity location renders embolization via the middle meningeal artery relatively low risk. Likewise, surgical resection of skull base meningiomas, and other vascular tumors, can be challenging due typically to narrow surgical corridors and firm tumor consistency. Tumor softening and necrosis can make surgical resection easier by minimizing the need for brain retraction and/or reducing mechanical injury to adjacent cranial nerves. Unfortunately, skull base meningiomas often have higher embolization risks as feeding arteries are often associated with the cranial nerve blood supply and dangerous anastomoses.

Paragangliomas

Paragangliomas are rare tumors of neural crest cell origin that typically arise from the temporal bone, carotid body, or nodose ganglion (i.e., glomus tympanicum, glomus jugulare, carotid body tumor, intravagal paraganglioma). Because these tumors develop where neural crest cells are located, the anatomical pattern of the feeding arteries may be predicted by the tumor size and location. Frequently involved arteries include the ascending pharyngeal, lingual, posterior auricular, stylohyoid, and occipital. In addition, the deep cervical artery and the thyrocervical trunk may contribute blood supply.43Advanced paragangliomas can seize blood supply from the anterior tympanic (branch of internal maxillary), caroticotympanic (branch of internal carotid), and superior tympanic (branch of middle meningeal) arteries.30 When visualized on angiography, these hypervascular tumors are characterized by an intense blush.

For larger paragangliomas, the benefits of preoperative embolization appear to outweigh the associated risks. Perioperative blood loss can be reduced and surgical time decreased.44 It may be prudent to limit preoperative embolization to those paragangliomas greater than 3 cm in diameter as smaller tumors can often be resected with less intraoperative risk. Small tumors are typically more difficult to embolize. They are associated with smaller feeding arteries that render injection of embolic material more difficult without reflux into the parent vessel. In select cases, the DPT can overcome this challenge.30,45 In the case of carotid body tumors, balloon protection of the ICA during embolization is often helpful.

Paragangliomas may be effectively embolized with various materials (Fig. 16.3). Embolization is most commonly performed transarterially with PVA particles or liquid embolic agents.30 DPT with NBCA or Onyx has yielded good results and appears to be effective and safe.31,46,47 In one report, the DPT resulted in some degree of devascularization in more than 90% of patients without permanent complications.48

Juvenile Nasopharyngeal Angiofibromas

Juvenile nasopharyngeal angiofibromas (JNAs) are benign, yet highly aggressive and infiltrating, neoplasms that are almost exclusively seen in adolescent males. These tumors contain vessels that do not have a normal smooth muscle wall. JNAs are commonly supplied by the internal maxillary, ascending palatine, ascending pharyngeal, accessory meningeal, and internal carotid arteries.49 JNAs have significantly larger shunts than most other head and neck tumors, which may limit the achievable extent of devascularization.50 Characteristically, angiography demonstrates a reticulated pattern in the arterial phase and a dense tumor blush that continues into the venous phase.

The advantages of preoperative embolization for JNAs are compelling. Studies show diminished intraoperative blood loss, less blood transfusion needs, more complete resection, and fewer tumor recurrences.51,52 Blood loss reduction during postembolization resection is considerable compared to the other head and neck tumors. JNAs are less likely to recur when the entire tumor is removed en bloc. Complete devascularization makes this type of removal easier. DPT may be a useful method for devascularization if all branches cannot be embolized through the transarterial route (Fig. 16.4).31

Similar to paragangliomas, multiple embolic materials can be used to treat JNAs. As JNAs tend to have large arterial shunts, particles greater than 150 µm may be advantageous. Larger particles may be needed if significantly larger shunts are discovered during angiography. The operator should, therefore, be prepared to make rapid intraoperative adjustments if necessary. Particles that travel through a large shunt may cause pulmonary complications. One potential solution to these high-flow shunts is to use balloon-augmented embolization to decrease the flow through the target vessels at the time of embolization.1,2

Hemangiopericytoma

Previously termed angioblastic meningiomas, hemangiopericytomas are rare, smooth muscle pericyte cell–derived tumors found around meningeal capillaries. Angiographically, these tumors are characterized by large arterial pedicles with many tiny corkscrew-like feeding vessels entering the tumor. The vascular stain is intense and fluffy with lingering contrast in venous channels. The techniques for the embolization of hemangiopericytomas parallel those of meningiomas.53

Hemangioblastoma

Hemangioblastomas are benign vascular tumors typically found during infancy that occur predominantly in the spinal cord and cerebellum. Cerebellar hemangioblastomas are also one of the most common posterior fossa primary central nervous system tumors found in adults. Cerebellar hemangioblastomas derive most of their blood supply from the cerebellar arteries (as opposed to the external carotid circulation) as they are intra-axial in location. Meningeal, tentorial, and vertebral arteries may supply additional blood.53 Hemangioblastomas typically display irregular vessels with intensely staining nodules exhibiting homogeneous or mottled appearance on angiography.

Preoperative embolization has been very successful in reducing intraoperative blood loss during hemangioblastoma surgery.54 Reduced blood loss and improved outcomes were reported in tumors that had almost complete embolization. However, partial embolization resulted in increased transfusions and more operative complications in some cases.55 Hemangioblastomas less than or equal to 1.5 cm do not typically warrant preoperative embolization as the procedural risks can outweigh those of bleeding during the surgical resection.56 Embolization with particles greater than 150 µm or liquid NBCA may be safest.57

POTENTIAL COMPLICATIONS

Both major and minor complications can occur during embolization of vascular tumors of the head and neck. Major complications may include cranial nerve palsy, skin or mucosal tissue necrosis, stroke, intracranial hemorrhage, death, inadvertent embolization of pulmonary vasculature, and contrast-induced nephropathy.23

A recent meningioma embolization literature review identified 36 reports published between 1990 and 2011, including 459 patients who underwent meningioma embolization. Of these, 21 patients (4.6%) had complications related to embolization and 3 experienced a major complication or death (0.7%).58 Several studies demonstrating even higher complication rates were eliminated from the analysis due to strict exclusion criteria. One excluded study evaluated 167 patients with skull base meningiomas. The authors documented an immediate postembolization complication rate of 21.6%, with 9% of patients sustaining permanent disability.59

Hemorrhagic complications may occur due to mechanical injury of the feeding artery by the microcatheter and wires or upon catheter retrieval when using liquid embolics. Hemorrhagic complications are also thought to occur in higher frequency when substantial devascularization of the tumor results in significant necrosis. This risk may be exacerbated by using very small particles that penetrate deep into the tumor bed.5 Other theories suggest that compromised venous outflow may increase the risk of hemorrhage in high-flow tumors.25,60,61

Complication Avoidance

Reflux of small particles or liquid material may occur even during the most precise and careful procedure. Several steps may be taken to reduce this risk. Catheters should be placed distal to the origin of vessels that need to be preserved. Particle size should be considered carefully for controlled infusion as smaller particles are more likely to flow around the catheter. Balloon catheters may be deployed before delivery of embolic material to prevent or reduce the amount of refluxed substance.15 Additionally, care should be taken to avoid proximal rupture of the microcatheter. Proximal rupture may allow particles to enter and occlude vessels not intended for embolization.6

Ischemia of the vasa nervorum and resultant cranial nerve palsies can occur due to reflux of embolic material or penetration of unknown anastomoses. For example, delivery of embolic material into the stylomastoid branch of the occipital artery may result in facial nerve palsy. This happens most frequently with liquid agents but has occurred with PVA particles as well.30 Careful and thorough angiography of targeted, contralateral, and nearby vessels before embolic infusion can reveal possible unexpected anastomoses and aberrant vascular architecture. If a concern for losing blood supply to cranial nerves exists, provocative testing using lidocaine may be used.62 The appearance of a new neurologic deficit during testing indicates the possibility of cranial nerve palsy following embolization. Repositioning of the microcatheter, as close to the tumor bed as possible, will decrease the likelihood of obstructing the blood supply to normal tissues.15

Minor Complications

Common minor complications include arterial access site issues such as hematoma formation, localized pain, and fever. Transient headache or temporofacial pain is the most common complication observed after embolization.16 This can be caused by tumor swelling or, in the case of intracranial tumors, irritation of the meninges.3 Pain is typically managed with analgesics.15 Preoperative steroids may limit edema and reduce the likelihood of resultant complications.30 Dexamethasone 10 mg can be given intravenously during preoperative assessment before the embolization procedure. If the tumor is large and a significant amount of embolization has been achieved, then continuing the dexamethasone at 4 mg every 6 to 8 hours (intravenous or oral) is advisable. A relatively rapid taper over the next 10 to 14 days is then prescribed. Bradycardia can develop after manipulation of the branches of the ECA, and sometimes the internal maxillary artery, which can evoke the trigeminocardiac reflex.63

Tumor-Specific Complications

One important potential complication specific to catecholamine-secreting paragangliomas is a life-threatening vasomotor attack.64 If a paraganglioma of this type is discovered, α-antagonist agents should be used instead of β-antagonists, which are contraindicated.6 Carotid sinus syndrome is another serious complication that can occur after carotid body tumor embolization.65 In addition, embolization of a jugular paraganglioma has reportedly caused hypoglossal nerve palsy.66 Accurate preoperative diagnosis and assessment of paragangliomas can help in preparing for and anticipating potential hemodynamic instability.

TIPS AND TRICKS

• In addition to bilateral selective catheter angiography of the external and internal carotid arteries, superselective catheterization of the external carotid branches is useful to reveal dangerous anastomoses.

• Balloon occlusion testing during catheter angiography can determine if carotid sacrifice is an option during surgical resection of some tumors.

• DPT for embolization may be the only option for vascular tumors with impossible endovascular access.

• Eighty percent reduction of tumor blush following embolization should be the minimum goal.

• Provocative testing of targeted vasculature with Amytal (grey matter) and lidocaine (white matter) can help predict cranial nerve palsy and other neurologic deficit that could be at risk during embolization. As a result, embolization under conscious sedation where neurologic examination can be performed should be considered.

• The goals of preoperative embolization should be discussed extensively with the surgeon.

• Balloon-augmented or protected embolization can help prevent complications and negate the risks associated with high-flow shunting.

• Great care should be taken in selecting the embolic agent. The experience of the operator with the agent may be the most critical factor.

• Particles should always be mixed with contrast agent to allow for visualization at the time of injection.

• Sizing of particles during particle embolization is extremely important. Small particles (45–150-µm diameter) may pose an increased risk of complications. Particle diameters ranging from 150 to 350 µm may be optimal, except in high-flow shunting where larger particles may be necessary.

• Particles should be injected with the flow of the blood and not pushed against resistance. This will help avoid traversing through dangerous anastomoses or reaching small terminal vessels that supply cranial nerves.

• If Onyx is used for embolization, the tumor surgeon should be notified that sparks can be generated with use of the Bovie monopolar cautery.

• Coils can be used to occlude a dangerous anastomotic channel, allowing preferential embolization of the target vessel without reflux into the dangerous anastomosis.

• The embolization catheter should be placed as distal as possible in the vessel feeding the tumor and must be distal to the origin of vessels that need preservation.

• Close clinical surveillance postembolization is important to rapidly identify any major procedure-related complications. Rapid identification and treatment of these types of complications can drastically improve patient outcome.

CONCLUSION

In conclusion, the outcome of preoperative embolization for vascular tumors of the head and neck depends on many factors, including the type and characteristics of the tumor, the location of the tumor, the vascular architecture of the patient, the technique implemented, the embolic material chosen, and the knowledge and experience of the operator. Careful consideration of all of these factors along with a thorough and thoughtful workup ensures the best chance of success.

REFERENCES

 1. Spiotta AM, Miranpuri AS, Vargas J, et al. Balloon augmented Onyx embolization utilizing a dual lumen balloon catheter: utility in the treatment of a variety of head and neck lesions [published online ahead of print September 11, 2013]. J Neurointerv Surg. doi:10.1136/neurintsurg-2013-010833.

 2. Jagadeesan BD, Grigoryan M, Hassan AE, et al. Endovascular balloon-assisted embolization of intracranial and cervical arteriovenous malformations using dual-lumen coaxial balloon microcatheters and Onyx: initial experience. Neurosurgery. 2013;73:238–243.

 3. Wakhloo AK, Juengling FD, Van Velthoven V, et al. Extended preoperative polyvinyl alcohol microembolization of intracranial meningiomas: assessment of two embolization techniques. AJNR Am J Neuroradiol. 1993;14:571–582.

 4. Bendszus M, Monoranu CM, Schütz A, et al. Neurologic complications after particle embolization of intracranial meningiomas. AJNR Am J Neuroradiol. 2005;26:1413–1419.

 5. Carli DF, Sluzewski M, Beute GN, et al. Complications of particle embolization of meningiomas: frequency, risk factors, and outcome. AJNR Am J Neuroradiol. 2010;31:152–154.

 6. Morris P. Interventional and Endovascular Therapy of the Nervous System: A Practical Guide. New York, NY: Springer-Verlag; 2002.

 7. Hamada J, Ushio Y, Kazekawa K, et al. Embolization with cellulose porous beads, I: an experimental study. AJNR Am J Neuroradiol. 1996;17:1895–1899.

 8. Kai Y, Hamada JI, Morioka M, et al. Clinical evaluation of cellulose porous beads for the therapeutic embolization of meningiomas. AJNR Am J Neuroradiol. 2006;27:1146–1150.

 9. Bendszus M, Klein R, Burger R, et al. Efficacy of trisacryl gelatin microspheres versus polyvinyl alcohol particles in the preoperative embolization of meningiomas. AJNR Am J Neuroradiol. 2000;21:255–261.

10. Rutka J, Muller PJ, Chui M. Preoperative Gelfoam embolization of supratentorial meningiomas. Can J Surg. 1985;28:441–443.

11. Shi ZS, Feng L, Jiang XB, et al. Therapeutic embolization of meningiomas with Onyx for delayed surgical resection. Surg Neurol. 2008;70:478–481.

12. Kim LJ, Albuquerque FC, Aziz-Sultan A, et al. Low morbidity associated with use of n-butyl cyanoacrylate liquid adhesive for preoperative transarterial embolization of central nervous system tumors. Neurosurgery. 2006;59:98–104.

13. Gobin YP, Murayama Y, Milanese K, et al. Head and neck hypervascular lesions: embolization with ethylene vinyl alcohol copolymer—laboratory evaluation in Swine and clinical evaluation in humans. Radiology. 2001;221:309–317.

14. Gemmete JJ, Chaudhary N, Pandey A, et al. Usefulness of percutaneously injected ethylene-vinyl alcohol copolymer in conjunction with standard endovascular embolization techniques for preoperative devascularization of hypervascular head and neck tumors: technique, initial experience, and correlation with surgical observations. AJNR Am J Neuroradiol. 2010;31:961–966.

15. Lazzaro MA, Badruddin A, Zaidat OO, et al. Endovascular embolization of head and neck tumors. Front Neurol. 2011;2:64.

16. Bilbao JI, Martinez-Cuesta A, Urtasun F, et al. Complications of embolization. Semin Intervent Radiol. 2006;23:126–142.

17. Feng L, Kienitz BA, Matsumoto C, et al. Feasibility of using hyperosmolar mannitol as a liquid tumor embolization agent. AJNR Am J Neuroradiol. 2005;26:1405–1412.

18. Jungreis CA. Skull-base tumors: ethanol embolization of the cavernous carotid artery. Radiology. 1991;181:741–743.

19. Kubo M, Kuwayama N, Hirashima Y, et al. Hydroxyapatite ceramics as a particulate embolic material: report of the physical properties of the hydroxyapatite particles and the animal study. AJNR Am J Neuroradiol. 2003;24:1540–1544.

20. Kubo M, Kuwayama N, Hirashima Y, et al. Hydroxyapatite ceramics as a particulate embolic material: report of the clinical experience. AJNR Am J Neuroradiol. 2003;24:1545–1547.

21. Probst EN, Grzyska U, Westphal M, et al. Preoperative embolization of intracranial meningiomas with a fibrin glue preparation. AJNR Am J Neuroradiol. 1999;20:1695–1702.

22. Yasui K, Shoda Y, Suyama T, et al. Preoperative embolization for meningioma using lipiodol. Interv Neuroradiol. 1998;4(suppl 1):63–66.

23. Duffis EJ, Gandhi CD, Prestigiacomo CJ, et al. Head, neck, and brain tumor embolization guidelines. J Neurointerv Surg. 2012;4:251–255.

24. Geibprasert S, Pongpech S, Armstrong D, et al. Dangerous extracranial-intracranial anastomoses and supply to the cranial nerves: vessels the neurointerventionalist needs to know. AJNR Am J Neuroradiol. 2009;30:1459–1468.

25. Mack W, Vinuela F. Diagnostic evaluation and embolization of meningiomas. In: DeMonte F, McDermott MW, Al-Mefty O, eds. Al-Mefty’s Meningiomas. New York, NY: Thieme Medical Publishers; 2011.

26. Chun JY, McDermott MW, Lamborn KR, et al. Delayed surgical resection reduces intraoperative blood loss for embolized meningiomas. Neurosurgery. 2002;50:1231–1235.

27. Kai Y, Hamada J, Morioka M, et al. Appropriate interval between embolization and surgery in patients with meningioma. AJNR Am J Neuroradiol. 2002;23:139–142.

28. Dowd CF, Halbach VV, Higashida RT. Meningiomas: the role of preoperative angiography and embolization. Neurosurg Focus. 2003;15:E10.

29. Casasco A, Houdart E, Biondi A, et al. Major complications of percutaneous embolization of skull-base tumors. AJNR Am J Neuroradiol. 1999;20:179–181.

30. Willing SJ. Transarterial embolization of vascular tumors in the head and neck. Semin Interv Radiol. 2003;20:3–12.

31. Casasco A, Herbreteau D, Houdart E, et al. Devascularization of craniofacial tumors by percutaneous tumor puncture. AJNR Am J Neuroradiol. 1994;15:1233–1239.

32. Nakamura M, Roser F, Michel J, et al. The natural history of incidental meningiomas. Neurosurgery. 2003;53:62–70.

33. Yano S, Kuratsu J; Kumamoto Brain Tumor Research Group. Indications for surgery in patients with asymptomatic meningiomas based on an extensive experience. J Neurosurg. 2006;105:538–543. doi:10.3171/jns.2006.105.4.538.

34. Chan RC, Thompson GB. Morbidity, mortality, and quality of life following surgery for intracranial meningiomas. A retrospective study in 257 cases. J Neurosurg. 1984;60:52–60.

35. Awad IA, Kalfas I, Hahn JF, et al. Intracranial meningiomas in the aged: surgical outcome in the era of computed tomography. Neurosurgery. 1989;24:557–560.

36. Bendszus M, Rao G, Burger R, et al. Is there a benefit of preoperative meningioma embolization? Neurosurgery. 2000;47:1306–1311.

37. Macpherson P. The value of pre-operative embolisation of meningioma estimated subjectively and objectively. Neuroradiology. 1991;33:334–337.

38. Dean BL, Flom RA, Wallace RC, et al. Efficacy of endovascular treatment of meningiomas: evaluation with matched samples. AJNR Am J Neuroradiol. 1994;15:1675–1680.

39. Bendszus M, Martin-Schrader I, Warmuth-Metz M, et al. MR imaging- and MR spectroscopy-revealed changes in meningiomas for which embolization was performed without subsequent surgery. AJNR Am J Neuroradiol. 2000;21:666–669.

40. Grand C, Bank WO, Balériaux D, et al. Gadolinium-enhanced MR in the evaluation of preoperative meningioma embolization. AJNR Am J Neuroradiol. 1993;14:563–569.

41. Jungling FD, Wakhloo AK, Hennig J. In vivo proton spectroscopy of meningioma after preoperative embolization. Magn Reson Med. 1993;30:155–160.

42. Koike T, Sasaki O, Tanaka R, et al. Long-term results in a case of meningioma treated by embolization alone—case report. Neurol Med Chir (Tokyo). 1990;30:173–177.

43. van den Berg R, Wasser M, van Gils A, et al. Vascularization of head and neck paragangliomas: comparison of three MR angiographic techniques with digital subtraction angiography. AJNR Am J Neuroradiol. 2000;21:162–170.

44. Westerband A, Hunter GC, Cintora I, et al. Current trends in the detection and management of carotid body tumors. J Vasc Surg. 1998;28:84–92.

45. Tikkakoski T, Luotonen J, Leinonen S, et al. Preoperative embolization in the management of neck paragangliomas. Laryngoscope. 1997;107:821–826.

46. Wanke I, Jäckel MC, Goericke S, et al. Percutaneous embolization of carotid paragangliomas using solely Onyx. AJNR Am J Neuroradiol. 2009;30:1594–1597.

47. Chaloupka JC, Mangla S, Huddle D, et al. Evolving experience with direct puncture therapeutic embolization for adjunctive and palliative management of head and neck hypervascular neoplasms. Laryngoscope. 1999;109:1864–1872.

48. Abud DG, Mounayer C, Benndorf G, et al. Intratumoral injection of cyanoacrylate glue in head and neck paragangliomas. AJNR Am J Neuroradiol. 2004;25:1457–1462.

49. Wilms G, Peene P, Baert AL, et al. Pre-operative embolization of juvenile nasopharyngeal angiofibromas. J Belge Radiol. 1989;72:465–470.

50. Schroth G, Haldemann AR, Mariani L, et al. Preoperative embolization of paragangliomas and angiofibromas. Measurement of intratumoral arteriovenous shunts. Arch Otolaryngol Head Neck Surg. 1996;122:1320–1325.

51. Roberson GH, Price AC, Davis JM, et al. Therapeutic embolization of juvenile angiofibroma. AJR Am J Roentgenol. 1979;133:657–663.

52. Siniluoto TM, Luotonen JP, Tikkakoski TA, et al. Value of pre-operative embolization in surgery for nasopharyngeal angiofibroma. J Laryngol Otol. 1993;107:514–521.

53. Krajina A, Cesak T, Zelenak K, et al. Therapeutic embolization of cranial tumors. In: Abujamra AL, ed. Diagnostic Techniques and Surgical Management of Brain Tumors. Rijeka, Croatia: InTech; 2011.

54. Eskridge JM, McAuliffe W, Harris B, et al. Preoperative endovascular embolization of craniospinal hemangioblastomas. AJNR Am J Neuroradiol. 1996;17:525–531.

55. Shigekazu T, Ruichi T, Yukihiko F, et al. Surgical treatment of hemangioblastomas with presurgical endovascular embolization. Neurologic Med Chir (Tokyo). 2001;41:246–252.

56. Glasker S, Van Velthoven V. Risk of hemorrhage in hemangioblastomas of the central nervous system. Neurosurgery. 2005;57:71–76.

57. Cornelius JF, Saint-Maurice JP, Bresson D, et al. Hemorrhage after particle embolization of hemangioblastomas: comparison of outcomes in spinal and cerebellar lesions. J Neurosurg. 2007;106:994–998. doi:10.3171/jns.2007.106.6.994.

58. Shah AH, Patel N, Raper DM, et al. The role of preoperative embolization for intracranial meningiomas. J Neurosurg. 2013;119:364–372.

59. Rosen CL. Ammerman JM, Sekhar LN, et al. Outcome analysis of preoperative embolization in cranial base surgery. Acta Neurochir (Wien). 2002;144:1157–1164. doi:10.1007/s00701-002-0965-y.

60. Kallmes DF, Evans AJ, Kaptain GJ, et al. Hemorrhagic complications in embolization of a meningioma: case report and review of the literature. Neuroradiology. 1997;39:877–880.

61. Yu SC, Boet R, Wong GK, et al. Postembolization hemorrhage of a large and necrotic meningioma. AJNR Am J Neuroradiol. 2004;25:506–508.

62. Barr JD, Mathis JM, Horton JA. Provocative pharmacologic testing during arterial embolization. Neurosurg Clin N Am. 1994;5:403–411.

63. Lv X, Li Y, Lv M, et al. Trigeminocardiac reflex in embolization of intracranial dural arteriovenous fistula. AJNR Am J Neuroradiol. 2007;28:1769–1770.

64. Kremer R, Michel RP, Posner B, et al. Catecholamine-secreting paraganglioma of glomus jugulare region. Am J Med Sci. 1989;297:46–48.

65. Eskridge JM, Harris AB, Finch L, et al. Carotid sinus syndrome and embolization procedures. AJNR Am J Neuroradiol. 1993;14:818–820.

66. Maier W, Marangos N, Laszig R. Paraganglioma as a systemic syndrome: pitfalls and strategies. J Laryngol Otol. 1999;113:978–982.