3 Embolization of Skull Base Tumors
Daniel A. Tonetti and Brian T. Jankowitz
Summary
This chapter will review the different methods of embolizing skull base tumors including common pitfalls and perils.
Keywords: Embolization, particles, PVA, liquid embolic, Onyx, NBCA, coils
3.1 Key Learning Points
●Preoperative tumor embolization can decrease intraoperative blood loss and increase the chance of successful tumor resection.
●Embolization is predicated entirely on the avoidance of complications.
●There should be a clear understanding of the goals of tumor embolization agreed upon between the surgeon and the neurointerventionalist.
●Safe embolization requires knowledge of patient-specific anastomotic connections and the risk/benefit profile of available embolysates, given the relevant anatomy.
3.2 Introduction
Endovascular embolization can be utilized in conjunction with surgery to improve chances for successful skull base tumor resection by decreasing tumor vascularity. Significant advances have been made in technique and embolic materials since the first descriptions of such procedures in 1973.1 The most common agents currently used are ethylene vinyl alcohol copolymer (Onyx), n-butyl cyanoacrylate (NBCA), coils, particles, ethanol, or a combination of the above.2
Of paramount importance to the clinical team caring for a patient with a skull base tumor is the awareness that the primary goal of tumor embolization is to enhance the chances of a successful surgical resection. Tumors of the skull base can be exceedingly vascular and may have difficult-to-access vascular pedicles; therefore, embolization can play a direct role in decreasing the difficulty of the resection for the surgeon. Ideally this allows for increased surgical field visualization with decreased morbidity of the surgical procedure.3 However, tumor embolization should be approached with extreme caution as it will rarely significantly influence the overall outcome of surgery, and, though prior literature has supported the efficacy of tumor embolization to reduce both intraoperative blood loss4 , 5 , 6 and recurrence,7 there are no tumors that absolutely require preoperative embolization.
Commonly treated, highly vascular tumors of the skull base include some meningiomas, hemangiopericytomas, juvenile nasopharyngeal angiofibromas (JNAs), hemangioblastomas, and paragangliomas (glomus tumors). Although this list is not exhaustive, these are the most common vascular skull base tumors and represent the majority of a neurointerventionalist’s referrals for tumor embolization.
Direct intratumoral puncture techniques have been described for skull base tumors accessible percutaneously or via natural orifices.8 This technique may be of use in patients with superficial, easily accessible, hypervascular tumors, but is not without risk of major complications.9 The most useful application of this technique is for previously embolized, recurrent JNAs. When all safe arterial pathways to a tumor have been surgically occluded or embolized, direct puncture may be the only method of access. This has been described in small case series for certain carotid body, glomus jugulare, and glomus vagale paragangliomas.10 , 11 , 12 This chapter will focus on the role of preoperative transarterial embolization in the management of vascular skull base tumors, as transarterial embolization is more common and the role for direct tumoral puncture has yet to be well established. However, many of the same guidelines, risks, and recommendations with regard to procedural safety apply for direct tumor techniques.
3.3 Goal of Embolization and Injury Avoidance
Prior to skull base tumor embolization, it is of critical importance to identify patient-specific vascular anatomy including anastomotic connections and have a complete understanding of the following:
●Tumoral blood supply.
●Involved cerebral and cranial nerve blood supply.
●Associated blood supply of end-organs including skin and retina.
Common arterial feeders of skull base tumors can arise from branches of the internal carotid arteries (ICAs), the external carotid arteries (ECAs), the vertebral arteries (VAs), or any combination of these arteries and/or their branches. Tumors arising from the skull base meninges are classically supplied by dural feeders at the site of dural attachment, which may include branches from the ECA/ICA/VA, and by cortical or pial branches at the tumor’s periphery. Blood supply to dural tumors has been well described in the literature;13 a complete understanding of a given patient’s specific anatomy prior to embolization is a prerequisite to avoid complication from errant embolization.
We advocate for a presurgical diagnostic cerebral angiogram for most skull base tumors, even if there is no plan for embolization. The benefit is multifold. The vascularity of these tumors can be hard to predict, even with extensive noninvasive imaging such as magnetic resonance imaging (MRI) or computed tomography (CT). Knowing about aberrant parasitized feeding arteries, overall vascularity, collateral flow through the circle of Willis, and venous drainage patterns and involvement can aid in the operative approach, prepare for blood loss, and help predict the safety of vessel sacrifice. A balloon test occlusion can be easily planned in conjunction with the diagnostic angiogram when deemed necessary. If embolization is planned, a separate diagnostic procedure in an awake patient can avoid the embarrassment of putting someone under general anesthesia only to discover the absence of accessible arterial feeders. Furthermore, some straight-forward pedicles may be amenable to an awake embolization, which then allows for provocative Wada testing—selective injection of a temporary neuroanesthetic agent such as sodium amytal, propofol, or lidocaine—to simulate neurologic deficit.
Super-selective catheterization of ECA and ICA branches is needed to define the blood supply to any given tumor and to identify any potential intracranial-extracranial anastomoses which may prove dangerous if misunderstood and embolized. Combination blood supply of some skull base tumors from complex ICA and ECA anastomoses of the meninges can often make embolization both challenging and risky. Anastomotic pathways between intracranial and extracranial circulations are well-described.14 Generally, there are three regions that serve as major extracranial-to-intracranial anastomotic connections: the orbital region via the ophthalmic artery, the petrous-cavernous region, and the upper cervical region with the posterior circulation.
Special attention should be paid to any potential anastomoses with the ophthalmic artery, a common source of ICA–ECA anastomosis. Although the ophthalmic artery typically anastamoses with ethmoidal arteries, it may arise from the middle meningeal artery (MMA);15 in this circumstance, MMA sacrifice can lead to visual loss. The occipital artery can anastomose with the vertebral artery via C1 and C2 radicular branches, as can ascending and deep cervical arteries with the C3–C7 radicular branches. Key ICA–ECA anastomoses in the petrous-cavernous region include the vidian artery of the petrous ICA with the internal maxillary artery, and anastomoses between the inferolateral trunk (ILT) and meningohypophyseal trunk (MHT) with the ascending pharyngeal artery (APA). Careful consideration should also be paid to the ILT, MHT, and APA because of their complicated supply to the cranial nerves at the base of the skull; in our experience, it is generally unwise to embolize major branches of these vessels.
The decision to embolize a skull base tumor prior to surgical resection requires a holistic team-based approach with all parties involved taking an active role in the decision. There should be a clear understanding of the goals of tumor embolization, and these goals and the timing of embolization should be agreed upon by both the surgical team and the neurointerventionalist prior to any intervention. Specific goals of tumor embolization may include:
●Occlusion of a deep feeding artery on the side opposite to the surgical trajectory.
●Deep penetration with small particles to soften and induce necrosis within surgically hard-to-reach tumors, augmenting ease of tumor resection.
●Proximal occlusion of select dominant feeding artery/arteries with coils to reduce blood loss during operative exposure or debulking.
It is advantageous for the endovascular team to know the surgeon’s specific requirements and how embolization specifically can influence the outcome of a proposed surgery, and the goals of both teams should be aligned and congruent. For example, special attention must be paid to preserving the septal branch of the sphenopalatine artery (SPA) if a nasoseptal flap will be necessary for skull base reconstruction during an endonasal tumor. Nasoseptal flaps are frequently pedicled on the posterior septal artery, the terminal branch of the SPA, and the preservation or sacrifice of this branch should be discussed with the entire surgical team prior to embolization.
It is common for an overzealous interventionalist at the time of embolization to pursue the often-unreachable “perfect” radiographic outcome. In light of this aspect of human nature, we have found it useful to have a predetermined embolization stopping point, beyond which represents deteriorating gains and rapidly increasing risk to the patient. Knowing when to quit is a skill gained through experience, and we have found predetermined stopping points useful for complication avoidance. Specific stopping points that we have used in our practice include:
●Surpassing a predefined amount of radiation (>5 Gy) or fluoro time (>60 min).
●Reflux of liquid embolic into feeding arteries, with careful attention to avoid bilateral internal maxillary artery reflux and occlusion if the harvest of a nasoseptal flap is necessary.
●Following occlusion of deep, surgically inaccessible feeding arteries.
●Following occlusion of a single dominant feeder.
Skull base tumors often have a dominant feeding artery that offers the best chance of meaningful devascularization. These are frequently dural-based, and in most cases vessel sacrifice conveys very low risk to the patient. In contrast, most occipital artery or cavernous carotid branches supplying a given skull base tumor rarely provide large conduits and are typically not worth the risk of embolization.
3.4 Available Embolysates
Choice of embolysate can have a major impact on injury avoidance. We have found the following agents, listed in decreasing order of safety, to be beneficial: coils, large particles (e.g., polyvinyl alcohol [PVA]), Onyx, NBCA, small particles (e.g., embospheres), and ethanol. The size of embolysate matters, both in terms of efficacy and complication rates.16 , 17 In general, liquid embolics and small particles can penetrate tumor capillary beds more distally than coils or large particles; this allows for reduced surgical vascularity but increases the chance of complication from intracranial-extracranial anastomoses or nerve palsy from occlusion of cranial nerve vasa nervorum. Coils or large particles may be sufficient for proximal pedicle embolization and generally are safer due to their increased ability for control. The choice of embolysate should be carefully considered to avoid complications and should address the goal of embolization. Pros and cons of certain commercial embolysates are outlined in Table 3.1.
Embolysate type (examples) | Advantages | Disadvantages |
Coils ●Tornado® (Cook Medical, Bloomington, IN) ●Axium™ (Medtronic, Santa Rosa, CA) ●Target® (Stryker Neurovascular, Fremont, CA) ●Barricade™ (Balt USA, Irvine, CA) | ●Simple to use and deploy ●Very controllable in low- or moderate-flow states ●Proximal flow arrest | ●No distal penetration |
Large particles ●Polyvinyl alcohol (PVA) | ●Relatively safe ●Proximal flow arrest ●Causes significant inflammatory reaction and vessel fibrosis | ●No distal penetration ●Significant recanalization rate ●Clumping/aggregation may occur, occluding vessel more proximal than expected based on size |
n-Butyl cyanoacrylate (NBCA) | ●Excellent distal penetration ●Forms permanent cast of the vessel, progressing to chronic inflammation and fibrosis | ●Difficult to control in high-flow fistulae ●Requires experience to aid in tailoring an NBCA/Ethiodol mixture ratio resulting in an appropriate polymerization time ●Recanalization can occur if only partial embolization is achieved |
Ethylene vinyl alcohol copolymer (Onyx) ●Onyx18 ●Onyx34 | ●Easy to control ●Excellent distal penetration ●Used commonly, well-understood ●Nonadhesive, allowing for longer injection times and temporarily suspending injection if necessary ●Provides body to the tumor and delineates operative margins to facilitate surgical manipulation and resection | ●High radiation exposure and time commitment ●Dimethyl sulfoxide (DMSO) can be neurotoxic and rapid injection may cause vasospasm and necrosis, which may increase chances of cranial neuropathy ●Can cause sparking with electrocautery during surgery |
Small particles ●Tris-acryl Gelatin ●Microspheres (Embospheres) | ●Excellent distal penetration ●Generally won’t aggregate/clump ●Causes significant inflammatory reaction and vessel fibrosis ●Consistent particle size | ●Need for intermittent agitation to maintain suspension ●Can be difficult to control ●High risk of capillary penetration which may cause ischemia and cranial neuropathy |
Ethanol | ●Excellent distal penetration | ●Rarely used ●Difficult to control, disseminates widely ●Rapidly diluted by vascular inflow |
3.5 Case Examples
Case 1. A 15-year-old boy with a new diagnosis of a large JNA was referred for preoperative tumor embolization (Fig. 3.1). Preprocedure anteroposterior (AP) and lateral right ECA injection demonstrated intense tumor blush from the distal internal maxillary artery (Fig. 3.2), and this vessel was selected for embolization with Onyx18. Intraprocedural, super-selective right distal internal maxillary artery injection demonstrated extensive tumor blush (Fig. 3.3). Postembolization AP and lateral digital subtraction angiography (DSA) of the right ECA demonstrates no residual tumor supply from the right ECA (Fig. 3.4); however, ICA injection reveals persistent tumor blush from several cavernous carotid branches (Fig. 3.5). Given the elevated risk with super-selective catheterization and embolization of these intracranial cavernous ICA branches, the embolization procedure was terminated. The patient underwent successful endonasal surgical resection with resultant gross total resection the following day.
Case 2. A 54-year-old man presented to his otolaryngologist with 3 months of right-sided hearing loss and facial hemiparesis and was found on MRI to have an avidly-enhancing posterior fossa tumor in the region of the right cerebellopontine angle (Fig. 3.6) with a presumed diagnosis of hemangiopericytoma. At the request of his neurosurgeon he underwent preoperative embolization. Right ECA injection revealed multiple feeding arteries (Fig. 3.7, red arrows) to the tumor (black arrow) from the right internal maxillary and middle meningeal arteries. Super-selective injection of the right MMA revealed significant tumor blush (black arrow, Fig. 3.8), and the patient then underwent Onyx18 and Barricade coil embolization of the right MMA with no residual filling from the MMA at the end of the procedure (Fig. 3.9).
Additional tumor vascular supply was identified from cavernous branches of the right ICA (Fig. 3.10) and from the right superior cerebellar artery (SCA) and anterior inferior cerebellar artery (AICA) (Fig. 3.11). The right SCA was super-selectively catheterized and embolized with Onyx18. Postembolization angiography of the posterior circulation demonstrated no residual tumor filling from the right SCA; residual filling from AICA remained (Fig. 3.12). At this point two large pedicles supplying the tumor had been successfully embolized and total fluoroscopy time had exceeded 60 minutes; the neurointerventionalist and the neurosurgeon jointly elected to end the embolization procedure. The patient awoke from the procedure with no new neurologic deficits, and he underwent gross total tumor resection the following day. The pathology revealed that the tumor was a hemangioblastoma rather than the presumed diagnosis of hemangiopericytoma.