Embolization Technique

Diagnostic angiography and tumor embolization are performed 1 to 2 days before the scheduled surgical resection to allow time for tumor necrosis while avoiding neovascularization. However, some report waiting as long as 7 days between embolization and surgery.² The patient should be well hydrated before the commencement of angiography to protect renal function from the contrast material.

The diagnostic angiogram is extremely important to identify not only the vascular supply to the tumor but also dangerous anastomoses. In-depth knowledge of anatomy and potential external carotid–to–internal carotid anastomoses is essential for performing tumor embolization safely and effectively.⁴ The most common anastomoses that one must evaluate are listed in Table 110-1. The other pitfall that must be avoided is embolizing the vascular supply to the cranial nerves and roots. Knowledge of the anatomy is essential; however, one should exercise caution and know that vascular distributions are highly variable. If any doubts remain, administering 3 mL of lidocaine and testing for cranial nerve deficits can be performed before embolization.² Table 110-2 lists the common vascular supply to the cranial nerves and roots. In addition, amobarbital may be used to assess the arterial blood supply to the brain parenchyma.^5,6 Monitored anesthesia care is necessary to perform provocative testing. However, some patients cannot tolerate monitored anesthesia care and therefore require general anesthesia. Although general anesthesia negates the use of provocative testing, it does provide some benefits, such as increasing the accuracy of angiography (less motion artifact) and patient comfort (manipulation inside the middle meningeal artery can produce extreme discomfort). Continuous electroencephalographic monitoring along with somatosensory evoked potentials can provide insight that a complication has occurred when general anesthesia is used.

TABLE 110-2 Cranial Nerve Blood Supply from Potentially Embolized Vessels

ICA, internal carotid artery.

Once the diagnostic angiogram is performed and it is deemed safe to continue with the embolization, the patient is given 10 mg of dexamethasone and fully heparinized before insertion of the microcatheter and guide catheter. Dexamethasone is administered to help with the potential postoperative edema, and the patient should be heparinized to at least two times the baseline activated clotting time to prevent the formation of emboli from the catheters.

A microcatheter and microguidewire are selectively placed, under digital subtraction angiography and road map guidance, into a feeding vessel as close to the tumor as possible. The guidewire is removed and the embolic agent injected under continuous road map imaging to ensure that it does not reflux around the catheter, travel through anastomoses previously not visualized, be deposited in brain parenchyma, or travel beyond the tumor bed into the venous system. Once this feeding arterial supply is completely embolized, the catheter is then selectively placed into another feeding vessel (that is safe to embolize), and the process is repeated. The embolization procedure is complete when no tumor blush is visualized or no other feeding vessel can be safely embolized. It is important to emphasize that embolization should take place at the tumor bed itself and not just at the proximal feeding artery. Occlusion of the proximal feeding artery alone will result only in the formation of collateral blood supply and ineffective embolization. After embolization, the patient is maintained on steroid therapy and admitted for observation.

Embolic Agents

Several different agents can be used for tumor embolization (Table 110-3). The agents fall into one of three main categories: liquids, particulates, or coils. The agent selected depends on the presence or possibility of a dangerous anastomosis, the ability to navigate the microcatheter to the ideal location, vascular supply to the cranial nerves, and operator preference. The vasa nervorum are usually less than 150 to 200 µm; therefore, if cranial nerves are at risk, it is recommended that embolic agents larger than 200 µm in size be used.⁴ The best embolization results are achieved with small or liquid agents that can penetrate the tumor bed and embolize at the capillary level. These agents are also the most dangerous to use because they can damage normal structures as well. Large embolic agents, such as coils or particles larger than 500 µm, are relatively safe but are ineffective if used alone. A good mixture of safety and efficacy is achieved when embolic agents ranging in size from 300 to 500 µm are used.⁴

TABLE 110-3 Classification of Embolic Agents

ETOH, ethyl alcohol; NBCA, N-butylcyanoacrylate; PVA, polyvinyl alcohol.

Efficacy

The efficacy of tumor embolization is debatable. Several small series published in the literature support the use of tumor embolization and its benefits,^7–11 but there are also reports that question the efficacy and utility of preoperative tumor embolization, most notably for meningiomas.¹² Currently, the overall consensus within the field of neurosurgery is that preoperative tumor embolization is beneficial in reducing intraoperative blood loss in patients with vascular tumors. However, no large randomized study has demonstrated that preoperative embolization improves outcome or increases surgical success rates.

Meningiomas

Meningiomas are extra-axial tumors that arise from arachnoid cells in the leptomeninges and account for approximately 15% of all intracranial neoplasms.¹³ These tumors are usually quite vascular because they arise from the dura, which is a heavily vascularized structure.¹⁴ Convexity meningiomas seem to have a greater vascular supply than do skull base meningiomas, and the closer the convexity meningioma to the midline, the greater the chance of bilateral supply.⁴

The complication rate for embolization of meningiomas is low. Lasjaunias and Bernstein reported that 3 of 185 (1.6%) patients had a permanent neurological deficit after embolization,¹⁵ and Halbach and colleagues reported a morbidity rate of less than 0.5% after embolization of several hundred meningiomas.⁴

A convexity meningioma is seen in Figure 110-1A. Diagnostic angiography revealed the vascular supply to this tumor to be from branches of the middle meningeal artery (see Fig. 110-1B). Under digital subtraction angiography and road map guidance, a microcatheter was navigated into one of the feeding vessels (see Fig. 110-1C). Embospheres (300 to 500 µm) were then injected into the tumor bed until the tumor blush dissipated (see Fig. 110-1D). This was repeated in all the feeding vessels until tumor blush was no longer visualized.

FIGURE 110-1 A, T1-weighted contrast-enhanced magnetic resonance image of a meningioma. B, Lateral angiogram of the right external carotid artery demonstrating tumor blush. C, Microcatheter in a branch of the middle meningeal artery demonstrating tumor blush. D, Angiogram after embolization demonstrating the absence of tumor blush.

Juvenile Nasopharyngeal Angiofibroma

Juvenile nasopharyngeal angiofibromas are rare, highly vascular, benign tumors that occur most commonly in young males.^4,16,17 Patients usually complain of epistaxis and nasal obstruction. These tumors originate in the nasopharynx but may extend into the nose or orbit and intracranially.¹⁸

Treatment options for juvenile nasopharyngeal angiofibroma are surgical resection, radiation therapy, or a combination of the two. However, most agree that surgery is the treatment of choice.^19,20 The role of embolization is debated, but because of the extreme vascular nature of these tumors, most recommend preoperative embolization before surgical resection. However, some argue against preoperative embolization because they believe that it contributes to increased recurrence rates and leads to poor surgical resection.^21,22

The vascular supply to these tumors primarily arises from branches of the internal maxillary artery, facial artery, ascending pharyngeal artery, and internal carotid artery. These tumors frequently have a bilateral vascular supply, and therefore both carotids should be evaluated.²

Paragangliomas

Paragangliomas are highly vascular tumors that arise from paraganglion cells of the parasympathetic nervous system.²³ In the head and neck, these tumors are most commonly located at the jugular fossa, carotid bifurcation, and vagus nerve.^2,4

Clinical findings depend on the location of the tumor. For paragangliomas located at the jugular bulb, patients may have dysfunction of cranial nerves IX to XII. Tumors in this location are often referred to as glomus jugulare tumors. Tumors located at the carotid bifurcation, called a carotid body tumor, may be manifested as a painless neck mass, hoarseness, and dysfunction of cranial nerve XII. Tumors in the middle ear, known as tympanic paragangliomas, can cause tinnitus and dysfunction of cranial nerves VII and VIII. Paragangliomas that occur along the vagus nerve are referred to as vagal paragangliomas and can cause a painful neck mass. Paragangliomas can secrete catecholamines and serotonin regardless of their location, which can result in episodic arrhythmias, hypertension, diaphoresis, headaches, and potential hypertensive crises. Any manipulation of the tumor, such as with surgery, angiography, embolization, or even palpation of the mass, could release these vasoactive substances and precipitate a hypertensive crisis. For this reason, patients suspected of having an actively secreting tumor should be screened preoperatively by testing their urine for vanillylmandelic acid and 5-hydroxyindoleacetic acid. Patients with actively secreting paragangliomas must be premedicated with alpha blockers such as phenoxybenzamine or phentolamine.

The blood supply to these tumors most commonly arises from the ascending pharyngeal artery, as well as other branches from the external and internal carotid arteries. The structures at risk from embolization of these vessels are listed in Tables 110-1 and 110-2. Occasionally, a large number of branches from the internal carotid artery will supply the tumor, and in patients able to tolerate it, consideration of carotid sacrifice is entertained.

A paraganglioma located at the carotid bifurcation in seen in Figure 110-2A. The diagnostic angiogram revealed that the vascular supply was from both the external and internal carotid arteries. A microcatheter was selectively placed into multiple feeding vessels (see Fig. 110-2B). Polyvinyl alcohol particles were injected into multiple feeding arteries until the tumor blush dissipated (see Fig. 110-2C).

FIGURE 110-2 A, Tumor blush of a paraganglioma at the carotid bifurcation. ECA, external carotid artery; ICA, internal carotid artery. B, Microcatheter located in a feeding vessel demonstrating tumor blush. C, Paraganglioma status after embolization with polyvinyl alcohol particles.

Schwannomas

Schwannomas are slowly growing neoplasms that arise from Schwann cells. They occur on cranial and spinal/peripheral nerves and are the most common tumor found at the cerebellopontine angle. The majority of these tumors are hypervascular, but with an inhomogeneous blush seen on angiography because of areas of avascularity mixed within areas of hypervascularity.⁴ The ascending pharyngeal artery is the most common arterial blood supply for intracranial schwannomas. These tumors are treated similar to meningiomas, as described earlier.

Hemangiopericytoma

Central nervous system hemangiopericytomas are a rare occurrence and represent less than 1% of all intracranial tumors.²⁴ These tumors were once thought to be a malignant version of meningiomas; however, they do not have the same genetic characteristics as meningiomas, and the World Health Organization has classified them as a separate entity.^13,24 These tumors behave much more aggressively than typical meningiomas. They have no gender predilection, occur in a younger age group, and have a tendency to recur with the development of late metastasis when compared with meningiomas.¹³

In a study evaluating seven patients with hemangiopericytoma, Akiyama and associates reviewed the radiographic images of these tumors. They reported that computed tomography (CT) and magnetic resonance imaging (MRI) in all seven patients revealed contrast enhancement (four homogeneous on CT and five homogeneous on MRI). Via angiography they found that the feeding vessels to the tumors arose from the pial-cortical vessels in all seven patients, as well as the meningeal-dural vessels in six of the seven patients.²⁴ Only one of the seven patients had a corkscrew vessel within the tumor. All seven tumors were surgically resected, with five of the seven patients sustaining more than 1 L of blood loss, thus revealing how vascular these tumors are.

In other literature, these tumors have been reported to have an arterial supply from branches of the internal carotid artery and vertebrobasilar circulation, as well as from branches of the external carotid artery. The classic angiographic features of these tumors are described as an intense tumor blush with a long-lasting venous phase and corkscrew vessels seen in the tumor itself.²

Conclusion

Tumor embolization is a well-known and frequently used adjunctive therapy for treating vascular pathology in the central nervous system. Most neurosurgeons today agree that embolization of certain vascular tumors decreases intraoperative blood loss and makes surgical resection easier.

Multiple agents and catheters are available to provide safe and effective embolization, provided that the endovascular physician is aware of potential pitfalls, such as external carotid–to–internal carotid anastomosis and the cranial nerve vascular supply. As endovascular technology advances, the safety and efficacy of tumor embolization should continue to improve.