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Embolization of Tumors: Brain, Head, Neck, and Spine
Acknowledgments
The authors thank the staff of Neuroscience Publications at Barrow Neurological Institute for assistance with manuscript preparation.
Hypervascular neoplasms of the central nervous system can be formidable surgical challenges associated with significant morbidity and mortality, with excessive intraoperative blood loss prompting termination of the surgery before achieving its goals. Multiple reports have suggested preoperative embolization reduces intraoperative blood loss, the need for transfusions, operative time, and the length of hospitalization. Embolization also may reduce mass effect and alleviate pain. Furthermore, preoperative embolization can facilitate a complete surgical extirpation by clarifying the surgical field, enhancing tumor boundaries, and shrinking the tumor.
In most cases, preoperative embolization of arterial pedicles in various vascular central nervous system tumors is technically feasible, regardless of the tumor’s origin and location ( Table 63.1 ). The goals of tumor embolization are sacrificing the feeding vessels and obliterating the tumor capillary bed to the greatest extent possible. These goals must be balanced against the risks of embolization, which include occlusion of en passage vessels, pulmonary emboli, retained microcatheters, and compression of eloquent neural tissues by expanding intratumoral edema or hemorrhage. There has been mixed evidence suggesting reduced blood loss and reduced surgical times; the ongoing debate about the utility of preoperative embolization is based on variable case selection criteria and variable quality of embolization. , Judicious selection of patients, safe embolization technique, and adequate devascularization are critical to achieving a favorable risk-benefit profile for embolization.
Table 63.1
Barrow Neurological Institute Series of 129 Embolized Central Nervous System Tumors (1995–2009)
| Tumors | No. |
|---|---|
| Meningiomas | |
| Olfactory groove | 2 |
| Convexity | 10 |
| Skull base | 1 |
| Parasagittal | 3 |
| Frontal | 5 |
| Sphenoid | 3 |
| Paraganglioma | |
| Glomus jugulare | 17 |
| Glomus tympanicum | 1 |
| Carotid body tumors | 7 |
| Hemangioblastoma | 12 |
| Juvenile nasal angiofibroma | 25 |
| Hemangiopericytoma | 3 |
| Others | |
| Plasmacytoma (spinal) | 1 |
| Aneurysmal bone cyst (spinal) | 2 |
| Thyroid carcinoma met (spinal) | 1 |
| Hemangioma (skull base) | 1 |
| Hemangioma (facial) | 2 |
| Hemangioma (spinal) | 4 |
| Renal carcinoma met (spinal) | 12 |
| Renal carcinoma met (cranial) | 1 |
| Giant cell tumor | 3 |
| Vestibular schwannoma | 1 |
| Jugular foramen nerve sheath tumor | 1 |
| Synovial cell sarcoma (spinal) | 1 |
| Osteogenic sarcoma (spinal) | 1 |
| Schwannoma (spinal) | 2 |
| Pharyngeal carcinoma | 2 |
| Chordoma (spinal) | 1 |
| Nasal polyp | 1 |
| Thyroid carcinoma | 1 |
| Melanoma (spinal) | 1 |
| Dural cavernous malformation | 1 |
| Total | 129 |
Broad Principles of the Arterial Supply
Vessels of the head, neck, and spine supply the soft tissue surrounding the neural axis, the dural covering, the proximal nerves, and the parenchyma of the brain and spinal cord. Tumors may recruit supply from any of these sources, depending on both the origin and location of the tumor. Many tumors can grow quite large before disrupting tissue planes and recruiting vascular supply from tissue distinct from the site of origin. Vessels supplying the parenchyma of the brain, the pial vessels, include the intradural branches of the internal carotid artery (ICA) and vertebral arteries as well as the anterior spinal artery. Embolization in these vessels carries the risk of off-target embolization to the parenchymal vessels. Embolization via pial vessels focuses on distal catheterization to minimize the at-risk territory. Catheterization and removal of the catheter also present risk of dissection with associated hemorrhagic and ischemic complications of pial vessel embolization. In our experience, tumors supplied mostly by pial vessels have limited devascularization without significant risk of embolic complications.
Dural vessels derive from branches of the external carotid artery (ECA) as well as proximal branches of the ICA and vertebral artery. Before supplying the dura, these branches often supply the cranial nerves as they traverse the cranial foramina. Embolization is therefore safer after distally catheterizing these vessels. However, reflux of embolisate or solvent can still result in cranial nerve palsy. Within the dura, the ease of distal catheterization corresponds with the caliber of the vessel, although the tentorial arteries derived from the meningohypophyseal trunk are notably tortuous and typically difficult to catheterize even when dilated due to pathologic recruitment. In our experience, distal catheterization of the middle meningeal artery (MMA) offers effective embolization of the tumor capillary bed when the tumor is dural based. The structural support of the dura also reduces the risk of vessel avulsion during catheter removal.
The dural and pial vessels do not exist in isolation but as an interconnected network, with anastomoses that have variable calibers. The flow through these anastomoses varies from patient to patient and also varies with physiologic and therapeutic changes. Alterations of flow during embolization can result in recruitment of previously angiographically occult anastomotic channels. These anastomoses are most frequently observed at the anterior skull base between the ethmoidal arteries and the ophthalmic artery, as well as in the spinal vascular supply. The approaches to each type of tumor depend on the specific vascular supply from this broad framework.
Tumors of the Head and Neck
Meningiomas
Meningiomas originate from arachnoid cap cells and can be hypervascular. They are slightly more common in women than men and account for 13% to 18% of all intracranial tumors. Symptomatic or growing lesions are primarily managed with extirpation. Recurrence is dependent on the pathologic grade but is also inversely proportional to the extent of surgical resection, as classified by the Simpson grade. The resection of many large meningiomas has been aborted due to heavy intraoperative blood loss, a complication that can be mitigated with the judicious use of preoperative embolization. Angiography and preoperative embolization of intracranial meningiomas are common practices used to improve the likelihood of complete resection and cure. Angiography is also essential for surgical planning to delineate the vascular supply to the tumor, the encasement and patency of vascular structures (arteries or dural venous sinuses), the degree of displacement of neuronal elements, and the site of dural attachment.
Vascular Targets
The blood supply to meningiomas is typically twofold: large dural arterial pedicles and pial and cortical arteries. Classically, large arteries supply the site of dural attachment and the bulk of the tumor, creating a sunburst appearance on angiography. The epicenter of the sunburst is usually the site of dural attachment. The pial and cortical vessels usually supply the tumor capsule, with their vascular contribution increasing as the tumor enlarges. Large arterial pedicles typically arise from branches of the ECA, but they may also arise from the ICA. Dural pedicles arising from the ECA include the MMA, accessory meningeal artery, neuromeningeal artery (arising from the ascending pharyngeal artery), and stylomastoid artery (arising from the occipital artery). The ICA occasionally supplies meningiomas via ethmoidal, cavernous, clival, or tentorial branches.
The location of the meningioma suggests which vessels warrant scrutiny during angiography. Anterior fossa meningiomas can be supplied by both the ICA and the ECA bilaterally. Diaphragmatic or tuberculum sellae meningiomas frequently derive blood supply from branches of the supraclinoid ICA. High-convexity and parasagittal tumors tend to feed from the MMA, superficial temporal artery, and the artery of the falx cerebri and warrant angiography of the bilateral anterior circulation. Tumors of the anterior falx or frontal convexity frequently receive their blood supply from the meningeal branches of the ethmoidal artery and anterior falcine branches or, occasionally, from the anterior cerebral artery or a tentorial branch of the ophthalmic artery. Bilaterally, the anterior or posterior ethmoidal arteries often supply olfactory groove lesions, and evaluation of the ophthalmic and distal internal maxillary arteries must be meticulous due to occult collateral supply and risk to the central retinal artery.
Branches of the ECA, specifically the artery of the foramen rotundum, vidian arteries, or accessory meningeal artery, usually supply middle fossa meningiomas. The vascular supply of meningiomas involving the sphenoid wing often derives from the recurrent meningeal branch of the ophthalmic artery or branches of the MMA. Parasellar meningiomas tend to be fed by branches of the petrous, cavernous, or supraclinoid branches of the ICA, and the arteries of the foramen rotundum, and foramen ovale, or the neuromeningeal branch of the ascending pharyngeal artery.
The vascular supply of posterior fossa meningiomas is usually from the posterior meningeal artery, MMA, or accessory meningeal artery. Classically, tentorial meningiomas receive arterial feeders from the tentorial branch of the meningohypophyseal trunk, but they can be supplied by the infratentorial trunk, MMA, or accessory meningeal artery. Petroclival lesions are often supplied by the MMA (frequently from the petrosal, petrosquamosal, or occipital branches), transmastoid branches of the posterior auricular or occipital arteries, anterior inferior cerebellar artery (via the subarcuate branch), or neuromeningeal branch of the ascending pharyngeal artery.
The common vascular origins shared by posterior fossa meningiomas and cranial nerves require diligent attention when embolization of these lesions is considered. For example, cranial nerves III to VI share blood supply with tentorial meningiomas via the MMA, meningohypophyseal trunk, or accessory meningeal artery branches. Provocative testing before embolization can minimize the risks of inadvertently injuring the cranial nerves. Furthermore, extracranial-to-intracranial (EC-to-IC) arterial anastomoses, particularly between posterior auricular or occipital arteries and the high cervical spinolaminar segment of the vertebral artery, may be present.
Meningiomas commonly invade the dural venous sinuses. Patency of the adjacent sinus and surrounding cortical veins is an important consideration and should be evaluated to facilitate surgical planning. Complete occlusion of the venous sinus may allow aggressive surgical resection through excision of the involved portion of the sinus.
Considerations
Many meningiomas do not require preoperative embolization because they often can be easily devascularized at surgery. At our institution, we recommend preoperative embolization of giant meningiomas, meningiomas involving the skull base, and those involving the pineal region ( Fig. 63.1 ). In these meningiomas, the vascular pedicle may be obscured until the tumor is debulked. In patients who are poor surgical candidates, embolization may be offered as a palliative measure to slow tumor growth.
The most common pedicle for embolization in our experience is the MMA. This arterial pedicle has the lowest risk profile and achieves significant penetration of the liquid embolisate into the capillary bed, with retrograde penetration into other arterial feeders. Although this pedicle is amenable to early surgical ligation, embolization offers significant penetration into the tumor for substantial hemostatic benefit if there is more than one arterial pedicle. The boundaries of the tumor must be well delineated on control angiography due to the risk of retrograde transtumoral embolization of pial feeders. At our institution, we assess all feeding pedicles at initial control angiography and then initiate embolization via the MMA. If the MMA embolization does not achieve adequate devascularization, we turn our attention to other feeders. Embolization of deep-feeding arteries such as the inferolateral trunk of the cavernous ICA and the meningohypophyseal trunk can be technically challenging due to their small caliber and acute angle of origin. Technological advances in microcatheters and microguidewires have facilitated superselective catheterization of these blood vessels and have expanded the range of treatable intracranial lesions through embolization. Even so, the potential for reflux of the embolisate into the ICA remains a serious concern, and such lesions continue to present major challenges. The inferolateral trunk occasionally has collaterals with the ophthalmic artery via the deep recurrent ophthalmic artery. During embolization of the inferolateral trunk, extreme caution is warranted to minimize the risk of potential blindness. Various neurosurgeons have begun pursuing balloon-modulated embolization from the ICA, with reported success in case reports. However, the risk-benefit profile of these complex maneuvers is not well understood. We have not found the evidence convincing enough to suggest to patients that the risk from these embolization techniques is less than that of the surgical approach. , Although previous reports have suggested effective embolization via branches of the ICA, these authors worked with first-generation embolic agents and assessed embolization using angiographic blush. The risks and complications of embolization with liquid embolisates do not follow the same profile as that of particulate embolisates, and extrapolation from earlier studies may lead to unsatisfactory outcomes. More importantly, the assessment of successful embolization continues to be debated within the broader debate of preoperative embolization for meningiomas, but angiographic blush is likely to result in underrepresentation of tumor vascularity during the surgical approach, and angiographers may overstate the extent of embolization. At our institution, we avoid embolization via pial branches; unlike in arteriovenous malformations, there are rarely dilated arterial pedicles terminating in the meningioma. Although in vascular malformations, a small cerebellar infarct from the distal sacrifice of the superior cerebellar artery (SCA) is clinically tolerated, stroke can typically be avoided during resection of a meningioma and would add significant morbidity.
Embolization of pial or ophthalmic branches is usually considered too perilous to undertake. However, some neurosurgeons have reported cases of successful ophthalmic artery or distal cortical branch embolization. , Based on their experience, they recommend that embolization of pial or cortical vessels only be undertaken if the following conditions are met: (1) The tumor is supplied exclusively by the ICA; (2) the tumor is in a noneloquent portion of the brain; (3) the patient has a negative sodium amytal test; (4) superselective catheterization is performed with the catheter directly abutting the tumor capsule ; and (5) particulate, rather than glue-based, embolisate is used, although other groups have had increasing success with liquid embolisates.
Pineal region meningiomas are rare, accounting for 0.3% of intracranial meningiomas and 6% to 8% of pineal region tumors. These uncommon lesions draw their blood supply from a variety of sources, including meningeal branches of the ECA, the tentorial artery, medial or lateral posterior choroidal branches, branches of the superior vermian or SCA, meningeal branches of the posterior inferior cerebellar artery, or vertebral arteries. Arguably some of these vascular pedicles suggest a confusion of falcotentorial meningiomas with pineal meningiomas. Sagoh et al. reported successful embolization of a pineal region meningioma with estrogen alcohol and polyvinyl alcohol (PVA) via the bilateral MMAs.
Optic nerve meningiomas are seldom amenable to endovascular treatment because of the shared blood supply between the tumor and the optic nerve. Terada et al. concluded that if the microcatheter can be positioned distal to the origin of the central retinal artery, embolization is possible. However, the risk of causing blindness is high if reflux occurs into the central retinal artery. In many cases, aggressive embolization of optic nerve meningiomas is neither beneficial nor advisable.
Indications for Embolization
The primary rationale for the embolization of meningiomas is to reduce blood flow to the tumor, thereby facilitating more extensive surgical resection. Several studies have attempted to compare the risks associated with preoperative embolization for meningioma resection with its benefits. Bendszus et al. concluded that intraoperative blood loss was reduced only in patients who underwent complete tumor embolization as defined by the absence of tumor blush on angiography. At our institution, we routinely obtain postoperative gadolinium-enhanced magnetic resonance imaging (MRI) the night after embolization to evaluate the extent of devascularization. Although some groups have investigated the utility of blood flow and perfusion sequences to evaluate tumor vascularity after embolization, routine T1 enhancement is very effective and widely available.
Dean et al. performed a retrospective study to determine the risk-to-benefit profile of preoperative embolization of meningiomas. In the study, 33 patients underwent preoperative embolization followed by surgical resection. These patients were compared to an appropriately matched group with 193 nonembolized meningiomas that were extirpated. Preoperative embolization significantly reduced intraoperative blood loss and the need for transfusion. The operative time, total cost, length of hospital stay, and complication rates were similar in both groups. Other authors have found similar findings. ,
Complications
The overall risk associated with endovascular embolization of meningiomas is low, and a recent large meta-analysis estimated a 4.6% complication rate with a major complication rate of 0.2%. Major complications include stroke, blindness, intratumoral edema, or hemorrhage. Migration of embolic material via reflux or an unappreciated EC-to-IC anastomosis is the most common cause of major morbidity associated with embolization. The neurointerventionalist must have a working knowledge of the highly variable anatomy of EC-to-IC anastomoses and must constantly remain vigilant for the possibility of proximal reflux. Cataclysmic intratumoral swelling can follow embolization, particularly when performed with particulate embolisates, and can require emergency resection. Our practice is to resect meningiomas the day after embolization. Tumor swelling can sometimes be mitigated by the administration of corticosteroids.
Minor complications occur in as many as 30% of patients and include facial pain, trismus, or both. These adverse effects can be managed symptomatically with corticosteroids or analgesics and are usually self-limiting. Rare complications such as cranial nerve damage (thought to be related to occlusion of the vasa vasorum of the cranial nerves), subarachnoid hemorrhage, or retinal embolus have been reported. , Scalp necrosis is a rare but serious complication occasionally associated with embolization of ECA vessels. Several authors recommend preserving the superficial temporal artery as a donor vessel for a free tissue transfer in the event of massive scalp necrosis. ,
Patients with skull base meningiomas often become symptomatic with some degree of cranial nerve dysfunction. Embolization can exacerbate this dysfunction, which should be emphasized during preoperative patient counseling. Embolization of the petrous branches of the MMA (which frequently supplies lesions of the posterior fossa or posterior parasellar region) can result in damage to the facial nerve. Embolization of branches of the ascending pharyngeal artery (which supplies clival or petroclival meningiomas) risks damage to the lower cranial nerves. The practice of superselection of tumor blood vessels as distally as possible, ideally with the microcatheter immediately adjacent to the tumor capsule, decreases the risk of inadvertent embolization of vessels supplying normal tissue. If there is any uncertainty, provocative testing may help define the shared vascular supply to the cranial nerves.
Paragangliomas
Paragangliomas are typically benign, slow-growing tumors of neural crest origin arising from chemoreceptors located in blood vessel walls. A rare tumor with an incidence of 1:30,000, they occur sporadically more commonly in women in the 5th decade of life and also present in familial clusters with a male predominance at a younger age. Certain familial patterns or associations with genetic syndromes (multiple endocrine neoplasia II, neurofibromatosis 1, von Hippel-Lindau disease, familial paraganglioma, or Carney triad) have been associated with the diagnosis of paragangliomas. Multiple paragangliomas have been found in 22% and 87% of sporadic and familial paragangliomas, respectively. , Less than 10% of paragangliomas are malignant. Indium-111 octreotide, a radioisotopic somatostatin analog, has been used as a labeling tracer to selectively identify multiple or metastatic paragangliomas.
Paragangliomas, which are highly vascular tumors, are often referred to a neurointerventionalist for presurgical embolization at the neurosurgeon’s request. In the head and neck, the most common location is at the carotid body, followed by the temporal bone (glomus jugulare or glomus tympanicum) and upper pharyngeal space (glomus vagale). Although histologically similar to pheochromocytomas, only 4% of paragangliomas of the head and neck are associated with catecholamine hypersecretion. Clinical evidence of paroxysmal catecholamine surges must be evaluated preoperatively by 24-hour urine collection for fractionated catecholamine and metanephrine measurements.
Carotid body tumors arise from the carotid body, which is located at the posterior aspect of the carotid bifurcation. The chemoreceptive cells of the carotid body are located in the periadventitia of the carotid bifurcation and are primarily responsive to hypoxia. Conditions of chronic hypoxia, such as living in high altitudes (more than 1500 m above sea level), chronic obstructive pulmonary disease, and cyanotic heart disease are known risk factors for the development of carotid body tumors.
The most common presentation associated with carotid body tumors is painless, slowly enlarging neck mass. These tumors can cause lower cranial nerve dysfunction (i.e., hoarseness, stridor, or hypoglossal palsy) due to local mass effect, but they rarely grow larger than 4 cm. The diagnosis of carotid body tumors can be confused with glomus vagale. The latter lesions typically arise from paraganglionic tissue rests within the nodose ganglion and are found immediately rostral to the carotid bifurcation. The angiographic appearance of carotid body tumors and glomus vagale tumors differs in that carotid body tumors characteristically splay the ICA and ECA ( Fig. 63.2 ), whereas vagal paragangliomas tend to displace the carotid arteries anteriorly and medially.
Glomus jugulare tumors arise from glomus rests within the jugular foramen. Patients often complain of progressive unilateral hearing loss or pulse-synchronous tinnitus. Otoscopic examination of the external auditory canal may reveal a red or blue pulsatile mass. If seen on computed tomography (CT), bone-remodeling phenomena (e.g., demineralization, erosion, and destruction of bony structures) can be suggestive of the presence of a paraganglioma within the temporal bone. Gadolinium-enhanced MRI remains the predominant, noninvasive diagnostic imaging modality. On both T1- and T2-weighted sequences, these lesions typically appear as intensely gadolinium-enhancing masses with “salt-and-pepper” flow voids.
Angiography of these lesions must identify the intracranial and extracranial supply to the tumor, as well as the involvement of the dural venous sinus system. The patency of both transverse and sigmoid sinuses must be evaluated to determine whether the sacrifice of the involved sinus is feasible without causing venous hypertension and infarction. The blood supply to a carotid body tumor is typically derived from proximal ECA branches or is derived directly from the bifurcation. The blood supply to tympanojugular tumors is almost uniformly derived from the ascending pharyngeal artery. Glomus tympanicum tumors usually receive blood supply from the inferior tympanic branch of the ascending pharyngeal artery, while branches of the neuromeningeal trunk supply the hypoglossal canal and jugular fossa lesions. These lesions tend to be small and rarely require preoperative embolization. Glomus tumors within the temporal bone are often fed by branches of the petrous (via the vidian artery) or cavernous (clival branch of the meningohypophyseal trunk) segments of the ICA.
Glomus jugulare tumors, particularly those that extend into the intracranial compartment, require preoperative embolization. These lesions frequently are multicompartmentalized, with a separate arterial supply to each compartment. Historically, these lesions were approached with direct puncture since each arterial feeder would need to be serially catheterized for embolization. With the increased use of liquid precipitate embolisates, transfemoral transarterial embolizations are more successful at tumor devascularization via penetration of the capillary beds and retrograde embolization of noncatheterized arterial pedicles. In general, the ascending pharyngeal artery supplies the inferomedial compartment, while the stylomastoid branch of the occipital or posterior auricular artery contributes to the posterolateral compartment. The anterior compartment tends to be supplied by branches of the internal maxillary artery or the caroticotympanic artery. Branches of the MMA typically feed the superior compartment. If the sacrifice of the jugular vein or sigmoid sinus will be necessary during the surgical approach, the intracranial venous outflow system should also be evaluated during angiography.
Superselective catheterization of the arterial pedicles is crucial for evaluating the angioarchitecture of the tumor and for identifying EC-to-IC anastomoses. Many such superselective microcatheterizations may be required to opacify or embolize the entire tumor. Tumors with a substantial blood supply from the ICA or significant encasement of the ICA may not be amenable to surgical resection and can be evaluated for possible vessel sacrifice with balloon test occlusion.
Embolization reduces operative time and intraoperative blood loss. , In the hands of an experienced neurointerventionalist, the risk of embolization for carotid body tumors is acceptably low, although the yield is probably too low to justify embolization of lesions smaller than 2 cm. Due to the local soft-tissue inflammatory response, surgery within 48 hours of embolization is strongly recommended.
Complications
Most severe complications associated with embolization of head and neck paragangliomas are related to the inadvertent migration of embolisate into the intracranial circulation either through reflux or through the rich and highly variable EC-to-IC anastomotic network. Embolization of glomus jugulare tumors can cause lower cranial nerve palsies, presumably from embolization of the vasa vasorum supplying these nerves. Facial nerve palsies and even herniation syndromes have also been reported as rare complications of glomus jugulare tumor embolization. , Temporary facial nerve paresis is common, about 6.6%, after embolization because the facial nerve often receives its blood supply from the stylomastoid artery and the petrosal branches of the MMA or accessory meningeal artery. Recovery of facial nerve paresis is more common when PVA is used as the embolic agent because the vessels tend to recanalize. Occasionally, n -butyl cyanoacrylate ( n- BCA) and dimethyl sulfoxide (DMSO) may result in transient palsy from toxicity or vasospasm. Provocative testing may elucidate the risks of cranial nerve injury, although it has not been formally studied in the embolization of paragangliomas. Anesthesiology support and close monitoring are prudent with secreting tumors due to rare reports of catecholamine release and hypertensive crisis during embolization. Overall, the risk of complications from embolization is less than that of surgical management.
Hemangioblastomas
Hemangioblastomas are benign, hypervascular neoplasms primarily found in the cerebellum or spinal cord. They account for 1% to 2% of craniospinal tumors and occur most commonly within the cerebellar hemispheres, followed by the vermis, cerebellopontine angle, or brain stem. Most hemangioblastomas are sporadic, but 20% are associated with von Hippel-Lindau disease. The disease has an autosomal dominant inheritance pattern with incomplete penetrance. Multiple hemangioblastomas are common in patients with von Hippel-Lindau disease.
Operative morbidity is high because of uncontrollable bleeding, so naturally, these lesions have been targeted for preoperative embolization. The blood supply to cerebellar hemangioblastomas is typically from the posterior inferior cerebellar artery, but the anterior inferior cerebellar artery or SCA branches can also contribute. Pontomedullary lesions often derive their blood supply from SCA branches, while cervicomedullary lesions are supplied by branches of the vertebral artery or anterior spinal artery. Superficial lesions can draw blood supply from dural branches of the vertebral artery (i.e., posterior meningeal artery). Due to the highly vascular nature of these lesions, the caliber of the feeding artery can exceed that of the basilar artery.
The risk associated with embolization of hemangioblastomas is high, on the order of 11% in a recent systematic review but previously as high as 50% in single series because the feeding arteries are often pial vessels. Suboptimal penetration of the embolisate into the tumor nidus offers little in terms of reducing operative blood loss, particularly in posterior fossa lesions. The patient is thereby typically exposed to the risk of the embolization procedure without incurring any benefit. However, some hemangioblastomas may have significant surgical complications, including aborted extirpation due to intraoperative blood loss; there may be an indication for identifying microsurgically difficult pedicles in challenging hemangioblastomas. Some authors postulate that postembolization hemorrhage is related to venous outflow obstruction. ,
Between 1995 and 2009, we successfully embolized 13 posterior fossa hemangioblastomas. One patient suffered a nonfatal complication (stroke) as a result of embolization. Therefore, the morbidity rate was 7.7%. In 3 cases, embolization was aborted due to the lack of tumor vessels suitable for embolization. This situation underscores one of the tenets of safe embolization of posterior fossa hemangioblastomas: Judicious tumor selection is key to minimizing complications. Only a small percentage of hemangioblastomas resected at our institution are deemed suitable for preoperative embolization. Embolization is reserved for large lesions, lesions with arterial feeders that are difficult to access surgically, or lesions that cannot be resected due to intraoperative hemorrhage. By placing the microcatheter tip beyond normal vessels directly into the tumor vasculature, the risks associated with embolization can be mitigated.
The potential for postembolization hemorrhage or swelling exists and can be especially precipitous in the posterior fossa. However, we strongly believe that by meticulously adhering to the tenets of superselective catheterization and intracranial tumor embolization, hemangioblastomas of the posterior fossa can be safely embolized to aid surgical resection.
Solitary Fibrous Tumor (Previously Named Hemangiopericytoma)
Solitary fibrous tumors (SFTs) are aggressive mesenchymal tumors arising from the contractile pericytes of Zimmerman, which are leiomyoblastic cells surrounding capillaries and postcapillary venules. These intracranial extra-axial neoplasms account for less than 1% of intracranial tumors. They commonly appear similar to meningiomas on imaging, although they may have a heterogeneous enhancement pattern on T2-weighted imaging and prominent intratumoral flow voids as well as diffusion restriction. On magnetic resonance spectroscopy, they show increased choline and decreased creatinine and n -acetylaspartate, and they are typically more heterogeneous than meningiomas. They are associated with high rates of recurrence and have the potential for metastasis despite combined surgical and radiation therapies.
SFT are highly vascular lesions, and intraoperative hemorrhage can be significant. Hemorrhage is the most common cause of subtotal resection or operative morbidity. Gross total resection has a significant advantage over subtotal resection for recurrence (38% vs. 84%, respectively). Embolization substantially reduces intraoperative bleeding and facilitates resection. However, embolization can be technically difficult because these tumors tend to parasitize cortical vessels. Embolization via these vessels has a higher risk of complication, so embolization is often completed using direct puncture techniques. We have also had success with Onyx, n- BCA, and PVA through transarterial approaches. Postembolization swelling is common with these lesions; therefore, resection within 48 hours of embolization is recommended.
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