Chapter 89 Embolization of Tumors
Brain, Head, Neck, and Spine
Hypervascular neoplasms of the central nervous system (CNS) can be formidable surgical challenges associated with significant morbidity and mortality. Vascular tumors can result in excessive intraoperative blood loss, prompting termination of the surgery before achieving its goals. Multiple reports have suggested preoperative embolization can reduce intraoperative blood loss, the need for transfusions, operative time, and the length of hospitalization.1–4 Embolization also may reduce mass effect and alleviate pain.5 Furthermore, preoperative embolization can facilitate a more 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 CNS tumors is technically feasible, regardless of the tumor’s origin and location (Table 89-1). 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.
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 |
Tumors of the Head
Meningiomas
Meningiomas originate from arachnoid cap cells and can be hypervascular. They are slightly more common in females than in males and account for 13% to 18% of all intracranial tumors.6 Typically, they are benign, with the potential for a surgical cure with complete resection. Recurrence rates are inversely proportional to the extent of surgical resection. Angiography and preoperative embolization of intracranial meningiomas are common practices used to improve the chances obtaining complete resection and a cure. The resection of many large meningiomas has been aborted due to heavy intraoperative blood loss, a complication that can be mitigated with judicious use of preoperative embolization. Angiography can also assist surgical planning by delineating 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.
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 (MHT), 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 (AICA, via the subarcuate branch), or neuromeningeal branch of the ascending pharyngeal artery.
Outcomes
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 middle cranial fossa or skull base, falcine or parasagittal meningiomas, or meningiomas of the pineal region (Fig. 89-1). During surgery, the vascular supply to skull base meningiomas is frequently obscured until a substantial portion of the tumor has been excised, emphasizing the beneficial utility of embolization in these cases. In patients who are poor surgical candidates, embolization may be offered as a palliative measure to slow tumor growth.
Large, hypervascular skull base tumors whose vascular supply is not readily accessible via surgery should be evaluated for preoperative embolization. Embolization of deep-feeding arteries such as the inferolateral trunk and MHT 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 expanded the range of treatable intracranial lesions through embolization. Even so, the potential for reflux of embolic material into the ICA remains a serious concern, and these lesions continue to present major challenges for even the most experienced neurointerventionalists. Abdel Kerim et al. described a technique of inflating a balloon in the MHT distal to the exit of a tumoral feeding artery to improve the penetration of Onyx (ev3 Endovascular, Irvine, CA) into the feeding vessel.7 Several authors have successfully embolized middle fossa tumors with deep-feeding arteries with good surgical and radiographic outcomes.8–10 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.
Embolization of pial or ophthalmic branches is usually considered too perilous to undertake. However, Kaji et al. reported two cases in which distal cortical ICA branches were successfully embolized with Gelfoam (Pharmacia & Upjohn Company LLC, Peapack, NJ) before surgery.11 Based on their experience, these authors 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 located 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. (5) Particulate, rather than glue-based, embolisate is used.
Pineal region meningiomas are rare, accounting for 0.3% of intracranial meningiomas and 6% to 8% of pineal region tumors.12 These uncommon lesions can 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 superior cerebellar artery (SCA), meningeal branches of the posterior inferior cerebellar artery (PICA), or VAs. Sagoh et al. reported successful embolization of a pineal region meningioma with estrogen alcohol and polyvinyl alcohol (PVA) via the bilateral MMAs.13
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.14 In many cases, aggressive embolization of optic nerve meningiomas is neither beneficial nor advisable.
Indications for Embolization
In general, the primary rationale for the embolization of meningiomas is to reduce blood flow to the tumor, thereby facilitating a more complete 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 absence of tumor blush on angiography.15
We 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 of 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 stay, and rates of complication were similar in both groups. Other authors have found similar findings.16,17
Complications
The overall risk associated with endovascular embolization of meningiomas is low.18,19 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 follows embolization, particularly if performed with particle embolisates, and can require emergent 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.19 These side effects can be managed symptomatically with corticosteroids or analgesics and are usually self-limited. Rare complications such as cranial nerve damage (thought to be related to occlusion of the vaso vasorum of the cranial nerves), subarachnoid hemorrhage, or retinal embolus have been reported.20,21 Scalp necrosis is a rare but serious complication occasionally associated with embolization of ECA vessels. Several authors recommend preserving the STA as a donor vessel for a free tissue transfer in the event of massive scalp necrosis.22,23
Paragangliomas
Certain familial patterns or association with genetic syndromes (multiple endocrine neoplasia II, neurofibromatosis 1, von Hippel-Lindau (VHL) 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.24,25 Indium-111 octreotide, a radioisotope somatostatin analogue, has been used as a labeling tracer to selectively identify multiple or metastatic paragangliomas.26
The most common presentation associated with carotid body tumors is a 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. 89-2), whereas vagal paragangliomas tend to displace the carotid arteries anteriorly and medially.27
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 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.28 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 MHT) segments of the ICA.
Glomus jugulare tumors, particularly those that extended into the intracranial compartment, require preoperative embolization.29 These lesions frequently are multicompartmentalized, with a separate arterial supply to each compartment. To achieve complete embolization of a glomus jugulare tumor, the neurointerventionalist must selectively catheterize and embolize each arterial feeding vessel. 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 sacrifice of the jugular vein or sigmoid sinus will be necessary, the intracranial venous outflow system should 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 substantial 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.30,31 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 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 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 vaso vasorum supplying these nerves. Facial nerve palsies and even herniation syndromes have also been reported as rare complications of glomus jugulare tumor embolization.32,33 Temporary facial nerve paresis is common 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. Provocative testing should be undertaken before glue embolization because this embolisate is relatively permanent and may lead to irreversible deficits.
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.6 Most hemangioblastomas are sporadic, but 20% are associated with VHL disease. The disease has an autosomal dominant inheritance pattern with incomplete penetrance. Multiple hemangioblastomas are common in patients with VHL disease.
Operative morbidity is high because of uncontrollable bleeding, so naturally these lesions have been targeted for preoperative embolization.34 The blood supply to cerebellar hemangioblastomas is typically from PICA, but AICA 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 VA or anterior spinal artery. Superficial lesions can draw blood supply from dural branches of the VA (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 because the feeding arteries are often pial vessels. Suboptimal penetration of embolisate into the tumor nidus offers little in terms of reducing operative blood loss, particularly in posterior fossa lesions. The patient is thereby exposed to the risk of the embolization procedure without incurring any benefit.35 Embolization of posterior fossa hemangioblastomas has been associated with complication rates as high as 50%, although some studies have shown preoperative embolization to be a helpful adjunct to resection.36,37 Some authors postulate that postembolization hemorrhage is related to venous outflow obstruction.38,39
Hemangiopericytomas
Hemangiopericytomas are highly vascular lesions, and intraoperative hemorrhage can be significant. Hemorrhage is the most common cause for subtotal resection or operative morbidity. Embolization substantially reduces intraoperative bleeding and facilitates resection.40–42 However, embolization can be technically difficult because these tumors tend to parasitize cortical vessels. Ethanol and direct surgical puncture have been successfully employed in the past, although we have had success with Onyx, n-BCA, and PVA. Postembolization swelling is common with these lesions; therefore, resection within 48 hours of embolization is recommended.
Juvenile Nasal Angiofibromas
Juvenile nasal angiofibromas (JNAs) are benign, extremely vascular, nonencapsulated neoplasms consisting of vascular and connective tissue. They usually arise from the superior posterior margin of the sphenopalatine foramen. JNAs are the most common benign tumor of the nasopharynx and account for 0.05% to 0.5% of all head and neck tumors.43 These tumors almost exclusively affect adolescent boys; the mean age at diagnosis is 14 years. JNAs rarely metastasize but display locally malignant behavior and exhibit high rates of recurrence after subtotal resection.44 Approximately 30% of JNAs manifest with intracranial extension.45 The most common presenting symptoms are epistaxis and prolonged nasal obstruction.
The unique appearance of JNAs on CT and MRI eliminates the need for biopsy, which can result in uncontrollable bleeding. Angiography demonstrates multiple tortuous feeding vessels followed by a dense, homogeneous blush in the capillary phase (Fig. 89-3). Prominent draining veins are apparent immediately in the early venous phase. JNAs are typically supplied by branches of the internal maxillary artery, with contributions from the ascending pharyngeal artery in as many as 33% of cases.46 Bilateral carotid angiography is mandatory in all cases, particularly if there is intracranial extension, because these tumors can recruit blood supply from the ophthalmic artery, contralateral internal maxillary artery, and branches of either ICA.
Surgical resection is regarded as the primary treatment modality.47