Microsurgical and Endovascular Treatment of Giant Intracavernous Aneurysms

Microsurgical and Endovascular Treatment of Giant Intracavernous Aneurysms Hyeong Joong Yi, MD* and Michael Horowitz, MD† Treatment of giant intracavernous carotid artery aneurysms (ICCA), rare but formidable challenging lesions, requires scrupulous review of the clinical and radiographic studies and involves several different or successive surgical approaches. To attain complete permanent exclusion of the ICCAs from the circulation while preserving the parent carotids, microsurgical or endovascular techniques should be employed. Three kinds of surgical approaches can be addressed: (1) direct surgical aneurysm obliteration with parent artery preservation, (2) indirect obliteration using parent artery sacrifice, and (3) indirect aneurysm obliteration followed by extracranial-to-intracranial bypass or interposition grafts. In most instances, however, endovascular intervention with or without vessel reconstruction is now the initial treatment. When one considers parent carotid occlusion, balloon test occlusion should be performed irrespective of surgical options. Oper Tech Neurosurg 8:74-77 © 2005 Elsevier Inc. All rights reserved. KEYWORDS giant aneurysm, intracavernous carotid artery aneurysms (ICCA), microsurgical approach, endovascular intervention, balloon test occlusion (BTO), extracranial-to-intracranial (EC-IC) bypass

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iant intracavernous carotid artery aneurysms (ICAAs) are uncommon clinicopathological entities yet their large size and anatomic complexity mandate full utilization of the neurovascular armamentarium. Direct and indirect surgical attack and the use of adjuvant endovascular procedures are often required to address these lesions. Direct surgical obliteration of the giant ICAAs has been possible but remains a formidable challenge. With Dolenc’s introduction of detailed microsurgical anatomy and with subsequent combined epi- and subdural approach to the cavernous sinus (CS), operative results have been favorable.1,2 These outcomes are attributed to more thorough knowledge of the microsurgical anatomy of the CS; improved diagnostic imaging, including magnetic resonance imaging (MRI), angiography, and xenon computed tomography (CT) or single photon emission computed tomography (SPECT); intraoperative neuroelectrophysiological monitoring with pharmacological brain protection, and technical refinements in surgical skills. When a patient is diagnosed with a giant ICAA and treatment is considered, permanent exclusion of the aneurysm

*Department of Neurosurgery, Hanyang University Medical Center, Haengdangdong, Sungdong-gu, Seoul, South Korea. †Department of Neurosurgery, University of Pittsburgh Medical Center, Pittsburgh, PA. Address reprint requests to Hyeong Joong Yi, MD, Assistant Professor, Department of Neurosurgery, Hanyang University Medical Center, Haengdangdong, Sungdong-gu, 133-792, Seoul, South Korea; E-mail: [email protected].

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from the circulation with preservation of the ICA is the preferred goal. Nevertheless, endo- and exovascular surgical treatment of giant ICAAs can be divided into three approaches: (1) direct surgical aneurysm obliteration with parent artery preservation, (2) indirect obliteration using parent vessel sacrifice, and (3) indirect aneurysm obliteration followed by extracranial-to-intracranial (EC-IC) bypass or interposition grafts. Initial treatment is usually endovascular intervention, with or without sacrifice of the ICA. If, however, endovascular treatment is refused, unsuccessful, or too dangerous, direct surgical occlusion or trapping and cerebral revascularization with EC-IC bypass is the treatment of choice.3 Giant ICAAs are most often located outside the subarachnoid space. Rupture may lead to symptomatic or asymptomatic direct cavernous-carotid fistula or severe intractable epistaxis. Subarachnoid hemorrhage can occur when the lesion erodes through the dura or dural rings of the carotid artery. Lesions can also produce mass effect on surrounding neural structures leading to facial pain or ophthalmoplegia/paresis. The risk of thromboembolic phenomenon to the distal vasculature is another concern if partial aneurysmal thrombosis occurs. The decision to treat a giant ICAA should hinge on the aneurysm’s morphology and the patient’s mode of presentation. All symptomatic aneurysms (hemorrhage, progressive neurological deterioration, and intractable pain) and some asymptomatic aneurysms that extend into the subarachnoid space and sphenoid sinus should be treated.4,5

Microsurgical and endovascular treatment of ICAAs

Direct Microsurgical Approaches to the CA Before a surgical attack on a giant ICAA, all patients should undergo a balloon test occlusion (BTO) with some form of provocative testing or measurement of cerebral blood flow (CBF). Even if the surgeon thinks that permanent vessel occlusion will be unnecessary, it is important to determine the patient’s ability to tolerate permanent occlusion or prolonged temporary occlusion should the need arise. To further reduce surgical morbidity and avoid complications, a clear understanding of the multiple points of access to the CS is crucial. Ten anatomic triangles have been described through which the CS can be accessed, but only a few bear surgical importance.1,2,6 The anteromedial triangle is situated between the lateral aspect of the extradural optic nerve, the medial aspect of the oculomotor nerve, and the tentorial edge from the entry point of the optic nerve into the optic canal. Through this window the horizontal intracavernous portion and the anterior genu of the ICA can be explored. The size of this triangle is small but it can be enlarged substantially by drilling the anterior clinoid process, dissecting the proximal dural ring from the oculomotor nerve, and incising the dura propria along the longitudinal axis of the optic nerve. The paramedian triangle is defined by the lateral aspect of the oculomotor nerve, the medial aspect of the trochlear nerve, and the tentorial edge running from the entry point of the oculomotor posteriorly to the entry point of the trochlear nerve. It is the usual site of origin of the meningohypophyseal trunk and the medial loop of the intracavernous ICA. Parkinson’s triangle is bordered medially by the lateral aspect of the trochlear nerve, laterally by the medial aspect of the ophthalmic division of the trigemenal nerve (V1) and posteriorly by the gasserian ganglion and the dural edge between the entry point of the trochlear and trigeminal nerves. Through this narrow triangle with judicious retraction of the trochlear and V1 nerves in opposite directions, the abducens nerve and the entire segment of the ICA from the lateral ring to the proximal ring can be visualized. This triangle can be used to expose the cavernous ICA during lateral intradural and extradural approaches. The posterolateral or Glasscock’s triangle is bordered by the superior petrosal nerve medially, the posterior aspect of the mandibular nerve anteriorly, and an imaginary line between the foramen spinosum and arcuate eminence of the petrous bone posteriorly. This triangle is exposed during the lateral extradural approach (of Dolenc) and is of particular importance for obtaining proximal control of the petrous ICA while dissecting an aneurysm or repairing the ICA in the CS.6 Preoperative and perioperative preparation is the same as that used for surgery of an anterior circulation aneurysm. General endotracheal anesthesia is used for all patients. Intraoperative electrophysiological monitoring, electroencephalography, and somatosensory evoked potentials can be useful for providing intraoperative warning of impending cerebral injury, especially if temporary occlusion is anticipated. A portable C-arm should also be readily available for intraoperative angiography. For positioning, the patient is placed on the operating

75 table in the supine position with the head elevated 15 to 30° and rotated 15 to 20° away from the lesion side by using a radiolucent graphite pin headholder. The patient’s neck and scalp should be prepared in the same operative field in case proximal control of the cervical ICA or revascularization using the cervical ICA or external carotid artery is required. The scalp and temporalis muscle are elevated. The posterior division of the superficial temporal artery (STA) is preserved, and a standard frontotemporal or orbitozygomatic craniotomy is performed. In principle, the combined epi- and subdural exposure of the frontotemporal region, as originally described by Dolenc,1,2 is performed. First, the anterior clinoid process is accessed through an extradural approach and the foramen rotundum and foramen ovale are identified. Through wide removal of the anterior clinoid process and reduction of the optic strut, the anteromedial triangle is exposed. This exposure is attained by complete skeletonization of the optic canal with a high-speed drill. If the posterior ethmoid sinus or the sphenoid sinus is entered, the area must be sealed to avoid postoperative CSF rhinorrhea. The falciform ligament around the optic nerve is transected sharply, and the optic nerve is mobilized superomedially. The distal dural ring should be fully incised from its dorsal to inferior extent to permit mobilization of the proximal ICA segment and separation of the ophthalmic artery from the aneurysm. Further removal of the lesser sphenoid wing and anterior clinoid process is followed by the intradural approach. The dura is incised and retracted forward. Once the sylvian fissure is dissected completely, a retractor can be applied gently to split the temporal and frontal lobes widely. The opticocarotid cistern arachnoid is incised to allow CSF to escape and the brain to relax. Dissection then proceeds posteriorly to the tentorial edge. Great care is exerted to identify the dural penetration points of the oculomotor and trochlear nerves. These nerves are mobilized, and further dissection of the anteromedial and paramedian triangles enables the cavernous ICA to be exposed. The CS is opened anteriorly to posteriorly, from the space between the oculomotor nerve and supraclinoid ICA to the posterior clinoid process. Bleeding from the CS can be controlled using oxidized cellulose or absorbable gelatin. However, extreme care must be taken to avoid excessive packing, which can cause unwanted compression of the neural and vascular structures within the CS. To obtain proximal and distal vascular control, the carotid canal can be unroofed by drilling over Glasscock’s triangle.6 It is important to maintain thin adventitial coverings when the ICA is mobilized in this triangle. When this maneuver is completed, the ICA is available for application of temporary clips and for anastomosis of a saphenous vein graft as in the Fukushima bypass procedure.7 If the aneurysm has ruptured before or during the exposure, compression of the cervical ICA may suffice. However, better control is assured by exposing the cervical ICA before the craniotomy is begun. When clip ligation is contemplated, the basic principles of circumferential definition of the aneurysm neck, visual identification of all arterial branches, and

H.J. Yi and M. Horowitz

76 maintenance of parent vessel patency should be strictly applied.

Indirect Surgical Obliteration With or Without EC-IC Bypass A giant ICAA with a wide neck-to-dome ratio or fusiform shape may preclude successful coil embolization or clip reconstruction. In these cases, surgical or endovascular trapping with or without cerebral revascularization should be the primary treatment. BTO of the ICA is an important preoperative diagnostic tool to determine the patient’s cerebrovascular reserve. It is essential for deciding the need for a revascularization procedure.8 Temporary carotid occlusion tests are used with measurements of cerebral perfusion such as xenon cerebral blood flow (CBF), xenon-enhanced CT or SPECT, or transcranial Doppler measurements. The level of residual CBF after temporary occlusion of the ICA that is considered safe for carotid ligation, however, is still controversial. To perform the BTO, a double-lumen occlusion balloon catheter is introduced into the femoral artery and advanced within the ICA to the level of the C1 to 2 vertebral bodies.9 The patient is heparinized to an activated clotting time (ACT) ⬎250 seconds, and the endovascular balloon is inflated under direct fluoroscopic visualization. After complete arterial occlusion is confirmed by distal contrast injection and lack of contrast washout, the patient undergoes continuous neurologic evaluations for 10 minutes. The balloon should be deflated if the patient becomes symptomatic. If no neurologic deficits occur during the 10-minute clinical BTO, the patient is transferred to the CT or SPECT scanner where CBF is analyzed using radionuclide, Xenon, or CT measurement. The balloon needs to remain inflated for CT Xenon, radioactive Xenon, and CT perfusion studies. Once the radionucleotide is injected for a SPECT scan, the balloon can be deflated and the study performed soon after the injection. Based on stable Xenon CBF testing, patients are grouped into one of three categories reflecting a minimum CBF value in any vascular territory: high-risk group (failed clinical BTO), moderate-risk group (passed the clinical BTO but developed quantitative BTO values less than 30 mL/100g/min), and low-risk group (passed both the clinical and quantitative BTO). If the ICA must be killed to treat the aneurysm, highrisk patients undergo high-flow revascularization (70-140 mL/min, up to 250 mL/min) with saphenous vein or radial artery grafts followed by carotid occlusion. Moderate-risk patients undergo low-flow EC-IC revascularization (15-25 mL/min, up to 90 mL/min) usually using STA-to-MCA (middle cerebral artery) bypass, followed by carotid occlusion. Low-risk patients may undergo carotid sacrifice only.8 In addition to bypass grafts, cerebral revascularization has been performed with interposition grafts placed between the high cervical or petrous carotid artery and the carotid siphon. In this procedure the proximal cervical or petrous ICA and the ICA siphon segments are exposed, and end-to-side anastomosis of a 5- to 7-cm-long saphenous vein interposition graft is performed. The distal ICA ligation should be made immediately proximal to the origin of the ophthalmic artery to prevent intraluminal dead space that can be a potential source of embolic thrombi.6

Operative Results Dolenc has provided the most extensive reports on the direct surgical treatment of ICAAs.10 According to his experience with 109 patients harboring ICAAs, the rate of temporary minor morbidity (cranial neuropathy) was 89% (resolved 4 to 6 months after surgery). The rate of permanent morbidity was 5%. However, all morbidities included minor deficits (minor visual loss, minor hemiparesis, and persistent cranial nerve palsies). There was no major persistent morbidity and the mortality rate was 3%. Others have reported a temporary morbidity rate of 63%, a minor persistent morbidity rate of 38%, and no major permanent morbidity and no mortality.5

Endovascular Approaches The indications for endovascular management of large and giant ICAAs are no different from those used for open surgical repair. They include symptomatic hemorrhage either into the nasal sinuses with epistaxis or intracranially into the subarachnoid space from aneurysmal erosion through the dura of the CS, symptomatic direct carotid-cavernous fistula, mass effect with compression of the CS cranial nerves leading to pain or ophthalmoplegia or paresis, or both. Once the decision has been made to proceed with endovascular treatment, the surgeon must consider the options. Almost all treatment plans begin with an ICA BTO test. We favor Xenon CBF evaluation during balloon inflation. Others use a hypotensive challenge, SPECT blood flow, CT perfusion, and radioactive Xenon CBF evaluation. If the patient passes the BTO, a decision is made either to attempt vessel reconstruction or simple arterial ligation with or without aneurysm trapping. If reconstruction is chosen, it is usually performed with intravascular uncovered stents and platinum detachable coils. When a case is anticipated, patients are heparinized to an ACT of 250 seconds during the procedure and are pretreated with IIb/IIIa platelet inhibitors (Plavix 300-500 mg load followed by 75 mg daily). When emergent treatment is needed or intraprocedural IV IIb/IIIa inhibitors are administered during the procedure, we use such medications whether or not a stent is inserted into the parent vessel because most large and giant aneurysms have wide necks, which place a large amount of platinum coil in contact with flowing blood. The IIb/IIIb inhibitors (Plavix 75 mg daily) and aspirin (81-325 mg daily) are taken by mouth for 30 days at which time the Plavix is eliminated. If ICA vessel occlusion is undertaken, we favor aneurysm trapping with coils placed from just below the level of the ophthalmic artery to the petrous ICA. Detachable coils are typically used for the distal occlusion while less expensive fibered coils are used for the proximal occlusion. We perform all trapping and occlusion procedures using a balloon occlusion catheter as our proximal guide catheter so that anterograde blood flow is arrested during coil deposition. This strategy reduces both the risk of distal coil migration and the risk of thromboembolic complications from thrombus forming on the coils and then being washed distally to the brain before trapping and coil-mediated flow arrest are completed. All patients are heparinized during the procedure and given IIb/IIa inhibitors as described above. Trapped or occluded

Microsurgical and endovascular treatment of ICAAs patients, however, remain on therapeutic heparin for 12 to 24 hours after the procedure in an attempt to reduce the risk of thromboembolic events related to ICA thrombosis and stump emboli. If reconstruction and trapping are not possible from an endovascular route, we recommend open surgical trapping if the surgeon believes that a clip can be placed proximal to the ophthalmic artery. Occlusion proximal to the ophthalmic artery is important because the ICA BTO permits ophthalmic artery flow to the supraclinoid ICA, which may be an important source of collateral blood flow when the ICA is occluded. If proximal occlusion cannot be achieved, patients are counseled that distal clip applications are associated with a 10 to 15% risk of visual loss from occlusion of the ICA origin ophthalmic artery. Although they may have passed the BTO, they may still have ischemic complications once the ophthalmic artery collateral flow is sacrificed. If surgical trapping is impossible or the risk is too high, proximal endovascular or exovascular ICA occlusion is performed. Close follow-up is needed to be sure that the aneurysm thromboses and neither remains patent nor re-opens from retrograde flow or collateral reconstitution of the ICA. In terms of outcomes, patients are told that they have a 33% chance of improving with treatment, a 33% chance of remaining the same, and a 33% chance of worsening from the aneurysm swelling after treatment. No literature, however,

77 documents these numbers; they are based on personal findings alone.

References 1. Dolenc V: Direct microsurgical repair of intracavernous vascular lesions. J Nenurosurg 58:824-831, 1983 2. Dolenc V: A combined epi- and subdural approach to carotid-ophthalmic artery aneurysms. J Neurosurg 62:667-672, 1985 3. Russell SM, Jafar JJ: Microsurgical treatment of intracavernous carotid artery aneurysms, in Le Roux PD, Winn HR, Newell DW (eds): Management of Cerebral Aneurysms. Philadelphia, PA: Saunders, 2004, pp 711-729 4. Linskey M, Sekhar LN, Hirsch BW, et al: Aneurysms of the intracavernous carotid artery: Natural history and indications for treatment. Neurosurgery 26:933-937, 1990 5. Linskey ME, Sekhar LN, Horton JA, et al: Aneurysms of the intracavernous carotid artery: A multidisciplinary approach to treatment. J Neurosurg 75:525-534, 1991 6. Dolenc V: Surgery of vascular lesions of the cavernous sinus. Clin Neurosurg 36:240-255, 1990 7. Spetzler RF, Fukushima T, Martin N, et al: Petrous carotid-to-intradural carotid saphenous vein graft for intracavernous giant aneurysm, tumor, and occlusive cerebrovascular disease. J Neurosurg 73:496501, 1990 8. Lawton M, Hamilton M, Morcos J: Revascularization of aneurysm surgery: Current techniques, indications, and outcome. Neurosurgery 38: 83-94, 1996 9. Field M, Jungreis CA, Chengelis N, et al: Symptomatic cavernous sinus aneurysms: management and outcome after carotid occlusion and selective cerebral revascularization. AJNR 24:1200-1207, 2003 10. Dolenc V: Intracavernous aneurysms, in Kaye A, Black P (eds): Operative Neurosurgery, Vol 2. New York: Harcourt, 2000