| OCR Text |
Show ORIGINAL CONTRIBUTION Endovascular Treatment of a Bilateral Ophthalmic- Ethmoidal Artery Dural Arteriovenous Fistula Vasilios Katsaridis, MD, PhD, Chrysanthi Papagiannaki, MD, and Constantinos Violaris, MD Abstract: A 76- year- old man developed blurred vision, and cerebral angiography disclosed an anterior skull base dural arteriovenous fistula ( DAVF) supplied by both ethmoidal branches of the ophthalmic arteries and draining through a single cortical vein. Selective catheterization of both ophthalmic arteries distal to the origin of the central retinal arteries and occlusion the fistula feeders with injections of « - butyl cyanoacrylate glue led to complete occlusion of the fistula with preservation of retinal perfusion. The visual symptoms are attributed to impaired retinal perfusion as the result of a steal phenomenon. With care, a DAVF in this location can be successfully treated endovascularly while preserving retinal perfusion by embolizing the ophthalmic artery distal to the origin of the central retinal arteries and avoiding any backflow of embolizing material. (/ Neuro- Ophthalmol 2007; 27: 281- 284) Dural arteriovenous fistulas ( DAVFs) account for 10%- 15% of intracranial arteriovenous malformations ( 1). They are commonly classified according to the pattern of venous drainage by the systems of Cognard et al ( 2) and Borden et al ( 3). DAVFs rank higher ( higher risk of rupture) if they drain through leptomeningeal or cortical venous branches. The system of Cognard et al ( 2) also includes the criterion of venous ectasia, which further increases the risk of rupture. DAVFs of the ophthalmic- ethmoidal artery are rare. We present a case of a bilateral ophthalmic-ethmoidal artery DAVF that had caused an intracerebral Neurosurgical Department, Papanikolaou General Hospital, Thessa-loniki, Greece. Address correspondence to Vasilios Katsaridis, MD, PhD, Neurosurgeon, Neurosurgical Department, Papanikolaou General Hospital, 15 Papanikolaou Avenue, Thessaloniki GR- 57010, Greece; E- mail: vkats@ iname. com hematoma ( ICH) and presented challenges in endovascular management. CASE REPORT A 76- year- old man was admitted to our hospital after an episode of loss of consciousness that had lasted a few minutes. Upon admission he was mildly disorientated and complained of headache. His family informed us that during the last month he had been complaining of blurred vision in both eyes but had not consulted an ophthalmologist. Brain CT scanning showed a small ICH in the cortex of the left frontal lobe not requiring urgent surgical evacuation. MRA revealed a dilated and tortuous vascular structure coursing over the left frontal parasagittal cortex, raising the suspicion of a vascular malformation. Digital subtraction angiography ( DSA) disclosed a high- flow DAVF supplied by both anterior ethmoidal arteries arising from both ophthalmic arteries. The DAVF was supplied by a single feeder from the right ethmoidal artery ( Fig. 1 A) and by multiple feeders from the left ethmoidal artery ( Fig. IB). The draining vein exhibited an aneurysmal dilatation at its proximal part, coursed tortuously, and drained to the superior sagittal sinus. We proceeded to embolize the DAVF. Initially, we placed a guiding catheter in the petrous segment of the right internal carotid ( ICA) and catheterized the right ophthalmic artery ( OA). We navigated the tip of a Marathon micro-catheter ( Micro Therapeutics Inc., Irvine, CA) distal to the origin of the central retinal artery ( CRA) and proximally to the origin of the ethmoidal artery ( EA). Ultraselective angiography confirmed the correct position of the micro-catheter tip with no opacification of the retina. We proceeded to occlude the segment of the OA that supplied the feeder of the DAVF with a very limited injection ( 0.1 mL) of a 15% mixture of « - butyl cyanoacrylate ( NBCA) glue ( Histoacryl; B. Braun, Melsungen, Germany) diluted in lipiodol/ Ethiodol ( Guerbet, Roissy, France). Immediate postinfection angiography showed no visualization of the DAVF and normal perfusion of the retina ( Fig. 2). J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 281 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Katsaridis et al FIG. 1. A. Digital subtraction angiography ( DSA) of the right internal carotid artery ( ICA), lateral projection. It demonstrates a dural arteriovenous fistula ( DAVF, arrow) supplied by the anterior ethmoidal branch of the right ophthalmic artery with drainage through a cortical vein that is aneurysmally dilated in its proximal portion. B. DSA of the left ICA, lateral projection. It demonstrates that the DAVF is also supplied by the anterior ethmoidal branch of the left ophthalmic artery with drainage through the same aneurysmally dilated cortical vein { arrow). We then placed the guiding catheter in the left ICA and attempted to perform the same procedure on the left side. Despite using different combinations of micro-catheters and guidewires, catheterization of the left OA proved impossible because of the reverse catheterization angle. We placed a second guiding catheter in the left vertebral artery and, under road mapping from both guiding catheters, we managed to catheterize the left OA, navigating the microcatheter through the basilar, left posterior cerebral, left posterior communicating, and left ICAs. The catheterization of the OA was achieved with little effort because the trajectory of the microcatheter in the posterior communicating, internal carotid, and the ophthalmic arteries was almost in a straight line ( Fig. 3). After navigation of the i FIG. 2. Postembolization digital subtraction angiography of the right internal carotid artery, lateral projection, early arterial phase. The dural arteriovenous fistula is no longer visualized. FIG. 3. Unsubtracted angiography of the left internal carotid artery, lateral view. The ophthalmic artery has been selectively catheterized through a second guiding catheter in the left vertebral artery following a course through the basilar, left posterior cerebral, left posterior communicating, and left internal carotid arteries. 282 © 2007 Lippincott Williams & Wilkins Dural Fistula J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 microcatheter tip in the OA distal to the origin of the central retinal artery, we occluded the multiple DAVF feeders with an injection of 0.4 mL of a 10% mixture of NBCA glue in lipiodol/ Ethiodol that reached the beginning of the draining vein. The final postembohzation DSA of the left ICA showed complete occlusion of the DAVF with no visualization of the draining vein but normal perfusion of the retina of the left eye ( Fig. 4). The patient was extubated immediately postoperatively and was discharged 5 days later in excellent condition, claiming that he no longer experienced blurring of vision. CT angiography 6 months later showed no evidence of flow in the DAVF. The patient reported completely normal vision with a best- corrected visual acuity of 20/ 20 in both eyes and no abnormalities on ophthalmoscopy. DISCUSSION DAVFs are abnormal shunts within the dura. They are mostly idiopathic in origin, although trauma, infection, and hormonal disturbances have been implicated as etiologic factors. They are usually supplied by meningeal branches but are also supplied from cutaneous or osseous ones. They most frequently drain into venous sinuses; cortical drainage is very rare ( 4). The pattern of cortical venous drainage seen in our patient carries a substantially higher risk of rupture and intracranial bleeding, warranting more aggressive treatment ( 4,5). DAVFs of the anterior cranial fossa almost constantly drain through cortical veins. Arterial supply arises from the anterior meningeal artery when the fistula is located FIG. 4. Postembolization digital subtraction angiography of the left ICA, lateral projection, early arterial phase. The DAVF is no longer visualized. laterally and from the anterior and posterior EAs when it is located by the midline ( 4). The DAVF of our patient was located in the anterior cranial fossa near the midline and posterior to the left frontal sinus. It was supplied by both anterior EAs, branching from the OAs, with the right one crossing the midline. The DAVF was drained exclusively by a left frontal cortical vein that exhibited an aneurysmal dilatation ( ectasia) at its proximal part. The investigation of such lesions includes CT and MRI as well as MRA, but the definitive diagnosis is made with DSA. A novel method of discovery of DAFVs of the anterior skull base was described by Fiori et al ( 6) with the use of pulse- wave Doppler. The draining vein in our patient had ruptured and caused an ICH. A similar case of DAVF supplied by both EAs was described by Tiyaworabun et al ( 7) with the difference that the drainage was through a cerebral vein into the vein of Rosenthal and the straight sinus. It is interesting that the proximal part of the draining vein exhibited an aneurysmal dilatation exactly as in our patient and had also caused an ICH. Unlike our patient, the patient of Tiyaworabun et al ( 7) was treated surgically ( and with success). Two other cases of DAVFs of the anterior cranial fossa supplied by the anterior and posterior EAs have been reported by Ito et al ( 8), differing from our patient in that they had additional arterial supply from the external carotid system. The draining vein had an aneurysmal dilatation in those patients as well. Our patient had been complaining of blurred vision during the month before the rupture of the DAVF. This could be attributed to a steal phenomenon from both central retinal arteries. Steal phenomena are common in DAVFs and can cause a variety of symptoms such as cranial nerve palsies because most cranial nerves are supplied by meningeal arteries ( 4). Xiong et al ( 9) reported a case of monocular amaurosis fugax due to a DAVF of the falcine artery originating from the OA and attributed the symptomatology to a steal phenomenon. The endovascular treatment we attempted resulted in resolution of the fistulous communication while preserving the supply to both retinas. The improvement in the patient's vision can be attributed to increased perfusion of the retinas due to the cessation of the steal phenomenon. In a series of vascular lesions involving the OA, Lefkowitz et al ( 10) reported the successful embolization of four DAVFs of the anterior cranial fossa with preservation of vision. In that series, the authors relied on Amytal testing to assess the safety of the point of injection of embolic material. We did not perform an Amytal test and relied solely on angiographic findings. We injected the NBCA mixture only when we were certain that the microcatheter tip was distal to the origin of the central retinal artery, and the retina was not opacified by contrast injections from that point. 283 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Katsaridis et al The integrity of the central retinal artery was achieved by slow and careful injection of the material, not allowing it to backflow into the OA. An alternative to endovascular treatment of this DAVF would have been surgical coagulation and disconnection of the fistula, a straightforward, well- proven, and established form of therapy. Surgical treatment of DAVFs has yielded excellent results but can be tedious, with the risk of morbidity from blood loss due to injury to fragile and engorged vessels in the adjacent brain ( 11). Furthermore, craniotomy has inherent risks of infection and postoperative hemorrhage and constitutes major discomfort for the patient compared with endovascular embolization. Intra- arterial embolization of this particular DAVF had a significant risk of central retinal artery occlusion by embolic backflow or ophthalmic artery injury during the microcatheterization. Our experience with the use of liquid embolic agents influenced our decision to perform endovascular embolization of the lesion. The risk of compromise of the blood supply to the retina was constantly evaluated during the intervention, and we were ready to abort the endovascular treatment if it was considered dangerous. Fortunately we were able to embolize the DAVF and preserve the blood supply to both retinas. REFERENCES 1. Newton TH, Cronqvist S. Involvement of dural arteries in intracranial arteriovenous malformations. Radiology 1969; 93: 1071- 8. 2. Cognard C, Gobin YP, Pierot L, et al. Cerebral dural arteriovenous fistulas: clinical and angiographic correlation with a revised classification of venous drainage. Radiology 1995; 194: 671- 80. 3. Borden JA, Wu JK, Shucart WA. A proposed classification for spinal and cranial dural arteriovenous fistulous malformations and implications for treatment. JNeurosurg 1995; 82: 166- 79. 4. Dural arteriovenous malformations ( DAVMs). In: Lasjaunias P, Berenstein A, eds. Surgical Neuroangiography Vol 2: Endovascular Treatment of Craniofacial Lesions. Berlin: Springer- Verlag; 1987: 273- 315. 5. Lasjaunias P, Chiu M, ter Brugge K, et al. Neurological manifestations of intracranial dural arteriovenous malformations. J Neurosurg 1986; 64: 724- 30. 6. Fiori L, Parenti G, Puglioli M, et al. Anterior fossa dural arteriovenous malformation discovered by means of PW- Doppler examination. Neurol Res 1995; 17: 226- 8. 7. Tiyaworabun S, Vonofakos D, Lorenz R. Intracerebral arteriovenous malformation fed by both ethmoidal arteries. Surg Neurol 1986; 26: 375- 82. 8. Ito J, Imamura H, Kobayashi K, et al. Dural arteriovenous malformations of the base of the anterior cranial fossa. Neuroradiology 1983; 24: 149- 54. 9. Xiong L, Li J, Jinkins JR. Amaurosis fugax caused by a dural arteriovenous fistula from the ophthalmic artery. AJNR Am J Neuroradiol 1993; 14: 191- 2. 10. Lefkowitz M, Giannotta SL, Hieshima G, et al. Embolization of neurosurgical lesions involving the ophthalmic artery. Neurosurgery 1998; 43: 1298- 303. 284 © 2007 Lippincott Williams & Wilkins |
