Indian Journal of Vascular and Endovascular Surgery

: 2015  |  Volume : 2  |  Issue : 3  |  Page : 125--129

Endovascular Approach for Treatment of Frontal Dural Arteriovenous Fistula through the Ophthalmic Arteries using Glue: A Case Presentation with Review of Literature

Santosh PV Rai1, Keerthiraj Bele2, Harikiran Reddy1,  
1 Department of Radiodiagnosis, KMC, Manipal University, Mangalore, Karnataka, India
2 Department of Neurointerventional Radiology, KMC, Manipal University, Mangalore, Karnataka, India

Correspondence Address:
Santosh PV Rai
Department of Radiodiagnosis, KMC, Manipal University, Mangalore, Karnataka


A rare case of right frontal bleed in elderly gentleman secondary to anterior cranial fossa dural arteriovenous fistula was detected on computed tomography angiogram, and complete endovascular embolization was achieved through ophthalmic arteries using glue as embolic material. Successful endovascular treatment along with surgical evacuation of subdural hematoma resulted in excellent recovery of the patient. Quick in-and-out approach using flow directed microcatheters and fast embolizing potential of glue may allow for rapid, safe, and successful embolization of such fistulas. The rarity of the location and the transarterial glue embolization of the nidus by micro catheter through both ophthalmic arteries makes this an interesting case for discussion.

How to cite this article:
Rai SP, Bele K, Reddy H. Endovascular Approach for Treatment of Frontal Dural Arteriovenous Fistula through the Ophthalmic Arteries using Glue: A Case Presentation with Review of Literature.Indian J Vasc Endovasc Surg 2015;2:125-129

How to cite this URL:
Rai SP, Bele K, Reddy H. Endovascular Approach for Treatment of Frontal Dural Arteriovenous Fistula through the Ophthalmic Arteries using Glue: A Case Presentation with Review of Literature. Indian J Vasc Endovasc Surg [serial online] 2015 [cited 2020 Feb 22 ];2:125-129
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Full Text


We present a rare case of a frontal dural arteriovenous fistula (DAVF) detected on computed tomography (CT) angiogram and presenting with right frontal bleed. The fistula was treated by a unique endovascular arterial approach through the ophthalmic arteries using glue as the embolic material.

DAVFs are abnormal connections between dural arterial feeders and dural venous sinus or leptomeningeal vein with fistulous site located within the dural leaflets. Dural arteriovenous shunts (DAVSs) are classified as dural sinus malformations, infantile DAVSs, and adult types of DAVSs.[1] The dural sinus malformation is the one having true congenital origin. The acquired causes of DAVS include dural sinus thrombosis, intracranial infection, trauma, surgery, or mostly idiopathic.[2],[3],[4],[5],[6],[7],[8] DAVSs are also seen in hypercoagulation states and pregnancy.[9] Chronic venous hypertension is the most important etiologic factor.[10] Abnormal angiogenic activity is induced directly or indirectly by venous hypertension through decreasing cerebral perfusion and increasing ischemia.[11] These are mediated through abnormal expression of endothelial-cell vascular growth factors which are demonstrated in DAVS.[12]

DAVS are associated with pial arteriovenous fistulas (AVFs) in some cases. The relation between two is such that DAVS can induce formation of pial arteriovenous malformation and vice versa. Both dural and cortical veins open directly into the dural sinus. Increased venous pressure or thrombosis of sinus results in abnormal arteriovenous shunts (AVSs) between dural arteries and veins without intervening capillaries in the wall of the dural sinus.[13] These results in increased flow of blood into the low-resistance system of dural sinus which can exert a venous steal effect on the upstream cortical veins opening directly into the dural sinus.[1] The result of steal effect cause hypoxia in the regions drained by these cortical veins which result in up-regulation of the angiogenic factors that act on the capillo-venous endothelial-cells and other cellular process involved in the remodeling of the vascular system for a significant period of time triggering the formation of the pial AVFs. Pial AVFs inducing DAVSs have been proposed in some high-flow pial AVFs associated with DAVSs upstream from their drainage into the dural sinus.[14] This could be explained by a similar sump effect created by the high-flow venous drainage of the pial AVF downstream. The venous changes by high-flow pial AVS on the venous sinuses, such as increased venous pressure or venous outflow obstruction, can also be triggering factors.

 Case Report

A 63-year-old gentleman presented with sudden onset of headache and vomiting while driving. There was no history of trauma. There was no history of seizures, loss of consciousness, and weakness of limbs. The patient was a known hypertensive, and he was on regular medications and not on anticoagulants. General physical examination was within normal limits. On neurological examination, the patient was drowsy but oriented to time and place. He was normotensive on examination. Routine blood parameters are within normal limits.

CT study was done which showed right frontal hematoma and adjacent extra axial subdural hemorrhage [Figure 1]a. Later CT angiogram was done which showed prominent cortical vessels in the right frontal region and prominent dural vessels along the right fronto-parietal region [Figure 1]a and [Figure 1]c and a prominent venous channel in the right frontal lobe suspicious of DAVF. Bilateral ophthalmic arteries were prominent and supplying the fistula [Figure 1]b and [Figure 1]d. Patient was subsequently taken up for digital subtraction angiography which showed dural AVF in right basifrontal region fed by anterior ethmoidal branches of bilateral ophthalmic arteries [Figure 1]e draining into the cortical veins with venous aneurysm formation and draining in turn into mid Superior sagittal sinus, basal vein of Rosenthal, superficial middle cerebral vein, vein of Labbe, and transverse sinus.{Figure 1}

He was counseled for both surgical and endovascular embolization of dural AVF and patient relatives opted for endovascular management. Under all aseptic precautions under general anesthesia, using 6 French (F) guiding catheter (Neuron – Penumbra Inc., San Leandro, CA, USA) placed in the right cavernous internal carotid artery (ICA), (Marathon-EV3) micro catheter with (Mirage-EV3) micro guidewire was taken into the right ophthalmic artery and placed as close to fistula as possible and 20% histoacryl glue was injected under road map guidance with good percolation of glue into the fistula and no filling of the fistula from right ophthalmic artery [Figure 2]. Later 6F catheter (Neuron – Penumbra Inc., San Leandro, CA, USA) as guiding catheter was placed in the left cavernous ICA, (Marathon-EV3 micro catheter with (Mirage-EV3) micro guidewire was taken into the left ophthalmic artery and placed as close to fistula as possible and 17% histoacryl glue was injected under road map guidance with good percolation of glue and no filling of the fistula from left ophthalmic artery. Check bilateral middle meningeal artery angiogram that showed no filling of the fistula. Subdural hemorrhage was drained after 2 days by burr hole surgery. The patient's condition improved dramatically within 3 days and was discharged in a week.{Figure 2}


Among the dural arteriovenous (AV) malformations of the brain, AVFs located in the anterior cranial fossa are rarely seen. Halbach et al.[15] published a study in 1990, reviewing 33 new cases since 1963, Lepoire et al.[16] described their first three encounters with this entity. Since then DAVFs of the anterior cranial fossa have been reported with increasing frequency. DAVFs of the anterior cranial fossa occur more commonly in men than in women (ratio of 7:1) and usually in the elderly. The most common presentation is hemorrhage, either subarachnoidal, subdural, or intracranial. DAVFs of the anterior cranial fossa have occasionally been observed incidentally during imaging for other diagnostic purposes.[17]

Dilated cortical veins are seen on CT or magnetic resonance studies and suggest DAVF,[18] but bilateral external and internal carotid angiography is gold standard to establish the diagnosis and to map arterial feeders and venous drainage. Some DAVF gets feeders from ophthalmic artery via anterior ethmoidal branches hence called anterior ethmoidal DAVF. Usually, both ophthalmic arteries are hypertrophic and feed the DAVF via the anterior ethmoidal arteries. Deshmukh et al. reported the first case of a patient with bilateral ethmoidal DAVF in 2005.[19] The second case of bilateral ethmoidal DAVF was reported by Komotar et al. in 2007.[20] External carotid feeders from penetrating septal branches of the sphenopalatine arteries are seen in most of the cases. The DAVF usually drains into the superior sagittal sinus via a frontal cortical vein. Venous outflow directly to basal veins or to the cavernous sinus has been described in some cases.[21],[22],[23]

DAVFs of the anterior cranial fossa are high-risk factors for hemorrhage because of their cortical venous drainage (types III and IV).[24] In view of their aggressive nature, DAVFs of the anterior cranial fossa require treatment which includes surgical or endovascular approach. Neurosurgical approach includes disconnection of the vascular shunt between dural arteries of the cribrosal plate and pial veins of the frontobasal lobe. A low frontal craniotomy with electrocoagulation and transection of the vascular connection and eventually excision of the fistula site is usually the procedure performed.[25] Surgical complications include cerebrospinal fluid leakage and intradural infections as in performing a low frontal craniotomy, the frontal and ethmoidal sinuses may be opened.

Transorbital ligature of the anterior ethmoidal artery should not be done, as distal collaterals will reinject the DAVF at the level of the lamina cribrosa.[23] Transarterial embolization has not been very successful in DAVF for similar reasons. Occlusive agents such as polyvinyl alcohol (PVA) particles and N-butyl 2-cyanoacrylate will be caught in the ethmoidal web of tiny feeders proximally to the fistula site and will not reach the venous portion. Also approaching the DAVF of the anterior cranial fossa through the ophthalmic artery carries a substantial risk of retinal infarction.

With the development of flow directed micro catheters, super selective catheterization of small distal arteries can be reached, and Embolization agents can be injected just proximal to fistulous site so than nontargeted embolization can be prevented. Alvarez et al. reported an uncomplicated embolization of an ethmoidal DAVF using histoacryl in 1990.[26] They demonstrated that origin of central retinal artery is proximal to arteries that supply ethmoidal DAVFs and that embolization risk could be minimized by catheterization beyond this safety point. Lefkowitz et al. performed provocative tests with lidocaine/amytal to assess the risk of embolization during the ophthalmic artery embolization in a series of 12 lesions involving the ophthalmic artery including three ethmoidal DAVFs.[27] Though all of the three ethmoidal DAVFs was not endovascularly obliterated and required subsequent surgery, embolization could be successfully performed without any complications.

Common embolization agents include PVA available in 350-um particle diameter ranges, n-butyl cyanoacrylate (NBCA) glue, platinum or stainless steel coils, absolute alcohol, or Onyx. PVA is the easiest material to use, but it is known for its impermanent nature. NBCA is a more permanent agent than PVA, but it is more difficult to administer. Furthermore, its injection time would be limited by the polymerization time. Onyx (ev3 Neurovascular, Irvine, California, USA) is a nonadhesive embolic agent, which is supplied in ready-to-use vials. Onyx is mechanically occlusive but nonadherent to the vessel wall, allowing prolonged feeder injections. Onyx is a preferred embolic agent due to its cohesive and nonadhesive nature which helps in controlled penetration and obliteration of the fistula. Onyx has significant drawbacks such as reflux proximally along microcatheters and slow injection with delayed penetration, and prolonged stay of microcatheters in ophthalmic arteries increasing risk of thromboembolism and central retinal artery occlusion.

Other therapeutic approach is targeting the venous compartment of DAVFs. Surgical disconnection of retrograde draining veins has proved to be a promising procedure for management of aggressive DAVFs.[28],[29] A transvenous endovascular approach to DAVFs involving the cavernous and dural sinuses has been performed successfully with low risk.[30] The microcatheter should be advanced over the guidewire very gently to avoid spasm and rupture of the draining vein or, eventually, a venous aneurysm.

Fiber helical platinum microcoils have been replaced by mechanically or electrolytically detachable coils.[31] Detachable coils have the advantage of retrievability when misplaced or when coil dimensions do not fit the diameter of the vein.

To summarize, DAVFs are abnormal connections between dural arterial feeders and dural venous sinus or leptomeningeal vein with fistulous site located within the dural leaflets.[32] Although anterior cranial fossa DAVFs are rare (5.8%),[6],[15] they have a very high incidence of sudden massive intracranial hemorrhage (62–91%)[33] particularly if the fistula is draining into leptomeningeal vein and in presence of aneurysmal varix formation. Patients presenting with hemorrhage, symptomatic DAVF, and pial drainage vessel with varix require aggressive management of fistula by surgical or endovascular management.[33]

Treatment of DAVF involves disconnection of AVs fistulous site by occlusion of the nidus, venous drainage or occlusion of all arterial supply, and can be achieved by endovascular approach, surgical or a combination of both.[34],[35] Endovascular embolization of fistulae although feasible is not technically easy due to difficulty in navigating microcatheters across small tortuous ophthalmic arteries and risk of occlusion of central retinal artery resulting in permanent blindness,[34] and transvenous access is difficult due to small bridging vein which are fragile.

Although at present microsurgical obliteration of the fistulae is considered preferred treatment for anterior cranial fossa DAVF, endovascular embolization is possible and could be considered as an alternative for patients who are not candidates for surgery or who are not willing for surgery.[36]

Endovascular embolization through the ophthalmic arteries using glue can be done safely and successfully in patients with good vascular access with reasonable success rate and low risk of complications. In those patients with safe access through ophthalmic arteries, endovascular embolization could be the treatment of choice, followed by open surgery in cases of failure of embolization.

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1Lasjaunias P. Vascular Diseases in Neonates, Infants and Children. Berlin: Springer-Verlag; 1997. p. 321-71.
2Houser OW, Campbell JK, Campbell RJ, Sundt TM Jr. Arteriovenous malformation affecting the transverse dural venous sinus – An acquired lesion. Mayo Clin Proc 1979;54:651-61.
3Chaudhary MY, Sachdev VP, Cho SH, Weitzner I Jr, Puljic S, Huang YP. Dural arteriovenous malformation of the major venous sinuses: An acquired lesion. AJNR Am J Neuroradiol 1982;3:13-9.
4Graeb DA, Dolman CL. Radiological and pathological aspects of dural arteriovenous fistulas. Case report. J Neurosurg 1986;64:962-7.
5Sakaki T, Morimoto T, Nakase H, Kakizaki T, Nagata K. Dural arteriovenous fistula of the posterior fossa developing after surgical occlusion of the sigmoid sinus. Report of five cases. J Neurosurg 1996;84:113-8.
6Awad IA, Little JR, Akarawi WP, Ahl J. Intracranial dural arteriovenous malformations: Factors predisposing to an aggressive neurological course. J Neurosurg 1990;72:839-50.
7Bito S, Ohnishi T, Takimoto N, Sakaki S, Gohma T, Motozaki T. Dural arteriovenous fistulae found after removal of a meningioma – A case report (author's transl). No Shinkei Geka 1978;6:397-400.
8Vilela P, Willinsky R, terBrugge K. Dural arteriovenous fistula associated with neoplastic dural sinus thrombosis: Two cases. Uroradiology 2001;43:816-20.
9Berenstein A, Lasjaunias P, editors. Endovascular treatment of cerebral lesions. Surgical Neuroangiography. Vol. 4. Berlin: Springer-Verlag; 1992. p. 6-81.
10Terada T, Higashida RT, Halbach VV, Dowd CF, Tsuura M, Komai N, et al. Development of acquired arteriovenous fistulas in rats due to venous hypertension. J Neurosurg 1994;80:884-9.
11Lawton MT, Jacobowitz R, Spetzler RF. Redefined role of angiogenesis in the pathogenesis of dural arteriovenous malformations. J Neurosurg 1997;87:267-74.
12Uranishi R, Nakase H, Sakaki T. Expression of angiogenic growth factors in dural arteriovenous fistula. J Neurosurg 1999;91:781-6.
13Hamada Y, Goto K, Inoue T, Iwaki T, Matsuno H, Suzuki S, et al. Histopathological aspects of dural arteriovenous fistulas in the transverse-sigmoid sinus region in nine patients. Neurosurgery 1997;40:452-6.
14Valavanis A, Yasargil MG. The endovascular treatment of brain arteriovenous malformations. Adv Tech Stand Neurosurg 1998;24:131-214.
15Halbach VV, Higashida RT, Hieshima GB, Wilson CB, Barnwell SL, Dowd CF. Dural arteriovenous fistulas supplied by ethmoidal arteries. Neurosurgery 1990;26:816-23.
16Lepoire J, Montaut J, Bouchot M, Laxenaire M. Intrafrontal arteriovenous aneurysms vascularized by the anterior ethmoidal artery. Apropos of 3 cases. Neurochirurgie 1963;9:159-66.
17Bioh S, Nakagawa H, Arita N, Fujiwara M. Dural arteriovenous malformation in the anterior fossa. Case report. Neurol Med Chir (Tokyo) 1981;21:131-4.
18Ito J, Imamura H, Kobayashi K, Tsuchida T, Sato S. Dural arteriovenous malformations of the base of the anterior cranial fossa. Neuroradiology 1983;24:149-54.
19Deshmukh VR, Chang S, Albuquerque FC, McDougall CG, Spetzler RF. Bilateral ethmoidal dural arteriovenous fistulae: A previously unreported entity: Case report. Neurosurgery 2005;57:E809.
20Komotar RJ, Connolly ES Jr, Lignelli AA, Mack WJ, Mocco J, Harbaugh RE. Clinicoradiological review: Bilateral ethmoidal artery dural arteriovenous fistulas. Neurosurgery 2007;60:131-5.
21Kobayashi H, Hayashi M, Noguchi Y, Tsuji T, Handa Y, Caner HH. Dural arteriovenous malformations in the anterior cranial fossa. Surg Neurol 1988;30:396-401.
22Abumiya T, Kamiyama H, Murata J, Nunomura M, Chono Y, Kobayashi N, et al. Dural arteriovenous malformation with uncommon draining veins in the anterior fossa. Case report. Neurol Med Chir (Tokyo) 1987;27:1195-200.
23Lasjaunias P, Chiu M, ter Brugge K, Tolia A, Hurth M, Bernstein M. Neurological manifestations of intracranial dural arteriovenous malformations. J Neurosurg 1986;64:724-30.
24Cognard C, Gobin YP, Pierot L, Bailly AL, Houdart E, Casasco A, et al. Cerebral dural arteriovenous fistulas: Clinical and angiographic correlation with a revised classification of venous drainage. Radiology 1995;194:671-80.
25Martin NA, King WA, Wilson CB, Nutik S, Carter LP, Spetzler RF. Management of dural arteriovenous malformations of the anterior cranial fossa. J Neurosurg 1990;72:692-7.
26Alvarez H, Rodesch G, Garcia-Monaco R, Lasjaunias P. Embolisation of the ophthalmic artery branches distal to its visual supply. Surg Radiol Anat 1990;12:293-7.
27Lefkowitz M, Giannotta SL, Hieshima G, Higashida R, Halbach V, Dowd C, et al. Embolization of neurosurgical lesions involving the ophthalmic artery. Neurosurgery 1998;43:1298-303.
28Borden JA, Wu JK, Shucart WA. A proposed classification for spinal and cranial dural arteriovenous fistulous malformations and implications for treatment. J Neurosurg 1995;82:166-79.
29Davies MA, Ter Brugge K, Willinsky R, Wallace MC. The natural history and management of intracranial dural arteriovenous fistulae. Part 2: Aggressive lesions. Interv Neuroradiol 1997;3:303-11.
30Halbach VV, Higashida RT, Hieshima GB, Mehringer CM, Hardin CW. Transvenous embolization of dural fistulas involving the transverse and sigmoid sinuses. AJNR Am J Neuroradiol 1989;10:385-92.
31Terada T, Kinoshita Y, Yokote H, Tsuura M, Tanaka Y, Itakura T, et al. Clinical use of mechanical detachable coils for dural arteriovenous fistula. AJNR Am J Neuroradiol 1996;17:1343-8.
32Newton TH, Cronqvist S. Involvement of dural arteries in intracranial arteriovenous malformations. Radiology 1969;93:1071-8.
33Tanei T, Fukui K, Wakabayashi K, Mitsui Y, Inoue N, Watanabe M. Dural arteriovenous fistula in the anterior cranial fossa: Four case reports. Neurol Med Chir (Tokyo) 2008;48:560-3.
34Hoh BL, Choudhri TF, Connolly ES Jr, Solomon RA. Surgical management of high-grade intracranial dural arteriovenous fistulas: Leptomeningeal venous disruption without nidus excision. Neurosurgery 1998;42:796-804.
35van Dijk JM, TerBrugge KG, Willinsky RA, Wallace MC. Selective disconnection of cortical venous reflux as treatment for cranial dural arteriovenous fistulas. J Neurosurg 2004;101:31-5.
36Kim JH, Kwon OK, Lee KJ, Koh SB, Yoo H, Koh YC, et al. Surgical management of dural arteriovenous fistula of the anterior cranial fossa after failure of embolization therapy: Case report. J Korean Neurosurg Soc 2002;31:271-3.