|Year : 2015 | Volume
| 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
|Date of Web Publication||8-Oct-2015|
Santosh PV Rai
Department of Radiodiagnosis, KMC, Manipal University, Mangalore, Karnataka
Source of Support: None, Conflict of Interest: None
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.
Keywords: Dural arteriovenous fistula, endovascular, glue
|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;2:125-9
|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 2021 Feb 28];2:125-9. Available from: https://www.indjvascsurg.org/text.asp?2015/2/3/125/166938
| Introduction|| |
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. 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.,,,,,, DAVSs are also seen in hypercoagulation states and pregnancy. Chronic venous hypertension is the most important etiologic factor. Abnormal angiogenic activity is induced directly or indirectly by venous hypertension through decreasing cerebral perfusion and increasing ischemia. These are mediated through abnormal expression of endothelial-cell vascular growth factors which are demonstrated in DAVS.
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. 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. 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. 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: Axial computed tomography angiogram (a) shows right frontal hematoma (long black arrow) and prominent cortical vessels in the right frontal region and prominent dural vessels along the right frontoparietal region (short black arrows). (b) Axial computed tomography angiogram shows bilateral ophthalmic arteries are prominent (black arrows). (c) Coronal computed tomography angiogram shows prominent dural vessels (black arrow). (d) Volume rendered image shows that bilateral ophthalmic arteries are prominent (white arrows) and (e) confirms the dural arteriovenous fistula (short black arrows) supplied by the ophthalmic artery (long black arrow)|
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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: Digital subtraction angiography images in “road map” mode shows serial images (a-f) demonstrating the percolation of glue (double black arrows c and f) into the arteriovenous fistula administered through the micro catheter (thin black arrow b) in the nidus passed co-axially through the guiding catheter in the intracranial internal carotid (thick black arrow a)|
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| Discussion|| |
Among the dural arteriovenous (AV) malformations of the brain, AVFs located in the anterior cranial fossa are rarely seen. Halbach et al. published a study in 1990, reviewing 33 new cases since 1963, Lepoire et al. 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.
Dilated cortical veins are seen on CT or magnetic resonance studies and suggest DAVF, 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. The second case of bilateral ethmoidal DAVF was reported by Komotar et al. in 2007. 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.,,
DAVFs of the anterior cranial fossa are high-risk factors for hemorrhage because of their cortical venous drainage (types III and IV). 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. 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. 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. 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. 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., A transvenous endovascular approach to DAVFs involving the cavernous and dural sinuses has been performed successfully with low risk. 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. 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. Although anterior cranial fossa DAVFs are rare (5.8%),, they have a very high incidence of sudden massive intracranial hemorrhage (62–91%) 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.
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., 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, 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.
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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