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 Table of Contents  
CASE REPORT
Year : 2013  |  Volume : 3  |  Issue : 4  |  Page : 168-172

Central retinal vein occlusion after gamma knife radiosurgery for cavernous sinus dural arteriovenous fistula


1 Department of Ophthalmology, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan
2 Department of Diagnostic Radiology, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan
3 Department of Neurosurgery, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan

Date of Web Publication20-Nov-2013

Correspondence Address:
Yan-Ming Chen
Department of Ophthalmology, E-Da Hospital, 1, E-Da Road, Yan-Chao District, Kaohsiung City 824
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.1016/j.tjo.2013.05.001

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  Abstract 


A 70-year-old man presented to our clinic complaining of binocular diplopia and persistent redness in the left eye for 5 months. Conjunctival vessels were dilated and tortuous in both eyes. Intraocular pressure was 16 mmHg in the right eye and 23 mmHg in the left eye. Complete bilateral sixth cranial nerve and partial left third cranial nerve palsies were noted. Brain computed tomography and cerebral angiography revealed a Barrow Type C dural arteriovenous fistula. The patient underwent gamma knife radiosurgery (GKRS) at a dose of 18 Gy and a target volume of 3.3 mL. Within 1 month of GKRS, the patient reported an improvement in diplopia, but 4 months following the procedure, he experienced micropsia, metamorphopsia, and darkness in his left eye. Prominent flame-shaped hemorrhages and retinal edema, the typical picture of central retinal vein occlusion (CRVO), developed in his left eye. Intraocular pressure in this eye was controlled with antiglaucoma topical medication. 5 months later, the left retina had appeared normal. Antiglaucoma drops were gradually tapered and eventually discontinued. The GKRS, used in recent decades, is noninvasive and effective in the treatment of dural arteriovenous fistula. However, CRVO can occur after GKRS. Here, we present, in detail, a clinical course of CRVO that developed after GKRS. Our findings may be useful for further understanding of this rare complication.

Keywords: central retinal vein occlusion, dural arteriovenous fistula, gamma knife radiosurgery


How to cite this article:
Lin YC, Ou CH, Liang CL, Hsu HC, Tsai SH, Chen YM. Central retinal vein occlusion after gamma knife radiosurgery for cavernous sinus dural arteriovenous fistula. Taiwan J Ophthalmol 2013;3:168-72

How to cite this URL:
Lin YC, Ou CH, Liang CL, Hsu HC, Tsai SH, Chen YM. Central retinal vein occlusion after gamma knife radiosurgery for cavernous sinus dural arteriovenous fistula. Taiwan J Ophthalmol [serial online] 2013 [cited 2019 Nov 13];3:168-72. Available from: http://www.e-tjo.org/text.asp?2013/3/4/168/203916




  1. Introduction Top


Dural arteriovenous fistulas (DAVFs) are arteriovenous shunts from a dural arterial supply to a dural venous channel. They are typically supplied by pachymeningeal arteries and located near a major venous sinus. Recent studies have shown that gamma knife radiosurgery (GKRS) is a safe and effective treatment for intracranial DAVFs when used alone or in combination with other treatment modalities.[1],[2],[3],[4]

Central retinal vein occlusion (CRVO) refers to sluggish or blocked central retinal vein blood flow. Retinal veins upstream from the obstruction accumulate extra blood and become dilated and torturous. The increased intravenous pressure subsequently drives blood and fluid into the retina, causing retinal hemorrhages and retinal and macular edema.[5],[6],[7],[8],[9] Herein, we report a case of CRVO after GKRS in a patient with cavernous sinus DAVFs.


  2. Case report Top


A 70-year-old man presented to our ophthalmic clinic on January 12, 2011, complaining of diplopia and persistent redness in his left eye for 5 months. Best-corrected visual acuity was 6/15 in the right eye and 6/10 in the left eye. Intraocular pressure (IOP) was 16 mmHg in the right eye and 23 mmHg in the left eye. Conjunctival vessels were dilated and torturous in both eyes. Complete bilateral sixth cranial nerve and partial left third cranial nerve palsies were noted and a fundus examination revealed a slight retinal vessel dilatation in the left eye. Intracranial DAVFs were suspected and brain computed tomography showed prominent bilateral cavernous sinuses, especially on the left, and an engorged left superior ophthalmic vein (SOV; [Figure 1]A and [Figure 1]B, consistent with bilateral cavernous sinus DAVFs. Cerebral angiography revealed a Barrow Type C DAVF that was supplied by multiple arterial feeders, including the bilateral middle meningeal artery, the left accessory middle meningeal artery, and branches of the bilateral internal maxillary artery [Figure 1]C and [Figure 1]D. Azopt (1% brinzolamide ophthalmic suspension; Alcon Inc., Fort Worth, TX, USA) was administered twice a day in the left eye and after 2 weeks of treatment IOP was 14 mmHg in the right eye and 18 mmHg in the left eye. The patient underwent GKRS on February 12, 2011, with a dose of 18 Gy to the 50% isodose line and a target volume of 3.3 mL.
Figure 1: Brain computed tomography showed (A) prominent bilateral cavernous sinuses, especially on the left side, and (B) an engorged left superior ophthalmic vein. (C, D) Cerebral angiograms revealed a Barrow Type C dural arteriovenous fistula that was supplied by multiple arterial feeders including the bilateral middle meningeal artery, left accessory middle meningeal artery, and branches of the bilateral internal maxillary artery.

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Within 1 month of GKRS, the patient reported an improvement in diplopia. Additionally, the left third cranial nerve and right sixth cranial nerve palsies had completely resolved, but the left sixth cranial nerve palsy persisted. Retinal vessels in the left eye returned to normal, but conjunctival vessels remained engorged and torturous in both eyes. No changes in visual acuity had occurred and IOP was 18 mmHg in the right eye and 19 mmHg in the left eye. The antiglaucoma medication for the left eye was changed to twice-daily Cosopt (dorzolamide hydrochloride–timolol maleate ophthalmic solution; Merck & Co., Inc., Whitehouse Station, NJ, USA) for better IOP control.

On April 15, 2011, the patient again presented to our clinic complaining of color perception changes in his left eye. Although visual acuity and IOP had not changed since the previous visit, the retinal vessels had again become engorged and multiple blot hemorrhages were found in the mid-peripheral retina. A partial third cranial nerve palsy had again developed in the left eye and the persistent, complete left sixth cranial nerve palsy remained. Intraocular pressure was 16 mmHg in both eyes and the patient was instructed to continue Cosopt use.

On June 15, 2011, the patient returned to our clinic complaining of micropsia, metamorphopsia, and darkness in his left eye. Best-corrected visual acuity had decreased to 6/30 and typical characteristics of CRVO, including prominent flame-shaped hemorrhages and retinal edema, had developed in his left eye [Figure 2]A. The patient had no history of systemic disease associated with CRVO, including hypertension, diabetes mellitus, blood dyscrasias, clotting disorders, vasculitis, and autoimmune disease. Although IOP in the left eye was well controlled with Cosopt, we added twice-daily Alphagan P (brimonidine tartrate ophthalmic solution 0.15%; Allergan Inc., Irvine, CA, USA) to his regime because elevated IOP could have led to CRVO development.
Figure 2: Fundus photos of the left eye. (A) Typical picture of central retinal vein occlusion on June 15, 2011. (B) Partial resolution of retinal hemorrhages on September 7, 2011. (C) Nearly total resolution of retinal hemorrhages on November 30, 2011. (D) No sign of central retinal vein occlusion on July 18, 2012.

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Fivemonths later, retinal hemorrhages in thelefteyehadresolved [Figure 2]B,[Figure 2]C,[Figure 2]D and best-corrected visual acuity had returned to 6/10 with no further treatment. Retinal edema, as precisely monitored with optical coherent tomography, did not completely resolve until 10 months later [Figure 3]. On February 29, 2012, a year after GKRS, magnetic resonance angiography was performed, which showed no obvious residual DAVFs and a normal caliber SOV bilaterally.
Figure 3: Serial optical coherent tomography (macula) of the patient's left eye. (A) The patient was noted to have central retinal vein occlusion on June 15, 2011. Optical coherent tomography showed mild retinal edema. (B) Macular edema was demonstrated on September 7, 2011. (C) Most of the retinal edema subsided on November 30, 2011. (D) Complete resolution of retinal edema on July 18, 2012.

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The last patient visit took place on August 15, 2012, at which time the retina of the left eye appeared normal on both ophthalmoscopy and optical coherent tomography, but the patient continued to experience some micropsia and metamorphopsia. At this point, anti-glaucoma drops were gradually tapered and eventually discontinued. The patient still suffered from diplopia because of persistent left third and sixth cranial nerve palsies.


  3. Discussion Top


The development of CRVO has been previously noted as a rare complication of cavernous sinus DAVFs.[5],[6],[7],[8],[9],[10],[11],[12],[13] It can occur as part of the natural course of cavernous sinus DAVFs in patients receiving conservative treatment,[5],[7],[8],[9],[10] after transvascular embolization,[6],[8],[11],[13] and after GKRS.[12] Predisposing factors for CRVO development in patients with cavernous sinus DAVFs are not currently known, but several theories have emerged. Pollock et al[7] and Brunette et al[5] suggested that increased IOP may be an important factor, but Suzuki et al[9] reported a case of occlusion even though IOP was well controlled. They suggested that the fistula resulted in an increased intracavernous sinus pressure, which was conducted to the SOV and, subsequently, to the retinal vasculature. This increased intravascular pressure eventually impaired the retinal circulation and the CRVO developed. Nevertheless, Komiyama et al[6] reported one case of CRVO 4 months after DAVF embolization. In this case, cerebral angiography revealed only minimal shunted flow to the cavernous sinus and SOV. Thus, increased pressure in the cavernous sinus and SOV cannot be the sole factor contributing to the occurrence of CRVO. Several clinical reports have indicated that SOV thrombosis is connected with CRVO. Chen et al[11] described one patient whose ocular symptoms worsened 3 days after palliative embolization. Angiography revealed an incomplete SOV thrombus, as well as severe orbital venous congestion. Preechawat et al[13] performed embolization in 60 patients with DAVF, three of whom developed a CRVO, and subsequent severe visual defects, from SOV thrombosis. Aside from angiographic evidence, SOV thrombosis also occurred in one patient as documented on magnetic resonance imaging, with paradoxical worsening after GKRS.[12]

After GKRS, radiation-induced vessel injuries and subsequent healing processes could obliterate vessels. Theoretically and ideally, the nidus should be obliterated first. Unfortunately, the draining vein is occasionally occluded prior to the nidus, and an early draining vein occlusion (EDVO) develops. There are only a few reports on the incidence and characteristics of EDVO in DAVFs treated by GKRS, but EDVO in patients with cerebral arteriovenous malformations (AVMs) after GKRS is well described by Yen et al.[14] In this series of 1400 cerebral AVM patients, 12 developed early thrombosis in the draining vein between 6 months and 25 months (median = 11.6 months) after GKRS.[14] Although DAVFs and AVMs are different disease entities both pathologically and clinically, the mechanisms leading to EDVO after GKRS might be similar. According to Yen et al,[14] the post-GKRS AVM obliteration process is generally slow, allowing the vasculature surrounding the nidus to develop collateral venous drainage pathways. However, in unusual situations, an acute/subacute thrombosis within the draining vein can develop prior to nidus obliteration, possibly because of direct radiation damage to draining veins and venous stasis within turbulent flow eddies.[14]

Few reports have noted ocular complications of GKRS in patients with cavernous sinus DAVFs. Lau et al[12] reported CRVO development in one patient 1 month after GKRS, which had completely resolved 1 month later. In the largest series of 146 DAVF patients treated with GKRS, Wu et al[4] reported a transient deterioration of ocular symptoms in 14 DAVF patients between 2 weeks and 11 months following GKRS, with SOV thrombosis documented in nine of these patients. Unilateral vision impairment associated CRVO, intraocular hemorrhage, and SOV thrombosis developed in two cases. Overall, SOV thrombosis occurred in 11 (7.5%) of 146 cases and permanent vision impairment occurred in two (1.4%) of 146 cases. In the case ofbilateral cavernous sinus DAVFs presented here, the patient’s right eye recovered completely and his left eye only partially recovered following GKRS. A CRVO developed and a resolved third cranial nerve palsy returned in the left eye 4 months after treatment. Fortunately, the CRVO spontaneously resolved and the patient had a good visual recovery 5 months later. Unfortunately, the cranial nerve palsy and double vision persisted.

The clinical features of the fistula are determined not only by the supplying arteries, but also by the draining veins.[15],[16] In patients with exophthalmos and dilated episcleral veins, the main venous drainage from the cavernous sinus is the superior ophthalmic vein, whereas in patients presenting with third, fourth, and sixth cranial nerve palsies, the venous drainage is from the cavernous sinus to the pericarotid plexus, pterygoid plexus, and inferior petrosal sinus. Because our patient had persistent cranial nerve palsy, despite the absence of an obvious DAVF on MR angiography, minor DAVF residual, not visible on the image study, may have remained or the cranial nerve injury by DAVF was irreversible. Changes in the clinical presentation of this case may have indicated venous drainage changes after GKRS. Although this may have happened with no treatment, Yen et al[14] believe that GKRS contributed to this rare occurrence of obliteration caused by draining vein thrombosis. Furthermore, our patient reported a symptom duration of5 months prior to seeking medical attention and all changes took place within 6 months following GKRS. Although no direct evidence implicates GKRS as a cause of CRVO, we believe that radiosurgery was a significant contributor to CRVO development in this patient.

GKRS has the advantages of being noninvasive, accurate, and effective, and has changed DAVF treatment in recent decades. However, given the slower fistula occlusion process following GKRS than following traditional embolization procedures, longer follow-up times are likely to be needed to determine the procedure efficacy. Moreover, EDVO with accompanying CRVO could occur as long as 6 months following GKRS and DAVF patients undergoing the procedure should be informed of this possibility. Herein, we have summarized the clinical courses of the few reported CRVO cases that have developed after GKRS. This may be useful for better understanding of this rare complication.



 
  References Top

1.
Paul AR, Colby GP, Huang J, Tamargo RJ, Coon AL. Selection of treatment modalities or observation of dural arteriovenous fistulas. Neurosurg Clin N Am 2012;23:77–85.  Back to cited text no. 1
    
2.
See AP, Raza S, Tamargo RJ, Lim M. Stereotactic radiosurgery of cranial arteriovenous malformations and dural arteriovenous fistulas. Neurosurg Clin N Am 2012;23:133–46.  Back to cited text no. 2
    
3.
Sheehan J. Gamma knife surgery for dural arteriovenous fistula. J Neurosurg 2006;104:864–5.  Back to cited text no. 3
    
4.
Wu HM, Pan DH, Chung WY, Guo WY, Liu KD, Shiau CY, et al. Gamma knife surgery for the management of intracranial dural arteriovenous fistulas. J Neurosurg 2006;105(Suppl.):43–51.  Back to cited text no. 4
    
5.
Brunette I, Boghen D. Central retinal vein occlusion complicating spontaneous carotid-cavernous fistula. Case report. Arch Ophthalmol 1987;105:464–5.  Back to cited text no. 5
    
6.
Komiyama M, Yamanaka K, Nagata Y, Ishikawa H. Dural carotid-cavernous sinus fistula and central retinal vein occlusion: a case report and a review of the literature. Surg Neurol 1990;34:255–9.  Back to cited text no. 6
    
7.
Pollock S, Miller NR. Central retinal vein occlusion complicating spontaneous carotid-cavernous fistula. Arch Ophthalmol 1986;104:331.  Back to cited text no. 7
    
8.
Sergott RC, Grossman RI, Savino PJ, Bosley TM, Schatz NJ. The syndrome of paradoxical worsening of dural-cavernous sinus arteriovenous malformations. Ophthalmology 1987;94:205–12.  Back to cited text no. 8
    
9.
Suzuki Y, Kase M, Yokoi M, Arikado T, Miyasaka KD. Development of central retinal vein occlusion in dural carotid-cavernous fistula. Ophthalmologica 1989;199:28–33.  Back to cited text no. 9
    
10.
Barke RM, Yoshizumi MO, Hepler RS, Krauss HR, Jabour BA. Spontaneous dural carotid-cavernous fistula with central retinal vein occlusion and iris neo-vascularization. Ann Ophthalmol 1991;23:11–7.  Back to cited text no. 10
    
11.
Chen Z, Zhu G, Feng H, Liu Z. Worsening of cavernous sinus dural arteriovenous fistula with incomplete superior ophthalmic thrombosis after palliative transarterial embolization. Neurol India 2007; 55:390–2.  Back to cited text no. 11
    
12.
Lau LI, Wu HM, Wang AG, Yen MY, Hsu WM. Paradoxical worsening with superior ophthalmic vein thrombosis after gamma knife radiosurgery for dural arteriovenous fistula of cavernous sinus: a case report suggesting the mechanism of the phenomenon. Eye 2006;20:1426–8.  Back to cited text no. 12
    
13.
Preechawat P, Narmkerd P, Jiarakongmun P, Poonyathalang A, Pongpech S. Dural carotid cavernous sinus fistula: ocular characteristics, endovascular management and clinical outcome. JMed Assoc Thai 2008;91:852–8.  Back to cited text no. 13
    
14.
Yen CP, Khaled MA, Schwyzer L, Vorsic M, Dumont AS, Steiner L. Early draining vein occlusion after gamma knife surgery for arteriovenous malformations. Neurosurgery 2010;67:1293–302.  Back to cited text no. 14
    
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Kurata A, Takano M, Tokiwa K, Miyasaka Y, Yada K, Kan S. Spontaneous carotid cavernous fistula presenting only with cranial nerve palsies. Am J Neuroradiol 1993;14:1097–101.  Back to cited text no. 15
    
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Stiebel-Kalish H, Setton A, Nimii Y, Kalish Y, Hartman J, Huna Bar-On R, et al. Cavernous sinus dural arteriovenous malformations: patterns of venous drainage are related to clinical signs and symptoms. Ophthalmology 2002;109: 1685–91.  Back to cited text no. 16
    


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