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Taiwan Journal of Ophthalmology 2 (2012) 151e154 Contents lists available at SciVerse ScienceDirect Taiwan Journal of Ophthalmology journal homepage: www.e-tjo.com Case report Central retinal vein occlusion with secondary cilioretinal artery occlusion treated with intravitreal bevacizumab (Avastin) Yu-Chien Chung a, Shih-Jen Chen a, b, *, Shih-Yun Lee a, Fenq-Li Lee a, b, Sui-Mei Lee a, b a b Department of Ophthalmology, Taipei Veterans General Hospital, Taipei, Taiwan School of Medicine, National Yang-Ming University, Taipei, Taiwan a r t i c l e i n f o a b s t r a c t Article history: Received 17 May 2012 Received in revised form 6 August 2012 Accepted 30 August 2012 Available online 2 October 2012 Two young male patients experienced acute visual disturbance in one eye, with central scotoma showing central retinal vein occlusion with cilioretinal artery occlusion (CLRAO). Optical coherent tomography (OCT) revealed inner retinal edema at areas of retinal infarction. An intravitreal injection of Avastin was administered to these two patients with improvement of symptoms within 4e8 weeks. These two cases suggested that OCT may help detect CLRAO by showing inner retinal edema, and demonstrated that intravitreal injection of Avastin may improve venous engorgement and retinal hemorrhage, as well as circulation of cilioretinal artery, thus shortening the disease course. Copyright Ó 2012, The Ophthalmologic Society of Taiwan. Published by Elsevier Taiwan LLC. All rights reserved. Keywords: bevacizumab (Avastin) central retinal vein occlusion cilioretinal artery occlusion 1. Introduction Central retinal vein occlusion (CRVO) is a frequent primary vascular disorder of the retina with vein blockage in the optic nerve head. Some eyes with CRVO, at its onset, may have associated cilioretinal artery occlusion (CLRAO). Oosterhuis in 19681 and then Hayreh in 19712 first reported this condition. The pathogenesis of CLRAO in patients with CRVO was unknown. In one study, retinopathy resolved in 70% of the eyes with nonischemic CRVO and CLRAO in a median time of 8 months.3 2. Case reports 2.1. Case 1 A healthy 38-year-old man presented with two episodes of transient blackout in the left eye for 1 day prior to coming to our clinic. On ophthalmic examination, visual acuity was 6/6 in both eyes, and visual field (VF) revealed cecocentral scotoma in the left eye. Dilated fundus examination showed venous engorgement of four quadrants, disc hemorrhage, and sectoral retinal whitening over the territory of one artery, with optical coherent tomography * Corresponding author. Department of Ophthalmology, Taipei Veterans General Hospital, Shih-Pai Road, Taipei 112, Taiwan. E-mail address: [email protected] (S.-J. Chen). (OCT) showing inner retinal edema (Fig. 1). Fluorescein angiography (FA) disclosed pulsatile filling of the artery with area of hypoperfusion above the fovea (Fig. 2). Carotid angiography revealed no thrombus or filling defect in the carotid or vertebral artery as well as in the ophthalmic or central retinal artery. Other systemic evaluation, including blood chemistry, inflammatory markers (erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)), blood coagulation profile, and autoimmune markers, were normal. The obstructed retinal artery was suspected to be a cilioretinal artery with secondary obstruction by increased intramural pressure due to CRVO. Intravitreal injections of Avastin (1.25 mg/0.05 mL) and triamcinolone (0.25 mg/0.05 mL) were given on the day of presentation, and the patient was treated with two more intravitreal injection of Avastin (1.25 mg/0.05 mL) in the following 2 months. In the following months, although the retinal whitening did not improve, the venous engorgement and artery circulation delay ameliorated with smaller scotoma on VF 1 month later. The artery circulation normalized with persistent distal ischemic area 2 months later. However, atrophy of inner retina was noted on OCT (Fig. 1). 2.2. Case 2 A 22-year-old man had newly diagnosed hypertension for 2 weeks prior to onset of ocular symptoms, and was on medical treatment. He presented to our clinic with gray vision in the left eye for 2 weeks. On ophthalmic examination, the best-corrected visual 2211-5056/$ e see front matter Copyright Ó 2012, The Ophthalmologic Society of Taiwan. Published by Elsevier Taiwan LLC. All rights reserved. http://dx.doi.org/10.1016/j.tjo.2012.08.007 152 Y.-C. Chung et al. / Taiwan Journal of Ophthalmology 2 (2012) 151e154 Fig. 1. Color fundus picture, OCT, and visual field of Case 1 (A) at presentation, and (B) 4 and (C) 8 weeks after intravitreal Avastin injection. The color fundus picture showed ameliorated venous engorgement and retinal whitening. Vertical OCT showed inner retinal swelling at the location of CLRAO (arrows) without macular edema, which regressed with inner retinal atrophy 8 weeks after therapy. Visual fields revealed gradual improvement of central scotoma. CLRAO ¼ cilioretinal artery occlusion; OCT ¼ optical coherent tomography. acuity was 6/6 in both eyes, with an intraocular pressure of 18/17 mmHg. Anterior segment was normal. Dilated fundus examination revealed disc swelling with retinal hemorrhage and faint retinal infarction in the left eye. OCT on the same day showed no macular edema but inner retinal swelling in the upper portion of fovea. VF demonstrated a central scotoma compatible with the location of retinal infarction (Fig. 3). One week later, he was administered an intravitreal injection of Avastin (1.25 mg/0.05 ml). Two weeks later, FA disclosed a minimal hypoperfusion patch superior to the fovea with mild artery and venous delay in the left eye (Fig. 2). One month later, OCT showed atrophy of inner retina and VF showed ameliorated central scotoma in the left eye (Fig. 3). 3. Discussion Hayreh reported a case series of 38 patient having CRVO with CLRAO from 1974 to 1999.3 Most reported cases of nonischemic CRVO with CLRAO were young adults (mean 45.8 16.0 years; range, 19e80 years), compared to those of CRVO alone that increased with age.4 Nearly all patients had disc edema with hemorrhage at initial visit, and all eyes had variable degrees of venous engorgement during acute phase. Generally, FA showed only transient hemodynamic block and not the typical CLRAO. Without intervention, resolution time of retinopathy in nonischemic CRVO was mostly 8 months (mean 42 101.0 months; median, 8.1 months; range, 0.7e472.3 months). In our cases, improved retinopathy could be observed after administration of intravitreal Avastin, with resolution at 1e2 months of follow-up. To our knowledge, this is the first report of treatment of CRVO with CLRAO with intravitreal Avastin. Two hypotheses have been proposed for the pathogenesis of CRVO with CLRAO.5,6 The first hypothesis is the development of CLRAO secondary to the raised capillary pressure caused by CRVO.7e12 The second hypothesis suggests a primary reduction in perfusion pressure of the cilioretinal and retinal arteries, leading to decreased retinal circulation and subsequent venous stasis and thrombosis.8,9,11 In our cases, venous engorgement alleviated after intravitreal Avastin treatment, with subsequent improvement of retinal infarction. The clinical picture supported the first hypothesis. Retinal vein occlusion leads to an increased expression of vascular endothelial growth factors (VEGFs) in retina and retinal pigment epithelium and an increased release into the vitreous, causing neovascularization and vascular hyperpermeability with subsequent breakdown of the blooderetina barrier.13 Intraocular VEGF is elevated in patients with both ischemic CRVO and nonischemic CRVO.14 The possible role of anti-VEGF agents in these two patients with nonischemic CRVO, nonmacular edema, but CLRAO is, first, to decrease the hyperpermeability status of retinal vein induced by venous stasis, which, hopefully, will decrease the edema surrounding the occluded vein and thus improve the circulation of the corresponding or nearby artery. Another role of Avastin injection is to decrease the inflammation. A recent study has shown that Avastin can not only prevent the upregulation of VEGF, but also decrease the proinflammatory cytokine.15 Nonischemic CRVO in young healthy patients had been suggested to be associated with inflammatory reaction with secondary occlusion.13 Y.-C. Chung et al. / Taiwan Journal of Ophthalmology 2 (2012) 151e154 153 Fig. 2. Color fundus picture, OCT, and visual field of Case 2 (A) at presentation, and (B) 1 week and (C) 4 weeks after intravitreal Avastin injection. Arrows point to the area of retinal infarction in the fundus picture and OCT. The inner retina became atrophy at 4 weeks, as shown by the OCT. Visual fields showed gradual improvement of scotoma. OCT ¼ optical coherent tomography. Fig. 3. (A) Baseline FA of Case 1 and (B) 2-week follow-up FA of Case 2. Both images showed area of hypoperfusion above the fovea as well as the retinal hemorrhage, disc swelling, venous congestion, and leakage. FA ¼ fluorescein angiography. Hence, Avastin was worth a trial in these two patients in order to improve the arterial as well as venous circulation, and the results seemed promising. Larger case series are needed to confirm this hypothesis of treatment effects. Unlike CRVO with macular edema, inner retina swelling, as demonstrated by OCT, was the feature of CRVO complicated with CLRAO. In Case 2, with faint retinal infarction in the fundus because of the mild symptoms and delayed visit (2 weeks after onset), significant inner retinal edema was still demonstrated by OCT. OCT is a valuable tool for CRVO not only for the evaluation of macular edema but also for the differential diagnosis of combined artery occlusion. In conclusion, nonischemic CRVO with disc hemorrhage may obscure the detection of secondary CLRAO. OCT may help in the detection of CLRAO by revealing the presence of inner retinal edema. Intravitreal injection of Avastin may improve venous engorgement and retinal hemorrhage as well as circulation of cilioretinal artery. References 1. Oosterhuis JA. Fluorescein fundus angiography in retinal venous occlusion. In: Henkes HE, editor. Perspective in ophthalmology. Amsterdam: Excerpta Medica Foundation; 1968. p. 29e47. 2. Hayreh SS. Pathogenesis of occlusion of the central retinal vessels. Am J Ophthalmol 1971;72:998e1011. 3. Hayreh SS, Fraterrigo L, Jonas J. Central retinal vein occlusion associated with cilioretinal artery occlusion. Retina 2008;28:581e94. 4. Rogers S, McIntosh RL, Cheung N, Lim L, Wang JJ, Mitchell P, et al. The prevalence of retinal vein occlusion: pooled data from population studies from the United States, Europe, Asia, and Australia. Ophthalmology 2010;117:313e9. 154 Y.-C. Chung et al. / Taiwan Journal of Ophthalmology 2 (2012) 151e154 5. Kim IT, Lee WY, Choi YJ. Central retinal vein occlusion combined with cilioretinal artery occlusion. Korean J Ophthalmol 1999;13:110e4. 6. Bottós JM, Aggio FB, Dib E, Farah ME. Impending central retinal vein occlusion associated with cilioretinal artery obstruction. Clin Ophthalmol 2008;2:665e8. 7. Zylbermann R, Rozenman Y, Ronen S. Functional occlusion of a cilioretinal artery. Ann Ophthalmol 1981;13:1269e72. 8. Glacet-Bernard A, Gaudric A, Touboul C, Coscas G. Occlusion of the central retinal vein with occlusion of a cilioretinal artery: apropos of 7 cases. J Fr Ophtalmol 1987;10:269e77 [in French, English abstract]. 9. Brazitikos PD, Pournaras CJ, Baumgartner A. Occlusion of a cilioretinal artery associated with occlusion of the central retinal vein. Klin Monatsbl Augenheilkd 1991;198:374e6 [in French, English abstract]. 10. Schatz H, Fong ACO, McDonald HR, Johnson RN, Joffe L, Wilkinson CP, et al. Cilioretinal artery occlusion in young adults with central retinal vein occlusion. Ophthalmology 1991;98:594e601. 11. Keyser BJ, Duker JS, Brown GC, Sergott RC, Bosley TM. Combined central retinal vein occlusion and cilioretinal artery occlusion associated with prolonged retinal arterial filling. Am J Ophthalmol 1994;117:308e13. 12. Noble KG. Central retinal vein occlusion and cilioretinal artery infarction. Am J Ophthalmol 1994;118:811e3. 13. Buehl W, Sacu S, Schmidt-Erfurth U. Retinal vein occlusions. Dev Ophthalmol 2010;46:54e72. 14. Koss MJ, Pfister M, Rothweiler F, Michaelis M, Cinatl J, Schubert R, et al. Comparison of cytokine levels from undiluted vitreous of untreated patients with retinal vein occlusion. Acta Ophthalmol 2011 Nov 8. http://dx.doi.org/ 10.1111/j.1755-3768.2011.02292.x. 15. Drechsler F, Köferl P, Hollborn M, Wiedemann P, Bringmann A, Kohen L, et al. Effect of intravitreal anti-vascular endothelial growth factor treatment on the retinal gene expression in acute experimental central retinal vein occlusion. Ophthalmic Res 2012;47:157e62.