A 59-year-old woman with history of noninsulin dependent diabetes mellitus and systemic hypertension presented with decreased vision in her left eye since 2 months ago. Bestcorrected visual acuity (BCVA) was 20/20 and 20/400 in the right and left eyes respectively.Relative afferent pupillary defect was negative.Anterior segment examination was unremarkable except for mild posterior subcapsular cataracts bilaterally. Funduscopy (Fig. 1) revealed sectoral retinal hemorrhage with macular edema and neurosensory retinal detachment due to inferotemporal branch retinal vein occlusion (BRVO). Basic laboratory tests, cardiologic consultation,fluorescein angiography (Fig. 2) and optical coherence tomography (Fig. 3) were obtained,followed by two intravitreal injections of 1.25 mg bevacizumab (IVB) in the left eye 2 months apart. BCVA improved to 20/80 in the left eye 2 months after the second injection.Post-treatment features are shown in Figures 4 to 6.One year later the patient presented with reduced vision in the same eye and visual acuity of 20/800. Funduscopy disclosed diffuse retinal hemorrhage and macular edema due to central retinal vein occlusion (CRVO, Fig. 7). Fluorescein angiographic findings are shown in Fig. 8.
Figure 1.
Pretreatment red-free photograph reveals acute inferotemporal branch retinal vein occlusion with sectoral intraretinal hemorrhage.
Figure 2.
Pretreatment fluorescein angiography shows venous engorgement (inferotemporal), mild perifoveal capillary drop out and blocked fluorescence due to branch retinal vein occlusion.
Figure 3.
Pretreatment optical coherence tomography demonstrates marked increase in foveal thickness (596 μm) and neurosensory detachment.
Figure 4.
Two months after treatment; red-free photograph shows decreased intraretinal hemorrhage.
Figure 5.
Two months after treatment; fluorescein angiography shows decreased venous engorgement and perifoveal capillary dilatation.
Figure 6.
Two months after treatment; optical coherence tomography shows marked improvement in neurosensory detachment and reduction in foveal thickness (211 μm).
Figure 7.

Fundus photograph one year after initial presentation. Diffuse retinal hemorrhage and venous engorgement due to central retinal vein occlusion.
Figure 8.
One year after initial presentation, fluorescein angiography shows diffuse venous engorgement, retinal neovascularization with leakage due to old branch retinal vein occlusion and blocked fluorescence due to retinal hemorrhage resulting from central retinal vein occlusion.
DISCUSSION
The pathogenesis of BRVO remains obscure.The occlusion commonly occurs at arteriovenous crossings, where the artery and vein share a common tunica adventitia. Changes in the arterial wall, especially atherosclerotic changes, are considered to be important risk factors for BRVO, which have been similarly shown for CRVO. However, progression of atherosclerotic changes appears to be less intense in BRVO as compared to CRVO, suggesting the possible role of other factors such as hypertension and hypercoagulability in the pathogenesis of the former condition.1 By investigating the mechanism of CRVO in monkeys,Hayreh et al2 reported that characteristic funduscopic appearance of retinal hemorrhage and retinal capillary bed obliteration are observed only following simultaneous ligation of the central retinal vein and artery. They concluded that circulatory failure in the artery is the most important factor in the development of CRVO.Atherosclerosis is likely to be involved in the development and progression of CRVO and diabetes mellitus is significantly associated with the condition.3 On the other hand, systemic hypertension seems to be a more important risk factor for BRVO.
Despite similar pathogenesis and risk factors,it is unclear why BRVO and CRVO do not occur simultaneously in the same eye. The patient presented herein developed BRVO followed by CRVO in the same eye within a one year interval. To the best of our knowledge no such case has been reported in the literature.
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