Retina Today - Imaging Options in Retinal Vein Occlusion (April 2018)

摘要

Retinal vein occlusion (RVO) is the second leading cause of retinal vascular disease, with reported cumulative annual incidence of 1.8% for branch RVO (BRVO) and 0.5% for central RVO (CRVO),1,2 and bilateral or subsequent incidences of 6.4% and 0.9%, respectively.1,3,4 AT A GLANCE • OCT is the gold standard imaging modality in the management of patients with RVO. • Fundus photography and fluorescein angiography are acceptable and helpful alternatives. • Newer imaging methods are promising but should be employed with caution until more data are available. The postulated mechanism of action involves impingement of venules at the shared adventitial sheath by crossing arterioles leading to turbulence, stasis, thrombosis, and occlusion.5,6 Response to anti-VEGF and antiinflammatory agents has empirically demonstrated that inflammatory factors play a more important role in RVO than previously presumed, beyond the obvious ischemia. These processes, seemingly mediated by released VEGF, induce retinal edema, retinal hemorrhages, and ischemia, thereby compromising visual function (Figure 1).7-9 Figure 1. The BRVO seen in this fundus photograph features intraretinal blot hemorrhages and soft exudates in the distribution of the occluded superotemporal vein. Because diabetes, hypertension, hypercoagulable states, and vasculitis are associated with a higher incidence of RVO, cooperation with an internist is advised. History of CRVO in the same or fellow eye, open-angle glaucoma, or retrobulbar external compression, as in thyroid orbitopathy or other orbital masses, also predispose an individual to RVO.10-12 Objectively assessing RVO severity and determining prognosis of the condition depend on imaging studies. All clinical trials in RVO have relied heavily on various imaging modalities to standardize eligibility and treatment monitoring. This article reviews the use of some established imaging modalities in these important clinical trials and looks ahead at some promising new imaging technologies. ESTABLISHED TREATMENT OPTIONS Management of RVO with laser photocoagulation, anti-VEGF agents, and corticosteroids has been well established (Tables 1 and 2).13-29 Laser Photocoagulation The Branch Vein Occlusion Study (BVOS) recommended focal laser photocoagulation for BRVO causing visual acuity of 20/40 or worse and macular edema.13,14 Evidence of center-involving macular edema on fluorescein angiography (FA) was the critical entry criterion. Separately, scatter photocoagulation to the involved segment was found to prevent occurrence of vitreous hemorrhage if neovascularization developed. The Central Vein Occlusion Study (CVOS) reported that panretinal photocoagulation reduced visual loss when 2 or more clock hours of iris neovascularization or more than 10 disc areas of capillary nonperfusion was present, but macular grid photocoagulation did not reduce visual acuity loss caused by macular edema.3,15-18 FA provided the gold standard for eligibility and monitoring of edema and extent of capillary nonperfusion (Figure 2). Figure 2. An 80-year-old woman with diabetes and hypertension presented with decreased visual acuity (20/200) and CRVO in her left eye. Fundus photograph shows the presence of disc edema, venous tortuosity, and diffuse retinal hemorrhages (A). FA of the left eye highlights corresponding areas of disc leakage, vessel wall staining, flame-shaped blocked fluorescein, and diffuse capillary nonperfusion (B). OCT of the macula shows cystoid maculopathy with neurosensory detachment (C). OCT at 1-year follow-up after patient received five intravitreal ranibizumab (Lucentis; Genentech) injections with marked resolution of cystoid changes and neurosensory detachment (D). The patient’s visual acuity at last follow-up visit improved to 20/60. Anti-VEGF Therapy Anti-VEGF agents antagonize the effect of VEGF and generally arrest or even reverse disease progress