Retina Today - Management Trends in Retinal Vascular Occlusive Diseases (April 2018)

摘要

Retinal vascular occlusive diseases constitute a significant cause of visual impairment in the elderly worldwide. This article focuses on strategies for managing patients with retinal vein occlusion (RVO) and retinal artery occlusion (RAO). RVO IN A NUTSHELL Central RVO (CRVO) and branch RVO (BRVO) are caused by thrombosis of a retinal vein. RVO is the second most common vision-threatening retinal vascular disease after diabetic retinopathy.1-3 Systemic risk factors include arteriosclerosis, hypertension, diabetes, lipid abnormalities, and vascular inflammatory diseases.4 Because of characteristic alterations in the arteriovenous crossing anatomy, hypertension is the leading risk factor for BRVO,4 yet the necessity for hypercoagulability testing in younger patients and patients with bilateral RVO remains controversial.5 AT A GLANCE • RVO is the second most common vision-threatening retinal vascular disease after diabetic retinopathy. • Although giant cell arteritis is a relatively uncommon cause of central retinal artery occlusion, it is essential to rule it out in patients 50 years and older. • Multiple therapeutic interventions for RVO have emerged with significant potential for clinical improvement, whereas optimal therapies with proven visual benefit for retinal artery occlusions have yet to be found. Move Over Laser The most common cause of vision loss in patients with RVO is macular edema (ME). Coexisting macular ischemia is the primary determinant of visual outcomes in patients with RVO.1-3 Historically, grid laser photocoagulation was the gold standard therapy for BRVO; however, intravitreal pharmacotherapy has largely replaced laser as the intervention of choice for both BRVO and CRVO. Intravitreal injection of anti-VEGF agents has become first-line therapy for ME secondary to RVO since numerous prospective studies revealed their remarkable therapeutic effects.6-19 More than half of patients with nonischemic RVO will achieve rapid improvement in visual acuity and reduction in retinal thickness shortly after initiation of anti-VEGF therapy, and these improvements are largely maintained with adequate retreatment.6-19 Visual acuity changes from baseline and number of injections required in selected prospective clinical trials are outlined in Figures 1 and 2. Early initiation (ie, 3 months from onset) of anti-VEGF therapy appears to lead to the greatest improvement in visual acuity.12,17,19 Figure 1. Changes in best corrected visual acuity (BCVA) in selected prospective clinical trials for BRVO (A) and CRVO (B). The numbers adjacent to the colored dots indicate mean change in BCVA (ETDRS letter score) from baseline at follow-up visits. This graph is intended to give a rough estimate of visual changes with each treatment modality. Treatment arms in different clinical trials cannot be directly compared due to differences in study populations, disease duration, and inclusion and treatment criteria. Figure 2. Scatter plot illustrating the relationships between mean number of anti-VEGF injections per year and mean changes in BCVA from baseline in BRVO (A) and CRVO (B). This graph is intended to provide a rough estimate of the number of anti-VEGF injections required to gain or maintain visual acuity each year. Treatment arms in different clinical trials cannot be directly compared due to differences in the study populations, disease duration, and inclusion and treatment criteria. An Anti-VEGF Drug is an Anti-VEGF Drug? At this point, evidence from randomized controlled trials has not shown definitive differences in efficacy and safety among anti-VEGF agents.18,20 The SHORE study demonstrated that an as-needed (PRN) regimen with monthly follow-up, after 7 monthly injections, was as effective as a monthly treatment regimen.11 Although many trials mandate a loading period, one to two injections might be sufficient before switching to PRN in cases that demonstrate compl