The main objective is to determine the efficacy of intravitreal administration of Ranibizumab combined with intravitreous injection of expansile gas and induction of posterior vitreous detachment on best-corrected visual acuity and ocular coherence tomography (OCT) macular thickness in subjects with neovascular age-related macular degeneration (AMD) with posterior vitreomacular adhesion (VMA).

Secondary objectives are to assess the safety and tolerability of the intravitreal administration of Ranibizumab combined with intravitreous injection of expansile gas.

Age-related macular degeneration (AMD) is the leading cause of severe visual loss in industrialized countries. In recent years, the advent of anti-vascular endothelial growth factor (VEGF) therapies, such as ranibizumab and bevacizumab, has revolutionized neovascular AMD treatment and anti-VEGF has become the standard treatment for choroidal neovascularization (CNV) with a better visual outcome than previous therapies such as photodynamic therapy (PDT). However, one study reported that up to 45% of cases (20 out of 44 eyes) were non-responders showing resistance to anti-VEGF. In these cases, visual acuity did not improve and persistent subretinal fluid remained despite the usual monthly injection of anti-VEGF. A current focus of anti-VEGF treatment is how to determine which eyes will respond to treatment. To date, three genetic studies into the response to treatment for wet AMD have shown that specific genotypes for complement factor H and LOC genes are associated with treatment response. Previous studies have described the relationship between the posterior vitreous and the macula in AMD and have suggested that vitreomacular adhesion (VMA) plays an important role in the development of exudative AMD. In a recent paired eye study, we controlled confounding variables by selecting only patients with unilateral exudative AMD, and showed that eyes with exudative AMD had a significantly higher incidence of posterior VMA than paired normal eyes (P=0.0007). This result indicates that VMA is a possible risk factor for exudative AMD. In another recent study, Mojana and co-workers reported improvement in VA after 25-gauge trans pars plana vitrectomy (TPPV) with hyaloid removal in five patients who had a history of demonstrable VMA and poorly responsive CNV despite aggressive anti-VEGF therapy. We postulated that a subpopulation of exudative AMD cases do not respond to anti-VEGF therapy and that VMA may play a role in this resistance to therapy. The recent results of our study indicate that posterior VMA has a negative effect on visual outcome after intravitreal anti-VEGF treatment for exudative AMD. BCVA did not improve in eyes with posterior VMA despite anti-VEGF treatment. Posterior hyaloid removal by intravitreous injection of expansile gas and induction of posterior vitreous detachment may be considered as a treatment option in patients with VMA who are poor responders to anti-VEGF treatment.

Inclusion Criteria:

1. Age > 50 years old
2. Exudative AMD proven by fundus photograph and fluorescein angiography (FA)with VMA proven by OCT
3. Ability to provide written informed consent and comply with study assessments

Exclusion Criteria:

1. Previous anti-VEGF treatment
2. More than three prior treatment with PDT
3. Previous subfoveal focal laser photocoagulation in the study eye
4. Laser photocoagulation (juxtafoveal or extrafoveal) in the study eye within 1 month preceding day 0
5. Subfoveal fibrosis or atrophy in the study eye
6. History of vitrectomy surgery in the study eye
7. Significant concurrent ocular or macular diseases in the study eye
8. medical Hx such as myocardial infarction, cerebrovascular accident, ischemic cardiomyopathy, non ocular hemorrhage
9. History of Ranibizumab hypersensitivity
10. Presence of active periocular infection and/or endophthalmitis