Abstract

Purpose: To report the significant worsening of Vitreomacular Traction (VMT), following the intravitreal injection of Bevacizumab (Avastin) in an Age Related Macular Degeneration (AMD) eye; thereby raising the awareness of this possibility. Method: Retrospective observational case report. Results: After 3 monthly doses of intravitreal injection of 1.25 mg/0.05 cc bevacizumab for treatment of AMD, a post injection OCT revealed the presence of VMT and an increased central macular thickness (CMT) by additional 268 microns compared to pre injection levels. Conclusion: Worsening of VMT and increase in CMT following injection of intravitreal drugs can occur. This VMT worsening effect of intravitreal injections is under recognized. It demands greater attention since it is seen with a new common route of ocular drug delivery and may be responsible for cases of pharmacological failure.

Highlights

  • There is evidence to support the clinical association of age related macular degeneration (AMD) and vitreomacular adhesion (VMA) or vitreomacular traction (VMT); this association occurs commonly [1] [2] [3]

  • Intravitreal anti VEGF is established as the treatment of choice for wet Age Related Macular Degeneration (AMD) and its effectiveness and safety has been validated by several randomized trials

  • We propose a mechanical theory for this increase in central macular thickness (CMT) following intravitreal anti VEGF injection

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Summary

Introduction

There is evidence to support the clinical association of age related macular degeneration (AMD) and vitreomacular adhesion (VMA) or vitreomacular traction (VMT); this association occurs commonly [1] [2] [3]. Published data suggests that it is common to find VMA/VMT occurring in AMD eyes when compared to age matched non-AMD control eyes [5] [6]. This association perhaps is more common with exudative AMD when compared to non-exudative AMD eyes. VMT adversely worsens AMD possibly due to the tractional forces that are exerted on the macular inducing inflammation or other mechanisms [6]. There is a suggestion that tractional forces of the VMT may antagonize the effect of intravitreal anti VEGF therapy and cause pharmacological treatment failure and resistance [7]

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