Diagnosing and Treating Vitreomacular Adhesion

Abstract

Perifoveal vitreous detachment with residual vitreofoveal adhesion is considered as the first stage of posterior vitreous detachment. A key point is the transition from an innocuous vitreomacular adhesion (VMA) to a pathological vitreomacular traction (VMT). By using optical coherence tomography (OCT), VMA is defined as adhesion of the posterior hyaloid cortex involving the centre of the foveal region with or without a hyper-reflective signal on the inner surface of the retina. VMT is diagnosed when the inner macular surface slopes steeply, or sharp angulation and localised deformation of the retinal profile is detected at the VMA site. Otherwise, VMA is simply considered to be persistent adherence of the cortical vitreous. The tractional effects of perifoveal vitreous detachment cause a variety of macular pathologies determined by the size and the strength of the residual vitreoretinal adhesion. Vitreomacular adhesion plays a major role in the development of diseases such as vitreomacular traction syndrome (VMTS), macular hole, epiretinal membrane, tractional macular oedema and myopic macular retinoschisis. In addition, clinical evidence supports the theory that the course of diabetic retinopathy and age-related macular degeneration may be strongly influenced by an incomplete posterior vitreous separation. The current standard of care of vitreomacular interface pathologies is vitrectomy and membrane peeling – a procedure that is thought to relieve epiretinal traction – followed by regeneration of the retinal architecture and recovery of visual function. Over the last few years, with the introduction of 25-gauge (0.50mm) and 23-gauge (0.72mm) instruments, there has been another major shift toward transconjunctival microincisional vitrectomy surgery (MIVS). Pharmacological induction of posterior vitreous detachment (PVD) can become a further step toward a real ‘minimally invasive vitreous surgery’ for VMTS.