Entry site neovascularisation after diabetic vitrectomy

When scleral entry sites over the pars plana were first used for vitrectomy access, concerns were raised that anterior vitreous complications might compromise surgical outcomes.1 2 After all, it had long been recognised that, in chronic uveitis or in inflammation complicating a penetrating injury, the non-pigmented ciliary epithelium might undergo proliferation and fibrous metaplasia, accompanied by a stroma derived vascular component, to form a “cyclitic” membrane using the anterior surface of the vitreous as a scaffold; this could lead to traction on the ciliary processes and peripheral retina, hypotony, and phthisis.3 The retrolental membrane might also include glial and retinal pigment epithelial cells in cases of concomitant rhegmatogenous retinal detachment or an “ingrowth” of episclera derived fibrovascular tissue at sites of penetration. Happily, such foreboding over pars plana vitrectomy has proved largely unfounded, presumably reflecting in part the dispersion of any inflammatory mediators involved. But vitrectomy for the ischaemic retinopathies, especially for proliferative diabetic retinopathy (PDR), has been a notable exception.

Following vitrectomy for PDR, any residual new vessels located posterior to the vitreous base usually undergo regression,4 but some eyes develop florid basal neovascularisation as a supplement to the normal wound healing process at the sclerotomies.2 5 6 Such entry site neovascularisation (ESNV) may arise as an isolated event after otherwise successful surgery when it represents one of a number of possible sources of “delayed” diabetic vitreous cavity haemorrhage (DVCH)—that is, bleeding after an initial haemorrhage-free period of 3 or more weeks post-vitrectomy. Other possible culprits for delayed DVCH include “secondary haemorrhage” from shedding of thrombus …