The Role of the Vitreous Body in Various Ocular Changes and Following Cataract Surgery
The close connection between the vitreous body and retina can result in reti-nal tears in vitreous detachment, which in turn can lead to rhegmatogenousretinal detachment (from the Greek word “rhegma,” breakage.
These retinal defects provide an opening for cells from the retinal pigment epithelium to enter the vitreous chamber. These pigment cells migrate along the surface of the retina. As they do so, they act similarly to myofibroblasts and lead to the formation of subretinal and epiretinal membranes and cause con-traction of the surface of the retina. This clinical picture is referred to aspro-liferative vitreoretinopathy (PVR). The rigid retinal folds and vitreous mem-branes in proliferative vitreoretinopathy significantly complicate reattach-mentoftheretina. Usually this requires modern techniques of vitreous surgery.
Retinal vascular proliferation can occur in retinal ischemia in disorders such as diabetic retinopathy, retinopathy in preterm infants, central or branch reti-nal vein occlusion, and sickle-cell retinopathy. Growth of this retinal neovascu-larization into the vitreous chamber usually occurs only where vitreousdetachment is absent or partial because these proliferations require a sub-strate to grow on. Preretinal proliferations often lead to vitreous hemorrhage.Fibrotic changes produce traction of the retina resulting in a tractional retinal detachment.
Increased postoperative inflammation in the anterior segment can progress through the hyaloid canal to the posterior pole of the eye and a cystoid macu-lar edema can develop. This complication occurs particularly frequently fol-lowing cataract surgery in which the posterior lens capsule was opened with partial loss of vitreous body. (Hruby-Irvine-Gass syndrome is the develop-ment of cystoid macular edema following intracapsular cataract extraction with incarceration of the vitreous body in the wound).