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).
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