Proliferative vitreoretinopathy (PVR) is a disease entity related to a
number of intraocular diseases, including retinal detachment (RD).
Several studies have confi rmed the hypothesis that PVR occurs as a
reparative process induced by retinal breaks and excessive infl amma-
tory reaction. A survey of recently published series suggested that the
frequency of PVR remains largely unchanged in primary RD, with the
incidence ranging from 5.1 to 11.7%.
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PVR is the most common cause
of failed repair of rhegmatogenous RD and risk factors for PVR are
related to several, well-known pre-, intra-, and postoperative clinical
situations. Currently, surgery such as pneumatic retinopexy, scleral
buckling, and pars plana vitrectomy (PPV) is the mainstream therapeu-
tic modality for RD and PVR. The goal of surgery is to create chorioreti-
nal adhesion around all the retinal breaks and to relive all the tractional
force. Single-operation reattachment rates were 73% for pneumatic reti-
nopexy and 82% for scleral buckling after 6 months, and multiple-
operation reattachment rates at 2 years were 99% for pneumatic
retinopexy and 98% for scleral buckling for RD. Surgical success rates
for PVR have improved as techniques and instruments of vitrectomy
evolved. The introduction of ancillary techniques such as longer-acting
gases and long-term vitreous substitutes like silicone oil elevated the
success rate from 35 – 40% to approximately 60 – 75% at 6 months. Despite
these advances, more than one-fourth of initially successful cases results
in redetachment due to recurrent retinal traction. Furthermore, visual
results are less satisfactory and only 40 – 80% of cases with anatomic
success achieve ambulatory vision. As a result, PVR remains a diffi cult
problem to manage and continuing efforts have been made to develop
other forms of therapy to inhibit the pathologic response causing trac-
tion. Recent efforts have been directed toward the chemical inhibition
of cellular proliferation and membrane contraction in PVR.