Risk factors and prevention of proliferative vitreoretinopathy

Abstract

Proliferative vitreoretinopathy (PVR) is the most common complication after repair of a retinal detachment. It is a clinical syndrome characterized by fibrocellular proliferation resulting in the formation of fibrotic epiretinal (i.e., preretinal and subretinal) membranes. Despite improvements in surgical techniques and anatomical outcomes, the treatment of PVR remains a challenge to preserve functional vision. PVR represents a wound healing response and multiple cytokines and growth factors may play a key role in its development. One of the most critical steps in the development of PVR is transformation of retinal pigment epithelium cells into fibroblastic and myofibroblastic phenotypes, which results in proliferation of fibrocellular membranes. Contraction of the membranes causes tractional retinal detachment. Treatment of PVR includes meticulous removal of fibrocellular membranes, relieving traction on all retinal breaks and intraocular tamponade. Several pharmacologic agents have demonstrated effectiveness in preventing the contraction of fibrocellular membranes in experimental models of PVR.

Keywords:

• animal model of proliferative vitreoretinopathy treatment
• pathogenesis
• proliferative vitreoretinopathy
• scleral buckle
• silicone oil
• tamponade
• vitrectomy

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Proliferative vitreoretinopathy has been reported to occur in 5–10% of cases of rhegmatogenous retinal detachment and is responsible for 75% of all surgical failures.

• Despite recent improvements in anatomical success, visual prognosis continues to be poor in re-operated eyes.

• Understanding pathophysiologic processes driving the development of proliferative vitreoretinopathy has been rapidly expending in recent years and multiple complex intracellular pathways for proliferation and contraction of these membranes have been elucidated.

• Surgery remains the mainstay therapy for proliferative vitreoretinopathy, however, multiple promising drugs are on the horizon.