15.1 Features
Proliferative vitreoretinopathy (PVR) is a disease where epiretinal membranes form on the surface of the retina, creating traction and ultimately retinal detachment (RD). PVR is the most common cause of failed primary rhegmatogenous RD repair, causing recurrent tractional or combined tractional and rhegmatogenous RD. The molecular pathophysiology is poorly understood. Surgical histopathology studies identify retinal pigment epithelial (RPE) cells, glial cells, and macrophages within the epiretinal membranes. The current hypothesis is that RPE cells undergo transdifferentiation into glial or fibroblast-like cells on the surface of the retina, proliferate, and ultimately contract, causing tractional RD or creating retinal stretch holes, leading to combined tractional and rhegmatogenous RD.
15.1.1 Common Symptoms
Painless vision loss, sometimes associated with flashing lights or floaters in the vision. In the setting of chronic RD with PVR, symptoms include peripheral visual field loss that may progress centrally. Due to the predilection for inferior pathology, superior visual field loss may be a presenting symptom. The most frequent time of presentation is 1 to 3 months after primary RD surgery.
15.1.2 Exam Findings
Examination begins with assessment of the lens. Due to the need to maximize vitreous base shaving and peripheral membrane peeling, phakic individuals are typically made pseudophakic. Next, the vitreous is assessed, identifying haze and pigment clumps in the vitreous or on the retina surface (▶ Fig. 15.1, white circle), which are defining features of grade A PVR (▶ Table 15.1). In patients with recurrent RD, identification of residual vitreous strands/traction and evaluation of the vitreous base for contracture or anterior displacement define grade CA PVR (▶ Table 15.1). Careful scrutiny of the retinal surface in patients with grade B PVR will identify wrinkling of the retinal surface (▶ Fig. 15.2a, white arrowhead), retinal stiffness, vessel tortuosity (▶ Fig. 15.2a, white arrow), and rolled or irregular edges (▶ Fig. 15.1; ▶ Fig. 15.2a, white arrows) of the retinal break(s) (▶ Table 15.1). In patients with grade C PVR, full-thickness retinal folds often called star folds (▶ Fig. 15.1, white arrowhead) and subretinal strands (▶ Fig. 15.3c) can be identified. Assessment of the location of star folds, will classify grade C PVR as anterior (grade CA) or posterior (grade CP) to the equator (▶ Table 15.1).
Fig. 15.1 Ultra-widefield fundus photograph of a postvitrectomy eye with partial silicone oil fill with the arcuate meniscus visible across the middle of the image. Areas of grade A proliferative vitreoretinopathy (PVR) are highlighted by the white circle with pigment clumps on the retina surface. Areas of grade B PVR are shown by the white arrow, demonstrating rolled edges of the inferior retinal break. An area of grade CP PVR with a full-thickness star fold is identified by the arrowhead.
Fig. 15.2 (a) Ultra-widefield fundus photograph of a post-vitrectomy eye with a large temporal retinal break with rolled edges (arrow), retinal wrinkling (arrowhead), and vessel tortuosity (dashed arrow). (b) B-scan ultrasonography shows thickened retina (between white arrows) and stiffness of this area on kinetic ultrasound.
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