OBJECTIVES: To determine the intraretinal and periretinal pathological changes in early anterior proliferative vitreoretinopathy (APVR). DESIGN: Observational case series. PARTICIPANTS: Eighteen patients undergoing retinectomy for APVR. METHODS: Retinectomy specimens removed at vitrectomy surgery were analysed by (a) semithin light microscopy, (b) immunohistochemistry and (c) electron microscopy. RESULTS: The specimens showed consistent outer retinal degenerative changes, marked Muller cell hypertrophy and glial continuity to epiretinal membranes. Photoreceptor outer and inner segments were markedly disrupted and occasional photoreceptor nuclear had pyknosis and chromatin clumping consistent with apoptosis. Muller cells expressed upregulated levels of glial fibrillary acid protein (GFAP) and extended through glial bridges to complex epiretinal membranes which in some areas had a bilaminar structure with a glial-negative inner lamina. CONCLUSION: Retinal degeneration and photoreceptor apoptosis occur in retinal detachment complicated by proliferative vitreoretinopathy (PVR), although during the early stages of the process neural retinal cells remain present, suggesting potential for recovery. The intraretinal glial response appears to be centrally involved in the formation of contractile epiretinal membranes. The retina retains the capacity for a degree of functional recovery following surgery for PVR. Surgical separation of anterior epiretinal membranes in PVR may be difficult and incomplete and alternative surgical strategies may be necessary to prevent recurrence.
OBJECTIVES: To determine the intraretinal and periretinal pathological changes in early anterior proliferative vitreoretinopathy (APVR). DESIGN: Observational case series. PARTICIPANTS: Eighteen patients undergoing retinectomy for APVR. METHODS: Retinectomy specimens removed at vitrectomy surgery were analysed by (a) semithin light microscopy, (b) immunohistochemistry and (c) electron microscopy. RESULTS: The specimens showed consistent outer retinal degenerative changes, marked Muller cell hypertrophy and glial continuity to epiretinal membranes. Photoreceptor outer and inner segments were markedly disrupted and occasional photoreceptor nuclear had pyknosis and chromatin clumping consistent with apoptosis. Muller cells expressed upregulated levels of glial fibrillary acid protein (GFAP) and extended through glial bridges to complex epiretinal membranes which in some areas had a bilaminar structure with a glial-negative inner lamina. CONCLUSION:Retinal degeneration and photoreceptor apoptosis occur in retinal detachment complicated by proliferative vitreoretinopathy (PVR), although during the early stages of the process neural retinal cells remain present, suggesting potential for recovery. The intraretinal glial response appears to be centrally involved in the formation of contractile epiretinal membranes. The retina retains the capacity for a degree of functional recovery following surgery for PVR. Surgical separation of anterior epiretinal membranes in PVR may be difficult and incomplete and alternative surgical strategies may be necessary to prevent recurrence.
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