A proposed new classification for diabetic retinopathy: The concept of primary and secondary vitreopathy

Abstract

Background:Many eyes with proliferative diabetic retinopathy (PDR) require vitreous surgery despite complete regression of new vessels with pan retinal laser photocoagulation (PRP). Changes in the vitreous caused by diabetes mellitus and diabetic retinopathy may continue to progress independent of laser regressed status of retinopathy. Diabetic vitreopathy can be an independent manifestation of the disease process.Aim:To examine this concept by studying the long-term behavior of the vitreous in cases of PDR regressed with PRP.Materials and Methods:Seventy-four eyes with pure PDR (without clinically evident vitreous traction) showing fundus fluorescein angiography (FFA) proven regression of new vessels following PRP were retrospectively studied out of a total of 1380 eyes photocoagulated between March 2001 and September 2006 for PDR of varying severity. Follow-up was available from one to four years.Results:Twenty-three percent of eyes showing FFA-proven regression of new vessels with laser required to undergo surgery for indications produced by vitreous traction such as recurrent vitreous hemorrhage, tractional retinal detachment, secondary rhegmatogenous retinal detachment and tractional macular edema within one to four years.Conclusion:Vitreous changes continued to progress despite regression of PDR in many diabetics. We identifies this as “clinical diabetic vitreopathy” and propose an expanded classification for diabetic retinopathy to signify these changes and to redefine the indications for surgery.

Retinal Changes Induced by Epiretinal Tangential Forces

“…Functionally, advanced glycation end (AGE) cross-links in the collagen fibrils of vitreoretinal interface cause reduced solubility, tissue rigidity, a decreased susceptibility of proteins to enzymatic digestion, aggregation of collagen fibers, and dissociation of collagen from hyaluronan, resulting in vitreous destabilization and alterations of PVC and hyalocytes [ 40 , 42 ]. Stitt et al [ 40 ] suggested that AGE-derived cross-links on the vitreous collagen network may cause earlier age-related vitreous degeneration in patients with diabetes than in those without diabetes and may cause anomalous PVD, vitreoschisis, and vitreoretinal traction [ 40 , 43 ]. Furthermore, proliferative diabetic retinopathy (PDR) alters the vitreous tissue by inclusion of fibrous tissue and vasogenic cells [ 43 ].…”

“…Stitt et al [ 40 ] suggested that AGE-derived cross-links on the vitreous collagen network may cause earlier age-related vitreous degeneration in patients with diabetes than in those without diabetes and may cause anomalous PVD, vitreoschisis, and vitreoretinal traction [ 40 , 43 ]. Furthermore, proliferative diabetic retinopathy (PDR) alters the vitreous tissue by inclusion of fibrous tissue and vasogenic cells [ 43 ]. Structural changes at the vitreoretinal interface promote migration and proliferation of vasogenic cells in the vitreous and the consequent contraction can produce macular edema and vitreous hemorrhage [ 43 ].…”

Intravitreal ziv-aflibercept in diabetic vitreous hemorrhage

“…In about a third of cases, retinal new vessels either continue to grow or do not regress despite full PRP leading to recurrent VH [14,15]. The natural history of diabetic VH in eyes with previous PRP is still undefined in the literature but appears more favorable than in eyes without PRP [4].…”

Systematic Review and Meta-Analysis of 16 Randomized Clinical Trials of Radix Astragali and Its Prescriptions for Diabetic Retinopathy

“…Diabetic retinopathy can be managed by improved control of glucose and blood pressure [15, 16], pharmacological, laser, and surgical approaches [17, 18]. Principal pharmacological therapies include drugs that inhibit neovascularization, such as anti-VEGF derivatives (Avastin & Lucentis [19–21]), or drugs to relieve macular swelling such as steroidal anti-inflammatory drugs (triamcinolone acetonide [22]).…”