Take-home: Peeling of the internal limiting membrane with staining of retinal tissues might help macular hole closure and resolve retinal schisis.
Performing a vitrectomy might accomplish more than meets the eye. Recent observations indicate that vitrectomy with peeling of the internal limiting membrane (ILM) and use of vitreoretinal dye might actually activate the retinal glia.
“The cases in which the macular holes close under these circumstances are not just the result of relieving traction,” Tongalp Tezel, MD, said. “There must be something else that is happening.”
Dr. Tezel, the Chang Family Professor of Ophthalmology, and director, Vitreoretinal Division, Columbia University Medical Center, New York, hypothesized that ILM peeling goes over-and-above removing traction and might induce the wound-healing response by activating the retinal glia postoperatively–with resultant closure of macular holes and resolution of retinal schisis in patients with high myopia
To study this, Dr. Tezel and colleagues studied the causes of retinal glial activation in freshly enucleated human eyes obtained from an eye bank. The investigators mimicked vitrectomy and ILM peeling in these eyes.
Using Western blotting and quantitative polymerase chain reaction, they studied the changes in various genes and proteins, such as vimentin, SERPINA-3, glial fibrillary acidic protein (GFAP), and endothelin receptor type B, bone morphogenetic protein 7, and secreted phosphoprotein-1, that are associated with retinal glial activation.
The dyes used during the procedures were indocyanine green (ICG), Brilliant blue G (BBG), trypan blue, and triamcinolone.
The findings indicated that vitrectomy alone activates the glia. When the researchers looked at what happens without vitrectomy, but with dye injection alone, they were surprised to find that genes indicating astrocyte and Muller cell activation, such as GFAP and SERPINA-3, seemed to be widely expressed when BBG or ICG was used.
Staining and peeling boosts up the individual effects on the expression levels of glial activation genes. Dr. Tezel also noted that BBG resulted in a robust Müller cell reactivity, which manifested itself with an increased expression of vimentin or GFAP compared to all other dyes.
Another observation was the induction of retinal gliosis with kenalog, which is expected to exert an antifibrotic effect like all steroids. Dr. Tezel and associates attribute this paradoxical outcome to the particulate nature of the drug.
“Overall, in this study, protein and glial activation genes seem to have increased,” Dr. Tezel said.
The investigators also correlated their observations with the inner retinal dimpling seen after chromovitrectomy with these dyes. Initially, investigators had thought that dimpling resulted from destruction of nerve fibers, or that the densities of the Muller cells were thought to be unequal.