[Relationship between vitrectomy and the morphology and function of the retina].
Pathological processes in the vitreous will be reflected in the morphology and function of the retina, and these processes can originate from sources outside the vitreous. The purpose of vitreous surgery is to remove the qualitatively and/or morphologically diseased vitreous. Successful vitrectomy will be manifested by an improvement in the structure and/or function of the retina. We have evaluated the morphology of the vitreoretinal interface, and the function of the retina before and after vitreous surgery. Plasmin-assisted vitrectomy was used in some cases to remove the diseased vitreous more efficiently and less invasively. The effect of this procedure was assessed by examining the morphology and function of the retina. First, the relationship between the qualitative and structural abnormality of the vitreous in macular diseases was studied. In aphakic/pseudophakic eyes with cystoid macular edema, there was a depression of retinal function over the entire retina which may have been caused by chemical mediators released into the vitreous. These mediators may have been produced by inflammation in the anterior segment of the eye. In eyes with an idiopathic macular hole, optical coherence tomographic (OCT) images suggested that the progression of the macular hole might depend on a balance between foveal adhesion and the posterior vitreous. Second, the efficacy, surgical damage, and limitations of vitreous surgery were investigated. The recovery of macular function was assessed by focal macular electroretinograms (FMERGs) after vitrectomy for epiretinal membrane, choroidal neovascularization, and diabetic macular edema. The concurrent examination by optical coherence tomography (OCT) suggested that a decrease in retinal thickness contributed to the functional recovery. Macular functional recovery was delayed and limited after macular translocation, diabetic macular edema, and internal limiting membrane peeling. Third, we studied the effect of plasmin-assisted vitrectomy on the retina. The plasmin was used to remove the vitreous more completely and less invasively. In rabbits, ERG, OCT, and histological examinations demonstrated that the use of commercially-available plasmin at a concentration used on human patients resulted in temporary adverse effects on the retina. For human patients, we purified the plasmin from the patients' serum at the Nagoya University Hospital and the activity was about the same as in previous reports. The purified plasmin was approved by our hospital's institutional review board, and written informed consent was obtained from each patient. Patients with macular edema, idiopathic macular hole, and epiretinal membrane without posterior detachment underwent plasmin-assisted vitrectomy and were evaluated morphologically and electrophysiologically. The efficacy of the plasmin in separating the vitreo-retinal interface was demonstrated by an occasional spontaneous posterior vitreous detachment with or without core vitrectomy, and the presence of less vitreous cortex attached to the internal limiting membrane that was removed during vitrectomy. This was the first histological demonstration of the effectiveness of plasmin in the living eye. Full-field ERGs before and after surgery demonstrated clear evidence that no alteration of retinal functional had occurred, although we did detect a possible osmotic effect by an increase in OCT-determined retinal thickness by the high-molecular weight autologous plasmin. In future studies, the proper concentration and reaction time for each condition of the vitreous should be determined. In conclusion, the pathophysiology of the vitreous should reflect the retinal function. The recovery of the structure of the retina is important for the recovery of retinal function. This should always be the primary goal of surgeons who perform quality surgery.
Terasaki
Hiroko
H
Department of Ophthalmology, Nagoya University School of Medicine.
D000818:Animals; D005341:Fibrinolysin / Q000502:physiology; D006801:Humans; D008266:Macula Lutea / Q000473:pathology; D008269:Macular Edema / Q000601:surgery; D011817:Rabbits; D012160:Retina / Q000033:anatomy & histology* / Q000502:physiology*; D012164:Retinal Diseases / Q000473:pathology; D012167:Retinal Perforations / Q000503:physiopathology; D014821:Vitrectomy; D014822:Vitreous Body / Q000503:physiopathology
D005341:Fibrinolysin