Treatment is usually indicated for symptomatic vitreomacular traction (VMT) with or without a full thickness macular hole (FTMH) and without spontaneous resolution. Ultrastructural parameters are evaluated by SD-OCT, in order to classify the vitreoretinal interface and to estimate the success rate of treatment. The resolution rate after therapy with intravitreal Jetrea® (Ocriplasmin) is high (up to 70 %) in patients with symptomatic focal vitreomacular traction (≤ 1500 µm) with or without a macular hole (≤ 250 µm) and with no epiretinal membrane (ERM), but depends on the exact baseline analysis. All other patients with idiopathic traction retinopathy should be treated by minimal invasive pars plana vitrectomy (MIVI). Vitreoretinal surgery effectively removes traction and gives a high closure rate of a full thickness macular hole (FTMH, 90 to 100 %). It is now a very safe procedure with few side effects. Despite a low risk profile (cataract, retinal tear etc.) the indication for surgery needs to take the safety profile into account. Therefore vitrectomy is only indicated in symptomatic patients complaining of blurred vision, VA reduction and metamorphopsia. Vitrectomy is also indicated in patients whose treatment by pharmacologic vitreolysis has failed.
In this ongoing study there was a high percentage of resolution of vitreomacular traction (71 %) 1 month after intravitreal operative injection of Jetrea® and closure of two out of five macular holes. This was further associated with stabilization of visual acuity and reduction of foveal thickness. Further investigations are necessary to document the effectiveness of the pharmacological vitreolysis in a clinical setting.
When traction is ≤ 1500 μm, enzymatic vitreolysis with ocriplasmin is a therapeutic option. In the presence of VMT >1500 μm or ERM, surgical treatment with vitrectomy is associated with better outcomes. In small macular holes with VMT and in the absence of ERM, enzymatic vitreolysis with ocriplasmin is an option. In cases of holes >400 μm, or in the absence of evident VMT, or in the presence of ERM, vitrectomy is the first choice.
A 76-year-old patient presented with a reduced visual acuity of 0.8. The clinical examination revealed rubeosis iridis and dilated retinal veins. In fluorescein angiography peripheral retinal ischemia could be observed and panretinal laser coagulation was immediately started. A comprehensive internistic counselling on the risk factors particularly for ocular ischemic syndrome was refused by the patient. Over time there was a progression of loss of visual acuity to complete visual loss. Magnetic resonance angiography revealed a profound stenosis of the internal carotid artery with complete closure of the left ophthalmic artery and percutaneous transluminal angioplasty was performed in vascular surgery.
This high-resolution SD-OCT-based retrospective study showed that fellow eyes of patients with VMT or FTMH were at increased risk of demonstrating pathological changes in the morphology of the VRI.
This article describes the case of a 22-year old female patient, who first presented with holocephalic headaches and bilateral loss in vision. After diagnosis of a complete Vogt-Koyanagi-Harada syndrome, high-dose corticosteroid therapy was initiated. Due to recurrent headaches 6 weeks later, immunosuppressive therapy was initiated with cyclosporine A. Because of an adverse effect (hirsutism) treatment was changed to azathioprine. In a long-term follow-up over 2 years the patient showed stable clinical findings with good visual acuity.
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