Objective To summarize the visual outcome of patients with severe ocular trauma treated with vitreous surgery. Methods Clinical data of 188(191 eyes) with severe ocular trauma treated with vitreous surgery in a period from November 1996 to April 1998 were analysed retrospectively. Results The study included penetrating injury in 56 eyes, foreign bodies in the posterior segment in 70 eyes, blunt injury in 41 eyes , and globe rupture in 24 eyes. Main complications included endophthalmitis in 35 eyes, choroidal bleeding in 20 eyes, retinal detachment in 60 eyes, and vitreous hemorrhage in 97 eyes. Post-opera-tively, out of 188 eyes, except for 3 of patients too young to examine, visual acuity improved in 133(70.7%), including 85(45.2%) with visal acuity 0.02-1.0, 46(24.5%) remained unchanged; and 9(4.8%) had worse vision. Among 34 with no-light-perception, 12 had light-perception or over. Conclusion A majority of severe trauma eyes can be salvaged with considerable visual recovery after adequate and timely vitreous surgery. (Chin J Ocul Fundus Dis,1999,15:4-6)
Microcystic macular edema (MME) represents a pathological change that can be observed in the inner layer of the retina in patients diagnosed with glaucoma. This phenomenon is particularly prevalent in individuals with moderate to advanced glaucoma. The majority of research in this field has focused on primary open-angle glaucoma. The occurrence of MME in glaucoma has been demonstrated to be associated with younger age, advanced stage and disease progression. MME occurs in the parafoveal region, most frequently located in the inferior perimacular region, which corresponded with the most vulnerable area of ganglion cells in glaucoma. The presence of MME may affect the automatic layering of optical coherence tomography images, suggesting that clinicians should be mindful of the occurrence of MME to avoid misdiagnosis of the disease. It is hypothesised that the occurrence of MME in glaucoma may be related to macular vitreous traction, mechanical stress of the stent, and Müller cell dysfunction. A comprehensive investigation of the precise pathophysiological mechanism of MME in glaucoma will facilitate the development of a novel perspective and a scientific foundation for the diagnosis, disease monitoring and evaluation of treatment efficacy in glaucoma.