Diabetic retinopathy: pathogenesis, clinical grading, management and future developments.

Decades of research into the pathophysiology and management of diabetic retinopathy have revolutionized our understanding of the disease process. Diabetic retinopathy is now more accurately defined as a neurovascular rather than a microvascular disease as neurodegenerative disease precedes and coexists with microvascular changes. However, the complexities of the pathways involved in different stages of disease severity continue to remain a challenging issue for drug discovery. Currently, laser photocoagulation is the mainstay of treatment for proliferative diabetic retinopathy, but is gradually being superseded for diabetic macular oedema. However, it is destructive and at best results in a gradual but modest improvement in vision in the long term. So, diabetic retinopathy remains the most prevalent cause of visual impairment in the working-age population despite established screening programmes, early diagnosis and treatment of the condition. The recent discovery of inhibitors of vascular endothelial growth factor is revolutionizing the management of diabetic retinopathy, particularly diabetic macular oedema. However, not all patients respond to anti-vascular endothelial growth factor agents, reinforcing the fact that diabetic retinopathy is a multifactorial disease. Studies are still required to improve our understanding of how retinal structure correlates with visual function. It is hoped that these will lead to better characterization of the disease phenotype based on treatment responses to different agents and allow an algorithm to be developed that will guide the management of diabetic retinopathy and diabetic macular oedema at different stages of severity.

Vitreoretinal interface changes in acute-onset postoperative endophthalmitis.

BACKGROUND: The aim of this study was to assess the significance of different clinical appearances of the vitreoretinal interface in the surgical management of acute postoperative endophthalmitis. PATIENTS AND METHODS: 22 patients underwent vitrectomy and were divided intraoperatively in 3 groups according to the degree of vitreoretinal interface changes: 10 patients had white infiltrates in the vitreous cortex but no retinal hemorrhages (group A), eight patients had white infiltrates in the vitreous cortex and retinal hemorrhages (group B) and four patients had advanced vitreous opacification, strong vitreoretinal adhesions and retinal hemorrhages (group C). In group A vitrectomy was performed and the vitreous cortex was removed cautiously, while in groups B and C the vitreous cortex was not removed in the first procedure. RESULTS: Visual acuity improved in 14 patients, remained stable in 2 patients and deteriorated in 6 patients. The visual prognosis was better in group A. None of the cases was complicated with retinal detachment following vitrectomy, but in groups B and C 37.5 % and 50 % of the patients, respectively, went into phthisis. CONCLUSIONS: Intraoperative assessment of the vitreoretinal interface insult in acute postoperative endophthalmitis contributes to an optimal surgical management, and it also has a prognostic value.