. Purpose:  To compare macular thickness following uncomplicated phacoemulsification with foldable acrylic lens and manual small incision cataract surgery (MSICS) with non‐foldable polymethyl methacrylate (PMMA) lens implantation. Methods:  Prospective study was carried out with one eye each of 224 patients with senile cataract randomized into two groups, phacoemulsification and MSICS, by simple 1:1 randomization. Following surgery by either of the two methods, macular thickness was measured by optical coherence tomography (OCT) on the 1st, 7th, 42nd and 180th postoperative day. Main outcome measure was postoperative macular thickness. Results:  On the first postoperative day, central subfield mean thickness (CSMT) in MSICS group was 192.8 ± 17.9 μm and that in phacoemulsification group was 192.1 ± 27.4 μm, with no significant difference (p = 0.12). On the 7th day, CSMT in MSICS group (198.9 ± 21.4 μm) was significantly (p = 0.04) more than that in phacoemulsification group (193.1 ± 19.3 μm). On the 42nd day, CSMT in MSICS group was 207.8 ± 26.3 μm and that in phacoemulsification group was 198.3 ± 23 μm, the difference being significant (p = 0.007). Clinically macular oedema was not diagnosed in any of the patients at any visit. The increase in macular thickness was sub‐clinical and did not affect final visual outcome in any patient. Conclusion:  In spite of the greater theoretical risk of increased postoperative inflammation following MSICS, there was no evidence of cystoid macular oedema, either clinically or on OCT. However, chance of sub‐clinical increase in CSMT was more following MSICS compared to phacoemulsification.

Objective:To identify the sociodemographic characteristics, degree and cause of visual disability among certified visually disabled individuals in a rural district of West Bengal, India and to identify possible lacunae, if any, in the existing certification system.Materials and Methods:A cross-sectional study by secondary data analysis of medical records of 155 visually disabled individuals and their 310 eyes. Demographical features, diagnosis, percentage of visual disability and work activity status of each individual were analyzed.Results:One hundred and thirty one (84.52%) individuals had 100% disability. The number of males was significantly higher than that of females. Fifty eight (37.42%) individuals were below 21 years of age. Phthisis bulbi was the most common cause followed by microphthalmos. Further, 81.29% patients had the same lesion bilaterally.Conclusion:Patients with higher grades of disability have attended certification boards. A large number of disabled individuals comprised children and young adults. Male gender bias demands concern.

Purpose:Despite the disease having similar glycemic status and duration microangiopathy in some patients develop within few years whereas it doesn't appear as a health complication in some diabetics for a considerable period. This study is undertaken to assess the hyperglycemia-induced biochemical background behind the development of diabetic retinopathy (DR) in type 2 diabetes mellitus (DM).Methods:Following proper diagnosis, 100 patients of type 2 DM of 10–12 years duration having no DR, and 42 patients of type 2 DM of the same duration and glycemic status as the second group, with mild retinopathy were recruited in the study. Lactic acid, glutamate, malondialdehyde (MDA), nitrate, advanced glycation end-products (AGEs), peripheral blood mononuclear cell reactive oxygen species (ROS), vascular endothelial growth factor (VEGF), and its receptor 2 (VEGFR2) in these two groups were produced in an assay following standard methodology.Results:Biochemical markers of anaerobic glycolysis, lipid peroxidation, AGEs, glutamate concentration, oxidative stress, and expression of VEGF and its VEGFR2 with significantly elevated markings were found in them who developed earliest stage of DR rather than them who had not.Conclusion:Hyperglycemia-induced anomalous glucose metabolism, lipid peroxidation, advanced glycation, glutamate toxicity, and oxidative stress create a background where apoptosis of retinal capillary endothelial cells invite increased expression of VEGF and VEGFR2, these being the crucial factors behind the development of diabetic microangiopathy.