Diabetic retinopathy, a secondary microvascular complication of diabetes mellitus is the leading cause of blindness in the Unites States amongst individuals age 20 to 64. Two major retinal problems cause most of the diabetes-related vision loss: diabetic macular edema and complications from abnormal retinal blood vessel growth, angiogenesis. Secondary to angiogenesis, increased retinal blood flow is of pathogenic importance in the progression of diabetic retinopathy. Understanding the role of hyperglycemia seems to be the most critical factor in regulating retinal blood flow, as increased levels of blood glucose are thought to have a structural and physiological effect on retinal capillaries causing them to be both functionally and anatomically incompetent. High blood glucose induces hypoxia in retinal tissues, thus leading to the production of VEGF-A (vascular endothelial growth factor protein). Hypoxia is a key regulator of VEGF-induced ocular neovascularization. Secondary to the induction of VEGF by hypoxia, angiogenesis can be controlled by angiogenic inducers and inhibitors. The balance between VEGF and angiogenic inhibitors may determine the proliferation of angiogenesis in diabetic retinopathy. Since VEGF-A is a powerful angiogenic inducer, utilizing anti-VEGF treatments has proved to be a successful protocol in the treatment of proliferative diabetic retinopathy.

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Ains-A retrospective analysis of children with post-traumatic endophthalmitis was performed to determine if microbiological differences exist between this disease in the paediatric population compared with this disease in adults. Method Herein, we report our experience with posttraumatic endophthalmitis in children with emphasis on microbiological differences that occur between this group and adults. Materials and methodsWe reviewed the medical records of 12 consecutive cases of post-traumatic endophthalmitis in patients 18 years and younger presenting to our institution. For each case we obtained the patient's age, sex, type of injury, initial visual acuity, vitreous culture results, treatment regimen, and final visual acuity.Those patients presenting with posttraumatic endophthalmitis who had not had primary repair were immediately placed on intravenous cefazolin and gentamicin. During primary repair corneal wounds were repaired before conjunctival peritomy. Prolapsing subconjunctival uvea and/or subconjunctival blood, suggesting a scleral perforation, were attended to first. Conjunctiva and Tenon's capsule were locally dissected away from the wound. If vitreous prolapse was evident, a manual vitrectomy was performed using a dry cotton tip applicator and scissors. Scleral lacerations were uniformly repaired with 8.0 nylon suture. After repair of wounds involving the cornea and anterior sclera, a 360 degree peritomy was performed and the globe was explored. Routinely we first examined the four quadrants of the globe between recti muscles using the Schepens retractor and a cotton tip swab. Each of the recti muscles was then isolated and retracted to allow for visualisation underneath the muscle. If a scleral perforation was seen at the insertion of the recti muscle, the muscle was removed from the globe and then reinserted after repair.Following repair of the globe, conjunctival, anterior chamber, and vitreous cultures were obtained. Anterior chamber taps were performed using a 30 gauge needle at the surgical limbus. Vitreous taps were obtained using a 23 gauge needle at the pars plana. Intravitreal injections of vancomycin 1I0 mg and amikacin sulphate 0 40 mg were given in all cases.For all cases ocular fluids were plated on sheep blood agar, chocolate agar, thioglycolate broth, and Sabouraud's dextrose. Gram and Giemsa stains were performed on all scrapings.In select cases a pars plana vitrectomy was performed to clear the ocular media and obtain ocular fluids for culture and examination. The decision to perform a pars plana vitrectomy was made by the attending vitreoretinal surgeon treating the patient. At our institution, criteria for performing a vitrectomy as an 888 on 9 May 2018 by guest. Protected by copyright.

The Early Treatment Diabetic Retinopathy Study (ETDRS) identified important risk factors for progression to high risk proliferative diabetic retinopathy (PDR) including retinopathy severity, decreased visual acuity, and high levels of hemoglobin A1C (HbA1c). Additional risk factors for progression to PDR are decreased hematocrit and increased serum lipids. The long-term benefit of improving glycemic control was evaluated by three large studies: the Diabetes Control and Complications Trial (DCCT), the Stockholm Interventional Study, and the UK prospective study. Several small studies, notably the Kuwamoto study, also evaluated the relationship between the glycemic control and diabetic retinopathy. Intensive glycemic control reduces the risk of any retinopathy by approximately 27%. Intensive therapy is most effective when initiated early in the course of the diabetes, demonstrating a beneficial effect over the course and progression of retinopathy. The long term benefits of the intensive glycemic control greatly outweigh the risk of "early worsening." Lowering elevated serum lipid levels has been shown to decrease the risk of cardiovascular morbidity. The ETDRS data suggest that lipid lowering may also decrease the risk of hard exudate formation and associated vision loss in patients with diabetic retinopathy. Preservation of vision may be an additional motivating factor for lowering serum lipid levels in persons with diabetic retinopathy and elevated serum lipid levels.

To quantify the amount of optic nerve axonal loss associated with the presence of a mild relative afferent pupillary defect (RAPD) in an experimental monkey model. Methods: The right macula of 5 rhesus monkeys (Macaca mulatta) was treated with concentrically enlarging diode laser burns until an RAPD was detected using a transilluminator light and measured with neutral density filters. Intervals between treatments were 3 to 7 days over a period of 2 months. Pupillary responses to light stimulation were recorded with a monocular infrared television pupillometer. Two months after detection of an RAPD, 5 treated and 4 control monkeys underwent euthanasia and enucleation. Histopathologic analysis and quantification of optic nerve axon counts using an image analysis system were performed. Results: No RAPD was observed despite an estimated ganglion cell loss of up to 26%. A 0.6 log unit RAPD was present in 5 monkeys when the laser scar incorporated the entire macula within the temporal vascular arcades. One eye had progressive vitreomacular traction with worsening of the RAPD to 1.8 log units without further laser treatment. Histopathologic evaluation disclosed complete loss of the normal retinal architecture within the macula. The average fiber loss for the 4 treated eyes with 0.6 log unit RAPDs compared with fellow eyes was 53.3% (95% confidence interval [CI], 45.0%-61.6%). The average difference in axon counts between untreated pairs of optic nerves was 12.8% (95% CI, 10.0%-15.6%). Optic nerve axon loss between pairs of experimental and control eyes was statistically significant (PϽ.001). Conclusion: In rhesus monkeys, an RAPD develops after an approximate unilateral loss between 25% and 50% of retinal ganglion cells. Clinical Relevance: Owing to redundancy in the anterior visual pathways, unilateral retinal ganglion cell loss may occur prior to the observation of an RAPD. The presence of an RAPD measuring 0.6 log units implies that significant retinal ganglion cell injury has occurred.