Aim: To determine if uncomplicated phacoemulsification cataract surgery is associated with an accelerated rate of progression of diabetic retinopathy or maculopathy postoperatively. Methods: A prospective trial of 50 type 2 diabetics undergoing monocular phacoemulsification cataract surgery by a single consultant surgeon. The grade of diabetic retinopathy and diabetic maculopathy in the operated and non-operated fellow eye was assessed preoperatively and for 12 months postoperatively. Results: Overall, retinopathy progression was observed in 11 patients. In seven the retinopathy progressed in both eyes, in three it progressed in the operated eye alone, and in one it progressed in the fellow eye alone. Macular oedema was observed in 13 eyes postoperatively. Four had transient pseudophakic cystoid macular oedema and nine true diabetic maculopathy. Where maculopathy progressed it did so symmetrically in five patients, it progressed in the operated eye alone in four patients, and the fellow eye alone in two patients. There was no significant difference in the number of operated and fellow eyes whose retinopathy or maculopathy progressed postoperatively. In both the operated (OE) and non-operated (NoE) eyes retinopathy progression was associated with a higher mean HbA 1 C (OE p=0.003; NoE p=0.001) and insulin treatment (OE p=0.008, NoE p=0.04). Conclusion: Uncomplicated phacoemulsification cataract surgery does not cause acceleration of diabetic retinopathy postoperatively and any progression that is observed probably represents the natural history of the disease. Although macular oedema is common after cataract surgery it may follow a benign course and in many patients the development of clinically significant macular oedema postoperatively probably represents natural disease progression rather than being a direct effect of surgery.

The incidences of infectious and noninfectious endophthalmitis after IVT were low, and the risk did not increase with each successive injection. We found higher rates of noninfectious endophthalmitis with bevacizumab compared with ranibizumab or aflibercept. Three quarters of cases with infectious and two thirds of cases with noninfectious endophthalmitis retained vision within 10 letters of the pre-endophthalmitis level.

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RA-associated PUK often has a poor visual outcome and its appearance may herald the transformation of a patient's RA into the systemic vasculitic phase. RA-associated PUK should be managed with aggressive immunosuppression if the associated morbidity and mortality are to be avoided. Cell-mediated mechanisms appear to be important in the aetiopathogenesis of PUK and a combination of corticosteroids and cyclosporin is therefore probably the regimen of choice.

Pseudophakic cystoid macular oedema (PCMO) remains a significant cause of compromised postoperative vision in contemporary cataract surgery. Well‐established risk factors include intraoperative complications such as posterior capsule rupture and preoperative factors including: diabetes mellitus, uveitis, retinal vein occlusion, epiretinal membrane. The role of topical glaucoma medications in PCMO continues to be debated. Current treatment strategies largely target suppression of inflammation. Topical NSAIDs remain the mainstay in prophylaxis and treatment of PCMO. Topical corticosteroids are commonly used as monotherapy or in combination with NSAIDs. Unfortunately, high‐quality trials are notably lacking for other PCMO treatment modalities such as: periocular corticosteroids, orbital floor triamcinolone, intravitreal triamcinolone, corticosteroid implants, intravitreal bevacizumab and pars‐plana vitrectomy. A lack of consistency in defining PCMO and resolution of PCMO explains why even large systematic reviews may come to contradictory conclusions. This review explores the varied contemporary evidence‐base in relation to the aetiology, diagnosis, prophylaxis and treatment of PCMO.

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Diabetic retinopathy is a vascular disease of the retina characterised by hyperglycaemic and inflammatory processes. Most animal models of diabetic retinopathy are hyperglycaemia-only models that do not account for the significant role that inflammation plays in the development of the disease. In the present study, we present data on the establishment of a new animal model of diabetic retinopathy that incorporates both hyperglycaemia and inflammation. We hypothesized that inflammation may trigger and worsen the development of diabetic retinopathy in a hyperglycaemic environment. Pro-inflammatory cytokines, IL-1β and TNF-α, were therefore injected into the vitreous of non-obese diabetic (NOD) mice. CD1 mice were used as same genetic background controls. Fundus and optical coherence tomography images were obtained before (day 0) as well as on days 2 and 7 after intravitreal cytokine injection to assess vessel dilation and beading, retinal and vitreous hyper-reflective foci and retinal thickness. Astrogliosis and microgliosis were assessed using immunohistochemistry. Results showed that intravitreal cytokines induced vessel dilation, beading, severe vitreous hyper-reflective foci, retinal oedema, increased astrogliosis and microglia upregulation in diabetic NOD mice. Intravitreal injection of inflammatory cytokines into the eyes of diabetic mice therefore appears to provide a new model of diabetic retinopathy that could be used for the study of disease progression and treatment strategies.

Compared with microperimetry, BCVA seems to significantly underestimate the change in visual function experienced by patients treated with ranibizumab.