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Diabetic Macular Oedema

This develops as a result of hyperglycaemia-induced vascular damage resulting in breakdown of the inner blood-retinal barrier and leakage of fluid into the retina. Risk factors for progression include raised HbA1c, increased diastolic blood pressure and gross proteinuria. Once started, the condition tends to progress. Usually, the condition is treated with laser, but improvements in vision are rarely observed.

Prevention
Intensive control of blood sugar with HBA1c below or equal to 7% has been shown to prevent progression.  Switching type 2 diabetics to insulin increases the incidence of diabetic macular oedema in the short term. We believe that angiotensin II converting enzyme inhibitors and fenofibrate may slow progression, but convincing data is not yet available.

Treatment
Triamcinolone can improve diabetic maculopathy (DMO), but needs repeated injection or to be used in combination with other treatment modalities like laser. Anti-VEGF drugs are currently being investigated - so far the evidence suggests that Avastin is not as effective as triamcinolone in reducing DMO. Laser is thought to work by stimulating the release of chemical mediators. The ETDRS study showed that early treatment of DMO affecting the peri-foveal area reduced the incidence of severe visual loss more effectively than delayed treatment. Recent advances in laser treatment include the use of micropulse lasers, in which the duration of the laser pulse is of the order of 0.3 milliseconds (standard laser pulse duration is 100 milliseconds). This reduces heat build up and collateral thermal damage and scarring of the surrounding retina. This should help to preserve colour vision, field of vision, contrast sensitivity and reduce the small risk of choroidal neovascularisation associated with conventional grid laser photocoagulation.

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