Diabetic macular edema (DME) results from abnormal leakage of macromolecules into the extracellular space from microaneurysms and incompetent blood vessel walls due to small vessel damage from high blood glucose levels. Oncotic forces then allow water into the extracellular space. Abnormalities in the retinal pigment epithelium (RPE) may reduce normal outflow of fluid from the retina to the underlying choriocapillaris via the pump mechanism (Ferris et al. 1984). This leads to retinal edema in the macula with accompanying loss of vision. There is evidence suggesting that vascular endothelial growth factor (VEGF) plays a part in vessel wall permeability with subsequent retinal edema (Aiello et al. 1997).