Main features of nonproliferative diabetic retinopathy are capillary dilatation, tortuosity and microaneurysm formation, leading to haemorrhages, exudation and lipid deposition on the retina. Increased vascular permeability leads to exudation and extravasation of fluid in the retina. The retina looks grey and thickened. Initially the oedema is limited to the outer plexiform and inner nuclear layer. Fluorescein angiogram of the mild retinopathy shows a group of hyperfluorescent dots within the confined of the lipid exudates. These increase in fluorescence and produce a small amount of localised leak. In more severe cases the cotton-wool spots shows as areas of capillary closures. Initially they are hypofluorescent but during the late phase show hyperfluorescence due to staining from the leakage of dye. The intraretinal microvascular abnormality shows increase fluorescence during the arteriovenous phase that produces a small amount of leak towards the late phase. The haemorrhage masks fluorescence through the entire sequence of angiography. The late phase shows beading, dilatation, and staining of the lateral walls of the veins. The areas of retina with oedema also show moderate degree of hyperfluorescence due to leakage of dye. In cases of proliferative diabetic retinopathy neovascularization commonly occurs around the posterior pole to the equator, usually along the course of major retinal vessels, which is described as neovascularisation elsewhere. If there is severe ischaemia new vessels grow from the optic disc, which is referred as new vessels of the disc. During the early phase of the transit the capillary closure areas show hypofluorescence. Gradually the new vessels fill to demonstrate the architectural detail. During the progress of the transit and towards the late phase considerable degree of leakage of dye occur from the defective new vessels and the underlying details are lost leaving a huge area of hyperfluorescence. The leakage may be so severe that it can spill out into the vitreous obscuring the retinal vascular detail. On the contrary long standing new vessels may no longer exude and produce leakage. Diabetic maculopathy may be sub-classified as focal, diffuse, and ischaemic. A mixture of microaneurysms, lipid exudates and oedema is confined to a localised area. The vision may be affected due to spread of oedema into the macula itself. Focal diabetic maculopathy shows increased hyperfluorescence dots and the oedema collects a fair amount dye towards the late phase. The venous phase shows the capillary dilatation and tortuosity with evidence of early leak. The diffuse types, as the name suggests, affects a wider area of the macula. There is wide spread microaneurysms, vascular changes, haemorrhage and retinal oedema due to increased permeability of the retinal capillaries involving the posterior pole. In long-standing cases the neuroretina of the macula separates due to collection of oedema fluid in the outer plexiform layer (Henle’s). This gives rise to a typical clinical picture of cystoid macular oedema. The early phase of the angiogram masks the choroidal background fluorescence but soon the clusters of microaneurysms begin to fluoresce and produce leakage affecting a wider area of the macula. The late picture shows ample leakage from the capillary bed. In a long standing case a typical flower petal pattern of leakage around the macula fills the cystoid spaces. This is called cystoid macular oedema. Capillary closure and decreased perfusion around the foveal avascular zone is the prominent feature of ischaemic maculopathy. The perifoveal arcade is severely distorted. The oedema and microangiopathy are distributed in a similar fashion to that seen clinically in diffuse type. Angiography is the only way to differentiate between the diffuse and the ischaemic maculopathy. In case of ischaemic type large area of capillary closure is seen affecting the macular area. The perifoveal arcade is no longer preserved and the foveal avascular zone widen with marked distortion. Diffuse leakage of dye may occur during the late phase that includes the fovea.