The former causes a higher incidence and greater severity of retinopathy. The retinopathy begins when the capillary basement membrane thickens, leading to vessel closure. There's a dropout of pericytes, the cells that keep normal capillaries tight. The capillary walls weaken, causing microaneurysms that then rupture, with leakage of serum proteins, lipids and blood. Blood accumulates as dot and blot hemorrhages in the retina's inner nuclear and outer plexiform layers, and flame-shaped hemorrhages form in the nerve fiber layer.
Serum lipids aggregate as exudates, and a build-up of serous fluid causes retinal edema.
Venous beading results, and further capillary closure leads to focal hypoxia and cotton wool spots. More widespread hypoxia causes a release of a vascular endothelial growth factor, stimulating neovascularization either from the disc or the capillaries of the retina or iris. Neovascularization of the disc or elsewhere on the retina poses risk for vitreal hemorrhage and subsequent tractional retinal detachment. Iris neovascularization may cause neovascular glaucoma with secondary angle closure. Intraretinal microvascular abnormalities may be a precursor to retinal neovascularization.