Diabetic retinopathy is among the important problems that develop in patients with diabetes mellitus. The prevalence today amoung diabetics is substantially lower than in earlier periods, due to better treatment of diabetes and related disorders. Diabetic retinopathy is thus among the excellent reasons for diabetics to assiduously control their hyperglycermia and reduce their risk factors.
There are two types of diabetic retinopathy, non-proliferative and proliferative. "Proliferative" in this context means that small blood vessels are growing abnormally. Usually, the non-proliferative type develops first and then may ultimately lead to the more serious proliferative form. But sometimes the proliferative develops first.
Damage to blood vessels and neurons accounts for much of the pathogy of diabetes mellitus, including diabetic retinopathy. In the non-proliferative form, damage to small blood vessels underlying the retina cause them to become leaky, so that fluid and lipoproteins leaves the blood vessels, leading to macular edema and lipid deposits.
Depending on the degree, macular edema can reduce contrast sensitivity, visual field and, if it involves the central macula, visual accuity.
Direct damage to neurons, including the rods and cones, can be occuring too.
As described above, the more serious proliferative form involves angiogenesis. The angiogenesis begins at the optic disc, with tufts of highly permeable capillaries developing. See the figure referenced in Patient F to see examples of the abnormal vessels. All this causes serious damage to the retina and substantial loss of visual accuity if the fovea is damaged.
The edema and damage to the retina can also lead to retinal detactment.
The single most important treatment is to control the hyperglycemia of diabetes mellitus and reduce the related risk factors.
Then if the retinopathy becomes sufficently severe, the abnormal blood vessels were treated with laser photocoagulation, as discussed with Patient F.
In the past, this was where the treatment ended. More recently, the role of VEGF has been recognized and anti-VEGF antibody is sometimes injected into the eye. Glucocorticoid (corticosteroid) drugs may also be injected to reduced inflammation.
Vitrectomy may also be necessary if the vitreous body becomes cloudy due to small hemorrhages from the abnormal blood vessels. The eye is filled with fluid to replace to vitreous body. This might also reduce the likelihood of retinal detachment if the vitreous body is pulling on the retina.