Macular edema can occur in NPDR, but it is more common in more severe cases of DR due to the leakiness of the new blood vessels ( Wani 2003).ĭiabetics can also have problems located more anteriorly in the eye. While the effects of neovascularization in PDR can be devastating, the most common cause of vision loss in diabetics is macular edema. If the retina is not re-attached soon, especially if the macula is involved, vision may be permanently compromised. This is another mechanism by which DR can cause sudden vision loss. If enough force is created, a tractional retinal detachment may occur. These vessels may also scar down, forming strong anchors between the retina and vitreous causing traction on the retina. As the vitreous shrinks with age, it pulls on these fragile vessels and can cause them to tear, resulting in a vitreous hemorrhage and sudden vision loss. They may even grow off the retina and into the vitreous. This may sound like a good idea, but the new vessels are leaky, fragile, and often misdirected. In PDR, the fibrovascular proliferation extends beyond the ILM. This is referred to as neovascularization. Angiogenic factors, like VEGF, stimulate growth of new retinal blood vessels to bypass the damaged vessels. PDR – As mentioned earlier, the retina has a high metabolic requirement, so with continued ischemia, retinal cells respond by releasing angiogenic signals such as vascular endothelial growth factor (VEGF). Within one year, 52-75% of patients falling into this category will progress to PDR ( Aiello 2003). It is diagnosed using the "4-2-1 rule." A diagnosis is made if the patient has any of the following: diffuse intraretinal hemorrhages and microaneurysms in 4 quadrants, venous beading in ≥2 quadrants, or IRMA in ≥1 quadrant. Severe NPDR – In the most severe stage of NPDR, you will find cotton wool spots, venous beading, and severe intraretinal microvascular abnormalities (IRMA). Moderate NPDR – Characterized by multiple microaneurysms, dot-and-blot hemorrhages, venous beading, and/or cotton wool spots. NPDR is further subdivided based on retinal findings:Įarly NPDR – At least one microaneurysm present on retinal exam. This obstruction may cause infarction of the nerve fiber layer, resulting in fluffy, white patches called cotton wool spots (CWS). As NPDR progresses, the affected vessels eventually become obstructed. This sediment is composed of lipid byproducts and appears as waxy, yellow deposits called hard exudates. Resolution of fluid lakes can leave behind sediment, similar to a receding river after a flood. Fluid deposition under the macula, or macular edema, interferes with the macula's normal function and is a common cause of vision loss in those with DR. The weakened vessels also become leaky, causing fluid to seep into the retina. Because of their dot-like appearance, they are called "dot-and-blot" hemorrhages. Microaneurysms eventually rupture to form hemorrhages deep within the retina, confined by the internal limiting membrane (ILM). This weakens the capillary walls and results in small outpouchings of the vessel lumens, known as microaneurysms. NPDR – Hyperglycemia results in damage to retinal capillaries. As the disease progresses, it may evolve into proliferative diabetic retinopathy (PDR), which is defined by the presence of neovascularization and has a greater potential for serious visual consequences. The word "proliferative" refers to whether or not there is neovascularization (abnormal blood vessel growth) in the retinaEarly disease without neovascularization is called nonproliferative diabetic retinopathy (NPDR). Jesse Vislisel and Thomas Oetting, MS, MDĭiabetic retinopathy falls into two main classes: nonproliferative and proliferative. Diabetic Retinopathy: From One Medical Student to Another
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