Diabetic retinopathy

Microangiopathy of the retina caused by chronic hyperglycemia, leading to capillary leak and occlusion with microaneurysms, hemorrhages, exudates, and in advanced stages neovascularization that threatens vision.

• Very common complication of diabetes and the leading cause of blindness in working-age adults. Largely preventable with early detection (screening) and treatment, so exams often test screening guidelines and management to prevent vision loss.

• Often asymptomatic in early phases; vision may remain normal until macular edema or vitreous hemorrhage develops. Symptoms can include blurred vision (especially if macula is involved), floaters, or scotomas in later stages.
• Fundoscopic hallmarks in nonproliferative DR: multiple microaneurysms (tiny red dots), dot-and-blot hemorrhages in the retina, hard exudates (yellow lipid deposits from leaky vessels), and cotton-wool spots (white "soft" exudates from nerve fiber infarcts). Venous beading and IRMA (intraretinal microvascular abnormalities) appear as NPDR becomes severe.
• Proliferative DR is marked by neovascularization – fragile new blood vessels on the optic disc or retina. These can bleed into the vitreous (causing sudden floaters or vision loss) and form scar tissue, leading to traction retinal detachments if untreated.
• Diabetic macular edema (DME) can occur at any stage (NPDR or PDR) when leaky capillaries cause macular swelling. DME is a major cause of vision blurring in diabetes (often indicated by hard exudates at the macula) even without proliferative changes.

1. Detect early: perform regular dilated fundus exams (direct ophthalmoscopy or retinal photography) in all diabetics. Use OCT (optical coherence tomography) to confirm macular edema and fluorescein angiography to map retinal nonperfusion or leaks when planning laser treatment.
2. Classify severity of NPDR (mild, moderate, severe) vs PDR. NPDR severity is assessed by the extent of hemorrhages, venous beading, and IRMA (use the "4-2-1 rule" for severe NPDR: ≥4 quadrants of hemorrhages, ≥2 quadrants of venous beading, ≥1 quadrant of IRMA). Any neovascularization = proliferative DR.
3. Aggressively control risk factors to slow progression: maintain tight glycemic control (goal HbA1c ~7% if possible) and blood pressure control. Good control significantly lowers the risk of onset and progression of retinopathy (as shown by DCCT/UKPDS studies).
4. Plan timely intervention for advanced disease: refer to an ophthalmologist if moderate NPDR or any worse findings. Do not wait for vision symptoms. Early ophthalmology referral allows for laser or injection therapy before irreversible vision loss occurs.

1. Optimize systemic factors: strict glucose control and blood pressure control to slow retinopathy progression (also treat dyslipidemia; e.g., adding fenofibrate has shown benefit in slowing DR in some studies).
2. Laser photocoagulation: panretinal photocoagulation (PRP) for proliferative DR to induce regression of neovascular vessels (by ablating ischemic peripheral retina and reducing VEGF drive); focal or grid laser can be used for focal leaking microaneurysms in DME.
3. Anti-VEGF injections: intravitreal anti–vascular endothelial growth factor agents (e.g., ranibizumab, bevacizumab, aflibercept) are first-line for diabetic macular edema (reduce macular swelling and improve vision) and are also effective alternative therapy for proliferative DR (can cause neovascular regression).
4. Vitrectomy surgery: indicated for advanced complications – e.g., a non-clearing vitreous hemorrhage or a tractional retinal detachment from PDR. Vitrectomy can remove hemorrhagic vitreous and relieve traction to restore some vision.

• Mnemonic: 4-2-1 rule for severe NPDR (≥4 quadrants of hemorrhages, ≥2 quadrants venous beading, ≥1 quadrant IRMA).
• Remember: Neovascularization = Proliferative DR. Any new vessels on fundus means the disease has progressed to proliferative stage (requires prompt treatment).

• Any diabetic with sudden vision loss, new-onset floaters, or a curtain falling over vision → urgent evaluation for vitreous hemorrhage or retinal detachment due to proliferative DR (immediate ophthalmology referral).
• Detection of neovascularization of the iris (rubeosis iridis) in a diabetic → indicates severe retinal ischemia and high risk for neovascular glaucoma; requires prompt treatment (PRP laser) to prevent permanent vision loss and painful glaucoma.

1. All patients with diabetes → ensure dilated screening eye exams at recommended intervals (Type 1 DM: start ~5 years after diagnosis (around age 10 or puberty) and then annually; Type 2 DM: start at diagnosis and annually). Pregnant diabetics need an eye exam early in pregnancy due to rapid DR progression risk.
2. If no retinopathy or mild NPDR is found → follow-up eye exam in 1 year (or up to 2 years if no DR and good control per some guidelines). Continue optimal glycemic and BP control.
3. If moderate NPDR (multiple hemorrhages, cotton wool spots) or any DME is present → refer to ophthalmology within a few months for closer monitoring. If severe NPDR or PDR is identified → refer to a retina specialist urgently (within weeks) for possible laser or injection treatment.
4. Ophthalmologist performs detailed evaluation (fundus exam, OCT, angiography) and initiates therapy if needed: e.g., laser photocoagulation for high-risk PDR or anti-VEGF injections for DME. The eye specialist will schedule more frequent follow-ups (every 3–4 months for active disease) to monitor response.
5. Maintain long-term follow-up: even after treatment, diabetic patients require regular eye exams for life. Emphasize patient education on the importance of annual screenings and early treatment to prevent blindness.

• Middle-aged diabetic with years of poor glycemic control, now on fundoscopic exam has numerous microaneurysms, dot-blot hemorrhages, and hard exudates → nonproliferative diabetic retinopathy (background retinopathy).
• Diabetic patient complaining of sudden vision loss with floaters; fundus is hard to visualize due to a large vitreous hemorrhage, and proliferative neovascular vessels are seen on parts of the retina → proliferative diabetic retinopathy (vitreous hemorrhage from neovascularization).