Proliferative Diabetic Retinopathy (PDR)

Proliferative diabetic retinopathy is an advanced eye problem caused by long-standing diabetes. High blood sugar damages tiny retinal blood vessels. Parts of the retina become starved of oxygen and release distress signals (especially VEGF). Those signals make new, fragile blood vessels grow on the retina and optic nerve. These vessels break easily, bleed into the eye (vitreous hemorrhage), and pull on the retina, sometimes causing a tractional retinal detachment. Without timely treatment, PDR can lead to permanent vision loss. The main goals are to stop abnormal vessel growth, prevent bleeding and scarring, protect central vision, and keep you safely followed up. Stanford Medicine

Proliferative diabetic retinopathy means the retina has started to grow new blood vessels. The retina is the light-sensing film at the back of your eye. In diabetes, long-term high blood sugar damages small retinal vessels. Damaged vessels cannot bring enough oxygen. The retina becomes “hungry” for oxygen. In response, your eye releases growth signals (mainly a protein called VEGF). These signals tell the eye to grow new vessels on the retinal surface and sometimes on the colored part at the front (the iris).

These new vessels are not normal. They are thin, weak, and leaky. They bleed into the clear gel inside the eye (the vitreous). Blood in the gel blocks light and causes sudden floaters or dark curtains. Over time, the new vessels grow with scar tissue. Scar tissue shrinks like a tight band and pulls the retina away from the back wall (tractional retinal detachment). New vessels can also grow in the eye’s drainage angle and raise eye pressure, causing neovascular glaucoma, which is painful and dangerous.

PDR is serious but treatable. Timely laser, eye injections, or surgery can save sight. The most important daily action is good diabetes control and regular eye exams.

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How PDR develops

1. Sugar damage: Years of high blood sugar injure the lining of tiny retinal vessels.

2. Blockage and leaks: Vessels close off and others leak fluid and fats. Areas of retina get poor blood flow.

3. Oxygen shortage: Starving retina sends out distress signals (VEGF and others).

4. Abnormal new vessels: Fragile new vessels sprout on the retina and optic disc.

5. Bleeding and scars: New vessels bleed into the gel. Healing makes fibrous scar tissue.

6. Pulling and detachment: Scars pull the retina off (traction). Tears can form. Fluid slips under the retina.

7. Pressure rise: New vessels can clog the drainage angle, raising pressure (neovascular glaucoma).

8. Vision loss: Bleeding, detachment, and high pressure reduce or destroy sight.

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Types of PDR

1. Early or “non–high-risk” PDR
   New vessels are present but small and without major bleeding. Vision can still be fine. Close follow-up is needed.

2. High-risk PDR
   New vessels are large or there has been a vitreous or pre-retinal bleed. This form has a much higher risk of sudden severe vision loss, so treatment is urgent.

3. PDR with vitreous or pre-retinal hemorrhage
   Blood leaks in front of the retina or into the vitreous gel. You may see floaters, haze, or a dark curtain. Doctors often see a fresh red layer over the retina or free blood in the gel.

4. PDR with tractional retinal detachment
   Scar tissue pulls the retina off its normal position. Vision becomes distorted or missing in parts. If the macula (the sharp-vision center) lifts off, central vision drops quickly.

5. Combined tractional–rhegmatogenous detachment
   The pulling force causes a retinal tear. Fluid then goes under the retina through the tear. This mix is more complex and often needs surgery sooner.

6. PDR with diabetic macular edema (DME)
   Swelling in the central retina can exist with PDR. Swelling causes blurred central vision even when there is no bleeding.

7. PDR with neovascular glaucoma
   New vessels grow on the iris and into the drainage angle. This blocks the outflow of eye fluid and raises eye pressure. Pain, redness, and severe vision loss can follow.

8. Inactive or regressed PDR
   After good treatment (laser or injections) and better systemic control, new vessels shrink and scars become quiet. Ongoing monitoring is still needed.

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Causes

These are things that cause PDR to appear or push it to get worse. Many are controllable.

1. Long duration of diabetes
   The longer you live with diabetes, the more time sugar has to damage retinal vessels.

2. Poor blood sugar control (high HbA1c)
   Higher average sugar leads to more vessel damage. Keeping HbA1c near your target lowers risk.

3. Large swings in blood sugar
   Rapid ups and downs also stress vessels and can speed retinopathy.

4. High blood pressure
   Pressure damages tiny vessels and reduces healthy blood flow in the retina.

5. High cholesterol and high triglycerides
   Fatty particles leak into the retina and worsen swelling and damage.

6. Kidney disease (diabetic nephropathy)
   Kidney damage and eye damage often move together. Kidney issues raise the risk of PDR.

7. Pregnancy in a person with diabetes
   Eye disease can progress faster during pregnancy, especially if diabetes was not well controlled before.

8. Puberty and rapid growth in teens with diabetes
   Hormone changes can make retinopathy appear or progress more quickly.

9. Obesity and metabolic syndrome
   These conditions cluster with high sugar, pressure, and lipids, which harm vessels.

10. Smoking
    Smoking reduces oxygen and harms blood vessel health, worsening ischemia.

11. Obstructive sleep apnea
    Night-time oxygen dips trigger more VEGF and oxidative stress, raising PDR risk.

12. Anemia
    Low red blood cells mean less oxygen to the retina, which drives new vessel growth.

13. Systemic inflammation
    Ongoing body inflammation injures vessel linings and promotes scarring.

14. Cardiovascular disease
    Vascular disease elsewhere often reflects vessel injury in the eye.

15. Delayed or skipped eye exams
    Missing routine dilated exams allows silent disease to advance into PDR.

16. Rapid initial drop in HbA1c from very high levels
    When very poor control improves very quickly, retinopathy can temporarily worsen before it stabilizes.

17. Cataract surgery in eyes with severe untreated retinopathy
    Surgery itself does not “cause” PDR, but inflammation after surgery may unmask or accelerate active disease if PDR was not controlled first.

18. Genetic susceptibility
    Some people develop PDR earlier or more severely even with similar sugar control.

19. Male sex and certain ethnic backgrounds
    Some groups show higher risk in studies; this is not destiny but a reminder to screen closely.

20. Poor control of other diabetes complications
    Neuropathy, fatty liver disease, and hypertension together signal high overall vascular risk, which includes the retina.

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Symptoms of PDR

Many people have no symptoms until late. That is why regular eye exams are so important.

1. No symptoms at first — vision can look normal while dangerous new vessels are forming.

2. Floaters — spots, cobwebs, or strings that move with your eye.

3. Sudden blurry vision — often from a fresh bleed into the vitreous gel.

4. Dark curtain or shadow — bleeding or detachment can block part of your view.

5. Flashing lights — pulling on the retina can trigger brief flashes.

6. Distorted vision (straight lines look bent) — traction or macular swelling.

7. Patchy or missing areas in the field of view — from bleeding or detachment.

8. Poor night vision — low-light sight drops with advanced damage.

9. Colors look faded or washed out — macular involvement can dull colors.

10. Trouble focusing or reading — central blur from macular edema or blood haze.

11. Frequent changes in clarity — vision may clear and blur as small bleeds settle.

12. Glare and halos — light scatters through blood or scar tissue.

13. Eye pain or headache — possible with high eye pressure in neovascular glaucoma.

14. Red eye — may occur with bleeding or high pressure.

15. Sudden severe vision loss — large hemorrhage or macula-off detachment is an emergency.

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Diagnostic Tests

A) Physical Exam (whole-person and eye-focused)

1. Medical history and symptom review
   The clinician asks about diabetes duration, HbA1c, blood pressure, kidney health, pregnancy, sleep apnea, smoking, and symptoms like floaters or vision loss. This finds risk and urgency.

2. Blood pressure measurement
   High pressure worsens retinopathy. Measuring it helps guide whole-body care to protect the eyes.

3. General exam for diabetes complications
   Signs of kidney disease, nerve disease, or cardiovascular disease raise concern for faster eye progression.

4. External eye inspection
   The doctor looks for red eye, iris new vessels, or pain suggesting high pressure or inflammation.

B) Manual / Clinical Eye Tests

5. Visual acuity (eye chart) with and without pinhole
   This measures how sharp your vision is and whether blur is from the eye’s optics or from retinal disease.

6. Refraction
   Checking the lens prescription helps separate simple focus problems from retinal causes of blur.

7. Pupil exam and relative afferent pupillary defect (RAPD) check
   Pupil reactions help detect significant retinal or optic nerve dysfunction.

8. Confrontation visual fields
   The clinician screens for missing areas in side vision that suggest hemorrhage or detachment.

9. Intraocular pressure (tonometry)
   High pressure can point to neovascular glaucoma. Normal pressure does not rule out PDR.

10. Slit-lamp biomicroscopy with dilated pupil
    After dilation, the doctor inspects the lens, vitreous gel (looking for blood), and front structures for iris new vessels.

C) Lab and Pathology-Related Tests

11. HbA1c
    Shows average blood sugar over ~3 months. Lowering toward your target reduces risk of progression.

12. Fasting plasma glucose or time-in-range from CGM
    Helps understand daily control and sugar swings that affect eye health.

13. Lipid profile (cholesterol and triglycerides)
    Abnormal lipids worsen retinal leakage and swelling.

14. Kidney function tests (creatinine, eGFR) and urine albumin-to-creatinine ratio
    Kidney damage often travels with eye damage. Poor kidney function signals higher eye-risk.

15. Complete blood count (CBC)
    Finds anemia, which reduces oxygen delivery to the retina and can worsen PDR.

D) Electrodiagnostic Tests

16. Electroretinography (ERG)
    Measures the retina’s electrical response to light. In advanced disease, ERG can show reduced function, helping with prognosis.

17. Visual evoked potentials (VEP)
    Measures the brain’s response to visual signals. It helps when vision is poor but the cause is unclear, separating retinal from optic nerve problems.

E) Imaging Tests

18. Dilated fundus examination (indirect ophthalmoscopy) with scleral depression when needed
    This is the core eye exam. The doctor directly views the retina, looks for new vessels on the disc (NVD) or elsewhere (NVE), pre-retinal or vitreous hemorrhage, scar bands, and any detachment.

19. Color fundus photography (including ultra-widefield photos)
    Photos document disease. Widefield images capture far-peripheral new vessels and ischemia.

20. Optical coherence tomography (OCT)
    OCT is a non-contact scan that shows cross-sections of the retina. It detects macular edema, traction on the macula, and layers lifted by detachment.

21. OCT Angiography (OCTA)
    OCTA maps blood flow in retinal layers without dye. It shows areas lacking capillaries and can highlight abnormal new vessels.

22. Fluorescein angiography (FA) — standard or ultra-widefield
    A small dye is injected into a vein. A special camera tracks dye flow in the retina. Leaks, blocked areas, and new vessels light up. Ultra-widefield FA shows far-peripheral disease that guides laser.

23. B-scan ocular ultrasound
    When the view is blocked by dense blood, ultrasound checks for retinal detachment or large scar bands and guides the need for surgery.

24. Gonioscopy
    A tiny mirrored lens lets the doctor view the drainage angle. New vessels here suggest neovascular glaucoma and call for urgent treatment.

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Non-pharmacological treatments (therapies & “other” care)

Each item explains what it is, why it’s done (purpose), and how it helps (mechanism)—in very simple English.

1. Tight glucose control (personalized A1C target).
   Purpose: Lower the risk that retinopathy worsens.
   Mechanism: Steadier, lower blood sugar reduces toxic stress on retinal vessels. (In landmark trials, intensive control greatly lowered retinopathy progression, a “metabolic memory” benefit that persisted for years.) The New England Journal of MedicinePMC

2. Blood-pressure control (if you have hypertension).
   Purpose: Reduce new damage to retinal vessels and lower risk of DR starting or getting worse.
   Mechanism: Lower pressure means less strain on fragile capillaries; benefits are clearest if you already have high BP. PMC

3. Cholesterol & triglyceride control.
   Purpose: Fewer fatty deposits (“hard exudates”) and potentially fewer laser/surgery needs.
   Mechanism: Better lipid levels reduce leakage from damaged vessels and may support retinal health. (Systemic lipid management is part of standard DR care.) Diabetes Journals

4. Smoking cessation.
   Purpose: Improve blood vessel health everywhere, including the retina.
   Mechanism: Quitting reduces oxidative stress and improves blood flow, supporting healing. Diabetes Journals

5. Regular dilated eye exams with a retina specialist.
   Purpose: Catch new bleeding or traction early—before vision drops.
   Mechanism: Careful follow-up allows timely laser, injections, or surgery when needed. (Visit frequency is individualized; PDR needs close follow-up.) Stanford Medicine

6. Medical nutrition therapy (dietary coaching).
   Purpose: Help you meet glucose, BP, and weight goals you can actually live with.
   Mechanism: A fiber-rich, lower-glycemic eating plan smooths spikes in blood sugar and reduces vascular stress. Diabetes Journals

7. Physical activity plan (safe & regular).
   Purpose: Improve insulin sensitivity, weight, BP, lipids, and overall eye health.
   Mechanism: Exercise helps glucose control and cardiovascular health, which supports the retina. Ask your eye doctor about limits if you’ve recently bled. Diabetes Journals

8. Weight management.
   Purpose: Make glucose and BP easier to control.
   Mechanism: Losing even a modest amount of weight improves insulin action and inflammation. Diabetes Journals

9. Sleep apnea detection and treatment (CPAP when indicated).
   Purpose: Reduce nighttime oxygen drops that may aggravate retinal ischemia.
   Mechanism: CPAP improves oxygenation and cardiovascular health, indirectly supporting the eye. Diabetes Journals

10. Kidney-disease co-management.
    Purpose: Kidney and retinal vessels are cousins—protecting one helps the other.
    Mechanism: Treating albuminuria, adjusting BP meds (e.g., ACEi/ARB) and dialysis timing helps fluid balance and vascular stability. Diabetes Journals

11. Anemia correction when present.
    Purpose: Better oxygen delivery to the retina.
    Mechanism: Treating iron deficiency or other causes improves tissue oxygenation and may reduce ischemic drive. Stanford Medicine

12. Vision safety education (warning signs).
    Purpose: Get urgent care if trouble starts.
    Mechanism: Knowing that “a shower of floaters,” “a dark curtain,” or sudden blur needs same-day care can save sight. Stanford Medicine

13. Low-vision rehabilitation (if vision remains reduced).
    Purpose: Maximize remaining vision for daily life.
    Mechanism: Training, magnifiers, lighting, and contrast aids help you work, read, and move safely. Stanford Medicine

14. Home vision awareness (simple checks).
    Purpose: Notice changes between appointments.
    Mechanism: Brief, regular checks of each eye’s vision and distortion can flag new problems quickly. Diabetes Journals

15. Medication adherence support (pill boxes, reminders, CGM).
    Purpose: Stay on track with glucose/BP medicines, which protects the retina.
    Mechanism: Fewer missed doses = steadier control. Diabetes Journals

16. Tele-retina screening when appropriate.
    Purpose: Easier access to screening where specialists are scarce (not a full substitute for in-person dilated exams when PDR is present).
    Mechanism: Remote retinal photos help triage and accelerate needed care. Diabetes Journals

17. Stress management & adequate sleep.
    Purpose: Support steadier glucose and BP.
    Mechanism: Lower stress hormones and better sleep reduce swings that strain vessels. Diabetes Journals

18. Avoid heavy straining right after a hemorrhage or procedure (ask your surgeon).
    Purpose: Lower the chance of re-bleeding.
    Mechanism: Avoiding Valsalva-type strain reduces sudden eye pressure spikes that can disturb fragile vessels. Stanford Medicine

19. Pregnancy planning if you have diabetes.
    Purpose: Pregnancy can accelerate DR; planning protects you.
    Mechanism: Pre-pregnancy eye check and tighter glucose targets, with more frequent exams during pregnancy, lower risk. Diabetes Journals

20. Prompt treatment of any eye bleeding.
    Purpose: Prevent scarring and retinal detachment.
    Mechanism: Early laser/injection/surgery interrupts the cascade of bleeding → scarring → traction. Stanford Medicine

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Drug treatments

Doses here are for clinician reference, not for self-use. All injections are done in-office by eye surgeons.

1. Ranibizumab (anti-VEGF).
   Class: VEGF-A inhibitor. Dose/Timing: For DR on the U.S. label: 0.3 mg intravitreal, often monthly initially; in the major PDR trial (Protocol S) specialists used 0.5 mg with a structured retreatment plan. Purpose: Stop new vessels and reduce bleeding risk; also helps if macular edema co-exists. Mechanism: Blocks VEGF, the growth signal for abnormal vessels. Side effects: Eye pain, pressure rise, inflammation; very rare infection; systemic risks are low but discussed individually. FDA Access DataPMC

2. Aflibercept (anti-VEGF “trap”).
   Class: VEGF-A/VEGF-B/PlGF blocker. Dose/Timing: 2 mg intravitreal, typically every 4 weeks at first, then extended per response. Purpose: Suppress neovascularization; strong effect on DR severity and macular edema. Mechanism: Binds VEGF family ligands to stop abnormal vessel growth/leak. Side effects: Similar to other anti-VEGF injections. PMC

3. Bevacizumab (anti-VEGF; off-label in the eye).
   Class: VEGF-A antibody. Dose/Timing: Commonly 1.25 mg intravitreal at intervals directed by the specialist. Purpose/Mechanism: As above. Side effects: Similar class effects; it is widely used off-label due to cost and availability. vivahealth.com

4. Faricimab (dual-pathway anti-VEGF/anti-Ang-2).
   Class: VEGF-A and Angiopoietin-2 inhibitor. Dose/Timing: 6 mg intravitreal; monthly loading then extend in DME; improves DR severity scores. Purpose: Reduce neovascular activity and edema with potential for longer durability. Mechanism: Dual pathway “stabilizes” leaky, inflamed vessels. Side effects: As with other intravitreal biologics. FDA Access DataPMC

5. Dexamethasone intravitreal implant (0.7 mg).
   Class: Corticosteroid (biodegradable implant). Dose/Timing: Single in-office implant; effect often lasts ~3–4 months; can be repeated. Purpose: Helpful when diabetic macular edema co-exists or anti-VEGF is not enough. Mechanism: Strong anti-inflammatory/anti-leak effect. Side effects: Eye-pressure rise, cataract progression; infection risk is rare but serious. Molina Healthcare

6. Triamcinolone acetonide (intravitreal).
   Class: Corticosteroid. Dose/Timing: Commonly 4 mg/0.1 mL intravitreal as a clinician-directed adjunct, especially for DME. Purpose/Mechanism/Side effects: Similar to dexamethasone; shorter acting; pressure/cataract risks. Diabetes Journals

7. Fluocinolone acetonide implant (0.19 mg).
   Class: Corticosteroid (nonbiodegradable, very long acting). Dose/Timing: One implant can release drug for up to 3 years in chronic DME. Purpose: Reduce chronic edema that worsens vision in DR. Mechanism/Side effects: Long-term steroid effect; monitor for ocular hypertension and cataract. ILUVIEN

8. Fenofibrate (oral).
   Class: PPAR-α agonist for dyslipidemia. Dose/Timing: Common doses 145–200 mg once daily (per trials/regulatory use). Purpose: In large trials, fenofibrate reduced DR progression and need for laser/surgery in type 2 diabetes with existing DR—used as a systemic adjunct (not a substitute for eye treatment). Mechanism: Improves lipid metabolism and may have direct retinal anti-inflammatory/anti-angiogenic actions. Side effects: Monitor kidney function and for drug interactions. Imperial EndocrinologyPMC

9. Blood-pressure medications (e.g., ACE inhibitors/ARBs) when indicated.
   Class: Antihypertensives. Dose/Timing: Individualized to BP targets. Purpose: Lower incidence/progression risk of DR in those with hypertension. Mechanism: Reduce vascular strain; protect kidney/retina microcirculation. Side effects: Vary by drug; your primary doctor individualizes therapy. PMC

10. Glucose-lowering therapy (insulin and/or non-insulin agents).
    Class: Antihyperglycemics. Dose/Timing: Personalized to reach safe A1C goals. Purpose: Strongest systemic lever to slow DR worsening over time. Mechanism: Lower glucose reduces toxic effects on retinal capillaries (“metabolic memory”). Side effects: Vary by agent; hypoglycemia is prevented with careful planning. The New England Journal of Medicine

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Dietary “molecular” supplements

Evidence for supplements in treating PDR is limited. Use them only as complements to proven medical/surgical care and with your doctor’s approval (interactions and kidney/liver issues matter).

1. Omega-3 (EPA/DHA): often 1–2 g/day combined. Function: anti-inflammatory; supports vascular health. Mechanism: pro-resolving lipid mediators may calm retinal inflammation.

2. Lutein + Zeaxanthin: e.g., 10 mg + 2 mg/day. Function: macular antioxidants. Mechanism: filter blue light/oxidative stress; not a substitute for injections/laser.

3. Alpha-lipoic acid: 300–600 mg/day. Function: antioxidant; may help oxidative pathways in diabetes.

4. Resveratrol: 100–500 mg/day (formulation dependent). Function: antioxidant; possible anti-angiogenic signaling in lab models.

5. Curcumin (enhanced bioavailability forms): label dosing varies. Function: anti-inflammatory; theoretical vascular benefits.

6. Quercetin: 250–500 mg/day. Function: antioxidant flavonoid; mechanistic anti-VEGF signals in preclinical work.

7. Benfotiamine (vitamin B1 derivative): 150–300 mg/day. Function: reduces advanced glycation pathway activity.

8. Vitamin D (repletion to sufficiency): dose per lab result. Function: general vascular/immune support.

9. Coenzyme Q10: 100–200 mg/day. Function: mitochondrial antioxidant.

10. N-acetyl-cysteine: 600–1200 mg/day. Function: replenishes glutathione; antioxidant.

Bottom line: these can support whole-body health but do not reverse PDR. Your clinician will prioritize glucose/BP/lipids, laser/surgery, and eye injections—the things proven to protect sight. Diabetes Journals

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Regenerative & stem-cell drugs

There are no approved stem-cell drugs or “immunity boosters” for PDR. In fact, unapproved stem-cell eye injections have caused severe, permanent blindness in patients treated outside controlled trials. If you ever see these marketed for PDR, avoid them. Only consider research options within regulated clinical trials. FDA Access Data

What’s being researched (no approved dosing):

1. Gene therapy to deliver anti-VEGF long-term (e.g., ABBV-RGX-314). Early trials are exploring whether a one-time procedure could suppress neovascular signals for years. ClinicalTrials.govregenxbio.gcs-web.com

2. Intravitreal AAV vectors encoding aflibercept (e.g., ADVM-022): durability is promising in lab/early studies, but safety signals (including hypotony) have paused/altered some DME programs. CGTlive™

3. Other sustained-delivery anti-VEGF platforms.

4. Cell-based vascular support therapies (research stage only).

5. Anti-inflammatory/anti-fibrotic biologics under study.

6. Ang-Tie pathway modulators (beyond faricimab) in development.

Discuss any trial with your retina specialist to weigh potential benefits/risks and ensure the site is legitimate and regulated. PMC

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Surgeries/procedures

1. Panretinal photocoagulation (PRP, “scatter laser”).
   Procedure: The doctor places many tiny laser spots in the peripheral retina in one or more sessions.
   Why: PRP reduces the retina’s oxygen demand and shuts down the growth drive for new vessels, lowering bleeding and detachment risks. PRP is a long-proven, durable treatment for PDR, though it can reduce night/peripheral vision. Stanford Medicine

2. Pars plana vitrectomy (PPV).
   Procedure: The surgeon removes the vitreous gel (and blood), peels scar tissue, applies endolaser, and may place gas/silicone oil to stabilize the retina.
   Why: Done for non-clearing vitreous hemorrhage, tractional retinal detachment, or dense membranes threatening the macula—situations common in advanced PDR. Stanford Medicine

3. Endolaser PRP during vitrectomy.
   Procedure: Laser is applied from inside the eye at surgery.
   Why: Finishes or reinforces PRP when the view was blocked by blood before surgery. Stanford Medicine

4. Focal/grid macular laser (select cases with macular edema).
   Procedure: Precisely targets leaking microaneurysms or diffuse edema zones.
   Why: Today it’s used more selectively (often as an adjunct to injections), but it can help stabilize macular swelling in some eyes. Stanford Medicine

5. Pre-/intra-operative anti-VEGF around surgery (adjunct).
   Procedure: Injection shortly before vitrectomy.
   Why: Prunes fragile new vessels and can make surgery cleaner with less bleeding; timing is individualized by the surgeon. Stanford Medicine

Laser vs anti-VEGF for PDR—what studies show: At 2 years and 5 years, ranibizumab (anti-VEGF) produced visual acuity outcomes similar to PRP, with less peripheral visual-field loss and fewer macular edema problems in the ranibizumab group—but it requires frequent, reliable follow-up and injections. Your doctor will help choose based on your eye, life, and ability to keep appointments. PMC+1

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Prevention habits

1. Keep glucose near your individualized target (the #1 lever for the retina). The New England Journal of Medicine

2. Treat hypertension if present; check BP at home. PMC

3. Manage cholesterol/triglycerides with lifestyle and medications when needed. Diabetes Journals

4. Don’t smoke. Diabetes Journals

5. Keep your scheduled retina visits—even if your vision “seems fine.” Stanford Medicine

6. Exercise most days (as cleared by your clinicians). Diabetes Journals

7. Follow a fiber-rich, lower-glycemic diet pattern. Diabetes Journals

8. Address sleep apnea and snoring. Diabetes Journals

9. Manage kidney and heart health—these systems are connected. Diabetes Journals

10. In pregnancy (or planning), arrange extra eye checks. Diabetes Journals

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When to see a doctor urgently

• New floaters or a “cobweb,” sudden blur, flashes, or a dark curtain in your vision (possible bleeding or detachment).

• After an injection/laser/surgery if you have severe pain, sudden vision drop, pus-like discharge, or worsening redness.

• If you miss injections or visits: call to reschedule—anti-VEGF works best with regular care. (PDR managed with injections alone needs good adherence.) Stanford MedicineJAMA Network

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What to eat & what to avoid

1. Eat: non-starchy vegetables at most meals (fiber helps steady glucose). Diabetes Journals

2. Eat: lean proteins (fish, poultry, legumes) to reduce glycemic spikes. Diabetes Journals

3. Eat: whole grains over refined grains (slower glucose rise). Diabetes Journals

4. Eat: nuts/seeds in small portions (healthy fats; satiety). Diabetes Journals

5. Eat: fish rich in omega-3s (e.g., salmon) 1–2×/week, if not contraindicated. Diabetes Journals

6. Avoid/limit: sugar-sweetened drinks and fruit juices (fast spikes). Diabetes Journals

7. Avoid/limit: ultra-processed snacks and desserts (high glycemic load). Diabetes Journals

8. Avoid/limit: trans fats and excessive saturated fat (vascular strain). Diabetes Journals

9. Avoid/limit: heavy alcohol intake (glucose swings and BP effects). Diabetes Journals

10. Avoid/limit: high-sodium packaged foods if you have hypertension. Diabetes Journals

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Frequently asked questions

1) Can PDR go away on its own?
No. It usually progresses without treatment. Laser and injections can control it and protect vision. Stanford Medicine

2) Which is “better,” laser or injections?
They’re both effective. Anti-VEGF injections and PRP had similar vision results at 5 years; injections preserve more peripheral field but need regular visits; PRP is durable with fewer visits. Your life and eye decide. PMC

3) Will I lose my night or side vision with PRP?
Some reduction in night/peripheral vision is common after scatter laser. Doctors balance this risk against the benefit of preventing bleeding and detachment. Stanford Medicine

4) Are eye injections safe?
Serious infection is very rare. Most people do well, but you’ll be monitored for inflammation, pressure changes, and rare complications. FDA Access Data

5) If I miss injections, can my eye get worse?
Yes. Anti-VEGF works only if kept up; lapses can allow vessels to regrow and bleed. If you must miss, call to rebook quickly. JAMA Network

6) Do I need surgery if I have a big bleed?
Maybe. Some bleeds clear on their own, but non-clearing hemorrhage or a tractional detachment often needs vitrectomy. Stanford Medicine

7) Does aspirin make eye bleeding worse?
In the large ETDRS trial, aspirin did not worsen bleeding or DR progression. If you need aspirin for the heart, it’s not an eye contraindication. Always follow your cardiologist’s advice. PubMed

8) Can diet or vitamins cure PDR?
No. Diet and supplements support overall health, but they don’t replace laser/injections/surgery for PDR. Diabetes Journals

9) Is PDR in both eyes?
Often yes, though severity may differ. Each eye gets its own plan. Stanford Medicine

10) Can I work or exercise with PDR?
Usually yes—with guidance. Avoid heavy straining right after a bleed or procedure; ask your surgeon about limits and return-to-activity steps. Stanford Medicine

11) Is pregnancy risky for my eyes?
DR can worsen faster in pregnancy. Pre-pregnancy counseling and extra eye exams during pregnancy help protect vision. Diabetes Journals

12) What if I’m far from a retina clinic?
Tele-retina photos can help triage, but in-person retina care is needed for PDR treatment. Plan transport/support for follow-ups. Diabetes Journals

13) How many PRP sessions will I need?
Often 1–3, sometimes more. Doctors tailor to the eye’s response. Stanford Medicine

14) How long do anti-VEGF injections continue?
Months to years. Intervals may lengthen if the eye stays quiet; you and your doctor decide together. FDA Access Data

15) Are “stem-cell shots” helpful?
No approved stem-cell eye injections for PDR exist. Unapproved treatments have blinded patients. Stick with proven care or regulated trials. FDA Access Data

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 19, 2025.