Neovascular glaucoma happens when the retina does not get enough oxygen for a period of time (this is called retinal ischemia). In response, the eye releases a strong growth signal called VEGF (vascular endothelial growth factor). VEGF tells new blood vessels to grow on the iris (the colored part of your eye) and over the drainage angle (the tiny filter at the edge of the cornea and iris that lets fluid leave the eye). These new vessels are abnormal. They are thin, leaky, and come with scar-like tissue (fibrous membranes). As the membrane tightens, it closes the drainage angle. When the angle is closed, the eye fluid (aqueous humor) cannot leave. Pressure in the eye rises sharply. High pressure injures the optic nerve, the cable that carries vision signals to the brain. Without quick care, NVG can cause severe pain and permanent vision loss within days to weeks.
Neovascular glaucoma (NVG) is a dangerous type of glaucoma that happens when new, fragile blood vessels grow in the wrong place inside the eye. These new vessels grow on the colored part of the eye (the iris) and in the tiny drainage angle where the eye’s fluid is supposed to leave. The new vessels are not normal. They come with a thin scar-like tissue. This tissue pulls and covers the drainage angle. When the drainage angle is covered, the fluid in the eye (called aqueous humor) cannot leave easily. The fluid then builds up. The eye pressure rises. The high pressure damages the optic nerve, which is the cable that carries vision to the brain. If the pressure stays high, vision can be lost quickly and permanently.
NVG does not start in the front of the eye. It usually starts in the back of the eye, in the retina, when the retina is not getting enough oxygen and nutrients. We call this retinal ischemia. A starved retina sends out strong chemical signals (most importantly VEGF—vascular endothelial growth factor) asking the body to grow new blood vessels to bring more oxygen. The problem is that these new vessels do not only grow on the retina. They also grow on the iris and in the angle. This is why NVG is often called an “anterior segment complication of retinal ischemia.”
In short, NVG = retinal ischemia → VEGF surge → abnormal new vessels on iris/angle → blockage of drainage → very high eye pressure → optic nerve damage.
How NVG develops
A problem reduces blood flow to the retina. This problem can be diabetes, a blocked retinal vein, a blocked retinal artery, or poor blood flow from narrowed neck arteries, and several other causes.
The retina becomes starved of oxygen (ischemic). A starved retina releases VEGF and other growth signals to “call for help.”
Abnormal new vessels appear. New vessels first show on the iris surface. Doctors call this rubeosis iridis. These vessels are delicate and leaky.
A thin fibrovascular membrane forms in the drainage angle. This sheet slowly creeps over the angle structures like a film.
At first, the angle is still partly open (open-angle phase). The membrane increases outflow resistance and the pressure begins to rise.
Then the membrane contracts and pulls the iris forward. This causes peripheral anterior synechiae (PAS), which are stuck adhesions that close the angle.
The angle becomes sealed (angle-closure phase). Now the fluid has almost nowhere to go, and eye pressure can jump to very high numbers.
High pressure damages the optic nerve. If not treated fast and correctly, vision can be lost in days to weeks in severe cases.
Types of neovascular glaucoma
You may hear doctors describe NVG by stage or by underlying cause. Both views are helpful.
By stage (what is happening in the angle)
Pre-glaucoma stage (rubeosis stage). New vessels are seen on the iris or at the pupil edge, but eye pressure may still be normal. This is a warning stage. If the cause is found and treated early (for example with laser to the retina and anti-VEGF injection), glaucoma may be prevented.
Open-angle neovascular glaucoma. The angle looks open, but a clear fibrovascular sheet is covering the drainage meshwork. Outflow is blocked. Pressure rises. This stage can be painful or sometimes silent.
Angle-closure neovascular glaucoma. The fibrovascular sheet tightens. The iris sticks to the angle (peripheral anterior synechiae). The angle is closed. Pressure often becomes very high. Pain, corneal swelling, and fast vision loss are common.
By underlying cause (why the retina became ischemic)
Ischemic retinal vein occlusions (especially central retinal vein occlusion).
Proliferative diabetic retinopathy and other severe diabetic eye disease.
Ocular ischemic syndrome from severe carotid artery narrowing and poor eye perfusion.
Other causes of severe retinal ischemia (listed in detail under “Causes” below).
This two-way naming helps because early stage disease can sometimes be reversed if the cause is treated quickly.
Causes of NVG
In almost all cases, the common pathway is retinal ischemia leading to VEGF release and abnormal new vessel growth on the iris and angle.
Proliferative diabetic retinopathy (PDR). Long-standing, poorly controlled diabetes causes large areas of retinal oxygen shortage. The retina releases VEGF, which drives abnormal new vessels in the retina and on the iris/angle, leading to NVG.
Central retinal vein occlusion (CRVO)—ischemic type. A main retinal vein gets blocked, blood flow backs up, and the retina becomes severely ischemic. High VEGF levels then trigger rubeosis and NVG.
Branch retinal vein occlusion (BRVO) with large ischemic areas. A branch vein blockage can also cause wide ischemic zones. If the area is big enough, VEGF rises and NVG can develop.
Ocular ischemic syndrome (severe carotid artery disease). Narrowed neck arteries reduce blood to the eye. The whole eye, including the retina, becomes under-perfused, which promotes new, abnormal vessels and NVG.
Central retinal artery occlusion (CRAO). A sudden stop of blood to the retina causes extreme ischemia. The VEGF surge that follows may lead to iris neovascularization and NVG, especially if the retina remains poorly perfused.
Long-standing retinal detachment. A detached retina is not nourished well. Chronic detachment can drive ischemia, VEGF release, and rubeosis, which may progress to NVG.
Chronic uveitis with retinal ischemia. Long inflammation can damage retinal vessels. If enough retina is starved, VEGF increases and abnormal vessels can grow on the iris and angle.
Retinopathy of prematurity (ROP) with ischemic retina. In some children born very early, abnormal vessel growth and peripheral retinal ischemia can lead to anterior segment neovascularization and NVG later if untreated.
Sickle cell retinopathy. Sickled red cells block tiny retinal vessels. The retina becomes ischemic and produces VEGF, which may lead to neovascularization and NVG.
Radiation retinopathy (after eye or head radiotherapy). Radiation can damage retinal vessels. Over time this can cause ischemic retinopathy, high VEGF, and iris/angle neovascularization.
Intraocular tumors (e.g., retinoblastoma in children, uveal melanoma in adults). Tumors may cause local ischemia, inflammation, or VEGF release, leading to rubeosis and NVG.
Carotid-cavernous fistula and other high-venous-pressure states. Abnormally high venous pressure in the eye can impair retinal circulation and oxygen delivery, promoting ischemia and neovascularization.
Penetrating ocular trauma with retinal damage. Severe trauma can injure retinal vessels, cause detachments or scarring, and lead to ischemia and subsequent NVG.
Toxoplasmosis retinochoroiditis with ischemic scars. Some infections damage retinal vessels or create scars that reduce perfusion, causing VEGF release and neovascularization.
Coats disease (in children and young adults). Abnormal, leaky retinal vessels lead to exudation and areas of non-perfusion, which can trigger neovascularization and NVG in advanced cases.
Persistent fetal vasculature / persistent hyperplastic primary vitreous (PFV/PHPV). This developmental problem can leave the eye with disordered vessels and ischemic retina, predisposing to anterior segment neovascularization.
Retinal vasculitis (e.g., Eales disease). Inflammatory closure of retinal veins causes non-perfusion and VEGF-driven neovascularization that can extend to the iris and angle.
Hyperviscosity syndromes (e.g., polycythemia vera, multiple myeloma, Waldenström macroglobulinemia). Very thick blood flows poorly through retinal capillaries, causing ischemia and neovascularization.
Leukemia or other hematologic disorders with retinal ischemia. Abnormal white cells or anemia can impair retinal blood flow and oxygen delivery, promoting new vessel growth and NVG.
Idiopathic retinal capillary non-perfusion (rare). Sometimes, widespread retinal non-perfusion occurs without a clear diagnosis. The ischemia itself can be enough to drive rubeosis and NVG.
Common symptoms and signs
Symptoms vary by stage. Early on, there may be no pain and vision may be only slightly blurred. In later stages, pain and fast vision loss are common.
Blurred vision. The image looks foggy or out of focus, often worse in the affected eye.
Sudden or stepwise drop in vision. Vision can fall quickly if pressure spikes or the cornea swells.
Eye pain. The eye can ache deeply, especially when pressure is very high.
Headache on the same side. Pain can spread to the forehead or temple.
Red eye. The white part looks injected because surface vessels are dilated.
Light sensitivity (photophobia). Bright light becomes uncomfortable.
Halos around lights. Corneal swelling makes lights look like they have colored rings.
Tearing or watery eye. The irritated cornea makes more tears.
Nausea or vomiting. Very high eye pressure can trigger these systemic symptoms.
Seeing floaters or dark spots. If there is bleeding inside the eye, small moving shadows may appear.
Eye feels hard to gentle touch. The globe may feel unusually firm when the eyelid is closed (not a diagnostic test for the public, but people sometimes notice this sensation).
Poor night vision. Low-light vision may worsen with retinal disease and corneal haze.
Loss of side (peripheral) vision. Glaucoma damages the optic nerve in a way that first affects side vision.
Pain that wakes you from sleep. Pressure spikes can be severe at night or early morning.
Pupil looks irregular or sluggish. As new vessels and scar tissue change the iris, the pupil may not move normally (often noticed by clinicians, sometimes by patients in photos).
Diagnostic tests
The goal of testing is to confirm neovascularization, measure eye pressure, check the angle, assess the retina, find the cause of retinal ischemia, and plan treatment.
Below are 20 tests across five groups.
A) Physical exam tests
Visual acuity (distance and near). You read letters on a chart. This shows how clear your vision is now and helps track change after treatment.
External eye examination. The doctor looks at the eyelids, conjunctiva, and cornea for redness, swelling, and corneal haze, which can occur when the pressure is high.
Pupil examination (shape and reaction to light). The doctor checks for small, irregular vessels at the pupil edge and looks for sluggish reaction or a relative afferent pupillary defect, which hints at optic nerve or severe retinal damage.
Slit-lamp biomicroscopy of the anterior segment. A special microscope shows fine detail. The clinician looks for rubeosis iridis (tiny new vessels on the iris) and for signs of inflammation or blood in the front chamber.
Corneal clarity assessment. The doctor looks for corneal edema (water logging) caused by very high pressure, which explains halos and pain.
B) Manual / office-based functional tests
Applanation tonometry (Goldmann). This is the gold standard to measure intraocular pressure (IOP). It gently flattens a tiny area of the cornea to read an accurate pressure number.
Gonioscopy. A mirrored contact lens is placed on the eye (with anesthetic drops) to look directly at the drainage angle. The doctor can see new vessels in the angle, membranes, and peripheral anterior synechiae that mark angle closure.
Indentation (dynamic) gonioscopy. The doctor applies gentle pressure with the gonio lens to see whether the angle opens with pressure (suggesting a membrane that might be moved) or if it is truly sealed by synechiae.
Dilated fundus examination with indirect ophthalmoscopy. After dilating drops, a bright light and lens are used to view the retina for vein or artery occlusions, diabetic changes, widespread non-perfusion, or tumors.
Central corneal thickness (pachymetry). A quick probe measures corneal thickness. Very thick or very thin corneas can skew pressure readings. This helps interpret IOP more correctly.
C) Laboratory and pathological tests
Blood glucose and HbA1c. These tests check for diabetes and how well it is controlled. Poor control is a major driver of retinal ischemia and NVG.
Complete blood count (CBC). This looks for anemia, very high white cells, or platelet problems that can cause hyperviscosity or other blood issues linked to retinal ischemia.
Hemoglobin electrophoresis (sickle screen). This checks for sickle cell disease or trait when the history or exam suggests it, because sickling can cause retinal ischemia and NVG.
ESR and CRP (in selected patients). These inflammation markers are used when a doctor suspects giant cell arteritis or other vasculitides that could cause artery occlusion and retinal ischemia.
D) Electrodiagnostic tests
Electroretinogram (ERG). This test measures the electrical response of the retina to light. A very reduced ERG may confirm widespread retinal damage and poor retinal reserve, which affects prognosis.
Visual evoked potential (VEP). This test measures the electrical signal reaching the brain from visual stimuli. It helps assess optic nerve function when pressure has been high or when the optic nerve looks damaged.
E) Imaging tests
Fluorescein angiography (FA). Dye is injected into a vein in the arm, and rapid photos of the retina are taken. FA shows areas of non-perfusion, leaky neovascularization, and helps guide laser treatment.
Optical coherence tomography (OCT) of the macula and optic nerve. OCT uses light to make cross-section images. It shows macular edema, traction, and optic nerve fiber loss, all of which affect vision and treatment choices.
OCT-angiography (OCT-A). This non-invasive scan maps blood flow in retinal layers without dye. It can show capillary loss and neovascular complexes that explain the VEGF drive.
B-scan ocular ultrasonography (when the view is blocked). If corneal swelling, cataract, or blood blocks the view, ultrasound can detect retinal detachment, vitreous hemorrhage, or tumors that may be causing ischemia and NVG.
Non-pharmacological treatments
(Each item: Description • Purpose • How it helps)
Urgent ophthalmology care — Description: Same-day or next-day eye specialist assessment. Purpose: Stop pressure spikes and save vision. Mechanism: Rapid diagnosis, anti-VEGF injection, laser planning, and pressure-lowering steps.
Panretinal photocoagulation planning (PRP) — Description: Wide-field retinal laser (often performed urgently). Purpose: Reduce the retina’s oxygen demand. Mechanism: Laser “turns down” VEGF production by treating ischemic retina.
Head elevation & rest during pain spikes — Description: Sit up or sleep with extra pillows. Purpose: Ease pressure-related pain. Mechanism: Improves venous outflow, may slightly lower eye pressure and reduce corneal edema symptoms.
Avoid Valsalva/straining — Description: Prevent heavy lifting, forceful coughing, or constipation. Purpose: Reduce sudden pressure rises. Mechanism: Less spikes in venous pressure → less IOP surges.
Stool softeners & hydration habits — Description: Fiber, fluids, and gentle stool softeners. Purpose: Reduce straining. Mechanism: Keeps abdominal pressure down → fewer IOP spikes.
Stop smoking — Description: Smoking cessation plan. Purpose: Improve oxygen delivery to the retina. Mechanism: Better vascular health lowers ischemia and VEGF drive.
Sleep apnea evaluation & CPAP use if needed — Description: Screen for obstructive sleep apnea. Purpose: Improve night-time oxygen levels. Mechanism: Less hypoxia → less VEGF signaling.
Tight diabetes control (with your medical team) — Description: A1c goals, diet, meds, and follow-up. Purpose: Slow retinal damage. Mechanism: Less ischemia → less neovascular drive.
Blood pressure & lipid optimization — Description: Follow your clinician’s targets. Purpose: Protect retinal circulation. Mechanism: Better perfusion reduces VEGF triggers.
Review of systemic medicines — Description: Check steroids and other drugs with your doctor. Purpose: Avoid IOP-raising or angle-narrowing risks. Mechanism: Minimizes drug-induced pressure issues.
Eye protection & activity adjustments — Description: Safety glasses; avoid high-impact sports until stable. Purpose: Prevent trauma to fragile new vessels. Mechanism: Lowers risk of hyphema (bleeding).
Cool, dark environment for comfort — Description: Sunglasses, dim light, cold compress over closed lids. Purpose: Reduce photophobia and aching. Mechanism: Calms ciliary body and trigeminal pain pathways.
Glycemic-friendly, anti-inflammatory eating pattern — Description: Vegetables, lean proteins, whole grains; limited refined sugars. Purpose: Support retinal and vascular health. Mechanism: Better metabolic control → less ischemia.
Moderate, doctor-approved exercise — Description: Walking and cardio approved by your physician. Purpose: Heart and vessel health. Mechanism: Improved circulation; may modestly lower IOP.
Low-vision aids if vision is reduced — Description: Magnifiers, high-contrast lighting, accessibility settings. Purpose: Maximize remaining vision. Mechanism: Improves daily function and safety.
Home safety & fall prevention — Description: Clear walkways, night lights, handrails. Purpose: Prevent injuries with reduced vision. Mechanism: Environmental risk reduction.
Frequent follow-up schedule — Description: Often every 1–2 weeks early on. Purpose: Catch re-bleeds or pressure rebounds. Mechanism: Early tweaks to meds/laser/surgery plans.
Care coordination — Description: Eye doctor + primary care + vascular specialist. Purpose: Treat the whole problem. Mechanism: Fixing systemic blood flow issues lowers eye VEGF.
Education about warning signs — Description: Learn pain, redness, halos, nausea signs. Purpose: Prompt action during flares. Mechanism: Faster care prevents nerve damage.
Advance planning for surgery — Description: Pre-op clearance, stop blood thinners only if your doctors approve. Purpose: Safer surgery, fewer bleeds. Mechanism: Optimizes healing and pressure results.
Drug treatments
Always individualized by your ophthalmologist. Doses below are typical starting points—not personal medical advice.
Bevacizumab (anti-VEGF biologic, intravitreal)
Dose/Timing: 1.25 mg injected into the eye; often at diagnosis, then as needed (weeks to months).
Purpose: Rapidly regress new vessels on iris/angle.
How it works: Neutralizes VEGF so vessels shrink and stop leaking.
Side effects: Rare infection (endophthalmitis), transient IOP rise, small bleeding risk.Ranibizumab (anti-VEGF, intravitreal)
Dose/Timing: 0.5 mg intravitreal; repeated per response.
Purpose/Mechanism: Same as above; designed for intraocular use.
Side effects: Similar to bevacizumab.Aflibercept (VEGF-trap, intravitreal)
Dose/Timing: 2 mg intravitreal; may last longer in some cases.
Purpose: Strong VEGF binding; helps quiet neovascularization.
Side effects: Similar intravitreal injection risks.Timolol 0.25–0.5% (topical beta-blocker)
Dose/Timing: 1 drop twice daily (unless contraindicated).
Purpose: Lower IOP.
How it works: Reduces aqueous humor production.
Side effects: Wheezing, slow heart rate, fatigue; avoid in asthma/COPD/heart block.Brimonidine 0.2% (topical alpha-2 agonist)
Dose/Timing: 1 drop three times daily.
Purpose: Lower IOP in combination therapy.
How it works: Decreases production and increases uveoscleral outflow.
Side effects: Dry mouth, fatigue, allergic redness; caution with MAO inhibitors.Dorzolamide 2% (topical carbonic anhydrase inhibitor)
Dose/Timing: 1 drop three times daily (often combined with timolol).
Purpose: Additional IOP reduction.
How it works: Lowers aqueous production by blocking carbonic anhydrase in ciliary body.
Side effects: Stinging, bitter taste; rare corneal issues.Acetazolamide (oral carbonic anhydrase inhibitor)
Dose/Timing: 250 mg 4×/day or 500 mg ER 2×/day short-term.
Purpose: Rapid IOP drop while planning procedures.
How it works: Systemic inhibition of aqueous production.
Side effects: Tingling, frequent urination, fatigue, kidney stones, low potassium; avoid in sulfa allergy or severe kidney disease; pregnancy caution.Mannitol (IV hyperosmotic agent)
Dose/Timing: 1–2 g/kg IV over 30–60 min in acute crisis.
Purpose: Emergency pressure reduction.
How it works: Pulls fluid out of the eye by osmotic gradient.
Side effects: Headache, dehydration, heart failure overload risk; hospital use only.Netarsudil 0.02% (topical Rho-kinase inhibitor)
Dose/Timing: 1 drop once nightly.
Purpose: Additional IOP lowering, even with compromised trabecular meshwork.
How it works: Increases trabecular outflow; may soften/relax the outflow tissues.
Side effects: Conjunctival redness, small corneal verticillata; usually mild.Latanoprost 0.005% (topical prostaglandin analog)
Dose/Timing: 1 drop at bedtime.
Purpose: Sustained IOP lowering.
How it works: Increases uveoscleral outflow.
Side effects: Darker iris/eyelash growth, eye redness; avoid if there is active inflammation.
Supportive meds often added: topical prednisolone acetate 1% (to calm inflammation) and atropine 1% (to rest the ciliary muscle and reduce pain/photophobia). Your doctor will decide if these are appropriate.
Dietary “molecular” supplements
Discuss with your clinicians—some interact with blood thinners or have dose limits.
Omega-3 (EPA+DHA) — Dose: 1–2 g/day. Function: Supports vascular health. Mechanism: Anti-inflammatory lipid mediators may improve blood flow characteristics.
Nicotinamide (Vitamin B3) — Dose: 0.5–1 g/day unless your doctor supervises higher research doses. Function: Mitochondrial support for retinal ganglion cells. Mechanism: Boosts NAD⁺ pathways linked to cell energy.
Citicoline — Dose: 500–1,000 mg/day (oral) or as drops in some regions. Function: Neuro-support for optic nerve signaling. Mechanism: Aids phospholipid and neurotransmitter pathways.
Coenzyme Q10 — Dose: 100–200 mg/day. Function: Antioxidant for mitochondria. Mechanism: Supports ATP production; may protect retinal ganglion cells.
Alpha-lipoic acid — Dose: 300–600 mg/day. Function: Antioxidant; helpful in diabetes-related oxidative stress. Mechanism: Recycles other antioxidants; improves endothelial function.
Magnesium (glycinate/citrate) — Dose: 200–400 mg at night. Function: Vascular and neural relaxation; sleep support. Mechanism: Smooth-muscle modulation and NMDA receptor effects.
Ginkgo biloba (EGb 761) — Dose: 120 mg/day. Function: Microcirculation support. Mechanism: Antioxidant/vasoregulatory effects; caution with anticoagulants.
Resveratrol — Dose: 100–250 mg/day. Function: Antioxidant/vascular signaling. Mechanism: Sirtuin pathways; anti-inflammatory effects.
Curcumin (with piperine or enhanced forms) — Dose: 500–1,000 mg/day. Function: Anti-inflammatory/antioxidant. Mechanism: NF-κB modulation; limited bioavailability unless formulated.
Melatonin — Dose: 0.3–3 mg at bedtime. Function: Sleep and possible nocturnal IOP modulation. Mechanism: Melatonin receptors in ciliary body may influence aqueous dynamics.
Reality check: Supplements can support general eye and nerve health, but they do not replace anti-VEGF, laser, or glaucoma surgery in NVG.
Regenerative / stem-cell / ‘immunity-booster’” approaches
Important truth: There is no proven “immunity booster” drug that treats neovascular glaucoma. The options below are experimental and should only be considered within regulated clinical trials.
Mesenchymal stem cell (MSC) intravitreal therapy — Function: Potential neuroprotection/anti-inflammation. Mechanism: Paracrine factors may support retinal ganglion cells. Dose: No approved dose; study-only.
MSC-derived exosome eye drops/injections — Function: Cell-free regenerative signaling. Mechanism: Micro-RNAs and proteins may reduce inflammation and support repair. Dose: Investigational only.
Trabecular meshwork stem cell transplantation — Function: Restore outflow tissue. Mechanism: Rebuild/repair the eye’s natural drain. Dose: Preclinical/early research.
AAV-based anti-VEGF gene therapy — Function: Long-term VEGF suppression. Mechanism: Retina makes its own anti-VEGF protein after one procedure. Dose: Trial-defined; not approved for NVG.
Encapsulated cell therapy (neurotrophic factors like CNTF/BDNF) — Function: Continuous delivery of protective proteins. Mechanism: Supports optic nerve survival. Dose: Trial devices; not standard care.
Rho-kinase–modulating regenerative strategies — Function: Beyond pressure lowering, may remodel outflow tissues. Mechanism: Cytoskeletal and extracellular matrix effects. Dose: Approved drops exist for IOP, but the “regenerative” aspect remains under study.
Procedures & surgeries
Panretinal photocoagulation (PRP) — Procedure: A laser treats many peripheral retinal spots. Why: Decreases VEGF production by shrinking ischemic retina; helps stop the growth of abnormal vessels on the iris and angle.
Glaucoma drainage implant (tube shunt: Ahmed, Baerveldt, etc.) — Procedure: A small tube is placed to carry fluid from inside the eye to a plate under the conjunctiva, where it is absorbed. Why: Lowers IOP when the angle is scarred closed.
Trabeculectomy (usually with mitomycin-C) — Procedure: Creates a new drainage pathway (a “bleb”) under the upper eyelid. Why: Powerful pressure lowering when anatomy and scarring allow.
Cyclophotocoagulation (transscleral or endoscopic) — Procedure: Laser treats the ciliary body (the fluid-making tissue). Why: Reduces aqueous production when outflow is blocked and other options fail or pain relief is needed.
Pars plana vitrectomy with endolaser ± anti-VEGF — Procedure: Removes the gel (vitreous), treats the retina with internal laser, and may add anti-VEGF. Why: Clears hemorrhage, applies definitive PRP, and helps quiet neovascular drive.
Prevention strategies
Control diabetes carefully (A1c goals from your clinician).
Treat high blood pressure and cholesterol to vascular targets.
Stop smoking and avoid secondhand smoke.
Keep regular dilated eye exams, especially if you have diabetes or vascular disease.
Seek prompt care for retinal vein occlusion symptoms (sudden blur, distortion).
Evaluate carotid arteries if your doctor suspects low ocular perfusion.
Use medications exactly as prescribed; do not overuse steroids.
Manage sleep apnea if present.
Protect your eyes from trauma.
Maintain heart-healthy nutrition and activity to support circulation.
When to see a doctor (red flags)
Severe eye pain, headache, or nausea/vomiting with a red eye.
Sudden blurred vision, halos around lights, or new floaters.
A “curtain” or dark shadow in your vision.
Any rapid change after an injection or laser (pain, pus, vision drop).
If you have diabetes/vein occlusion and notice new redness or light sensitivity.
Do not wait—neovascular glaucoma can progress in days.
What to eat and what to avoid
Helpful choices (eat more of these):
Leafy greens (spinach, kale) • 2) Berries • 3) Citrus fruits • 4) Tomatoes • 5) Fatty fish (salmon, sardines) • 6) Nuts (walnut, almond) • 7) Olive oil • 8) Whole grains • 9) Beans/lentils • 10) Low-fat dairy or fortified alternatives.
Why: Heart-healthy, glucose-steady foods support blood vessels and reduce oxidative stress.
Things to limit/avoid:
Sugary drinks • 2) Refined carbs (white bread, pastries) • 3) Excess salt • 4) Processed meats • 5) Deep-fried foods • 6) Trans fats • 7) Heavy alcohol • 8) Smoking/nicotine • 9) Herbal “blood thinners” before procedures (e.g., high-dose ginkgo/garlic—only if your doctors advise) • 10) Unsupervised mega-doses of supplements.
Why: These worsen metabolic control, blood pressure, bleeding risk, or medication safety.
Frequently asked questions
Is neovascular glaucoma curable?
It is controllable, but not “curable.” We can shut down abnormal vessels, lower pressure, and protect remaining vision. Early action matters most.Will anti-VEGF injections alone fix it?
They help quickly, but laser (PRP) and often surgery are usually needed for durable control.If pressure becomes normal, am I safe?
Lower pressure helps, but you also need the VEGF drive reduced and the root cause treated. Keep follow-ups.Can vision return to normal?
Some vision can improve if swelling or bleeding clears, but optic nerve damage is permanent. The goal is to save what you have and keep you comfortable.Why do I still need surgery after injections?
Scar tissue may already have closed the angle. A tube or other surgery creates a new drainage path.Are the surgeries painful?
Anesthesia and pain control are standard. Soreness is common, but severe pain is not expected. Report strong pain right away.How often will I need injections or laser?
It varies. Some eyes quiet after one to two injections plus PRP; others need repeat treatments based on exams.Can both eyes be affected?
Yes—if the underlying condition (like diabetes or carotid disease) affects both eyes. Regular checks of both eyes are important.Do glaucoma drops still work if the angle is closed by scar tissue?
Drops help, but may not be enough. That’s why tubes or cyclophotocoagulation are often required.Are steroids bad for glaucoma?
Steroids can raise pressure in some people, but short-term, carefully monitored steroids may be used to control inflammation. Your doctor balances risks and benefits.Can I exercise?
Usually yes, once stabilized—prefer moderate cardio. Avoid heavy lifting or inverted poses that spike pressure until your doctor clears you.Should I change my diet?
Follow a heart-healthy, diabetes-friendly pattern. Diet supports the root disease, but it does not replace medical or surgical care for NVG.Will I need life-long follow-up?
Almost always yes. NVG can recur if the ischemia returns. Ongoing care keeps you safe.Are stem-cell treatments available?
Currently experimental. Consider only within regulated clinical trials—not routine care.What if I cannot tolerate multiple drops?
Tell your doctor. There are fixed-combination drops, oral medicines, laser, and surgical options to simplify the plan.
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 14, 2025.
