A choroidal vasoproliferative tumor—more commonly called a retinal vasoproliferative tumor (VPT)—is a benign (non-cancer) lump made mostly of new blood vessels and support cells in the peripheral retina (the retina is the thin, light-sensing layer that lines the inside of the eye). The word “vaso-proliferative” means “blood vessels growing more than they should.” These extra vessels are leaky, so fluid and fat-like deposits (exudate) seep out. That leak can blur vision, distort straight lines, and sometimes lift the retina off the back of the eye (exudative retinal detachment, which is an emergency).
A retinal vasoproliferative tumor is a small, usually solitary lump of abnormal blood vessels and reactive glial tissue that grows in the far edge of the retina, most often in the lower outer quadrant. It’s benign (not cancer), but it can leak (exude) fluid and lipids, cause swelling (macular edema), tug on the retina and form membranes, or bleed into the eye. Those effects—not the tumor itself—are what harm vision. VPTs may be primary (appear in otherwise healthy eyes) or secondary (develop in eyes with other diseases or past injuries). Nature+1PMC
Although “choroidal” appears in the name you gave, the growth usually starts in the retina, not the choroid (the choroid is the vascular layer under the retina). Many doctors therefore prefer “retinal vasoproliferative tumor.” The lump itself does not spread (no metastasis), but the leaking fluid and secondary changes (like swelling of the central retina called cystoid macular edema) can seriously harm sight if untreated.
Typical features you might hear your eye doctor describe:
Color/appearance: a pink-yellow or reddish-orange dome-shaped mass in the far retinal periphery, often inferotemporal (lower outer quadrant).
Feeder vessels: small arteries and veins going in and out of the mass.
Exudation: yellowish deposits and pockets of subretinal fluid (fluid under the retina).
Secondary membranes: scar-like layers that can tug on the retina.
VPTs can be primary (idiopathic)—meaning no known trigger—or secondary to another eye condition that has been present for a while (for example, long-standing inflammation).
The retina gets injured or stressed (sometimes silently). In response, it releases growth signals (like VEGF and others). These signals tell nearby cells to sprout new capillaries (tiny blood vessels) and call in glial cells (retinal support cells) to “patch” the area. The repair goes too far, building a solid, leaky mound. Because these new vessels are immature and fragile, they ooze fluid and sometimes bleed. The leaked fluid spreads, especially downhill with gravity, so we often see problems in the lower retina.
Types
Primary (Idiopathic) VPT
“Idiopathic” means no clear cause is found. The tumor arises in an otherwise healthy eye. It is usually single and appears in middle-aged adults. It is benign but can leak a lot.Secondary VPT
“Secondary” means it develops because of another eye disease or damage. The tumor may be single or multiple, and it often appears in a retina with long-standing inflammation, scarring, or degeneration. Because the underlying problem remains, leakage and recurrence can be more stubborn.Solitary vs Multiple
Many people have one tumor; some have two or more. Multiple lesions are more often secondary.Active (exudative) vs Inactive (fibrotic/scarred)
Active tumors leak a lot and cause swelling. Inactive or fibrotic ones look paler and harder, with less leakage, but can still pull on the retina.Small vs Large / Peripheral vs Mid-peripheral
Size and position matter because bigger and more posterior (closer to the center) tumors are more likely to threaten central vision.
Causes
In many patients the cause is unknown. When we do find a link, it is usually a long-standing retinal problem that triggered abnormal vessel growth.
Idiopathic (no known cause) – The body overgrows vessels in a small retinal area for reasons we cannot identify.
Intermediate uveitis / pars planitis – Chronic inflammation near the peripheral retina; inflammation means constant chemical signals that push vessel growth.
Retinitis pigmentosa (RP) – A retinal degeneration that stresses tissue; stressed retina releases pro-growth factors.
Coats disease (adult form) – Abnormal leaky retinal vessels lead to chronic exudation, priming further reactive growth.
Old retinal tears or detachments – Scarring and ischemia (low oxygen) after tears/detachments stimulate new vessel sprouting.
Prior retinal surgery or intense laser/cryotherapy – Any healing response can sometimes overshoot and create a reactive mass.
Retinopathy of prematurity (ROP) – Earlier life abnormal vessel growth can leave the retina unstable, later fostering a VPT.
Toxoplasma scars – Infectious scars alter local anatomy and oxygen balance, driving reactive vascular growth.
Familial exudative vitreoretinopathy (FEVR) – A genetic vascular development disorder predisposing to peripheral ischemia and neovascular growth.
Stickler syndrome – A connective-tissue disorder that weakens the vitreous-retina interface and promotes peripheral degeneration.
Ocular trauma – Injury starts a big healing response; new vessels over-grow in the damaged zone.
Radiation retinopathy – Prior radiation causes capillary drop-out (ischemia) and then abnormal vessel proliferation.
Sickle cell retinopathy or other hemoglobinopathies – Blocked retinal capillaries starve tissue of oxygen; low oxygen drives neovascular growth.
Sarcoidosis – A granulomatous inflammation that can affect the eye; chronic inflammation promotes proliferation.
Retinal vein occlusion – A blocked vein raises back-pressure, causing leak and ischemia, both stimulating a VPT.
Choroidal hemangioma nearby – A vascular mass in the choroid can disturb fluid balance, indirectly triggering retinal reactive growth.
Long-standing epiretinal membrane – Tugging and micro-injury from a membrane can lead to chronic low-grade inflammation.
Tuberculosis or syphilis uveitis – Chronic infectious inflammation sets up the same pro-growth chemical environment.
High myopia with peripheral degeneration – Thinned, stressed peripheral retina can become ischemic and reactive.
Post-inflammatory scars of any cause – Wherever the retina has a healed scar, the border zone can overproduce vessels later.
Symptoms
Some people notice nothing until leakage reaches the macula (the central sharp-vision area). Others have early hints.
Blurred or dim central vision – From macular swelling (fluid in central retina).
Distortion (metamorphopsia) – Straight lines look wavy because the retina is puffed or pulled.
A “gray shadow” or curtain from the side – Suggests subretinal fluid spreading or an exudative detachment.
Floaters – Dark specks or cobwebs caused by cells or blood in the gel (vitreous).
Flashes of light (photopsia) – Retinal tugging or irritation can trigger brief light flashes.
Peripheral blind spot – A localized scotoma where the tumor and exudate distort the retina.
Poor night vision – If the surrounding retina is stressed, rod cells struggle in low light.
Color fading or subtle color shift – Swollen macula makes colors seem off.
Increased glare and light sensitivity – Edema (swelling) scatters light, making glare worse.
Eye ache or dull discomfort – Not classic, but inflammation or raised pressure can cause it.
Redness – If there is active inflammation in the front of the eye as well.
Headache around the eye – From eye strain or inflammation.
Sudden blur after heavy activity – More fluid leak can temporarily worsen vision.
Reading difficulty – Letters smear or dance when the macula is involved.
No symptoms at all – Many tumors are found incidentally during a routine dilated exam.
Diagnostic tests
Doctors combine history, examination, and tests. Imaging shows leakage, fluid, and mass features. Electrodiagnostics check retinal function. Labs look for underlying causes when a VPT is secondary.
A) Physical exam (general, no machines beyond basics)
Visual acuity test
Reading letters on a chart tells how sharp your central vision is. A drop suggests macular edema or fluid from leakage.Pupil examination
The doctor shines a light to see how pupils react. An afferent defect (one eye responds less) hints at retinal or optic nerve trouble.Confrontation visual fields
You cover one eye and report when you see fingers moving in the side vision. Missing areas can match the tumor location.Amsler grid at the slit lamp
A checkerboard grid helps you spot wavy lines or blank spots, classic for macula swelling.
B) Manual, clinician-performed eye tests (with simple tools)
Slit-lamp biomicroscopy with contact or non-contact fundus lens
A microscope with bright light lets the doctor inspect the retina, see the mass, the feeder vessels, exudates, and fluid pockets.Indirect ophthalmoscopy
Wearing a headlight and lens, the doctor scans the far periphery (where VPTs love to hide). This is key to finding the lesion.Scleral depression
Gentle pressing on the white of the eye (with numbing drops) brings far-peripheral retina into view, revealing small tumors and exudation.Applanation tonometry (eye pressure check)
Measures intraocular pressure. Very high pressure could mean secondary glaucoma from inflammation or steroid treatment.Color vision testing (Ishihara)
Simple color plates test for color loss, which can happen if macula function is affected by edema.
C) Laboratory and pathological tests (to search for secondary causes)
General inflammation panel (CBC, ESR, CRP)
Looks for systemic inflammation that might align with uveitis or other inflammatory drivers.Infectious screening (toxoplasma, syphilis, TB/IGRA as indicated)
Finds treatable infections that can cause retinal scars and chronic inflammation.Autoimmune markers (ANA; ± ACE/lysozyme for sarcoid)
Helps detect autoimmune or granulomatous conditions linked with secondary VPT.Genetic testing when inherited disease is suspected (e.g., FEVR, Stickler)
Confirms hereditary retinal disorders that set the stage for peripheral ischemia and VPT.
Note: Tissue biopsy is rare because VPT can usually be diagnosed clinically and by imaging. Pathology (if ever obtained) shows capillaries + glial tissue.
D) Electrodiagnostic tests (how well the retina works)
Full-field electroretinogram (ERG)
Measures electrical responses of rod and cone cells. Global weakness supports underlying degenerations (like RP).Multifocal ERG (mfERG)
Maps local function across the retina. Reduced signals near the tumor/exudate show regional damage.Visual evoked potential (VEP)
Checks the pathway to the brain. Usually normal in isolated VPT, but helpful if the doctor suspects optic pathway issues.
E) Imaging tests (to see the mass, leakage, and fluid)
Color fundus photography
High-resolution pictures document the tumor’s size, color, and exudates. Useful for before-after comparisons.Fluorescein angiography (FA)
A dye in the vein lights up retinal vessels. In VPT, FA shows early filling of the mass and late leakage—proof of leaky capillaries.Optical coherence tomography (OCT)
A light-based scan that slices the retina into layers. OCT shows cystoid macular edema, subretinal fluid, and sometimes the edge of a peripheral lesion if imaged properly.B-scan ocular ultrasonography
A gentle ultrasound probe on the closed eyelid shows a solid, dome-shaped mass with medium reflectivity and can detect fluid under the retina, even when the view is clouded.
Other imaging your specialist may add: OCT-angiography (OCT-A) to view blood flow without dye, indocyanine green angiography (ICGA) for deeper choroidal detail, and ultrasound biomicroscopy if the tumor is very anterior.
Non-pharmacological treatments
Observation with close follow-up. Tiny, quiet tumors without macular threat can be safely watched, with OCT and widefield photos every few months. Purpose: avoid overtreatment and track for change. Mechanism: none—monitoring only. Nature
Peripheral laser photocoagulation to the tumor. Aims to cauterize and shrink the lesion, reduce leakage. Works by thermal coagulation of abnormal vessels. Useful in small, accessible tumors. ScienceDirect
Cryotherapy (freezing). A probe applied externally through the sclera freezes the tumor; it often works well for small (<2 mm thickness) lesions. Purpose: destroy vascular tissue; Mechanism: ice-crystal–mediated cellular necrosis and vascular closure. PMC
Repeat cryotherapy (staged). Larger lesions sometimes need more than one session to fully involute. Mechanism and purpose as above; staged to limit collateral damage. PMC
Photodynamic therapy (PDT) with verteporfin. Light-activated drug targets abnormal vessels and closes them selectively. Useful when laser/cryotherapy are hard to apply or when there’s heavy exudation. Limitation: very anterior tumors can be hard to reach. Healio JournalsRetina Today
Plaque brachytherapy (localized radiation). A tiny radioactive “plaque” is sutured to the sclera over the tumor for several days, delivering a precise dose that shrinks the mass and dries exudation—especially for larger (>2.5 mm) or refractory tumors. JAMA NetworkPMC
Indirect laser to surrounding exudation pools. Not for the tumor core but to wall off or stabilize areas of threatened macula when appropriate.
Diathermy (rarely used). Controlled cautery for abnormal vasculature when other methods aren’t possible. Purpose: vascular closure; Mechanism: heat coagulation. PMC
Transpupillary thermotherapy (TTT). Low-energy infrared laser to heat the lesion gently. Purpose: reduce leakage; Mechanism: sub-photocoagulative hyperthermia causing vessel closure. (Adjunct in select cases.)
Anti-VEGF-sparing intervals (structured monitoring). After procedures, a planned observation period gauges whether leakage has quieted before adding injections—minimizing burden.
Targeted treatment of macular epiretinal membrane (non-surgical prep). Pre-surgery counseling, lubrication, and anti-inflammatory non-drug measures (cool compresses, rest) to reduce irritation and photophobia while planning definitive care.
Low-vision rehabilitation. If vision is reduced, training with magnifiers, enhanced contrast, and lighting helps daily tasks. Purpose: maximize function regardless of tumor status.
Smoking cessation support. Smoking worsens retinal microvascular health. Stopping can improve overall ocular outcomes. Purpose: reduce ischemic drive.
Blood pressure optimization (with primary care). Hypertension can aggravate retinal leakage and hemorrhage; good control helps stabilization.
Blood sugar control (if diabetic). Hyperglycemia impairs capillaries; tight control supports healing.
Protective eyewear. Prevents additional trauma to a vulnerable peripheral retina.
UV/blue-light hygiene (sunglasses outdoors). General comfort and glare reduction for photophobia; indirect support during recovery.
Sleep apnea screening when indicated. Untreated OSA is linked to retinal vascular dysregulation; treating it can aid overall eye health.
Patient-held monitoring (Amsler/phone reminders). Early flagging of worsening distortion or new floaters speeds re-treatment.
Shared decision-making pathways. Written plans for when to escalate from observation → laser/cryotherapy → PDT or plaque radiation, based on size, location, and macular threat. Retina TodayScienceDirect
Practical rule of thumb (from the literature): small tumors often respond to cryotherapy, while larger or refractory lesions may need PDT or plaque radiation (and sometimes vitrectomy—see surgeries). PMCJAMA Network
Drug treatments
Important: Drug use here is largely adjunctive—to dry macular edema, calm inflammation, and control exudation. Many regimens are off-label and individualized.
Bevacizumab (anti-VEGF) intravitreal injection
Class: anti-VEGF antibody. Dose: 1.25 mg/0.05 mL, typically every 4–6 weeks initially. Purpose: reduce leakage, macular edema; bridge or complement laser/cryotherapy/PDT. Mechanism: blocks VEGF-A so vessels leak less. Side effects: transient eye pressure rise, rare infection (endophthalmitis), very rare systemic effects. Anti-VEGF is reported useful in VPT and in VPT-like peripheral exudative disorders. PMCScienceDirectRanibizumab (anti-VEGF) intravitreal
Dose: 0.5 mg monthly or PRN. Similar purpose/mechanism/risks as bevacizumab; sometimes chosen for regulatory/sterility reasons. ScienceDirectAflibercept (anti-VEGF/Trap) intravitreal
Dose: 2 mg every 4–8 weeks initially. Mechanism: traps VEGF-A/B and PlGF, potentially stronger drying in some eyes. Risks: similar intravitreal risks. ScienceDirectTriamcinolone acetonide (intravitreal steroid)
Dose: 2–4 mg; used sparingly. Purpose: tamp down inflammation and macular edema. Mechanism: broad anti-inflammatory; tightens blood-retina barrier. Side effects: pressure rise, cataract acceleration, infection risk.Dexamethasone intravitreal implant (0.7 mg)
Purpose: sustained steroid effect for edema; Mechanism and risks as steroids; benefit is controlled release over months, fewer injections overall. ScienceDirectTopical NSAID drops (e.g., bromfenac 0.09% once daily)
Purpose: adjunct for macular edema symptoms; Mechanism: COX inhibition reduces prostaglandin-mediated leakage. Side effects: stinging, rare corneal issues with overuse.Oral acetazolamide (250 mg 1–2×/day)
Purpose: sometimes used short-term for cystoid macular edema; Mechanism: carbonic anhydrase inhibition improves retinal pigment epithelium (RPE) fluid pumping; Side effects: tingling, taste change, kidney stone risk.Short course topical steroid (prednisolone acetate 1% QID, tapered)
Purpose: quiet surface/intraocular inflammation if present; Risks: pressure rise, cataract with prolonged use.Periocular steroid injection (sub-Tenon’s triamcinolone 20–40 mg)
Purpose: anti-inflammatory effect without entering the vitreous in some cases; Risks: IOP rise, ptosis, rare globe perforation.Immunomodulatory therapy (e.g., methotrexate, mycophenolate, biologics) only when there’s a clear underlying uveitis/systemic inflammatory disease driving a secondary VPT. Dose: disease-specific. Purpose: treat the root inflammation so the reactive tumor and leakage calm down. Risks: systemic (liver, marrow, infection) and require specialist co-management. PubMed
Reality check from the literature: many VPT cases are managed with procedure-first strategies (cryotherapy/laser/PDT/plaque). Anti-VEGF and steroids are often adjuncts to control macular edema and exudation. ScienceDirectPMC
Hard immunity / regenerative / stem cell” drugs
For VPT specifically, there are no approved immune-boosting, regenerative, or stem-cell drug therapies. Research in retina is active (gene therapy, cell replacement) but focuses on other diseases (e.g., age-related macular degeneration, inherited dystrophies), not VPT. Any use here would be off-target and not recommended outside clinical trials. Briefly:
Anti-VEGF gene therapy (e.g., RGX-314, Ixo-vec/ADVM-022)—investigational to make the eye produce its own anti-VEGF; not studied for VPT.
RPE stem-cell patches (pluripotent-derived)—trialed in macular diseases, not for peripheral VPT nodules.
Photoreceptor precursor cell therapy—experimental for degenerations (e.g., RP), not VPT.
CRISPR/gene editing approaches—target specific mutations in inherited diseases; not a VPT therapy.
Neuroprotective biologics (e.g., CNTF implants)—studied in RP; not for VPT.
Autologous bone marrow–derived cell infusions—no evidence for VPT; avoid outside trials.
Bottom line: do not pursue these for VPT outside IRB-approved studies; there is no dosing to recommend for VPT. (If you’re interested in trial-level options for an underlying dystrophy, I can pull current listings.)
Surgeries
Pars plana vitrectomy (PPV) with membrane peel/ILM peel when the macula has a tight epiretinal membrane or tractional changes. Why: to relieve pulling, improve macular shape, and help vision.
Vitrectomy with endolaser and gas/oil tamponade when there’s extensive exudation, subretinal fluid, or peripheral breaks. Why: reattach/flatten retina, then stabilize with internal tamponade.
External drainage of subretinal fluid (selected cases). Why: rapidly relieve large peripheral detachment threatening the macula.
Local tumor resection (trans-scleral) in highly selected, accessible lesions (rare today). Why: remove mass when other modalities aren’t feasible or malignancy is suspected. JAMA Network
Scleral buckle (occasionally) if the tumor’s traction or associated breaks produce a rhegmatogenous detachment. Why: support the retina mechanically while adjunct treatments control the tumor.
For large or refractory tumors with persistent leakage or detachment, many centers combine PPV with adjuncts (endolaser, cryo/PDT) or consider plaque brachytherapy for tumor control. The plaque itself is not a “surgery” on the tumor but is often placed in the OR. PMC
Prevention strategies
Strictly speaking, there’s no proven way to prevent VPT from forming. These steps aim to reduce complications, stabilize the retina, and catch changes early:
Keep follow-up appointments and imaging intervals.
Control blood pressure and blood sugar with your primary care team.
Stop smoking; seek support programs if needed.
Protect eyes from trauma (sports eyewear).
Treat uveitis or inflammation promptly to minimize reactive proliferation.
Adhere to post-procedure instructions (eye drops, activity limits).
Use an Amsler grid weekly if macula has been threatened.
Manage sleep apnea if present; use CPAP as prescribed.
Avoid unsupervised blood thinners/herbal anticoagulants around procedures; always discuss with your doctor.
Report new flashes/floaters/curtain immediately—don’t wait.
When to see a doctor
Right away if you notice a shower of new floaters, flashes, a curtain, sudden blur, or eye pain—possible bleeding or retinal tear/detachment.
Soon (days) if you develop new distortion, worsening blur, or new dark spot off to the side.
Routine: keep scheduled OCT/photography follow-ups even if you feel fine—peripheral disease can change silently.
What to eat” and “what to avoid”
Eat more of:
Leafy greens (spinach, kale): lutein/zeaxanthin support macular health.
Colorful veggies/berries: antioxidants may help counter oxidative stress.
Fish (2–3×/week): omega-3s support retinal membranes.
Nuts/legumes: healthy fats and minerals for microvascular health.
Hydration: supports general ocular perfusion and medication tolerance.
Limit/avoid:
6) Excess sodium (worsens blood pressure, fluid balance).
7) Added sugars (glycemic spikes harm small vessels).
8) Trans fats / ultra-processed foods (pro-inflammatory).
9) Excess alcohol (bleeding risk, BP effects).
10) Unregulated herbal “blood thinners” (ginkgo, high-dose garlic) around procedures unless your retina specialist okays them.
Diet can’t “shrink” a VPT. It’s supportive—the heavy lifting is done by laser/cryotherapy/PDT/plaque and, when needed, injections or surgery.
Frequently asked questions
1) Is VPT cancer?
No. It’s benign. The complications (leakage, swelling, bleeding, traction) are what reduce vision. PMC
2) Why does mine threaten the macula if it’s in the periphery?
Because fluid and lipids can travel toward the macula, and traction can ripple across the retina. That’s why OCT of the macula is monitored closely. JAMA Network
3) What’s the first-line treatment?
It depends on size and location. Small tumors often respond to cryotherapy; bigger or stubborn ones may need PDT or plaque radiation. Clinicians often mix approaches to dry the macula fastest. PMCHealio JournalsJAMA Network
4) Do anti-VEGF shots cure the tumor?
They usually don’t make the mass disappear, but they can reduce leakage and macular edema and buy time while a definitive procedure works. PMC
5) How successful is plaque brachytherapy?
In a classic series of 30 eyes, 97% had tumor regression, 65% had retinal detachment resolve, and over a third recovered to 20/40 or better—great for larger lesions. PMC
6) Can VPT come back after treatment?
It can reactivate or new exudation can occur—especially in secondary disease. Regular follow-up is key. JAMA Network
7) Is laser safer than cryotherapy?
Both are safe in expert hands. Choice is about tumor size, thickness, and accessibility. Very peripheral or thicker tumors often favor cryo; suboptimally accessible ones may need PDT or plaque. PMCRetina Today
8) Will I need surgery?
Only if there’s significant traction, epiretinal membrane, non-resolving detachment, or hemorrhage that procedures and injections can’t settle. JAMA Network
9) How is VPT different from choroidal hemangioma or PEHCR?
VPT is a retinal mass; choroidal hemangiomas are choroidal vascular tumors; PEHCR is a peripheral degenerative process that can mimic a mass and cause hemorrhage. The location, imaging, and angiography patterns differ. PMCEyeWikiAAO
10) Can I go blind from this?
Severe vision loss is uncommon with modern care, but it can happen if macular edema or detachment isn’t controlled. Early, tailored treatment reduces risk. JAMA Network
11) How many treatments will I need?
Often more than one. Cryotherapy can require repeat sessions; PDT may be repeated; injections are commonly series-based. Plan is individualized. PMC
12) Does it affect both eyes?
Primary VPT is usually one eye, but secondary VPT can be bilateral or multiple. PMC
13) Can lifestyle changes fix it?
No. They support eye health but don’t replace procedures or injections.
14) Are there clinical trials?
Typically not VPT-specific, but trials for macular edema therapies or inflammatory eye disease may be relevant in secondary VPT. I can look up current options on request.
15) What’s the prognosis?
Good when macular threats are treated promptly. Each case depends on tumor size/location, whether it’s primary vs secondary, and response to therapy. JAMA Networ
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 07, 2025.
