A retinal angioma, also known as a retinal capillary hemangioma, is a rare, non-cancerous (benign) growth made up of extra blood vessels in the retina—the light-sensing layer at the back of the eye. In very simple terms, imagine the retina as a delicate wallpaper of cells that captures images. A retinal angioma is like a tiny cluster of new, extra wires (blood vessels) growing where they shouldn’t. These extra vessels can leak fluid, cause swelling, or pull on the retina, leading to vision problems if left untreated. Most often, retinal angiomas occur in people with von Hippel–Lindau (VHL) disease, a genetic condition, but they can also appear on their own without any inherited cause JAMA Network.
A retinal angioma (the medical label is retinal capillary hemangioblastoma) is a tiny ball-shaped over-growth of blood-vessel cells inside the light-sensing layer (the retina) at the back of the eye. Think of it as a “sponge-like” knot of capillaries that keeps letting blood plasma leak into the surrounding retina. Although the tumour is benign (it does not spread like cancer), the extra fluid, fats, and traction it causes can blur or even destroy vision if nothing is done. Scientists first linked this lesion to the inherited von Hippel–Lindau (VHL) gene change more than a century ago, and today we know that roughly half of all people with a retinal angioma carry that gene mistake, while the other half develop one for reasons doctors are still untangling. EyeWiki
Main types you may hear about
| Type name (plain term) | What it means in simple English |
|---|---|
| Peripheral capillary angioma | The commonest form. It grows out in the far edges of the retina. Often seen first in teenagers or young adults and is easiest to treat with laser. Retina Today |
| Juxtapapillary capillary angioma | The growth hugs the optic-nerve head (“the cable entry”). It can mimic optic-nerve swelling and is trickier to treat because laser risks nerve damage. EyeWiki |
| Cavernous hemangioma | These look like bunches of red grapes hanging from a vein. They leak far less fluid, so many remain quiet for years. Linked to “cerebral cavernous malformation” genes (CCM 1-3). Retina Today |
| Racemose (AV) angioma / Wyburn-Mason | A rare tangle where an artery flows straight into a vein with no capillary bed. It usually involves the brain as well. Vision loss often comes from bleeding, not exudate. NCBI |
| Acquired vasoproliferative tumour | A secondary angioma-like mass that appears after long-standing retinal injury (e.g., uveitis, degeneration, trauma). It is “reactive,” not genetic. Retina Today |
| Sporadic single angioma | A one-off knot in an otherwise healthy person with no VHL gene change and no family history. Doctors still do not fully know why it happens. |
Causes & risk factors
VHL gene mutation (inherited) – the tumour-suppressor gene on chromosome 3 is faulty from birth; retinal angioma is often the first warning sign. EyeWiki
New (de-novo) VHL mutation – the same gene mistake appears for the first time in a child whose parents are unaffected.
CCM-1, 2 or 3 mutations – genes that also cause cavernous malformations in the brain can create grape-like retinal angiomas. Retina Today
Somatic (“second-hit”) VHL loss in the eye – in sporadic cases, only retinal cells lose the second good copy of VHL later in life, triggering a local angioma.
Congenital AV malformation (Wyburn-Mason) – a developmental slip when artery and vein channels form before birth.
Chronic low oxygen inside the eye (e.g., long-standing retinal detachment, sickle-cell ischemia) – low oxygen up-regulates VEGF, pushing capillaries to over-grow.
High-altitude hypoxia in infancy – rare reports suggest babies reared at very high altitudes may develop abnormal retinal vessels, though proof is scarce.
Prematurity & past ROP – healed retinopathy of prematurity leaves ischemic patches that may later sprout vasoproliferative tumours.
Previous penetrating eye trauma – scarred retina can secrete growth factors that drive vessel knobbing.
Chronic uveitis – long-lived inflammation feeds angiogenic (blood-vessel-growing) signals.
Old retinal infections (toxoplasmosis scars) – similar mechanism to trauma.
Radiation exposure – therapeutic or accidental radiation can damage vessel walls, prompting abnormal regrowth.
Uncontrolled diabetes – ischemic drive and VEGF storm may rarely tip over into a focal angioma rather than diffuse neovascularisation.
Severe carotid disease – low ocular perfusion pressure promotes collateral vessel sprouting.
Hormonal surges (pregnancy, estrogen therapy) – extra estrogen can boost VEGF; a few case reports note tumour growth during pregnancy.
Long-term corticosteroid use – indirect; steroids may quiet inflammation but thin collagen support, letting vessels pouch out.
Systemic polycythemia or high EPO – thicker blood and higher growth factors nurture vascular lumps.
Hypertensive retinopathy scars – after micro-infarcts, reparative vessels may ball up.
Ocular irradiation for other tumours – secondary effect years later.
Unknown / idiopathic factors – half of solitary angiomas still have no clear trigger despite testing.
Common symptoms
Blurred vision – fluid leaks from the knot, making the retina swell and images smudge.
Distorted or “wavy” lines – swelling pulls the photoreceptor layer unevenly (metamorphopsia).
Central blind spot – if leakage hits the macula, a dark patch blocks reading vision.
Flashes of light – traction on the retina can tickle photoreceptors, producing brief sparks.
Floaters – tiny blood droplets or lipid clumps drift in the vitreous.
Peripheral shadow – large exudative detachments raise the retina like a bubble at the edge of sight.
Reduced night vision – swollen rods work poorly in dim light.
Washed-out colours – macular edema dulls colour discrimination.
Eye ache or pressure – rare, but if leakage drives neovascular glaucoma the eye can hurt.
Red eye – small surface vessels react when internal bleeding irritates tissues.
Photophobia – glare sensitivity rises because retinal cells are stressed.
Double vision – uncommon; may occur if secondary strabismus develops from asymmetric vision loss.
Sudden vision drop – happens when the knot bleeds into the vitreous.
Pulsing image (visual shimmer) – turbulent flow in feeder vessels can create a rhythmic shimmer.
Total vision loss in one eye – end-stage after untreated chronic leakage, detachment, or glaucoma.
Diagnostic tests
A. Physical-exam–based
Visual-acuity chart – simple letter reading shows how sharp the central retina is today.
Colour-vision plates – Ishihara dots pick up early macular stress from fluid.
Pupil light reflex – a sluggish pupil hints at optic-nerve or severe macular injury.
Confrontation visual field – waving fingers from the side maps large blind zones from detachments.
External eye inspection with magnifier – looks for surface redness or neovascular glaucoma signs linked to severe leakage.
B. Manual, in-office viewing tests
Direct ophthalmoscopy – the doctor peers through the pupil; the angioma glows red-orange with big feeding vessels.
Indirect ophthalmoscopy + scleral depression – a brighter head-mounted view that shows the far periphery where most tumours hide. EyeWiki
Amsler grid – a hand-held square of lines; wavy or missing lines warn of macular edema.
Tonometry – measures eye pressure; high pressure may appear if VEGF triggers angle-blockage vessels.
C. Laboratory & pathological tests
VHL gene sequencing (blood or saliva) – pinpoints inherited or new VHL changes; positive result pushes doctors to scan kidneys, brain, and pancreas for other tumours. AAO
CCM gene panel – checks for KRIT-1, CCM-2, CCM-3 mutations when the lesion looks cavernous.
Serum VEGF level – not a routine test, but research shows spikes when multiple angiomas flare.
Histopathology of excised tissue – rarely done; microscope confirms a ball of capillaries plus “foamy” stromal cells with absent VHL protein. EyeWiki
D. Electro-diagnostic tests
Full-field electroretinogram (ERG) – records the retina’s electrical flash response; widespread edema can dampen the b-wave.
Pattern visual-evoked potential (VEP) – measures brainwaves from a checkerboard; reduced amplitude hints that the optic pathway is suffering from chronic macular input loss.
E. Imaging tests
Colour fundus photography – creates a baseline picture; later shots reveal growth or leak changes.
Fundus fluorescein angiography (FFA) – dye video that lights up the feeding artery, the bright-white tumour, and dye leakage. It spots “pin-point” tumours too small to see otherwise. Retina Today
Indocyanine-green angiography (ICG) – infrared dye penetrates deeper; helpful for larger or hidden lesions.
Spectral-domain optical coherence tomography (SD-OCT) – cross-section scan that shows the mound in the retinal layers and the pocket of fluid around it. EyeWiki
Optical coherence tomography angiography (OCT-A) – a dye-free map of moving blood; it outlines the capillary web inside the lesion and tracks flow drop after treatment. PMCPubMed
Non-Pharmacological Treatments
These physical or procedural therapies help control or remove the abnormal blood vessels without relying on medicines. Each treatment is described in plain English, with its purpose and basic way of working (mechanism).
Observation (Watchful Waiting)
Purpose: To monitor small, stable angiomas that aren’t causing problems.
Mechanism: Regular eye exams check for growth or fluid leakage. No active treatment until needed.
Laser Photocoagulation
Purpose: To seal leaking vessels and shrink small tumors.
Mechanism: A focused laser beam burns and closes abnormal capillaries in the lesion AAO.
Cryotherapy
Purpose: To freeze and destroy angioma tissue, especially in peripheral retina.
Mechanism: A probe applied to the outside of the eye freezes the lesion, causing cell death in the abnormal vessels AAO.
Photodynamic Therapy (PDT)
Purpose: To target and close vessels in tumors that are too close to critical structures for laser.
Mechanism: A light-sensitive drug is injected, collects in the angioma, and is activated by low-energy laser light, sealing vessels AAO.
Plaque Brachytherapy
Purpose: To use localized radiation for tumors not reachable by surface therapies.
Mechanism: A small radioactive “plaque” is sewn onto the eye wall next to the tumor, delivering focused radiation over days.
Transpupillary Thermotherapy (TTT)
Purpose: To heat and damage tumor vessels with minimal damage to surrounding retina.
Mechanism: Infrared laser delivers low-power heat through the pupil, causing vessel collapse.
Diathermy
Purpose: To coagulate the lesion with electric current.
Mechanism: An electrode probe applies high-frequency current to burn and seal vessels.
External-Beam Radiotherapy
Purpose: To treat multiple or large tumors when other methods are not suitable.
Mechanism: Radiation beams from outside the body focus on the angioma over several sessions.
Stereotactic Radiosurgery
Purpose: Single-session, high-precision radiation for small to medium tumors.
Mechanism: Multiple radiation beams converge on the lesion, delivering a high dose to the angioma while sparing healthy tissue.
Proton Beam Therapy
Purpose: To use charged particles for very precise tumor targeting.
Mechanism: Proton particles deposit most energy at a defined depth (“Bragg peak”), minimizing collateral damage.
Endolaser Photocoagulation (During Surgery)
Purpose: To treat lesions that require vitrectomy first.
Mechanism: During surgery, a laser probe inside the eye directly photocoagulates the angioma.
Pars Plana Vitrectomy
Purpose: To remove vitreous gel and ease traction if the angioma causes retinal detachments or hemorrhage.
Mechanism: Small incisions allow removal of gel, blood, and membranes, relieving pulling on the retina.
Retinal Resection
Purpose: To physically remove the angioma when other methods fail.
Mechanism: Surgical excision of the lesion through a small retinal cut, followed by reattachment of the retina.
Subretinal Fluid Drainage
Purpose: To remove fluid under the retina secondary to leaking angiomas.
Mechanism: A tiny tube drains fluid under the retina, allowing it to re-stick to underlying layers.
Transscleral Thermotherapy
Purpose: To heat tumors through the sclera (white coat of the eye).
Mechanism: A probe placed on the sclera heats the underlying angioma, similar to TTT but external.
Subthreshold Micropulse Laser
Purpose: To minimize retinal damage while treating exudation.
Mechanism: Laser delivers very short pulses below the threshold of visible burns, stimulating cell repair.
Scleral Buckling
Purpose: To treat retinal detachments caused by angioma traction.
Mechanism: A silicone band is placed around the eye’s equator, pushing the wall inward to reattach the retina.
Photocoagulation Array Scanning (Pattern Laser)
Purpose: To speed up treatment of multiple small lesions.
Mechanism: A patterned laser array delivers multiple burns in one pulse.
Brachytherapy with Radioactive Seeds
Purpose: To allow flexible placement for tumors of various shapes.
Mechanism: Tiny radioactive seeds implanted near the angioma deliver continuous local radiation.
Enucleation (Last Resort)
Purpose: Removal of the entire eye when tumor threatens life or unbearable pain.
Mechanism: Surgical removal of the eyeball, followed by prosthetic fitting.
Drug Treatments
Medicines can help shrink vessels, reduce swelling, or slow tumor growth. Each drug is listed with its class, typical dose, timing, purpose, how it works, and possible side effects.
Ranibizumab (Lucentis)
Class: Anti-VEGF antibody fragment
Dosage & Timing: 0.5 mg injected into the eye every 4 weeks.
Purpose: Reduce leakage and swelling from tumor vessels.
Mechanism: Blocks vascular endothelial growth factor (VEGF), a protein that fuels new vessel growth PMC.
Side Effects: Eye pain, inflammation, increased eye pressure.
Bevacizumab (Avastin)
Class: Anti-VEGF monoclonal antibody
Dosage & Timing: 1.25 mg intravitreal injection monthly.
Purpose: Similar to ranibizumab at a lower cost.
Mechanism: Binds VEGF to stop new vessels.
Side Effects: Rare inflammation, floaters.
Aflibercept (Eylea)
Class: VEGF trap fusion protein
Dosage & Timing: 2 mg intravitreal every 8 weeks after loading.
Purpose: Longer-acting VEGF inhibition.
Mechanism: Acts as a decoy receptor for VEGF and PlGF.
Side Effects: Mild eye irritation, headache.
Pegaptanib (Macugen)
Class: Anti-VEGF aptamer
Dosage & Timing: 0.3 mg intravitreal every 6 weeks.
Purpose: Early anti-VEGF therapy for angiomas.
Mechanism: Binds VEGF_165 isoform to block angiogenesis.
Side Effects: Conjunctival hemorrhage, vitreous floaters.
Sirolimus (Rapamune)
Class: mTOR inhibitor (anti-proliferative)
Dosage & Timing: 2 mg orally once daily.
Purpose: Slow tumor cell division.
Mechanism: Blocks mTOR pathway to reduce endothelial proliferation PentaVision.
Side Effects: Mouth ulcers, high cholesterol.
Propranolol (Inderal)
Class: Nonselective β-blocker
Dosage & Timing: 40 mg orally twice daily.
Purpose: Off-label use to shrink hemangiomas.
Mechanism: Reduces VEGF production and vasoconstriction PMC.
Side Effects: Low blood pressure, fatigue.
Interferon-α
Class: Immunomodulator
Dosage & Timing: 3 million IU subcutaneously 3 times weekly.
Purpose: Inhibit angioma growth by immune activation.
Mechanism: Stimulates immune cells to attack abnormal vessels.
Side Effects: Flu-like symptoms, low blood counts.
Triamcinolone Acetonide
Class: Corticosteroid
Dosage & Timing: 4 mg intravitreal injection every 3 months.
Purpose: Reduce retinal swelling and exudation.
Mechanism: Anti-inflammatory action decreases vessel permeability.
Side Effects: Increased eye pressure, cataract formation.
Thalidomide
Class: Anti-angiogenic immunomodulator
Dosage & Timing: 100 mg orally once daily.
Purpose: Slow vessel growth in resistant cases.
Mechanism: Inhibits TNF-α and VEGF pathways.
Side Effects: Nerve damage (neuropathy), constipation.
Sunitinib
Class: Multi-targeted tyrosine kinase inhibitor
Dosage & Timing: 50 mg orally once daily, 4 weeks on/2 weeks off.
Purpose: Experimental systemic therapy for VHL-related tumors.
Mechanism: Blocks VEGF receptors and platelet-derived growth factor receptors.
Side Effects: High blood pressure, hand-foot syndrome.
Dietary Molecular & Herbal Supplements
Certain nutrients may support eye health, reduce inflammation, or protect blood vessels. Use these under doctor guidance; dosages are general.
Vitamin A (Retinol) – 5,000 IU/day; supports retinal cell repair by maintaining healthy photoreceptor membranes.
Vitamin C – 500 mg twice daily; antioxidant that protects vessels from damage.
Vitamin E – 400 IU/day; lipid-soluble antioxidant guarding cell membranes.
Zinc – 80 mg/day; cofactor in antioxidant enzymes, supports retinal pigment.
Lutein & Zeaxanthin – 10 mg + 2 mg daily; carotenoids that filter harmful light and reduce oxidative stress.
Omega-3 Fatty Acids (DHA/EPA) – 1 g/day; anti-inflammatory effect stabilizes vessels.
Bilberry Extract – 160 mg twice daily; contains anthocyanins that strengthen capillaries.
Ginkgo Biloba – 120 mg/day; improves microcirculation and prevents vessel leakage.
Curcumin (Turmeric) – 500 mg twice daily; anti-inflammatory and anti-angiogenic properties.
Resveratrol – 250 mg/day; polyphenol that inhibits VEGF expression.
Green Tea Extract (EGCG) – 300 mg/day; antioxidant that reduces new vessel growth.
Astaxanthin – 12 mg/day; powerful antioxidant protecting retina cells.
Coenzyme Q10 – 100 mg twice daily; supports mitochondrial health in retinal cells.
Alpha-Lipoic Acid – 300 mg/day; regenerates other antioxidants and reduces inflammation.
N-Acetylcysteine – 600 mg twice daily; precursor to glutathione, the body’s master antioxidant.
Regenerative & Stem Cell-Based Approaches
Although still experimental, these therapies aim to repair retinal damage and restore function.
hESC-RPE Transplantation
Dose: Transplant of 200,000 retinal pigment epithelium cells.
Function: Replace damaged supporting cells under the retina.
Mechanism: Human embryonic stem cell–derived RPE integrates into retina to nourish photoreceptors BioMed Central.
iPSC-Derived RPE Patch
Dose: Surgical placement of a cell sheet under retina.
Function: Provide structural and metabolic support to photoreceptors.
Mechanism: Induced pluripotent stem cells differentiate into RPE and form a monolayer.
Mesenchymal Stem Cell (MSC) Intravitreal Injection
Dose: 1 × 10^6 cells injected into vitreous cavity.
Function: Secrete growth factors that aid repair.
Mechanism: MSCs release neurotrophic and anti-inflammatory cytokines PMC.
Bone Marrow–Derived CD34+ Cells
Dose: 1 × 10^6 CD34+ cells intravitreal.
Function: Promote blood vessel normalization.
Mechanism: Endothelial progenitor cells help remodel abnormal vessels.
Umbilical Cord MSC (UC-MSC) Intravenous
Dose: 2 × 10^6 cells/kg body weight.
Function: Systemic support for retinal repair.
Mechanism: Homing of MSCs to damaged retina and release of protective factors PMC.
Retinal Progenitor Cell (RPC) Subretinal Injection
Dose: 5 × 10^5 cells delivered under retina.
Function: Replace lost neuronal cells.
Mechanism: Differentiate into photoreceptors and interneurons.
Surgical Procedures
When other treatments fail or complications arise, surgery can directly address structural issues.
Pars Plana Vitrectomy
Procedure: Removal of the eye’s vitreous gel.
Why: To clear hemorrhage or relieve retinal traction from angioma.
Retinal Tumor Resection
Procedure: Microsurgical removal of the angioma through a small retinal incision.
Why: For tumors that resist other therapies and cause ongoing problems.
Transscleral Resection
Procedure: Excision of tumor through the sclera (white of the eye).
Why: When the lesion is located close to the eye wall.
Endoresection
Procedure: Surgical shaving of the tumor from inside the eye.
Why: For lesions not reachable by external resection.
Enucleation
Procedure: Removal of the entire eye.
Why: Last resort when vision cannot be saved or for painful blind eye.
Prevention Strategies
While many angiomas are genetic, these steps may help slow their effects or catch them early:
Genetic Counseling: For families with VHL history.
Regular Eye Exams: Annual dilated fundus exams to spot early lesions.
Blood Pressure Control: High pressure can worsen bleeding.
Smoking Cessation: Smoking damages vessels and increases leak risk.
Healthy Diet: Rich in antioxidants to protect eye cells.
UV Protection: Wear sunglasses to reduce light-related damage.
Maintain Healthy Weight: Obesity can worsen vascular stress.
Manage Diabetes: High blood sugar weakens capillaries.
Limit Alcohol: Excess alcohol promotes inflammation.
Avoid High-Impact Activities: To reduce eye trauma risk.
When to See a Doctor
Seek prompt medical care if you notice any of these signs:
Sudden blurred vision or blind spots.
Floaters (specks moving across your vision).
Flashes of light in peripheral vision.
Distorted or wavy lines (metamorphopsia).
Sudden loss of peripheral vision.
Eye pain or redness.
Family history of VHL or angiomas.
Any new visual disturbance.
Early treatment can preserve sight.
Diet: What to Eat and What to Avoid
Eat:
Leafy greens (spinach, kale) for lutein/zeaxanthin.
Fatty fish (salmon, mackerel) for omega-3s.
Citrus fruits for vitamin C.
Nuts and seeds for vitamin E.
Berries for antioxidants.
Avoid:
Processed foods high in trans fats.
Excessive salt that raises blood pressure.
Sugary drinks that increase inflammation.
Alcohol in excess, which can damage blood vessels.
Foods lacking nutrients (empty calories).
Frequently Asked Questions
What causes retinal angioma?
A genetic mutation in the VHL gene or, less often, spontaneous vessel growth without genetics JAMA Network.Can retinal angioma turn into cancer?
No. It is benign but can still harm vision by leaking or pulling the retina.How is retinal angioma diagnosed?
Eye exam with fundus photography and fluorescein angiography (dye test) shows the lesion.Is treatment always needed?
Small, non-leaking lesions can be watched. Treatment is for leaking, growing, or vision-threatening tumors aapos.org.Can laser cure it?
Laser photocoagulation can shrink small angiomas and seal leaking vessels.What are the risks of cryotherapy?
Possible swelling, bleeding, or damage to nearby healthy retina.Are injections safe?
Anti-VEGF injections carry small infection risk but often reduce edema and vision loss PMC.Can supplements alone treat it?
Supplements support eye health but cannot replace medical or surgical treatment.Does diet really matter?
A nutrient-rich diet keeps blood vessels healthy and may slow disease progression.Is stem cell therapy approved?
Not yet; still in clinical trials, with safety and efficacy under study BioMed Central.Can retinal angioma recur after treatment?
Yes. Regular follow-up is essential to catch new or returning lesions.Does everyone with VHL get retinal angiomas?
About 50–60% of VHL patients develop retinal angiomas during their lifetime.Can vision fully recover?
Early treatment often preserves vision; damage from chronic edema or detachment may be permanent.How often should I have eye exams?
At least once a year, or more often if you have known lesions or VHL.Are there gene therapies?
Research is underway, but no approved gene therapy exists yet for retinal angioma.
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.
