A circumscribed choroidal hemangioma is a benign (non-cancerous) blood-vessel tumor that grows inside the choroid, the spongy, vascular layer underneath your retina (the “film” at the back of the eye).
“Circumscribed” means the tumor is well-outlined and round/oval, usually like a small orange-red mound on eye exam. Unlike cancers, it does not spread to other parts of the body. The main problem is that it leaks fluid and can lift or swell the retina (serous retinal detachment and/or macular edema). That fluid—not the tumor itself—is what blurs vision, causes distortion (straight lines look wavy), or reduces contrast and color clarity.
Most CCHs are present from birth but only get noticed in young or middle adulthood when fluid starts to build. They’re different from diffuse choroidal hemangiomas (which are broader, often linked to Sturge-Weber syndrome). Here we focus on circumscribed ones.
The choroid feeds the retina. A CCH has abnormal, thin-walled vessels that leak. That leakage creates subretinal fluid and macular edema. The retina works best when dry and flat; fluid makes the light-sensing cells misfire, so you notice blur, gray patches, or distortion.
A circumscribed choroidal hemangioma (CCH) is a benign (non-cancerous) lump made of blood vessels that sits inside the choroid, the spongy, blood-rich layer under your retina (the “film” at the back of the eye). “Circumscribed” means the tumor is well-defined and localized—a single, round or dome-shaped spot rather than a large sheet. On eye exam it often looks orange-red and usually lies behind the center of vision (the macula) or nearby. It tends to be solitary (one eye, one lesion). The tumor itself is harmless, but it can leak fluid under the retina and cause vision problems if it sits near the center of sight or starts to ooze. (Key clinical descriptions summarized from major reviews and practice articles. PMCLippincott Journals)
Think of the choroid as a dense garden of tiny blood vessels that feeds the retina. In CCH, a small patch of those vessels overgrows and packs together more than usual—like a bunch of grapes under the retina. The overgrown vessels have thin, leaky walls, so fluid can seep out, collecting under the retina (subretinal fluid), which blurs or distorts vision. The tumor usually does not spread to other parts of the body and does not turn into cancer.
Most people only discover a CCH when changes in vision appear—commonly blur, wavy lines, or a dark/gray spot in central sight. The tumor may be quiet for years and then starts leaking, especially if it’s close to the macula. The good news: once correctly identified, the lesion is treatable if it’s causing vision loss (for example, with targeted light-based therapy). Diagnosis usually relies on its very typical look on imaging tests (see the “Diagnostic tests” section). (Clinical presentation and typical location summarized from ophthalmology reviews. Lippincott Journals)
Types
CCH itself is one type of choroidal hemangioma (the other big category is diffuse hemangioma, usually linked to Sturge–Weber syndrome, which is not what we’re discussing here). Within circumscribed lesions, eye doctors often describe “types” in practical ways that affect symptoms and testing:
By location to the fovea (center of sharp vision)
Subfoveal: sitting right under the center—most likely to blur central vision.
Juxtafoveal: near the center—can still distort vision.
Extrafoveal: off to the side—may cause fewer symptoms unless leaking widely.
By activity (“quiet” vs “leaky”)
Inactive (dry): the lump is there but no fluid is seen under the retina; vision may be normal.
Active (with subretinal fluid): fluid pockets appear; vision often drops or looks wavy.
By apparent shape on imaging
Dome-shaped: the classic smooth hill-like bump.
Broader/flat-topped: still well-outlined but flatter, sometimes harder to spot without imaging.
By visibility on routine exam
Obvious clinical lesion: clearly orange-red on dilated exam.
Subtle/“masked” lesion: color blends with the fundus; imaging (like OCT or angiography) is key to prove it.
These “types” are descriptive—they help explain symptoms and guide testing—but they’re all the same underlying benign vascular tumor.
Causes
Important truth first: doctors believe CCH is a developmental vascular anomaly—basically a localized birth-time quirk in the choroid’s blood vessels. We do not know a single, proven “cause” like an infection or a behavior. So below are the best-understood base causes plus factors that likely influence when/why a CCH shows up or starts leaking. Think of #1 as the core cause; the rest are contributors/triggers/associations rather than hard causes.
Developmental vascular overgrowth (core cause)
A small area of choroidal vessels overdevelops early in life, forming a compact, benign hamartoma (a tissue that grows in a disorganized but non-cancerous way).Local vessel wall weakness
The tiny channels inside the tumor often have thin, leaky walls, making fluid seepage more likely over time.Abnormal choroidal blood flow
Slight flow imbalances (e.g., venous congestion) in that spot can increase pressure and promote leakage.Aging of the retinal pigment epithelium (RPE)
As the RPE (the retina’s support layer) thins with age, it becomes less efficient at pumping out fluid, so leakage near a CCH is more noticeable.Proximity to the fovea
Lesions near the center are noticed earlier because even small amounts of fluid hurt central vision.Spikes in blood pressure
Sudden or chronic high blood pressure may increase leakage from already fragile tumor vessels.Hormonal shifts
Pregnancy and other hormonal changes can temporarily increase vascular leakiness, making CCH more symptomatic.Inflammation in or around the eye
Local inflammation can destabilize blood vessel walls, tipping a quiet CCH into leak mode.Vigorous Valsalva/venous pressure swings
Heavy lifting/straining briefly raises venous pressure, which can worsen seepage in a fragile patch.Choroidal thickness changes
People with naturally thicker choroids may have higher baseline choroidal pressure, stressing weak vessels.Minor, unnoticed trauma
A small bump to the eye won’t create a CCH, but it might trigger leakage in an existing one.Systemic fluid retention
Conditions or medicines that retain fluid (e.g., some steroids) can tip the balance toward more subretinal fluid.Sunlight/oxidative stress (indirect)
Long-term light exposure and oxidation can age the RPE, reducing fluid-clearing capacity overlying a CCH.Poor sleep/apnea (indirect)
Repeated oxygen dips may stress vessels and the RPE pump, making leakage more likely to show.High altitude exposure (temporary)
Hypoxia and pressure changes could transiently increase choroidal congestion and fluid.Dehydration/overhydration swings
Large fluid balance changes can shift choroidal volume and leakage patterns.Coexisting retinal diseases
Other macular problems (e.g., epiretinal membrane) may magnify distortion from a small fluid pocket.Genetic background (nonspecific)
While no single gene explains CCH, genetic differences likely influence how choroidal vessels form in that spot.Metabolic health
Diabetes, lipid disorders, or obesity can affect vessel health and RPE function, nudging leakage.Time
Even a quiet CCH can change slowly—tiny vessels remodel, and the RPE tires—so leakage can appear years later.
Bottom line: #1 is the main cause; the others are modifiers that may unmask or worsen a pre-existing, benign vascular patch.
Symptoms
Blurred central vision – Fluid under the macula softens focus like moisture under wallpaper.
Metamorphopsia (wavy lines) – Straight lines look wavy/bent because the retina is slightly lifted.
Micropsia or macropsia – Things look smaller or larger because the retinal image is stretched.
Central gray/dim spot (scotoma) – A patch of missing/weak vision where the retina is most lifted.
Reduced contrast sensitivity – Fine details and shades of gray become harder to see.
Color fading – Colors, especially reds, can look washed out when the macula is affected.
Visual fatigue – Reading or close work tires the eyes faster due to subtle distortion.
Difficulty reading small print – Letters blur or double from macular fluid.
Glare sensitivity – Bright lights wash out detail more than before.
Worse vision on waking – Overnight fluid shifts can temporarily increase macular swelling.
Improved vision after a while upright – Sitting/standing lets fluid redistribute, sometimes sharpening sight.
Peripheral vision generally fine – Unless the tumor is farther out, side vision is often normal.
Floaters usually unrelated – Floaters are common in many people; CCH doesn’t usually cause them directly.
No pain – CCH doesn’t hurt; pain suggests another problem.
Slow change – Symptoms often creep in over weeks to months, not overnight (unless leakage surges).
Diagnostic tests
Big idea: doctors confirm CCH by looking at the back of the eye and by imaging how the lesion and its blood vessels behave. CCH has a very recognizable pattern on several tests.
A) Physical exam
History and symptom mapping – When vision got blurry, which tasks are hard, whether lines look wavy—this targets the macula as the trouble spot.
Best-corrected visual acuity – Standard eye chart with the best glasses correction shows how much central vision is affected.
Amsler grid – A square grid you view at reading distance; wavy/missing boxes point to macular swelling.
Color vision and contrast checks – Simple book/chart tests show subtle macular dysfunction from fluid.
B) Manual/clinical tests at the slit lamp
Dilated fundus exam with slit-lamp + special lens – The doctor examines the retina with a 90D/78D lens: a CCH often looks like a smooth, orange-red, dome-shaped mound, sometimes with shiny fluid tracking away from it. (Typical appearance summarized from clinical reviews. PMC)
Indirect ophthalmoscopy – A head-mounted light and lens give a wide view to see the lesion’s edges and any retinal detachment.
Manual perimetry (Goldmann) – A slow, careful mapping of visual field picks up central or paracentral dips that match the lesion’s location.
Contact lens biomicroscopy/3-mirror – Lets the doctor hover over the lesion optically to judge height and borders more precisely.
C) Lab & pathological tests
No routine blood tests – CCH is not an infection or systemic cancer; labs aren’t usually needed unless another diagnosis is suspected.
Biopsy (rare) – Because CCH has very typical imaging, a biopsy is almost never needed; it’s considered only in very atypical cases where melanoma or metastasis cannot be ruled out otherwise.
D) Electrodiagnostic tests
Full-field ERG (electroretinogram) – Measures the retina’s overall electrical response; often normal or only mildly changed because CCH is localized.
Multifocal ERG (mfERG) – Maps local retinal function; can show reduced signals over the macula where fluid collects.
EOG (electro-oculogram) – Looks at RPE function; can be slightly abnormal if the RPE pump is stressed by chronic fluid.
VEP (visual evoked potentials) – Checks the visual pathway to the brain; usually normal, helping rule out nerve pathway problems when vision is down.
E) Imaging tests
Optical Coherence Tomography (OCT) – A non-contact scan that shows a cross-section of retina and choroid. In CCH it typically shows a smooth, dome-shaped elevation under the retina and pockets of subretinal fluid; enhanced-depth OCT can show choroidal details. (Key OCT features supported by ophthalmic literature. canadianjournalofophthalmology.ca)
Fundus Fluorescein Angiography (FA/FFA) – A small dye injection with serial photos. CCH usually shows early and persistent brightness (hyperfluorescence) and leakage into surrounding tissue in later frames—evidence of leaky vessels. (Angiographic patterns summarized from reviews. PMC)
Indocyanine Green Angiography (ICGA/ICG) – A deeper-choroid dye test. Classic CCH shows rapid early filling and a “late washout” pattern (it looks bright early and then less bright later compared to surrounding choroid). This signature pattern helps separate CCH from other tumors. (ICG early hyperfluorescence and late washout are widely reported. Retina TodayLippincott JournalsPMC)
B-scan ultrasonography (with A-scan reflectivity) – An eye ultrasound shows a solid, dome-shaped mass with high internal reflectivity (bright echoes), unlike melanoma which often looks hollow/darker. This difference is very helpful in diagnosis. (Ultrasound reflectivity differences and dome shape documented in reviews. PMC)
Fundus autofluorescence (FAF) – A blue-light photo that highlights lipofuscin and RPE changes. Over a CCH you may see bright or dark patterns that track fluid or RPE stress. (FAF patterns over CCH summarized in clinical series. Lippincott Journals)
MRI of the orbits (selected cases) – Not routine, but helpful when melanoma/metastasis is a concern. CCH often appears hyperintense on T1 relative to vitreous and shows strong contrast enhancement; T2 can be iso- to hyperintense. These features support CCH over melanoma in the right context. (MRI signal characteristics reported in radiology references and series. RadiopaediaBMJ Blogs)
Non-pharmacological treatments
Plain truth: Only procedures (like PDT, laser, or radiation) dry the retina reliably by sealing/shrinking leaky tumor vessels. The items below help with safety, monitoring, and day-to-day vision, but they don’t remove the tumor.
Watchful waiting with structured follow-up
If your tumor is small, away from the macula, and not causing fluid/vision loss, your doctor may monitor with scheduled checks (exam + OCT ± ultrasound). Purpose: avoid overtreatment while catching any fluid early. Mechanism: careful observation; treat if/when leakage threatens vision.Scheduled OCT/OCT-A imaging
Regular OCT scans map retinal thickness and fluid. OCT-A shows flow patterns. Purpose: detect even tiny recurrences. Mechanism: non-contact light scanning.B-scan ultrasonography
Ultrasound confirms the lesion’s dome shape and internal reflectivity and tracks stability. Purpose: objective baseline and follow-up. Mechanism: sound waves.Low-vision rehabilitation
If vision is reduced, specially trained therapists tailor magnification, contrast tools, and reading strategies. Purpose: maximize remaining vision. Mechanism: optical aids + training.Task lighting and contrast optimization
Brighter, glare-free lighting and high-contrast materials make reading/close work easier. Purpose: better function despite mild blur. Mechanism: boosts signal-to-noise for the retina.Tinted filters/anti-glare lenses
Amber/yellow filters can improve contrast; polarized sunglasses reduce outdoor glare. Purpose: comfort and clarity. Mechanism: cut scattered light and blue haze.Electronic magnifiers/apps
Handheld video magnifiers or phone apps enlarge text and adjust contrast. Purpose: easier reading. Mechanism: digital enlargement.Amsler grid self-checks
Weekly checks at home to spot new distortion or blind spots early. Purpose: prompt clinic visit if change appears. Mechanism: simple square grid test.Driving safety counseling
If vision dips, discuss driving rules and alternatives. Purpose: safety for you and others. Mechanism: legal/functional guidance.Smoking cessation
Smoking worsens vascular leak and delays recovery in many eye diseases. Purpose: support retinal health. Mechanism: reduces oxidative and vascular stress.Blood pressure control
High BP stresses fragile tumor vessels. Purpose: minimize leakage risk. Mechanism: steadier choroidal perfusion.Sleep apnea screening & treatment
Sleep apnea can thicken the choroid and worsen fluid in some retinal disorders. Purpose: steadier oxygenation and perfusion. Mechanism: CPAP or other therapy reduces nocturnal hypoxia.Diabetes optimization (if present)
High glucose harms retinal barriers. Purpose: less edema-prone retina. Mechanism: glycemic control.Hydration and salt sense
Extreme high-salt diets can favor fluid retention. Purpose: avoid systemic fluid shifts that might aggravate edema. Mechanism: common-sense balance; not a cure.Careful use of blood thinners (only if medically indicated)
Do not stop prescribed anticoagulants without your physician. But if you take them without a clear need, discuss risk/benefit with your doctor. Purpose: avoid unnecessary bleeding risk. Mechanism: medication review.Protective eyewear for sports/at-risk jobs
Trauma can worsen retinal problems. Purpose: protect the eye. Mechanism: impact protection.Psychological support
Vision changes can be stressful. Purpose: reduce anxiety and improve adherence. Mechanism: counseling or peer groups.Workplace/reading ergonomics
Larger monitors, bigger fonts, and correct screen distance. Purpose: reduce eye strain. Mechanism: ergonomic adjustment.Head-of-bed elevation during acute fluid episodes
Some people feel less morning blur with slight head elevation. Purpose: comfort; evidence limited. Mechanism: venous outflow position.Sunlight discipline after PDT (anticipatory counseling)
If PDT is planned, you’ll need 48 hours of strict light protection after the infusion. Purpose: prevent whole-body photosensitivity reactions. Mechanism: limits activation of the photosensitizer outside the eye.
Drug treatments
Key idea: PDT with verteporfin is the best-studied definitive option for many vision-threatening cases, but it is a drug-plus-light procedure. Anti-VEGF and steroid injections are often adjuncts that dry the fluid; they usually do not shrink the tumor itself.
Safety note: All dosing below is typical, off-label in CCH unless noted, and must be individualized by your retina/ocular oncology specialist.
Verteporfin (photosensitizer used for PDT)
Class: Photosensitizing drug for photodynamic therapy.
Typical dose/time: 6 mg/m² IV over ~10 minutes; laser activation (689 nm) follows per protocol in clinic.
Purpose: Primary treatment to seal/close abnormal tumor vessels and dry the retina.
Mechanism: Verteporfin is activated by a specific laser wavelength, creating reactive oxygen species that damage leaky vascular endothelium → thrombosis of the tumor’s vessels while largely sparing normal retina.
Key side effects/precautions: Whole-body photosensitivity for ~48 hours (avoid sun/bright indoor light), infusion-site pain, back pain during infusion (rare), transient vision changes.Bevacizumab (intravitreal, 1.25 mg)
Class: Anti-VEGF monoclonal antibody.
Schedule: Injection into the eye; often monthly x1–3, then as needed.
Purpose: Reduce subretinal/intraretinal fluid; may improve vision short-term or as an adjunct to PDT.
Mechanism: Neutralizes VEGF, reducing vascular permeability.
Key risks: Rare endophthalmitis, transient IOP spike, small risk of retinal tear/detachment; systemic vascular events are rare with ocular dosing.Ranibizumab (intravitreal, 0.5 mg)
Class: Anti-VEGF Fab.
Schedule: Similar to bevacizumab.
Purpose/mechanism/risks: As above; sometimes chosen for regulatory/pharmacy reasons.Aflibercept (intravitreal, 2 mg)
Class: VEGF-trap fusion protein.
Schedule: Injection, often q4–8 weeks initially; tailored to response.
Purpose: Dry the retina; may work in cases not responding to other anti-VEGF agents.
Mechanism: Binds VEGF-A, VEGF-B, and PlGF, reducing leak.
Key risks: Same injection-related risks as above.Triamcinolone acetonide (intravitreal, ~4 mg)
Class: Corticosteroid.
Purpose: Reduce macular edema; sometimes used when PDT/anti-VEGF are insufficient.
Mechanism: Suppresses inflammation and vascular permeability.
Key risks: Cataract progression, steroid-induced ocular hypertension/glaucoma, injection risks.Dexamethasone implant (0.7 mg, “Ozurdex®”)
Class: Sustained-release corticosteroid implant.
Duration: Often 2–4+ months of effect.
Purpose: Longer-lasting edema control when recurrent fluid limits vision.
Mechanism: Local steroid release → stabilizes blood–retina barrier.
Key risks: IOP rise, cataract with repeated use; injection risks.Acetazolamide (oral, 250–500 mg 1–2× daily)
Class: Carbonic anhydrase inhibitor (systemic).
Purpose: Sometimes reduces retinal edema; supportive, not definitive.
Mechanism: Alters fluid transport across retinal pigment epithelium (RPE), promoting fluid resorption.
Key side effects: Tingling in fingers/toes, metallic taste, fatigue, kidney stones, low potassium; avoid in sulfa allergy; caution in pregnancy and kidney disease.Dorzolamide 2% (topical, 1 drop 2–3× daily)
Class: Carbonic anhydrase inhibitor (eye drop).
Purpose: Modest help for cystoid edema in some cases.
Mechanism: Similar to acetazolamide but topical.
Key side effects: Eye irritation, bitter taste; rare allergy.Topical NSAID (e.g., nepafenac 0.1% 3× daily or bromfenac 0.09% 1–2× daily)
Class: Non-steroidal anti-inflammatory (ocular).
Purpose: Supportive option for mild cystoid edema or to maintain dryness after a definitive procedure.
Mechanism: Blocks COX → fewer prostaglandins → less vascular leak.
Key side effects: Surface irritation; very rare corneal complications with prolonged use.Propranolol (oral; adult starting 20–40 mg 2–3× daily; pediatric by mg/kg/day)
Class: Non-selective beta-blocker.
Purpose: Experimental in CCH (well-established for infantile skin hemangiomas). May reduce vascular activity in selected, carefully monitored cases.
Mechanism: Vasoconstriction, anti-angiogenic signaling.
Key cautions: Not routine for CCH; avoid in asthma, severe bradycardia/heart block; monitor BP/HR; dizziness/fatigue common.
Reality check: In most vision-threatening CCH, your specialist will discuss PDT first, and may add anti-VEGF or a steroid if fluid is stubborn or recurs.
Dietary, molecular, and herbal supplements
(Supportive only. None of these shrink the tumor. Always tell your ophthalmologist what you take; several interact with blood thinners or affect surgery/procedures.)
Lutein (10–20 mg/day) — Carotenoid that concentrates in the macula; supports antioxidant defense and contrast sensitivity.
Zeaxanthin (2–10 mg/day) — Works with lutein; filters blue light and supports macular pigment.
Omega-3s (EPA+DHA ≥1 g/day) — May support retinal cell membranes and anti-inflammatory balance.
Vitamin C (≈500 mg/day) — Antioxidant supporting collagen and vascular walls.
Vitamin E (≈400 IU/day) — Antioxidant; avoid high doses if on anticoagulants or before eye procedures.
Zinc (25–80 mg elemental/day) + Copper (2 mg/day) — Cofactors in antioxidant enzymes; do not exceed without medical advice.
Bilberry extract (80–160 mg, 1–2×/day) — Anthocyanins may aid night/contrast vision; evidence modest.
Saffron (20–30 mg/day standardized crocin/crocetin) — Small studies show retinal functional support in other diseases; supportive only.
Curcumin (500–1000 mg/day; enhanced bioavailability) — Anti-inflammatory signaling; may slightly reduce edema tendency.
Resveratrol (150–250 mg/day) — Antioxidant/vasoactive; bleeding risk with warfarin/antiplatelets.
Coenzyme Q10 (100–200 mg/day) — Mitochondrial support; safe adjunct.
Taurine (500–1000 mg/day) — Important amino sulfonic acid in retina; supportive only.
Green tea catechins (EGCG 150–300 mg/day or 1–2 cups/day) — Antioxidant; avoid late evening (caffeine).
Grape seed extract / Pycnogenol (50–150 mg/day) — Flavonoids that may reduce capillary leak; bleeding caution.
Multicolor produce pattern (dietary, not a pill) — Leafy greens, orange/yellow veggies, berries, and citrus provide a broad antioxidant mix naturally.
Again: these do not treat the tumor. Think of them as retina-friendly habits while definitive eye therapy does the heavy lifting.
Regenerative / stem-cell drugs” — what’s real today?
There are no approved immune, regenerative, or stem-cell drugs for CCH. Below are research concepts you might see in headlines; they are not standard care for CCH:
RPE cell therapy (transplant) — Experimental for advanced macular degeneration, not CCH. No approved dosing.
Photoreceptor progenitor cells — Early research; aim to replace lost cells; not for fluid from CCH.
Mesenchymal stem cell injections — Investigational; safety/efficacy concerns; not recommended outside trials.
Gene therapy delivering anti-VEGF — Being tested for other retinal diseases; no approved CCH indication.
Sustained in-eye biologic expression (e.g., RGX-314/ADVM-022-like approaches) — For AMD/DR; not tested/approved for CCH.
mTOR/other pathway inhibitors — Hypothetical for vascular tumors; no clinical standard in CCH.
Bottom line: If someone markets “stem-cell cures” for CCH, be skeptical and ask your retina oncologist.
Procedures / “surgeries”
Many of these are clinic-based laser/light/radiation procedures, not cuts/sutures. Your team chooses based on tumor location, size, and macular involvement.
Photodynamic Therapy (PDT) with verteporfin
Procedure: IV verteporfin → precisely targeted 689 nm laser to the tumor.
Why it’s done: It’s the go-to for subfoveal/juxtafoveal CCH with fluid; it dries the retina and often preserves or improves vision with relatively low collateral damage.Transpupillary Thermotherapy (TTT)
Procedure: 810 nm diode laser delivers gentle heat to the tumor.
Why: Useful for extrafoveal lesions; can reduce leakage. It’s less selective than PDT and used more selectively today.Focal/Confluent Laser Photocoagulation (argon/green)
Procedure: Thermal laser spots to the tumor surface.
Why: Historically used, still considered for well-outside-the-fovea lesions. Risk of scotoma if near the macula, so it’s not used there.Plaque Brachytherapy (I-125 or Ru-106)
Procedure: A small radioactive “plaque” is sutured to the outside of the eye over the tumor for a set time, then removed.
Why: For refractory CCH not responding to PDT/laser, or for larger lesions. Can control fluid; carries radiation risks (e.g., radiation retinopathy) that are carefully weighed.Proton Beam Radiotherapy
Procedure: Highly targeted external radiation delivered in a few sessions.
Why: An option for large or resistant tumors when other methods are unsuitable.
Prevention tips
You can’t prevent being born with a CCH, but you can reduce the chance of vision damage:
Keep scheduled follow-ups (exam + OCT).
Report new symptoms early (distortion, gray patch, sudden blur).
Treat promptly when fluid threatens the macula.
Don’t smoke.
Control blood pressure and manage diabetes if present.
Treat sleep apnea if you have it.
Use sunglasses outdoors to reduce glare/strain.
Avoid unnecessary anticoagulants/supplements that thin blood (only with your doctor’s guidance).
Protect eyes during sports/at-risk work.
Adhere to post-procedure instructions (especially light protection after PDT).
When to see a doctor
New or worsening blur, wavy lines, or a gray/black spot in your central vision.
Sudden drop in vision in one eye.
New floaters/flashes or a curtain in your vision (possible retinal tear/detachment—urgent).
After PDT, any severe pain, marked light reaction, or a red, painful eye after any injection.
If you’re pregnant or planning pregnancy and need treatment—tell your retina specialist to adjust timing/choices.
H) What to eat and what to avoid
Eat more of:
Leafy greens (spinach, kale) for lutein/zeaxanthin.
Oily fish (salmon, sardines, mackerel) 2×/week for omega-3s.
Colorful vegetables & berries (carrots, oranges, bell peppers, blueberries) for broad antioxidants.
Nuts/legumes/whole grains for minerals and steady energy.
Citrus & kiwifruit for vitamin C.
Adequate water for general hydration.
Go easy on / avoid:
Very salty, ultra-processed foods (can worsen general fluid retention).
Trans fats and excessive fried foods (vascular stress).
Excess alcohol (healing/medication interactions).
Mega-doses of single vitamins/herbals without your doctor’s okay (interaction/bleeding risks, especially around procedures).
Smoking/vaping (hurts retinal perfusion).
Frequently asked questions
1) Is CCH a cancer?
No. It’s benign. It does not metastasize. The main issue is leaky fluid affecting vision.
2) Will it keep growing?
Most CCHs are relatively stable in size; what changes over time is leakiness. Treatments aim to shut down leakage.
3) Can it go away by itself?
The tumor remains, but fluid can wax and wane. If the macula is threatened, treatment is recommended to protect vision.
4) What is the best treatment?
For many macula-involving cases, PDT with verteporfin is first choice because it’s effective and selective. Your situation (size, location, prior treatment) may point to another option.
5) Do anti-VEGF injections cure it?
They often dry fluid and improve vision short-term, but they usually don’t shrink the tumor. They are adjuncts or bridges.
6) What happens during PDT?
You get an IV infusion of verteporfin, then a targeted laser shines onto the tumor to activate the drug only there. You then follow strict light-avoidance for about 48 hours.
7) How soon will vision improve?
If fluid clears, people often notice improvement over days to weeks; full stabilization may take 1–3 months. Some changes (like long-standing macular damage) may be only partly reversible.
8) Can I need more than one treatment?
Yes. Recurrences can happen. Your doctor may repeat PDT, switch to another laser/radiation, or add injections.
9) Is treatment painful?
In-office lasers and injections use numbing drops; most patients feel pressure, not pain. Radiation options involve anesthesia for plaque placement.
10) Will glasses fix my vision?
Glasses help refractive blur, but they can’t remove retinal fluid. Drying the retina is key; after that, glasses or low-vision aids can fine-tune clarity.
11) Is the other eye at risk?
CCH is usually unilateral. The other eye is monitored, but risk is low.
12) Can I fly or exercise?
Yes, typically safe. After certain procedures (e.g., specific gases used in other eye surgeries) flying may be restricted—but that’s not typical for CCH treatments.
13) What about pregnancy?
Tell your specialist. Some drugs and procedures (e.g., verteporfin, certain injections) may be timed or modified during pregnancy.
14) Will insurance cover it?
Vision-threatening CCH treatments are generally considered medically necessary; coverage varies by country/plan. Your clinic will help pre-authorize.
15) What if I do nothing?
Some lesions stay quiet, but macular fluid can damage vision over time. Regular monitoring is essential so you can treat before permanent harm.
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.
