Coats’ disease is a rare eye condition where some of the tiny blood vessels in the retina (the “film” at the back of the eye that senses light) are abnormal, fragile, and leaky. Because they leak, fatty fluid and cholesterol collect in and under the retina. This buildup can blur vision and, in more serious cases, lift the retina off the back wall (an exudative retinal detachment). The core features doctors look for are retinal telangiectasia (twisted, dilated, “telangiectatic” vessels), micro-aneurysms, and yellow-white “hard” exudates in the retina. Most of the time only one eye is affected. In children, it’s more common in boys; adults can get it too, but that’s less common. The exact cause is unknown. NCBIGenetic & Rare Diseases Info Center
Coats’ disease is a rare eye condition where tiny blood vessels in the retina (the light-sensing tissue at the back of the eye) grow abnormally, become twisted and ballooned (telangiectasia and small aneurysms), and leak fluid and fats (lipids). That leakage soaks the retina, creates yellow “hard exudates,” and can lift the retina off the eye wall (an exudative retinal detachment) if the fluid builds up. It usually affects one eye and is more common in boys, often starting in childhood. It is not typically inherited. The main problem is the leaky vessels, not a tumor. Doctors treat the leaky spots and try to dry the retina so vision can be protected. EyeWiki
Pathology
Think of the retinal circulation like a neatly woven net. In Coats’, parts of that net are poorly built: the vessel walls are weak and lose their tight, waterproof seal (the blood–retina barrier). Fluid and cholesterol-rich particles seep out into the retina (like a slow leak through a thin garden hose). Over time:
Yellow deposits (hard exudates) collect around the leaky areas.
Fluid pockets (cysts) form within the retina.
If leakage is heavy or long-lasting, fluid collects under the retina, lifting it up (exudative retinal detachment).
The body tries to clean up the mess with immune cells, which can leave scars and traction that further distort the retina. NCBI
How doctors describe disease severity
Clinicians often use the Shields classification to stage Coats’ disease from mild to very advanced:
Stage 1: Abnormal (telangiectatic) vessels only.
Stage 2: Vessels plus exudation (2A extrafoveal; 2B involving the fovea).
Stage 3: Exudative retinal detachment (3A subtotal; 3B total).
Stage 4: Total detachment with secondary glaucoma.
Stage 5: End-stage, often a blind/painful eye. PubMed
This staging is practical: early stages often keep vision good with timely treatment; late stages have a higher risk of severe, permanent vision loss. PubMed
“Types” of Coats’ disease
There isn’t a strict, universally agreed “type 1, type 2…” system for Coats’ the way some diseases have. But in everyday practice, doctors talk about patterns that help set expectations:
Classic childhood Coats’ disease.
The common pattern: a boy with one eye affected, showing telangiectasia and yellow exudates in the peripheral retina. Progression can be slow or step-wise; careful follow-up is crucial. AAOAdult-onset Coats’ disease.
Same process, but showing up later. It often progresses more slowly and sometimes responds well to focused treatment of the leaky areas. PMCPosterior (macular) variant.
Some patients show macula-centered telangiectasia/exudation early, which more directly threatens central vision even if the overall area involved is small.Bilateral Coats’ (rare).
True both-eye Coats’ is uncommon. When both eyes look “Coats-like,” doctors are careful to rule out other conditions that can mimic Coats’. Genetic & Rare Diseases Info CenterCoats-like retinopathy (mimics, not true Coats’).
A “Coats-like” picture can appear in other diseases (for example, some inherited retinal diseases or inflammatory/vascular problems). These are not true Coats’ but can look similar on exam, so the label prompts a thorough check for masqueraders (like retinoblastoma in a child with a white pupil). NCBI
Causes
Doctors do not know the root cause of Coats’ disease. It is sporadic and not inherited in the great majority of cases. What we do know is how it behaves—and we can list key processes and contributors that cause the leakage and damage inside the eye. Think of the items below as disease drivers and worseners, not proven genetic causes. Genetic & Rare Diseases Info Center
Abnormally formed tiny retinal vessels (telangiectasia).
These are structurally weak and tend to leak fluid and lipids, setting everything else in motion. NCBILoss of the blood–retina barrier.
Normally, vessel walls are “watertight.” In Coats’, that seal is broken, so fluid seeps into the retina. NCBIMicro-aneurysms.
Outpouchings along vessels act like tiny sacs that ooze fluid into retinal layers. NCBICapillary non-perfusion (areas that don’t get blood).
Poor flow around abnormal vessels causes local low oxygen, which can increase leakiness.Local retinal hypoxia.
Low oxygen levels “tell” blood vessels to leak more and grow abnormally.VEGF signaling (a leakage/growth signal).
Hypoxic retina can elevate VEGF, a factor that increases leakage and abnormal vessel behavior.Pericyte loss.
Pericytes are “support cells” wrapped around capillaries; when they are scarce, capillaries become fragile and leaky.Endothelial dysfunction.
The inner lining cells of blood vessels (endothelium) don’t hold tight junctions well in Coats’, so fluid escapes.Cholesterol-rich exudation.
Lipid-heavy fluid collects and becomes hard exudates, which damage and “poison” nearby retinal cells.Retinal cysts and edema.
Chronic leakage forms fluid pockets that disrupt the precise alignment of light-sensing cells.Subretinal fluid accumulation.
Enough leakage lifts the retina, causing exudative detachment and sudden drops in vision. NCBIInflammatory clean-up response.
As the body tries to mop up fat and fluid, immune cells arrive and can leave scarring behind.Formation of fibrous tissue.
Scarring can tug on the retina (traction), worsening distortion.Vitreous changes.
The gel in the eye (vitreous) can pull on leaky areas or carry exudates more centrally.Macular involvement.
Leakage that reaches the fovea directly blurs fine central vision.Secondary glaucoma (late).
In advanced disease, the eye’s pressure can rise, adding pain and optic nerve damage. PubMedCataract (late).
Chronic inflammation and treatments can cloud the lens, further reducing vision. Genetic & Rare Diseases Info CenterVitreous hemorrhage (sometimes).
Fragile vessels can bleed into the eye’s gel, suddenly clouding vision.Amblyopia in children.
When one eye is blurry for months, the brain “turns it down,” creating “lazy eye,” which can persist without treatment.Delay in diagnosis.
Because Coats’ can be painless and one-sided, kids may not complain; late detection allows more damage to build up.
Symptoms and signs
Blurry or reduced vision in one eye.
The commonest complaint. Leaked fluid and exudates scatter light and blur the image reaching the brain. Genetic & Rare Diseases Info CenterLeukocoria (“white pupil”) in photos.
Parents may notice a white glow instead of a red reflex in flash photos—an urgent reason to see an eye doctor because retinoblastoma can look similar. NCBIStrabismus (“eye turn” or crossed eye).
When one eye sees poorly, it may drift inward or outward. Genetic & Rare Diseases Info CenterLoss of side (peripheral) vision.
Peripheral fluid/exudates can chew away at the visual field long before central vision drops.Distorted or wavy lines (metamorphopsia).
Swollen or scarred macula bends straight lines.Dark spot or missing patch in vision (scotoma).
A cluster of exudates or a small detachment can make a “blank” area.Poor night or dim-light vision.
Edema and exudates reduce the retina’s sensitivity in low light.Color fading (desaturation).
Macular involvement washes out colors, making them look less vivid.Floaters or flashes.
Bleeding or vitreous traction can create moving specks or brief light flashes.Sudden big drop in vision.
If the retina detaches exudatively, vision can fall rapidly (like a shade coming down).Eye redness or irritation.
Usually mild or absent—Coats’ is often painless—but late complications can make the eye red.Eye pain (late).
High pressure (secondary glaucoma) in advanced disease can be painful. PubMedNystagmus (rare).
Rapid, small eye movements can appear in severe, early, one-eye vision loss during infancy.Head tilt or closing one eye.
Kids may try to “optically” improve vision by tilting the head or shutting the bad eye.School performance issues.
Subtle one-eye vision loss can show up as trouble reading or copying from a board.
Diagnostic tests
A) Physical exam
History and visual behavior observation.
The exam starts with simple questions: When did you notice a white pupil in photos? Any eye turn? Does the child prefer one eye? In small children, how they fixate and follow is a crucial “test.”Visual acuity testing (age-appropriate).
Older kids read a chart; younger ones match pictures or symbols. Doctors compare eyes and look for large differences that suggest amblyopia risk.Pupil exam and the “swinging flashlight test.”
Checking the pupils finds an afferent pupillary defect (RAPD) if one retina/optic nerve is underperforming.Red reflex test.
In a dark room, a scope shines light to see the red/orange reflex from the retina. An asymmetric or white reflex is a red flag that triggers urgent retinal evaluation. NCBIOcular alignment and motility checks (cover tests).
Simple cover–uncover and alternate cover tests reveal a hidden or constant strabismus (common in one-eye diseases).Anterior segment exam (slit-lamp).
The front of the eye (cornea, anterior chamber, iris, lens) is checked for inflammation, cataract, or signs of high pressure that can accompany advanced disease. Genetic & Rare Diseases Info CenterIntraocular pressure measurement (tonometry).
Pressure is measured because secondary glaucoma can develop in late stages; elevated pressure needs its own treatment. PubMedDilated fundus examination (indirect ophthalmoscopy).
With dilating drops and a head-mounted light, the doctor surveys the entire retina, searching for telangiectatic vessels, micro-aneurysms, hard exudates, and exudative detachment. This is the core clinical exam for Coats’. NCBIScleral depression (when needed).
A gentle external tool temporarily indents the eye wall to bring far-peripheral retina into view—helpful for spotting subtle telangiectasia in the periphery.Amsler grid (for old enough patients).
A simple square grid helps patients describe distortion or missing areas that hint at macular involvement.
B) “Manual” office tests
Confrontation visual fields.
The clinician moves fingers in different directions to map gross side-vision loss—a quick screen that can show peripheral damage.Color vision testing (Ishihara or similar).
Poor color discrimination can happen with macular involvement; comparing eyes is informative.Pinhole test.
Looking through a small pinhole reduces blur from refractive errors; if vision stays poor with the pinhole, retinal causes are more likely.Near vision and reading tasks.
Simple near-vision tasks can expose macular trouble earlier than distance charts.RAPD quantification (neutral density filters).
Beyond a yes/no pupil test, filters can grade how much the affected eye under-signals the brain.
C) Lab and pathological tests
No routine lab test confirms Coats’.
There is no specific blood test for Coats’ disease. Labs are used only when the doctor suspects another condition that can mimic Coats’ or travel with similar signs (infections, inflammations, or systemic issues). This section is short on purpose—to stay accurate. NCBIPathology (rare; only if an eye is removed).
In very advanced, painful, blind eyes—or when retinoblastoma cannot be safely ruled out—surgery to remove the eye (enucleation) may be considered. The pathologist then sees lipid-laden exudates, foamy macrophages, and abnormal retinal vessels—findings that fit Coats’. This is not routine but explains what “pathology” would show. EyeWiki
D) Electrodiagnostic tests
Electroretinography (ERG).
ERG measures the retina’s electrical response to flashes of light. In Coats’, ERG may be reduced in areas with heavy exudation or detachment. It helps quantify overall retinal health and can assist with prognosis and surgical planning. NCBIVisual evoked potential (VEP).
VEP looks at electrical signals from the visual cortex after a checkerboard or flash stimulus. It helps confirm that reduced sight is retinal/ocular rather than brain-based and can be useful in children who cannot do standard vision charts.Electro-oculography (EOG).
EOG assesses the retinal pigment epithelium (RPE) function. It is not specific for Coats’ but may be part of a broader work-up in atypical or very advanced cases. NCBI
E) Imaging tests
Wide-field fundus photography.
High-resolution photos (often with an ultra-wide-field camera) document the abnormal vessels and exudates over time, making it easy to track if the disease is better, stable, or worse.Fluorescein angiography (FA).
After a small dye injection in the arm, rapid retinal photos show where vessels leak or don’t perfuse. In Coats’, FA lights up telangiectasia, micro-aneurysms, and late leaking—it’s one of the signature tests. EyeWikiOptical coherence tomography (OCT).
OCT is like a retinal ultrasound with light that cross-sections the macula. It shows intraretinal cysts, edema, and subretinal fluid—crucial for macular decision-making and for checking treatment response. EyeWikiOCT angiography (OCTA).
Without dye, OCTA maps blood flow and can reveal telangiectatic channels, capillary dropout, and the health of deep and superficial plexuses. Helpful when dye FA isn’t possible.B-scan ocular ultrasound.
If the media are cloudy (blood, cataract) and the retina can’t be seen, B-scan shows whether the retina is detached and, importantly, can help differentiate a solid tumor (retinoblastoma) from an exudative detachment. It’s an essential safety test in a child with leukocoria.Ultrasound biomicroscopy (UBM).
High-frequency ultrasound images the front of the eye and ciliary body—useful in late disease to look for angle closure or other causes of high eye pressure.MRI of the orbits/brain (selected cases).
If a child has leukocoria and the fundus can’t be seen well, an MRI can help exclude retinoblastoma before any invasive treatment. CT is less favored due to radiation, especially in kids. NCBIColor fundus autofluorescence (FAF).
FAF can highlight lipofuscin and RPE stress, sometimes outlining zones of chronic exudation and damage invisible in standard photos.Serial photo/OCT “treat-and-track.”
Repeating images at each visit lets doctors quantify improvement (“less fluid,” “fewer exudates”) after laser or other therapies.Staging-guided imaging plan.
Imaging is matched to the Shields stage: earlier stages focus on FA mapping and macular OCT; advanced stages add B-scan and pressure checks to guide whether surgery is needed. PubMed
Non-pharmacological treatments (therapies & supportive care)
These are “no-pill/no-injection” options or procedures that don’t rely on systemic drugs. I’ll explain purpose and mechanism plainly.
Observation with close follow-up – In very mild, non-threatening cases, watching carefully is reasonable. Purpose: avoid overtreatment. Mechanism: the eye is monitored until treatment is clearly needed. EyeWiki
Laser photocoagulation (focal) – A precise laser “cauterizes” the abnormal, leaking retinal vessels to seal them. Purpose: stop leakage and exudates; Mechanism: heat closes telangiectasia and light-bulb aneurysms. Often repeated. EyeWikiBioMed Central
Laser to ischemic (non-perfused) retina (scatter) – Treats empty, avascular areas that fuel vessel leakage. Purpose: reduce VEGF drive and leakage; Mechanism: laser ablates non-perfused retina, lowering leak stimulus. EyeWiki
Cryotherapy – A freezing probe is applied outside the eye to freeze the abnormal peripheral vessels when thick fluid blocks laser from reaching them. Purpose: close deep, leaky vessels; Mechanism: cold-induced vessel closure. AAO
Photodynamic therapy (PDT) – A light-activated therapy that targets abnormal vessels near the posterior pole when laser is risky. Purpose: shrink/close leaky vessels near the center; Mechanism: light activates drug within vessels to shut them down. (Used off-label in selected cases.) PMC+1
Wide-field fluorescein angiography-guided treatment – Purpose: map all leaking/ischemic areas; Mechanism: dye study shows exactly where to laser/cryo. EyeWiki
Optical coherence tomography (OCT)-guided care – Purpose: track fluid/exudates at the macula; Mechanism: micrometer-level scans guide timing of repeat treatments. PMC
Amblyopia therapy (patching the healthy eye) – For children with reduced vision from prolonged blur. Purpose: push the brain to use the weak eye; Mechanism: structured patching hours per day as directed by pediatric ophthalmology. (Drug penalization uses atropine, a medication; patching alone is the non-drug part.) General pediatric eye practice.
Full refractive correction (glasses/contacts) – Purpose: give the best possible focus to the affected eye once the retina is drier; Mechanism: lenses reduce refractive blur so brain gets the clearest signal. Standard clinical care.
Low-vision rehabilitation – When permanent damage remains, training with magnifiers, high-contrast materials, and lighting can improve function. Purpose: maximize remaining vision; Mechanism: optical and behavioral strategies. Standard low-vision care.
Monocular safety counseling – If one eye sees poorly, protect the better eye. Purpose: prevent injuries; Mechanism: polycarbonate safety glasses for sports/activities. Standard safety guidance.
School accommodations – Preferential seating, larger print, assistive tech. Purpose: reduce learning barriers; Mechanism: accessibility tools. Standard vision-education practice.
UV-blocking eyewear outdoors – Purpose: general retinal protection and comfort; Mechanism: filters UV/blue light, reduces glare. General eye-health practice.
Photography-based home awareness (pictures/videos of “white pupil”) – Parents sometimes first notice “leukocoria” in flash photos; Purpose: prompt early evaluation; Mechanism: education. Public health awareness.
Tele-follow-up where appropriate – Purpose: keep close tabs when clinic trips are hard; Mechanism: remote review of symptoms and timing of in-person imaging. Adjunct to in-person care.
Smoking avoidance / smoke-free home – Purpose: support vascular health; Mechanism: removes vascular irritants; not disease-specific but eye-healthy. General public health.
Systemic health optimization – Treat any coexisting issues (rare associations reported); Purpose: stabilize overall health; Mechanism: coordinated pediatric care. EyeWiki
Prompt evaluation of any new strabismus or vision change – Purpose: catch reactivation early; Mechanism: early clinic visit triggers imaging/treatment. EyeWiki
Long-term surveillance of both eyes – Even though usually unilateral, the fellow eye can rarely show abnormalities; Purpose: detect subtle fellow-eye changes; Mechanism: periodic dilated exams ± wide-field imaging. Retina Today
Pain control and comfort measures in end-stage eyes – If vision is gone and the eye is comfortable, supportive care may be chosen; Purpose: quality of life; Mechanism: lubricants, protective eyewear; if painful, see surgery section below. EyeWiki
Medicine (drug) treatments
*Doses are typical ophthalmic doses used off-label in Coats’ disease and must be individualized by a retina specialist. Frequency varies by response.
Bevacizumab (anti-VEGF) – intravitreal injection
Class: anti-VEGF biologic.
Typical dose: ~1.25 mg/0.05 mL into the vitreous; sometimes lower doses in small children.
When: as an adjunct to laser/cryo in eyes with heavy exudation or detachment.
Purpose/mechanism: lowers VEGF to reduce leakage and help the retina dry, often to make laser/cryo safer and more effective.
Key side notes: Helps many, but there are reports of fibrosis/traction after anti-VEGF in exudative diseases—used with caution and close follow-up.
Side effects: rare infection (endophthalmitis), pressure spikes, inflammation; theoretical systemic risks are low with ocular dosing. Unbound MedicineAAOPMCRanibizumab (anti-VEGF) – intravitreal
Class: anti-VEGF biologic.
Typical dose: 0.5 mg/0.05 mL.
Use: adjunct, case-by-case like bevacizumab.
Mechanism/side effects: as above. EyeWikiAflibercept (anti-VEGF) – intravitreal
Class: VEGF-trap biologic.
Typical dose: 2 mg/0.05 mL.
Use: off-label adjunct similar to above.
Mechanism/side effects: as above. AAO JournalTriamcinolone acetonide – intravitreal steroid
Class: corticosteroid.
Typical dose: 1–4 mg intravitreal (varies by surgeon); some use 4 mg/0.1 mL.
When: to quickly reduce exudation/edema so that laser/cryo can be applied.
Mechanism: anti-inflammatory, stabilizes vessel permeability.
Side effects: cataract and glaucoma risk, need for pressure checks. AAO JournalLippincott JournalsDexamethasone implant (Ozurdex) – intravitreal
Class: biodegradable steroid implant.
Typical dose: 0.7 mg device.
When/purpose: adjunct in stubborn exudation; can dry the macula and help other treatments.
Mechanism: sustained steroid release.
Side effects: IOP rise, cataract over time. PMC+1Verteporfin (for Photodynamic Therapy)
Class: photosensitizer used during PDT procedure.
Dose/timing: standard PDT dosing/protocols (weight-based infusion), then activated by laser.
Use: selected cases with posterior vascular lesions where thermal laser would harm central vision.
Mechanism: light-activated endothelial damage to seal abnormal vessels.
Side effects: photosensitivity precautions after infusion. PMCIOP-lowering eye drops (e.g., timolol, brimonidine, dorzolamide, prostaglandin analogs)
Class: glaucoma medicines.
Use: only when stage 4 disease causes high pressure (neovascular glaucoma) or steroid-related IOP rise; not a primary Coats therapy.
Mechanism: reduce aqueous production or increase outflow to lower pressure/pain.
Side effects: vary by class (beta-blockers can cause fatigue/bronchospasm, alpha-agonists sedation/dry mouth, CAIs stinging; PGAs redness/darkening of iris/lashes). AAONCBIShort course oral acetazolamide (selected cases)
Class: carbonic anhydrase inhibitor.
Use: short-term adjunct for IOP spikes or severe edema in selected contexts; not routine.
Mechanism: reduces fluid production in the eye.
Side effects: tingling, GI upset, fatigue; avoid long-term use in kids without specialist oversight. Review of OptometryTopical steroids (surface)
Class: corticosteroid drops.
Use: only if anterior segment inflammation occurs after procedures; not a treatment for the retinal leak itself.
Mechanism: reduces inflammation at the front of the eye. General ophthalmic practice.Cycloplegics (e.g., atropine) for comfort in painful inflamed eyes
Class: anticholinergic drops.
Use: relieve ciliary spasm pain in selected inflamed eyes; also used for amblyopia penalization (that’s the drug version of amblyopia therapy).
Mechanism: relaxes focusing muscle and dilates pupil. Standard ophthalmic practice.
Important caution on anti-VEGF: Although anti-VEGF injections often help exudation, there are documented cases of vitreoretinal fibrosis and tractional retinal detachment after treatment in ischemic retina. Retina specialists weigh risk vs benefit and monitor closely. AAOPMCNature
Dietary, molecular & herbal supplements
There’s no supplement proven to treat Coats’ disease. Nutrition can support overall retinal health, but it does not replace laser, cryo, injections, or surgery. Where possible, I’ll tie to strong eye-nutrition evidence (mostly from AMD studies), and note typical doses used in those contexts.
Lutein (10 mg/day) – Function: macular pigment; Mechanism: antioxidant filtering of blue light; Evidence base comes from AMD/AREDS2, not Coats. PubMedNational Eye Institute
Zeaxanthin (2 mg/day) – Often paired with lutein; Function/Mechanism: as above. PubMed
Omega-3 (DHA/EPA; food-first, or ~1 g/day combined if advised) – Function: supports photoreceptor membranes and anti-inflammatory signaling; Evidence mixed in AMD; use food-first (fatty fish). PMCNational Eye Institute
Vitamin C (≈500 mg/day if supplementing) – Antioxidant; mechanism: scavenges free radicals. Evidence strong for general eye antioxidant support (AREDS used 500 mg). National Eye Institute
Vitamin E (≈400 IU/day in AREDS) – Antioxidant; mechanism: lipid membrane protection. AMD data, not Coats. National Eye Institute
Zinc (≈80 mg zinc oxide in AREDS with copper 2 mg) – Function: retinal enzyme cofactor; mechanism: antioxidant pathways; include copper to avoid deficiency. AMD data. National Eye Institute
Copper (2 mg/day with high-dose zinc) – Prevents copper-deficiency anemia when using high-dose zinc. AMD protocols. National Eye Institute
Beta-carotene (avoid in smokers) – Replaced by lutein/zeaxanthin in AREDS2 due to lung cancer risk in smokers; in general, avoid mega-doses. PubMed
Bilberry/anthocyanins – Function: antioxidant; mechanism: vascular support; evidence in retinal disease is limited; consider food sources (berries).
Saffron (20–30 mg/day trials in AMD) – Neuroprotective signals suggested in small studies; no Coats-specific data.
Curcumin (turmeric extract, standardized) – Anti-inflammatory; potential vascular effects; limited eye-specific evidence.
Resveratrol – Antioxidant; lab data on angiogenesis modulation; clinical evidence in retinal disease remains limited.
CoQ10 – Mitochondrial support; limited ocular trial data.
Alpha-lipoic acid – Antioxidant; peripheral neuropathy data; retinal evidence limited.
Multivitamin (balanced, not megadoses) – Insurance for dietary gaps; mechanism: broad micronutrient sufficiency.
Bottom line: prioritize food-first (leafy greens, colored veggies, fish, nuts, legumes, fruit) and discuss any supplements with your clinician, especially for children. Supplements don’t treat Coats’ disease but can support general eye health. National Eye Institute
Regenerative / stem-cell drugs
There are no approved immune-boosting or stem-cell drugs for Coats’ disease. Regenerative therapies (RPE or photoreceptor cell transplants) are being studied for degenerative retinal diseases (like AMD or inherited dystrophies), not for Coats’ vascular leakage. If you see “stem cell cures” advertised for Coats, that’s not evidence-based. Here’s the honest snapshot:
RPE cell therapy (embryonic/iPSC-derived) – In clinical trials for AMD/Stargardt; not established for Coats. PMCPentaVision
Photoreceptor precursor transplantation – Early research; not a clinical option for Coats. ScienceDirect
MSC (mesenchymal stem cell) approaches – Investigational neuroprotection in degenerations; no Coats indication. BioMed Central
Cell-derived exosomes – Experimental; not a therapy for Coats today. BioMed Central
Gene/cell combo strategies – In trials for other retinal diseases; nothing established for Coats. Cell
“Immune boosters” (general) – No evidence they change Coats’ course; avoid unregulated products in children.
Surgeries
Surgery is reserved for advanced disease (typically stages 3–4) when fluid detachment is extensive or when glaucoma or pain develops.
Pars plana vitrectomy (PPV) – Surgeon removes the gel (vitreous), may make a small retinal opening (retinotomy), drains subretinal fluid, applies internal laser, and uses a tamponade (gas or silicone oil) to hold the retina flat. Why: reattach retina and enable vessel ablation when the detachment is too big for laser/cryo alone. PMC+1
External (trans-scleral) drainage of subretinal fluid – A controlled drain from outside the eye to remove thick exudative fluid; often combined with laser/cryo. Why: flatten retina to allow effective treatment and improve anatomic outcomes. Nature
Scleral buckle (sometimes with PPV) – A silicone band indents the eye wall to support the retina; can be combined with PPV and drainage in complex cases. Why: mechanical support to maintain reattachment. Turkish Journal of Ophthalmology
Cyclophotocoagulation (cyclodiode) for neovascular glaucoma – Laser reduces the ciliary body’s fluid production when pressure is uncontrolled and painful. Why: pain control and pressure reduction in stage 4 eyes. PMC
Enucleation (eye removal) – Considered for painful, blind eyes or when retinoblastoma can’t be excluded safely. Why: relieve pain and protect life/health when vision is already lost. EyeWiki
Practical prevention & protection ideas
We can’t “prevent” Coats’ disease from arising, but we can prevent delays, protect the better-seeing eye, and protect quality of life.
Learn the signs: new strabismus, poor tracking, or a “white pupil” in photos → get checked quickly. EyeWiki
Keep scheduled follow-ups and imaging; reactivation can happen. Cleveland Clinic
Use polycarbonate protective eyewear for sports if one eye is weak (monocular precautions).
Ensure good classroom lighting, larger print, and front-row seating when needed.
Don’t smoke and keep the home smoke-free (vascular health).
Eat a retinal-healthy diet (see next section). National Eye Institute
Sun/UV protection outdoors (comfort and general eye safety).
Seek care fast if pain, redness, or sudden vision drop occurs (possible pressure rise or inflammation).
Keep emergency contacts for your retina clinic; small changes in kids can be big.
If a doctor mentions retinoblastoma in the differential, do the imaging promptly to stay safe. PMC
When to see a doctor
Right away (urgent): a “white pupil” in photos, sudden eye pain/redness, sudden big drop in vision, light sensitivity with headache, eye looks bigger, or the child is very fussy touching the eye. These can signal retinal detachment or pressure rise (glaucoma). EyeWiki
Soon (next available): new drifting eye (strabismus), school noticing trouble seeing, new floaters or flashes, or missed follow-up. EyeWiki
What to eat and what to avoid
Diet won’t cure Coats’ disease, but it supports overall retinal and vascular health.
What to eat
Leafy greens (spinach, kale) for lutein/zeaxanthin.
Colorful veggies & fruits (orange/yellow peppers, citrus, berries) for vitamins C/A.
Fatty fish (salmon, sardines) 1–2×/week for omega-3s.
Nuts & seeds (almonds, walnuts) for vitamin E and healthy fats.
Legumes (lentils, beans) for zinc and protein.
Eggs (yolks contain lutein/zeaxanthin).
Whole-grain, Mediterranean-style pattern overall. National Eye Institute
What to limit/avoid
- Ultra-processed, very salty snacks (fluid retention isn’t the cause here, but overall health matters).
- Smoking/vaping exposure (vascular harm).
- Mega-dose single supplements without medical advice—especially beta-carotene in smokers (AREDS2 replaced it with lutein/zeaxanthin). PubMedt be excluded or media are too opaque to see in. EyeWikiPMC+1
FAQs
1) Is Coats’ disease cancer?
No. It’s a vascular leak problem, not a tumor. Doctors still rule out retinoblastoma early because the two can look similar. PMC
2) Can both eyes be affected?
Usually it’s one eye, but the other eye should still be checked regularly. Rare fellow-eye vascular changes have been reported. Retina Today
3) Who gets it most?
Mostly boys, typically starting in childhood; adults can be affected too. EyeWiki
4) What causes it?
Exact cause is unknown. It’s considered idiopathic (no proven genetic pattern), with abnormal retinal vessels that leak. EyeWiki
5) How do doctors pick a treatment?
By stage and what threatens vision: laser/cryo for leaky vessels; injections or steroids as adjuncts if exudation is heavy; surgery if the retina is widely detached or pressure is high. EyeWikiPMC
6) Will my child need more than one treatment?
Often yes. Coats’ lesions can re-leak; multiple laser/cryo sessions or combined treatments are common. BioMed Central
7) What are the biggest risks of anti-VEGF shots here?
In some ischemic eyes, anti-VEGF can be followed by fibrosis and traction; that’s why retina specialists use them judiciously and monitor closely. AAOPMC
8) Do steroids help?
They can dry exudation and make laser possible in advanced eyes, but they can raise eye pressure and speed cataract. EyeWiki
9) When is surgery needed?
If there’s a large exudative detachment that won’t settle with laser/cryo (± injections), or if there’s painful high pressure or non-resolving fluid. PMC
10) Will my child lose vision?
Outcomes vary with stage at diagnosis and how quickly treatment dries the macula. Earlier, milder cases do better than advanced cases. Cleveland Clinic
11) Can Coats’ disease come back after treatment?
Yes, it can reactivate. That’s why long-term follow-up is important. Cleveland Clinic
12) Is there a way to prevent it?
There’s no known prevention. The key is early detection and protecting the better eye with safety measures. EyeWiki
13) Are stem-cell or “regenerative” cures available now?
No—not for Coats’ disease. Cell therapies are in trials for other retinal conditions; nothing proven for Coats yet. PentaVision
14) What about diet or vitamins?
A healthy, Mediterranean-style diet supports retinal health, but there’s no supplement that treats Coats. Use AREDS-style nutrients only if your doctor recommends, and avoid beta-carotene if you smoke. National Eye InstitutePubMed
15) When should we call urgently?
New eye pain/redness, sudden vision drop, the eye looking “bigger,” or a new white pupil in photos—get urgent care. EyeWiki
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The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: August 07, 2025.
