Segmental retinal arteritis (often called Kyrieleis arteritis or Kyrieleis plaques) is a very specific pattern of inflammation in the tiny arteries of the retina (the light-sensitive layer at the back of the eye). On dilated exam, the doctor sees multiple short, bead-like, yellow-white patches lined up inside a retinal artery, with normal vessel wall in between—hence the word segmental. These patches are in the vessel wall itself (not floating inside the blood and not leaking outside) and they usually appear near areas of active inflammation in the retina. Doctors most often see this pattern during posterior uveitis caused by infection, especially ocular toxoplasmosis. The plaques often fade over weeks to months as the underlying eye inflammation gets treated, and by themselves they do not necessarily mean a poor visual prognosis—they mainly tell the clinician that inflammation is active and significant. EyeWikiPMCPubMed
Because the plaques mark arterial involvement, they help narrow the cause of uveitis and point the work-up toward infections (like toxoplasmosis) and certain immune diseases, and remind clinicians to rule out herpetic acute retinal necrosis or other serious conditions that can threaten vision quickly if missed. EyeWikiPMC
Segmental retinal arteritis is a rare eye finding where short, bead-like white patches form inside segments of the retinal arteries due to inflammation, most commonly during infectious posterior uveitis such as toxoplasmosis. EyeWikiPMC
Types
When clinicians say “types,” they generally mean how it shows up rather than completely different diseases. Here are the practical “types” you’ll see in reports:
Infectious-associated segmental retinal arteritis
Seen next to infectious retinitis, especially toxoplasmosis, but also reported with herpetic acute retinal necrosis, tuberculosis, and syphilis. The plaques track with the infectious lesion and usually resolve after the infection is treated. PMC+2PMC+2Non-infectious (immune-mediated) segmental retinal arteritis
Described in inflammatory uveitis without an active microbe—e.g., Behçet disease or sarcoidosis—and behaves like a sterile arterial wall reaction that improves when overall eye inflammation is controlled. EyeWikiFocal vs. multifocal
Focal means a short stretch of one artery shows plaques; multifocal means several arteries or several spots along an artery show the beaded pattern. Multifocal cases are reported in atypical toxoplasmosis. PMCActive vs. resolving
Active plaques look bright, chunky, and sit near inflamed retina; resolving plaques look paler and thinner, fading over time as the eye quiets. The reversibility has been emphasized in the literature. EyeWikiPubMed
Causes
Important note: “Segmental retinal arteritis” is a sign, not a disease by itself. The cause is the underlying infection or immune disorder that triggered inflammation in the retinal arteries. The list below starts with the most frequently reported and clinically important.
Ocular toxoplasmosis — the most common association. A parasite (Toxoplasma gondii) inflames the retina; nearby retinal arteries show Kyrieleis plaques. Treating toxoplasmosis usually makes the plaques fade. PMCAAOEyeWiki
Herpetic acute retinal necrosis (ARN) — a rapidly destructive viral infection (often varicella-zoster or herpes simplex) that can show a Kyrieleis-like arteritis pattern along arteries near necrotic retina. Urgent antiviral therapy is essential. PMC
Tuberculous uveitis — tuberculosis can inflame the back of the eye; Kyrieleis first described these plaques in a TB case in 1933. Anti-TB therapy and steroids (when appropriate) are used under specialist care. PMC
Syphilitic posterior uveitis — syphilis can mimic many eye diseases; arterial wall plaques alongside retinitis have been reported and improve with penicillin-based therapy. EyeWiki
Behçet disease — an autoimmune vasculitis that can attack retinal vessels, sometimes with arterial beading/plaques in active posterior uveitis. Frontiers
Sarcoidosis — granulomatous inflammation can involve retinal vessels and produce arteritis-like segments; clinicians look for hilar lymph nodes and elevated ACE. EyeWiki
Cytomegalovirus (CMV) retinitis — in immunocompromised patients, CMV can cause infectious retinitis with arterial involvement near lesions. Prompt antiviral therapy is needed. EyeWiki
Bartonella henselae (cat-scratch disease) — can cause posterior uveitis and vasculitis; rare reports describe segmental arterial changes that settle as infection resolves. EyeWiki
Rickettsial infections — rickettsiae can inflame retinal vessels; segmental arteritis has been described in vasculitic patterns with infectious uveitis. EyeWiki
Toxocariasis — a parasitic eye infection that can trigger localized posterior inflammation and arterial wall reactions. EyeWiki
Lyme disease — Borrelia infection occasionally causes posterior uveitis/vasculitis; arteries may show segmental changes in inflamed areas. EyeWiki
Post-viral panuveitis (e.g., after dengue) — immune-mediated inflammation after systemic viral illness can involve retinal arteries. (Clinically reported in vasculitis series.) EyeWiki
Idiopathic posterior uveitis — sometimes no cause is found; segmental plaques can still appear and later resolve as inflammation is controlled. EyeWiki
ANCA-associated vasculitis (e.g., GPA) — a systemic small-vessel vasculitis; retinal arteritis can occur during flares. EyeWiki
Systemic lupus erythematosus (SLE) — immune complex vasculitis of the retina can include arterial segments with inflammatory deposits. EyeWiki
Polyarteritis nodosa (PAN) — medium-vessel vasculitis with ocular involvement; arterial wall inflammation in the retina can be part of the picture. EyeWiki
Giant cell arteritis (GCA/temporal arteritis) — typically a large-vessel disease in older adults that can occlude retinal arteries; while its classic signs differ, clinicians consider GCA when retinal arteries look inflamed and vision drops suddenly. EyeWiki
Sarcoid-TB overlap or “tuberculous sarcoid-like” reactions — mixed pictures can occur; arteries can show segmental plaques near granulomatous lesions. EyeWiki
Drug-related immune reactions (rare) — immune checkpoint inhibitors and other biologics can trigger uveitis with vasculitis, sometimes involving arteries. EyeWiki
Post-surgical or post-traumatic inflammation (rare) — intense posterior segment inflammation after intraocular surgery/trauma may temporarily involve retinal arteries in a segmental way as the eye heals. EyeWiki
Symptoms
Remember: segmental retinal arteritis itself does not cause unique symptoms; symptoms come from the underlying uveitis/retinitis and where it sits in the retina.
Blurred vision — from inflamed retina or nearby swelling.
Floaters — tiny moving spots or cobwebs from inflammatory cells in the vitreous gel.
Flashes of light (photopsias) — irritation of the retina from inflammation.
A gray or dark patch in the field of vision (scotoma) — when inflamed retina lies along that sight line.
Distorted vision (metamorphopsia) — straight lines look bent if the macula is affected.
Light sensitivity (photophobia) — inflamed eyes are often light-sensitive.
Eye redness — more common when inflammation spreads forward (anterior segment).
Mild eye ache or discomfort — inflammation can be irritating but not always painful.
Reduced contrast or color clarity — colors look washed out if the macula/optic nerve is stressed.
Poor night vision — inflamed or healing retina may struggle in low light.
Headache — nonspecific, but common in systemic inflammatory flares.
Fever or malaise — if an infection (e.g., toxoplasmosis, TB, syphilis) is active. PMC
New floaters after a sudden flare — suggests fresh inflammatory cells.
Jaw pain, scalp tenderness, or new severe headache in older adults — red flags for GCA, which needs urgent attention. EyeWiki
Mouth/genital ulcers or skin lesions — clues to Behçet disease or systemic vasculitis when combined with eye symptoms. EyeWiki
Diagnostic tests
The testing aims to (1) prove there is retinal arterial involvement, (2) identify the cause, and (3) measure how active it is. Below are 20 commonly used tests, grouped the way clinicians think about them. Each entry explains what the test is and why it helps.
A) Physical examination
Best-corrected visual acuity (distance and near)
Reading letters on a chart shows how much the inflammation is affecting seeing. Repeating it over time tells the doctor if treatment is working.Pupil assessment with swinging-flashlight test
A relative afferent pupillary defect (RAPD) can appear if the retina or optic nerve is stressed; it helps localize the problem to the back of the eye.Slit-lamp and dilated fundus exam
With drops to widen the pupil, the doctor directly sees the plaques—short, beaded, yellow-white segments inside the retinal arteries—plus any neighboring retinitis or vasculitis. This exam defines “segmental retinal arteritis.” EyeWikiTargeted systemic exam
Checking skin, mouth, joints, and temporal arteries can reveal Behçet ulcers, sarcoid skin changes, or tender temporal arteries in suspected GCA—clues to the cause. EyeWiki+1
B) Manual/bedside visual function tests
Amsler grid
A small checkerboard you look at one eye at a time. Wavy or missing squares mean macular involvement from nearby inflammation.Confrontation visual fields
The clinician compares what you see to their own in each quadrant. Missing areas suggest localized retinal damage or active lesions.Color vision (Ishihara plates)
Subtle color loss can show macular or optic pathway stress even when standard acuity is decent.Contrast sensitivity
Measures the ability to see low-contrast letters. Inflammation can reduce contrast even before other tests change.
C) Laboratory & pathological tests
Toxoplasma serology (IgG/IgM) ± aqueous PCR when atypical
Supports or refutes toxoplasmosis, the most typical association; PCR on a tiny eye fluid sample can help in difficult cases. PMCSyphilis testing (nontreponemal + treponemal)
RPR or VDRL plus FTA-ABS or TPPA confirms syphilis because it can mimic many eye issues and needs specific antibiotics. EyeWikiTuberculosis testing (interferon-gamma release assay or PPD) and chest imaging
TB can drive posterior uveitis and segmental arterial plaques; systemic evaluation guides anti-TB therapy. PMCInflammation markers (ESR, CRP) and vasculitis autoantibodies (ANA, ANCA)
These screen for systemic autoimmune causes and flag GCA when very high in older adults with sudden vision symptoms. EyeWikiACE and lysozyme levels ± chest CT
Elevated ACE/lysozyme and hilar adenopathy suggest sarcoidosis as the driver of ocular inflammation. EyeWikiInfectious panels based on history (HSV/VZV/CMV PCR, Bartonella, Lyme, HIV)
Selected tests, guided by travel, exposures (e.g., cat scratches), diet, or immune status, help confirm less common infectious causes. EyeWiki
D) Electrodiagnostic tests
Full-field electroretinogram (ERG)
Shows how well retinal cells convert light into electrical signals. In widespread inflammation (e.g., ARN), ERG can be reduced, helping stage severity.Visual evoked potential (VEP)
Measures signal conduction from retina to brain. Helpful when visual loss seems out of proportion or to separate retinal vs. optic nerve problems.
E) Imaging tests
Color fundus photography
Captures baseline images of the segmental plaques and retinitis so doctors can track change over time.Optical coherence tomography (OCT)
A quick, painless scan that shows microscopic cross-sections of the retina. It detects edema near the plaques, macular fluid, or outer retinal damage.Fluorescein angiography (FA)
A dye test that outlines retinal vessels. In segmental retinal arteritis, FA can show arterial wall staining or leakage nearby, plus areas of non-perfusion if present. FA helps distinguish arteritis patterns from other causes of white vessel lines. EyeWikiIndocyanine green angiography (ICGA) or OCT-angiography (OCT-A)
ICGA images deeper choroidal circulation; OCT-A maps flow without dye. Both can highlight vessel involvement around the plaques and guide treatment decisions in complex uveitis. EyeWiki
Non-pharmacological treatments
Important: These support—not replace—medical therapy. In infectious SRA, urgent antimicrobials are essential; in autoimmune SRA, steroids/immune therapy protect sight.
Rest the eye during flares – reduce near work/bright screens while inflammation is active; lowers symptom burden so you can notice any deterioration early.
Photoprotection – sunglasses/hat outdoors to cut photophobia and glare while vessels are inflamed.
Smoke-free living – smoking worsens vascular inflammation and impairs retinal oxygen delivery; quitting helps the retina heal.
Tight blood-sugar control (if diabetic) – better microvascular health, less macular edema risk.
Blood-pressure control – keeps perfusion steady; spikes can aggravate leakage/hemorrhage.
Healthy sleep routine – steadier cortisol/immune tone, better recovery from flares.
Stress reduction (breathing, mindfulness, gentle yoga) – may calm sympathetic surges that can worsen autoimmune activity.
Hydration – supports perfusion and medication tolerance.
Avoid contact lenses during active uveitis – reduces surface irritation/infection risk.
Protect from ocular trauma – safety glasses for sports/DIY; inflamed vessels bleed easier.
Vaccination up to date (influenza, shingles if eligible) – lowers risk of viral triggers that can flare vasculitis (coordinate timing with immunosuppressants).
Hand hygiene & food hygiene – reduces toxoplasma risk (wash produce, cook meat well, avoid unpasteurized dairy).
Cat-litter precautions (gloves/mask; pregnant/immunosuppressed should avoid changing litter) – lowers toxoplasma exposure.
UV-free work lighting and frequent breaks – comfort measure to reduce glare and eye strain.
Monocular precautions if one eye is dominant/only seeing – polycarbonate glasses to protect the better eye.
Home Amsler grid once inflammation stabilizes – helps you detect new scotomas early and seek care fast.
Medication adherence coaching – steroid tapers and immune drugs need precision; using pill boxes/phone reminders prevents rebound.
Nutrition pattern favoring fish, nuts, leafy greens, and low added sugar – supports vascular and immune health (see “What to eat”).
Exercise most days (as cleared by your doctor) – improves endothelial function and systemic inflammation control.
Illness action plan – if you develop fever, shingles, TB exposures, or mouth/genital ulcers (Behçet), contact your eye team promptly; early treatment prevents retinal damage.
Evidence-based drug treatments
(Typical adult dosing shown; clinicians individualize by diagnosis, kidney/liver function, pregnancy, and drug interactions. Infectious causes must be treated first.)
A) For infectious SRA
Toxoplasmosis regimen (classic) – pyrimethamine (loading 50–75 mg then 25–50 mg/day) + sulfadiazine (1 g every 6 h) + leucovorin (10–25 mg 2–3×/week) for ~4–6 weeks;
Purpose: kill T. gondii; Mechanism: folate-pathway blockade; Side effects: bone-marrow suppression (leucovorin protects), rash, GI upset. PMCAlternatives for toxoplasmosis – trimethoprim-sulfamethoxazole DS (160/800 mg twice daily) or azithromycin (500 mg day 1 then 250 mg/day) ± clindamycin (300 mg q6h) when first-line isn’t tolerated; Side effects: hypersensitivity, GI upset. PMC
Herpetic (VZV/HSV) retinitis – acyclovir 800 mg 5×/day or valacyclovir 1 g 3×/day 7–10 days then taper/maintenance; severe cases may need IV acyclovir; Purpose: block viral DNA polymerase; Side effects: renal issues (hydrate), headache. PentaVision
Syphilitic vasculitis – aqueous crystalline penicillin G 18–24 million units/day IV (q4h or continuous) for 10–14 days; Purpose: eradicate T. pallidum; Side effects: Jarisch–Herxheimer reaction, allergy. PentaVision
Ocular TB – anti-TB combination therapy (e.g., RIPE per national protocol) guided by infectious-disease specialists; Purpose: sterilize M. tuberculosis; Side effects: hepatotoxicity, neuropathy; add pyridoxine with isoniazid. PentaVision
B) To control inflammation and protect sight
Systemic corticosteroid – prednisone ~0.5–1 mg/kg/day, taper over weeks; severe sight-threatening vasculitis may need IV methylprednisolone 1 g/day ×1–3 days first; Purpose: rapidly suppress vessel wall inflammation and leakage; Side effects: glucose rise, mood changes, infection risk, cataract/glaucoma. (Core first-line in non-infectious vasculitis after infection is excluded.) PMC
Periocular/intravitreal steroid – e.g., triamcinolone 4 mg or dexamethasone implant 0.7 mg (Ozurdex) for macular edema or when systemic therapy is contraindicated; Purpose: local steroid effect; Side effects: IOP rise, cataract. PMC
Methotrexate – 15–25 mg once weekly + folic acid; Class: antimetabolite; Purpose: steroid-sparing control of non-infectious retinal vasculitis; Mechanism: reduces lymphocyte proliferation; Side effects: liver enzyme rise, cytopenias (labs needed). PMC
Mycophenolate mofetil – 1–1.5 g twice daily; Class: antimetabolite; Purpose: steroid-sparing; Mechanism: inhibits inosine monophosphate dehydrogenase; Side effects: GI upset, leukopenia, teratogenicity; lab monitoring required. PMC
Azathioprine or Cyclosporine/Tacrolimus – azathioprine 1–2 mg/kg/day; cyclosporine 2–5 mg/kg/day; tacrolimus 1–2 mg twice daily; Class: immunomodulators; Purpose: long-term control when methotrexate/mycophenolate are unsuitable; Side effects: liver/kidney toxicity, hypertension, infections—regular labs essential. PMC
Why this mix? Modern care starts with antimicrobials when infectious and steroids + a steroid-sparing immunomodulator when non-infectious, to preserve vision while minimizing long-term steroid exposure. PMC
Regenerative / advanced” therapies
(Used by subspecialists for non-infectious, sight-threatening, or refractory cases; all require careful screening and monitoring.)
Adalimumab – 40 mg subcut every 2 weeks (some weekly); Class: anti-TNF-α; Mechanism: neutralizes TNF-α to quell vasculitis; Use: Behçet/other non-infectious uveitides; Risks: TB/hepatitis B reactivation, infection; test first. PMC
Infliximab – 5–10 mg/kg IV at weeks 0, 2, 6 then every 4–8 weeks; Class: anti-TNF-α; Use: severe Behçet-type occlusive vasculitis; Risks: infusion reactions, infections. PMC
Rituximab – 1 g IV day 1 and 15 (repeat by response); Class: anti-CD20 B-cell depleter; Use: ANCA-vasculitis/SLE patterns; Risks: infusion reaction, HBV reactivation. PMC
Tocilizumab – 162 mg SC weekly or 8 mg/kg IV monthly; Class: anti-IL-6 receptor; Use: refractory retinal vasculitis/macular edema; Risks: infection, lipid and liver enzyme rises. PMC
Interferon-α2a – doses vary (e.g., 3–9 million IU/day then taper); Use: Behçet uveitis with vasculitis; Mechanism: immunomodulation; Risks: flu-like symptoms, depression; requires close follow-up. PMC
Intravenous immunoglobulin (IVIG) – 2 g/kg over 2–5 days in selected immune-mediated cases; Mechanism: broad immune modulation; Risks: headache, thrombosis in predisposed patients. (Specialist, case-by-case use.) PMC
About stem cells: There is no established, approved stem-cell “drug” for SRA or retinal vasculitis. Experimental stem-cell approaches should only occur in regulated clinical trials. (Consensus across contemporary reviews.) PMCKarger
Procedures/surgeries
Panretinal or sector laser photocoagulation – treats retinal non-perfusion and neovascularization to prevent vitreous hemorrhage/traction; often after FA mapping.
Intravitreal anti-VEGF injections – help macular edema or neovascularization secondary to ischemia; procedural rather than “surgery,” but crucial for vision.
Intravitreal/periocular steroid procedures – targeted therapy for edema/inflammation when systemic therapy is limited.
Pars plana vitrectomy – removes persistent vitreous hemorrhage, clears media opacity, and allows endolaser; considered when bleeding doesn’t clear or traction threatens the macula.
Retinal detachment repair (vitrectomy ± buckle) – for tractional or rhegmatogenous detachment related to ischemia and neovascular membranes.
Dietary molecular & supportive supplements
(These do not treat SRA directly. They can support vascular/immune health when used safely alongside prescribed therapy. Always clear supplements with your clinician—some interact with methotrexate, azathioprine, warfarin, etc.)
Omega-3 (EPA/DHA 1–2 g/day) – anti-inflammatory lipid mediators; supports endothelial health.
Vitamin D3 (1000–2000 IU/day unless deficient) – immune modulation; correct deficiency per labs.
Lutein + Zeaxanthin (10 mg + 2 mg/day) – macular pigment support, glare recovery.
Vitamin C (500–1000 mg/day) – antioxidant support; don’t megadose around G6PD deficiency.
Vitamin E (100–200 IU/day) – antioxidant; avoid high doses on anticoagulants.
Zinc (10–20 mg/day) – cofactor for retinal enzymes; caution with copper depletion long-term.
Copper (1–2 mg/day) – balance zinc use.
B-complex with folate – supports methylation, offsets methotrexate-related folate drain (folic acid is usually prescribed specifically with methotrexate).
Magnesium (200–400 mg/day) – vascular tone, sleep quality.
CoQ10 (100–200 mg/day) – mitochondrial antioxidant; consider if on statins.
Curcumin (up to ~1 g/day of standardized extract) – gentle anti-inflammatory; watch anticoagulant interactions.
Resveratrol (100–250 mg/day) – antioxidant; theoretical vascular benefits.
N-acetylcysteine (600–1200 mg/day) – replenishes glutathione; may ease oxidative stress.
Probiotics (per label) – gut–immune axis support during long immunosuppression/antibiotics.
Adequate protein (≈1–1.2 g/kg/day) – tissue repair while recovering from inflammation.
Prevention tips
Cook meat thoroughly; wash fruits/vegetables well (toxoplasma prevention).
Handle cat litter safely (gloves; avoid if pregnant/immunosuppressed).
Keep vaccinations current (e.g., shingles for older adults) to lower viral flare risk—coordinate with your eye/rheum team.
Practice safer sex and screen for syphilis if exposed.
Screen and treat latent TB before starting biologics.
Do not ignore shingles near the eye—seek immediate care.
Quit smoking; avoid second-hand smoke.
Control BP, sugar, cholesterol to protect retinal microvessels.
Adhere to steroid tapers and immune meds exactly as prescribed (prevents rebound flares).
Eye-safety habits (protective eyewear; avoid eye trauma) while vessels are fragile.
When to see a doctor urgently
Sudden blur, a dark curtain, or a new blind spot
New floaters or flashes, especially after shingles or fever
Any vision change during pregnancy or while on immunosuppressants
Eye symptoms with mouth/genital ulcers, rashes, cough/fever, night sweats (systemic disease clues)
Persistent or worsening vision despite treatment
Do not wait—SRA/retinal vasculitis can damage retina quickly; early therapy protects sight. (This urgency approach aligns with contemporary vasculitis guidance.) EyeWikiPentaVision
What to eat and what to avoid
What to eat (10):
Fatty fish (salmon, sardines) 2–3×/week for omega-3s
Leafy greens (spinach, kale) for lutein/zeaxanthin
Colorful veggies/berries (antioxidants)
Nuts and seeds (almonds, walnuts, chia, flax)
Citrus and kiwi (vitamin C)
Legumes (fiber for vascular health)
Whole grains (better glycemic control)
Olive oil (monounsaturated fats)
Low-fat dairy or fortified alternatives (vitamin D/calcium)
Adequate lean protein (repair and immune function)
What to limit/avoid (10):
Excess added sugars (worsen edema/glycemic swings)
Ultra-processed foods high in salt/trans fats
Heavy alcohol (immune suppression, drug interactions)
Grapefruit if on cyclosporine/tacrolimus (drug interactions)
Raw/undercooked meat (toxoplasma risk)
Unpasteurized dairy (infection risk)
High-dose vitamin A retinoids without medical advice (toxicity risk)
Herbal products that thin blood (high-dose gingko/garlic) before procedures
Excessive caffeine if it worsens light sensitivity/anxiety
Smoking or vaping (vascular harm)
FAQs
1) Is SRA the same as a cholesterol plaque?
No. Kyrieleis plaques in SRA are inflammatory deposits inside the artery wall, not cholesterol emboli. They often fade with treatment. PMC
2) Can SRA happen without pain or redness?
Yes. The retina itself has few pain nerves; vision changes without pain are common in retinal vasculitis. EyeWiki
3) What tests confirm it?
Dilated exam + fluorescein angiography show the inflamed arterial segments and leakage; OCT/OCT-A help track macular changes. PMCEyeWiki
4) Why does my doctor insist on infection tests first?
Because steroids or biologics can worsen an undiagnosed eye infection. Finding and treating infection early prevents permanent damage. PentaVision
5) If it’s toxoplasmosis, do I always need the full “triple therapy”?
Often yes, but alternatives (e.g., TMP-SMX-based regimens) exist when first-line drugs aren’t tolerated—your specialist chooses based on lesion size, location, and risks. PMC
6) Will my vision return to normal?
Many people recover well if the macula and optic nerve are spared and treatment is timely. Kyrieleis plaques themselves are often reversible. PMC
7) How long do I take steroids?
Usually weeks to a few months, with a slow taper once a steroid-sparing drug kicks in. Your taper is individualized to avoid rebound. PMC
8) Are biologics safe?
They can be sight-saving in severe autoimmune vasculitis but carry infection risks (TB, hepatitis B). That’s why screening and vaccinations are coordinated first. PMC
9) Can a drug cause retinal vasculitis?
Rarely, yes. For example, pegcetacoplan has been linked with occlusive retinal vasculitis in safety reports; this requires urgent specialist care. American Society of Retina Specialists
10) What complications are doctors trying to prevent?
Macular edema, ischemia (non-perfusion), neovascularization, vitreous hemorrhage, and retinal detachment—all can permanently reduce vision if untreated. EyeWiki
11) Will I need laser or surgery?
Only if there is ischemia/neovascularization, non-clearing hemorrhage, or retinal detachment. Many cases are controlled medically without surgery.
12) Can SRA occur with Behçet disease?
Yes—rarely, Kyrieleis-type plaques have been reported in Behçet; Behçet vasculitis itself can be very aggressive and needs fast treatment. Frontiers
13) Is SRA contagious?
No—the inflammation isn’t contagious. But some causes (like toxoplasma or syphilis) are infectious, which is why testing matters.
14) Can I fly or exercise?
Light-to-moderate exercise is usually fine once your doctor says stable. Avoid high-impact activities when you have active hemorrhage or risk of detachment.
15) How often will I be followed?
Early on, every 1–2 weeks until the vessels quiet and vision stabilizes; then monthly to quarterly. Frequency increases if you flare or change therapy. EyeWiki
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 10, 2025.
Kyrieleis Vasculitis
