Pediatric uveitic glaucoma is optic-nerve damage from long-lasting or repeated eye inflammation in a child, often with high eye pressure (IOP). The inflammation can clog or scar the eye’s drainage angle. Sometimes the steroid medicines used to calm the inflammation can also raise the pressure. Both the disease and the treatment can play a role. PMCEyeWikiPentaVisionNCBI
Inside the front of the eye there is a tiny drain called the trabecular meshwork. When the eye is inflamed, cells, proteins, and fibrin float in the eye fluid. These can block the drain. Over time the inflammation can also scar the angle where the drain sits. A scarred angle does not open or work well. Pressure builds up. High pressure squeezes the delicate optic nerve fibers at the back of the eye. That slow squeeze causes permanent vision loss if not controlled. Even when pressure is not very high, chronic inflammation can still harm the drainage tissue and the nerve. Some children also over-respond to steroid drops and get a sharp pressure rise during treatment. PentaVisionAAOPMCNCBI
Types
Doctors describe types by how the angle behaves and what is causing the pressure:
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Open-angle uveitic glaucoma – the angle looks open, but inflammatory debris or swelling inside the drain slows outflow. Pressure rises. This is the most common mechanism in uveitis. PentaVision
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Angle-closure from peripheral anterior synechiae (PAS) – scar tissue sticks the iris to the angle over time. The drain becomes physically closed. EyeWiki
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Pupillary block with iris bombe – the pupil edge sticks to the lens (posterior synechiae). Fluid cannot pass through the pupil, the iris bows forward, and the angle closes. Pressure may rise quickly. EyeWiki
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Steroid-induced ocular hypertension/glaucoma – steroids used to control inflammation can raise IOP, and children are often strong “steroid responders.” This can happen with drops, injections, or implants. NCBIGlaucoma Today
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Mixed-mechanism glaucoma – more than one of the above is present (for example, steroid response on top of angle scarring). PMC
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Acute vs. chronic – acute rises happen during flare-ups; chronic damage builds over months or years when inflammation or angle scarring continues. PMC
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By uveitis location – usually anterior uveitis carries the highest angle risk, but intermediate, posterior, and panuveitis can also lead to glaucoma, especially with repeated inflammation or steroid treatment. EyeWiki
Causes
These are underlying conditions or triggers that can cause uveitis in children and lead to glaucoma through the mechanisms above.
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Juvenile idiopathic arthritis (JIA) – common cause of chronic anterior uveitis in children. Long-lasting inflammation and long treatment courses increase glaucoma risk. AAOBioMed Central
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HLA-B27–related uveitis (often linked to juvenile spondyloarthritis) – tends to be sudden and recurrent; each flare can spike the pressure. AAO
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Intermediate uveitis (pars planitis) – inflammation near the ciliary body can disturb aqueous production and outflow and may be long-standing. EyeWiki
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Herpetic anterior uveitis (HSV) – the virus inflames the trabecular meshwork (trabeculitis), causing painful pressure spikes. EyeWiki
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Varicella-zoster uveitis (VZV) – similar to HSV; pressure elevation can be prominent during active episodes. EyeWiki
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Cytomegalovirus (CMV) anterior uveitis – less common in healthy children but can cause recurrent pressure rises through trabeculitis. EyeWiki
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Toxoplasmosis uveitis – retinal chorioretinitis with spillover anterior inflammation; repeated inflammation can scar the angle. EyeWiki
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Toxocariasis – parasitic inflammation in kids; can lead to chronic intraocular inflammation and secondary glaucoma. EyeWiki
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Tuberculosis-related uveitis – granulomatous inflammation can damage the angle; treatment often needs steroids, adding steroid-response risk. EyeWiki
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Syphilitic uveitis – less common in children but important to test; inflammation can involve the anterior chamber and raise IOP. EyeWiki
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Sarcoidosis / early-onset sarcoidosis (Blau syndrome) – granulomas and chronic inflammation can produce PAS and pressure rise. EyeWiki
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Behçet disease – relapsing uveitis with vasculitis; frequent flares raise cumulative risk. EyeWiki
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Vogt–Koyanagi–Harada disease – panuveitis; steroid treatment courses are long, so steroid-response can add to risk. EyeWiki
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Post-traumatic uveitis (including sympathetic ophthalmia) – inflammation after injury can be intense and prolonged, with angle scarring. EyeWiki
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Lens-induced uveitis – leakage of lens proteins after trauma or surgery can trigger inflammation and secondary glaucoma. EyeWiki
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Corticosteroid-induced pressure rise during uveitis treatment – a treatment effect that can turn ocular hypertension into glaucoma if unrecognized. Children are often strong responders. NCBIGlaucoma Today
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Inflammatory bowel disease–associated uveitis – systemic inflammation can involve the eye and angle over time. EyeWiki
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Psoriatic arthritis–associated uveitis – another juvenile arthritis subtype with eye inflammation risk. AAO
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Post-surgical uveitis (after cataract or retinal surgery) – inflammation after surgery can create synechiae and angle closure in a small child. PMC
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Idiopathic chronic anterior uveitis – no clear systemic cause, but persistent low-grade inflammation still scars the angle and threatens the nerve. EyeWiki
Symptoms
Remember: some children have few symptoms, and vision loss can be silent. These are common clues:
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Red eye that keeps coming back or never fully clears.
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Light sensitivity (child hides from light or squints).
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Eye pain or discomfort, sometimes deep aching.
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Blurred vision that may change day to day.
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Tearing or watery eye without a cold.
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Headache, especially around the eyes or brow.
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Halos around lights, often with corneal swelling from high IOP.
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Nausea or vomiting when pressure rises quickly.
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Floaters (small spots or cobwebs), more with posterior inflammation.
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Small or irregular pupil, or a pupil that seems “stuck” (posterior synechiae).
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Eye rubbing or squeezing the lids shut.
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Squinting or frequent blinking while reading or using screens.
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One eye looks bigger or the cornea looks larger in a very young child (rare in uveitis, but high pressure in infants can enlarge the eye).
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No obvious complaints, but screening shows high pressure or optic-nerve changes during routine rheumatology/uveitis visits.
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School or play difficulties from blurred or fluctuating vision.
(These symptoms match how inflammation and pressure behave in uveitis and glaucoma in children; sometimes the only “symptom” is what the doctor finds during routine screening.) PMCAAO
Diagnostic tests
A) Physical exam–based tests
1) Age-appropriate visual acuity testing
For toddlers, doctors use picture charts, Lea symbols, Teller cards, or matching games. For older kids, a standard letter chart works. The goal is to measure how clearly each eye sees on its own. Vision can drop from inflammation, from glaucoma nerve damage, or from complications like macular swelling. AAO
2) Slit-lamp exam with cell and flare grading
A microscope light is used to look for cells and protein “flare” in the front chamber. This tells the doctor how active the uveitis is. Active inflammation increases the chance of pressure spikes and angle damage. A simple 0 to 4+ grading helps track progress over time. EyeWiki
3) Pupil exam for synechiae and iris bombe
The doctor checks pupil shape, reaction to light, and whether the pupil edge is stuck to the lens (posterior synechiae). If the pupil is stuck all around, fluid cannot move forward and the iris balloons (iris bombe), closing the angle. EyeWiki
4) Dilated optic-nerve evaluation
After dilating drops, the doctor studies the optic disc for thinning or cupping that suggests glaucoma damage. Comparing drawings or photos over time helps detect change early. AAO Journal
B) Manual / in-office functional tests
5) Tonometry (eye-pressure measurement)
Pressure is checked with tools like Goldmann applanation, Icare rebound, or Tono-Pen. In small children, crying or squeezing the lids can artificially raise the reading, so calm measurement techniques or an exam under anesthesia (EUA) may be needed. Pressure is the key number for glaucoma risk. AAOEyeWiki
6) Gonioscopy (angle examination)
A tiny mirrored lens lets the doctor see the drainage angle. They look for inflammatory debris, PAS (scars), or narrow/closed angle. Gonioscopy guides treatment and tells whether the mechanism is open-angle, angle-closure, or mixed. In younger children this is often done during EUA. AAO
7) Pachymetry (central corneal thickness)
A quick ultrasound or optical probe measures corneal thickness. Thick or thin corneas can skew IOP readings, so thickness helps interpret pressure correctly and improves risk assessment. AAO Journal
8) Visual field testing (perimetry)
Older children can do Humphrey or Goldmann visual fields. Younger kids may need simpler, kinetic methods. Visual fields show blind-spot enlargement or peripheral vision loss from glaucoma. Results can be variable in kids, so repeated testing helps. AAO JournalAAO
9) Laser flare photometry
This device quantifies protein “flare” in the front chamber. It is helpful for monitoring JIA-related uveitis, even when the slit-lamp looks quiet, and can guide how aggressively to control inflammation to protect the angle. PubMed
C) Laboratory and pathological tests
10) ANA (antinuclear antibody)
This blood test helps support a diagnosis of JIA-associated uveitis, especially in younger girls with chronic, quiet anterior uveitis. It also helps coordinate care with pediatric rheumatology. AAO
11) HLA-B27 typing
A blood test that supports HLA-B27–associated uveitis in children with back or joint problems or recurrent painful red eyes. It points to a tendency for acute pressure spikes during flares. AAO
12) ACE and lysozyme
Blood tests that, together with clinical signs and imaging, support sarcoidosis in the right setting. Early-onset sarcoidosis (Blau) is a pediatric form that can cause chronic uveitis. EyeWiki
13) Tuberculosis testing (IGRA or PPD)
Used when TB exposure or risk factors exist. Treating the infection is essential to control inflammation and protect the angle. EyeWiki
14) Syphilis serology (non-treponemal + treponemal tests)
Important in unexplained uveitis because syphilis can mimic many eye diseases. Identifying it changes treatment and protects vision. EyeWiki
15) Aqueous humor PCR (targeted)
In selected cases, a tiny fluid sample from the front chamber is tested for HSV, VZV, CMV, Toxoplasma or other pathogens. Pinpointing the cause helps choose the right therapy and limit steroid exposure. EyeWiki
D) Electrodiagnostic tests
16) Visual evoked potential (VEP)
VEP measures brain responses to visual patterns or flashes. It is useful when a child is too young or unable to do reliable vision charts or fields. It can objectively estimate visual function, and research shows VEP can help detect optic-pathway dysfunction and may pick up changes earlier than standard fields, though protocols vary and it is not a stand-alone glaucoma test. MDPI+1PMC
17) Electroretinography (ERG, including pattern ERG)
ERG measures retinal electrical activity. Pattern ERG reflects retinal ganglion cell function, the cells harmed in glaucoma. ERG helps separate retinal from optic-nerve causes of vision loss in hard pediatric cases. Some payers consider ERG investigational for routine glaucoma diagnosis, so clinicians use it selectively. NCBIIOVSCenters for Medicare & Medicaid Services
E) Imaging tests
18) Optical coherence tomography (OCT) of the optic nerve and RNFL/macula
OCT gives painless cross-section pictures. It measures nerve-fiber layer thickness and ganglion-cell layers. Thinning over time suggests glaucoma damage. Macular OCT also shows cystoid macular edema from uveitis, which lowers vision even when pressure is controlled. AAO Journal
19) Anterior-segment OCT (AS-OCT)
This OCT looks at the cornea, iris, and drainage angle. It helps confirm angle closure, iris bombe, or PAS, and guides whether laser or surgery is needed. AAO
20) Ultrasound biomicroscopy (UBM)
UBM uses high-frequency ultrasound to image the angle structures through cloudy corneas or small pupils. It is very helpful when the angle view is blocked by inflammation or scars. AAO
Non-pharmacological treatments
Each item includes what it is, why we do it (purpose), and how it helps (mechanism)—in simple English.
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Education & care plan (family + school).
Purpose: Make treatment doable every day.
Mechanism: Clear schedules for drops/shots, side-effect watch lists, and school accommodations reduce missed doses and flare-ups that raise pressure. -
Drop-giving skills & routines.
Purpose: Ensure the medicine actually reaches the eye and stays there.
Mechanism: Proper instillation and punctal occlusion (pressing the inner eyelid for 1–2 minutes) improve effect and cut body absorption, lowering systemic side-effects from pressure drops and steroids. -
Written flare-action plan.
Purpose: Act fast at the first sign of a flare (redness, light sensitivity, floaters, eye ache, haloes).
Mechanism: Rapid anti-inflammatory steps prevent scarring of the drain and sudden pressure spikes. -
Frequent follow-up & home symptom logs.
Purpose: Tight monitoring is crucial in kids because damage can be silent.
Mechanism: Trend IOP, optic nerve status, and activity; catch steroid-induced IOP rises early—especially with potent drops like difluprednate. PubMed -
Protective eyewear for sports/play.
Purpose: Prevent trauma that can trigger inflammation or angle damage.
Mechanism: Polycarbonate goggles reduce risk during ball sports or rough play. -
Blue-blocking and glare-reducing sunglasses outdoors.
Purpose: Improve comfort and reduce photophobia.
Mechanism: Tinted lenses decrease light-induced ciliary spasm and squinting. -
Warm compresses + preservative-free lubricants for surface comfort.
Purpose: Calm irritation that can mimic or worsen symptoms.
Mechanism: Stabilize tear film and reduce reflex inflammation on the eye surface. -
Healthy sleep and pain control (acetaminophen/ibuprofen as advised).
Purpose: Reduce stress hormones and inflammatory signaling.
Mechanism: Better sleep and comfort lower the systemic “inflammation tone.” -
Screen-time breaks.
Purpose: Limit eye strain and dryness that can make light sensitivity worse.
Mechanism: “20-20-20” rule maintains blinking and tear quality. -
Smoking-exposure elimination.
Purpose: Reduce extra oxidative stress and tear film instability.
Mechanism: Secondhand smoke raises inflammatory mediators that can aggravate uveitis. -
Vaccination review (with rheumatology).
Purpose: Keep infections down when on immunosuppressants.
Mechanism: Use inactivated vaccines on schedule; avoid live vaccines during significant immunosuppression (doctor-directed). -
TB & hepatitis screening before biologics.
Purpose: Make biologics safer.
Mechanism: Detect latent infections that TNF- or IL-6–blocking drugs could reactivate. (Standard rheumatology practice.) -
Allergy control (if relevant).
Purpose: Minimize extra eye itching/rubbing and surface inflammation.
Mechanism: Environmental control + antihistamine/mast-cell stabilizer drops (non-steroidal) reduce triggers. -
Systemic disease optimization.
Purpose: The eye calms when JIA is well-controlled.
Mechanism: Coordinated methotrexate/biologic therapy reduces autoimmune attack in the eye drain and iris. American College of Rheumatology -
Nutrition pattern: “anti-inflammatory plate.”
Purpose: Support immune balance and tissue repair.
Mechanism: Omega-3–rich fish, colorful produce, whole grains, and adequate vitamin D may help systemic inflammation (see supplement section for safe, pediatric-appropriate targets). Office of Dietary Supplements+1 -
Eye-drop preservatives minimization when possible.
Purpose: Reduce surface toxicity from benzalkonium chloride in chronic therapy.
Mechanism: Preservative-free or low-BAK options lower surface inflammation. -
Medication interaction check (grapefruit, St. John’s wort, etc.).
Purpose: Avoid drug-food/herbal interactions with calcineurin inhibitors or other agents.
Mechanism: Prevents under- or over-dosing from CYP3A or P-glycoprotein effects. -
Contact lens holiday during active inflammation.
Purpose: Reduce mechanical irritation and infection risk.
Mechanism: Supports corneal health while the uvea calms. -
Psychosocial support.
Purpose: Long treatments stress families.
Mechanism: Counseling and peer groups improve adherence and quality of life. -
Sun-safety + outdoor time (balanced).
Purpose: Encourage general health and vitamin D sufficiency while protecting eyes.
Mechanism: Short, protected outdoor time supports overall well-being; sunglasses and hats protect sensitive eyes. HealthyChildren.org
Drug treatments
Important pediatric note: Doses below are common clinical ranges. Children need individualized dosing by weight or body-surface area and specialist oversight. Never start/adjust these without your child’s ophthalmologist/rheumatologist.
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Topical corticosteroids (e.g., prednisolone acetate 1% q1–2h then taper; difluprednate 0.05% qid then taper).
Purpose: Rapidly shut down uveal inflammation.
Mechanism: Blocks multiple inflammatory pathways.
Side effects: Steroid-induced IOP rise (more likely and earlier in children, especially with difluprednate), cataract, infection risk—hence close IOP checks and early transition to steroid-sparing therapy. PubMedPMC -
Cycloplegics/mydriatics (e.g., atropine 1% qd–bid; homatropine 2–5% bid–qid).
Purpose: Pain relief and prevention/breaking of iris-lens adhesions (posterior synechiae).
Mechanism: Paralyzes ciliary muscle and dilates pupil to rest inflamed tissues and keep the pupil moving. EyeWiki -
Topical beta-blocker (timolol 0.25–0.5% qd–bid; use punctal occlusion; avoid in asthma/heart block).
Purpose: Lower IOP.
Mechanism: Decreases aqueous humor production.
Side effects: Bradycardia, bronchospasm (systemic absorption); use the lowest effective dose with punctal occlusion in children. -
Topical carbonic anhydrase inhibitor (dorzolamide 2% tid or brinzolamide 1% bid–tid).
Purpose: Lower IOP.
Mechanism: Reduces aqueous production in the ciliary body.
Side effects: Stinging, rare corneal edema (especially in endothelial disease). -
Prostaglandin analog (latanoprost 0.005% qhs; consider in quiescent uveitis).
Purpose: Lower IOP when inflammation is controlled.
Mechanism: Increases uveoscleral outflow.
Note: Contemporary pediatric data do not show increased risk of new uveitis with PGAs in children; they are reasonable once the eye is quiet. EyeWiki -
Alpha-2 agonist (brimonidine 0.1–0.2% bid–tid).
Purpose: Lower IOP.
Mechanism: Lowers aqueous production and increases uveoscleral outflow.
**Caution: Avoid in children <2 years and use extreme caution in <6 years or <20 kg due to risk of central nervous system depression, apnea, and lethargy. Ophthalmology TimesNature -
Oral carbonic anhydrase inhibitor (acetazolamide ~5–10 mg/kg/dose up to q6–8h short-term or 10–15 mg/kg/day divided; specialist dosing).
Purpose: Short-term IOP control (e.g., before surgery or during severe spikes).
Mechanism: Strong systemic reduction of aqueous production.
Side effects: Tingling, appetite loss, acidosis, kidney stone risk—monitor electrolytes, avoid with sulfonamide allergy. PMC -
Methotrexate (MTX) 10–15 mg/m² once weekly (often subcutaneous at higher doses for better absorption) + folic acid.
Purpose: Steroid-sparing anchor for JIA-associated and idiopathic non-infectious uveitis.
Mechanism: Down-regulates folate-dependent immune cell pathways; calms T-cell–driven inflammation.
Side effects: Nausea, liver enzyme rise, marrow suppression (rare at JIA doses); lab monitoring needed. BioMed CentralScienceDirect -
Adalimumab (ADA) 20 mg q2 weeks if <30 kg or 40 mg q2 weeks if ≥30 kg (often with MTX).
Purpose: First-line biologic when MTX is not enough; proven to reduce treatment failure and keep uveitis quiet.
Mechanism: Monoclonal antibody blocking TNF-α.
Side effects: Injection-site reactions, infection risk (screen TB, hepatitis). New England Journal of MedicinePubMed -
Other steroid-sparing immunomodulators/biologics (individualized):
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Mycophenolate mofetil (e.g., 600 mg/m² bid, max per specialist): purine synthesis blocker; GI upset, leukopenia.
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Cyclosporine (e.g., 3–5 mg/kg/day in divided doses): calcineurin inhibitor; monitor BP/creatinine.
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Infliximab (5–10 mg/kg IV at weeks 0, 2, 6, then q4–8wk): anti-TNF mAb; infusion reactions/infection risk.
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Tocilizumab (typical 8 mg/kg IV q4wk or 162 mg SC regimens): IL-6 receptor blocker; data support use in anti-TNF–refractory JIA-uveitis, especially with macular edema.
(These are chosen when MTX/ADA are inadequate or not tolerated, under pediatric rheumatology.) The LancetPMC
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Dietary molecular supplements
Big caveat: Evidence in children with uveitis is limited. Use a food-first approach. If supplements are considered, do it with your pediatric team. Doses below reflect typical pediatric-appropriate ranges or general public health guidance—not medical prescriptions.
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Vitamin D3: 400–600 IU/day for most children; higher only if deficient and prescribed. Function: bone/immune support. Mechanism: modulates T-cell responses. HealthyChildren.orgOffice of Dietary Supplements
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Omega-3 (EPA+DHA): aim for dietary fish; supplements for older kids/teens often 250–500 mg/day total EPA+DHA if intake is low. Function: pro-resolving lipid mediators. Mechanism: shifts eicosanoids toward anti-inflammatory pathways. Office of Dietary Supplements
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Probiotics (strain-specific, e.g., Lactobacillus/Bifidobacterium): ~10⁹ CFU/day commonly used; avoid in seriously ill or immunocompromised children unless advised. Function: gut–immune tuning. Mechanism: strengthens barrier, reduces LPS-driven inflammation. PMCAAFP
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Curcumin: pediatric data are limited; small studies show tolerability over a wide range—use modest doses (e.g., 250–500 mg/day in teens) only with clinician guidance. Function: NF-κB modulation. Mechanism: down-regulates cytokines. PubMedPMC
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Lutein/Zeaxanthin: typically food-based (greens/eggs). Function: macular pigment/antioxidant. Mechanism: quenches free radicals in retinal tissues.
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Vitamin C (diet-first; supplement only if intake is low): antioxidant recycling.
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Vitamin E (diet-first; avoid high-dose pills in kids): membrane antioxidant.
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Zinc (meet RDA via food; supplements only if deficient): supports innate and adaptive immunity.
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Selenium (meet RDA via food): selenoprotein antioxidant roles.
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Prebiotic fiber (inulin/oligosaccharides from foods or supplements): Function: feeds beneficial bacteria; Mechanism: boosts short-chain fatty acids that dampen inflammation.
Immune-modulating immunity/regenerative
Plain talk: There are no approved “stem-cell drugs” for pediatric uveitis or uveitic glaucoma. What is evidence-based are immune-modulating (“steroid-sparing”) medications that calm the disease safely. Experimental cell-based therapies exist only in research programs.
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Methotrexate (weekly, 10–15 mg/m²).
Function: First steroid-sparing backbone; reduces flares and protects the drain from inflammatory scarring.
Mechanism: Folate pathway inhibition reduces autoreactive lymphocytes. BioMed Central -
Adalimumab (q2wk, weight-based).
Function: Proven to prevent treatment failure in JIA-uveitis when MTX alone falls short.
Mechanism: TNF-α blockade reduces uveal cytokine storm. New England Journal of Medicine -
Infliximab (IV mAb anti-TNF).
Function: For fast control in severe or ADA-refractory cases.
Mechanism: Neutralizes TNF-α; often used with MTX. -
Tocilizumab (IL-6 receptor blockade).
Function: Useful after anti-TNF failure, and for uveitic cystoid macular edema.
Mechanism: Shuts down IL-6–driven inflammation; IV or SC regimens. PMC -
Cyclosporine or tacrolimus (calcineurin inhibitors).
Function: Add-on steroid-sparing control.
Mechanism: Blocks T-cell activation via calcineurin pathway (monitor kidney/BP). -
Experimental/regenerative approaches (research only):
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Mesenchymal stromal cell (MSC) therapies / exosomes: Early animal and small human case-series suggest anti-inflammatory effects in autoimmune uveitis, but this is not standard care and should be done only in clinical trials.
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Hematopoietic stem cell transplantation (HSCT): Considered only for extreme, refractory systemic JIA (not for typical eye-limited disease) because of serious risks; rarely relevant to uveitis itself. PMC+1Frontiers
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Surgeries
Context: Surgery is considered when, despite quieting the inflammation, pressure remains unsafe or optic nerve damage progresses. The eye should be as quiet as possible before and after surgery.
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Angle surgery (goniotomy or trabeculotomy).
Procedure: Opening or cannulating the eye’s natural drain from inside the eye (goniotomy) or from the white of the eye (trabeculotomy).
Why: Works best when the angle is open but clogged with inflammatory debris or synechiae are limited; often an early choice in children. EyeWiki -
Gonioscopy-assisted transluminal trabeculotomy (GATT).
Procedure: A suture or micro-catheter is threaded 360° through the drain and pulled to open it.
Why: Restores native outflow with an ab interno approach; useful when angle is accessible. -
Trabeculectomy with antimetabolite (e.g., mitomycin-C).
Procedure: Creates a new drain under the conjunctiva (a “bleb”).
Why: For eyes needing very low target pressures; children scar vigorously, so antimetabolites and meticulous inflammation control matter. -
Glaucoma drainage devices (GDD) (e.g., Ahmed, Baerveldt).
Procedure: A small plate and tube shunt fluid to a plate reservoir.
Why: Often preferred in pediatric uveitic glaucoma; good long-term success when inflammation is controlled. EyeWiki -
Cyclophotocoagulation (CPC: diode or micropulse).
Procedure: Laser (outside the eye) reduces ciliary body fluid production.
Why: Rescue procedure for refractory eyes or when other surgeries are not possible; micropulse aims to be gentler. (Use cautiously in uveitis; decisions are individualized.)
Prevention strategies
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JIA uveitis screening on schedule (per pediatric rheum/ophthalmology guidance). Early detection prevents silent damage. American College of Rheumatology
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Aim for “no cells.” Keep anti-inflammatory therapy strong enough to fully suppress uveitis. ScienceDirect
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Minimize steroid exposure long-term. Transition to MTX/adalimumab early to avoid steroid-induced pressure rise. New England Journal of MedicinePubMed
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IOP checks after any steroid change (start, increase, potent formulation). Kids can spike quickly—especially with difluprednate. PubMed
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Teach punctal occlusion to reduce systemic side effects from drops.
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Check for infections before biologics (TB/hepatitis) and keep inactivated vaccines up to date.
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Protect eyes during sports with shatter-resistant eyewear.
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Medication reconciliation at every visit (watch CYP3A interactions with calcineurin inhibitors).
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Healthy lifestyle (sleep, nutrition, outdoor time with sun protection). HealthyChildren.org
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Rapid access pathway for flares or pressure spikes (same-week urgent slots).
What to eat” & “what to avoid
Diet does not replace medicines, but it supports the immune system and overall eye health.
Eat more of:
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Fatty fish (2 child-size servings/week: salmon, sardines) for omega-3s. Office of Dietary Supplements
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Colorful vegetables & fruits (rainbow plate daily) for carotenoids and antioxidants.
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Whole grains & legumes for fiber that feeds a healthy gut microbiome.
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Greek yogurt or fermented foods if tolerated (natural probiotics; choose low sugar). PMC
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Vitamin D sources (fortified milk, eggs) and a doctor-guided supplement if intake/levels are low. HealthyChildren.org
Limit/avoid:
- Sugary drinks and ultra-processed snacks that amplify systemic inflammation.
- Very salty/instant foods that worsen fluid retention and blood pressure.
- Energy drinks/caffeine (teens) that can cause palpitations alongside beta-blocker drops.
- Grapefruit (juice or whole) if taking cyclosporine/tacrolimus (interaction—ask doctor).
- Herbal supplements without medical review (e.g., St. John’s wort lowers calcineurin inhibitor levels; turmeric/curcumin can thin blood at high dose).
When to see the doctor now
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New eye pain, redness, light sensitivity, haloes, headache/nausea, or sudden blur.
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Any IOP spike symptoms or home device flags (if available).
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Side-effects after drops: unusual sleepiness, lethargy/apnea in a small child after brimonidine; wheeze/bradycardia after beta-blockers; tingling/lethargy after acetazolamide. Ophthalmology Times
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Missed biologic dose with new floaters/redness.
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Before sports seasons for eyewear updates.
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Immediately after any eye injury.
FAQs
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Is pediatric uveitic glaucoma contagious?
No. It’s an immune problem, not an infection (unless a specific infection is identified). -
Can my child “grow out of it”?
Some children achieve long remissions, but long-term monitoring is essential because uveitis can recur—even when arthritis is quiet. Hopkins Medicine -
What’s the vision goal?
Protect the optic nerve and keep vision development normal. That means zero eye inflammation and safe pressure at every visit. ScienceDirect -
Why move off steroids so quickly?
Kids are strong “steroid responders.” Early steroid-sparing agents lower the risk of steroid-induced glaucoma and cataract. PubMed -
Is adalimumab safe in children?
In the SYCAMORE randomized trial, adalimumab (weight-based dosing q2 weeks, added to MTX) reduced treatment failures in JIA-uveitis versus placebo. Screening for TB/hepatitis is required. New England Journal of Medicine -
Are prostaglandin drops risky in uveitis?
Modern pediatric data do not show increased risk of new uveitis with PGAs; your doctor may add them once the eye is quiet to help pressure. EyeWiki -
Why can’t my toddler use brimonidine?
It can depress the central nervous system in young/small children—hence contraindicated under 2 years and used very cautiously under 6 years or <20 kg. Ophthalmology Times -
How often will labs be needed?
MTX and other immunomodulators require periodic blood tests (liver enzymes, blood counts). Frequency depends on the drug and your child’s age/weight. -
Will surgery cure glaucoma?
Surgery controls pressure; it doesn’t cure the tendency to high pressure. Inflammation control still matters before and after surgery. -
Which surgery is “best”?
It depends on the eye’s angle, scarring, age, and disease control. Angle surgeries and shunts (Ahmed/Baerveldt) are common choices in children with uveitis when medicine isn’t enough. EyeWiki -
Can my child play sports?
Yes, with protective eyewear and good disease control. Avoid contact sports during active flares or right after eye surgery. -
Do screens worsen the disease?
Screens don’t cause uveitis, but long sessions can worsen dryness and discomfort. Use the 20-20-20 rule and frequent blinking. -
What about vaccines while on biologics?
Inactivated vaccines are encouraged; live vaccines are usually avoided during significant immunosuppression—coordinate with rheumatology/pediatrics. -
Is there a role for stem-cell treatments now?
Not in standard care. Cell-based approaches remain experimental and limited to clinical trials; HSCT is reserved for extreme systemic JIA, not typical eye-limited disease. PMCFrontiers -
What’s the long-term outlook?
With early screening, zero-tolerance for inflammation, smart steroid-sparing therapy (MTX ± ADA), and timely surgery when needed, many children maintain good vision into adulthood. New England Journal of Medicine
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The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: August 20, 2025.
