Uveitic Glaucoma

Uveitic glaucoma is high pressure inside the eye that happens in a person who has uveitis (inflammation inside the eye). The uvea is the “middle coat” of the eye—made of the iris (the colored part), ciliary body (the focusing muscle and fluid factory), and choroid (the blood-vessel layer behind the retina). When the uvea becomes inflamed, it releases cells, proteins, and chemical messengers into the clear fluid inside the front of the eye (aqueous humor). This inflammation can block the eye’s drainage meshwork (the trabecular meshwork) or can make the iris stick to nearby structures. Either problem slows down the outflow of fluid and makes the internal eye pressure (called intraocular pressure, IOP) rise. If high pressure continues, it damages the optic nerve (the cable that sends vision signals to the brain) and causes glaucoma—a pattern of vision loss that usually starts in the side (peripheral) vision and can move inward if untreated.

Uveitic glaucoma is a type of secondary glaucoma that happens in people who have uveitis, which is inflammation inside the eye. The uvea includes the iris (the colored part), the ciliary body (which makes fluid), and the choroid (the blood vessel layer). When these tissues get inflamed, they release immune cells and inflammatory chemicals that make the eye’s drainage tissue swell, clog, or scar. Eye fluid (called aqueous humor) cannot leave the eye normally, so the eye pressure becomes too high. High eye pressure damages the optic nerve, which is the cable that sends visual signals from the eye to the brain. Over time, this damage causes blind spots and can lead to permanent vision loss if not treated. Uveitic glaucoma may be short-term during a flare, long-lasting if scarring occurs, or come and go with repeated inflammation. Steroid medicines used to control uveitis can also raise eye pressure in some people, so care must balance control of inflammation with safe eye pressure.

How does uveitic glaucoma happen?

Inside the eye, clear fluid flows from the ciliary body into the front chamber and drains out through tiny filters: the trabecular meshwork (main route) and the uveoscleral pathway (secondary route). In uveitis, immune cells and proteins flood the front chamber. They clog and swell the trabecular meshwork (called trabeculitis) and can create sticky adhesions called synechiae. Posterior synechiae glue the iris to the lens and can block the pupil (pupillary block), while peripheral anterior synechiae (PAS) glue the iris to the angle, physically closing the drain. The iris can also swell (iritis), the ciliary body can inflame (cyclitis), and steroid drops or injections can trigger a steroid response that further raises pressure. Repeated flares lead to permanent scarring of the angle. The optic nerve suffers from pressure-related stress and poor blood flow, losing nerve fibers and thinning the retinal nerve fiber layer. The final common pathway is optic neuropathy, which shows up as visual-field loss.

Inflammation can raise eye pressure in several ways. First, the inflammatory cells and proteins can swell or clog the trabecular meshwork (trabeculitis), so fluid cannot exit easily, leading to secondary open-angle glaucoma. Second, inflammation can make the iris form synechiae—sticky scars—either behind the iris (posterior synechiae, causing pupillary block and “iris bombe,” where the iris bows forward) or in front between the iris and the drainage angle (peripheral anterior synechiae, or PAS), both of which can cause secondary angle-closure glaucoma. Third, the medicines used to calm uveitis—especially steroids—can themselves raise eye pressure in susceptible people, creating steroid-induced ocular hypertension or steroid-induced glaucoma. Fourth, long-standing inflammation can starve eye tissues of oxygen and trigger new, fragile blood vessels to grow in the angle (neovascularization), which can close the angle with scar tissue and cause very high pressures.

Uveitic glaucoma is particularly challenging because the doctor must balance two goals at the same time: quiet the inflammation and lower the pressure. Treating only one often worsens the other. For example, avoiding steroids may let inflammation run wild and scar the angle; using too much steroid without monitoring may spike the pressure.

Types

1. Secondary open-angle uveitic glaucoma
   The drainage angle looks open on gonioscopy, but inflammation has swollen or clogged the trabecular meshwork (cells, proteins, debris), so fluid does not drain well and the pressure rises.

2. Secondary angle-closure from posterior synechiae with pupillary block
   Inflammation makes the iris stick to the lens behind it, closing the pupil. Fluid made behind the iris cannot pass forward, so pressure builds in the back of the iris, bowing it forward (“iris bombe”) and closing the angle.

3. Secondary angle-closure from peripheral anterior synechiae (PAS)
   Repeated or severe inflammation causes scar bridges between the iris and the angle wall. These bridges progressively seal the angle shut, reducing drainage and raising pressure.

4. Steroid-induced ocular hypertension/glaucoma
   Some people are “steroid responders.” Topical, injected, implant, or systemic steroids stiffen the trabecular meshwork, slow outflow, and raise IOP. In uveitis, steroids are often needed, so careful monitoring is essential.

5. Neovascular (rubeotic) glaucoma secondary to chronic uveitis
   Chronic inflammation can lead to oxygen stress and growth of new vessels on the iris and angle. These vessels contract and form scar tissue that closes the angle.

6. Acute uveitic IOP spikes (trabeculitis pattern)
   In viral anterior uveitis (e.g., herpes simplex, zoster, CMV), the trabecular meshwork itself becomes inflamed, causing sudden, large pressure spikes even with only mild eye redness.

7. Chronic uveitic glaucoma with optic nerve damage
   Long-standing, low-grade inflammation with persistent medium-high pressure slowly damages the optic nerve and narrows side vision.

8. Posner–Schlossman syndrome (glaucomatocyclitic crisis)
   Recurrent, brief attacks of mild uveitis plus very high pressure in one eye. Often linked to viral triggers. Between attacks the eye can be quiet.

9. Fuchs heterochromic iridocyclitis-related glaucoma
   Chronic, mild anterior uveitis with little pain, fine white deposits on the cornea, loss of iris color, and a silent, gradual pressure rise.

10. Juvenile idiopathic arthritis (JIA)-associated uveitic glaucoma
    Often a chronic, “quiet” anterior uveitis in children that forms synechiae and PAS over time; glaucoma may be discovered late unless screened.

11. HLA-B27-associated uveitis with pressure elevation
    Sudden, painful anterior uveitis with fibrin, sometimes hypopyon, and IOP fluctuations during flares.

12. Viral anterior uveitis (HSV, VZV, CMV) with IOP spikes
    Unilateral high pressure during flares, sector iris atrophy, and reduced corneal sensation (especially herpetic).

13. Lens-induced uveitis with secondary glaucoma (phacolytic, phacoantigenic)
    Leaking lens proteins or immune reaction to lens material inflame the anterior chamber, clog outflow, and raise pressure.

14. Trauma-related uveitis with secondary glaucoma
    Blunt or penetrating injury triggers inflammation and/or synechiae; angle damage can coexist, compounding pressure rise.

15. Post-surgical uveitis-glaucoma (e.g., UGH syndrome)
    An intraocular lens rubs the iris or ciliary body (Uveitis-Glaucoma-Hyphema), causing chronic inflammation and pressure spikes.

16. Sarcoidosis-associated uveitis
    Granulomatous inflammation creates heavy protein/cell load and synechiae; steroid treatment may add a pressure rise.

17. Tubercular uveitis-related glaucoma
    Chronic granulomatous uveitis with PAS and pressure elevation; systemic evaluation is needed.

18. Syphilitic uveitis with pressure changes
    Can mimic many patterns of uveitis; pressure may rise during active inflammation.

19. Behçet disease/Vogt-Koyanagi-Harada (VKH)-related uveitis
    Recurrent or diffuse inflammation can damage outflow or form synechiae, eventually raising pressure.

20. Masquerade syndromes (e.g., intraocular lymphoma) presenting like uveitis with glaucoma
    Cancer cells in the eye imitate uveitis, cause inflammation-like debris, and elevate pressure; biopsy may be required.

Causes

1. Active anterior uveitis itself – cells and proteins block the drainage meshwork.

2. Trabeculitis – the drain tissue is inflamed and swells shut.

3. Posterior synechiae – iris sticks to lens, causing pupillary block and iris bombe.

4. Peripheral anterior synechiae (PAS) – scar bridges close the angle permanently.

5. Steroid response – steroid medicines stiffen the meshwork and slow fluid outflow.

6. Neovascularization of the angle – new vessels and membranes pull the angle closed.

7. Herpes simplex or zoster anterior uveitis – viral irritation causes sharp IOP spikes.

8. Cytomegalovirus (CMV) anterior uveitis – recurrent IOP spikes with mild redness.

9. Posner–Schlossman syndrome – episodic mild iritis with very high IOP.

10. Fuchs heterochromic iridocyclitis – quiet, chronic inflammation with slow IOP rise.

11. Juvenile idiopathic arthritis (JIA) uveitis – silent uveitis causes synechiae and PAS.

12. HLA-B27 uveitis – fibrin and debris clog outflow during flares.

13. Sarcoidosis – granulomas and protein-rich fluid block outflow.

14. Tuberculosis – chronic granulomatous uveitis forms PAS.

15. Syphilis – protean uveitis patterns with pressure elevation.

16. Lens-induced uveitis (phacolytic/phacoantigenic) – lens proteins and immune reaction clog the drain.

17. Trauma – inflammatory debris and synechiae after injury.

18. Post-operative irritation (e.g., UGH) – mechanical rubbing triggers uveitis and pressure spikes.

19. Silicone oil in the eye (after retinal surgery) – can block the angle and inflame tissues.

20. Masquerade/intraocular tumor – malignant cells mimic uveitis and obstruct outflow.

Symptoms

1. Eye pain or ache – a dull, deep pain from inflammation and pressure.

2. Redness – inflamed blood vessels on the white of the eye (ciliary flush may ring the cornea).

3. Blurred or foggy vision – from corneal swelling, inflammatory haze, or optic nerve stress.

4. Halos around lights – corneal edema bends light and creates rainbow rings.

5. Sensitivity to light (photophobia) – inflamed iris and ciliary body react painfully to light.

6. Headache or brow ache – referred pain from high pressure.

7. Tearing and discomfort – surface irritation from inflammation.

8. Floaters – inflammatory cells drifting in the visual jelly (vitreous) if posterior uveitis is present.

9. Glare and reduced contrast – scatter from corneal edema or inflammatory haze.

10. Nausea and vomiting – possible with very high pressure spikes.

11. Small, irregular, or stuck pupil – synechiae alter pupil shape and movement.

12. Color desaturation or dim vision – optic nerve stress can reduce color depth.

13. Side-vision loss – classic glaucoma pattern; often silent at first.

14. Asymptomatic high pressure – some people feel nothing until damage has progressed.

15. Recurrent “attacks” in one eye – especially in viral or Posner–Schlossman patterns.

Diagnostic tests

Below are 20 key tests. I’ve grouped them by the type of test and kept the language simple. Doctors choose a subset based on your history and exam.

Physical Exam

1. Visual acuity test (Physical Exam)
   Reading letters on a chart measures how sharp your central vision is. It sets a baseline and shows how much inflammation or pressure is affecting sight.

2. External and slit-lamp inspection for redness pattern (Physical Exam)
   The doctor looks for ciliary flush (a violet-red ring around the cornea) that signals internal inflammation rather than simple surface irritation.

3. Pupil exam for size, shape, and reactivity (Physical Exam)
   A small, irregular, or non-moving pupil suggests posterior synechiae; poor light reaction or pain on light can reflect active uveitis.

4. Confrontation visual fields (Physical Exam)
   A bedside check for side-vision loss can reveal glaucoma damage even before formal machine testing.

5. Digital IOP palpation (Physical Exam)
   Gently pressing the closed eyelid with fingertips gives a rough sense of pressure when tools aren’t yet used; a “rock-hard” eye suggests very high IOP and urgent care.

Manual/Clinical Tests

6. Goldmann applanation tonometry (Manual Test)
   The gold standard pressure measurement. A blue light and a small prism gently touch the numbed cornea to measure IOP accurately.

7. Slit-lamp biomicroscopy with anterior chamber cell/flare grading (Manual Test)
   A microscope with a bright beam lets the doctor count cells (inflammatory cells) and flare (protein) in the chamber using SUN grading, confirming active uveitis.

8. Gonioscopy (Manual Test)
   A mirrored contact lens shows the drainage angle. The doctor looks for open vs closed angle, PAS, neovascularization, inflammatory debris, and signs of iris bombe.

9. Dilated fundus exam (Manual Test)
   After dilating the pupil, the doctor examines the optic nerve for cupping (glaucoma damage), checks the macula for swelling, and looks for posterior uveitis.

10. Central corneal thickness (pachymetry) (Manual Test)
    A quick touch probe or OCT measures corneal thickness. Thick or thin corneas can make pressure readings look lower or higher than the true value and influence risk estimates.

11. Automated perimetry (visual field test) (Manual Test)
    You press a button when you see spots of light. The pattern shows typical glaucoma field loss and helps track progression over time.

12. IOP diurnal curve or home tonometry (Manual/Monitoring)
    Repeated pressure checks through the day can reveal pressure spikes tied to inflammation or steroid use that a single clinic reading might miss.

Laboratory and Pathology

13. Basic inflammatory and infectious screen (Lab/Pathological)
    Tests may include CBC, ESR/CRP, syphilis serology (RPR/VDRL and treponemal test), Quantiferon-TB, ACE/lysozyme (sarcoid clues), and sometimes HIV testing—guided by history and local patterns.

14. Autoimmune markers when indicated (Lab/Pathological)
    HLA-B27, ANA, RF, or others are chosen based on symptoms (e.g., back pain with HLA-B27 disease, childhood arthritis in JIA).

15. Aqueous humor PCR (Lab/Pathological)
    A tiny fluid sample from the front of the eye can be tested for HSV, VZV, CMV, or toxoplasma DNA if viral or infectious uveitis is suspected, especially in one-eyed, recurrent, high-IOP cases.

16. Cytology / flow cytometry for masquerade (Lab/Pathological)
    If cancer masquerade is suspected, specialized testing on fluid or tissue can look for malignant cells (e.g., lymphoma).

Electrodiagnostic

17. Visual evoked potential (VEP) (Electrodiagnostic)
    Measures the speed and strength of signals from eye to brain. It helps when optic nerve function is uncertain or when media (cornea/lens) are cloudy.

18. Electroretinography (ERG), including photopic negative response (Electrodiagnostic)
    Tests the retina’s electrical response. The photopic negative response can reflect ganglion cell health, complementing visual field and OCT in advanced or complex cases.

Imaging

19. Optical coherence tomography (OCT) of the optic nerve and macula (Imaging)
    A light-based scan measures retinal nerve fiber layer (RNFL) and ganglion cell thickness (glaucoma markers) and checks for macular edema from uveitis that can also blur vision.

20. Anterior-segment OCT or ultrasound biomicroscopy (UBM) (Imaging)
    These show the angle and iris in cross-section. They confirm iris bombe, PAS, plateau iris, lens position, and how much the angle is closed—useful for choosing laser or surgery.

Non-pharmacological treatments (therapies and others)

1. Strict flare control plan: The most important non-drug step is a personalized plan to recognize triggers (stress, infections) and seek early care. Purpose: prevent angle damage. Mechanism: earlier anti-inflammatory action prevents scarring.

2. Protective sunglasses and dim-light strategies: Reduce light sensitivity and ciliary spasm. Mechanism: lowers photophobia-related discomfort that worsens inflammation behaviors (squeezing, rubbing).

3. Cold compress during painful flares: Brief, clean cold packs reduce surface vessel dilation and discomfort. Mechanism: vasoconstriction reduces ache.

4. Warm compress and lid hygiene (if blepharitis): Calmer lids reduce surface inflammation that can aggravate uveitis. Mechanism: improves tear film and lowers cytokine load.

5. Correct drop-instillation technique: One drop at a time, 5 minutes apart, no bottle-tip touch. Mechanism: ensures proper dosing and reduces contamination.

6. Punctal occlusion (digital pressure) after drops: Gently press inner corner for 2–3 minutes. Mechanism: keeps medicine in the eye and reduces systemic side effects.

7. Preservative-minimizing strategy: Use preservative-free lubricants or lower-BAK regimens. Mechanism: reduces ocular surface toxicity that can worsen inflammation.

8. Contact lens holiday during flares: Prevents microtrauma and infection risk. Mechanism: reduces friction and inflammatory triggers.

9. Smoking cessation: Smoking increases oxidative stress and worsens vascular supply to the optic nerve. Mechanism: improves microcirculation and healing.

10. Regular aerobic exercise (when eye is quiet): Moderate exercise may slightly lower IOP and improve vascular health. Mechanism: enhances outflow and perfusion (avoid heavy straining).

11. Blood pressure and sleep apnea control: Nocturnal hypotension and untreated OSA can harm optic-nerve perfusion. Mechanism: stabilizes optic-nerve blood flow.

12. Anti-inflammatory diet pattern (Mediterranean-style): Emphasize fish, leafy greens, legumes, whole grains, nuts. Mechanism: lower systemic inflammation and oxidative stress.

13. Hydration and caffeine moderation: Adequate fluids with moderate caffeine (avoid large boluses). Mechanism: avoids transient IOP spikes from dehydration or sudden caffeine loads.

14. Stress-reduction practice (breathing, yoga, CBT): Lowers sympathetic surges that can trigger flares. Mechanism: reduces inflammatory signaling via neuro-immune pathways.

15. Blue-light and glare management: Night driving filters and screen adjustments. Mechanism: reduces ciliary strain.

16. Eye protection at work and sport: Goggles prevent trauma-induced flares. Mechanism: avoids secondary inflammation and bleeding.

17. Systemic disease co-management: Coordinate with rheumatology/infectious disease. Mechanism: treating the root disease lowers eye inflammation burden.

18. Regular follow-up with visual fields/OCT: Early detection of nerve change guides treatment. Mechanism: prevents silent progression.

19. Adherence aids (alarms, apps): Missed drops are a common cause of failure. Mechanism: improves dosing consistency.

20. Education on steroid risks: Understand that steroids help uveitis but can raise IOP. Mechanism: prompts timely pressure checks and dose adjustments.

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Drug treatments

Doses are typical adult ranges; individual plans vary. Infectious uveitis requires targeted antimicrobials plus careful pressure control. Always treat the inflammation and the pressure together.

1. Topical corticosteroids (e.g., prednisolone acetate 1% q1–4h, then taper): Purpose: calm uveitis fast. Mechanism: suppresses cytokines and leukocytes. Side effects: steroid response (raised IOP), cataract, delayed healing, infection risk.

2. Cycloplegics (e.g., homatropine 5% bid; atropine 1% qd–bid during flares): Purpose: relieve pain, prevent posterior synechiae. Mechanism: relax ciliary muscle and dilate pupil. Side effects: light sensitivity, dry mouth, rare angle-closure in narrow angles.

3. Topical beta-blockers (e.g., timolol 0.5% qd–bid): Purpose: lower IOP quickly. Mechanism: decreases aqueous production. Side effects: fatigue, bradycardia, bronchospasm (avoid in asthma/COPD, caution in heart block).

4. Topical carbonic anhydrase inhibitors (e.g., dorzolamide 2% tid; brinzolamide 1% tid): Purpose: reduce IOP. Mechanism: lowers aqueous production. Side effects: bitter taste, corneal irritation; caution in sulfonamide allergy.

5. Alpha-2 agonists (e.g., brimonidine 0.2% tid): Purpose: reduce IOP and possibly offer neuroprotection. Mechanism: decreases production and increases uveoscleral outflow. Side effects: fatigue, dry mouth, allergy, caution in children.

6. Rho-kinase inhibitors (netarsudil 0.02% qhs): Purpose: lower IOP when others are not enough. Mechanism: improves trabecular outflow and reduces episcleral venous pressure. Side effects: conjunctival redness, corneal verticillata.

7. Systemic carbonic anhydrase inhibitor (acetazolamide 250–500 mg bid–qid short term): Purpose: rapid pressure drop in spikes or pre-op. Mechanism: reduces aqueous production. Side effects: tingling, fatigue, GI upset, kidney stones, metabolic acidosis; avoid in sulfa allergy and severe kidney disease.

8. Steroid-sparing immunomodulators (e.g., methotrexate 10–25 mg weekly with folic acid; mycophenolate 1–1.5 g bid; azathioprine 1–2 mg/kg/day): Purpose: control non-infectious uveitis long term to reduce steroid burden. Mechanism: dampen aberrant immune activity. Side effects: liver toxicity, bone-marrow suppression, infection risk; lab monitoring required.

9. Biologics for non-infectious uveitis (e.g., adalimumab 40 mg sc q2w; infliximab 5–10 mg/kg IV q4–8w; tocilizumab 4–8 mg/kg IV q4w): Purpose: control refractory inflammation. Mechanism: block TNF-α or IL-6 pathways. Side effects: serious infections, reactivation of TB/hepatitis; screening and specialist oversight needed.

10. Antivirals for herpetic/CMV uveitis (e.g., acyclovir/valacyclovir; valganciclovir for CMV): Purpose: remove infectious trigger and reduce trabeculitis-related IOP spikes. Mechanism: inhibit viral replication. Side effects: kidney toxicity (acyclovir), bone-marrow suppression (valganciclovir); dosing adjusted for renal function.

Note on prostaglandin analogs: These are powerful glaucoma drops (e.g., latanoprost qhs). In active uveitis, some clinicians avoid them due to concern for inflammation or cystoid macular edema, especially with herpetic disease; others use them cautiously in quiet eyes. Decisions should be individualized.

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Dietary molecular supplements

These are supportive, not cures; discuss with your doctor, especially if pregnant, on blood thinners, or with kidney/liver disease.

1. Nicotinamide (vitamin B3) 1–3 g/day in divided doses: Function: supports retinal ganglion cell energy. Mechanism: boosts NAD+ pools and mitochondrial resilience.

2. Omega-3 fatty acids (EPA/DHA) 1–2 g/day: Function: anti-inflammatory support. Mechanism: shifts eicosanoid balance toward less inflammatory mediators.

3. Coenzyme Q10 (100–200 mg/day): Function: antioxidant and mitochondrial cofactor. Mechanism: improves oxidative phosphorylation and scavenges free radicals.

4. Alpha-lipoic acid (300–600 mg/day): Function: broad antioxidant. Mechanism: regenerates other antioxidants and improves redox balance.

5. Ginkgo biloba extract (120–240 mg/day): Function: microcirculatory support. Mechanism: vasoregulatory and antioxidant effects; caution with anticoagulants.

6. Curcumin (turmeric extract) 500–1000 mg/day with piperine: Function: systemic anti-inflammatory support. Mechanism: NF-κB and cytokine modulation.

7. Resveratrol 100–250 mg/day: Function: antioxidant/anti-inflammatory. Mechanism: SIRT pathways and oxidative stress reduction.

8. Magnesium 200–400 mg/day (elemental): Function: vascular tone and nerve function. Mechanism: smooth-muscle relaxation and NMDA modulation; adjust in kidney disease.

9. Vitamin D3 1000–2000 IU/day (per labs): Function: immune modulation and bone/nerve health. Mechanism: nuclear receptor effects on immune cells.

10. Vitamin C 500–1000 mg/day: Function: aqueous-phase antioxidant. Mechanism: scavenges free radicals; large boluses may transiently affect IOP—use steady daily dosing.

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Regenerative / stem-cell” drugs

There are no approved “stem-cell drugs” for uveitic glaucoma. In non-infectious uveitis, we use immunomodulatory (immune-suppressing, not boosting) therapies to stop the harmful eye inflammation that leads to glaucoma damage. Below are six evidence-based agents used by specialists; they temper the immune system to protect the eye.

1. Methotrexate (10–25 mg weekly + folic acid): Function: steroid-sparing control of chronic uveitis. Mechanism: inhibits folate-dependent cell proliferation and cytokine production.

2. Mycophenolate mofetil (1–1.5 g bid): Function: long-term control in many uveitis types. Mechanism: inhibits lymphocyte purine synthesis.

3. Azathioprine (1–2 mg/kg/day): Function: alternative steroid-sparing agent. Mechanism: purine analog that reduces lymphocyte activity.

4. Adalimumab (40 mg sc every 2 weeks): Function: FDA-approved biologic for non-infectious uveitis. Mechanism: neutralizes TNF-α, a key inflammatory cytokine.

5. Infliximab (5–10 mg/kg IV): Function: powerful control for refractory cases (e.g., Behçet). Mechanism: monoclonal antibody to TNF-α.

6. Tocilizumab (4–8 mg/kg IV q4w or sc forms): Function: for uveitis with macular edema or resistant inflammation. Mechanism: blocks IL-6 signaling.

Experimental note: Mesenchymal stem-cell therapy and neuroprotective cell-based approaches are being studied for optic-nerve diseases, but they are not standard care for uveitic glaucoma.

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Surgeries

1. Laser peripheral iridotomy (LPI): A small laser hole is made in the iris to bypass a blocked pupil in pupillary block (iris bombe). Why: reopens fluid flow from back to front, preventing angle closure.

2. Trabeculectomy with antimetabolites (e.g., MMC): Creates a new drainage pathway under the conjunctiva. Why: lowers IOP when drops and lasers fail; antimetabolites fight scarring in inflamed eyes.

3. Glaucoma drainage devices (Ahmed, Baerveldt): A tube shunts fluid to a plate under the eye’s surface. Why: reliable pressure control in uveitic eyes prone to scarring.

4. Cyclophotocoagulation (traditional or micropulse): Laser applied to ciliary body reduces fluid production. Why: for eyes uncontrolled by other means or as a safer option in scar-prone tissues.

5. Goniosynechialysis and angle procedures (selected cases): Mechanical breaking of fresh PAS and angle-based MIGS/goniotomy in carefully chosen, quiet eyes. Why: reopen blocked angle when scarring is not permanent.

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Preventions

1. Early treatment of every uveitis flare: Prevents angle scarring.

2. Adherence to steroid tapers: Too-fast taper invites rebound; too prolonged invites steroid pressure rise.

3. Scheduled pressure checks during steroid therapy: Catch steroid response early.

4. Vaccination and infection control per doctor advice: Lowers infectious triggers; screen for TB before biologics.

5. Systemic disease control: Keep arthritis, sarcoid, or other drivers quiet with the right specialist.

6. Avoid unnecessary steroid exposure: Use the lowest effective dose and add steroid-sparing agents when needed.

7. Eye protection and injury avoidance: Trauma can trigger uveitis.

8. Stop smoking and control vascular risks: Protects optic nerve perfusion.

9. Maintain healthy sleep and treat sleep apnea: Stabilizes nighttime blood flow to the nerve.

10. Keep all follow-ups for OCT/fields: Detect silent glaucoma progression early.

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When to see a doctor (red flags)

• Immediately for severe eye pain, sudden vision drop, halos with headache and nausea, or a very red eye with light sensitivity.

• Urgently (within 24–48 hours) for new floaters/flashes, irregular or stuck pupil, or if pressure was recently high.

• Promptly if you are on steroids or immunosuppressants and feel an infection (fever, cough, sores), or if your drops run out or seem to stop working.

• Routinely for pressure checks, OCT, and visual fields even when the eye feels “normal.”

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What to eat and what to avoid

Eat more:

• Leafy greens and colorful vegetables (spinach, kale, peppers, berries) for antioxidants and nitrates that support microcirculation.

• Fish twice a week (salmon, sardines, mackerel) for omega-3s that balance inflammation.

• Whole grains, legumes, nuts, and seeds for steady energy and micronutrients.

• Hydration throughout the day (small, regular sips) to avoid dehydration-related eye discomfort.

Limit or avoid:

• Large caffeine boluses (big energy drinks at once) that can transiently spike IOP; moderate coffee/tea is usually fine.

• High-salt, ultra-processed foods that worsen vascular risk and fluid balance.

• Excess alcohol which disturbs sleep and vascular control.

• Smoking and secondhand smoke which harm optic-nerve blood flow and increase oxidative stress.

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Frequently asked questions

1. Is uveitic glaucoma permanent?
   The optic-nerve damage is permanent, but future damage is preventable with good inflammation control, safe pressure levels, and regular monitoring.

2. Can steroid drops cause glaucoma?
   They can cause steroid-induced pressure rise in susceptible people. Doctors balance steroid dose with pressure-lowering treatment and may add steroid-sparing drugs.

3. Are prostaglandin drops safe in uveitis?
   Often used cautiously. In active uveitis or herpetic disease they may be avoided; in quiet eyes they may be used if benefits outweigh risks.

4. Will I need surgery?
   Not always. Many patients do well with medicines and disease control. Surgery is considered when pressure stays high or angle scarring limits outflow.

5. Can exercise help?
   Moderate aerobic activity can slightly lower IOP and improve blood flow. Avoid heavy straining or inverted poses during active disease.

6. Do blue-light filters help?
   They do not treat glaucoma, but can make light sensitivity more comfortable during or after flares.

7. Is uveitic glaucoma the same as primary open-angle glaucoma?
   No. The cause is inflammation (and sometimes steroids). Management focuses on both inflammation and pressure, whereas primary glaucoma focuses on pressure alone.

8. Can diet cure it?
   Diet cannot cure glaucoma or uveitis, but an anti-inflammatory, nutrient-rich pattern supports overall eye health and treatment success.

9. What if my pressure is normal but I still have uveitis?
   You still need care. Each flare can create scar tissue that later raises pressure; prevention and monitoring are essential.

10. How often should I be checked?
    During flares, sometimes every few days. When quiet and stable, every 1–3 months, plus periodic OCT and visual-field testing as directed.

11. Are biologics safe?
    They can be very effective but suppress the immune system. Screening for TB and hepatitis and ongoing monitoring reduce risks.

12. Can I wear contact lenses?
    Avoid during active inflammation. In quiet periods, daily disposables with excellent hygiene may be acceptable per your doctor.

13. Do supplements replace drops?
    No. Supplements are supportive only and should never replace prescribed anti-inflammatory or pressure-lowering therapies.

14. Why does my vision blur after drops?
    Some drops (e.g., cycloplegics, viscous lubricants) temporarily blur vision. This usually clears; ask about timing doses when vision demands are lower.

15. Can uveitic glaucoma affect both eyes?
    Yes. Some causes are bilateral, and even unilateral disease needs monitoring of the fellow eye.

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 29, 2025.