Synechiae

Synechiae means “sticking together.” In the eye, it means parts that should glide smoothly now stick together and will not separate easily. The most common kind is when the colored part of the eye (the iris) sticks to the front window of the eye (the cornea) or to the clear capsule of the lens. When the iris sticks to the cornea it is called anterior synechiae. When the iris sticks to the lens it is called posterior synechiae. These sticky bands can be small and soft at first, or they can become strong, broad, and permanent with time. Synechiae can block the normal flow of fluid inside the eye. This blockage can raise eye pressure and can damage the optic nerve if not treated. Synechiae are a sign that the eye has been inflamed, injured, or otherwise stressed.

Synechiae are sticky adhesions that make parts of the eye abnormally attach to each other after inflammation, injury, or angle crowding. Think of them as “scar-like sticking.” Two common forms matter most:

• Posterior synechiae: the iris (the colored part) sticks to the front of the lens. This can make the pupil irregular, keep it from opening well, and block fluid flow from the back to the front of the eye (pupillary block). That blockage can raise inner eye pressure and set off angle closure. EyeWiki

• Peripheral anterior synechiae (PAS): the iris edge sticks forward to the drainage area (the trabecular meshwork/cornea) at the angle. This can permanently close parts of the angle, reduce fluid outflow, and cause angle-closure glaucoma if enough of the angle is sealed.

Synechiae usually appear after inflammation in the eye (uveitis), trauma or surgery, or a pressure attack in angle-closure disease. They matter because they can distort the pupil, keep light from entering normally, cause pain and light sensitivity, and raise eye pressure that threatens vision. EyeWiki+1

Why synechiae form

Inside a calm, healthy eye, tissues are smooth, the fluid is clear, and surfaces do not touch for long. Inflammation changes this delicate balance. Inflammation makes the iris “sticky” because proteins, inflammatory cells, and a mesh of fibrin appear in the front chamber of the eye. If the pupil is kept small during inflammation, the iris spends more time touching the lens in the center or the cornea near the edge, and it can glue itself there. Fresh synechiae can sometimes be gently pulled apart by dilating the pupil. Old synechiae get scarred and fibrous and are much harder to release. When the iris sticks all the way around the pupil, fluid cannot pass from the back chamber to the front chamber. Pressure then pushes the iris forward like a bulging dome. This is called iris bombe. The bulging iris can stick to the drainage angle and create peripheral anterior synechiae, which block fluid outflow and can cause secondary angle-closure glaucoma. In short, inflammation plus contact equals sticking, and sticking plus blockage equals pressure problems.

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Types of synechiae

1. Posterior synechiae (focal): Small points where the iris sticks to the lens at one or more spots.

2. Posterior synechiae (broad): Large patches where the iris sticks widely to the lens.

3. Ring synechiae (seclusio pupillae): The iris sticks all the way around the pupil edge, sealing the pupil like a gasket.

4. Occlusio pupillae: A membrane grows over the pupil and blocks it, sometimes along with ring synechiae.

5. Peripheral anterior synechiae (PAS, focal): Small areas where the iris sticks to the cornea at the drainage angle.

6. Peripheral anterior synechiae (broad or 360°): Wide or complete angle adhesions causing long-standing outflow blockage.

7. Inflammatory PAS: PAS formed mainly after uveitis or iritis.

8. Neovascular PAS: PAS formed when new, fragile blood vessels grow on the iris and angle (for example in diabetes or vein occlusion) and pull the iris forward.

9. Traumatic synechiae: Adhesions formed after blunt or penetrating eye injury or surgery.

10. Congenital or developmental adhesions: Rare adhesions present from birth or due to developmental angle anomalies; these are uncommon and differ from classic inflammatory synechiae.

Causes of synechiae

1. Acute anterior uveitis (iritis): Inflammation makes the iris sticky and likely to adhere to the lens or cornea.

2. Chronic uveitis (e.g., HLA-B27 diseases): Repeated or long inflammation gives more time for strong adhesions to form.

3. Granulomatous uveitis (e.g., sarcoidosis, tuberculosis): Thick inflammatory material and fibrin promote firm synechiae.

4. Herpes simplex keratouveitis: Viral inflammation of the cornea and iris increases fibrin and sticky contact.

5. Herpes zoster ophthalmicus: Varicella-zoster virus causes intense inflammation that favors synechiae.

6. Endophthalmitis (severe intraocular infection): Heavy inflammation and fibrin commonly lead to broad adhesions.

7. Post-operative inflammation (e.g., after cataract surgery): Early post-op iritis can create fresh synechiae if not controlled.

8. Blunt trauma: Contusion can trigger inflammation and bleeding, allowing iris to adhere at the angle (PAS).

9. Penetrating trauma: Direct tissue damage and healing create abnormal adhesions.

10. Chemical injuries (alkali/acid burns): Surface and internal inflammation make the iris and cornea prone to sticking.

11. Corneal ulcers or severe keratitis: Nearby inflammation spills into the anterior chamber and encourages synechiae.

12. Hyphema (blood in the anterior chamber): Clots can organize and glue the iris to the angle (PAS).

13. Neovascularization of the iris (rubeosis iridis): New vessels and scar tissue pull and stick the iris to the angle.

14. Advanced diabetic eye disease: Ischemia drives rubeosis and PAS formation.

15. Retinal vein occlusion (ischemic): Severe ischemia can cause rubeosis and subsequent PAS.

16. Chronic angle crowding or intermittent angle closure: Repeated contact encourages permanent iris-angle adhesions.

17. Lens-induced inflammation (e.g., phacolytic or phacoanaphylactic): Lens proteins leak and trigger sticky uveitis.

18. ICE syndrome (iridocorneal endothelial syndrome): Abnormal endothelium creeps over angle and iris, creating PAS.

19. Long-term strong miotic use (e.g., high-dose pilocarpine): A very small pupil keeps the iris pressed to the lens and favors posterior synechiae in inflamed eyes.

20. Juvenile idiopathic arthritis uveitis: Often quiet yet sticky inflammation that easily forms posterior synechiae in children.

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Symptoms

Synechiae themselves may be silent, especially early, but they often travel with inflammation and pressure changes. Each item below is written plainly.

1. Eye pain or aching: The inflamed iris and rising pressure can hurt.

2. Redness: Blood vessels at the limbus dilate and create a deep red or violaceous ring.

3. Light sensitivity (photophobia): The inflamed iris spasms with light, which is painful.

4. Blurred vision: Inflammation, corneal swelling, or cataract can blur sight.

5. Halos around lights: Corneal edema from high pressure causes rainbow rings.

6. Headache around the eye: Eye pressure and ciliary body spasm can refer pain.

7. Small, irregular, or “peaked” pupil: The pupil edge is tethered by synechiae and looks misshapen.

8. Poor dilation in the clinic: Drops do not enlarge the pupil well because the iris is stuck.

9. Glare: An irregular pupil edge lets in stray light.

10. Reduced night vision: A small or fixed pupil limits light entry in the dark.

11. Eye tenderness to touch: Inflammation makes the eye sensitive.

12. Nausea or vomiting with severe pressure rise: High eye pressure can trigger systemic symptoms.

13. Tearing and irritation: Surface inflammation increases reflex tearing.

14. A feeling of heaviness or fullness: Pressure buildup can feel like weight behind the eye.

15. Sometimes no symptoms at all: Mild or old synechiae may be found only during an eye exam.

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Diagnostic tests

A) Physical examination tests (bedside observations)

1. Detailed history and symptom review: The doctor asks when pain, light sensitivity, or blur began and what makes it better or worse. A story of sudden pain and redness suggests acute inflammation that can form synechiae.

2. Visual acuity testing: Reading letters shows how much vision is affected. A change guides urgency and helps track recovery.

3. Pupil inspection in light and dark: The doctor looks for a small, irregular, or oval pupil. An uneven pupil edge that does not round out in the dark suggests posterior synechiae.

4. External examination for redness pattern: A deep red ring around the cornea (ciliary flush) points to iritis, which is the common driver of synechiae.

5. Penlight anterior chamber depth shadow test: A quick light from the side shows a shadow on the iris if the front chamber is shallow. A shallow chamber plus pain may mean angle crowding or angle closure related to PAS.

B) Manual and in-office instrument tests

6. Slit-lamp biomicroscopy: A bright microscope looks at the cornea, anterior chamber, iris, and lens. The doctor sees cells, flare, fibrin, keratic precipitates, and the exact points where the iris is stuck to the lens or cornea.

7. Pharmacologic dilation and cycloplegia test: Strong dilating drops (with or without a cycloplegic) are used to see whether fresh posterior synechiae can break. If the pupil stays notched or fixed, adhesions are likely mature.

8. Gonioscopy (three- or four-mirror lens): A special contact lens shows the drainage angle. The doctor sees if the iris is truly stuck to the angle (PAS) or simply pushing against it without scarring.

9. Indentation gonioscopy: Gentle pressure with a four-mirror lens temporarily shallows the central chamber. If the angle opens, the blockage was just contact; if it stays closed, PAS are present.

10. Tonometry (eye pressure measurement): Pressure is measured because synechiae can block fluid outflow and raise pressure. The number guides treatment and urgency.

C) Laboratory and pathological tests (to find the cause of inflammation)

11. Complete blood count (CBC) with differential: Looks for infection or systemic inflammation that could drive uveitis.

12. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP): General markers of inflammation that support an inflammatory cause of synechiae.

13. HLA-B27 typing: Identifies a genetic marker linked to acute, sticky anterior uveitis that often makes posterior synechiae.

14. Syphilis testing (nontreponemal and treponemal): Detects syphilitic uveitis, which can form synechiae and needs specific antibiotics.

15. Tuberculosis screening (IGRA or PPD) ± targeted workup: Helps uncover TB-related uveitis that causes chronic synechiae if untreated.

16. Aqueous humor analysis (PCR/culture for HSV, VZV, CMV, toxoplasma when indicated): A tiny fluid sample can confirm infectious causes of uveitis that tend to produce fibrin and adhesions.

D) Electrodiagnostic tests (used in special situations)

17. Visual evoked potential (VEP): Measures how quickly and strongly the brain responds to visual signals. It helps when vision remains poor even after pressure and inflammation improve, ruling out optic nerve problems.

18. Electroretinogram (ERG): Measures retinal function. It is used if long inflammation or a suspected retinal disease is also reducing vision and needs to be separated from the effect of synechiae.

E) Imaging tests (to map structure without touching the eye)

19. Anterior segment optical coherence tomography (AS-OCT): A non-contact light scan shows cross-sectional images of the cornea, iris, pupil, and angle. It can display iris–lens contact, iris bombe, and the width of the angle.

20. Ultrasound biomicroscopy (UBM): High-frequency ultrasound images the front of the eye even when the cornea is cloudy. It shows hidden adhesions, plateau iris, ciliary body changes, and the extent of angle closure caused by PAS.

Non-pharmacological treatments

Note: These steps support healing and comfort but do not “melt” synechiae. Breaking adhesions usually needs pupil-dilating drops and sometimes procedures (see below).

1. Education and early care: Learn warning signs (pain, light sensitivity, blur) and seek prompt care to stop inflammation before sticking occurs. Purpose: prevention. Mechanism: earlier anti-inflammatory treatment lowers fibrin that causes adhesions.

2. Sunglasses and hat: Reduce light sensitivity and ciliary spasm. Mechanism: lower photic trigging of pain.

3. Short rest in a dim room during flares: Comfort measure while medicines start working. Mechanism: relaxes iris/ciliary strain.

4. Cool compresses (brief, clean): Soothe surface irritation during active redness. Mechanism: vasoconstriction cools the surface.

5. Artificial tears (preservative-free): Ease surface irritation; do not treat synechiae but improve comfort. Mechanism: lubricate and dilute inflammatory mediators on the surface.

6. Eye shield at night (if advised): Prevent accidental rubbing when the eye is tender. Mechanism: mechanical protection to reduce micro-trauma in inflamed eyes.

7. Avoid contact lenses during flares: Reduce irritation and infection risk while the eye is inflamed. Mechanism: less friction and fewer microbes.

8. Avoid over-the-counter “redness reliever” vasoconstrictor drops: They can mask symptoms and sometimes aggravate rebound redness. Mechanism: does not treat inflammation and may complicate monitoring.

9. No miotic self-use (like pilocarpine) in uveitis unless prescribed: Miotics can tighten the iris and worsen sticking during inflammation. Mechanism: more iris–lens contact.

10. Manage systemic autoimmune disease (with your rheumatologist): Quiets eye flares at their source. Mechanism: systemic control reduces ocular inflammation.

11. Prompt treatment of infections that can trigger uveitis (e.g., syphilis, TB, herpes): Mechanism: remove the inflammatory trigger to cut adhesion risk.

12. Protective eyewear for sports/work: Prevent trauma-related inflammation and PAS. Mechanism: reduces blunt/penetrating injuries.

13. Smoking cessation: Tobacco smoke promotes inflammation and delays healing. Mechanism: lowers systemic inflammatory load that can amplify eye flares.

14. Healthy sleep and stress management: Poor sleep and stress sensitize pain and inflammation. Mechanism: calmer autonomic tone may lessen symptom perception.

15. Regular eye follow-ups after an attack: PAS can silently progress; mapping with gonioscopy and AS-OCT catches it early. Mechanism: surveillance to guide timely procedures.

16. Head-up posture if pressure is high (as advised): Mild, temporary comfort while medical therapy begins. Mechanism: may slightly reduce episcleral venous congestion.

17. Cold, clean tears after dilation if stinging: Comfort only. Mechanism: surface soothing; does not affect synechiae.

18. Allergy control if relevant: Avoid rubbing and surface inflammation that complicate exams. Mechanism: calmer surface allows better monitoring.

19. Systemic health basics (BP, blood sugar) optimized: Good control supports ocular healing. Mechanism: stable vascular and immune status.

20. Emergency plan: If severe pain, halos, nausea, sudden blur, treat as urgent—possible pressure crisis. Mechanism: faster relief prevents PAS from “setting.”

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Drug treatments

Exact dosing must be individualized by your clinician. Ranges below reflect typical regimens cited in ophthalmic references and labels.

1. Atropine 1% (cycloplegic): Purpose: relax spasm and prevent/break posterior synechiae. Typical use: 1–2×/day during active uveitis, then taper. Mechanism: blocks muscarinic receptors to paralyze the sphincter muscle and pull the pupil open. Side effects: blurry near vision, light sensitivity, rare systemic anticholinergic effects.

2. Homatropine 2–5% or Cyclopentolate 1% (cycloplegics): Purpose: same as atropine but shorter acting; often BID–QID early on. Mechanism/Side effects: as above.

3. Phenylephrine 2.5–10% (adrenergic mydriatic used in clinic): Purpose: extra iris dilation; sometimes helps lyse fresh posterior synechiae under supervision. Mechanism: alpha-1 agonist contracts dilator muscle. Safety note: 10% is contraindicated in infants <1 year and patients with hypertension or thyrotoxicosis; rare dangerous cardiovascular events reported—clinicians often prefer 2.5% when adequate.

4. Prednisolone acetate 1% (topical steroid): Purpose: mainstay to calm anterior uveitis. Typical use: start q1–2h for moderate–severe, then taper over weeks; milder cases q6h and taper (per response). Mechanism: suppresses inflammatory cytokines and cells. Side effects: cataract, IOP rise; needs monitoring.

5. Difluprednate 0.05% (topical steroid): Purpose: potent steroid alternative. Typical use: often QID, shown comparable to prednisolone 1% eight times daily in trials. Side effects: similar; watch IOP.

6. Timolol 0.25–0.5% (beta-blocker) for high IOP: Purpose: lower pressure when PAS or block raises IOP. Use: usually BID. Mechanism: reduces aqueous production. Side effects: can worsen asthma/bradycardia—disclose history.

7. Brimonidine 0.2% (alpha-2 agonist) for high IOP: Use: TID (or per label). Mechanism: cuts aqueous production and increases uveoscleral outflow. Side effects: fatigue, dry mouth.

8. Dorzolamide 2% (topical carbonic anhydrase inhibitor): Use: TID. Mechanism: lowers aqueous production. Side effects: bitter taste, stinging.

9. Acetazolamide (oral CAI) 250 mg Q6h or 500 mg SR BID (short-term): Purpose: rapid IOP reduction in acute pressure spikes. Mechanism: systemic CAI. Side effects: tingling, fatigue; avoid in sulfonamide allergy; monitor electrolytes.

10. Mannitol 20% IV (1–2 g/kg, acute): Purpose: emergency osmotic drop in IOP during angle-closure crisis while definitive laser/surgery is arranged. Side effects: fluid shifts—hospital supervision.

Special scenario—herpetic anterior uveitis: clinicians often add an antiviral, e.g., valacyclovir (typical adult induction 500 mg–1 g TID, then taper/maintenance), alongside steroids/cycloplegics, with tailored dosing by diagnosis and kidney function.

Prostaglandin analogs are often avoided in active inflammatory causes of angle problems because they may aggravate inflammation; choices are individualized.

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Dietary “molecular” supplements

Evidence for supplements treating synechiae is lacking. Some nutrients support general eye or immune health. Always ask your doctor—especially if pregnant, on blood thinners, or with kidney/liver disease.

1. Omega-3 fatty acids (EPA/DHA; e.g., ~1 g/day of combined EPA+DHA): Function: anti-inflammatory lipid mediators (resolvins). Mechanism: shifts eicosanoid balance toward resolution pathways.

2. Vitamin D (per clinician-checked level; common maintenance 600–800 IU/day, safe upper limit 4,000 IU/day for most adults): Function: immune modulation; deficiency links to some inflammatory conditions. Mechanism: nuclear receptor effects temper immune activity.

3. Curcumin (standardized extracts, doses vary: often 500–1000 mg/day in studies with enhanced-absorption forms): Function: antioxidant/anti-NF-κB actions explored in uveitis research; adjunct only. Mechanism: down-regulates inflammatory signaling.

4. Lutein/Zeaxanthin (e.g., 10 mg/2 mg/day as in AREDS2): Function: macular antioxidants supporting retinal health (not synechiae). Mechanism: filter blue light and quench reactive oxygen species.

5. Vitamin A (only if deficient; avoid excess): Function: supports ocular surface immunity. Mechanism: retinoid signaling for epithelial integrity.

6. Vitamin C (e.g., 200–500 mg/day): Function: aqueous antioxidant; supports collagen and capillaries. Mechanism: free-radical scavenging.

7. Vitamin E (e.g., 100–200 IU/day if no contraindication): Function: lipid antioxidant. Mechanism: protects membranes from peroxidation.

8. Zinc (e.g., 8–11 mg/day total intake; avoid excess): Function: cofactor in immune enzymes. Mechanism: supports antioxidant enzymes like superoxide dismutase.

9. Quercetin (doses vary in studies): Function: flavonoid with anti-inflammatory/antioxidant properties. Mechanism: may modulate mast-cell and NF-κB pathways (adjunct only).

10. N-acetylcysteine (600 mg/day commonly used in ocular surface studies): Function: glutathione precursor antioxidant. Mechanism: replenishes cellular antioxidant capacity.

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Immune-modulating or regenerative-type drugs

These are physician-supervised systemic therapies used to control non-infectious uveitis so synechiae stop forming. They do not dissolve existing adhesions. Doses below are typical starting ranges—your specialist individualizes therapy and monitors labs.

1. Methotrexate (e.g., 10–25 mg once weekly with folic acid): Function: steroid-sparing immunomodulator. Mechanism: antifolate effects reduce lymphocyte activity. Notes: monitor liver, blood counts; avoid in pregnancy.

2. Mycophenolate mofetil (e.g., 1–1.5 g twice daily): Function: decreases relapses in non-infectious uveitis. Mechanism: blocks lymphocyte purine synthesis. Notes: GI upset, infection risk; contraception required.

3. Cyclosporine (e.g., ~2–5 mg/kg/day in divided doses): Function: calcineurin inhibitor to control T-cell–driven uveitis. Notes: monitor kidney function and blood pressure.

4. Adalimumab (FDA-approved for non-infectious intermediate, posterior, and panuveitis): Typical adult dosing: 80 mg once, then 40 mg every other week starting 1 week later. Mechanism: anti-TNF-α biologic that dampens ocular inflammation. Notes: TB/hepatitis screening; infection risk counseling.

5. Infliximab (IV anti-TNF-α; dosing commonly 5 mg/kg at weeks 0, 2, 6 then q8w): Function: for refractory non-infectious uveitis in select cases. Notes: infusion reactions; infection screening required.

6. Tocilizumab (IL-6 inhibitor; SC or IV regimens vary): Function: option for macular edema or refractory uveitis in expert hands. Notes: monitor labs; infection risk counseling.

Important warning about “stem cell” therapies: There are no approved stem-cell drugs to treat synechiae or uveitis in routine practice. Unregulated eye injections marketed as “stem cell” treatment have blinded patients; the FDA explicitly warns consumers to avoid unapproved clinics. Consider only regulated clinical trials.

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Procedures/surgeries

1. Laser Peripheral Iridotomy (LPI): A tiny laser opening in the peripheral iris to bypass pupillary block, equalize pressure between back and front chambers, and prevent PAS after angle-closure attacks. It’s quick outpatient laser.

2. Argon Laser Peripheral Iridoplasty (ALPI): Laser spots shrink the peripheral iris to pull it away from the angle in certain angle configurations (e.g., plateau iris) when LPI alone is not enough.

3. Goniosynechialysis (GSL): A delicate procedure—often combined with cataract surgery—where the surgeon mechanically peels recent PAS off the drainage meshwork to reopen the angle. Best results are with “fresh” PAS; long-standing PAS respond less.

4. Cataract extraction with surgical synechiolysis: During cataract surgery, the surgeon uses viscoelastic and instruments to break posterior synechiae, reform the pupil, and restore access to the lens; this can also deepen the anterior chamber and help angle anatomy.

5. Filtering or MIGS procedures (e.g., trabeculectomy, goniotomy variants): If PAS is extensive and pressure remains high, glaucoma surgeries create new outflow paths or enhance existing ones to protect the optic nerve. Choice depends on anatomy and disease stage.

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Prevention tips

1. Treat uveitis flares promptly with prescribed drops to cut the “sticky window.”

2. Use cycloplegic/mydriatic drops as directed during flares to prevent posterior synechiae.

3. Attend follow-ups with gonioscopy after an angle-closure event to find and treat early PAS.

4. Consider LPI early when indicated for narrow angles to prevent future block and PAS.

5. Protect eyes from trauma at work/sports.

6. Control systemic autoimmune disease with your specialists to reduce eye relapses.

7. Avoid miotics during active uveitis unless specifically prescribed to prevent iris–lens sticking.

8. Never self-medicate with phenylephrine 10%; it’s clinic-only and risky in some patients.

9. Do not skip steroid tapers; stopping too early can re-ignite inflammation and adhesion.

10. Know emergency signs (severe pain, halos, nausea, sudden blur) and seek urgent care.

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When to see a doctor urgently

• Right away if you have severe eye pain, halos around lights, headache with nausea/vomiting, or sudden blurry vision—these can signal a pressure crisis (angle closure) that can cause permanent harm without fast care.

• Soon (within 24–48 hours) for red, painful, light-sensitive eyes that persist, because early uveitis treatment helps prevent synechiae.

• Immediately after eye trauma with pain or vision change.

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Foods to favor—and to limit

Diet won’t break synechiae, but a steady anti-inflammatory, nutrient-dense pattern supports ocular and systemic health.

What to eat (aim daily/weekly):

1. Leafy greens (spinach, kale) for lutein/zeaxanthin.

2. Fatty fish (salmon, sardines) for omega-3s.

3. Colorful vegetables (peppers, carrots) for carotenoids.

4. Citrus and berries for vitamin C.

5. Nuts and seeds for vitamin E and healthy fats.

6. Legumes for fiber and minerals.

7. Whole grains for steady energy.

8. Olive oil as main fat.

9. Adequate protein (fish, eggs, lean meats, tofu).

10. Hydration with water/unsweetened beverages.

What to limit:

1. Ultra-processed snacks and 2) sugary drinks (pro-inflammatory).

2. Excess salt (pressure/vascular health).

3. Excess alcohol.

4. Trans-fats and 6) repeatedly heated oils.

5. Very high-glycemic sweets.

6. Smoking (not food, but crucial to quit).

7. Mega-dosing supplements without guidance.

8. Self-use of “eye drops” promising quick whitening—they don’t treat inflammation.

(General principles; your clinician or dietitian can tailor advice.)

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Frequently asked questions (FAQs)

1) Can drops “melt” synechiae?
No. Drops like cycloplegics and phenylephrine in-clinic can pull the iris away if the adhesion is fresh, but old, fibrotic synechiae often need mechanical/laser/surgical help.

2) Why do doctors dilate my pupil during a flare?
To prevent the iris from sticking to the lens and to break early adhesions, and also to relieve spasm pain.

3) Are synechiae dangerous by themselves?
They are a warning sign—they can distort the pupil and close the angle, raising pressure that can damage the optic nerve.

4) How do doctors see PAS?
With gonioscopy (a contact lens exam) and sometimes AS-OCT or UBM to visualize the angle.

5) Does phenylephrine 10% work better than 2.5%?
It can dilate more, but 10% carries higher systemic risk and is contraindicated in certain patients; clinicians often use 2.5% unless stronger dilation is essential.

6) Will steroids harm my eyes?
Topical steroids are crucial to control inflammation; prolonged or potent use can raise IOP and cause cataracts, so doctors monitor and taper.

7) Do prostaglandin glaucoma drops help in uveitis-related angle issues?
They can lower IOP but are often avoided in active inflammation; your doctor chooses safer alternatives first.

8) Can PAS be peeled off?
Yes—goniosynechialysis can peel recent PAS to reopen the angle, often during cataract surgery; long-standing PAS respond less well.

9) Is laser iridotomy permanent?
The opening usually stays patent and prevents pupillary block, but you still need monitoring for PAS and overall angle health.

10) Will cataract surgery fix synechiae?
It can break posterior synechiae, reshape the pupil, and deepen the anterior chamber, improving angle anatomy—plus vision improves if the cataract was significant.

11) Are “stem cell” injections a cure?
No. Unapproved stem-cell eye injections have blinded patients; the FDA warns against them. Consider only regulated trials.

12) Will supplements cure synechiae?
No. Nutrients may support general eye health, but adhesions need medical/surgical care.

13) Can synechiae come back after being broken?
Yes, if inflammation returns or pressure crises recur. Ongoing prevention and follow-up matter.

14) How quickly should I be seen for a suspected flare?
Within 24–48 hours, sooner if pain is severe or vision worsens. Early treatment prevents sticking.

15) What’s the long-term outlook?
With prompt treatment, regular monitoring (including gonioscopy), and procedures when needed, many people maintain good vision and pressure control.

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 27, 2025.