Phacoanaphylactic Endophthalmitis (Phacoantigenic Uveitis)

Phacoanaphylactic endophthalmitis is a rare kind of sterile (non-infectious) inflammation inside the eye that happens after lens proteins leak out of the natural lens because the lens capsule is torn. The body usually ignores lens proteins because they are sealed away from the immune system. When the capsule breaks during an accident or an eye operation, those proteins can spill into the eye. The immune system “notices” them for the first time and overreacts, producing a granulomatous uveitis (a strong, clumpy, cell-based inflammation). Doctors today prefer the name phacoantigenic uveitis because it is not a true immediate “anaphylactic” allergy; it is more like a delayed immune reaction to lens protein. EyeWikiPMCScienceDirect

This condition is part of the broader family called lens-induced uveitis. It most often appears after cataract surgery or after eye trauma that opens the lens capsule, but it can also follow other procedures that disturb the lens. The inflammation can be mainly in the front of the eye (anterior uveitis) and, in some cases, can extend backward so the whole inside of the eye looks inflamed (an “endophthalmitic” picture). Typical signs are eye pain, redness, light sensitivity, blurry vision, and visible inflammatory “deposits” on the back of the cornea. Doctors may see large greasy-looking spots called mutton-fat keratic precipitates, fibrin, and adhesions between the iris and the lens (posterior synechiae). Eye pressure can rise if inflammatory cells or lens particles clog the drainage system. NCBIEyeWiki

The word “endophthalmitis” is usually used for infection inside the eye. Phacoanaphylactic endophthalmitis mimics an infection because the eye looks very inflamed, but here the trigger is immune, not bacterial or fungal. This difference matters because treatment choices differ, and the doctor will often sample eye fluid to rule out infection when the picture is unclear. EyeWikiNCBI

The reaction can start days to weeks after the capsule is opened. In teaching texts it is often described as appearing about 1 to 14 days after lens capsule injury, but there are reports showing it can also occur much later (even years) if lens material remains hidden and then leaks. The timing depends on how much lens material is exposed, where it sits, and how the person’s immune system responds. ScienceDirectPubMed

Phacoanaphylactic endophthalmitis is a strong, mistaken immune reaction inside the eye that happens after lens proteins are exposed to the immune system. This usually occurs after cataract surgery, eye injury, or when tiny pieces of the natural lens remain in the eye. Your immune system normally never “sees” lens proteins because they are sealed away. When that protective barrier breaks, the immune system can treat lens proteins as foreign and attacks them, causing painful inflammation. Doctors also call this phacoantigenic uveitis. It is not an infection by germs, but the symptoms can look similar to infectious endophthalmitis, which is why urgent expert assessment is critical.

The lens is “immune-privileged,” meaning the body’s defenses normally ignore it. Trauma or surgery can spill lens material into the front or back of the eye. The immune system then forms antibodies and immune cells that bind to lens proteins and release inflammatory chemicals (cytokines, complement). This causes redness, pain, light sensitivity, blurred vision, floaters, and sometimes high eye pressure. In some people the inflammation is granulomatous (tiny clumps of immune cells), and it can affect both the front (anterior) and back (posterior) parts of the eye.

How doctors think about it

1. This is a diagnosis of urgency. Doctors must quickly rule out infection because infection needs antibiotics or surgery right away.

2. Clues for this immune type include a history of lens trauma/surgery, retained lens fragments, and inflammation that improves when lens material is removed plus steroids or other immune-quieting medicines.

3. Imaging and slit-lamp exam look for residual lens matter, cells and flare, keratic precipitates, vitreous haze, synechiae (stuck iris), and pressure changes.

4. Treatment aims are simple: remove the trigger (lens material), calm the immune storm, protect the retina and optic nerve, and prevent scarring and glaucoma.

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Types

There is no single official “stages and grades” chart for phacoanaphylactic endophthalmitis. In everyday practice, doctors group cases by how it started, how far the inflammation has spread, and what else is going on in the eye. The labels below help you understand what a report may say.

1. Post-surgical phacoantigenic uveitis.
   This follows cataract surgery, secondary lens surgery, YAG capsulotomy, IOL exchange, or other intraocular procedures that open or disturb the lens capsule and let lens proteins escape. EyeWiki

2. Post-traumatic phacoantigenic uveitis.
   This follows a penetrating injury or a blunt injury that tears the capsule. It is historically the most common setting because trauma is unpredictable and can leave hidden lens material behind. PubMed

3. Anterior-predominant (classic) phacoantigenic uveitis.
   Inflammation is mainly in the front part of the eye (iris–ciliary body). Doctors see cells and flare in the anterior chamber, big greasy KPs, fibrin, and sometimes hypopyon. The back of the eye may be relatively quiet.

4. Endophthalmitic variant (pan-inflammation).
   Inflammation is more diffuse, with vitritis (cells in the back gel of the eye) and a clinical picture that can mimic infectious endophthalmitis, especially when media are cloudy and the view is limited. EyeWiki

5. With retained lens fragments.
   A chunk of lens or fine lens “powder” remains inside (front chamber, behind the iris, or in the vitreous). This tends to prolong and intensify inflammation until the material is removed. ScienceDirectEyeWiki

6. Without visible fragments (protein leak only).
   The capsule was opened briefly, or tiny amounts leaked and then sealed, so no big pieces are left. The immune system still reacts to dissolved lens proteins.

7. With secondary pressure rise (lens-induced glaucoma overlap).
   Inflammation and lens material can block the trabecular meshwork, raising eye pressure. This overlaps with the “lens-induced glaucoma” group and requires pressure control alongside anti-inflammatory care. EyeWikiNCBI

8. Recurrent or chronic course.
   If small fragments stay hidden or keep leaking, the eye can smolder with repeated flares, sometimes months later, until the material is located and removed. Karger

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20 causes (really, 20 common triggers/situations that let lens protein escape)

Each “cause” below is simply a situation that opens the lens capsule and gives lens proteins access to the immune system. The more spillage, the bigger the risk.

1. Standard cataract surgery with a torn posterior capsule.
   A rupture during phacoemulsification lets nucleus or cortex move out of place and leak proteins into the eye. EyeWiki

2. Dropped lens fragments into the vitreous during surgery.
   When pieces fall back, they can persist, slowly leaking protein and worsening inflammation. ScienceDirectEyeWiki

3. Extracapsular cataract extraction with capsular rent.
   A large opening or incomplete removal of cortex can leave inflammatory lens matter behind. PubMed

4. Intracapsular extraction with residual cortical “pearls.”
   Even older techniques can leave protein sources that trigger a delayed response. PubMed

5. Penetrating eye injury that tears the capsule.
   Any sharp trauma that opens the lens can cause a strong immune reaction days to weeks later. PubMed

6. Blunt trauma with occult capsule rupture.
   A hard blow can split the capsule without an obvious wound; later leakage drives inflammation. PubMed

7. YAG posterior capsulotomy with released lens material.
   A laser opening can free tiny retained cortical pieces, especially in complicated cases. EyeWiki

8. IOL exchange or repositioning that disturbs the capsule.
   Manipulation around the bag can uncover old cortex or stress a thin capsule. oculist.net

9. Secondary lens surgery in a uveitic eye.
   Prior inflammation makes tissues fragile; lens material can be harder to clear. EyeWiki

10. Retained small cortical flakes in the anterior chamber.
    White, fluffy cortical remnants can sit behind the iris or in the angle and keep the eye inflamed. CollaborativeEYE

11. Retained nuclear chips in the sulcus or vitreous.
    Denser pieces are slower to dissolve and can cause ongoing uveitis or pressure spikes. ScienceDirect

12. Hyper-mature cataract that leaks lens proteins.
    A very old, liquefied lens can leak through a weak capsule and provoke a strong reaction. Cybersight

13. Zonular weakness with lens subluxation and capsule stress.
    Conditions like pseudoexfoliation or trauma can shift the lens, making capsule tears more likely. EyeWiki

14. Wound dehiscence after surgery.
    If a surgical wound opens, lens material can migrate unexpectedly. oculist.net

15. Combined surgery (e.g., cataract + vitrectomy) with lens handling.
    More complex procedures increase the chance of small retained fragments. Karger

16. Capsular fibrosis that traps and then releases cortex.
    Scarred capsular bags sometimes hide cortex that later works loose.

17. Intraocular foreign body that injures the lens.
    Metal or glass can puncture the capsule and seed lens protein leakage after it is removed.

18. Prior infectious endophthalmitis treated but with unnoticed lens breach.
    Even after infection clears, a silent capsular tear can continue to leak proteins. EyeWiki

19. Complicated pediatric lens surgery for trauma or congenital cataract.
    Children can also mount strong reactions when cortex is retained.

20. Late capsular bag–IOL complex instability.
    Years after surgery, a shifting bag can expose old lens material and re-ignite inflammation. Karger

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15 symptoms (what patients commonly feel or notice)

1. Eye pain that may be throbbing.
   Pain comes from the inflamed iris and ciliary body and sometimes from high eye pressure when the drainage pathway is clogged. NCBI

2. Red eye.
   Blood vessels on the white of the eye become dilated because of the intense inflammatory signals. NCBI

3. Light sensitivity (photophobia).
   The inflamed iris muscles react painfully to light, so bright rooms hurt. NCBI

4. Blurry or foggy vision.
   Cells, protein (“flare”), and fibrin in the fluid scatter light, and swelling in the cornea or retina can add to the blur. NCBI

5. Floaters.
   If inflammatory cells reach the vitreous gel, small mobile shadows appear.

6. Headache or brow ache.
   Ciliary spasm and pressure rise can refer pain to the brow region.

7. Tearing and watering.
   The eye’s surface becomes irritated and watery because of the inflammatory process.

8. Mild discharge (usually watery, not thick pus).
   Because the cause is immune, discharge is often minimal compared with bacterial infection. If thick discharge appears, doctors think about infection. NCBI

9. Halos or glare.
   Corneal edema from high pressure or inflammation causes colored rings around lights.

10. Small or irregular pupil.
    Inflammation makes the iris sticky, causing posterior synechiae that change pupil shape. NCBI

11. Eye feels tender to touch.
    Inflamed tissues are sensitive, and pressure on the eyelids can be uncomfortable.

12. Rapid drop in vision after a procedure or injury.
    The timing—days to weeks after lens capsule opening—is a useful clue. ScienceDirect

13. Nausea with severe pressure spikes.
    Very high intraocular pressure can cause nausea and vomiting.

14. Feeling of “something in the eye.”
    Anterior chamber cells and corneal edema can create a gritty, foreign-body sensation.

15. Vision that improves a little with pinhole but remains poor.
    Pinhole may sharpen focus slightly, but inflammation limits clarity until it is treated.

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20 diagnostic tests (grouped the way doctors think at the slit-lamp)

The goal of testing is to confirm intense intraocular inflammation, look for lens material, check eye pressure, and rule out infection or other causes of uveitis. The mix below covers bedside observations, “manual” chair tests, lab and pathology checks, electrodiagnostics when needed, and imaging.

A) Physical examination (5 tests)

1. Visual acuity testing at distance and near.
   Tells how much vision is affected and helps track improvement with treatment.

2. External inspection of lids and conjunctiva.
   Looks for lid edema and diffuse redness that match a severe anterior segment reaction. This also helps differentiate from surface problems like conjunctivitis. NCBI

3. Pupil examination for size, shape, and reactivity.
   Finds posterior synechiae (sticky adhesions), irregular pupils, and any relative afferent pupillary defect if the back of the eye is also very inflamed. NCBI

4. Slit-lamp biomicroscopy of the anterior segment.
   Shows hallmark findings: cells and flare, fibrin, mutton-fat keratic precipitates, and sometimes hypopyon. The doctor also looks for retained cortical chips in the angle or behind the iris. NCBI

5. Dilated fundus examination when media are clear.
   Checks for vitritis, retinal edema, or other posterior signs of inflammation. If the view is hazy, the team moves to ultrasound.

B) Manual/bedside office tests (4 tests)

6. Applanation tonometry (Goldmann) to measure intraocular pressure.
   Pressure may be elevated when inflammatory cells and protein block the drainage system; monitoring guides treatment. NCBI

7. Gonioscopy.
   A contact lens lets the doctor look into the drainage angle to find retained lens fragments, inflammatory debris, or angle synechiae. This matters for pressure control and planning surgery. EyeWiki

8. Seidel test over surgical or traumatic wounds.
   A fluorescein strip helps detect wound leaks that could keep lens material moving into the eye.

9. Pinhole and color-vision/red-desaturation checks.
   These quick bedside maneuvers help separate optical blur from neuro-retinal dysfunction when inflammation is heavy.

C) Laboratory & pathological tests (5 tests)

10. Anterior chamber paracentesis for cytology, Gram stain, and cultures (as needed).
    If the picture looks like infection, the doctor may tap a small amount of fluid to look for bacteria or fungi and to examine inflammatory cell types. A negative culture in the right setting supports a lens-protein immune reaction. NCBI

11. Vitreous tap/biopsy when posterior involvement is suspected.
    Helps rule out infectious endophthalmitis when the eye is severely inflamed with a poor view. EyeWiki

12. Histopathology of removed lens capsule or fragments.
    On microscopy, classic phacoantigenic inflammation shows zonal granulomatous reaction with epithelioid histiocytes and giant cells wrapped around lens material—this is the gold-standard pattern that confirms the mechanism. PubMed

13. General inflammatory markers (CBC, ESR, CRP).
    Not specific, but helpful when building a full uveitis picture or excluding other systemic inflammatory diseases.

14. Targeted uveitis lab panel to exclude other causes (e.g., syphilis serology, TB testing, ACE/lysozyme for sarcoidosis) when the story is atypical or there is no clear lens trigger. This prevents missing another treatable condition.

D) Electrodiagnostic tests (2 tests)

15. Visual evoked potential (VEP).
    Rarely needed, but helpful when dense inflammation and media opacity make optic-nerve function hard to judge.

16. Electroretinogram (ERG).
    Assesses retinal function when the view is blocked or when chronic inflammation raises concern about retinal damage.

E) Imaging tests (4 tests)

17. B-scan ocular ultrasound.
    Essential when the front of the eye is cloudy. It can show vitritis, retained lens fragments settled low in the vitreous, retinal detachment, or choroidal thickening. It guides the decision to perform vitrectomy. PubMedEyeWiki

18. Ultrasound biomicroscopy (UBM).
    High-frequency ultrasound of the front of the eye helps locate small fragments in the anterior chamber, behind the iris, or in the sulcus. EyeWiki

19. Anterior segment optical coherence tomography (AS-OCT).
    Non-contact imaging to visualize the wound, capsule edges, fibrin strands, and the angle when gonioscopy is difficult.

20. Macular OCT.
    Checks for cystoid macular edema, a treatable cause of ongoing blurry vision after the inflammation quiets.

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Non-Pharmacological Treatments (Therapies & Others)

Below are 20 supportive, procedure-free or habit-based measures. Each item includes Description, Purpose, and Mechanism in plain language.

1. Protective eye shield

   • Description: Wear a rigid shield, especially during sleep and travel.

   • Purpose: Prevent accidental rubbing or bumps.

   • Mechanism: Physical barrier reduces mechanical irritation and risk of reopening wounds or dislodging healing tissues.

2. Strict “no eye rubbing” rule

   • Description: Avoid touching or rubbing the eye.

   • Purpose: Decrease irritation, infection risk, and pressure spikes.

   • Mechanism: Rubbing causes micro-injury and pressure surges that worsen inflammation.

3. Sunglasses and low-glare lighting

   • Description: Use UV-blocking sunglasses outdoors; reduce screen glare.

   • Purpose: Ease photophobia (light sensitivity).

   • Mechanism: Less light hitting inflamed tissues means less pain and lower inflammatory reflex responses.

4. Head-of-bed elevation (30 degrees)

   • Description: Sleep with head raised.

   • Purpose: Reduce eye congestion and morning discomfort.

   • Mechanism: Gravity-assisted drainage lowers tissue edema and pressure.

5. Cold compress (short, gentle)

   • Description: 10 minutes, clean cloth, not directly on sutures.

   • Purpose: Soothe pain and redness.

   • Mechanism: Vasoconstriction reduces swelling and inflammatory mediator diffusion.

6. Warm eyelid hygiene (only if advised)

   • Description: Gentle lid cleaning to maintain ocular surface.

   • Purpose: Keep tear film healthy; improve comfort.

   • Mechanism: Clears debris and oils; supports tear film stability, reducing secondary irritation.

7. Activity modification

   • Description: Avoid heavy lifting, straining, high-impact sports early on.

   • Purpose: Prevent pressure spikes and jolts.

   • Mechanism: Reduces Valsalva-related IOP rises and micro-trauma.

8. Tear film support with preservative-free artificial tears (non-drug status varies by region; here treated as a device/OTC support)

   • Description: Frequent lubricating drops without preservatives.

   • Purpose: Soothe surface irritation.

   • Mechanism: Dilutes inflammatory molecules on the surface and stabilizes tear layer.

9. Blood sugar control for people with diabetes

   • Description: Stick to diabetes plan and monitoring.

   • Purpose: Better healing and less inflammation.

   • Mechanism: Stable glucose reduces pro-inflammatory glycation and infection risk.

10. Smoking cessation

    • Description: Stop tobacco and vaping.

    • Purpose: Lower inflammation and improve healing.

    • Mechanism: Smoking promotes oxidative stress and vasoconstriction; stopping reverses these.

11. Alcohol moderation

    • Description: Avoid or limit alcohol, especially during steroid therapy.

    • Purpose: Protect liver and immune balance.

    • Mechanism: Less hepatic stress and more stable immunity improve drug handling and healing.

12. Adequate hydration

    • Description: Regular water intake unless restricted for medical reasons.

    • Purpose: Support tear production and systemic recovery.

    • Mechanism: Hydration supports tissue perfusion and metabolite clearance.

13. Sleep hygiene

    • Description: Regular sleep schedule; low light at night.

    • Purpose: Improve immune balance and pain control.

    • Mechanism: Good sleep normalizes cortisol and reduces inflammatory cytokines.

14. Stress reduction (breathing, gentle yoga, mindfulness)

    • Description: Daily short sessions.

    • Purpose: Lower pain perception and inflammation.

    • Mechanism: Parasympathetic activation dampens stress-driven inflammatory signals.

15. Dietary pattern: anti-inflammatory emphasis

    • Description: More colorful vegetables, fish, nuts, and whole grains.

    • Purpose: Support natural inflammation resolution.

    • Mechanism: Omega-3s, polyphenols, and fiber modulate immune pathways.

16. Allergen avoidance (if relevant)

    • Description: Reduce exposure to known eye irritants.

    • Purpose: Prevent extra inflammation piled onto the uveitis.

    • Mechanism: Fewer mast-cell triggers means fewer histamine cascades.

17. Glycemic-friendly meals during steroid use

    • Description: Lower simple sugars; steady carbohydrates.

    • Purpose: Steroids can raise blood sugar.

    • Mechanism: Stable glucose reduces secondary inflammation and infection risk.

18. Follow the drop schedule exactly

    • Description: Use a written chart or phone reminders.

    • Purpose: Maintain steady control of inflammation.

    • Mechanism: Consistent intraocular drug levels prevent rebound flares.

19. Prompt reporting of warning signs

    • Description: Call immediately for sudden pain, vision drop, pus-like discharge, or curtain-like shadow.

    • Purpose: Catch infection or retinal problems fast.

    • Mechanism: Early intervention saves vision.

20. Protective eyewear for life

    • Description: Use safety glasses for sports, tools, and risky tasks.

    • Purpose: Prevent future trauma that could re-expose lens material or harm the eye.

    • Mechanism: Impact resistance lowers injury risk.

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Drug Treatments

Important: Choice and dose depend on your eye exam, pressure, and whether infection is excluded. Never start steroid drops without medical supervision if infection is possible.

1. Prednisolone acetate 1% (topical corticosteroid)

   • Class: Corticosteroid (topical).

   • Dosage & Time: 1 drop every 1–2 hours while awake for severe inflammation, then gradual taper over weeks as directed.

   • Purpose: Rapidly calm the immune attack.

   • Mechanism: Suppresses cytokines, leukocyte migration, and capillary leakage.

   • Side effects: Elevated eye pressure, delayed wound healing, cataract progression, infection risk if misused.

2. Difluprednate 0.05% (topical corticosteroid)

   • Class: Corticosteroid (high-potency topical).

   • Dosage & Time: 1 drop QID (four times/day), then taper.

   • Purpose/Mechanism: Stronger steroid action for difficult inflammation; same mechanism as above.

   • Side effects: Similar to prednisolone; pressure checks are essential.

3. Atropine 1% (cycloplegic)

   • Class: Anticholinergic cycloplegic/mydriatic.

   • Dosage & Time: 1 drop BID–TID.

   • Purpose: Relieve ciliary spasm pain and prevent synechiae (iris sticking).

   • Mechanism: Paralyzes ciliary muscle and dilates pupil, reducing pain and scarring.

   • Side effects: Blurred near vision, light sensitivity; rarely systemic anticholinergic effects.

4. Homatropine 5% (cycloplegic)

   • Class: Anticholinergic.

   • Dosage & Time: 1 drop BID–TID as an alternative to atropine.

   • Purpose/Mechanism/Side effects: Similar to atropine but shorter action.

5. Topical NSAID (e.g., ketorolac 0.5%)

   • Class: Nonsteroidal anti-inflammatory (topical).

   • Dosage & Time: 1 drop QID as an adjunct to steroids.

   • Purpose: Additional control of prostaglandin-mediated inflammation; may help macular edema risk.

   • Side effects: Surface irritation, rare corneal issues (use under supervision).

6. Timolol 0.5% (IOP-lowering beta-blocker)

   • Class: Beta-blocker eye drop.

   • Dosage & Time: 1 drop BID if pressure rises.

   • Purpose: Control steroid-induced or inflammation-induced high IOP.

   • Mechanism: Decreases aqueous humor production.

   • Side effects: Can cause slow heart rate, bronchospasm; avoid in asthma/COPD unless okayed.

7. Brimonidine 0.2% or Dorzolamide 2% (IOP-lowering agents)

   • Class: Alpha-agonist (brimonidine), carbonic anhydrase inhibitor (dorzolamide).

   • Dosage & Time: 1 drop TID each, used singly or combined.

   • Purpose/Mechanism: Lower aqueous formation and/or enhance outflow to keep pressure safe.

   • Side effects: Local irritation; brimonidine—fatigue/dry mouth; dorzolamide—bitter taste.

8. Acetazolamide 250 mg (systemic CAI)

   • Class: Oral carbonic anhydrase inhibitor.

   • Dosage & Time: 250 mg QID or 500 mg SR BID, short course.

   • Purpose: Rapid IOP control when drops are not enough.

   • Mechanism: Blocks aqueous production systemically.

   • Side effects: Tingling, frequent urination, metabolic acidosis; avoid in sulfa allergy unless doctor agrees.

9. Oral corticosteroid (Prednisone)

   • Class: Systemic corticosteroid.

   • Dosage & Time: 0.5–1 mg/kg/day, short course with taper after infection is excluded and surgery planned/complete.

   • Purpose: Suppress severe or posterior inflammation.

   • Mechanism: Broad immune suppression of cytokines and cell trafficking.

   • Side effects: High sugar, mood change, sleep issues, stomach upset, bone loss with long use.

10. Immunomodulators for refractory cases (examples: Methotrexate, Mycophenolate, Cyclosporine)

    • Class: Steroid-sparing systemic agents (DMARDs).

    • Dosage & Time:

      • Methotrexate: 7.5–25 mg once weekly + folic acid.

      • Mycophenolate mofetil: 1–1.5 g BID.

      • Cyclosporine: 2–5 mg/kg/day in divided doses.

    • Purpose: Control chronic or relapsing inflammation to minimize steroid exposure.

    • Mechanism: Reduces lymphocyte activity and antibody production.

    • Side effects: Lab monitoring needed; risks include liver, kidney, blood count, and infection issues.

Note: Because phacoanaphylactic endophthalmitis is an immune reaction to lens proteins, the definitive treatment is removal of the residual lens material when present. Medicines control the inflammation and protect the eye before and after that procedure.

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Dietary Molecular Supplements

These do not replace medical or surgical care. Dosages are typical ranges from nutrition literature for adults; individual needs vary, and interactions (e.g., with blood thinners, immunosuppressants, diabetes drugs) must be reviewed by your clinician.

1. Omega-3 fatty acids (EPA/DHA)

   • Dose: 1–2 g/day EPA+DHA with meals.

   • Function: Anti-inflammatory support.

   • Mechanism: Shifts eicosanoids toward pro-resolving mediators.

2. Curcumin (with piperine for absorption)

   • Dose: 500–1000 mg/day standardized curcumin; ensure quality.

   • Function: Inflammation modulation.

   • Mechanism: NF-κB pathway down-regulation; antioxidant action.

3. Quercetin

   • Dose: 500 mg once or twice daily.

   • Function: Mast-cell stabilization, antioxidant.

   • Mechanism: Reduces histamine release; scavenges free radicals.

4. Resveratrol

   • Dose: 150–500 mg/day.

   • Function: Cytokine modulation.

   • Mechanism: Influences SIRT1 and inflammatory gene expression.

5. Lutein + Zeaxanthin

   • Dose: Lutein 10–20 mg/day, Zeaxanthin ~2 mg/day.

   • Function: Retinal antioxidant support.

   • Mechanism: Macular pigment antioxidants protect against oxidative stress.

6. Vitamin D3

   • Dose: Commonly 1000–2000 IU/day; individualized by blood levels.

   • Function: Immune balance.

   • Mechanism: Modulates T-cell responses; supports tissue health.

7. Vitamin C

   • Dose: 500–1000 mg/day total (diet + supplement).

   • Function: Collagen synthesis and antioxidant.

   • Mechanism: Scavenges oxidants; supports healing.

8. Vitamin E (mixed tocopherols)

   • Dose: Up to 200 IU/day unless contraindicated.

   • Function: Lipid membrane antioxidant.

   • Mechanism: Reduces lipid peroxidation in ocular tissues.

9. Zinc (as zinc gluconate or picolinate)

   • Dose: 10–25 mg elemental zinc/day short term; add copper if long term.

   • Function: Immune and wound-healing cofactor.

   • Mechanism: Supports enzyme systems and antioxidant defenses.

10. N-Acetylcysteine (NAC)

    • Dose: 600–1200 mg/day.

    • Function: Antioxidant precursor to glutathione.

    • Mechanism: Replenishes glutathione; may reduce oxidative signaling that fuels inflammation.

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Advanced” Immune-Modulating / Regenerative-Oriented Therapies

Transparency first: There are no approved stem-cell drugs for phacoanaphylactic endophthalmitis. The cornerstone is surgical removal of lens material plus anti-inflammatory therapy. The options below are specialist-guided for refractory uveitis to reduce steroid dependence; some are off-label in this exact condition.

1. Adalimumab (TNF-α inhibitor)

   • Dose: 40 mg subcutaneously every 2 weeks (some need weekly).

   • Function: Steroid-sparing control of chronic non-infectious uveitis.

   • Mechanism: Blocks TNF-α, a key inflammatory cytokine.

2. Infliximab (TNF-α inhibitor)

   • Dose: 5–10 mg/kg IV at weeks 0, 2, 6, then every 4–8 weeks.

   • Function: Rescue therapy in difficult uveitis.

   • Mechanism: Neutralizes TNF-α to calm inflammation.

3. Tocilizumab (IL-6 pathway inhibitor)

   • Dose: 4–8 mg/kg IV monthly or 162 mg SC weekly/biweekly.

   • Function: For uveitis with macular edema or TNF-refractory cases.

   • Mechanism: Blocks IL-6 signaling, reducing vascular leakage and cell activation.

4. Methotrexate (DMARD)

   • Dose: 7.5–25 mg once weekly + folic acid.

   • Function: Long-term steroid-sparing control.

   • Mechanism: Antimetabolite that decreases lymphocyte proliferation and inflammatory mediators.

5. Mycophenolate mofetil (Antimetabolite)

   • Dose: 1–1.5 g twice daily.

   • Function: Chronic control when steroids must be minimized.

   • Mechanism: Inhibits inosine monophosphate dehydrogenase, suppressing T/B cells.

6. Cyclosporine (Calcineurin inhibitor)

   • Dose: 2–5 mg/kg/day in divided doses.

   • Function: Alternative steroid-sparing agent.

   • Mechanism: Blocks calcineurin, reducing T-cell activation.

Investigational note: Cell-based therapies (e.g., mesenchymal stem cells) have no established role in this disease and should only be considered within approved clinical trials.

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Surgeries/Procedures

1. Removal of retained lens fragments (anterior approach)

   • Procedure: Through the front of the eye, the surgeon washes out and removes lens pieces left after cataract surgery or trauma.

   • Why: Eliminates the immune trigger (exposed lens proteins) quickly.

2. Pars plana vitrectomy (PPV) with posterior fragment removal

   • Procedure: From the back of the eye, the surgeon removes the vitreous gel and extracts lens material that fell behind.

   • Why: Clears inflammatory debris, improves visualization, and protects the retina.

3. Anterior chamber washout and synechiolysis

   • Procedure: Irrigation/aspiration of inflammatory debris; gentle separation of iris adhesions.

   • Why: Reduces inflammatory load, restores pupil shape, and improves fluid flow.

4. IOL assessment and, if necessary, IOL exchange or removal

   • Procedure: If the intraocular lens (IOL) is malpositioned or coated with inflammatory deposits that won’t clear, it may be repositioned, exchanged, or removed.

   • Why: Eliminates mechanical/immune irritation and allows better control of inflammation.

5. Glaucoma surgery (trabeculectomy or tube shunt) for secondary glaucoma

   • Procedure: Creates a new fluid pathway or places a drainage device to lower intraocular pressure.

   • Why: Protects the optic nerve when pressure stays high despite medicines.

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Prevention Strategies

1. Meticulous cataract surgery technique and cortical cleanup.

2. Early recognition and removal of retained lens fragments after surgery or trauma.

3. Protective eyewear during work, sports, and high-risk tasks to avoid eye injuries.

4. Avoid eye rubbing and follow post-op instructions exactly.

5. Prompt follow-up visits after cataract surgery or ocular trauma to detect inflammation early.

6. Manage systemic conditions (e.g., diabetes) that impair healing.

7. Pre-operative control of ocular surface disease (blepharitis, dry eye) to reduce post-op inflammation triggers.

8. Use of peri-operative anti-inflammatory plans as directed by the surgeon.

9. Immediate reporting of new floaters, pain, or vision drop after surgery or injury.

10. Keep a written medication schedule to avoid missed steroid tapers or drops.

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When to See a Doctor

• Seek urgent care now (same day) if you have sudden eye pain, marked redness, pus-like discharge, rapidly worsening vision, curtain-like shadow, many new floaters, flashes of light, or severe light sensitivity. These can mean infection, retinal tear/detachment, or uncontrolled inflammation.

• Book a prompt appointment if you have persistent blur, ongoing mild pain, halos, headaches, or difficulty using drops.

• After surgery or trauma, do not “wait and see”—call your surgeon for any new eye symptom.

Good Choices to Eat More Often

1. Fatty fish (salmon, sardines): omega-3s for inflammation resolution.

2. Leafy greens (spinach, kale): lutein/zeaxanthin for retinal antioxidant support.

3. Colorful vegetables and berries: polyphenols that calm oxidative stress.

4. Nuts and seeds (walnuts, flax, chia): plant omega-3s and minerals.

5. Olive oil: monounsaturated fats and polyphenols that favor anti-inflammatory pathways.

6. Citrus and kiwifruit: vitamin C for collagen and healing.

7. Eggs (if allowed): lutein/zeaxanthin and protein for repair.

8. Whole grains and legumes: fiber for stable blood sugar (helpful during steroid use).

9. Yogurt or fermented foods: gut support that may influence systemic inflammation.

10. Plenty of water: supports tear film and metabolism unless fluid-restricted.

Things to Limit or Avoid

1. Sugary drinks and sweets: push blood sugar up and may worsen inflammation.

2. Ultra-processed foods high in additives and trans fats.

3. Excess salt, especially if steroids cause fluid retention or high pressure.

4. Excess alcohol, which stresses the liver and sleep quality.

5. Smoking/vaping, which increases oxidative injury.

6. Very spicy or irritant foods if they worsen reflux during steroids/NSAIDs.

7. Large caffeine loads late in the day, which can disrupt sleep (needed for healing).

8. Mega-dosing supplements beyond medical advice (risk of interactions).

9. Herbal products that thin blood (e.g., high-dose ginkgo, garlic) before surgery—only with doctor approval.

10. High-vitamin A liver products in large amounts, which can be toxic if overused.

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Frequently Asked Questions

1. Is this an infection?
   No. Phacoanaphylactic endophthalmitis is immune-mediated. However, it mimics infection, and doctors will first exclude infectious endophthalmitis because the treatments are very different.

2. What causes the immune attack?
   Exposure of lens proteins—from surgery or trauma—breaks immune tolerance. The body then targets those proteins as if they were foreign.

3. Can it happen long after cataract surgery?
   Yes. If retained lens fragments remain or later move, inflammation can appear days to weeks after surgery, and rarely later. Any new symptoms after eye surgery deserve prompt evaluation.

4. What is the main treatment?
   The definitive step is to remove residual lens material that is triggering the reaction. Anti-inflammatory drops (steroids) and cycloplegics calm the eye before and after surgery.

5. Why are strong steroids used?
   Steroids are the fastest way to suppress the immune storm and protect vision. They must be supervised to watch for pressure rises and other side effects.

6. Will I need systemic medicines?
   Sometimes. If inflammation is severe, posterior, or persistent, doctors may use oral steroids or steroid-sparing immunomodulators to control it.

7. Can pressure in the eye go up?
   Yes. Inflammation and steroid drops can raise intraocular pressure. Doctors treat this with IOP-lowering drops or, rarely, glaucoma surgery.

8. What complications can occur if untreated?
   Risk includes permanent vision loss, cystoid macular edema, glaucoma, posterior synechiae, and optic nerve or retinal damage.

9. How quickly should I be seen?
   Immediately for severe pain, major redness, or sudden vision changes. For new or ongoing symptoms after surgery or trauma, same-day or next-day assessment is wise.

10. Is antibiotic treatment needed?
    Not for this immune form once infection is excluded. If there is any uncertainty, doctors may take fluid samples and start empiric antibiotics while awaiting results.

11. Will I keep my intraocular lens (IOL)?
    Often yes. If the IOL is stable and clean, it can stay. If it irritates tissues or is malpositioned, it may be repositioned, exchanged, or removed.

12. How long does recovery take?
    It varies. Many patients improve within days to weeks after lens material removal and proper drop schedules, but tapering steroids can take weeks to months to prevent rebound.

13. Can this happen in the other eye?
    It is eye-specific because it needs local lens protein exposure. However, your other eye may have cataract surgery risks of its own, so precise technique and careful follow-up matter for both eyes.

14. Are “immune boosters” helpful?
    This condition is caused by an over-active, misdirected immune response, so treatment aims to modulate or suppress immunity—not boost it. Be careful with any products marketed as “boosters.”

15. What can I do at home to help?
    Protect the eye, use drops exactly as prescribed, avoid rubbing, wear sunglasses, sleep with head elevated, eat anti-inflammatory foods, and keep all follow-ups. Report any worsening symptoms immediately.

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 21, 2025.