Sterile Endophthalmitis

Sterile endophthalmitis means that the inside of the eye becomes very inflamed, but there is no living germ causing an infection. The word “endophthalmitis” describes inflammation of the vitreous and aqueous parts inside the eye. The word “sterile” means that cultures and molecular tests for bacteria and fungi are negative. In simple words, the eye is angry, cloudy, and painful, but the eye is not infected. The inflammation is driven by a toxic trigger, a drug reaction, or an immune reaction. The condition can look like infectious endophthalmitis at first sight. The condition needs careful and fast evaluation because the two conditions are hard to tell apart early on. Sterile endophthalmitis often improves quickly after the trigger is removed and after anti‑inflammatory treatment is started. Infectious endophthalmitis usually worsens without antibiotics or surgery.

Sterile endophthalmitis means intense inflammation inside the eye that looks like endophthalmitis but is not caused by live germs. In other words, the eye’s inner fluids (the vitreous and aqueous) are inflamed, but cultures for bacteria or fungi are negative, and the inflammation settles when the trigger is removed and inflammation is suppressed. It often follows intravitreal injections (for example anti-VEGF medicines or steroids) or rarely certain surgical exposures to irritating substances. Clinically it can mimic infectious endophthalmitis (the dangerous germ-driven type), so doctors act fast and sort it out with exam, imaging, and sometimes fluid samples. PMCEyeWiki

Sterile endophthalmitis is most often reported after injections into the eye, after eye surgery, or after leakage of lens proteins. It can also follow exposure to toxins or particles that irritate the eye. The inflammation can be severe, but the clinical story and the test results help doctors to separate it from a true infection. This guide explains the condition in very simple language. Each sentence uses clear terms. Every section gives a long and practical description.

Types of sterile endophthalmitis

1) Post‑injection sterile endophthalmitis. This type happens after an intravitreal injection. The injection may be an anti‑VEGF drug, a steroid suspension, an antibiotic, or another agent. The eye reacts to the drug, the vehicle, a preservative, or small particles. Pain is often mild to moderate. Vision gets blurred. Floaters are common. Symptoms often begin within 24 to 72 hours. Cultures are negative. The inflammation often improves with topical or systemic steroids once infection has been excluded.

2) Drug‑induced immune inflammatory reaction (immunogenic IOI). Some drugs can trigger an immune reaction inside the eye. The drug itself can act like an antigen. The immune system then attacks parts of the retina or choroid. This reaction can be strong and may involve retinal vessels. It can present like sterile endophthalmitis, with vitritis and sometimes vasculitis. Cultures are negative. The course may be more prolonged than a simple toxic flare.

3) Toxic posterior segment syndrome (TPSS). This pattern mirrors toxic anterior segment syndrome (TASS), but the inflammation is in the vitreous and retina. The trigger can be a contaminant, a detergent residue, or an endotoxin from non‑living bacterial fragments. The eye becomes inflamed quickly. Pain may be mild. Vision drops fast. There is no replicating organism. Removing the toxic source and controlling inflammation helps.

4) Lens‑induced (phacoanaphylactic) endophthalmitis. This type follows leakage of lens proteins into the eye. The immune system sees the lens proteins as foreign. The eye mounts a granulomatous response. There is severe anterior and posterior segment inflammation. Cultures are negative. It can follow trauma or surgery with retained lens fragments. Clearing the lens material and calming the immune response improves the condition.

5) Particle‑induced sterile endophthalmitis. Tiny particles can make the vitreous angry. Examples include silicone oil microdroplets from syringes or tubing, crystalline steroid particles, or talc‑like fillers. These particles irritate immune cells. The vitreous gets cloudy. Vision falls. Removing the particles and using anti‑inflammatory therapy helps.

6) Preservative‑ or vehicle‑related endophthalmitis. Some drug lots have higher levels of preservatives, surfactants, or stabilizers. Some vehicles include polysorbates or other agents. These can activate inflammatory pathways. The eye reacts quickly after exposure. Cultures stay negative. Switching to preservative‑free or a different lot prevents repeat events.

7) Residual antiseptic or detergent–related inflammation. If an antiseptic like povidone‑iodine or a detergent residue accidentally enters the eye, the tissue becomes toxic and inflamed. The onset is rapid. Pain can be burning. The anterior chamber and vitreous show cells and flare. Thorough irrigation and supportive care are used after ruling out infection.

8) Post‑surgical sterile posterior segment inflammation. Instruments, tubing, or balanced salt solutions can rarely carry endotoxin or residues even when sterilized. The result is a sterile inflammatory storm after surgery. It can occur after vitrectomy, cataract surgery, or combined procedures. Careful investigation of surgical materials and lots is important in a cluster.

9) Suture or implant material reaction. The eye can react to certain suture materials, scleral buckle components, or an intraocular lens surface. The inflammation can extend to the vitreous. Cultures are negative. Removing or exchanging the offending material may quiet the eye.

10) Pseudoendophthalmitis from drug crystals. Suspensions like triamcinolone can leave white crystals in the anterior chamber or vitreous. The crystals can mimic pus. The eye can look like it has a hypopyon. Pain is minimal. Vision is hazy mainly from the crystals and cells. Cultures are negative. The finding resolves as crystals settle or are cleared.

11) Autoimmune posterior uveitis masquerading as endophthalmitis. Some autoimmune diseases cause a sudden, dense vitritis and retinal vasculitis. The first impression can be “endophthalmitis.” Microbiologic tests are negative. Systemic evaluation reveals an autoimmune driver. Steroid and immunomodulatory therapy control the inflammation.

12) Device‑associated sterile inflammation. Calcification on an intraocular lens, degradation of a cartridge, or shedding from tubing can trigger inflammation. The time course can be delayed. Cultures are negative. Exchange of the device or lens and control of inflammation are used.

13) Hemorrhage‑associated sterile vitritis. Blood breakdown products in the vitreous can irritate tissues. The inflammatory response can resemble low‑grade endophthalmitis. No infectious organism is found. Clearing the hemorrhage often improves the inflammation.

These overlapping patterns share one truth. The inflammation is strong. The tests do not find replicating germs. The story, timing, exam, and test results point away from infection and toward a toxic or immune cause.

Causes of sterile endophthalmitis

1) Intravitreal anti‑VEGF drug reaction. The eye reacts to an anti‑VEGF injection such as bevacizumab, ranibizumab, aflibercept, brolucizumab, or faricimab. The trigger can be the drug, the stabilizer, or tiny particles. Symptoms often start within 1–3 days. Pain is often mild. Vision drops due to cells and haze. Cultures are negative.

2) Intravitreal steroid suspension reaction. The eye reacts to triamcinolone crystals or the suspension vehicle. The crystals can cause a pseudo‑hypopyon. The vitreous can become very cloudy. Cultures are negative. The inflammation settles as crystals clear.

3) Endotoxin (pyrogen) exposure from non‑living bacterial fragments. Endotoxin can remain in solutions or on instruments even without live bacteria. The toxin triggers a strong inflammatory cascade. The onset is rapid. Cultures are negative because there is no live organism.

4) Silicone oil microdroplet contamination. Microdroplets can shed from syringes, tubing, or injection systems. They float in the vitreous and irritate cells. The eye becomes inflamed. Removing the source prevents recurrence.

5) Preservatives or surfactants in drug lots. Preservatives like benzalkonium chloride or surfactants like polysorbate can activate the immune system inside the eye. A higher than expected load can cause a cluster of cases. Cultures are negative.

6) Residual antiseptic inside the eye. If povidone‑iodine or chlorhexidine accidentally enters the eye, tissues are damaged and inflamed. The eye hurts and vision drops fast. There is no infection. Flushing and anti‑inflammatories are used after urgent assessment.

7) Detergent or cleaning residue on instruments. If instruments have residual detergent, the posterior segment can be injured and inflamed. The pattern can involve both anterior and posterior segments. Clusters raise suspicion of a process problem.

8) Lens‑protein leakage (lens‑induced uveitis). Trauma or surgery can spill lens proteins. The immune system attacks the proteins. Granulomatous inflammation follows. The vitreous becomes cloudy. Cultures are negative.

9) Retained lens fragments after cataract surgery. Small lens pieces can hide and continue to leak proteins. The eye stays inflamed. The vitreous can be involved. Removing the fragments settles the inflammation.

10) Retained ophthalmic viscosurgical device (OVD). Thick viscoelastic left in the eye can prolong inflammation and raise pressure. In some eyes it extends posteriorly. Clearing the OVD helps.

11) Suture material reaction. Some sutures can act as foreign bodies. They can rub, erode, or shed. The nearby tissues inflame. The vitreous can show cells if the reaction is strong. Removing the suture quiets the eye.

12) Intraocular lens (IOL) surface or material reaction. Rarely, an IOL surface film or calcification triggers inflammation that reaches the vitreous. Exchange of the lens solves the trigger.

13) Degraded tubing, cartridge, or injector material. Tiny bits of plastic or polymer can shed and reach the vitreous. The eye responds with inflammation. Process review prevents repeat events.

14) Drug compounding‑related particle load. Large particle loads from compounding can irritate the vitreous. The reaction is sterile. Careful sourcing and filtration reduce the risk.

15) Intraocular foreign body without infection. An inert fragment, such as glass or plastic, can sit in the eye and cause sterile inflammation. The vitreous stays angry until the fragment is removed.

16) Severe vitreous hemorrhage with breakdown products. Blood breaks down into iron and other molecules. These irritate tissues. The vitritis can resemble low‑grade endophthalmitis. Clearing the hemorrhage helps.

17) Autoimmune flare triggered by surgery or injection. A patient with a background autoimmune tendency can flare after an eye procedure. The flare involves the vitreous. Cultures are negative. Systemic workup may be needed.

18) Systemic drug‑induced uveitis. Some systemic medicines are linked with uveitis. The inflammation can extend to the vitreous. The timing with the drug is a clue. Stopping the drug helps if it is the driver.

19) Vaccine‑associated uveitis. Very rarely, vaccination can be followed by a transient immune uveitis. The vitreous can be cloudy. No organisms are found. The course is usually self‑limited with supportive care.

20) Reaction to intravitreal antibiotic without infection. An antibiotic placed in the vitreous can sometimes irritate tissues or cause an immune reaction even when no bacteria are present. The eye inflames. Cultures remain negative.

Symptoms and signs

1) Blurred vision. Vision becomes cloudy because cells and proteins fill the aqueous and vitreous. Light cannot pass cleanly to the retina. Reading and face recognition become hard.

2) New floaters. Patients see dark spots, strings, or cobwebs. These are clumps of inflammatory cells and debris moving in the vitreous.

3) Mild to moderate eye pain. Pain is often less severe than in infectious endophthalmitis, but the eye feels sore, achy, or pressured. Pain can worsen with movement or light.

4) Red eye. The white of the eye looks red because surface blood vessels are dilated from inflammation.

5) Photophobia (light sensitivity). Bright light hurts because the inflamed iris and ciliary body move when the pupil changes size. The retina is also irritated.

6) Tearing and watery discharge. The eye waters as a reflex to irritation. The discharge is usually watery, not thick, because there is no pus from bacteria.

7) Decreased contrast and glare. Haze in the media scatters light. Patients notice glare around lights and have trouble in bright settings.

8) Headache around the eye. The inflamed eye can cause a referred ache around the brow or temple.

9) Foreign body sensation. The eye can feel scratchy from surface inflammation and from frequent blinking.

10) Small hypopyon or pseudo‑hypopyon. A white layer can collect in the lower part of the anterior chamber. It can be true inflammatory cells or heavy drug crystals. It looks like pus but cultures are negative.

11) Vitritis and vitreous haze on exam. The doctor sees many cells and haze in the vitreous on slit‑lamp and indirect exam. The red reflex is dull.

12) Anterior chamber cells and flare. There are white cells and protein in the front of the eye. The light beam shows particles floating in the aqueous.

13) Retinal vascular sheathing or vasculitis. In immune‑mediated cases, blood vessels look white‑lined and inflamed. Leakage can be seen on angiography.

14) Mild eyelid swelling. The lids can look puffy from the surface inflammation and rubbing.

15) Intraocular pressure change. Pressure can rise from clogging of the drainage pathways by cells, or pressure can fall if the ciliary body shuts down during severe inflammation. The change can add to discomfort and blur.

Diagnostic tests

A) Physical examination tests

1) Visual acuity testing. The patient reads a chart to measure sharpness of vision. A drop from baseline suggests that cells and haze are blocking light or that the retina is affected. Measuring acuity at each visit tracks recovery. A quick pinhole test helps separate optical blur from retinal dysfunction. In sterile endophthalmitis, vision often improves quickly once inflammation calms.

2) Pupil examination and relative afferent pupillary defect (RAPD) check. The doctor shines a light in each eye and watches how the pupils react. A new RAPD points to retinal or optic nerve dysfunction. In sterile endophthalmitis, a strong RAPD is less common unless inflammation is very dense or there is associated vasculitis. The test is fast and needs no machines.

3) External inspection of lids, conjunctiva, and sclera. The doctor looks for redness, chemosis, lid swelling, discharge, wound leaks, or suture problems. A quiet wound with no leak argues against an infection entering through the wound. Diffuse redness with watery tearing is common in sterile inflammation.

4) Confrontation visual fields and color vision screening. The doctor tests side vision by finger counting and checks color plates. Diffuse haze reduces both. Focal field loss suggests another process. These bedside checks add functional context to acuity.

B) Manual clinical tests and procedures

5) Slit‑lamp biomicroscopy. A microscope with a bright slit beam allows close inspection of the cornea, anterior chamber, iris, lens, and anterior vitreous. The doctor grades cells and flare. Keratic precipitates, fibrin, or a small hypopyon may be seen. In pseudoendophthalmitis from crystals, shiny white particles are seen layering inferiorly. The slit‑lamp view documents severity and response over time.

6) Intraocular pressure measurement (tonometry). A gentle probe or a puff test measures eye pressure. Pressure can be high if inflammatory cells block the trabecular meshwork, or low if the ciliary body is shut down. Pressure tracking helps guide therapy and safety.

7) Dilated indirect ophthalmoscopy with scleral depression when safe. The pupil is dilated, and the doctor uses a head‑mounted light and lens to see the vitreous, macula, vessels, and periphery. Dense vitritis can hide details. Scleral depression can help view the far periphery, but it is avoided if the eye is very tender. The exam looks for retinal tears, hemorrhage, vasculitis, or foreign material.

8) Seidel test for wound leak. A fluorescein strip is placed at the wound, and blue light is used to see if aqueous is leaking. A negative Seidel test and a well‑sealed wound decrease the chance of an exogenous infection. The test is simple and bedside.

9) Anterior chamber paracentesis (sample collection). A tiny needle draws a small amount of aqueous under sterile conditions. The fluid is sent for stains, cultures, and PCR. The collection is a manual procedure; the analysis is done in the lab. In sterile endophthalmitis, all microbiologic tests are negative.

10) Vitreous tap or core vitrectomy for diagnostic sample. A small‑gauge needle or vitrector collects vitreous. The sample goes to the lab for stains, cultures, and PCR. In sterile cases, these tests do not grow organisms and PCR is negative. The procedure can also reduce inflammatory load.

C) Laboratory and pathological tests

11) Gram stain, cytology, and cell count of aqueous or vitreous. The lab looks for bacteria on Gram stain and for fungal forms on special stains. Cytology counts white cells and looks for crystals or foreign material. In sterile endophthalmitis, no organisms are seen. Crystals or particles may be identified if present.

12) Bacterial culture of intraocular fluids. Samples are placed on media to grow bacteria. In sterile endophthalmitis, cultures remain negative at all time points. A negative culture supports a non‑infectious diagnosis when the clinical course also fits.

13) Fungal culture of intraocular fluids. Samples are placed on fungal media. No growth occurs in sterile inflammation. This helps exclude fungal endophthalmitis, which often needs different therapy and has a different time course.

14) Broad‑range or targeted PCR for bacterial and fungal DNA. Molecular tests search for genetic material from organisms. In sterile cases, PCR is negative. PCR is very sensitive, so a negative result is strong supporting evidence when paired with the clinical picture.

15) Endotoxin (LAL) testing on implicated solution or drug lot if available. If a cluster occurs after a specific drug lot or balanced salt solution, a sample can be sent for endotoxin testing. A positive toxin test with negative cultures points to a toxic sterile outbreak. This test helps with quality control and public health actions.

D) Electrodiagnostic tests

16) Full‑field electroretinography (ffERG). Electrodes measure the electrical response of the retina to flashes of light. Severe vitritis or toxic injury can lower the amplitudes. In sterile inflammation that resolves, ERG often improves. The test assesses global retinal function when media clarity limits direct viewing.

17) Visual evoked potential (VEP). Electrodes on the scalp record responses from the visual pathway when the eye is stimulated. If visual acuity is poor but VEP is relatively preserved, media haze is a major factor. If VEP is very reduced, there may be deeper retinal or optic nerve dysfunction. The test helps separate optical from neuroretinal issues.

E) Imaging tests

18) B‑scan ocular ultrasound. A probe placed on the closed eyelid sends sound waves into the eye. The machine draws a picture from echoes. Dense vitreous opacities, membranes, or detachments can be seen even when the view is poor. In sterile endophthalmitis, dense low‑reflective opacities fill the vitreous without loculated abscesses. The test guides the need for vitrectomy.

19) Optical coherence tomography (OCT). OCT uses light to create cross‑sectional images of the retina. It shows macular edema, subretinal fluid, and hyper‑reflective dots from inflammatory cells. It tracks recovery as haze clears. OCT helps when acuity remains low despite a clearer view.

20) Fluorescein angiography (FA). A dye is injected into a vein, and rapid retinal photos are taken. FA shows leakage from inflamed vessels and areas of non‑perfusion. In immune‑mediated sterile cases, vasculitis or occlusion patterns can appear. FA helps tailor anti‑inflammatory care once infection has been excluded.

Non-pharmacological treatments (therapies and “other” supports)

1. Immediate, urgent reassessment. The most important “treatment” is rapid expert evaluation to rule out infection and start appropriate care; speed protects vision. American Academy of Ophthalmology

2. Close observation with safety-netting. If the eye is stable and infectious risk is low, doctors may monitor closely (often daily at first) while using anti-inflammatory measures; you’ll be told exactly when to call or return urgently.

3. Temporary activity modification. Light work is usually okay, but avoid dusty environments, swimming, eye makeup, and contact lenses until cleared, to minimize extra irritation and exposure.

4. Eye protection and sun-glasses. A shield at night prevents accidental rubbing; sunglasses reduce photophobia and help comfort.

5. Cold compresses for comfort. Short, clean cold packs can reduce surface soreness and lid swelling (avoid pressing on the eye).

6. Frequent preservative-free lubricants. Sterile, single-use tears soothe the surface, which is often irritated by antiseptics from the procedure, and reduce reflex tearing that blurs vision. American Society of Retina Specialists

7. Strict no-rub rule. Rubbing boosts inflammation and risks corneal abrasion.

8. Head elevation. Sleeping with your head up can lessen morning haze from inflammatory debris settling.

9. Screen-time pacing. Short, frequent breaks (20-20-20 rule) reduce glare and eye strain while vision stabilizes.

10. Smoke avoidance. Smoke inflames the ocular surface and worsens healing; staying smoke-free improves comfort and tear quality.

11. Humidified, clean air. Dry air and dust increase irritation; a clean, humidified room eases symptoms.

12. Nutrition and hydration basics. Adequate fluids and balanced meals support general healing and help avoid medication side effects (like steroid-related stomach upset).

13. Glycemic control in diabetes. Stable sugars reduce inflammatory noise and speed tissue recovery (work with your medical team).

14. Stress reduction and sleep. Good sleep lowers systemic inflammatory tone and helps the brain adapt to temporary visual fluctuations.

15. Allergy minimization. If you have seasonal allergies, controlling them lowers background ocular inflammation.

16. Blue-light filters or hats outdoors. Reduces glare while the retina is light-sensitive.

17. Adherence coaching. A simple dosing chart or phone alarm improves drop adherence and outcomes.

18. Caregiver education. Family members learn red-flag symptoms so they can help you seek care quickly if things worsen.

19. Avoid unsupervised OTC “redness” drops. Many contain vasoconstrictors that can irritate or mask changes; always ask your ophthalmologist first.

20. Avoid alternative injections or unregulated “treatments.” Especially avoid stem-cell injections offered by clinics without rigorous trials—such procedures have blinded patients. New England Journal of MedicineAmerican Academy of Ophthalmology

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Drug treatments

Doses below are typical starting points used by eye doctors; your regimen must be individualized by your ophthalmologist based on exam findings and test results.

1. Topical corticosteroid — Prednisolone acetate 1%
   Class: Corticosteroid drop. Dose/Time: 1 drop every 1–2 hours while awake for 24–48 h, then taper per response. Purpose: Rapidly calm intraocular inflammation. Mechanism: Blocks phospholipase A2 → less prostaglandin/cytokine signaling. Side effects: IOP rise, delayed epithelial healing, cataract with prolonged use.

2. Topical corticosteroid — Difluprednate 0.05%
   Class: Potent steroid drop. Dose/Time: 1 drop 4–6×/day, taper. Purpose: Stronger front-of-eye anti-inflammatory effect. Mechanism: High lipid solubility; potent glucocorticoid receptor agonism. Side effects: IOP spikes can be brisk; needs pressure checks.

3. Cycloplegic — Atropine 1%
   Class: Antimuscarinic. Dose/Time: 1 drop 1–2×/day. Purpose: Pain relief from ciliary spasm and prevention of posterior synechiae. Mechanism: Paralyzes ciliary muscle and iris sphincter. Side effects: Light sensitivity, near blur, rare systemic anticholinergic effects.

4. Topical NSAID — Bromfenac 0.07% or Nepafenac 0.1–0.3%
   Class: COX inhibitor drop. Dose/Time: 1 drop 1–3×/day as adjunct. Purpose: Complement steroid effect, reduce macular edema risk. Mechanism: Lowers prostaglandin synthesis. Side effects: Stinging; rare corneal issues with overuse.

5. Oral corticosteroid — Prednisone
   Class: Systemic steroid. Dose/Time: Often 0.5–1 mg/kg/day for short courses in severe vitritis or vasculitis patterns, then taper. Purpose: Suppress posterior segment inflammation when topical therapy is insufficient. Side effects: Glucose elevation, mood changes, GI upset; needs medical supervision.

6. Periocular corticosteroid — Sub-Tenon triamcinolone (e.g., 20–40 mg)
   Class: Depot steroid injection around the eye. Purpose: Longer-acting posterior anti-inflammatory effect when drops are not enough. Mechanism: Slow steroid diffusion to retina/choroid. Side effects: IOP rise, cataract progression.

7. Intravitreal corticosteroid — Dexamethasone implant (0.7 mg)
   Class: Steroid implant (Ozurdex®). Purpose: Potent, sustained suppression of vitritis or macular edema; used cautiously and not if infection is suspected. Side effects: IOP rise, cataract; rare migration in certain eyes.

8. Intravitreal triamcinolone (e.g., 2–4 mg)
   Class: Steroid injection. Purpose: Rapid posterior anti-inflammatory effect. Caution: Can itself cause crystal-related sterile inflammation; used selectively. Side effects: IOP rise, cataract.

9. Empiric intravitreal antibiotics — Vancomycin + Ceftazidime
   Class: Broad-spectrum intravitreal antibiotics. When used: At presentation when infection cannot be ruled out. Purpose: Protect vision while cultures are pending; stopped if infection is excluded and the course proves sterile. Side effects: Rare retinal toxicity; dosing is standardized by surgeons. American Academy of Ophthalmology

10. Immunomodulators (special situations) — e.g., Methotrexate or Mycophenolate
    Class: Steroid-sparing systemic agents. Use: Not routine for one-off sterile endophthalmitis; considered only if the picture actually represents underlying noninfectious uveitis that recurs or persists. Monitoring: Lab tests and coordinated care with uveitis specialists.

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Dietary “molecular” supplements

These do not treat sterile endophthalmitis. They may support general anti-inflammatory balance or ocular metabolism. Discuss with your doctor, especially if you’re on blood thinners, pregnant, or have chronic disease.

1. Omega-3 (EPA+DHA) — ~1–2 g/day with meals. Function: Anti-inflammatory lipid mediators; may support tear film and retinal metabolism. Mechanism: Competes with arachidonic acid pathways.

2. Vitamin D3 — 1000–2000 IU/day (adjust to serum 25-OH D). Function: Immune modulation. Mechanism: Nuclear receptor signaling that tempers inflammatory cytokines.

3. Vitamin C — 500–1000 mg/day. Function: Antioxidant recycling in aqueous humor. Mechanism: Scavenges reactive oxygen species.

4. Lutein + Zeaxanthin — 10 mg + 2 mg/day. Function: Macular pigment support. Mechanism: Blue-light filtering, antioxidant activity in photoreceptors.

5. Zinc (with copper) — 25–40 mg elemental zinc/day + 1–2 mg copper. Function: Enzyme cofactor, retinal metabolism. Mechanism: Supports antioxidant enzymes (e.g., superoxide dismutase).

6. Curcumin (with piperine) — 500–1000 mg/day. Function: Systemic anti-inflammatory adjunct. Mechanism: NF-κB pathway modulation.

7. Quercetin — 250–500 mg/day. Function: Flavonoid antioxidant. Mechanism: Inhibits lipid peroxidation and cytokine release.

8. Resveratrol — 100–250 mg/day. Function: Antioxidant; may support microvascular health. Mechanism: Sirtuin activation pathways.

9. N-Acetylcysteine (NAC) — 600 mg 1–2×/day. Function: Glutathione precursor. Mechanism: Replenishes cellular antioxidant defenses.

10. Coenzyme Q10 — 100–200 mg/day with fat-containing meal. Function: Mitochondrial electron transport support. Mechanism: Antioxidant within lipid membranes.

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Regenerative / stem-cell

1. There is no approved “immunity booster” drug to prevent or treat sterile endophthalmitis. The condition is local inflammation from toxicity or an immune reaction—not a weak immune system. Strengthening “immunity” is not a treatment target.

2. Stem-cell injections into the eye are not a treatment for sterile endophthalmitis and have caused blindness in unregulated clinics. Major cases published in the New England Journal of Medicine describe severe, permanent vision loss after intravitreal adipose-derived “stem cells.” Avoid any clinic offering this. New England Journal of MedicineAmerican Academy of Ophthalmology

3. Biologic anti-TNF or anti-IL-6 agents (e.g., adalimumab, tocilizumab) are not routine here. They are reserved for chronic, noninfectious uveitis under subspecialist care, not for a one-time sterile post-injection flare.

4. Autologous serum eye drops help corneal surface disease; they do not treat intraocular sterile endophthalmitis.

5. Corticosteroid implants (e.g., dexamethasone) can suppress sterile vitritis in selected cases after infection is excluded, but they are anti-inflammatory, not “regenerative.”

6. Experimental regenerative strategies belong only in regulated clinical trials with ethics approval and FDA/EMA oversight—never in cash-pay storefronts.

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Procedures and surgeries

1. Diagnostic/therapeutic tap and inject. The surgeon takes tiny samples of aqueous or vitreous for culture/PCR and injects intravitreal antibiotics immediately if infection is possible. Why: It buys time and vision while proving whether germs are present. If tests later confirm a sterile reaction, antibiotics are stopped and anti-inflammatory therapy continues. American Academy of Ophthalmology

2. Pars plana vitrectomy (PPV). The vitreous gel is partially or completely removed and replaced with sterile fluid. Why: Reduces inflammatory load, clears visual axis, allows larger samples, and treats complications (e.g., retinal tears).

3. Anterior chamber washout (TASS). Surgeons irrigate and exchange the anterior chamber fluid. Why: Flushes out toxic residues and reduces the inflammatory “fuel.” PMC

4. IOL explantation or exchange (selected TASS cases). Why: If an intraocular lens is implicated (e.g., contaminated surface), removing or replacing it eliminates the trigger.

5. Surgery for complications. If sterile inflammation leads to retinal detachment, persistent vitreous opacities, or membranes, PPV with membrane peeling or retinal repair restores structure and vision.

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Prevention strategies

1. Use silicone-free syringes and proper filters for intravitreal drugs to minimize microdroplets/particles.

2. Maintain strict cold-chain and gentle handling of biologics to avoid aggregation.

3. Avoid preservatives inside the eye; use preservative-free preparations for intraocular use.

4. Use correctly mixed, physiologic irrigating solutions (right pH/osmolarity).

5. Meticulous instrument processing—complete rinsing, no enzyme residue, correct sterilization—to prevent TASS. PMC

6. Standardized compounding in accredited pharmacies when splitting vials; avoid bedside repackaging where not permitted.

7. Single-use vials when possible to reduce handling variables.

8. Avoid shaking/foaming of protein drugs; follow manufacturer handling.

9. Comprehensive team training and checklists; board-certified clinicians and consistent protocols lower risks. PMC

10. Rapid reporting of clusters to public-health and professional bodies for investigation if multiple cases occur on one day. EyeWiki

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When to see a doctor

• Same day or immediately if you have new blur, floaters, pain, redness, or light sensitivity after an eye injection or surgery—even if you think it might be “just irritation.”

• Immediately if pain is moderate to severe, vision drops quickly, or you notice a white fluid level (possible hypopyon).

• Urgently if symptoms worsen after starting treatment or if the other eye starts to hurt.
  Early assessment lets your doctor treat as infection until proven otherwise, which is the safest route for your vision. EyeWiki

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What to eat — and what to avoid

Eat more of:

1. Colorful vegetables and leafy greens (lutein/zeaxanthin) to support retinal metabolism.

2. Fatty fish (omega-3s) 2–3×/week or use a vetted supplement after medical advice.

3. Citrus and berries (vitamin C) for antioxidant support.

4. Nuts and seeds for vitamin E and trace minerals.

5. Plenty of water to stay hydrated for comfort.

Avoid or limit:

6. Excess salt and ultra-processed foods, which can worsen fluid balance and systemic inflammation.

7. Smoking and secondhand smoke—they inflame ocular tissues.

8. Excess alcohol, which disturbs sleep and healing.

9. Mega-doses of unvetted supplements without doctor approval (interactions are real).

10. Unregulated “immune boosters” marketed online; these won’t help and can harm.

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FAQs

1) Is sterile endophthalmitis an infection?
No. It looks like infection but cultures are negative and it responds to anti-inflammatory treatment once infection is excluded. PMC

2) Why do doctors sometimes inject antibiotics if it’s sterile?
Because at the start they can’t be sure. The safest plan is to treat as infection until tests and the clinical course prove otherwise. American Academy of Ophthalmology

3) How soon after an injection can it start?
It can be within hours to a couple of days for many sterile reactions; some delayed immune reactions (for example with brolucizumab) occur weeks later. PMC

4) Does it always hurt?
No. Pain can be mild or absent in many sterile cases; severe pain raises concern for infection and needs immediate care. EyeWiki

5) Can it happen after cataract surgery?
Yes. A TASS-type sterile anterior inflammation can occur from residues or toxic exposures and typically begins 12–48 hours after surgery. PMC

6) Will I lose vision permanently?
Most sterile cases recover well with prompt anti-inflammatory care and stopping the trigger. Visual outcome depends on how fast it’s recognized and treated and on any complications.

7) Could I get it again?
If the trigger repeats (for example, the same drug or syringe type), it can recur. Your doctor may switch agents, use silicone-free syringes, or change protocols.

8) Do I need surgery?
Often no. Surgery is considered if inflammation is severe, not clearing, or if complications (like retinal detachment) appear.

9) Are steroids safe?
They are the mainstay for sterile inflammation but require pressure and cataract monitoring. Your ophthalmologist will tailor the taper to you.

10) Should I continue my anti-VEGF shots?
That’s individualized. Many patients can switch to a different agent or resume later after the eye has calmed, depending on the specific trigger and risk–benefit discussion.

11) Do I need oral antibiotics?
Not for a proven sterile case. Antibiotics are used up front only when infection is possible. American Academy of Ophthalmology

12) Can eye drops from the pharmacy fix this?
No. Do not self-treat. You need a specialist exam and a plan that may include prescription drops and procedures.

13) Can supplements cure it?
No supplement cures sterile endophthalmitis. Diet and supplements are adjuncts at best; the core treatment is medical/surgical.

14) Are stem-cell injections helpful here?
No—and they can be dangerous. Unregulated stem-cell eye injections have blinded patients. Avoid them. New England Journal of Medicine

15) What’s the single best prevention step for clinics?
Meticulous handling of drugs and instruments (silicone-free syringes, correct solutions, residue-free instruments) and team protocols—these measures reduce risk dramatically. PMC

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 26, 2025.