Intravitreal Endophthalmitis

Intravitreal endophthalmitis is a severe, sight-threatening infection inside the eye that happens after a tiny needle is used to place medicine into the vitreous gel (the clear jelly that fills most of the eye). “Intravitreal” means “into the vitreous.” “Endophthalmitis” means “inflammation inside the eye caused by germs.” In this condition, bacteria (and less commonly fungi) get into the eye and multiply. The body reacts with a strong inflammatory response. Pus-like cells and toxins cloud the vitreous, the retina becomes swollen and unhappy, and vision can drop very quickly. Symptoms usually include sudden pain, redness, light sensitivity, and a rapid drop in vision hours to a few days after an intravitreal injection. This is an emergency. It can lead to permanent vision loss if not treated immediately with intravitreal antibiotics (antibiotics delivered directly into the eye) and sometimes surgery. The standard first treatment is to take a small sample and inject antibiotics right away, commonly vancomycin (for Gram-positive bacteria) plus ceftazidime (for Gram-negative bacteria). These drugs are used in precise tiny doses directly into the eye to achieve bactericidal levels fast. EyeWikiAmerican Academy of Ophthalmology

Intravitreal endophthalmitis is a severe infection and inflammation inside the eye. The germs live and grow in the eye’s clear fluids: the vitreous gel in the back and the aqueous fluid in the front. Because the inside of the eye is a closed space with very little immune protection, germs can multiply fast. The eye then fills with pus-like inflammatory cells, and the normally clear media turn cloudy. If diagnosis is delayed, the infection can scar or destroy delicate tissues like the retina and optic nerve, causing permanent vision loss. In medical words, endophthalmitis is a purulent (pus-forming) inflammation of the intraocular fluids, usually caused by bacteria or fungi. NCBIEyeWiki

Pathophysiology

When bacteria or fungi get into the eye, they release toxins and trigger a very strong immune response. White blood cells rush in, proteins leak from small blood vessels, and strands form in the vitreous gel. This clouding is called vitritis and is the hallmark of endophthalmitis. The pressure in the eye may go up or down. The retina can be damaged directly by the germs and indirectly by the body’s own inflammatory reaction. The pace of damage depends on the specific germ and the number of organisms. Some bacteria (for example Bacillus cereus after trauma) can destroy vision within hours, while many fungal infections are slower and more insidious. EyeWikiPMC

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Types

Doctors classify endophthalmitis mainly by how the germs enter the eye and by which organisms are involved.

1. Exogenous endophthalmitis (germs come from outside the body)

• Post-operative: occurs after intraocular surgery, most often after cataract surgery with lens implantation. Skin bacteria like coagulase-negative Staphylococcus are common in acute cases; chronic cases months later are often due to Cutibacterium acnes hiding in the capsular bag. EyeWikiMoran COREMDPI

• Post-intravitreal injection: follows injections for retinal diseases. It can present very rapidly and sometimes more aggressively than routine post-surgical cases. Oropharyngeal Streptococcus species are a well-recognized cause. EyeWiki

• Post-traumatic: follows penetrating eye injury, especially with a retained foreign body. Environmental organisms like Bacillus cereus are classic and can progress with frightening speed. PMC

• Bleb-associated: occurs months to years after glaucoma filtering surgery when an infected bleb allows microbes to enter the eye. Late cases frequently involve streptococci and gram-negative bacteria like Haemophilus influenzae. EyeWiki

• Keratitis-associated spread: a severe corneal ulcer that perforates or tracks inward can seed the anterior chamber and then the vitreous. (This route is less common but documented in severe bacterial or fungal keratitis.) AAO Journal

2. Endogenous endophthalmitis (germs come from the bloodstream)
   Germs travel in the blood from an infection elsewhere (for example a liver abscess, infected IV line, or heart valve infection) and seed the eye. Candida species and gram-negative bacteria like hypervirulent Klebsiella pneumoniae are classic causes; the latter is strongly linked with pyogenic liver abscess, especially in parts of Asia. NCBINature

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Causes

Important note: “Cause” here means the entry event or source plus typical organisms that lead to infection.

1. Recent cataract surgery — small numbers of skin bacteria can enter through the surgical wound and multiply in the eye; coagulase-negative Staphylococcus is common in acute cases. EyeWiki

2. Chronic infection after cataract surgery due to Cutibacterium acnes — this slow, indolent bacterium can hide on the lens capsule and flare up months later with recurrent inflammation. Moran CORE

3. Intravitreal injection for retinal disease — a needle passing through the eye wall can carry bacteria inward; droplet contamination from talking/coughing nearby has been implicated in streptococcal cases. EyeWiki

4. Penetrating eye trauma — dirt or plant material can push environmental organisms into the eye; Bacillus cereus is notorious for rapid, severe damage. PMC

5. Retained intraocular foreign body (IOFB) — a tiny metal or organic fragment left inside the eye is a nidus for infection and biofilm. (Often linked with Bacillus or gram-negative rods.) BMJ Open

6. Glaucoma filtering bleb infection — a thin, leaking bleb can let streptococci or H. influenzae in, leading to late, dangerous endophthalmitis. EyeWiki

7. Vitreoretinal surgery — any intraocular procedure carries a small risk of inoculation if microbes reach the vitreous during or just after surgery. EyeWiki

8. Keratitis that perforates or tracks inward — a deep corneal ulcer (bacterial or fungal) can extend into the anterior chamber and back into the vitreous cavity. AAO Journal

9. Contaminated instruments, solutions, or medications (rare outbreaks) — if a solution or instrument is contaminated, many patients may be affected; strict sterilization and quality control aim to prevent this. ESCRS

10. Endocarditis or bacteremia (bloodstream infection) — Staphylococcus aureus or streptococci in the blood can seed the eye and start infection from the inside. NCBI

11. Pyogenic liver abscess due to hypervirulent Klebsiella pneumoniae — this organism can spread from a liver abscess to the eye and cause aggressive endogenous endophthalmitis. Nature

12. Indwelling IV catheters or total parenteral nutrition with candidemia — Candida in the blood can settle in the choroid and vitreous, especially in hospitalized or immunocompromised patients. NCBI

13. Intravenous drug use — unsterile injections can lead to bloodstream infections with bacteria or fungi that travel to the eye. NCBI

14. Uncontrolled diabetes mellitus — raises infection risk and is linked to worse outcomes in some endogenous cases. ScienceDirect

15. Immunosuppression (steroids, chemotherapy, transplant) — weak immune defenses make fungal or unusual bacterial infections more likely to reach the eye. NCBI

16. Neonatal or ICU sepsis — premature or critically ill patients are at risk of Candida or gram-negative bloodstream infections that can involve the eyes. NCBI

17. Dental or ENT sources with bacteremia — oral streptococci can enter the bloodstream and seed the eye, and they also feature in some post-injection cases. EyeWiki

18. Urogenital or gastrointestinal sepsis — urinary or GI infections can cause bacteremia that occasionally leads to endogenous endophthalmitis. NCBI

19. Bleb leaks after glaucoma surgery — a persistent leak is a direct pathway for microbes from the ocular surface to the anterior chamber and then posteriorly. EyeWiki

20. High-virulence trauma organisms (e.g., Bacillus cereus) — included separately because their toxins can destroy retinal tissue extremely fast, making early recognition crucial. PMCFrontiers

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Symptoms

1. Sudden drop in vision — vision becomes blurry or dim because the vitreous fills with inflammatory cells. EyeWiki

2. Eye pain — pain ranges from aching to severe, often worse with eye movement. NCBI

3. Eye redness — the white of the eye is very red from inflamed surface vessels. EyeWiki

4. Light sensitivity (photophobia) — bright light hurts because the inflamed iris and ciliary body react painfully. NCBI

5. Floaters or hazy view — clumps in the vitreous cast shadows and make moving spots in vision. NCBI

6. Lid swelling and conjunctival chemosis — the tissues around the eye get puffy and boggy from inflammation. EyeWiki

7. Thick discharge or tearing — surface irritation and inflammation can cause watering and mucus. NCBI

8. Headache around the eye — referred pain from inflamed ocular structures. NCBI

9. Nausea — severe ocular pain or pressure changes can trigger nausea. NCBI

10. Fever or malaise (especially endogenous cases) — whole-body infection can cause systemic symptoms along with eye signs. NCBI

11. Rapid worsening over hours (high-virulence bacteria) — with organisms like Bacillus, vision can crash in less than a day after trauma. PMC

12. Slower, smoldering course (fungal or C. acnes) — symptoms can be subtle and intermittent for weeks to months. EyeWikiMoran CORE

13. Hypopyon (a white layer in the front of the eye) — visible pus-like fluid settles inferiorly in the anterior chamber. EyeWiki

14. Pain on moving the eye — inflammation of tissues and high pressure can make movement painful. NCBI

15. Very poor vision at presentation (e.g., light perception only) — in severe cases, only the ability to detect light remains at first exam. NCBI

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Diagnostic tests

The goals of testing are to recognize the emergency, confirm the organism, and check for a source when infection comes from the bloodstream.

A) Physical examination at the slit lamp and in clinic

1. Visual acuity (Snellen/ETDRS)
   Reading letters at distance gives a baseline. A sudden drop compared with the other eye is a red flag for intraocular infection. NCBI

2. Pupil exam and RAPD
   Checking the light reflex and for a relative afferent pupillary defect helps judge retinal or optic nerve involvement in severe cases. NCBI

3. External inspection
   Lid swelling, conjunctival chemosis, and discharge support a diagnosis of severe intraocular inflammation or infection. EyeWiki

4. Intraocular pressure (tonometry)
   Pressure can be high from inflammation or low from ciliary shutdown. (Avoid tonometry if an open-globe injury is suspected.) NCBI

5. Slit-lamp anterior segment exam
   Doctors look for corneal edema, anterior chamber cells/flare, fibrin, and hypopyon—classic visible signs in endophthalmitis. EyeWiki

6. Dilated fundus exam (indirect ophthalmoscopy)
   When the media permit, the retina is inspected for dense vitritis, retinal infiltrates, or chorioretinal lesions. Often the view is too hazy, which itself is a key clue. EyeWiki

B) Manual/bedside functional checks

7. Pinhole test
   If vision does not improve with a pinhole, the problem is not simple refractive blur and may reflect media opacity or retinal dysfunction from infection. NCBI

8. Color vision
   Loss of color discrimination suggests optic or macular involvement when inflammation is severe. NCBI

9. Seidel test with fluorescein (for leaks)
   After trauma or surgery, dye highlights a leaking wound or bleb that can be the entry point for germs. EyeWiki

C) Laboratory and pathological tests to identify the organism

10. Aqueous humor tap for Gram stain and culture
    A small fluid sample from the anterior chamber can show bacteria on stain and grow them on culture media. Results guide targeted therapy. NCBI

11. Vitreous tap/biopsy for stain and culture
    Sampling the core vitreous usually yields higher positivity than aqueous sampling in acute cases. It is the key microbiologic test. NCBI

12. Fungal stains and culture (e.g., KOH with calcofluor; Sabouraud agar)
    Especially in slow, endogenous, or immunocompromised presentations, these tests look for yeasts like Candida or molds like Aspergillus. EyeWiki

13. Broad-range molecular tests (16S/18S/ITS rRNA PCR)
    PCR can detect bacterial or fungal DNA when cultures are negative or slow, often identifying an organism within a day and increasing diagnostic yield substantially. PubMed+1Ajo

14. Blood cultures (especially if endogenous is suspected)
    Two or more sets increase the chance of catching the bloodstream source (for example, Klebsiella from a liver abscess or Staph aureus from endocarditis). NCBI

15. Systemic inflammatory labs (CBC, CRP/ESR) and organ-specific tests
    These help corroborate infection and guide the search for a source (urine culture for UTI, imaging or ultrasound for liver abscess, echocardiography for endocarditis when indicated). NCBIAjo

D) Electrodiagnostic tests (used selectively)

16. Electroretinography (ERG)
    When the media are opaque and the retina cannot be seen, ERG helps estimate whether retinal function is still present, which informs prognosis. NCBI

17. Visual evoked potential (VEP)
    If there is a question about the optic pathway when the fundus view is blocked, VEP can show whether signals are reaching the brain. (This is not routine but occasionally helpful.) NCBI

E) Imaging (ocular and orbital)

18. B-scan ocular ultrasonography
    This is the frontline imaging when the view is hazy. It can show dense vitreous opacities, membranes, retinal detachment, choroidal thickening, or even a hidden foreign body. NCBI

19. CT of the orbits (and sometimes head/face)
    CT is excellent for metallic or glass foreign bodies after trauma and for detecting gas-forming organisms. It also screens for orbital complications. (Avoid MRI if metal may be present.) BMJ Open

20. MRI of the orbits and brain
    When fungus or extension beyond the eye is suspected, MRI helps define soft-tissue involvement, scleral spread (panophthalmitis), or intracranial complications. NCBI

Non-pharmacological treatments

Below are supportive and procedural steps that do not involve taking systemic medicines. Many are done together with intravitreal antibiotics, because antibiotics are the core of care. I explain each item with the description, purpose, and mechanism in plain English.

1. Urgent triage and referral
   Description: Same-day evaluation by a retina specialist or eye emergency service.
   Purpose: Time is retina; earlier therapy saves vision.
   Mechanism: Rapid assessment leads to immediate intravitreal therapy and surgery when needed, reducing bacterial load before irreversible retinal damage occurs.

2. Aseptic field preparation in clinic or OR
   Description: Thorough eyelid skin and conjunctival cleansing with povidone-iodine 5–10% and sterile draping of lashes and lids; sterile speculum to keep eyelids open.
   Purpose: Minimize new contamination during any eye procedure (tap, injection, or surgery).
   Mechanism: Povidone-iodine rapidly kills a broad range of microbes on the ocular surface, lowering inoculum at the time of intraocular entry.

3. Vitreous tap/biopsy (diagnostic sampling)
   Description: Using a needle or vitrector to remove a small sample of vitreous for microbiology before antibiotics.
   Purpose: Identify the causative organism and its drug sensitivities.
   Mechanism: Culture/PCR tells the team which bug is present, enabling targeted antibiotic adjustments.

4. Core vitrectomy (pars plana vitrectomy) as a primary procedure when indicated
   Description: Microsurgery to remove infected vitreous gel and inflammatory debris.
   Purpose: Lower the number of organisms and toxins; improve oxygenation and drug penetration.
   Mechanism: Physically clears the bacterial “soup,” reduces inflammatory mediators, and creates space for light to reach the retina.

5. Repeat vitrectomy or repeat tap if clinical course worsens
   Description: A second surgical clean-out or sampling after initial therapy.
   Purpose: Address persistent infection or inadequate response.
   Mechanism: Further reduces microbial burden and provides fresh cultures to guide changes in therapy.

6. Wound revision and sealing of any entry leaks
   Description: Tightening or suturing any leaking injection track or surgical incision.
   Purpose: Stop ingress of surface fluid and microbes.
   Mechanism: A sealed wound prevents reflux of contaminated tears into the eye.

7. Intraocular lens (IOL) and capsular bag washout/removal in post-cataract cases with in-the-bag infection
   Description: For post-surgical cases where biofilm on lens material is suspected, remove or thoroughly clean.
   Purpose: Eliminate a hidden reservoir of bacteria that shields them from drugs.
   Mechanism: Biofilms protect microbes from antibiotics; removing the nidus helps eradicate infection.

8. Removal of sustained-release intravitreal implants if colonized
   Description: Taking out an infected steroid or drug implant.
   Purpose: Remove reservoirs that seed ongoing infection.
   Mechanism: Similar to IOL biofilm logic—no surface, no sanctuary for bacteria.

9. Intensive vision-directed monitoring
   Description: Frequent checks of acuity, pain, intraocular pressure (IOP), and slit-lamp/ultrasound findings.
   Purpose: Detect improvement or early failure to escalate care.
   Mechanism: Clinical trend tracking guides timing of repeat injections or surgery.

10. Ultrasound B-scan when media are opaque
    Description: A gentle probe images the retina through closed lids when the view is blocked.
    Purpose: Confirm if the retina is attached and assess vitreous debris.
    Mechanism: High-frequency sound waves bounce off structures to create a picture when you can’t see in.

11. IOP control with non-drug measures
    Description: Gentle ocular massage avoidance, head elevation, and careful fluid management during surgery.
    Purpose: Keep pressure safe to protect the optic nerve.
    Mechanism: Mechanical and positional steps assist outflow and avoid ischemic spikes.

12. Pain and light management (non-drug)
    Description: Sunglasses, dim lighting, and rest.
    Purpose: Reduce photophobia and discomfort during healing.
    Mechanism: Less light stimulation calms inflamed tissues and reduces reflex tearing.

13. Protective eye shield
    Description: Rigid shield over the eye outside of exams.
    Purpose: Prevent accidental rubbing or trauma.
    Mechanism: Physical barrier protects a vulnerable globe.

14. Hygiene education for the patient and caregiver
    Description: Clear instructions: no eye rubbing, careful handwashing, drop technique, and return-warning signs.
    Purpose: Reduce re-contamination and ensure early re-presentation if worse.
    Mechanism: Behavior change lowers exposure and raises vigilance.

15. Systemic stabilization in the medically ill
    Description: Coordinate with internal medicine if the patient is septic or immunocompromised.
    Purpose: Improve host defenses and antibiotic pharmacokinetics.
    Mechanism: Treating systemic disease (e.g., diabetes control) supports ocular recovery.

16. Addressing eyelid margin disease and blepharitis (between procedures)
    Description: Warm compresses, lid hygiene, and, if needed, later medical therapy after acute phase.
    Purpose: Reduce bacterial load on lids for future procedures.
    Mechanism: Fewer bacteria at the margin means less risk of re-inoculation.

17. Speech minimization during procedures
    Description: “No-talking” or masked talking policy for staff and patient during injections/tap.
    Purpose: Reduce aerosolized oral flora (notably streptococci).
    Mechanism: Fewer droplets near the needle entry lowers risk of introducing virulent mouth bacteria. Evidence suggests no-talking and/or masking policies may reduce post-injection endophthalmitis. AAO JournalPubMed

18. Use of prefilled syringes and single-use supplies
    Description: Factory-filled, sterile drug syringes and avoidance of multi-use vials when possible.
    Purpose: Lower compounding and handling contamination risk.
    Mechanism: Reduces the number of steps where microbes can enter.

19. Strict hand hygiene and glove use
    Description: Alcohol-based hand rub before gloving; fresh sterile gloves for each eye.
    Purpose: Block transfer of organisms from hands to instruments or patient.
    Mechanism: Hand sanitizers rapidly kill transient pathogens and gloves provide a physical barrier.

20. Post-procedure follow-up within 24–48 hours if concerning symptoms
    Description: Early, scheduled check or emergency access.
    Purpose: Catch early infection while salvageable.
    Mechanism: The earlier the re-entry for treatment, the better the prognosis.

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Drug treatments

Key point: The backbone is intravitreal antibiotics at precise doses. These go directly into the eye to reach bactericidal concentrations quickly. A commonly used empiric pair is vancomycin (1 mg/0.1 mL) for Gram-positive coverage and ceftazidime (2.25 mg/0.1 mL) for Gram-negative coverage; alternatives exist for allergies. Antifungals are chosen when fungus is suspected. EyeWikiAmerican Academy of Ophthalmology

1. Vancomycin — intravitreal
   Class: Glycopeptide antibiotic (Gram-positive, including MRSA and streptococci).
   Typical dose/time: 1 mg in 0.1 mL, injected intravitreally at diagnosis; may repeat based on response and culture guidance.
   Purpose: Kill Gram-positive organisms frequently implicated in post-injection endophthalmitis.
   Mechanism: Blocks cell-wall synthesis, causing bacterial death at high intraocular levels.
   Notable side effects: Rare retinal toxicity with standard dosing is uncommon; systemic reactions minimal due to local delivery.

2. Ceftazidime — intravitreal
   Class: Third-generation cephalosporin (Gram-negative coverage including Pseudomonas).
   Typical dose/time: 2.25 mg in 0.1 mL, intravitreal at diagnosis; repeat per course and sensitivities.
   Purpose: Complement vancomycin to cover Gram-negatives.
   Mechanism: Inhibits cell-wall synthesis of susceptible Gram-negatives.
   Side effects: Rare retinal toxicity with standard doses; watch for allergy history.

3. Amikacin — intravitreal (for beta-lactam allergy)
   Class: Aminoglycoside (Gram-negative).
   Typical dose/time: 0.4 mg in 0.1 mL intravitreal; used when ceftazidime cannot be used.
   Purpose: Alternative Gram-negative coverage.
   Mechanism: Binds 30S ribosome, causing misreading and bacterial death.
   Side effects: Risk of macular infarction at higher doses or in susceptible eyes; used cautiously.

4. Dexamethasone — intravitreal (adjunct, selected cases)
   Class: Corticosteroid.
   Dose/time: ~0.4 mg in 0.1 mL intravitreal at the time of antibiotics (practice varies).
   Purpose: Calm intense inflammation that itself can damage retina.
   Mechanism: Suppresses cytokine cascade; reduces edema.
   Side effects: Possible IOP rise, theoretical risk of dampening host defenses—use is individualized.

5. Voriconazole — intravitreal (if fungus suspected/confirmed)
   Class: Triazole antifungal.
   Dose/time: Often 100 µg in 0.1 mL intravitreal; may repeat per fungal response.
   Purpose: Treat Candida/Aspergillus endophthalmitis.
   Mechanism: Inhibits ergosterol synthesis in fungal membranes.
   Side effects: Potential retinal toxicity at high levels; careful dosing and culture guidance essential.

6. Amphotericin B — intravitreal (fungal)
   Class: Polyene antifungal.
   Dose/time: 5–10 µg in 0.1 mL intravitreal.
   Purpose: Alternative/adjunct for fungal organisms.
   Mechanism: Binds ergosterol, forming pores that kill fungi.
   Side effects: Retinal toxicity risk increases with dose; dosing precision is critical.

7. Systemic moxifloxacin — oral (select post-injection cases; evidence mixed)
   Class: Fluoroquinolone antibiotic.
   Dose/time: Commonly 400 mg once daily for several days when chosen.
   Purpose: Add systemic Gram-negative and streptococcal coverage in select scenarios (practice patterns vary).
   Mechanism: Inhibits bacterial DNA gyrase/topoisomerase IV.
   Side effects: Tendon issues, QT prolongation, GI upset; not universally required and evidence of benefit after cataract surgery is limited compared with intravitreal therapy. PMC

8. Systemic antifungals (voriconazole, fluconazole)
   Class: Triazoles.
   Dose/time: Voriconazole often 200 mg twice daily (adjusted), fluconazole dose per organism.
   Purpose: Essential if fungal endophthalmitis or systemic fungemia.
   Mechanism: Systemic levels treat concurrent bloodstream/tissue infection and support intravitreal therapy.
   Side effects: Liver enzyme elevations, visual disturbances (voriconazole), drug interactions.

9. Topical fortified antibiotics (adjunct)
   Class: High-concentration topical vancomycin/ceftazidime or fluoroquinolones.
   Dose/time: Frequent drops early.
   Purpose: Treat surface and anterior chamber contamination; adjunct to intravitreal therapy.
   Mechanism: High tear/aqueous levels decrease surface bacterial load and anterior segment involvement.
   Side effects: Surface irritation; rare allergy.

10. Cycloplegic drops (e.g., atropine) — symptom control
    Class: Antimuscarinic.
    Dose/time: Once or twice daily as ordered.
    Purpose: Reduce ciliary spasm pain and prevent posterior synechiae.
    Mechanism: Temporarily “freezes” the focus muscle and opens the pupil.
    Side effects: Light sensitivity from dilation; systemic absorption is minimal with proper punctal occlusion.

Why intravitreal dosing matters: Delivering antibiotics inside the eye immediately achieves levels that killing bacteria require—levels that are very hard to reach quickly with pills or IV alone. This is a major principle drawn from decades of clinical practice and studies. American Academy of Ophthalmology

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Dietary molecular supplements

Diet does not cure endophthalmitis. These options are supportive for overall healing and general eye health and should never delay proven treatments. Discuss with a clinician—especially if you take blood thinners or have kidney/liver disease.

1. Vitamin C (ascorbic acid) — 500–1000 mg/day
   Function: Antioxidant support during inflammation.
   Mechanism: Regenerates other antioxidants; supports collagen synthesis in healing tissues.

2. Vitamin E (natural mixed tocopherols) — 200–400 IU/day
   Function: Lipid membrane antioxidant.
   Mechanism: Limits oxidative damage to cell membranes in inflamed tissues.

3. Omega-3 fatty acids (EPA/DHA) — 1–2 g/day combined EPA+DHA
   Function: Anti-inflammatory lipid mediators.
   Mechanism: Competes with arachidonic acid, shifting toward pro-resolving mediators.

4. Zinc (as zinc gluconate) — 15–30 mg elemental/day
   Function: Immune enzyme cofactor; supports epithelial repair.
   Mechanism: Helps DNA/RNA synthesis and barrier function.

5. Vitamin A (as beta carotene or retinyl palmitate) — 2,500–5,000 IU/day (avoid high doses in pregnancy)
   Function: Epithelial integrity and immune signaling.
   Mechanism: Retinoids regulate gene expression involved in mucosal defense.

6. Lutein + zeaxanthin — 10–20 mg + 2–4 mg/day
   Function: Macular antioxidants.
   Mechanism: Concentrate in photoreceptors and filter high-energy light; supportive for retinal stress.

7. N-acetylcysteine (NAC) — 600–1200 mg/day
   Function: Precursor to glutathione.
   Mechanism: Replenishes intracellular antioxidant defenses.

8. Probiotics (e.g., Lactobacillus rhamnosus GG) — per label
   Function: Gut immune tone support.
   Mechanism: Modulates mucosal immunity; may reduce systemic inflammatory noise.

9. Curcumin (with piperine for absorption) — 500–1000 mg/day
   Function: Anti-inflammatory polyphenol.
   Mechanism: Inhibits NF-κB signaling pathways; adjunct only.

10. Coenzyme Q10 (ubiquinone) — 100–200 mg/day
    Function: Mitochondrial cofactor; antioxidant.
    Mechanism: Supports cellular energy production during recovery.

Again: supplements are optional, supportive, and not a substitute for intravitreal therapy or surgery.

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Regenerative / stem-cell drugs

You asked for this category specifically. Here’s the honest, safe, evidence-based answer in simple English.

1. There are no approved “stem-cell drugs” to treat intravitreal endophthalmitis.
   Why: Endophthalmitis is an acute infection. The proven lifesaving steps are intravitreal antibiotics and vitrectomy when indicated. Experimental intraocular cell therapies target chronic retinal diseases, not acute intraocular infections. Using unproven stem-cell products in the eye can cause scarring, detachment, or even blindness.

2. Intravenous immunoglobulin (IVIG) is not standard for endophthalmitis.
   Why: The infection is compartmentalized inside the eye, and the fastest way to kill germs is direct intravitreal antibiotics. IVIG has no proven role here.

3. Systemic “immune boosters” (herbs, megavitamins) do not clear bacteria in the vitreous.
   Why: Even if they modulate immunity, they cannot replace the bactericidal levels achieved by intravitreal antibiotics within minutes.

4. Systemic corticosteroids as “immune modulators” are not used to boost immunity; if used at all, they’re carefully timed adjuncts to reduce inflammation after antibiotics are started—and only in selected cases.
   Why: Giving steroids before killing microbes can worsen infection.

5. Cytokine modulators or biologics (e.g., anti-TNF) have no role in acute infectious endophthalmitis and could be harmful.
   Why: They suppress host defenses during active infection.

6. Safe reality check: The closest thing to “regenerative” support is prompt source control (vitrectomy) plus nutritional support and visual rehabilitation later. This promotes the eye’s natural recovery capacity. Any clinic offering stem cells for endophthalmitis is outside accepted standards.

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Surgeries

1. Diagnostic/therapeutic vitreous tap + intravitreal injection (“tap and inject”)
   Procedure: Under sterile conditions, a small volume of vitreous is aspirated for culture, immediately followed by intravitreal antibiotics.
   Why: You get both a lab diagnosis and immediate drug delivery without delay.

2. Pars plana vitrectomy (PPV)
   Procedure: Through tiny ports, a vitreous cutter removes infected vitreous gel; antibiotics are injected at the end.
   Why: Reduces the number of microbes and toxins quickly, improves drug spread, and helps salvage vision—especially when the initial vision is very poor or the view is too cloudy to assess. (Modern practice often favors earlier PPV in severe presentations.) PMC

3. IOL/capsular bag removal or washout (post-cataract cases)
   Procedure: Remove or scrub biofilm from the lens implant and capsular bag.
   Why: Bacteria can hide on plastic surfaces; removing the hiding place helps cure the infection.

4. Removal of infected intravitreal implants
   Procedure: Take out the colonized device.
   Why: To eliminate a persistent source of organisms.

5. Wound repair / scleral patching if there is a leak
   Procedure: Close and reinforce any leaky track or incision.
   Why: Prevents ongoing ingress of surface fluid and microbes and improves globe integrity.

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Practical prevention

1. Povidone-iodine to lids and conjunctival sac before any intravitreal injection.

2. No-talking and/or masking policy during injections to reduce oral droplet spread. AAO JournalPubMed

3. Sterile technique: sterile speculum, lash isolation, and single-use supplies.

4. Prefilled syringes when available; avoid multi-dose vials and unnecessary compounding steps.

5. Hand hygiene with alcohol rub before gloving; new sterile gloves for each eye.

6. Manage blepharitis and heavy lid crusting before elective injections.

7. Avoid needle contact with lashes or lid skin; never pass over non-prepped areas.

8. Do not apply prophylactic topical antibiotics routinely (they do not reduce risk and may increase resistance); rely on povidone-iodine.

9. Educate patients to report pain, vision drop, or increasing floaters promptly.

10. For cataract surgery context: intracameral cefuroxime (1 mg/0.1 mL) at the end of surgery reduces postoperative endophthalmitis risk. (Different setting, same principle of rapid intraocular drug levels.) ESCRSPMC

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When to see a doctor

• Same day if you’ve had an intravitreal injection in the last few days and now have increasing eye pain, redness, light sensitivity, or vision worsening.

• Immediately if you notice a sudden shower of floaters, a “milk-white” view, or a curtain-like shadow.

• If you are immunocompromised or had a recent eye surgery, be even more cautious—seek care with any worrying symptom.

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What to eat and what to avoid

Eat:

• Hydrating foods and fluids: water, broths—dehydration worsens discomfort.

• Protein-rich foods: eggs, fish, lentils—to support tissue healing.

• Colorful fruits and vegetables: berries, citrus, leafy greens—for antioxidants (vitamin C, carotenoids).

• Healthy fats: nuts, seeds, olive oil, and omega-3-rich fish (salmon, sardines) for anti-inflammatory support.

• Whole grains for steady energy and micronutrients.

Avoid (for now):

• Excess alcohol (dehydrates; interferes with healing).

• Very salty foods that may worsen swelling.

• Smoking/vaping (impairs tissue oxygenation and healing).

• Uncontrolled high-sugar intake if you have diabetes (infection outcomes are worse with poor glycemic control).

Remember: diet is supportive only. It cannot replace intravitreal therapy or surgery.

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Frequently asked questions

1) Is intravitreal endophthalmitis common?
It’s rare, but because intravitreal injections are very common, every retina practice has protocols to prevent and treat it rapidly.

2) How fast can vision drop?
Sometimes within hours. That’s why new pain or vision loss after an injection is treated as urgent.

3) What is the first treatment?
A vitreous sample is taken and intravitreal antibiotics are injected immediately—most often vancomycin + ceftazidime as empiric coverage while cultures are pending. EyeWiki

4) Do I always need surgery?
Not always. If the infection is milder, doctors may do a tap and inject and monitor closely. If the infection is severe (very poor vision or dense opacity), or not improving, they often perform pars plana vitrectomy early. Modern practice trends favor earlier vitrectomy in worse presentations. PMC

5) Do eye drops alone help?
No. Drops cannot reach high enough levels inside the vitreous to cure an established infection. They may be used as adjuncts for surface control.

6) Are systemic antibiotics (pills/IV) enough?
For post-injection/post-surgical cases, systemic antibiotics alone are not enough; the eye needs direct intravitreal therapy. Evidence for routine systemic antibiotics after injections is mixed; practice varies and is individualized. PMC

7) What about fungal endophthalmitis?
Doctors use intravitreal antifungals (e.g., voriconazole or amphotericin B) and often systemic antifungals as well, guided by cultures and clinical features.

8) Can steroids help?
Intravitreal dexamethasone may be added after antibiotics to limit damaging inflammation in select cases; this is individualized because suppressing inflammation too early can be harmful.

9) How long until I know if treatment worked?
Often you’ll see signs within 24–48 hours (less pain, clearer media, small vision gains). If not, your team considers repeat injection or vitrectomy.

10) Could my own mouth bacteria cause this?
Yes—streptococcal species from the mouth can be implicated. That’s why many teams use no-talking or masking during injections. AAO Journal

11) Can this happen again?
The risk is still low, but it can. Preventive steps (povidone-iodine, sterile technique, speech control, prefilled syringes) keep the risk very small.

12) Will I lose my eye?
That is rare, but the condition is serious. Prompt, aggressive treatment usually saves the eye, and many patients recover meaningful vision—especially with early care.

13) Can I use herbal/“immune” remedies instead of antibiotics?
No. These cannot kill bacteria inside the vitreous. Use only as adjuncts with your doctor’s guidance.

14) Should I stop my blood thinners before injections to prevent infection?
No. Blood thinners affect bleeding risk, not infection. Doctors generally do not stop them for injections; always follow your prescriber’s advice.

15) What’s the single most important prevention step?
Povidone-iodine antisepsis on the eye surface before the needle goes in, plus a no-talking/masking policy during the injection. For cataract surgery (a different setting), intracameral cefuroxime at the end of surgery reduces infection risk. AAO JournalESCRS

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.