Surgically-Induced Necrotizing Scleritis (SINS)

Surgically-Induced Necrotizing Scleritis, or SINS, is a very severe inflammation that eats away the white wall of the eye called the sclera, and it happens after eye surgery near the area of the surgical wound. Doctors believe it is mostly an autoimmune reaction, which means the body’s own defense system starts to attack the eye tissue after surgery, probably because surgery exposes hidden tissue proteins and changes blood flow in a way that sets off a delayed immune response. This reaction causes painful, rapidly progressing tissue damage of the sclera, sometimes spreading forward or backward, and it can appear weeks, months, or even years after different kinds of eye operations like pterygium removal, cataract surgery, trabeculectomy, scleral buckling, pars plana vitrectomy, or strabismus surgery. In almost all cases it begins right next to the incision or the operated area, which is a big clue to the diagnosis. Doctors must always rule out infection and toxic or ischemic scleral necrosis from things like mitomycin C, beta-irradiation, or heavy cautery, because these conditions can also cause scleral melting after surgery and may look very similar, but they are treated differently and should not be called SINS. SINS is rare but dangerous, and it can threaten vision if not recognized quickly and treated with immunosuppression once infection is excluded. EyeWikiPMCAmerican Academy of OphthalmologyLippincott Journals

Why SINS happens

In SINS, the immune system likely forms immune complexes that deposit in the small blood vessels of the sclera near the surgical site. These immune complexes trigger vasculitis, which is inflammation of those vessels, and that cuts down blood supply and oxygen to the sclera. Reduced blood supply and direct immune attack cause the tissue to thin, break down, and die (this is what “necrotizing” means). The surgical cut and the healing process may expose antigens, change local proteins, and disturb the balance between breakdown and repair, so the immune system becomes misdirected. This is why SINS often occurs in people who have had more than one eye surgery and in some people who have autoimmune diseases elsewhere in the body. PMCScienceDirect+1

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Types of SINS

Doctors use practical, descriptive groupings that help them recognize and manage SINS. These are not strict universal labels, but they are useful ways to think about the problem.

1) By location in the eye wall

• Anterior SINS means the melting is in the front white of the eye that you can see when you look in the mirror, near the surgical wound on the surface. This is the most common form, because most surgeries create incisions in the front. PMC

• Posterior SINS means the inflammation and tissue damage extend toward the back of the eye wall, sometimes after procedures like scleral buckle or vitrectomy, and may cause deep pain and signs seen best on ultrasound or MRI. PMCNature

2) By extent and pattern

• Focal SINS is a localized patch of melting right next to the wound, which can spread if not treated.

• Diffuse SINS is a broader area of thinning and necrosis that involves a longer segment of sclera and can threaten the structural stability of the eye.

3) By timing after surgery

• Early-onset SINS appears within weeks to a few months after the operation.

• Delayed-onset SINS appears many months or even years later, which can make the link to surgery less obvious unless you look closely at the wound area and history. PMC

4) By procedure association (helpful for suspicion)

• SINS has been reported after pterygium surgery, cataract surgery, trabeculectomy, scleral buckling, pars plana vitrectomy, and strabismus surgery. Knowing the operation helps the clinician look carefully along old incision lines for the first signs of melting. SpringerOpenPMC

5) By the immediate differential to exclude

• Autoimmune SINS is the classic form once infection and toxic ischemia are excluded and is treated with systemic immunosuppression.

• Infectious scleral necrosis is not SINS, but it can follow surgery and must be ruled out because it needs antimicrobial treatment first.

• Toxic/ischemic scleral necrosis from mitomycin C, beta-irradiation, or excessive cautery can mimic SINS and must be excluded because the cause is impaired healing and tissue blood supply rather than a systemic autoimmune attack. Lippincott JournalsFrontiers

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Causes

Below are 20 practical “causes and triggers” that increase the chance of scleral necrosis after surgery or make SINS more likely. Some are true triggers of autoimmune SINS, while others are look-alikes or cofactors that must be ruled out. I phrase each cause in plain terms, and doctors then test to separate autoimmune SINS from infection and toxic ischemia.

1. Recent or past eye surgery with a scleral or limbal incision near the melting area, because the immune system may misreact to the surgical site. PMC

2. Multiple eye surgeries in the same eye, which stack up immune triggers and tissue changes, making SINS more likely. PMC

3. Pterygium surgery with a wound at the nasal sclera, which is a common surgical site later linked to SINS. PMC

4. Cataract surgery with a limbal or scleral tunnel, which can sometimes precede SINS in the incision area. SpringerOpen

5. Trabeculectomy where tissue is removed and a flap is made, which can later be a focus for immune damage. SpringerOpen

6. Scleral buckle surgery for retinal detachment, which manipulates the sclera, and later SINS has been reported. SpringerOpen

7. Pars plana vitrectomy (PPV) using sclerotomies, which can be followed by SINS at those ports. Nature

8. Strabismus (squint) surgery, which uses muscle reattachment on the sclera and can later trigger SINS, sometimes even bilaterally. ScienceDirect

9. Adjunctive mitomycin C at surgery, which can cause toxic ischemic scleral necrosis that mimics SINS and must be excluded first. Lippincott Journals

10. Adjunctive beta-irradiation for pterygium, which can impair healing and blood supply and cause necrosis that resembles SINS. Lippincott Journals

11. Excessive cautery at surgery, which can burn vessels and reduce blood flow, leading to ischemic necrosis that looks like SINS. Lippincott Journals

12. Exposed or irritating sutures, which can rub and inflame local tissue and start a harmful immune cycle at the wound edge. (Clinical inference supported by surgical case series focusing on wound adjacency.) PMC

13. Underlying autoimmune disease such as rheumatoid arthritis or granulomatosis with polyangiitis, which raises the baseline risk of necrotizing scleritis and can be unmasked by surgery. NCBI

14. Older age with thin sclera or poor wound healing, which lowers tissue reserve and makes melting more likely after an immune hit. (Mechanistic inference from necrotizing scleritis pathophysiology.) ScienceDirect

15. Systemic vascular disease like long-standing diabetes or severe hypertension, which can reduce micro-circulation and delay healing, making necrosis worse if immunity is triggered. (Mechanistic inference plus general scleral vasculitis data.) ScienceDirect

16. Severe dry eye or ocular surface disease, which weakens the conjunctival cover and exposes sclera to breakdown. (Clinical reasoning; often noted around pterygium wounds.) PMC

17. Prior ocular trauma that scars the sclera and changes local immune responses, which can prime the eye for a later post-surgical reaction. SpringerOpen

18. Postoperative infection at or near the wound, which must be excluded because it can cause infectious scleritis that looks similar but is not SINS and requires antimicrobials first. Frontiers

19. Cosmetic conjunctivectomy or conjunctival surgeries, which have also been followed by necrotizing scleritis in reports. Ajo

20. Long delay between surgery and new eye pain right at the old wound site, which is a “cause-revealing clue” that the surgery is the key trigger even if it happened long ago. PMC

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Symptoms

1. Deep, boring eye pain that feels severe and constant and often wakes the person at night or gets worse with eye movement. This is a classic scleritis pain signal. NCBI

2. Redness around the old surgical site that can spread and looks more violaceous than bright red, which hints the deep sclera is inflamed. NCBI

3. Marked tenderness when the eye is gently touched, which is typical of scleritis and helps separate it from milder surface inflammation. NCBI

4. A visible white patch turning thin and gray-blue, which means the sclera is thinning and the dark uveal tissue is showing through. This is a serious warning sign. PMC

5. A crater or ulcer at the wound edge that looks “dead” or melted, which is the necrosis that defines SINS. PMC

6. Worsening light sensitivity because inflamed tissues make bright light painful and the iris may react. NCBI

7. Tearing and irritation, which are nonspecific but often accompany severe surface and deep inflammation. NCBI

8. Blurry or reduced vision, which can result from irregular corneal surface, astigmatism from scleral distortion, or involvement of deeper structures. NCBI

9. Pain with eye movements, because the inflamed sclera is where the muscles attach, so movement pulls on inflamed tissue. NCBI

10. A non-healing wound area, where the conjunctiva does not close well or re-opens, which is a clue to ongoing necrosis. PMC

11. Minimal or no discharge compared with the level of pain, which points more toward immune scleritis than a frank infection (though infection must still be ruled out). Frontiers

12. Raised red nodules near the wound in some cases, which can merge into necrosis as disease progresses. NCBI

13. A blue-black “uveal show” through very thin sclera, which means the eye wall is dangerously thin. PMC

14. Headache around the eye and brow, which often travels along branches of the trigeminal nerve due to deep inflammation. NCBI

15. Symptoms in both eyes after surgery in one eye, which is uncommon but reported, and it reflects the systemic immune nature of the problem. ScienceDirect

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Diagnostic Tests

Doctors group the evaluation into what we see and feel, quick bedside maneuvers, blood and tissue tests, electrodiagnostic checks when needed, and imaging. The first goal is to prove scleral necrosis and inflammation, the second goal is to exclude infection and toxic ischemia, and the third goal is to look for a related autoimmune disease that changes treatment.

A) Physical Exam

1. Visual acuity test checks how well each eye can see letters, because vision loss suggests deeper involvement or complications that need urgent control. NCBI

2. Slit-lamp examination of the wound maps the exact location of redness, thinning, and necrotic edges right next to the old incision, which is the classic hallmark of SINS. PMC

3. Palpation for focal tenderness with a gentle instrument confirms deep scleral pain and helps distinguish scleritis from episcleritis, which is usually less tender. NCBI

4. Intraocular pressure (IOP) measurement checks for pressure changes due to inflammation or steroid treatment and monitors risk if the wall is thin. NCBI

5. Dilated fundus exam looks for signs of posterior spread such as choroidal folds or retinal changes, which can occur with posterior scleritis. PMC

6. Complete ocular surface check looks for suture exposure, conjunctival defects, and corneal melt, which help separate SINS from toxic or infectious causes and show where tissue support is failing. Lippincott Journals

B) Simple Bedside / Manual Tests

7. Phenylephrine blanching test places a drop of phenylephrine to see if redness blanches; episcleritis blanches more, but true scleritis redness persists, which supports a deep inflammatory process. NCBI

8. Fluorescein dye and Seidel test paints the surface to find epithelial defects or leak if the sclera is dangerously thin; a positive leak means an emergency. (General ophthalmic practice applied to scleral melts.) NCBI

9. Gentle transillumination of thin areas shows blue-black uveal glow under thin sclera and helps map the extent of melt. (Clinical exam technique.) PMC

10. Extraocular movement-induced pain check asks the patient to look in different directions; pain with movement supports scleritis because the muscles pull on inflamed sclera. NCBI

11. Localized pressure with a cotton tip differentiates superficial tenderness from deep, boring pain and helps judge how imminent the risk of perforation may be. (Clinical exam principle.) NCBI

C) Laboratory and Pathology Tests

12. Complete blood count (CBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) look for systemic inflammation that supports an autoimmune process. NCBI

13. Rheumatoid factor (RF) and anti-CCP antibodies check for rheumatoid arthritis links, which are classically associated with necrotizing scleritis. NCBI

14. ANCA testing (especially c-ANCA/PR3) screens for granulomatosis with polyangiitis, which can cause severe necrotizing scleritis and needs specific systemic therapy. NCBI

15. Syphilis serology (RPR/VDRL and treponemal test), TB tests (IGRA or PPD), and fungal/bacterial culture if discharge is present help exclude infectious scleritis, which changes treatment completely. Frontiers

16. Antinuclear antibody (ANA) and complement levels help screen for other autoimmune connective tissue diseases. NCBI

17. Urinalysis and kidney function tests look for blood or protein and renal inflammation that point to a systemic vasculitis associated with ocular disease. NCBI

18. Scleral biopsy with histopathology and microbiology is reserved for unclear or refractory cases to distinguish autoimmune necrotizing scleritis with vasculitis from infectious or toxic causes; it looks for immune complex vasculitis and organisms. PMC

D) Electrodiagnostic Tests

19. Visual evoked potentials (VEP) can be used when vision is poor and the doctor needs to check the optic nerve pathway function if posterior scleritis or compressive swelling is suspected; this is not routine but can help in complex cases. (Selective use based on posterior disease.) PMC

20. Electroretinogram (ERG) or pattern ERG is rarely needed, but in atypical cases with posterior involvement and unclear retinal function, these tests can help separate retinal dysfunction from visual loss due to pain or optics. (Occasional adjunct.) PMC

21. Electro-oculogram (EOG) is also rarely used and is mainly supportive if there is concern about widespread retinal pigment epithelium effects in unusual posterior disease presentations; most SINS cases do not need this. (Adjunctive rationale.) PMC

E) Imaging Tests

22. B-scan ultrasonography looks through the eye wall for posterior scleritis signs like scleral thickening and the classic “T-sign,” which shows fluid in the Tenon’s space; it helps when back-of-the-eye involvement is suspected. PMC

23. Anterior segment OCT (AS-OCT) measures scleral and corneal thickness and shows intrascleral dark spaces consistent with inflammation; it helps monitor thinning over time without touching the eye. Taylor & Francis Online

24. Ultrasound biomicroscopy (UBM) gives high-resolution images of the very front sclera at the wound and maps how deep and wide the melt is. (Imaging rationale; commonly used in anterior segment disease.) Taylor & Francis Online

25. MRI of the orbits with contrast shows scleral enhancement and thickening and can reveal posterior extension and inflammation around the eye; it is very helpful when the exam is limited by pain or swelling. PMC

26. CT of the orbits is less sensitive than MRI for soft tissues but can show buckle position, calcifications, or complications and helps in surgical planning. PMC

27. Fluorescein angiography (FA) and indocyanine green angiography (ICG) can show leakage and staining patterns in scleral and episcleral vessels and help differentiate types of scleritis and look for choroidal involvement. Medscape

Non-pharmacological treatments (therapies & others)

1. Protective eye shield and strict “no-rub” rule
   Purpose: prevent accidental trauma to thin sclera.
   Mechanism: physical barrier reduces shear and impact.

2. Frequent preservative-free lubrication (drops + gel at night)
   Purpose: keep the surface moist; reduce friction.
   Mechanism: stabilizes the tear film and cushions fragile tissue.

3. Moisture chamber glasses or humidifier
   Purpose: decrease evaporation.
   Mechanism: maintains local humidity, improving epithelial healing.

4. Cold compress (brief, gentle)
   Purpose: symptom relief of pain.
   Mechanism: mild vasoconstriction can reduce superficial discomfort.

5. Activity modification
   Purpose: avoid heavy lifting, bending, dusty/windy exposure.
   Mechanism: reduces strain and environmental irritation.

6. UV-blocking eyewear outdoors
   Purpose: protect inflamed tissues from UV.
   Mechanism: reduces phototoxic stress and squint-related pressure.

7. Bandage contact lens (specialist-placed)
   Purpose: cover small epithelial defects and improve comfort.
   Mechanism: physical scaffold for surface healing.

8. Punctal occlusion (temporary plugs) when dry eye is severe
   Purpose: retain natural tears longer.
   Mechanism: decreases drainage to keep the eye wetter.

9. Eyelid hygiene and warm (not hot) lid care for meibomian dysfunction
   Purpose: improve oil layer of tears.
   Mechanism: better tear stability → better healing.

10. Smoking cessation
    Purpose: improve microcirculation and wound healing.
    Mechanism: nicotine cessation widens vessels and increases oxygen delivery.

11. Nutrition upgrade (protein + vitamin C–rich foods)
    Purpose: supply collagen building blocks.
    Mechanism: amino acids and ascorbate support collagen cross-linking.

12. Stress and sleep optimization
    Purpose: lower systemic inflammatory tone.
    Mechanism: cortisol rhythm balance improves immune regulation.

13. Blood sugar and blood pressure control
    Purpose: protect small vessels feeding sclera.
    Mechanism: better perfusion → better healing.

14. Discontinue toxic topical regimens (e.g., excessive preserved drops) under doctor guidance
    Purpose: remove chemical irritation.
    Mechanism: lowers surface toxicity load.

15. Education and early-warning plan
    Purpose: catch progression early.
    Mechanism: patients report new pain, color change, or discharge immediately.

16. Careful contact lens avoidance (unless therapeutic bandage lens is prescribed)
    Purpose: prevent mechanical trauma.
    Mechanism: reduces rubbing and micro-injury.

17. Shielding during sleep
    Purpose: prevent night-time eye rubbing.
    Mechanism: mechanical barrier.

18. Targeted physical rest during flares
    Purpose: reduce sympathetic spikes that can worsen pain/inflammation.
    Mechanism: calmer autonomic tone.

19. Post-op wound care adherence (if recently operated)
    Purpose: optimize healing environment.
    Mechanism: proper hygiene and scheduled checks.

20. Co-management with rheumatology even if not yet diagnosed with autoimmune disease
    Purpose: find and control a hidden systemic driver.
    Mechanism: systemic disease control lowers ocular relapse risk.

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Drug treatments

Safety note: The doses below are typical clinician starting points. Actual dosing must be individualized by your doctor based on weight, kidney/liver function, other medicines, pregnancy status, and lab results. Do not self-start or adjust without medical supervision.

1. Prednisone (oral corticosteroid)
   Class: systemic steroid.
   Dose/time: commonly 0.5–1 mg/kg/day; taper slowly over weeks to months.
   Purpose: rapidly suppress inflammation and pain.
   Mechanism: blocks multiple inflammatory pathways (cytokines, immune cells).
   Side effects: high sugar/pressure, mood changes, insomnia, infection risk, bone loss, stomach upset.

2. Methylprednisolone (IV “pulse” steroid)
   Class: systemic steroid.
   Dose/time: 500–1000 mg IV daily for 3 days in severe vision-threatening cases, then switch to oral taper.
   Purpose: fast control when the melt is aggressive.
   Mechanism: immediate high-level immunosuppression.
   Side effects: as above; transient metallic taste, flushing; needs monitoring.

3. Cyclophosphamide
   Class: alkylating immunosuppressant.
   Dose/time: 1–2 mg/kg/day orally or IV pulses (specialist protocol).
   Purpose: strongest steroid-sparing agent in vasculitis-associated necrotizing disease.
   Mechanism: suppresses rapidly dividing immune cells.
   Side effects: low blood counts, infection, bladder irritation, infertility risks; requires strict lab monitoring and protective measures.

4. Methotrexate
   Class: antimetabolite immunosuppressant.
   Dose/time: 10–25 mg once weekly (oral or subcutaneous) + folic acid daily.
   Purpose: long-term control and steroid-sparing.
   Mechanism: reduces lymphocyte proliferation; anti-inflammatory.
   Side effects: liver enzyme elevation, mouth sores, cytopenias; avoid in pregnancy; monitor labs.

5. Azathioprine
   Class: antimetabolite immunosuppressant.
   Dose/time: 1–2 mg/kg/day orally; check TPMT/NUDT15 activity where available.
   Purpose: maintenance therapy and steroid-sparing.
   Mechanism: inhibits purine synthesis in immune cells.
   Side effects: low blood counts, liver enzyme rise, infection risk.

6. Mycophenolate mofetil
   Class: antimetabolite immunosuppressant.
   Dose/time: 1–1.5 g twice daily.
   Purpose: alternative steroid-sparing agent with ocular evidence.
   Mechanism: blocks lymphocyte nucleotide synthesis.
   Side effects: GI upset, low blood counts, infection risk.

7. Cyclosporine
   Class: calcineurin inhibitor.
   Dose/time: 2–5 mg/kg/day in divided doses; target levels may be monitored.
   Purpose: useful in immune-mediated scleritis when others are intolerable.
   Mechanism: reduces T-cell activation.
   Side effects: kidney strain, high blood pressure, gum changes, tremor; drug interactions.

8. Rituximab
   Class: anti-CD20 B-cell depleting biologic.
   Dose/time: 375 mg/m² weekly ×4 or 1 g ×2 two weeks apart; repeats per specialist.
   Purpose: for refractory necrotizing scleritis, especially with ANCA-vasculitis or RA.
   Mechanism: removes B-cells that produce harmful antibodies.
   Side effects: infusion reactions, infections (screen for hepatitis B), rare PML; vaccinations and monitoring needed.

9. Infliximab / Adalimumab
   Class: anti-TNF biologics.
   Dose/time: Infliximab 3–5 mg/kg IV at weeks 0, 2, 6 then every 6–8 weeks; Adalimumab 40 mg SC every 2 weeks (some need weekly).
   Purpose: for resistant cases, particularly with systemic autoimmune disease.
   Mechanism: blocks TNF-α, a key inflammatory signal.
   Side effects: infections (screen TB/hepatitis), injection or infusion reactions; avoid in certain demyelinating/heart failure conditions.

10. Topical corticosteroid (e.g., prednisolone acetate 1%) plus pain control
    Class: local steroid (adjunct only) and oral analgesics as prescribed.
    Dose/time: drops every 1–4 hours initially, then taper; always combined with systemic therapy in necrotizing disease.
    Purpose: surface comfort and adjunct inflammation control.
    Mechanism: local anti-inflammatory effect.
    Side effects: higher eye pressure, delayed surface healing with prolonged use—requires monitoring.

Antibiotics/antifungals: used only when infection is proven or strongly suspected. SINS itself is sterile; treating the wrong way can harm.

Protective co-meds with steroids: proton pump inhibitor for stomach, calcium + vitamin D for bone, consider bisphosphonate for long steroid courses—doctor decides.

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Dietary molecular supplements

These can support general healing and lower overall inflammatory tone. They do not replace medical therapy.

1. Omega-3 (EPA/DHA): 1000–2000 mg/day combined EPA+DHA.
   Function/mechanism: pro-resolving mediators; may reduce inflammatory signals and improve tear film.

2. Vitamin D3: 1000–2000 IU/day (adjust to lab level).
   Function: immune modulation; low levels link to higher autoimmunity risk.

3. Vitamin C: 500–1000 mg/day in divided doses.
   Function: collagen synthesis cofactor; supports wound repair.

4. Protein (whey or collagen peptides): 15–25 g/day if diet is low.
   Function: provides amino acids for tissue rebuilding.

5. Zinc: 10–20 mg/day (short term unless deficient).
   Function: epithelial and immune support; cofactor for many enzymes.

6. Curcumin (turmeric extract): 500–1000 mg/day standardized curcuminoids with piperine if tolerated.
   Function: down-regulates NF-κB inflammatory pathways.

7. N-Acetylcysteine (NAC): 600–1200 mg/day.
   Function: antioxidant precursor to glutathione; may help mucous quality.

8. Lutein + Zeaxanthin: 10 mg + 2 mg/day.
   Function: ocular surface and retinal antioxidant support.

9. Probiotics (mixed strains): per label daily.
   Function: gut-immune axis balancing; may modestly reduce systemic inflammatory tone.

10. Magnesium: 200–400 mg/day (citrate or glycinate).
    Function: supports neuromuscular relaxation and sleep, indirectly improving recovery.

Check interactions (e.g., curcumin can interact with blood thinners). Your clinician should approve supplements, especially when you’re on immunosuppressants.

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Advanced” immuno-regenerative options

In everyday language: these are strong immune-targeted or regenerative therapies used only by specialists for stubborn cases. Some are off-label for scleritis; some are experimental. Clear informed consent is essential.

1. Rituximab (B-cell depletion)
   Dose: see above.
   Function/mechanism: removes antibody-producing cells; helps in ANCA-vasculitis–linked SINS.

2. Tocilizumab (IL-6 receptor blocker)
   Dose: commonly 162 mg SC weekly or every 2 weeks, or IV per protocol.
   Function: blocks IL-6 signaling; case series show benefit in refractory ocular inflammation.

3. Abatacept (CTLA-4–Ig)
   Dose: weight-based IV monthly or 125 mg SC weekly.
   Function: turns down T-cell co-stimulation; used when TNF blockers fail.

4. JAK inhibitors (e.g., tofacitinib, upadacitinib)
   Dose: e.g., tofacitinib 5 mg BID; upadacitinib 15 mg daily (rheum protocols).
   Function: blocks intracellular cytokine signaling; promising case reports in stubborn scleritis.

5. Intravenous immunoglobulin (IVIG)
   Dose: 2 g/kg divided over 2–5 days per cycle.
   Function: resets immune balance; used rarely for refractory autoimmune disease.

6. Autologous biologics for surface healing (adjunctive, not immune suppression): autologous serum tears or platelet-rich plasma (PRP) eye drops
   Dose: per compounding protocol.
   Function: growth factors that support epithelial repair when the surface is very dry or non-healing.

True stem-cell therapy for SINS is experimental and not standard of care. If discussed, it should be in the setting of a regulated clinical trial.

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Surgeries

Rule of thumb: control inflammation first with medicines. Surgery is for tectonic support—to prevent perforation or to close a hole.

1. Tectonic scleral patch graft
   Procedure: a donor scleral (or corneal) patch is sutured over the thinned area.
   Why: adds thickness and rigidity to prevent rupture.

2. Lamellar scleral reinforcement (sclerectomy + graft)
   Procedure: removes dead sclera edges and overlays healthy graft.
   Why: removes non-viable tissue and rebuilds the wall.

3. Conjunctival advancement or rotational flap
   Procedure: mobilize nearby conjunctiva to cover an avascular scleral bed.
   Why: brings new blood supply to promote healing.

4. Amniotic membrane transplantation
   Procedure: one or multiple layers of amniotic membrane are sutured or glued over melts.
   Why: provides growth factors and a biological bandage to encourage re-epithelialization.

5. Corneoscleral lamellar keratoplasty or tissue adhesive with bandage lens (for tiny perforations)
   Procedure: either a tailored lamellar graft or cyanoacrylate glue plus a bandage lens.
   Why: seals leaks fast and preserves globe integrity.

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Prevention strategies

1. Pre-op autoimmune screening if history suggests it; involve rheumatology early.

2. Prefer conjunctival autograft for pterygium; avoid bare-sclera technique when possible.

3. Judicious use of mitomycin-C (lowest effective dose/time) and avoid beta irradiation.

4. Gentle tissue handling and minimal cautery to preserve blood flow.

5. Bury or remove irritating sutures promptly.

6. Plan incisions away from previously weakened areas if re-operating.

7. Post-op steroid regimen tailored and tapered slowly; do not stop abruptly.

8. Aggressive dry-eye care around the time of surgery.

9. No smoking, good nutrition, and control of diabetes/hypertension.

10. Early follow-up and patient education on warning signs (pain, color change, sudden blur).

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When to see a doctor urgently

• Severe, boring eye pain, especially after prior eye surgery.

• New blue-gray zone or visible “hole/notch” on the white of the eye.

• Sudden vision drop, halos, or light sensitivity.

• Any sign of leakage (tears that “taste salty” with a constant wet spot can be a clue).

• Fever, cough, joint pains, skin rash, or blood in urine suggesting a systemic autoimmune flare.

• While on steroids or immunosuppressants: any fever, cough, sores, or unusual bruising.

Do not delay—SINS can progress fast.

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What to eat and what to avoid

What to eat (10 ideas):

1. Lean proteins (fish, eggs, legumes, tofu) for collagen building.

2. Vitamin C–rich fruits/veggies (citrus, berries, kiwi, bell peppers).

3. Leafy greens (spinach, kale) for micronutrients.

4. Orange/yellow produce (carrots, pumpkin) for antioxidants.

5. Omega-3 sources (fatty fish like salmon, or flax/chia if plant-based).

6. Nuts and seeds (almonds, walnuts) for healthy fats.

7. Whole grains (oats, brown rice) for steady energy.

8. Dairy or fortified alternatives (for calcium + vitamin D).

9. Plenty of water—hydration supports the tear film.

10. Yogurt/kefir (if tolerated) for gut support.

What to avoid (10 tips):

1. Smoking and second-hand smoke (major blood-flow blocker).

2. Excess salt (especially on steroids—salt worsens swelling/pressure).

3. Excess sugar and ultra-processed foods (raise systemic inflammation).

4. Heavy alcohol (impairs healing and raises infection risk).

5. Very spicy or reflux-trigger foods if steroids upset the stomach.

6. Grapefruit with certain drugs like cyclosporine (ask your doctor).

7. Herbal products that thin blood (e.g., high-dose ginkgo) without approval.

8. High-dose vitamin A or E without indication (fat-soluble vitamin risks).

9. Energy drinks that spike blood pressure.

10. Unverified “immune boosters” online—can clash with immunosuppressants.

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Frequently asked questions (FAQs)

1. Is SINS the same as an infection?
   No. SINS is usually sterile inflammation driven by the immune system. Infection can look similar, so doctors test to tell them apart.

2. How soon after surgery can SINS appear?
   Any time—from weeks to years. Many cases appear within the first year.

3. Why does it hurt so much?
   The sclera has rich nerves, and deep inflammation causes severe, boring pain.

4. Can SINS make me blind?
   It can threaten vision if thinning leads to perforation or if inflammation spreads. Early treatment greatly reduces this risk.

5. Will I need strong medicines?
   Often, yes. Necrotizing disease usually needs systemic steroids and a steroid-sparing immunosuppressant.

6. How long is treatment?
   Weeks to months, sometimes longer, with slow tapering and close monitoring.

7. Are biologics safe?
   They can be very effective when used correctly, but they carry infection risks and need screening and lab monitoring.

8. Can diet alone fix SINS?
   No. Diet is supportive only. Medical therapy is essential.

9. Will I need surgery again?
   Only if tectonic support is required (dangerous thinning or a leak). Doctors try to calm inflammation first.

10. Is the other eye at risk?
    If there is an underlying autoimmune disease, the other eye can be at risk for scleritis. Systemic control lowers that risk.

11. Can SINS come back?
    It can recur, especially if systemic disease is active or if strong medicines are stopped too quickly.

12. Are contact lenses safe?
    Avoid normal cosmetic/contact lenses. A therapeutic bandage lens may be placed only by your doctor.

13. Can I work or exercise?
    Yes, but avoid heavy lifting, dusty/windy environments, and eye-rubbing until your doctor clears you.

14. Which specialist should I see?
    An ophthalmologist (preferably a cornea/external disease or uveitis specialist). Rheumatology often co-manages.

15. What are danger signs at home?
    New severe pain, sudden blur, blue-gray area expanding, or any fluid leak—seek urgent care immediately.

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The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 27, 2025.