Proliferative Vitreoretinopathy (PVR)

Proliferative vitreoretinopathy—usually shortened to PVR—is a scarring response that can happen after a retinal detachment. Cells in and around the retina begin to grow and form thin membranes on the surface of the retina, under the retina, and sometimes within the retina itself. These membranes are not flexible. They can contract like tiny shrink-wrap bands and pull on the retina. This pull can make the retina wrinkle into fixed folds or even detach again after surgery. PVR is therefore the most common reason a repaired retinal detachment comes back. It develops in about 5–10% of rhegmatogenous retinal detachments (detachments caused by a break or tear). In simple terms: a retinal detachment injures the eye, the eye tries to “heal,” the scar tissue over-heals, and that over-healing can tug the retina off again. EyeWiki

Proliferative vitreoretinopathy—usually shortened to PVR—is a scarring process that can happen after a retinal detachment or serious eye injury. Cells in and around the retina start to multiply, move, and lay down thin sheets of scar tissue on the surface of the retina (on top, underneath, or even within the retinal layers). Those sheets then shrink and pull, creating fixed folds and traction that can re-detach the retina or keep it from lying flat even after surgery. In short: PVR is the eye’s “overactive wound-healing response,” and it is the most common reason a retinal detachment repair fails. EyeWikiPMC+1

When the retina detaches, the normal barrier between the blood and retina leaks. Signaling proteins and inflammatory messengers flood in. Retinal pigment epithelium (RPE) cells, glial cells, fibroblasts, and immune cells become activated. Some RPE cells change their identity (epithelial-to-mesenchymal transition), migrate, and form contractile membranes. As those membranes contract, they stiffen and shorten the retina, and the traction can lift the retina back off the eye wall. EyeWiki

Pathophysiology

After a detachment, the normal barrier between the bloodstream and the retina leaks. Chemical signals that drive inflammation and healing surge into the eye. Retinal pigment epithelial (RPE) cells, glial cells, fibroblasts, and immune cells move, multiply, and lay down matrix. Some RPE cells change their identity (a process called epithelial-to-mesenchymal transition) and gain the ability to crawl and contract. The result is a network of thin, contracting membranes that stiffen and shorten the retina. This “over-healing” is why PVR can pull a retina back off after a seemingly successful repair. EyeWikiPMC

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Types and clinical classification

Doctors describe PVR by how far it has progressed and where the membranes sit.

1. By severity (Retina Society/updated scheme)

• Grade A (early/minimal): tiny pigment clumps or haze in the vitreous showing very early proliferative activity.

• Grade B (moderate): the retina looks “cellophane-like” and slightly stiff, with fine surface wrinkling and vessel tortuosity.

• Grade C (severe): fixed retinal folds from contracting membranes; folds can be star-shaped, broad and diffuse, or caused by subretinal “clothesline/napkin-ring” bands.
  The 1991 update also labels location as posterior (P) or anterior (A) and records extent in clock hours (for example CP12 means posterior, Grade C, 12 clock hours). PubMedAAO JournalEyeWiki

2. By location

• Posterior PVR: membranes and folds behind the vitreous base; may show star-folds radiating from a central area.

• Anterior PVR: traction at the vitreous base and ciliary body; in severe cases it can circle 360°. Anterior disease is important because it can drive tractional redetachment and hypotony; ultrasound biomicroscopy (UBM) helps visualize it. EyeWikiPubMed

3. Intraretinal PVR (newer concept)
   PVR is not only on top of or under the retina. In some cases, glial proliferation inside the retina stiffens and shortens it. Swept-source OCT can highlight these intraretinal changes. EyeWikiOphthalmology Retina

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Causes and risk factors

PVR is best thought of as a complication or “scar response” that is triggered or worsened by certain situations. Below are common, evidence-linked factors.

1. The retinal detachment itself (RRD): any RRD can start the cascade that leads to PVR, because the detachment opens the blood-retina barrier and releases growth signals. EyeWiki

2. Long-standing detachment: the longer the retina is off, the stronger the inflammatory and scarring response becomes. EyeWiki

3. Inferior detachment: gravity lets cells and inflammatory debris settle inferiorly, so inferior RDs more often show PVR. EyeWiki

4. Large or multiple retinal breaks: more exposed RPE and more inflammation means more risk. Review of Ophthalmology

5. Giant retinal tear: a very large flap tear exposes a big area of RPE, markedly raising risk. EyeWiki

6. Vitreous hemorrhage: blood in the vitreous is pro-inflammatory and increases risk of postoperative PVR. ResearchGate

7. Choroidal detachment: adds inflammation and alters fluid dynamics, favoring proliferation. PMC

8. Pre-existing PVR: once present, it predicts more PVR after surgery unless fully relieved. EyeWiki

9. Previous failed RD surgery or multiple surgeries: each operation can release cells and cytokines and can add to scarring risk. EyeWiki

10. Aphakia or pseudophakia: some analyses link lens status to higher postoperative PVR risk. ResearchGate

11. Extensive RD area (e.g., ≥50% of retina): large detachments imply more injury and more risk. Ophthalmology Retina

12. Macula involvement: macula-off detachments are associated with higher PVR risk in some studies. Lippincott Journals

13. Preoperative retinal folds or stiffness: signs of early proliferation suggest a head start toward PVR. EyeWiki

14. Intra- or postoperative hemorrhage: blood products feed the scarring response. EyeWiki

15. Extensive cryotherapy or laser: necessary treatments can, when extensive, add inflammatory drive. EyeWiki

16. Retinectomy or broad vitrectomy: tissue manipulation can liberate cells and cytokines. EyeWiki

17. Injection of intraocular gas/air (context-dependent): in some settings has been listed among operative risk factors. EyeWiki

18. Uveitis or other intraocular inflammation: inflammatory eyes are biologically primed for proliferation. EyeWiki

19. Open-globe trauma: trauma-related RDs carry high PVR risk; smoking further raises it. PubMed

20. Cigarette smoking: associated with higher rates of PVR after RD repair, even beyond trauma-related cases in some series. IOVSLippincott Journals

Notes from newer data: recent database and multicenter studies continue to explore systemic factors (e.g., diabetes, hypertension) and myopia as possible contributors; results vary by cohort and methodology. Treat these as possible modifiers rather than core causes. OvidOphthalmology RetinaPMC

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Symptoms

1. Blurry vision: vision becomes unclear and stays that way. It may worsen over days to weeks.

2. A dark curtain or shadow: a gray or black edge moves into the field of view; this is typical when the retina is off again.

3. Peripheral vision loss: side vision becomes missing or dim.

4. Flashes of light (photopsia): brief sparkles or lightning shapes appear, especially in dim light.

5. Floaters: small spots or cobwebs drift, sometimes increasing suddenly.

6. Wavy or distorted lines (metamorphopsia): straight lines look bent, due to retinal wrinkling.

7. Poor central detail: reading and recognizing faces become hard.

8. Reduced contrast or color vividness: colors look dull and gray.

9. Worse vision in low light: night driving and dim rooms feel harder.

10. Slow visual recovery after RD surgery followed by decline: vision may improve after repair, then worsen again as PVR contracts. EyeWiki

11. A sensation that the eye is “pulling”: not painful, but an awareness of strain.

12. In some cases, mild aching or discomfort: pain is not a key feature, but irritation can occur.

13. Increased light sensitivity: glare or photophobia may appear.

14. Unequal pupils or a relative afferent defect (found by the doctor): a sign that the retina or optic nerve is under stress.

15. No symptoms at first: early Grade A/B changes can be silent and only visible to the examiner. PubMed

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Diagnostic tests

Doctors combine history, careful eye examination, and targeted tests. Below are common tests used to confirm PVR, define its extent, find triggers, and plan surgery.

A) Physical exam tests (chair-side basics)

1. Best-corrected visual acuity (distance and near): measures how clearly each eye sees, monitors change over time, and helps set urgency. A sudden drop after RD repair signals possible PVR-related redetachment.

2. Pinhole acuity: checks if blur is mostly optical (improves with pinhole) or retinal (stays poor); persistent poor pinhole acuity points toward retinal disease.

3. Pupillary light responses (look for a relative afferent pupillary defect): a weaker response on the affected side suggests reduced retinal input.

4. Confrontation visual fields: maps missing areas of side vision at the bedside and guides more detailed perimetry if needed.

B) Manual/clinical examination tests (at the slit lamp and with lenses)

5. Slit-lamp biomicroscopy of the anterior segment and vitreous: looks for inflammatory cells and Shafer’s sign (“tobacco dust”)—tiny brown pigment granules suggesting a retinal break and ongoing activity. It documents lens status (phakic/pseudophakic/aphakic) and any surgical wounds. NCBIJABFM

6. Intraocular pressure (tonometry): PVR can drive low IOP (hypotony) from ciliary body traction in anterior disease or, less often, high IOP; measuring pressure adds context. Nature

7. Dilated indirect ophthalmoscopy with scleral depression: the gold standard to examine the far peripheral retina, find breaks, and see fixed folds that define PVR. Depression helps reveal small, hidden tears and membrane traction. NCBI

8. Contact lens fundus biomicroscopy (e.g., with a three-mirror lens): gives a high-magnification view of membranes, star-folds, and vitreous base traction to plan surgery. PubMed

9. Amsler grid at near (symptom mapping): documents metamorphopsia and helps track changes after repair; while simple, it gives the patient a daily self-check.

C) Laboratory and pathological tests (selected, when inflammation or infection is suspected)

10. Complete blood count and inflammatory markers (ESR/CRP): useful when history or exam suggests uveitis, infection, or systemic inflammation contributing to PVR risk.

11. Targeted infectious work-up (e.g., syphilis, TB, toxoplasma) guided by history and local prevalence: used in atypical or inflamed eyes to address treatable triggers before or after surgery.

12. Autoimmune/uveitis panel (e.g., ANA, HLA-B27) when indicated: helps if a systemic inflammatory disorder is suspected.

13. Aqueous or vitreous sampling (PCR/cytology) in select cases: rarely needed, but valuable when infection or masquerade is on the differential; can direct therapy and reduce recurrence risk.

D) Electrodiagnostic tests (functional tests of the retina and pathway)

14. Full-field electroretinography (ffERG): records the retina’s electrical response to flashes of light. It helps estimate how healthy the retina is (globally) in chronic detachment and after reattachment, informing prognosis when PVR is severe. PMCAmerican Academy of Ophthalmology

15. Multifocal ERG (mfERG): maps macular function in many small zones at once; useful when OCT shows macular distortion from membranes and we need a functional correlate. BioMed Central

16. Visual evoked potential (VEP): measures the brain’s response to visual stimuli; helpful when media opacity or complex disease makes acuity hard to judge and we need an objective measure of visual potential. MDPI

E) Imaging tests (to confirm, map, and plan)

17. B-scan ultrasonography: essential when the view is hazy from hemorrhage or cataract; confirms detachment, reveals fixed folds, and checks macular status if the fundus is not visible. Dynamic scanning helps distinguish mobile RD from stiff, PVR-related membranes. American Academy of Ophthalmology+2American Academy of Ophthalmology+2

18. Optical coherence tomography (OCT): high-resolution cross-sections show epiretinal and intraretinal changes, macular traction, subretinal bands, and retinal thickening; swept-source OCT is being used to better classify intraretinal PVR. Ophthalmology RetinaScienceDirect

19. Fundus photography/ultra-widefield imaging: documents star-folds, contraction patterns, and extent by clock hours to track over time and communicate with the surgical team. EyeWiki

20. Ultrasound biomicroscopy (UBM) for anterior PVR: a high-frequency ultrasound that visualizes the ciliary body and vitreous base to uncover epiciliary membranes and anterior traction not seen with standard methods—particularly useful when hypotony or recurrent inferior redetachment are present. PubMedEyeWiki

Non-pharmacological treatments

1. Urgent, expert follow-up — After any retinal detachment repair, tight follow-up catches early PVR changes before they lock in. Purpose: protect vision. Mechanism: early detection → timely re-intervention reduces traction time on the macula. (General clinical practice)

2. Head positioning exactly as instructed — Face-down or side positioning keeps the gas or oil bubble pushing on the right area. Purpose: maximize reattachment. Mechanism: buoyant tamponade keeps retina apposed, limiting the “space” where membranes can contract.

3. Avoid air travel/high altitude while gas is in the eye — Gas expands with lower cabin pressure. Purpose: prevent dangerous pressure spikes and loss of tamponade effect. Mechanism: Boyle’s law; stable bubble size is crucial for retinal apposition.

4. Protective eye shield & no eye rubbing — Purpose: prevent micro-trauma and accidental pressure. Mechanism: reduces mechanical stress that can worsen tiny breaks or inflammation.

5. Sleep posture care — Use pillows to maintain the advised position through the night. Purpose: maintain tamponade hours. Mechanism: prolonged contact of gas/oil with targeted retina supports healing.

6. Strict drop adherence (steroid/antibiotic/cycloplegic as prescribed) — Though drops are “medications,” the actionable habit is non-pharm adherence. Purpose: control inflammation & comfort. Mechanism: calmer eye = lower pro-scarring signals.

7. Inflammation-reducing habits — Cool compresses, gentle eyelid hygiene, smoke avoidance. Purpose: keep ocular surface quiet. Mechanism: fewer inflammatory inputs entering the eye.

8. Systemic health optimization — Good glucose, blood pressure, and lipid control. Purpose: heal better. Mechanism: improved microvascular function supports retinal recovery.

9. Quit smoking — Purpose: lower PVR risk & improve healing. Mechanism: nicotine and smoke products raise inflammatory and fibrotic signals; smoking has been linked to higher PVR after trauma. EyeWiki

10. Activity modification early on — No heavy lifting/straining while gas is present and the retina is healing. Purpose: reduce sudden pressure spikes. Mechanism: less Valsalva = steadier intraocular pressure.

11. Prompt attention to new symptoms — New floaters, flashes, curtain, pain, or drop in vision → call right away. Purpose: early rescue. Mechanism: faster action limits scarring time.

12. Visual rest and light management — Breaks from screens and bright light, use of sunglasses outdoors. Purpose: comfort and glare control. Mechanism: calmer ciliary body & ocular surface.

13. Hydration and balanced diet — Not a cure, but supports healing. Purpose: provide nutrients. Mechanism: adequate vitamins/minerals aid general tissue repair.

14. Home Amsler or simple “one-eye-at-a-time” checks — Purpose: self-monitor distortion or new shadows. Mechanism: early detection of traction changes.

15. Adherence to silicone oil care plan — If oil is used, keep scheduled checks and removal when advised to reduce complications. Purpose: safer long-term course. Mechanism: oil helps reattach but should not be permanent in many cases. Lippincott Journals

16. Infection prevention basics — Hand hygiene before drops; avoid contaminated water to the eye early post-op. Purpose: reduce endophthalmitis risk. Mechanism: fewer pathogens near incisions.

17. Manage associated uveitis (with your doctor) — The action is attending all visits and reporting flares. Purpose: limit pro-fibrotic cytokines. Mechanism: less intraocular inflammation → less stimulus for membrane growth. EyeWiki

18. Protect the fellow eye — Quick care if symptoms occur in the other eye and regular exams if you had PVR once. Purpose: reduce risk in second eye. Mechanism: surveillance matters; PVR in one eye raises risk after RD in the other. Ophthalmology Retina

19. Realistic vision rehab planning — If vision remains limited, occupational therapy, contrast-enhancing lighting, and low-vision aids help you function better. Purpose: quality of life. Mechanism: compensate for residual distortion.

20. Education & support — Understanding the plan reduces anxiety and improves adherence. Purpose: success. Mechanism: informed patients follow the program more closely.

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Drug treatments

Important: As of today, surgery is the mainstay of PVR management. Medicines are mainly adjuncts studied to reduce scarring or recurrences. Many are off-label and used only by retina specialists. Review of Ophthalmology

1. Methotrexate (antimetabolite / immunomodulator)
   Dose/Timing: Common research regimens use 200–400 µg intravitreal per injection; often given intra-op and then weekly or every 2–3 weeks for multiple doses. Purpose: reduce cell proliferation and inflammation that drive scarring. Mechanism: inhibits dihydrofolate reductase; anti-proliferative and anti-inflammatory. Side effects: corneal toxicity/epithelial defects, rare inflammation; requires specialist dosing and monitoring. Healio JournalsPubMed+1

2. Triamcinolone acetonide (steroid)
   Dose/Timing: e.g., 2–4 mg intravitreal; sometimes used in silicone-oil–filled eyes as an adjunct. Purpose: suppress postoperative inflammation. Mechanism: broad cytokine suppression, reduces edema. Side effects: eye pressure rise, cataract, infection risk. Evidence is mixed; some trials show benefit as adjuncts. EyeWiki

3. Dexamethasone implant (steroid, slow-release)
   Dose/Timing: 0.7 mg intravitreal implant (Ozurdex®) at or after surgery in some studies. Purpose/Mechanism: sustained steroid to calm inflammation and possibly reduce membrane formation. Side effects: IOP rise, cataract; not universally adopted for PVR. EyeWiki

4. 5-Fluorouracil + Low-Molecular-Weight Heparin (5-FU/LMWH) (antimetabolite + anti-adhesion)
   Dose/Timing: Delivered as a dilute intra-operative infusion during vitrectomy in trials. Purpose: try to lower postoperative PVR. Mechanism: 5-FU inhibits cell division; heparin can reduce cell adhesion/fibrin. Side effects: corneal toxicity, hypotony (rare). Results are mixed—benefit in some high-risk groups, no clear benefit in established PVR. FrontiersPubMed

5. Daunorubicin (anthracycline antimetabolite; investigational/limited use)
   Dose/Timing: very low intraocular concentrations studied; narrow safety window. Purpose: directly block proliferating cells. Mechanism: DNA intercalation/antimitotic. Side effects: retinal toxicity risk; because of safety window, routine use is limited. ScienceDirectPMC

6. Bevacizumab / Ranibizumab (anti-VEGF; not standard for PVR)
   Dose/Timing: standard anti-VEGF intravitreal doses in selected cases. Purpose: occasionally considered to modulate vascular/permeability components or co-existing conditions; evidence for PVR prevention is limited/experimental. Side effects: rare infection, transient pressure rise. EyeWiki

7. Atropine (cycloplegic)
   Dose/Timing: topical, short course after surgery. Purpose: pain/photophobia relief, stabilize the iris. Mechanism: relaxes ciliary spasm. Side effects: light sensitivity, near blur. (Supportive comfort measure.)

8. Topical NSAIDs (e.g., ketorolac/nepafenac)
   Dose/Timing: standard post-op courses if cystoid macular edema is present. Purpose: reduce macular swelling. Mechanism: COX inhibition → lower prostaglandins. Side effects: surface irritation; rare corneal problems with prolonged use. (Adjunct for edema rather than PVR itself.)

9. Systemic steroids (short, specialist-directed)
   Dose/Timing: carefully selected cases. Purpose: dampen severe inflammation. Mechanism: systemic cytokine suppression. Side effects: glucose/pressure elevation, mood/sleep changes, infection risk; used judiciously. EyeWiki

10. Experimental anti-fibrotic pathway agents (research use only)
    Examples: TGF-β pathway blockers (e.g., decorin), ROCK-pathway modulators. Purpose/Mechanism: target the scarring biology at its source. Status: preclinical/early clinical; not approved for routine care. Side effects: under study. SpringerLinkPMC

Take-home: There is no universally approved drug that reliably prevents or cures PVR. Medicines are adjuncts; surgery fixes the mechanics. PubMed

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Dietary “molecular” supplements

(dose • function • mechanism — not proven PVR treatments)

Evidence supports some nutrients for macular degeneration or general retinal health; none are proven to prevent/treat PVR. Discuss your case with your surgeon before taking anything.

1. Lutein 10 mg + Zeaxanthin 2 mg daily — Function: macular pigment support. Mechanism: antioxidant carotenoids concentrate in the macula; AREDS2 favored L/Z over beta-carotene (especially for former smokers). National Eye InstituteJAMA Network

2. Omega-3s (DHA/EPA 1–2 g/day combined) — Function: membrane health/anti-inflammatory. Mechanism: DHA is abundant in photoreceptor outer segments; supports retinal cell membranes. NCBI

3. Vitamin C (≈500 mg/day) — Function: antioxidant support. Mechanism: scavenges reactive oxygen species.

4. Vitamin E (≈200 IU/day; avoid high doses unless advised) — Function: lipid antioxidant. Mechanism: protects membranes from peroxidation.

5. Zinc (up to 25 mg/day unless otherwise directed) — Function: cofactor in retinal enzymes. Mechanism: supports antioxidant pathways; high doses can upset copper balance.

6. Copper (≈2 mg/day when taking zinc) — Function: balance with zinc to avoid deficiency.

7. Astaxanthin (4–12 mg/day) — Function: antioxidant carotenoid; may help eye strain. Mechanism: quenches singlet oxygen.

8. Alpha-lipoic acid (300–600 mg/day) — Function: antioxidant recycling. Mechanism: regenerates glutathione.

9. Curcumin (500–1,000 mg/day with pepperine for absorption) — Function: general anti-inflammatory; theoretical antifibrotic signals. Mechanism: NF-κB modulation (evidence in PVR is preclinical at best).

10. Resveratrol (100–250 mg/day) — Function: antioxidant; vascular support. Mechanism: SIRT pathways.

Notes: In AREDS2, adding omega-3s to the original formula did not further lower AMD progression overall; L/Z are preferred to beta-carotene due to lung-cancer risk in former smokers. Supplements can interact with meds (e.g., blood thinners). National Eye Institute

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Regenerative / stem-cell” drug concepts

Reality check: There are no approved immune-booster or stem-cell drugs that treat PVR in routine practice. Below are research/adjunct approaches your specialist might discuss in select cases or clinical trials.

1. Intravitreal Methotrexate — Immunomodulator/antiproliferative. Function: dampen inflammatory and proliferative drivers. Mechanism: antimetabolite blocking DNA synthesis and cytokine signaling in PVR cells. Dose (research): 200–400 µg per injection in series. Healio JournalsPubMed

2. mTOR inhibition (Sirolimus) — Regenerative-friendly anti-inflammatory concept. Function: broad anti-proliferative/anti-fibrotic signaling. Mechanism: blocks mTOR; reduces T-cell activity and fibrosis signals; used in uveitis, being explored in retinal disease—not established for PVR. AAO Journal+1

3. ROCK inhibitors (e.g., netarsudil) — trial stage — Function: reduce cell contraction/migration. Mechanism: Rho-kinase pathway drives cytoskeleton and fibrosis. Early lab/clinical-trial interest; outcomes pending. CenterWatchPMC

4. TGF-β pathway blockade (e.g., decorin; receptor inhibitors) — Function: antifibrotic; oppose EMT of RPE. Mechanism: interrupts central pro-scarring signal. Evidence so far is preclinical. SpringerLinkPubMed

5. Sustained-delivery antimitotics (e.g., daunorubicin in porous silicon carriers) — Function: longer, safer anti-proliferative exposure. Mechanism: controlled micro-dose delivery; still research. PMC

6. Biologic scaffolds (e.g., amniotic membrane patching as an adjunct) — Function: provide a bioactive barrier/anti-scarring environment during complex re-operations. Mechanism: physical and biochemical modulation of wound healing; early reports only. EyeWiki

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Surgeries

1. Pars plana vitrectomy (PPV) with meticulous membrane peeling
   Procedure: remove vitreous gel; stain and peel epi-retinal and subretinal membranes; relieve all traction; laser around retinal breaks. Why: this is the core fix—remove the scaffolds that pull on the retina so it can lie flat. Review of Ophthalmology

2. Relaxing retinotomy/retinectomy
   Procedure: when the retina is shortened and cannot lie flat, surgeons make a cut (retinotomy) or remove a strip of stiffened retina (retinectomy) to release contraction. Why: relieve intractable traction so the remaining retina can reattach smoothly. Success rates are good in experienced hands, but re-operations are common. PMC+1

3. Tamponade choice: silicone oil or long-acting gas
   Procedure: fill the eye with silicone oil or gas (e.g., C3F8) at the end of surgery. Why: the bubble presses the retina into place as laser scars seal. In complex PVR, surgeons often prefer silicone oil; outcomes can be favorable with either, depending on case details. PMC

4. Adjuncts inside the eye
   Procedure: perfluorocarbon heavy liquid (PFCL) to flatten retina during surgery; endolaser or cryopexy to seal breaks. Why: make the retina flat and watertight so it can heal without traction. Retina Today

5. Silicone oil removal (later stage)
   Procedure: once the retina is stable, oil is often removed to avoid late complications; sometimes combined with additional membrane work if needed. Why: minimize long-term risks from retained oil and optimize optics. Lippincott Journals

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Preventions

1. Seek care quickly for flashes, floaters, or a “curtain.”

2. Fix retinal tears promptly before they progress.

3. Avoid delays in repairing a large detachment.

4. Don’t smoke (especially after trauma-related detachments). EyeWiki

5. Control inflammation (e.g., uveitis) with your ophthalmologist.

6. Control diabetes and blood pressure.

7. Follow post-op positioning and restrictions closely.

8. Keep all follow-ups—early scar signs can be addressed faster.

9. Protect the fellow eye—know symptoms and get fast care. Ophthalmology Retina

10. Avoid eye trauma—use protective eyewear for risky activities.

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When to see a doctor urgently

• New or worsening floaters or light flashes

• Any shadow, gray curtain, or crooked/distorted vision

• Sudden drop in vision, or eye pain/redness after surgery

• Change in the size/position of the gas bubble view
  These can mean traction has returned, the retina has lifted again, or pressure is off. Get same-day advice from your retinal surgeon.

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What to eat” and “what to avoid

Eat more of:

1. Fatty fish (salmon, sardines, mackerel) 2–3×/week for DHA/EPA.

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

3. Citrus and berries for vitamin C.

4. Nuts/seeds (almonds, walnuts, flax, chia) for vitamin E and omega-3 precursors.

5. Colorful vegetables (peppers, carrots, squash) for carotenoids and vitamin A.

Limit/avoid:

1. Smoking & secondhand smoke (strong risk amplifier). EyeWiki
2. Excess alcohol (worsens inflammation and healing).
3. Ultra-processed foods high in trans-fats/sugars (pro-inflammatory).
4. Megadoses of supplements without medical guidance (side-effect risks; e.g., beta-carotene in former smokers). National Eye Institute
5. Dehydration—stay well hydrated for general health.

Note: These nutrition ideas come from broader eye-health and AREDS/AREDS2 evidence for retinal well-being (AMD), not PVR-specific trials. National Eye Institute

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FAQs

1) Is PVR the same as a new tear?
No. PVR is scarring that pulls on the retina; a new tear is a hole. PVR can create traction that leads to new tears if not relieved.

2) Can eye drops cure PVR?
No. Drops help with inflammation and comfort, but surgery fixes the traction. Medicines are adjuncts. Review of Ophthalmology

3) If my retina reattaches, why is my vision still blurry?
The macula may have been off too long or developed folds/edema. Anatomic success does not always equal perfect vision. BioMed Central

4) Will I need more than one operation?
Possibly. PVR often needs staged or repeat surgery to fully release traction. PMC

5) Gas or silicone oil—which is better?
Depends on the case. In advanced PVR, many surgeons choose oil; outcomes can be good with either. Your surgeon will pick based on traction location, positioning needs, and lifestyle factors. PMC

6) Can methotrexate prevent PVR?
Studies suggest serial low-dose intravitreal methotrexate (given by a surgeon) may help as an adjunct in some cases, but it’s not a stand-alone cure. Healio Journals

7) What about 5-FU with heparin?
Results are mixed: benefit signals in certain high-risk groups, but not helpful for established PVR in an RCT. It’s not routine for everyone. FrontiersPubMed

8) Is PVR more likely if I already had it in the other eye?
Yes—history of RRD with PVR in one eye increases second-eye risk if it later detaches. Ophthalmology Retina

9) Can diet or vitamins stop PVR?
No direct proof. Healthy nutrition supports healing, but PVR treatment is surgical. AREDS/AREDS2 nutrients are for AMD, not PVR. National Eye Institute

10) How long must I position my head a certain way?
Your surgeon will tailor this. Many patients need strict positioning for days to weeks until the retina is stable.

11) Is PVR contagious or hereditary?
No. It’s a scarring response. Some genetic and inflammatory factors may influence susceptibility, but it is not contagious. EyeWiki

12) How soon can I travel?
Avoid flying or high altitude with an intraocular gas bubble. If silicone oil was used, travel rules differ—ask your surgeon.

13) Will the silicone oil stay forever?
Often no—it is usually removed once the retina is stable, to reduce long-term complications. Lippincott Journals

14) What are warning signs after surgery?
New floaters/flashes, curtain, sudden blur, severe pain/redness, or major pressure change in the gas bubble view—call immediately.

15) What’s the outlook?
With modern techniques, many eyes are reattached, though some need multiple surgeries and vision may remain limited. Early detection, careful surgery, and strong follow-up give the best chance. Review of Ophthalmology

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 23, 2025.

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