Peripapillary Intrachoroidal Cavitation

Peripapillary Intrachoroidal Cavitation, often shortened to PICC, is a pocket or hollow inside the choroid (the vascular layer under the retina) that forms right next to the optic nerve. On a dilated eye exam, doctors often see a yellow-orange patch sitting at the outer edge of the myopic crescent (the pale zone around the optic disc that is common in highly myopic eyes). On modern OCT scans, the pocket shows up as a dark (hyporeflective) space beneath the normal line of Bruch’s membrane and the retinal pigment epithelium, meaning the retina over the area is usually still attached and looks structurally intact, while the “cavity” sits deeper in the wall of the eye. This finding is most common in people with high (axial) myopia, and it can sometimes cause visual field defects that look very similar to glaucoma, which is why recognizing it is important. PubMedDove Medical PressPentaVision

Historically, this lesion was first thought to be a detachment of the retinal pigment epithelium in pathological myopia and was called peripapillary detachment of pathologic myopia (PDPM). With better OCT technology, researchers realized the pocket lies within or just behind the choroid, not under the retina itself—so the more accurate name became peripapillary intrachoroidal (or suprachoroidal) cavitation. PentaVisionNature+1

Many people with PICC do not notice symptoms at all. Others have blind-spot–like missing areas in the side vision (visual field) that can be mistaken for glaucoma. Several studies show that visual field defects are common in eyes with PICC, and the pattern can mimic early glaucoma, creating confusion and anxiety. Recognizing PICC prevents mislabeling a patient as “glaucomatous” when the field loss may actually result from this structural peripapillary lesion. PMCDove Medical Press

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Types

Because there is no single official “staging system,” it is helpful to describe patterns doctors commonly use to communicate about PICC:

1. By location around the disc

   • Inferior PICC: sitting under the optic nerve (most reported).

   • Temporal PICC: sitting toward the temple side, often in eyes with tilted discs.

   • Nasal or superonasal PICC: less common; still possible in very myopic eyes.
     These patterns reflect where the eye wall is most stretched and where the myopic conus and posterior staphyloma are most pronounced. Nature

2. By depth/plane on OCT

   • Intrachoroidal pocket: the classic dark cavity lies within the choroid.

   • Suprachoroidal pocket: newer work shows many lesions actually occupy the suprachoroidal space (a natural potential space between choroid and sclera). In practice, both are part of the same spectrum and are imaged similarly. Dove Medical Press

3. By associated features

   • With “sinkhole” or full-thickness defects in border tissue: a visible communication or gap in the peripapillary tissues on OCT.

   • With posterior staphyloma or tilted disc: common co-findings in high myopia.

   • With macular traction or retinoschisis nearby: occasionally present in highly myopic eyes and relevant to prognosis. PMC

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Causes

No single on/off “cause” has been proven for everyone. PICC seems to happen when several mechanical and structural factors in a highly myopic eye come together. Below are 20 evidence-informed contributors that likely make PICC more likely; each item is explained in plain English:

1. High axial myopia
   A long eyeball stretches the tissues around the optic nerve. This stretch can split the choroid and create a pocket. PMC

2. Posterior staphyloma
   A bulging, thinned area in the back of a myopic eye changes the local curvature and tensile forces, favoring cavitation next to the disc. Nature

3. Tilted optic disc
   When the optic disc is slanted, the peripapillary tissues are pulled unevenly. That asymmetry increases stress points where a cavity can form. PMC

4. Parapapillary gamma zone / conus expansion
   Large bare areas around the disc in myopia signal tissue loss and slippage; the border of this zone is a frequent site for PICC. Dove Medical Press

5. Scleral thinning near the disc
   A thinner, weaker sclera provides less support for the choroid, allowing it to bow and split.

6. Suprachoroidal separation
   The natural plane between choroid and sclera can be pulled open under stress, creating a persistent space that we see as a cavity on OCT. Dove Medical Press

7. Traction from the dura/optic nerve sheath during eye movements
   In highly myopic eyes, the optic nerve sheath can tug on the peripapillary wall when the eye moves, adding repetitive micro-strain that opens a pocket.

8. Border tissue defects (“sinkholes”)
   Tiny full-thickness gaps in the peripapillary support tissues can connect the cavity to adjacent spaces and help the cavitation persist. PubMed

9. Uneven intraocular pressure (IOP) load across a tilted disc
   Even with normal IOP, a slanted optic nerve head concentrates stress on one side, encouraging cavitation, field defects, or both.

10. Choroidal vessel rearrangement in myopia
    Enlarged “pachyvessels” and remodeling may weaken the surrounding stroma, making splitting easier.

11. Age-related connective tissue changes
    With age, collagen and elastin quality decline, so stretched tissue is less likely to rebound and more likely to split.

12. Rapid progression of axial length in young adulthood
    Fast elongation can outpace the ability of peripapillary tissues to adapt, predisposing to a tear-like separation.

13. Peripapillary atrophy (PPA)
    When the support layers thin near the disc, they bend more under everyday forces, promoting cavitation.

14. Local choroidal hypoperfusion
    Reduced blood support may weaken tissue maintenance and repair, allowing a pocket to form.

15. Vitreopapillary traction
    Subtle traction from the posterior hyaloid near the disc edge can add shear forces to the peripapillary wall.

16. Repeated micro-trauma from eye rubbing
    Chronic rubbing briefly raises pressure and deforms the globe, potentially aggravating peripapillary stress in a vulnerable, highly myopic eye.

17. Genetic predisposition to pathologic myopia
    Genes that increase the risk of axial elongation indirectly raise the risk of peripapillary structural changes like PICC.

18. Thin border tissue of Elschnig
    A congenitally thin or stretched “border tissue” ring where the retina meets the optic disc can be a weak point for cavitation. PubMed

19. Disc–sclera angle mismatch
    If the optic disc inserts at a steep angle into an already curved staphyloma, the “corner” bears high strain and may split.

20. History of macular traction disorders in high myopia
    Eyes with tractional problems (like foveoschisis) demonstrate that the whole posterior pole is under abnormal mechanical load, which can extend to the peripapillary region.

Notes on certainty: Items 1–4, 6–8 have the strongest imaging and clinical associations in the literature. Others are plausible contributors supported by biomechanical reasoning in myopic eyes and by case-series observations. PMC+1NatureDove Medical Press

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Symptoms

1. No symptoms at all (very common; the finding may be incidental).

2. A faint “missing patch” near the natural blind spot in one eye.

3. Side-vision gaps that look like glaucoma on testing.

4. Blurred areas in the vision that come and go with fatigue.

5. Reading feels patchy, as if a few letters vanish off the page.

6. Trouble finding small objects in certain parts of the visual field.

7. Mild distortion (metamorphopsia) if traction involves the nearby macula.

8. More glare or reduced contrast in the area close to the blind spot.

9. “Shadow” or arc-shaped smudge just next to the center of vision.

10. Eye strain or awareness of the affected eye during prolonged near work (from myopia and coexisting changes rather than the cavitation itself).

11. Colors look slightly washed out near the scotoma (rare).

12. Slow adaptation from light to dark when the field defect encroaches on more sensitive areas.

13. Difficulty with quick saccades when scanning text because the small scotoma interrupts smooth tracking.

14. Headaches from squinting or compensating (non-specific).

15. Anxiety after being told “possible glaucoma” when the fields look glaucomatous but the pressure and nerves are borderline—recognition of PICC can relieve this.

Clinically, visual field defects are frequent in PICC, and their pattern can overlap with early glaucoma. This overlap is what makes careful imaging essential. PMCDove Medical Press

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Diagnostic tests

A) Physical examination

1. Best-corrected visual acuity
   Measures how clearly you see with the best glasses. PICC may not reduce acuity unless other myopic problems are present.

2. Pupil exam and relative afferent pupillary defect (RAPD) check
   Most PICCs do not cause RAPD; if present, it suggests broader optic nerve involvement or another diagnosis.

3. Confrontation visual fields
   A quick bedside check that can hint at scotomas near the blind spot.

4. Color vision testing (Ishihara or similar)
   Usually normal; a defect suggests associated optic nerve pathology or macular disease rather than PICC alone.

5. Intraocular pressure (IOP) measurement
   Important to avoid misdiagnosing glaucoma; many patients with glaucoma-like fields from PICC have normal IOP.

B) Manual/clinical tests at the slit-lamp

6. Dilated fundus examination with a high-power lens
   The examiner looks for a yellow-orange peripapillary patch at the edge of the myopic conus, often inferior or temporal to the disc.

7. Indirect ophthalmoscopy (wide-field view)
   Helps judge how the lesion relates to posterior staphyloma, lattice areas, and other myopic degeneration.

8. Amsler grid
   A simple square grid to check for distortion or missing lines, useful if there is macular traction along with PICC.

9. Serial fundus photography
   Side-by-side photos over time help track stability or slow expansion of the lesion.

C) Laboratory and pathological tests

10. No routine lab test diagnoses PICC
    PICC is an imaging diagnosis. However, labs can rule out inflammatory or infectious causes if the appearance is atypical.

11. Autoimmune/inflammatory panel when needed
    If the clinician worries about peripapillary inflammation or uveitis masquerading as a detachment, targeted labs may be ordered.

12. Oncologic workup only if the lesion mimics a tumor
    Rarely, a peripapillary cavitation is mistaken for a mass; in that situation, limited labs or referral can be used to exclude choroidal tumors. (Good imaging usually prevents this.)

D) Electrodiagnostic and functional tests

13. Standard automated perimetry (e.g., Humphrey 24-2/30-2)
    Maps visual field defects, which in PICC can imitate glaucoma arcuate or paracentral patterns. Tracking over time shows stability or change. PMC

14. Microperimetry
    Relates sensitivity to a fundus map, showing how the scotoma aligns with the peripapillary lesion.

15. Visual evoked potentials (VEP) or pattern ERG
    Used when there’s diagnostic doubt about optic neuropathy; often normal or only subtly changed in isolated PICC.

E) Imaging tests

16. Spectral-domain or swept-source OCT (peripapillary scans and enhanced-depth imaging)
    The key test. It shows a dark cavity beneath Bruch’s membrane at the disc edge, often with wedge-shaped posterior bowing of the choroid/sclera and sometimes a border-tissue defect (“sinkhole”). OCT distinguishes PICC from true RPE detachment. PubMedPentaVision

17. OCT-A (optical coherence tomography angiography)
    Useful to look for choroidal neovascularization (CNV) if vision drops or the fundus changes. It helps decide if anti-VEGF therapy is needed (for CNV, not for PICC itself).

18. Fundus autofluorescence (FAF)
    Highlights RPE health; in PICC, FAF helps confirm that the RPE overlying the cavity is often intact, supporting the intrachoroidal/suprachoroidal nature of the lesion.

19. Fluorescein angiography (FA) and indocyanine green angiography (ICGA)
    These dye tests can show early hypo- and late staining without leakage over the peripapillary patch (typical for PICC) and are good for detecting CNV if suspected.

20. Axial length measurement / ocular biometry
    Documents high myopia, a major context for PICC, and helps correlate changes with progression of myopic anatomy.

Non-pharmacological treatments

Important context: none of the following “fixes” the cavity. They reduce risk, improve safety and comfort, and catch complications early. For each, you’ll see Description → Purpose → Mechanism in simple terms.

1. Structured OCT follow-up
   Description: Regular dilated eye exams with OCT around the optic nerve and macula.
   Purpose: Track stability and catch schisis, detachment or PP-CNV early.
   Mechanism: OCT provides cross-sectional “slices” that show changes in fluid or tissue over time. Dove Medical Press

2. Visual field (perimetry) monitoring
   Description: Automated tests that map side-vision sensitivity.
   Purpose: Separate PICC-related field changes from true glaucoma progression.
   Mechanism: Serial fields plus OCT nerve fiber measurements prevent over- or under-treating suspected glaucoma. Dove Medical PressPLOS

3. OCT-angiography (OCT-A) when indicated
   Description: Dye-free imaging of micro-blood flow near the disc and macula.
   Purpose: Look for new abnormal vessels (CNV) without injections.
   Mechanism: Flow maps reveal tiny vessel networks that suggest CNV. PMC

4. High-myopia comorbidity check
   Description: Review for posterior staphyloma, lattice, traction.
   Purpose: Identify structural stress that can drive retinoschisis/detachment.
   Mechanism: Mapping the posterior eye guides timing of retina referrals. Dove Medical Press

5. Glaucoma evaluation (when fields/OCT look suspicious)
   Description: Baseline and periodic intraocular pressure (IOP), corneal thickness, optic nerve exam.
   Purpose: Avoid mislabeling PICC as glaucoma—or missing real glaucoma.
   Mechanism: Combining structure (OCT) and function (fields) with IOP trends improves diagnostic accuracy. Dove Medical Press

6. Amsler grid or self-monitoring for central distortion
   Description: Simple at-home grid test.
   Purpose: Early alert for macular involvement from PP-CNV or schisis.
   Mechanism: Distortion or blank spots prompt urgent reassessment.

7. Optimal spectacle/contact lens correction
   Description: Keep prescriptions updated; consider high-index lenses or specialty contacts for very high powers.
   Purpose: Maximize clarity and reduce eyestrain.
   Mechanism: Clear optics improve functional vision despite structural changes.

8. Low-vision strategies when field loss matters
   Description: Lighting tweaks, contrast enhancement, magnifiers, orientation training.
   Purpose: Improve reading/safety if field defects are bothersome.
   Mechanism: Enhancing contrast and magnification compensates for local sensitivity loss.

9. Work/reading ergonomics
   Description: Use the 20-20-20 rule and maintain >30–40 cm working distance.
   Purpose: Reduce near-work fatigue common in high myopia.
   Mechanism: Breaks limit accommodative strain and dryness.

10. Dry-eye care if symptomatic
    Description: Blinks, humidifiers, preservative-free tears, warm compresses.
    Purpose: Comfortable eyes maintain steadier fixation for testing and daily tasks.
    Mechanism: Stabilizing the tear film improves vision quality.

11. UV and glare protection
    Description: Sunglasses and hats outdoors.
    Purpose: Reduce light discomfort and oxidative stress.
    Mechanism: Filters limit high-energy light exposure to retinal tissues.

12. Smoking cessation
    Description: Stop tobacco exposure.
    Purpose: Support overall ocular vascular health and reduce risk for other retinal diseases.
    Mechanism: Less oxidative and vascular stress benefits retinal tissues.

13. General cardiovascular risk management
    Description: Control blood pressure, diabetes, lipids.
    Purpose: Protect ocular microcirculation.
    Mechanism: Healthier vessels = more resilient retina/choroid.

14. Protective eyewear for sports/DIY
    Description: Polycarbonate glasses during impact-risk activities.
    Purpose: Highly myopic eyes are more vulnerable to injury.
    Mechanism: Shields reduce blunt/penetrating trauma.

15. Home fall-prevention
    Description: Declutter floors, improve lighting, mark stair edges.
    Purpose: Compensate for localized field defects.
    Mechanism: Environmental design reduces trip risk.

16. Patient education (written/visual aids)
    Description: Clear explanations of what PICC is and isn’t.
    Purpose: Reduce anxiety and improve adherence to follow-up.
    Mechanism: Understanding why we monitor boosts engagement.

17. Family screening for high myopia in children
    Description: If parents are highly myopic, get kids regular eye checks.
    Purpose: Early myopia control reduces later pathologic risks.
    Mechanism: More outdoor time and proven pediatric myopia strategies lower the odds of severe axial elongation. JAMA Networkwspos.org

18. Increase outdoor time (for children/adolescents in the family)
    Description: Aim for ~2 hours per day outside.
    Purpose: Lowers risk of developing myopia or slows early progression.
    Mechanism: Bright outdoor light modulates retinal dopamine and eye-growth signals. JAMA NetworkPMC

19. Axial length tracking in high myopes
    Description: Annual biometry where available.
    Purpose: Objective measure of eye growth.
    Mechanism: Millimeter-level changes flag risk of future pathology.

20. Rapid-access plan for sudden symptoms
    Description: Know your urgent clinic/ER route.
    Purpose: Minutes matter if detachment or CNV develops.
    Mechanism: Early anti-VEGF or surgical care preserves vision. SAGE Journals

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Drug treatments

Evidence point: There is no medication that heals the PICC cavity. Medicines are used only if a complication develops, most commonly peripapillary CNV or if coexisting glaucoma needs treatment. Doses below are typical for the condition treated; your retina or glaucoma specialist will individualize therapy.

1. Ranibizumab (anti-VEGF)
   Class: VEGF-A inhibitor (intravitreal).
   Dose/Timing: 0.5 mg/0.05 mL injection; often monthly loading, then PRN/treat-and-extend for CNV.
   Purpose/Mechanism: Shrinks leaky neovessels and reduces fluid.
   Side effects: Transient eye irritation/pressure rise; rare endophthalmitis or retinal tear. SAGE Journals

2. Aflibercept (anti-VEGF)
   Class: VEGF-A/PlGF trap (intravitreal).
   Dose/Timing: 2.0 mg/0.05 mL; monthly x3 then q8w or treat-and-extend for CNV.
   Purpose/Mechanism: Potent blockade of neovascular growth and leakage.
   Side effects: Similar to ranibizumab. SAGE Journals

3. Bevacizumab (anti-VEGF, off-label intraocular use)
   Class: VEGF-A inhibitor.
   Dose/Timing: 1.25 mg/0.05 mL, PRN series for CNV.
   Purpose/Mechanism: Cost-effective anti-VEGF; many PP-CNV case series show control.
   Side effects: As above; off-label intraocular use discussed with informed consent. SAGE Journals

4. Faricimab
   Class: Bispecific anti-VEGF/anti-Ang-2.
   Dose/Timing: 6 mg/0.05 mL, extended dosing after loading in neovascular conditions.
   Purpose/Mechanism: Dual-pathway vascular stabilization may increase durability.
   Side effects: Similar intraocular risks to other anti-VEGFs. (Evidence extrapolated from neovascular macular disease.)

5. Brolucizumab
   Class: Anti-VEGF (small single-chain antibody).
   Dose/Timing: 6 mg/0.05 mL in approved neovascular AMD regimens; off-label in other CNV.
   Purpose/Mechanism: Higher molar dose can permit longer intervals.
   Side effects: Rare but serious retinal vasculitis/occlusion risk—specialists use with caution.

6. Verteporfin (for Photodynamic Therapy, PDT)
   Class: Photosensitizer (IV), activated by a specific laser.
   Dose/Timing: Weight-based IV infusion with laser activation to the PP-CNV zone.
   Purpose/Mechanism: Light-activated drug shuts down abnormal vessels with less collateral damage near the optic nerve than thermal laser in many reports.
   Side effects: Photosensitivity for 48 h, infusion reactions. PMCPubMedNature

7. Latanoprost (if true glaucoma coexists)
   Class: Prostaglandin analog (topical).
   Dose/Timing: 1 drop nightly (0.005%).
   Purpose/Mechanism: Lowers IOP to protect optic nerve when glaucoma is present; does not treat PICC.
   Side effects: Conjunctival redness, lash growth, iris darkening.

8. Timolol (if glaucoma coexists)
   Class: Topical beta-blocker.
   Dose/Timing: 1 drop once or twice daily (0.25–0.5%).
   Purpose/Mechanism: Decreases aqueous production to lower IOP.
   Side effects: Can affect breathing/heart rate—medical review is essential.

9. Brimonidine (if glaucoma coexists)
   Class: Alpha-2 agonist (topical).
   Dose/Timing: 1 drop twice daily (0.2% or 0.15%).
   Purpose/Mechanism: Lowers IOP and may have neuroprotective roles under study.
   Side effects: Allergy, dry mouth, drowsiness.

10. Low-dose atropine (for children in the family with progressive myopia, not to treat PICC)
    Class: Antimuscarinic drop.
    Dose/Timing: 0.01–0.05% nightly for 1–3+ years, per specialist.
    Purpose/Mechanism: Slows axial elongation in many—but not all—studies; mixed evidence at 0.01%, with stronger effects seen at 0.05%.
    Side effects: Mild light sensitivity/near blur at higher doses. JAMA Network+1MDPI

They haven’t shown reliable benefit for PICC, and can add risk. Treatment is targeted to complications—especially CNV—using anti-VEGF or PDT. PMC

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Dietary “molecular” supplements

Straight talk: No supplement has been proven to reverse PICC. Some eye-healthy nutrients have evidence in other retinal conditions (notably AMD). Discuss any supplement with your clinician, especially if you smoke or take blood thinners.

1. Lutein 10 mg/day
   Function: Macular pigment carotenoid; filters blue light, antioxidant.
   Mechanism: In AMD studies, helps retinal resilience; not shown to alter myopia/PICC. PubMedPMCFrontiers

2. Zeaxanthin 2 mg/day
   Function/Mechanism: Partner carotenoid to lutein; similar rationale. PubMed

3. AREDS2 formulation (for people with intermediate AMD, not for PICC)
   Typical daily amounts: Vitamin C 500 mg, Vitamin E 400 IU, Zinc 80 mg (as zinc oxide), Copper 2 mg, plus lutein/zeaxanthin.
   Function/Mechanism: Slows AMD progression; not preventive for people without AMD and not a PICC therapy. JAMA Network

4. Omega-3 (EPA+DHA 1 g/day)
   Function: Anti-inflammatory membrane support; mixed results in AMD; general cardiovascular benefits.
   Mechanism: May support retinal cell membranes. JAMA Network

5. Vitamin D (per deficiency only, per doctor)
   Function: Systemic health; ocular evidence is mixed; correct deficiency for overall wellbeing.
   Mechanism: Immune and tissue support.

6. Vitamin C (up to 500 mg/day if diet is poor)
   Function/Mechanism: Antioxidant; part of AREDS2 (for AMD). Not a PICC treatment. JAMA Network

7. Vitamin E (up to 400 IU/day if advised)
   Function/Mechanism: Antioxidant; in AREDS2 for AMD; avoid excess. JAMA Network

8. Zinc with copper (AREDS2 ratios, if AMD and advised)
   Function/Mechanism: Antioxidant/enzymatic support; large doses only under medical guidance. JAMA Network

9. Astaxanthin (6–12 mg/day)
   Function: Potent carotenoid antioxidant; small studies suggest benefit for eye fatigue; no PICC data yet.
   Mechanism: Free-radical scavenging.

10. General Mediterranean-style diet (not a pill, but powerful!)
    Function/Mechanism: Fruits, leafy greens, fish, nuts—broad cardiovascular and retinal support; in AMD evidence, diet patterns help, though not a PICC therapy. Mayo Clinic Press

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Regenerative or stem-cell drugs

Short, transparent answer: There are no approved immunity-boosting or stem-cell drugs for PICC. Using unregulated “stem cell shots” inside the eye has caused devastating blindness in case reports. If you see such offers, avoid them unless they’re part of an ethics-approved clinical trial. BioMed Central

That said, here are research directions (informational only; no dosing outside trials):

1. Cell therapies for retinal degeneration (RPE/photoreceptor cells) – Explored in AMD, retinitis pigmentosa, Stargardt; not for PICC. Early trials show feasibility but remain investigational. PMCBioMed Central

2. Gene therapy (e.g., RS1 for X-linked retinoschisis) – Gene replacement is being tested for genetic retinoschisis, a different disease than PICC. MalaCards

3. Scleral cross-linking (riboflavin/UVA or genipin) to slow myopic eye growth – Animal and pilot human work suggest biomechanical strengthening; not standard care. PMCPLOStvst.arvojournals.org

4. Posterior scleral reinforcement (PSR) surgery – A mechanical graft to buttress the myopic eye; meta-analyses suggest potential benefit in children with progressive high myopia, not PICC itself; still debated. SpringerLink

5. Paracrine/neuroprotective stem-cell strategies – Being studied for photoreceptor survival in other retinal diseases; not applicable to PICC today. Lippincott Journals

6. Targeted anti-fibrotic/ECM remodeling agents – Preclinical ideas tied to scleral biomechanics; no clinical protocols yet. PMC

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Procedures/surgeries

1. Photodynamic therapy (PDT) with verteporfin for peripapillary CNV
   Procedure: IV verteporfin + targeted laser to the CNV near the disc.
   Why done: To close PP-CNV while minimizing optic nerve damage compared with thermal laser. Small series show good outcomes. PubMedEyeWiki

2. Intravitreal anti-VEGF injections (office procedure)
   Procedure: Injection of ranibizumab/aflibercept/bevacizumab into the eye.
   Why done: First-line for many CNV types, including peripapillary CNV; reduces leakage and hemorrhage. SAGE Journals

3. Pars plana vitrectomy (PPV) for macular retinoschisis/detachment associated with PICC
   Procedure: Microsurgery to relieve vitreoretinal traction; sometimes peel membranes.
   Why done: Case reports/series show PPV can resolve schisis/detachment linked to cavitation-related traction. Healio JournalsDove Medical Press

4. Posterior scleral reinforcement (PSR) for progressive high myopia (select pediatric cases)
   Procedure: A reinforcing graft sutured on the posterior globe.
   Why done: To try to slow axial elongation in aggressive childhood myopia; not a PICC fix, but may reduce future risk landscape in select cases. SpringerLink

5. Glaucoma surgery (e.g., trabeculectomy, minimally invasive options) — only if true glaucoma coexists
   Procedure: Various surgeries to lower IOP.
   Why done: Protect the optic nerve when medications fail. This is for glaucoma, not for PICC. (General standard of care context.)

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Prevention

Prevention here means reducing future risk, mainly by curbing high-myopia progression in children and avoiding secondary damage.

1. For kids in the family: aim for ~2 hours outdoors daily. JAMA Networkwspos.org

2. Schedule regular pediatric vision checks if there’s a family history of high myopia.

3. Use evidence-based myopia control in children (clinician-guided low-dose atropine, optical strategies). MDPI

4. Limit prolonged near work and follow the 20-20-20 rule.

5. Ensure good indoor lighting for reading/study.

6. Wear UV-blocking sunglasses outdoors.

7. Don’t smoke (and avoid secondhand smoke).

8. Protect eyes during impact-risk activities with proper eyewear.

9. Control systemic health (BP, glucose, lipids).

10. Know urgent warning signs (new distortion, sudden blur, new blind spot, flashes/floaters with a curtain)—and seek care fast.

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When to see a doctor urgently

• Sudden distortion or a gray spot near the center of vision.

• New or increasing floaters/flashes or a curtain-like shadow (possible tear/detachment).

• New peripapillary hemorrhage or any rapid drop in vision.

• If you’ve been told you have “glaucoma” based only on the field test but your OCT shows a PICC—get a glaucoma/retina co-review to avoid misdiagnosis. Dove Medical Press

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What to eat and what to avoid

Food supports overall eye health; it does not shrink a PICC.

1. Leafy greens daily (spinach, kale): natural lutein/zeaxanthin.

2. Colorful vegetables & citrus: vitamin C and antioxidants.

3. Fatty fish 1–2×/week (salmon, sardines): omega-3s.

4. Nuts and seeds: vitamin E and healthy fats.

5. Whole grains/legumes for steady energy and vascular health.

6. Hydrate well to help dry-eye comfort.

7. Limit ultra-processed, high-salt foods that can nudge BP up.

8. Avoid smoking; limit alcohol.

9. If you have intermediate AMD, ask about AREDS2—but remember, it’s for AMD, not PICC. JAMA Network

10. Don’t mega-dose supplements beyond recommended daily values unless your doctor advises it. Mayo Clinic Press

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Frequently Asked Questions

1) Is PICC a tumor?
No. It’s a structural pocket next to the optic nerve in highly myopic eyes; imaging distinguishes it from tumors. Dove Medical Press

2) Will it make me go blind?
The cavity itself usually doesn’t threaten central vision. Risk comes from complications like PP-CNV or schisis/detachment—which are treatable if caught early. Dove Medical Press

3) Do I need treatment right now?
Most cases are observed. Treatment is reserved for complications (anti-VEGF injections or PDT for PP-CNV; surgery for schisis/detachment). SAGE JournalsPubMed

4) Can glasses or contacts fix it?
They correct blur from refractive error, not the cavity. They help you see your best day-to-day.

5) Is PICC the same as glaucoma?
No. It can mimic glaucoma on visual fields, so your team uses OCT and IOP to sort this out. Dove Medical Press

6) Could I have both PICC and glaucoma?
Yes. That’s why careful evaluation and follow-up are important.

7) What’s peripapillary CNV—and why is it a big deal?
It’s abnormal new blood vessels near the optic nerve that can leak or bleed. It needs anti-VEGF or PDT to protect vision. SAGE JournalsPubMed

8) If I get injections, how many will I need?
It varies. Many people need a short monthly series, then less frequent injections as the eye stabilizes. Your retina specialist tailors the plan. SAGE Journals

9) Is PDT safe so close to the optic nerve?
Small series report good outcomes without optic-nerve damage when protocols are followed. PubMed

10) Can low-dose atropine drops help my PICC?
No—they’re for slowing myopia in children, not treating PICC. Evidence for 0.01% is mixed; 0.05% shows stronger effects. JAMA NetworkMDPI

11) Do supplements help?
They don’t heal PICC. AREDS2 helps some people with AMD; discuss with your doctor if that applies to you. JAMA Network

12) Are there stem-cell “cures” I can buy?
No approved cures exist; unregulated stem-cell injections have blinded patients. Only join vetted clinical trials. BioMed Central

13) Can surgery remove the cavity?
No. Surgery addresses complications (e.g., vitrectomy for traction, PDT/anti-VEGF for PP-CNV). Healio JournalsPubMed

14) How often should I be checked?
Your clinician will set an interval (often every 6–12 months, sooner if changes). OCT and fields guide timing.

15) What’s the single most important thing I can do?
Keep your follow-up appointments and seek care fast for any sudden vision changes.

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

Last Updated: August 21, 2025.