Pachydrusen

Pachydrusen are small mounds of waste material that collect under the retinal pigment epithelium (RPE) in the back of the eye. They look yellow-white on photographs of the retina. They are usually large (often bigger than 125 micrometers), have sharp edges, and their shapes can be a bit irregular or complex. They tend to sit in the posterior pole (the central back part of the eye) and may appear alone, in tiny clusters, or scattered across a wide area. Doctors first used the word “pachydrusen” to point out that these deposits happen in eyes with a thick choroid (the spongy, blood-rich layer under the retina) and with dilated choroidal vessels (“pachyvessels”)—a family of problems called the pachychoroid spectrum. Pachydrusen are not the same as the soft drusen of classic age-related macular degeneration (AMD): they look different, sit in different patterns, and are tied to a thick choroid, not the thin choroid often seen in AMD. EyeWikiPMCNature

Pachydrusen are large, yellow-white deposits that sit under the retinal pigment epithelium (RPE) and ride on top of a thickened choroid (the blood-vessel layer beneath the retina). They belong to the pachychoroid family of conditions, such as central serous chorioretinopathy (CSC) and polypoidal choroidal vasculopathy (PCV). Pachydrusen themselves usually do not need treatment. Doctors focus on watchful monitoring and treating complications (for example, fluid or new leaky vessels) if they appear. EyeWikiNature

Pachydrusen were named in 2018 to describe a distinct type of drusen seen in eyes with a thick choroid and enlarged “pachy-vessels.” They’re typically >125 µm across, can be isolated or in small clusters, look irregular but sharply bordered, and tend to scatter across the posterior pole (back of the eye). Unlike the soft drusen in classic age-related macular degeneration (AMD), pachydrusen live in eyes with increased choroidal thickness and pachyvessels that may compress the tiny choroidal capillaries. EyeWikiPMCSpringerLink

In pachychoroid eyes, the choroid is thicker and the large choroidal veins are expanded. Those big veins can compress the tiny choriocapillaris above them, which lowers oxygen delivery to the RPE and outer retina. Over time, that stress can lead the RPE to shed lipids and proteins that collect under it as deposits—the pachydrusen. In many people, these deposits do not cause symptoms on their own. The trouble is that the same “thick-choroid” environment can also lead to leaky fluid (like in central serous chorioretinopathy) or new, fragile vessels (pachychoroid neovasculopathy or polypoidal choroidal vasculopathy), which can blur or distort vision. PMC+2PMC+2

Pachydrusen show up in people with pachychoroid pigment epitheliopathy (PPE), central serous chorioretinopathy (CSC), pachychoroid neovasculopathy (PNV), and polypoidal choroidal vasculopathy (PCV). They act like a fingerprint that the choroid is thick and the choroidal vessels are enlarged, even if the person has no fluid or bleeding today. Their look, size, and spread help doctors separate them from soft drusen or pseudodrusen seen in typical AMD. Nature+1

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Types of pachydrusen

There is no rigid “official” list of subtypes that every doctor must use, but the descriptions below reflect how clinicians commonly talk about pachydrusen in practice:

1. Solitary pachydrusen
   A single, large, sharply-edged, yellow-white deposit under the RPE in a thick-choroid eye. It may be near the macula or closer to the optic nerve. The Retina Society

2. Clustered pachydrusen
   Several deposits sit close together, often in small groups. Each deposit keeps its distinct border, and together they form a small patch. EyeWiki

3. Scattered pachydrusen across the posterior pole
   Multiple deposits spread out over the back of the eye, sometimes sparing the exact foveal center. The pattern is wider than typical soft drusen. EyeWiki

4. Peripapillary pachydrusen
   Deposits that favor the area next to the optic nerve (the “peripapillary” region). This distribution helps hint at pachychoroid. The Retina Society

5. Pachydrusen with PPE
   Deposits appear along with RPE mottling but no subretinal fluid, a pattern often called pachychoroid pigment epitheliopathy. Retina Specialist

6. Pachydrusen with CSC history
   Pachydrusen may be found in eyes with a past or present central serous chorioretinopathy, reinforcing that the choroid is thick and hyperpermeable. PMC

7. Pachydrusen with neovascular complications (PNV/PCV)
   Pachydrusen can coexist with abnormal new vessels under the retina (pachychoroid neovasculopathy) or polypoidal lesions. Their presence can signal a pachychoroid background to the neovascular disease. PMCNature

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Causes

Think of “causes” here as drivers and risk factors that create a thick-choroid environment or stress the RPE, allowing deposits to build up. Not every person will have all of these.

1. Thick choroid (pachychoroid)
   A thicker-than-usual choroid crowds the tiny choriocapillaris and stresses the RPE, encouraging deposit buildup. PMC

2. Dilated choroidal veins (pachyvessels)
   Enlarged deeper veins can compress upper layers that feed the RPE, nudging it toward waste accumulation. PMC

3. Choroidal hyperpermeability
   “Leaky” choroidal vessels swell the tissue and disturb normal nutrient flow, which can promote sub-RPE deposits. PMC

4. Pachychoroid pigment epitheliopathy (PPE)
   RPE stress without fluid is a setup for deposits to appear and persist. Retina Specialist

5. Central serous chorioretinopathy (CSC)
   CSC reflects the same thick, hyperpermeable choroid. Even when the fluid dries, the underlying milieu favors deposits. PMC

6. Polypoidal choroidal vasculopathy (PCV)
   PCV grows out of a pachychoroid background in many eyes, and pachydrusen may coexist. PMC

7. Pachychoroid neovasculopathy (PNV)
   New vessels develop on top of pachychoroid changes; pachydrusen can be part of the landscape. PMC

8. Age
   Pachydrusen are usually found in middle-aged and older adults, because time adds up the stress on RPE and choroid. (General observation in pachychoroid and drusen literature.)

9. Genetic background (different from classic AMD)
   Pachydrusen and pachychoroid seem to have different genetic patterns than typical AMD drusen, suggesting a separate pathway. (Ongoing research; current reviews highlight phenotypic and possible genotypic differences.) PubMed

10. Thick-choroid anatomy by ethnicity
    Some populations show more pachychoroid features, which may raise the chance of pachydrusen; prevalence data suggest notable rates in Asian cohorts. (Population data and reviews describe prevalence and differences.) PMCScienceDirect

11. Male sex in pachychoroid conditions
    Some pachychoroid diseases (like CSC) are more common in men, which can indirectly increase the chance of pachydrusen in those groups. PMC

12. Corticosteroid exposure (systemic or local)
    Steroids can worsen choroidal leakage and trigger CSC; the same environment can favor deposits over time. PMC

13. Psychosocial stress and catecholamines
    Stress relates to CSC risk; sustained high stress may sustain a pachychoroid state, supporting deposits. PMC

14. Sleep disturbance or sleep apnea (CSC link)
    Poor sleep and sleep apnea are linked with CSC in studies; the downstream pachychoroid state may favor pachydrusen. PMC

15. Hypertension or vascular dysregulation
    Blood pressure and vascular tone can affect choroidal flow, contributing to chronic RPE stress. (Supported across pachychoroid/CSC pathophysiology discussions.) PMC

16. High sympathetic drive (type-A traits)
    A “wired” autonomic state is often discussed with CSC; long-term vascular effects can favor deposits. PMC

17. RPE metabolic load
    When the RPE works harder to clear waste in a low-oxygen or crowded choroid, leftover material can build up as deposits. PMC

18. Choroidal remodeling over time
    Choroidal veins can remodel and shift pathways; the changing flow pattern can sustain RPE stress and promote deposits. SpringerLink

19. Light-exposure and oxidative stress (general retinal risk)
    The outer retina faces oxidative stress daily; if the choroid cannot clear by-products efficiently, deposits can grow. (General retinal physiology; consistent with RPE/choroid stress frameworks.) PMC

20. Lipid handling in Bruch’s membrane
    Drusen are lipid-rich. In pachychoroid eyes, altered lipid turnover at the RPE–Bruch’s interface can favor sub-RPE build-up. (Drusen biology and pachydrusen reviews.) PMC

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Symptoms

Many people with pachydrusen have no symptoms at all. Problems usually arise from other pachychoroid issues that may come with them (fluid, bleeding, or new vessels). Still, here are the symptoms to watch for:

1. No symptoms
   Common. Pachydrusen are often an incidental finding on retinal imaging. EyeWiki

2. Blurred central vision
   If fluid, bleeding, or scarring develops in a pachychoroid eye, fine detail fades.

3. Wavy or bent lines (metamorphopsia)
   Straight lines on a page may look warped when the macula is stressed.

4. A gray or dim spot (scotoma)
   A small blind or dim patch can appear in the center or near-center.

5. Poor contrast
   Letters may be harder to pick out against the background.

6. Difficulty reading small print
   Fine letters break up or seem faded.

7. Colors look dull
   Color saturation drops, especially for reds and greens.

8. Glare sensitivity
   Light feels harsh, and headlights bloom.

9. Slow recovery in bright light
   After a flash or outdoor glare, vision clears more slowly.

10. Trouble in dim light
    Signs and faces are harder to see in low light.

11. Micropsia or macropsia
    Objects may seem smaller or larger than they are.

12. Intermittent blur
    Vision may vary day to day if fluid comes and goes.

13. Headache or eye strain
    People squint or strain to overcome subtle blur.

14. Reduced reading speed
    Words swim or lose crisp edges.

15. Anxiety about vision changes
    Fluctuating vision can cause worry, which can feed back into stress—a known issue in pachychoroid conditions. PMC

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Diagnostic tests

A) Physical examination

1. Visual acuity (distance and near)
   You read letters on a chart. This measures how sharp your vision is today and helps track change over time.

2. Pupil examination
   The doctor looks for equal, brisk reactions to light. An abnormal response can signal deeper retinal or optic nerve problems (usually normal in isolated pachydrusen).

3. Intraocular pressure (tonometry)
   While not specific to pachydrusen, measuring eye pressure helps rule out other issues and sets a baseline for safe care.

4. Dilated slit-lamp fundus exam with a handheld lens
   After dilating drops, the doctor inspects the retina and RPE directly. Pachydrusen appear yellow-white with sharp borders and a scattered or clustered pattern across the posterior pole. EyeWiki

B) Manual/bedside functional tests

5. Amsler grid
   You stare at a small central dot on a square grid to check for wavy lines or missing areas, which can reveal macular distortion.

6. Pinhole test
   Looking through a pinhole quickly shows whether blur is optical (like uncorrected glasses) or retinal.

7. Confrontation visual fields
   You cover one eye while the examiner brings in small targets from the side to check for obvious field gaps near the center.

8. Color vision plates (Ishihara or similar)
   Simple dot-plate booklets check for color desaturation that sometimes accompanies macular stress.

C) Laboratory & pathological tests

9. Lipid profile (cholesterol and related measures)
   Not diagnostic by itself, but it can contextualize drusen biology, which is lipid-rich, and helps overall vascular risk management. (Supportive, not required.)

10. Genetic testing (research setting)
    Classic AMD genes (like CFH, ARMS2) do not map cleanly onto pachydrusen; testing is not routine but may be used in studies exploring differences. PubMed

11. Histopathology of drusen (rare, research or post-mortem)
    Microscopy can confirm sub-RPE, lipid-protein deposits, but this is not done in routine care. PMC

D) Electrodiagnostic tests

12. Full-field ERG (electroretinogram)
    Measures global retinal function. Usually normal in isolated pachydrusen; useful if diffuse retinal disease is suspected.

13. Multifocal ERG
    Maps macular function area by area. It can show reduced signals in spots of chronic stress.

14. Electro-oculogram (EOG)
    Assesses RPE function. Abnormalities can support RPE stress in complex or atypical cases.

E) Imaging tests (the core workup)

15. Spectral-domain OCT with enhanced-depth imaging (EDI-OCT)
    This is the key test. It gives cross-section pictures through the retina. In pachydrusen you see sub-RPE mounds with steep edges. EDI lets you measure choroidal thickness and see pachyvessels pressing upward. PMC

16. Swept-source OCT (SS-OCT)
    A deeper-penetrating OCT that visualizes the choroid even better, confirming thickness and dilated vessels. PMC

17. OCT-angiography (OCT-A)
    A non-dye scan that shows blood-flow maps. It helps exclude or detect new vessels (PNV/PCV) that may form on a pachychoroid background. PMC

18. Fundus autofluorescence (FAF)
    This maps RPE health using its natural glow (lipofuscin). Pachydrusen may show mixed autofluorescence signals, and FAF can reveal stressed RPE around them. PMC

19. Fluorescein angiography (FA)
    A dye test that shows retinal circulation and leaks. In pachychoroid settings, FA helps document fluid or leakage if present. PMC

20. Indocyanine green angiography (ICGA)
    A dye test that images choroidal circulation. It is excellent for showing choroidal hyperpermeability, pachyvessels, and polypoidal lesions, all of which help distinguish pachychoroid-related disease from classic AMD. PMC

Non-pharmacological treatments

Important: these support overall eye health and pachychoroid control. They do not dissolve pachydrusen. Your doctor tailors a plan based on your eye scans.

1. Observation with scheduled OCT.
   Purpose: catch early changes (fluid, bleeding).
   Mechanism: high-resolution scans track the RPE and choroid over time. ScienceDirect

2. Medication cleanup (steroid stewardship).
   Purpose: reduce CSC-type flares.
   Mechanism: lowering or avoiding corticosteroids (when medically safe) removes a strong trigger for choroidal leakage. Coordinate with your prescribing doctors. EyeWiki

3. Stress reduction and sleep hygiene.
   Purpose: tame sympathetic overdrive.
   Mechanism: stress raises cortisol/adrenergic tone; CBT, mindfulness, exercise, and regular sleep may reduce CSC risk. ophthalmologyretina.org

4. Sleep apnea evaluation and treatment (CPAP if needed).
   Purpose: improve oxygenation and autonomic balance.
   Mechanism: treating OSA has been linked to better choroidal status in CSC-type eyes. AjoAAO

5. Cardiometabolic tune-up (BP, glucose, lipids).
   Purpose: support microvascular health.
   Mechanism: healthier vessels may lessen choroidal congestion.

6. Smoking cessation.
   Purpose: protect retinal and choroidal circulation.
   Mechanism: less oxidative and vascular stress; smoking is a risk factor across retinal diseases. (In CSC cohorts, smoking often tracks with higher risk.) ResearchGate

7. Caffeine and stimulant moderation.
   Purpose: avoid adrenergic surges.
   Mechanism: fewer transient spikes that could favor choroidal leakage in sensitive eyes.

8. Weight management & regular exercise.
   Purpose: reduce OSA risk and improve vascular tone.
   Mechanism: weight loss lowers OSA severity and improves systemic hemodynamics linked to pachychoroid states. PMC

9. Blue-light and UV awareness (sunglasses outdoors).
   Purpose: reduce light-related RPE stress.
   Mechanism: quality UV-blocking lenses cut retinal light load; helpful for general retinal health.

10. Healthy-eye diet pattern.
    Purpose: provide antioxidants and carotenoids.
    Mechanism: leafy greens (lutein/zeaxanthin), colorful veg/fruit, and fish (omega-3s from diet) support the macula’s antioxidant defenses (see “What to eat” below). (AREDS2 applies to intermediate AMD; not proven for pachydrusen.) National Eye Institute

11. Avoid unnecessary “steroid-like” supplements.
    Purpose: prevent hidden triggers.
    Mechanism: some bodybuilding/“herbal” products contain androgenic or corticosteroid-like compounds that can aggravate CSC-type disease. EyeWiki

12. Treat reflux and manage nighttime acid if symptomatic.
    Purpose: improve sleep quality and reduce nocturnal stress/awakening.
    Mechanism: better sleep complements OSA and stress care (evidence on reflux itself is mixed for CSC). ScienceDirect

13. Protective habits for screens and close work.
    Purpose: reduce eye strain signals that can mask subtle new symptoms.
    Mechanism: regular breaks (20-20-20 rule) help you notice new distortion early.

14. Home Amsler grid monitoring.
    Purpose: self-detect new wavy lines or missing spots.
    Mechanism: fast trigger to call your doctor if changes appear.

15. Sunlight/photosensitivity precautions after PDT sessions.
    Purpose: avoid verteporfin-related light reactions (if you ever have PDT).
    Mechanism: strict light protection for ~48 hours post-PDT prevents skin reactions. BauschPubMed

16. Manage anxiety and mood.
    Purpose: break the stress–vision spiral.
    Mechanism: counseling/CBT lowers sympathetic tone that aggravates CSC susceptibility. ophthalmologyretina.org

17. Coordinate care across specialties.
    Purpose: align steroid plans, OSA therapy, and eye follow-up.
    Mechanism: fewer mixed signals to the choroid.

18. Prompt attention to new visual symptoms.
    Purpose: early treatment of complications.
    Mechanism: faster control of fluid/bleeding gives better outcomes.

19. Educate family for symptom watching.
    Purpose: extra eyes to notice changes.
    Mechanism: quick reporting if you overlook gradual distortion.

20. Keep all imaging records.
    Purpose: compare scans across time.
    Mechanism: doctors can spot tiny shifts in pachydrusen, RPE, or choroid that matter.

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Drug treatments

These medicines treat complications (like PCV/PNV fluid or bleeding), not pachydrusen themselves. Doses below are typical reference regimens; your retina specialist will tailor a plan.

1. Ranibizumab (anti-VEGF).
   Class: anti-VEGF-A monoclonal fragment; Dose/Time: 0.5 mg intravitreal, often monthly loading then treat-and-extend.
   Purpose/Mechanism: dries leakage and shrinks abnormal vessels.
   Notes: In PCV, ranibizumab + verteporfin PDT improved vision and polyp closure more than ranibizumab alone in EVEREST II. Side effects: eye infection (rare), pressure rise, inflammation. PubMedJAMA Network

2. Aflibercept (anti-VEGF “trap”).
   Class: VEGF-A/PlGF decoy receptor; Dose/Time: 2 mg monthly for 3 doses, then usually every 8 weeks and extend as stable.
   Purpose/Mechanism: potent drying and polyp regression data in PCV.
   Side effects: similar to other anti-VEGFs. NatureMDPI

3. Faricimab (dual Ang-2/VEGF-A).
   Class: bispecific antibody; Dose/Time: 6 mg with monthly loading then extend (often q8–16 wk when stable).
   Purpose/Mechanism: blocks VEGF-A and Ang-2 to stabilize vessels; growing real-world experience and subgroup data support use in PCV/nAMD.
   Side effects: as for anti-VEGF; monitor for inflammation. NaturePMCFrontiers

4. Bevacizumab (anti-VEGF, off-label).
   Class: anti-VEGF-A; Dose/Time: 1.25 mg intravitreal, typically monthly then extend.
   Purpose/Mechanism: dries leakage from neovascular complications; widely used off-label.
   Side effects: as above. The Open Ophthalmology Journal

5. High-dose aflibercept (8 mg).
   Class: anti-VEGF “trap”; Dose/Time: 8 mg after loading then extend; used when durability is needed.
   Purpose/Mechanism: longer intervals vs 2 mg in many nAMD/PCV practices.
   Side effects: similar class effects; specialist decision. MDPI

6. Brolucizumab (anti-VEGF).
   Class: small anti-VEGF single-chain; Dose/Time: 6 mg on specialist discretion.
   Purpose/Mechanism: strong drying; Caution: higher risk of intraocular inflammation and occlusive vasculitis than other agents—used selectively with informed consent. AAO+1JAMA Network

7. Verteporfin (Visudyne) for PDT (drug used during a light-based procedure).
   Class: photosensitizer; Dose/Time: 6 mg/m² IV over 10 min, then 689 nm light at 50 J/cm² for 83 s starting 15 min after infusion begins; often half-dose/half-fluence for CSC.
   Purpose/Mechanism: selectively closes abnormal choroidal vessels and calms choroidal leakage.
   Side effects: 48 h photosensitivity, infusion extravasation can injure skin; follow strict light precautions. EyeWikiBauschWiley Online Library

8. Topical NSAIDs (adjunct, selective use).
   Class: anti-inflammatories; Dose/Time: per label.
   Purpose/Mechanism: may reduce mild surface inflammation or discomfort after procedures; not a core pachychoroid therapy.

9. Carbonic anhydrase inhibitors (e.g., oral acetazolamide, selective use).
   Class: diuretic; Purpose/Mechanism: sometimes used to promote subretinal fluid resorption in other macular conditions; evidence in pachychoroid complications is limited—specialist-only use.

10. Mineralocorticoid antagonists (eplerenone/spironolactone) — no longer recommended for chronic CSC.
    Class: MR antagonists; historically tried for CSC.
    Evidence: the VICI randomized trial showed no benefit over placebo for chronic CSC; most experts do not use them for this purpose. Side effects: electrolyte changes, blood-pressure effects, breast tenderness (spironolactone). PubMedThe LancetNature

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Dietary “molecular” supplements

There is no supplement proven to treat pachydrusen. The only strong supplement evidence in retina is the AREDS2 formula for people with intermediate AMD, which pachydrusen is not. Use supplements only after discussion with your eye doctor.

1. AREDS2 blend — Vitamin C 500 mg, Vitamin E 400 IU, Zinc 80 mg + Copper 2 mg, Lutein 10 mg, Zeaxanthin 2 mg daily.
   Function/Mechanism: antioxidant and carotenoid support for macula; benefit shown only for intermediate AMD to slow progression. Smokers should avoid β-carotene versions. National Eye Institute+1

2. Lutein (10 mg) & 3) Zeaxanthin (2 mg) (as in AREDS2).
   Function: pigments concentrate in the macula and filter blue light; helpful within AREDS2 for the right AMD stage; unproven for pachydrusen. JAMA Network

3. Zinc (80 mg with copper 2 mg) (AREDS2 component).
   Function: cofactor for retinal enzymes; must include copper to avoid deficiency. National Eye Institute

4. Vitamin C (500 mg) & 6) Vitamin E (400 IU) (AREDS2 components).
   Function: antioxidants; the AREDS/AREDS2 dose is safe under trial oversight, but confirm with your physician if you take blood thinners. National Eye Institute

5. Omega-3s (DHA/EPA) from diet rather than pills.
   Function: membrane support and anti-inflammatory tone; supplement pills showed no added AMD benefit in AREDS2, so focus on fish intake instead. National Eye Institute+1

6. Saffron (trial-level interest in macular function).
   Function: antioxidant spice with exploratory macular data; no pachydrusen-specific evidence.

7. Astaxanthin (carotenoid).
   Function: antioxidant; human retinal evidence is limited—discuss risks and interactions first.

8. CoQ10 or resveratrol (general antioxidants).
   Function: cellular energy/antioxidant roles; no proven retinal benefit for pachydrusen—avoid unless your doctor agrees.

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Regenerative / stem-cell drugs

There are no approved “immunity booster,” regenerative, or stem-cell drugs for pachydrusen or the broader pachychoroid spectrum. Experimental RPE cell or gene therapies are being studied mainly for advanced AMD, not for pachydrusen, and should only be received in regulated clinical trials. Many commercial “stem-cell clinics” are unsafe and have caused severe harm.
Safer alternative: if you’re interested in research, ask your retina specialist to screen you for legitimate clinical trials (ClinicalTrials.gov) that fit your actual diagnosis, such as PCV or nAMD studies of new anti-angiogenic approaches. ClinicalTrials.gov

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Procedures and why they’re done

1. Photodynamic therapy (PDT) with verteporfin.
   Why: top choice for chronic CSC and sometimes combined with anti-VEGF in PCV.
   How: verteporfin IV then eye is illuminated with 689 nm light; half-dose/half-fluence variants reduce adverse events in CSC.
   Goal: settle choroidal hyperpermeability and shrink abnormal complexes. Wiley Online LibraryBioMed Central

2. Anti-VEGF intravitreal injection series.
   Why: treat pachychoroid neovasculopathy or PCV with fluid/bleeding.
   How: small injection of anti-VEGF medicine; often monthly loading, then treat-and-extend.
   Goal: dry the macula, improve/maintain vision; sometimes combined with PDT in PCV. PubMed

3. ICGA-guided focal laser (select CSC cases).
   Why: when a leak point is outside the fovea and PDT is unavailable.
   Goal: seal the leak safely away from the center. BioMed Central

4. Subthreshold/micropulse laser (backup option).
   Why: where PDT isn’t available or suitable; lower burn risk than conventional laser.
   Goal: stimulate RPE pump without scarring; less effective than PDT, but sometimes used. BioMed Central

5. Surgery for large submacular hemorrhage (rare PCV events).
   Why: if dense blood threatens the fovea.
   How: options include pneumatic displacement with tPA or limited vitrectomy per specialist judgment.
   Goal: move blood off the fovea and preserve vision.

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Prevention tips

1. Avoid unnecessary steroids (all forms) and discuss safer alternatives with your doctors. EyeWiki

2. Screen for sleep apnea if you snore, feel unrefreshed, or your partner notices pauses in breathing. Treat if present. Ajo

3. Manage stress with structured tools (CBT, mindfulness, exercise). ophthalmologyretina.org

4. Don’t smoke; seek cessation help if needed. ResearchGate

5. Keep BP, sugar, and lipids controlled.

6. Maintain healthy weight to lower OSA risk. PMC

7. Eat a macula-friendly diet (greens, colorful veg, fruit, fish, nuts).

8. Protect eyes from intense sunlight with proper sunglasses.

9. Check an Amsler grid weekly and report changes.

10. Keep regular retina visits and bring prior images for comparison.

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When to see a doctor urgently

• Sudden blur or central dark spot (scotoma).

• New distortion (straight lines look wavy).

• Flashes, many new floaters, or a “curtain” of vision loss.

• Eye pain or redness after an injection or procedure.

• Any vision change in your only good-seeing eye.
  Prompt care improves outcomes when complications develop.

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What to eat, and what to avoid

Eat more of these

1. Dark leafy greens (spinach, kale): rich in lutein/zeaxanthin that concentrate in the macula. National Eye Institute

2. Colorful vegetables and fruit (orange, yellow, red): broad antioxidants.

3. Fatty fish (salmon, sardines, mackerel) 1–2×/week: dietary omega-3s support retinal membranes (supplement pills didn’t help AMD progression in trials). National Eye Institute

4. Nuts and seeds (almonds, walnuts): healthy fats and micronutrients.

5. Whole grains and legumes: steady energy and vascular health.

Limit or avoid

1. Smoking and vaping: harmful to ocular blood supply.
2. Excess alcohol: can worsen overall health and sleep quality.
3. Highly processed, high-salt foods: unhelpful for blood pressure and sleep.
4. Energy drinks/stimulants late in the day: may worsen sleep/adrenergic tone in sensitive people.
5. Self-prescribed “eye” supplements not vetted by your doctor: many are unproven or interact with medicines.

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Frequently asked questions

1) Are pachydrusen the same as AMD drusen?
No. They’re both sub-RPE deposits, but pachydrusen live in thick-choroid eyes and have a different look and spread from soft AMD drusen. EyeWiki

2) Do pachydrusen always lead to vision loss?
Usually no. The risk comes from complications like CSC fluid, PNV, or PCV. PMC

3) Can pachydrusen turn into AMD?
They flag a pachychoroid biology rather than classic AMD biology. Some people may have overlapping features; your doctor separates them with imaging. PubMed

4) What is the best test to track pachydrusen?
OCT with choroidal measurements, sometimes plus OCTA/ICGA if PCV is suspected. ScienceDirect

5) Is there a pill to dissolve pachydrusen?
No. Management focuses on monitoring and treating complications if they arise. PMC

6) Do supplements help?
AREDS2 helps intermediate AMD, not pachydrusen. Use only if your doctor confirms AMD-stage eligibility. National Eye Institute

7) Why do doctors care about sleep apnea?
OSA relates to CSC and thick choroids; treating OSA may steady the disease environment. Ajo

8) Are steroid creams or inhalers a problem?
They can be. Any steroid can tip CSC physiology, so discuss safer options with prescribers. EyeWiki

9) What is PDT and will I need it?
Photodynamic therapy uses verteporfin plus light to calm choroidal leakage; top evidence exists in chronic CSC and as combo therapy in PCV. Your doctor decides based on scans. Wiley Online LibraryPubMed

10) If I need injections, which anti-VEGF is best?
All major agents work; choices depend on your response and visit burden. In PCV, ranibizumab+PDT produced better polyp closure than ranibizumab alone in EVEREST II, and aflibercept and faricimab are widely used too. PubMedNature+1

11) Is brolucizumab safe?
It can control fluid but carries a higher risk of inflammation and retinal vasculitis than other agents—specialists use it selectively. AAO+1

12) Can laser fix pachydrusen?
No. Focal or micropulse laser may be used for certain CSC leaks when PDT isn’t an option. BioMed Central

13) Can pachydrusen disappear?
They can change slowly over time, but the main point is watching for new fluid or vessels rather than “clearing” the deposits. PMC

14) How often should I be checked?
Your doctor sets the interval (often every 3–12 months when quiet) and sooner if symptoms change, guided by OCT findings. ScienceDirect

15) What’s the single most helpful thing I can do?
Control triggers (steroids, untreated OSA, high stress), show up for OCT checks, and call early for any new distortion or blur. EyeWikiAjo

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Last Updated: August 19, 2025.