Submacular Hemorrhage 

Submacular hemorrhage means bleeding under the central part of the retina called the macula. The macula is the tiny spot that gives you sharp, detailed, central vision—the vision you use to read, drive, recognize faces, and see fine detail. When blood collects beneath the retina at the macula, it blocks light, poisons nearby cells with iron from blood, and pushes on fragile light‑sensing cells (photoreceptors). These three problems—blocking, poisoning, and pressure—can quickly damage the macula if the bleed is large or lasts too long.

• “Submacular” means the bleeding sits under the macula. Depending on the exact layer, it may be subretinal (under the light‑sensing tissue) or sub‑RPE (beneath the retinal pigment epithelium, a support layer).
• “Hemorrhage” simply means bleeding or pooled blood.

A submacular hemorrhage is a pool of blood that leaks under the center of the retina (the macula). The macula is the tiny spot in the back of your eye that gives you sharp, straight-ahead vision for reading, faces, and fine detail. When blood slips under this area, it lifts and poisons the light-sensing cells (photoreceptors). That can blur or block central vision, sometimes very quickly.

Why this matters: animal and human data show that blood under the macula can damage photoreceptors within hours to days, mainly because (1) the clot contracts and shears the delicate outer segments, (2) iron from the blood is toxic, and (3) the clot blocks nutrient exchange between the retina and its support layer (RPE). Treating early can help limit permanent damage. PubMed+1American Academy of OphthalmologyEyeWiki

Why it is urgent: The macula is delicate. Red blood cells break down and release iron and other by‑products that are toxic to photoreceptors. A thick, sticky clot can also press on and suffocate these cells. The longer the blood stays, the higher the chance of permanent scar and permanent central vision loss. Even small bleeds can cause serious blurring if they sit right under the fovea (the exact center of the macula).

Common triggers: The most frequent cause in older adults is abnormal new blood vessels under the retina (called choroidal neovascularization, or CNV) linked to age‑related macular degeneration (AMD). Other causes include polypoidal choroidal vasculopathy (PCV), retinal arterial macroaneurysm (RAM), high myopia (very long eyeball with fragile tissues), trauma, and inflammatory or infectious conditions that produce fragile vessels that can leak or burst.

What you may notice: Many people feel sudden blurring, a dark or gray spot in the center (a central scotoma), or wavy lines (metamorphopsia). Colors can look washed out. Reading becomes difficult. Pain is usually absent unless there was serious eye injury.

What doctors aim to do: First, they confirm the diagnosis and measure how deep and wide the blood is. Then they look for the underlying cause (for example, CNV from AMD). Treatment choices depend on cause, size, depth, and how long the blood has been there. (This article focuses on definition, types, causes, symptoms, and diagnostic tests, as requested.)

Types of Submacular Hemorrhage

Doctors often describe SMH by where the blood sits, how much there is, how old it is, and what caused it. Using simple words:

1. By Eye Layer

• Subretinal SMH: Blood sits between the photoreceptors and the retinal pigment epithelium (RPE). It directly touches the light‑sensing cells, so vision can drop quickly. Fresh blood looks bright red; older blood looks darker and clotted.
• Sub‑RPE SMH: Blood is beneath the RPE, so it may look darker and dome‑shaped. It can hide details on fluorescein angiography but shows better on indocyanine green angiography or optical coherence tomography (OCT). It can still damage the macula by lifting and starving it of nutrients.
• Mixed‑plane SMH: Blood is both subretinal and sub‑RPE. This often happens with strong leakage or rupture of abnormal vessels, and it can be harder to manage.

2. By Size (How much blood)

• Small (focal) SMH: A small spot under the fovea or beside it. Even a tiny spot can cause big symptoms if it sits exactly under the fovea.
• Moderate (patch) SMH: A larger patch covering part of the macula. Reading is often difficult; faces may blur.
• Massive (extensive) SMH: A large collection that can extend beyond the macula. Thick clots raise the retina and threaten long‑term scarring.

3. By Time (How old the blood is)

• Acute (fresh) SMH: Hours to days old. Blood appears bright red on exam. Urgency is high because early damage can still be reduced if the cause is treated quickly.
• Subacute SMH: Several days to a few weeks old. The blood darkens, becomes thicker, and can trap toxic by‑products against the photoreceptors.
• Chronic (organized) SMH: Weeks to months old. The blood clots, breaks down, and may form subretinal fibrosis (scar tissue). Vision recovery becomes more limited.

4. By Cause

• Neovascular (CNV‑related) SMH: Due to fragile new vessels in AMD, PCV, high myopia, inflammatory CNV, or idiopathic CNV. These are common and often recur without controlling the underlying process.
• Macroaneurysm‑related SMH: From a weak, ballooned section of a retinal artery (RAM) that leaks or bursts near the macula.
• Traumatic SMH: From direct or indirect eye injury (for example, a ball to the eye) that ruptures choroidal or retinal vessels.
• Other vascular or systemic SMH: From blood disorders, very high blood pressure, or medication effects (for example, strong blood thinners) that tilt the balance toward bleeding.

5. By Thickness (How raised the retina is)

• Thin layer: A film of blood that still allows some light through.
• Thick clot: A lumpy, elevated mass under the macula that blocks light and presses on photoreceptors.

6. By Location relative to the fovea

• Foveal SMH: Directly under the center of the macula; symptoms are most severe.
• Parafoveal/juxtafoveal SMH: Just next to the very center; symptoms vary based on exact position.

Causes

Below are 20 causes that can lead to bleeding under the macula. For each cause, you will see a plain‑English description of what it is, how it leads to bleeding, and why it matters.

1. Neovascular (wet) Age‑Related Macular Degeneration (AMD)
   In wet AMD, fragile new vessels grow from the choroid under the retina. These vessels leak fluid or bleed easily. A sudden break can dump blood under the macula, causing a submacular hemorrhage. Without control of the neovascular growth, bleeds may recur.
2. Polypoidal Choroidal Vasculopathy (PCV)
   PCV is a choroidal condition with grape‑like bulges (polyps) in a branching vascular network. These abnormal vessels can burst and cause repeated submacular bleeding. It often affects middle‑aged to older adults and may cause large, dark, dome‑shaped bleeds.
3. Retinal Arterial Macroaneurysm (RAM)
   A RAM is a balloon‑like bulge in a retinal artery, often in older people with high blood pressure. The thin wall can leak or rupture, spilling blood in different retinal layers, including under the macula. Vision loss depends on how close the bleed is to the fovea.
4. Pathologic (High) Myopia with Choroidal Neovascularization
   In very nearsighted eyes, the eyeball is elongated. The support layers thin and crack, and new, fragile vessels may form under the retina (myopic CNV). These can bleed and create submacular hemorrhage, sometimes in younger adults.
5. Trauma (Direct or Indirect Eye Injury)
   A blunt hit, fall, or projectile can tear or rupture choroidal or retinal vessels. Even indirect pressure waves can burst vessels under the macula. Bleeding may be immediate and large, and other injuries (like choroidal rupture) can coexist.
6. Ocular Histoplasmosis Syndrome (OHS)
   Old scars in the choroid from histoplasma infection can later develop CNV. Those new vessels are fragile and can bleed under the macula. Patients may have no active infection—only the after‑effects that set the stage for bleeding.
7. Angioid Streaks
   These are cracks in Bruch’s membrane (a support layer under the retina). The cracks can allow CNV to grow and bleed. Angioid streaks can be linked to systemic conditions like pseudoxanthoma elasticum.
8. Choroidal Osteoma
   A rare, bony tumor in the choroid can trigger CNV at its edges. These new vessels bleed easily, causing submacular hemorrhage, often in young women.
9. Multifocal Choroiditis and Punctate Inner Choroidopathy (PIC)
   These are inflammatory conditions in the back of the eye. The inflammation disrupts normal layers and can stimulate CNV, leading to submacular bleeds. Vision can fluctuate with disease activity.
10. Serpiginous Choroiditis
    Another inflammatory disease with spreading patches of chorioretinal damage. CNV may grow at the borders of old lesions and bleed under the macula.
11. Central Serous Chorioretinopathy (CSCR) with Secondary CNV
    Most CSCR cases are fluid‑based, but long‑standing cases can develop secondary CNV. These fragile vessels can bleed under the macula, particularly in chronic or recurrent CSCR.
12. Idiopathic Choroidal Neovascularization (no clear cause)
    Sometimes CNV appears in otherwise healthy eyes with no obvious trigger. These vessels still have the same problem—they are fragile and can bleed under the macula.
13. Sickle Cell Retinopathy and Other Hemoglobinopathies
    Blood disorders can cause abnormal fragile retinal vessels. With sickle cell disease, sea‑fan‑shaped neovascularization can bleed; in rare cases, bleeding can track under the macula.
14. Retinal Vein Occlusion (Branch or Central)
    Blocked retinal veins cause high venous pressure and leakage. Most bleeding is within the retina, but occasionally blood can collect under the macula, especially if secondary CNV develops.
15. Leukemia and Other Hematologic Disorders
    Abnormal blood counts, such as very low platelets or high white cells, can cause spontaneous bleeding in the eye. If the macula is involved, blood may settle beneath it.
16. Uncontrolled Hypertension (Very High Blood Pressure)
    High pressure damages vessel walls and makes them leaky or prone to rupture. A sudden spike can trigger bleeding, including under the macula, particularly when other risks are present.
17. Anticoagulant/Antiplatelet/Thrombolytic Medications
    Drugs that thin blood or prevent clots (like warfarin, DOACs, aspirin, clopidogrel, or tPA) can worsen or trigger bleeding from fragile macular vessels. They are often necessary for heart or stroke conditions but can tip the balance toward an eye bleed when other risks exist.
18. Radiation Retinopathy
    After radiation therapy to the eye or nearby areas, blood vessels can become weak and leaky. New vessels can form and bleed, sometimes under the macula.
19. Toxoplasmosis or Other Chorioretinal Infections with Secondary CNV
    Old chorioretinal scars from infection can later develop CNV at the edges. These vessels can bleed and place blood under the macula.
20. Valsalva‑Related Events in Predisposed Eyes
    A sudden pressure increase from heavy lifting, coughing, or vomiting usually causes preretinal bleeds, but in predisposed eyes (for example, with existing CNV), this added strain can trigger a submacular bleed.

Symptoms

Not everyone gets all symptoms. Severity depends on how big the bleed is, how close it is to the fovea, how deep it sits, and how long it has been there.

1. Sudden central blur
   Vision in the center becomes foggy or out of focus, often over hours to days.
2. A dark or gray spot in the center (central scotoma)
   People describe a fixed smudge or missing patch in the middle of what they are trying to look at.
3. Wavy or bent lines (metamorphopsia)
   Straight lines look kinked or wavy, especially when reading or looking at door frames.
4. Reduced reading speed
   Letters seem broken or missing; words fade or jump, making reading tiring or impossible.
5. Faded or washed‑out colors
   Colors look less rich, especially reds and greens, because the macula is disturbed.
6. Difficulty recognizing faces
   The central details of faces are missing or blurred, so people rely on voice or context.
7. Poor contrast sensitivity
   Gray‑on‑gray details are hard to see (for example, steps in dim light).
8. Micropsia or macropsia (size distortion)
   Objects can look smaller or larger than they are, because the retina is lifted or distorted by the blood underneath.
9. Light sensitivity in some cases
   Bright light may feel uncomfortable when the macula is irritated or swollen.
10. No pain
    Most SMH is painless, which can be misleading. Lack of pain does not mean the eye is fine.
11. Sudden change after a trigger
    Some people notice a sharp drop in vision after a cough, bending, or minor bump, especially if fragile vessels were already present.
12. A shadow that does not move
    Unlike a floater, the central dark patch stays put and matches the area of blood under the retina.
13. Unequal vision between the two eyes
    One eye may be much worse than the other if only one macula is affected.
14. Trouble with fine tasks
    Sewing, reading small print, or phone use becomes challenging due to missing central detail.
15. Anxiety about rapid worsening
    People often worry because changes are sudden and serious. This stress is understandable and should be acknowledged during care.

Diagnostic Tests

Doctors choose tests to confirm bleeding under the macula, locate the exact layer, measure size and thickness, and find the root cause (for example, CNV, macroaneurysm, or inflammation). Below are 20 tests divided into five practical groups.

A) Physical Examination

1. Best‑Corrected Visual Acuity (BCVA)
   What it is: Reading letters on a standardized chart with your best glasses correction.
   Why it’s used: Tells how much central vision is reduced at baseline and during follow‑up.
   What it shows in SMH: A drop in central lines is common. Changes over time help judge whether the bleed is clearing or if treatment is helping.
2. Pupil Exam for Relative Afferent Pupillary Defect (RAPD)
   What it is: Shining a light in each eye and watching how pupils react.
   Why it’s used: Checks if the retina‑to‑brain signal is imbalanced.
   What it shows in SMH: Most SMH does not cause RAPD, but if present, it suggests more widespread or deeper retinal/optic nerve issues needing careful evaluation.
3. Slit‑Lamp Exam with Dilated Fundus Examination
   What it is: A microscope exam after dilating drops to look at the retina and macula directly.
   Why it’s used: Directly sees the blood, estimates location (subretinal vs sub‑RPE), and notes size and thickness.
   What it shows in SMH: Fresh red or darker clotted blood under the macula, elevation of the retina, and any scars, drusen, or signs of CNV.
4. Intraocular Pressure (Tonometry)
   What it is: A quick pressure check of the eye.
   Why it’s used: Ensures pressure is safe and looks for complications if steroids or surgery are considered.
   What it shows in SMH: Usually normal, but baseline pressure helps guide safe care.

B) Manual / Functional Office Tests

5. Amsler Grid
   What it is: A small square grid of straight lines you look at one eye at a time.
   Why it’s used: Maps distorted or missing central vision at home or in clinic.
   What it shows in SMH: Wavy lines, missing boxes, or a central gray patch that matches the bleed area.
6. Pinhole Test
   What it is: Viewing through a tiny pinhole to reduce blur from focusing errors.
   Why it’s used: Separates refractive blur (helped by pinhole) from retinal disease (not helped).
   What it shows in SMH: Little or no improvement, supporting a macular cause of blur.
7. Contrast Sensitivity (e.g., Pelli‑Robson)
   What it is: Reading letters that get lighter on a gray chart.
   Why it’s used: Detects subtle central function loss not seen on standard acuity charts.
   What it shows in SMH: Lower contrast scores, especially when blood covers the fovea.
8. Color Vision Testing (e.g., Ishihara, D‑15)
   What it is: Identifying colored numbers or arranging colored caps.
   Why it’s used: Checks macular function because the macula handles fine color detail.
   What it shows in SMH: Reduced color discrimination when the fovea is affected.

C) Lab and Pathological Tests

9. Complete Blood Count (CBC) with Platelets
   What it is: A blood test that measures red cells, white cells, and platelets.
   Why it’s used: Looks for anemia, leukemia, or low platelets that make bleeding more likely.
   What it shows in SMH: Abnormal counts may explain easy bleeding or guide safe treatment.
10. Coagulation Profile (PT/INR and aPTT)
    What it is: Blood tests showing how fast your blood clots.
    Why it’s used: Checks the effect of blood thinners or clotting problems.
    What it shows in SMH: An elevated INR or prolonged times mean higher bleeding risk and influence treatment timing.
11. Hemoglobin A1c (HbA1c)
    What it is: A 3‑month average of blood sugar control.
    Why it’s used: Poorly controlled diabetes raises risk of retinal disease and bleeding.
    What it shows in SMH: High values suggest a systemic contributor that needs attention.
12. Lipid Profile
    What it is: Blood fats, including LDL, HDL, and triglycerides.
    Why it’s used: Vascular health affects eye vessels; high lipids track with vascular fragility.
    What it shows in SMH: Elevated lipids add to overall risk and guide systemic care.

D) Electrodiagnostic Tests

13. Full‑Field Electroretinogram (ffERG)
    What it is: A test that measures the electrical response of the entire retina to light.
    Why it’s used: Checks overall retinal health; severe widespread disease lowers responses.
    What it shows in SMH: Usually near‑normal unless there is broader retinal damage, but it provides a baseline when vision is worse than the bleed size suggests.
14. Multifocal ERG (mfERG)
    What it is: Measures localized electrical signals from many tiny areas of the macula.
    Why it’s used: Directly assesses how the central retina is functioning.
    What it shows in SMH: Reduced signals in the area under and around the hemorrhage, tracking recovery over time.
15. Pattern ERG (PERG)
    What it is: Electrical test using patterned stimuli (like checkerboards).
    Why it’s used: Sensitive to macular and ganglion cell function.
    What it shows in SMH: Depressed responses when the fovea is compromised, with potential improvement as blood clears.
16. Visual Evoked Potential (VEP)
    What it is: Measures the brain’s response to visual stimuli.
    Why it’s used: Ensures the visual pathway beyond the eye is intact when exam findings and vision do not match.
    What it shows in SMH: Usually normal if only the macula is affected, helping rule out optic nerve pathway issues.

E) Imaging Tests

17. Optical Coherence Tomography (OCT) of the Macula
    What it is: A non‑contact scan that creates cross‑section pictures of the retina.
    Why it’s used: Shows exact location (subretinal vs sub‑RPE), thickness of the blood, and retinal swelling.
    What it shows in SMH: A hyper‑reflective or shadowing layer under the macula, elevation of the retina, presence of CNV signs, and changes over time as blood clears.
18. Fluorescein Angiography (FA)
    What it is: A dye is injected into a vein, and rapid photos track dye flow in retinal vessels.
    Why it’s used: Maps leakage, blockage, and CNV activity.
    What it shows in SMH: Blood may block fluorescence (appears dark), and active CNV may show leakage at the edges.
19. Indocyanine Green Angiography (ICGA)
    What it is: Another dye test that highlights choroidal circulation better than FA.
    Why it’s used: Excellent for finding PCV polyps or networks hiding under blood or pigment.
    What it shows in SMH: Polypoidal lesions or choroidal hot spots that explain recurrent bleeding.
20. OCT Angiography (OCTA)
    What it is: A non‑dye scan that detects moving blood cells to visualize vessels.
    Why it’s used: Finds CNV without dye and tracks changes over time.
    What it shows in SMH: A neovascular network under the macula, with reduced signal where thick blood causes shadowing.

Non-pharmacological treatments

These are supportive or procedural steps that don’t involve systemic drugs. Some are done with medicines; some are lifestyle/rehab changes. Evidence quality varies—procedures are supported by clinical series; lifestyle steps come from AMD/vascular risk guidance.

1. Observation with tight follow-up – For small/thin bleeds and good vision, especially if the cause is already controlled. Purpose: avoid unnecessary risk; Mechanism: spontaneous clot retraction/absorption. EyeWiki

2. Post-procedure positioning after intravitreal gas (pneumatic displacement) – commonly face-down or downward gaze for a few days; some biomechanical analyses favor face-forward gaze—clinics vary. Purpose: gas bubble nudges blood off the fovea. American Academy of OphthalmologyPMCJAMA Network

3. Pneumatic displacement (gas injection) without drugs – Office procedure using SF6/C3F8 gas to push blood away; often paired with tPA and/or anti-VEGF. Purpose: move clot off fovea to reduce toxicity. American Academy of Ophthalmology

4. Low-vision rehabilitation – Devices, lighting, contrast tips to maximize remaining vision; Purpose: preserve independence; Mechanism: adaptive training.

5. Amsler grid home monitoring – Daily 10-second check to catch new distortion early. Purpose: trigger urgent care if changes appear. American Academy of Ophthalmology

6. Smoking cessation – Strong AMD risk reducer; Purpose: fewer bleeds/progression over time; Mechanism: improves choroidal blood flow/oxidative stress. nei.nih.gov

7. Blood pressure control – Especially important for RAM and PCV. Purpose: reduce re-bleed risk; Mechanism: less vessel stress. PMC

8. Avoid heavy straining/Valsalva (lifting, severe constipation) during healing. Purpose: lower sudden venous spikes; Mechanism: less chance of new multilayer hemorrhage. NCBI

9. Protective eyewear (if trauma risk). Purpose: prevent traumatic re-bleed.

10. UV-blocking sunglasses & stable lighting – Comfort and glare control; may aid function.

11. Nutritional optimization (see diet section) – Mediterranean-style patterns support retinal health; AREDS2 supplements for the right AMD stages. nei.nih.gov+1

12. Weight, lipids, and exercise management – Lower vascular risks that feed the problem. nei.nih.gov

13. Medication review with your cardiologist/GP – Do not stop blood thinners on your own. Purpose: balance eye bleeding risk vs stroke/MI risk.

14. Head-of-bed elevation (first days) – Can reduce pooling and morning blur.

15. Timed follow-up OCT (e.g., 1 day, 1–2 weeks, 4–6 weeks) – Purpose: confirm displacement/absorption and plan injections.

16. Education about gas safety – No air travel and no nitrous-oxide anesthesia until gas fully gone; prevents dangerous eye-pressure spikes. PubMedRetina TodayThe Royal College of Ophthalmologists

17. Fall-prevention/home safety – If vision is impaired, reduce injury risk.

18. Driving guidance – Pause driving if central scotoma/vision below legal threshold; resume per clinician advice.

19. Work/reading ergonomics – Larger fonts, higher contrast, e-readers; reduces eye strain while healing.

20. Psychological support – Sudden vision loss is stressful; counseling and peer support help coping and adherence.

Drug treatments

These are the evidence-based medicines most commonly used for SMH due to nAMD/PCV/RAM. Doses below are the labeled/typical intravitreal doses for their approved retinal uses; schedules are customized by your retina specialist (loading→“treat-and-extend”).

1. Ranibizumab (anti-VEGF-A mAb fragment) • 0.5 mg/0.05 mL IVT • often monthly x3 then treat-and-extend • Purpose: shut down leaking new vessels; reduce re-bleed risk • Mechanism: binds VEGF-A • Side effects: eye irritation, floaters, rare infection/IOP rise; very rare arterial thromboembolic events. FDA Access Data

2. Bevacizumab (anti-VEGF-A mAb; off-label in eye) • 1.25 mg/0.05 mL IVT • monthly then extend • Purpose/mechanism as above • Side effects as above (compounded drug; sterility standards matter). (widely used off-label; dose standard in retina literature)

3. Aflibercept (VEGF-trap for VEGF-A/B & PlGF) • 2 mg/0.05 mL IVT • monthly x3 then q8w or extended • Purpose: dries macula, stabilizes CNV • Side effects: similar to other anti-VEGF. RegeneronFDA Access Data

4. Faricimab (bispecific anti-VEGF-A/anti-Ang-2) • 6 mg/0.05 mL IVT • monthly x4 then q8–16w • Purpose: longer durability in many eyes • Side effects: injection-related; monitor for inflammation. FDA Access Datagene.com

5. Brolucizumab (anti-VEGF single-chain antibody) • 6 mg/0.05 mL IVT • monthly x3, then q8–12w • Purpose: intensive drying; caution: small risk of retinal vasculitis/occlusive vasculitis—discuss risk-benefit. Novartis

6. Alteplase (rtPA, “tPA”) intravitreal (fibrinolytic) • ~25–50 µg IVT often with gas + positioning • Purpose: dissolve the clot so gas can push it off the fovea • Mechanism: converts plasminogen→plasmin (clot breakdown) • Side effects: re-bleed, retinal toxicity at high doses, rare endophthalmitis. PMC

7. Alteplase (rtPA) subretinal (during vitrectomy) • ~10–40 µg under the retina • same purpose/mechanism • Side effects: surgical risks + same pharmacologic cautions. PMC

8. Verteporfin (Photodynamic Therapy, “PDT”) (photosensitizer drug + 689-nm laser) • 6 mg/m² IV infusion then timed light • Purpose: close down PCV polyps/CNV especially in PCV or RAM-related bleeding, often combined with anti-VEGF • Side effects: infusion pain, back pain; photosensitivity for 48 h—avoid sun. Lippincott Journals

9. Topical IOP-lowering drops (e.g., timolol, brimonidine) as needed • Purpose: handle pressure spikes after gas/injection • Mechanism: reduce aqueous production/increase outflow • Side effects: drug-specific (e.g., fatigue with beta-blockers).

10. Antibiotic povidone-iodine prep (not a “treatment” for SMH, but standard before injections) • Purpose: lower endophthalmitis risk • Mechanism: strong antisepsis • Side effects: transient irritation.

Note: Intravitreal gas (SF6/C3F8) is a tamponade agent/procedure, not a “drug,” and appears under procedures below. Evidence suggests earlier displacement (<~14 days) and anti-VEGF control of the underlying CNV improve the odds of better vision. Nature

Regenerative / immune / stem-cell” drugs

These are not standard treatments for SMH itself. They aim at the underlying AMD biology and remain investigational:

1. Gene therapy anti-VEGF (e.g., RGX-314) – subretinal or suprachoroidal AAV gene delivering anti-VEGF protein for long-term suppression; clinical trials only; dose/schedule per protocol; goal: reduce injection burden. Retina Today

2. Gene therapy anti-VEGF (e.g., ADVM-022 / Ixo-vec) – intravitreal AAV; trials only; aims similar to above. ScienceDirect

3. RPE cell therapy (embryonic-stem-cell derived patches) – for late AMD/atrophy in trials; not targeted to acute hemorrhage; early safety/feasibility data only. PMC

4. Complement-pathway inhibitors (for GA) – (e.g., pegcetacoplan/avacincaptad) help geographic atrophy progression, not SMH; listed here only to avoid confusion.

5. Neuroprotectives/anti-ferroptosis (preclinical) – targeting iron-driven cell death after bleeds; no approved therapy yet. ScienceDirect

6. “Immune boosters” – There are no immune-strengthening drugs proven to help SMH; avoid unproven products that may thin blood or interact with anticoagulants.

Surgeries / procedures

1. Pars plana vitrectomy (PPV) + subretinal tPA + gas

   • Procedure: remove vitreous gel; inject tPA under the retina to liquefy the clot; fill eye with gas; positioning to shift blood off the fovea.

   • Why: For thick/large bleeds or when office-based techniques fail. Retina Today

2. PPV + intravitreal tPA + gas (no subretinal cannula)

   • Procedure: tPA placed into vitreous (diffuses through retina), gas fill, positioning.

   • Why: Simpler than subretinal cannulation; may work better when hemorrhage is older/thicker. Nature

3. Office pneumatic displacement (no vitrectomy)

   • Procedure: intravitreal expansile gas only (sometimes followed by anti-VEGF shortly after), plus positioning.

   • Why: Minimally invasive option for recent bleeds. JAMA Network

4. Photodynamic therapy (PDT) ± anti-VEGF (especially in PCV/RAM)

   • Procedure: IV verteporfin + laser to shut down culprit vessels.

   • Why: PCV often responds well; reduces re-bleeding. Lippincott Journals

5. Historic submacular clot extraction / macular translocation

   • Procedure: older surgeries to physically remove clot or move the macula.

   • Why not common now: The Submacular Surgery Trial did not show better vision than observation for hemorrhagic AMD; modern care favors anti-VEGF ± tPA/gas. EyeWiki

Risks across procedures: re-bleeding, retinal detachment, RPE tear (especially with large PEDs), infection, pressure spikes. ScienceDirect

Dietary / molecular and other supportive supplements

(These do not dissolve an acute clot. They may support retinal health or AMD care. Only AREDS2 has strong evidence—and only for intermediate AMD to slow progression, not to treat a fresh hemorrhage.)

1. AREDS2 formula (per day): Vit C 500 mg, Vit E 400 IU, Zinc 80 mg (with Copper 2 mg), Lutein 10 mg, Zeaxanthin 2 mg. Mechanism: antioxidant/anti-inflammatory support; benefit: slows AMD progression in the right stages. Talk to your doctor if you smoke or are on blood thinners. nei.nih.gov+1

2. Lutein (10 mg) + Zeaxanthin (2 mg) – carotenoids concentrated in the macula; filter blue light; antioxidant. (Are also in AREDS2.) nei.nih.gov

3. Omega-3s (DHA/EPA ~1 g/day) – heart-healthy; retinal cell membrane support. AREDS2 showed no added AMD benefit when added to the formula, but fish intake is part of healthy diet. nei.nih.gov

4. Saffron (20–30 mg/day) – small studies in early AMD suggest functional gains; evidence is limited.

5. Vitamin D (per deficiency status) – general vascular/immune health; check levels.

6. B-complex (B6/B12/folate) – homocysteine metabolism; avoid excess; can interact with meds.

7. CoQ10 (100–200 mg) – mitochondrial support; limited eye-specific evidence.

8. Alpha-lipoic acid (300–600 mg) – antioxidant; limited macular data.

9. Taurine (500–1,000 mg) – photoreceptor cell health (preclinical/limited clinical).

10. Resveratrol (150–250 mg) – antioxidant; clinical AMD evidence limited.

11. Curcumin (turmeric extract 500–1,000 mg) – anti-inflammatory; may thin blood at high doses.

12. Zinc (if not using full AREDS2 dose) – do not double; excess causes copper deficiency/anemia.

13. Copper (with zinc) – prevents copper-deficiency anemia from zinc.

14. Bilberry/anthocyanins – mixed data; safe in food amounts; supplements may thin blood.

15. Vitamin A/β-carotene – avoid β-carotene if you smoke (lung cancer risk); AREDS2 removed it. nei.nih.gov

Always discuss supplements with your doctor, especially if you take warfarin, DOACs, or antiplatelets—some “natural” products increase bleeding risk.

Prevention tips

1. Don’t smoke (or quit). nei.nih.gov

2. Control blood pressure and cholesterol (helps RAM/PCV risk). PMC

3. Eat Mediterranean-style: leafy greens, colorful veg, nuts, whole grains, fish. nei.nih.gov

4. Use AREDS2 if you have intermediate AMD (per eye doctor). nei.nih.gov

5. Keep diabetes in range (A1c goals personalized).

6. Protect eyes from trauma (sports/tools).

7. Avoid heavy straining; treat constipation/cough. NCBI

8. Monitor with an Amsler grid; call if new waves/blank spots. American Academy of Ophthalmology

9. Take anti-VEGF on schedule if you have wet AMD—reduces recurrence risk.

10. Medication review—never stop anticoagulants on your own; decisions are team-based (retina + cardiology).

When to see a doctor

• Same-day/next-day: sudden central blur, a new dark spot, or new distortion (straight lines look bent).

• Immediately (ER if after hours): sudden vision loss after eye injury; severe eye pain; a curtain/veil (possible detachment).

• Promptly (24–48 h): if you are on blood thinners and notice new central changes; after any procedure if vision worsens.

• Routine but soon: any new Amsler grid changes, new floaters/flashes.

What to eat / what to avoid

Lean into:

1. Leafy greens (spinach, kale, collards) – lutein/zeaxanthin. nei.nih.gov

2. Fatty fish 1–2×/week (salmon, tuna, sardine) – omega-3s. nei.nih.gov

3. Colorful veg & fruit (orange/yellow/reds) – antioxidants.

4. Nuts/legumes – healthy fats and minerals.

5. Whole grains & olive oil – heart-healthy base.

Go easy on / avoid:

1. Highly processed, high-sugar foods – spike vascular risk.
2. Excess salt – pressure control.
3. Excess alcohol – vascular/med interactions.
4. Supplements that thin blood (e.g., high-dose fish oil, ginkgo, high-dose garlic) if you’re on anticoagulants—discuss first.
5. β-carotene supplements if you smoke (lung-cancer risk). nei.nih.gov

FAQs

1. Can a submacular hemorrhage go away on its own?
   Sometimes small/thin bleeds absorb, but waiting too long can harm photoreceptors. Retina specialists often act early to move blood off the fovea. PubMed

2. What’s the time window for best results?
   Sooner is better. Many centers aim to displace within days; outcomes tend to be better when the hemorrhage is <~14 days old. Nature

3. Is gas injection always needed?
   No. Options range from anti-VEGF alone to gas ± tPA, to vitrectomy. The plan depends on size/thickness, cause (nAMD/PCV/RAM), and your overall health. American Academy of Ophthalmology

4. Do anti-VEGF injections cure it?
   They treat the cause (leaky new vessels) and help prevent re-bleeding; the blood itself may still need displacement with gas/tPA if thick or central. American Academy of Ophthalmology

5. Is there a role for surgery?
   Yes for larger/thicker bleeds or failures of office therapy. Modern surgery usually means vitrectomy + tPA + gas, not the old clot-extraction operations. Retina Today

6. Is PDT still used?
   Yes, especially when PCV is the driver—often combined with anti-VEGF. Lippincott Journals

7. How will my head be positioned after gas?
   Your team will tell you; many advise face-down/downward gaze for days, though some analyses favor face-forward. Follow your surgeon’s exact instructions. American Academy of OphthalmologyPMC

8. Can I fly after a gas injection?
   No—do not fly until the gas is completely gone. Also avoid nitrous-oxide anesthesia; both can dangerously raise eye pressure. PubMedRetina Today

9. Will I need many injections later?
   Often yes—anti-VEGF is ongoing for wet AMD/PCV, but intervals may lengthen (treat-and-extend). Regeneron

10. Could this happen again?
    Yes, especially if the underlying CNV/PCV isn’t controlled or if blood pressure is high. Staying on your treatment plan helps. Lippincott Journals

11. Are there vitamins that fix a hemorrhage?
    No vitamin removes a fresh clot. AREDS2 can help slow AMD progression in certain stages; it is not an acute treatment. nei.nih.gov

12. Is bevacizumab (Avastin) safe if it’s off-label?
    It’s widely used by retina specialists; safety depends on sterile compounding and standard injection precautions.

13. What if I’m on warfarin or a DOAC?
    Do not stop on your own. Your retina specialist will coordinate with your cardiologist about risks/benefits for eye procedures.

14. How is the cause confirmed if blood blocks the view?
    OCT shows where the blood sits; ICGA can reveal PCV; OCTA/FA help uncover CNV once blood thins. Lippincott Journals+1

15. What’s the long-term outlook?
    Depends on bleed size/thickness, speed of treatment, and how well the underlying disease is controlled. Early action improves the odds. American Academy 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 12, 2025.

Previous

Ocular Graft-Versus Host Disease (GVHD)

Next

Choroidal Effusions 

Related Articles

Added to wishlistRemoved from wishlist 0

Choroiditis

Added to wishlistRemoved from wishlist 0

Tapetochoroidal Dystrophy

Added to wishlistRemoved from wishlist 0

Choroideremia

Added to wishlistRemoved from wishlist 0

Regional Choroidal Atrophy and Alopecia