Vitreous Hemorrhage (VH)

Vitreous hemorrhage means bleeding into the vitreous, the clear gel that fills most of the inside of the eye between the lens at the front and the retina at the back. In a healthy eye, this gel is transparent like water, so light can pass through to the retina and you see clearly. When blood leaks into this gel, even in tiny amounts, the gel is no longer fully clear. Light gets blocked or scattered, and vision can suddenly look cloudy, smoky, or full of dark spots (often called floaters).

Vitreous hemorrhage means bleeding into the clear gel (vitreous) that fills the back of your eye. When blood leaks into this gel, it blocks light from reaching the retina, so vision can look foggy, smoky, reddish, full of floaters, or suddenly very dark. VH is a symptom of another problem in or around the retina (for example, a new retinal tear, fragile new blood vessels from diabetic retinopathy, vein blockage, blunt trauma, or a burst small vessel). The first job for the eye doctor is to find and treat the cause and to check urgently that the retina is not torn or detached. If the retina cannot be seen clearly, a B-scan ultrasound helps to look through the blood. Some hemorrhages clear on their own over weeks, but others need laser or surgery (most often pars plana vitrectomy)—especially if the view is blocked, the cause is dangerous, or vision does not improve. EyeWiki

The blood usually comes from retinal blood vessels or fragile new vessels that grow because the retina is not getting enough oxygen (this is called retinal ischemia). Sometimes bleeding happens after traction (pulling) on a normal vessel or after trauma. The blood can be fresh and bright red, clotted and dark, or broken down over time into brownish “dust” that still interferes with vision.

Vitreous hemorrhage is not a diagnosis by itself—it is a sign of an underlying problem such as diabetic eye disease, a retinal tear, retinal vein occlusion, or injury. The goals are to (1) find the cause, (2) look for dangerous problems like a retinal tear or detachment, and (3) treat both the bleeding and the underlying cause to protect vision.

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What happens in the eye

1. A blood vessel breaks or leaks (from disease, traction, or trauma).

2. Blood enters the vitreous gel (or the potential spaces right in front of the retina) and blocks light.

3. Vision drops: you may see floaters, haze, or a curtain.

4. Inflammation and clots form; the blood can contract and stick to the gel.

5. Sticky blood and contracting gel can pull on the retina (traction). That can tear the retina or even cause a retinal detachment, which is an emergency.

6. Over weeks, the body can slowly clear the blood, but if the cause continues (like new fragile vessels in diabetes), rebleeding is common.

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Types of vitreous hemorrhage

Doctors often group bleeding by where it sits, how much there is, and how it started. These “types” help predict symptoms, tests, and treatment.

1. Preretinal (subhyaloid) hemorrhage

   • Where: Between the retina and the posterior hyaloid face (the back “skin” of the vitreous).

   • Look: A boat-shaped, horizontal blood level when you look at the retina; often sharply outlined.

   • Meaning: Common with retinal vein occlusion, diabetic retinopathy, Valsalva retinopathy, and Terson syndrome.

   • Effect: Can severely blur central vision if it sits over the macula.

2. Intravitreal (intragel) hemorrhage

   • Where: Within the vitreous gel itself, mixed like smoke in fog.

   • Look: Diffuse haze and many floaters; the fundus view is often very poor.

   • Meaning: Happens with posterior vitreous detachment (PVD) with a retinal tear, diabetic neovascularization, and trauma.

   • Effect: Vision ranges from mildly hazy to very poor depending on how dense it is.

3. Sub–internal limiting membrane (sub-ILM) hemorrhage

   • Where: Under the ILM (the retina’s innermost “cellophane” layer).

   • Look: A round, sharply bordered dark puddle; can look like a blister of blood.

   • Meaning: Seen in Valsalva retinopathy, blood disorders, or trauma.

   • Effect: May need laser or surgery if it threatens the macula or fails to clear.

4. Mixed-type hemorrhage

   • Where: Combination of preretinal + intravitreal + sub-ILM blood.

   • Meaning: Common in severe diabetic eye disease or major trauma.

   • Effect: Often more severe symptoms and slower natural clearing.

5. By timing

   • Acute (hours to days): fresh red blood, sudden floaters, haze.

   • Subacute (days to weeks): clotting, color darkens, vision may slowly improve.

   • Chronic/recurrent (weeks to months): repeated bleeds, brown “hemosiderin dust,” risk of traction and scar (fibrovascular) membranes.

6. By severity

   • Mild: a few floaters, partial fundus view.

   • Moderate: significant haze, hard to see the retina.

   • Severe/dense: no fundus view; must rely on ultrasound.

7. By cause

   • Tractional/ischemic (e.g., diabetic neovascularization)

   • Tear-related (e.g., PVD with retinal break)

   • Pressure-related (e.g., Valsalva, Terson)

   • Traumatic (blunt or penetrating injury)

   • Vascular occlusion–related (e.g., CRVO/BRVO)

   • Medication/bleeding diathesis–related (e.g., anticoagulants, low platelets)

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Common causes

1. Proliferative diabetic retinopathy (PDR)
   High sugar damages retinal vessels → retina becomes oxygen-starved → eye grows fragile new vessels that bleed easily into the vitreous.

2. Posterior vitreous detachment (PVD) with retinal tear
   The vitreous gel separates from the retina with age; if it pulls too hard, it can tear the retina and rip a vessel, causing bleeding.

3. Retinal vein occlusion (CRVO/BRVO)
   A blocked retinal vein raises pressure in retinal capillaries → leakage and hemorrhage; fragile collateral vessels may bleed into vitreous.

4. Blunt ocular trauma
   A hit to the eye or head shakes the gel and tears vessels; can also tear the retina, cause angle recession, or lead to retinal detachment.

5. Penetrating injury / intraocular foreign body (IOFB)
   A sharp object or metal fragment enters the eye, directly injuring retinal vessels and causing bleeding; often a surgical emergency.

6. Valsalva retinopathy
   Heavy lifting, coughing, vomiting, or straining suddenly raises venous pressure → burst superficial retinal vessels, often sub-ILM/subhyaloid blood.

7. Terson syndrome
   Intracranial hemorrhage (like subarachnoid bleed) causes a sudden spike in venous pressure transmitted to the eye → vitreous/preretinal bleeding.

8. Retinal arterial macroaneurysm rupture
   An outpouching of a retinal artery in older adults (often with hypertension) can burst → multilayered retinal and vitreous bleeding.

9. Sickle cell retinopathy
   Sickled red cells block small vessels, causing peripheral ischemia and sea-fan neovascularization that bleeds into vitreous.

10. Eales disease (idiopathic retinal vasculitis)
    Inflammation and occlusion of peripheral retinal vessels lead to neovascularization and repeated vitreous hemorrhages (often in young adults).

11. Ocular ischemic syndrome
    Severe carotid artery narrowing → poor blood flow to the eye → retinal ischemia → fragile new vessels that bleed.

12. Retinopathy of prematurity (advanced stages)
    Abnormal vessel growth in premature infants can bleed and form fibrovascular membranes that contract and bleed again.

13. Neovascularization from chronic retinal detachment
    Long-standing detachment drives ischemia and new, weak vessels that can bleed into the vitreous.

14. Age-related lattice degeneration with atrophic holes/tears
    Thinned peripheral retina (lattice) is prone to tears; torn edges bleed, especially during acute PVD.

15. High myopia (pathologic myopia)
    A very long eyeball stretches tissues; lacquer cracks, posterior staphyloma, and fragile vessels can bleed, sometimes reaching the vitreous.

16. Inflammatory chorioretinitis (e.g., toxoplasmosis)
    Inflammation damages retinal vessels; leaky fragile vessels can bleed; inflammation also clouds the vitreous.

17. Leukemia and other blood dyscrasias
    Abnormal platelets or very high white cells cause retinal hemorrhages that may break through into the vitreous.

18. Anticoagulant or antiplatelet medications (e.g., warfarin, DOACs, aspirin, clopidogrel)
    These reduce clotting; fragile retinal vessels or minor traction can bleed more easily and longer.

19. Severe hypertension
    High pressure damages small retinal vessels → leakage and hemorrhage that can sometimes track into the vitreous.

20. Post-operative bleeding (after cataract surgery, vitrectomy, or retinal laser)
    Surgical manipulation or new vessels can bleed shortly after or weeks later (called delayed postoperative hemorrhage).

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Symptoms

1. Sudden floaters
   Dark spots, cobwebs, or strings that move as the eye moves—these are clumps of blood and tiny particles in the gel.

2. Vision haze or smoke
   The world looks like looking through fog or smoke; fresh blood scatters light strongly.

3. Blurry or dim vision
   Less light reaches the retina; fine detail and contrast drop.

4. Dark curtain or shadow
   A fixed dark area may mean dense hemorrhage or, more urgently, a retinal detachment—this needs urgent care.

5. Red or brown tint
   Some people notice a reddish hue or brownish haze, especially in bright light.

6. Photopsia (flashes of light)
   Flashes suggest vitreoretinal traction; often seen with PVD and retinal tears.

7. Increase of floaters over hours or days
   More spots can appear as bleeding continues or clots break up.

8. Worse vision in the morning
   Blood can settle overnight; as you sit up and move, vision may slightly improve.

9. Better vision in one head position
   Tilting the head can sometimes move pooled blood away from the center.

10. Reduced contrast sensitivity
    Whites look gray, and reading low-contrast prints is hard.

11. Glare and light sensitivity
    Stray light from blood particles increases glare and photophobia.

12. Monocular symptoms
    Usually affects one eye at first; compare eyes by alternately covering each eye.

13. No pain (usually)
    Most vitreous hemorrhages are painless. Pain suggests trauma, high pressure, or inflammation.

14. New floaters after a hit or strain
    A clear link to trauma or Valsalva maneuver points to the cause.

15. Recurring episodes
    Repeat bleeds hint at an ongoing source like diabetic neovascularization.

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Diagnostic tests

A) Physical exam

1. Visual acuity (distance and near)
   Reading letters on a chart shows how much the hemorrhage blocks vision. Tracking changes over time helps monitor clearing or rebleeding.

2. Pupil exam with swinging flashlight test
   Checks for relative afferent pupillary defect (RAPD). An RAPD can signal significant retinal damage or optic nerve involvement, not just blocked light.

3. Intraocular pressure (IOP) measurement (tonometry)
   Measures eye pressure. High pressure may occur with ghost-cell glaucoma or neovascular glaucoma; low pressure can follow trauma or retinal detachment.

4. External and anterior segment inspection
   Looks for eyelid lacerations, hyphema (blood in the front chamber), inflammation, lens issues—clues to trauma or surgical causes.

5. Confrontation visual fields
   A quick bedside test for missing areas (scotomas). A peripheral field loss may suggest retinal detachment beyond what can be seen through blood.

B) Manual office tests

6. Slit-lamp biomicroscopy with dilation (78D/90D lens)
   A microscope view of the anterior vitreous and central retina. Detects sub-hyaloid pools, sub-ILM bleeds, and signs of neovascularization near the optic disc.

7. Indirect ophthalmoscopy (with scleral depression when safe)
   A wide-field look at the peripheral retina for tears, holes, lattice degeneration, and traction. Scleral depression helps find small breaks that cause bleeding.

8. Gonioscopy
   A mirrored contact lens shows the drainage angle. Finds angle recession (after blunt trauma) and angle neovascularization, which can raise eye pressure.

9. Amsler grid
   A simple check of central vision and metamorphopsia. Persistent central distortion after clearing may point to macular disease under or after the bleed.

C) Laboratory and pathological tests

10. Complete blood count (CBC)
    Looks for anemia and platelet count. Low platelets increase bleeding risk; very high white cells (e.g., leukemia) can cause retinal hemorrhages.

11. Coagulation profile (PT/INR, aPTT)
    Checks clotting ability. High INR (e.g., on warfarin) or coagulation disorders make bleeding more likely and slower to stop.

12. Blood glucose and HbA1c
    Confirms diabetes control. Poor control increases risk of neovascularization and recurrent vitreous hemorrhage.

13. Sickle cell screen / hemoglobin electrophoresis
    Detects sickle cell disease or trait in relevant patients. Guides retinal laser decisions and overall risk management.

14. Inflammation/autoimmune work-up (ESR, CRP; ANA/ANCA when indicated)
    Looks for vasculitis or systemic inflammatory disease that can inflame retinal vessels and trigger bleeding.

D) Electrodiagnostic tests

15. Electroretinography (ERG)
    Measures retinal electrical responses. Helps judge retinal function when blood blocks the view—for example, to plan surgery if the retina may be very weak.

16. Visual evoked potentials (VEP)
    Measures signal from eye to brain. Useful when vision is poor but we need to know if the visual pathway is intact beyond the hemorrhage.

E) Imaging tests

17. B-scan ocular ultrasonography
    Key test when the fundus cannot be seen. Ultrasound can detect retinal detachment, large tears, vitreous traction, intraocular foreign bodies, and the amount and location of blood.

18. Optical coherence tomography (OCT) and OCT-angiography (OCT-A)
    OCT shows retinal layers, sub-ILM pockets, and macular edema. OCT-A can map capillary nonperfusion and neovascularization once media clarity improves.

19. Fluorescein angiography (FA)
    Dye test to highlight leaks, ischemia, microaneurysms, and new vessels. Often performed after partial clearing to plan laser treatment.

20. CT or MRI of orbits/brain (selected cases)
    CT is useful in trauma to find foreign bodies or fractures. MRI assesses soft tissues and optic nerve (avoid MRI if metal IOFB is suspected). In Terson syndrome, brain imaging looks for intracranial hemorrhage.

Non-pharmacological treatments (therapies & “other” measures)

Below are practical, medicine-free steps used alongside medical/surgical care. Each item includes description, purpose, and mechanism in plain English.

1. Urgent dilated eye exam and ultrasound (B-scan)
   What: Full pupil dilation and, if needed, ultrasound imaging.
   Purpose: Make sure there’s no retinal tear or detachment and look for the cause of bleeding.
   How it helps: Finds problems hidden behind the clouded vitreous so the right treatment (laser/surgery) can be done in time. EyeWiki

2. Watchful waiting (short, cautious observation)
   What: Give mild VH a little time to settle if the retina is safe.
   Purpose: Some bleeds clear by themselves; avoiding unnecessary procedures.
   How it helps: Blood clots slowly break down and the eye clears naturally (roughly ~1% absorption per day is often cited in classic literature). EyeWiki

3. Head-of-bed elevation during rest
   What: Sleep with the head up 30–45°.
   Purpose: Let gravity pull blood away from the central vision.
   How it helps: May reduce morning blur when blood settles over the macula overnight. EyeWiki

4. Retinal detachment precautions
   What: Learn warning signs—new flashes, a shower of floaters, a curtain/shadow.
   Purpose: Get immediate help if detachment starts.
   How it helps: Early repair saves sight. EyeWiki

5. Activity modification (avoid heavy straining / Valsalva)
   What: Avoid heavy lifting, forceful coughing, constipation straining (use stool-softening diet), and strenuous exercise until cleared.
   Purpose: Reduce pressure spikes that can re-bleed fragile vessels.
   How it helps: Lower mechanical stress on fragile retinal neovessels or tears. EyeWiki

6. Protective eye shield for recent trauma
   What: Rigid shield after eye injury or post-op as instructed.
   Purpose: Prevent accidental pressure or further injury.
   How it helps: Guards the healing eye while the cause is treated. EyeWiki

7. Systemic blood pressure and glucose control
   What: Tight but safe control with your primary doctor/endocrinologist.
   Purpose: Reduce ongoing ischemia and new fragile vessels in diabetic retinopathy or vein occlusion; lower re-bleed risk.
   How it helps: Stabilizes blood vessels and slows disease driving VH. EyeWikiAmerican Academy of Ophthalmology

8. Smoking cessation
   What: Stop smoking; seek formal cessation help.
   Purpose: Improve microvascular health and oxygen delivery to retina.
   How it helps: Less ischemia → less drive for abnormal vessel growth. EyeWiki

9. Regular follow-up schedule
   What: Frequent checks until the view clears or surgery is done.
   Purpose: Catch hidden retinal tears or early detachment.
   How it helps: Timely intervention if things worsen. EyeWiki

10. Optimize anticoagulation with the prescribing physician (do not self-stop)
    What: Discuss risks/benefits of blood thinners with the doctor who prescribed them.
    Purpose: Balance clotting/bleeding safely; usually do not stop solely to clear VH.
    How it helps: EyeWiki and ETDRS show aspirin didn’t increase VH risk; indiscriminate stopping can be dangerous. EyeWiki

11. Treat sleep apnea if present
    What: Evaluation for OSA and use of CPAP when indicated.
    Purpose: Reduce hypoxic spikes that can drive neovascularization.
    How it helps: Better oxygenation → lower VEGF drive over time. (Supportive vascular risk factor control principle.) EyeWiki

12. Glycemic index diet patterns (part of systemic control)
    What: Steady-carb meals, fiber, and balanced diet.
    Purpose: Fewer glucose swings that damage retinal capillaries.
    How it helps: Supports long-term diabetic eye stability with medical care. American Academy of Ophthalmology

13. Fall prevention & home safety
    What: Improve lighting, remove trip hazards.
    Purpose: Reduce new ocular trauma that could trigger hemorrhage.
    How it helps: Trauma is a common cause of VH in younger people. EyeWiki

14. Prompt treatment of retinal tears (office laser/cryotherapy)
    What: If a tear is found, seal it early.
    Purpose: Prevent detachment and further bleeding.
    How it helps: Laser “spot-welds” the retina. EyeWiki

15. Education about the fellow eye
    What: The other eye often gives clues; keep both eyes monitored.
    Purpose: Catch symmetric/asymmetric disease early.
    How it helps: Improves diagnosis and timing of treatment. EyeWiki

16. Avoid high-risk contact sports or wear proper eye protection
    What: Goggles/face shields as recommended.
    Purpose: Prevent re-injury.
    How it helps: Reduces new bleeds from blunt trauma. EyeWiki

17. Manage anemia or platelet problems with your medical team
    What: Hematology workup if blood disorders suspected.
    Purpose: Correct systemic contributors to bleeding.
    How it helps: Low platelets or clotting disorders can worsen VH. EyeWiki

18. Sun/light comfort strategies
    What: Sunglasses/hat for glare from red blood-tinged vision.
    Purpose: Comfort and safety outdoors.
    How it helps: Reduces photophobia and improves function while healing. (Supportive.)

19. Driving and work safety adjustments
    What: Avoid driving until vision is stable and legally safe; adjust job tasks that need sharp depth perception.
    Purpose: Prevent accidents while vision is hazy.
    How it helps: Safety during recovery.

20. Psychological support
    What: Counseling/reassurance about temporary vision loss.
    Purpose: Reduce anxiety; improve adherence to follow-up and rehab.
    How it helps: Better coping and outcomes.

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Drug treatments

Important: No pill or drop “dissolves” vitreous blood. Medicines are used to treat the cause (e.g., fragile new vessels), prepare for surgery, control complications (e.g., high eye pressure), or treat inflammation. Dosages below are typical; doctors tailor them to you.

1. Bevacizumab (anti-VEGF), intravitreal 1.25 mg/0.05 mL
   Class: Monoclonal antibody to VEGF. When: Before vitrectomy in PDR (1–7 days), or for neovascular AMD-related VH.
   Purpose/Mechanism: Shrinks abnormal vessels, reduces leakage/bleeding.
   Side effects: Rare infection (endophthalmitis), pressure rise, inflammation. Evidence: widely used; timing around surgery varies by surgeon. EyeWiki

2. Ranibizumab (anti-VEGF), 0.5 mg/0.05 mL intravitreal
   As above; labeled for ocular neovascular diseases; used similarly. Side effects as above. EyeWiki

3. Aflibercept (anti-VEGF decoy), 2 mg/0.05 mL intravitreal
   Binds VEGF-A/B and PlGF; used for AMD/PDR complications with similar goals and risks. EyeWiki

4. Triamcinolone acetonide (intravitreal), 2–4 mg
   Class: Corticosteroid. When: Inflammatory causes or as adjunct (e.g., with surgery).
   Purpose: Reduce inflammation and vascular permeability.
   Side effects: Cataract acceleration, intraocular pressure (IOP) rise, infection risk. EyeWiki

5. Dexamethasone intravitreal implant (0.7 mg)
   Longer-acting steroid implant for inflammation/edema control in selected cases. Same steroid risks. EyeWiki

6. Timolol ophthalmic 0.25–0.5% (1 drop BID)
   Class: Beta-blocker drop. When: Secondary IOP rise (e.g., ghost-cell glaucoma from VH).
   Purpose: Lowers aqueous production → lowers pressure.
   Side effects: Slow heart rate, bronchospasm (systemic absorption in sensitive patients). (Standard glaucoma management principle.)

7. Brimonidine 0.2% (1 drop TID)
   Class: Alpha-2 agonist drop. Purpose: Additional IOP lowering.
   Side effects: Dry mouth, fatigue, allergy. (Glaucoma management principle.)

8. Dorzolamide 2% (1 drop TID)
   Class: Topical carbonic anhydrase inhibitor. Purpose: More IOP reduction if needed.
   Side effects: Stinging, bitter taste, rare sulfa-related issues. (Glaucoma management principle.)

9. Acetazolamide 250 mg PO QID or 500 mg SR BID (short term)
   Class: Oral carbonic anhydrase inhibitor. Purpose: Temporarily lower high IOP until definitive care.
   Side effects: Tingling, fatigue, GI upset, kidney stone risk; avoid in sulfa allergy. (Glaucoma/IOP management principle.)

10. Analgesic choice: Acetaminophen (paracetamol) as needed; avoid nonessential NSAIDs unless prescriber approves
    Purpose: Pain relief without extra bleed risk.
    Note: ETDRS found aspirin did not raise VH risk, but many clinicians still prefer acetaminophen for short-term comfort to avoid confounders. Always follow your doctor’s plan, especially if you’re on antiplatelets. EyeWiki

Studies in diabetic post-vitrectomy eyes are mixed (some trials show no clear benefit, some small/abstract data suggest possible reduction of early rebleeds). Routine use for VH is not standard; discuss in specialized settings only. PMCtransfusionevidencelibrary.comeuretina.orgPentaVision

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Dietary “molecular” supplements

No supplement clears existing VH. These may support overall retinal and vascular health when used appropriately with medical care. Always check for drug–supplement interactions (bleeding risk with some herbs; effect on anticoagulants).

1. Lutein (10 mg/day) & Zeaxanthin (2 mg/day)
   Function/mechanism: Carotenoids concentrate in macula as antioxidants; general retinal support. (Evidence mostly from AMD; supportive, not VH treatment.)

2. Omega-3 DHA/EPA (≈1 g/day)
   Function: Anti-inflammatory effects on microvasculature; may support vascular health.

3. Vitamin C (≈500 mg/day)
   Function: Antioxidant; supports collagen and vessel integrity; avoid very high doses without guidance.

4. Zinc (25–40 mg elemental/day, short courses unless deficient)
   Function: Cofactor in antioxidant enzymes; long-term high doses can cause copper deficiency—use prudently.

5. Vitamin D (dose to blood level, often 1000–2000 IU/day)
   Function: Immune modulation and vascular health support; correct deficiency.

6. B-complex (esp. B12/folate if low)
   Function: Lowers homocysteine when deficient; supports neuroretinal metabolism.

7. Magnesium (200–400 mg/day as tolerated)
   Function: Vascular tone and metabolic support; adjust for kidney function.

8. Anthocyanin-rich bilberry/blueberry extracts (standardized)
   Function: Antioxidant/vasoactive polyphenols; evidence limited; avoid if on strong anticoagulation without clearance.

9. CoQ10 (100–200 mg/day)
   Function: Mitochondrial support, antioxidant; limited ocular evidence but generally safe.

10. Curcumin (absorption-enhanced forms, 500–1000 mg/day)
    Function: Anti-inflammatory; can interact with anticoagulants—ask prescriber first.

(Again: these are supportive for general eye/vascular wellness, not proven treatments for VH.)

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Regenerative / stem cell” drugs

There are no approved stem-cell or “immunity booster” drugs to treat vitreous hemorrhage. Stem-cell approaches (e.g., retinal pigment epithelium or photoreceptor cell therapies) are experimental for certain degenerative retinal diseases and not used to clear VH. For VH, outcomes depend on fixing the cause (retinal tears, neovascularization from diabetes/vein occlusion, AMD, trauma). Offering “stem cell drugs” for VH outside clinical trials is not evidence-based and can be harmful. Safer, proven options are anti-VEGF, laser, and vitrectomy as indicated. EyeWikiAmerican Academy of Ophthalmology

If you’re interested in cutting-edge care, ask your retina specialist about registered clinical trials for your underlying disease—not for VH itself.

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Surgeries/procedures

1. Pars plana vitrectomy (PPV)
   What: Microsurgery to remove the blood-filled vitreous, relieve traction, repair tears, and apply endolaser to the retina. Gas/air may be added at the end.
   Why: Non-clearing VH, suspected/confirmed retinal tear or detachment, dense VH of unknown cause, or VH with iris/angle neovascularization or ghost-cell glaucoma. It both diagnoses and treats the problem when the view is blocked. EyeWiki

2. Panretinal photocoagulation (PRP) laser
   What: Many small laser burns in the peripheral retina to treat proliferative diabetic retinopathy or ischemic vein occlusion.
   Why: Shrinks abnormal new vessels and reduces future bleeding risk; often combined with vitrectomy if the view was blocked. PRP remains a core therapy for PDR. American Academy of OphthalmologyAAO Journal

3. Focal laser/cryotherapy to retinal tears
   What: Laser “spot-welds” or cryo freezes around a tear.
   Why: Seal the tear to prevent detachment and stop bleeding from that site when visible. EyeWiki

4. Nd:YAG hyaloidotomy (a.k.a. membranotomy) for premacular subhyaloid hemorrhage
   What: A clinic laser creates a small opening in the thin membrane over a pocket of blood so it drains into the vitreous, away from the macula.
   Why: Speeds clearing when a large premacular (subhyaloid) pool blocks central vision—e.g., Valsalva retinopathy or some macroaneurysms—especially if done early. Evidence shows high success in selected cases. PMC+1NatureJAMA Network

5. Endolaser during vitrectomy
   What: Laser delivered from inside the eye during PPV.
   Why: Treats neovascularization/tears once blood is removed and the retina is clearly visible; often part of PPV for diabetic VH. EyeWiki

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Preventions

1. Control diabetes carefully (A1c target individualized).

2. Treat high blood pressure to target with your doctor.

3. Quit smoking (formal cessation program).

4. Eye protection during risky work/sports.

5. Know warning signs (flashes, floaters burst, curtain) and seek urgent care.

6. Keep regular dilated exams, especially if you have diabetes or vein occlusion.

7. Manage anticoagulants only with prescriber guidance—do not self-stop.

8. Treat sleep apnea if present (CPAP).

9. Heart-healthy diet and exercise (as cleared by your doctors).

10. Prompt treatment of retinal tears/holes when found. EyeWikiAmerican Academy of Ophthalmology

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When to see a doctor

• Immediately (same day / emergency): Sudden burst of floaters, flashes, a dark curtain or shadow, serious eye trauma, or pain with major vision loss. These can signal a retinal tear or detachment, which needs urgent treatment. EyeWiki

• Soon (within days): New foggy/red-brown haze, slower-onset floaters, or decreased vision without pain.

• Ongoing: If you have diabetes/retinal vein occlusion/AMD, keep scheduled visits—even if vision seems okay.

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What to eat” and “what to avoid

What to eat (supportive):

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

2. Oily fish 2–3×/week (salmon/sardine: omega-3).

3. Citrus & berries (vitamin C/anthocyanins).

4. Colorful vegetables (carotenoids/antioxidants).

5. Nuts & seeds (vitamin E, minerals).
   Why: General retinal and vascular support; helps systemic control (diabetes, BP). American Academy of Ophthalmology

What to limit/avoid (safety):

1. Excess added sugars/refined carbs (worsen glucose).
2. Excess salt (worsens BP).
3. Heavy alcohol (vascular stress, falls).
4. High-dose unneeded supplements that increase bleeding risk (e.g., large doses of vitamin E, ginkgo, garlic capsules) unless your prescriber agrees
5. 10) Nonessential NSAIDs for pain if alternatives exist (follow prescriber, especially if you’re on antiplatelets/anticoagulants). (ETDRS: aspirin didn’t raise VH risk, but coordination with your doctors is essential.) EyeWiki

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 FAQs

1) Can vitreous hemorrhage go away on its own?
Sometimes yes—small bleeds can clear over weeks. Larger/dense bleeds or those from dangerous causes often need laser or surgery. EyeWiki

2) How do I know if it’s an emergency?
If you see flashes, many new floaters, or a dark curtain, or had eye trauma, seek urgent care—these can mean a retinal tear/detachment. EyeWiki

3) Will eye drops or pills dissolve the blood?
No. Drops/pills don’t dissolve vitreous blood. Treatment focuses on fixing the cause and letting the eye clear naturally or with vitrectomy. EyeWiki

4) Do anti-VEGF injections help?
Yes—for VH from neovascular diseases (diabetic retinopathy, AMD) and often around vitrectomy timing. They shrink fragile vessels and reduce leakage, but they do not instantly remove blood already present. EyeWiki

5) Is panretinal photocoagulation (PRP) still important?
Yes. PRP remains a cornerstone for proliferative diabetic retinopathy to prevent new bleeding and complications. American Academy of OphthalmologyAAO Journal

6) What if the doctor can’t see my retina because of the blood?
They use ultrasound to check for tears/detachment. If it’s not clearing quickly or the cause is worrisome, they may do vitrectomy to treat and to see inside. EyeWiki

7) Are blood thinners always the cause? Should I stop them?
Not necessarily. Classic evidence shows aspirin didn’t increase VH risk; do not stop anticoagulants/antiplatelets without your prescriber’s plan—stopping can be dangerous. EyeWiki

8) Can a laser in the clinic help if the blood sits under a membrane in front of the macula?
Yes, in selected premacular (subhyaloid) hemorrhages, a Nd:YAG hyaloidotomy can drain the blood into the vitreous and speed recovery. It’s case-by-case. PMCNature

9) Is vitrectomy safe?
Modern PPV is common and often very effective, especially for non-clearing VH, but like any surgery it has risks (infection, cataract, retinal detachment). Your surgeon explains your risk–benefit. EyeWiki

10) Will I get VH again after surgery?
Early rebleeds can occur in diabetic eyes; surgeons may use techniques (endolaser, careful tissue handling). Medications like TXA have mixed evidence and are not routine. PMCtransfusionevidencelibrary.com

11) How long until I can drive/work?
Only when vision meets legal and safety needs and your surgeon clears you. Depth perception can be off during healing.

12) Can pressure in the eye go up because of VH?
Yes—ghost-cell glaucoma and inflammation can raise IOP. Pressure-lowering drops or oral medicines may be used temporarily. (Glaucoma management principle.)

13) Does diet matter?
Diet supports overall vascular health and diabetic/BP control but doesn’t clear blood. A heart-healthy pattern with leafy greens and fish helps the long game. American Academy of Ophthalmology

14) What if my VH is from trauma?
You’ll likely use eye protection, limit activity, and may need surgery if there’s a tear, detachment, or foreign body. Follow-up is crucial. EyeWiki

15) What’s the long-term outlook?
It depends on the cause and whether the macula and optic nerve are healthy. VH from PVD/tear that’s treated promptly often does well; VH from advanced diabetic retinopathy or AMD can have a more guarded prognosis. EyeWiki

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

Last Updated: August 30, 2025.