RETINA COMPANION NOTE

Vitreous Haemorrhage

Types, causes, clinical evaluation and management

Vitreous haemorrhage is a clinical finding, not the final diagnosis. The priority is to identify the source and, particularly in an acute spontaneous haemorrhage, exclude an associated retinal tear or retinal detachment.

Retina Companion Note

Watch the Insight Ophthalmology lecture, then use the companion note below for structured revision and updated clinical interpretation.

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What is vitreous haemorrhage?

Vitreous haemorrhage is the presence of blood within the vitreous cavity. It may produce anything from a few new floaters to profound, painless visual loss depending on the amount, distribution and location of blood. [1]

The vitreous cavity lies behind the lens and is occupied by the normally transparent vitreous gel. Because the vitreous itself is essentially avascular, blood within it originates from neighbouring retinal, choroidal or anterior-segment structures. [1]

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Types of vitreous haemorrhage

Vitreous haemorrhage can be classified according to the anatomical location of the blood.

Type Anatomical location Typical appearance Useful clinical point
Subhyaloid haemorrhage Between the posterior hyaloid and the retinal surface Often sharply demarcated, dome-shaped or boat-shaped, sometimes with a horizontal fluid level Appearance may overlap with sub-ILM haemorrhage. OCT can help identify the anatomical plane. [3]
Sub-ILM haemorrhage Between the retina and the internal limiting membrane (ILM) Frequently well defined and boat-shaped or dome-shaped OCT can demonstrate blood beneath the ILM. A positional shifting test should not be used as a definitive discriminator. [3]
Intravitreal haemorrhage Blood dispersed within the vitreous gel Usually diffuse or irregular rather than forming a sharply defined collection Fresh blood appears red; its appearance changes with erythrocyte degeneration and haemoglobin breakdown. [1]

Premacular haemorrhage may occur in conditions such as Valsalva retinopathy, Terson syndrome and retinal arterial macroaneurysm. [1] [3]

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How does vitreous haemorrhage occur?

Most causes of vitreous haemorrhage can be understood through four main mechanisms. [1]

1

Fragile abnormal vessels

Retinal ischaemia → VEGF upregulation → neovascularisation → fragile new vessels → bleeding

The classic example is proliferative diabetic retinopathy (PDR).

2

Disruption of a normal retinal vessel

Posterior vitreous detachment → vitreoretinal traction → vessel disruption ± retinal tear → vitreous haemorrhage

This mechanism is clinically important because an associated retinal tear may be present. [2]

3

Breakthrough haemorrhage

A large retinal or subretinal haemorrhage may extend through the retina and enter the vitreous cavity.

Examples: retinal arterial macroaneurysm, neovascular AMD and polypoidal choroidal vasculopathy.

4

Trauma or another ocular source

Blunt or penetrating trauma, intraocular surgery or, less commonly, anterior-segment bleeding may allow blood to enter the vitreous cavity.

Important causes of vitreous haemorrhage

The causes are easier to remember when grouped by their underlying mechanism rather than as one long list. [1]

Neovascular / ischaemic
  • Proliferative diabetic retinopathy
  • Retinal vein occlusion with neovascularisation
  • Eales disease
  • Proliferative sickle-cell retinopathy
  • Ocular ischaemic and other proliferative retinal vascular disorders

In these conditions, retinal ischaemia promotes neovascularisation. These newly formed vessels are fragile and may bleed into the vitreous.

PVD and retinal breaks
  • Acute posterior vitreous detachment
  • Retinal tear
  • Associated retinal detachment

Acute vitreoretinal traction may avulse a retinal vessel or create a tractional retinal tear. This group is especially important because an occult retinal break may progress to rhegmatogenous retinal detachment. [2]

Retinal / choroidal bleeding
  • Retinal arterial macroaneurysm
  • Neovascular age-related macular degeneration
  • Polypoidal choroidal vasculopathy

A sufficiently large retinal or subretinal haemorrhage may break through into the vitreous cavity. [1]

Trauma
  • Blunt ocular trauma
  • Penetrating or perforating injury
  • Retinal tear, dialysis or giant retinal tear
  • Choroidal rupture
  • Intraocular foreign body

In traumatic cases, the associated posterior-segment injury may be more important than the vitreous haemorrhage itself.

Other important associations

Terson syndrome refers to intraocular haemorrhage associated with acute intracranial haemorrhage or a sudden rise in intracranial pressure.

Sudden rise in intracranial pressure → pressure transmitted around the optic nerve sheath → impaired retinal venous outflow → retinal venous hypertension → rupture of retinal vessels → intraocular haemorrhage

The haemorrhage may be intraretinal, sub-ILM, subhyaloid or intravitreal. The precise pathogenesis remains debated, but this venous-congestion mechanism is preferred over the older concept of subarachnoid blood simply tracking into the vitreous. [7]

Other less common causes include intraocular surgery, inflammatory disease and systemic haematological or coagulation disorders. [1]

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Important

The diagnosis you must not miss

Acute spontaneous vitreous haemorrhage with a poor fundus view should be considered potentially associated with a retinal tear or retinal detachment until these have been adequately excluded. [2]

In an acute posterior vitreous detachment, the presence of vitreous haemorrhage substantially increases concern for an accompanying retinal break.

Ask specifically about flashes and sudden new floaters.
Ask about a curtain, shadow or visual-field defect.
Examine the peripheral retina carefully whenever the view permits.
If the retina cannot be adequately visualised, perform B-scan ultrasonography.
Arrange appropriate early reassessment if the initial retinal view remains limited.
Poor view ≠ no retinal tear. An obscured fundus should never be assumed to be an uncomplicated vitreous haemorrhage.
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Clinical presentation

Vitreous haemorrhage usually presents with a sudden, painless disturbance of vision. The severity depends mainly on the density and location of the haemorrhage. [1]

Floaters
Patients may notice new spots, cobwebs or mobile shadows, especially with a smaller haemorrhage.
Haze or dark streaks
A moderate haemorrhage may produce hazy vision, dark streaks or a reddish tint to vision.
Reduced visual acuity
Dense blood within the visual axis may cause a marked reduction in visual acuity.
Photopsia
Flashes of light suggest associated vitreoretinal traction, such as an acute posterior vitreous detachment, rather than being caused by the blood itself. [2]
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Clinical evaluation

Evaluation should answer two questions: What caused the haemorrhage? and is there urgent retinal pathology behind it?

History
  • Onset and progression of visual symptoms
  • Flashes, new floaters or a curtain / field defect
  • Recent ocular trauma
  • Diabetes and systemic vascular disease
  • Previous retinal disease or intraocular surgery
  • Anticoagulant or antiplatelet medication
  • Known haematological or coagulation disorder

Anticoagulant use should not be accepted as an explanation that removes the need to identify the ocular source of bleeding.

Visual acuity & IOP

Document visual acuity and measure intraocular pressure (IOP).

Anterior segment

Look for:

  • hyphema;
  • iris neovascularisation;
  • inflammation;
  • surgical or traumatic clues.
Dilated fundus examination

If the view permits, identify the source of bleeding and examine the peripheral retina carefully.

  • Retinal neovascularisation
  • Retinal tear
  • Retinal detachment
  • Retinal vascular occlusion
  • Retinal arterial macroaneurysm
  • Other retinal or choroidal pathology

Scleral depression should be used when clinically appropriate because a causative retinal tear may lie in the far periphery. [2]

Gonioscopy

Perform gonioscopy when angle neovascularisation is suspected, particularly in eyes with an ischaemic retinal vascular disorder.

When the fundus cannot be seen

Dense vitreous haemorrhage may make direct retinal examination impossible. In this situation, B-scan ultrasonography becomes a key investigation. [1]

Retinal detachment
The most important pathology to exclude when the posterior segment cannot be visualised.
Posterior vitreous detachment
B-scan can help demonstrate a detached posterior hyaloid and associated vitreous mobility.
Tractional membranes
Useful when proliferative retinal disease or tractional retinal pathology is suspected.
Mass or trauma-related pathology
Ultrasound may also identify an intraocular mass or traumatic posterior-segment abnormality when clinically relevant.
Clinical Pearl

A retina that cannot be seen is not the same as a retina that is attached. Dense vitreous haemorrhage should not be labelled uncomplicated simply because no retinal tear or detachment is visible clinically.

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What happens to the blood?

Once blood enters the vitreous cavity, it undergoes a gradual process of clot formation, erythrocyte breakdown and clearance. [1]

Vitreous haemorrhage
↓
Clot formation
↓
Erythrocyte degeneration and haemolysis
↓
Dispersion and cellular clearance
↓
Gradual clearing

Because the vitreous is avascular, cellular clearance is relatively slow, and erythrocytes or their breakdown products may persist for prolonged periods. [1]

Long-standing haemorrhage

Chronic vitreous haemorrhage may occasionally be associated with synchysis scintillans or secondary glaucoma due to blood-cell breakdown products.

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Can vitreous haemorrhage cause glaucoma?

Yes. Long-standing intraocular haemorrhage can occasionally produce secondary open-angle glaucoma when blood-cell breakdown products reach and obstruct the trabecular meshwork. [6]

Ghost-cell glaucoma

With long-standing vitreous haemorrhage, erythrocytes lose haemoglobin and become relatively rigid, khaki-coloured ghost cells.

Old vitreous haemorrhage → degenerated RBCs → ghost cells → trabecular obstruction → raised IOP

When these cells gain access to the anterior chamber, they may obstruct aqueous outflow and produce ghost-cell glaucoma. [6]

Haemolytic glaucoma

Following intraocular haemorrhage, erythrocyte breakdown releases haemoglobin. Haemoglobin-containing macrophages and erythrocytic debris may accumulate in the trabecular meshwork and impair aqueous outflow. [6]

Exam Pearl
Ghost-cell glaucoma Degenerated erythrocytes obstruct the trabecular meshwork.
Haemolytic glaucoma Haemoglobin-laden macrophages and erythrocytic debris obstruct outflow.

IOP-lowering therapy is therefore used when raised IOP or secondary glaucoma is actually present; prophylactic anti-glaucoma medication is not routinely required for every vitreous haemorrhage.

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Do Not Confuse

Synchysis scintillans vs asteroid hyalosis

Both can produce multiple reflective vitreous particles, but their composition, behaviour and clinical setting are different.

Feature Synchysis scintillans Asteroid hyalosis
Composition Cholesterol crystals Calcium-lipid deposits
Typical setting Often associated with a chronically diseased eye and may follow long-standing vitreous haemorrhage Commonly an incidental finding in an otherwise stable eye
Mobility Crystals are freely mobile within liquefied vitreous Asteroid bodies remain relatively suspended within the vitreous gel
Effect of gravity Settle inferiorly when the eye becomes still Do not characteristically settle inferiorly
Relationship to vitreous haemorrhage May occur after chronic or old intraocular haemorrhage Not a consequence of vitreous haemorrhage
Exam Pearl

Synchysis scintillans settles with gravity. Asteroid bodies remain suspended within the vitreous.

Management starts with the cause

There is no single treatment for vitreous haemorrhage. Management is directed primarily at the underlying pathology, while also considering the density of haemorrhage, retinal visibility and visual needs. [1]

Observation

Observation may be appropriate when:

  • the retina has been adequately assessed;
  • no retinal tear, retinal detachment or other urgent pathology is present;
  • the underlying cause does not require immediate treatment;
  • spontaneous clearing is reasonably expected.

Head elevation may allow blood to settle inferiorly and can improve the patient's functional superior field of vision, but it does not treat the underlying cause.

Clinical Update

Routine vitamin C has no established role in modern vitreous-haemorrhage management, and prophylactic timolol is not indicated unless raised IOP or secondary glaucoma is actually present.

Treat the retinal cause

Retinal tear
An acute symptomatic tractional retinal tear generally requires prompt retinopexy, usually with laser photocoagulation or cryotherapy, to reduce the risk of retinal detachment. [2]
Neovascular retinal disease
Where haemorrhage results from retinal neovascularisation, treatment must reduce the underlying ischaemic and angiogenic drive. Depending on the disease, this may involve PRP, intravitreal anti-VEGF therapy, vitrectomy, or a combination of these approaches.
Associated retinal detachment
If a retinal detachment is present, management is directed at the detachment itself rather than simply waiting for the vitreous haemorrhage to clear.
Clinical Pearl

Do not treat the blood and forget the disease. Clearing the haemorrhage is secondary to identifying and controlling its source.

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PDR-related vitreous haemorrhage

Proliferative diabetic retinopathy (PDR) is one of the major causes of spontaneous vitreous haemorrhage. Management must address both the haemorrhage obscuring vision and the underlying proliferative retinal disease. [4]

PRP
Panretinal photocoagulation remains an important treatment for proliferative disease when sufficient retina can be visualised and treated. [4]
Anti-VEGF
Intravitreal anti-VEGF therapy can suppress active neovascularisation and is an important component of contemporary PDR management. [4]
Vitrectomy
Pars plana vitrectomy clears the haemorrhage, permits direct retinal assessment and allows endolaser treatment when required. [5]
Modern evidence

DRCR Retina Network Protocol AB compared initial aflibercept with vitrectomy plus PRP for vitreous haemorrhage from PDR. Mean visual acuity over the primary 24-week period was not significantly different between the two initial strategies, although vitrectomy produced faster early visual recovery in many eyes. [5]

Clinical Pearl

PDR-related vitreous haemorrhage does not have one mandatory treatment pathway. The choice between anti-VEGF, PRP and vitrectomy depends on retinal visibility, disease activity, traction and the need for visual rehabilitation.

When is vitrectomy considered?

Pars plana vitrectomy (PPV) clears the haemorrhagic vitreous, allows direct assessment of the retina and permits treatment of associated retinal pathology. The timing depends on the cause, retinal findings and clinical context. [1]

Retinal detachment requiring surgical repair
Significant tractional retinal pathology requiring intervention
Dense vitreous haemorrhage preventing necessary retinal assessment or treatment
Persistent / non-clearing vitreous haemorrhage
Recurrent vitreous haemorrhage
Selected PDR-related haemorrhage where earlier visual rehabilitation or definitive retinal treatment is desirable [4] [5]
Trauma or other associated posterior-segment pathology requiring surgery
Exam Pearl

Traditional cutoff: approximately 6 months

Older examination teaching may quote a non-clearing vitreous haemorrhage persisting for about 6 months as an indication for vitrectomy.

This is an older arbitrary exam cutoff, not a modern universal waiting period. Contemporary surgery may be considered much earlier depending on the underlying cause, retinal status, recurrence, fellow-eye status and the patient's visual requirements.

Historically, the Diabetic Retinopathy Vitrectomy Study compared early vitrectomy with prolonged deferral in severe diabetic vitreous haemorrhage. [8]

A practical approach to vitreous haemorrhage

The first decision is whether the retina can be adequately visualised. From there, management follows the underlying cause.

Vitreous haemorrhage detected
↓
Can the retina be adequately visualised?
YES
Identify the source of bleeding
↓
Look specifically for a retinal break or retinal detachment
↓
Treat the underlying cause
NO
Perform B-scan ultrasonography
↓
Exclude retinal detachment and other significant posterior-segment pathology
↓
Determine the likely cause
↓
Decide between close reassessment and intervention according to clinical risk
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Take-home points

1
Vitreous haemorrhage is a finding, not a diagnosis. Always identify the underlying source of bleeding.
2
Anatomically, haemorrhage may be preretinal / premacular or intravitreal.
3
Major clinically important causes include PDR, acute PVD with or without a retinal tear, and trauma.
4
In acute spontaneous vitreous haemorrhage, always consider an occult retinal tear or retinal detachment.
5
When the fundus cannot be adequately visualised, B-scan ultrasonography is central to evaluation.
6
Long-standing haemorrhage can occasionally cause secondary glaucoma, particularly ghost-cell or haemolytic glaucoma.
7
Management is cause-directed; the aim is not simply to wait for the blood to clear.
8
The traditional 6-month cutoff for non-clearing haemorrhage is useful for examinations, but modern vitrectomy timing is cause- and patient-specific.
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References

  1. 1.

    Shaikh N, Srishti R, Khanum A, et al. Vitreous hemorrhage — causes, diagnosis, and management. Indian J Ophthalmol. 2023;71(1):28–38.

    doi:10.4103/ijo.IJO_928_22
  2. 2.

    American Academy of Ophthalmology Preferred Practice Pattern Retina/Vitreous Committee. Posterior Vitreous Detachment, Retinal Breaks, and Lattice Degeneration Preferred Practice Pattern®. Ophthalmology. 2025;132(4):P163–P196.

    doi:10.1016/j.ophtha.2024.12.023
  3. 3.

    Brar AS, Ramachandran S, Takkar B, Narayanan R, Mandal S, Padhy SK. Characterization of retinal hemorrhages delimited by the internal limiting membrane. Indian J Ophthalmol. 2024;72(Suppl 1):S3–S10.

    doi:10.4103/IJO.IJO_266_23
  4. 4.

    American Academy of Ophthalmology Preferred Practice Pattern Retina/Vitreous Committee. Diabetic Retinopathy Preferred Practice Pattern®. Ophthalmology. 2025;132(4):P75–P162.

    doi:10.1016/j.ophtha.2024.12.020
  5. 5.

    Antoszyk AN, Glassman AR, Beaulieu WT, et al; DRCR Retina Network. Effect of intravitreous aflibercept vs vitrectomy with panretinal photocoagulation on visual acuity in patients with vitreous hemorrhage from proliferative diabetic retinopathy: a randomized clinical trial. JAMA. 2020;324(23):2383–2395.

    doi:10.1001/jama.2020.23027
  6. 6.

    Campbell DG, Simmons RJ, Tolentino FI, McMeel JW. Glaucoma occurring after closed vitrectomy. Am J Ophthalmol. 1977;83(1):63–69.

    doi:10.1016/0002-9394(77)90193-3
  7. 7.

    Hayreh SS. Pathogenesis of Terson syndrome. Indian J Ophthalmol. 2022;70(12):4130–4137.

    doi:10.4103/ijo.IJO_1359_22
  8. 8.

    Diabetic Retinopathy Vitrectomy Study Research Group. Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy: two-year results of a randomized trial. Diabetic Retinopathy Vitrectomy Study Report 2. Arch Ophthalmol. 1985;103(11):1644–1652.

    doi:10.1001/archopht.1985.01050110038020

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