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.
Watch the Insight Ophthalmology lecture, then use the companion note below for structured revision and updated clinical interpretation.
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]
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]
How does vitreous haemorrhage occur?
Most causes of vitreous haemorrhage can be understood through four main mechanisms. [1]
Fragile abnormal vessels
Retinal ischaemia → VEGF upregulation → neovascularisation → fragile new vessels → bleeding
The classic example is proliferative diabetic retinopathy (PDR).
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]
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.
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]
- 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.
- 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 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]
- 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.
Terson syndrome refers to intraocular haemorrhage associated with acute intracranial haemorrhage or a sudden rise in intracranial pressure.
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]
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.
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]
Clinical evaluation
Evaluation should answer two questions: What caused the haemorrhage? and is there urgent retinal pathology behind it?
- 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.
Document visual acuity and measure intraocular pressure (IOP).
Look for:
- hyphema;
- iris neovascularisation;
- inflammation;
- surgical or traumatic clues.
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]
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]
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.
What happens to the blood?
Once blood enters the vitreous cavity, it undergoes a gradual process of clot formation, erythrocyte breakdown and clearance. [1]
Because the vitreous is avascular, cellular clearance is relatively slow, and erythrocytes or their breakdown products may persist for prolonged periods. [1]
Chronic vitreous haemorrhage may occasionally be associated with synchysis scintillans or secondary glaucoma due to blood-cell breakdown products.
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.
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]
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.
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 |
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.
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
Do not treat the blood and forget the disease. Clearing the haemorrhage is secondary to identifying and controlling its source.
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]
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]
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]
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.
Take-home points
Related Videos
References
-
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.
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.
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.
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.
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.
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.
Hayreh SS. Pathogenesis of Terson syndrome. Indian J Ophthalmol. 2022;70(12):4130–4137.
doi:10.4103/ijo.IJO_1359_22 -
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






