Vitreous Haemorrhage

Definition

Causes

Clinical Features

Symptoms

• Mild VH: sudden-onset floaters and diffuse visual blurring; visual acuity may be preserved
• Dense VH: severe visual loss (vision may be reduced to light perception)
• Patients often describe red or dark haze, "cobwebs," or a "blood-red" curtain

Signs

• Red reflex is reduced or absent
• Fundus view is partially or completely obscured
• In trauma/PVD context, "tobacco dust" (pigment cells — Shafer's sign) in the anterior vitreous indicates probable retinal break

Investigations

B-scan Ultrasonography ⚠️ Mandatory with dense VH

• Non-clotted VH: uniform appearance on B-scan
• As cellular aggregates form: small particulate echoes
• Critical to exclude retinal tear or detachment and choroidal melanoma when the fundus cannot be visualised

Tip: Always perform B-scan ultrasonography when a dense vitreous haemorrhage prevents fundal view — to exclude retinal detachment or choroidal melanoma. — Kanski's Clinical Ophthalmology, 10th ed.

Fundus Appearance

Management

Conservative

• Many cases (e.g., Terson syndrome, mild PVD-related) resolve spontaneously within weeks to months
• Head elevation / bed rest: promotes gravitational settling of blood inferiorly
• Avoid anticoagulants/aspirin where possible
• Control systemic disease (e.g., blood glucose, blood pressure)

Medical / Laser

• Panretinal photocoagulation (PRP): for underlying proliferative retinopathy once media clears
• Intravitreal anti-VEGF (e.g., aflibercept): an alternative to early vitrectomy for PDR-related VH. DRCR.net Protocol AB showed that vitrectomy + PRP achieves faster visual recovery than initial aflibercept, but 2-year visual outcomes are similar — either is a reasonable first-line approach
• Nd:YAG laser hyaloidotomy: for persistent premacular (retrohyaloid) haemorrhage — disperses blood into the vitreous cavity for faster absorption

Surgical — Pars Plana Vitrectomy (PPV)

1. Severe persistent VH that precludes adequate PRP (most common indication)
2. In type 1 diabetics (absent rubeosis): traditionally considered after 3 months; earlier surgery may improve outcomes
3. Bilateral VH
4. VH with tractional retinal detachment threatening the macula — treat urgently
5. Combined tractional + rhegmatogenous RD — treat urgently
6. Dense premacular retrohyaloid haemorrhage (risk of ERM / tractional macular detachment)
7. VH with concurrent retinal detachment

Special Scenarios

Terson Syndrome

• Intraocular haemorrhage + subarachnoid haemorrhage (usually ruptured anterior communicating artery aneurysm)
• Haemorrhage is typically bilateral, usually intraretinal/preretinal; may break into vitreous
• Mechanism: retinal venous stasis from elevated cavernous sinus pressure
• Most resolve spontaneously; early vitrectomy in selected cases

Traumatic VH

• Often associated with PVD; pigment cells in anterior vitreous (tobacco dust) warrant urgent peripheral retinal examination
• Chorioretinitis sclopetaria (high-velocity projectile near globe) may cause VH ± retinal detachment

Proliferative Diabetic Retinopathy (PDR)

• Most common cause of VH requiring vitrectomy
• Vitrectomy combined with extensive endolaser PRP
• Anti-VEGF pre-treatment can reduce intraoperative bleeding

Prognosis

• Depends heavily on the underlying cause and presence of complications (retinal detachment, neovascular glaucoma)
• Spontaneous absorption is common in non-proliferative causes
• PDR-related VH carries a guarded prognosis without treatment; good outcomes with timely vitrectomy + PRP
• Terson syndrome: long-term visual prognosis is generally good

Vitreous Haemorrhage — 20-Mark Answer

Definition (1 mark)

Anatomy & Pathophysiological Basis (2 marks)

• The ora serrata anteriorly
• The optic nerve head posteriorly
• Along the major retinal vessels

Aetiology (3 marks)

Paediatric note: In infancy and childhood, consider birth trauma, non-accidental injury (shaken baby), congenital X-linked retinoschisis, pars planitis, and bleeding dyscrasias.

Clinical Features (3 marks)

Symptoms

• Sudden, painless loss of vision
• Sudden appearance of floaters, cobwebs, black spots, or a red/dark haze
• Dense VH: severe visual loss down to light perception

Signs

• Reduced or absent red fundus reflex
• Partial/total obscuration of fundus view
• Red blood cells visible in anterior vitreous on slit-lamp
• Chronic VH: yellow-ochre appearance (haemoglobin breakdown)

• Mild RAPD may be present with dense haemorrhage
• "Tobacco dust" (Shafer's sign) — pigment cells in anterior vitreous — indicates likely retinal break
• Dependent layering of blood inferiorly
• Iris neovascularisation (rubeosis) in PDR

Fundus photograph: vitreous and preretinal haemorrhage from PDR — Wills Eye Manual

Differential Diagnosis (1 mark)

• Vitritis (uveitis): WBCs, not RBCs; not sudden onset
• Retinal detachment without VH: similar visual symptoms
• Vitreous amyloidosis: glass-wool opacities, bilateral, systemic history
• Asteroid hyalosis: calcium pyrophosphate deposits — not true haemorrhage; moves with vitreous but does not sediment

Investigations / Workup (3 marks)

1. History

• Systemic disease: diabetes, hypertension, sickle cell, bleeding disorder
• Trauma, recent surgery, headache (Terson)
• Prior episodes, anticoagulant use

2. Ocular Examination

• Slit-lamp (undilated): look for iris neovascularisation, anterior chamber red cells
• IOP measurement (ghost cell glaucoma risk)
• Dilated fundus examination (indirect ophthalmoscopy ± scleral depression)
• Examine contralateral eye — may give clues to the diagnosis (e.g., diabetic changes, AMD, sickle cell "sea fan" neovascularisation)

3. B-scan Ultrasonography ⚠️ Mandatory when fundus is obscured

• Acute/mild VH: scattered low-amplitude mobile opacities (small dots)
• Mature/organised VH: thick mobile membranes, multiple large echoes; blood layers inferiorly
• Key clinical use: exclude retinal detachment, retinal tear (elevated flap), or choroidal melanoma
• Differentiating VH from RD on B-scan:
  • RD — hyperechoic membrane moves with eye movements and is fixed at the optic disc
  • VH — echoes remain horizontal (gravitational), found in the middle of the posterior chamber

4. Fluorescein Angiography (IVFA)

• Aids in defining aetiology once media clarity permits
• Useful to define extent of neovascularisation or ischaemia

5. Systemic Investigations

• Blood glucose, HbA1c (diabetes)
• FBC, clotting screen, INR (if on warfarin, haematological disease)
• Sickle cell screen in appropriate demographics
• CT/MRI head if Terson syndrome suspected

Management (5 marks)

A. Conservative (Observation)

• Head of bed elevated — promotes inferior settling of blood, clearing visual axis superiorly (also the most common site for retinal breaks)
• Restrict: no heavy lifting, straining, or bending
• Discontinue aspirin, NSAIDs, and anticoagulants unless medically necessary
• Treat the underlying cause as soon as possible:
  • Retinal break → laser photocoagulation or cryotherapy
  • Proliferative retinopathy → anti-VEGF or PRP
  • Detached retina → surgery

B. Laser

• Panretinal photocoagulation (PRP): for underlying PDR once adequate view obtained; reduces neovascularisation
• Nd:YAG laser hyaloidotomy: for persistent premacular retrohyaloid haemorrhage — disperses blood into vitreous cavity for faster absorption; reduces risk of ERM/tractional macular detachment

C. Intravitreal Anti-VEGF

• Agents such as aflibercept, bevacizumab, ranibizumab used for PDR-related VH
• DRCR.net Protocol AB: eyes treated with early vitrectomy + PRP regained vision faster than those given initial aflibercept; however, 2-year visual outcomes were similar — both are acceptable first-line options for VH from PDR
• Pre-operative anti-VEGF reduces intraoperative bleeding in complex vitrectomy

D. Pars Plana Vitrectomy (PPV) — Surgical

1. Severe persistent VH precluding adequate PRP (most common indication)
2. Type 1 diabetics without rubeosis — traditionally within 3 months; earlier surgery may improve outcomes
3. Bilateral VH (most cases)
4. VH with tractional retinal detachment threatening the macula → treat without delay
5. Combined tractional + rhegmatogenous RD → treat urgently
6. Dense premacular retrohyaloid haemorrhage (risk of fibrovascular scaffold formation)
7. Non-clearing VH of unknown aetiology — two-thirds of such cases will have retinal tears or detachment
8. VH with iris neovascularisation (rubeosis)
9. Hemolytic or ghost cell glaucoma

Tip: Persistent VH or progressive tractional RD threatening the macula should be treated as soon as possible with pars plana vitrectomy. — Kanski's Clinical Ophthalmology, 10th ed.

Complications of VH (1 mark)

• Ghost cell glaucoma: degenerated erythrocytes (ghost cells) obstruct the trabecular meshwork
• Hemolytic glaucoma: macrophages laden with haemoglobin products obstruct outflow
• Tractional retinal detachment: fibrovascular proliferation along the posterior hyaloid
• Epiretinal membrane (ERM)
• Amblyopia in children
• Persistent severe visual loss

Prognosis (1 mark)

• Depends on underlying cause and presence of complications
• PVD-related and Terson syndrome VH: generally good prognosis with spontaneous resolution
• PDR-related VH: guarded without treatment; good functional outcomes with timely vitrectomy + PRP
• VH + retinal detachment or neovascular glaucoma: worse prognosis

Panretinal Photocoagulation (PRP) — 20-Mark Answer

1. Definition (1 mark)

2. Mechanism of Action (2 marks)

1. Destruction of ischaemic peripheral photoreceptors — the most metabolically demanding cells in the retina — reducing total retinal oxygen demand
2. Improved oxygenation of inner retina — by eliminating the oxygen-consuming outer layers, oxygen from the choroid can diffuse further inward, reducing inner retinal hypoxia
3. Reduction of VEGF production — the ischaemic peripheral retina is the major source of VEGF; ablating this tissue dramatically reduces VEGF secretion
4. Regression of neovascularisation — lowered VEGF leads to closure and fibrosis of new vessels (NVD, NVE, NVI)
5. Possible RPE scar-mediated effects — laser scars may directly alter cytokine production from the RPE

The net result: ischaemic drive for neovascularisation is eliminated → existing new vessels regress → risk of vitreous haemorrhage and tractional retinal detachment is reduced.

3. Indications (3 marks)

Primary Indication: Proliferative Diabetic Retinopathy (PDR)

• Severe NVD (new vessels at disc) without haemorrhage: 26% risk of severe visual loss at 2 years → reduced to 9% with PRP
• NVD with haemorrhage, or NVE > ½ disc area with haemorrhage: high-risk characteristics requiring prompt PRP

• NVD ≥ ¼–⅓ disc area
• Any NVD with preretinal or vitreous haemorrhage
• NVE ≥ ½ disc area with preretinal or vitreous haemorrhage

Other Indications:

4. Pre-Treatment Evaluation (1 mark)

• Dilated fundus examination (indirect ophthalmoscopy + slit-lamp biomicroscopy)
• Fluorescein angiography (FA): delineates extent of NV, identifies areas of capillary non-perfusion, guides treatment boundaries
• Wide-field FA: accurately maps peripheral capillary non-perfusion for targeted/selective treatment
• OCT: assess for co-existing diabetic macular oedema (DMO) before PRP
• IOP measurement; iris neovascularisation check (undilated slit-lamp)

Key principle: If co-existing clinically significant macular oedema (CSMO) or central-involving DMO is present, treat the oedema first (with anti-VEGF or focal/grid laser), then perform PRP — to avoid exacerbation by PRP.

5. Informed Consent (1 mark)

• Visual field loss: PRP reduces peripheral field; may be severe enough to legally preclude driving — though most patients with initially good vision maintain the binocular field standard required
• Risk to central vision: PRP can worsen or precipitate macular oedema — reduced by fractionating treatment over 2–3 sessions
• Night vision impairment: destruction of peripheral rod photoreceptors
• Colour vision changes
• Alternative: Anti-VEGF therapy (DRCR.net Protocol S, CLARITY studies) is as effective as PRP at 5 years for PDR; patient may choose this route, but must understand the need for repeated injections and shorter-term follow-up data

6. Equipment and Setup (1 mark)

Laser Sources

• Argon green (514 nm): historically standard
• Diode (810 nm): penetrates media opacity better; absorbed by melanin preferentially
• Frequency-doubled Nd:YAG (532 nm): common in modern systems
• Pattern scan laser (PASCAL): delivers pre-programmed multispot arrays with very short pulses, allowing rapid delivery of large numbers of burns

Contact Lenses

• Panfundoscopic lens (e.g. Volk SuperField, Mainster PRP 165): preferred; provides wide-field view of peripheral retina
  • ⚠️ With panfundoscopic lenses: actual retinal burn diameter is twice the interface setting (200 μm selected → 400 μm retinal burn)
• Three-mirror (Goldmann) lens: alternative; requires more repositioning
• High-magnification lens (Mainster, Area Centralis): for posterior component of treatment near arcades

Anaesthesia

• Topical (proxymetacaine drops): adequate in most cases
• Sub-Tenon or peribulbar block: for patients with severe discomfort, especially peripheral/horizontal meridian treatment

7. Laser Parameters (3 marks)

Burn intensity: only a light (grey-white) burn is desired — heavy/intense burns increase complication risk without additional benefit.

8. Treatment Pattern and Extent (2 marks)

Boundaries of Treatment

• Posteriorly: outside the temporal macular vascular arcades (approximately 2 disc diameters from the foveal centre)
• Nasally: usually 2 disc diameters nasal to the optic disc are left untreated (to preserve paracentral field)
• Anteriorly: extends to ora serrata

Technique

1. Apply a "barrier" row of laser burns just temporal to the macula early in the procedure — protects against accidental macular damage
2. In severe PDR: treat the inferior fundus first — any subsequent vitreous haemorrhage gravitates inferiorly and would otherwise obscure this area
3. Avoid areas of vitreoretinal traction — laser over traction sites can precipitate haemorrhage or tractional detachment
4. Review at 4–6 weeks after completing adequate burns; additional sessions applied as needed

Multispot / Pattern Scan (PASCAL)

• Short pulses (e.g. 20 ms), very short intervals, pre-programmed arrays
• Delivers large number of burns rapidly
• Shorter pulse duration may require a greater total number of burns for equivalent response

Targeted Retinal Photocoagulation (TRP)

• Wide-field FA guides selective treatment of only the ischaemic/non-perfused peripheral zones
• Achieves NV regression while minimising collateral damage to perfused retina
• Reduces side effects compared to conventional full PRP

9. Indicators of Successful Regression (1 mark)

• Blunting of neovascular vessel tips
• Shrinking and disappearance of NV — leaving "ghost" vessels or fibrosis
• Regression of intraretinal microvascular abnormalities (IRMA)
• Decreased venous beading and dilation
• Absorption of retinal haemorrhages
• Disc pallor (in some cases)

Wide-field fundus photograph: established PRP scars in the mid-periphery with sparing of the posterior pole and macula

Regression of disc neovascularisation and fibrovascular membrane 10 days after PRP

10. Complications (2 marks)

Immediate / Short-term

Long-term / Chronic

11. PRP vs. Anti-VEGF — Current Evidence (2 marks)

• PRP remains preferred when anti-VEGF compliance is uncertain (single treatment course)
• Anti-VEGF preferred when co-existing DMO is present (DRCR Protocol S: 28% vs 42% DMO rate with anti-VEGF vs PRP)
• Anti-VEGF does not replace PRP in patients lost to follow-up — PRP provides more durable protection
• PRP + anti-VEGF combined may be used in severe PDR with co-existing DMO

12. Special Situations (1 mark)

• With co-existing DMO: treat macular oedema first with anti-VEGF (or focal/grid laser for non-central CSMO) before PRP. If focal laser to macula is needed, apply it before PRP in the same session.
• Before cataract surgery in PDR: PRP reduces risk of post-operative rubeosis and NVG
• Intraoperative (endolaser): applied during PPV via intraocular probe, allowing treatment despite media opacity
• Terson syndrome / vitreous haemorrhage: if PRP cannot be completed due to VH → proceed to early vitrectomy + intraoperative endolaser
• Rubeosis/NVG: PRP combined with anti-VEGF injection (intravitreal) for rapid NVI regression; PRP for long-term stability