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Simulate central retinal vein occlusion (CRVO) — obstruction of the central retinal vein at or immediately posterior to the lamina cribrosa, producing the most dramatic and visually devastating fundus appearance in retinal vascular disease: diffuse 360° flame-shaped and dot-blot haemorrhages across all four retinal quadrants (sometimes described as a "blood and thunder" fundus), markedly dilated and tortuous retinal veins in all quadrants, optic disc swelling (papilloedema), multiple cotton-wool spots (focal retinal nerve fibre layer infarcts), and severe macular oedema from diffuse venous hypertension and upstream capillary bed congestion. With a population prevalence of approximately 0.8 per 1,000 individuals (increasing to 4.6 per 1,000 over age 64), CRVO is the second most common retinal vascular occlusion after BRVO. The critical clinical dichotomy — established by Hayreh's landmark studies and the Central Vein Occlusion Study Group — divides CRVO into two prognostically distinct forms: Non-ischaemic (perfused) CRVO — venous stasis retinopathy with intact capillary perfusion on FFA, mild-to-moderate initial vision loss, variable natural history (up to 30–33% convert to ischaemic over 3 years); and Ischaemic CRVO — extensive capillary non-perfusion (>10 disc areas on FFA), profound vision loss (CF to HM), high risk of anterior segment neovascularisation (rubeosis iridis) and neovascular glaucoma ("100-day glaucoma", so named because neovascular glaucoma historically developed within ~100 days of ischaemic CRVO onset before anti-VEGF treatment was available). The common anatomical bottleneck for CRVO is the lamina cribrosa — where the central retinal artery and vein share a rigid scleral canal, making venous compression by arteriosclerotic arterial wall thickening or raised intraocular pressure possible at this single anatomical point. Risk factors: systemic hypertension (most important, present in 60–73% of CRVO patients), glaucoma (elevated IOP compresses the vein at the lamina cribrosa — 20–25% of CRVO patients have glaucoma or elevated IOP), hypercholesterolaemia, diabetes, thrombophilia (antiphospholipid antibody syndrome, factor V Leiden — especially in young CRVO patients under 50), hyperviscosity syndromes, and vasculitis. Simulate three presentations with ΔE colour shift, CIE xy chromaticity, and image simulation.

Central retinal vein occlusion colour science simulation by Auric Artisan.

Base color
CRVO subtype & settings
Venous congestion / macular oedema severity 50%
Image simulation
Upload JPG/PNG (max 1200 × 1200). See how a scene appears through non-ischaemic CRVO (diffuse macular oedema with moderate central blur, relative peripheral preservation), ischaemic CRVO (profound central and paracentral vision loss from macular oedema + inner retinal ischaemia), or neovascular complication (severe vision loss from advanced glaucoma and secondary angle closure).
Research notes
Non-ischaemic vs ischaemic CRVO — the key clinical distinction: The Central Vein Occlusion Study (CVOS) group established the diagnostic criteria for ischaemic CRVO: ≥10 disc areas of capillary non-perfusion on fluorescein angiography (FFA). Relative afferent pupillary defect (RAPD) and electroretinography (ERG) b-wave/a-wave ratio reduction are useful clinical surrogate markers when FFA is not immediately available. Approximately 25–34% of non-ischaemic CRVOs convert to the ischaemic subtype within 36 months of presentation, necessitating close monitoring. The most feared complication — neovascular glaucoma — occurs in approximately 45% of untreated ischaemic CRVOs within 15 months; this risk is dramatically reduced by pan-retinal photocoagulation (PRP) and anti-VEGF treatment.
Swatches
Normal
HEX: — • RGB: — • xy: —
CRVO affected
HEX: — • RGB: — • xy: —
ΔE (CIE76)
—
ΔE (CIEDE2000)
—
Deep preview
Normal
CRVO (deep)
Chromaticity (CIE xy)
Central venous congestion chromaticity shift
D65 white point: 0.313, 0.329
Image simulation

CRVO simulations model the retinal oedema, haemorrhagic signal attenuation, and inner retinal ischaemia from central venous congestion in the sRGB colour space. Non-ischaemic CRVO: models diffuse macular oedema as moderate central cone signal degradation with intraretinal fluid causing contrast loss — the haemorrhagic component adds a warm red-brown chromaticity bias from deoxyhaemoglobin absorption across all four retinal quadrants (greater chromaticity shift than BRVO due to 360° involvement). Ischaemic CRVO: adds inner retinal ischaemic attenuation to the oedema model, simulating the combined effect of macular oedema and retinal ganglion cell layer infarction on visual signal processing — greater luminance reduction and desaturation. Neovascular complication: models advanced secondary glaucoma as severe diffuse attenuation with peripheral constriction. ΔE2000 per Sharma et al. (2005). Not for clinical diagnosis — CRVO requires dilated fundoscopy, fluorescein angiography (FFA), SD-OCT, full-field ERG, and systemic cardiovascular and thrombophilia workup.

Multi-condition comparison
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Compare non-ischaemic CRVO (venous stasis retinopathy, intact perfusion, moderate macular oedema), ischaemic CRVO (capillary non-perfusion, severe macular oedema + inner retinal ischaemia), and neovascular complication (rubeosis iridis, neovascular glaucoma from anterior segment neovascularisation).