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Simulate central retinal artery occlusion (CRAO) — an ophthalmic emergency characterised by sudden painless monocular vision loss from embolic or thrombotic occlusion of the central retinal artery (CRA) at the lamina cribrosa. CRAO produces profound inner retinal ischaemia within minutes: the inner retina (ganglion cell layer through inner nuclear layer) depends entirely on the CRA blood supply and has an ischaemic tolerance of only approximately 90–100 minutes in primate models (Hayreh et al., 1980). The hallmark fundus sign is the cherry-red spot at the macula — the thin foveola (which has no inner retinal layers and is nourished by the underlying choriocapillaris) remains its normal red-orange colour while the surrounding inner retina becomes opaque whitish from cytotoxic oedema, creating the characteristic contrast. Non-arteritic CRAO (atherosclerotic/embolic) accounts for approximately 95% of cases and requires urgent carotid duplex ultrasound, echocardiography, and Holter monitoring to identify the embolic source. Arteritic CRAO from giant cell arteritis (GCA) occurs in approximately 5% and is the most urgent — requiring immediate high-dose IV methylprednisolone (1 g/day × 3 days) to prevent fellow eye involvement and systemic vasculitis. Branch retinal artery occlusion (BRAO) affects a sectoral distribution with better visual prognosis. Simulate three clinical presentations with ΔE colour shift, CIE xy chromaticity, and image simulation.

Central retinal artery occlusion colour science simulation by Auric Artisan.

Base color
CRAO subtype & settings
Retinal ischaemia / oedema severity 50%
Image simulation
Upload JPG/PNG (max 1200 × 1200). See how a scene appears through non-arteritic CRAO (near-complete central vision loss with cherry-red spot — profound inner retinal ischaemia), arteritic CRAO (GCA-related, bilateral risk, combined optic nerve + retinal ischaemia), or BRAO (sectoral altitudinal field defect with preserved central vision if fovea spared).
Research notes
Cherry-red spot — anatomy explains the sign: The foveola has no inner retinal layers — it consists only of cone photoreceptor outer segments, Henle fibre layer, and foveolar Müller cell processes, all nourished by the choriocapillaris (not the CRA). When the CRA is occluded, the inner retina surrounding the fovea becomes oedematous and opaque white from cytotoxic swelling of ganglion cells and inner nuclear layer neurons. The thin foveola, still perfused by the choroid, retains its normal red-orange colour — creating the pathognomonic cherry-red spot sign by contrast against the surrounding pale oedema. This sign is also seen in storage diseases (Tay-Sachs, Niemann-Pick) where lipid storage in ganglion cells produces similar perifoveal opacification.
Swatches
Normal
HEX: — • RGB: — • xy: —
CRAO affected
HEX: — • RGB: — • xy: —
ΔE (CIE76)
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ΔE (CIEDE2000)
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Deep preview
Normal
CRAO (deep)
Chromaticity (CIE xy)
Ischaemic retinal chromaticity shift
D65 white point: 0.313, 0.329
Image simulation

CRAO simulations model the profound inner retinal ischaemia following central retinal artery occlusion. Non-arteritic CRAO: models near-total cone signal loss from inner retinal infarction — the inner retina (ganglion cell layer, inner plexiform layer, inner nuclear layer) undergoes cytotoxic oedema within minutes, producing the characteristic pale whitish retinal appearance. The foveola (nourished by choriocapillaris) retains function → cherry-red spot. Arteritic CRAO (GCA): combined CRA + posterior ciliary artery ischaemia → even more severe with choroidal hypoperfusion. BRAO: sectoral involvement with better prognosis if fovea spared. ΔE2000 per Sharma et al. (2005). Not for clinical diagnosis — CRAO is an ophthalmic emergency requiring immediate dilated fundoscopy, FFA, ESR/CRP (GCA exclusion), carotid duplex, echocardiography, and neurological assessment.

Multi-condition comparison
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Compare non-arteritic CRAO (embolic, profound VA loss, cherry-red spot), arteritic CRAO (GCA, bilateral risk, urgent steroids), and BRAO (sectoral, better VA if fovea spared).