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Simulate vitreous haemorrhage (VH) — the extravasation of blood into the vitreous cavity, one of the most common causes of acute painless vision loss in ophthalmology. The vitreous body is normally an optically clear gel, and blood dispersed within it acts as a spectral absorption filter — haemoglobin within red blood cells (RBCs) has characteristic absorption peaks: the Soret band at ~415 nm (deepest absorption), the α-band at ~540 nm, and the β-band at ~576 nm. This means that blue and green wavelengths are preferentially absorbed by haemoglobin, while red wavelengths are relatively spared — producing the characteristic warm red-brown visual haze that patients with VH describe. At low concentrations, VH produces a mild reddish-brown tint with preserved fundus view; at high concentrations, VH is so dense that no light reaches the retina and vision drops to light perception (LP) only. Acute VH from retinal tear/PVD — the most urgent cause — occurs when vitreous separation avulses a retinal blood vessel at a horseshoe tear, releasing blood directly into the vitreous cavity (must exclude retinal tear and retinal detachment urgently). Proliferative diabetic retinopathy (PDR) VH — the most common cause worldwide — occurs when fragile neovascular vessels (NVD at the disc, NVE elsewhere) bleed into the vitreous, often recurrently. Dense non-clearing VH — blood that persists for weeks to months, requiring pars plana vitrectomy (PPV) for clearance and to visualise and treat the underlying pathology. Model haemoglobin spectral absorption, warm chromaticity shift, ΔE colour difference, CIE xy chromaticity, and image simulation.

Vitreous haemorrhage colour science simulation by Auric Artisan.

Base color
VH aetiology & settings
Haemorrhage density / severity 50%
Image simulation
Upload JPG/PNG (max 1200 × 1200). See how a scene appears through vitreous haemorrhage: acute VH (dispersed RBCs producing a warm red-brown optical density haze — haemoglobin Soret/α/β absorption preferentially attenuates blue and green wavelengths, relatively sparing red), diabetic PDR VH (recurrent VH from neovascular vessel rupture — may have layered component with denser inferior blood and clearer superior vitreous from gravity-dependent settling), or dense non-clearing VH (complete media opacity — virtually no light transmission at maximum severity, vision LP only).
Research notes
Haemoglobin absorption spectrum — the physics of VH colour: The characteristic red-brown visual haze of VH is a direct consequence of the absorption spectrum of oxyhaemoglobin (OxyHb) and deoxyhaemoglobin (DeoxyHb). OxyHb has three absorption peaks: the Soret band at ~415 nm (blue — deepest absorption, ε ≈ 131,000 M⁻¹cm⁻¹), the α-band at ~540 nm (green), and the β-band at ~576 nm (yellow-green). This absorption profile means that blue and green photons are preferentially absorbed as they traverse the haemorrhagic vitreous, while red/orange photons (>600 nm) pass through with less attenuation. The result: the patient sees through a warm (red-biased) spectral filter. As haemorrhage density increases (higher Hb concentration × longer path length through the vitreous), the transmission drops across all wavelengths and the warm shift becomes more pronounced — at maximum density, essentially no light reaches the retina and vision is LP only.
Swatches
Normal
HEX: — • RGB: — • xy: —
VH affected
HEX: — • RGB: — • xy: —
ΔE (CIE76)
—
ΔE (CIEDE2000)
—
Deep preview
Normal
VH (deep)
Chromaticity (CIE xy)
Haemoglobin-mediated chromaticity shift
D65 white point: 0.313, 0.329
Image simulation

Vitreous haemorrhage simulations model the optical media opacity caused by dispersed red blood cells in the vitreous cavity. Haemoglobin spectral absorption is the primary mechanism: oxyHb absorption peaks at 415 nm (Soret), 540 nm (α), and 576 nm (β) produce preferential blue and green attenuation — the patient sees through a warm red-brown spectral filter whose density is proportional to haemoglobin concentration and vitreous path length. Acute VH (retinal tear/PVD): models dispersed fresh blood as a uniform warm-shift spectral filter. The model uses a simplified warm spectral bias (a*+ red shift, b*- blue attenuation) rather than full spectral integration through the Hb absorption curve. Diabetic PDR VH: same spectral model but with assumptions for recurrent haemorrhage and potentially layered blood (gravity-dependent settling creates denser inferior and clearer superior vitreous — not spatially modelled in swatch mode). Dense non-clearing VH: maximum haemorrhage density — at s=1.0, essentially total light absorption (LP vision only). ΔE2000 per Sharma et al. (2005). Not for clinical diagnosis — all acute VH requires urgent dilated fundus examination or B-scan ultrasonography to exclude retinal tear/detachment.

Multi-condition comparison
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Compare acute VH (fresh dispersed RBCs — warm red-brown haze from oxyHb absorption), diabetic PDR VH (recurrent neovascular haemorrhage — deoxyHb component shifts absorption profile slightly), and dense non-clearing VH (maximal media opacity — near-total light absorption at high severity). All three share the characteristic haemoglobin warm spectral signature but differ in density, chronicity, and associated clinical urgency.