Base color

Model & settings

Cyanopsia model

Blue shift severity50%

Perceptual severity curve Multi-pass deep simulation UV-leak overlay (aphakic)

Image simulation

Choose image Upload JPG/PNG (max 1200 × 1200). Blue-bias simulation rendered next to original.

Research notes

Cyanopsia (from Greek kyanos = blue + opsis = sight) is a form of chromatopsia in which the visual field acquires a blue tint. It is the most common post-cataract chromatopsia: removal of the yellowed crystalline lens (which progressively absorbs short wavelengths with age) dramatically increases blue-violet retinal irradiance, overwhelming S-cone pathways before chromatic adaptation recalibrates. PDE5 inhibitors (sildenafil, tadalafil, vardenafil) produce transient cyanopsia by cross-inhibiting retinal PDE6 (phosphodiesterase-6), altering rod and cone phototransduction kinetics with preferential effect on S-cone pathways. Aphakic patients (lacking any lens) experience permanent increased short-wavelength sensitivity unless a UV-blocking IOL is implanted. "Spectral blue bias" shifts color balance toward 440-475 nm; "contrast lift" increases perceived brightness in blue-dominant regions. The UV-leak overlay models the additional ultraviolet sensitivity present in aphakic eyes.

Swatches — Reference vs Cyanopsia

Reference

HEX: — • RGB: — • xy: —

Cyanopsia Sim

HEX: — • RGB: — • xy: —

ΔE (CIE76)

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ΔE (CIEDE2000)

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Deep preview

Reference

Simulated

Chromaticity (CIE xy)

Blue shift axis (toward S-cone dominant locus)

D65 white point: 0.313, 0.329

Image simulation

Simulations operate in linear sRGB for perceptual correctness. ΔE2000 implemented locally. Cyanopsia is modeled as an S-cone spectral bias (blue channel gain increase, red/green attenuation) reflecting the increased short-wavelength retinal irradiance after removal of the yellowed crystalline lens. PDE5-inhibitor cyanopsia is modeled as transient retinal PDE6 cross-inhibition altering cone phototransduction kinetics. Contrast lift mode increases local contrast in the blue band. Combined mode applies both spectral bias and contrast enhancement. The UV-leak overlay models additional ultraviolet sensitivity present in aphakic eyes. For perceptual optics research and design accessibility — not clinical diagnosis.

Multi-condition comparison

Condition A

Condition B

Steps

Compare normal, Condition A and Condition B across multiple severities. If an image is loaded it will be processed into the grid, otherwise color swatches are shown.

Advanced mode

Etiology model

Blue gain factor

145%

IOL type

Etiology notes: The natural crystalline lens progressively yellows with age (brunescence), absorbing short wavelengths (<500 nm). Cataract extraction removes this filter. Clear IOLs block UV (<400 nm) but transmit blue freely — producing acute cyanopsia. Yellow-tinted IOLs (e.g. AcrySof Natural) mimic the young adult lens and reduce post-operative blue shift. PDE5 inhibitors (100 mg sildenafil dose) cross-inhibit retinal PDE6 with IC₅₀ approximately 10× that of PDE5, producing transient S-cone pathway hyperactivity.

Model assumptions & limits

Blue bias is implemented as S-cone proxy (blue channel gain) with complementary R/G attenuation. Real post-surgical cyanopsia involves complex spectral transmission changes across the entire visible and near-UV range.
PDE5 inhibitor effects are dose-dependent and subject-variable; the 3-11% incidence figure applies to standard doses.
Chromatic adaptation (von Kries) would normally reduce perceptible cyanopsia within hours to days — the simulator shows the acute pre-adaptation state.
IOL spectral transmission curves are simplified; real IOLs have specific cutoff wavelengths varying by manufacturer.