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Simulate hypertensive retinopathy — the spectrum of retinal microvascular changes induced by chronic systemic hypertension, ranging from subtle arteriolar narrowing to the life-threatening emergency of malignant hypertension with optic disc swelling. The retina is the only tissue where blood vessel morphology can be directly observed non-invasively in vivo, making the fundus a unique "window" into systemic vascular health. The Keith-Wagener-Barker (KWB) classification — introduced in 1939 and still widely used clinically — grades hypertensive retinopathy from Grade 1 to Grade 4 based on the severity of retinal arteriolar changes and their correlation with systemic cardiovascular and renal disease prognosis. Hypertension affects the retinal microvasculature through two interacting mechanisms: (1) Chronic adaptive autoregulation — the retinal arterioles respond to chronically elevated systemic blood pressure by undergoing smooth muscle hypertrophy and intimal fibrosis ("arteriosclerosis"), producing three characteristic ophthalmoscopic signs: increased arteriolar light reflex (the normal thin white "reflex streak" along the arteriolar surface broadens and brightens — progressing from copper-wire reflex [arteriolar wall thickening] to silver-wire reflex [fibrotic, non-transparent wall]), generalised arteriolar attenuation (the arteriole-to-vein (A/V) ratio decreases from the normal ~0.67–0.75 to <0.67 and eventually <0.5 in severe cases), and arteriovenous (AV) nicking/nipping with Gunn's sign (the thickened arteriolar wall compresses the underlying venule at crossing points where they share a common adventitial sheath — the "deflection" and "banking" (Bonnet's sign) of the vein at these crossings is the most important sign for diagnosing hypertensive arteriosclerosis). (2) Acute hypertensive crisis — when blood pressure exceeds the autoregulatory capacity of the retinal vasculature (typically diastolic BP >120 mmHg in accelerated hypertension or >130 mmHg in malignant hypertension), the arteriolar barrier breaks down, producing focal arteriolar spasm/leakage, flame-shaped haemorrhages (superficial RNFL), cotton-wool spots (focal RNFL infarcts from arteriolar occlusion), hard exudates (lipoprotein extravasation into the outer retina — forming a macular star when arranged around the fovea in Henle's fibre layer), and — in the most severe cases — optic disc oedema/papilloedema from raised intracranial pressure or direct optic nerve ischaemia. Simulate three KWB-grade clusters with ΔE colour shift, CIE xy chromaticity, and image simulation.

Hypertensive retinopathy colour science simulation by Auric Artisan.

Base color
KWB grade & settings
Hypertension severity / vascular damage 50%
Image simulation
Upload JPG/PNG (max 1200 × 1200). See how a scene appears through mild hypertensive retinopathy (arteriolar changes without significant visual effect — near-normal vision, fundus changes visible only on ophthalmoscopy), moderate hypertensive retinopathy (hard exudates + cotton-wool spots causing partial contrast loss near haemorrhage zones — macular star may cause central visual distortion), or severe/malignant hypertensive retinopathy (papilloedema + dense macular exudates causing moderate-to-severe central blurring, enlarged blind spot, and constricted visual field).
Research notes
Macular star — classic sign of severe hypertension: The macular star (or "star figure") is a ring of hard exudates arranged in a stellate pattern around the fovea, following Henle's fibre layer — the radiating oblique photoreceptor axons that form a star pattern when lipid-protein exudate leaks from damaged parafoveal capillaries and tracks along this anatomical layer. The star may also appear in other conditions (neuroretinitis, diabetic maculopathy) but in the context of malignant hypertension it is the hallmark of severe systemic hypertension requiring urgent blood pressure control. Hard exudates differ from cotton-wool spots: hard exudates are white-yellow, sharply defined (intraretinal lipid), while cotton-wool spots are fluffy white (nerve fibre layer infarcts). Both may coexist in Grade 3 hypertensive retinopathy.
Swatches
Normal
HEX: — • RGB: — • xy: —
HR affected
HEX: — • RGB: — • xy: —
ΔE (CIE76)
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ΔE (CIEDE2000)
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Deep preview
Normal
HR (deep)
Chromaticity (CIE xy)
Hypertensive microvascular chromaticity shift
D65 white point: 0.313, 0.329
Image simulation

Hypertensive retinopathy simulations model the retinal photoreceptor and inner retinal functional changes from vascular damage using KWB-grade-specific models in the sRGB colour space. Mild HR (Grade 1–2): models near-physiological function with minimal cone signal disruption — arteriolar attenuation and AV nicking are structural signs without direct visual consequence; only subtle contrast reduction at affected vascular territories. Moderate HR (Grade 3): models the combined effects of focal retinal ischaemia (cotton-wool spots), and intraretinal lipid exudate (hard exudates absorbing and scattering light at the outer plexiform layer) — adding a mild warm-yellow chromaticity bias from the yellow lipid deposits plus localised contrast loss. Severe/malignant HR (Grade 4): models papilloedema-related optic nerve dysfunction as diffuse luminance and contrast attenuation affecting the entire visual field, with enlargement of the blind spot and progressive visual field loss simulated as increased peripheral desaturation. ΔE2000 per Sharma et al. (2005). Not for clinical diagnosis — hypertensive retinopathy requires dilated fundoscopy with grading, OCT, and urgent blood pressure measurement.

Multi-condition comparison
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Compare mild hypertensive retinopathy (KWB Grade 1–2: arteriolar attenuation, AV nicking, copper/silver wiring — near-normal vision), moderate (KWB Grade 3: flame haemorrhages, cotton-wool spots, hard exudates, macular star), and severe/malignant (KWB Grade 4: disc oedema, papilloedema, severe vision loss).