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Simulate posterior vitreous detachment (PVD) — the separation of the posterior vitreous cortex from the internal limiting membrane (ILM) of the retina, the single most common vitreoretinal event in human ageing. The vitreous body is a transparent gel composed of a sparse meshwork of type II collagen fibrils suspended in a hydrated hyaluronic acid (hyaluronan) matrix filling the posterior 4/5 of the globe (~4 mL volume). With age, the vitreous undergoes progressive syneresis (liquefaction) — the collagen-hyaluronic acid network degrades, collagen fibrils aggregate into visible strands and sheets, and the gel transitions from a uniform optically-clear phase into a heterogeneous mixture of liquid vitreous (lacunae) and collapsed collagen condensations. When the degree of liquefaction is sufficient, the posterior hyaloid face (posterior vitreous cortex) separates from the ILM — this is PVD. The separation typically initiates at the perifoveal macula and propagates anteriorly, with the final detachment point being the vitreous base (the firm annular vitreoretinal adhesion 2 mm anterior and 3 mm posterior to the ora serrata). The pathognomonic clinical sign is the Weiss ring (Vogt's ring) — a ring-shaped opacity of glial tissue avulsed from the optic disc margin when the peripapillary vitreous separates, visible as an annular floater on slit-lamp biomicroscopy and on B-scan ultrasound. Patients typically present with acute onset of floaters (vitreous condensations casting shadows on the retina), photopsia (tractional flashes of light from residual vitreoretinal adhesion points pulling on the retina during eye movement), and occasionally a curtain/veil sensation if complicated by retinal detachment. PVD itself is benign in ~85–90% of cases; however, 10–15% of acute symptomatic PVDs are complicated by retinal breaks (horseshoe tears at sites of persistent vitreoretinal adhesion) and 1–3% progress to rhegmatogenous retinal detachment. Model uncomplicated PVD with floaters and photopsia, PVD with vitreous haemorrhage, and PVD-associated retinal tear/hole using ΔE colour shift, CIE xy chromaticity, and image simulation.

Posterior vitreous detachment colour science simulation by Auric Artisan.

Base color
PVD presentation & settings
Vitreous opacity / haemorrhage severity 50%
Image simulation
Upload JPG/PNG (max 1200 × 1200). See how a scene appears through PVD: uncomplicated PVD (discrete floater shadows from vitreous condensations and Weiss ring — focal translucent opacities drifting across the visual field with eye movement), PVD with vitreous haemorrhage (diffuse red-brown haze from dispersed red blood cells in the vitreous cavity — dense VH at high severity may obscure fundus view entirely), or PVD with retinal tear complication (combined floaters + haemorrhage + potential curtain/veil visual field obstruction from developing retinal detachment).
Research notes
PVD clinical significance — the 5-minute "floater history": Acute symptomatic PVD is one of the most common urgent presentations in ophthalmology. The critical clinical question is whether an acute PVD is uncomplicated (benign) or complicated by a retinal tear (surgical emergency). Key red flags for complicated PVD: (1) shower of small floaters (pigment cells — "tobacco dust" or Shafer's sign in the anterior vitreous on slit-lamp), (2) dense vitreous haemorrhage obscuring the fundus view — assume a retinal tear until proven otherwise, (3) subjective curtain/shadow across the visual field (developing retinal detachment), (4) sudden decrease in visual acuity. All patients with acute symptomatic PVD require urgent dilated fundus examination (within 24–48 hours), peripheral retinal examination with scleral depression to exclude retinal tears, and B-scan ultrasound if VH obscures the fundus view.
Swatches
Normal
HEX: — • RGB: — • xy: —
PVD affected
HEX: — • RGB: — • xy: —
ΔE (CIE76)
—
ΔE (CIEDE2000)
—
Deep preview
Normal
PVD (deep)
Chromaticity (CIE xy)
Vitreous opacity chromaticity shift
D65 white point: 0.313, 0.329
Image simulation

Posterior vitreous detachment simulations model the optical media opacity caused by vitreous structural changes. Uncomplicated PVD: models discrete vitreous condensation floater shadows as a mild, non-uniform luminance reduction — the actual spatial distribution of floaters (drifting opacities, Weiss ring) cannot be replicated in a uniform swatch simulation but the average luminance and mild contrast impact is represented. In uncomplicated PVD, photopsia (tractional flashes) is a neural phenomenon from mechanical retinal stimulation and is not a colour/luminance change — not modelled. PVD with vitreous haemorrhage: models dispersed RBCs in the vitreous cavity as a warm red-brown optical density filter — haemoglobin absorption (peak ~540–576 nm) attenuates green and blue transmission, producing a characteristic red-brown chromatic haze with marked luminance reduction at high severity. PVD with retinal tear: combines haemorrhage opacity model with the assumption that the tear itself introduces an additional local scotoma from developing subretinal fluid. ΔE2000 per Sharma et al. (2005). Not for clinical diagnosis — acute PVD requires urgent dilated fundus examination to exclude retinal tears.

Multi-condition comparison
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Compare uncomplicated PVD (mild floater opacity), PVD with vitreous haemorrhage (red-brown haemoglobin-mediated optical density), and PVD complicated by retinal tear (combined VH + developing retinal detachment). Observe how vitreous haemorrhage produces a distinctly warm (red-brown) chromaticity shift unlike the neutral opacity of simple floaters.