Vitreous Anatomy

Overview

The vitreous body is the clear, avascular gel that fills the posterior segment of the eye, bounded anteriorly by the lens and ciliary body and posteriorly by the retina. It occupies roughly four-fifths of the eye's volume. Far from a passive filler, its gel consistency maintains ocular shape, supports the retina mechanically against the choroid and sclera, and, being nearly avascular itself, provides a clear optical path for light traveling from the lens to the photoreceptors.

Vitreous anatomy comes down to two related facts. The gel is not uniform: its density and its adhesion to the retina both vary by region. And its molecular composition changes with age, which is what ultimately drives liquefaction and separation from the retina. Both threads lead to the same endpoint, the single most common vitreous event of adult life: posterior vitreous detachment (PVD).

Regional Anatomy: Base, Body, Cortex

The vitreous is conventionally described as having a central body and a peripheral cortex, plus one specific zone of anchoring, the vitreous base, that behaves differently from every other part of the gel.

Vitreous Base

The vitreous base straddles the ora serrata, the scalloped junction where the neurosensory retina ends and the non-photoreceptive epithelium of the pars plana begins. It extends a few millimeters both anterior and posterior to the ora serrata, overlying the peripheral retina and pars plana at once. This is the single strongest point of vitreoretinal adhesion anywhere in the eye, well beyond the attachment over the rest of the retina, and that strength is what makes it clinically important. When the vitreous gel is subjected to traction, whether from a PVD, blunt trauma, or ordinary eye movement acting on a gel that has not fully liquefied, the vitreous base is the last place to let go. Traction concentrates instead at its posterior edge, over the peripheral retina, which is why retinal tears cluster at the vitreous base.

Vitreous Body and Cortex

The central vitreous body is the bulk gel occupying most of the posterior segment volume. Surrounding it is the vitreous cortex, a thin, comparatively dense peripheral shell where collagen fibrils pack more tightly than in the central gel. The cortex is subdivided by location into an anterior cortex, adjacent to the lens and ciliary body and contributing to the anterior hyaloid face, and a posterior cortex, applied against the retinal surface and contributing to the posterior hyaloid face (covered in its own section below). Aside from the vitreous base, the cortex adheres most firmly to the retina at the optic disc margin and, to a lesser degree, along the major retinal vessels and at the macula. These are the sites where a detaching posterior cortex can transiently tug on the retina before it finally separates.

The Posterior Hyaloid

The posterior hyaloid, also called the posterior vitreous cortex, is the condensed layer of vitreous collagen fibrils that lines the retinal surface and adheres to the internal limiting membrane (ILM), the basement-membrane-like structure formed by the footplates of Müller cells at the innermost retina. This posterior hyaloid face is denser than the central vitreous body because it is part of the cortex described above. Its adhesion to the ILM, apart from the reinforced sites at the disc margin, vessels, and macula, is comparatively weak and diffuse across most of the posterior pole. That weak, diffuse adhesion is exactly why the posterior hyaloid can separate cleanly during a PVD, unlike the vitreous base.

Molecular Composition

The vitreous is roughly 98–99% water by volume. Its gel behavior, though, comes from a dilute meshwork of two other components suspended in that water: type II collagen fibrils and hyaluronic acid (hyaluronan), a large, highly hydrophilic glycosaminoglycan.

The collagen fibrils form a loose three-dimensional scaffold that gives the vitreous its structural framework. Hyaluronic acid molecules are interspersed throughout that scaffold, and because each hyaluronan molecule can bind an enormous number of water molecules, they hold water within the collagen network rather than letting it separate out as free fluid. That is what gives the vitreous its viscous, gel-like consistency instead of the behavior of plain water. Collagen is densest at the vitreous base and in the cortex and sparsest in the central vitreous.

Aging changes this balance directly. Collagen fibrils progressively aggregate into thicker bundles, and the hyaluronan-water complex that had been holding the gel together begins to separate from the collagen scaffold. This process is called synchysis. The practical result is liquefaction: pockets of liquid vitreous, called lacunae, form within an otherwise still-gelled matrix. It is this age-related liquefaction, not a single acute event, that sets up the eventual collapse of the gel described below under posterior vitreous detachment.

Posterior Vitreous Detachment

Posterior vitreous detachment is the separation of the posterior hyaloid face from the internal limiting membrane of the retina. It is overwhelmingly age-related, and its mechanism follows directly from the composition changes described above. Progressive liquefaction (synchysis) creates a fluid-filled space within the central vitreous. Once enough of the gel has liquefied, the remaining collagen scaffold can no longer hold its shape against gravity and eye movement, and it collapses forward (syneresis). That collapse pulls the weakly adherent posterior cortex away from the ILM, and liquefied vitreous seeps through a break in the cortex, often near the optic disc, into the newly created retrohyaloid space, completing the separation.

The posterior hyaloid separates cleanly from most of the retina but remains firmly anchored at the vitreous base and, transiently, at the disc margin and along the vessels. The detaching gel can exert focal traction at those sites during the process. Traction at the vitreous base, where the retina is thinnest and adhesion is strongest, is what can produce a retinal tear. Traction at the disc margin as the cortex finally releases classically produces the ring-shaped floater, a Weiss ring, that patients report as a new, single dark floater. Traction on a retinal vessel can tear it and cause a vitreous hemorrhage. A PVD without any of these complications is simply the normal endpoint of vitreous aging and needs no treatment. A new PVD warrants a dilated exam specifically to rule out the tear it can cause at the vitreous base.

High-Yield Pearls

• The vitreous is ~98–99% water; its gel consistency comes from a dilute type II collagen scaffold holding hyaluronan-bound water in place.
• The vitreous base (straddling the ora serrata) is the strongest vitreoretinal adhesion site: traction there during a PVD is the anatomic basis for peripheral retinal tears.
• The posterior hyaloid = posterior vitreous cortex; its separation from the ILM is the event that defines a PVD.
• A Weiss ring (a single new ring-shaped floater) reflects the cortex finally releasing from the optic disc margin, a reassuring sign that the separation there is complete, though it doesn't rule out a tear elsewhere.
• Embryologically, the neurosensory retina and RPE both arise from the two layers of the optic cup (neuroectoderm), relevant context for why the ILM the vitreous adheres to is a retinal, not vitreous, structure.

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