CHAPTER 18

THE VITREOUS: BIRD'S EYE VIEW

A. NEETENS

The vitreous is a simple connective tissue. The postnatal vitreous contains cells-hyalocytes-that synthesize hyaluronic acid, collagen, and probably other vitreous components. The hyalocytes have func­tional characteristics of a macrophage. The question arises as to wheth­er they may develop actine filaments and show evidence of contractil­ity, like cells invading the vitreous from adjacent tissues. Fibroblasts, retinal pigment epithelial cells, and vascular endothelial cells are all capable of proliferating along vitreoretinal membranes and can pene­trate into the vitreous cavity through a discontinuity in the internal limiting lamina that may result from damage to Miiller cells.

The hyalocytes are present in highest concentration in the vitreous cortex, especially at the vitreous base and in its posterior part. Their lowest concentration is around the equator.

The first vitreous formed embryologically (primary vitreous) is thought to be derived from the retina, lens, and cells of the hyaloid system. The secondary vitreous appears to be derived from the Miiller cells, which play an important role in maintaining the vitreoretinal adhesion.

The most important vitreoretinal adhesion is at the vitreous base. In this location the vitreoretinal interface consists of a complex formed by the basal laminae of the adjacent cells, and the vitreous cortex. This is where collagen fibers and hyaluronic acid occur in highest concentra­tion.

Other attachments of the vitreous are at the disc and the macula. "Attachment plaques" between Miiller cells and the internal limiting lamina have been described in the basal and equatorial regions but not in the posterior pole, except around the fovea. Vitreoretinal adhesions also exist at the level of meridional retinal folds, equatorial pigment clumps, and around progressive latticelike degeneration. Firm vitreore-

C. L. Schepens et al. (eds.), The Vitreous and Vitreoretinal Interface© Springer Science+Business Media New York 1987

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tinal adhesions may also form along peripheral retinal vessels, which explains the common presence of a bridging blood vessel across an arrowhead-shaped retinal tear.

The vitreous gel is formed by insoluble type II collagen composed of three similar alpha I polypeptide chains arranged as a meshwork. The interaction of these chains maintains the gel structure. The most impor­tant properties of the vitreous, transparency and viscoelasticity, are derived from this gel structure that is stabilized by a viscous solution of hyaluronic acid.

The vitreous acts as a barrier against the entry of cells and macro­molecules. It has an inhibitory effect upon lymphocyte transformation and phagocytosis by macrophages. The latter property possibly modu­lates the diffusion of immunologic and angiogenic factors in the eye. The vitreous also appears to inhibit the proliferation of cells involved in inflammatory, proliferative, and neovascular responses.

Physical factors such as increased temperature (by diathermy and photocoagulation), production of free radicals, and practically all forms of high-energy radiation may cause the collagen gel to shrink.

Sodium hyaluronate is the vitreous substitute of choice at the mo­ment, because it is water miscible and offers the unique property of viscoelasticity, protecting the delicate retina from mechanical shock by acting as a shock absorber. Hyaluronate interferes little with wound healing because it does not affect the movement of fibroblasts. Its high viscosity helps to prevent it from escaping under the retina in cases of rhegmatogenous retinal detachment. It is therefore a good adjunct to flatten rigid retinal folds.

The vitreous is a difficult structure to study clinically because of its relative transparency and low reflectivity. The clinician should spend sufficient time on vitreous examination, and it is essential to record the findings on paper. Dynamic vitreous studies following ocular move­ments are best performed with a slitlamp biomicroscope and the pow­erful convex precomeal lens of El Bayadi-Kajiura. This lens causes minimal distortion and glare and provides a large field of view. Photo­graphic documentation is possible with this instrumentation. In cases with opaque media, ultrasound A- and B-scan is helpful for the detec­tion of retinal detachment and vitreoretinal traction sites.

Vitreous liquefaction reduces the size of the vitreous gel. This may result in collapse and detachment of the posterior vitreous cortex, allowing the liquid vitreous to enter the subhyaloid space, anterior to the retina. Intravitreous strands may develop in degenerated vitreous.

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This process is age related. In myopic eyes and in associated systemic connective disorders, vitreous degeneration appears at an earlier age. Other factors that precipitate vitreous detachment are vitreous hemor­rhage, trauma, posterior segment inflammation, aphakia, diabetes mel­litus, and abiotrophic hereditary vitreoretinal diseases.

The availability of liquid vitreous is almost as important as vitreous traction in the pathogenesis of rhegmatogenous retinal detachment. Animal experiments have shown that retinal ischemia is also a signifi­cant factor in the pathogenesis of vitreous detachment. This is illus­trated by the fact that posterior vitreous detachment is most frequent in areas overlying retinal hypoxia.

Vitreous detachment allows the migration of cells and macromole­cules into the vitreous cavity. Their proliferation being no longer inhi­bited by the presence of vitreous gel, preretinal and vitreous mem­branes can grow freely.

Some vascular diseases often lead to neovascular proliferation into the vitreous cavity; examples are diabetic retinopathy, sickle-cell reti­nopathy, venous obstruction, and radiation retinopathy. Other vascular diseases, such as arteriolar obstruction, Coats' disease, and angiomato­sis retinae (Von Rippel-Lindau disease), rarely do. In retinal branch vein occlusion, liquefaction of the cortical gel, present in 80 % of the eyes, is more severe in the area of the occluded vessels. When the posterior vitreous detachment is partial, the prognosis of subsequent vitreous hemorrhage and retinal detachment is worse than in cases with complete posterior detachment.

The strong adhesions that exist normally between the vitreous cortex and the macula may playa role in the pathogenesis of certain macular diseases, particularly macular breaks and cystoid macular edema. The macula and the vitreous base are particularly vulnerable to ocular con­tusion because the vitreoretinal adhesion is exceptionally firm in these areas.

Vitreodonesis after cataract surgery creates a corresponding turbu­lence within the aqueous. The concussive effect upon tissues of aqueous and fluid vitreous results in endophthalmodonesis. This effect has been proposed as a cause of corneal decompensation (Fuchs' syndrome), cys­toid macular edema (Irvine-Gass syndrome), and rhegmatogenous reti­nal detachment. These pathological changes are facilitated by decreased hyaluronic acid content in the vitreous of aphakic patients, increased collagen cross-linking, and decreased viscoelasticity.

There is evidence that an extracapsular cataract extraction with

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intact posterior capsule decreases the incidence of retinal detachment. A capsulotomy seems to negate the beneficial effect of an intact poste­rior capsule in preventing retinal detachment. These clinical impres­sions will require longer observation and a larger series of cases before they can be confirmed.

Tractional retinal detachment is produced by changes in the vitreous cavity due to contractile structures. These contractile elements are con­tained in extraretinal vasoproliferative tissue. The total retinal detach­ment in severe retinopathy of prematurity exhibits the characteristics of massive proliferative vitreoretinopathy.

The vitreous body and the retina may be affected by degenerative conditions of obscure etiology but with definite hereditary patterns, suggesting a genetic defect. Although the vitreous shows pathological changes, it is not certain whether the concomitant retinal changes are the cause or the result of the condition.

Some hereditary vitreoretinal degenerative diseases may be accom­panied by poorly known systemic manifestations. Since the vitreous is a connective tissue, its participation in these disorders is expected, and concomitant retinal disorders are frequent.

The exact pathogenesis and mechanisms that explain how vitreous changes can precipitate the development of retinal disease are not yet fully known for three main reasons: no appropriate animal model is available; the morphological changes that occur in the vitreous are only partly visible in vivo; and the accompanying biochemical changes in the vitreous, when retinal disease develops, are almost completely unknown.

In spite of many careful clinical observations and much laboratory research, vitreous physiology and the pathogenesis of vitreous changes remain largely unexplored. However, a close relationship has been established between vitreous changes and retinal disease in many instances. This emphasizes the need for considering closely the changes at the vitreoretinal interface.