ANATOMY AND PHYSIOLOGY

Anatomy

The vitreous is a transparent elastic hydrogel (Figure 14-1). It occupies about 80% of the volume of the eye (Figure 14-2). During embryonic development, primary, secondary, and tertiary vitreous are formed and laid down (Figure 14-3). Their genesis is described in detail in Chapter 2. Briefly, the primary vitreous is associated with the hyaloid vascular supply system, which nourishes the lens during development. The secondary vitreous is laid down around the primary vitreous and forms the definitive (adult) vitreous, whereas the tertiary vitreous contributes to the formation of the lens zonules.

Figure 14-1 Vitreous after dissection of the sclera, choroid, and retina. A band of dark tissue can be seen posterior to the ora ciliaris retinae, circling the dorsal two thirds of the vitreous. This is neural retina that was firmly adherent to the vitreous base and could not be dissected. The vitreous also remains attached to the anterior segment (ciliary body, iris, and lens). The vitreous is almost entirely gel and thus is solid, maintaining its shape even though situated on a surgical towel exposed to room air.

(From Yanoff M, Duker JS [2004]: Ophthalmology, 2nd ed. Mosby, St. Louis).

Figure 14-2 The vitreous body (shaded area) occupies the posterior compartment of the eye.

(Modified from Fine BS, Yanoff M [1979]: Ocular Histology. Harper & Row, New York.)

Figure 14-3 Stages of vitreous development. Primary vitreous and hyaloid vessels nourishing the embryonic lens. B, The secondary vitreous laid down around the primary vitreous, which condenses into Cloquet’s canal. The secondary vitreous will become the adult vitreous. C, Tertiary vitreous (lens zonules or ligaments) at the lens periphery.

(Courtesy Dr. G.A. Severin.)

The vitreous body is divided into the following zones (Figure 14-4):

1. Anterior vitreous, located anterior to the ora ciliaris retinae (see Figure 14-4, area 5)

2. Posterior vitreous, located posterior to the ora ciliaris retinae (see Figure 14-4, area 7)

3. Cortex, which comprises the peripheral vitreous (see Figure 14-4, area 12), including:

a. Vitreous base, which is the attachment of the vitreous at the ora ciliaris retinae (see Figure 14-4, area 6)

b. Peripapillary vitreous, located adjacent to the optic disc (see Figure 14-4, area 10)

4. Central vitreous, including Cloquet’s canal (see Figures 14-3 and 14-4, area 13). Cloquet’s canal, which is a cleft in the vitreous where the hyaloid vasculature passed during embryonic development, is visible with the biomicroscope (see Figure 14-3, B and C).

Figure 14-4 Relations and attachments of the vitreous body: 1, attachment of anterior zonular fibers to the lens; 2, attachment of posterior zonular fibers to the lens; 3, attachment of anterior vitreous face to posterior lens capsule; 4, anterior extremity of Cloquet’s canal (Mittendorf’s dot); 5, anteriormost attachment of vitreous base to mid pars plana; 6, region of vitreous “base”; 7, region of diminishing adherence of vitreous base to retinal surface; 8, vitreous-retinal attachment; 9, vitreous-retinal attachment at margin of fovea centralis (absent in domestic animals); 10, attachment of posterior vitreous around optic disc; 11, posterior extremity of Cloquet’s canal (Bergmeister’s papilla); 12, cortical vitreous; 13, central vitreous. Density of lines indicates approximate relative degrees of strength of attachment.

(Modified from Fine BS, Yanoff M [1979]: Ocular Histology. Harper & Row, New York.)

Composition

Vitreous is a complex gel with the following constituents:

• Water (99%)

• Collagen fibers, which serve as a skeleton for the gel

• Cells (hyalocytes)

• Hyaluronic acid

Collagen fibrils form a meshwork internal to the retina (the vitreous cortex) and intermingle with the fibers of the internal limiting membrane of the retina, thus forming a firm attachment between the vitreous cortex and the retina (Figure 14-5). Therefore anterior movement of the vitreous (such as occurs after lens luxation) may pull the retina off the retinal pigment epithelium (RPE) and cause traction retinal detachment. A potential space exists between the vitreous and the inner surface of the retina. Blood and exudates may accumulate in this space if the vitreous and retina separate, resulting in subhyaloid hemorrhage.

Figure 14-5 The vitreous base near the peripheral retina. The MŸller cells (a) have a basement membrane (b) that forms the inner limiting membrane of the retina. The collagen fibrils (c) of the vitreous base form a meshwork internal to the retina. These fibrils join the internal limiting membrane.

(From Hogan MJ, et al. [1971]: Histology of the Human Eye. Saunders, Philadelphia.)

The collagen fibrils are also responsible for the numerous attachments of the vitreous to the adjacent structures—the posterior lens capsule, the ora ciliaris retinae (the vitreous base), and the optic nerve head (see Figure 14-4). Collagen fibrils are present in greater concentrations at the vitreous bases and around the optic disc, where attachment is the strongest.

The lens sits in a depression in the anterior face of the vitreous cortex, the hyaloid fossa (patella fossa). Collagen fibrils form attachments between the posterior lens capsule and the anterior vitreous. These attachments are especially significant in dogs. Removal of the posterior lens capsule, as in intracapsular lens extraction, results in loss of vitreous.

Hyalocytes are numerous within the vitreous and are more numerous near the cortex. The functions of these cells are unclear, but they may possess secretory and phagocytic capabilities as well as the potential for reversion to primitive fibroblasts able to form scar tissue. Mucopolysaccharides, containing a high proportion of hyaluronic acid, are intimately related to the collagen fibrils and hyalocytes and are present in higher concentration where hyalocytes are common. Hyaluronic acid provides the viscoelasticity of the vitreous body.

With the exception of collagen and hyaluronic acid, aqueous humor and vitreous are similar in composition, with free movement of many substances between them. The principles that govern entry of substances, including drugs, from the vascular circulation into the aqueous humor generally apply to the vitreous as well.

Function

The vitreous does not have a specific and clearly defined role in ocular physiology of the adult. It contributes to maintaining ocular volume and possibly the shape of the globe. It also helps maintain some ocular structures, notably the lens and retina, in their correct anatomic locations. Also, it forms part of the optical pathway that light must pass on its way to the retina. However, the vitreous does not have a significant role in refraction of this light, because its refractive index is similar to that of the lens.

PATHOLOGIC REACTIONS

Because of its simple structure and lack of vascular and lymphatic supply, the vitreous has a limited range of pathologic reactions, as follows:

• Liquefaction: Because of its high water content, the vitreous gel may liquefy (syneresis) in response to many stimuli (e.g., infection, trauma, uveitis, senile changes). After liquefaction, the vitreous separates from the retina, encouraging retinal detachment from the underlying RPE. Liquified vitreous may also enter the subretinal space through retinal holes, predisposing to rhegmatogenous retinal detachment.

• Cicatrization: After inflammation of surrounding tissues or infection, scar tissue may form in the vitreous. These vitreous bands may contract and detach the retina (traction detachment).

• Proliferative vitreoretinopathy: This reaction occurs in association with retinal disease. In response to retinal disease, glial or RPE cells proliferate on the innermost retina or in the vitreous and form scars. Subsequently, these fibrotic membranes may form that pull on the retina, causing it to tear and detach.

• Vascularization: The vitreous has no blood supply, but blood vessels may grow into it from an inflamed or malformed retina (neovascularization). These vessels often are incomplete or fragile and are a source of vitreous hemorrhage (e.g., in the collie eye anomaly).

• Infection and inflammation: These reactions are discussed later.

• Elongation: Elongation of the vitreous body causes elongation of the axial length of the eye and, consequently, of the pathway that light must pass on its way to the retina. As a result, light that was previously focused on the retina is now focused in front of the retina, thereby causing shortsightedness (myopia). Such elongation occurs as a result of visual deprivation during the neonatal period. It may be induced by lid suturing and other deprivation techniques during the critical developmental period in animal models of myopia. It may also occur naturally, as a result of neonatal cataracts or corneal opacities that cause visual deprivation, resulting in neonatal myopia (as well as abnormalities in the visual cortex). This is another reason why congenital ocular opacities should be corrected as soon as possible, before irreparable changes occur in the eye, and why third eyelid flaps and tarsorrhaphies should be carefully considered in neonates.

Congenital and Developmental Abnormalities

Persistent Hyaloid Artery

The hyaloid artery is part of the embryonic vascular supply of the lens, which is described in Chapter 2. In most species, the hyaloid artery atrophies within a few weeks after birth (see Figure 14-3). An exception is ruminants, in which remains of the artery may be observed in a significant number of adults. However, persistent remnants of varying extent may be found in any species. The remnants of the artery origins on the surface of optic disc, which are surrounded by glial tissue, are called Bergmeister’s papilla (see Figure 14-4, area 11). These appear ophthalmoscopically, end-on, as red to white tufts originating from the optic disc and extending anteriorly a variable distance into the vitreous (see Figure 2-10, B, in Chapter 2). Similarly, at the distal end of the artery, remains of its attachment to the posterior lens capsule may be seen. The remains are known as Mittendorf’s dot (see Figure 14-4, area 4). It does not interfere with vision, except for rare occasions when it induces focal, posterior cataracts. A persistent artery, however, may extend from the disc all the way to the posterior lens. Persistence of the hyaloid artery may be hereditary in the Doberman pinscher and Sussex spaniel. In rats, the hyaloid artery may bleed into the vitreous during normal atrophy.

A persistent hyaloid artery and its attachment to the posterior lens capsule must be differentiated from the following conditions by the following means:

• Posterior capsular and subcapsular cataracts: By accurate localization of the opacity. In the golden retriever and Labrador retriever, Mittendorf’s dot is differentiated from a cataract on the basis of its smaller size and location on the posterior lens capsule. The cataract is much larger and is usually triangular, and careful examination may determine that it is located in the posterior lens cortex, rather than capsule. Mittendorf’s dot usually has the anterior remnant of the hyaloid artery attached as a small white “tail” visible biomicroscopically.

• Normal lens sutures (especially in cattle and horses): By familiarity with the normal appearance

• Vitreous bands: By the linear appearance of the bands, which are usually located outside Cloquet’s canal as well as by the presence of other signs of injury or inflammation (see Acquired Disorders)

• Persistent tunica vasculosa lentis and persistent hyperplastic primary vitreous: By the more extensive nature of the opacity on the posterior lens capsule (see following sections)