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The last three decades of the twentieth century saw an explosion of interest in the vitreous because of the development of vitreoretinal surgery. Prior to this period, large numbers of patients were blinded by inoperable vitreoretinal diseases. One goal of this chapter is to help the medical student, intern, resident, general ophthalmologist and optometrist become aware of the indications for vitreoretinal surgery, many of which are time sensitive. Many vitreoretinal conditions have implications for the family medical practitioner, internist, and emergency physician.

The vitreous fills the space between the lens and the retina and consists of a three-dimensional collagen fiber matrix and a hyaluronan gel (Figure 9–1). (The older term, “vitreous humor” is less commonly used today.) The outer surface of the vitreous, known as the cortex, is in contact with the lens (anterior vitreous cortex) and adherent in varying degrees to the surface of the retina (posterior vitreous cortex) (Figure 9–2).

Figure 9-1.

The vitreous consists of a three-dimensional matrix of collagen fibers and a hyaluronan gel.

Figure 9-2.

The vitreous cortex is adherent to the lens and especially to the retinal surface to varying degrees.

Aging, hemorrhage, inflammation, trauma, myopia, and other processes often cause hypocellular contraction of the vitreous collagen matrix. The posterior vitreous cortex then separates from areas of low adherence to the retina and may produce traction on areas of greater adherence. The vitreous base extends from the equator anteriorly and is a zone of great adherence. The vitreous virtually never detaches from the vitreous base. The vitreous is also adherent to the optic nerve and, to a lesser extent, the macula and retinal vessels. Adherence to the macular region is a significant factor in the pathogenesis of epimacular membrane, macular hole, and vitreomacular traction syndrome.

Previously it was taught that the vitreous developed cavities from a process known as syneresis, ultimately resulting in “collapse” of the vitreous. It is now believed that collagen cross-linking and selective loss of retinal adherence rather than cavity formation are the primary events. Even though the vitreous may migrate inferiorly when separated from the retina, this process causes less force at the zones of vitreoretinal adherence than the traction caused by saccadic eye motion. Saccadically induced, dynamic forces play a significant role in the development of retinal breaks (tears), damage to the retinal surface, and bleeding from torn vessels (Figure 9–3). Further contraction of the vitreous caused by invasion of retinal pigment epithelial, glial, or inflammatory cells may result in sufficient static traction to detach the retina without retinal tears.

Figure 9-3.

Motion of partially detached vitreous (white arrow), induced by saccades (black arrow) and resulting in a retinal break (arrowhead).


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