Contact lenses are an important but underused tool in the management of many corneal disorders. Conceived by Leonardo da Vinci in 1508, as outlined in three of his sketches (1), proof of principle of the ability of rigid (glass) scleral contact lenses to neutralize irregular corneal astigmatism was provided by Fick and Kalt in 1888 (2). Scleral lenses were revived in 1936 by Feinbloom, a New York optometrist, who was the first to use plastic in their construction. However, their usefulness was limited by the rapid development of microcystic corneal edema (Sattler’s veil) in the short term and the development of corneal neovascularization that accompanied their longer-term use. In a seminal paper, Smelser and Ozanics in 1952 established the importance of ambient air as the primary source of oxygen needed to maintain the metabolism of corneal tissue, and scleral lens-induced corneal edema was shown to be a consequence of corneal oxygen deprivation (3). Efforts to avoid this complication by increasing the transport of oxygen-saturated tears to the underlying cornea through the introduction of fenestrations, slots, and channels were unsuccessful, and scleral lenses were virtually abandoned when rigid corneal and soft contact lenses became available.

Contact lenses are classified as rigid (hard) and flexible (soft). Their designs are described as corneal (supported entirely on the cornea), corneoscleral (supported by the cornea and sclera), and scleral (supported entirely by the sclera).

Rigid contact lenses have the unique capability to improve the optics of the damaged corneal surface by neutralizing irregular corneal astigmatism. However, exploiting their optical benefits in eyes with damaged corneas has posed significant obstacles. Because their fitting characteristics depend on the distorted geometries of diseased corneas on which they rest, it is often not possible to achieve a satisfactory result.

The inability of soft contact lenses to neutralize irregular corneal astigmatism relegates their non-cosmetic use to protecting damaged corneal surfaces from desiccation and the friction of blinking. However, this function depends on the availability of an adequate supply of tears to maintain their hydration and avoid lens adhesion that can create shearing forces at the corneal surface during blinking.

The physiologic tolerance of contact lenses depends on their ability to maintain an adequate supply of corneal oxygen (estimated to be in the order of 75 mm Hg) (4) and avoid the accumulation of carbon dioxide. The rate of gas transmission through a contact lens is directly related to the Dk (gas permeability constant) of the contact lens material and inversely to its average thickness (L) (5). Their ratio, Dk/L, is known as the gas transmissibility of a particular lens and reflects the respiratory constraints that it places on the cornea. If the gas transmissibility of a contact lens is insufficient, corneal edema will result owing to the toxic effects of the resulting acidosis (6,7). The edema threshold of Dk/L varies among normal corneas, and is significantly lower in those with impaired endothelial function (8). Prolonged lid closure, as occurs during sleep, imposes an additional hypoxic burden on the cornea and requires a significantly greater oxygen transmissibility to avoid increasing the incremental corneal swelling that normally occurs during sleep.
Chronic corneal hypoxia can induce corneal neovascularization and endothelial polymegethism (9). Moreover, it is believed that a hypoxic corneal environment increases the risk of bacterial keratitis (10).

The surface properties of contact lenses also have important clinical implications. Although the surfaces of rigid gas-permeable (RGP) and hydrogel lenses are inherently wettable, it is more accurate to describe them (and that of the mucin layer of the cornea) as transitional. Such surfaces are hydrophilic (water-attracting) when exposed to an aqueous medium and become hydrophobic (waterrepellant) when in contact with air. Most contact lenses, including soft lenses (Holden BA, personal communication), become adherent during overnight wear because of the accumulation of a sticky mucinous material that binds them to the cornea. It can be reasoned that during periods of lens immobility and stagnation of the fluid compartment between the lens and cornea, the corneal mucin layer fills the space between these two surfaces. In the absence of tear flow, the lipid content and hydrophobicity of the mucin increase. This is accompanied by the expelling of its aqueous component and, as it shrinks, this gluelike material pulls the lens against the cornea. When the adherent lens breaks free as blinking and normal tear production is reestablished on awakening, shear forces are generated at the corneal surface that can detach loosely bound epithelium (11). This phenomenon is accelerated in dry eyes and, most likely, in the presence of silicon-containing polymers.

This role has been traditionally been limited to hydrogel contact lenses. The goals are to protect the corneal epithelial surface from the desiccating effects of exposure to air and the shearing forces of blinking, and to provide relief from pain. However, their effectiveness as a corneal bandage requires an adequate tear supply to maintain lens hydration and avoid corneal adhesion. This limits their usefulness in dry eyes. Although soft lenses that have a greater bulk and lower water content are more resistant to dehydration, lower oxygen transmissibility compromises their physiologic tolerance during extended wear.

A new generation of silicon-containing hydrogel polymers offers higher gas transmissibility and better physiologic tolerance during extended wear (12). It is unclear whether their hydrophilic coating is effective in reducing the incidence of overnight adhesion.

Use of soft bandage lenses in corneal disorders requires close monitoring. The extended wear of soft contact lenses has been shown to increase the risk of microbial keratitis (13), which is probably further increased in the presence of epithelial defects.