Mechanical epithelial defects
The contact lens is a foreign body that rubs across and is pressed against the corneal epithelium with each blink, thousands of times each day. Surprisingly, this only occasionally results in an abrasion. Corneal abrasions from contact lens wear need to be recognized and treated because they indicate chronic epithelial stress due to the contact lens. Epithelial defects can allow bacteria to penetrate the cornea, resulting in a stromal infection. Chronic corneal epithelial trauma can stimulate subepithelial fibrosis in the absence of an infection. The specific abrasion pattern often provides the necessary clues to indicate what problem can be corrected to improve the comfort and safety of the patient.
Manipulation of a contact lens during insertion and removal can traumatize the epithelium creating painful abrasions of various shapes and sizes. These abrasions usually heal quite rapidly with simple lubrication or patching. Debris trapped under a contact lens or a chip or tear in the edge of a contact lens can produce dramatic curvilinear abrasions. Removal of the debris or replacement of the damaged contact lens is all that is needed to treat this problem.
Punctate epithelial erosions occur commonly with contact lens wear and have several causes. Three staining patterns are characteristic for rigid lenses, as follows: central, peripheral, and 3- and 9-o’clock positions. If a lens is too flat for the particular cornea, it may produce central punctate staining. A steep cornea, such as in keratoconus where the lens rubs on the tip of the cone, is a typical example. A lens that is too steep for the cornea can produce peripheral punctate staining patterns, often in a superior arcuate shape. A poorly moving lens or one with a large optical zone may produce superior arcuate staining.
The most common staining pattern occurs between the lens and the limbus in the interpalpebral fissure (at the 3- and 9-o’clock positions). This epitheliopathy is caused by the contact lens lifting the lid away from the cornea and poor tear stability with subsequent drying of the cornea. This often is exacerbated by an incomplete blink. A small amount of staining (at the 3- and 9-o’clock positions) is benign, but persistent epithelial erosions can lead to dellen formation, neovascularization, Salzmann-type elevated lesions, and pseudopterygium formation. This type of punctate staining is alleviated by decreasing the distance from the lens to the limbus with a larger lens, reducing edge lift with a thinner-edged lens or steeper fit, or refitting with a lens that rests under the upper lid (alignment fit).
Punctate staining by soft lenses is not as common as with rigid lenses but can occur. Soft lenses that cause excessive desiccation can cause an inferior central or inferior arcuate pattern. Usually, these patients have minor symptoms of mild irritation or slightly decreased vision. Refitting with a higher water content lens or RGP lens usually eliminates the problem.
Epithelial splitting is a common finding in asymptomatic soft contact lens wearers. This finding often is overlooked on a routine examination because it usually does not cause severe symptoms and may be covered by the upper lid. Epithelial splits are horizontal, linear, white, faintly staining epithelial defects in the superior cornea, which often are asymptomatic during lens wear and produce mild foreign body sensation after the lens has been removed. The splits usually heal after the lenses have been out for 24 hours and refitting with RGP lenses prevents recurrence.
Chemical epithelial defects
Various contact lens chemical solutions can produce a range of epithelial defects from marked erosions to less extensive punctate defects. Surfactant cleaning solutions that are left on the lens after cleaning usually cause immediate pain, redness, photophobia, and tearing upon lens insertion. These symptoms typically disappear after 1-2 days.
If hydrogen peroxide is placed on the eye, it can cause intraepithelial and subepithelial gas bubbles. These bubbles have a dramatic appearance and can cause significant but usually temporary vision loss. The bubbles typically resolve without permanent sequelae within minutes to hours. However, hydrogen peroxide can cause a permanent refractive change by altering the shape of the cornea.
Enzyme cleaner and chemical disinfection solutions can cause more subtle and intermittent punctate epithelial defects. This condition may require careful investigation and systematic elimination of various lens care products to identify and remove the offending agent. Use of preservative-free solutions and proper use of hydrogen peroxide disinfection usually solves this problem.
Hypoxia
Because the oxygen requirements of the cornea are met by direct diffusion of oxygen from the corneal surface, the barrier of the contact lens reduces the amount of available oxygen. Contact lens wear (especially with a closed lid during sleep) can cause acute hypoxia. If mild, hypoxia produces epithelial edema and temporary blurred vision; if severe, it can cause epithelial cell death and desquamation. Patients usually experience discomfort and remove the contact lenses before the acute hypoxia becomes severe. Typically, the conjunctiva is hyperemic, and the epithelium has fine punctate defects, producing temporary decreased vision and photophobia.
Chronic hypoxia produces a variety of more subtle effects, such as epithelial microcysts. Contact lens users who sleep in their lenses are prone to developing epithelial microcysts. These transparent epithelial inclusions of degenerated epithelium are about 10-15 µm, begin in the deep epithelium, and slowly migrate anteriorly. Upon reaching the surface, they rupture, creating depressions that pool with fluorescein. Epithelial microcysts seldom produce any significant symptoms other than a mild decrease in vision. Surprisingly, it takes several weeks for the microcysts to disappear after discontinuation of the contact lenses. Either the mitotic rate is reduced below normal or the microcysts continue to be produced long after the contact lenses are removed.
One of the hallmarks of chronic corneal hypoxia is superficial neovascularization, especially along the superior limbus. Neovascularization of less than 2 mm from the limbus is not visually significant and generally is well tolerated but is a sign of hypoxia and may be a harbinger of more significant problems. Rarely, deep stromal neovascularization can occur. Changing to lenses that are thinner or contain materials with greater oxygen permeability, have greater lens movement, and decreasing wear time (especially eliminating overnight wear) can greatly reduce the risk of progression.
Chronic hypoxia has been implicated as a cause of the decreased corneal sensitivity that occurs with prolonged contact lens wear and may be partly the reason why some patients have increased comfort with long-term wear and why they often have decreased comfort with a change from polymethyl methacrylate (PMMA) to gas-permeable contact lenses.
The corneal epithelium is thinner in contact lens wearers. This change may be due to chronic hypoxia and decreased mitotic activity. In addition to thinning of the epithelium, extended wear is associated with decreased epithelial shedding, increased cell size, and increased binding of Pseudomonas aeruginosa to the cell surface. All of these effects could reduce the resistance of the cornea to bacterial infection. The thinner epithelium poses less of a barrier to bacterial penetration. The reduced shedding of epithelial cells allows the attached bacteria to remain on the eye for longer periods of time. The increased binding of bacteria, such as P aeruginosa, enables greater numbers of bacteria to attach to the epithelial surface.
The physiology of the corneal epithelium also is altered by contact lens wear. The barrier function of the epithelium is reduced, and the permeability to fluorescein is doubled after as little as 2 weeks of soft contact lens wear. Similarly, rigid contact lenses can alter the epithelial permeability.
Superficial immunologic reactions
A variety of chemicals in contact lens solutions can elicit superficial toxic or immune reactions. The typical response is a fine punctate keratopathy, conjunctival injection, tearing, itching, and occasionally chemosis.
The preservative, thimerosal, which is now rarely used, produced a keratoconjunctivitis in as many as 10% of contact lens wearers who used thimerosal-preserved products. Essentially, it has disappeared from use, but other chemicals used as preservatives or disinfectives can produce similar pathology, so recognition of this condition is helpful.
The earliest symptoms are mild and nonspecific (eg, foreign body sensation, conjunctival hyperemia, variable mixed follicular-papillary hypertrophy), which present gradually after weeks or years of uneventful contact lens wear. The superior limbus becomes progressively more hyperemic and a triangle of punctate keratopathy extends downward from the involved limbus toward the central cornea. If allowed to proceed, the epitheliopathy may progress to an opaque pannus with microcysts.
A problem associated with the use of chemical disinfection systems and seen with increasing frequency is the development of small, gray, epithelial, granular opacities that resemble the epithelial opacities of Thygeson superficial punctate keratopathy. The round, gray-white granules appear to be on the surface of the epithelium and are scattered randomly across the cornea. They are similar to Thygeson superficial punctate keratopathy, but they tend to be small and stain less intensely with fluorescein. These opacities are associated with symptoms of foreign body sensation, tearing, photophobia, lens intolerance, and conjunctival injection. The symptoms resolve over a few days after the chemical disinfecting solution is discontinued.
Thimerosal and other chemicals used in disinfection systems also can produce subepithelial infiltrates similar to those seen in adenoviral conjunctivitis. Changing to a preservative-free hydrogen peroxide based disinfection system or to gas-permeable lenses allows these deposits and infiltrates to resolve. However, it may take weeks for the pathology to disappear.
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