Contact Lens-induced
Neovascularization
BY ROBERT CAMPBELL, M.D. & PATRICK CAROLINE, C.O.T., F.A.A.O.
APR. 1996
As we all know, the human cornea is avascular except for a one-millimeter area adjacent to the limbus where there are small superficial capillaries called marginal arcades. These arcades originate from the episcleral branches of the anterior ciliary artery.
Contact lens-induced neovascularization is a common and perplexing complication found mostly in soft lens wearers. Its presence indicates some form of corneal distress, i.e., hypoxia, lens irritation or adverse response to a solution.
This month's case history involves a 41-year-old female who wore PMMA lenses from 1965 to 1982. Since 1982, she has been wearing daily wear soft contact lenses, most recently CSI lenses 8.6, -8.50, 14.8 OD; 8.6, -7.50, 14.8 OS. She uses a preservative-free, hydrogen peroxide disinfecting system due to a history of thimerosal sensitivity. Visual acuity with her present lenses is 20/20- OU with a wearing time of 14 hours a day. She is free of ocular symptoms.
Slit lamp examination showed that both lenses were centered and moving well, with approximately 0.25mm of blink-induced movement in primary position. The central corneas were clear. Peripherally, we noted 0.75mm of vascularization in the superior, inferior and temporal quadrants of both eyes (Fig. 1). On the left cornea, we noted a superior temporal area of lipid deposition with faint opacification and scarring (Fig. 2). In contact lens wearers, multiple factors can contribute to vascularization.
FIG. 1: PERIPHERAL VASCULARIZATION. |
FIG. 2: LIPID DEPOSITION AND FAINT SCAR, SECONDARY TO PERIPHERAL VASCULARIZATION. |
MECHANICAL FACTORS
Chronic dilatation of limbal vessels may be a precursor to new vessel growth. This may occur secondary to a tight or decentered soft contact lens. The tight-fitting hydrogel lens may restrict venous drainage resulting in lactic acid accumulation, a possible stimulus to corneal vascularization. Epithelial damage secondary to a damaged or deposited lens may be associated with the production of vasostimulating factors.
HYPOXIA
Corneal edema from contact lens wear can increase lactic acid production and reduce compactness of the corneal tissue. However, corneal edema with accompanying lactic acid production and loss of tissue compactness appear to be insufficient stimuli for corneal vascularization. Current theories suggest that the additional stimulus of epithelial microtrauma may also be necessary. With epithelial trauma, enzymes are released that are chemotactic for inflammatory cells. When the cells reach the site of epithelial injury, they release angiogenic factors that induce new vessel growth toward the site of the injury.
SOLUTION SENSITIVITY
The toxic effects of solution preservatives can cause vascularization in contact lens wearers. Therefore, practitioners should prescribe preservative-free lens care products for individuals who are at risk of developing vascularization.
RECOMMENDATION
Our patient discontinued wearing the low water content lenses, and we immediately refit her with PBH Precision UV lenses (74 percent water content). We instructed her to continue her present care regimen and to wear the lenses on a daily wear basis with disposal every two weeks. We'll see this patient every three months to monitor the vascularization, and if we note additional vessel growth, we'll consider the high Dk RGP lens alternative. CLS
Dr. Campbell is medical director of the Park Nicollet Contact Lens Clinic & Research Center, Minnetonka, Minn. Patrick Caroline is director of contact lens research at Oregon Health Sciences University, Portland, Ore.