VLK in Veteran GP Lens Wearers
BY WILLIAM L. MILLER, OD, PHD, FAAO
Vascularized limbal keratitis (VLK) was first described and staged in 1989 by Grohe and Lebow. Only a few publications have since described it and few if any have discussed its role in GP contact lens dropouts. One report in the literature describes VLK's association with an early generation GP contact lens that had undergone crazing. Some have referred to VLK as a pseudopterygium, while others have suggested a relation to Salzmann's nodular degeneration. The latter is due in part to its histopathological appearance as described by Caroline and André in their Contact Lens Case Reports column in February 2006.
VLK is an adverse inflammatory event that occurs primarily in GP lens wearers and is related to mechanical irritation. The limbal area contains immunological cells such as Langerhans and stem cells that make it vulnerable and sensitive to constant mechanical irritation regardless of the source. Mechanical irritation caused by lens edge trauma can result from a large diameter lens, an inadequately shaped lens edge, a lens with excessive apical clearance or one with an inadequate edge clearance.
Patients who have VLK will present with ocular irritation, the level of which will vary widely among patients. Most will complain of moderate irritation or pain with an ever increasing area of redness at the VLK site, usually presenting as a unilateral anomaly. They will also experience varying levels of photophobia and lacrimation. GP lens wearing time will be reduced.
Biomicroscopy will reveal a raised, semiopaque lesion bridging the limbal border with prominent vascularization of the lesion and adjacent conjunctival hyperemia (Figure 1). The surface of the lesion, depending on its stage, will exhibit epithelial erosion.
Figure 1. VLK lesion.
The life cycle of VLK is broken down into four stages, with increasing symptoms for each successive stage: Stage 1, hyperplasia; Stage 2, inflammation; Stage 3, vascularization; Stage 4, epithelial erosion. VLK can be confused with phlyctenules, but the mechanical etiology, vascularization and overall general appearance aids in the differential diagnosis.
VLK is self-limiting and will resolve with scarring and residual vascularization. However, this resolution may take several days and is likely to discourage GP contact lens wearers. I prefer a more aggressive management with topical therapeutics and eventual GP parameter changes.
Many of my patients dislike ceasing lens wear, but because the evolution of VLK lesions is mechanically induced, patients must discontinue wear. I then prefer a mild topical steroid like Lotemax, Alrex (both Bausch & Lomb) or Flarex (Alcon), but depending on the magnitude of the problem you can also prescribe topical nonsteroidal inflammatories such as Voltaren (Novartis) or Acular (Allergan) or stronger steroids such as Pred Forte (Allergan).
You may also wish to add a non-preserved tear supplement, especially if you suspect that a patient will continue to wear his GP contact lens regardless of your best advice to cease wear. GP modifications include decreasing the overall diameter of the lens and increasing the peripheral curve to increase the edge lift.
Bill the initial visit and follow-up visits for patients who have VLK with the appropriate 992XX code. CLS
Dr. Miller is the Director, Cornea and Contact Lens Service at the University of Houston College of Optometry. He is a member of the American Optometric Association and serves on its Journal Review Board. You can reach him at email@example.com.