Vascularized Limbal Keratitis
BY ROBERT CAMPBELL, M.D. & PATRICK CAROLINE, C.O.T., F.A.A.O.
Almost daily, we examine patients who wear rigid contact lenses who have some degree of peripheral corneal complication. This can include 3 and 9 o'clock staining, corneal vascularization, dellen formation, contact lens-induced pseudopterygia, and the new kid on the block -- vascularized limbal keratitis (VLK).
SIGNS OF VLK
Grohe and Lebow first adequately described and differentiated VLK from other peripheral corneal anomalies in 1989. The condition is hallmarked by an ill-defined, elevated, opaque limbal mass. The lesion occurs along the horizontal axis at 3 and 9 o'clock or at 4 and 8 o'clock. There can be extensive corneal staining at the lesion site with a lesser degree of limbal staining. Both superficial and deep vascularization may be present, especially in the more advanced stages.
Patients with active VLK typically complain of increased lens awareness and reduced wearing time. Many patients report they can see a 'white spot' on the cornea with localized conjunctival injection.
AN OLD MYSTERY SOLVED
This month's case history describes two rigid contact lens wearers who had unidentified elevated peripheral lesions. The patients were examined and photographed in 1977 and 1978. The records indicated that both patients had been wearing PMMA lenses successfully for more than five years before the onset of symptoms. Today, the diagnosis would most likely be vascular limbal keratitis.
VLK begins as a heaping of hyperplastic corneal tissue secondary to lateral lens movement with eye excursion. This is followed by conjunctival hyperemia and corneal infiltration. Ultimately, a vascular leash emanating from the conjunctiva leads to the elevated epithelial mass. There may be erosions of the elevated nodule with significant corneal staining and hyperemia.
FIG. 1: PMMA-INDUCED VASCULARIZED LIMBAL KERATITIS, 1977
FIG. 2: PMMA-INDUCED VASCULARIZED LIMBAL KERATITIS, 1978.
The etiology of VLK appears to be related primarily to large lens diameters with minimal peripheral clearance. This may explain why VLK occurs more frequently with modern RGP lens designs versus traditional PMMA designs that often incorporated smaller posterior optical zone diameters with wide, flat peripheral curves.
The condition can be treated by improving the peripheral lens-to-cornea relationship. Initial design modifications should include flatter and wider peripheral curves to reduce epithelial chafing, and smaller overall diameters to reduce peripheral impingement. Ocular lubricants can relieve some of the symptoms and aid in corneal wetting.
In more advanced stages, it may be necessary to temporarily discontinue lens wear and initiate antibiotic/steroid therapy.
Temporarily discontinuing lens wear along with appropriate lens design modifications often resolves the condition. To date, most VLK patients we have treated have successfully returned to RGP lens wear with no recurrence of the condition.
This month's case history describes two patients with unidentified peripheral corneal lesions who sought treatment from university cornea specialists in the late 1970s. The etiology, differentiation and treatment of these lesions remained a mystery until 1989 when two private practitioners pieced together a syndrome they called vascularized limbal keratitis. CLS
Dr. Campbell is medical director of the Park Nicollet Contact Lens Clinic & Research Center, Minnetonka, Minn. Patrick Caroline is an assistant professor of optometry at Pacific University, Forest Grove, Ore., and director of contact lens research at Oregon Health Sciences University, Portland, Ore.