Living Library

Vascularized Limbal Keratitis (VLK)

CLINICAL DESCRIPTION:
Figure 2Figure 1Vascularized limbal keratitis (VLK), as coined by Grohe and Lebow in1989, is a unique, inflammatory rigid lens complication that involves the conjunctiva, limbus and cornea.    Objectively, the practitioner observes an elevated, semi-opaque epithelial lesion with a diffuse ill-defined border that bridges the limbus (Figure 1).  Localized conjunctival injection, adjacent and overlying corneal epithelial staining and corneal vascularization are also observed with the condition (Figure 2). 
SYMPTOMS:
Patients typically complain of discomfort, photophobia, lacrimation, lens awareness, decreased wearing times and often visualization of the lesion.
INCIDENCE: 
The phenomenon occurs with both daily and extended rigid lens wear of PMMA, silicone/acrylate and fluorosilicone/acrylate materials. The common denominator is most often a large diameter, steep fitting and/or low edge lift lens design.
ETIOLOGY:
The condition is a result of chronic irritation usually secondary to desiccation, abnormal tear wetting or distribution, and mechanical impingement. A mechanism for the immunological response in VLK has been postulated.  However, complete histological studies of the lesions have not been reported. The limbus has been identified as an immunologically sensitive tissue that, due to its close proximity to the conjunctival vascular plexus, serves as the transition zone to the cornea with a predisposition towards an inflammatory response.   Mast cells within limbal tissue provide a pathway for the release of vasoactive substances which dilate blood vessels, produce peripheral and conjunctival edema and attract inflammatory cells. Most notably, the attraction of eosinophils to the region may induce the symptoms of discomfort and lens awareness. 
Also implicated in the immune response is the greater concentration of Langerhans cells in the peripheral cornea that represent a significant factor in the development of ocular hypersensitivity and the development of peripheral corneal infiltration. Finally, the role of edema in serving as a precursor to inflammation has been postulated through involvement of the corneal stem cells.  The stem cells, which are primarily located in the limbus, are the source for the differentiation and proliferation of the corneal epithelium. Any substantial insult, such as contact lens induced mechanical impingement near the limbus could compromise the cornea's ability to heal.
MANAGEMENT:
Grohe and Lebow categorized the disease process into clinical stages that aid in establishing appropriate treatment protocols.  A summary of the key stages are as follows.
  •  Stage I - Hyperplasia
    • Patients are usually asymptomatic
    • Epithelial chafing 
    • Micro superficial punctate keratitis (SPK)
    • Epithelial heaping
  • Stage II - Inflammatory Response
    • Subjective mild ocular irritation
    • Hyperemia
    • Infiltration
    • Coalesced SPK
  • Stage III - Vascularization
    • Moderate hyperemia
    • Vascular leash extends to the mass
    • Collar around the infiltrate
    • Wear time decreased
  • Stage IV - Erosion
    • Increase in symptomology
    • Erosion of the epithelial mass
    • CL wear may be unbearable
Ocular lubricating, decongestant and antioxidant drops have been described as providing relief in early stages; the vasoconstrictive effect of ocular decongestants can limit progression to more advanced stages by reducing vascular permeability and vessel engorgement.  Advanced cases with infiltration and vascularization often respond best with corticosteroid treatment.  Corticosteroids can prevent or suppress the responses associated with inflammation, such as pain, redness, swelling, and local heat. 
The management plan after resolution of each stage is the same. A reduction in mechanical irritation and/or an increase in tear distribution must be established by one or more of the following changes to the RGP lens:  decreasing the overall diameter, flattening the base curve and/or, increasing edge lift.
Another key management factor in preventing recurrence of the VLK phenomenon is maintenance of the precorneal tear film and lens wettability through the prevention of organic and inorganic deposition on the lens surfaces.
KEY REFERENCES:
Grohe RM and Lebow KA.  Vascularized limbal keratitis. ICLC 1989;16(7&8): 197-208. 
Davis L and Lebow K.  Noninfectious corneal staining.  In Silbert JA (ed):  Anterior Segment Complications of Contact Lens Wear,Second Edition. Butterworth-Heinemann 2000;78-9.
OTHER REFERENCES:
McMonnies CW. Contact lens induced corneal vascularization. ICLC 1983;10(1):12-21. Lebow KA. Reduce three-and-nine corneal staining with moderateedge-lift profiles. Contact Lens Spectrum 1990 29-33.
Edwards K, Hough T. Contact-lens related case studies: Vascularised limbal keratitis. Optician 1998, 216 (5680): 36-37.

Cornea and Contact Lens Living Library
Vascularized Limbal Keratitis (VLK)

Edited by:
Jennifer Smythe, O.D., Pacific University College of Optometry
Ronald Watanabe, O.D., New England College of Optometry