CLINICAL DESCRIPTION:
Vascularized 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
o Patients are usually asymptomatic
o Epithelial chafing
o Micro superficial punctate keratitis
(SPK)
o Epithelial heaping
Stage II - Inflammatory Response
o Subjective mild ocular irritation
o Hyperemia
o Infiltration
o Coalesced SPK
Stage III - Vascularization
o Moderate hyperemia
o Vascular leash extends to the mass
o Collar around the infiltrate
o Wear time decreased
Stage IV - Erosion
o Increase in symptomology
o Erosion of the epithelial mass
o 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
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