Association of Optometric Contact Lens Educators

Contact Lens-Induced Superior Limbic Keratoconjunctivitis (CLSLK)

CLINICAL DESCRIPTION:
Contact Lens-Induced Superior Limbic Keratoconjunctivitis (CLSLK) is a contact lens-related, inflammatory condition involving the corneal epithelium and stroma, the limbus, and the bulbar and tarsal conjunctiva.  CLSLK should be differentiated from Theodore’s Superior Limbic Keratoconjunctivitis, which has an almost identical presentation but is unrelated to contact lens wear.

Clinical findings are usually bilateral and include:  fine papillary hypertrophy with scattered petechiae on the superior tarsal conjunctiva; injection, edema, and staining (rose bengal and fluorescein) of the superior bulbar conjunctiva and limbus; rose bengal and fluorescein staining of the superior cornea; epithelial dulling or irregularity of the superior cornea; and epithelial and subepithelial infiltration of the superior cornea.  More advanced cases may have U or V-shaped patterns of subepithelial haze or fibrovascular pannus in the superior cornea.  Some references indicate that corneal filaments are rarely seen in cases of CLSLK, while common with Theodore’s SLK. 

SYMPTOMS:
Patients with CLSLK may complain of increased lens awareness, lens intolerance, burning, itching, photophobia, redness, or increased lacrimation.  Reduced vision is uncommon, but may occur in extremely advanced cases with extensive pannus formation.

INCIDENCE:
CLSLK generally occurs in individuals who have worn soft contact lenses from two months to three years.1  Although the incidence and prevalence of CLSLK in the general population are not known, there is some idea as to the prevalence of the condition among symptomatic contact lens wearers.  Wilson-Holt and Dart2, in a 1989 retrospective evaluation, found that 17.6% of contact lens complications were attributed to CLSLK.  A similar study in 1992 reported the percentage as 6.5%.3  The decline in cases of CLSLK over this time period corresponds with the increase in frequent replacement lenses and the decline in use of solutions containing thimerosal.  Thimerosal was commonly used as a preservative in contact lens solutions up until the mid-1980’s. 

ETIOLOGY:
At the present time, CLSLK is a condition with an uncertain multifactorial etiology.  Suggested causes include mechanical irritation, hypoxia, and hypersensitivity.  Immune reactions to contact lens deposits or preserved care regimens have been implicated.  When combined with upper eyelid motion, excessive contact lens movement, deposits on the posterior contact lens surface, and contact lens design all appear to play some part in developing CLSLK. 

An hypoxic environment is created at the superior limbus by the combined effects of the contact lens and the lid, which may play a role in CLSLK development.  The preservative thimerosal has historically been known to cause an intense delayed hypersensitivity reaction in contact lens patients.  Many patients were reported to have developed CLSLK due to thimerosal hypersensitivity. Thimerosal, however, has practically been eliminated from contact lens care products and CLSLK has not been eradicated.  Based on the clinical signs, an immune component to CLSLK is most strongly indicated. 

MANAGEMENT:
Lens wear should be discontinued and ocular lubrication should be prescribed until signs and symptoms improve. The current pair of lenses should be discarded.  Prostaglandin inhibitors have some therapeutic value, but are not necessary for resolution of CLSLK.  With CLSLK, symptoms should quickly disappear upon lens removal; this finding has been used to differentiate CLSLK from Theodore’s SLK, where symptoms continue.

When signs and symptoms have resolved, the patient can be refit with a different lens design or polymer to reduce possible mechanical irritation and increase oxygen supply to the superior limbus.  A preservative-free care system, daily replacement lenses, and contact lens rewetting drops should be considered as well. 
 

KEY REFERENCES:

1. Abel R, Shovlin JP, DePaolis MD.  A Treatise on Hydrophilic Lens Induced Superior Limbic Keratoconjunctivitis.  Int Contact Lens Clin 1985; 12(2): 116, 119-123.
2. Wilson-Holt N, Dart JKG.  Thimerosal Keratoconjunctivitis, Frequency, Clinical Spectrum and Diagnosis.  Eye 1983; 3:581.
3. Stapleton F, Dart J, Minassian D.  Nonulcerative Complications of Contact Lens Wear.  Arch Ophthalmol 1992; 110:1601.

1. Campbell R, Caroline P.  Contact Lens Induced Superior Limbic Keratoconjunctivitis.  Spectrum 1996; 2: 56.
2. Efron N.  Superior Limbic Keratoconjunctivitis.  In:  Efron N.  Contact Lens Complications.  Woburn, MA: Butterworth-Heinemann, 1999: 50-57.
3. Efron N. Contact Lens-Induced Superior Limbic Keratoconjunctivitis.  Optician 1997; 213 (5599): 20-26.
4. Sendele D, Kenyon K, Mobilia E.  Superior Limbic Keratoconjunctivitis in Contact Lens Wearers.  Ophthalmol 1983; 90: 616-622.
5. Silbert JA.  Contact Lens-Induced SLK vs. Theodore’s SLK.  Review of Optometry 1996; 133(4): 95-96.
6. Stenson S.  Superior Limbic Keratoconjunctivitis Associated with Soft Contact Lens Wear. Arch Ophthalmol 1983; 101(3): 402-404.