Superior limbic keratoconjunctivitis is characterized as an inflammation of the superior bulbar conjunctiva with predominant involvement of the superior limbus, an adjacent epithelial keratitis, and a papillary hypertrophy of the upper tarsal conjunctiva.
In 1963, Thygeson and Kimura described it as a chronic, localized, filamentary conjunctivitis. Contemporaneously, this condition was given its name, superior limbic keratoconjunctivitis (SLK), by Theodore. Five years later, Tenzel and Corwin each reported an association between thyroid abnormalities and SLK.[2, 3] A mimicking disorder has been encountered in soft contact lens (SCL) wearers, typically with exposure to thimerosal-preserved solutions.[4, 5]
In the US, The frequency of superior limbic keratoconjunctivitis has been reported to be 3% in a cohort of Graves ophthalmopathy patients, but it is much lower in the general population. Although no racial predilection exists, middle-aged people (range, 4-81 y) and women are predominantly affected.
In general, the prognosis for superior limbic keratoconjunctivitis is excellent, with remission as the natural history and eventual total resolution, although symptoms may last for years.
See the following for more information:
- Acute Hemorrhagic Conjunctivitis
- Allergic Conjunctivitis
- Atopic Keratoconjunctivitis
- Bacterial Conjunctivitis
- Emergent Treatment of Acute Conjunctivitis
- Epidemic Keratoconjunctivitis
- Giant Papillary Conjunctivitis
- Keratoconjunctivitis Sicca
- Neonatal Conjunctivitis
- Viral Conjunctivitis
Etiology and Pathophysiology
The cause of superior limbic keratoconjunctivitis (SLK) is unknown, but inflammatory changes from mechanical soft tissue microtrauma are the final common pathway. This condition is also associated with thyroid dysfunction but has been known to develop in association with scarring of the palpebral conjunctiva in euthyroid patients.
Other potential risk factors for development of superior limbic keratoconjunctivitis include prolonged eyelid closure with associated hypoxia or reduced tear volume, as well as morphologic or functional changes in superior conjunctival apposition to the globe following upper eyelid procedures.
Superior limbic keratoconjunctivitis is believed to be present secondary to superior bulbar conjunctiva laxity, which induces inflammatory changes from mechanical soft-tissue microtrauma. In settings in which the physiologic tolerance of mechanical forces on the delicate ocular surface is exceeded, chronic inflammation results in thickening of the conjunctiva and keratinization, which is then cyclical in perpetuating the inflammation. Eventually, a filamentary response may be induced on the affected cornea. Factors inducing conjunctiva laxity include thyroid eye disease, tight upper eyelids, and prominent globes. Immunochemical histopathologic examination of the abnormal conjunctiva in superior limbic keratoconjunctivitis lends credence to microtrauma being of most significance to the development of superior limbic keratoconjunctivitis.