Keratoconjunctivitis, Superior Limbic
This disorder 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.1 It was given its name, superior limbic keratoconjunctivitis (SLK), by Theodore, contemporaneously. Five years later, Tenzel and Corwin reported an association with thyroid abnormalities and SLK.2,3 A mimicking disorder has been encountered in soft contact lens wearers, typically with exposure to thimerosal-preserved solutions.
SLK is believed to be present secondary to superior bulbar conjunctiva laxity, which induces inflammatory changes from mechanical soft tissue microtrauma4 In settings where the physiological 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 SLK lends credence to microtrauma being of most significance to the development of SLK.
The frequency of SLK has been found to be 3% in a cohort of Graves ophthalmopathy patients, but it is much lower in the general population.
The international frequency is unknown.
The natural history of the disorder is remission and eventual total resolution but only after a prolonged clinical course.
No racial predilection exists.
Women are predominantly affected.
Typically, middle-aged people are affected; however, this entity has been reported to occur in patients aged 4-81 years.
Patients present with complaints of burning and irritation of the affected eye.
Some patients may present with redness. Upgaze may elicit these symptoms.
Typically, usage of moisturizing medications only provides minimal relief.
Symptoms remit and exacerbate and are variable in degree, but no diurnal pattern to the worsening of symptoms exists.
In most cases, the condition is present bilaterally, although one eye may be more symptomatic.
Patients with filaments are usually extremely symptomatic.
Commonly, a history of thyroid dysfunction is elicited upon questioning. The natural history of SLK is prolonged, with gradual clearing.
Patients often have numerous eye specialists for their symptoms. Unless the doctors have specifically examined the upper bulbar conjunctivae or everted the upper eyelids, they may have missed the diagnosis.
Marked inflammation of the upper lid tarsal conjunctiva, adjacent inflammation of the upper bulbar conjunctiva, and punctate rose bengal staining of the cornea at the upper limbus are signs of SLK.
The conjunctiva extending from the upper limbus to the insertion of the superior rectus muscle also demonstrates thickening, hyperemia, and typical rose bengal staining. It stands out in stark contrast to the normal appearance of the inferior conjunctiva and cornea.
Approximately one third of patients present with filaments on the upper cornea or along the superior limbus.
The cause of SLK is unknown, but inflammatory changes from mechanical soft tissue microtrauma are the final common pathway.
SLK is associated with thyroid dysfunction.
SLK has also developed in association with scarring of the palpebral conjunctiva in euthyroid patients.
Prolonged eyelid closure with associated hypoxia or reduced tear volume may be a risk factor for SLK development.
Morphological or functional changes in superior conjunctival apposition to the globe following upper eyelid procedures may induce SLK.5