|Superior Limbic Keratoconjunctivitis (SLK of Theodore)
Signs and Symptoms
Individuals presenting with SLK typically report symptoms of ocular
discomfort, including burning, foreign-body sensation, or non-descript pain. Additionally,
patients may complain of photophobia and excessive tearing. Gross clinical signs often
include mild lid swelling and pseudoptosis as well as blepharospasm. Visual acuity is
usually not affected.
Inspection of the ocular surface in SLK reveals a sectoral inflammation
and injection of the superior bulbar conjunctiva. The limbal margin of the cornea may be
inflamed as well. Eversion of the upper lid reveals a uniform papillary hypertrophy along
the tarsus, which may be mild to marked. Vital dye staining is standard in SLK, with
patients displaying punctate epithelial disruption of the affected region; this is evident
with both sodium fluorescein dye as well as rose bengal or lissamine green solutions.
Filaments are encountered within the precorneal tear film in roughly half of all patients
with SLK. The condition is typically bilateral but often asymmetric. In most instances,
the diagnosis of SLK is based solely upon the characteristic presentation. The only known
laboratory confirmation is the presence of keratinized epithelial cells from scrapings of
the affected superior bulbar conjunctivae.
The exact etiology and pathogenesis of SLK remains unclear. Infectious
agents such as bacteria, viruses, fungi, and other intracellular parasites appear to be
unrelated to this condition. An autoimmune etiology has been considered, based upon the
pattern of the disorder (i.e., exacerbations and remissions), the female predominance, and
an association with thyroid disease and other autoimmune diseases.
The most widely accepted theory regarding the pathogenesis of SLK is
that it results from mechanical irritation of the superior limbal region, as loose
conjunctival tissue rubs against the limbus during blinking. Factors such as tight lids,
prominent globes, and thyroid disease have been offered as potential instigators of this
A newer theory regarding the etiology of SLK implicates a local tear
deficiency to the superior keratoconjunctiva. Researchers have proposed that this
deficiency results in significantly reduced levels of vital tear-based nutrients to the
affected region, as well as increased mechanical friction from the superior lid.
SLK is a chronic, recurrent and sometimes recalcitrant disorder. While no
treatment has yet been shown to be 100 percent effective, many modalities have been
employed successfully. The treatment of choice for most practitioners has been 0.5 to 1.0%
silver nitrate solution, applied topically to the superior bulbar and tarsal conjunctivae.
This treatment chemically cauterizes the irregular tissue, promoting regrowth of new,
healthy epithelium. Unfortunately, recurrences have been known to occur after using silver
nitrate, and retreatments are common.
Pressure patching has been employed for severely symptomatic cases of
SLK, as well as the use of subsequent bandage hydrogel lenses to alleviate the mechanical
irritation. Thermal cauterization as well as surgical recession or resection of the
superior bulbar conjunctiva has also been employed as treatment modalities for SLK. The
use of topical preparations, including vitamin A eyedrops, 4% cromolyn sodium solution,
and Alomide (0.1% lodoxamide tromethamine solution, Alcon) have also been somewhat
effective in managing SLK. Most recently, lacrimal punctal occlusion therapy has been
advocated for this disorder.
Other reports in this section
- In managing this disorder, topical agents should be employed in the early
stages of all mild and moderate presentations; thermocautery, chemocautery, and surgical
resection should be employed only when less invasive means have failed.
- Lacrimal occlusion therapy may prove to be a viable option for SLK; while
additional research is needed in this area, recent studies have shown great potential.
- SLK of Theodore should not be confused with contact lens-induced SLK
(CL-SLK), a condition that is occasionally observed in young, otherwise healthy hydrogel
lens wearers. An association with thimerosal-preserved solutions has been seen in some of
these patients. The typical presentation of CL-SLK consists of increasing contact lens
intolerance, superior tarsal and bulbar injection, and significant superior corneal
staining with stromal hazing. Corneal involvement may be noted as far inferiorly as the
superior pupillary margin. Treatment for CL-SLK consists of temporarily discontinuing
contact lens wear, along with the liberal use of preservative-free ocular lubricants. Upon
resolution, contact lens wear may be resumed with a fresh pair of lenses, however all
thimerosal-preserved solutions should be terminated. In more severe or recurrent cases,
patients may need to be refit with RGP materials.
- Refer all patients presenting with SLK for a systemic workup, including a
serologic thyroid panel. A 1995 study demonstrated a 65 percent correlation between SLK
and systemic thyroid disease. Other disorders such as rheumatoid arthritis and
Sjögrens syndrome may also have similar associations.