Band keratopathy derives its name from the distinctive appearance of calcium deposition in a band across the central cornea. This corneal degeneration can occur from a variety of causes, both systemic and local.
Band keratopathy is the result of precipitation of calcium salts on the corneal surface (directly under the epithelium). Serum and normal body fluids (eg, tears, aqueous humor) contain calcium and phosphate in concentrations that approach their solubility product. Evaporation of tears tends to concentrate solutes and to increase the tonicity of tears; it is especially true in the intrapalpebral area where the greatest exposure of the corneal surface to ambient air occurs. Elevated serum calcium or serum phosphate can tip the balance in favor of precipitation. Topical medications that contain phosphates also may contribute to this problem. Finally, elevation of the surface pH out of the physiologic range changes the solubility product and favors precipitation. This type of tissue pH change can be seen in chronically inflamed eyes and may explain, in part, why patients with uveitis are at risk for the development of band keratopathy.
Endothelial function may play a role in the formation of calcium deposition. Compromise of endothelial function and corneal edema are sometimes seen in patients who have silicone oil inside the eye when it comes into contact with the posterior cornea. Although this association has been noted, the exact reasons remain uncertain.
The exact incidence of calcific band keratopathy is unknown.
Patients with band keratopathy may experience a decrease in vision as the deposition progresses across the visual axis. A foreign body sensation and irritation associated with an irregular surface are common symptoms. The ocular discomfort may worsen to the point of becoming disabling. The plaque itself often is visible and of cosmetic concern to the patient and family members.
No known difference exists in the incidence of band keratopathy between men and women.
No known association of band keratopathy exists with increasing age.
Patients with band keratopathy complain of the following:
Foreign body sensation
Visual acuity will be decreased in proportion with the density of deposition of calcium salts in the central cornea. Slit lamp examination often reveals a whitish-grayish plaquelike deposition that occurs in a band across the cornea. The very periphery of the cornea may be spared because of the buffering effect of limbal blood vessels. Holes in the plaque may be apparent; these holes represent spaces where the corneal nerves are traversing the Bowman membrane to the epithelial surface.
The calcium deposition typically begins in the periphery and progresses centrally but, occasionally, may begin centrally.
The calcium may be very fine or thick and plaquelike. When it is thick, it may flake off, causing epithelial defects and painful symptoms.
The following systemic conditions are associated with band keratopathy:
Hypercalcemia due to the following:
Excessive vitamin D intake
Other systemic conditions
Discoid lupus erythematosus
Local ocular conditions
Juvenile idiopathic arthritis with uveitis
Anterior mosaic dystrophy
Drug-associated calcium deposition
Steroid phosphate preparations
Pilocarpine containing mercurial based preservatives
Viscoelastic agents (rare, early formulations; may be related to phosphate buffers)
Topical medications containing phosphate buffers (especially in the setting of chemical eye burns)
Chemical fume related
Calcium bichromate vapor
Intraocular use of recombinant tissue-plasminogen activator (rt-PA)