Calcific band keratopathy (calcium hydroxyapatite deposition) is a calcific degeneration of the superficial cornea that involves mainly Bowman layer. It is often idiopathic. There are 6 main known causes:
chronic ocular disease (usually inflammatory) such as uveitis in children, interstitial keratitis, severe superficial keratitis, and phthisis bulbi
hypercalcemia caused by hyperparathyroidism, vitamin D toxicity, milk–alkali syndrome, sarcoidosis, and other systemic disorders
hereditary transmission (primary hereditary band keratopathy, with or without other anomalies)
elevated serum phosphorus with normal serum calcium, which sometimes occurs in patients with renal failure
chronic exposure to mercurial vapors or to mercurial preservatives (phenylmercuric nitrate or acetate) in ophthalmic medications (the mercury causes changes in corneal collagen that result in the deposition of calcium)
silicone oil instillation in an aphakic eye
Other rare associated disorders have been reported, including iris melanoma. Band keratopathy may also result from the deposition in the cornea of urates, which appear brown, unlike the gray-white calcific deposits, and may be associated with gout or hyperuricemia.
Calcific band keratopathy begins as fine, dustlike, basophilic deposits in Bowman layer. These changes are usually first seen peripherally. A peripheral clear zone representing a lucid interval is seen between the limbus and the peripheral edge of the keratopathy. Eventually, the deposits may coalesce to form a horizontal band of dense calcific plaques across the interpalpebral zone of the cornea (Fig 12-12).
A reasonable first step in managing this condition would be a workup (eg, serum electrolytes and urinalysis) to rule out associated metabolic/renal disease. Underlying conditions, such as keratoconjunctivitis sicca or renal failure, should be treated or controlled as much as possible, which may reduce or control the deposition of calcium or at least help reduce the recurrence of band keratopathy. The calcium can usually be removed from Bowman layer by chelation with a neutral solution of disodium ethylenediaminetetraacetic acid (EDTA; usual concentration 0.5%–1.5%), which can be warmed to speed up the chemical chelation of calcium. (Disodium EDTA is no longer commercially available but can be obtained through a compounding pharmacy.) The epithelium overlying the calcium needs to be removed prior to applying the chelating solution. Any cylindrical tube that approximates the corneal diameter can facilitate the process by acting as a reservoir to confine the chelating solution to the desired treatment area, although this is not always necessary. With the reservoir in place, very gentle surface agitation with truncated Weck-Cel sponges may further enhance the release of the impregnated calcium. If used at all, scraping should be gentle so as to prevent damage to Bowman layer. A fibrous pannus may be present along with extensive calcific band keratopathy, especially if silicone oil is responsible, and neither EDTA nor scraping will remove such fibrous tissue. A soft contact lens can be helpful postoperatively until the epithelium has healed. The problem can recur but may not do so for years, at which time the treatment may be repeated. Phototherapeutic keratectomy (PTK) using excimer laser is not advised as a primary treatment because calcium ablates at a different rate from stroma, which could produce a severely irregular surface. If residual opacification remains after the initial EDTA chelation, then PTK may be employed.
. Corneal and conjunctival calcification. In: Roy FH, Fraunfelder FW, Fraunfelder FT. 6th ed. Current Therapy series. Philadelphia: Elsevier/Saunders; 2008:337–338.