Treating and Managing Calcific Changes in the Cornea
By William L. Miller, OD, PhD, FAAO
Calcific band keratopathy is related to either a hypercalcemic state in a patient or local factors that cause calcium deposition on the cornea. Uveitis, dry eye disease, sarcoidosis, multiple myeloma, trachoma, Paget disease and hyperparathyroidism have been implicated in this condition, and it has been reported in as many as one-third of patients who have juvenile rheumatoid arthritis (Wolf et al, 1987). Topical ophthalmic drops have also been implicated, and there may be idiopathic causes. It has also been found secondary to the intraocular placement of silicone oil in the treatment of retinal detachments (Sharma et al, 2011; Ozdek et al, 2011).
Several theories have been proposed for the mechanism behind calcium deposition found in band keratopathy, including local evaporative effects on the tear film and an overall increase in tissue pH. Calcium may form intra- or extracellularly, depending on the etiology of the disease.
Signs and Symptoms
In its early stages, calcific band keratopathy is characterized by a whitish gray deposit proximal to the anterior limiting lamina. Deposition starts nasally and temporally with a clear zone between the keratopathy and the limbus. As the disease progresses, it usually involves the central cornea, but in some cases, the central cornea is affected first. As the disease advances, the deposition appears chalky white and tends to become denser, with increasing penetration into the more anterior epithelial layers.
Most patients with early disease are asymptomatic. As it worsens, they may complain of foreign body sensation, decreased vision, pain, irritation, grittiness, tearing and photophobia. Typically, patients do not complain of pain until the disease has worsened and the calcium salts have penetrated the anterior epithelium. At this stage, the patient has a greater risk for recurrent corneal erosions.
When you detect calcific band keratopathy, you should conduct a careful history and review of systems. If you suspect systemic etiologies, consider ordering serum calcium, phosphorus, renal function, uric acid, parathyroid hormone and angiotensin-converting enzyme tests, which can be coordinated with your patient's primary care physician or internist.
For early disease, address the eye irritation with nonpreserved tear supplements and possibly ointment at bedtime. Contact lenses may be used as bandages to protect the ocular surface. As the disease progresses, additional treatment may be necessary to free the corneal surface of the deposited salts. This may include application of the chelating agent edetate disodium (EDTA). Because EDTA will not penetrate an intact epithelium, it is applied after the cornea is anesthetized and the superficial epithelium debrided. Other treatments include scraping the area with a blade or diamond burr, phototherapeutic keratectomy or a combination of both. Amniotic membrane transplantation has been used after surgical removal of the calcium to enhance healing. Some clinicians have reported using all three methods to achieve a satisfactory clinical outcome (Anderson et al, 2001; Im et al, 2010; Jhanji, 2011). At least one group has reported using laser-assisted subepithelial keratectomy combined with EDTA, with the subsequent placement of a bandage contact lens to increase comfort and achieve good clinical results (de Ortueta et al, 2006). CLS
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Dr. Miller is an associate professor and the chair of the Clinical Sciences Department at the University of Houston College of Optometry. He is a member of the American Academy of Optometry and the American Optometric Association, where he serves on its Journal Review Board. You can reach him at email@example.com.