Band Keratopathy

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Background

Band keratopathy is characterized by the appearance of a band across the central cornea, formed by the precipitation of calcium salts on the corneal surface (directly under the epithelium).[1] This form of corneal degeneration can result from a variety of causes, either systemic or local, with visual acuity decreasing in proportion to the density of the deposition (see the image below). (See Etiology.)


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Band keratopathy. Note the bandlike whitish-grey lesion across the corneal surface, sparing the superior and inferior cornea.

Superficial debridement generally restores vision and comfort for most patients with band keratopathy, although failure to manage the source of the condition often leads to recurrence. (See Prognosis, Treatment, and Medication.)

Etiology

Corneal deposition of calcium salt

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; this 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.

In addition, 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.[2, 3, 4]

Endothelial function may also play a role in calcium deposition. Compromise of endothelial function and corneal edema are sometimes seen in patients who have silicone oil inside the eye, when the oil comes into contact with the posterior cornea. The exact reasons for this association remain uncertain.[5, 6]

Band keratopathy was one of the main long-term complications (8% of patients) in a study of 50 ophthalmologic patients treated with silicone oil in whom the oil remained inside the eye for an unusually long period of time (median, 30 months).[7]

Systemic risk factors

The following conditions are associated with hypercalcemia, a risk factor for band keratopathy:

Discoid lupus erythematosus and tuberous sclerosis are other systemic conditions associated with band keratopathy.

Local ocular risk factors

Local ocular conditions associated with band keratopathy include the following:

Chemically associated risk factors

Drug-associated calcium deposition can result from the following:

Chemical fume ̶ related risk factors include the following:

Prognosis

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.

As previously mentioned, unless underlying conditions have been addressed, removing the calcium deposits in band keratopathy will be associated with a high incidence of recurrence. In general, however, superficial debridement restores vision and comfort for most patients with band keratopathy, with the incidence of adverse outcomes following this procedure being very low.

History and Physical Examination

History

Patients with band keratopathy complain of the following:

Physical examination

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 grayish white, 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 represent spaces where the corneal nerves are traversing the Bowman membrane to the epithelial surface. (See the image below.)


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Band keratopathy. Note the bandlike whitish-grey lesion across the corneal surface, sparing the superior and inferior cornea.

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.

Approach Considerations

Laboratory Studies

Patients who present with band keratopathy should have a serum calcium and phosphate level drawn unless the deposition has been documented previously and the underlying cause is known.

Renal function tests, such as blood urea nitrogen (BUN) and creatinine, should be performed as well. Renal failure and the need for dialysis can be associated with an elevation in serum phosphate and calcific band keratopathy.[14, 15]

If sarcoid is suspected, an angiotensin-converting enzyme (ACE) should be obtained. In otherwise idiopathic cases, parathyroid hormone levels should be checked.

Histologic Findings

Band keratopathy is characterized by calcium deposition involving the Bowman layer and the superficial stroma of the cornea. The earliest changes include basophilic staining of the Bowman layer. Amorphous, eosinophilic connective tissue and a fibrous pannus often are present between the calcium deposition and the overlying epithelium in more advanced cases. (See the image below.)


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Total calcification of the cornea. Deep and superficial layers of the cornea are involved with this process.

Calcium is deposited intracellularly when hypercalcemia is the cause; extracellular deposits are characteristic of local ocular disease.

Approach Considerations

Superficial debridement in band keratopathy is usually effective in restoring normal vision. Various adverse outcomes can result from the procedure, including corneal scarring and vision loss, but the incidence of such complications is very low.

Although medical therapy is ineffective in treating band keratopathy, underlying conditions associated with elevated levels of calcium or phosphate should be treated to prevent deposition from recurring.

Diet

As noted, excessive vitamin D intake has been associated with band keratopathy, as has milk-alkali syndrome. Excessive absorption and serum elevation of calcium is the consequence of these 2 diet-related problems.

Superficial Debridement

Superficial debridement can be performed in a minor operating room under topical anesthesia. Proparacaine or tetracaine drops can be used for this purpose. Use of an operating microscope is recommended.

Procedure

Place a lid speculum to hold open the eyelids, and debride the epithelium overlying the calcium with an ophthalmic surgical blade or spatula.

Apply 0.05 mol, 1.5% neutral disodium ethylenediaminetetra-acetic acid (EDTA) to the corneal surface. Weck-cel sponges soaked in this solution can be used for this purpose. Alternatively, the solution can be placed in a water bath over the cornea to limit ocular exposure.

Calcium deposits are then removed with firm scraping of the corneal surface with a blunt spatula. (A Paton spatula works well.) Often, it is necessary to apply solution, followed by scraping several times to remove the plaque. The primary goal is to clear the visual axis. Thin calcium deposits may come off in 5 minutes, while thick plaques may take 30-45 minutes to dissolve.

Once the deposits have been scraped, an assessment of the smoothness of the underlying stroma can be made. If the surface is very irregular, phototherapeutic keratectomy with an excimer laser can be performed to smooth the surface. Ideally, this procedure is performed in the same setting.

Note that the excimer laser should not be used to remove calcium. Attempting to remove band keratopathy with the excimer laser alone will result in significant irregular astigmatism, since the cornea, not calcium, will be ablated preferentially. The role of the excimer is to polish the surface after the plaque has been removed.[16]

Irrigate the eye thoroughly following the procedure to remove EDTA solution from the conjunctival surface and fornices.

Place a bandage contact lens over the cornea. Alternatively, pressure patching or frequent antibiotic ointment can be used.

Postoperative care

Postoperative care includes the insertion of a bandage contact lens that is left in place until the epithelium heals. Topical nonsteroidal agents are useful for pain control immediately following the procedure and for the first few days afterwards.

An antibiotic drop should be prescribed with the bandage contact lens in place. Use of a topical steroid drop (eg, prednisolone acetate [not phosphate]) is helpful for comfort and treatment of the inflammation and corneal edema that are often present in the early postprocedure period. These medications can be stopped when the epithelium is healed and the bandage contact lens is removed (usually within the first 1-2 wk).

Complications

The main complications related to the removal of calcium deposits on the corneal surface include the following (it is also possible that additional procedures will be needed):

Occasionally, a mild subepithelial haze can be seen weeks after EDTA chelation. This may resolve on its own. A mild topical steroid (eg, fluorometholone 0.1%) may help to resolve this haze. If there is significant damage to the Bowman membrane, the haze may be permanent.

Medication Summary

The goals of pharmacotherapy are to reduce plasma calcium levels, to prevent complications, and to reduce morbidity. As previously mentioned, 0.5 mol, 1.5% neutral disodium EDTA is applied to the corneal surface to aid in superficial debridement for band keratopathy. Weck-cel sponges soaked in this solution can be used for this purpose, or the solution can be placed in a water bath over the cornea to limit ocular exposure. After debridement, the eye should be thoroughly irrigated to remove EDTA solution from the conjunctival surface and fornices.

Edetate calcium disodium (Calcium Disodium Versenate)

Clinical Context:  This compound chelates with many divalent and trivalent metals. Because of its affinity for calcium, it lowers serum calcium levels during intravenous (IV) infusion. Slow infusion causes mobilization of extracirculatory calcium stores. Edetate calcium disodium also chelates with other polyvalent metals, therefore increasing urinary excretion of magnesium, zinc, and other trace elements. Although it does not chelate with potassium, it may reduce the serum potassium level. Do not use this medication for lead toxicity.

Edentate calcium disodium is indicated for the emergency treatment of hypercalcemia but is rarely used, since newer drugs are now available to treat this indication. It must be specially compounded and buffered for topical formulation.

Class Summary

This is used to lower serum calcium levels.

Author

Michael Taravella, MD, Director of Cornea and Refractive Surgery, Rocky Mountain Lions Eye Institute; Professor, Department of Ophthalmology, University of Colorado School of Medicine

Disclosure: AMO/VISX None Consulting

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Stephen D Plager, MD, FACS Chief, Department of Ophthalmology, Dominican Hospital; Assistant Clinical Professor, Department of Ophthalmology, Stanford University Hospital

Stephen D Plager, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, and California Medical Association

Disclosure: Nothing to disclose.

Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Institute

Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, International Society of Refractive Surgery, and Pan-American Association of Ophthalmology

Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; Inspire Honoraria Speaking and teaching; RPS Ownership interest Other; Vistakon Honoraria Speaking and teaching; EyeGate Pharma Consulting; Inspire Consulting fee Consulting; Bausch & Lomb Honoraria Speaking and teaching; Bausch & Lomb Consulting fee Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References

  1. Jhanji V, Rapuano CJ, Vajpayee RB. Corneal calcific band keratopathy. Curr Opin Ophthalmol. Jul 2011;22(4):283-9. [View Abstract]
  2. Bernauer W, Thiel MA, Kurrer M, et al. Corneal calcification following intensified treatment with sodium hyaluronate artificial tears. Br J Ophthalmol. Mar 2006;90(3):285-8. [View Abstract]
  3. Doostdar N, Manrique CJ, Hamill MB, Barron AR. Synthesis of calcium-silica composites: a route toward an in vitro model system for calcific band keratopathy precipitates. J Biomed Mater Res A. Nov 2011;99(2):173-83. [View Abstract]
  4. Daniel E, Pistilli M, Pujari SS, Kaçmaz RO, Nussenblatt RB, Rosenbaum JT, et al. Risk of Hypotony in Noninfectious Uveitis. Ophthalmology. Jul 12 2012;[View Abstract]
  5. Federman JL, Schubert HD. Complications associated with the use of silicone oil in 150 eyes after retina-vitreous surgery. Ophthalmology. Jul 1988;95(7):870-6. [View Abstract]
  6. Sternberg P Jr, Hatchell DL, Foulks GN, et al. The effect of silicone oil on the cornea. Arch Ophthalmol. Jan 1985;103(1):90-4. [View Abstract]
  7. Morphis G, Irigoyen C, Eleuteri A, Stappler T, Pearce I, Heimann H. Retrospective review of 50 eyes with long-term silicone oil tamponade for more than 12 months. Graefes Arch Clin Exp Ophthalmol. May 2012;250(5):645-52. [View Abstract]
  8. Porter R, Crombie AL. Corneal and conjunctival calcification in chronic renal failure. Br J Ophthalmol. May 1973;57(5):339-43. [View Abstract]
  9. Kennedy RE, Roca PD, Landers PH. Atypical band keratopathy in glaucomatous patients. Am J Ophthalmol. Nov 1971;72(5):917-22. [View Abstract]
  10. Taravella MJ, Stulting RD, Mader TH, et al. Calcific band keratopathy associated with the use of topical steroid- phosphate preparations. Arch Ophthalmol. May 1994;112(5):608-13. [View Abstract]
  11. Kompa S, Redbrake C, Dunkel B, et al. Corneal calcification after chemical eye burns caused by eye drops containing phosphate buffer. Burns. Sep 2006;32(6):744-7. [View Abstract]
  12. Moisseiev E, Gal A, Addadi L, Caspi D, Shemesh G, Michaeli A. Acute calcific band keratopathy: case report and literature review. J Cataract Refract Surg. Feb 2013;39(2):292-4. [View Abstract]
  13. Smolin G. Corneal dystrophies and degenerations. The Cornea. 1994;500-503.
  14. Anderson SB, de Souza RF, Hofmann-Rummelt C, et al. Corneal calcification after amniotic membrane transplantation. Br J Ophthalmol. May 2003;87(5):587-91. [View Abstract]
  15. Klaassen-Broekema N, van Bijsterveld OP. Limbal and corneal calcification in patients with chronic renal failure. Br J Ophthalmol. Sep 1993;77(9):569-71. [View Abstract]
  16. Sharma N, Mannan R, Sinha R, Kaushal S, Titiyal JS, Kumar A, et al. Excimer laser phototherapeutic keratectomy for the treatment of silicone oil-induced band-shaped keratopathy. Eye Contact Lens. Sep 2011;37(5):282-5. [View Abstract]
  17. Najjar DM, Cohen EJ, Rapuano CJ, Laibson PR. EDTA chelation for calcific band keratopathy: results and long-term follow-up. Am J Ophthalmol. Jun 2004;137(6):1056-64. [View Abstract]

Band keratopathy. Note the bandlike whitish-grey lesion across the corneal surface, sparing the superior and inferior cornea.

Calcium deposition associated with the use of dexamethasone phosphate. The calcium plaques appear as elevated white lesions at the edge of a persistent epithelial defect.

The image shown is of a patient who developed a calcium plaque following a corneal transplant and the use of a topical steroid phosphate preparation.

Band keratopathy. Note the bandlike whitish-grey lesion across the corneal surface, sparing the superior and inferior cornea.

Total calcification of the cornea. Deep and superficial layers of the cornea are involved with this process.

Band keratopathy. Note the bandlike whitish-grey lesion across the corneal surface, sparing the superior and inferior cornea.

Calcium deposition associated with the use of dexamethasone phosphate. The calcium plaques appear as elevated white lesions at the edge of a persistent epithelial defect.

Total calcification of the cornea. Deep and superficial layers of the cornea are involved with this process.

The image shown is of a patient who developed a calcium plaque following a corneal transplant and the use of a topical steroid phosphate preparation.