BASICS

DESCRIPTION

A degenerative corneal disorder characterized by a gray or white band of opacity in the interpalpebral fissure, most commonly caused by the gradual precipitation of calcium in the anterior layers of the cornea (Bowman’s membrane, epithelial basement membrane, and anterior stroma).

EPIDEMIOLOGY

Incidence

Unknown

Prevalence

Unknown

RISK FACTORS

• Chronic eye disease

• Abnormal calcium and phosphate metabolism

• Mercury exposure

• Ocular surgery using silicone oil

• Gout (causes a pigmented noncalcific band keratopathy)

Genetics

Rare cases of a familial calcific band-shaped keratopathy, probably autosomal recessive, have been reported (1).

GENERAL PREVENTION

Management of chronic eye inflammation or other disease; management of systemic calcium and phosphate abnormalities

PATHOPHYSIOLOGY

Precipitation of calcium below the corneal epithelium, thought to be caused by tear film hypertonicity, pH elevation, or changes in calcium or phosphate concentration. In mercury exposure and silicone keratopathy, calcium deposition occurs because of degenerative corneal changes.

ETIOLOGY

• Chronic eye disease: Chronic uveitis, end-stage glaucoma, phthisis bulbi. Severe dry eye disease may increase risk of band keratopathy because of tear hypertonicity.

• Abnormal calcium and phosphate metabolism or levels: Hyperparathyroidism, malignancy, sarcoidosis, Paget’s disease, vitamin D overdose, renal failure, milk-alkali syndrome

• Chemical or drug exposure: Mercury vapor, topical medications containing phosphates or mercurial preservatives, silicone oil

• Gout (causes deposition of urate crystals in the anterior cornea)

COMMONLY ASSOCIATED CONDITIONS

See the Etiology section.

DIAGNOSIS

HISTORY

• Decreased vision (if opacity is in visual axis)

• Foreign body sensation (if epithelium is compromised)

• Ocular and systemic risk factors (see the Risk Factors section)

• Toxic exposures

PHYSICAL EXAM

• Grayish plaque in superficial cornea in the interpalpebral zone, often with clear lacunae, creating a “Swiss-cheese” appearance. Opacity starts at 3 and 9 o’clock positions, separated from the limbus by clear cornea, and slowly progresses centrally. If calcium deposits break through epithelium, fluorescein staining will detect an epithelial defect.

• In gout, the deposits are yellow and crystalline.

DIAGNOSTIC TESTS & INTERPRETATION

Lab

Initial lab tests

• Complete slit lamp examination (see the Physical Exam section for typical features). Look for evidence of underlying ocular disease, including corneal edema, cell and flare in anterior chamber, synechiae, elevated intraocular pressure or hypotony, glaucomatous optic neuropathy, silicone oil, phthisis.

• In the absence of ocular conditions accounting for the band keratopathy, check for elevated serum calcium, phosphate, BUN, creatinine.

• Check for elevated serum uric acid, if gout is suspected.

Follow-up & special considerations

If systemic abnormalities detected, further lab tests may be indicated (e.g., parathyroid hormone level to investigate hypercalcemia).

Pathological Findings

• Basophilic stippling of Bowman’s layer, progressing to linear deposits of calcium in the superficial cornea. Calcium deposits are intracellular in hypercalcemia and extracellular in ocular disease.

• In gout, urate crystals are seen in epithelial cell nuclei.

DIFFERENTIAL DIAGNOSIS

• Corneal scar

• Interstitial keratitis

• Calcareous corneal degeneration (posterior stromal or full thickness calcium deposition which may occur in eyes with chronic ocular disease or inflammation)

TREATMENT

MEDICATION

• For mild foreign body sensation, topical lubrication with artificial tears or ophthalmic ointments may be helpful. (For decreased vision or more severe foreign body sensation or pain, surgical debridement is indicated. See the Surgery/Other Procedures section below.)

• Medical therapy for underlying ocular or systemic causes as indicated.

ADDITIONAL TREATMENT

Issues for Referral

Follow-up as needed based on symptoms and underlying ocular or systemic disease

SURGERY/OTHER PROCEDURES

• Surgical debridement is indicated if pain or decreased vision becomes significant.

– Ethylenediamine tetraacetic acid (EDTA) chelation of calcium deposits: Debridement or removal of corneal epithelium, followed by application of EDTA to the exposed corneal surface in order to remove the calcium deposits by chelation (2)[C]

– Excimer laser phototherapeutic keratectomy (PTK). May be used primarily (3)[C] or in combination with EDTA chelation (4)[C]

– Mechanical debridement of deposits, e.g., by scraping with a surgical blade (5)[C]

ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

• As needed for symptoms (decreased vision, foreign body sensation)

• As needed for management of underlying ocular or systemic causes

• After EDTA chelation, close follow-up until epithelium is healed, and then as needed.

DIET

As indicated by any systemic etiologies (renal failure, vitamin D overdose, milk-alkali syndrome)

PROGNOSIS

Likely to recur or progress, but because progression is usually very gradual, symptoms of decreased vision and foreign body sensation may not reappear for months to years.

COMPLICATIONS

• Corneal infection due to epithelial breakdown

• Following EDTA chelation, PTK, or other surgical debridement, corneal haze or scarring may develop.

• PTK may cause myopic shift.

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