BLOG: When to treat band keratopathy
Like spotting a tube of Preparation H in your mother-in-law’s bathroom, band keratopathy is a common finding that can give profound insights into a patient’s systemic situation.
We all see this condition frequently, but many eye care providers do not understand its significance — especially its frequent association with diseases that lead to extreme levels of calcium in the blood.
Calcific band keratopathy (CBK) manifests as an opaque interpalpebral band of calcium deposition at the level of Bowman’s layer. The deposits begin as a gray haze, usually confined to small islands nasally and temporally, but can slowly grow into a dense and pebbly white plaque that completely reaches across the cornea. There is always a clear zone at the limbus. Scattered holes — the result of penetration by corneal nerves — give CBK a “Swiss cheese” appearance.
CBK is caused by calcium and phosphate precipitating out of the tear film and is exacerbated by three factors: an acidic tear film that causes precipitation of the alkaline calcium salt, an increased osmolarity from tear film evaporation and an abnormal level of serum calcium. The conjunctiva provides a buffering effect to the tear film at the limbus, which explains CBK’s peripheral clear zone.
In its early stages, CBK looks like small grey peripheral parentheses at 3 and 9 o’clock and is simply known as a type 1 limbal girdle of Vogt; this is present in nearly 100% of individuals older than 80 years and can safely be ignored. However, when CBK enlarges beyond the peripheral cornea, you must be able to explain why you think this is happening.
Ophthalmic causes
When trying to explain a large or growing CBK, the first conditions to consider are ocular, including chronic uveitis, intraocular silicone oil or other forms of very sick eyes. Both increased tear film evaporation and chronic ocular surface inflammation encourage precipitation, so dry eye will make CBK formation more likely.
The most common ocular association is with chronic uveitis, especially juvenile rheumatoid arthritis.
Systemic causes
If you see an unusual case of CBK and there is no significant ocular explanation, it is likely that your patient is in a state of systemic hypercalcemia. The most common causes are chronic renal failure, which will almost always have already been diagnosed, and hyperparathyroidism, which may have escaped notice.
The parathyroid glands — pea-sized glands adjacent to the thyroid glands — regulate blood calcium levels through the action of parathyroid hormone (PTH). PTH secretion increases calcium levels, primarily by pulling stored calcium from the bones. Hyperparathyroidism, characterized by excessive production of PTH, pulls too much calcium into the blood stream. Symptoms of hyperparathyroidism also include kidney stones, nervous system problems and osteoporosis.
The presence of hyperparathyroidism is concerning, since the most common causes are parathyroid adenomas and other tumors. These neoplasms occur in 100,000 Americans each year (Michels et al).
If you are worried about a systemic cause of CBK, order tests or ask your patient’s primary care provider to investigate. At minimum, tests should include serum calcium, phosphorus and uric acid, as well as renal function tests and PTH.
Surgical treatment
In severe cases of CBK, symptoms include decreased vision, foreign body sensation, tearing and photophobia, and at this point surgery should be considered. The surgical treatment for CBK is simple and usually results in an excellent improvement in vision.
The treatment depends on chelation with ethylenediaminetetraacetic acid, known as EDTA. Chelation is a method of tightly bonding a molecule to a target metal to facilitate its removal, a process originally pioneered as an antidote to mustard gas during World War II.
A cornea specialist debrides the protective epithelium, soaks the calcium deposits with EDTA and cleanly scrapes them off Bowman’s layer to reveal the smooth surface underneath. The cornea is then thoroughly rinsed and allowed to heal, similar to other epithelium-off techniques.
Hyperparathyroidism is often treated with surgical resection of the parathyroids, even in the absence of symptoms.
Understand the principles behind this common finding, and you will not only provide superior care for your patient, but you may also discover a systemic condition overlooked by other doctors. Tiny peripheral islands of CBK can be ignored, but larger instances should be thoroughly investigated to determine the cause of excessive serum calcium, with symptomatic cases sent to a cornea surgeon.
References:
- Jhanji V, et al. Curr Opin Ophthalmol. 2011;doi:10.1097/ICU.0b013e3283477d36.
- Krachmer JH, Mannis MJ, Holland EJ. Cornea: Fundamentals, Diagnosis and Management. Vol. 1. 3rd ed. Mosby Elsevier; 2001:908-910.
- Michels TC, et al. Am Fam Physician. 2013;88(4):249-257.
- Moisseiev E, et al. J Cataract Refract Surg. 2013;doi:10.1016/j.jcrs.2012.12.020.
For more information:
Kuhn-Wilken is a staff optometrist at Pacific Cataract and Laser Institute’s Tualatin Clinic in Oregon.
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