Band Shaped Keratopathy

Band Shaped Keratopathy (Calcific band keratopathy, or band keratopathy) is a non-specific corneal condition characterised by chronic deposition of calcium salts (principally hydroxyapatite) within the basement membrane, Bowman’s layer and anterior stromal lamellae of the corneal epithelium (leaving remainder of the cornea clear). Initially, corneal degenerative changes begin near the limbus, either on nasal, temporal or both sides together in exposed palpebral fissure at 3 to 9 o’clock position. Calcific band is concentric with the limbus but is separated from it by a clear zone (representing a lucid interval) due to lack of Bowman’s layer at the periphery, or due to buffering action at the limbus. Keratopathy appears as a superficial greyish-white corneal opacity having frosted or ground glass appearance. The opacity is covered by clear epithelium with lacunae of uninvolved tissue. There are numerous holes where corneal nerves penetrate the Bowman’s layer. The disease progresses toward the corneal center and thickens as well in its anterior and posterior dimensions, resulting in more opaque, whitish surface with increased nodularity. Calcium deposits thicken and may cause breakdown of the overlying epithelium, resulting in the appearance of spontaneous and recurrent corneal epithelial erosions.

Band shaped keratopathy may occur as isolated condition or in association with a variety of disease entities. The corneal involvement is described as band shaped keratopathy because of the band-like distribution of the deposits across the interpalpebral zone. Unlike band shaped keratopathy, calcareous degeneration usually spares the basement and Bowman’s membrane and is characterised by clumps of calcium salts in the superficial and deep stroma.

Patients with keratopathy may remain relatively asymptomatic for a considerable length of time in early stages of the disease, as long as the central visual axis of the cornea remains clear. With progression of the disease, there is diminution of visual acuity and pain in the eyes due to disruption of the corneal epithelium.

Identification of corneal and conjunctival degenerations has improved with the use of confocal microscopy, immuno-histochemical staining and genetic testing.

 

References:

Agarwal Sunita, Agarwal Athiya, Apple David J, Buratto Lucio, Alio Jorge L, Pandey Suresh K and Agarwal Amar. Textbook of Ophthalmology Volume 1. First Edition. Jaypee Brothers Medical Publishers (P) Ltd.. 2002. New Delhi. P. 1080- 1081.

Basak Samar K. Jaypee Gold Standard Mini Atlas Series: Diseases of the cornea. Jaypee Brothers Medical Publishers (P) Ltd. 2011. P 175 – 177.

Biswas Jyotirmay, Krishnakumar S, Ahuja Shweta. Manual of Ocular Pathology. Jaypee Brothers Medical Publishers (P) Ltd. 2010. P 37.

Badrinath SS, Padmanabhan Prema. Sankara Nethralaya Clinical Practice Patterns in Ophthalmology. Second Edition. Jaypee Brothers Medical Publishers (P) Ltd. 2012. P 115 – 116.

Selvakumar Ambika, Noronha Veena, Sundaram Padmaja Minakshi. Sankara Nethralaya Atlas of Imaging in Ophthalmology. Jaypee Brothers Medical Publishers (P) Ltd. 2014. P 113.

Yanoff Myron, Sassani Joseph W. Ocular Pathology. Sixth Edition. Mosby Elsevier. 2009. P 279.

Roy Frederick Hampton. Master Techniques in Ophthalmic Surgery. Second Edition. Jaypee Brothers Medical Publishers (P) Ltd. 2015. P 101- 106.

Roy Frederick Hampton, Fraunfelder Frederick W, Fraunfelder Frederick T. Roy and Fraunfelder’s Current Ocular Therapy. Sixth Edition. Saunders Elsevier. 2008. P 337.

Prajna N Venkatesh. FAQs in Ophthalmology. Jaypee Brothers Medical Publishers (P) Ltd. 2013. P 88- 90.

Wright Kenneth W, Spiegel Peter H. Pediatric Ophthalmology and Strabismus. Second Edition. Springer. 2003. P 407.

Tasman William, Jaeger Edward A. The Wills Eye Hospital – Atlas of Clinical Ophthalmology. Second Edition. Lippincott Williams & Wilkins. 2001. P 57.

Naumann GOH, Apple DJ. Pathology of the eye. Springer-Verlag. 1986. P 329- 330.

http://emedicine.medscape.com/article/1194813-overview

http://webeye.ophth.uiowa.edu/eyeforum/cases/214-band-keratopathy.htm

http://www.aao.org/bcscsnippetdetail.aspx?id=1430bd5e-635d-4bad-92e6-c56668055790

Basak Samar K. Atlas of Clinical Ophthalmology. Second Edition. Jaypee Brothers Medical Publishers (P) Ltd. 2013. P 118.

Sihota Ramanjit, Tandon Radhika. Parson's Diseases of the Eye. Reed Elsevier India Private Limited. 22nd Edition. 2015. P. 215.

Nema H V, Nema Nitin. Textbook of Ophthalmology. Sixth Edition. Jaypee Brothers Medical Publishers (P) Ltd. 2012. P 167 – 168.

Saxena Sandeep. Clinical Ophthalmology: Medical & Surgical Approach. Second Edition. Jaypee Brothers Medical Publishers (P) Ltd. 2010. P 117.

Eagle Ralph C,Jr. Eye Pathology: An Atlas and Text. Second Edition. Lippincott Williams & Wilkins. 2011. P 85.

Sundaram Venki, Barsam Allon, Alwitry Amar, Khaw Peng T. Oxford Specialty Training: Training in Ophthalmology- the essential clinical curriculum. Oxford University Press. 2009. P 30.

Dixon J. Diseases of the eye. First Edition. London: J Churchill; 1848. P114.

Patients with band shaped keratopathy are asymptomatic in the early stages of the disease.

Patients with band shaped keratopathy may complain of:

  • Ocular (eye) irritation.
  • Foreign body sensation.
  • Diminution of vision.
  • Lacrimation or watering of eyes.
  • Pain.
  • Epithelial defects.
  • Photophobia (increased sensitivity to light).
  • Visible plaque in the eye.
  • Redness (less common).

 

Numerous mechanisms, whether systemic or local to the eye, by which the balance of the calcium phosphate solubility product are tilted toward abnormal tissue calcification resulting nonspecific finding of band keratopathy. As such, there are many diseases associated with this condition. Though we tend to think first of conditions such as uveitis and systemic hypercalcaemia, in a recent series the most commonly associated causes of calcific band keratopathy were chronic corneal oedema, phthisis bulbi, and even idiopathic cases.

Systemic disease associations:

Hypercalcaemia (elevated serum calcium level) may be due to:

  • Hyperparathyroidism.
  • Over treatment for hypoparathyroidism.
  • Vitamin D intoxication.
  • Sarcoidosis.
  • Multiple myeloma.
  • Paget’s disease.
  • Milk-alkali syndrome.
  • End stage renal disease: In end-stage renal disease, elevation of either serum calcium, phosphate, or both may disrupt the equilibrium towards precipitation.
  • Hypophosphatasia: Hypophosphatasia, an in