Xerophthalmia

Xerophthalmia (from Ancient Greek xērós (ξηρός) meaning dry and ophthalmos (οφθαλμός) meaning eye) is a medical condition in which the eye fails to produce tears. It may be caused by vitamin A deficiency, which is sometimes used to describe that condition, although there may be other causes.

Xerophthalmia
Pronunciation
  • /ˌzɪərɒfˈθælmiə/ (listen)
SpecialtyOphthalmology

Xerophthalmia caused by a severe vitamin A deficiency is described by pathologic dryness of the conjunctiva and cornea. The conjunctiva becomes dry, thick and wrinkled. If untreated, it can lead to corneal ulceration and ultimately to blindness as a result of corneal damage.

Xerophthalmia usually implies a destructive dryness of the conjunctival epithelium due to dietary vitamin A deficiency—a rare condition in developed countries, but still causing much damage in developing countries. Other forms of dry eye are associated with aging, poor lid closure, scarring from a previous injury, or autoimmune diseases such as rheumatoid arthritis and Sjögren's syndrome, and these can all cause chronic conjunctivitis. Radioiodine therapy can also induce xerophthalmia, often transiently, although in some patients late onset or persistent xerophthalmia has been observed.[1]

The damage to the cornea in vitamin A associated xerophthalmia is quite different from damage to the retina at the back of the globe, a type of damage which can also be due to lack of vitamin A, but which is caused by lack of other forms of vitamin A which work in the visual system. Xerophthalmia from hypovitaminosis A is specifically due to lack of the hormone-like vitamin A metabolite retinoic acid, since (along with certain growth-stunting effects) the condition can be reversed in vitamin A deficient rats by retinoic acid supplementation (however the retinal damage continues). Since retinoic acid cannot be reduced to retinal or retinol, these effects on the cornea must be specific to retinoic acid. This is in keeping with retinoic acid's known requirement for good health in epithelial cells, such as those in the cornea.

Cause

The condition is not congenital and develops over the course of a few months as the lacrimal glands fail to produce tears. Other conditions involved in the progression already stated include the appearance of Bitot's spots, which are clumps of keratin debris that build up inside the conjunctiva and night blindness, which precedes corneal ulceration and total blindness.

WHO CLASSIFICATION:

XN-Night blindness

X1A-Conjunctival xerosis

X1B-Bitot spots

X2-Corneal xerosis

X3A-Corneal ulceration/keratomalacia, involving less than one-third of the cornea

X3B-Corneal ulceration/keratomalacia, involving more than one-third of the cornea

XS-Corneal scar due to xerophthalmia

XF-Xerophthalmic fundus

Prevention

Prophylaxis consists of periodic administration of Vitamin A supplements. WHO recommended schedule, which is universally recommended is as follows:

  • Infants 6–12 months old and any older children weighing less than 8 kg – 100,000 IU orally every 3–6 months
  • Children over 1 year and under 6 years of age – 200,000 IU orally every 6 months
  • Infants less than 6 months old, who are not being breastfed – 50,000 IU orally should be given before they attain the age of 6 months

Treatment

Treatment can occur in two ways: treating symptoms and treating the deficiency. Treatment of symptoms usually includes the use of artificial tears in the form of eye drops, increasing the humidity of the environment with humidifiers, and wearing wraparound glasses when outdoors. Treatment of the deficiency can be accomplished with a Vitamin A or multivitamin supplement or by eating foods rich in Vitamin A. Treatment with supplements and/or diet can be successful until the disease progresses as far as corneal ulceration, at which point only an extreme surgery can offer a chance of returning sight.

Epidemiology

Xerophthalmia usually affects children under nine years old and "accounts for 20,000–100,000 new cases of childhood blindness each year in the developing countries." The disease is largely found in developing countries like many of those in Africa and Southern Asia.

See also

References
  1. Solans, R.; Bosch, J.A.; Galofre, P.; others (2001), "Salivary and lacrimal gland dysfunction (sicca syndrome) after radioiodine therapy.", Journal of Nuclear Medicine, 42 (5): 738–43, PMID 11337569

Further reading
Classification
External resources
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