Vitamin A Deficiency, Prevention and Treatment
Vitamin A is very essential for our proper growth and fitness.Deficiency: The signs of vitamin A deficiency are predominantly ocular. They include night blindness, conjunctival xerosis, Bitot’s spots, corneal xerosis and keratomalacia. The term ‘xerophthalmia” (dry eye) comprises all the ocular manifestations of Vitamin A deficiency ranging from nightblinddness to keratomalacia. Given belows in a short description of the ocular manifestations.
Date: 11/24/2006 4:47:32 AM ( 16 y ) ... viewed 3303 times
(a) Night blindness: Lack of vitamin A first causes night blindness or inability to see in dim light. The mother herself can detect this condition when her child cannot see in late evenings or find her in a darkened room. Night blindness is due to impairment in dark adaptation. Unless vitamin A intake is increased, the condition may get worse, especially when children also suffer from diarrhoea and other infections.
(b) Conjunctional xerosis: This first clinical signs of Vitamin A deficiency. The conjunctiva becomes dry and non-wet table. Instead of looking smooth any shiny, it appears muddy and wrinkled. It has been well described as “emerging like sands banks are receding tide” when the child ceases to cry.
(c) Bitot’s Spots: Bitot’s spots are triangular, pearly-white or yellowish, foamy spots on the bulbar conjunctiva on either side of cornea. They are frequently bilateral. Bitot’s spots in young children usually indicate vitamin A deficiency. In order individuals, these spots are often inactive sequelae of earlier disease.
(c) Corneal xerosis: This stage is particularly serious. The cornea appears dull, dry and non-wet table and eventually opaque. It does not have a moist appearance. In more severe deficiency there may be corneal uncertain. The ulcer may heal leaving a corneal scar, which can affect vision.
(d) Keratomalacia: Keratomalacia or liquefaction of the cornea is a grave medical emergency. The cornea (a part or the whole) may soft and may burst open. The process is a rapid one. If the eye collapses, vision is lost. Keratomalacia is one of the major causes of blindness in India and is frequently associated with protein energy malnutrition.
Prevention: Prevention and/or control take two forms:
(a) Improvement of people’s diet so as to ensure a regular and adequate intake of foods rich in Vitamin A, and
(b) Reducing the frequency and severity of contributory factors, e.g., PEM, respiratory tract infections, diarrhoea and measles.
Since vitamin A can be stored in a body for 6 to 9 months and liberated slowly, a short-term, simple technology had been evolved by the National Institute of Nutrition at Hyderabad (India) for community based intervention against nutritional blindness, which has subsequently been adopted by other countries. The strategy is to administer a single massive does of 200,000 IU in vitamin A in oil (retinol palminate) orally every 6 months to preschool children (1 year to 6 years), and half that dose (100,000 IU) to children between 6 months and one-year age. In this way, the child would be, as it were “immunized” against xerophthalmia. The protection afforded by six-monthly dosing seems very adequate as measured by clinical signs of deficiency. In a longitudinal study in Hyderabad city, the incidence of keratomalacia in area covered by the programmed decreased by about 80 percent.
Treatment: Vitamin A deficiency should be treated urgently. Nearly all of the early stages of xerophthalmia can be reversed by administration of a massive does (200,000 IU or 110 mg of retinol palmitate) orally on two successive days (30). All children with corneal ulcers should receive vitamin A whether or not a deficiency is suspected.
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