Vitamin A deficiency

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Compiled by: Dr. Iddi Ndyabawe
XEROPHTHALMIA
They term xerophthalmia is now reserved (by a joint WHO and USAID Committee, 1976) to
cover all the ocular manifestations of vitamin A deficiency, including not only the structural
changes affecting the conjunctiva, cornea and occasionally retina, but also the biophysical
disorders of retinal rods and cones functions.
Etiology
It occurs either due to dietary deficiency of vitamin A or its defective absorption from the gut. It
has long been recognised that vitamin A deficiency does not occur as an isolated problem but is
almost invariably accompanied by protein-energy malnutrition (PEM) and infections.
WHO classification (1982)
The new xerophthalmia classification (modification of original 1976 classification) is as follows:
Clinical features
1. X N (night blindness). It is the earliest symptom of xerophthalmia in children. It has to be
elicited by taking detailed history from the guardian or relative.
2. X1A (conjunctival xerosis). It consists of one or more patches of dry, lustreless, nonwettable
conjunctiva (Fig. 19.1), which has been well described as ‘emerging like sand banks at receding
tide’ when the child ceases to cry. These patches almost always involve the inter-palpebral area
of the temporal quadrants and often the nasal quadrants as well. In more advanced cases, the
entire bulbar conjunctiva may be affected. Typical xerosis may be associated with conjunctival
thickening, wrinkling and pigmentation.
3. X1B (Bitot’s spots). It is an extension of the xerotic process seen in stage X1A. The Bitot’s
spot is a raised, silvery white, foamy, triangular patch of keratinised epithelium, situated on the

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bulbar conjunctiva in the inter-palpebral area. It is usually bilateral and temporal, and less
frequently nasal
4. X2 (corneal xerosis). The earliest change in the cornea is punctate keratopathy which begins
in the lower nasal quadrant, followed by haziness and/or granular pebbly dryness (Fig. 19.3).
Involved cornea lacks lustre.
5. X3A and X3B (corneal ulceration/keratomalacia), Stromal defects occur in the late stage due
to colliquative necrosis and take several forms. Small ulcers (1-3 mm) occur peripherally; they
are characteristically circular, with steep margins and are sharply demarcated (Fig. 19.4). Large
ulcers and areas of necrosis may extend centrally or involve the entire cornea. If appropriate
therapy is instituted immediately, stromal defects involving less than one-third of corneal surface
(X3A) usually heal, leaving some useful vision. However, larger stromal defects (X3B)
commonly result in blindness.
6. XS (corneal scars). Healing of stromal defects results in corneal scars of different densities
and sizes which may or may not cover the pupillary area. A detailed history is required to
ascertain the cause of corneal opacity.
7. XFC (Xerophthalmic fundus). It is characterized by typical seed-like, raised, whitish lesions
scattered uniformly over the part of the fundus at the level of optic disc.
Treatment
It includes local ocular therapy, vitamin A therapy and treatment of underlying general disease.
1. Local ocular therapy. For conjunctival xerosis artificial tears (0.7 percent hydroxypropyl
methyl cellulose or 0.3 percent hypromellose) should be instilled every 3-4 hours. In the stage of
keratomalacia, full-fledged treatment of bacterial corneal ulcer should be instituted.
2. Vitamin A therapy. Treatment schedules apply to all stages of active xerophthalmia viz. XN,
X1A, X1B, X2, X3A and X3B. Oral administration is the recommended method of treatment.
However, in the presence of repeated vomiting and severe diarrhoea, intramuscular injections of
water-miscible preparation should be preferred. The WHO recommended
schedule is as given below:
i. All patients above the age of 1 year (except women of reproductive age): 200,000 IU of
vitamin A orally or 100,000 IU by intramuscular injection should be given immediately on
diagnosis and repeated the following day and 4 weeks later.
ii. Children under the age of 1 year and children of any age who weigh less than 8 kg should be
treated with half the doses for patients of more than 1 year of age.

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iii. Women of reproductive age, pregnant or not:
(a) Those having night blindness (XN), conjunctival xerosis (X1A) and Bitot’s spots (X1B)
should be treated with a daily dose of 10,000 IU of vitamin A orally (1 sugar coated tablet) for 2
weeks.
(b) For corneal xerophthalmia, administration of full dosage schedule (described for patients
above 1 year of age) is recommended.
3. Treatment of underlying conditions such as PEM and other nutritional disorders, diarrhoea,
dehydration and electrolyte imbalance, infections and parasitic conditions should be considered
simultaneously.
Prophylaxis against xerophthalmia
The three major known intervention strategies for the prevention and control of vitamin A
deficiency are:
1. Short-term approach. It comprises periodic administration of vitamin A supplements. WHO
recommended, universal distribution schedule of vitamin A for prevention is as follows:

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A revised schedule of vitamin A supplements being followed in India since August 1992, under
the programme named as ‘Child Survival and Safe Motherhood (CSSM)’ is as follows:
2. Medium-term approach. It includes food fortification with vitamin A.
3. Long-term approach. It should be the ultimate aim. It implies promotion of adequate intake of
vitamin A rich foods such as green leafy vegetables, papaya and drum- sticks (Fig. 19.8).
Nutritional health education should be included in the curriculum of school children.
Note. The short-term approach has been mostly in vogue especially in Asia. The best option
perhaps is a combination of all the three methods with a gradual weaning away of the short-term
approach.