2. Etiology and Pathogenesis
• Vitamin A is a fat-soluble substance that is essential for immunity, growth,
maintenance of mucosal surfaces, cell differentiation, reproduction, and vision.
• Rich sources of preformed vitamin A include liver, cod liver oil, butter, eggs,
and cheese.
• Provitamin A carotenoids, such as β-carotene, are found in dark green leafy
vegetables, carrots, and certain orange and yellow fruits and vegetables. β-
carotene is converted in the gut to vitamin A.
• Vitamin A is largely transported in to the liver, which stores about 90% of the
vitamin A in the body
3. Etiology and Pathogenesis
• Retinol is required:
– For the elaboration of rhodopsin or “visual purple” by the
rods,
– For maintenance of normal differentiation of the epithelial
lining of several structures throughout the body, and
– For a full competency immune response
4. Etiology and Pathogenesis
• Changes in vitamin A deficiency :
Keratinization of the epithelium of mucous membranes harder &
resist wetting
Loss of goblet cells which secrete mucusdry eye
Rhodopsin is not formed night blindness
• Thus, vitamin A deficiency can affect the tear layer, the conjunctiva, the
cornea, and the ability to see at night
5. Many factors can contribute to vitamin A deficiency
• Decreased intake
• Impaired absorption, altered storage
• Decreased circulation
• Increased utilization and uptake by tissues
• Increased metabolic losses of vitamin A
6. Epidemiology
• Nutritional blindness is primarily a problem of developing countries
• 250 million pre-school-age children are subclinically vitamin A deficient
• 3 million have clinical xerophthalmia
• 300,000 are blind from xerophthalmia (about 10% of all blind children)
• Nutritional blindness can occur at any age, but particularly among young
children and pregnant women.
7. Epidemiology
• Xerophthalmia is most common among 1- to 6-year-old
children, although severe, blinding forms are concentrated in
those 6 months to 3 years of age.
• At least four factors account for this pediatric age distribution:
1. Children often are born to vitamin A-deficient mothers
2. Childhood is a period of rapid growth, placing heavy demands
on vitamin A stores
3. The young child is in the dangerous weaning period.
4. Childhood also is the age of greatest morbidity (and mortality)
from measles, chickenpox, pertussis, respiratory infections,
and especially gastroenteritis.
8. CLINICAL CLASSIFICATION
• XN: Night blindness
• X1A:Conjunctival xerosis
• X1B:Bitot's spots
• X2:Corneal xerosis
• X3A:Corneal ulceration/keratomalacia involving less than
one third of the corneal surface
• X3B:Corneal ulceration/keratomalacia involving one third or
more of the corneal surface
• XF: Xerophthalmic fundus
• XS: Corneal scars presumed secondary to xerophthalmia
14. Diagnosis
• Diagnosis requires a high degree of suspicion
• Treatment is most practical way to confirm the diagnosis.
• Xerophthalmia is a clinical diagnosis.
• For children, serum or plasma vitamin A levels less than
0.35 µmol/L are considered to indicate vitamin A deficiency
• Histologic examination of the conjunctival epithelium for
squamous metaplasia and loss of goblet cells has been used
15. Treatment
• Xerophthalmia is a medical emergency that should be treated
promptly with vitamin A therapy.
• Individuals with xerophthalmia are at increased risk of blindness,
and because of the effects of vitamin A deficiency on the immune
system, they are also at increased risk of infections and death.
• Night blindness usually improves within 24 hours, and corneal and
conjunctival xerosis responds within days.
• High-dose vitamin A therapy is recommended by WHO for children
with measles
16. Treatment schedule for xerophthalmia
or measles
Timing of dose Age Dose in IU
On diagnosis < 6 months 50, 000
6 – 12 months 100, 000
>12 months 200, 000
Following day same age-specific dose
2-4 weeks later same age-specific dose
17. Treatment indications
• All children with any active corneal ulceration
• All children with signs of xerophthalmia
• All children with measles
• All severely ill or malnouished children from
areas where xerophthalmia occurs, even if there is
no clinical evidence of xerophthalmia
18. Prevention
• Distribution of massive dose of vit A
• Fortification of food with Vit.A
• Horticulture and agriculture to grow & eat the
right sort of food
• Nutrition and health education
• Immunization especially for measles
19. Periodic oral vitamin A
supplementation
• Infants <6 months 50,000 IU
– Non-breast-fed infants, breast-fed infants
– whose mothers have not received supplemental vitamin A
• Infants 6-12 months 100,000 IU
– Every 4-6 months
• Children >12 months 200,000 IU
– Every 4-6 months
• Mothers 200,000 IU
– Within 8 weeks of delivery
