Vitamin A deficiency (VAD), till recently, was the commonest cause of preventable blindness in Indian children. Although the prevalence of severe disease has markedly declined in recent years due to preventive supplementation programs, sub clinical Vitamin A deficiency continues to be a major public health problem, with an estimated prevalence of —1-3% in pre-school children.


Vitamin A is a fat-soluble vitamin, existing in two forms —

a) Pre-formed vitamin e.g. retinol, present in animal sources; and

b) Pro-vitamin e.g. /3-carotene, present in plant sources, which is converted to retinol in the gut.

Retinol is actively accumulated in liver (as retinyl palmitate) during last trimester of pregnancy and breastfeeding. Postnatally, retinol is better absorbed than 3-carotene and transported in blood, bound to a retinolbinding protein.

Vitamin A is essential for — a) retinal functions i.e. regeneration of Rhodopsin — a chromoprotein, essential for night vision, b) maintenance of epithelial integrity with cellular regeneration (resistance to infections), and c) removal of toxic free-radicals from body (anti-oxidant).

Vitamin A deficiency

Etiology Vitamin A deficiency is most common in toddlers and preschool children from low socioeconomic status. Common causes of VAD include —

a) Dietary deficiency

b) Mal absorptive states e.g. chronic diarrhea, worm infestations etc.

c) Impaired metabolism e.g. in chronic liver disease

d) Reduced transport proteins e.g. in malnutrition, nephrotic syndrome etc.

e) Higher requirements in infections e.g. measles.

t) Less intrauterine stores e.g. in pre terms

g) Darner disease – a genetic defect (Vitamin A dependency)

Clinical manifestations of Vitamin A deficiency may be divided into two broad groups – ophthalmic (xerophthalmia) and extra-ophthalmic manifestations.

A) Xerophthalmia denotes a spectrum of ocular signs in Vitamin A deficiency including — Night blindness i.e. inability to see clearly in dim- light or slower dark-adaptation.

• Conjunctival Xerosis i.e. dry, wrinkled, lusterless, muddy conjunctiva due to cornified epithelium and Bitot’ spots – chalky gray triangular plaques, generally near the temporal limbus, due to heaped-up dry epithelium.

• Cortical lesions of variable severity Xerosis i.e. dull, dry and cloudy comea, Ulcers, limited to few layers of cornea, or keratomalcia i.e. liquefaction and rupture of full-depth cornea, leading to loss of vision. Even milder cases may lead to comeal scarring on recovery.

• Fundal changes e.g. retinal xerosis and detachment.

B) Extra-ocular manifestations include —

• Phrynoderma (Follicular hyperkeratosis), presenting as dry and scaly skin with toad-like texture, especially over extensor aspects of extremities e.g., dorsum of tibia, knees and elbows. Phrynoderma is also associated with essential fatty acid deficiency.

• Recurrent respiratory infections, due to squamous metaplasia of respiratory mucosa,

• Recurrent urinary tract infections, pancreatitis or parotitis due to epithelial metaplasia of urinary or exocrine tracts.

• Rarely, atrophy of genital epithelium may lead to reproductive dysfunction in adults.

Diagnosis of Vitamin A deficiency is largely clinical, though subclinical deficiency may be identified by —

a) Conjuctival impression cytology (dC), to detect loss of mucus-secreting goblet cells and epithelial metaplasia on special staining,

b) Dark-adaptation test, and

c) Low plasma carotene levels (<20 j.tgIL).


As per WHO recommendation, Standard treatment of Vitamin A deficiency includes 3 doses of concentrated Vitamin A (1 lac lU/nil), given orally, on day 1, 2 and 14. In cases with mal absorption/persistent vomiting, IM therapy (strength: 50,000/mi) may be used, given as half of the oral dose with same schedule.

All cases treated should receive dietary counseling and Vitamin A prophylaxis till 6-8 years of age (2 lac TU every 6 month) to prevent the recurrence.

Local ophthalmic treatment of corneal lesions, with antibiotics, mydriatics and eye-padding is equally important.

Prevention of Vitamin A deficiency includes nutritional counseling, Vitamin A supplements and prevention of precipitating illnesses e.g. measles.

National program for prevention of nutritional blindness due to it.

This program was launched in 1971 as a separate health program but later incorporated in child survival and safe motherhood or CSSM program (1992) and subsequently, in Reproduction & child health or RCH program (1997).

Objectives: To decrease the incidence of Vitamin A deficiency and subsequent blindness.

Beneficiary: Children from 6 months to 5 years. Components of this program include —

– Regular prophylaxis with 6-monthly administration of Oral Vitamin A 1,00,000 IU (< 1 year) and 2,00,000 IU in older children; from 6 months to 5 years of age. This protocol was first developed by National institute of nutrition, Hyderabad and later adopted by WHO as global strategy. Under RCH program, routine Vitamin A supplementation is limited to two doses, first with measles vaccine at 9 months and second with first DPT/OPV boosters at 15-18 months.

– Additional doses of Vitamin A, after illnesses e.g. measles, severe PEM, chronic diarrhea and long febrile illnesses.

– Dietary counseling, to encourage consumption of cheap and locally available Vitamin A rich foods

– Prevention of precipitating illnesses e.g. measles by vaccination coverage and breast feeding promotion.

– Periodic monitoring and evaluation

Note: In national program, Oral Vitamin A is supplied as multi-dose liquid preparation (1 lac lU/mi), with a special 2 ml spoon. Only this spoon should he used and not the regular 5 ml spoons, to avoid over dosage.

Hyper-vitaminosis A

Being fat-soluble, excess Vitamin A is not readily excreted in urine and accumulates in tissues with following presentations —

Acute hypervitaminosis, due to acute preventive or therapeutic overdose (>3, 00,000 IU), presents as Pseudotumor cerebri i.e. transient, self-limiting, benign intracranial hypertension with headache, vomiting, drowsiness, bulging fontanels and/or papilledema. Exact mechanism is unknown, probably relates to massive rupture of lysosomal membranes.

Chronic hypervitaminosis due to prolonged Vitamin A deficiency therapy e.g. for acne, presents with – anorexia, weight loss, dry pruritic skin, alopecia, tender extremities (hyperostosis on X-ray), hepatosplenomegaly and pseudotumor cerebri.

Hypercarotenemia – asymptomatic, transient yellowish discoloration of skin/body fluids, due to excess consumption of (3-carotene containing fruits.

Massive Vitamin A deficiency administration in first trimester may also have severe teratogenic effects on fetus.