Vitamin A
deficiency
Β·
The risk of vitamin A deficiency is small in
children who are getting vitamin A
(retinol) or its precursors. Deficiency states are common in
many developing countries and are often associated with global malnutrition.
Barring impoverished populations, deficiency of vitamin A is rare in developed
countries. Vitamin A deficiency may also be seen as a complication with various
chronic disorders or diseases in children. Medical history related to dietary
habits may be important in identifying nutritional disorders.
Β·
In eye, vitamin A is metabolised to form rhodopsin
(retinal visual pigment). Action of light on rhodopsin is the initial step in
the visual process.
Β·
Pre-formed vitamin A is available in foods of
animal origin only. Vitamin A may be obtained from carotenes, which are present
in green and coloured vegetables and yellow fruits. Carotenes provide vitamin A
to the vegetarians.
Β·
Malnutrition, especially protein deficiency, may
also cause vitamin A deficiency. Clinical or sub-clinical zinc deficiency may
also increase the risk of vitamin A deficiency.
Β· Except for vitamin A, toxicity from excess intake of vitamins is less common. Excessive intake of carotene (precursor of vitamin A) may lead to pigmentation of skin (hypercarotenosis). This gets reduced and fades away when intake of carotene is reduced.
Symptoms:
- Symptoms of vitamin A deficiency are associated with the requirement of vitamin A for the maintenance of epithelial functions.
- Symptoms include:
- Delayed dark adaptation (an early symptom).
- Night blindness or nyctalopia (seen in more advanced cases).
- Photophobia (sensitivity to light).
- Diminution of vision.
- Dry and scaly cornea (xerophthalmia).
- Conjunctival plaques (Bitotβs spot).
- Corneal degeneration (Keratomalacia and corneal ulceration).
- Besides eye lesion, child with vitamin A deficiency
may have systemic features such as growth retardation,
susceptibility to infections, anaemia, diarrhoea, mental retardation, apathy,
increased intracranial pressure, and wide separation of the cranial bone at the
sutures.
Causes:
- There are low levels of vitamin A in plasma, liver, and extra-hepatic tissues of neonates, as compared to adults. Normal plasma levels increase gradually as child grows.
- Vitamin A deficiency and xerophthalmia still occur
throughout much of the developing countries and are linked to under-nourishment. Vitamin A
deficiency may also be seen as complication in
children with various chronic disorders or diseases. Malnutrition, particularly
protein deficiency, may cause vitamin A deficiency because of the impaired
vitamin A carrying protein.
- Eye lesions are the most specific
and characteristic features of vitamin A deficiency, but
these may manifest rather late in
the progression of deficiency. Lesions caused by vitamin A deficiency develop
insidiously and rarely manifest before two years of age.
- Besides the important features such as delayed dark adaptation, night blindness, and photophobia, the corneal/ conjunctival epithelium is severely affected.
Pathology
- Characteristic changes as a result of vitamin A deficiency in epithelial cells include proliferation of basal cells, hyperkeratosis, and formation of cornified squamous epithelium. The combination of defective epithelial barrier to infection, low immune response, and lowered response to inflammatory stress leads to associated health problems.
- Delayed adaptation to the dark is due to reduced re-synthesis of visual pigment rhodopsin in retina.
- The retinal pigment epithelium degenerates, pigment containing retinal rods and cones loose support and thus break down, resulting in blindness.
Diagnosis
- Diagnosis depends upon history, clinical examination and laboratory investigations.
- A dietary history is important in diagnosis or ruling out low intake, being the aetiological factor.
- Early vitamin A deficiency shows delayed dark adaptation.
- Keratinised conjunctiva shows Bitotβs spots at a relatively early stage.
- Cornea shows dry and scaly layers of cells known as xerophthalmia. Cornea may degenerate and produce keratomalacia, corneal ulceration, necrosis, and permanent corneal scars.
Β·
Clinical
criteria by ocular signs
o XN
Night blindness
o X1A
Conjunctival xerosis
o X1B
Bitotβs spot
o X2
Corneal xerosis
o X3A
Corneal ulceration/keratomalacia <1/2 corneal
surface
o X3B
Corneal ulceration/keratomalacia β₯1/2 corneal surface
o XS
Corneal scar
o XF
Xerophthalmic fundus
Β·
Biochemical
criteria
o Serum vitamin
A (retinol) less than 10ΞΌg/100 ml (0.35ΞΌmol/liter)
Β·
Measurement of plasma retinol level is not an accurate indicator of
vitamin A status. However, measurement of plasma levels of retinol may be important in cases with severe vitamin A deficiency and with depleted stores in liver.
Β·
Clinical or even subclinical vitamin A deficiency
is associated with immunodeficiency leading
to increased chances of infection such as measles and increased risk of
mortality, especially in developing countries.
Management should be carried out under medical supervision.
Β· Xerophthalmia and vitamin A deficiency requires urgent treatment.
- Supportive therapy:
- Topical artificial tears: Topical artificial tears may be used to lubricate eyes in xerophthalmia.
- Wrap around glasses: These prevent against infections and prevent air from further drying the eyes.
- Air humidifier: Air humidifier maintains humidity and thus prevents dryness.
- Topical therapy:
- Topical retinoic acid: Topical retinoic acid (0.1%) in arachis oil, even with concomitant systemic vitamin A therapy, was found to be associated with more rapid healing of corneal lesions in substantial number of patients. A three times a day application of retinoic acid was not associated with conjunctival congestion, corneal vascularisation, or any scarring. Retinoic acid has limited human trials.
- Systemic medical therapy:
- Vitamin A supplementation for deficiency state depends upon safety and efficacy of its use
- A daily supplement of 1500ΞΌg of vitamin A is normally sufficient for latent cases of vitamin A deficiency, but recommended dietary allowance (RDA) levels may be the goal after this intake (which covers needs of >97% of population).
- Xerophthalmia cases may require 1500ΞΌg/kg of body weight orally for five days followed by 7500ΞΌg of vitamin A in oil given intramuscularly, till recovery.
- World Health Organisation (WHO) is giving high priority to prevention of vitamin A deficiency in communities where xerophthalmia occurs. They have recommended giving single prophylactic oral dose of retinyl palmitate (an ester of retinol or vitamin A) to pre-school children
- Surgical therapy:
- Surgery plays limited role in the management of xerophthalmia. It is of no use when there is complete corneal necrosis.
- Keratoplasty: Keratoplasty for keratomalacia may be associated with poor visual outcome even in those where graft survives.
- Amniotic membrane transplantation: Amniotic membrane transplantation may be done in cases with corneal perforation due to xerophthalmia, as an alternative to keratoplasty.
Complications:
- This may produce complications and leave sequelae such as corneal opacity and blindness.
Prevention
- Prevention may involve
- Free distribution of vitamin A capsule under medical guidance to children and pregnant women.
- Fortification of food with vitamin A.
- Nutrition and health education of the target population.
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