Year : 1981 | Volume
: 29 | Issue : 4 | Page : 477--478
Malnutrition and corneal blindness
R P Dhanda
|How to cite this article:|
Dhanda R P. Malnutrition and corneal blindness.Indian J Ophthalmol 1981;29:477-478
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Dhanda R P. Malnutrition and corneal blindness. Indian J Ophthalmol [serial online] 1981 [cited 2020 Aug 7 ];29:477-478
Available from: http://www.ijo.in/text.asp?1981/29/4/477/30958
Inspite of fair amount of research work done on the nutritional studies of the populations in different countries, different regions of the country and different economic strata of the population, the subject has not been as critically understood as it needs to be. For example, it has been often emphasised that mass therapy with 50,000 units of vitamin-A given twice at six months interval to the school and pre-school children will eradicate keratomalacia. This particular aspect of vitamin A deficiency and its relation to keratomalacia needs to be critically evaluated on a clinical as well as research basis.
According to the text book description, the eye manifestations of the vitamin-A deficiency are :
Changes in the conjunctiva : brown pigmentation and Bitot's spots.Corneal involvement : Keratomalacia.Night blindness.
Clinical experience has established that there may be cases with conjunctival changes and no night blindness, and vice versa, there may or may not be night blindness and no conjunctival changes, Furthermore conjunctival changes may not respond to vitamin-A therapy. It is not uncommon to come across cases of Bitot's spots which have persisted inspite of massive vitamin-A therapy. Biochemical studies have indicated that vitamin-A level in blood is well above the minimum threshold level in cases of conjunctival xerosis. These observations are suggestive that conjunctival changes are not necessarily due to vitamin-A deficiency alone. It is not likely to be the only cause of this conjunctival pathology.
Corneal liquefaction is a serious effect of malnutrition, and is common in many developing countries. In India, keratomalacia has been reported largely from two southern states possibly because these areas are not only economically poor but their dietary habits are such that the diet is largely comprise of rice and starch and totally devoid of proteins and is poor in fat and calories. Rows of keratomalacia cases seen in the district of Madurai and around in Tamil Nadu are rare to come across in northern India, In the northern parts of India cases of keratomalacia are occasionally seen and reported but most such cases of keratomalacia are precipitated by acute diarrhoea, parasitic infestation and severe anemia.
It is also necessary to emphasise that diagnosis of keratomalacia should be based on the criteria clinically present and not on presumption. It would not be correct that any corneal opacity is due to keratomalacia, simply because the child presents picture of severmalnutrition. These illnourished children are also common victims of bacterial infections, small pox, and many other tropical systemic diseases. Vitamin-A deficiency in such cases contributes to the corneal pathology because of low tissue viability, while principal cause of corneal pathology is the infection, local or systemic. It will, therefore, not be correct that all cases of corneal opacity in endemically illnourished population are cases of keratomalacia due to malnutrition.
It is interesting to report that I visited some severely drought and scarcity affected areas of Gujarat and examined many hundred children, women and men, living in such conditions or working on scarcity project. Nearly 50% of the children had suffered from night blindness for some time during the scarcity months. Distribution of vitamin-A among these populations had quickly cured them all of the symptoms of night blindness. Interestingly enough, I did not come across a single cases of keratomalacia in this area.
More recently it has been emphasised that satisfactory level of retinol binding protein in blood is essential for transport of vitamin-A and deficiency of this protein may be responsible for manifestations of vitamin-A deficiency even though the diet may contain adequate vitamin-A. To this may be added the importance of the absorption factors so that not only vitamin A should be ingested but it should be absorbed from the intestines, carried in the circulation, stored in the liver and metabolished and utilised properly. It may be hypothesised that cases deficient in retinol binding proteins may develop night blindness, while children with adequate retinol binding proteins but deficient in other proteins may develop keratomalacia. The relationship of retinol binding proteins to transport, storage and utilisation of vitamin-A in the body, however, needs a more critical study to establish acceptable conclusions.
Electro-retinographic studies have further revealed that night blindness on one side and conjunctival and corneal involvement on the other are not as closely interlinked to vitaminA as has been emphasised in the literature. E.R.G. is completely extinguished in most cases of night blindness due to vitamin-A deficiency. E.R.G. has been recorded as perfectly normal in cases of conjunctival xerosis. A good electrical potential has been recorded even in cases of keratomalacia.
It has been further observed that vitamin-A level in blood must fall below minimum threshold level of 20 i.u. per 100 ml. before it can cause night blindness. Many of these cases of night blindness do not have conjunctival and corneal manifestations. It is therefore unbelievable that vitamin-A in blood may fall below the minimum threshold level and cause night blindness and yet it may not cause conjunctival and corneal involvement. The only interpretation of this can be that night blindness is the only true clinical manifestation of vitamin A deficiency while conjunctival and corneal involvements are more complex deficiency syndromes.
It is therefore only right that effort. should be made to understand the effects of malnutrition more clearly before framing and planning national programmes in a vast country like India involving huge financial committments which may not give expected results in the absence of a clear understanding of the subject. As stated above, it will not be correct to say that two doses of 50,000 unit of vitamin-A repeated at six months interval among preschool and school-going children and pregnant mothers will eradicate keratomalacia. Keratomalacia and conjunctival involvements are complex deficiency syndromes involving deficiencies of proteins, calories and ofcourse vitamin-A, but probably also other nutritional factors. Extensive biochemical studies in representative groups of population in different developing countries is, therefore, important for evolving national and international programmes in developing countries.