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Year : 1981  |  Volume : 29  |  Issue : 4  |  Page : 477-478

Malnutrition and corneal blindness

Indore, India

Correspondence Address:
R P Dhanda
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Source of Support: None, Conflict of Interest: None

PMID: 7201977

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How to cite this article:
Dhanda R P. Malnutrition and corneal blindness. Indian J Ophthalmol 1981;29:477-8

How to cite this URL:
Dhanda R P. Malnutrition and corneal blindness. Indian J Ophthalmol [serial online] 1981 [cited 2021 Jan 18];29:477-8. Available from: https://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 :­

  1. Changes in the conjunctiva : brown pigmentation and Bitot's spots.
  2. Corneal involvement : Keratomalacia.
  3. 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.


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