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issue. An increased susceptibility and a diminished power of resistance against infections are therefore present.

The eye lesion does not appear, as a rule, until late in the disease. It first occurs in the form of night blindness (hemeralopia) and dryness of the ocular conjunctiva (xerosis). The dryness later extends over the cornea, which becomes hazy, shrivels up, and shortly after

[graphic]

Fig. 1.-Diseased condition of the eye resulting from a deficiency of fat-soluble A.

pieces of it become necrosed (keratomalacia). In most cases the ocular conjunctiva is infected; the child then has photophobia, the conjunctiva is red and swollen, and the eye begins to water. When the cornea necroses the inflammation spreads to the interior of the eye. The inflammation may be so intense and widespread in many cases that it almost obscures the original xerosis. The eye lesion can be distinguished only with difficulty from the destructive inflammation in such cases. If the disease is not recognized in time the

child becomes blind. If the child does not then die of a secondary infection first, the most frequent cause of death is broncho-pneumonia.

In Figure 1 such a patient is seen, a boy of about 2 years. He appears to be a healthy child, the eyes only being swollen and kept tightly closed. He is, however, of small size and weighs less than normal. He also has a catarrhal infection.

In Figure 2 his eyes are seen to be completely destroyed. The conjunctiva is swollen and red, both corneæ are necrotic and there is

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pus in the anterior chamber. The child was cured but became totally Dlind, as the cornea never heals with clear transparent tissues. The scar's are always bazy and opaque, as will be observed from the succeeding pictures of children who were cured. (Figs. 3 and 4.) In cases where the cornea is only partly damaged the child, however. may usually be saved from complete blindness.

if a small child receives no milk whatever, not even separated milk or buttermilk, but is given only water, tea, gruel, and the like for a prolonged period on account of diarrhea or other malady, the child will diminish in size and become atrophic, with dry, wrinkled

skin, but otherwise it will resemble the first type, as will be seen from Figure 5. In this case, in addition to the absence of the fat-soluble A factor, several others are missing, but it is essentially the primary wasting disease—in this instance the intestinal trouble which dominates the entire clinical picture. Such a case answers most nearly to the xerophthalmia described by the older authors. When the child is a little older and stronger, and not ill, it can apparently thrive for a long time on an essentially carbohy

[graphic]

FIG. 3.—The patient has been cured but is totally blind, as the cornea never heals with

clear transparent tissues

drate diet, but sooner or later the tissues become edematous, and if the child has received no fresh milk, xerophthalmia and bronchopneumonia, etc., may supervene just as in the first type.

the child has had only a little butter in addition to the carbohydrate diet, edema, like that in Bright's disease, can certainly occur, but neither xerophthalmia nor marked changes in resisting power are observed, and the child is easily restored to health when it receives milk. Figure 6 shows such a case with an enormous amount of edema, but with no eye lesion.

Besides the xerophthalmia, the characteristic symptoms in this disease, which arises in consequence of the absence of the fat-soluble A factor, are therefore inhibition of growth and diminished iminunity and vitality. In bigger children and adults, who hardly

[graphic][merged small][merged small]

utilize so much fat-soluble A factor as the small child, the disease may be merely represented by the latter symptoms. It is only when

[graphic]

Fig. 5.-Showing a primary wasting disease due to entire lack of milk in the diet.

the lack of the fat-soluble A factor in the food has been almost absolute for a long time, or when the consumption of it has been very great, e. g., in chronic infectious diseases, that the bigger chil

dren get xerophthalmia also. It is chiefly the small children—that is to say, those under 2 to 3 years of age—who get xerophthalmia, and this may happen even though there has been some fat-soluble A factor in their food.

During the war there was much sickness among the bigger children in central Europe, which took the form especially of inhibition of growth and a large number of infectious diseases running a grave course. Thus many children were attacked by tuberculosis. The smaller children, on the other hand, were remarkably little affected and xerophthalmia was hardly seen at all in them. This

[graphic]

Fig. 6.--Edema without eye lesions due to a deficiency of butterfat.

state of affairs was due to the fact that during the war all the milk and milk products in Germany were rationed so that every little child obtained a certain amount daily. If the child was being suckled by the mother, she got the milk, and xerophthalmia was never observed in children suckled by a mother capable of yielding sufficient milk.

In Denmark the conditions, as mentivued, were different; before, and especially during the war, there were many cases of xerophthalmia. In a recent investigation undertaken for the Danish Ophthalmological Society by Olaf Blegvad, from 600 to 700 cases of xerophthalmia were found to have occurred between the years 1909 and

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