It is everyday knowledge that fresh vegetables are of great value in the protection from, and cure of, scurvy. The first experimental investigation of this subject was that of Holst and Froelich, published in 1907, and continued in a series of papers extending to 1916. These investigators tested the potency of a large number of vegetables by feeding them in varying quantities to guinea-pigs. They found that all vegetables have antiscorbutic value but to a markedly varying degree. Cabbage, sorrel leaves, endive, head salad, and dandelion leaves, were found to be of most avail in protecting againstscurvy, whereas carrots, cooked potatoes and cooked turnips, and cauliflower proved to be of less value. In general, it may be stated that the leafy vegetables have more antiscorbutic power than the roots or the tubers. This generalization, we shall see, is not without exception,e.g., the swede. Similar experimental work has been recently carried on by a group of investigators at the Lister Institute, who have added considerably to our knowledge in this field. In all this experimental work cabbage has been found to be the most potent of the vegetables, and therefore experiments have centered about it just as in considering fruits the work has centered about orange juice or lemon juice. We shall, therefore, discuss in detail its reaction to heat and dehydration.
Cabbage.—Holst and Froelich found that 1 g. daily of fresh cabbage afforded nearly complete protection to guinea-pigs, and Delf has corroborated this work. This amount is sufficient to prevent the development of manifest scurvy, although it does not induce satisfactory growth. In this respect it is comparable to giving 1.5 c.c. of orange juice daily. If guinea-pigs take only 0.5 g. of raw cabbage, scurvy will develop; whereas 2 g. or more will promote satisfactory growth and no scorbutic changes will be found on microscopic examination.
Effect of Heating.—Vegetables are of decidedly less antiscorbutic value when cooked than raw; cabbage, for instance, on being boiled is weakened about one-half. Heating to 110° C. for an hour destroys almost all of its antiscorbutic factor. Delf’s tests did not show so great a loss. She came to the conclusion, of theoretical and practical value, that slow cooking at a low temperature is much more deleterious than rapid cooking at a higher temperature. Hess and Unger found that carrots lostmuch of their antiscorbutic power after boiling, and that this was the result of a true destruction, the vitamine not having been merely dissolved in the water of boiling; for if guinea-pigs consumed 40 c.c. per capita of this water, they were not protected against scurvy (Fig. 11). Acidulating the water with 10 per cent. vinegar did not reduce the loss, an experience similar to that of others using citric acid or lemon juice.
Vegetables cannot be considered from an antiscorbutic standpoint as a standard and uniform foodstuff, as they vary in their content of this factor according to their freshness and age.This was demonstrated by means of feeding experiments with carrots. For example, 35 g. of old carrots, such as were used for feeding the laboratory animals, afforded but little protection after having been cooked in an open vessel for about 45 minutes, whereas the same amount of young carrots cooked this way protected the guinea-pigs. It is obvious that this distinction is of importance in evaluating the antiscorbutic content of the various foods, and in considering whether individuals and groups of individuals are receiving an adequate quota of antiscorbutic vitamine. It will be noted later that it is also of importance in connection with the potency of dehydrated vegetables. Recent experiments indicate that not only age, but thedegree of ripenessmust be considered in appraising the food value of vegetables. Feeding experiments showed that tomatoes which were fully ripe were more potent than those which were slightly green. Probably many other factors play a rôle in determining the richness of vegetables in vitamine. It may not be immaterial whether they are allowed to ripen on the vine or shrub, or mature subsequently. The nature of the soil may also affect the antiscorbutic quality ofthe vegetables or fruit. So that it is evident that we must not be schematic in considering this question, and must realize that a table of antiscorbutic values, such as accompanies this text (Table 3), does not furnish definite and inflexible values.
There is a marked difference betweenvegetables and vegetable juicesin keeping quality, and in their reaction to heat and to acid. In general, it may be stated that the juices are much more sensitive. Holst and Froelich brought out this point in 1912 and enlarged upon it in their publication of 1916. The different juices vary greatly in this respect; for example, dandelion juice is acutely sensitive to heat, whereas sorrel leaves withstand high temperatures very well. In regard to these differences an analogy may be drawn to the fruit juices. Lemon, orange and raspberry juices are markedly thermostable, but lime juice is weakened markedly by heat. Many of these juices are protected by the addition of acid—5 per cent. of lemon juice increasing the thermostability of cabbage juice—whereas, as we have stated, little is gained by cooking vegetables in an acid medium.
Potato.—The civilized world is dependent for its quota of antiscorbutic foodstuff largely upon the potato. It might be thought, therefore, that this would signify that the potato is endowed with great antiscorbutic power. Such is not the case, however, as demonstrated both by laboratory tests and clinical experience. Considering its importance, there have been surprisingly few feeding experiments carried out with potato. Holst and Froelich (1912) found that 17 g. of potatoes, steamed at 100° C. for 30 minutes, afforded but slight protection, and that it required 20 g. to fully protect a guinea-pig. Givens and Cohen failed to ward off scurvy by means of cooked potatoesfed to the equivalent of 5 g. of the raw vegetable (guinea-pigs will not eat raw potatoes). There are no accurate figures as to the quantity of potatoes needed to protect a human being from scurvy. The statement of Doctor Guy, however, who after careful study of convicts’ diets, concluded that 14 ounces daily would protect them from scurvy (if the ration included one ounce of other fresh vegetable and 4 ounces of meat), is probably close to the mark.41With the experience that potatoes play such a significant rôle in the prevention of scurvy, how are we to interpret the fact that they are only mildly antiscorbutic? Potatoes are consumed in very large amounts; in the Temperate Zone probably twice as many pounds of potatoes are consumed during the winter as of all other vegetables combined (Fig. 1). It is evident, therefore, that in a practical evaluation of antiscorbutic foodstuffs, not only the intrinsic antiscorbutic potency must be considered, but also the quantity of the vegetable or fruit consumed.
Swede.—We cannot leave the consideration of vegetable antiscorbutics without adding a few words as to the value of swede juice,42which has been recently highly recommended by Chick and Rhodes, who found it comparable to the cabbage and the onion, and even to orange juice. For example, 25 c.c. of raw swede juice were equivalent to 1.5 g. of raw cabbage. It is, therefore, more potent than the juice of raw carrot, and far more efficacious than the juice of the beetroot (Table 3). Tests carried out with this antiscorbutic in infant feedingseemed to show that it is of value in this field. The authors believe that the potency of vegetables is closely associated with certain botanical species, and that in this way the marked virtue of the swede can be explained, as it belongs to the natural order of Cruciferæ, which includes also the cabbage, the scurvy grass and the cresses. If, however, this is a rule of nature, it is difficult to explain the marked difference between the lime and the lemon, which are both varieties of Citrus Medica.
Dehydrated Vegetables.—For hundreds of years fresh vegetables have been dried to serve as food during the winter months and have fulfilled a useful purpose on account of their small bulk and great food value. The question for us to consider, however, is whether dehydrated vegetables still retain their antiscorbutic quality and can be counted on to supply this factor in the dietary. At present this subject is engaging the attention of laboratory workers as well as of practical dietitians and food hygienists. The experience of the past is not happy in this regard. In the Medical and Surgical History of the War of the Rebellion we read as follows: “A scorbutic tendency was developed at most of our military posts during the winter season, after the troops had been confined to the use of the ordinary ration with desiccated vegetables. The latter in quantities failed to repress the disease.” In spite of this and similar military experiences43the employment of dehydrated vegetables was urged recently for rationing our soldiers, the claim being made that “by simply soaking in water and boiling in thesame water these vegetables are brought back to the condition of fresh vegetables.” Both in this country and in England there was strong propaganda during the war to dehydrate vegetables on an enormous scale and to substitute them for the fresh food.
Dehydrated vegetables as a cause of scurvyFig. 12.—Hay, oats, waterad libitum, and 7 g. of dehydrated carrots dried at a room temperature of about 130° F. about 1 month previously. All animals developed scurvy. The marked gain in weight when an equivalent amount of fresh carrots was substituted for the dehydrated vegetable corresponded to the disappearance of scorbutic signs. Guinea-Pig B 951 did not receive fresh carrots, as it was evidently ailing at the time the second period began.
Experimental investigation on this subject may be summarized as showing that vegetables dried according to present methods lose their antiscorbutic value as the result of dehydrating (Fig. 12), and that they become still more impoverished as the result of aging. We should not sweepingly condemn the principle of dehydration, as very possibly some slight modifications in the process may be devised which will counteract the deteriorating influence. In their paper of 1912, to which reference has been made so often, Holst and Froelichreported that potatoes, carrots, peas, lentils and almonds have practically no protective value after they are thoroughly dried. In two reports—one giving the results of feeding various brands of dehydrated carrots to guinea-pigs, and the other of an attempt to cure scurvy in babies by means of these carrots—we also came to the conclusion that the antiscorbutic factor had been almost completely destroyed. Givens and Cohen (1918) found that even cabbage dried at a low temperature retained only a small amount of its potency after a month, and Delf and Skelton came to practically the same conclusion, also noting that the cabbage on being kept, steadily lost what little of the antiscorbutic factor had survived the drying process. The same was true of the fat-soluble factor. These authors made an observation which may prove of value in helping to solve this problem, namely, that “the residual amount is distinctly greater if the cabbage is plunged into boiling water before drying.” This protective action of heat they suggest may indicate that: “Some at least of the destruction may be due to the activity of an enzyme or other body originally present in the living tissue.”
Another observation which may prove of practical value in rendering dehydrated vegetables the nutritional equivalent of the fresh vegetable is that when the carrots selected for dehydration are young and fresh a product is obtained which possesses decided antiscorbutic power. In this connection the following statement by Falk and his co-workers in a study of the enzyme action of vegetables and the effect of dehydration is significant: “In considering these enzyme results, it may be pointed out that the state of ripeness and the age of the vegetable undoubtedly influence the activities.”
The most promising dehydration experiment has beenconducted by Holst and Froelich and was published in 1916 in a paper which has passed unnoticed. They dried white cabbage so that it retained its antiscorbutic properties, and, to a large extent, its color and taste, for a period of two years. This result was accomplished by keeping out all moisture and preventing hydrolysis,44a method which is employed in preserving antitoxins, toxins and agglutinins. It is by far the most encouraging test reported, and should be made the basis of further work by those actively interested in perfecting dehydration.
Cure of scurvy by addition of canned tomatoFig. 13.—Cure of scurvy by the addition of canned tomato. In this case, as frequently, the alleviation of symptoms preceded the gain in weight.
Canned Food (Tomatoes).—In the course of canning, as in dehydrating, most vegetables and fruits lose their antiscorbutic properties. A general denunciation, however, of all canned foods is incorrect, as there are exceptions to this rule. It has been shown by Hess and Unger thatcanned tomatoes possess a high degree of antiscorbutic power (Fig. 13), and it is probable that most of the acid fruits and vegetables are able to withstand the canning process. It was found, in an experiment embracing many series of guinea-pigs, that 4 c.c. daily of strained, canned tomato are sufficient to afford protection, even when a lot was used which had been prepared a year previously. This is indeed remarkable, considering that the food undergoes a two-fold heating in the course of canning, during one of which (“processing”) the temperature is raised to fully 230° F. Tomatoes have another advantage over most other vegetables in that they are richly endowed with the water-soluble vitamine, as shown by our tests on pigeons suffering from polyneuritis, and by the experiments on rats of Osborne and Mendel, who found tomatoes far superior in this respect to turnips, onions, beetroots or beans. They are also rich in the fat-soluble vitamine. In view of the availability of canned tomatoes and their excellent keeping quality they are well suited to an extended use as an antiscorbutic. In the subsequent chapter we shall discuss their employment in infant feeding and in the army ration.
Germinated Cereals and Pulses.—In 1912 Fuerst reported that although the resting seed—the cereal grain, the pea, bean and lentil—are poor in antiscorbutic vitamine, they develop this principle as soon as they germinate. They possess, in other words, latent antiscorbutic properties, and are potentially antiscorbutic. This observation is not only of scientific interest but of practical value, as these pulses are well suited for transport and do not readily deteriorate. For this reason, Chick and her co-workers at the Lister Institute, who were searching for an antiscorbuticfoodstuff for the army, directed their attention to the utilization of the pulses. In the course of a thorough investigation (1919) they found that although it required 30 to 40 g. daily of dry green peas to prevent scurvy in the guinea-pig, a consumption of 10 g. of the germinated peas afforded satisfactory protection.45The soaked seeds have an antiscorbutic value comparable to many of the fresh vegetables; by no means as great as cabbage, but somewhat greater than that of carrots. As the result of cooking, their potency was found to be reduced about 75 per cent. We shall have occasion to refer to this antiscorbutic food in the chapter on treatment in connection with the rationing of armies.
Meat and Eggs.—As has been stated, animal tissues are distinctly inferior to fruits and vegetables in the antiscorbutic principle. As there has been no accurate evaluation of these foods—the only test being one by Chick, Hume and Skelton, where 10 c.c.ofraw beef juice failed to protect guinea-pigs—we have to depend upon clinical experience for our knowledge. Beef juice is highly rated by physicians in the prevention of infantile scurvy, but it is probably far less potent than vegetables or fruit juices. The Arctic explorers, and many who have lived in the Arctic regions, agree that the inhabitants are protected from scurvy during the winter months by their diet of fresh meat and fish. The Admiralty Enquiry on the outbreak of scurvy in the Arctic Expedition of 1875 reported that a large ration of meat is necessary to afford protection. Curran (1847) described three cases admitted to the hospital in the great Irish epidemic of that year, wherethe diet previously had included three-quarters of a pound of meat on five days of the week. From these and similar experiences the conclusion is manifest that the divergence of opinion regarding the value of meat is based upon quantitative differences in the rations. Evidently, if sufficient meat is provided, the development of scurvy will be obviated. Another factor which must be borne in mind is that those who refer to meat in the Arctic regions refer to fresh raw meat, which is a far more valuable antiscorbutic than the ordinary cooked meat.
There is almost no experimental data on the antiscorbutic value ofeggs. Hard-boiled eggs were fed to guinea-pigs and it was found that 9 g. per capita daily was insufficient to protect them. An attempt was also made to cure infantile scurvy with a daily addition of one raw egg to the dietary, but without avail. It is possible that fresh raw eggs have an antiscorbutic value comparable to meat, but the large quantity required makes dependence upon them impracticable.
Beer and Alcoholic Beverages.—For generations beer has been highly regarded as an antiscorbutic. Captain Cook prized it greatly and always supplied his men with a freshly-made infusion of malt called “sweetwort.” Lind writes: “Beer and fermented liquors of any sort will be found the best antiscorbutic remedies” (p. 76). He refers at different times to the value of spruce beer, ale, wine and other vinous liquors. In his excellent book on “Military Hygiene,” Munson writes: “Good beer and wine have decided value, also vinegar.” On the other hand, recent scientific experiment has shown that beer has practically no antiscorbutic value. There is but one study on this subject, that of Harden and Zilva, which is quite convincing.They found that guinea-pigs and monkeys developed scurvy in spite of the fact that they received, respectively, 50 c.c. and 180 c.c. of beer daily. They conclude, as a result of their experiments, that “bottled ale and stout and fined beer as brought on to the market, are lacking both in antineuritic and antiscorbutic accessory factors, and that kilned material is also wanting in these two principles.” The apparent contradiction between practical experience and laboratory investigation in regard to beer is due to a difference in the process of brewing. Cook and Lind and the older authors refer to freshly-made beer, whereas the modern beer which was tested in the laboratory was made from “high-dried” material. The antiscorbutic potency of beer as formerly used was due to its preparation from freshly-germinated grain and its consumption shortly after brewing. Dyke tells us of an interesting incident illustrating the importance of this distinction. In the recent war an outbreak of scurvy occurred among the Kaffir labor battalion in France. At home these natives consume a large amount, as much as three gallons a day, of Kaffir beer, which is made from freshly-germinated corn, and is consumed shortly after it is made. The French prepared a similar fermented beverage for their South African laborers, the sole difference in preparation being that the process of germination had been omitted for reasons of convenience. Scurvy resulted, a disorder which is practically unknown among the natives at home.
Miscellaneous Foodstuffs.—During the past few years a great many different kinds of foods have been tested in the laboratory for their antiscorbutic value. It will be well for completeness’ sake to say a word about them,although they have been found to possess little or no antiscorbutic properties. The studies of Holst and Froelich showed definitely that all the cereals—oat, barley, rye, maize, and preparations made from the bran or from the endosperm—are devoid of antiscorbutic vitamine. Cohen and Mendel added 3 per cent. of calcium lactate or sodium chloride, or 5 per cent. of butter, without enhancing the value of oats in this respect.
Failure of yeast as prophylacticFig. 14.—Failure of yeast as a prophylactic; latent scurvy promptly yielding to orange juice.
As is well known, yeast possesses the water-soluble vitamine in marked concentration. It is natural, therefore, that its antiscorbutic power was put to the test, especially as it has been accorded therapeutic value. Hess and Unger showed that autolyzed yeast was of no value in the cure of infantile scurvy (Fig. 14); Chick and Hume (1917) and Cohen and Mendel (1918) came to the sameconclusion in regard to guinea-pig scurvy, making use of autolyzed yeast, yeast extract and dried brewers’ yeast.
In view of the fact that cod liver oil is practically a specific for human rickets, Hess and Unger tried the effect of this oil both in infantile scurvy and in that of guinea-pigs. It proved to have no protective or curative value. The animal experiments were confirmed by Cohen and Mendel. The use of olive oil also proved futile.
Pitz in 1918 reported that in animal experiments he had found that lactose was able to protect against scurvy, and attributed this result to its power to alter the intestinal flora. We shall not enter into a detailed discussion of this question, as the study was carried out on a ration embodying unlimited and uncontrolled amounts of milk, and it has since been shown that the apparent cure was due to an increased consumption of milk by the animals in the progress of the experiment. Cohen and Mendel, Harden and Zilva, Hart, Steenbock and Smith (1919) all failed to protect or to cure their animals with lactose when they were placed on a ration which was definitely measured and limited. Hess and Unger failed to cure infantile scurvy by means of lactose.
It has been suggested that scurvy is due to a lack of secretion of the endocrine glands, a question which will be referred to again in considering the relation of scurvy to other “deficiency diseases.” With this idea Ingier added thyroid, hypophysis, thymus and parathyroid to the food of guinea-pigs, or gave it parenterally. She was unable to observe any beneficial results. Jackson and Moore met with the same result on feeding desiccated thyroid gland. We may add that we gave dried thyroid and also parathyroid glands in the treatment of infantile scurvy without effect.
Any consideration of the question of antiscorbutic foodstuffs brings into sharp relief the difference between empiricism and scientific investigation. For well over a hundred years it was generally known that scurvy could be cured by fruits or vegetables, and yet no further progress was made toward a more complete understanding of the value of these foodstuffs. As far back as 1847 Budd ascribed the action of antiscorbutic foods “to an essential element, which, it is hardly too sanguine to state, will be discovered by organic chemistry or the experiments of physiologists in a not far distant future.” Busk, in giving his testimony in 1877 before the British Scurvy Commission, said that it was his belief “that scurvy was due to the fact that the diet was lacking in a peculiar and as yet little-understood factor.” The question remained in this hypothetical and inactive state until it was attacked recently by experimental methods. Decided advance has been made only in the past few years, since these foodstuffs have been studied from a quantitative viewpoint.
The antiscorbutic factor is abundant in fresh foods, especially in vegetables and fruits, and to a considerably less extent in animal foods, such as milk, meat and fish. Among the vegetables there is a marked distinction in potency. A beginning has been made in standardizing these various foodstuffs, in grading them approximately according to their antiscorbutic efficacy (Table 3). It should be remembered, however, that the importance of an antiscorbutic food depends not only on its intrinsic content of the antiscorbutic factor, but quite as much on the amount of the food which is eaten. For example, although potatoes possess only moderate virtue compared withorange juice, they are of greater practical value in view of the large quantities which are consumed and their availability when green vegetables are lacking. Furthermore, the fact recently brought out that the various vegetables, and perhaps the fruits as well, have considerably more value when they are fresh and young than when they are old, warns us not to carry our quantitative standardization too far.
Fruits and vegetables which are dehydrated have been found to have lost their antiscorbutic properties. This generalization is not without its exception, for it has been found that cabbage and tomato withstand drying well, and that if milk is dried under favorable conditions it retains a very large part of its antiscorbutic value. It may be stated that the outlook is bright in regard to dehydration, as the problem has not yet been thoroughly studied, and the process may be so improved that there will be little difference in the nutritional value between the fresh and the dehydrated food.
The study of antiscorbutic values points a lesson in regard to the methods of cooking vegetables. It has demonstrated that short cooking, associated with a high degree of temperature, is less deleterious than longer cooking at a low degree. In other words, that less damage is brought about by boiling or by steaming vegetables than by stewing them. Here age and freshness again play a rôle; in fact, a double rôle, as the older and tougher vegetables contain not only less antiscorbutic, but require more prolonged cooking.
In general, the belief is correct that canning destroys the antiscorbutic value of foods, but once more an exception must be made, for it has been found that acid foods,such as the tomato, withstand the canning process with but little loss of potency.
The field of antiscorbutic foodstuffs is one which is fertile for future investigation. The antiscorbutic status of milk heated to various heights of temperature and subjected to various degrees of aging furnishes problems of great practical importance. A lack of growth has been noted when antiscorbutics are given which have been subjected to a high degree of heat (e.g., autoclaved orange juice). Whether this is due to the destruction of some other growth factor is a question which has been raised by several experimental studies and requires an answer.
It is quite possible that we shall find useful antiscorbutic foods which at present are unknown or unappreciated. The recent introduction of the swede, of the canned tomato and of germinated pulses suggests and even renders this probable. On the other hand, the recognition of the comparative poverty of the antiscorbutic factor in lime juice shows the importance of putting each foodstuff to the experimental test.
The identity of scurvy in the infant, in the young child and in the adult is thoroughly established and requires no further substantiation. There are, however, sufficient differences between the symptoms of adult scurvy and those of Barlow’s disease to render it advisable to consider them separately. These distinctions are due largely to the fact that the former disorder affects mature tissues, whereas the latter is engrafted upon tissues which are in the process of rapid growth and development. The symptomatology is influenced also by the striking differences in environment—the passive, shielded existence of the infant, contrasted with the active and exposed life of the adult. Although we shall, therefore, treat adult and infantile scurvy separately, it should be borne in mind that, from an etiologic and pathologic viewpoint, such a division is artificial and is resorted to merely for purposes of clarity.
Adult Scurvy.—The earliest sign of scurvy is usually a change in the complexion of the individual. His color becomes sallow or muddy, an aspect difficult to describe, but one which is characteristic, and constitutes an important danger signal to the eye of the experienced physician. About the same time the patient loses his accustomed vigor, seemingly becomes indolent and complains of tiring quickly, and of breathlessness. He may experience fleeting pains in the joints and limbs, especially in the legs, symptoms which are frequently attributed to rheumatism. At this early stage the appetite may stillbe normal, there is usually no loss in weight, but merely a general malaise which is significant, although in no way distinctive. Very soon the gums become sore, bleed readily, and are found to be congested, spongy, and somewhat hemorrhagic at their edges. Absolute reliance must not, however, be placed on this sign for early diagnosis, as at times it does not appear until later. Careful examination at this stage will disclose petechial spots on the body, more especially on the legs, at the site of the hair follicles, or even larger ecchymoses, depending upon the hemorrhagic tendency of the individual, his exposure to bruising, the adequacy of his diet, and secondary infection. Less frequently bleeding from the nose occurs early, or the eyelid suddenly becomes swollen and purple, or the urine shows the presence of blood.
These signs progress steadily with a varying degree of rapidity. The complexion becomes more dingy and somewhat brownish, the weakness increases so that the slightest exertion causes breathlessness and palpitation, and the gums become spongy and even fungous. If there is infection of the gums and the teeth are carious, the breath is extremely foul—a sign long associated with scurvy. Later the teeth become loose and may fall out, and the alveolar process undergoes necrosis. The surface hemorrhages increase in severity, large effusions appearing on the trunk, on the extremities, and less often beneath the mucous membrane of the mouth. A bloody diarrhœa may take the place of the constipation which is generally noted earlier in the disease. There are at this time hemorrhages into the muscles and deeper tissues, especially into the calves of the legs, giving rise to hard, brawny, tender swellings which have been termed “scurvy sclerosis.” This is sometimes the earliest sign noted bythe patient and may puzzle the physician who has not met with it before. The swelling may be found in the popliteal space or at the site of the tendo Achilles, and result in lameness and contracture of the neighboring joint. Frequently there is slight edema of the ankles associated with a glossiness of the extensor surfaces of the legs. This infiltration differs from ordinary edema in being firm and not pitting on pressure. The skin is dry and rough, the follicles being unusually elevated;46the hair likewise is dry and loses its lustre. Not infrequently subperiosteal hemorrhages occur, giving rise to exquisitely tender swellings, especially of the tibia or of the femur, or of the ramus of the lower jaw, as has been noted in connection with guinea-pig scurvy. If there are wounds or ulcers they assume a hemorrhagic aspect, the edges becoming bluish or livid and showing no tendency to heal; even scars which have existed for many years change in color and show an altered state of nutrition, and ulcers long healed break out afresh.
Nowadays, the disease usually does not reach this stage, and rarely progresses further. If, however, the patient remains untreated, he becomes progressively weaker and more lethargic; there is frequent palpitation, shortness of breath, and increasing loss of weight. The pains in the limbs render him helpless and an object of pity. Marked edema may be added to the picture as the result of starvation, so that the legs become swollen, and even the face becomes bloated. Hemorrhages into theskin as large as the palm of the hand appear on different parts of the body. The gums swell to such an extent that they overlap and may even hide the teeth and protrude from the mouth as foul fungoid growth. Death comes about in various ways. Frequently sudden and fatal syncope occurs, due to heart weakness or to the pouring out of fluid into the pleural or the pericardial cavities. Another frequent cause of death is secondary infection, resulting in pneumonia, which finally ends the suffering of the patient. The fatal outcome is thus described in the narrative of Lord Anson’s voyage:
“Many of our people, though confined to their hammocks, ate and drank heartily, were cheerful, and talked with much seeming vigor, and in a loud, strong tone of voice; and yet, on their being the least moved, though it was only from one part of the ship to another, and that in their hammocks, they have immediately expired; and others, who have confided in their seeming strength, and have resolved to get out of their hammocks, have died before they could well reach the deck. And it was no uncommon thing for those who could do some kind of duty, and walk the deck, to drop down dead in an instant, on any endeavor to act with their utmost vigor; many of our people having perished in this manner during the course of this voyage.”
“Many of our people, though confined to their hammocks, ate and drank heartily, were cheerful, and talked with much seeming vigor, and in a loud, strong tone of voice; and yet, on their being the least moved, though it was only from one part of the ship to another, and that in their hammocks, they have immediately expired; and others, who have confided in their seeming strength, and have resolved to get out of their hammocks, have died before they could well reach the deck. And it was no uncommon thing for those who could do some kind of duty, and walk the deck, to drop down dead in an instant, on any endeavor to act with their utmost vigor; many of our people having perished in this manner during the course of this voyage.”
The disease may develop and progress in various ways. It may remain latent for a long period and be cured by some accidental change of diet, or, as more frequently occurs, it runs a moderately acute course, and is promptly cured by means of antiscorbutics. In the days when scurvy was common and widespread it sometimes became chronic, developing into the “inveterate scurvy”of the older authors, which was notably resistant to treatment. Harvey, in his treatise published in 1685, states that “a mild scurvy may continue or be protracted to ten, twenty, or thirty years.”
In addition to the general picture of the disease which we have presented, mention should be made of other less common symptoms. As is well known, one of the characteristic signs of scurvy ishemorrhage. Indeed, in many of the systematic treatises of medicine it is classified as a hemorrhagic disease. Besides the bleeding into the gums, skin and bones, hemorrhage into the stomach may take place, giving rise to hæmatemesis, or there may be hemorrhage into the eye, under the conjunctiva or into the anterior chamber, leading to the destruction of the eyeball. A very unusual form is meningeal bleeding, giving rise to symptoms of apoplexy. It may be stated in general that hemorrhage dominates the picture of scurvy. Eruptions which in normal individuals are simply macular or papular, assume a hemorrhagic character when occurring in a scorbutic individual. This phenomenon was noted in the recent war in connection with the eruption of typhus fever, and has been observed by military and naval surgeons in numerous expeditions.
Scurvy reduces the nutritional state of probably all the cells and tissues of the body. If the resistance is still further lowered by exposure, nutritional disturbances will result more readily than where the tissues are normal and well nourished. For this reason we believe that scurvy may predispose tofrostbite. Reports of congelations occurring in the trenches in the course of the World War tend to confirm our opinion that scurvy was a predisposing factor in many of these cases. This has been true in other wars. For example, Munson writesthat “during the Crimean War the temperature was never very low and a report of the times suggests that the large number of congelations observed among the soldiers might well be regarded as gangrene owing to a scorbutic tendency exaggerated by the cold.”
In connection with the involvement of the gums, another typical symptom of scurvy, it should be remembered that this sign may appear late and therefore fail to be of value for early diagnosis, and that it occurs also in purpura and thus may lead to error. This is especially the case if there is pyorrhœa. As is well known, hemorrhages of the gums appear only where teeth are present, and are absent in the edentulous gums of old people as well as in babies who have no teeth. Immerman is probably correct in believing that an injury is always necessary to produce a hemorrhagic lesion in scurvy, and that this explains the early involvement of the gums and also their non-implication in the absence of teeth.
It is a common belief that separation of the epiphyses occurs only in infants and young children, and not in the scurvy of adults. This, however, is not correct, as in severe adult scurvy there is frequently a separation of the epiphyses of the long bones of the lower extremities or of the ribs, the latter resulting in a sinking of the sternum.
The pulse is sometimes slow and feeble, having been recorded as low as 40 beats per minute, but more frequently is rapid, in the neighborhood of 140. It is, however, almost invariably unduly excited by emotion or by mild physical activity. Frequently there is a low type of fever, which has been termed “scorbutic fever,” but which probably should be regarded as a complication of the disease rather than as an intrinsic symptom.
There is little tendency to the formation of pus. Althoughthe lymphatic glands are frequently enlarged and effusions into the tissues and into cavities of the body are by no means uncommon, they show little tendency to become purulent. In the severe cases described by the older authors, the breaking down of the glands in the inguinal region—buboes—is frequently noted. The urine is apt to be scanty, becoming much more profuse following treatment. Perspiration is also retarded.
A peculiar symptom reported in connection with numerous epidemics of scurvy, both on sea and on land, isnyctalopia or night-blindness. The patients can see fairly well during the day, but have very little vision as soon as darkness develops. This phenomenon has puzzled many observers, as nothing abnormal has been found on examination of the eyes. Recently O’Shea, who met with many cases of this nature among soldiers, has reported that in an ophthalmic examination of 22 cases the only abnormality was pallor of the optic disc in 3 cases. This weakness of sight is due to the general nutritional weakness and has been reported in connection with other exhausting and nutritional diseases—for example, hunger edema. More rarely there is day-blindness.
As a complication, dysentery may be mentioned. This has been described by Schreiber and others in scurvy epidemics occurring in the course of the World War. Jaundice may appear, and might be expected to occur more often in view of the marked congestion of the upper duodenum found so frequently at necropsy.
Pericarditis, hydrothorax, pleurisy with effusion, pneumonia, are common complications of severe forms of scurvy. Lind reports that the dominant complication varies in different epidemics; that on one cruise manycases of diarrhœa would occur and on another many pulmonary infections.
O’Shea reports the exceptional case of a man who was operated upon for acute appendicitis. A large hemorrhage in the wall of the cæcum was found, as well as some other hemorrhages in the peritoneal cavity. This report is interesting, not so much from a diagnostic standpoint as because “contrary to what might have been expected, scorbutic cases when operated upon showed no particular tendency to hemorrhage.”
Infantile Scurvy.—The stereotyped picture of infantile scurvy and the one which this term commonly suggests, is that of the acute form of the disease. Inacute infantile scurvywe have to do generally with a poorly-nourished, pale infant with a peculiarly alert and worried expression. As we approach its bed it whimpers or cries out in terror. Frequently its posture is characteristic, as it lies quietly on its back with one thigh everted and flexed on the abdomen. Examination shows that one or even both thighs are swollen and exquisitely tender, or that there is merely tenderness, the baby shrieking at the slightest pressure upon the lower end of the femur. If teeth are present, the adjacent gums are red, swollen and bleed readily. This is the syndrome which the medical student is taught to carry away to guide him in his everyday practice. It is the acute, florid type, and presents a striking picture, but must not be regarded as the common form of the disorder. If we are to diagnose infantile scurvy early and not overlook its more subtle manifestations, the classic textbook description must be augmented by portrayals of types of the disorder which are less crude and more difficult to recognize—of “subacute” and of “latent” scurvy.
The commoner form, which we have termed “subacute infantile scurvy,” comprises a large number of symptoms which are inconclusive individually, and frequently escape correct interpretation. The affected baby is usually in the second half of the first year of life, and does not gain in weight or gains but slightly for weeks. It may be fairly well nourished, but is pale or sallow, with perhaps slight edema of the upper eyelids. The mother or nurse complains that the child is irritable and peevish, and that the appetite is poor or capricious. The gums show a lividity or slight peridental hemorrhage, which on subsequent examination may be no longer visible, and may have consisted merely of a rim of crimson edging the borders of the upper gum, perhaps behind an upper incisor, as Still pointed out. On closer examination it may be observed that the papillæ of the tip of the tongue are markedly congested, and that a petechial spot is to be seen on its frenum, on the palpebral conjunctiva, or here and there on the surface of the body, more especially where there are erosions, eczema or other skin lesions. Attention may be called to tenderness of the lower thighs, which in some instances is definite, in others so ill-defined and fleeting that it is impossible to convince oneself of its significance or even reality. There may be slight edema over the crests of the tibia, of a kind which does not pit on pressure. The knee-jerks are almost always markedly exaggerated. The urine is diminished in volume but is generally normal or contains a trace of albumen and red and white blood-cells. The pulse is frequently rapid, and becomes markedly rapid and irregular on the slightest excitement. The respirations are also rapid (Fig. 15).
These symptoms do not constitute a rigid entity, but are subject to manifold variations. The syndrome maybe rendered less typical and clear by the fact that the infant has gained steadily rather than lost in weight, as is sometimes the case if the food has been insufficient during the first few months of life. Roentgenograms of the bones may show the “white line” at the epiphyses first described by Fraenkel (Fig. 20) or a thickening of the periosteum. However, too great reliance should not be placed on these signs in making an early diagnosis of this disorder, as neither is invariably present.
An instance of subacute scurvy, which in many respects is typical, is the following:
I. F., girl, was seen when 3 months old, weighing somewhat over 8 pounds. She was given Schloss milk, 4 ounces, and then 5 ounces every three hours, and did well, weighing 11¼ pounds two months later. As she failed to gain for some weeks, although getting 6 ounces of food, it was thought that this might be due to the fact that she was getting pasteurized milk and had never received an antiscorbutic. Autolyzed yeast had been tried as a prophylactic antiscorbutic, but failed to bring about a gain. When, however, orange juice was substituted for the yeast, a prompt growth-reaction resulted, a gain of 1¼ pounds in four weeks. Accompanying this lack of gain in weight there were many of the other symptoms enumerated above; irritability, pallor, slight tenderness of the lower ends of the femora, albumin and a few red and white cells in the urine. The pulse- or heart-beat was frequently over 150, and the respiration 60 (Fig. 15). The diagnosis of subacute scurvy was substantiated by the prompt subsidence of all symptoms when orange juice was administered.
I. F., girl, was seen when 3 months old, weighing somewhat over 8 pounds. She was given Schloss milk, 4 ounces, and then 5 ounces every three hours, and did well, weighing 11¼ pounds two months later. As she failed to gain for some weeks, although getting 6 ounces of food, it was thought that this might be due to the fact that she was getting pasteurized milk and had never received an antiscorbutic. Autolyzed yeast had been tried as a prophylactic antiscorbutic, but failed to bring about a gain. When, however, orange juice was substituted for the yeast, a prompt growth-reaction resulted, a gain of 1¼ pounds in four weeks. Accompanying this lack of gain in weight there were many of the other symptoms enumerated above; irritability, pallor, slight tenderness of the lower ends of the femora, albumin and a few red and white cells in the urine. The pulse- or heart-beat was frequently over 150, and the respiration 60 (Fig. 15). The diagnosis of subacute scurvy was substantiated by the prompt subsidence of all symptoms when orange juice was administered.