THE MALNUTRITION OF TUBERCULOSIS.* By FLOYD M. Crandall, M.D., New York. The discussion before the Section on Pediatrics is upon malnutrition in children, and to me has been assigned the malnutrition of tuberculosis. A discussion of the various other symptoms of that condition would be, therefore, out of place. I may, however, call attention to the fact that tuberculosis is one of the most protean of diseases in its manifestations. In some cases it begins abruptly with clearly defined local symptoms, as in tubercular pneumonia. As far as diagnosis is concerned, the malnutrition is then of minor importance; as far as the welfare of the child is concerned, it is of vital importance. Wasting and anemia are constant accompaniments of active tubercular processes. It is sufficient to say that the anemia accompanying tuberculosis is usually simple in character. That is, it is marked by diminution both of the red corpuscles and the hemoglobin and is not due to disease of the blood making organs. It is secondary, not primary. Occasionally, however, it approaches a chlorotic type, particularly in girls in later childhood. It will be most profitable in the short time allotted to this subject, to consider those forms of concealed or generalized tuberculosis, so common in young children, in which local disease is found very late and sometimes not at all. These types have received much attention from recent writers. Jacobi refers to the "afebrile condition and chronic emaciation" of some cases. Holt classifies general tuberculosis, first, as those cases resembling infantile marasmus, and second, cases in older children resembling a continued fever. Comby refers to the tendency of tuberculosis to be generalized in infants and describes five clinical types in early childhood, the first of which he denominates as "apyretic tuberculosis," which runs the course of an ordinary athrepsia or dyspepsia, the symptoms being emaciation, vomiting, and diarrhea. In watching cases of this character, the question sometimes arises in the mind as to whether there is such a thing as a pretubercular stage, as has been suggested. Children sometimes waste away and die without showing the signs of any organic lesion. They seem to be suffering from simple marasmus, but at the au *Read before the Section on Pediatrics, the New York Academy of Medicine, December 12, 1901. topsy, death is found to have been due to tuberculosis. Hoit asserts that he has seen at least a dozen such cases. Here, then, we find tubercular cases pursuing their full course without showing local evidence of tuberculosis. In other cases after the symptoms of marasmus have existed for a greater or less period, the signs of organic disease develop, usually in the lungs. It is in such cases especially that the theory of a pretubercular stage has been evolved. If by this term is meant a specific stage of tuberculosis marked by wasting and anemia, before the formation of tubercles, the theory is not tenable. If, however, a condition of anemia is meant which predisposes to tuberculosis, the term pretubercular anemia may be permissible, but it should be understood that it is no integral part of tuberculosis. It is nothing more than a state of impaired nutrition which renders the patient susceptible to any infectious diseases. The so-called pretubercular stage is probably nothing else than the early stage of tuberculosis which has not been recognized. Even in adults it is not uncommon to find general infection and the disease under full headway when the lesions in the lungs are first detected. Infancy and childhood are the periods in life in which tuberculosis tends most strongly to hide itself in deep-seated and inaccessible tissues. The deeper lymph nodes are the most common seat of concealed tuberculosis. Here the disease may go on producing its constitutional symptoms without giving any evidence upon which a diagnosis of the true underlying cause may be made. These deep-seated nodes may be seriously affected without involvement of the superficial nodes. On the other hand, enlargement of the superficial nodes, if fever, anemia, and other constitutional symptoms be absent, offers no evidence of the infection of the deeper nodes. But superficial adenitis, accompanied by anemia and fever, not otherwise explained, is very suspicious of tubercular involvement of the deep lymphatic structures. Is the malnutrition of tuberculosis characteristic? Can the diagnosis of tuberculosis be made from the anemia and malnutrition alone without the discovery of local lesions or of bacilli in the sputa? The anemia is certainly not characteristic. It is that which accompanies many other conditions of lowered vitality. Loss of weight is common but it does not necessarily progress uninterruptedly. There may be even gain of weight temporarily. If watched for some time, however, wasting will invariably be found. Progressive wasting, however, is common in many other conditions. Cachexia rarely occurs early enough or is sufficiently dis tinctive to be a symptom of value in making a diagnosis before other more positive symptoms have developed. In my experience, neither the classical scrofulous nor tubercular diathesis has been particularly common among tubercular children. It is difficult for many practitioners to dissociate in their minds coughs and tuberculosis. And yet cough is utterly lacking in many patients and does not develop until late in others. In many cases of glandular tuberculosis the lesions are so located as not to produce cough. Even after pulmonary invasion, the cough may be so slight for a time as to attract but little attention, and after repeated visits, the physician may fail to hear it. In involvement of the bronchial lymph nodes, the cough may be so paroxysmal as to mislead the physician. In older children suffering from the more chronic forms of consumption, similar to those in adults, the cough occasionally assumes such a paroxysmal character as to simulate pertussis. Fever is also absent in the early stages of many cases of the marasmic type. It may, in fact, never be a prominent symptom, and when it does occur it may be erroneously attributed to indigestion or taking cold. Marked febrile action may not occur until late in the disease, when local signs are also present. The indigestion, loss of appetite, diarrhea, and vomiting, so often seen in these cases, are by no means characteristic. There is still another type of tuberculosis in children—that which resembles typhoid or continued fever, in which there is often a preliminary stage of malnutrition without diagnostic symptoms. This apyretic stage may continue for several weeks, to be followed by a stage of low, irregular fever, which may run for two or three weeks or longer, before any local symptoms develop. These are usually pulmonary. In this type wasting in the first stage, and wasting and fever in the second stage are symptoms never absent. Cases of this character form some of the most difficult and trying problems, which are presented to the practitioner. Unfortunately even after pulmonary signs have developed, it is not possible to be too dogmatic in one's statements, for a marasmic child may contract a simple bronchopneumonia and die after passing through a very similar series of symptoms. Consolidation in such cases is often so slow to develop that there may be a febrile stage of considerable duration before positive signs can be elicited. Autopsy may show such a case free from tuberculosis, while another running a very similar course may show abundant evidence of it. I am aware that I am not adding much light to the subject, but rather, perhaps, discouragement. The fault, however, is not mine; it lies rather with the conditions, for the malnutrition, both of the earlier and later stages of tuberculosis, has little about it by which a diagnosis can be made. Still it must be said that while these symptoms are none of them characteristic, taken together they form a clinical history which should put a practitioner upon his guard and should make him very careful in his progress. The question has been well summarized by Holt in the following words: "Early wasting without adequate cause followed by gradual development of low fever, and finally the appearance of signs of subacute bronchopneumonia, form the most characteristic features of general tuberculosis in early infancy. Yet all these symptoms are occasionally met with in cases in which the autopsy shows none of the lesions of tuberculosis." Anemia and wasting in a young child in which thorough examination reveals no adequate cause should always arouse the suspicion of incipient tuberculosis. I have thus far referred to infants and young children only, but desire to add a word regarding older children and adolescents, in whom anemia and malnutrition should always receive prompt attention. Tuberculosis rarely develops at this age in the well nourished and vigorous. In families with the tubercular tendency, the children between the ages of fourteen and twenty should receive particular care, and the first appearance of anemia and impaired nutrition should receive prompt treatment. I have come to regard chlorosis as a much more grave condition than many seem to do, though I think I have had my share of brilliant results in its treatment. Many cases improve promptly and continue in good health, while others continue to be more or less anemic and relapse easily. Where there is a family history of tuberculosis, chlorotics show a peculiar susceptibility to tubercular invasion. Rachford, who has made considerable study of this subject, asserts that the menstrual function is established somewhat earlier in girls with a tubercular family history than in those without such a history; that a scant and pale menstrual flow, followed by a leucorrheal discharge is very suspicious of concealed tuberculosis. Certain it is that a chlorotic girl is a candidate for almost any infectious or wasting disease, of which tuberculosis is first and foremost. When to this is added inherited tubercular tendency, her danger is very great. The thoughts which I have thus briefly presented may be thus summarized: 1. Wasting, anemia, and other evidences of malnutrition are constant accompaniments of tuberculosis in children. 2. These symptoms may occur in infants long before local disease can be detected and occasionally no local signs whatever are manifest before death. 3. In infants, tuberculosis shows a special tendency to be disseminated or to conceal itself in the deep tissues, as the lymph nodes. The disease may then run a course identical with simple marasmus. 4. In some cases a period of anemia and wasting is followed by a stage of irregular fever, after which local lesions appear, usually in the lungs. 5. In other cases tuberculosis in children begins with wellmarked local manifestations, particularly pneumonia. In these, evidences of malnutrition appear promptly and are usually progressive. 6. The anemia of tuberculosis, whether it appears before or after the occurrence of other symptoms, is usually a simple anemia and presents nothing characteristic. 7. A diagnosis of tuberculosis cannot be made alone from the character of the anemia or the malnutrition. However, persistent and increasing malnutrition in a child without discoverable cause is always suggestive of tuberculosis. 8. Anemia in adolescents should receive prompt and active attention, for it vastly increases the danger of tubercular invasion, which is particularly common at that period of life.-From "Archives of Pediatrics," January, 1902. WHY IS NEW BREAD INDIGESTIBLE? New bread is commonly considered indigestible, and with reason; but, according to an editorial writer in "The Lancet" (London), it is not necessarily so. Hot rolls when masticated properly should not offer any difficulty to the digestive organs. The writer goes on to say: "A slice of stale bread on being broken with the teeth resolves into more or less hard gritty particles which, unless they were softened by the saliva, would be almost impossible to swallow. The particles would irritate the throat and the gullet. The fact is, therefore, that man is compelled thoroughly to masticate and to impregnate stale bread with saliva before he swallows it. This act, of course, partially digests the bread and thus makes it in a fit state for digestion and absorption farther on in the alimentary tract. This is why stale bread appears to be more digestible than |