ACUTE MILIARY TUBERCULOSIS.
BY JOHN S. LYNCH, M.D.
Acute miliary tuberculosis may be defined to be an acute disease characterized by an eruption in one or all of the organs of the body of small nodular or granular masses called tubercles, attended with fever and various other functional disturbances.
The fact which Villemin and Klebs were the first to show,1 and which hundreds of others have since verified, that tuberculosis can be conveyed by inoculation to certain animals, and the additional fact that Koch and his followers seem to have identified the infective material in the micro-organism which he has named bacillus tuberculosis, would seem to justify our placing tuberculosis, along with variola, measles, etc., among the acute contagious infectious diseases. But since some able pathologists still deny the correctness of Koch's conclusions; since in certain animals indifferent irritants have excited a disease which could not be distinguished from tuberculosis by the ablest pathologists of Europe and America; since to some species of animals even more nearly allied to man by their organism than rabbits and guinea-pigs the disease cannot be conveyed at all, and that even to some of the latter inoculation fails to transmit it; and, above all, since there is, as far as we know, not one single case on record in which the disease has been clearly and unmistakably traced from man to man in the order of infection,—we do not think that as yet we are justified in defining it as a contagious infectious disease purely and only. Everybody will take small-pox if not protected by vaccination or inoculation, and this disease may be transmitted in a modified form to many of the lower animals. The same may be said of measles, scarlatina, and nearly all other diseases known to be contagious and infectious. Since, then, so few persons take tuberculosis that the evidence of its contagiousness rests upon a vague popular belief, and since even some animals of a species known to be peculiarly susceptible to the disease fail to take it even by inoculation, we think that we are justified in assuming that there must be something else besides a contagium required to produce the disease. This is evidently a predisposition which depends upon some peculiar diathesis, cachexia, or dyscrasia, congenital or acquired. It has been assumed that scrofula constitutes the particular diathetic condition which predisposes to tuberculosis, and it is common for scrofulosis and tuberculosis to be spoken of as convertible terms. In the article on SCROFULA in this work we have already given our reasons for dissent from this view, and to that article the reader is referred. Farther on we shall give our views as to what constitutes the tubercular diathesis when we shall speak of the mode of formation of tubercle.
1 But Buhl had long before advanced the doctrine that tuberculosis was a resorption disease.
While, then, we cannot as yet admit that acute miliary tuberculosis is always and only set up by a contagium, it is unquestionably true that it is in a large majority of instances caused by an infective material, which, however, does not come from without, but is produced within the system. This material is the purulent detritus resulting from the softening and breaking down of the inflammatory and other cellular hyperplasias which have undergone the caseous degeneration. It seems to make little difference whether the caseous product was derived from scrofulous glandular hyperplasia, catarrho-pneumonia, inflammation of serous membranes with a cellular exudation, or ordinary cellular inflammation; the only essential prerequisites being that there shall exist a cellular exudation or proliferation, and that these cells shall undergo the caseous degeneration.
The inoculation of this material into certain species of the lower animals or its absorption into the blood of a human being predisposed to tuberculosis will, as a rule, produce tuberculosis. Koch and his disciples add to the foregoing another prerequisite—viz. that the caseous matter must contain the bacillus tuberculosis. But as the bacillus is generally found in all the cheesy inflammatory products we have mentioned, they have (ignoring Virchow's definition of tubercle) declared that all these are tubercle, thus very much enlarging the hitherto accepted doctrine upon this subject. But if any of the cheesy products are found not to contain the bacillus, then such product is not tubercle, whatever may be the apparent identity or dissimilarity in their etiology, microscopical appearances, or clinical history. This seems to us to be a begging of the whole question of the relation of the bacillus to tubercle, and in the absence of fuller experimentation and investigation involves an assumption which cannot yet be admitted.
While the absorption of caseous pus is undoubtedly by far the most frequent cause of miliary tuberculosis, it cannot be inferred that all who may happen to have foci of caseous degenerations will necessarily be attacked by tuberculosis. On the contrary, a vast majority escape, and it is almost surprising how few of those who suffer from scrofulous inflammation of glands, joints, etc. become the subjects of miliary tuberculosis. Many cases of pulmonary phthisis also, originating as a cheesy pneumonia, run their course without any distinct tubercular complication. We can only explain these exemptions from the tubercular process by supposing that in such cases the predisposition to tuberculosis does not exist—they do not have the tubercular diathesis—or that such persons possess a peculiar means of resistance to the entrance of the infecting material into their blood.
Other diseases are supposed to favor the tubercular process, either by directly exciting or increasing the predisposition to it. Among others, measles, whooping cough, and typhoid fever have been regarded as specially liable to be followed by tuberculosis. Bad air, poor or insufficient food, onanism or other forms of sexual excess, severe study with insufficient exercise, and, in short, anything which impairs the strength or lowers the vitality, have been heretofore considered as excitants or predisposers of the disease. Admitting all these causes as effective in either exciting it or increasing the predisposition to it, there still remains quite a large residuum of cases in which the disease can be traced to none of these causes, and which, for the want of more accurate knowledge, we are compelled to call idiopathic or spontaneous. Such are those cases of tubercular meningitis occurring in young children heretofore in apparent good health, and in whom no traces of caseous degeneration can anywhere be found. It is true that it may be asserted that these children may have been infected through kissing by persons suffering from pulmonary consumption; but if this were so the disease ought to be far more frequent than it is, since the habit of kissing babies is universal and consumption the most prevailing of all diseases. In the absence of any proof to the contrary, we think that we are justified in believing that these are cases of spontaneous tuberculosis, occurring in consequence of intensity of the diathesis, either inherited or acquired.
Miliary tubercles are found in the form of small roundish nodules ranging in size from 1/500 to 1/250 inch (submiliary tubercles), up to the size of a millet-seed or even of a pea. When of the latter size they are always made up of a number of submiliary tubercles. Much larger masses are found usually in the lungs and in the mesentery, but these will generally be found to consist not of miliary or submiliary tubercles alone, but of cellular new formations derived from endothelial or lymphatic proliferations excited by the presence of tubercles, and therefore mixed with them. When first formed they are grayish in color, somewhat translucent, and tolerably firm to the touch (gray granulations). They soon, however, undergo partial fatty degeneration (this degeneration usually commencing in the centre of the mass), and subsequently are converted into a dry, yellowish-white, and somewhat crumbly mass which from its resemblance to cheese is called caseous. This sooner or later softens (the softening process beginning also in the centre), and the mass breaks down into a fluid detritus—tubercular pus. In some situations they never reach the caseous and purulent stage (notably in the cerebral meninges), because the interference with the organs or nerve-centres of animal life excited by their presence destroys the patient before there is time for the accomplishment of these changes. The subsequent history of tubercle depends upon the condition of the patient, his powers of resistance, the intensity of the tubercular diathesis, the injury inflicted by the first eruption, and the appearance of secondary eruptions. If all conditions are favorable, the patient placed under proper hygienic conditions and properly treated, the first eruption will also be the last, and the tubercle dries up into an earthy mass (calcareous degeneration), or it may remain for months, and even years, in its caseous stage without undergoing the softening process.
If we examine a fresh tubercle under the microscope, we find, according to Woodward2 and Zeigler,3 that it is usually made up of three different kinds of cells: first and most abundantly, lymphoid cells (Woodward) or white blood-cells (Zeigler); second, endothelioid cells; and third, embryonic cells. In addition to these there is often found (but not always) a few so-called giant-cells, generally occupying the centre or circumference of the tubercle, and sometimes both. These cells, which usually contain two or more nuclei and are much larger than the ordinary lymphoid cell, were thought at one time to constitute an essential histological feature of tubercle, and have been named tubercular cells. But the frequent absence of these cells in genuine tubercle has led to the conclusion that they do not possess any special significance and are purely accidental. Each submiliary tubercle is usually surrounded by a proliferating zone in which multinuclear (giant) cells and fibro-plastic or spindle-form elements can be distinguished (Cornil and Ranvier4). According to Rindfleisch,5 Woodward,6 and Zeigler,7 the cellular elements of tubercle are always found included in a trabeculum of fine fibrillar (connective) tissue, while Cornil and Ranvier deny the existence of any such trabeculum, maintaining that its appearance is due to the action of hardening agents used for preparing it for microscopic examination. Virchow and Woodward believed that tubercle always takes its origin in a lymphatic vessel, while Rindfleisch, partially agreeing with this view, maintains that they most generally occur in the lymphatic sheaths of the blood-vessels and follow the course of the latter, and that the cells which compose the tubercle are formed by proliferation of the endothelia of the lymphatics.
2 Medical and Surgical History of the War of the Rebellion, Part 2, Medical Volume, p. 593.
3 General Pathological Anatomy, London, 1883, p. 171.
4 Pathological Histology, Philadelphia, p. 116.
5 Textbook of Pathological Histology, Philadelphia, 1872, p. 125.
6 Op. cit.
7 Op. cit., p. 168.
Zeigler has not been able to demonstrate this relation of the tubercle to a blood-vessel—that is, to an artery—but leaves us to infer that they always arise from a capillary vessel, since he maintains that the tubercle is primarily and principally made up of emigrated leucocytes.
Such is a brief résumé of our knowledge as to the histology and mode of formation of tubercle, and such are the opinions—in some particulars agreeing, in others discordant—of those whose investigations and observations the world regards as most complete and accurate. This résumé is doubtless unnecessary and out of place in this article, since this question (the histology and mode of formation of tubercle) has been already discussed in the first volume of this work; but, as in the explanation which is to follow of our views as to what constitutes the tubercular diathesis and what is the mode of formation of tubercle we shall have to frequently refer to the facts above stated, we have thought it best, in order to save repetition and too frequent reference to authorities, to give the above résumé of the present state of the views of pathologists upon the histology of tubercle.
A careful consideration of the foregoing facts ought, it seems to us, to enable us to arrive at a rational and probably correct conclusion as to the mode of formation, as well as the principal etiological factors concerned in the causation, of the miliary tubercle; and we venture to offer the following explanation of the subject as more in consonance with the facts above related than any view which we have seen upon this question:
1. Miliary tubercles always occupy a lymph-space surrounding a capillary blood-vessel. When found, as they quite often are, occupying the wall of a larger vessel, artery or vein, it is still in the lymph-sheath of a capillary of the vasa vasorum that they primarily originated. And it may be said that this is the most dangerous site a tubercle can occupy, because when softening takes place it is so apt to burst into the lumen of the vessel and so produce a general infection.
2. The tubercular process consists at first of an undue or excessive emigration of leucocytes through the walls of a capillary which runs through a lymph-space, and where, of course, the walls of the vessel are less firmly supported. Those cells whose vitality is lowered by the causes which have preceded and excited the process can neither undergo any process of differentiation nor wander on through the lymphatics; they remain in the lymph-space, which they crowd and block up, and finally by their pressure occlude, the capillary vessel from which they emigrated. Until this event occurs they still retain a feeble vitality, and even abortive attempts at proliferation are seen, which, however, only reach the stage of division of the nucleus, the body of the cell meanwhile swelling up by imbibition and thus forming the so-called giant-cell. As soon as the capillary vessel becomes occluded further addition to the incipient tubercle from this source ceases; nutrition is now entirely cut off, and the cells, dying, become a foreign substance, and soon undergo the caseous degeneration. But by their presence they now excite a quasi-inflammatory process in the endothelia lining the lymph-space, and hence we have a secondary addition to the tubercle derived from the proliferating endothelia. Lastly, the inflammatory process extends to the connective-tissue cells around the lymph-space, and embryonic cells (the only cells capable of resulting from connective-tissue inflammation) are added to the mass. This constitutes the proliferating zone, consisting of many nucleated cells and fibro-plastic and spindle-form elements, described by Cornil and Ranvier.8
8 Loc. cit.
As soon as one capillary vessel becomes entirely occluded, the neighboring ones become distended by a collateral hyperæmia, and the same process of cell-exudation or emigration begins; and thus the process goes on until all the capillaries supplied by a single arterial twig take part in the process, and one of the larger tubercles is thus formed by an almost innumerable number of smaller (submiliary) ones. It would seem to be quite probable that the trabeculum which Rindfleisch, Woodward, and Zeigler described, and which Cornil and Ranvier denied, consists of the remains of the connective-tissue fibres which originally existed between the capillaries successively attacked by the tubercular process.
In the lungs this process is usually complicated by a true catarrho-pneumonic inflammation. The tubercle deposited beneath the lining membrane of the air-sacs sets up inflammation in that membrane, giving rise to abundant proliferation of the endothelia as well as emigration of leucocytes, so that the air-sac becomes packed with cells which may finally undergo caseation, and then cannot be distinguished from the original tubercle which started the process. If the eruption of tubercles should be very abundant, life may be destroyed by the pneumonic process before caseation has even begun in the inflammatory products. We have quite recently observed a case of this kind. A man came to the city hospital (Baltimore, Md.) who presented all the rational and physical signs of tuberculosis of the lungs. After about three weeks, during which there was only moderate fever, no notable dulness, and only a few scattered crepitant râles, the temperature suddenly rose to 104° F.; dulness appeared first over the lower third of the right lung, which rapidly extended over that side, and subsequently to the left side, and the man speedily died, comatose and cyanotic. The autopsy showed the most extensive miliary tuberculosis we had ever seen in the human lung; but in addition to the tubercles, which were found in almost every lobule of the right lung, the air-sacs were almost universally filled with a soft, purulent-like matter which oozed from the cut surface, and which could be squeezed out in enormous quantities; myriads of Koch's bacilli were found. It was interesting to note that the apparent starting-point of this tuberculosis was two small cavities in the apex of the left lung surrounded by firmly-indurated walls. Neither of these cavities was larger than the kernel of an ordinary-sized almond, and, as the induration surrounding them did not extend to the surface of the lung, their existence was not recognized before death. The man gave a history of cough and fever, which had lasted several weeks, about three years before his admission to the hospital.
More frequently, however, the reverse of the process above described takes place. That is, a catarrho-pneumonia terminating in caseation and softening sets up tuberculosis through absorption of the caseous pus. Indeed, in the case above related the order of pathological processes was, first, a catarrho-pneumonia of limited extent, a cavity or rather cavities; second, general tuberculosis; and lastly, a secondary catarrho-pneumonia caused by the tubercles. We believe, therefore, that Niemeyer's remark, that "the greatest danger for the majority of consumptives is that they are apt to become tuberculous," is not so absurd as a distinguished American author would have us believe.
The formation, then, of tubercle we believe to be an inflammatory process, in which we have—1st, an exudation of lymphoid cells (leucocytes) into the lymph-spaces, and occlusion by pressure of the capillary vessel from which the cells have escaped; 2d, inflammation and proliferation of the endothelium lining the lymph-space; and 3d, inflammation of the tissues nearest adjacent to the space. If this is simple areolar connective tissue, we have a "proliferating zone consisting of many-nucleated cells and fibro-plastic and spindle-form elements;" if a mucous or serous membrane, the usual products of inflammation of such membrane in other and ordinary cases.
But behind these processes there must exist something else which stands in the relation to them of predisposing and exciting causes. This we believe to be some anatomical and histological peculiarity, congenital or acquired, which gives to the individual that defective organization which is denominated the tubercular diathesis. It seems probable that this diathesis comprises two factors—viz.: 1st, an unusual thinness, and consequently weakness, of the walls of the capillary blood-vessels, which permits and favors a too facile emigration of the leucocytes; and 2d, a diminished or lowered vitality of the leucocytes themselves.
Both of these factors may exist at the birth of the individual as an inheritance from his progenitors, or both may be produced by causes which impair the general nutrition during either intra-uterine life or during the earlier infancy of the subject. Or one of them may exist without the other, and the animal thus escape for a long time, though exposed to the exciting causes of the disease. Sternburg's guinea-pigs (animals peculiarly susceptible to tuberculosis) remained healthy while enjoying the freedom of grassy fields, although inoculated with Koch's bacilli, which were found in their blood and tissues when killed, while those that were confined in cages under bad hygienic conditions speedily succumbed after a similar inoculation.9 If the first of these factors exist, any exhausting disease producing a dyscrasia, habits or hygienic conditions which tend to impair the nutritive functions, even psychological and emotional influences which take away the appetite for food or impair the functions of digestion—anything, in fact, which tends to degrade the quality of the blood and diminish the functional activity of the white blood-cell—may furnish the second factor constituting the tubercular diathesis. Both factors being present, it only requires an uncertain increase of the blood-pressure, causing a dilatation of the capillaries, to ensure that increased leucopedesis which constitutes the first step in the tubercular process.10 A protracted fever, therefore, of any kind, may furnish both the second factor in the tubercular diathesis and the exciting cause of the tubercular process itself; while any fever or any irritant capable of exciting fever or reaction against its presence occurring in man or other animal that happens to have the complete tubercular diathesis may excite tuberculosis. Koch's bacillus will undoubtedly excite tuberculosis in animals (and probably also in man) that have the tubercular diathesis complete; but it does so only by exciting that inflammatory and febrile reaction against its presence in the blood which other and perhaps indifferent irritants may also excite. In rabbits and guinea-pigs confined in cages, and therefore under unnatural and unhygienic conditions, it suffices to excite the disease only to introduce the bacillus into any part of their tissues: that it will not do so in guinea-pigs that are healthy and kept under natural conditions and surroundings Sternburg's experiments, alluded to above, clearly prove. It is true that other animals that are regarded as ordinarily non-tuberculous can also be inoculated with the bacillus with affirmative results, provided the bacillus is introduced into the eye or other serous membranes; but we must not forget that the pain and injury of such an operation will almost inevitably produce that deterioration of the health and impairment of cell-vitality which we maintain constitutes so essential a part of the tubercular diathesis. That the bacillus tuberculosis is always found in tubercle is undoubtedly true; but it is there because tubercle furnishes the most favorable and congenial breeding-place for it. Some special microbe is found in almost every special inflammatory product—vibriones in the pus of abscess, gonococcus in urethral inflammation, micrococcus in diphtheria, etc.—but no one, we believe, now holds that these various microbes are the causes of these diseases, since inoculation with pure cultures have given entirely negative results. While we believe, therefore, that the bacillus of Koch can excite tuberculosis in man or animal having the tubercular diathesis, we also believe that it does so because of its property of exciting that amount of irritation and reaction necessary to initiate the tubercular process—a property, however, possessed by many other irritants; and while it is probable that a few cases may be thus produced in man, a vast majority of the cases arise independently of its presence. And hence we maintain that tuberculosis is not a specific contagious disease in the sense that it is only produced by a special contagion, as small-pox and other similar diseases are.
9 Journal of the American Medical Association, vol. iv. No. 12, p. 314.
10 We hold that leucopedesis is a normal physiological process that is always going on during the period of active growth of the individual, as well as during the process of repair.
Primary acute miliary tuberculosis occurs only in the young or early adult period of life, for the reason, perhaps, that persons of the tubercular diathesis can hardly long escape the exciting causes of the disease, and so are attacked early. Persons possessing what may be called the incomplete or partial diathesis may be attacked by a secondary miliary tuberculosis at any, even the most advanced, age; but it will be found that in all such cases of late tubercularization there has occurred a direct infection of the blood by absorption of caseous detritus from a softening cheesy pneumonia or cavity. "In 28 out of 52 cases collected by Litten, it was associated with pulmonary phthisis, and this accords with general experience" (Roberts11).
11 Practice of Medicine, 5th ed., p. 301.
Acute primary general miliary tuberculosis—that is, in which all or nearly all the vascular tissues are attacked at once—must be one of the rarest diseases. Such cases can only occur when the tubercular diathesis is strongly marked and exciting causes of the most active character have been applied. As a rule, tubercular eruptions occur in successive crops, attacking the more vascular organs, as the lungs, cerebral meninges, spleen, liver, serous and mucous membranes, and bones, first and usually in the order given. Laennec's law, that if tubercle is found in any other organ it will also be found in the lung, is undoubtedly true, with the single exception perhaps of tubercular meningitis. If our explanation of the causes and mode of formation of tubercle is correct, we must a priori expect to find that a tissue so soft and spongy as the lung, and which is so vascular and subject to such great and sudden alterations of pressure and relaxation, would naturally be the site of the first formation of tubercle.
SYMPTOMS AND COURSE.—It is impossible to give a clear or lucid description of acute miliary tuberculosis, since there cannot be said to be any constant or pathognomonic symptoms produced by the disease per se. The symptoms present in any given case depend upon the organs involved, and may be said to consist merely of those furnished by such organs when invaded by inflammation. Fever is present in all cases. The grade or height of this fever will depend upon the number and extent of tubercular formations, and to some extent upon the organs involved. It will generally be highest in tubercle of the serous membranes, and of the lungs next. In general miliary tuberculosis the fever is highest, and can be distinguished with difficulty from enteric fever. If the intestinal mucous membranes are involved, and diarrhoea consequently exist, the differential diagnosis will be almost impossible. The fever, following the law of nearly all inflammatory and symptomatic fevers, is usually remittent, and the remissions and exacerbations correspond to the normal diurnal variations of temperature—lowest in the morning, highest in the evening. The remissions are also usually attended with perspiration, sometimes profuse, at others moderate. The patient early falls into that condition of prostration and general exhaustion which speedily comes on in all fevers of high temperature and protracted duration expressed by the term typhoidal state. Even the pains ordinarily complained of in inflammation of various organs are not felt, or if felt at all are seldom mentioned; which perhaps helps to render the diagnosis more difficult. Almost the only exception to this is when the cerebral meninges are early affected, in which case unusually severe headache may be complained of. Cough may be present, but is not more troublesome than in many cases of enteric fever, and is quite out of proportion to the lesions found in the lungs and pulmonary mucous and serous membranes. The expectoration varies, and is sometimes entirely absent. Generally, it is moderate and consists of frothy serum, occasionally streaked with blood. Hæmoptysis is said to be occasionally present, but must be extremely rare. Respiration is notably frequent early in the disease, and in the absence of pronounced physical signs of pulmonary lesions is perhaps one of the most reliable and pathognomonic signs present. Respirations are often as frequent as 60, seldom less than 30, per minute. The pulse is usually rapid, generally hard at first, but soon becoming soft and weak. The rate varies between 110 to 120 to 160 or more late in the disease.
The disease runs a rapid and invariably fatal course, often ending within the first fortnight, seldom lasting as long as two months.
Tubercles, miliary and submiliary, are found after death in almost all the vascular organs, varying much, however, in number in various organs, and often presenting different stages of development. In some, and especially in the lungs, tubercles will be found already in a state of incipient softening, others still firm and yellow (caseous), and others still grayish and semi-translucent, showing, we think, a different period of eruption, and demonstrating the correctness of our observation that miliary tubercles are always formed in successive crops.
If the tuberculosis is associated with inflammatory phthisis, and, as is the case in a majority of instances, has been caused by absorption of caseous detritus, large masses of caseous matter may be found in the lung, either in a softening condition, or cavities will be met with empty or partially filled with pus, and surrounded by indurated walls the result of interstitial pneumonia. These caseous masses and cavities are, in our view, the result of precedent catarrhs or croupous pneumonias, and not a result of the tubercular process.
Partial or local miliary tuberculosis is a much more frequent occurrence than the general disease above described. It occurs most frequently in persons under twenty-five years of age, and in a very large majority of cases between the ages of two and twenty. It occurs also most generally in the lungs first in point of frequency, in the mesentery next, and last in the cerebral meninges. Of course a secondary general tuberculosis may result in any of these cases from resorption, except in the meningeal variety, which generally destroys life before there is time for secondary infection.
Acute miliary tuberculosis may occur in the young as a consequence of measles and other exanthematous fevers, whooping cough, typhoid fever, and various other affections which seriously impair nutrition. According to our own observation, it is most likely to attack boys and girls soon after puberty who are pursuing too severe a course of study in school with insufficient exercise in the open air, and perhaps also those evil practices unfortunately too common in both sexes. Tubercular meningitis as an idiopathic affection (that is, without the previous or concurrent deposit of tubercles elsewhere) is almost exclusively met with in children between two and seven years, but secondary tuberculosis of the meninges may occur at any age. We have seen two cases of pulmonary phthisis, one of three and one of three and a half years' duration, and who bid fair to live for a long time, suddenly carried off by tubercular meningitis. Both of these persons were past thirty years of age.
Tuberculosis of the mesentery, peritoneum, and liver (for they are sometimes found in all three of these organs) is invariably either coincident with a general tuberculosis or the secondary consequence of scrofulous inflammation of the intestinal glands. Quite often here the tubercular process is associated with the scrofulous process, and large masses of caseous material will be found in the mesenteric system of glands.
As in general miliary tuberculosis there are no symptoms by which the disease can be positively recognized, so too in the partial or local disease there are absolutely no pathognomonic signs. We may say in general terms that if a person who is known to have had a pneumonia which has ended in a permanent consolidation of any considerable portion of one or both lungs, and who has for some time presented the symptoms, however slight, of chronic pulmonary phthisis, is suddenly attacked with fever and night-sweats; or, if fever has already existed, the temperature rises considerably above the previous average, with increase of cough; or if an uncontrollable diarrhoea sets in; or if headache and delirium should suddenly occur—delirium out of proportion to the fever,—then we are justified in believing that tuberculosis of the lungs, mucous membrane of the bowels, or arachnoid has occurred. Or if a young person of either sex, such as above described, should, after becoming pale and anæmic, begin to have slight fever with a dry, hacking cough, at first without expectoration or with a frothy muco-serous expectoration, which for an unusual length of time continues to retain this characteristic, and this fever and cough cannot be otherwise accounted for, then the existence of pulmonary tuberculosis is rendered extremely probable, although there is neither history nor evidence of preceding pneumonia or scrofulous glandular degeneration. If a few scattered and slight crepitant râles can be heard over one or both lungs without alteration of pulmonary resonance, and the respiratory rate is much too frequent for the temperature and pulse, then the diagnosis becomes almost absolutely certain. Unfortunately, this scattered or diffuse crepitant râle is often absent, and there are absolutely no physical signs whatever of the deadly mischief going on in the lungs.
Prolonged expiratory movement is spoken of by some as one of the reliable signs of tuberculosis, but as this sign is usually present in almost all forms of chronic pulmonary disease, its significance cannot be relied upon. Or if a child over two and under ten years of age, after showing evidences of malnutrition, should suddenly be attacked with fever of moderate temperature, become restless and fretful, should frequently vomit and retch even when the stomach is empty, and begin to have convulsions, with squinting and trismus, and if old enough complain of severe pain in the head, have a rapid, frequent, but irregular or slow and intermitting pulse,—if these symptoms become exaggerated at night and somewhat mitigated in the daytime, the diagnosis of tubercular meningitis may be made with tolerable certainty.
It would take more space than is allotted to this article to describe all the phases of tuberculosis: we shall therefore summarize the symptoms of this disease by saying again that the signs and symptoms of tuberculosis are simply those of inflammation with fever and such derangements of function and other local disorders as would be furnished by inflammation of any given organ under other circumstances, except that the pain produced by tubercular inflammation is not usually so severe as in other inflammations, and hence diagnosis is not always so easy as in the latter. For it is a remarkable fact that in tubercle of the peritoneum—an organ which in a state of inflammation usually gives such excruciating pain—this symptom is often not complained of, and the existence of tuberculosis not suspected until after a post-mortem. The same may be said of tubercle of the meninges. Pain is often not complained of, and is never so severe as in ordinary meningitis.
TREATMENT.—In acute general tuberculosis no treatment will be of any avail. All that can be done is to moderate the fever and support nutrition by appropriate food. For the first, quinia in large doses is undoubtedly the best remedy. It should be given in one or at most two doses daily. Twenty grains should be given early in the morning, and this dose repeated at 1 o'clock P.M., or thirty to forty grains may be given in a single dose about 8 or 9 o'clock A.M. Antipyrine should prove a valuable antipyretic in these cases, and, being probably equally effective, produces less disorder of the nervous system and digestive functions than the salt of cinchona. Judging from what we have seen of its effects in other fevers and inflammations, fifteen to twenty grains repeated about four times in the twenty-four hours should keep the temperature very near normal.
For the second indication milk and raw eggs constitute the best diet. Brandy or whiskey in the form of eggnog or milk-punch is useful, and in the latter stages indispensable. It should not be forgotten that according to the latest observations muriatic acid disappears from the gastric juice of fever patients, and that its power to digest animal food is therefore very much impaired. This should be supplied, therefore, by giving after every ingestion of milk, eggs, or other animal food ten to fifteen drops of dilute hydrochloric acid in a sufficient quantity of water. Peptone will also aid in the proper digestion of protein substances, and should therefore be added to the acid. Some of the liquid peptone sold by manufacturing chemists contains hydrochloric acid, and would therefore meet both these indications.
By these means we may doubtless prolong the life of the patient and promote his comfort or at least diminish his suffering, and if a cure is possible secure it. Tuberculosis of the mesentery and peritoneum, as well as tuberculosis of the cerebral meninges, will generally prove fatal, the one by impairing the chylo- and hæmatopoietic functions, the other by injury to the central nervous system, though Hartshorne of Philadelphia reports one case of the latter in which temporary recovery lasting one month took place, and quotes two cases by Guersant in the Dictionnaire de Médecine (1839) in which also partial recovery, lasting five weeks and two months respectively, occurred. "May we not imagine, however," says Hartshorne, "that if such convalescence could last two months, it might in a case affected with nearly similar lesions be prolonged indefinitely?"12 I am informed that a case of permanent recovery has been reported in England, but I have not been able to obtain the reference. To these I have to add a case of my own in which recovery has been maintained for a little more than nine months. In this case, a boy of twenty-six months, the convulsions were controlled for many days by hypodermic injections of morphia, while quinia was given by the mouth when possible, and otherwise by the rectum; and, though he had left hemiplegia and was for a time both blind and deaf, he recovered entirely in about six weeks, and has remained well.
12 Reynolds's System of Medicine, Am. ed., Philadelphia, 1880, vol. i. pp. 826, 827.
In pulmonary miliary tuberculosis the treatment is by no means so hopeless if the disease is promptly recognized and actively treated. The thing to be accomplished in this case is to prevent secondary eruptions and the softening of the tubercles already formed. We know that this last can be done in caseous deposits resulting from catarrho-pneumonia, and we also know that tubercle can be maintained in a quiet state or be made to dry up by calcareous impregnation or degeneration for an indefinite time, since post-mortems often show old tubercles in one or the other of these conditions. We know of one man who carried a caseous lung for nineteen years, coughing more or less during all that time, but in a sufficiently good state of health and strength to follow his occupation of ship-carpenter, but who died at last from phthisis; while another, a farmer living in one of the Southern States, has lived in fair health, with his left lung indurated from top to bottom, for twenty-four years. There cannot be a doubt, therefore, that if secondary crops of tubercles are prevented, and a perfect state of health and general nutrition maintained, the tubercles may remain quiescent in their cheesy condition or may undergo calcareous degeneration and dry up into inert and innocuous masses incapable of further harm.
The first and most important indication, therefore, in the treatment of tuberculosis is to suppress the fever; for as long as this continues new tubercles will continue to form, since the fever is both a predisposing and exciting cause. Quinia, therefore, or antipyrine, should be given as directed in general tuberculosis. The patient should be put to bed and not permitted to go about until the arrest of fever seems permanent. Nutrition should be supported and promoted also by the same means already indicated. As soon as the fever is permanently arrested (but not before) the patient should be permitted to take gentle exercise in the open air, and should be encouraged to spend as much time as possible out of doors, and if able to do so should be sent during the winter to that climate or place where, on account of its warmth and dryness, the most time can be spent in the open air.
Hypophosphites of lime and soda should be given constantly, and cod-liver oil also if the stomach can tolerate it. Large doses of the oil are useless, and often hurtful, a dessert-spoonful being quite as much as most stomachs can bear without exciting unpleasant eructations and nausea. The appetite and digestion are best excited by tincture or extract of cinchona and nux vomica. Iron we have found to be of little use, and often hurtful. We much prefer small doses of arsenic (two to five drops of Fowler's solution), and if there is much bronchitis this will be found especially useful. Some persons, however, cannot tolerate arsenic in any dose. The patient should carry a clinical thermometer, and as soon as the slightest fever is detected he should go to bed and active antipyretic treatment should be instituted, the tonics and alteratives being meanwhile suspended. If cough is troublesome (but not otherwise), one to two grains of codeia should be given two or three times a day or as often as may be found necessary. This is much preferable to morphia or other preparations of opium, which constipate the bowels, dry the mouth, impair the appetite, and so stupefy the patient that all inclination or even ability to take exercise in the open air is destroyed. Codeia is amenable to none of these objections.
Guided by these principles, we think we have successfully treated many cases of primary pulmonary tuberculosis—many in which the hereditary predisposition was strongly marked and the diagnosis unquestionable. It is true that many of these cases have relapsed and died after a variable period, but others have remained well for several years, and still others permanently.