Chapter XXXII: Part 32

ETIOLOGY. (See article on INTESTINAL WORMS, by Leidy.)--Hydatids have been found in the human subject in all countries, but especially in France, Germany, and in the north of Europe. They are rarely found in North America, and the fact that the majority of cases seen here have occurred in foreigners favors the probability of the hydatid disease having been imported. But there are two countries where it may be said to be endemic--Iceland and Australia. Finsen found 1 out of every 43 inhabitants affected with this disease in the district of Ofjord in Iceland. Hydatids are communicated to the human race through the system of the dog, and in Iceland the proportion of these animals to the population is probably more than 1 to 3, a recent census recording 20,000 dogs to 70,000 inhabitants. Hydatids usually enter the system through the digestive and respiratory organs. The Icelanders are excessively uncleanly and careless of the laws of ventilation. In the winter season both men and women are confined to the house in company with their dogs, and in consequence the air is impregnated, and oftentimes the drinking-water contaminated, through their dejecta, which contain thousands of the eggs of the echinococci. The largest {467} number of cases occur in the agricultural districts, since the dogs are more required there than on the sea-coast.

In Australia large numbers of dogs are maintained to guard the sheep. The droppings of these animals, dried by the hot winds, are inhaled as dust. It is curious to note that in Australia, where the high winds prevail, the proportion of pulmonary hydatids is very large, while in Iceland, where the drinking-water is the principal medium of communication, the lungs are less often affected than other viscera. Finsen's records in the latter country show 255 cases; of these, 176 occurred in the liver, and only 7 in the lungs. In both Iceland and Australia women are more subject to echinococci than men. This is possibly accounted for by the facts that the women take care of the dogs and wash the vessels from which they eat, and are also less protected by hair about the mouth and nose than men.

The disease occurs most often between the ages of twenty and thirty years, but it has been found in children of four years of age. Before ten and after sixty the proportion of cases in both sexes is equal. The malady is not hereditary, but uniformity of environment accounts for the propagation in communities. Pulmonary hydatids occur as primary formations in the lungs, but may be secondary to similar growths elsewhere, especially in the liver. There is, however, scarcely a tissue in the body in which hydatids have not been found.

MORBID ANATOMY.--Hydatid cysts consist of sacs of various sizes, from that of a pea to an orange or even an adult head. They are usually globular in shape, and attached by a vascular membrane to the organ in which they are situated. The walls of the cysts are composed of a few laminæ of indeterminate membrane of varying thicknesses, commonly depending on the age of the cyst. In young cysts they occur in direct contact with the lung, but as they grow larger a thicker investment is formed, and large old cysts which have generally undergone spontaneous rupture often have a dense leathery sac. Walsh asserts that the parent cyst lies in direct contact with the lung-tissue, and, unlike that of the liver, is rarely surrounded with a thick shell or cyst-wall of pseudo-areolar tissue. The interior of the pouch is smooth and of the aspect of serous membrane without epithelial covering. The parent cyst contains daughter cysts which are single or multiple, and a liquid the proportion of which is variable. This liquid is nearly limpid, and non-coagulable by heat or acids; it deposits by evaporation crystals of chloride of sodium.

Commonly, only one hydatid tumor is found in the human lungs, although in animals multiplicity of cysts is the rule. They are usually located in the base of the lungs, and are thought to be more common on the right side, but they may occupy any portion of one or both lungs. They have been found in the pleura, the bronchi, the pericardium, and the thyroid gland. In the pleural cavity they may be attached to both the costal and the visceral pleura; in the latter case they may form an outgrowth from the lung into the pleural cavity. Authorities differ as to the condition of the neighboring lung-tissue, some stating that the cysts are rarely surrounded by healthy lung-substance, while others assert the contrary. Since the growth of the cysts is often very slow, the accommodating power of the lung is remarkable when no constitutional mischief exists. In some instances the rapid enlargement of a cyst has been accompanied by certain forms of pneumonia, secondary inflammatory lesions, congestion of the neighboring tissue, splenification, or even gangrene.

Hydatids situated either in the lung or pleura may rupture into the bronchial tubes, and thence be discharged by cough and expectoration, or they may open externally like a pleural empyema, or even rupture through the diaphragm into the intestines or peritoneum. None of the above accidents are necessarily fatal, not even the latter, unless the fluid be puriform. {468} Empyema with pneumothorax usually follows rupture into the pleura. Finsen observes that a general urticaria may follow the rupture of a cyst into a serous cavity. In old cases, after rupture of cysts, pulmonary changes may almost always be found. The ruptured cyst may become a suppurating cavity, suggesting the possible development of phthisis. In some cases hydatid formations have been described with coexisting catarrhal or tubercular disease, or these processes may occur as a complication without rupture of the cyst.

SYMPTOMS.--The symptoms of hydatid cysts are obscure, and the physical signs difficult to analyze when the cysts are small. They are more suggestive when the cyst becomes large enough to contain a pint or more of fluid. The outline of the cyst is usually globular, and is imbedded in healthy or nearly healthy lung-tissue. According to Bird, the physical signs correspond with those familiar to us in pleural effusions: absolute dulness or flatness on percussion, with absence of respiratory murmur over a space of the chest-wall not smaller than the palm of the hand; vocal fremitus and resonance are also abolished. The expansion of the chest is more or less deficient upon the affected side, but seldom with any change on mensuration.

The area of the above physical signs usually presents a rounded outline, limited by a line of demarcation so exact that it can be mapped out with pen and ink, but is unaltered by position. Their location is generally in the lateral or infra-clavicular regions; beyond the boundary-line percussion is vesiculo-tympanitic resonant or normal, and the respiratory sounds begin at the very margin of the pen-and-ink line, and, though probably harsh and puerile in character, are indicative of healthy lung-tissue.

Pulmonary hydatids can seldom be examined by palpation, but all authors allude to a frémissement or peripheral fluctuation which may sometimes, but not invariably, be detected by palpation over the intercostal spaces. Davaine directs palpation as one would palpate an abdominal cyst. The sensation of fluctuation is as though the fluid were gelatinous; when the quantity of liquid is excessive this movement is not perceptible. It is most recognizable when there is but a single hydatid in the parent cyst (Jobert). The frémissement cannot be felt when the sac has undergone atheromatous degeneration, because there is then no liquid, and the cysts are withered, agglutinated to one another, and the tumor is inelastic and hard. By auscultating the tumor while practising percussion one may hear more or less positive vibrations resembling those produced by a bass string (Briançon).

The general symptoms of pulmonary hydatids are of mechanical origin: pain, dyspnoea, cough, with duskiness of the surface, all of which are more or less marked according to the size and location of the tumor and its rapidity of growth. A phthisical appearance is possible, with deterioration of the blood-crasis and progressive loss of flesh. Marked clubbing of the finger-ends and incurvation of the nails have been noticed, all of which symptoms have disappeared after the hydatid cyst has been tapped or expectorated. Cough nearly always accompanies this disease, as it does a large pleural effusion. The expectoration is a glairy mucus, sometimes stained with blood; when local bronchitis occurs as a complication, it may become muco-purulent. There is much diversity of opinion as to the frequency of hæmoptysis, many authors looking on it as a rare symptom. According to Bird, there is seldom or never profuse hæmoptysis, though several ounces have been expectorated at a time in an aggravated case where tapping had been long delayed. The cause of hæmoptysis is usually pressure of the growing cyst upon the pulmonary veins, leading to extravasations of blood.

If dyspnoea with deficient aëration of the blood, wasting, clubbed fingers, and expectoration persist after the expulsion or death of the hydatid, the probability is in favor of some associated pulmonary inflammation. When {469} a hydatid cyst ruptures into the bronchial passages, there is serious likelihood that the patient may choke or suffocative dyspnoea supervene. The quantity of entozoal substance voided at any one time varies from a few microscopical fragments up to a pint or more of unbroken acephalocysts. The expectoration of acephalocysts may continue several months. Serious general pulmonary symptoms precede and follow this accident. When rupture has taken place into a bronchial tube, there are the usual physical signs of a pulmonary abscess or large vomica. The sac usually suppurates, and there is a constant expectoration of blood, pus, and half-putrid acephalocysts of excessive fetor, and often portions of gangrenous lung-tissue. With these symptoms the temperature is sometimes of a low, remittent type, with hectic and sweats. The symptoms resemble those of empyema or advanced phthisis, and may continue for months, until the patient, in most cases, sinks from exhaustion, unless relieved by the evacuation of the sac and its contents. When hydatids develop in the pleural cavity the signs are identical with a localized pleural effusion.

Nothing has been said to differentiate pulmonary-hydatid expectoration from cases where an hepatic hydatid cyst has burst into the lungs, and the diagnosis may be very difficult. The physical signs of enlarged liver are present, also the antecedent symptoms of disordered hepatic action, especially intestinal indigestion and the staining of the sputa with bile. If the cyst has undergone suppuration, the symptoms may be allied to those of hepatic abscess.

The nucleation of testimony favors the view that a latent or slow growth is by far the most common history of hydatids. Their duration is very variable: patients may harbor them for a long time unconsciously, even over a period of sixty years. This is corroborated by Finsen, who reports cases in which the disease lasted sixteen, eighteen, and fifty-two years, proving this by stating that these individuals had left the country where the disease was endemic, and were residing during these periods where the malady was rare.

TERMINATIONS.--30 or 40 per cent. of cases terminate in recovery if the cysts spontaneously burst, death being caused in others by suppuration and exhaustion. There is, in addition, the risk of sudden death from the rupture of a large cyst in the lung, and consequent filling up of the air-passages by its contents. The cysts may sometimes undergo atheromatous changes in which the hydatids resemble crushed grape-seeds. Microscopically, one finds a puriform fluid, plates of cholesterin, crystals of hæmatoidin, hooklets of echinococci, and débris of membranes. Again, the cysts may resemble a caseous or cretaceous tubercle without special characteristics. This may be looked on as a species of spontaneous cure. The growth of hydatid cysts may bring about by pressure such a state of chronic pulmonary engorgement that it affords a predisposing condition favoring the development of tubercular phthisis.

DIAGNOSIS.--The differential diagnosis is necessarily difficult. The nationality of the subject and the presence of a predisposing environment should always be remembered. If the disease progresses rapidly without interference, the diagnosis may be complicated by the development of patches of bronchitis or pneumonia with rusty sputa. The bronchitis is, however, local, which, taken with the physical signs of a cyst, may be suggestive. The only absolute evidence of the existence of hydatids in the lungs, whether primary or secondary, is the appearance in the sputa of the characteristic cysts or portions of them, such as fragments of the hooklets of the echinococci. This, unfortunately, occurs as a late accident in their history. If the boundaries of the cyst can be recognized, it is justifiable to resort to paracentesis, and thereby withdraw some fluid for examination. The physical signs of local serous effusion, globular in shape, not evenly {470} distributed around the circumference of the chest, is one of the best differential evidences between hydatids and pleural effusion. Moreover, there is no fever in hydatids unless after rupture, or with extensive phthisical complication, while there is a history of fever in some stage of most cases of pleurisy. Hydrothorax is differentiated through its being bilateral and by its etiology. From local encysted pleurisy the only resort is exploratory puncture and the question of the probabilities in each case. In the same way paracentesis removes doubt whether there be mediastinal tumor, solid tumor of the lung, or circumscribed pneumonic abscess; in the latter the general history of each case is helpful. From phthisis we must have recourse to the physical diagnosis already mentioned as belonging to hydatids. An unbroken cyst in the liver, high up and far back on its convex surface, may not be distinguishable from one in the base of the lung immediately over the liver or one in the cavity of the pleura.

PROGNOSIS.--According to Reynaud, this depends on--1, whether the hydatid is single or multiple; 2, whether the pressure is exercised on blood-vessels or bronchi; 3, if hydatids are discovered elsewhere; 4, size of cyst; 5, alterations in the walls of cysts; 6, whether complicated with any other disease or independent.

If there is a tendency to pulmonary phthisis, inherited or acquired, or if this disease exists as a complication, it forms an unfavorable element in the prognosis. Persons once affected with hydatids are more susceptible to a second invasion of the parasite. The practicability of treatment by tapping is also an element in the prognosis.

TREATMENT.--Naturally, the preventive treatment rationally deduced from the now distinctly-understood causes should be practised. The water-supply should be protected from sources of contamination, and in addition the inhabitants of countries where the disease is prevalent should, as far as practicable, use boiled or stone-filtered water and refrain from eating water-cresses or plants of like character wherever these are liable to be contaminated.

Many drugs have been administered, among them the bromide and iodide of potassium; solutions of salt are also said to be deleterious to the life of the echinococcus; Laennec even prescribed salt baths. Tincture of kamela has been recommended by Hjaltelin, a physician in the employ of the Danish government in Iceland. He administered it in doses of thirty drops daily to adults, continuing its use during a month or more. It has a distinctly irritating and destructive effect on the acephalocyst (Bird). Turpentine, from its well-known anthelmintic powers and ready diffusibility, has naturally suggested itself as a remedy, and according to some has proved of great service in many instances, while in others it has signally failed.

Paracentesis is generally regarded as the most efficacious treatment, and may be carried out upon the principles usually applied in the treatment of hydrothorax. Bird recommends that the trocar should be not less than six inches long and of the smallest diameter that is made, always providing that it is strong enough to bear the strain of a firm pressure. Cysts can be tapped in this manner even when they are separated from the chest-wall by quite a deep layer of lung-substance. This treatment should be practised at the earliest possible period in the life of the cyst. Speaking of the aspirator, he says that cases always do so well if tapped early enough with the simple trocar and canula that aspiration is not required. The gradual expansion of the lung as the cyst is emptied is sufficient to expel all the fluid, especially if aided by the effects of coughing. In exceptional cases of old standing, where there is a thick adventitious external wall to the cyst, which is generally closely adherent to the ribs, or again in cysts of the pleura, a free antecedent incision of the external tissues is sometimes required. It has been suggested by different authors that tincture of iodine should be injected after {471} aspiration to secure the obliteration of the cyst by inflammation. The injection of carbolic or salicylic acid under the same conditions has been practised with success by Mosler and others.

The treatment of old suppurating cysts is rather different. The centre of the sac, as nearly as can be judged, is fixed upon, and an incision is then made through the skin and muscles, and the largest-sized trocar and canula that will pass between the ribs is introduced into the sac. This gives exit to a quantity of pus, even chalky substances and fragments of cysts of different sizes. The opening must be free and kept patulous for some weeks, and the sac should be daily washed out with some disinfecting solution through the drainage-tube. Some delay is always necessary to allow of the separation of the parent cyst from its nidus and the gradual expansion of the lung. Immediate attempts at its removal by forceps are generally unsuccessful, and portions are very apt to be left behind. Several complications may interfere with the success of the operation. One is the unavoidable piercing of a small bronchus by the trocar. After the operation the wound of the bronchus may remain patulous and a violent paroxysmal cough comes on, with subsequent possible evacuation of the cyst through this channel. The bronchial tubes, however, have been opened in operative treatment of pulmonary cavities without serious result. When the parent cyst has progressed to maturity quite unhindered, and is stuffed full of daughter cysts, it has been recommended in such cases to introduce the stylet and endeavor with its sharp point to stir up and break down the smaller cysts as much as possible. The thermo-cautery has recently been used successfully by Mosler to afford a means of penetrating the cyst in the treatment of pulmonary hydatids. The tissues of the thoracic wall must be first divided down to the pleura, as recommended in the opening of pulmonary vomica by the thermo-cautery. Resection of the ribs should be practised in case sufficient drainage cannot be accomplished through an interspace.

Before applying to these operative measures it is desirable that adhesions should have occurred between the visceral and the parietal pleura. Fenger and Hollister recommend the introduction of a needle as a means of diagnosis: if there be adhesions, it is unaffected by respiration; if no adhesions exist, it is moved synchronously with the breathing. There are, however, no absolutely reliable signs by which this adhesion can be determined. Paracentesis of suppurating sacs has been performed in cases in which the pleural surfaces have not been adherent. In some instances the lung has been stitched to the opening in the pleura, and after partial adhesion has occurred the purulent collection has been punctured. In certain other cases, when pleural adhesions have been absent, paracentesis has not been followed by serious pneumothorax, possibly because the apposition of the pleural surfaces is maintained by the tendency to cohesion which exists, and after operative interference these surfaces are united by adhesive inflammation.

{472}

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.

[Footnote 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, {473} 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.

{474} 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 Woodward[2] 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 Ranvier[4]). 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.

[Footnote 2: _Medical and Surgical History of the War of the Rebellion_, Part 2, Medical Volume, p. 593.]

[Footnote 3: _General Pathological Anatomy_, London, 1883, p. 171.]

[Footnote 4: _Pathological Histology_, Philadelphia, p. 116.]

[Footnote 5: _Textbook of Pathological Histology_, Philadelphia, 1872, p. 125.]

[Footnote 6: _Op. cit._]

[Footnote 7: _Op. cit._, p. 168.]

{475} 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]

[Footnote 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 {476} 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 {477} 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 {478} 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.

[Footnote 9: _Journal of the American Medical Association_, vol. iv. No. 12, p. 314.]

[Footnote 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" (Roberts[11]).

[Footnote 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, {479} 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.

{480} 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.