Volume 3 — DISEASES OF THE RESPIRATORY SYSTEM. (continued 18)

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 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 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 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.

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.

DISEASES OF THE PLEURA.

BY FRANK DONALDSON, M.D.

Pleurisy.

DEFINITION.—Inflammation, partial or general, of one or both pleuræ.

SYNONYMS. Pleuritis ([Greek: pleuritis]) morbus lateralis; Morbus pleuriticus (Celsus); Pneumona pleuritis (Cullen). Fr. Pleurésie; Ger. Seitenstich.

HISTORY.—Pleurisy derives its name from the accompanying pain in the side, usually its most prominent symptom. In the sense in which Hippocrates used the word [Greek: pleuritis], it meant all kinds of pain in the side, especially such as are of a violent character. Pleurisy was mentioned by Celsus, and was still better defined by Galen. Æctæus, however, was the first to describe it with precision and to speak of its treatment. These ancient authors viewed the disease as seated in the layer of the pleura lining the ribs or external parietes of the chest. More modern writers contended that the disease was more frequently in the expansion of the pleura over the lungs and other parts. Boerhaave and Van Swieten contended for the separate and distinct affection of the pleura. Sydenham, Hoffman, and Morgagni believed that the pleura and the substance of the lung were generally both implicated. Pinel was the first to definitely establish the difference between pleurisy and pneumonia from the anatomical lesions. Laennec laid the foundation of our present knowledge. He was followed by Andral, Chomel, Louis, and Cruveilhier in Paris, and by Forbes and Williams of London and Stokes of Dublin. They demonstrated, by the physical signs and general symptoms during life and by the post-mortem lesions, that inflammation may commence in and be limited to the pleura in some cases, and in others that it may extend to and involve the lungs. Again, they showed that in some instances the lung may be inflamed without involving the pleura generally, yet that in the large proportion of cases the disease may originate in one organ and extend in a greater or less degree to the other, thus implicating both of them. Previous to Laennec the incomplete anatomical knowledge of the nature of the serous membrane, the pleura, as a capsule of the lungs, and the thoracic organs and walls, as well as the theoretical views of the nature of inflammation as a morbid process, led to erroneous views. Their diagnoses were made from general symptoms only. Pleurisy was considered the more common disease. Avenbrugger, Corvisart, and Laennec, by their discoveries of the accurate physical modes of exploration of chest diseases, gave far more reliable data for differential diagnosis. Now we have, in addition to the general symptoms, the modern refinements in auscultation and percussion, the delicate measurements of Woillez's cyrtometer, Ransome's stethometer, and Pravaz's and Alex. Wood's hypodermic exploring-needles to enable us to attain great accuracy in the diagnosis.

CLASSIFICATION.—Pleurisy is one of the most common diseases of the respiratory apparatus. Though apparently simple, careful study shows it to be extremely complex. It occurs in very different forms and in a great many modifications, according to the producing causes and the numerous lesions which follow its course. We might classify the forms of pleurisy, according to their causes, as primary or secondary, tubercular, traumatic, etc.; or we could designate them according to their anatomical lesions, as dry pleurisy, pleurisy with effusion, general or parietal pleurisy, encysted, multilocular, purulent, hemorrhagic, etc. A methodical classification of all these forms is difficult if we attempt to base it upon the prominent characteristics or the lesions. We prefer a classification which enables us to study separately the clinical varieties which are most frequently met with, and therefore the most important. The symptomatology shows that the inflammatory process in pleurisy is of different degrees of intensity. We propose for our study to divide them into two main groups, according to the nature of the exudation:

Fibro-serous pleurisy, Acute, Chronic.

Purulent pleurisy, Acute, Chronic.

They may be local or general. When they result from disease of neighboring parts, they are generally local. Each of these groups comprehends primary and secondary varieties.

In the first, we have an exudation resembling the plasma of the blood. The effusion is not serous, for the fluid is spontaneously coagulable, whereas serum is not. It is not properly termed fibrinous, for it contains more albumen than fibrin. Fibro-serous is the most accurate term by which to designate it. The watery portion gravitates to the lowest part of the cavity, while the plastic deposit is thrown out over the two surfaces of the pleura. In the most acute forms the general symptoms, especially the pain and fever, are well marked. The exudation is at first largely fibrinous, but it is afterward more fluid in its character. In milder cases, the latent variety of the older authors, frequently designated as the subacute form, the subjective symptoms are so slight that the individual is not aware of his condition until the exudation, which is largely sero-fibrinous, mechanically interferes with his respiration. When first recognized these cases are really often chronic. They frequently remain sero-fibrinous in their character for a long time. Sometimes they become sero-purulent (the intermediary variety), and later purulent. Purulent pleurisies (empyema) are those where pus is the product of the inflammatory action. They may be acute (empyema d'emblée) or the result of transformation of acute or chronic fibro-serous pleurisies.

By this division we shall be able to take into consideration the fundamental causes of all the forms of pleurisy. Starting from the simple primary form, we shall be able to study special varieties of secondary pleurisies, such as tubercular and rheumatic.

Next, we shall examine separately the hemorrhagic variety as distinct from hæmothorax. The localized forms, such as the interlobular, diaphragmatic, and mediastinal, will be studied as varieties caused by their development in different localities.

The simplest plan to elucidate the whole subject of pleurisy is to analyze carefully, in the first place, the unquestionably acute disease, primary pleurisy, and afterward to connect with it the study of the several forms and varieties. Acute primary pleurisy has a sero-fibrinous exudation, and is the most common form of the disease. In it are best defined the usual characteristics of this inflammation. We consider this the principal type of this class, and with it shall study the development and character common to all the varieties of inflammation of the serous membrane of the thoracic cavity.

PATHOLOGICAL ANATOMY OF FIBRO-SEROUS PLEURISY.—The anatomical changes in all forms of pleurisy begin by hyperæmia of the vessels of the serous membrane and of the subserous connective tissue. This is followed by an exudation of a liquid, a pseudo-membranous deposit. In acute primary cases this is first noticed on the costal pleura. The pleura itself shows, by puffiness and oedema with red points and small ecchymosed spots, that the inflammatory process has affected it. In a few hours, in acute cases, there is found a thin deposit of fibrinous lymph of a reddish-yellow tinge, with more ecchymosed spots, resulting from the rupture of fine capillary vessels. The pleura is somewhat thickened and loses its transparency, and is studded with very fine granulations. Under the microscope it is shown that the epithelial cells are swollen, that their number has been largely increased by proliferation, and that they have been detached in great quantities. The granulations are scattered over the pleural surfaces, and separate the pleura from the fibrinous deposit. The connective tissue is loaded with liquid, in which are found in increased quantity leucocytes which have migrated through the walls of the blood-vessels.

Over the surface of the pleura there is a tissue of granulations composed of embryonic cells, which are derived from the proliferation of the elements of the connective tissue. In this tissue of new formation we find new blood-vessels coming from those belonging to the subserous tissue, which advances through small points, even to the free surface of the granulations. These vessels are very thin and brittle. They sometimes rupture and cause ecchymoses of the pleura and of the false fibrinous membranes—sometimes effusions of blood, which, becoming mixed with the serum in the pleural cavity, cause hemorrhagic pleurisies. This new tissue is susceptible of organization, and of transformation progressively into a tissue analogous to that of a cicatrix. Under the plastic exudation we find abundance of embryonic cells, which become elongated and spindle-shaped in the formation of new connective tissue. This is at first tender, but may become dense and fine over circumscribed points, so as to produce bands which enclose and touch the effusion. This is the origin of the organized neo-membranes which are found on the surface of the pleura. It is, moreover, this tissue of granulations which constitutes the bands which unite the parietal to the visceral pleura, the adhesions being produced by the contact and the union of vegetations or neo-membranes developed on the two opposed layers of the pleura. The membranes form the filamentous thin bands which draw obliquely together portions of the pleural sac. These lesions are very often slight and rudimentary in simple acute pleurisy, but are found well developed in purulent pleurisy, especially when it is chronic. These are hyperplastic parenchymatous lesions of the pleura. Acute inflammation of the pleura gives rise to two distinct forms of exudation—the plastic, deposited on the free surface of the serous layers or formed in flakes in the fluid; and the serous, which falls into the dependent portions of the cavity. The plastic may exceptionally exist alone. Their formation together is the rule. Anstie questions whether the serous effusion ever occurs without the fibrinous. The plastic exudation takes the form of granulations more or less prominent, constituting a bed of very irregular rough points. So long as the period of inflammation continues, new plastic deposits are formed over the old ones. They thus increase in thickness. The neo-membranes which play such an important rôle in the natural history of pleurisies increase very rapidly. Little by little, they are transformed into firm, very resisting tissues. They may become fibrous, cartilaginous, or even calcareous in their structure. These false membranes develop more freely at first when the opposing surfaces are kept apart by the effused liquids. The rubbing of the two pleuræ together seems to impede the process of organization. According to Wagner, the lymphatics are dilated and contain a liquid poor in corpuscles. The newly-organized and vascular tissues often become the starting-points of fresh inflammatory processes and of new products.

Exudations are of two kinds—liquid and pseudo-membranous. When the inflammation extends over a limited surface, the fibro-plastic exudation may be the only one; in which case the disease soon terminates with local adhesions. This is dry pleurisy, which is rarely primary in its origin. Ordinarily, the principal lesion of acute pleurisy consists in a sero-fibrinous effusion which collects in the cavity of the pleura; almost always the liquid effusion exists in decided quantity. In it there are suspended fibrinous flocculi, and on the surface of the pleura are found false membranes. The nature of the effused liquids has been thoroughly studied, ample opportunities having been furnished since thoracentesis has been so extensively used. The quantity of liquid is very variable, from a few grammes up to several liters. The terms small, moderate, and abundant are used to designate the quantity—one-half of a liter is considered a small quantity; moderate, one to one and a half liters; abundant effusion, two to two and a half liters; very abundant, when the effusion goes beyond three liters. The liquid is transparent and of yellowish-amber color. It is darker when the fluid has been some time in the chest, and resembles that of bouillon. Sometimes it has a rose tint when the liquid contains a sufficient quantity of red globules, or it may be somewhat opaque when it encloses a large proportion of leucocytes.

The presence of a few red globules does not constitute a hemorrhagic pleurisy, nor does the presence of a small quantity of leucocytes make a purulent pleurisy. It is only when they are very abundant that they severally give those characters to the effused fluid. Dieulafoy states,¹ after frequent examinations of aspirated serous fluid of acute pleurisy, simple and frank, that it contains the smallest quantity, from 500 to 600 red globules to the cubic millimeter, while the white globules were from fifteen to twenty times more numerous. In some instances he counted 1500, 2000, and even 3000, red globules to the cubic millimeter without the coloration of the liquid being sensibly modified. He adds that the liquid from the pleura has not a perceptible rose tint unless it contains from 5000 to 6000 red globules to the cubic millimeter. He concludes that there is no tendency to transformation into purulent pleurisy unless the number of red globules reaches 4000 or 5000 to the cubic millimeter. Rindfleisch (ed. 1869, Leipzig) states also that upon their number and that of the proliferated epithelial cells, with the floating flocculi, depends the convertibility of the serous into purulent effusions.

¹ De la Thoracentèse par Aspiration dans la Pleurisie aigue, p. 42, Paris, 1878.

Chemical Character of Effused Fluid.—Mehu² gives the composition of the fluid as closely resembling that of the serum of the blood. He found in it the same elements—water, albumen, fibrinogenous matter, salts, red globules, and leucocytes. The proportion of these principal constituents of the blood was greatly modified in the pleuritic liquid. The quantity of water was always increased. On the other hand, the quantity of substances in solution was greatly diminished. The exudation was really blood-plasma, more or less diluted, in which the relative proportion of the constituent elements varied according to the intensity of the inflammation. It has the same alkaline reaction, and it is spontaneously coagulable, owing to the presence of the fibrin which is in solution in the serum, the proportion of fibrin making it coagulate more or less rapidly. Mehu found the quantity of fibrin to vary from 09.073 to 19.276 to the kilogramme. The same mineral substances were found, but in less quantity, than in plasma of blood. The intensity of the inflammation causes alterations in the composition of the exudations. The more acute the inflammation, the greater is the quantity of albumen and of fibrinogen. The fibrinogenous matter contained in the exudation is coagulated only by contact with the air. One portion of it becomes concrete in the interior of the body in the form of fibrinous flocculi, which float in the fluid, and in the false membranes, which are deposited in successive layers on the surface of the inflamed pleuræ. This coagulation takes place in a manner analogous to that of the coagulation of the fibrin in a drop of blood. These false membranes are almost always found in acute pleurisies, but their development is very variable. Sometimes they are very thin, friable, and readily disappear; again, when the inflammation is intense, they last a long time and cover thickly both pleuræ. Occasionally they envelop the effusion and produce veritable cysts and localized pleurisies. Their color is opaline or semi-transparent when recently formed, but opaque when old. Their consistence varies according to the duration of the disease. At first they are soft, impregnated with fluid, easy to tear or break; later on they become resistant and almost dry. The microscope shows these false membranes to be formed of crossed fibrillæ, with intervals containing white blood-corpuscles, with voluminous, swollen epithelial cells of serous membrane, proliferated and detached.

² Arch. général de Méd., 1872.

When the pleural inflammation subsides, the exudation is destined to disappear. Usually the cure is produced by the reabsorption of the effused products. The liquid part of the exudation, the serosity, is absorbed by the lymphatics, which are found frequently dilated, and some of them are filled with fibrinous coagulations and the leucocytes. The solid parts, the false membranes, concrete fibrin, and cells disappear with more difficulty. They undergo granulo-fatty metamorphosis, and are then taken up by the lymphatics.

These fibrinous false membranes are not, as was formerly supposed, susceptible of organization. It is only the neo-membranes, formed by the proliferation of the elements of the pleura, which are organized or organizable. It is these that form bridles or ligaments which attach the lung to the thoracic wall, and are susceptible of transformation into cartilage or even into bone. In chronic cases these new membranes bind the lung down, impair its expansive powers, and inflict great damage upon the respiratory force.

Care must be taken to distinguish between the neo-membranes and the plastic and liquid exudations. These last contain transitory-formed elements entangled in the fibrinous layers. They are principally lymph-corpuscles, containing solitary nuclei, together with a few epithelial cells, almost always in process of disintegration, and isolated blood-corpuscles (Fraentzel).

Distribution of Fluid.—The situation and form in which the effusions are found in the pleural cavity furnish important data for study as applicable especially to diagnosis. At the commencement of the disease the effused plastic products form a thin covering to the pleural surface—a slight cushion interposed between the lung and the thoracic wall. Later, the fluid products gravitate by their weight to the lowest portion of the cavity of the pleura; then, as they increase in quantity, they gradually rise or are drawn to the superior portion of the thorax. Once formed, these effusions are but slightly movable and but little displaced by the varying positions of the patient, unless the quantity be very great and no adhesions or bands have been made. If the effusions be of viscid consistence, or if false membranes exist, they are mechanically prevented from moving. The serous transudations of hydrothorax always occupy the most dependent portion of the cavity, but observation shows how frequently the pleuritic effusions are immovable, being maintained and suspended between the diaphragm and the lungs, and imprisoned in the situation where they form by the false membranes.

Previous to 1843 the authorities universally taught that the effused fluids in the pleural cavity obeyed, as they would in an open vessel or in a vacuum, the law of gravity. They never appeared to question but that the fluid would necessarily assume its hydrostatic level, and consequently that it would reach a horizontal line in all parts of the chest. The distribution and the form which the effusions take were first studied by Damoiseau.³ Fernet and D'Heilly⁴ maintain that Damoiseau perfectly established the form and disposition which the effusions take in pleurisy. To study them well we must bear in mind, they say, three facts: the irregularly conical form of the pleural cavity; the effect of gravity; and the habitual position of the patient when lying down. Damoiseau and these authors utterly ignored the retractile force of the lung, as well as that of the diaphragm, and the resiliency of the thoracic walls, as effecting the position of the fluids in the pleural sac. If we observe that the patient at the commencement lies ordinarily on his back, the thorax being raised and more or less inclined to the horizontal position, we easily appreciate that the effusion ought to accumulate, at first, behind, in the most dependent portion of the costo-vertebral gutter, below the inferior angle of the scapula; then, as it increases in quantity, it rises and obliquely strikes the conoidal cavity, which encloses it, and makes on its surface curves resembling those of an oblique conic section (Damoiseau). As Damoiseau described the pleuritic line of flatness as a parabola, it was highest in the axillary region, where it first appears; thence, as its summit rises, its branches advance downward and outward to the sternum and the vertebral column.

³ Thèse de Paris, 1845.

⁴ Nouveau Dict. de Méd. et Chir., Paris, tome xxviii., 1880.

Since Damoiseau's first paper⁵ it has been generally acknowledged that the line of flatness over the upper surface of a moderate effusion is not horizontal when the patient is in the sitting or erect posture. There has been considerable difference of opinion among the English⁶ and continental writers as to the exact disposition of the fluid: some partially assent to Damoiseau's views; others, again, very materially modify them. Wintrich,⁷ who was one of the first among the Germans to emphasize the percussion line of demarcation between a pleuritic effusion and a contracted lung, says: "As the exudation gradually increases, the level of the fluid does not present a line which is horizontal or parallel to the ground, but one which descends toward the ground at a more or less acute angle." Fraentzel says that the line is never horizontal. Leichtenstein and Ferber⁸ maintain that the line depends upon the position of the patient early in the disease. Gee⁹ holds very much to this opinion. He states that the upper limit of the surface of liquid, when it reaches as high as two inches above the nipple, is horizontal. When lower than this, the dulness forms irregular parabolic curves, which become smaller and smaller as they descend. Austin Flint¹⁰ says, in his more recent edition: "The upper limit of the dulness or flatness, the position of the body being vertical, is not in a continuous horizontal line extending over the posterior, lateral, and anterior aspects of the chest." Flint, Wintrich, and Fraentzel speak of the line being highest behind. Calvin Ellis of Boston in two very suggestive papers¹¹ described a curve-line made by the upper line of the effused fluid, which radically differed from any one previously mentioned. "This curve begins, with medium effusions, relatively low down on the back, passes outward from the vertebral column, and soon turns upward and proceeds obliquely across the back to the axillary region, where it reaches its highest point. Thence it advances in a straight line, but with a slight descent, to the sternum." Powell, however, does not find that the curve invariably commences at a lower level behind. G. M. Garland,¹² in consequence of the resemblance of this curve to the italic letter S, has named it, very appropriately, the letter S curve. He adds that, according to his experience, "this curve, as described first by Ellis, may be traced, by proper percussion, in any case of free, uncomplicated pleurisy when the patient's body is erect and the amount of fluid present is not excessive. As any effusion increases in amount, the curve of its distribution gradually rises and tends to flatten out, so that it no longer presents its characteristic S feature after it reaches the second rib. At this point, when the fluid occupies nearly the entire side, the curve comes quite near to the horizontal, but if some of the fluid be withdrawn by aspiration or absorption the letter S curve will reappear and retreat downward in the inverse order of its advance, until with entire absorption it becomes merged into the normal boundary of the lung."¹³ Garland quotes from two recent German authorities—Heitler of Vienna and Rosenbach of Breslau—to the effect that the line of flatness of the effusion extends lower on the back than it does on the side, and that there is a triangle bounded by the vertebral column, the upper curve from the bottom, and a line drawn from the summit of the curve, where there is impaired resonance over the lung from adhesions and oedema of the lung, but where there is no fluid and no flatness. Garland had previously called attention to this space, and had named it the dull triangle. He had warned all who sought to trace the true line of pleuritic flatness to be careful not to overlook this region. Heitler had likened it to a monk's hood cut longitudinally through the centre and hanging apex down. Rosenbach made this dull space, clearing up in exercise and deep breathing, as distinctive between pleurisy and pneumonia. We must expect impaired resonance on the posterior wall above the fluid, for the fibrinous deposits from exudation collect there when the patient is in the recumbent position. Garland¹⁴ calls attention to the confused views caused by confounding the two physical signs of dulness (or impaired resonance) and flatness (absence of resonance), the latter only indicating the presence of fluid. If the differential diagnosis between the dulness on percussion over the dull triangle and the flatness over the fluid be not carefully made by delicate, light percussion, the two may easily be confounded and the fluid be thought to have arisen to a much higher level than it has. In some cases, owing to greater thickness in the walls and coverings of the chest and adhesions, it may be more difficult to draw nice distinctions in percussion sounds. This distinction can, however, be made if the percussion-stroke is used with proper delicacy and lightness, and a comparison made between the two signs, and not between them and vesicular resonance. If the percussion be strong, the vibrations are communicated from the resonant lung above the fluid, and deceive the examiner. The most effective manner of percussing is at right angles to the general direction of the curve, which is transverse across the chest. Thus examining, we have had ample opportunities of confirming the statement of Ellis and Garland that the curve line is never highest behind, even with the largest effusion. Wintrich and his German followers hold a different view. In moderate effusions it is highest in the axilla, from which point it turns downward posteriorly to touch the vertebral column at the interscapular region. In front it extends downward toward the sternum. R. Douglass Powell¹⁵ reports cases with drawings, showing that in typical cases the fluid does not take a water-level, "but a curve, having its convexity upward in the lateral region." When the effusion becomes excessive and fills the whole cavity, there is flatness on percussion everywhere. As the fluid subsides, however, from absorption or from mechanical removal, the distribution again resumes, to a greater or less degree, its previous shape. In moderate effusions there is, ordinarily, the dull triangle posteriorly, and Skodaic resonance under the clavicle in front in the anterior triangle. On the left side the lower limit of the effusion can be recognized by the flatness being in the shape of the arch of the diaphragm. In cases complicated by adhesions or by pathological changes in the lung itself the curve is changed, and in some the Ellis curve is straighter than in others. Adhesions form sometimes early in the disease. They mechanically interfere with the usual distribution of the fluid, as do catarrhal, tubercular, or pneumonic consolidations, and, indeed, emphysematous conditions. All these physical alterations of structure modify the elastic force of the lungs. According to Mohr's statistics, adhesions were wanting in 47 per cent. of the cases analyzed by himself. Garland's experiment of injecting glue and plaster of Paris, and subsequently cocoa-butter, into the pleura of living and dead dogs, and by moulds testing the curves formed, showed that if the dogs were suspended by the head the curve of flatness on percussion was very similar to the Ellis curve. On removing the casts after they had solidified, he found they closely corresponded to the shape and position indicated by the physical signs elicited before opening the chest.

⁵ Archives générale de Méd., 1843.

⁶ See Hyde Salter, Lancet, 1865; Powell, Trans. Roy. Med. and Chir. Soc., vol. lix.; W. N. Stone, Lancet, 1877; Le Gros Clarke, Roy. Soc. Med. and Chir., 1872.

⁷ Quoted by Garland, N.Y. Med. Journal, 1879.

⁸ Ibid.

⁹ Auscultation and Percussion, 1877.

¹⁰ Practice of Medicine, 1880, p. 130.

¹¹ Boston Med. and Surg. Journ., 1874 and 1876.

¹² Pneumono-Dynamics, New York, 1878.

¹³ N.Y. Med. Journal, Nov., 1879.

¹⁴ Pneumono-Dynamics.

¹⁵ Med. Times and Gazette, Oct., 1882.

Ellis's observations, and those of Garland with his experiments, have given us the most accurate views as regards the form of the curved line of flatness.

Nearly all modern authorities, including Peter, Gerhardt, and Paul Niemeyer, admit that fluids in the pleural sac assume more or less irregular curves, and not a hydrostatic, horizontal level. Whatever may be the nature and consistence of the effusion, fibro-serous, sero-purulent, or purulent, it does not behave in its distribution as if it were in an open vessel. But few writers, however, have troubled themselves to ascertain the causes of this apparently abnormal condition. They appear to have completely overlooked the facts that had been discovered in regard to the mechanics of the chest in connection with respiration and the circulation. Physiology had shown, especially by Marry's researches, the negative force of the lungs in aspirating the blood from the large venous trunks into the right side of the heart, and thus assisting the whole venous circulation. John Hutchinson¹⁶ drew attention to the antagonism existing between the expansion of the chest by muscular action and that of the lungs and the chest-walls. Hyde Salter¹⁷ showed that at the commencement of inspiration thoracic elasticity was favorable to inspiration, but as it advanced it became an expiratory force with lung-tension against further expansion. R. Douglass Powell¹⁸ drew further attention to these facts in connection with respiration and its modification by disease. Le Gros Clarke¹⁹ showed that atmospheric pressure over the abdomen kept the diaphragm in a condition of arched passive tension. He claimed that this negative force resisted the elasticity of the lung, and was the means of retaining the supplemental air in the lung and limiting the encroachment of abdominal organs.

¹⁶ Trans. Med. and Clin. Soc., 1846.

¹⁷ Lancet, Aug., 1865.

¹⁸ Trans. Clin. Soc., 1870.

¹⁹ Trans. Roy. Soc., 1872.

Douglass Powell in March, 1876,²⁰ in an elaborate and very suggestive paper on "Some Effects of Lung Elasticity," gives the practical bearing of these physiological facts in clinical medicine, as indicating a better insight as to the true mechanism and relative value in diagnosis of some signs of chest diseases, especially as to the importance of thoracic resilience as a force in respiration.

²⁰ Trans. Roy. Med. and Clin. Soc., vol. lix.

W. H. Stone early in 1877²¹ reported his experiments on sheep as to the amount of negative pressure exerted by the lungs, and concluded that it was equal to four to five inches of water. He moreover showed that even when the effusion was considerable in the pleural cavity, the lung still had contractile force sufficient to support two inches of water, so that to evacuate the fluid it was necessary to use external suction sufficient to overcome this lung-traction. In December, 1877, G. M. Garland²² gave to the public the results of his observations and experiments in regard to the form of the curve of distribution assumed by the pleural fluid, and its causes. He demonstrated that "the lung, by virtue of the strength of its contractility, takes the effusion along with it in its retraction, and that thereby assumes a pneumono-dynamic instead of a hydrostatic level," and that the Ellis curve was the true line of the upper level of the fluid in free, uncomplicated pleuritic effusion. Thus the physical cause of this condition was the retractile force of the lung lifting up the fluid. This is aided by the elastic resistance of thoracic walls and the negative pressure exercised by the effused liquid. The normal line on right side of demarcation between lung and liver is the letter S curve drawn out, the summit being high and the anterior branch correspondingly depressed. The modifications of this normal line in pleuritic effusions represent the effect of the negative pressure of the fluid. The decline in the Ellis curve toward the sternum shows that the elastic energy of the anterior part of the lung is feeble compared with that in the axillary region. "The layer of fluid is of less thickness above than at the base of the lung against the diaphragm. The upper surface takes its shape from the lung, which lifts it up by its retractility, and the effusion by its weight exerts a negative pressure upon the lung. The mass of the fluid is held when in moderate quantity in the supplemental space between the lower border of the lung and the diaphragm" (Garland). The atmospheric pressure from the interior of the lungs and from the exterior of the chest-wall keeps the costal and parietal surfaces of pleura together. Skoda, Powell, Stone, Homolle, and Quincke have shown the retractile energy of the lung, but the credit of drawing especial public attention to it, and of afterward elucidating the subject in its practical application to the study of pleurisy and in putting the whole subject upon a scientific basis, is unquestionably due to G. M. Garland of Boston.

²¹ London Lancet.

²² Pneumono-Dynamics, Boston, 1878.

ETIOLOGY OF FIBRO-SEROUS PLEURISY.—The etiology of acute primary pleurisy is frequently obscure. It may be hæmatic in origin, or it may be secondary, arising from pathological causes or antecedent disease. It is difficult to state with certainty whether it occurs in perfectly healthy persons, because there may be occult pathological conditions which cannot be appreciated. However, individuals are attacked with acute pleurisy who to all appearance, both to themselves and to those around them, are healthy. Authors differ very widely as to the disease being ever caused in healthy persons by exposure to cold. The older writers bring many proofs that such is the case. Ziemssen states that he could not trace the disease to exposure to cold in a single instance in 54 cases. Anstie holds the same view. Loomis states that in all instances where it (pleuritis) has followed upon exposure he has been able to find some predisposing cause. It is undeniable that pleuritis very frequently indicates the existence of some constitutional cachexia. Vital statistics show that it is more frequent in winter and spring than at other seasons. The vicissitudes of the weather, of temperature, and other atmospheric conditions have unquestionably a marked influence on the prevalence of the disease. Drafts of air passing over the chest or over other parts of the body, particularly when the subject is surrounded in-doors with a warmer atmosphere, wet clothing, intensely cold or a raw, damp atmosphere inhaled by persons coming out of a comparatively high temperature, especially if they are improperly protected by clothing, appear to be direct causes of primary pleuritis. If individuals thus exposed are debilitated by fasting, by such medicines as mercury, iodine, iodide of potassium, by over-exertion, by free perspiration, or by previous disease, they will be still more liable to contract the disease. Overheated apartments, especially at night during the sleeping hours, frequently are the direct cause of acute pleurisies or of croupal pneumonias. These cases are of such frequency that we are obliged to differ from the high authorities who consider the pleura as free from acute idiopathic inflammations as is the peritoneum.

There are numerous predisposing causes which, when examined, are found to lessen the power of resistance of the organism. Senility is an important one; so is childhood. Formerly it was supposed that pleurisy rarely attacked children. This view was prevalent because the disease often escaped detection. Of all chest diseases in children, mistakes in diagnosis are most frequently made with pleuritis.

We might suppose that this disease would be frequently met with in children, because they are oftentimes ill protected against the vicissitudes of the weather; besides, their feebleness predisposes them to feel keenly such shocks to their powers of endurance. The disease may occur at any age, and is more common under two years than was formerly supposed (Eustace Smith). Empyema is the form most frequently found in children, the effusion soon becoming purulent in them. Ziemssen tabulates the ages of 54 children whom he treated for primary pleuritis: first year of life, 3; second, 1; third, 7; fourth, 4; the remaining 39 between the ages of five and sixteen years.

Pleurisies are more frequent in males than in females, in the proportion of 5 to 3, owing to the greater exposure of the former to the exciting causes, and notwithstanding their stronger organisms. Among the predisposing causes we must not fail to give due importance to the malhygienic conditions which so powerfully impair the forces of the body. Prominent among these are sedentary occupations, imperfect alimentation, city lives, overwork of mind and body, deficient sunlight, overcrowded houses, and dampness of soil. These and many others interfere with the formative forces and lessen the power of resistance to exciting causes of pleurisy.

Traumatic pleurisies are caused by injuries or other mechanical causes. Injuries to the walls of the chest, contusions, burns, scalds, and lacerations which are superficial, frequently give rise to primary traumatic pleurisies. If the ribs are fractured, or blood, air, or pus gets into the pleural cavity, we have what has been termed secondary traumatic pleurisies.

Secondary Pleurisies.—The exciting causes of secondary pleurisies are numerous. They are pathological, and more readily appreciated than the causes of primary pleurisies. Owing to the anatomical connection between the lungs and the pleura, diseases, acute and chronic, of the former frequently give rise to pleurisies.

Among acute affections of the lungs, the several forms of pneumonia are the most frequent causes of pleurisies. Fraentzel states that we always find fibroid pneumonia associated with pleurisy as pleuro-pneumonia, even when the inflammation of the lung-tissue itself does not reach the pulmonary pleura. There is an intimate connection also between caseous pneumonia and pleurisy. This is sometimes quite circumscribed, and leads to adhesion of the pleural layers at the affected spot; sometimes it is diffused over a great part of the pleura, and it is then not infrequently associated with a considerable outpouring of different kinds of effusions. Catarrhal pneumonia rarely occurs without secondary pleuritis (Fraentzel). Pleurisies may also be caused by violent bronchial catarrhs or by hemorrhagic infarctions.

There are cases where, from the presence of tubercles under the parietal pleura, inflammatory action is set up and pleuritis ensues. Vomicæ bursting into the pleural cavity or tubercular perforation in pulmonary phthisis gives rise to pleurisies. Inflammation of the liver, cellular abscesses, and pericarditis may cause secondary pleurisies. Diffuse peritonitis is often complicated with pleurisy, the inflammatory process extending from the peritoneum to the pleura, through the diaphragm, by means of the serous canaliculi. This frequently occurs in puerperal peritonitis, and is almost invariably fatal (Fraentzel). The author had a case of fatal peritonitis in a man sixty-five years of age, which originated from an empyema. There was no rupture nor perforation of the diaphragm, so that the inflammatory process must have extended from the pleura to the peritoneum by means of these canals. Malignant diseases of the mammæ, oesophagus, lungs, and hydatids produce secondary pleurisies. Eruptive fevers, especially scarlatina, variola, typhoid fevers, are among the most frequent pathological causes of secondary pleurisies. It is doubtful whether their germs pass through the circulation or through the lymph-canals, and produce local inflammation of the same nature as their own, or whether they render the pleura more sensitive to shocks of various kinds. Rheumatism, gout, and nephritic diseases are frequently followed by pleurisies. As we have rheumatic endocarditis and pericarditis, in like manner there are rheumatic and uræmic pleurisies. Alcoholism and pyæmia, septicæmia and the puerperal state, especially during the first month after parturition, are powerful predisposing causes of pleurisies, as are also any morbid conditions of the skin, kidneys, or intestinal canal which interfere with their eliminating or depurating functions. This includes all forms of blood-poisoning. Hutchinson says that children suffering from congenital syphilis are especially liable to serous inflammations, and that pleurisy is in them a not uncommon cause of death. Niemeyer denounces the impropriety of giving the name of secondary pleurisy to all cases of pleurisy occurring in subjects with broken-down constitutions or weakened by other diseases. We often meet with such cases when Bright's disease exists. Niemeyer holds that it is not dependent upon renal disease, but upon the increased predisposition for all kinds of inflammatory disease. A trifling cause will sometimes excite a pleurisy when the resistance of the organism is materially lessened by previous disease.

SYMPTOMATOLOGY.—Rational Symptoms.—These vary according to the severity of the disease. Ordinarily, attacks of acute pleurisy come on suddenly, and it rarely happens that there is any appreciable feeling of malaise. Usually the first symptom is an acute pain in the side, which alarms the patient. The significance of this severe stitch is generally appreciated, as the subject at once calls attention to his sufferings. The pain is sharp, cutting, stabbing, that causes him to hold his breath as long as possible. When he is forced to breathe, it is by the action of the superficial intercostal muscles. He endeavors to fix his diaphragm and hold it rigid in order to prevent the surfaces from coming in contact and thus increasing his agony. This causes him, necessarily, to breathe frequently in order to get sufficient air. The greater the intensity of the pain, the more frequent and shorter are the respiratory acts. The dyspnoea and the effort to lessen the pain give the patient an expression of great suffering. Usually, the pain is felt over a circumscribed spot under the nipple of the affected side. Sometimes it is experienced as low as the sixth or seventh intercostal space, but rarely posteriorly below or under the scapula or in the axilla. In children the seat of pain is not always in the chest. Their lower intercostal nerves are often affected, and the sensation being referred to the ends of these nerves where they ramify on the abdominal wall, the pain is often seated in the abdomen. Such being the case in children, care must be taken not to confound pleurisies in them with epigastric or hypochondriac irritations. In adults, the pain is rarely located in the abdomen when it is caused by pleuritis in the lower portion of the pleural surface or in that part covering the diaphragm. In children there is also much tenderness on pressure. In what has been termed subacute or latent pleurisy the stitch may be entirely absent. Valleix found pain in 40 cases out of 46. Sometimes it is absent in ordinary breathing, but is brought on by sneezing or violent coughing or strong percussion. In severe cases, the effusion coming on rapidly, the pain may subside by the second day. If the effusion comes on slowly, the pain may keep up for six or eight days. The continuance of the pain always shows that the inflammatory process in the pleura is continuing, although the pulse and the temperature may be normal. The renewal of the sensation of pain after the pleurisy has passed away justifies us in the conclusion that there is a return of the inflammation. When the pain is agonizing, with signs of collapse, it is indicative of a secondary pleuritis arising in the course of a chronic caseous pneumonia. Tubercular and purulent exudations are distinguished from the sero-fibrinous by the longer duration and the greater intensity of the pain—two circumstances which afford a reliable basis for the diagnosis of such cases. The severe pain in pleuritis is probably caused by the inflammation extending to the sheaths of the nerves and to the nerve-texture itself (neuritis), as well as by inflammation of the pleura itself.

Severe attacks of acute exudative pleurisy may commence with a severe initiatory chill, followed by high fever, but ordinarily there are in pleurisy slight rigors, initial in their character. Some authors question whether they are not caused by the limited points of pneumonia connected with the pleuritis. If the rigors occur at regular intervals for days, we have reason to suspect tubercular trouble or empyema. The temperature does not run any regular course in pleurisy, nor does it bear any fixed relation to the pulse and the respiration. It usually varies from 100° to 102° F. In violent, acute cases it may reach 105° F.

Careful observations with the thermometer give us important indications by which to diagnose the nature of the pleurisies. In those of a tubercular nature the temperature continues high, from 100° to 104° F., for weeks. When the effusion becomes purulent the temperature becomes like that of hectic fever—in the morning normal, and in the evening rising to 102°, or even 103½° or 104° F. Sometimes the temperature is one or two degrees higher on the diseased side than it is on the healthy side.