Chapter XXXIII: Part 33

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 {481} 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.

[Footnote 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 {482} 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.

{483}

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 {484} 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 {485} 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 {486} 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.

[Footnote 1: _De la Thoracentèse par Aspiration dans la Pleurisie aigue_, p. 42, Paris, 1878.]

Chemical Character of Effused Fluid.--Mehu[2] 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 {487} 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.

[Footnote 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 {488} 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'Heilly[4] 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.

[Footnote 3: _Thèse de Paris_, 1845.]

[Footnote 4: _Nouveau Dict. de Méd. et Chir._, Paris, tome xxviii., 1880.]

Since Damoiseau's first paper[5] 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 English[6] 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 Ferber[8] maintain that the line depends upon the position of the patient early in the disease. Gee[9] 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 Flint[10] 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 papers[11] 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 {489} 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. Garland[14] 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 Powell[15] 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. {490} 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.

[Footnote 5: _Archives générale de Méd._, 1843.]

[Footnote 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.]

[Footnote 7: Quoted by Garland, _N.Y. Med. Journal_, 1879.]

[Footnote 8: _Ibid._]

[Footnote 9: _Auscultation and Percussion_, 1877.]

[Footnote 10: _Practice of Medicine_, 1880, p. 130.]

[Footnote 11: _Boston Med. and Surg. Journ._, 1874 and 1876.]

[Footnote 12: _Pneumono-Dynamics_, New York, 1878.]

[Footnote 13: _N.Y. Med. Journal_, Nov., 1879.]

[Footnote 14: _Pneumono-Dynamics_.]

[Footnote 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 Hutchinson[16] 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 Salter[17] 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 Powell[18] drew further attention to these facts in connection with respiration and its modification by disease. Le Gros Clarke[19] 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.

[Footnote 16: _Trans. Med. and Clin. Soc._, 1846.]

[Footnote 17: _Lancet_, Aug., 1865.]

[Footnote 18: _Trans. Clin. Soc._, 1870.]

[Footnote 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.

[Footnote 20: _Trans. Roy. Med. and Clin. Soc._, vol. lix.]

W. H. Stone early in 1877[21] 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 {491} fluid it was necessary to use external suction sufficient to overcome this lung-traction. In December, 1877, G. M. Garland[22] 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.

[Footnote 21: _London Lancet_.]

[Footnote 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 {492} 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 {493} 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 {494} 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.

As in other inflammations, the pulse in this disease varies considerably. The researches of H. Newell Martin show that there is ordinarily a constant ratio between the pulse-rate and the temperature. If the temperature be high (over 102° F.), we must expect the pulse to be as frequent as 115 or even 120 per minute. In mild cases, where the temperature does not go beyond 99.5° or 100° F., the pulse will not exceed 90 to 96. In slight cases, where the fibrinous exudation is very limited, the pulse may not exceed 80. In tubercular and purulent pleurisies the pulse may vary between 100 and 120. When there is a relapse the pulse advances as the temperature rises. Anstie has called attention to the quality of the pulse, which follows a uniform course on the whole, regard being had to the general vital condition of the patient. In the first stage of acute pains, with more or less tendency to shivering, the pulse, as tested with the sphygmograph, presents the algid form--_i.e._ the pulse-waves are very small and nearly devoid of secondary markings. As soon, however, as flushing of the face occurs, and a general sense of burning heat of the skin, the pulse passes to the true pyrexial type; the waves become large and dicrotic. The sphygmograph uniformly shows that the large and somewhat bounding pulse is always less resistant than that of health.