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.
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.
Jaffé-Duval23 states that he found the temperature of the diseased side raised above that of the healthy chest. Subsequently, Peter,24 after a long series of researches, reported some very important results as to the localized parietal temperature in cases of pleuritic effusions: (1) He found that the parietal temperature, as tested by the thermometer, is always higher on the side of the pleurisy than that of the body as tested in the axilla; (2) that the elevation of the temperature increases as the effusion augments, the highest local temperature corresponding to the period of secretory activity of the inflamed pleura; (3) the rise affects both sides, but is greater over the diseased pleura; (4) the temperature falls by degrees as the effusion is reabsorbed—less on morbid side; (5) the absolute elevation of local temperature is greatest in the sixth intercostal space; (6) after paracentesis the parietal temperature is increased: this falls in a few hours where the effusion is not re-formed, but when such is the case it continues for some days. This local rise of temperature, he considers, is from hyperæmia and cell-production, caused by the traumatism from the needle added to the already-existing hyperæmia. This excessive congestion, caused by the accumulation of blood occurring when a large quantity of fluid is rapidly withdrawn, produces the syncope, pulmonary congestion, consecutive albuminous expectoration, the pain, and the oppression amounting sometimes to suffocation, and occasionally ending in death.
23 Thèse de Paris, 1875.
24 La France médicale, 4th May, 1878.
At the commencement in acute cases the respiratory acts become very frequent, even going to 40 or 50 per minute. They are short, interrupted, and superficial. Their frequency makes up for their incompleteness in furnishing sufficient air. The painfulness of each act forces the individual not to expand the walls of his chest more than he can avoid. Moreover, the high fever in itself produces frequent respiration. As the temperature falls the respiration becomes less abnormal. If the effusion forms rapidly, the patient may become oppressed, even when the quantity is not large. If it is thrown out gradually, the breathing is not so much interfered with until a large quantity forms, the organism becoming accustomed to the interference with the play of the lungs. The strength of the individual and the activity of his nutritive functions are materially lowered. Sometimes he breathes with difficulty, especially when he takes active exercise. The dyspnoea is very painful and alarming. The aëration of the blood is so materially interfered with that there results a large quantity of carbonic acid, which irritates excessively the respiratory nerve-centres.
During the acute stage the patient sometimes lies on his back, but more frequently on the well side, and exceptionally on the diseased side. He avoids lying on the side where the inflammation exists, because the weight of his body increases the pain. I have, however, seen patients who would persist in lying on the painful side and supporting it with their hand. It sometimes happens that a patient lies on the affected side, and will not move, because the movement gives him such acute pain. Ordinarily, he prefers to lie on the healthy side, even after the fluid has been poured out to a moderate degree, because his pain is less. When, however, the effusion has become great enough to deprive him of the use of the diseased side, he instinctively turns on that side, so as to avoid the weight of the fluid pressing upon the lung on the sound side. Moreover, he wishes to expand as much as possible the side whose respiratory force now needs to do double work. This change of position in patients has an unmistakable significance. It shows that the sufferer is aware that he is more comfortable lying on the diseased side. His physician's attention is drawn to the condition of the chest as influenced by the increased quantity of fluid pressing the air out of the lung.
Cough is not a constant symptom in pleurisy, but ordinarily it occurs at some stage of the disease. It is short, dry, and suppressed in character. It is painful, and therefore is avoided when possible, especially previous to the effusion. It disappears generally about the fourth or fifth day, when the effusion has attained a considerable amount. The cause of the cough has been generally supposed to be the exalted sensibility of the inflamed pleura, but Nothnägel maintains that such is not the case. Fraentzel holds that the cough is caused by the strain on the lung-tissue and the finer bronchi when there is a slight effusion. Cough brought on by change of position is one of the characteristic symptoms of large effusions into the pleura. If the lung is completely compressed by the pleuritic effusion, then no actual strain on the alveoli or the bronchi can exist. In such cases there is no cough, but it returns when the effusion decreases in quantity, and quite violently, if this occurs suddenly, as, for instance, in puncture of the chest (Fraentzel). In the latter case the cough is probably caused by the rush of blood and the sudden expansion of the chest.
Slight frothy expectoration may exist, but ordinarily there is none whatever, unless from bronchial catarrhal complications. In that case sero-mucous fluid is expectorated in small quantity. If it becomes viscid and tinged with blood, it is caused by pulmonic involvement.
In empyema, if the expectoration becomes purulent, we ought at once to suspect the presence of some circumscribed spots of necrosis of the pleuritic covering of the lung, which have allowed the pus from the pleural cavity to filter through the lung-tissue. By careful physical examination of the chest we can ascertain whether there has been any diminution in the quantity of fluid. When, as sometimes occurs, there is actual perforation of the lung, the pus from an empyema comes in quantity, through the bronchial tubes, out of the mouth. Patients may sink from exhaustion following this discharge, or if the discharge be excessive it may fill up the bronchial tubes too rapidly for its removal by expectoration, thus causing suffocation. This danger is increased if the discharge takes place during sleep.
Cyanosis is a symptom which should cause serious alarm, for it shows that the effusion is so great as to interfere very materially with the due arterialization of the blood. When the cyanosis is accompanied by pallor, coming on suddenly in the course of a pleurisy, we may infer with considerable probability that there is a hemorrhagic exudation. But if the paleness comes on slowly during weeks or months, it may also be dependent on a simple sero-fibrinous effusion (Fraentzel). Protracted cases of effusion, especially if purulent, are associated with emaciation and loss of strength. There may exist more or less oedema of the lower extremities and of parts of the body where the patient lies down, as we have in the chronic diseases of the chest. When this oedema is limited to the affected side of the chest, whether it be extensively developed and spread over the entire half of the chest or confined to certain spots, it almost invariably justifies the diagnosis that the effusion is purulent. The effusion may, however, be purulent without the presence of this localized oedema. Occasionally, cases are met with of effusion in the left pleura where there are visible and palpable systolic pulsations in the intercostal spaces arising from the impulse of the heart or of the larger blood-vessels passing through the fluid.
Physical Signs.—Perhaps in no other disease of the chest are physical signs so important for purposes of diagnosis as they are in pleurisy. Even at the very beginning of the attack they give us valuable information. In later stages, when the effusion is in the pleural sac, they furnish, as we shall hereafter show, trustworthy data for diagnosis, prognosis, and also very valuable indications for treatment. There is no other disease of the chest where the physical changes made by the inflammatory process are so pronounced and so accessible to the senses of hearing, sight, and touch. The physical signs are so marked that, almost by themselves, they give us the pathological condition. They have been so carefully studied, and their correlative value insisted upon, that they are readily interpreted. One is often tempted to rely too much upon them to the exclusion of the proper consideration of the general symptoms.
As the physical condition of the pleuræ varies much in the several stages of the disease, the physical signs must necessarily vary accordingly.
At the very beginning of the attack the sensibility of the pleuræ is augmented by the inflammation. Consequently, on inspection, it will be observed that the patient is careful to avoid the pain caused by the inflamed pleuræ rubbing together. He not only tries to avoid using the ordinary muscles (especially the intercostals) for enlarging the capacity of the lower portion of the chest, where the disease is generally found, but he retracts his chest and keeps the pleuritic side almost motionless. The well side has double work to do, and is seen to expand more fully. The patient will frequently press the lower ribs in, on the affected side, with his hand, or he will lie on that side, so as to control the expansion of the chest, or he will lie on the healthy side and bend his body over.
The respiratory movements are marked by an irregular and jerking rhythm, and are quickly made. The pain felt on inspiration is of a catching or stabbing character, and produces dyspnoea, the subject struggling for air. The diaphragm is held as fixed as possible, so as to prevent the movement of the inflamed surfaces over each other. The patient restrains as far as possible the respiratory movements, especially those of expansion and retraction. This is the condition not only at the initiation of the disease, but at the next stage, that of effusion. We meet with the same painful respiration also in dry tubercular pleurisy. Mensuration shows that the sound side of the thoracic cavity is slightly enlarged by the extra work it has to perform in the first stage. The elevation movement is noticed to be restrained when the effusion has increased to the extent of overcoming the retractility of the lung, for the diaphragm is no longer drawn up by the lung, and the effusion rises and separates the parietal and pulmonary pleuræ. The diaphragm bags from the quantity of fluid, and contracts but feebly. This condition forces the liver and the spleen down in the abdominal cavity. Gradually the jerking rhythm ceases as the effusion advances, and the characteristic stitch in the side disappears. If the effusion increases until it reaches as high as the second rib, the respiratory movements are scarcely perceptible to the eye. When it reaches its maximum, the clavicle, they appear to be arrested, but the vertical diameter is slightly altered by the action of the intercostal muscles as they endeavor to elevate the ribs, and of the diaphragm as it feebly contracts and relaxes. The pleural cavity, which in health is lubricated by about two drachms of moist serous secretion, is frequently filled to the extent of seventy, eighty, or more—even to one hundred and twenty—ounces. We cannot wonder that it should be changed in shape and diameter. All available space is filled with the fluid, and yet the serous membranes continue to throw out the secretions. The lung must lose in size by its retractile force, and when that is overcome the fluid must press in all directions. The fluid gradually rises from the surface of the pleura over the diaphragm, and the lung, by negative pressure, draws it and the fluid upward. As long as the diaphragm is arched, although the lung recedes before the effusion, it is not really compressed. When, however, the diaphragm yields and falls from the large quantity of fluid, then the fluid conquers the lung. Ordinarily, the fluid, when in excessive quantities, presses upon the lung and the bronchi until it forcibly expels the air; the lung is compressed against the vertebral column, occupying a very small space corresponding to the surface under the scapula, often not larger than from three and a half to four inches square. Inspection shows that the spaces between the ribs become flattened out, that the ribs are more widely separated, and that the spaces themselves frequently bulge. The first observable indication of great distension of the pleural cavity, sufficient to cause intra-thoracic pressure, is the depression of the diaphragm, and next the flattening of the spaces between the ribs. This last is followed by increased pressure, which causes more general and marked enlargement. "This levelling of the intercostal spaces is due partly to paralysis of the intercostal muscles from serous inflammatory infiltration, and partly to the limited range of movement now possessed by the lung, which is reduced in volume by the effusion, and is no longer in contact with the thoracic parietes" (Guttman). This is especially noticed in children and young persons before the ribs become firm and resisting, the negative pressure exerted by the lung being in part annulled by the presence of the fluid. The diaphragm is notably depressed, and pushes the liver, the spleen, and the stomach below their usual point. So great is this centrifugal force that the heart's impulse may be felt in the epigastrium. The heart, when the effusion is on the left side, is frequently found over to the right of the sternum, and, in extreme cases, even in the right axilla. When the effusion is on the right side, the mediastinum is drawn over with it, and the heart is forced to the left until the apex-beat is perceived as far as one and a half inches to the left of the line drawn through the nipple, or, in some cases, to the left axilla. This rarely occurs unless we have fluid intra-thoracic pressure on the diseased side in addition to lung-traction of the healthy side. Even the costal pleura, projecting above the clavicle, may yield to pressure. Inspection reveals to the observer these striking physical alterations. Hippocrates did not fail to notice them.
1st. Mensuration shows that the semicircular, antero-posterior, and vertical measurements of the side are generally increased. According to Douglass Powell, the total circumference of the chest is always increased in effusion. 2d. Except in children, the bulging of the intercostal spaces does not occur until after the adjacent organs have been displaced by the fluid. When the effusion is large, it becomes evident, by inspection and by pressing the hand over the sides of the chest below the armpits, that there is almost immobility of the diseased side. We insist upon the importance of daily and repeated comparative measurements of the two sides as aids to diagnosis and prognosis in pleurisy. A full inspiration or a prolonged expiration will sometimes show a marked difference by measurement when it is not discovered during ordinary breathing. Woillez's cyrtometer, as perfected by Samuel Gee, is the best instrument for testing the circumference of the chest, and a pair of callipers for the diameter. The cyrtometer tracings give us the altered shape as well as circumference. It is especially valuable in the diagnosis of local empyema from basic pulmonary cavities. Care should be taken not to confound congenital deformities in the shape of the chest, such as the alar, flat or pigeon-breasted, or rachitic, with alterations produced by internal disease. It must also be borne in mind that the semi-circumference of the right side is normally greater by one-quarter to half an inch than that of the left side. By inspection of cases where large effusions have remained for long periods of time slowly absorbing—often, perhaps, not recognized—we discover marked unilateral retraction of the chest-walls, with torsion of the spine and shoulders. The adhesions preventing the lung from expanding, the alveoli become obliterated, and we have, in fact, atelectasis of the lungs. This is particularly the case in children, where the disease prevents the proper development of the side, the healthy side becoming, from supplementary work, more enlarged. Care must be taken not to confound with these the anatomical depressions met with sometimes in the anterior wall of the chest, especially at the lower portion of the sternum. The amplification of the chest takes place, to a greater or less degree, at its lower portion as soon as an appreciable quantity of liquid collects, long before it is possible to have any intra-thoracic pressure. The lung by its elasticity collapses, and the fluid is drawn upward in contact with the lung. The thoracic wall, consequently, has not, at that point, the retractile force of the lung to counteract its excentric resilience. It is not then drawn in in expiration by the lungs, while it is continually being drawn outward in inspiration. The lung-traction of the parietes of the chest is feeble from the diminished size of the lung. The greater the amount of fluid, the less lung-tension; consequently, the greater the enlargement of the chest, as shown by the cyrtometer. If the lung is contracted to its utmost limit (one-third of its size, according to Powell; one-eighth, according to Rokitansky), then there could be no suction force exercised by it upon the parietes of the chest, for, being disabled in its elasticity, it literally has no power. The whole parietes of the chest on the diseased side have nothing to antagonize their elasticity, so it is kept enlarged. In addition, at this stage the fluid of itself presses against the walls of the chest in all directions.
The elastic pulmonary tissue is always, to a certain extent, on the stretch. It is striving to pull asunder the pulmonary from the parietal pleura; but this it cannot do, because the air can have no access to the pleural cavity. The five mm. of mercury elasticity of the lungs can be increased by a distension of the chest from a forcible inspiration to thirty mm. of mercury. Anything which lessens this elasticity of the lungs takes off so much from the force which interferes with the rebound of the thoracic resilience, and consequently increases the circumference of the chest. Such is the case in emphysema, oedema of the lungs, pulmonary congestion, and, curious to relate, at the outset during the pyrexial stage of acute diseases, such as pneumonia, variola, bronchitis. The enlargement of the thoracic circumference is appreciable. It, however, gradually decreases and becomes normal. This yielding of the thoracic walls is attributable to temporary engorgement of the lungs, lessening their retractile force.
At the very commencement immediate results of percussion are negative, but by delicate taps over a pleximeter there is a sound at the margins, owing to the deficient expansion, of impaired resonance and of higher pitch, and the vibrations are less full. There is also a sense of pain, owing to the increased sensibility of the costal pleuræ. As the fibrinous coatings form, the sound becomes less and less full and the normal vibrations of sound are less diffused, more circumscribed, giving to the finger, used as a pleximeter, a sense of resistance from the diminished elasticity of the lung. This is especially the case at the base over the attachment of the diaphragm. As the effusion rises from the base, the sound on percussion becomes flat. The fluid being a non-resonant body, the vibrations of the percussion taps do not extend. The sound is of high pitch, but not resonant. It has been properly designated by Skoda an empty sound, for it conveys to the ear the condition beneath, which is one of perfect airlessness. It is not simply a dull sound or one where there is not the normal resonance, but it is destitute of all resonance: it is absolutely flat. The confusion of dulness with flatness has in the past led to erroneous conclusions as to the line showing the level of the fluid in pleurisy. As high an authority as Woillez, in reference to fluid flatness, speaks of dulness as complete, absolute, or very incomplete sub-dulness! The muscular coverings of the walls of the chest or unusual amount of adipose tissue or pleuritic coatings or bands produce impairment of resonance, and sometimes marked dulness on percussion. But when the percussion wave penetrates to the lungs, there is more or less resonance. When the lung is solid from pneumonia or tubercular deposits, the sound is often very dull, but rarely flat, because it seldom happens that all of the alveoli are filled up, and even when they are the vibrations are communicated to the bronchial tubes which contain air, and in this way there is some resonance. We call particular attention to the importance of these distinctions and to the necessity of light and delicate percussion in order to test the resonance or non-resonance of the thoracic cavities. If the percussion be strong, the vibrations are conveyed by the thoracic walls to the portions where there is no fluid, and thus we have impaired air-resonance, and not flatness. We have frequently seen errors of diagnosis in cases of pleurisy owing to the physician percussing with too much force. To secure accuracy, Garland25 lays down the simple rule of percussing with great care and always in straight lines, and of percussing each line to its terminus before taking up another. Powell26 compares the peculiar flat percussion sound of pleuritic effusion to that elicited on striking against a brick wall. The flatness is characteristic and more marked than the dulness of lung-consolidation. If we are not careful to make the distinction between impaired resonance and non-resonance, we may easily draw erroneous conclusions as to the rise and extent of the fluid in the chest. We have shown elsewhere (Pathological Anatomy of Pleurisy—[Distribution of Fluid]) that, as the fluid collects in the cavity, the lung contracts before it. The border above the level of the liquid contains less air, the capillary circulation is less active, and frequently there is more or less oedema, owing to its being the most dependent portion. These physical conditions impair, to a greater or less extent, the pulmonary resonance. Thus at the base above the fluid we might, on reflection, naturally expect some dulness on percussion, lessening as we recede from the fluid. Several observers have called attention to the impaired resonance over the lowest portion of lung posteriorly when the person is standing. Garland27 termed it the dull triangle. Heitler28 of Vienna observed this same condition in that locality, and likened it to a monk's hood cut longitudinally through the centre and hanging apex down. Rosenbach29 of Breslau noticed that this non-resonant triangle in pleurisy would often clear up on exercise or by breathing; this fact he considered distinctive between pleurisy and pneumonia.
25 Loc. cit.
26 Med. Times and Gazette.
27 Ziemssen's Supplement.
28 Wien. med. Wochenschr., 1878, quoted by Garland.
29 "Ein Beitrag zur phy. Diag. der Pleur.," Berlin klin. Wochenschrift, 1878, No. xii.
Although the fluid first collects over the posterior portion of the diaphragm, flatness on percussion is first observed over the axillary portion of the diaphragm, because, as explained by Calvin Ellis, the conditions there are more favorable for percussion. As the effusion increases the line of flatness, when the patient is in the upright position, advances, not directly up the back and horizontally across the chest, as was formerly supposed, but across the back in a curve reaching its highest point in the axilla, from which it descends toward the sternum.30 R. Douglass Powell31 says the upper margin of the effusion in typical cases is not a water-level, but presents a curve having its convexity upward and in the lateral region. Since the attention of the author was first called to a careful examination of the curve of flatness as ascertained by light and delicate percussion (in the erect position), he has found it to be more or less of an Ellis curve at an early stage of the effusion. The line is sometimes better defined than at others. All observers, however, must acknowledge that at the stage of the disease when cases of chronic fibro-serous pleurisy are first seen the letter S curve is not well marked. Mason states that although in some of his 200 cases this peculiarity was observed, in others the line was horizontal. When fluid fills the chest to excess and overcomes the elasticity of the lung, it gives flatness on percussion high up, even to the clavicle, and behind to the supra-spinous fossa. The fluid filling the cavity, the line of flatness becomes nearly horizontal. Then it is that percussion reveals the displacement of the diaphragm and abdominal organs. On removing the excess of fluid by aspiration or by absorption, this curved line reappears, and continues as previously.
30 See section on Pathological Anatomy of Pleurisy, distribution line.
31 London Med. Times and Gazette, Oct., 1882.
Contrary to the general belief, when the fluid is moderate in quantity change of position of the patient modifies but little the area of flatness, owing to its being retained between the lung and diaphragm. Woillez32 noticed slight mobility (never more than to the extent of one intercostal space) only in 5 of his 82 cases. He concluded that the conditions were very different from what they were in ordinary vessels outside the body. Woillez does not attempt to explain what these conditions are. Skoda acknowledged that in the majority of cases the fluid does not change its position as the patient moves. Skoda and Wintrich attribute the non-movement of fluid to adhesions. Garland, and subsequently W. H. Stone and Douglass Powell, showed that the effusions were immovable when in moderate amounts, because they were kept so by the retractility of the lung, and that the large amounts were movable because the retractility had been overcome by them. When in large quantities the fluid accumulates in depending positions of the chest. Later on in the disease, adhesions and bands mechanically interfere with the line of flatness; or if there be any disease of the lung interfering with its retractive force, the fluid may not take its usual line. These peripheral adhesions frequently occur at the upper margin, and are sometimes wavy and irregular. They often occur early in the disease, and prevent in a marked degree the fluid from yielding to the negative lung-traction.
32 Mal. Aigues des Org. Resp., Paris, 1872.
By these bands the pleuritic fluids become sacculated in different parts of the thorax—between the lungs and the walls of the chest, between the diaphragm and lungs and the pericardium, the mediastinum, the vertebral column, and actually between the lobes of the lung. Fraentzel holds that the percussion sound is dull over the thorax whenever the effusion attains the depth of from one inch and a half to two inches between the lung and the chest wall. Garland by his experiments on dogs shows that the fluid does not thus rise between the lung and parietes, except a very thin layer, by capillary attraction, not sufficient to cause flatness on percussion or to interfere with the expansion of the lung unless the amount is very excessive, and not until the lifting power of the lung is completely overpowered. When the effusion is very large, it fills up the posterior portion of the thorax, compressing the lung against the uppermost portion of the spine or the mediastinum. The percussion sound is absolutely flat, provided the force of the blow be not too great; in that case the ribs are thrown into vibration or the vibrations extend to the sound lung. This materially impairs the dulness and may lead to error of diagnosis.
The lung may be prevented from contracting by reason of various kinds of adhesions or by means of widespread infiltrations, by emphysema, and by laryngeal stenosis. In such cases, as the effusion increases, it quickly rises in the thinner layers without displacing the organs. Fraentzel warns us that sometimes, in left-sided effusions, the lung having become adherent to the heart, the heart is drawn back with the lung away from the wall of the chest, and then it cannot be felt anywhere: the absence of the apex-beat and the feebleness of the heart-sounds may lead us to assume, incorrectly, that there is effusion in the pericardium. If the fluid collects between the external layer of the pericardium and the mediastinum, the heart is surrounded and pressed by the pleuritic effusion.
The Skodaic resonance is a remarkable tubular quality of resonance heard on percussion when the effusion extends up to the fourth rib or beyond it, nearly filling the pleural cavity. It is a high-pitched, long vibration, semi-tympanitic sound, rarely absent when, from an effusion, the lung is retracted to a very small size, but still contains some air. It is most frequently found anteriorly under the clavicle, near the sternum, because to that point the lung withdraws as long as it has any retractility left. If the air be forced out of the lung by pressure, this sound is no longer heard. Flint called this peculiar tympanitic sound, heard above the level of the fluid in pleurisy, by the descriptive name vesiculo-tympanitic resonance. The vesicular, though feeble, is combined with the tympanitic quality, and the intensity of the resonance is abnormally increased. This subclavicular tympanitic sound is not peculiar to pleurisy. It exists in pneumonia preceding hepatization, and was noticed by Hudson, Graves, and Williams before Skoda called attention to it in pleurisy. Skoda's explanation of this phenomenon is now generally accepted—namely, that it comes from diminished tension of the lung-tissue, caused by diminution in the quantity of air, and consequently relaxation of lung-tension. The residuary air in the alveoli does not mix properly with the tidal column: it is indeed pent up by the narrowed diameter of the minute bronchi. Thus it becomes surcharged with carbonic-acid gas; this relaxes the air-sacs and lessens their tension. In fact, the percussion sounds are invariably tympanitic when the parietes of the organ which contains air are not stretched. When they are firmly stretched, the sound elicited by percussion becomes less and less tympanitic, and finally dull: such, we know, is the case in striking a drumhead. The chief characteristic of the sign relates to the quality of the sound; the resonance is nearly devoid of vesicular quality. A resonance absolutely non-vesicular is always tympanitic (Flint). This tympanitic sound is so constant under the clavicle that although it may be from other causes, its appearance would lead us to suspect effusion, especially in children. It is not only at the apex, but wherever the lung shrinks from pleuritic exudation and loses in tension, the percussion sound has the tympanitic quality. We find it occasionally near the sternum, and sometimes in sacculated effusions we observe it in different parts of the thorax. Traube, and subsequently Fraentzel (Ziemssen's Cyc.), called attention to the fact that sometimes a long expiration would cause a temporary abolition of this tympanitic sound at the apex. Their explanation is that the sound is heard over the compressed lung. Garland urges that this explanation cannot be a satisfactory one, for a certain amount of pulmonary expansion is essential to the production of tympanitic resonance.
This exaggerated resonance elicited by percussion has received its name from the eminent German who wrote so much about it; but it did not escape the accurate ear of the discoverer of percussion, Avenbrugger, who clearly defined the subclavicular tympanitic resonance in pleurisy.33 Skoda's sign, however, is not unique, for observation proves, when the lung is contracted with fluid below, that there are several varieties of resonance. Notta,34 who was not aware of Skoda's ideas, describes the sound as hydroaérique where the lung is above the level of the fluid. Roger,35 who called especial attention to Skoda's views, admitted that there were several varieties of tympanitic resonance heard above the fluid. He compares them to those heard on percussing over the stomach of the cadaver. Woillez36 describes five varieties or types of sonorousness, according to their intensity, their tone, and their quality. He noticed these under the clavicle at different points above the liquid—ordinarily on the level of the second or the third rib. (1) The most common and the best defined was a short sound, dry and superficial; the tone of this was acute, with exaggeration of intensity. Williams37 in 1841 called attention to these peculiarities. With this variety we frequently have a reverberation, pointed out by Stokes in 1837—a cracked-jar sound more or less marked. Woillez noticed this variety in 11 of his 82 cases; of this number 9 were in pleurisy of left side. (2) There was exaggeration of intensity or tympanism with a grave tone: 7 of Woillez's cases showed this variety, of which 6 were on left side. (3) A subclavicular resonance, unnaturally acute, but with exaggerated intensity. (4) Exaggeration of intensity, with equal tone on both sides; only 2 patients out of 82 showed this variety. (5) Exaggerated abnormal resonance, more acute than healthy side, and with normal fulness of sound. These are all modifications of percussion sounds elicited in pleurisy and other pathological physical conditions resembling it, where there are variations of tension together with other modification of the structure of the lung. The bruit de pôt fêlé is sometimes clearly marked, as it is also in hepatization of lung.
33 Avenbrugger, Ouv., ed. de Corvisart, 1808, Paris.
34 Arch. gén. de Méd., 1850, t. xxii.
35 Ibid., 1852, t. xxix.
36 Mal. Aig. des Org. Resp., Paris, 1872.
37 The Path. and Diagnosis of Dis. of the Resp. Organs, 1841.
Traube's Semi-lunar Space.—There is a point on the left side where we find normally a vesiculo-tympanitic sound, first pointed out by Traube and enforced by Fraentzel. It is situated at the anterior base of the left side, and is of a half-moon shape. It is bounded inferiorly by the margin of the thorax, and superiorly by a curved line whose concavity is turned downward. It begins in front, below the fifth or sixth costal cartilage, and extends backward along the margin of the chest as far as the top of the ninth or tenth rib. Its greatest breadth is from four to four and a half inches. This tympanitic sound is caused by the air in the stomach, which lies well up against the diaphragm. When the stomach is pushed down by the falling of the diaphragm, from excessive fluid, the tympanitic sound disappears. The value of this semi-lunar space in the diagnosis of pleuritic effusions has been variously estimated. Fraentzel considers it of great significance in the differential diagnosis between pleurisy and pneumonia; Ferber and Garland do not. Weil suggests that the area of this space may be diminished by filling the stomach and colon with solid or fluid food. Garland shows that as the diaphragm's depression depends upon the excess of fluid overcoming the lifting force of the lung, we may have, with a vigorous, unimpaired lung, a large amount of effusion in the pleural cavity, yet the resonance of the semi-lunar space may remain tympanitic. The condition of this semi-lunar space is of most diagnostic value in extensive left-sided effusions. The more the diaphragm is pressed down by the effusion, the smaller becomes the space of tympanitic resonance. It may gradually disappear altogether.
Auscultatory percussion may sometimes be advantageously employed to detect fluid in the pleura, especially in the younger subjects, for intercostal fluctuation may frequently be appreciated when we press carefully with the palm or surface of the finger between the ribs while the percussion shock is applied to another part of the same side. If we auscultate with a stethoscope, the chest extremity of which is made to fit in between the ribs, while another person percusses the chest, we can sometimes detect the fluctuation within the cavity of the chest.
We thus see that in the diagnosis of pleuritic effusions percussion is very valuable, perhaps the most valuable of the physical signs. We must not, however, forget that its significance may deceive us if the fluid is prevented from gravitating by pre-existing adhesions, or if it is encapsuled between the diaphragm and lung or between the lobes. Cases occasionally occur where, from fibrinous bands, the fluid is kept in the posterior part of the thorax, consequently there is pronounced clearness and fulness in front. Percussion does not enable us to diagnose the consistence of the contents of the pleura, or its nature, whether it be fibro-serous or purulent. To do this we must resort to Bacelli's method, or, still better, to exploratory punctures by the hypodermic syringe.
Palpation.—The sense of touch gives valuable physical signs in pleurisy. At the commencement, before there is any effusion of fluid, even of fibrinous deposit, we notice by palpation the decreased movement of the walls of the chest, and also the sensitiveness of the walls. When the eye cannot notice modifications of the expansion and elevation movements or movements of the ribs, correct views may be formed by palpation, especially in regard to the amount of local expansion in the upper part of the chest. In the lower part, by inserting a finger in the intercostal space we notice the modification of local expansion, also the convergence of the ribs taking place coincidently with the continuance of the elevation movement. We are thus furnished with additional presumptive proofs of the impermeability of the pulmonary tissue. When fibrinous effusion exists, the hand, early in the disease, recognizes the pleuritic friction or grazing. Later on, palpation perceives the rubbing when the muscles have recovered from their temporary paresis.
As soon as the effusion begins to form we detect a lessening of the delicate vibrations of the voice as communicated to our hands, always guarding ourselves against error by remembering that the normal sound is greater in the infra-clavicular region of the right side, and that it is always weaker in children and women, unless they have shrill, weak voices, in which case it may be entirely absent. It, indeed, requires a certain sonority of voice to be felt through the walls of the chest. When we find that both sides convey the vocal vibrations to our touch, we may be sure there is no effusion of fluid. Errors are often made by applying palpation over too extensive a surface, thus reaching beyond the fluid. It is important to use light, delicate palpation, employing the finger-tips instead of the whole hand, in order to exclude the vibrations from above as we approach the confines of the effusion. This vocal fremitus is entirely lost from the base up to the point to which the fluid reaches, and later on when it separates the two pleural surfaces. This absence of vocal fremitus is one of the most valuable physical signs of pleuritic effusion. It enables us to diagnose it from nearly all cases of lung-consolidation except when caused by malignant disease. When there are considerable pleuritic adhesive bands, they interfere with the complete absence of fremitus; but in children this sign is not so reliable. With them vocal fremitus is often scarcely perceptible in health. In dry tubercular pleurisy palpation gives us the characteristic friction. Palpation detects also the rubbing of the two lymph-covered surfaces after the absorption of the fluid. When there are thick fibrinous bands extending between the parietal and pulmonary pleuræ, there may be a vocal fremitus notwithstanding the presence of a quantity of fluid in the pleural cavity.
Displacement of Adjacent Organs.—The displacement of the heart as a physical sign indicating the presence of fluid in pleurisy is one of great significance. It is indeed a cardinal sign, second only in value to percussion flatness. It is almost invariably met with. Stokes38 stated that it was observed at an early period, and was one of the very first signs of effusion; "that it may exist even before the upper portions of the chest have become dull, and is a circumstance of constant occurrence long before any yielding of the muscular portions of the thoracic walls." The heart is displaced at the very commencement of the effusion, and its dislocation increases pari passu with the effusion. The absence of the displacement, unless it can be explained by some special circumstance which rarely occurs, such as the retention of the pericardium by old adhesions or consolidation of the opposite lung, would negative the diagnosis of unilateral effusion. In this condition there is a marked contrast with the displacement and depression of the diaphragm and the resulting alterations of position of liver, spleen, and stomach. These only occur when the effusion is in great excess—not until from the large quantity of fluid the retractility of the lung is overcome, and it is consequently unable to lift up the fluid and the diaphragm. This altered position of the diaphragm drags the heart downward by means of the ligamentous attachment of the pericardial sac to its tendinous portion. The deviations from the normal positions of the heart in slight effusions can always be noticed if the exact point of the apex-beat is sought for by palpation and listened for with the stethoscope. Careful percussion will show the shifting area of flatness.
38 Dis. of Heart and Aorta, 1854, Dublin.
Powell calls attention to a fallacy with reference to cardiac displacements in the earlier stages of effusion—that, as the base of the lung retracts, the left or the right margin of the heart, as the case may be, becomes uncovered. This may lead to an apparent delay in the displacement of the organ, the more extreme left or right boundary being now within reach of palpation. The axis of the heart is not greatly changed by an ordinary degree of effusion. It becomes a little more vertical, and in extreme cases it may become slightly twisted. Only in rare and extreme cases does the axis of the heart become altered in direction beyond the vertical line. Powell39 found at a post-mortem a heart that had become so twisted as to present itself obliquely edgeways in front. Sibson had previously pointed out this disposition of the heart to turn over and to present its posterior surface forward in cases of effusion.
39 Consumption and Dis. of Lung, London, 1878.
In examining into the cause and significance of the displacement of the heart in pleurisy we find that until within a few years, it was, and indeed very generally now it is, believed that the sole cause was from direct pressure of the fluid actually pushing the heart away from its normal position. Skoda, Traube, Stokes, Powell, and Garland were, we believe, the first authors to show that such was not the case, certainly in moderate effusions. The displacements take place when the amount is very small—too small to exert any positive pressure. It is true that nature places the heart in such a position that it can yield readily to slight forces. It hangs in the pericardial sac, which is suspended by the aorta, and which is bound by ligaments to the body of the third dorsal vertebra. Every change of position of the body causes certain anatomical alterations of the heart's position. Wintrich, Skoda, and Braune think that the heart swings like a pendulum from its base, and that its apex is therefore elevated with every deviation to the right or left. Lebert says the heart is first depressed by the sinking of the diaphragm, and then elevated by being pushed to the right. Fraentzel says that in displacements to the right the heart is simply pushed over, and is never elevated as Wintrich describes it. The mediastinum offers but slight resistance, and is very easily pushed to the right side, where there is no compact organ to resist, and where the cavity is larger; whereas it is with more difficulty pushed to the left, where the heart occupies so large a space.
It has been satisfactorily demonstrated that until the pleura is about two-thirds full of fluid no positive pressure is exercised upon the lungs or heart. According to Rokitansky, the lung cannot be compressed until seven-eighths of the pleural cavity is occupied by fluid. The fluid cannot be drawn off by a canula unless air enters to replace the fluid. Unless the pressure on the fluid from within the cavity is greater than that of the atmosphere we cannot draw off a large quantity: if the pressure balances that of the atmospheric air, only a few drops of fluid are discharged externally, except by forced expirations and coughs. This is the case even when the quantity reached several liters. The feebler the expiratory force the less fluid escaped. Yet the heart is displaced as soon as the effusion appears. The significance of the displacement is that it shows the presence of fluid, but does not show the measure of intra-thoracic pressure (Powell).
Garland's explanation is that the heart, with the sac and its connections, "is placed between two highly elastic bodies (the lungs) which are striving to retract in opposite directions. The heart, therefore, being acted upon on either side by opposing forces, occupies a position where these forces just balance each other; and this is the status of physiological repose in the vertical position of the body. Now, when an effusion is poured into either chest, the lung of that side contracts, and thereby exhausts a certain amount of its retractile energy. The opposing lung, however, still remaining normal, immediately begins to draw the heart toward itself, and the degree of displacement thereby induced will be proportional to the diminution of energy in the compromised lung." Stokes divided displacements of the heart into excentric and concentric. The former he considered due to direct pressure of the fluid, and the latter, when from any cause there was diminution in volume of one lung, the other lung, by its increased volume, forced it over. The concentric displacements, he thought, were generally the result of some chronic disease producing atrophy of lung.
Thus we see that displacements of the heart occur at three distinct periods in the course of pleurisy, and from different causes in each case: (1st) As soon as fluid forms in the pleural sac. At this period the displacement is caused by the presence of the fluid which occupies part of the pleural cavity. The lung by its elasticity retracts. It is, consequently, of less volume and exerts less negative force upon the mediastinum and its contents than the healthy lung. The two lungs having by their equal tractile energy previously kept the heart in situ, the healthy lung draws the mediastinum out of its position in a transverse direction. Necessarily, the displacement of the heart from this cause is in proportion to the amount of fluid effused. This is the most frequent mode of displacement of the heart. It can be said to be almost always present. (2d) When the quantity of fluid is great enough to overcome the retractility of the lung and exert intra-thoracic pressure, it forcibly expels the air from the alveoli of the lung and by direct positive pressure pushes the heart aside. The displacement of the heart in this case can only be produced when the pleural sac is two-thirds or more filled by fluid. When this condition is met with, the displacement is very great, because the heart has been already displaced by lung-traction. Previous to the researches of Garland, Stone, and Powell, this was supposed to be the only manner of explaining the displacement of the heart from pleurisy. (3) Where, as illustrated by Stokes',40 Hunt's,41 and Chew's42 cases, the heart is displaced toward the diseased side. This occurs more as a sequel of pleurisy in the course of the absorption of chronic or suppurative pleurisy, where by non-expansion of lung a partial vacuum is produced. The external atmosphere presses in the thoracic walls of the diseased side, and the internal atmospheric pressure from the healthy side is exerted against the mediastinum and presses the heart in that direction. Marked displacements from this cause are rare; slight displacements are more frequent. Cicatrices from healing of large cavities would have this effect. Mere consolidation of lung could not cause it.
40 Dis. of Resp. Organs.
41 J. W. Hunt, Dub. Med. Journ., loc. cit.
42 S. C. Chew, case reported to Med. and Chi. Soc. of Md., 1883.
Displacement of Lung.—The lung in cases of effusion is drawn up by its own retractile energy. It has been demonstrated that this force is considerable. As the effusion advances the lung recedes to a certain point, when the fluid, having overcome the retractility of the lung and having a fixed point below, actually exerts positive pressure upon the lung (Garland), and compresses the air out of the alveoli and the compressible bronchi. This compression cannot take place until the diaphragm is no longer elevated into the thorax, but is bagged down by the excessive weight of the fluid. There can be no compression of lung until its elasticity has been exhausted. The gradual effect of the continued contraction of the lung is to straighten out the letter S curve. The force of lung necessarily diminishes gradually as it contracts in volume. On the other hand, the immediate effect of compression is to obliterate that curve. So long, therefore, as we are able to trace a well-marked letter S on the chest, we may be certain that the lung is well out of reach of compression (Garland). Peyrot43 showed by plaster-of-Paris injections into the chests of cadavers, and then making cross-sections, that deformities of the chest are not due to a development of one side, the other remaining normal, but that they consist of a mutual adjustment of all parts. The simultaneous movement of the sternum toward the left in left-sided effusions makes the displacement of the heart appear greater than it actually is.
43 Arch. gén., Juill., 1876.
The Diaphragm and Intercostal Spaces.—The diaphragm is not depressed below the edges of the ribs, nor do the intercostal spaces bulge until the weight of the fluid exceeds the lifting force of the lung. The admission of air into the pleural sac produces the same result. The depression of the diaphragm is due in part to the weight of the fluid, but chiefly to the diminished contractile energy of the retracted and diminished lung. The displacement of the mediastinum depends upon similar conditions. Since the traction of the lungs always affects both sides of the thorax, the movable mediastinum must follow the lung, which is still capable of contracting, and therefore with right-sided exudations the left lung will draw the parts over to itself. Only with excessive effusions in the pleural cavity does the pressure of the fluid come into activity.
The liver and spleen may be pushed below their normal position by excessive effusion after the diaphragm yields to the weight of the fluid. Woillez found the liver displaced downward in the abdominal cavity in one-fourth of the right pleurisies and only once in left-side pleurisies. The extent on the right side was from two or three centimeters to three fingers' breadth, even as far as the umbilicus.
The stomach, when the diaphragm sinks, may be pushed downward; thus the so-called semi-lunar space of Traube may be obliterated. Ferber noticed a peculiar displacement of the stomach in two cases where he had produced an artificial hydrothorax of the left side. The fundus was pushed to the right, and the stomach was folded over on itself to a certain extent. A second and marked folding-in of the greater curvature occurred near the pylorus. This condition of stomach, with left-sided pleural exudations, has been hitherto entirely neglected by authors. May not the vomiting which is often observed with excessive effusion, and which has been attributed to violent acts of coughing, be due to this doubling over of the stomach?
Auscultation.—At the commencement of acute pleurisy, when hyperæmia exists with dryness of the pleural surfaces, auscultation shows a respiratory murmur lessened in intensity and duration. There is also a jerking unevenness in the rhythm of respiration, and weakness or indistinctness of the vesicular murmur consequent upon the imperfect and irregular expansion of the lung. On the healthy side the respiratory murmur is hypervesicular, and becomes puerile and noisy in character. In from twelve to eighteen hours the plastic fibrinous deposit on one or both pleuræ causes us sometimes to hear, over circumscribed spots, at the end of inspiration and the beginning of expiration, a fine friction sound, which varies in intensity over the points of contact of the surfaces. This is especially the case in the infra-mammary, infra-axillary, and infra-scapula regions. Woillez heard friction sounds in 52 of his 82 cases. The pain in respiration makes it very jerking and irregular. The contact of the surfaces pushes aside the lymph, and thus we hear the sound at a given point at one inspiration and not at another. It is heard more distinctly during inspiration than expiration. The reason of our not hearing the friction sound at the early stage of pleurisy continuously, but with interruptions in inspiration and expiration, is because the opposed rough pleural surfaces do not continuously rub against one another, but remain adherent for a few moments, until a deeper inspiration tears them asunder. The effusive stage comes on so rapidly in acute pleurisy that often when patients are examined the friction sound of the first stage has disappeared. It has been generally taught that the cause of the disappearance of the friction sound, and its subsequent reappearance as convalescence commences, are owing to the fluid separating the surfaces and its reabsorption. We have seen, from Garland's experiments and from careful clinical percussion explorations, that the fluid does not come between the two surfaces unless in very great effusion, but that it occupies the cavity between the lung and diaphragm. Stokes long since showed that there was temporary paresis of respiratory muscles, and consequently loss of movement of the surfaces over each other, which movement was necessary to produce friction sound. The reappearance of friction sounds indicates recovery of this muscular power. When heard, the friction is of the grazing variety—the most delicate form. Walshe designates it as the attrition species, and says it is audible over a limited extent of surface, occurring with occasional respirations, dry, and limited strictly to inspiration. As the effusion appears, we find, beginning with the lower border, that the respiratory murmur disappears, becoming less distinct as the effusion advances in the pleural cavity. Ordinarily, we hear no breath sounds. The absence, however, of breath sounds as a sign of pleuritic effusion is by no means a constant one. When the fluid contains many fibrinous bands, binding the lung down to the costal pleura, or when the effusion is very large and forces the air nearly out of the pulmonary tissue, pressing it into a firm mass against the vertebral column (at a point corresponding to the spine of the scapula), or when the lung is solid simply from the residual air being pressed out of it, diffused bronchial tubular breathing is heard. The tubular sound is conveyed, not ordinarily through the fluid, but by the parietes of the chest and by the solid plastic linings and adhesions. The fluid, if in large quantity and filled with fibrinous bands, may also feebly conduct the sound, which, being produced on solid surfaces, is best conducted by solids. We hear, in fact, a respiratory sound of low pitch, but tubular in quality. It is bronchial, but it differs widely from the familiar bronchial respiration observed when the lung is consolidated in pneumonia. It is a diffused distant tubular sound unaccompanied by moist sounds, soft in its quality and muffled. It has not the brazen, harsh character of pneumonic bronchial respiration. In pneumonia this sound is immediately under the ear, the lung being in contact with the inner surface of the ribs, and rendered a good conductor by its solidity, and the sound rendered louder by the increased consonating properties of the walls of the bronchi; whereas, in pleurisy, the lung is contracted above the level of the fluid, or, when the effusion is excessive, is removed from the walls by an indifferent conductor of its sounds, and the sounds are conveyed from the compressed lungs at their base by the walls of the chest, and, in a degree, by the deposits on the pleural surfaces. The bronchial breath sound which we hear over the lung, compressed by fluid, near the vertebra continues sometimes a long time after the absorption of the fluid, because the lung, deprived of air, expands slowly. If the effusion be small, we do not hear bronchial respiration, because there is sufficient air in the alveoli to prevent the conduction of the sound, the air not being compressed out by the effusion, but the whole lung being lessened in volume. If, again, the mass of fluid be very large, it prevents the free transmission of the waves of sound, and we do not hear them.
The auscultatory phenomena necessarily vary according to the amount of fluid in the cavity, the extent of the adhesions, the retraction, and the compression of the lung-parenchyma. If the compression be sufficient to prevent the air from passing down the bronchi, we do not hear bronchial respiration, because where, as in health, it is not communicated to the ear (owing to its non-conduction by the lung-tissue), it cannot be produced. Douglass Powell44 calls attention to another unusual pressure effect—altered quality of voice and cough, a husky voice, and a laryngeal quality of cough undistinguishable from that so often heard in cases of mediastinal tumor or aneurism. These disappear after paracentesis.
44 Consumption and Dis. of Lungs and Pleura, 1878.
Above the level of the fluid, and again as absorption of fluid takes place, we have a return of the characteristic friction sound as the muscles of the chest recover their normal power. With care this sound will not be confounded with intra-pulmonary râles, which are moist sounds removed or modified by cough or expectoration. These convey to the ear the sound of bubbles of air as they pass through the mucus and the secretions of the bronchi; whereas the friction sounds are superficial noises from rough surfaces moving over each other. The mucous râles which are sometimes heard are not from the pleurisy, but from bronchial catarrh. The friction sounds heard in the stage of absorption are ordinarily coarser and more abrupt. They are unequally jerking in character, and in quality resemble osseous crepitation. In chronic pleurisy, and for a long time after the fluid is gone in acute pleurisies, we have pleuritic rubbing sounds when the walls of the chest are drawn out in full respiration. At the absorption stage we ordinarily hear the lung gradually expanding. The respiratory sounds are feeble, and frequently moist subcrepitant râles are heard in the bronchial tubes. If the effusion has been of long duration, we find the pleural surfaces so thoroughly coated with fibrinous deposit, and the lung so separated by bands from the costal pleura, that the expansion of the lung is very much impaired and the percussion dulness does not subside. Leaming and Camman of New York give numerous cases where there might well be difference of opinion as to whether the signs heard were intra-pulmonary or pleuritic. In cases where the intra-pulmonary adventitious râles resemble the extra-pulmonary frictions, the diagnosis is assisted by considering the length of the sound. The character and intensity of the friction murmur varies very much. It may be a slight grazing sound or a coarse, sharp creaking-of-leather noise. Walshe gives no less than six modifications of the friction sound, ranging from a feeble, scarcely audible noise to one of extreme loudness. Friction sound is mostly an isolated phenomenon—that is, it is not accompanied by any unnatural quality of respiratory or vocal sound. Advanced type friction consists of a series of jerking sounds, rarely exceeding three or four in number.
We must remember that sometimes, notwithstanding a considerable quantity of fluid, the lung expands, and, pushing the fluid aside, causes the rubbing of the pleural surfaces together. When unmistakable, these respiratory friction phenomena are pathognomonic of the results of pleurisy. Thus they are properly considered of great value in the diagnosis.
Pneumo-pericardial Friction Sounds.—On the left side the uneven pleural surfaces are sometimes forced together by the impulse of the heart; of course, the resulting friction sounds are cardiac in their rhythm. Then, again, fibrinous deposits on the outer surface of the pericardium are forced against those of the covering pleural layers, both by respiratory and heart impulses. Close attention to the rhythm and the positions where these sounds are heard will prevent their being considered pericardial in their nature.
The fluid may be nearly removed and yet the condensation of the superficial strata be sufficient to produce extensive and marked dulness. Under such circumstances the production of friction phenomena is inevitable. The retention of some portion of the lung surface in tolerably close proximity to the costal pleura by means of adhesions also renders the production of friction sound possible, although a considerable quantity of fluid be present in the pleura. It is common to find effusion signs in the back and friction signs in front. We most frequently have friction at the base when there is absolute flatness. If the walls be separated by fluid, there can be no friction from contact. But it rarely happens that the fluid rises between the surfaces. To produce friction sounds we must have motion of rough surfaces which are in contact.
If the patient talks while we are listening in cases of small effusion we hear over the scapula, toward the spine, and between the scapula and the spine, bronchophony, as we do also when the lung is nearly deprived of air, in which case the sound sometimes has the bleating, nasal resonance designated by Laennec ægophony. In his opinion this was of constant occurrence and of great diagnostic value, but now it has been demonstrated that this sound can be heard when there is no fluid whatever, but consolidated lung. Anstie calls it one of the fancy signs of pleurisy. Ægophony is an unimportant variety of bronchophony, and not a characteristic phenomenon of pleuritic effusions. Of itself, it is not diagnostic of effusion, yet it is none the less true that it is a modification of bronchophony, and is commonly met with in cases of moderate pleuritic effusion, usually toward the upper margin of the fluid. It is difficult to state definitely the amount of fluid which usually produces it. Guttman thinks it is probably produced by the vibration of the walls of the flattened, compressed bronchi; this vibration is excited by the voice and transmitted to the thin layer of fluid which, at the upper part of the exudation, lies between the lung and the chest-wall. This tremulous movement of the sides of the bronchi gives the voice sounds a quavering, interrupted character; and, as they have to pass through a fluid medium to reach the surface, they lose in clearness and precision and acquire a nasal twang.
When the effusion is large, and we have full dilatation of the chest, all vocal resonance ceases, because the vocal vibrations go through media of such different kinds that they are lost before they reach the ear. During absorption, before the lung recovers its normal volume, we again hear bronchophony. Pleural adhesions and thickening cause the sound to be heard through the effusion when we least expect it. It is not unusual to find ægophony and bronchophony in the same lung. They are also found in some cases of pneumonia, and in some individuals, especially in children, we have between the scapula a normal resonance of the voice, with an ægophonic resonance.
Bacelli's Sign (Pectoriloquie aphonique).—This, the reverberation of the whispered voice through the fluid, is a sign of considerable value. If well marked it indicates fibro-serous fluid; its absence, however, does not show that the fluid is not of this character. (See [Purulent Pleurisy].)
Auscultation is of great value as indicating with definiteness the position occupied by the effusion as it is being reabsorbed.
Heart Murmur.—From excessive accumulation of fluid in the pleural sac a systolic murmur over the base of the heart is very often heard. That it is produced by pressure or twisting of the aorta is evident from the fact that it ceases when the fluid is withdrawn.
Phonometry we have found of but little value in the diagnosis of pleurisy.
COURSE AND DURATION. Acute pleurisy is essentially a unilateral disease. It does not pursue a regularly-defined course, nor have we any critical stages, as in pneumonia. In mild cases of acute primary pleuritis the disease advances slowly and recovery is tardy. The febrile movement may be four or five days in reaching its height. It remains at this point for several days—from four to seven days; in rare instances as long as ten days.
The effusion sometimes comes on very rapidly, but ordinarily is one or two days in forming. When it appears it may be divided into (1) the stage of progress, (2) stationary period, and (3) resolution. For the examination of both of these we must employ percussion, and mensuration by means of the cyrtometer, which give us exact results. Woillez in a large number of observations found that the first period lasted from eleven to twenty-four days, most frequently from fifteen to twenty days. The stationary period he found varied from twenty-four hours to several days. Frequently the reabsorption commences suddenly without any interval. Resolution is initiated from the eleventh to the twenty-fifth day, and lasts over fifteen days.
As the effusion advances the acute symptoms—rapid pulse, the elevated temperature, acute pain, and superficial dyspnoea—are materially lessened. If, however, the effusion be very great, we shall have at first painful dyspnoea, especially when the patient makes unusual exertions. This dyspnoea is ordinarily in proportion to the amount of the effusion. If there is much displacement of heart or distortion of larger blood-vessels, there is imminent danger to life. After the first few days we are often surprised at the tolerance of the whole system of the excessive amount of fluid. Absorption, after the effusion has been thrown out, is at first rapid, then it occurs more gradually; part of the liquid portion disappears, and the fibrinous portion undergoes fatty degeneration previous to absorption. The physical signs of flatness, vocal fremitus, together with the return of the displaced organs, the heart, liver, and diaphragm, to their normal positions, give us accurate means of judging of the progress toward cure. The general health shows unmistakable signs of improvement. The appetite is better, as are also the color and strength. If the effusion remains undiminished in quantity, or if it becomes purulent in character, the general appearance will show evidences of weakness and lowered vitality.
The average duration of acute primary pleurisies varies, when the effusion has not reached any considerable height, from two to four weeks. It may continue thirty or thirty-eight days—minimum duration twenty days. The absorption requires many weeks if the effusion is large or if it becomes chronic. Two months may elapse before the fluid entirely disappears. In some cases it continues, unless thoracentesis be performed, for many months. We have given the symptoms manifested when there is any renewal of the inflammatory process. In pleuritis acutissimus death may occur in ten days or two weeks from syncope, or from thrombosis caused by pressure upon the large venous trunks and consequent twisting, especially of the ascending cava, where it perforates the central tendon of the diaphragm to reach the pericardium, or by torsion of the aorta. When the effusion remains for a long time, the lung may be permanently prevented from expanding by pleuritic thickenings resulting from inflammatory products. In acute primary pleurisy the tendency is toward resolution. Louis went so far as to state that pleurisies never caused death. Trousseau, Lacaze, and others give cases where sudden deaths were produced by the quantity of fluid pressing upon the heart and blood-vessels. In subacute pleurisy (latent pleurisy of the older writers) the course of the disease is so gradual, so unattended by pain or even discomfort to the patient, that he goes perhaps weeks with considerable fluid in the cavity without being aware of it. He has probably been able to continue his occupation without intermission. It is only when he begins to feel weak and to lose flesh, and finds that his respiratory force is impaired, that he consults a physician. The rational symptoms scarcely point to pleurisy, but the physical signs of the presence of fluid are very distinctive. In this form the effusion is ordinarily greater in quantity than in the acute variety, and unless some of the fluid be taken away by aspiration, absorption is very sluggish. In these cases, if the fluid remains long in the cavity, the lung may become permanently disabled by the long continuance of the compression.
In chronic pleurisy the effusions from the acute or subacute pleurisies remain unabsorbed. They ordinarily are purulent in character, but sometimes they remain sero-fibrinous many months. Purulent pleurisies may be primary as well as secondary. (See [Purulent Pleurisy].)
TERMINATIONS.—Pleurisy of a fibro-serous nature terminates in (1) convalescence, (2) becomes chronic, or (3) ends fatally. Among those who are cured there are some instances where the disease is of short duration and the recovery prompt and complete. With others the disease itself is of a severer type and lasts longer. If the attack of pleurisy be secondary to another disease, especially if the latter be of a nature to profoundly affect the nutrition, convalescence is very tedious.
Acute pleurisies which are primary but rarely become chronic, but when secondary they frequently are chronic from the beginning. Heyfelder states that chronic pleurisies are three times more frequent on the left side than on the right side.
Trousseau, Bowditch, Lacaze, Behier, and others have reported sudden and unexpected deaths in cases of fibro-serous pleurisies. Not only has this resulted in cases where the fluid was excessive in quantity, but also in cases where the amount was moderate. Wilson Fox (Brit. Med. Journ., Dec., 1877) gathered from medical literature between 50 and 60 sudden deaths from effusions of all kinds. Syncope has been the usually assigned cause of death. Négrié45 collected 12 cases of unexpected deaths from pleurisy, and there were but 2 of them where syncope could be assigned as the cause of the fatal termination. Of the remaining 10 cases, 3 were caused by what is invariably a grave complication, pericarditis, and 7 by clots formed in the heart or pulmonary artery. In the cases where pericarditis existed the deaths occurred as early as the eleventh or twelfth day. In the other cases death occurred as late as from the twentieth to the forty-fifth day. Woillez46 reports 2 cases where death was produced by supervening congestion of healthy lung.
45 Thèse de Paris, 1864.
46 Loc. cit.
COMPLICATIONS AND SEQUELÆ.—The inflammation may extend by contiguity to the lung-parenchyma, pneumonia supervening after a few days, or it may appear to come on simultaneously. It is, however, a rare complication. Lacaze47 reported one case, and that followed thoracentesis; Lugrol reported a similar case.
47 Loc. cit.
Pneumonia does not appear to commence after the effusion has reached the point of compressing the lung. The inflammations frequently are peribronchitic and broncho-pneumonic. The mediastinum may become involved. Fraentzel states that it can never be clearly proved that simple croupous pneumonia exists as a complication of primary pleuritis on the side affected; on the sound side it occurs occasionally. Laennec taught that the compression by the fluid always tended to prevent the occurrence of pneumonia. Anstie's opinion was that when the lung is compressed to carnification it is incapable of inflammation. The most formidable way in which pneumonia may complicate pleurisy is where, considerable effusion existing in one pleura, inflammation attacks the opposite lung. It may be doubted whether this ever occurs in truly primary pleurisies: kidney disease, specific fevers, pyæmia, etc. nearly always precede it. Hyperæmia or congestion of the opposite lung, without its amounting to pneumonia, does occur, and is a very grave complication. The same may be said of double pleurisy and peritonitis as resulting from blood-poisoning. It rarely happens in primary acute pleurisy that both pleuræ become involved. When such is the case, however, it is generally tubercular in its nature, and necessarily a very grave if not a fatal complication. Walshe reports having seen 4 cases of idiopathic bilateral pleurisy in persons thoroughly healthy and perfectly free from constitutional taint of any kind. In all the pericardium was involved, and in 1 the peritoneum. They were all fatal. Acute pericarditis from extension of the inflammatory process is a frequently-occurring complication. When the inflammation extends to the pericardium, the effusion is of the same character as that of the pleurisy, whether it be sero-fibrinous, purulent, or hemorrhagic. It is a complication of great gravity and is sometimes the cause of a fatal termination of the pleurisy. We have never met with endocarditis as a complication, but Fraentzel speaks of having seen it in acute pleurisy in children. Before complete carnification occurs oedema of the lungs may be produced on the diseased side or in the healthy lung. This pulmonary oedema, when it attacks the sound side, is acute, being produced by rapid pulmonary congestion, which causes free, albuminoid, and frothy expectoration, often ending in asphyxia. The serum and albumen of the blood by transudation pass into the bronchi and the alveoli, and fill them more rapidly than they can be expectorated: the subject dies by suffocation. Auscultation reveals fine vesicular râles, characteristic of oedema of the lungs, closely resembling the fine crepitation of pneumonia. Traube has named this oedema pneumonia serosa. Engorgement it certainly is, but it can scarcely be designated a pneumonia. It closely resembles the oedema we meet with after thoracentesis, which has been named by Hérard expectoration albumineuse.
Bronchial catarrhs, when complicating pleurisies, cause dyspnoea, add much to the discomfort, and protract the duration of the disease. Barth48 speaks of dilatation of bronchi as a complication of pleurisy. Woillez49 calls attention to a complication which has been generally overlooked by the authorities—a persistent pain which some patients suffer in the side of the chest a long time after the disease has been cured. The most dangerous complications are syncope, formation of clots, venous emboli, and exaggerated distension of the thoracic walls by the effusion.
48 Mém. de la Soc. Méd. d'Obs., Paris, 1856.
49 Article "Pleurisy," Mal. Aigu. Resp., 1872.
Sequelæ.—The connection of pleurisies, especially chronic, with subsequent tuberculosis, is very generally admitted. Bartholow says: "The importance of pleuritis as a cause of phthisis is hardly sufficiently recognized in inducing tubercular deposit, and by adhesion limiting the movements of the organs, and thus inducing diseases." Anstie says: "It is now well established not merely that pleurisy often occurs in phthisical lung disease, but that pleurisy itself is capable of setting up true tuberculosis even in previously healthy persons. This is specially apt to occur where purulent effusion has been allowed to remain too long in the pleura, or where paracentesis has been performed repeatedly for empyema, the wound being closed in the interval." Modern authors thus consider that a productive field is offered for the bacillus tuberculosis.
Flint states that "in an analysis of 47 cases, in 3 the subsequent development of phthisis was probable, although not demonstrated, and in 1 case only the occurrence of this disease as a sequel was certain." Of 53 cases reported by Blakiston, not one became phthisical during several years after recovery from the pleurisy. Flint says the effect of chronic pleurisy with effusion in a person already phthisical is to arrest or retard for a time the progress of phthisis. We have mentioned the retraction of the chest-walls with deformity of shoulders and spine, and the permanent dislocation of the heart and larger blood-vessels, as serious results, as also the orifices produced by the bursting of the empyemas outwardly. These may all in time, with judicious care and treatment, be very materially lessened, and even cured. Empyema sometimes causes destruction of the periosteum of the ribs and subsequent necrosis. It is questionable whether there are any cases of pleurisy which do not leave more or less extensive adhesions between the two pleural surfaces. In many cases they do not, it is true, seem to injure seriously the general health, yet they must impair the full functions of the lungs. How frequently this is the case is shown at autopsies of persons dying of other diseases, where we find extensive adhesions when we had no reason during life to suspect that such would be the case. Adhesive bands may interfere with the expansion of the lungs and cause chronic bronchial catarrhs, ending in death. Caseous pneumonias are among the sequelæ of pleurisy. When the false membranes are thick and numerous, the lung remains impervious to air and useless. This condition sometimes produces bronchiectasis. While it is true that the lungs, when the effusion is not great enough to actually compress them, sometimes retain their expansibility for three, six, or even eight months, yet there are cases where they do not expand after being bound down for months, and then we have depression of the walls of the chest. Woillez met with 6 such cases.
DIAGNOSIS AND PROGNOSIS.—The diagnosis of the several varieties of pleurisy ought easily to be made by the due appreciation of the general symptoms and physical signs we have enumerated. Cases occur where the differential diagnosis is not free from difficulties, even to the most careful of observers. Pleurisies on the left side are more easily diagnosed than those on the right side. Most of the signs are much more frequently observed on the left than on the opposite side: some of them are rarely met with except on the left. Before the discovery of the science of auscultation and percussion pleurisy and pneumonia were frequently confounded. By their aid the two diseases may ordinarily be diagnosed with precision. In both there are chilliness, fever, cough, and dyspnoea. At the initiation of acute pleurisies, we expect for several days more or less of chilliness, but in pneumonia one, or at most two, decided rigors. The temperature in primary pleurisy rarely goes beyond 100° F. in the first twenty-four hours, whereas in croupous pneumonia, in the same length of time, it not unfrequently rises to 103° F. or 104° F. In consequence of this high temperature in pneumonia the skin becomes hot and dry, with frequently a bright spot on the cheek corresponding to the side of the diseased lung. This is not the case in pleurisies, where, on the contrary, we have a pale, anxious expression of face. The comparatively mild fever of pleurisy is continuous. We have not, as in pneumonia, the marked changes, often of two or three degrees, between the morning and evening temperatures, nor have we critical days (between the fifth and eleventh) where the fever breaks with rapid defervescence.
Pleurisy is a more prolonged disease, and is not self-limited. The cough of pleurisy is short and quick, with no expectoration, unless it is thin, frothy mucus. In pneumonia the cough is longer, and is accompanied by a tenacious expectoration, more or less free, and generally (not always) tinged with blood. The rusty-colored sputa is almost characteristic of pneumonia. At first there is a marked difference in the dyspnoea in the two diseases. In pleurisy it is superficial, because the lungs are not freely expanded in consequence of the accompanying pain. In pneumonia it is deeper and the oppression is greater. The struggle for breath in the first stage of pneumonia is frequently alarming to witness. The relative frequency of pulse and respiration is more modified in pneumonia. The stitch-like, cutting pain in pleurisy is characteristic and very circumscribed, whereas in pneumonia, unless the pleura is involved, there is little or nothing beyond a dull soreness. We have in pleurisy the restrained movement of the side affected, and corresponding increase of movement of the healthy side. Not so in pneumonia. At the beginning of croupous pneumonia we generally have the crepitant râle heard in inspiration, but not observed in pleurisy. The friction sound, if present, heard in inspiration and expiration, is equally characteristic of pleurisy. If, as sometimes happens, we do not hear either the crepitant râle or the friction sound, we must be cautious in our diagnosis until we have the more definite symptoms of the next stage.
Later on in the clinical course of the diseases, in their second stage—consolidation in pneumonia and effusion in pleurisy—the physical signs enable us to make the differential diagnosis. We expect dulness in both diseases, but it is more absolute in pleuritic effusions, and to the finger, as a pleximeter, the resistance is greater. In pneumonia there is very seldom complete dulness over the whole side of the chest, for there are frequently lobules not consolidated, or spots where the solid deposit has been partially absorbed. Moreover, the area of dulness is not bounded by that peculiar curved line, with its concavity at the base behind, facing the vertebra, gradually becoming convex as it turns upward and forward toward the axilla, again descending toward the sternum, as is the case in pleuritic effusions. Changes of position of the patient may cause the fluid, when in large quantity, in pleurisy, unless prevented by fibrinous adhesions of the two surfaces, to gravitate to a greater or less degree, and thus alter the points where we have flatness on percussion. The enlargement of the thorax, the bulging of the intercostal spaces, the marked displacement of the organs, and the frequently complete obliteration of the semi-lunar space, are characteristic of excessive pleuritic effusions. The displacement of the neighboring organs, especially of the heart, is a very valuable diagnostic sign of pleurisy.
There are, however, other conditions besides the presence of fluid, such as new growths and pneumothorax, which, by increasing the contents of the chest, may produce the same result. We may also meet with cases of congenital malposition of heart or instances where infantile disease, or constrained position, necessitated by occupation, have caused malformation of the contents of the chest.
The most characteristic percussion sign of effusion in pleurisy is the semi-tympanitic (Skodaic) or amphoric resonance high up in front. In rare cases it is found in pneumonia, but it is most pronounced over the consolidated lung, whereas in pleurisy it is above the level of the fluid. The vesicular murmur is not heard below the level of the fluid, unless very feebly at its upper surface, nor indeed is the passage of the tidal column of air up and down the bronchial tubes. In pneumonia bronchial respiration and increased resonance of voice rapidly supervene; whereas in pleurisy the voice is obliterated. In pneumonia we find the characteristic loud, high-pitched, brazen bronchial respiration over the whole of the consolidated portion. When a tubular quality is given to the inspiratory murmur in pleurisy, it is a diffused, distant, and low-pitched sound from the compressed lung. There is a marked contrast between the increased vocal fremitus of pneumonia and its entire absence in pleurisy. In pneumonia there is strong bronchophony with a jarring thrill to the ear, but there is not the displacement of the adjacent organs, the increased volume of the affected side, nor the widening and bulging of the intercostal spaces, with sometimes fluctuations, perceived on auscultatory percussion, as in pleurisy.
Although both diseases are ordinarily unilateral, yet we more frequently meet with double pneumonia than with double pleurisy. It must be borne in mind that we may discover the coexistence of pneumonia and pleurisy. When this does occur special care must be taken in the diagnosis. In cases of pleurisy on the left side, sometimes the impulse of the heart forces the two surfaces of the pleura together, and causes us to hear a pleural, cardiac friction sound. It has the rhythm of the heart, and is heard when respiratory movements have been suspended. This sound is limited to the left border of the heart. Care is needed to prevent the error of diagnosing pericarditis.
The diagnosis of pleurisy from hydrothorax, or passive transudation of fluid into the cavity of the pleura from mechanical causes or blood-poisoning, depends upon the recognition of the fact that ordinarily the latter is not ushered in by fever—that it is bilateral, and is frequently accompanied with dropsy in other parts of the body. Transudations being slowly developed, the lung gradually contracts, and the presence of the fluid is tolerated for a considerable time; indeed, it is not until it is excessive that it compresses the lung. Thus, dyspnoea is not ordinarily produced until the accumulation is very great.
Sometimes the diagnosis between pleurisy and intercostal myalgia, or pleurodynia, is confused and uncertain. The pain may be as intense and the respiration as jerky where there is no pleurisy, if there is great soreness of the muscles between the ribs. The pain is, moreover, accompanied by more or less rise of temperature. Oftentimes the respiration is as painful as in pleurisy, for the individual instinctively refrains from causing the muscles to contract. Usually there is greater tenderness on pressure over the walls of the chest, less fever, and the area of pain is larger in this form of muscular rheumatism. The friction sound, if present, makes the diagnosis clear. We sometimes remain in doubt for twenty-four hours.
Intercostal neuralgia less closely resembles pleurisy. It occurs without fever, generally in anæmic subjects or in those debilitated by chronic general diseases, especially uterine. The tenderness is limited to several points along the course of a nerve, at the exit of the nerve from the spinal cord, in the axillary region, and near the sternum.
Pericardial effusions and aneurisms can ordinarily be readily diagnosed from pleurisies. Their positions in the cavity are so well defined, and the accompanying physical signs are so characteristic, that they ought not to be confounded with pleuritic effusions.
Solid tumors and cysts occupying a considerable portion of the pleura or bulging into it from the mediastinum may deceive us into thinking that there is an effusion. They displace organs, press upon the lungs, or intervene between the lung-texture and the walls of the chest, thus preventing us from hearing the entrance and exit of air and the vibrations of the voice. Not containing air, we have flatness on percussion. Being solid conductors, we have with them increased vocal fremitus, whereas in pleuritic effusions it is not perceived. Ordinarily, tumors are found at the superior or central portion of the chest, and cause an irregular bulging of the walls instead of the general enlargement caused by liquid effusions. Before the discovery of the present modes of physical diagnosis intra-thoracic growths, especially cancerous ones, were frequently confounded with pleurisies by even the most careful observers. Now such errors are only occasionally committed. The history of the case, the general symptoms, absence of fever, etc. will assist us in making the differential diagnosis. A careful examination by physical exploration will give us valuable aids. The bulging produced by malignant growths is not so marked nor is it so uniform. The dulness on percussion is not so pronounced. It does not vary from changes of position of patient. The displacement of heart and other organs is not so marked. Hunt50 calls attention to the considerable blood-stained expectoration from cancer. He calls it currant-jelly expectoration. We must look also for the characteristic signs of cancerous cachexia and enlargement of glands in the axilla and in the supra-clavicular fossa. The exploring aspirator-needle will generally enable us to arrive at an accurate diagnosis, with the assistance of a microscope to examine the fluid or solid matter withdrawn. The fluid thus obtained from cancer is generally blood-stained.
50 Loc. cit.
Inflammations of the pleuræ are sometimes caused by the presence of intra-thoracic tumors. Abscesses of the liver and echinococci cysts may ascend, and, pushing the diaphragm before them, occupy the pleural sacs, and thus simulate pleuritic effusions.
Pulmonary atelectasis, caseous inflammation of the tissue of the lung, aneurisms of the large thoracic blood-vessels, may, without care, be mistaken for pleurisies. It is very important to ascertain the nature of the fluid effused into the pleural cavity, whether or not it is serous, sero-fibrinous, purulent, or hemorrhagic. Generally this can be done by careful study of the accompanying general symptoms and the clinical history of the case. If there are repeated irregular rigors from the beginning, followed by high fever and free perspirations, there is every reason to fear that the fluid is purulent. If symptoms of blood-poisoning develop, we are still more confident that there is pus. Its hemorrhagic character may be inferred when great pallor, weakness, and lowered temperature suddenly appear during an acute attack.
Bacelli's physical sign known as pectoriloquie aphonique, or the passage through the effused fluid of the whispered voice, has considerable significance as a means of testing the nature and character of the fluid. His conclusion was that, when heard, it showed the fluid was fibro-serous; when not heard, it revealed to us that the effusion was purulent or sero-purulent. Laennec had noticed that in voiceless consumptives the whispers would sometimes resound as if the patient shouted in the ear of the auscultator. R. Douglass Powell reported51 10 cases bearing upon the value of this sign. In 6 of these, in which the fluid was clear, 5 yielded the sign, the sixth did not. In 2 acute cases, when the effusion was purulent, the sign was heard. He adds that he has heard the sign to perfection in fetid sero-purulent effusion. Mercadie52 claims that when pectoriloquie aphonique is heard in purulent effusions it is only at the uppermost part of the fluid near its limit, where it has become very thin from the weightier portion, the flocculi, and the leucocytes falling to the dependent portion of the sac. Care must be taken in listening for this sign. The patient must be ordered to speak each syllable slowly and in a whisper, distinctly counting up to twenty or thirty. If it be present we ought to be able to perceive that the syllables sound, to the ear, clearly articulated along the height of the effusion. The sound is caused by the transmission of the whisper without any buzzing and without continuous murmur. The maximum of intensity of this sound is heard along the vertebral gutters and along the posterior base of the pleural cavity. It becomes feeble in its distinctive character as we approach the axillary region and also immediately under the angle of the scapula. The theoretical objection has been made to this sign that its production is contrary to well-known physical laws of the conduction of sound-waves. It is said because the sound originates in the air it must be indifferently conducted by fluid; moreover, that its transmission ought to be in proportion to the density of the fluid, whereas this sound is best conducted by a thin fluid. Walshe's explanation of the greatly-increased sound-conducting power of a consolidated lung in croupous pneumonia was that it was owing to its homogeneity of structure. Bacelli avails himself of this principle to account for our hearing through a fibro-serous fluid the whispered sonorous waves, and our not hearing them when the fluid was sero-purulent or purulent. In the latter case the fluid is excessively heterogeneous, containing leucocytes in abundance, besides layers of membranes, flocculi, and blood-discs. The sound-waves are lost as they pass through these media of different density. We have found it to be a physical sign of value in the differential diagnosis of the nature of the fluid, yet its presence is not pathognomonic of serous effusions. In thin fluids it is generally heard, and ordinarily it is not found in purulent pleurisies. If well marked, it indicates a fibro-serous effusion. Its absence does not necessarily show purulent pleurisy. Its greatest value is as indicating the purulent transformation of a fibro-serous effusion.
51 Trans. Int. Med. Cong., 1881, vol. ii.
52 Thèse de Paris, 1876.
Thanks to modern investigations, we have in the very fine needle of the aspirator, or that of the hypodermic syringe, a delicate and sure means of accurate diagnosis, not only as to the nature of the fluids, but as to that of tumors and growths which may be confounded with them. We would not use for exploration a trocar and canula. We consider it best to employ a short needle in aspiration, for fear that a delicate hypodermic needle might break. Flint states that he has known several instances of this accident. Aspiration can be performed with perfect safety, and, indeed, without any fears of unpleasant results even if we perforate an aneurism. The orifice made is so small that the tissues close the moment the needle is withdrawn after making the exploratory puncture. If care be taken to cleanse the instrument and to use Listerism that no deleterious germ be introduced, the operation is harmless. (See [Purulent Pleurisy].)
Blunders in diagnosis, however, will rarely occur if an examination is conducted with great accuracy, and if we follow the course of the disease with care.
PROGNOSIS.—The prognosis of simple primary pleurisy is generally favorable, unless it is complicated with other diseases or occurs in enfeebled persons. The intrinsic tendency of the disease is to recovery. Laennec considered that the prognosis in acute pleurisy was always favorable. Pleurisy with scanty sero-fibrinous effusion is not in itself serious. Dry pleurisy is free from danger. Subacute pleurisy with large effusions, where the course of the disease is insidious and slow, is more apt to be followed by tuberculosis than the more acute cases. Louis's law, deduced from 150 cases, that patients never died from the effusion in acute pleurisies, was long since disproved by Trousseau. Lacaze du Thiers published in 1873, in his thesis, a number of cases of sudden death from large accumulation of fluid. These deaths were caused by a large amount of effusion being thrown out rapidly, and suddenly compressing the lung before the system had time to accommodate itself to the presence of the effusion. These cases, termed foudroyant, should be very carefully watched. There is danger of death from orthopnoea when the pleural cavity is completely filled, especially in latent pleurisies, where the patient, unaware of the risk, makes, perhaps, unusual physical exertions. Some deaths have been caused by oedema of the lungs and some by syncope; others, again, from thrombosis of the pulmonary artery. We must bear in mind the grave prognostic value of attacks of orthopnoea and severe dyspnoea, because they, more than the mere quantity of the fluid, show the want of tolerance in the organism. These cases demand prompt mechanical interference with the aspirator. The very rapid accumulation of the effused liquid, even if unattended by dyspnoea, is an unfavorable sign, for observation has proved that in such a case its absorption is attended with more difficulty. Bilateral pleurisies attended with considerable effusion are commonly fatal.
If there are complications with other acute diseases, such as pericarditis or pneumonia, the prognosis may be far from favorable, more particularly if pleurisies supervene when the organism has been exhausted by a long continuance of the primary disease.
If absorption begins soon after the acute symptoms subside (and we expect it to do so where the general health and strength are good), and goes on vigorously, we can with confidence predict a favorable result, especially if there be no contraction of the walls. The earlier the reabsorption takes place the more favorable the prognosis. If, however, four or five weeks pass without any perceptible diminution in the extent of the effusion, there is cause for uneasiness. Especially is it dangerous if, in addition, we have those ugly symptoms, emaciation, weakness, and hectic fever, which point to the conversion of the fluid into pus. There is the prospect of protracted formation of pus with its dangerous sequelæ, including tuberculosis from infective absorption.
That these dangers can in a great measure be obviated by prompt thoracentesis ought now to be universally admitted. Anstie predicts that the experience of the next twenty years will enable us to ensure an absolute immunity from fatal results from either of these serious complications. Symptoms of oedema of the lungs or of cyanosis are bad prognostic signs; so is diminution in the amount of urine secreted, which indicates that the arteries are incompletely filled. Still worse are the symptoms of over-distension of the veins, dropsy, and the appearance of albumen, casts, and blood in the urine.
The prognosis in secondary pleurisies is much more serious. In cases where the effusion is purulent at their commencement, the prognosis is graver than when it becomes purulent after remaining some time in the cavity. This is because they are often pyæmic in their origin.
With modern treatment, however, the percentage of recovery is greater than it formerly was. When we have to contend with chronic purulent cases occurring in cachectic constitutions or in those debilitated by other illnesses, especially tubercular, the prognosis is necessarily unfavorable. The most fatal of all secondary pleurisies are those supervening in the course of pyæmia or puerperal infection. Here death is the rule, recovery the rare exception.
Pleurisies supervening on Bright's disease or nephritis, following scarlatina and idiopathic fevers, have a high rate of mortality. The modern employment of the thermometer is of the greatest assistance to us in forming our prognosis. Marked variations of temperature, whether they be below the normal or constantly high or advancingly high, have grave significance. Anstie's valuable results from the use of the sphygmograph, as giving us the favorable and the unfavorable pyrexial pulse-forms, cannot be over-estimated. We fully concur with him, "that in the dangerous secondary pleurisies the combined use, for prognostic purposes, of the thermometer and the sphygmograph is more valuable than all the other modes of observation put together." It is so because they give us accurate physical data by which we can estimate the exact condition of the patients.
Relapses, with a rapid increase in the amount of fluid after reabsorption has been active and convalescence apparent, are frequently attended with danger, because they often denote a tubercular or hemorrhagic development. A very unfavorable sign is the rapid increase in the effusion after spontaneous or artificial discharges, especially if the fluid has become fetid in its character and has the dark appearance of unhealthy, purulent matter.
TREATMENT.—The study of the natural history of acute fibrino-genic pleurisy teaches us that there is always in it a tendency toward recovery unless there is some constitutional weakness behind the disease or a large fibro-serous effusion resulting from it. We have all met with cases where patients have recovered in the course of a month or six weeks spontaneously, without any treatment. Of A. L. Mason's 200 cases, 132 recovered without having to resort to thoracentesis. It is often a harmless disease when left, as far as medical treatment is concerned, entirely to itself. Of course the body-temperature and the physical evidence of the effusion ought always to be carefully observed. The hygienic treatment ought never to be neglected. We should insist upon rest in bed in the most comfortable position to the patient. The temperature of the room should be from 65° F. to 68° F., the approximate in-door winter degree for healthy adults.53 The body, especially the chest, should be kept quiet; all unnecessary movement should be avoided. The food ought to be nourishing in quality, easy of digestion, and in quantity sufficient to keep up healthy nutrition. Stimulants are unnecessary, but it is a mistake to withdraw water, which contributes so much to the comfort of the patient and cannot injure him in the first stage. We should take care that the patient has enough sleep. If necessary, mild hypnotics should be used. The effusion results from the inflammatory process, and not from simple transudation. If the pain is very severe, we must resort to the administration of opium by mouth or to hypodermics of from one-eighth to one-sixth of a grain of morphia; this, however, should be avoided when possible, as preparations of opium impair the appetite and depress the patient. The pain ordinarily passes off in 48 hours, and can often be relieved by application of hot-water bags, turpentine stupes, or anodyne liniments. Bloodletting, general or local, is rarely necessary. Leeches will give relief to the acute pain, but opium does that more effectively. Depletory remedies are hurtful and retard convalescence, and do not control the amount of the effusion, which in itself is depletory. If the patient is seen at the initiation of the disease, a large dose of quinia (from ten to fifteen grains), especially if the temperature goes to 101° F., often has a marked effect in controlling the temperature and also the tendency to effusion. Smaller doses may be repeated every few hours. Liq. ammonii acetatis, in fluidrachm j to fluidrachm ij doses every two hours, and Apollinaris or other alkaline drinks, relieve vascular tension and promote the action of the skin and kidneys. During the pyrexia, with the effusion increasing, we endeavor to lower arterial pressure within the pleural vessels by aconite, diaphoretics, mild salines, diuretics, with complete rest of the body. Hot applications (not heavy poultices, however) may sometimes be used at short intervals, with a view of dilating the superficial vessels and thus relieving those of the interior.
53 Boston City Hosp. Reports, 3d Series, 1882.
Under this simple treatment many patients are sufficiently well in a few weeks' time to sit up. They ought not to be permitted to move about unless there is a very small amount of effusion. Roberts54 of University College Hospital applies adhesive strips over the chest in all cases from the beginning. Mason prefers Martin's india-rubber bandage, three or four inches wide, extending from the lower border of the ribs to the axilla, as it adapts itself better to the chest-walls and supplies an easily-regulated elastic pressure. He considers it also useful in promoting absorption after tapping. Generally in three or four weeks, in favorable cases, the effusion has been absorbed and the patient is able to resume his ordinary duties. The writer cordially endorses Anstie and Bartholow's protests against the employment of mercury for any supposed aplastic properties. It really exhausts the recuperative forces of the organism, and probably injures instead of benefiting in pleurisy.
54 Quain's Medical Dictionary.
If the exudation be in considerable quantity, three or four weeks may be required for its absorption. If this process is sluggish, can we by medicines promote it? Mercury has lost its old reputation as a remedy for this purpose. Iodine externally, and iodide of potassium in decided doses, still retain, to a limited extent, the confidence of practitioners. Preparations of iron, especially the muriatic tincture, have had better effects in the hands of the writer than any other remedy. Large blisters cause great discomfort, and their utility is very questionable. Alkalies possess the power of dissolving exudation, and of these the most efficient is ammonia, especially carbonate of ammonium in doses of from five to ten grains. Saline laxatives, by producing watery stools, have some power in reducing the amount of fluid. Some authors recommend highly the acetate and citrate of potassium dissolved in a decoction of scoparium. J. W. Hunt55 places most reliance upon pilocarpus pinnatus, which has given him most marked and successful results, even where other remedies have failed. He pushes it to the extent of producing extreme diaphoresis. He commences with thirty minims of the fluid extract four times daily, rapidly increasing the quantity and the frequency of the doses to the extent of fluidrachm j every two hours. The one-eighth of a grain of its alkaloid, pilocarpine, given hypodermically, acts very promptly. He admits that the vital forces are so exhausted by this treatment as to require at once the administration of tonics, especially of iron with strong food. Grasset56 reported 5 cases of effusion treated by jaborandi. They were cases of pleurisy without fever or sign of inflammation—cases which ordinarily require several blisters to produce an effect.
55 Dublin Journal Med. Sci., Dec., 1882.
56 Journal de Thérapeutique, Avril, 1876.
Ernest Wernaere57 reported 7 cases of acute pleurisy where there was considerable febrile reaction. Jaborandi was effectual in every case, and the effusion rapidly disappeared after two doses of the infusion. The fever at the same time was diminished, and there was no return of it, as frequently occurs in non-inflammatory cases. It has less effect upon children than upon adults. In a case of Wernaere's only one dose was given.
57 Thèse de Paris, 1876.
The value of counter-irritants has been frequently questioned of late years. Fly blisters give relief in limited dry pleurisy. Many practitioners have great confidence in large blisters used over the chest after the febrile stage has subsided. Woillez, in tabulating the results of the various means of promoting absorption, puts purgatives first in utility, and blisters last. Blisters, he claims, had no effect in 90 per cent. of cases. The iodide of iron, in pills, or the compound syrup of the iodide of iron and manganese, with improved digestive powers, are the best means of promoting absorption. At this period of the disease it is an advantage to lessen, within certain limits, the amount of fluid taken into the stomach, forcing the blood to abstract water by absorption from the chest. Jaborandi has the same effect by withdrawing water from the blood.
There are cases of excessive quantity of fluid, and others which resist all drugs given to promote absorption. Among these are some acute cases, but many of a subacute and chronic nature, where the effusion remains stationary, injuring respiration and often mechanically endangering life. This occurred in nearly one-third of Mason's cases.
Thoracentesis.—In studying the history of this operation we have seen how frequently, since the time of Hippocrates, it has been in favor with practitioners, and then has fallen into discredit. During the past thirty years, thanks especially to Bowditch and Trousseau, its unquestionable value has been established, and is now universally recognized. Improved knowledge of pathology, safe and easily-applied instruments, together with the discovery, by Lister, of the means of securing the operation from septic dangers, have perfected this surgical treatment. Observation in hundreds of cases has proved that, properly used, it is almost without risk. As a means of diagnosis it is the most accurate we possess; as a treatment for affording positive relief it is a boon to suffering humanity; as a method of cure it has been most successful.
Such being the estimate of its value, let us study, 1st, the indications for its use; 2d, the manner of operating; 3d, and finally, the objections founded upon the accidents that have followed its application.
The indications are met with in two conditions—that of excessive accumulation of fluid, and where there is non-absorption of the effused liquid. In going over the symptoms we have seen the effects of large collections of fluid in the pleura—how the heart is pushed out of its normal position, and how the large blood-vessels are distorted. We have called attention to the retraction and compression of the lung until in many cases it is airless, and thus not able to perform its functions. We have shown that all the adjoining organs and cavities are sometimes forcibly thrown out of the position nature placed them in. The liver is pressed forward into the abdominal cavity, and the diaphragm is unable, from mechanical pressure, to ascend and contract. The mediastinum, with its contents, is materially interfered with. Observation has shown that such a state is a very dangerous one. Not only does it cause great dyspnoea, pain, and oppression, but the risk to life is imminent. In a number of instances it has caused death. Trousseau tells us of 3 deaths; Lacaze reports others. Bowditch, having seen several fatal cases produced by the quantity of fluid, worked with energy and perseverance until he was furnished by Wyman with his ingenious aspirator, of which he promptly availed himself, notwithstanding the objections he met with from others. "Ridicule," he says, "was pointed at me by some high in surgery: at first the whole medical profession was against me." He could not stand still and see men die whose lives could be saved. Chew had a patient die suddenly from this cause. Many authors mention cases of death from the large amount of fluid. Wilson Fox summed up from the records between 50 and 60 deaths from effusion in the pleural sac. Moreover, many patients have died where the disease was not recognized. The condition of the circulatory apparatus is such that we can readily understand that emboli would form in the heart, in the large blood-vessels, and in the parenchyma of the lung itself. These clots produce grave results. If they form in the pulmonary veins or in the left heart, they determine an embolic obstruction of the central artery, with all its consequences—apoplexy, hemiplegia, etc. If it forms in the right heart or in the pulmonary artery, it may produce rapid aphasia and death (Paget). Louis was certainly wrong when from his 150 cases of pleurisy he deduced the law that none died of this disease per se. It is thus a matter of the utmost importance that we should be able to recognize that there is a quantity of fluid capable of producing such serious results. The call for relief and diminution of the amount of fluid by thoracentesis is urgent. What amount is dangerous to life, and how can we arrive at an accurate estimate? To what extent can we judge by the subjective symptoms, especially by the dyspnoea? Andral and Trousseau both speak of it as a very fallacious and uncertain symptom, and by itself may be unimportant as an indication. In the beginning of the disease we find suffocating dyspnoea for a time when there is very little fluid. Diffusible stimulants and anodynes give relief. On the other hand, there are patients who with large amounts of fluid, even two quarts, walk about with but little difficulty in breathing, and attend to their pursuits unconscious of being in danger of sudden death. Bowditch58 speaks of several fatal cases in simple pleurisy from excessive amounts, "from sudden failure of the power of the heart, with or without more or less dyspnoea." This is especially the case where the fluid forms insidiously, without marked general symptoms. When, however, we meet with dyspnoea, together with other and more reliable symptoms, it is very significant of danger, and ought to force us to resort to thoracentesis to afford mechanical relief. If we rely upon general symptoms, we may be deceived as to the amount of fluid, and serious results may follow. However, we must bear in mind that the most imperative reasons for thoracentesis are the signs of threatened failure of cardiac power. Bowditch lays down the rule that "if the dyspnoea is excessive, so as to amount to permanent orthopnoea, or if I learn that within a few hours previous to my visit there has been even one attack of momentary orthopnoea during which the patient felt as if the breath would be wholly lost, I tap immediately, provided I am sure that there is even a small quantity of fluid in the pleural cavity, and that it is apparently the chief or perhaps only cause of the orthopnoea. I fear," he says, "death may occur before my next visit." This eminent American authority on this subject lays down as the result of his vast experience the rule that "when a patient comes under notice in whom a large quantity of fluid has been long effused, I advise thoracentesis as the first remedy." The author ventures to assert that where the amount is excessive there is imminent danger to life from the mechanical results of the presence of the fluid, even during the febrile stages; consequently thoracentesis is urgently necessary. I am confirmed in this view by Dieulafoy, Fernet, Clifford Allbutt, Marshall, and Cross. Barnes59 says in all cases where the effusion is large and where dyspnoea is urgent it is better to operate at once. "It is my practice to operate at once when the chest is two parts filled with water, without waiting for urgent dyspnoea." Dieulafoy, in discussing these questions, states,60 after consulting all the authorities accessible to him, that death has never been caused by less than two liters (equivalent to 62½ fluidounces), except in one instance reported by Blackey, where after death there was found 1500 grammes (47 fluidounces). In adults with well-formed chests he considers 1800 or 2000 grammes as the amount demanding surgical interference. He candidly acknowledges that he cannot make this an absolute rule, because the capacity of the pleural sacs must necessarily vary in different individuals according to their height, breadth, development of thoracic muscles, sex, etc.; consequently, the inconveniences and functional disturbances produced by a given quantity of fluid in the chest must be different in different persons. But how can we arrive at an accurate estimate of the amount in the chest? Dieulafoy,61 in calculating the quantity, states that if it amounts to 1200 grammes when it reaches the sixth intercostal space, it ought to be valued at 2000 grammes when it is found at the third intercostal space. This is only approximative and unreliable. The height of liquid is not always proportional to quantity. It varies with size of chest, resistance of organs and walls, and condition of lungs. Potain insisted upon the difficulties that the pulmonary hyperæmia caused in the diagnosis, the abundance of fluid, the variable degree of yielding of the lung, and the adhesions which have drawn the walls to the lung. The true way of judging of the necessity for the operation is from the grave functional disturbances and by the definite positive physical signs which give us unmistakable indications which we dare not neglect. We can calculate the amount of the effusion by the level of the flatness on percussion, by mensuration with the cyrtometer, and of the impaired thoracic movements by the stethometer. Physical examination reveals the extent of the displacement of the heart and other viscera. The displacement of the abdominal viscera, the liver, the spleen, and the stomach shows that there must be excessive amount of effused fluid in pleura—enough to produce serious intra-thoracic pressure. This is a condition demanding surgical interference. The Skodaic resonance under the clavicle, the complete flatness being horizontal instead of giving us the Ellis curve, impaired resonance over the posterior triangle becoming absolute dulness, the presence of cavernous or amphoric respiration near the sternal-clavicular articulation, and, in rare instances, subclavian murmur from pressure upon the subclavian artery,—all these signs give unmistakable evidences that the pleural cavity is full of fluid. It is important, in considering the treatment, to form a correct estimate of the degree of intra-thoracic pressure, for Erichson has shown that the mere collapse of a lung affects but little the facility of the circulation through it; its compression or forcible collapse necessarily retards the circulation and throws extra work upon the already overburdened heart. The more precise our physical diagnosis, the more appropriate will be our treatment. Douglass Powell found the intra-thoracic pressure to vary from a – pressure to ½ and 1½ inches of mercury at the commencement, and from –1/8 to –½, and even –1, inch mercury at the termination of paracentesis, there being in all cases a more or less considerable amount of fluid still remaining in the pleura. He states, as the result of his own observations, that in recent cases the period of effusion at which the intra-thoracic pressure is converted from a – pressure or zero to a positive pressure upon the lung and heart is marked clinically (1) by the flatness mounting up above the third cartilage (patient in sitting position), and (2) by the Skodaic resonance becoming changed from the full note to a more tubular quality. The extent of Skodaic resonance is a very valuable indication of the amount of fluid, and consequently of the propriety of operating. If this tympanitic resonance be down to the third rib, and the cyrtometer shows no decided enlargement, we had better not interfere. On the other hand, if the Skodaic sign is not heard, and instead there is flatness, we will be sure to find decided increased measurements and tubular breathing behind. Under such circumstances we may feel confident of positive intra-thoracic pressure of from one inch to one inch and a half of mercury—an amount sufficient to compress the lung and interfere with the heart's action. There is some danger of syncope, even if the patient remains motionless in bed, but if he moves about he is in imminent danger. The subject is annoyed by a straining retching cough with frothy, viscid sputa with perhaps some discolored points. The heart and the lung of the healthy side give warning of the danger, which ought never to pass unheeded. A murmur may be heard over the displaced heart, and over the lung on the unaffected side we may hear a fine crepitant râle, showing pulmonary hyperæmia and resulting oedema. The syphon or aspirator will afford, by withdrawing perhaps a quart, the necessary relief. Nature will do the rest in a large proportion of cases.
58 Unpublished MSS.
59 Brit. Med. Journal, Dec., 1877.
60 Nouveau Dict. Méd., vol. xxviii., art. "Thoracentesis."
61 Loc. cit.
We cannot always estimate accurately the quantity of fluid by the displacement of the heart and other organs. The retractile energy of the lung is a very important factor in producing this result. A very large effusion, associated with a very powerful lung, will produce but slight displacements, while small effusions, when the lung of the affected side has lost its elasticity, will cause relatively great displacements (Garland). If there be no adhesions present, the letter S curve of flatness becomes a sign of the greatest value. It marks accurately the height of the effusion. Knowing this, as well as the position of the heart and diaphragm, and the capacity of the chest, we can estimate the quantity of fluid in the pleural cavity. If in left pleurisies the heart be so pressed out of position that its apex beats to the right of sternum it is very diagnostic. With these signs, whether accompanied by dyspnoea or not, we must regard thoracentesis as imperatively called for. The presence of the febrile movement is not a counter-indication under these circumstances. The presence of a basic murmur, caused by the heart or aorta displacement, is an urgent indication for surgical interference.
There are attacks of fainting and syncope, suffocative paroxysms, with irregular and painful palpitations of the heart, with sometimes alarming threatenings of asphyxia—especially in pleurisy of the left side. These symptoms are probably due to the twisting of the inferior cava as it passes through the quadrilateral foramen of the diaphragm. The danger is necessarily increased by long continuance of the effusion. Prompt surgical treatment is indicated when we detect evidences of embarrassed circulation in the opposite lung, with a blowing quality of respiration and subcrepitant and oedemic râles.
In all cases of double pleurisy, where the total amount is sufficient to fill one whole cavity, we ought not to postpone operating. Even when the effusion is not very large, if there are other diseases of the respiratory or circulatory systems to cause grave complications, and danger of increased impairment of their functions, thoracentesis is rendered necessary. That these conditions justify thoracentesis we believe no one who has any practical experience will question. But two conditions exist where there is considerable difference of opinion in regard to the propriety of operating: 1st, during the febrile stage, and, 2d, where moderate effusion remains unabsorbed.
In regard to the first of these, many authorities, even among the most enthusiastic advocates of the operation, have contended that unless there is imminent danger to life from the excessive collection of fluid, it should not be withdrawn, as it would at once re-form, and additional inflammatory action might be excited by surgical treatment. Castiaux,62 however, strongly advocates the view that the operation by aspiration will hasten the cure of acute pleurisy and prevent the formation of the fibrinous deposits and bands which to a greater or less degree, even in moderate effusions, impair the expansion of the lungs. He relates 37 cases, almost all of which were operated upon by himself. He was successful in all of them, and the patients suffered no inconvenience or discomfort in consequence. In most of his cases the pulse and body-temperature fell (perhaps the same day, certainly the next morning), and even became normal after the operation, and the patients improved rapidly. He aspirated as soon as he detected the presence of fluid by exploratory punctures, believing that from the moment we have at our disposition sure means of relief which are harmless, it is useless to leave to nature the duty of removal—useless to leave to untrustworthy medication the relief which we can promptly give. He operated at the height of the first or inflammatory stage of the disease. He assigned as reasons for operating that he thereby relieved the lung of the compression which impairs expansion; that he removed a liquid rich in fibrin and capable of increasing the thickness of the neo-membranes; that by restoring the power to dilate he further prevented the lung from being compressed by the false membranes. These membranes cannot become organized unless they are separated by fluid. He states that he removed the fluid as completely as possible. As soon as the cavity was emptied respiration was made easy and the patient was relieved. Auscultation showed, by the vesicular murmur, that the lung had resumed its place without difficulty from top to bottom. The effusion returned, only in a few cases, with high temperature and frequent pulse, but another operation effectually arrested them. The pleurisy was cut short and puncture was considered the means of aborting the disease. The duration of the disease treated by this means was much shorter. Thus the patients were not forced to retain for months the liquid and false membranes in their chest. He states emphatically that there never supervened any accident, and especially that he never witnessed as a result the transformation of the serosity into pus, although it might appear theoretically likely to occur, as the serous membranes, already inflamed, ought to be more sensitive to injury.
62 Thèse de Paris, 1873.
This testimony is very strong. Moutard-Martin operated upon 12 patients with fibro-serous effusions where they had existed less than ten days, and where there was more or less of fever. Out of this number, 8 had no reproduction whatever of fluid, and in 4 there was only a slight re-formation, and there was no degeneration into purulent fluid in any of them. In the other cases operated upon, where the effusions dated from twenty to sixty days, the fluid was almost always reproduced, though ordinarily to a moderate extent. He urges the prompt withdrawal of the fluid as the most successful method, especially if there is reason to suspect the formation of false membranes.
Wedal's63 results confirm this view of the harmlessness of punctures during the febrile stage; and, more than this, they show that they hasten the cure. He operated on 17 patients from the second to the fifth day, and three times from the eighth to the tenth day. In cases of acute disease, where the patients were exempt from pulmonary or bronchial complications, the cure was not protracted beyond the twelfth day. Some were cured by the sixth day. His patients were, for the most part, vigorous men, young soldiers—very favorable subjects. Ordinarily, however, as shown by J. L. Mason's64 report of 132 cases where the operation was not performed, the duration of the attacks was weeks, and in some cases months. He considers the operation more apt to be successful if performed early in the disease, and that the existence of fever is no contraindication. The author has always pursued a more conservative course, and abstained from operating in the febrile stage unless, as in three instances, the effusion was so rapid in its formation that there was danger of serious consequences from the amount of the fluid. In these three instances the result was successful and without unpleasant sequelæ. Moutard-Martin65 states that aspiration made during the febrile stage is in no way prejudicial to the patient. Dieulafoy66 advises us to wait until the fever falls.
63 Étude clin. des épanchments pleurit., 1877.
64 Boston City Hospital Reports, 3d Series, 1882.
65 Loc. cit.
66 De la Thoracéntèse dans la Pleur. Aigue, 1878.
To remove the effusion during the inflammatory stage does not appear to be rational treatment unless the quantity is so excessive as to endanger the life of the patient. The fluid remains limpid unless exposed to air or contact with foreign substance. When, after a time, there is some coagulation, it is only of a thin layer which covers and protects the roughened surface of the pleura. A certain amount of effusion is useful; it separates and bathes in a bland fluid the tender and inflamed surfaces, and keeps at rest the affected portion of the lung. The lung in health exercises a constant traction upon the pleural sac, the vessels of which have therefore to sustain a negative or aspiratory pressure: this being so, it is physiological that if these vessels become temporarily weakened and congested by the inflammatory process, increased exudation proceeds from them. The effect of this exudation is to neutralize lung-traction, and therefore to lessen the afflux of blood to the weakened vessels. "Fluid effusion being thus both natural and salutary, in acute pleurisy we must be watchful, but not meddlesome" (Powell). We must not hurry, but we must try if nature will not by spontaneous absorption cause it to subside. We can ordinarily do this up to the end of two or even three weeks before resorting to artificial means.
The defervescence in pleurisy, we have seen, has no fixed period, as in pneumonia. In favorable acute cases the absorption begins as soon as the temperature begins to fall. Moreover, the liquid may be absorbed, notwithstanding the continuance of fever, and the effusion may continue notwithstanding the defervescence. In the subacute form the febrile period passes by unnoticed, although the effusion is often in large quantity.
When not urgent, how long should we wait for absorption of fluid? This is a question much discussed, and not yet settled. What becomes of the effusion in the acute pleurisies?
In the first days of its formation the liquid portions of the effusion are reabsorbed by the normal vessels of the serous membranes at the points left intact and the recent vessels of the neo-membranes, but the organization of these last demands, to be complete, from two to three weeks; it is not until the end of that time that they will be most favorable to reabsorption. Dybkowsky points to the anatomical fact that the lymph-vessels are found only in those parts of the costal pleura which cover the intercostal muscles, while the portions which are reflected over the ribs are destitute of such vessels.
On the other hand, the eccentric pressure made by a considerable effusion on the pleuræ may retard their vascularization and lengthen out the work of absorption. Moreover, during the time necessary for that organization a certain quantity of coagulable fibrin is deposited on the surface of the serous membranes. The pseudo-membranous bridles are not slow in forming, and cause the adhesions which press the lung against the costal wall, the vertebral gutter, and the superior parts of the thoracic cage, toward which the effusion tends to force them.
In very favorable cases the effusion may disappear by the twentieth day of the disease. In many cases, however, it lasts with the false membranes for several weeks, and not infrequently for many months. Cases are recorded by Powell and others where the effusion remained of a sero-fibrinous character for eighteen months and two years. Flint mentions two cases where the effusion was permanent, having lasted for years. Wilson Fox67 thinks that there is but slight danger of the fluid becoming purulent from mere lapse of time unless the patient should have another fresh inflammatory attack. It must be noted, however, that such is not the case in children. Voyet68 says that simple pleurisy in infants is transformed into purulent pleurisy with facility and extreme rapidity—so much so that when with these a serous effusion is slowly absorbed there is great danger of suppuration taking place. M. Vertiac69 states that chronic serous pleurisy may not exist among children. In 13,000 sick children in eleven years Barthez did not have a single case. Pathological anatomy has demonstrated to us that this fluid in separating these neo-membranes on the parietal and pulmonary pleuræ increases their development. The plastic rugosities collect the fibrils of fibrin on their surface, in the same manner as they are found on the twigs in whipping the blood, and as the atheromatous deposits on the interior of blood-vessels favor the formation of emboli. These false membranes may cause a number of complications by surrounding the lung with a thick, inelastic shell. The collapse of one part of the lung diminishes necessarily the field of hæmatosis, and consequently causes a compensatory congestion of that lung, and even of the lung of the other side. This occurring in an individual predisposed to tuberculosis or in a condition to develop and cultivate the bacillus tuberculosis may start the disease. Formad70 maintains that pleurisy is a very frequent cause of pulmonary tuberculosis. These imperfectly organized embryonic membranes cause deformities of the thorax; they are good ground for the growth of pathological products, such as cancer or tubercle; their fragile capillary vessels are the principal cause of a most troublesome form of hemorrhagic pleurisy. (See [HEMORRHAGIC PLEURISY].) If the lung be compressed but a short time, it does not undergo irreparable injury, but if for a considerable time, the thickened organized membrane, with the effusion, causes a more or less considerable atelectasis, binding down the lung and preventing its expansion. The author holds that the effusion, after the fever has subsided, is, in itself, a foreign and troublesome element; for even with a medium effusion we are not exempt from unpleasant results.
67 Brit. Med. Journ., Dec., 1877.
68 Thèse de Paris, 1870.
69 Ibid., 1865.
70 Paper read before the Baltimore Clinical Society, February, 1883.
Although, in moderate effusions, there is no compression of the lung, yet there is necessarily collapse of it pari passu with the amount of fluid. This interferes with its retractive power—the aspiration force, as it has been called—by which the venous blood is drawn into the right side of the heart. T. B. Curtis of Boston calls attention to this very important fact, and shows that the result must be disturbance of circulation, with imperfect blood-supply to the heart, interrupted cardiac action, feeble arterial tension, together with venous repletion and stagnation. In consequence of this condition there is a diminution of the quantity of urine, and, as generally occurs where there is venous congestion, a small quantity of albumen, cyanosis, etc. Fraentzel, Traube, and Lichtheim attribute the venous stagnation, etc. to obstruction in the pulmonary circulation resulting from pressure exercised by the effusion. Curtis and Garland hold that these bad symptoms are not caused by pressure, but by the diminished pulmonic retractility which exercises the negative pressure of emptying the large venous trunks.
Such being the ill-effects of the retracted lungs, is it well to allow even a moderate amount of fluid to remain in the pleural sac after Nature has failed to remove it? Besides, the presence of liquid alone displaces the organs, especially the heart and lungs; adhesions form and keep them in an abnormal condition. The retracted lung, bound down by bands, becomes enfeebled, loses its suppleness, and is rendered rigid, seriously impairing respiration. There exist three factors—false membranes, adhesions,71 and interstitial pneumonia—which tend to seriously disable the lung and even to produce complete atelectasis pulmonum. We must bear in mind that there is some danger of the fluid becoming purulent, especially if a fresh inflammatory attack should occur. The less time a pleurisitic effusion lasts, the sooner the patient will be placed beyond the probability of these serious injuries to the process of hæmatosis. It is but right to give Nature an opportunity, assisted by iron, salines, diuretics, iodine, and even blisters, in cases of moderate effusion. The rapidity of Nature's work in many cases in removing large quantities of fluid here and elsewhere is wonderful. But if she does not act, we ought not to let our patient become feeble and depressed in his nutrition, or perhaps maimed for life, by not withdrawing the fluid. Sometimes the absorbents only half do their work of removing the fluid, and leave a quantity in the chest. Under these circumstances tonics, good diet, and change of air will complete the absorption.
71 According to Wilson Fox, the density of the adhesions and false membranes is determined within the first fortnight of the effusion.
The question arises, How long shall we wait for absorption? Test first, by exploratory puncture, the nature of the fluid: if it is fibro-serous day after day, try by the cyrtometer the size of chest and by percussion the exact amount of flatness. If there is no evidence of any decline of the effusion in two weeks, slowly withdraw some of the fluid. This will start the absorbents into activity, for the natural absorbing power of the pleura is diminished when it has been unduly stretched for some time. The layer of lymphatics subjacent to the pleura and communicating by stomata with the pulmonary lymphatics, together with the other absorbent vessels, appear to be unable to remove the fluid. We maintain that the pressure on the orifices of the lymphatics is often too great for absorption to take place, and that by removing the pressure we can start the absorbents into activity. Aspiration under these circumstances shortens the duration by several weeks and hastens convalescence. J. W. Hunt72 advises that we should wait two or three weeks before operating. Loomis73 says if the fluid remains stationary for one week, or is increasing when the cavity is half filled, we must operate. Barnes74 would only wait a few days if the chest is half full, to see if absorption will begin to remove it. When the chest is two-thirds full, he advises immediate surgical interference. Oxley75 advises a delay of three or four weeks before operating. Anstie's76 rule is to postpone operating for one month. T. Clifford Allbutt's77 general rule is, if an effusion rises above the angle of the scapula, and abides in that quantity or increases for two or three weeks in spite of adequate treatment, it must be drawn off, whether the patient be embarrassed by it or not. Bowditch78 says: "If the effusion does not subside under the medical treatment, and the symptoms have not lessened after two or at the utmost four weeks, I have, after long experience, been led to the following general rules for my own guidance: 1st. I never allow any time to elapse before performing thoracentesis after a decided and prominent dyspnoea appears, or if a sudden and very threatening orthopnoea occur, or if I find the chest has become full or more than half full of fluid in a perfectly latent manner during a month of illness. 2d. After there is dulness to the angle of the scapula, with the other rational and physical signs of pleuritic effusions, I tap within four weeks, even if the patient seems quite comfortable, if the line of dulness does not get lower and seem to subside under the treatment. I think fatal mistakes are made by delaying too long before tapping." The author prefers ordinarily to wait for the subsidence of the fever in acute cases, unless the effusion is in dangerous quantity. The practitioner must continually use the thermometer as well as observe physical phenomena and general symptoms. Cyrtometric tracings give very valuable indications as to the activity or non-activity of the absorbent vessels. After the fever subsides the fluid may be regarded as a foreign body doing harm to the two principal organic functions upon which the nutrition of the animal frame is dependent—respiration and circulation. It is from this standpoint that Dieulafoy79 advises, if absorption is slow or difficult after two or three days, that the fluid should be aspirated. The greatest success has been obtained in cases where the fluid has been present but a short time. The number of fatal cases is increased by delay of operation. Toussaint's cases show this:
| 4 | deaths in | 176 | cases | operated | upon | between | 1st | and | 20th | day. |
| 6 | " | 80 | " | " | " | " | 20th | and | 60th | " |
| 1 | " | 7 | " | " | " | " | 60th | and | 120th | " |
In the quiet kind of pleurisy, formerly designated the subacute or latent, thoracentesis is especially applicable. Ordinarily, when the practitioner is consulted, there is considerable fluid, without any febrile movement. Here we are in duty bound to assist nature. Iron in the form of the tincture of the chloride and the syrup of the iodide are our best remedies. We cannot give the patients the tonic influence of outdoor air with exercise, because there is danger in their moving about; but they should have an abundant supply of nourishing food, with light wines. Absorption is very inactive and sluggish. Even with moderate effusion to the extent of one-third of the pleural cavity, we cannot let the fluid remain too long. Pidoux designated this form of pleurisy as the thoracentesis variety.
72 Loc. cit.
73 Dis. Resp. Org., etc., 1875.
74 Loc. cit.
75 N.Y. Med. Ex., Sept., 1882.
76 Syst. Med.
77 Quain's Dict. Med.
78 Unpublished MSS.
79 La Thoracent. par Asp. dans les Pleur. Aigues, 1878.
Conclusions.—1st. The author wishes to be distinctly understood as not advocating aspiration simply because there is an effusion, as a mere matter of routine, for its indiscriminate employment is undoubtedly attended with risk. He does claim that its performance is imperatively called for when the pleural cavity is full or nearly so; when there is much displacement of the heart or other viscera; when the patient is suffering from serious dyspnoea and danger of syncope, and when there are complications of disease of any kind of the other side or of the heart; finally, when there is double pleurisy. Bowditch states that he has seen thoracentesis give great relief in effusions following Bright's disease and cardiac diseases.
2d. He thinks that in acute cases, after the subsidence of the fever, if the pleura is one-third full of fibro-serous fluid, Nature will probably do her work of removal promptly. If she shows no sign of doing so, we should come to her assistance in about ten days or two weeks, and draw off a portion of the fluid—enough to relieve pressure and to encourage the absorption of what is left in the sac.
3d. In the subacute or chronic fibro-serous effusions it is not well to wait over three weeks before operating. As he shall show in the study of the dangers and objections, he considers the operation a perfectly safe one if the simple rules now generally observed by operators are faithfully carried out.
In studying the advisability of operating where there are not urgent indications we must ever bear in mind that while it takes a large quantity of fluid to compress the lung, the retracted lung may, by neo-membranes, be kept to its diminished volume. As long as the lung is able to lift up the fluid and the diaphragm it is in no danger of atelectasis. It is in a state of physiological rest. In a subject of bad constitution interstitial changes may indicate an earlier operation, but, if an effusion exists on the side on which there is already lung disease of a phthisical nature, we should be loath to interfere; for "experience has shown that an effusion checks, and sometimes arrests, the tubercular process" (Powell).
Contraindications.—These are principally in connection with the general condition of the patient. If it is such that there is no hope of his rallying, if he is very old, or if he has intervening croupal pneumonia, the operation is not justifiable. If the quantity of fluid is not large and does not interfere with organic functions, we can wait for some time.
Mode of Operating.—The old trocar method of operation is now abandoned. It was not always an easy one, was painful, and there was more or less danger of cutting the intercostal artery, of introducing air, and of establishing, by the size of the puncture, a fistulous orifice. If, perchance, the lung was perforated by the trocar, pneumothorax was established. In some cases of sacculated and limited effusions, and in chronic cases where the membranes were thick, it was not effectual, and if the fluid was not reached, the operator hesitated to introduce the trocar elsewhere. When the fluid flowed through the trocar, it came frequently in jets with painful coughs. The above operation was quite a formidable one. Now thoracentesis is always performed with very fine perforated needles attached to aspirators of some modern pattern, and guarded by Fitch's dome-trocar or Castiaux's protected point. We employ Dieulafoy's Potain's bottle-aspirator, Castiaux's of Paris, or Raumussen's of Copenhagen. Flint recommends the use of Davison's syringe. We fear it would be found too rough an instrument for so delicate an operation. The points of attachment of the bulb with the tubing are not sufficiently air-tight. The valves are very imperfect, and easily get out of order. In our efforts to pump out the fluid we might throw air in, and with it particles of organic matter.
The operator has his choice among no less than thirty-odd instruments similar to Dieulafoy's. They all work upon the same principle—the close operation, the withdrawal of the fluid by aspiration. The needle or trocar must be capillary: the smallest that is effective is the best—say a half millimeter in diameter—in order to make the orifice as minute as possible.
If we prefer the syphon, we must use a larger canula than we employ for aspiration—one of four millimeters in diameter. It should have two outlets—one straight, for the trocar, and one at an angle, for the attachment of the tubing. It should also be guarded by an air-tight collar. Into the syphon tubing a T-tube may be inserted for the purpose of attaching a side tube to be connected with a mercurial manometer, by means of which the exact intra-thoracic pressure may be observed during the operation. The syphon tube should be long enough to provide a fall of one, two, or three feet, as may be necessary. A fall of twelve to eighteen inches is usually enough, as we wish to remove the fluid slowly. We can easily increase the force by lengthening the tube. If the canula should become obstructed, lowering the basin suddenly will probably remove the piece of lymph. The trocar can be pushed again through the canula if necessary. In case the aspirator should be needed, the end should have a metallic joint affixed to it. In all the instruments used, absolute cleanliness should be observed. The tubing previous to operation should be filled with a solution of carbolic acid (1:40).
In cases of rapid effusion, especially during the febrile stage and when the intra-thoracic pressure of fluid is great, some prefer using the feeblest form of aspiration. Southey's capillary trocar, with drainage-tubes attached, is used as a syphon for this purpose. The fluid is drained off through a narrow india-rubber tubing which is placed under water to prevent air being drawn into it. Ordinarily, the use of the fine aspirating-needle without much force, and slowly drawing off the fluid, answers the same purpose. The fear some have expressed, of the danger of injuring the lung by the force of the rarefied space, is more theoretical than real. Even with a canula of the size that Southey employs there is some danger of leaving a fistulous orifice, for it has to be kept in for hours. If the smallest tube is used, from which the fluid simply comes in drops, the operation consumes five or even ten hours. Southey speaks of cases where the flow was kept up for twenty-four hours. Unless aspiration is resorted to, flocculi may easily stop up the canula, and then we are compelled to reintroduce the trocar, and afterward to reattach the tubing. Oxley, who thinks that the best results are obtained by the use of these tubes, acknowledges that so much time was consumed that he inserts four canulas, drawing off 44 fluidounces of fluid in one hour and ten minutes, thus defeating the object of using this method, which was to draw off the fluid very slowly, so as to enable the lung to expand gradually and healthfully.
There are cases where, to withdraw the fluid, more suction force than is usually employed with the syphon has to be used in order to antagonize the negative force exercised by the traction of the lung and the passive tension of the diaphragm. The author recently had a case where, notwithstanding the presence within the right pleural sac of a quantity of fluid large enough to obliterate the Skodaic resonance under the clavicle, not a drop could be drawn out by a syphon attached to a canula of 2 mm. in diameter. Having no additional tubing to increase the force of the syphon at hand, he used Dieulafoy's rack aspirator, ½ mm. in diameter, and drew off a quart of fluid—enough to relieve the symptoms of oppression. Stone reports a case of the kind where, although there were two quarts of fluid in the pleural sac, no fluid could be drawn out with a syphon exerting a force of 1½ pounds to the square inch, or one-tenth of an atmosphere. In the same case there was actually, in inspiration, a negative pressure exercised by the lung of two inches of water. Stone mentions another case where a boy fifteen years of age died from the quantity of fluid, which would not flow out when tapped. If he had had an instrument by which he could have used aspiration he would have saved the life.
The value of this syphon method has within a few years grown much in favor. It is simple and inexpensive. It allows the fluid to be drawn out with a uniform and feeble aspiratory force. The flow is very slow, which gives the lung time to expand gently, and the displaced organs to return gradually to their normal position. With the manometer attached we can judge accurately as to the intra-thoracic pressure. The size of the canula has to be larger than when we employ the aspirator—4 mm.—whereas with the latter we use ½ mm. or 1 mm. in diameter. If by any accident the lung should be perforated, the larger orifice would not be as harmless and insignificant as the smaller one. It must be borne in mind, especially in cases of long standing, that the neo-membranes are very vascular, and that with a 4 mm. perforator we may rupture the blood-vessels and complicate matters by the escape of blood into the pleural cavity. It is claimed that when the canula and syphon tubes have been introduced the patient can be left in charge of the nurse. This, the author thinks, should never be done, for nurses are rarely competent to judge whether a sufficient amount has been withdrawn, nor are they fit to assume the responsibility of acting in cases where promptness of treatment may be of the utmost importance. The operator or a competent substitute must remain until the operation is over. The withdrawal of fluid must, moreover, be slow, for slowness contributes in a great degree to lessen the dangers. Fraentzel recommends testing the force of the aspirator in the palm of the hand. Garland80 employs needles which are 1–2 mm. in diameter and remove only 50 to 100 grammes per minute. The thoracic pressure must be relieved by the withdrawal of only enough fluid to effect that purpose. It has been objected that the negative force of the aspirator is uncertain. It is a well-founded objection, yet we can employ with it a feeble force by exhausting only a portion of the air from the cylinder or bottle, and thus remove the fluid cautiously and very deliberately. It is admitted that if there is no intra-thoracic pressure the fluid will not flow out unless we introduce air or negative force. We claim that the syphon and the aspirator with capillary needles, employed with the precautions dictated by modern experience, are both safe and effective. Ordinarily, we prefer the bottle aspirator of Potain, or Dieulafoy's instrument with the manometer attachment.
80 "Dis. of Pleura," in Ziemmsen's Appendix.
Modern aspirators, if in perfectly good order, completely prevent the possibility of septic contamination by admission of air. Unclean needles and canulæ can—and we fear formerly often did—convert sero-fibrinous into purulent pleurisies. A case came under Powell's observation in which carelessness in this respect apparently led to decomposition of the fluid, suppurative pleurisy, and ultimately to the death of the patient. Before operating we ought always to test the instrument, and see that it works well by passing carbolized water through it. The points should be put in the flame of a spirit-lamp, and then dipped in carbolized water and glycerin—not in oil, which may be rancid. The hands and clothes of the operator should not be overlooked in this regard. The atmosphere of the room should previously be completely cleansed by ventilation, and afterward purified by atomization of disinfectants. We must not, in a word, incur the slightest risk of converting a simple inflammatory effusion of fibro-serous fluid, a mild disease, into a suppurative inflammation, a very troublesome, dangerous one.
A needle of not larger diameter than 1 millimeter (No. 2) should be connected with the end of the tubing. Next turn the stopcocks which shut off the barrel from the tubing on both sides, producing a vacuum in the receiver. The patient should then be placed in the recumbent position in bed, with his head and chest raised. We prefer this position, as the easiest for the patient at the time of operation and less apt to produce syncope or faintness. He can, without being moved, lie down in the horizontal position, which he should maintain for at least two hours. Bowditch has, without any accident, had his patients to sit during operation sidewise in a chair, with one arm resting upon a pillow placed upon the top of the back. The operation is accompanied with so little pain that it is not necessary to use either general or local anæsthesia. Some surgeons advise before operating the administration of a small dose of morphia hypodermically, or a stimulating drink of whiskey. We are not in the habit of using either. We have generally allowed patients to take a good meal of easily-digested food (milk if they consent) about two hours previous to the operation. Whiskey and ammonia we have ready in case of need. If we find it necessary to use a 4-mm. canula for syphon, it may be best to spare the pain of its introduction by local anæsthesia by ether, or by rhigoline in Richardson's spray, or by applying a piece of ice surrounded by salt, as suggested by Powell.
The point of puncture should vary according to the quantity of fluid. If the fluid is excessive, we can operate as high up as the fifth intercostal space on the right side and the seventh on the left. We can choose a lower intercostal, but as it is not proposed to draw off all the fluid, the higher operation is preferable. If the chest is two-thirds full, we can take the seventh or sixth intercostal space on the right side and eighth on the left. If only one-third of the cavity is occupied by fluid, we can go as low as the eighth intercostal on right and left sides, on a level with the angle of the scapula in the axillary line. If the quantity of liquid is so great as to force the abdominal viscera, especially the liver and the spleen, below their normal position, we may be safe in puncturing below the seventh intercostal space. But if such is not the case, the diaphragm may easily be touched on a level with even the seventh intercostal space. Aran plunged a trocar into the liver when operating through the seventh intercostal space. Ch. Bernard impinged upon the peritoneum at the same point. Woillez and Paul Barbille recommend the fifth intercostal space. Cruveilhier advises the third or fourth as being the point of the spontaneous openings. The author usually inserts the needle in the sixth intercostal space in the mid-axillary line: it is out of reach of the diaphragm and is accessible when the patient lies in the position in which he prefers placing him. The space is sufficiently wide and the parietes thin. Before operating the point must be examined carefully by percussion, auscultation, and palpation, so as to be accurate in the diagnosis that there is fluid at that point, and that nothing can be injured—lung, heart, or diaphragm.
Before inserting the needle the skin should be wiped over with an antiseptic solution. The skin being drawn up, the nail of the left index finger serving as a director, the point, having been first made aseptic, is introduced along the upper margin of the lower rib, taking care not to injure the periosteum—not by a boring motion, but by a sharp push, giving it a downward direction instead of a perfectly straight one, so as to avoid striking the lung. When the fluid is reached the stopcock is turned, so as to convert the needle into an aspirator. The index tells us whether we have struck the fluid, and its nature is shown. In chronic cases, where the bands are thick and partitions are firm, we may not find the fluid the first time. In such cases the needle is withdrawn and another point selected. The author had a case where he made no less than eight punctures before getting the fluid. At the last insertion of the needle he found it, and drew off a large quantity. The patient feels relieved in a very short time. As the fluid flows out the aspirating force should be only sufficient to draw it out slowly and gently. It is well to stop for a few minutes after aspirating about 4 fluidounces to watch the effects. The fluid running in a very small stream, we give the lung time to accommodate itself to its altered condition. The lung by this process is led, rather than forced, to resume its normal position. It is a difficult matter to fix the quantity that ought to be drawn off at one time. This must vary according to the circumstances of each case. Our rule has been to draw off more when the pleurisy is acute than when it is chronic. The long continuance of the fluid in the cavity has so impaired the lung's capability of expansion by the adhesive bands or compresses that the sudden withdrawal of a large quantity is attended with risk. If the patient bears the operation well, we may remove much more than if the contrary is the case. The amount withdrawn at the first operation should vary from 8 fluidounces to 16 fluidounces in a child, and 12 fluidounces to 24 fluidounces for an adult. We must bear in mind, as to the quantity to be removed, that ordinarily there is more or less danger of producing fresh engorgement of the capillaries and hyperæmia of the lung in removing a large quantity; and, moreover, it is unnecessary. We wish to remove the intra-thoracic pressure upon the lung and to promote the absorption of the fluid. The manometer will tell us accurately whether it is necessary to take out one, two, or three pints. If nature does not in due time remove what is left, the operation can be again resorted to. Slowness in the withdrawal of the fluid, as well as the small quantity drawn, lessens the probability of any unpleasant effects. Bowditch says: "I always draw with great deliberation. I pull so lightly upon the handle of the piston that it seems as if the fluid itself were pressing out from the chest and pushed the piston upward, my hand simply following that impulse. The instant that the patient becomes restless, especially if he have any constriction or sharp pain in the chest, I withdraw the tube, even if a large quantity of fluid remains. If I do this, I find the patient is soon relieved, and in most cases nature appears stimulated even by the withdrawal of a very small part of the effusion. The absorbents begin to act well, and the fluid that is left is speedily removed."
One point is of the utmost importance: the needle should be instantly withdrawn at the onset of dyspnoea, constriction, much cough, or any tendency to syncope. These symptoms are warnings we should never neglect. This is the time to administer stimulants, and ordinarily the patient soon recovers from these effects. We must not, especially in cases of long duration, expect to find much expansion of the lung until next day. The greatest success has followed cases treated by early operation and partial removals, repeated, if necessary, every day or two until absorption is commenced.
The needle should be taken out suddenly, the operator having previously turned the stopcock, and the skin allowed at once to fall over the orifice, which is so small that no air can enter. It is indeed obliterated at once. It may be well, however, to put some collodion over it, with a small compress. The patient ought not to be permitted to move for twenty-four hours after the operation. He should lie quietly in bed and partake of simple nourishment. The removal of fluid causes the return of friction sounds and of pleuritic pain. Nature slowly does her work of absorbing the fibrinous bands. The breath-sounds in some cases are not heard for weeks, or even months, after the operation. Complete recovery being slow, and the shock to the organism very serious, the patient should thoroughly re-establish his health and strength before reassuming his active duties. A protracted rest in an invigorating climate or a sea-voyage should be advised. If the lung is slow to expand, the patient should frequently practise long, deep inspirations.
Dangers of and Objections to the Operation.—Thoracentesis as a means of relieving suffering humanity has from time to time been praised and proscribed, even in this century. Boyer operated several times, and never saved a single case. Dupuytren had only 2 successful cases in 50. He said he preferred that his patients should die by the hand of God rather than by the hand of man. Sir Astley Cooper had only 1 successful case, Gendrin not 1 out of 20 cases. Davis saved two-thirds of his cases. The eminent W. W. Gerhard of Philadelphia looked upon the operation as nearly always attended by fatal results. What a contrast to modern views and clinical results! Since Bowditch and Trousseau popularized the operation, and Dieulafoy improved the aspirating instruments, there is now no difference of opinion as to the imperative necessity of operating in cases where there is, from the quantity of fluid, imminent danger to life. Up to Nov., 1882, Bowditch81 had operated 386 times in 245 cases, without a single fatal result, and with only 1 case in which alarming symptoms supervened. Dieulafoy's82 cases in 1878 amounted to 150, without the shadow of an accident. My colleague, S. C. Chew, has never met with any unpleasant result from his operations. The author has had 84 cases, with 138 operations, without any unpleasant result beyond temporary cough and slight dyspnoea. Fraentzel83 had 85 different cases, with 164 operations. A. L. Mason84 performed 122 operations in 70 cases, with no unfavorable result which could be attributed to the operation in any instance, but usually with great and permanent relief. In 42 of his cases 1 operation was all that was necessary. So common is the operation that cases are not reported unless there is something to attract attention to them. As illustrative of the great interest taken in the operation see the number of writers on the subject and the numberless articles in medical journals, and the modifications of instruments of all kinds connected with aspiration and drainage. Such being the case, we ought not to be surprised that some operators may have used the aspirator-needle when they ought not to have done so—that some should have neglected the simple rules now insisted upon as the result of experience.
81 Unpublished MSS.
82 Tho. Pleu. Aig., 1878.
83 Ziemssen's Cyc., vol. iv.
84 Loc. cit.
Although thoracentesis by aspiration is always a harmless operation in itself, there are dangers and accidents which may follow. They may be slight, serious, and sometimes even fatal. The number of deaths which have been the result of the operation, however, is small compared to that of persons dying from the effusion whose lives might have been saved by the withdrawal of fluid. Thoracentesis was frequently made use of without accident, and was considered a perfectly safe operation until Terrillon85 called attention to an accident which occurred sometimes after operating, a complication which Pinault86 had mentioned in 1853—the albuminoid expectoration. Terrillon reported 2 cases of sudden and rapid death with that symptom. Several similar cases, resulting in death, had been previously reported. Dieulafoy has collected from different sources reports of 6 deaths with albuminous expectoration, caused by acute oedema of the lungs brought on apparently by the operation of thoracentesis in twenty-four to thirty-six hours. In one of these cases (Gérard's) death occurred in ten minutes; in another (Gombault's) in fifteen minutes; in another (Bouveret's) in two hours; in Behier's in four hours. Terrillon's cases, where there was this frothy, albuminoid, and sometimes bloody expectoration, numbered 16, of which 6 were fatal. The patient is attacked with cough and oppression, with the characteristic expectoration. Auscultation shows the fine subcrepitant râles of oedema of the lungs, mingled with tubular quality and ægophony. Gradually, in favorable cases, the cough subsides, respiration is re-established, and in one hour the danger has passed. In fatal cases the cough becomes irregular and jerky, the agony increases, and the patient throws up the yellowish and albuminous expectoration in quantity varying from 50 grammes to (in one case reported by Moutard-Martin) 1 liter. The intensity of the dyspnoea and its duration vary very much—from twelve to twenty-four hours.
85 Thèse de Paris, 1872.
86 Ibid., 1853.
There has been considerable discussion among different authors as to what produce this serious condition. The view sustained by Hérard87 is the one generally admitted to be correct—viz. that it is from rapid congestion and acute oedema of the lung, and not from the passage of serous effusions of the pleura through the bronchi. Foucart88 relates a similar case of albuminous expectoration occurring in heart disease. This condition could not be produced by perforation of the lung, for the pre-existing vacuum renders the aspirator-needles the safest to introduce, because if there is fluid present it at once flows out and warns the operator not to push the implement farther in. In no autopsy has the orifice made by the needle been found, nor has it ever been known to produce pneumothorax. The quantity of albuminous sputa is out of all proportion to the orifice made. In several cases of reported perforation these symptoms did not occur. After the lung has been a long time compressed by an effusion, and when, in consequence of the expulsion of the liquid, it retakes its normal proportions, there occurs a rush of serum which is expelled by the bronchi. Hérard has seen patients in whom he could not find more than traces of liquid after the puncture, and who at the end of a half hour or an hour expectorated 500 to 1000 grammes of fluid which did not come from the pleura. That oedema of the lungs, or serous exudation from the capillaries into the walls and on the free surface of the alveoli, is a result of hyperæmia and pulmonary congestion is admitted by Robin, Bernard, Niemeyer, Jaccoud, and others. We have first congestion of the lung, then oedema resulting from it, ending in free albuminous expectoration, which comes not only sometimes from the diseased side, but from the healthy side, owing to pressure against the mediastinum and the other lung. This is an accident the possibility of which should be always before us in operating. No precaution ought to be neglected which will ward it off. It is instructive to analyze Terrillon's cases as to the cause of the oedema. As he considers that the aspirator, by draining out the lung, is likely to produce this unfortunate result, it is satisfactory to find that of the 16 cases where this unpleasant symptom was found, 12 were where the old trocar (Reybard's) was used without aspiration, and 4 where aspirators were used. Of the 6 fatal cases collected by Terrillon, 3 were with the trocar and 3 with the aspirator. Five out of the 6 fatal cases are found to have been not simple pleurisies, but pleurisies with complications, such as heart disease, bronchitis, tuberculosis, numerous adhesions, double pleurisy. The same may be said of the benign cases. In addition to these complications, large quantities of fluid had been drawn out at one time. Dieulafoy challenges his confrères to produce an instance of death from this cause when the fluid removed did not exceed 1200 grammes. His rule now is never to withdraw more than 1000 grammes of liquid at one time, and in large effusions to empty the sac by several operations. The older and more complicated the effusion, the more rigorous should be the rule, because there is great danger in thoracentesis when the fluid has existed long enough to have compressed the lung to a serious extent by bands. All careful operators now follow this rule. It is dangerous, and withal unnecessary, to draw off large quantities at a time. The gradual removal of fluid diminishes the risk of syncope where a sudden withdrawal may be serious in its effects. The effect is to suddenly deprive the lung of pressure which has for weeks perhaps made it anæmic. The blood rushes into the empty vessels, the air into the alveoli, and violent congestion and consequent oedema result. If, on the contrary, we draw out moderate quantities at different times with the capillary needle, which is so small that its introduction is harmless, the lung resumes progressively the functions it has lost, and the circulation gradually enters. Thus there is no risk of congestion.
87 Acad. Méd., 30 Juillet, 1872.
88 Thèse de Paris, 1875.
In examining the fatal cases reported by different authors, Foucart, Dieulafoy, Mercier, Lerebenthel, and Gagnet, we find other modes of death in addition to those by oedema of the lung, such as asphyxia and pulmonary emboli, and, as connected with the heart, syncope and cardiac thrombosis. In most of the cases these accidents resulted indirectly from the operation in twenty-four hours or a longer time. In a case reported by Guyot it occurred three days afterward. Congestion by itself may cause sudden and rapid death by determining asphyxia.
There are other lung causes which produce sudden death following thoracentesis, such as atelectasis, consecutive to effusion; secondary pneumonia, caseous or not; pulmonary tubercles. Besnier reports a case of gangrene of the lung following paracentesis. Of the 8 cases collected by Dieulafoy which may be put into this category, we find death from pericarditis, cardiac clot, and from thrombosis of the pulmonary artery. Death from the heart may be due to old lesions, to syncope, or to the presence of clots in the heart or small circulation. Stokes has given fatty degeneration of the heart as a cause of death in simple pleurisy without operation. Syncope, with death after operation, is caused by the sudden return of the heart to its normal position. The heart being pushed out of position, the larger blood-vessels are distorted, and the course of the circulation is severely interfered with. A very slight cause will arrest the circulation. By aspiration the mechanical cause is removed, but a small embolus, may, by the increased force of blood, be carried into the pulmonary circulation. Death by emboli in the capillaries of the lungs is very similar to death from clots in the right side of the heart and at the origin of the pulmonary artery. These clots may be formed in the pulmonary vessels, or may be transported in the small circulation to points more or less distant. Potain in 1861, and Vallin in 1869, reported sudden deaths from effusion in the pleural sac, causing embolism of the cerebral artery. How far aspiration is responsible for accidents of this kind it is difficult to decide. Were they caused by thoracentesis or notwithstanding the operation? They are unquestionably the cause of death without the operation in excessive effusions. The conditions which produce these results ought to be well considered previous to operation. We notice that in most of these cases large quantities of fluid were withdrawn—2000 grammes (Legroux), 3 liters (Vallin), 3500 grammes (Guyot), 1500 grammes (Chaillon and Goquel). The withdrawal in cases of long standing of such large quantities had, beyond a doubt, considerable influence in producing the fatal result. Bowditch89 addressed letters to 60 physicians, living in 31 of the States and 2 in Canada—representative men—asking if they had ever seen or heard of fatal results following thoracentesis by aspiration. Of this number, 53 replied in the negative, and 7 in the affirmative. "Upon an analysis, however," he states,89 "of the circumstances under which death occurred in these last, I found nothing to shake my confidence in the operation, provided it be performed with proper precautions during and subsequent to the tapping. In no one of these cases had the operation been the sole cause of the fatal result." "In 4 there was extra motion on the part of the patient after operation, and in the other 3 the disease had been allowed to continue without aid from a surgeon long after the operation was needed. In 1 the operation was a forlorn hope. One patient died on the table from anæsthetics." Bowditch adds: "These cases should not lessen our confidence in the operation, but simply teach us caution on three points—namely: do not delay too long; be very careful to direct the patient not to move, if possible, for twenty-four hours after operation; be cautious of using anæsthetics." Bowditch, from 29 fatal cases collected from Otto Leichtenstein,90 from his own knowledge, and from European literature, tabulates the causes of death in American and European practice: 7 of these cases were caused by extra-exertion after operation; 3 from cyanosis and coma; 4 from spray injections; only 1 from syncope; and 2 from albuminoid sputa. He quotes the final remark of Leichtenstein: "Death or any serious symptoms are so rare that they ought not to have the least influence upon our estimate of this most benign and blessed operation." Bowditch states that there were only 7 deaths in this country (as far as he could ascertain), and 29, or four times as many, in Europe, although the operation has been done much more frequently here and for a much longer time. Does not this show that in this country, in following Bowditch's precepts of great care and deliberation, the operation has been more successful? He never ceased in his lectures and writings to caution us to suspend the withdrawal of fluid the moment the patient begins to suffer in breathing, even in the slightest degree. Of course there may have been other cases occurring in American practice of fatal results, of which no reports were made to Bowditch.
89 Unpublished MSS., 1882.
90 Deutsches Arch. für klin. Med., vol. xxv., 1880.
The author has carefully gone over Leichtenstein's collected cases, and he finds a number of deaths mentioned by other European authors which are not included in his list. (The reader is referred to the theses of Terrillon,91 Foucart,92 Foster,93 Dieulafoy,94 Mercier,95 Pinault,96 Wilson Fox,97 and others.) Terrillon alone reports 6 deaths with symptoms of oedema of the lungs following thoracentesis. Leichtenstein does not mention any deaths from embolism, such as are quoted by Goquel, Chaillon, and Woillez. In his collection he gives only 1 death by syncope, whereas Dieulafoy comments upon 4 as found recorded by Trousseau and other French authorities. Toussaint's98 statistical tables of 300 cases, collected from other sources, give 14 deaths. Wilson Fox collected between 30 and 40 deaths connected with thoracentesis. Besnier stated in 1876 that the mortality from pleurisy in the French hospitals had greatly increased since the practice of thoracentesis had been largely followed. It is difficult to account for this in the face of the statements made by so many of its innocuousness when properly guarded: it may be explained by the fact that suppurative pleurisies are often confounded with those of a fibro-serous nature and treated by simple aspiration. Many fatal cases of empyema are complicated with phthisis; formerly these were added to the mortality for phthisis; where paracentesis was performed upon them they were added to the pleurisy column. Bearing in mind that chronic pleurisies, serous and purulent, are frequently consecutive to diabetes, Bright's disease, chronic alcoholism, cirrhosis of the liver, and other organic diseases, patients die of the primary lesions, though they have been relieved of the secondary ones. These statistics may record the deaths as resulting from pleurisy, for which there was operative interference, instead of from the organic diseases.
91 Loc. cit.
92 Loc. cit.
93 Clin. Obs.
94 Loc. cit.
95 Thèse de Paris, 1876.
96 Ibid., 1855.
97 Brit. Med. Journ., Dec., 1877.
98 Thèse de Paris, 1878.
Formerly, when trocars and canulas of considerable diameters were used, only extreme necessity from peril to life made surgeons consent to operate. We claim that by capillary needles, gentle force, and protected points all the old objections are obviated. As Anstie says, there is no opposition to the modern operation by men who have fairly tried Bowditch's practice. Only theorists who are afraid of its imaginary results and men too timid to act hesitate to make use of it. We have discussed elsewhere ([Purulent Pleurisy]) the danger of admitting air into the pleural cavity, but we insist that in the close method, with capillary needles, there is no danger whatever of air entering. The puncture is so very small that it closes at once by the elasticity of the structure of the chest, just as the knuckle of the intestine in hernia closes after the needle has drawn gases and fluid out of it.
Another objection urged against puncture of the pleura in such cases is the possibility of perforating the lung by fine needles, thus letting air into the cavity and causing cough.99 Marotte read a memoir on the subject to the Academy in 1872. He reported 4 cases, in all of which there were only temporary effects, no serious ones. Dieulafoy100 says: "I have been witness to the puncturing of the lung several times, and I have never seen any accident supervene under any circumstances. I have thoroughly convinced myself that punctures performed with a No. 1 needle, diameter half a millimeter, are harmless, and experiments on animals have given me the same results." He even suggests aspirating a few grammes of blood from a congested lung in the first stage of pneumonia, and thus practising local bloodletting. The author has 3 times pricked the lung in aspirating—twice with a No. 2 needle, diameter 1 millimeter, where a few drops of blood were drawn into the instrument, and they did not even produce a cough or the slightest inconvenience. The third time was with a No. 4 needle (2 millimeters). From this puncture some air escaped into the pleura, and for a few days there was evidence of pneumothorax. It then disappeared entirely, the air being absorbed. The case was a circumscribed empyema, which entirely recovered.
99 Allbutt, Quain's Dict. Med., 1883.
100 Treatise on Pneumatic Aspiration, Eng. trans., p. 256.
It will be noted that throughout the discussion of this important subject liberal use has been made of a valuable communication specially prepared by Henry I. Bowditch for this purpose, and embodying the mature results of his study and experience of thoracentesis. It seems not only to establish conclusively the claim that to him, in conjunction with Wyman, is due the great credit of introducing the principle of aspiration, but also to how great an extent it was through his persevering and skilful advocacy and performance of the operation that it became so firmly established in America upon a true scientific basis.
Purulent Pleurisy.
DEFINITION.—Purulent pleurisy is that disease in which the pleura secretes pus instead of fibro-serous fluid, as in simple pleurisy.
SYNONYMS.—Pyothorax; Empyema; Suppurative pleurisy.
HISTORY.—The term empyema was applied originally to any internal collection of pus—[Greek: en] and [Greek: pyon]. It is now restricted to pus in the pleural sac. The ancients, from the time of Hippocrates, diagnosed and treated empyema by thoracentesis and pleurotomy. They were familiar with the fact that it would sometimes discharge through the bronchi and make an orifice through the walls of the chest, and discharge outwardly. Their views of its pathology and its connection with other forms of pleurisy were necessarily crude and indefinite. Of late years, owing to the aids given by exploratory punctures, purulent pleurisies have been thoroughly investigated. Townsend101 divided the disease into four varieties, all of which are from degenerations of acute serous pleurisies, from increase of intensity of the inflammatory phenomena, or from modification of the secretion of the serous membrane. More modern researches have shown that frequently such is the case, and that purulent pleurisies often succeed serous pleurisies. The liquid when first thrown out is serous and limpid in character, and afterward becomes cloudy, opaline, then more and more opaque and purulent, owing to the pus being freely secreted and mixing with the fibro-serous effusion. In a certain number of cases, however, the effused liquid has from the first the appearance and anatomical composition of purulent fluid—d'emblée purulente. This has been shown by autopsies in cases of women who died in childbed from suppurating pleurisies, and in persons attacked with pyogenic fever, not simply from deposits of pus, but where an inflammatory period, of longer or shorter duration, preceded the deposit.102 Dieulafoy103 showed that in all effused liquids in the pleural sac there were present red globules and leucocytes.104 Laboulbène105 has established the fact that the exuded fluid in all pleurisies, even those apparently serous, contained, from the time of their formation, purulent globules. All cases, then, are historically purulent; but clinically serous and purulent pleurisies are distinct in their progress, termination, and treatment. Purulence is not always the sign of chronicity of pleural inflammation. It may, and does, show itself in many instances from the very commencement of the attack. Wilson Fox106 shows there is but little natural tendency in serous effusions to undergo purulent transformations. He thinks in the vast majority of cases suppurative pleurisies are so at early periods of disease. He states the proportion of primary suppurative pleurisies as from 14 to 20 per cent. It is when the number of leucocytes, from the intensity of the inflammation or modification of the process, discolors the fluid and gives to it its distinctive properties, that we use the name of purulent pleurisy. Verliac107 states that all chronic cases in infants become purulent.
101 Article "Empyema," Cyc. Prac. Med., vol. ii.
102 Pleurisie purulente, (Moutard-Martin), Paris, 1872.
103 "De l'Examen histologique des Liquides, etc.," Soc. Méd. des Hôp., 1878.
104 See section on [Hemorrhagic Pleurisies].
105 Traité d'Anatomie path., Paris, 1872.
106 Brit. Med. Journ., Dec., 1877.
107 Thèse de Paris, 1865.
ETIOLOGY.—The causes of purulent pleurisies are divided into local or traumatic, which are well ascertained and defined; and the general, the action of which is uncertain. Among the first are wounds of the chest, fractures or caries of the ribs, phlegmonous abscesses of the walls of the chest, effusions of blood, pathological liquids, pulmonary gangrene, rupture of tubercular cavities, and other injuries from adjacent organs, especially of those where pus is discharged into the cavity, for the presence of pus engenders pus. Thoracentesis has been accused of converting serous into purulent pleurisies by the admission of air into the pleural cavity. If the atmosphere admitted is contaminated by germs, we must acknowledge that such a result is possible. By the older methods, previous to the adoption of Reybard's protected canula, such a result may have been produced. We can thus, in a measure at least, account for the great mortality in cases operated upon. But since the adoption of the protected orifices of the small aspirating trocar of Wyman and the capillary perforating needles of Dieulafoy, we question whether, with such an insignificant puncture and the complete exclusion of air, thoracentesis can be justly accused of producing such serious mischief. Trousseau108 earnestly denied such a deleterious effect of the operation in his day. We have now not only the results obtained by Demarquay, Leconte, and Manotte of injecting air into the pleural cavities of inferior animals, but we have the bold experiments of Matice, who, convinced that air could not have any bad influence, actually had the audacity to perform the operation a number of times, allowing the air to enter freely through the canula. From numerous observations there resulted the fact, unsuspected by many, that air, penetrating freely to replace the liquid extracted, never gave rise to purulence in pleurisy; that, owing to its rapid absorption, it did not in the least interfere with the expansion of the lungs; in short, that it produced no accident whatever. While admitting the force of Matice's conclusions, we think it preferable to avoid the possibility of doing harm.
108 Loc. cit.
GENERAL CAUSES.—We have shown that secondary pleurisies frequently occur in the course of convalescence from eruptive diseases, measles, small-pox, and especially scarlet fever, and that they are purulent in their nature. The puerperal condition predisposes to suppurative inflammations of the serous membranes, and pleurisies in lying-in women are almost always purulent. In rheumatism, gout, and delirium tremens, and albuminuria as a rule, the pleuritic effusion is serous. It is purulent in persons suffering from severe injuries and among men exhausted by over-work or by alcoholic excesses, or protracted obscure diseases, such as typhoid fever and pyæmia. Analyses of the cases in which purulent transformation has occurred show that tubercles of the lung have only a minor influence in its production—only 34 per cent. of the whole number. Attimont's109 observations were founded upon 130 cases, 80 of which recovered; of the remaining 50 that died, he found tubercle in only 9 cases. Sometimes malhygienic conditions and insufficient alimentation may account for them. Men are more subject to this disease than women in the proportion of 8 to 1,110 and young children oftener suffer from purulent pleurisy than adults. It is not easy to explain the transformation of serum into pus in pleuritic effusions that have existed for some time where there have been no grave symptoms. Imprudent exposure, affecting the general health, may thus produce disastrous results. This occurs so frequently that purulent pleurisies are generally called chronic pleurisies. There are cases where neither local nor general conditions explain the transformation of serous into purulent effusions in the chest.
109 Thèse de Paris, 1869.
110 E. Moutard-Martin.
PATHOLOGICAL ANATOMY.—This is shown by an examination of the effused liquid, the different solid detritus that it contains, the false membranes, the pleura, the lung, and the thoracic wall itself. The liquid effused is purulent in character. It contains a greater or less number of leucocytes, some red globules, and voluminous granular cells, besides crystals of the fatty acids and plates of cholesterin. The pus is mixed with the serosity in varying quantities. The liquid may be slightly opaline or greenish-yellow, and sometimes gray. It may be thin or thick, with heavy flocculi, so as to pass with difficulty through a canula. The liquid is, ordinarily, inodorous, but it may be strong, and even fetid, where it has been in contact with air. In very few cases of old standing can the pus be regarded as active, the corpuscles being, as a rule, dead or having undergone fatty degeneration. Active suppuration is also more readily set up in a pleura which has already yielded pus.
Purulent effusions, independent of contact with air, may become in a short time the seat of putrid transformations. False membranes undergo alterations which produce fetid gases. The air, with its germs, its humidity, and heat, the three grand factors in putrefaction, is thrown in contact with substances of a putrescible composition. Marshall111 holds that sero-fibrinous effusions appear to have a greater tendency to quick decomposition when air is admitted into the pleural sac than the sero-purulent or purulent products. Pus, he considers, is more stable and less inclined to rapid putrefaction than sero-albuminous fluid. In quantity it varies from a very small number of grammes to five or even six liters. By examining the fluid first drawn out we can predict, by the number of leucocytes present, whether the pleurisy will continue to be serous or will become purulent. If subjected to the influence of ammonia, it will become thready, just as happens when pus is suspended in water, if the fluid contains many of these pus-elements. The purulent fluid may fill the whole or occupy but a small part of the cavity, or again the interlobular spaces only may contain the fluid, the cavity itself being empty. False membranes are almost constantly present and adherent to the parietal or pulmonary pleura; we find them also floating in the liquid. These false membranes may be more or less voluminous. The flocculi, which may be as large as an egg, undergo transformation when air is admitted, and become horribly fetid. They may give rise to septicæmic symptoms. When we see these enormous masses in the cavity, and are unable to get rid of them by suction, we do not wonder that their presence should poison the patient and the case become incurable. Pleurotomy is the only effective mode of getting rid of these dangerous masses, with sometimes gangrenous portions of pleural or lung-tissue. These false membranes frequently form pouches and divisions for isolated quantities of fluid. The false membranes are partly adherent and partly free, especially in cases where there are pulmonary or thoracic fistula. These false membranes differ in acute purulent pleurisies from those found in pleurisies of long standing. They are but feebly adherent to the pleura, and have a slight rose coloration. In old pleurisies the false membranes are of greater density, sometimes from 6 to 8 mm. in thickness. They are more adherent, and cannot be separated, and have a grayish color. The physical state and position of the lung and disposition of the adjoining structures are very similar to what they are in serous effusions. In but few cases do the false membranes envelop the whole of the lung. They pass over one part, and on to the costal pleura. The pulmonary tissue is condensed, sometimes absolutely impermeable to air, so that it will actually sink when dropped in water, being in a state of atelectasis. In cases of shorter duration it is found crepitant throughout its structure. Brouardet112 called attention to the inflammation in the under-pleural cellular tissue, as well as in the interlobular connective tissue, forming interstitial pneumonia, which determines condensation of this tissue and its retraction after the manner of cicatrices, and afterward its inextensibility. These explain the retraction of the thoracic walls and the narrowing of the chest.
111 Loc. cit.
112 "Interstitielle Pneumonie," Soc. Méd. des Hôp. Bullétin, 1872.
The most serious complication of this disease is the pleuro-bronchial fistula113 by which the fluid escapes through the lung. The firm adhesions between the lungs and walls, forming enclosed pockets, contribute in no small degree to the incurability of purulent pleurisy. These pockets cannot be emptied thoroughly, nor can the washings be made to penetrate them. The purulent secretion exercises a destructive action over the tissues surrounding it, as well as upon the viscera and walls of the chest: the soft parts become inflamed and abscesses form; the intercostal muscles suffer atrophy and undergo fatty degeneration, external openings occurring from ulceration. The latter are found less frequently than pleuro-bronchial fistula. This external perforation is habitually in front, in the upper intercostal spaces, which, near the sternum, are very wide and not protected by external intercostal muscles. The fifth intercostal is the most frequent locality. There may be one or several openings. They may be caused by the pus ulcerating through the parietal walls, or abscesses may be produced in the walls and burst externally. Exceptionally, the emptying of the liquid is by ulceration of the diaphragm into the abdomen, causing fatal peritonitis. Some years since the author saw, in consultation, a patient where the autopsy proved this condition. Rare cases have been reported where the fluid escaped into the pericardium, into the mediastinum, and into the opposite pleural cavity (Fernet114). Bouveret115 relates a number of cases in which the discharge of pus took place through such unusual channels as the oesophagus, the stomach, the intestines, and the pelvis of kidneys; also where the pus perforated the posterior cul-de-sac of the pleura and appeared in the posterior walls of the abdomen. In the last cases, he states, it may point in the groin, the lumbar region, the buttocks, or even in the thigh.
113 See section on [Pneumothorax].
114 Loc. cit.
115 Journal de Méd., Dec. 16, 1882; N.Y. Med. Rec., March, 1883.
SYMPTOMS.—In a large number of cases of purulent pleurisy the general symptoms do not differ materially from those of fibro-serous pleurisies. Sometimes, however, they do. This is according to whether they are acute purulent or chronic purulent pleurisies.
In acute purulent pleurisy the disease commences in the same way as the ordinary acute fibro-serous pleurisy. Indeed, the first effusion is ordinarily serous in appearance, and afterward it becomes purulent. We have the initial chilliness more or less marked, accompanied by the characteristic pain in the side and dry cough, the fever keeping up, even as high as 103° to 104° F.; and soon the signs of an effusion supervene. In a few days, ordinarily, in acute fibro-serous pleurisies, the febrile exacerbation disappears. Graves116 states that the extent of a pleurisy is not augmented after twenty-four hours. In acute purulent pleurisy the fever persists in spite of treatment; the effusion increases, sometimes less rapidly than in the serous variety, but in a continuous manner. If thoracentesis is performed about the eighth or tenth day, we notice that the fluid is opaline and contains a large quantity of pus. After this the fluid is reproduced, and as it forms the fever continues; the skin is hot and dry, the appetite impaired, and sweats appear during the night. In examining carefully the thoracic walls we find oedema of the diseased side. Later on there will probably be oedema of the lower extremities.
116 Clin. Méd., edited by Neligan.
Chronic purulent pleurisy is marked by symptoms somewhat different. It commences in a similar manner to that of acute pleurisy, with fever, but in a few days the fever disappears. In the evenings there may be some febrile action with slight chills. It is remarkable that frequently vast collections of purulent fluid do not give rise to chills. The fluid augments progressively, but sometimes very slowly, and often it appears to remain stationary for a long time. This condition continues sometimes for many months. The patients are pale and feeble, although they may get up and walk until the quantity is increased to such an extent as to impair their breathing capacity. Then the forces of the body by degrees diminish, and the appetite is impaired to a serious extent. The face becomes pale and the lips discolored. From time to time diarrhoea supervenes and oedema of the chest-walls is noticed, and general anasarca comes on without albumen in the urine. If nature does not open an orifice through the parietes of the chest or through the bronchi for the discharge, the patients finally succumb in the last degree of wasting with profuse sweats and fetid colliquative diarrhoea.
PHYSICAL SIGNS.—These, with some modifications, are very similar to those of ordinary sero-fibrinous pleurisy. We have the same dilatation of the chest, but it is more frequently localized. The oedema of the thoracic walls is almost characteristic of the presence of pus in the pleural cavity. We may, however, meet with it in fibro-serous pleurisy and in cachectic subjects on the side of decubitus. Then, again, there are cases of purulent pleurisy where it does not occur. It must be looked for with care, especially at the lateral portion beneath the armpit.
Mensuration and percussion afford especial evidences of purulent pleurisy, and frequently they discover encysted points.
The tubular quality of respiratory sounds is more pronounced, as are also the amphoric characters at the apex, caused by long-continued pressure of the compressed lung around the large bronchi. Ægophony is less frequently heard, the bronchophony is distant and less distinct, and vocal fremitus is more completely abolished. The non-transmission to the ear of the whispered voice through the walls of the chest (Bacelli's sound) in purulent pleurisy is a sign of considerable significance in tracing the transformation from serous fluid into pus. We must, however, bear in mind that when the sero-fibrinous effusion contains fibrinous flocculi, it has the same effect as a purulent fluid in interfering with the passage of the voice. (See article [ACUTE PLEURISY].)
DIFFERENTIAL DIAGNOSIS can be but indifferently reached by considering the points mentioned. An exploratory puncture enables us to decide with certainty as to the nature of the fluid. Without this the diagnosis is often very difficult. In acute purulent pleurisy the diagnosis is most difficult, especially at an early period, because the general symptoms and the local signs resemble closely those of ordinary pleurisy. When, however, the disease is further advanced, and we have the earthy aspect of countenance with oedema of the thoracic walls, we can be nearly positive in our opinion. Moutard-Martin117 speaks of this localized oedema at the level of the fluid as a certain indication of the purulent character of the fluid. But this oedema, as he admits, does not always exist. It is wanting in many cases, and it may be found in cases of sero-fibrinous effusion where the patient has been lying on the side, and in other cases of advanced cachectic disease. Formerly, there were many more errors of diagnosis, which were only discovered at autopsies, but now, thanks to aspiratory punctures, the diagnosis is much more accurate, and indicates to us the rational treatment. In both varieties of purulent pleurisy there is a tendency to discharge by making orifices through the walls of the chest or through the lung. This is nature's mode of spontaneous cure. The most common is the pleuro-bronchial fistula, and the period of the disease at which this accident may occur is very variable. Woillez118 cites a case where it occurred as early as the twenty-eighth day; ordinarily it occurs at a much later period, sometimes as late as the eightieth day. It comes on early in purulent pleurisy. In infants the perforations take place as early as in fifteen or twenty days, and are favorable to the cure in one-half of the cases. Saussier in 29 perforations of this kind counted 15 cures. The symptoms of this accident are easy of recognition. They vary according as the pleuritic effusion is diffused through the whole pleural cavity or is limited, encysted, or interlobular. In the first variety, where we have the physical evidences of the presence of pus, suddenly, during a paroxysm of coughing, the pus is forced up through the bronchi, and the patient in a very short time expectorates a considerable quantity, varying from a few grammes to a liter or more. The quantity thus thrown off depends upon the diameter of the fistula. It may be excessive, as in a case recently observed by the author where suffocation was produced, causing syncope, asphyxia, and death, the flow being so rapid as to fill up the bronchi to such an extent that the patient could not get rid of it. In many cases the pus is brought up more gradually, with successive coughs or with changes of position. Frequently vomiting is produced by the flow from the vomica. After the first instantaneous evacuation of pus (ordinarily continuous, sometimes intermitting) purulent expectoration takes place. The patient may pass hours without any discharge, when suddenly a severe cough brings up a quantity of pus, and again may spend days without further expectoration. Pleuro-bronchial fistulæ may have a valvular character, so that air may or may not be admitted into the pleural sac as the pus is discharged. With or without the formation of pneumothorax there is a tendency to cause putridity of pus. In cases of children, who swallow their expectoration, it often produces a very troublesome diarrhoea. The course of the disease and its prognosis are necessarily altered according to conditions met with. When the air does not penetrate, we observe that the diseased side becomes depressed and the swelling, previously noticed, disappears. The flatness on percussion diminishes or disappears entirely. On auscultation we have coarse râles, sometimes just inside the fistulous orifices, sometimes at a considerable distance. The general symptoms, as well as the physical signs, improve, and the case advances slowly toward cure. Ordinarily, the pus expectorated from the pleura, when free from contact with the air, is odorless, but it is rarely as unpleasant as in bronchial dilatations, unless it is long retained in the cavity, when putrefaction ensues. When the air enters from the bronchi, it frequently acquires a disgusting odor. If the air enters the pleura and takes the place of the pus, the chest remains enlarged. Indeed, it sometimes increases in size to such an extent as to cause suffocation unless the pus and gas are withdrawn. The valve made by the false membrane allowing the air to enter the cavity, but not to escape from it, causes the fluid to accumulate rapidly, and we have pneumothorax to a very painful degree. The diaphragm is pushed down, and, if the disease is on the right side, the liver is forced down, and descends to a level with the umbilicus.
117 Purulent Pleurisy, 1872.
118 Traité Clin. des Mal. Aigues des Organes Resp., 1872.
The collection of gas and fluid may be in such excess as to produce a concavity of the upper surface of the liver, while the organ is forced down into the abdomen. E. Moutard-Martin119 explains this extreme condition by the fact that the fistulous orifice being at the superior portion of the lung, the air having equalized the interior pressure with the exterior pressure, the liquid obeys the laws of gravity, and depresses the diaphragm. The fluid thus does not reach the level of the pulmonary fistula. Under these circumstances the expectoration may cease altogether unless the patient, by change of position, allows it to flow outward through the orifice.
119 Loc. cit.
The physical signs of this condition of pyo-pneumothorax are very marked and characteristic. Above the level of the fluid there is ordinarily a great exaggeration of resonance on percussion, especially at first. At the end of a few days, however, this resonance is sometimes materially modified, and we have obscurity of the percussion vibrations. Percussion, by itself, may lead us into error of diagnosis which the other modes of physical exploration will correct.
On auscultation we hear the amphoric murmur, which is sometimes of great intensity, and at others so feeble and distant as to require great attention on the part of the auscultator. These varieties of the amphoric respiratory sound appear to depend more upon the position of the pleuro-bronchial fistula, and upon the greater or less free circulation of air through the fistula, than upon the extent of the cavity (E. Moutard-Martin). This sound and the amphoric voice are the two principal auscultatory phenomena. There is also the vibrating metallic tinkling produced always in expiration. Although the physical cause may exist, this latter is by no means a constant sign. It may disappear for hours, and even days together, and then be heard for a short time. Sometimes it is only heard when the patient coughs suddenly and violently. When heard it is a very valuable indication of the presence of a pleuro-bronchial fistula. Auscultatory percussion gives us a still more valuable diagnostic phenomenon—the metallic amphoric reverberation—especially if we percuss with a metallic percussor over a metallic pleximeter. The Hippocratian splashing caused by succussion is a more characteristic sign of pyo-pneumothorax than any other we have mentioned. Other signs may fail, and often this is the only sign present. Almost all the symptoms and signs that have been considered characteristic of the presence of pus may coexist with a perfectly limpid sero-fibrinous effusion. We may even have in serous effusions a high, fluctuating temperature, profuse sweats, and quick pulse lasting several weeks. On the other hand, purulent effusions may be associated with symptoms of so mild a character as to lull suspicion. Previous to the application of exploratory punctures for purposes of accurate diagnosis, purulent pleurisies were confounded with the milder disease until so far advanced as to be too late for effective treatment. Now we can without risk discover purulent pleurisies at their very commencement, and before they reach the point of great danger to the subject we can relieve them by thoracentesis, and afterward pursue the treatment for a radical cure.
Limited, circumscribed pleurisies, such as are found at the base of the surface of the diaphragm and in the interlobular fissures, as well as those involving the pleural cavity itself, may empty their contents through the bronchi. As we have shown, the diagnosis of these forms is often very obscure and difficult. The fine capillary exploring-needle is a safe, and often a reliable, means of diagnosis. It may happen that we can only guess at the nature of the disease until, after a protracted cough, there is ejected by the mouth a quantity of pus, and the diagnosis is made clear. We may perhaps discover a point of flatness at the base or about the centre of the lung, but often this flatness is very incomplete, because the collection of pus does not always reach the thoracic wall. It may, indeed, be separated from it by healthy lung-texture. Auscultation may discover coarse râles or even gurgling with cavernous respiration. The voice sometimes has the character of pectoriloquy, at other times of bronchophony: the cavity is rarely large enough or the walls sufficiently firm to give the amphoric tone. Under these circumstances there is neither metallic tinkling nor Hippocratian succussion. The diagnosis of bronchial fistulas caused by encysted pleurisies may be confounded with tubercular cavities or with dilated bronchi. The exact position, however, of the lesion, the rapid manner of the first purulent expectoration, and the nature of the pus expectorated, will enable us always to arrive at an accurate diagnosis. We must remember that in bronchial dilatation the disease is developed by degrees, and the patients do not expectorate suddenly a notable quantity of pus; tubercular caverns are ordinarily at the summit. The mode of expectoration is different, and the matter expectorated does not present the same purulent and homogeneous characters. The general health is very different where encysted pleurisies exist from what it is in patients suffering from tubercular cavities. In the former case it is comparatively good; there are no profuse night-sweats, diarrhoea, etc. Perforation through the thoracic walls may take place at a period more or less remote from the commencement of the disease. The first indication of this result is, ordinarily, a pain over a limited point of one or two of the intercostal spaces, followed, in a few days or a week, by a raised sensitive point on the surface, without change of color of the covering skin. This may remain a long time in an unchanged condition, but generally it increases gradually until it becomes soft and fluctuating, reducible by pressure, but increased in size by efforts to cough or by forcible expectorations. The skin over the raised point becomes thin with a purplish tinge; suddenly, from some effort to cough or unusual exertion requiring suspension of breath, it bursts and gives exit to a quantity of pus far out of proportion to the size of the small tumor. Sometimes there are several such points in the same subject, appearing simultaneously or consecutively, especially if the discharge is not free through the first one. Ordinarily, there is but one which appears on the anterior portion of the chest about the fifth intercostal space or in the intra-mamillary line. These orifices sometimes close and then reopen. Of 18 cases of empyema necessitatis collected by John Marshall,120 1 occurred in the sixth intercostal space and 17 in the fifth, and 6 of his own cases in the fifth, beneath the nipple. This is, as he states, the weak point of the chest, relatively unprotected by the adjacent muscles. The internal intercostal muscle, the weakest portion of the great pectoral, and the thin fascia, are the only coverings at that point. There is valid reason why special bulging and spontaneous perforation should occur there. The spot also corresponds nearly with the middle of the pleural cavity when distended. The fifth intercostal space is wider than those below, and its limiting ribs, held to the sternum, give firmness to its borders—conditions which help the thinness of the walls in determining the place of perforation. In children perforation often takes place in the very wide second intercostal space. The perforation, although it may contract in size, persists and remains a fistulous canal, permitting air to enter and to escape. The fluid rarely becomes fetid unless there is a pleuro-bronchitic fistula or air is otherwise freely admitted. Sometimes when the orifice is oblique, the air does not enter at all. When the purulent effusion escapes through the thoracic walls, the patient experiences at once manifest relief. The respiration becomes better, the fever decreases, the sweats disappear, the appetite improves, and the general condition is decidedly ameliorated. This improvement persists as long as there is free discharge, but if from any cause it ceases, we have a return of serious symptoms. If no air enters, percussion and auscultation show the gradual disappearance of the evidences of disease; but if air enters we have the signs of pyo-pneumothorax, amphoric breathing, metallic and succussion sounds. The diagnosis of parietal openings is comparatively easy: the quantity of pus, its odor, with the physical signs, show its nature. With care this form of pleural opening is distinguishable from a fistula made by caries of the ribs or by vertebral abscesses, and not communicating with the pleura. The existence of a thoracic fistula does not prevent the formation of pleuro-pulmonary fistula, and reciprocally a parietal fistula can be found where the other has been previously formed. The abscesses following purulent pleurisies and empyema have been long recognized. Hippocrates mentioned them as contributing to a favorable prognosis in empyema.
120 London Lancet, March, 1882.
Pulsating empyema is where the lesion is situated in the neighborhood of the heart or of the aorta, which transmit their impulse. They are also sometimes called pulsating tumors, rising and falling with alternate movements of inspiration and expiration (Stokes, Graves, and Aran). These cases strongly simulate aneurisms. According to Fraentzel, the fluid is always purulent. In 1 case reported by him, and in 2 cases seen by Traube, pericarditis with effusion was present. Douglass Powell mentions two well-marked cases of pulsation in the left supra-mammary region where the diagnosis between effusion and aneurism was very difficult, but where paracentesis removed a large quantity of fluid and the signs of pulsation ceased. In these cases there was present neither pus nor pericarditis.
TERMINATIONS.—If allowed to take its natural course, pulsating empyema almost always ends in death from exhaustion or syncope, or by discharging through the lungs or through the intercostal spaces. Formerly, it was oftener fatal than now, but it is still justly considered the gravest form of pleurisy. We have seen that exceptionally it is cured by becoming encysted. It may be cured by spontaneous openings into the lungs, and more rarely by fistulous orifices121 through the walls of the chest. Is it possible for the disease to be cured by the absorption of the pus? The bearing of this inquiry upon the treatment cannot be over-estimated. If absorption can remove the pus, we may safely leave it in the pleural cavity. If the pus cannot be taken up by the absorbent vessels, we ought promptly to make use of radical measures and evacuate it. The literature on this point gives us few reliable cases. Spontaneous cure can rarely be produced by absorption. Douglass Powell122 writes that "the spontaneous disappearance of such effusions is too uncommon to be expected, and the process of reabsorption is one too full of peril to be anticipated with anything but dread. It is indeed an attempt at such absorption that occasions the most characteristic hectic symptoms." Surgical intervention is the rule. The writers previous to the introduction of exploratory punctures speak of cases where purulent pleurisies were diagnosed and the effusions were absorbed. We have shown that the differential diagnosis between serous and purulent effusions is very uncertain when made from the general symptoms and physical signs. Even Trousseau, with all his skill and vast experience, made the mistake of diagnosis, and performed the operation of pleurotomy in a case of serous effusion, and his patient died. There are well-authenticated cases where, after thoracentesis, small quantities of pus left behind have been absorbed, especially in children. That purulent pleurisies have been effectively cured by the pus becoming encapsuled has been demonstrated by autopsies of persons dying from other causes. E. Moutard-Martin reports a case where, after withdrawing with an exploratory trocar a few drops of pus, and thereby establishing the diagnosis of purulent pleurisy, he was unavoidably prevented from opening the chest. Two months afterward he found the effusion had entirely disappeared. He states that this was the only case he had ever seen of a spontaneous cure without evacuation. Douglass Powell has seen one case which has satisfied him as to the possibility of a local empyema becoming absorbed. Wilson Fox reports another similar case. Chronic pleurisies in childhood are almost invariably suppurative, yet Barthez and Rilliet report 7 out of 13 recovered. It must be, and generally is, admitted that cure by pus undergoing retrogressive fatty degeneration, and then being absorbed, is possible, but it rarely occurs. Should the more fluid portion be absorbed, the inspissated pus remaining on the pleural surface may at some future time, upon softening, give rise to secondary tubercular or purulent collections. It is also true that cure is quite often effected by spontaneous evacuation through the lungs and through the walls of the chest. This is especially the case in interlobular effusions and in cases sacculated by adhesions. Such cure is explained by the fact that adhesive inflammation, assisted by the elasticity of the lung on both sides, glues together the walls, isolates the fluid, and prevents air from entering, thus preventing the pus from putrefying.
121 In Andral's 8 cases of bronchial perforation there were only 3 deaths—a mortality less than by artificial opening previous to the application of Listerism.
122 Dis. of the Lungs and Pleura, London, 1878.
In cases of pulmonary perforations the probabilities of a favorable termination by absorption of gas, evacuation of fluid and the contents of the chest, are greater where air does not enter the cavity. The presence of air, especially if stagnant, in contact with the pus, makes a serious complication, causing putrefaction of the pus and consequent septicæmia, with all its dangers. The discharge of the purulent collection, through the parietes of the chest, after the manner of an ordinary abscess, is ordinarily made through the anterior part of the thorax, but it may take place in any part. At first this mode of evacuation, empyema necessitatis, is a great relief, but cures rarely result from it. Most frequently, owing to the imperfect evacuation through the tortuous canal and the entrance of air mingling with the pus, death supervenes unless the surgeon enlarges the orifice or produces a new one, and thoroughly empties the sac and persistently washes it out. From statistics collected by Wilson Fox, the mortality is not so great from spontaneous parietal openings as was formerly supposed. Of Andral's cases there were 2 deaths in 25. Goodhart had 11 cases, all of which recovered. Ewald lost 3 of his 6 cases. Cases of empyema necessitatis should be treated as artificial openings with every possible antiseptic precaution. The mortality would thus be decreased. The chances of cure by absorption are so small that when nature shows no tendency to either of the two spontaneous modes of cure, there is great danger of a fatal termination through hectic fever. The time for this result varies from a few weeks to months. When in empyema we have fistulous orifices they sometimes remain open for years. Near them are local points of depression, caused by external atmospheric pressure. When acute purulent pleurisy follows a low fever, such as typhoid or scarlet, a fatal termination may result in a short time; in other cases it is many months before the patient dies from exhaustion.
We cannot forbear to urge the importance of promptly and definitely settling the diagnosis by exploratory aspiratory punctures. Properly guarded, no evil can result, whereas a positive diagnosis enables us to act promptly with effective mechanical means of relief. It is undeniable that purulent effusions in the pleural cavity are very serious in their results, and are followed by death unless Nature or the surgeon evacuate them. Even when Nature does so, it is often imperfectly done, and the termination may be death unless we assist her to get entirely rid of the fluid.
PROGNOSIS.—Formerly the prognosis in every case was of extreme gravity. The condition was looked upon as of necessity fatal. Surgeons despaired of a successful result in operating. Now, thanks to thorough drainage and Listerism, unless the case is an old chronic empyema, we are hopeful of cure and a favorable prognosis may be given. We may look for good results where the disease is early recognized and promptly treated. J. G. Blake123 cured 16 in a total of 19 cases. Since 1869 he cured 9 out of 10 cases. Homer124 saved 26 out of 52. Feidler125 treated 112 patients, only 25 of whom died (all advanced tubercular cases); 21 were restored to good health; 66 (tubercular) were cured so far as return of effusion was concerned. Israel126 had 10 recoveries out of 11 cases. A. T. Cabot127 reports 11 recoveries out of 14 cases. Of the fatal cases, 2 died of phthisis; the third had existed four years.
123 Med. and Surg. Rep. Boston City Hospital, 2d Series.
124 Quoted from Med. Times, Philada., Aug., 1883.
125 Ibid.
126 Quoted from Dabney, Amer. Journ. Med. Sciences, Jan., 1883.
127 Bos. Med.-Surg. Journ., Aug. 16, 1883.
When purulent pleurisy follows fibro-serous effusions, and when it occurs in vigorous children, the prognosis is more hopeful than when it is preceded by scarlet fever or occurs in subjects debilitated by diseases which have exhausted the recuperative forces of the body. Empyema of tubercular origin has necessarily a grave prognosis. In persons in advanced life the prognosis is very unfavorable. If hectic fever or septicæmia occur, the prospects of cure are comparatively slight. In cases of empyema necessitatis much depends upon the power of resistance of the patient, and upon whether the matter is discharged before it has produced caries of the ribs, sternum, or spine, or has prostrated the vital powers. If these sequelæ have been produced, the condition of the body is most unfavorable to the restoration of health. If the pus in pyothorax has been discharged through the bronchi, though it may give temporary relief, it is attended with great danger, and if the discharge continues it will gradually wear out the patient's strength.
TREATMENT.—The diagnosis being established, we at once realize the great responsibility of treating a disease of such gravity. In many other diseases of serious import we trust Nature to do her part toward cure; here, as we have shown, we find her unable to come to our assistance. One of the large serous cavities, connected as it is with the lungs, is not only disabled, but contains a deleterious fluid which cannot remain in a closed cavity without sooner or later affecting the processes of nutrition. We can do little by medical treatment save to sustain the organism by tonics and reparatory agents; we can give wine, quinine, arseniate of soda, and cod-liver oil; we can administer a sustaining diet and place the patient in the best hygienic and sanitary condition. We cannot conscientiously hold out to the patient a prospect of cure by medicines.
There is danger in resorting to the expectant plan of treatment. We lose valuable time, and finally we shall be forced to resort to surgical operations, which in fact constitute the modern treatment of purulent pleurisy. By them only are we able to promote the primary objects of our treatment, which are to get rid of the purulent matter and to stop the suppurative inflammation. We thus endeavor to obliterate the pleural cavity and promote the expansion of the lungs.
Surgical Treatment.—This has been the treatment which has been most effectively used from the time of Hippocrates to modern times. There has been, and still is, great diversity of opinion as to the best modes of withdrawing the pus contained in the pleural cavity, but it is settled that when the diagnosis is certain the fluid must be removed—if not by spontaneous openings, by artificial means. We must except to this rule cases of suppurative pleurisy of phthisical origin. Bowditch years ago stated that in this class of cases it was advisable not to make permanent openings into the chest. In these the suppuration does not stop, and the operation appears to hasten the fatal issue of the disease. Wilson Fox demonstrates from statistics that the mortality in phthisical cases is increased by operations.
There is no room for discussion as to the indications, as in cases of simple sero-fibrinous pleurisy. There is only one thing necessary to be ascertained—the certainty of pus in the cavity. This is shown by the pointing or by pus abstracted by exploratory puncture. The more promptly we act, the greater the prospect of cure. As Powell128 emphatically says, "The prognosis is practically hopeless without surgical help. We must adopt some surgical measures or take upon ourselves responsibility for a large mortality." Bowditch, Trousseau, Hamilton Roe, Anstie, Parker, Marshall, and Moutard-Martin all concur as to the necessity of surgical interference. Clifford Allbutt129 says: "If pus or septic material be present in the body, we must not rest until it is removed. I therefore dislike and reprobate all tampering with an empyema."
128 Loc. cit.
129 Brit. Med. Journ., Dec., 1877.
We propose to mention, as briefly as we can in justice to the subject, the several modes of operating, together with our conclusions and the results obtained by us and by others of much larger experience.
Modes of Operating.—These are numerous, but they may be divided into three classes: First, the simple immediate evacuation of the fluid by subcutaneous thoracentesis with the ordinary trocar or with an aspirator of some kind, without allowing the flow to be continuous: this is the closed method; secondly, the open method—the operation by incision with a bistoury, and the introduction of permanent canulæ or of drainage-tubes of metal, of hard rubber, or of soft tubing; thirdly, the more radical treatment by free incision (pleurotomy) with or without washings or injections by the aid of syphons. With all these modes of operating the strictest antiseptic precautions should be taken.
Thoracentesis.—For this operation we have a choice between the ordinary hydrocele trocar, the trocar protected by a soft valve at the orifice (Reybard's instrument), Jules Guérin's or Wyman's aspirating pumps, Dieulafoy's previous-vacuum aspirator with capillary needles, and numerous modifications by others of Dieulafoy's, including Potain's, and Reynard's modification of Potain's, or we can have recourse to Potain's, Southey's, or Williams's syphon. If we select the trocar (Reybard's), we prepare the instrument by cleansing it thoroughly and Listerizing it. Reynard130 recommends a hypodermic of morphia previous to operation, to prevent the painful cough. The simplest method is to pass the aspirator needle through the flame of a spirit-lamp, and subsequently to plunge it in carbolic-acid solution. We spray with a carbolized solution the point of puncture, which should be at the sixth intercostal space, when possible, in the axillary line. Powell prefers a lower opening, in the seventh or eighth intercostal space and in the posterior axillary line. He wishes to completely empty the pleural cavity of pus and promote the obliteration of the abscess-sac by the descent of the lung as it re-expands, and by the return of the heart to its normal position: these processes converge toward the lower and postero-lateral position. We ordinarily prefer local anæsthesia by sprays of ether or rhigoline or by cocaine hypodermics to anæsthesia by inhalation. After drawing up the skin, so as to be able to close the orifice by the flap after the operation, we direct the trocar by the nail of the left index finger; we, with a quick movement, insert the trocar to the extent of three or four centimeters. By this quick insertion we do not run the risk of stopping the canula with the thick membranes. We allow the fluid to flow out slowly, but as completely as possible. In fibro-serous effusions we only draw off sufficient to remove intra-thoracic pressure, to avert the dangers caused by that pressure, and promote the process of absorption. In suppurative pleurisy, while we aim at relief from pressure, we wish to get rid of a fluid which is itself deleterious. Consequently, our object is to prevent absorption and to ward off the formation of fistulous outlets through the lungs or the parietes of the chest. Therefore we endeavor to completely evacuate the pus, and, as far as possible, to prevent its re-formation. While we desire to remove all the fluid if we can, we must not run any risk by doing so. If the cough annoys the patient, and the elasticity of the walls and the pressure from the displaced organs do not continue to force out the fluid, we had better stop the flow temporarily or renew the operation next day. We must desist if the cough becomes very persistent. We prefer Dieulafoy's aspirator or Potain's modification for the simple evacuation of the fluid, unless we wish to wash out the pleura; then we employ Potain's or Williams's (of Boston) syphon, because either can be applied with greater effect. It is best not to take needles of too small a diameter, for the flocculi may easily choke them. We prefer No. 2 (1 millimeter) or No. 3 (1 millimeter and a half). By using the small-sized dome-trocar we avoid the possibility of injuring the lung. Care must be taken in removing the canula to withdraw the aspiratory force by turning the stopcock; otherwise we may draw the pus into the texture of the walls and establish fistulous openings. In using the common trocar fistulæ have frequently been made, causing a serious complication.
130 Brit. Med. Journal, Sept., 1881.
Thoracentesis thus performed has often cured empyemas, especially in children. We find instances mentioned by Lacase, Duthiers, Dieulafoy, Lebert, Hamilton Roe, and others. It has been demonstrated that the operation is sometimes effective without resorting to injections and washings of the pleural cavity. Bouchet131 reports a case in a child following typhoid fever, where he aspirated thirty-three times and cured the patient; another case, a child four years of age, after two operations; another child, seven years of age, after six aspirations. Guérin132 reported several cases. M. Fouson133 reported 19 cases of children treated by aspiration with success. The younger the child, the greater are the chances of success. He advised complete emptying of the cavity. Lewis Smith134 prefers the use of an aspirator in operating upon children. He does not think it necessary to remove all the pus present. Cordet Gassicourt135 reports cases of three infants, each of whom was cured by one aspiration. C. Gerhardt of Würtzburg136 recommends in children complete evacuation of purulent fluid, through incisions and washings, avoiding entrance of air. Adolph Bajincke of Berlin137 states that aspiration with antiseptic treatment is often successful in children. He advises, if after two or three aspirations the fever returns and the fluid increases, that free incisions be made, with injections of salicylic acid (3 per cent.), with antiseptic dressings. He recommends the removal of only a portion of the fluid. A. Jacobi138 mentioned having in a single year 3 cases of empyema in young children, each of which required but a single aspiration; the quantity of pus in 1 case amounted to 300 or 400 grammes. The flexibility of the young ribs causes sufficient sinking in of the thorax to promote recovery. F. Richardson139 advises two aspirations before incisions. R. W. Parker,140 London, takes Richardson's view. He strongly advocates antiseptic precautions and injections of quinine (5 grs. to ounce j) and injection of filtered and carbolized air into the pleural cavity. Austin Flint141 advises that aspiration should be used first, but if not successful, then incisions should be made at the base of the thorax and a tent introduced to keep the orifice open. Anstie142 gives similar directions. According to Bowditch,143 "whenever the pus is pure there is no immediate call for thoracotomy, for patients at times get well after simple aspirations. Youth and recent uncomplicated disease favor this. Heretofore, after three aspirations the author has resorted to thoracotomy." Dabney144 says that aspiration occasionally gives good results, even in adults. S. C. Chew reported the case of an adult (twenty-five years of age) cured of empyema by one aspiration of sixteen ounces, and also a case of a child three years of age after three aspirations. Barnes145 reports a case of a patient nineteen years of age who recovered after four aspirations of large quantities of pus. J. G. Blake146 reports a case (boy ten years of age) where one aspiration of ten ounces accomplished a cure. He adds that in children repeated withdrawals of pus by aspiration are justifiable, but in adults after one unsuccessful operation he advises permanent opening. Dupuytren147 cured a case after seventy-three aspirations. The author has had 3 cases perfectly cured by aspiration: a child eleven months old, after three operations; a child of five years, after five operations; a boy sixteen years of age, after two operations.
131 London Lancet, 1860.
132 De la Thoracentèse par asp. dans la Pleu. Pur., 1871.
133 Thèse de Paris, 1877.
134 Diseases of Children.
135 Soc. de Thér., 26 April, 1882.
136 Trans. Int. Med. Con., vol. iv.
137 Ibid.
138 Ibid.
139 Ibid.
140 Ibid.
141 Clinical Medicine.
142 Reynolds's Sys., vol. ii.
143 Unpublished MSS.
144 Amer. Journ. Med. Sci., Oct., 1882.
145 Brit. Med. Journal, Dec., 1877.
146 Med. and Surgical Reports Boston City Hospital, 2d Ser., 1877.
147 Altimont, loc. cit.
Such being the record, we are in duty bound to try simple aspirations before making use of the more radical modes of treatment. The character of the fluid as drawn off by the exploring-needle furnishes valuable indications. Should it be found laudable and inodorous, we had better aspirate once or twice before resorting to the free incision. It can do no injury, and we thus enable the lung to expand, diminish the size of the cavity, and prepare for the more radical operation. In children we ought to try this mode repeatedly unless we have symptoms of emaciation and hectic approaching; in adults only two or three times. The operation is simple, painless, without danger, and occasionally perfectly effective. If the fluid re-forms quickly—and it sometimes does with astonishing rapidity—or there are evidences of depression from fever, sweats, and diarrhoea, we must promptly have recourse to one of the effective surgical methods producing free drainage. It is undeniable that the treatment by thoracentesis is frequently unsuccessful, notwithstanding repeated operations.
In sero-fibrinous effusions the close method is the most successful, but in purulent effusion this is not ordinarily the case, and we are forced to employ the open method to produce free, continuous discharges, as the purulent fluid re-forms rapidly.
Open Methods.—Of these we have—(1) drainage through a single orifice by the introduction of a permanent canula or soft india-rubber tube; (2) drainage through two openings; (3) use of syphon; (4) pleurotomy; (5) drainage by resection of ribs. Each of these modes has its advocates. They have all been frequently used with varying results. Each has its advantages and disadvantages.
The first point to be noted about these modes of operation is, that we cannot prevent the introduction of a greater or less amount of air to replace the fluid, and therefore it is of primary importance that we should always render the air aseptic. The incision must be made after thoroughly cleansing the point to be opened. The bistoury, the canula, the dressings, the receptacles of the pus, the sponges, and everything connected with the operation, should be purified to prevent the possibility of the contamination of the pleural cavity and its contents. At each subsequent dressing all these precautions should be renewed. Antiseptic gauze of six or eight layers in thickness, with finely-combed oakum or salicylated cotton, ought to be placed over and around the orifice for an area of twelve inches. In this way what little air enters after the operation may be rendered thoroughly aseptic.
Lister148 recommends that the coverings of gauze should be in eight folds if the drainage be excessive—that these be charged with a disinfectant composed of one part of carbolic acid to four parts of resin and pure paraffin. The dressings, he directs, should be kept in place by elastic bandages. This treatment stops suppuration promptly, and converts the discharge into one of a serous nature. His views have been amply confirmed. A. T. Cabot149 recommends that the dressings be covered with a piece of mackintosh large enough to project in every direction. In his cases he found it acted as a valvular fold, forcing the air and pus out and preventing air from entering.
148 "Lectures on Clin. Surgery, etc.," London Lancet, Dec., 1879.
149 Loc. cit.
Drainage by Canula through a Single Orifice.—The patient, having had about three hours previously a good substantial meal of easily-digested food, is placed in a semi-recumbent position, leaning over toward the healthy side. Before selecting the point of puncture, the side ought to be first washed with soap and water, so as thoroughly to remove all dirt and epithelium débris, and then bathed in a 1:20 solution of carbolic acid. As there is to be but one opening through which the fluid is to pass, it is desirable to have it low down. The eighth intercostal space, somewhat behind the posterior axillary line, is ordinarily the best point for the puncture. Lower than that we may encounter the diaphragm, and, as we must use a trocar of considerable size, we may inflict serious injury. As we desire to completely empty the pleural cavity, a higher point would not be as effective. After having satisfied ourselves of the presence of fluid at the point selected by the physical exploration, we ought always to insert, as a crucial test, a new exploratory hypodermic needle which has been rendered aseptic. Ordinarily, it is not necessary or expedient to resort to etherization, unless in case of a child, for local anæsthesia by cocaine hypodermically, by rhigoline or the ether spray, or by the application of a small piece of ice covered with salt (as suggested by Powell), will render the incision painless. It is needless to add that a weakened heart, a sluggish capillary circulation causing a cyanotic appearance, and marked dyspnoea contraindicate the employment of etherization. We prefer cutting through the integument with a bistoury, and then inserting the trocar, which must be pushed with a thrust through to the pleura. All of the pus should be allowed to escape, unless cough, oppression, or threatening syncope should be noticed, in which case it is better to insert the tube and arrest the flow by a cork. The outward flow should be rendered slow by covering the orifice with the dressings and allowing the fluid to soak into them. The tube should only be long enough to go well through the parietes into the pleural sac; otherwise it acts as an irritant, and interferes with the adhesion of the two pleural surfaces, which is necessary for the obliteration of the pus-secreting cavity and the expansion of the lung. The tube should be kept in position by a hard-rubber shield attachment, with bandages previously soaked in disinfectants applied around the body, and several layers of carbolized gauze. The firm canulæ, metallic or hard rubber, straight or curved, as proposed by Woillez and Dieulafoy, are now generally abandoned. These admit air either by the sides of the opening or through their canals, and they sometimes produce, at their extremities, local ulceration through the lung or even through the diaphragm, and cause peritonitis. Their only advantage consists in the facilities they offer for washing out the cavity. With canulæ made of soft india-rubber there is no danger of injuring the lung, etc. They are not painful to the patient, and they can be protected by valvular strips of gold-beater's skin or some soft substance at their orifices. Through these india-rubber tubes we can inject all fluids and washes, except those containing iodine. It has been proved by Dujardin-Beaumetz150 that iodine hardens india-rubber, renders it extremely brittle, and destroys its elasticity in a short time, even after a contact of forty-eight hours. In a case of Bucquoy's151 the tube underwent such alterations that it could only be extracted by a long and painful operation. If these tubes are in use when iodized fluid is to be injected, they must be temporarily removed, and a metallic one, with arrangements for a double current, substituted during the process of washing. If the canulæ are to be kept in permanently, they must be of large size, so as to allow free flow outward of fluid.
150 Quoted by Dieulafoy, Pneum. Asp., English ed.
151 Ibid.
After the operation the patient should always remain in bed in an easy, comfortable position, with the orifice covered by the dressings. His diet should be of an easily-digested and nutritious character. His temperature, pulse, and the condition of his secretions should be carefully watched. Ordinarily, it is not well to reopen the discharge-tube for three days. The same antiseptic precautions should be used then as at the operation, and a fresh tube inserted. The pus secreted ought, if the case be one of recent origin, to be small in quantity and without odor. After a few days it is best to allow the fluid to flow out on the dressings as it forms, which is done by turning the patient well over on his side. An occasional cough assists the discharge. Should the odor become putrid or gangrenous, or hectic symptoms show that the secretion is profuse and has no free exit, it becomes necessary at once to use washings and injections of simple warm water or warm water feebly alcoholized—1:45 or 1:80—or feebly iodized solutions. The greatest care should be taken with these washings that very gentle force be employed. (See [Pleurotomy].) This mode of operating is most effective in recent cases, for it gives the best opportunity to the lung to expand. It is the easiest to perform, and, subsequently, the least troublesome. If it be found ineffective, an additional orifice can be made and a fenestrated tube inserted, or the orifice can be enlarged by a free incision. There have been many successful cases of this mode of operating, but, as the author has sometimes found, it is difficult to establish free drainage, which is most important for the success of the treatment. The result of his experience has been that, in chronic cases especially, the two-opening drainage or free incision without tubes (pleurotomy) has finally to be employed. Powell recommends, after removing intra-thoracic pressure by aspiration or syphon, in a day or two to completely evacuate the fluid under the antiseptic spray and insert a tube for a few days only; then to allow the wound to heal, and await results, trusting nature to secrete a fibro-serous fluid which can be easily absorbed.
Drainage by two openings, as first effectively employed by Chassaignac, is made by the introduction, through a large covered canula, of a tube of india-rubber, perforated with holes, drawn out at another orifice. The tube has its two extremities on the outside, and one posterior, in the eighth or ninth intercostal space, and the other in front, in the seventh intercostal space, after the withdrawal of the canula. The anterior orifice is first made, and a long curved probe with a bulb at the end is passed through backward and downward until it strikes the posterior lowest intercostal space. The operator cuts down on the probe, which points outward. To this end the fenestrated drainage-tube is securely fastened, and is then drawn out through the first orifice. Both ends are retained out of their orifices, by a shield firmly fixed on the tube, for at least an inch. The pus flows out little by little, but continuously, through one or other orifice, according to the position of the patient. This is the most effective method to prevent accumulation. Unfortunately, false membranes and flocculi sometimes stop up the orifices in its walls, the pus does not flow out as it is formed, and there are all the evils of air and fluid mixed and retained in the serous cavity. It is, however, generally admitted that by this system of drainage a number of cases have been cured; but it is not often employed as a primary operation, as we wish to avoid, if possible, the irritation which may result from the presence of so much tubing in the chest. Moreover, it is not the best operation if there is any hope of the lung expanding again. In old chronic cases we cannot hope for more than very limited expansion.
Gross152 speaks of drainage-tubes as harsh and dangerous. Flint, Sr.,153 prefers free incisions, with introduction of tents, to drainage-tubes. Dabney154 considers continuous drainage in some form vastly preferable in the majority of cases. Israel155 had 10 cases recover out of 11 treated by thorough and continuous drainage. Cheadle believes that a large collection will certainly require a free opening in the end, and the sooner the pus is let out the better.
152 System of Surgery, vol. ii.
153 Clin. Med.
154 Amer. Journ. Med. Sci., Oct., 1882.
155 Quoted by Dabney.
Chassaignac's method of drainage will answer well unless, as frequently happens, the purulent pleurisies contain large fibrinous masses, hydatid pouches, or pieces of sphacelous débris.
Syphons, as used in purulent pleurisies, have some very decided advantages. Potain's ingenious instrument, based upon the syphon principle, enables us alternately to empty the pleural cavity into a basin of water, and, by reversing the instrument, to inject the water into the pleural cavity, thus washing out as often as necessary and with ease the purulent collection and cleansing the cavity. Potain's syphon is composed of an india-rubber tube 30 centimeters in length, to be introduced and remain in the pleural cavity. This tube is introduced through the canula, after the withdrawal of the trocar, to the depth of at least 20 centimeters, in order that its extremity should reach the posterior wall, the tube having been previously filled with water. The outer extremity is put into a basin containing water. The part of the tube at the outside of the orifice is closed by a serre-fine just beyond the shield, as is also the extremity in the water. Another tube is connected with the chest portion. This can be used for introducing water to wash out the pleura. The syphon of Potain has very decided advantages over the metallic and hard-rubber drainage-tubes. It prevents the introduction of air and enables us completely to empty the cavity; it permits us to wash out the cavity as frequently as is necessary without fatigue to the patient, without pain, and without change of position, and thus prevents attacks of coughing. All this is done slowly, and the flow can be arrested at any moment by means of the stopcocks. Where repeated washings are required the patient himself can perform them with ease. With the other modes the washings are practised with difficulty. The improved syphon by F. H. Williams of Boston is simple in construction, of small size, and inexpensive. Revilloid of Geneva (1882) reports 10 cases thus treated, of which 6 were cured. Bénard156 reports 8 cases treated by syphon, of which 4 were cured. Goodhart's157 statistics are not favorable to the use of the syphon. Of his 28 cases thus treated, 10 died; in only 6 did the syphon method alone effect the cure. Powell158 objects to the syphon method, because by it the chest cannot be drained unless the lung expands completely or air is freely allowed to enter the pleura. These conditions are impossible in such cases with a single opening and a single tube. Moutard-Martin, while speaking of the advantages of Potain's syphon, admits that in chronic cases where there are pieces of false membrane and flocculi floating in the fluid the tube may be clogged up, just as occurs in the metallic tubes and the drainage-tubes. The patient may thus die by retention of pus and by putrid absorption, unless pleurotomy is employed. It must be borne in mind that the syphon is a weak aspirating instrument. It ought to be 10 meters long to possess an aspirating force equal to that of a pneumatic pump (water being taken as the standard), and its long arm should measure from 7 to 8 meters, in order that its aspiratory force should equal that of a good pneumatic aspirator. Thus we see how weak is the aspirating power of a syphon which only measures the space which separates the bed of the patient from the floor. The ordinary aspirator can be easily changed into a syphon. The descending arm of the tube must be emptied by a stroke of the piston; the current is then established and the stream becomes continuous (Dieulafoy159).
156 Thèse de Paris, 1871.
157 Guy's Hospital Reports, 1877.
158 Loc. cit.
159 Trea. Pneum. Aspiration, Eng. trans., 1873.
While all prominent modern authorities admit the value in some cases of double metallic tubes, of those of hard rubber, of drainage-tubes, and of syphons, with thorough and complete antiseptic treatment, yet observation has taught us that there are many disadvantages and uncertainties. The drainage-tube may give rise to considerable irritation and prevent the closing of the sac—a very important aid to the cure. If the flow is retarded, the fluid may decompose. Therefore it is well to remove the tube frequently, to wash, cleanse, and renew it. The admission of air and stopping up of tubes, the feeble force employed, the putrid pseudo-membranes, and sometimes sphacelous débris, cause, in many instances, fatal results. It frequently happens that at first, when trying the simple aspirations, we find a whitish laudable pus which subsequently becomes thick and fetid. We use drainage-tubes and Williams's syphon, with strict adhesions to Listerism, and yet there may ensue continuous fever, emaciation, sweats, drawn face, and general oedema. We resort to detergent washes, with salicylate of sodium, of tincture of iodine, very diluted, yet the patients get worse and the tubes become obstructed. There is not sufficient free flow of the contents of the chest.
Pleurotomy.—We naturally shrink from freely opening the chest. It is right to try the simpler methods—aspiration, tubes to remain in the chest, drainage, use of syphons—but we are forced in many cases of chronic empyema to use pleurotomy, the thoracotomy of Bowditch, the operation of l'empyème of the ancients. It consists of a wide opening into the thorax between two ribs, permitting the escape of the effused liquids. If the orifice is large enough, we can remove from the cavity of the pleura not only the pus, but the large fibrous masses, gangrenous débris, hydatids, and putrefying material which produce septicæmia and death. The literature of this subject shows that bad results have ensued from this operation, and again and again it has been abandoned, but now that we can, by means of large openings, freely wash out the cavities, and can apply injections of antiseptic and alterative medicines to the suppurating surfaces, many lives are saved. Hippocrates' dogma as to the danger of free and rapid evacuation of pus had often a dangerous influence in preventing a thorough emptying of the sac. The object of this radical operation must be kept in view—to evacuate the pus by a free current, to permit the discharge of plastic products and organic débris, and to allow easy and frequent washings with healing and purifying injections. By these means we arrest suppuration, obliterate the sac, and allow the lung to expand. For this purpose wide orifices should be boldly made. They should be made where the chest bulges most, but not always at the most dependent portion. Ordinarily, the eighth intercostal space, somewhat behind the posterior axillary line, has been the one selected, because it has been supposed that thereby the cavity could be most effectually drained. The author has usually punctured higher, in the seventh intercostal space on the left and in the sixth on the right side, for the fifth and sixth ribs being more fixed, there is less danger of subsequent approximation. We cannot always determine the exact position of the diaphragm. The lung may be bound down by old adhesions to the diaphragm, and thus the latter may be injured by too low an incision; we can, moreover, better adapt the position of the patient to enable the matter to flow out from a higher orifice. Cases have occurred where the liver has been perforated on the right side by low punctures. In health the uppermost point of the diaphragm may be as high as the fifth space on the left side or the fourth space on the right. The cure does not depend upon the exact position of the puncture, because we expect to insert a mouth-tube to keep the orifice open, and probably resort to washings. It is not by its weight only that we expect the fluid to escape; incessant movements of the thorax assist in forcing the fluid through the tubes. Marshall160 urges the fifth space on the right side, and as near the weak point of the chest under the nipple as possible. On the left the pericardium must be carefully avoided. He advises that the operation should never be lower than the sixth or seventh intercostal interval. Douglass Powell prefers a lower puncture, in the seventh or eighth space in the posterior axillary line. In the punctures lower down the tube as it ascends rubs upon the diaphragm and protracts the healing, and the orifice closes too early. The emptying of the sac and the washings can be thoroughly attended to higher in the chest. The weak point selected by nature for empyema necessitatis ought always to be examined to see if there be any thinning of the wall, for if that be the case, the puncture should be made there. The incision should be made on a plane somewhat below that of the aponeurotic and muscular portions of the chest, to prevent the liquids from infiltrating into the subcutaneous cellular tissue. If we ascertain first by exploratory puncture that there is pus lower down, it is safe to operate at that point. The exterior orifice should be wider and larger than the interior, and not parallel with it, in order to avoid the gaseous infiltration in the tissues by the respiratory movements. Care must be taken that the bistoury should pass close to the upper border of the inferior rib, to avoid the intercostal artery. In making the incision—about 6 centimeters in length—should the artery be cut, it can easily be remedied by torsion. We raise the skin, and thus make a flap over the orifice. The bistoury should not be introduced with one cut through the soft textures, as recommended by Woillez, but layer by layer should be cut through. This secures avoiding the intercostal artery, and gives a larger exterior than interior cut, thus preventing danger of liquid infiltration. We can be guided by the index finger, and feel the textures as we cut down upon them. Under a continuous spray to thoroughly purify the air that may enter, a free opening should be made large enough to allow the finger to be introduced. As air enters the fluid contents escape through the orifice, protected by antiseptic dressings of gauze, oakum, and salicylated cotton. At first it is well to remove the dressings containing the pus twice daily; later, once daily will be sufficient. The orifice must be kept patent by a short, wide tube with a fine wire around it. We can thus, by changing the position of the patient, get rid of the contents of the chest cavity. If there should be fetidity, it is desirable to use washes of warm water first, and afterward of feebly-alcoholized water—a solution of salicylate of soda, chlorinated soda, or permanganate of soda. Cabot161 had most success in the use of sol. chlorinated soda, one part to twelve or fifteen of water, for purposes of injection. The average time that the tubes remained in, with his cases, was only twenty-four days. His favorable results he imputed to the mechanical action of the india-rubber covering over the antiseptic dressings.
160 Loc. cit.
161 Loc. cit.
Resection of Ribs.—The ancient operation of resection of ribs, dating back to Celsus, is strongly advocated by Pietavy, Thomas of Birmingham, Lane, and other modern writers as affording the best means of thoroughly evacuating the pleural cavity of its purulent contents and of keeping up constant drainage. John Marshall162 reports 4 cases where he resected the ribs to make permanent openings. In all of these cases the walls became gradually firm and new bone was formed. He concluded that the removal of a portion of one rib was not sufficient, but that a large space through four ribs is the proper size for the opening, that the sixth rib is the essential one to deal with, and that from one and a half to two inches of bone should be taken away. In one case he performed a subcutaneous division of costal cartilage with a view to weakening the thoracic walls and allowing them to fold in. A number of cases are reported of resection of ribs, with varying success, by Ewald,163 Taylor, House,164 and Thomas.165 Taylor166 advises the removal of the periosteum to prevent the rapid re-formation of bone. If after the puncture the rigidity of the ribs seems to keep up the discharge, and the lung does not expand to meet the rib, a resection of a considerable portion of two or three ribs may be made for relief. If, again, in the progress of the case the adjoining ribs have fallen in and have approximated, and thus become a source of pain in retaining a permanent drainage-tube, a portion of rib may be resected. The principal object of resection of ribs is to favor their falling in, for a sufficient orifice can thus be made between the ribs for the discharge. The upper two-thirds of the breadth of a rib may be trephined in order to give more room for exploration, evacuation, ablution, and prolonged drainage. This is the operation of Esthander,167 who thus treated successfully 5 of his 6 cases operated upon. Fenger of Chicago168 operated in this manner on fourth, fifth, and sixth ribs.
162 London Lancet, March, 1882.
163 "Med. Soc. Berlin," Lon. Med. Rec., 1876.
164 London Med. Record, Aug., 1876.
165 Trans. Clin. Soc., vol. xiii.
166 Brit. Med. Journ., Feb., 1881.
167 "Resection du Côltes de Emp.," Revue Mens. de Méd. et Surg., 1879, vol. B.
168 Med. News, Philada., Sept., 1882.
Jacobi169 says that resections ought not to be practised upon children. W. A. Lane,170 from the observation of 5 cases of empyema in children, strongly recommends that a portion of rib or ribs be removed at first, and the cavity thoroughly drained from the beginning. It assists, he argues, the cure by promoting the falling in of the ribs, the expansion of the lungs, and the ascent of the diaphragm. In children the difficulty in securing free drainage is that the spaces between the ribs are small, and after the cavity is opened they become much more contracted; soft tubes thus become compressed, and hard tubes cause much local irritation. Resection of ribs enables the operator to keep the orifice open and have perfect drainage. The opening should be large enough to allow the introduction of the finger and of an india-rubber tube of sufficient diameter to give free passage to the contents of the chest, without the tube being displaced by movement of the ribs. In only one of Lane's cases was trouble caused by rapid increase of bone. He operated as low as the ninth intercostal space in the axillary line, taking care always, by the hypodermic syringe, to ascertain that there was pus at that point. He divided the periosteum longitudinally, and removed with cutting forceps about three-quarters of an inch of rib. After he had thoroughly cleared out the cavity he introduced a short india-rubber tube, so that its inner end should not project into the cavity. Wire sutures were passed deeply through the intercostal tissues and tube, and, to render the position of the tube more secure, soft pins were fixed through the wall of the tube, and attached to them were pieces of elastic surrounding the chest.
169 N.Y. Med. Record, Jan., 1881.
170 Guy's Hospital Reports, vol. xli., 1882.
If necessary in order to have uninterrupted free drainage, children as well as adults should have their ribs resected. The important point in operating is to secure free exit to the fluid and purification of the cavity by the necessary washings by the open method. Pleurotomy by resection of ribs is almost universally acknowledged to be the most effective treatment, for it promotes most rapidly the agglutination of the pleural surfaces and the expansion of the lung.171
171 Lawson Tait strongly advocates this same method of treatment in peritonitis. He has performed laparotomy successfully in 20 cases, using washings and drainage-tubes (Bost. Med. and Surg. Journal, Aug. 16, 1883).
Good drainage is the essential consideration after the operation. We must prevent putrefaction or fetid decomposition in the pleural contents. So long as pus is retained within the sac, it does not putrefy, but putrefaction follows contact with the putrefactive agencies which abound in ordinary air, as shown by Pasteur and Tyndal. These are solid particles floating in the atmosphere. Although air must be admitted, it should be rendered aseptic. The drainage-tube, which should be just long enough to go thoroughly into the cavity, by itself is in many cases insufficient. The upper part of the cavity may retain on its surface pus and flocculi which may prove dangerous. By the syphon we can fill the cavity slowly with medicated tepid water without shock and without risk of tearing away the neo-membranes. Woillez172 advises that pleurotomy should be promptly used whenever pus is found. Béhier advocates the same treatment. E. Moutard-Martin,173 whose authority is high from his great experience and conservatism, advises us always to commence the treatment with thoracentesis by aspiration. He says, if the fever persists and the general condition grows worse, he does not hesitate to resort to pleurotomy. The author's more limited experience coincides with his. I. Marshall174 states as his opinion that purulent pleurisies require the immediate or early adoption of the open method. In fibro-serous pleurisy we wish to restore the physiological condition of the pleura, whereas in purulent cases the object is to obliterate the sac by adhesions throughout the surfaces, just as abscesses are cured. It is necessary that the costal and pulmonary pleura and that of the diaphragm should be brought closely in contact. This is produced simultaneously by the dilatation of the lung and the diminution in every way of the pleural cavity. The dilatation is produced by the disappearance of the intra-pleural pressure and the pressure in the opposite direction from the bronchial surfaces. This last depends upon the condition of the lung and of the visceral pleura. If the lung has been long compressed, it is almost carnified and reduced to a state of foetal atelectasis. It rarely happens that the bands which bind the lung down do not in time undergo granular fatty degeneration and disappear. This enables the lung to expand, if not to its original size, yet sufficiently to occupy the cavity, reduced in size by the approach of the walls. The heart, which previous to the operation was thrown more or less out of its normal position, comes back from the empty side, and often passes the position that it normally occupied. The lung follows the heart. The whole mediastinum finds itself altered in its position and in its contents. The depressed diaphragm rises promptly to its old position in the pleural cavity. The liver, spleen, and the rib-wall undergo striking modifications. We do not expect the lung to dilate to its full extent, as after aspirations in simple pleurisies. The lung, indeed, is already impaired in its movement. We admit air in order to secure treatment to these surfaces. When air is admitted into the normal chest, the lung is retracted to about one-half its size. In serous effusions we fear free admissions of air, because it assists in compressing the lungs, and may contain germs which promote suppuration. We must bear in mind that we may have double pleurisy from the pus producing pleural necrosis at the point of contact of the pleural sacs about the middle of the sternum opposite the middle of the third rib. Elsewhere there is no such danger, for the pleural surfaces remain a long distance from each other.
172 Bul. Soc. Méd. des Hôp., 26 April, 1872.
173 Pleurisie purulente, 1872.
174 Loc. cit.
Why should we postpone pleurotomy, with or without resection of ribs, until we have used the drainage-tube, canula, etc.? The impression is that this operation is attended with danger, whereas ordinarily, with care, such is not the case. In pleurotomy there is not the same danger of serious accidents as in thoracentesis, especially as performed by canulas and trocars. Pleurotomy never causes acute oedema of the lung. The forcible unfolding of the lung, with rush of blood to vessels that have been almost emptied by compression, does not occur under these circumstances. After the large openings of the chest the causes of the forced expansion of the lung do not exist. The diminution of the pressure on the mediastinum, the re-establishment of the thoracic aspiration, and consequently the more free access of venous blood into the right heart, favorably influence the general circulation. The pulse increases in force, the cyanosis is dissipated, frequently within a few hours, and the anasarca disappears in a few days.
Theory and observation show beyond a doubt that in all cases where there exists a decided intra-pleural tension pleurotomy of the thorax modifies efficiently the circulatory and respiratory functions. Instead of causing suffocation, it diminishes almost always, and that instantly and remarkably, the dyspnoea. In 1868, Maisonneuve175 made the startling announcement, which he claimed was nevertheless rigidly true, that of 100 patients who die after surgical operations, 95 are poisoned by organic substances absorbed. He claimed that the liquids exuded from the surface of wounds become corrupt when exposed to the external air, and that subsequently they undergo morbific changes and become formidable poisons. If, he said, we can prevent the dead liquids from putrefying, the gravest operations could be performed without danger. No one who studies the results of empyema in the past can question that the greatest danger is from the blood-poisoning known as septicæmia, caused by the absorption of the septic infection by the lymphatics.176 No matter what may be the nature of septicæmia, it is sufficient that the vast surfaces of the pleura produce certain prurient secretions, which, when absorbed and carried into the circulation, cause hectic fever with its results. We claim that there is less danger from putrid absorption when free incisions are made than from those only large enough to introduce a drainage-tube. Rome177 collected 49 cases, but of these 10 contained fetid pus; 9 of the number had been treated by one or many, even up to fifteen, aspirations. He concludes that the surgical interventions, other than pleurotomy, provoked in the purulent liquid of the pleura putrid fermentations in one-fifth of the cases. The products of this fermentation irritate actively the serous membrane, and cause an abundant suppuration intractable in its nature, and there is imminent danger of rapid exhaustion and hectic fever. One-third of Rome's cases contained solid pieces which could not be removed in any other way than by making free incisions. Although subserous cavities are not perfectly analogous to phlegmonous abscesses, yet they closely resemble each other. Histologically, the inflammatory process and its phases are the same, but there is this difference—absorption of the deleterious products is more active. Why allow a warm abscess to be transformed into a cold abscess, which will open later spontaneously after having caused grave disorders? We have seen how frequently large collections of pus sooner or later open either through the lung or through the chest-walls. If an opening has to be made, the more promptly the better. In the first stage, especially in acute purulent pleurisy, the slight neo-membranes and fibrinous deposits, barely solid, readily undergo granular fatty degeneration, and are absorbed if relieved of the pus. In this stage the two folds of the pleura are in their best condition for becoming adherent to each other, and by obliteration of the pleural cavity to end the disease. If acute empyema be treated early and gently before the lung is compressed or injured, with free opening and constant drainage, the patient being in a recumbent position on face or side, the pleura needs no washings. The orifices made spontaneously are frequently insufficient to completely empty and to keep up the current of pus as it forms. In bronchial fistula, unless the air is prevented from coming from the lung into the pleura by a valvular opening, we have frequently to resort to pleurotomy. If in empyema necessitatis the orifice partly closes or is not free enough, we must not hesitate to enlarge it or make a counter-opening to enable the matter to flow out. In tubercular pyo-pneumothorax, where the purulent fluid has been the primary lesion and has perforated the lung, the operation is not indicated. E. Moutard-Martin's treatise was founded upon 17 subjects, 5 of whom died and 12 were cured. Of the 12 cured, 2 had bronchial fistula in pneumothorax without any sign of tubercle; 5 had permanent fistulous openings and discharged occasionally a few drops of pus; 7 were cured without fistula. Blake178 reported 19 cases treated by permanent openings, with 15 "cured and much relieved." He operated by making incisions from one to two inches long, parallel with the ribs, between the seventh and eighth ribs, a little inside of the scapula. His practice was to keep the orifice open. He used either a spiral wire covered with gutta-percha or a gum-elastic catheter fastened to a shield and kept in position by adhesive plasters. Martin Oxley179 by pressing open the incision with a pair of dressing forceps introduced a silver or india-rubber tracheotomy-tube to keep the orifice open. He related several instances where pieces of tubing fell into the cavity and remained there without injury for months, and in one case as long as several years. Dabney180 urges with force the importance of our having a continuous discharge of pus as far preferable to its daily removal, "not only because it seems less liable to become fetid, but because, as the two surfaces of the pleura have to come together and heal by granulations, the retention of pus would delay this process by keeping the costal and pulmonary surfaces apart." Thorough drainage by two orifices or a wide incision kept open by two tubes is more effective than a simple drainage-tube. Antiseptic precautions are essential to ensure success at every stage of the operation.
175 London Prac., 1868.
176 Ranney, Annals of Anat. and Surgery, 1881.
177 Thèse de Paris, 1882.
178 Boston City Hospital Reports, 2d series.
179 Liverpool Medico-Chirurg. Journal, January, 1882; N.Y. Medical Abstract.
180 American Journal Med. Sciences, Oct., 1882.
Value of Injections and Washings.—The object of injections is to enable us thoroughly to wash out the cavity and to promote adhesions between the pleural surfaces. The chief danger being from septicæmia, it is of the greatest importance that the pus should not be allowed to remain in the cavity longer than can be avoided. The body-temperature, taken twice daily, is one of the best means of ascertaining the extent of the re-formation of pus. Stagnant pus, mingled with air, will undergo fermentation and cause putridity; hence the great value of incessant drainage through unobstructed tubes. When the pus is free from unpleasant odor and runs freely, it is not necessary to use washings or injections of any kind, for the cavity will purify itself. Washings and injections have sometimes been found very injurious and irritating, and sudden deaths have been attributed to them. If flocculi form, washings of tepid water with a very small percentage of alcohol or of salicylic acid (1 per cent.), used without force for fear of rupturing some of the recently-formed capillaries, are useful. When modifying injections are used, the patient ought to lie on the opposite side. In this way all the diseased parts are reached by the fluid. An ordinary syringe should not be used, but a Thudicum bottle or a fountain syringe: either of these can be raised sufficiently high to allow a gentle flow into the cavity. If the discharge becomes fetid, injections of solution of permanganate of potash (1 or 2 grains to ounce j) or of tinct. of iodine (1:4) in water ought to be used. The author has never seen any results of poisoning from the use of carbolic acid, but he has always used a feeble solution, 2 or 3 per cent. Dabney had symptoms of carbolic-acid poisoning in one of his cases where he used a 2 per cent. solution, notwithstanding the fact that he had taken every precaution to ensure its prompt return. A. T. Cabot181 mentions a case of carbolic poisoning in a boy four years of age produced by a feeble solution of one part to thirty of water used only to cleanse the instruments, tubes, and hand of the operator. Kuster's182 experiments show that anæmia and septic and pyæmic fevers predispose the system to carbolic-acid poisoning. He recommends an 8 per cent. solution of chloride of zinc. Chlorate of potassium drachm j to pint j has been used with benefit. The medical journals contain so many reports of the serious, and even fatal, results from absorption of carbolic acid when thrown into abscesses that we are compelled to abandon it in favor of other injections. B. W. Richardson long since showed the great value of iodine as a disinfectant. It not only corrects the fetor of decomposed pus, but at the same time lessens the secretion from the walls. The first injections should be weak, gr. 4 or 5 of iodine and iodide of potassium to a pint of water. Liq. iodinii com., ounce ss to ounce iv, ought not to be used until the surfaces have become accustomed to the action of iodine. Injections of medicated fluid ought not to be used unless they are absolutely necessary, because in some instances they have produced fainting attacks and epileptiform seizures with alarming convulsions. These results have followed injections of different fluids—borax, carbolic acid, iodine, permanganate of potassium, and even warm water. Similar phenomena have followed the injection of the bladder, the uterus, and even from passing a catheter. The shock may have been too sudden or the injection too forcible or the fluid too cold. A. L. Mason183 suggests that it is probably owing to sudden irritation of the lymphatics through the great splanchnic nerve, with anæmia of the brain. Paralysis of the limbs after convulsions makes the theory of embolic origin probable. These accidents must not make us underrate the great value of frequent washings with injections when rendered necessary by the approach of putrid infection. The number of these washings should depend upon the urgency of the symptoms, and antiseptic injections should not be employed unless we find evidences of fetor, because of one great objection: they do not favor the expansion of the lung.
181 Loc. cit.
182 Quoted by Dabney, loc. cit.
183 Boston City Hospital Reports, 2d Series.
Cases of long-standing compression of the lung could hardly result in complete re-expansion, but the general health will be recovered and the chest, contracted by approximation of the pleural surfaces from the walls being pressed in or ribs resected, will cease to secrete pus. If fever persists, with diarrhoea, sweats, emaciation, and fetid suppuration, it shows that the washings are not sufficient in number. They can be repeated as often as every three or four hours, to be decreased in frequency as the patient improves. Under frequent washings Feyrot184 reports favorable results in almost hopeless cases. Time is very precious when these symptoms of exhaustion or septicæmia set in, as it is of the utmost importance that we should endeavor to prevent promptly the absorption of the putrid products, the inevitable effects of which are to produce, before long, fatty and amyloid degeneration of the principal viscera. The most effective way of using detergent fluids is by syphons through two tubes perforated at their extremities and fastened with shields. A Thudicum douche-bottle or a fountain syringe can easily be used by patients themselves as often as is required. The orifice and the tubes should be protected by thorough and rigid antisepticism. As the case improves the cavity gradually gets smaller, the two pleuræ become adherent, and the quantity of fluid lessens until only a small amount flows out. Every eight or ten days we carefully draw out the tubes by degrees, until we have only a little canal beneath the walls. We can thus let the orifice heal slowly, for the sac is obliterated and the patient cured.
184 Thèse de Paris, 1876.
In the hands of Boyer, Delpech, Dupuytren, and Sir Astley Cooper the bistoury gave bad results, but as now used, with all modern appliances and antiseptic precautions, it affords infinite relief and many cures. We claim that by early pleurotomy, with Listerism scrupulously used at every stage of the operation, and if necessary with detergent washings, the mortality from this extremely grave disease can be very materially lessened.
Double Pleurisy.
Pleurisy may occur on both sides at the same time. Double pleurisies are secondary, not primary, and result from rheumatism, or still more frequently, according to Louis, from tuberculosis. In 150 cases of pleurisy quoted by him, there were no bilateral cases which were not produced by rheumatism, gangrene, or tuberculosis. A double pleurisy in a previously healthy person creates a strong suspicion of tubercular origin. There is generally an interval of some days before the attack of one side is followed by that of the other. When effusion takes place the dyspnoea is very great. Death is imminent unless the fluid is withdrawn by aspiration. Maintenon185 states that the inflammation may be so intense and the fever so high as to destroy life before the effusion is thrown out. The physical signs are the same as in unilateral cases. The effusion is never so great on one side as on the other. The progress of disease is rapid, and the result is almost always fatal.
185 Thèse de Paris, 1873.
Diaphragmatic Pleurisy.
The serous lining of the upper surface of the diaphragm may be involved in an ordinary pleurisy, or inflammation may be limited to it without involving either the pulmonary or the parietal membrane. In this latter case we have modifications of the characteristic symptoms and physical signs. Functional disturbances and special symptoms enable us to diagnose it. There is a febrile movement with occasional delirium, and some of the prominent symptoms, but without the physical signs to indicate the exact locality. The pain is intense, and dyspnoea exists even to the extent of orthopnoea and respiratory anguish, the respiration jerky and convulsive. The pain comes on suddenly in one of the hypochondriac regions, extending up to the attachments of the diaphragm to the costal surfaces. The pain is intense, and increased by full inspirations, by physical efforts, by vomiting, and even by the eructations of wind. The position of the patient attracts attention: as he sits with the trunk inclined forward, he has an anxious and distressed expression of countenance, sometimes accompanied by nausea and vomiting with singultus. Pressure elicits a characteristic tenderness; if applied under the false ribs, it causes suffering. The phrenic nerve is painful on pressure practised over the accessible points of its course, between the two inferior bands of the sterno-cleido-mastoid at the base of the neck. There are also painful irradiations in the cervical plexus above the clavicle and in the scapular region. Pressure over a circumscribed spot of the epigastric region causes a sharp agony of pain. This point is at the intersection of two lines—one, the external border of the sternum; the other, at the osseous portion of the second rib. Guéneau de Mussey186 has named this the diaphragmatic bottom. This pain extends sometimes to the vertebra and upward to the first intercostal space. Auscultation and percussion at the base of the lung give us some results: impaired expansion of the lung at the base and dulness on percussion; the diaphragm is in a great degree immobile, owing partly to the pressure upon it, and partly to a paresis from inflammation of its upper serous covering (Stokes187). When the inflammation is on the right side, we may find an icteroid tint, with vomiting, delirium, etc., with the liver pushed below its normal position in the abdomen. The inflammation of the pleural covering of the diaphragm may be caused by sero-hepatitis extending through the diaphragm (Copeland188).
186 Archiv. de Méd., 1879, vol. ii.
187 Dis. of Chest, 1837.
188 Dict. Med., vol. iii., edited by Lee.
If the effusion is confined to the space between the lung and diaphragm, the diagnosis is obscure. There may indeed be cases where we have but few of the symptoms already mentioned. If the fluid is not confined to this portion, but flows into the pleural cavity, it gives great relief, and the result is favorable. Diaphragmatic pleurisy may, however, end in death, either by its discharge into the peritoneal cavity or by constitutional disturbances.
Interlobular and Mediastinal Pleurisies.
The effusion is sometimes confined by adhesions between two lobes. The mediastinal variety is situated between the pleural boundary of the mediastinum and the adjacent portion of the pulmonary serous membrane. It is but rarely met with, and may be diagnosed by local symptoms. The flatness on percussion in the interlobular variety is very circumscribed. Both forms cause local pains, but in the mediastinal variety the pain is very deep and perceptible at the middle of the sternum, and is increased by the respiratory movements. In both varieties there is more or less fever. If either variety exist on the left side, the condition of the pericardium must be carefully examined, as pericarditis may be confounded with it. These limited collections of fluid may burst into a bronchus and be expectorated.
Multilocular Areolar Pleurisies.
Multilocular encysted collections of fluid in the pleural cavity are due to the partitions made by pseudo-membranes which divide the pleura into subcavities. These occur generally in subjects who have had previously dry or adhesive pleurisies. They are more serious than ordinary pleurisies. We meet with them in aspirating, when, after draining off the fluid from the base of the pleural cavity, we find the lung expanding, but above that point there is absence of respiratory murmur and of other physical signs indicating the presence of fluid. Reybard189 divides multilocular pleurisy into three varieties, with varying symptoms and physical signs, according to whether it exists at the upper, middle, or lower portion, right or left side. Owing to the thickness and distribution of neo-membranes, it is frequently difficult to localize the points of collections of fluid. Aspiration is the most accurate means of ascertaining the exact point and extension of the effusion.
189 Bullétin Acad. Méd., 1879.
Rheumatic Pleurisy.
HISTORY.—The recognition of the fact that we can have local manifestations of rheumatism in the texture of the lung itself, of the bronchi, and of the pleura is of comparatively recent date. There had been indefinite, loose statements, or rather suggestions, in some of the writers in the early part of the century, such as Chomel and Andral, as to the possibility of rheumatism appearing in the pulmonary textures; but we believe that the first definite description of the disease was made by T. H. Buckler of Baltimore in 1865.190 He claimed that the white fibrous tissue of the bronchi could be the seat of rheumatism, as well as similar textures about the joints. He illustrated his views by cases observed and reported by himself. He showed how, as a result, there were symptomatic engorgements, more or less solid, of the pulmonary parenchyma or rheumatic pneumonia. In 1854, Black191 found crystalline particles of uric acid and of urate of soda deeply imbedded in the thin white fibrous tissue of bronchi. Buckler showed the metastatic character of rheumatic inflammation in the bronchi and lungs as elsewhere. Buckler's subsequent papers192 published in connection with this subject, show remarkable success in treatment of fibro-bronchitis and rheumatic pneumonia based upon his views of their pathology.
190 Fibro-Bronchitis and Rheumatic Pneumonia.
191 Edin. Med. Journal, 1854.
192 Boston Med. Journal, 1882, and Amer. Med. Journal, Oct., 1882.
SYMPTOMS.—We find rheumatic pleurisy coming on in the course of rheumatic fever with the characteristic mobility of the points of inflammatory action. Laseque193 gives the symptom with accurate details—the acute pain in the side of the chest without cough or expectoration. He describes the pain as differing from that of ordinary pleurisy, in that the extent of pain is greater and not so limited, due to the fact that the rheumatism invades the aponeurotic tissue which forms the covering to the intercostal muscles. It persists longer and is wider spread. The dyspnoea is caused by the inability to move the respiratory muscles and by the disease invading the aponeurotic centre of the diaphragm.
193 "Pleurésie rheumatismale," Arch. Gén. de Méd., 1873.
The rapidity of the inflammation causes the sudden pain and the accompanying effusion in even a few hours. In a well-defined case recently seen by the writer in a lady forty-seven years of age the rheumatism literally jumped from a large joint to the pleura, giving rise to a severe pain, without cough or expectoration, with an increase of 2° of temperature and 20 beats of pulse. There was a moderate effusion. In forty-eight hours, under the influence of an initiatory dose of quinine (20 grains), followed by free doses of salicylate of sodium, the attack subsided and the friction sound at the base of the lung disappeared. This case did not follow the rule mentioned by Senx,194 that the disease, upon leaving the pleura of one side, appears in the same manner on the other. It sometimes goes to the pericardium and endocardium from the pleura. Chomel195 insisted upon the frequent examination of the heart to ascertain whether this had occurred.
194 De la Pleurésie rheumatismale, Paris, 1878.
195 Art. Pleurésie Dict., in 30 vols., 1842.
Rheumatism of the pleura does not always appear and disappear suddenly. It sometimes is gradual in progress and slow in recovery. It usually occurs when we have manifestations elsewhere, but the pleura may be the point first attacked, as is more frequently the case in pericarditis.
DIAGNOSIS.—The diagnostic signs are hereditary or personal tendency to the disease, the character of the local pain, the mobility of the disease, violence of pain and its rapid disappearance, and the existence of profuse sweats. Suppuration rarely occurs.
PROGNOSIS is in its nature serious, not from the intensity of the disease, but from its being a visceral rheumatic affection. It is, moreover, frequently double, and may recur often in the same subject.
TREATMENT is that of rheumatism elsewhere—salicylic acid and its salts, alkalies with opiates. Thoracentesis is rarely indicated, because mechanically the effusion does not seriously impede respiration: if the pericardium be involved, it may be necessary in order to relieve the pleura or the pericardium.
Hemorrhagic Pleurisy.
DEFINITION.—Pleurisy complicated by hemorrhage. Hemorrhagic pleurisy is the union of an ordinarily slight hemorrhage in the pleura with inflammation of that membrane (Laennec).
ETIOLOGY AND PATHOLOGY.—These must be studied together, because the pathology of the disease explains its etiology. While hæmothorax designates hemorrhage into the pleural cavity without inflammation, hemorrhagic pleuritis involves necessarily the idea of inflammation accompanied by effusion of blood, whether this occurs before, during, or subsequently to the inflammation. We cannot assign the name hemorrhagic pleurisy simply because there may be slight red coloration of the effusion. Microscopic researches have shown that all effusions, even the simplest, contain more or less white and red blood-corpuscles. The presence of a certain number of the red discs no more justifies us in calling the pleurisy hemorrhagic than the presence of the leucocytes would entitle us to call it purulent pleurisy. Dieulafoy196 states that there can be from 500 to 4000 red globules to the cubic millimeter without producing any coloration. They must reach 5000 before they will really attract attention. He says, however, that when the number of red corpuscles reaches 2000 the effusion is "histologically hemorrhagic," because the presence of blood is analogous to the state of engorgement or congestion of the first stage of pneumonia or other phlegmasia, and constitutes a particular phase of pleurisy which must produce purulent matter. The name hemorrhagic pleurisy ought to be used when the number of red blood-corpuscles is sufficient to enable us, by the unaided vision, to detect the presence of blood. We may, however, find a fluid in the pleural sac which is red and yet does not contain blood-discs, but their coloring principle, the dissolved hæmatin. Jaccoud197 designates this condition pseudo-hemorrhagic pleurisy. Vulpian and Charcot explain the slight discoloration by the presence of hæmatin crystals, which, having been imbedded in the false membranes, escape into the flow of the chest. Nolais198 included both of these discolored effusions among the varieties of hemorrhagic pleurisies: "Hemorrhagic pleurisies include all those of which the liquid borrows the red coloring matter of the blood." Moutard-Martin (R.)199 divides hemorrhagic pleurisy into three varieties: simple, as produced in simple, acute, or subacute pleurisy; tubercular; and cancerous. Trousseau200 considered all hemorrhagic pleurisies as caused by cancer. Beigel201 states positively that in cancerous pleurisy the effusion is limpid with a yellowish tinge. Walshe202 held the same views. Nolais, Moutard-Martin (R.), and Fernet satisfactorily demonstrated that such is not the case, but that the hemorrhagic effusion may be simple and independent of any organic disease. It may be produced by acute inflammations of the pleura as well as by cancer of the lung or pleura. It may be connected with pleuro-pneumonia or miliary tubercle. It comes, although more rarely, from fevers, such as measles, and from certain dyscrasiæ due to renal, hepatic, or even splenic lesions. When hemorrhagic pleurisy follows hæmothorax, the blood, after remaining liquid at least one or two hours, initiates the inflammatory action which has, according to Ch. Nélaton,203 for its object the encystment of the clot. Cornil and Ranvier204 claim that the cyst is caused by the retracted clot, and that after absorption of the serosity this cyst may become organized. The presence of air causes fetidity of the blood and purulent pleurisy.
196 De la Thoracentèse par Aspiration dans la Pleurésie aigue.
197 "De l'Humorisme ancien comparé à l'Humorisme moderne," Thèse de Concours, 1863; Gazette Méd., 1860, quoted by Nolais.
198 Thèse de Paris.
199 Thèse de Paris, 1878.
200 Clin. Méd.
201 Reynolds's Syst. of Med., 1871.
202 Dis. of the Chest.
203 Thèse de Paris, 1880.
204 Path. Anatomy.
We may have hemorrhagic effusions occurring simultaneously with acute pleurisy, with pulmonary congestions, pneumonias, and apoplexy of the lung. They are caused by the violence of the inflammation with local plethora, producing a sanguinary stasis—a mechanical result of intense congestion. Moutard-Martin (R.) states that in these cases the red globules come through the walls of the blood-vessels, as do the leucocytes, by diapedesis. Jaccoud205 admits that the blood-vessels are altered by the inflammation, perhaps also by the derangement in the vaso-motor innervation. The tissue of the pleura is penetrated by both red and white blood-corpuscles, and the blood-vessels and lymphatics are dilated, red corpuscles being found in lymphatics. By far the greatest number of hemorrhagic pleurisies are secondary to pleural inflammations, either resulting from acute causes or from cancerous or tubercular disease, or from diseases causing a dyscrasia of the blood, such as nephritic diseases, hepatic, cardiac, scorbutic affections, or alcoholic excesses. The secondary result of these pleurisies is the formation of neo-membranes, fibrous in their nature, which pathological anatomy shows contain, as they become organized, abundant blood-vessels with thin and brittle walls. A slight exciting cause is all that is necessary to produce their rupture. The primary cause is the false membrane, and, in some cases, vascular granulations, which have rapidly formed, perhaps in twenty-four hours—conditions eminently favorable to the production of hemorrhage. In cancerous, tubercular, and dyscrasial conditions of the blood, the blood-vessels are especially weak and easily give way, owing to the defective nutritive properties of the blood itself, just as, in typhoid fever, we have nasal and intestinal hemorrhage, and in typhus, petechiæ. In 200 cases collected by Moutard-Martin206 there was found intra-pleural effusion in three-eighths of the cases. Only one-third of that number were hemorrhagic. In 42 cancers observed between 1872 and 1876, 35 were without pleural effusion, 1 only was hemorrhagic. M. Moutard-Martin reports 34 observations of hemorrhagic pleurisy produced by cancer, 19 by tubercle, and 31 following simple pleurisy. Of these last there were 7 cases of effusion complicated with a pneumonia, 3 with a cirrhosis, 6 with a cardiac affection: all except 12 of these cases had some complication. Most of these (12) recovered, so he had not the autopsies to verify his diagnosis. Rayer207 cites 4 cases of bloody effusion in the pleura occurring in the course of a nephritis. Poutin208 reports 1 in renal sclerosis. M. Natalis-Guyon209 reports an epidemic of measles where many infants died of hemorrhagic pleurisy. Marguerite cites 13 cases complicating pneumonia, granulations, chronic pleurisy, small-pox, etc.
205 Clin. Méd.
206 Loc. cit.
207 Traité des Mal. des Reins.
208 Soc. Clin. de Paris, 1879.
209 Soc. Méd. des Hôpitaux.
Rilliet and Barthez210 say that it is common to find in infants considerable discoloration of effused serum in variolic and other organic poisons. It seems fair to conclude that hemorrhagic pleurisy may occur in a large number of cases where the blood has undergone alterations, but to produce it, it is necessary that the pleura should have been rendered vulnerable by pre-existing causes, because it ordinarily resists, better than many other membranes, the hemorrhagic tendency. If we admit the existence of tubercular or cancerous hemorrhagic pleurisies, we ought not to consider those as simple which are produced under the influence of the other causes that we have mentioned. The tubercular granulations are deposited either on the pleural surface or in the parenchyma of the lung near the surface, the most frequent locality being in the thickest parts of the organized false membranes. The rupture of their blood-vessels causes the escape of blood into the pleural cavity. The effusion, more or less discolored, rarely exceeds a liter in quantity. Effused blood from cancerous origin may either come from rupture of the vessels in the growths themselves by ulceration, or from the neo-membranes in their vicinity.
210 Traité des Mal. des Enfants, t. iii.
The primitive seat of the cancer is rarely in the pleura, but most frequently in the lung, the cancer being of secondary formation arising primarily from ganglions of the mediastinum. Hemorrhagic pleurisy may be caused by laceration of the newly-formed blood-vessels in the neoplasms by aspiration or by the lung expanding too suddenly. We conclude that hemorrhagic pleurisy is generally owing, directly or indirectly, to vascular neo-membranes which are produced in simple, in tubercular, and cancerous pleurisies.
SYMPTOMS.—The symptomatology of this form of pleurisy does not differ materially from that of other varieties. We cannot attach much importance to the initiatory symptoms nor to the march of the disease. If the quantity of blood be great, we must expect general weakness, pallor, and even fainting. We may have oedema of the walls, as in purulent pleurisy, and exceptionally in serous pleurisy. Ordinarily, however, hemorrhagic pleurisy is more extensive, and limited to the inferior part of the chest, owing to the interference with the venous circulation. If cancerous in its origin, we shall have dyspnoea and violent intercostal neuralgia from pressure of the tumor. When the effusion is formed in the pleural sac, the physical signs already enumerated indicate its presence. Some authors, especially Fernet, Moutard-Martin, Alcoud, and Guéneau de Mussey, attach considerable significance to Bacelli's whisper-pectoriloquy as showing that the effusion is not serous in character. Nolais questions this view, and says that this sound ought to be heard whenever there is blood, whereas they state it is heard only at the base or summit of fluid. When hemorrhagic pleurisy results from tuberculosis, it is never from the ordinary ulceration form, but always from the acute miliary, non-ulcerating variety. We must not, therefore, expect to be aided in our diagnosis by the progress and symptoms of pulmonary phthisis. We may, however, detect uncertain, indefinite symptoms which are hard to interpret as indicative of tuberculosis. The effusion is rarely excessive in this variety, whereas when resulting from cancer it is often very abundant and is rapidly reproduced.
DIAGNOSIS.—We may suspect the presence of hemorrhagic effusions, but only by exploratory punctures can we arrive at certainty of diagnosis. We must bear in mind that we may withdraw with the aspirator-needle some drops of blood at its insertion and at the close of the exploration from the highly vascular neo-membranes or from the lung itself. Having ascertained the nature of the fluid, the differential diagnosis must be made as to the cause, simple, tuberculous, or cancerous. We must study the manner of access of the disease, and especially ascertain if its invasion was violent, with a quantity of blood (d'emblée), or whether it came from the neo-membranes. In the simple variety there are the ordinary acute or subacute symptoms of pleurisy, without any preceding symptoms. In cases of tubercular origin we have to aid us a small quantity of fluid effused and the insidious character of symptoms. In cancerous cases we must expect to find traces of hereditary or of personal taint which may have affected the general health. We must look for cancer elsewhere, and examine carefully to see if there be any tumor of the mediastinum or intra-thoracic pressure, or any infiltration of the lymphatic glands, especially above the clavicle. The fluid drawn in the exploration ought to be examined microscopically, for we may detect evidences of cancer. Walshe211 cites a case where encephaloid débris was thus discovered. Other authors also give similar cases.
211 Diseases of the Chest.
PROGNOSIS.—This depends upon the nature of the disease producing it. When caused by the newly-formed membranes connected with simple serous pleurisy it is ordinarily not serious, for the mere presence of blood in the pleura has no bad influence over the restoration of health. It is more the intensity of inflammation, with the quantity of blood effused, that indicates gravity of prognosis. Dieulafoy212 considers the prognosis as unfavorable in the hémorrhagie d'emblée form, drawing the distinction between this and the histologically hemorrhagic. He thinks that every purulent pleurisy was at first hemorrhagic, and the presence of pus shows greater intensity of inflammation. Homolle213 also states that the pleurisies rich in red globules are ordinarily very acute, and, in consequence of that fact, predisposed to purulence. Purulency is not the sole cause of danger. We fear compression of the lungs, and still more septicæmia. In the tubercular and cancerous forms the prognosis must be very serious. When the hemorrhagic pleurisies arise in the course of organic diseases of the heart, kidney, and liver, they are of grave import.
212 Loc. cit.
213 Rev. des Sci. Méd., 1880.
TREATMENT.—If the quantity is excessive, local applications and ergot ought to be employed to arrest the flow. If the dyspnoea and oppression are great, it is best to draw off at least some of the fluid. If the quantity be not large enough to embarrass respiration, we must expect nature to absorb it, or by local inflammation to encyst it. Lacaze214 reports a case where a fistula was established, and the case was cured. Dieulafoy gives another case where six punctures were made, and no less than 6 liters, in all, were withdrawn. He injected afterward a solution of 4 grammes of sulphate of zinc to 400 grammes of water, and the patient was cured. In the first stage of the disease we use palliatives—morphia hypodermically, bromides, and chloral—if indicated. During febrile symptoms of acute cases we refrain from withdrawal of fluid unless it is excessive. The question of thoracentesis has been discussed in regard to simple pleurisies. The same rules apply, a fortiori, when the nature of the fluid is hemorrhagic. Ordinarily, the abundance of fluid, and the dyspnoea which results therefrom, indicate the operation. We prefer not to draw off the fluid completely—only enough to relieve the embarrassment of respiration—because we destroy the equilibrium of pressure on one side against the neo-membranes and the compressed lungs on the other. Congestion of the lung may thus be produced with albuminoid expectoration. Moutard-Martin (R.) coincides with Dieulafoy in limiting the amount to be withdrawn to one liter. Of course the fluid is slowly aspirated. After part of the fluid is withdrawn, what remains is absorbed, remains stationary, or increases in quantity. We repeat the operation, and slowly draw off greater quantities of fluid if it returns; especially in cancerous cases, where the effusion is often very large, the operation gives great relief. It is rarely large enough in tubercular cases to justify thoracentesis.
214 Thèse de Paris, 1851.
Tubercular Pleurisy.
Tubercular pleurisy may be acute or chronic. It may occur during the course of ordinary tubercular disease of the lung, by extension of the disease from the lung to its serous covering, or it may proceed from tubercular deposit on the pleura independently of any previous disease of the lung. Acute tubercular pleurisy may be dry and situated at the summit of the chest, or may be what is called accidental pleurisy. Dry pleurisy is almost constant in tuberculosis of the lung. Its existence is, in itself, a powerful presumption of pulmonary phthisis, especially when it is situated at the apex. In tuberculosis pleuritic inflammation is lighted up by slight and scarcely appreciable causes. Its commencement is insidious, with little or no pain or fever: indeed, it is with subacute symptoms that the disease slowly advances. The first intimation the patient has of the disease is the impairment of his breathing-power by the presence of fluid. The fluid is not generally in large quantities, and is serous or sero-fibrinous, and sometimes sero-purulent. Latent pleurisy of the older writers was frequently tuberculous in its origin. This form of tuberculosis may precede or follow the deposit of tubercles in the lung-tissue. The tubercles may be deposited to a slight extent in the tissue of the lung, and their presence is shown by an irritating cough only when the pleurisy approaches insidiously. The tubercular granulations over the visceral pleura are extended to the parietal surface also, and notably to the circumference of the fibrous leaflet of the diaphragm—an especial point of elevation for the secondary products.
This disposition of tubercular lesions of the pleura is one of the most striking examples of what is called infection from contiguity, and is a powerful proof of the infective property of tubercular products which from an initial nucleus is propagated from point to point. Acute tuberculosis of the pleura is one of the most common manifestations of acute phthisis. It more frequently causes acute than subacute pleurisy. Chronic tuberculosis almost always produces purulent pleural effusions. It is much more common in infants than in adults, and is sometimes met with in children from three to ten years of age (Barthez et Rilliet215). Tubercles may be developed in the intra- or extra-serous membrane. Among old people the tubercle sometimes appears first in the recent false membranes produced by pleuritis (as associated with caseous pneumonia, or genuine tuberculous processes in the lungs), or in connection with tubercles of other organs (Fraentzel216). The advance of this disease is habitually slow, or at least not accelerated by the development of other tubercular diseases. The diagnosis is often accompanied with great difficulties, for the disease may be confounded with chronic or with purulent pleurisy, especially if these are developed in a tuberculous subject. In both cases we have hectic, night-sweats, emaciation, etc. Thoracentesis alone can give definite results when the effusion is in considerable quantity. When suppurative pleurisy supervenes in tuberculous subjects, the prognosis is very grave. Should the pus be sufficient in quantity to embarrass respiration, it can be drawn off cautiously by aspiration. The open method of drainage and free incisions should not be used, for experience has shown that they injure instead of benefiting the patients.
215 Mal. des Enfants.
216 Ziemssen's Cyc., vol. iv.
Hydrothorax.
From [Greek: hydôr], water, and [Greek: thôrax], the chest.
DEFINITION.—Dropsy of the chest. The accumulated fluid in the pleural cavity which resembles the serum of the blood is not the product of inflammation, but is caused by mechanical obstruction to the circulation or by blood-poisoning. Hydrothorax is never idiopathic, but invariably secondary, resulting from disease, not of the pleura, but of the circulatory system or of the blood itself.
HISTORY.—Before pathological anatomy had been accurately studied, effusions resulting from inflammatory processes in the pleura were confounded with simple hydrothorax, which is not a variety of pleurisy. Royer217 and Laennec218 divided hydrothorax into idiopathic and symptomatic; Darwell219 adopted in a great measure their views. They did not draw the distinction between the passive transudation of serum, constituting the condition known as hydrothorax, and exudations resulting from idiopathic pleurisy. Before physical modes of exploring the chest were used there was great uncertainty in the diagnosis of collections of fluid in the pleural cavity.
217 Dict. de Méd., 1832.
218 Dis. of Chest, Forbes's edition.
219 Cyc. Pract. Med.
ETIOLOGY.—Dropsical effusion in the thorax is produced by the same causes which give rise to collections of watery fluid in other serous cavities and in the connective tissue, constituting general anasarca. Primary among the causes is obstruction of the venous circulation in the walls of the chest or in the lungs. Mitral disease, especially insufficiency with dilatation, deranges the normal circulation in the lung and its serous coverings, producing hyperæmia, oedema of the lung, and finally serous effusions into the pleural sac. General dropsy results. According to Fernet,220 in dropsies resulting from mitral disease oedema of the lungs and hydrothorax always precede all other oedemas. Fraentzel,221 on the contrary, states that it does not occur until there is no longer any room for the transuded fluid in the deeper portions of the subcutaneous tissues. Other diseases of the heart produce hydrothorax. Whenever there is abnormally high venous pressure, which invariably follows dilatation of the right side after compensatory hypertrophy has reached its limit, and the heart literally yields to the backed current of blood, we must expect dropsical results. Intra-thoracic tumors, aneurisms, emphysema, and sclerosis of the lung cause hydrothorax by pressing upon the venous trunks and upon the thoracic duct without producing general dropsy. Chronic diseases, such as cancerous disease, chronic malaria, etc., produce great exhaustion and give rise to general hydræmia. Especially is this the case in chronic disease of the kidneys, such as the several varieties of nephritis and amyloid degeneration, where there has been a loss of albumen for a long time and the blood-serum has been rendered poorer in solid constituents. Hydrothorax is not a disease, but a symptom resulting from a variety of causes which produce physical exosmosis of the serum of the blood.
220 Nouveau Dict. Méd., vol. xxviii.
221 Ziemssen's Cyc., Amer. trans., vol. iv.
PATHOLOGICAL ANATOMY.—Hydrothorax being merely dropsy of the thoracic cavity, there is no lesion of the pleura. There is a collection varying from 100 grammes to many liters of fluid in the cavity. It differs from the effusion in subacute pleurisy in its small quantity of fibrin, in having far less of albuminoid material, and no white blood-corpuscles. The water collects almost always in both sides of the chest, more on the side on which the patient lies in bed. In the recumbent position the fluid gravitates posteriorly more than the effusions of pleurisy. In the upright position it will follow Ellis's curved line more regularly than in effusions resulting from pleurisy, for there are no adhesion-bands interfering with its doing so. The fluid is limpid, of a light-yellow or citron color. Its composition resembles that of the plasma of the blood, but it contains more water and less of the constituent elements. Alex. James222 found that the amount of mineral matter was the same in dropsical fluids in all parts of the body, and that the organic albuminoid substances were larger in quantity in the pleura than in any other cavity. The amount of organic substances varied directly in accordance to the degree of pressure on the different capillary vessels. The anatomical changes in the pleura and the subpleural connective tissue are similar to those found in other collections of dropsical fluid. They are swollen and thickened by maceration with water. They become opalescent and less firm of texture. The lungs retract as the fluid increases in quantity. As the filtrates collect in both pleural sacs, the lungs do not forcibly collapse. The patient would sink at once were this the case. The arch-tension of the diaphragm is but rarely overcome, and consequently we must not expect to find the liver and spleen pushed down, especially when there is fluid in the peritoneal cavity. The position of the heart, unless there is a marked difference in the collections of the two sides, is but little altered, the retractive force of both lungs being impaired.
222 Med. Times and Gazette, Jan., 1880.
SYMPTOMS.—The general accumulation of watery fluid is not attended by any pronounced symptom until it has reached the point of interfering mechanically with the normal play of the lungs. At first dyspnoea is only perceptible on increased physical exercise. When the quantity is excessive, the individual suffers when perfectly quiet. The patient, until the fluid is excessive, lies on his back as the most comfortable position, but as the quantity increases he is often obliged to sit up in bed.
The dyspnoea is ordinarily much more oppressive than in pleuritic effusions, because both lungs are compressed. There is no rise of temperature, no pain in the side, no tenderness on pressure, no acceleration of the pulse, and but rarely any cough, as there is in pleurisy. The dyspnoea often becomes very painful, and may even produce orthopnoea, being accompanied by short and frequent acts of breathing. Where there are very large amounts of fluid the mechanical interference with the breathing is so great that cold sweats, cyanosis, and asphyxia follow, the pulse becoming smaller and more feeble until the patient dies.
The physical signs are, in general, the same as those of pleuritic effusions, especially the subacute form, with some slight variation. Inspection and mensuration do not aid us as in pleurisy, for in hydrothorax the accumulation of fluid is bilateral instead of unilateral. The tension is not sufficient to dilate the walls of the chest. Palpation shows absence of vocal resonance, but not invariably, for we are unable to compare the two sides. We must remember that we have oedema of the walls of the chest, which would partially prevent the thoracic vibrations from being felt. Percussion flatness is not as absolute as it is in pleurisy, unless the fluid is in excessive quantity, for the tension of the fluid is feebler and the lung contains more air. The lung is never completely compressed, as in pleurisy, there being no fibrinous bands to constrict it. The percussion vibrations, unless very lightly made, are communicated to the lung; and so there is dulness instead of flatness. The absence of fibrinous bands permits the fluid to change its position with the varying postures of the patient. This rarely occurs in pleuritic effusions after the first few days. Finally, Skodaic tympanic resonance at the apex is but seldom met with in simple hydrothorax.
Auscultation.—The presence of fluid between the lung and parietes prevents us from hearing the vesicular murmur. The distant bronchial respiration is rarely heard in hydrothorax, as it is in pleurisy, because the lungs are not completely deprived of air, and when present is less intense. Ægophony is frequently heard over the upper limit of the fluid, the whispering voice being transmitted through the fluid. Owing to pulmonary oedema there are subcrepitant râles, but never pleuritical friction sounds.
DIAGNOSIS.—Ordinarily, the diagnosis ought to be made without difficulty. The only disease with which there can be any danger of confounding it is subacute pleurisy. The principal points of differential diagnosis have been enumerated above. In subacute pleurisy (latent pleurisy) we have, in less intensity, the ordinary pleuritic symptoms. The pleuritic friction murmur is present, and a fluid containing the products of inflammation. Very exceptionally is subacute pleurisy double, whereas hydrothorax is almost invariably so.
The history of the case enables us to arrive at an accurate diagnosis. The withdrawal of a small quantity of fluid with a fine perforated needle, and its chemical and microscopical examination, will complete the diagnosis in doubtful cases.
Oedema of the lung can scarcely be confounded with hydrothorax. The absence of the physical evidences of water in the cavity, and the crackling sound heard in auscultation, are distinctive of oedema.
PROGNOSIS.—The prognosis is always serious, but it depends upon the nature of the disease producing the dropsy. If this can be removed, the collection of water may disappear. But, unfortunately, the circulatory diseases which produce it are generally chronic and incurable. The fluid can, by general treatment and mechanical means, be reduced, and the life of the patient prolonged and made comparatively comfortable. Sooner or later a large number of cases must succumb.
TREATMENT.—The treatment should first be directed to the primary disease causing the dropsy. If heart disease be the promoting cause, we must, by means of digitalis, endeavor to promote compensating hypertrophy, and by arsenic and iron improve the quality of the blood. If Bright's disease be the cause, the skimmed-milk diet, with iron and manganese, must be given with remedies which lessen the hydræmic condition of the blood. Digitalis, diuretics, jaborandi, and drastic purgatives give decided results. Of all purgatives, elaterium in decided doses (¼ grain), guarded by conium or hyoscyamus, causes most relief by producing free watery stools. Mechanical means must be resorted to without hesitation. It is best first to remove the fluid from the lower extremities by the insertion of Southey's capillary canula with caoutchouc tubing attached. Large quantities of water may thus be drawn off without local irritation, erysipelatous in its nature, being produced. Thoracentesis by aspiration averts death very often, and gives the greatest possible relief when the effusion is large enough to produce dyspnoea. In a case under the author's care life was prolonged many months and large quantities of fluid were removed. Altogether, there were twenty-two operations and 1563½ ounces of water removed. As often as every week one or other side had to be emptied, the quantity removed each time varying from 49 ounces to 112 ounces. For two months previous to death filtrates collected in the abdominal cavity also, and had to be frequently withdrawn.
Pneumothorax.
DEFINITION.—A collection of atmospheric air or of gas in the pleural cavity. Pneumothorax ([Greek: pneuma] and [Greek: thôrax]).
In ancient times gaseous collections were frequently noticed in serous cavities, especially on opening the chest for empyema and at post-mortem examinations. The presence of air resulting from laceration of the lungs by fractured ribs was known and designated as emphysema thoracis. Air in the pleura was considered as an accidental complication which occurred with empyema or as formed after death. Morgagni and others mentioned the presence of gas as formed in the pleural cavity. Itard223 was the first to speak of it as a disease and to name it pneumothorax. Owing to the imperfect knowledge of pathology at that period, he attributed the production of the air to the decay of the lung from chronic suppuration, and to the decomposition of the long-retained pus. Laennec was the first to give an accurate anatomical and clinical account of the disease.
223 Thèse de Paris, 1803.
HISTORY.—Pure pneumothorax—that is, pneumothorax caused by the presence of air alone in the pleura—is but rarely met with, except for a short time, when it has been introduced from without by traumatic injuries. The irritating effects of gas, unless it comes in small quantities through the ribs from wounds in the chest-walls, are very frequently followed in a short time by the production of a quantity of serosity or of pus. If air is introduced into the pleural cavity from perforation of the lung, there is also liquid matter from the lungs of such a character as at once to provoke inflammatory action. Such a condition is then denominated hydro-pneumothorax or pyo-pneumothorax. The latter was, in fact, recognized by Hippocrates by the sign of succussion, though not so designated.
ETIOLOGY.—Laennec divided pneumothorax into three distinct varieties: 1st, essential pneumothorax, resulting from the spontaneous formation of gas in the pleural cavity; 2d, pneumothorax from putrid decomposition of liquids effused into the pleura; 3d, pneumothorax by perforation, due to rupture into the pleura or to an accidental opening by which atmospheric air or gas from the lungs is introduced into the pleural cavity. This division, having Laennec's high authority, was for a long time generally received. It has now been established that the pleuræ cannot secrete air.
Proust224 collected 25 cases of so-called spontaneous pneumothorax, and showed that they could all be otherwise satisfactorily explained. In some cases errors of diagnosis had been made by mistaking tympanitic sonority at the anterior-superior portion of the chest, or the existence of the amphoric breathing found in pleurisy, for pneumothorax. Some were cases of pneumonia in which tympanitic percussion resonance deceived observers. Then, again, there was found, among the cases cited, pneumothorax resulting from rupture of a tubercular cavity or of a hydatid. In tubercular cases Proust found that the orifices made were so small—no larger, as Gairdner of Edinburgh had stated, than a pin's point—that they could not be detected, or that they had cicatrized before the post-mortem examination, or perhaps closed by adhesive false membranes. Other investigations by Ewald225 and Jaccoud226 have confirmed Proust's views that essential pneumothorax does not occur. Researches in pathological physiology disprove the possibility of a serous membrane producing a secretion of gas or of its passing from the blood through the capillary walls. We therefore conclude that pneumothorax from secretion of air within the pleura is contrary to physiological facts generally accepted, and is disproved by pathological investigations.
224 Ibid., 1862.
225 Quoted by Fraentzel, Ziemssen, vol. iv.
226 Gaz. hébd., 2ème serie, 1864.
The second variety in Laennec's division—namely, where the gas results from decomposition of fluid in the pleural cavity—has been supported by such high authorities as Hughes Bennett, Townsend, Wunderlich, and Jaccoud. Yet it is difficult to understand how it could occur. The contact of air appears to be necessary for the decomposition of serum and pus in the pleural cavity. While shut up in a cavity coated with neo-membrane, a fluid may certainly remain undecomposed for a long time, and undergo decomposition as soon as taken out of the cavity. Recent researches in regard to putrid fermentations appear to confirm the view that the presence of air is absolutely necessary to produce that effect.
We believe, therefore, that perforation, with rupture of the visceral or parietal layer of the serous membrane, causing the introduction of air into the pleural cavity, is the invariable cause of pneumothorax and of hydro-pneumothorax. The causes of the rupture are in the lung, in the pleura, or in the adjoining organs. They may be traumatic or non-traumatic: the latter may be perfectly designated pathological causes, because the pneumothorax is always secondary, following upon a pre-existing pathological condition.
Traumatic pneumothorax may take place in consequence of an injury to the thoracic walls, of an exterior injury, or of a penetrating wound. The parts may be so bruised that pleural necrosis gives rise to sloughs and resulting openings. Fracture of ribs may tear the lungs, and allow air to enter the connective tissue and produce local emphysema. Violent contusions, as in a case recently observed by the author, produce laceration of the lung without the rib or costal pleura being injured.
Non-traumatic or Pathological Causes.—Laennec taught that pulmonary tuberculosis was the most frequent cause of pneumothorax; and further observation has demonstrated the correctness of this view. Walshe states that such is the case in 90 per cent. of the cases of perforation of the lung. In 131 observations reported by Saussier,227 81 were from pulmonary phthisis, principally from caseous pneumonia. Fraentzel228 says, from his own observation, that 90 out of 96 cases of pneumothorax are produced by vomicæ on the surface of the lungs in the course of caseous pneumonia. Grisolle states that nine-tenths of the cases result from rupture of a lung-cavity. Fuller229 reports 22 cases, in 18 of which the disease was produced by tubercular ulceration. Chambers,230 at St. George's Hospital, reports that 21 out of 23 were tubercular. Fernet231 states that pneumothorax results in nine-tenths of the cases from some of the forms of pulmonary phthisis.
227 Thèse de Paris, 1841.
228 Ziem. Cyc., vol. iv.
229 Dis. of the Chest, p. 226.
230 Dec. Pathologicum, cap. v. sec. v.
231 Nouveau Dict., vol. xxviii.
Ordinarily, pneumothorax is unilateral; only exceptionally is it met with on both sides. In tubercular cases it is twice as common on the left side as on the right (Condrin232). In the total of 146 cases reported by Louis, Walshe, and Powell, 94 were on the left side; whereas when it is consecutive to a pleuritic effusion it is almost always on the right side—17 out of 18 (Saussier233).
232 Thèse de Paris, 1882.
233 Ibid., 1841.
In tubercular cases perforation of the lung may occur at any period of the disease; the most frequent time, however, is that of the softening or while excavations are being formed, where adhesions have not yet protected the two sides by binding them together with neo-membranes. It may come from a small cavity. Andral met with cases where only a few tubercles existed. Townsend reported a case where one tubercle burst immediately under the pleura. The superior lobe of the lung is where the perforation generally occurs, because it is there that the tubercular lesion ordinarily commences and is most advanced (Louis). It is least frequent in chronic fibroid phthisis and most often met with in acute pneumonic phthisis. Douglass Powell234 reports cases where sinuses extended from cavities, and finally burst into the pleura. Sometimes the rupture occurs at the base of the superior lobe, about the third or fourth rib; it may happen, however, at any point of the lung; it has even occurred at the base of the lung lying on the diaphragm (Houghton235).
234 Med. Times and Gaz., Jan. and Feb., 1869.
235 Cyc. Pract. Med., vol. iii.
Saussier236 shows by the following table the relative frequency of the principal causes of pneumothorax in 131 cases:
| Pneumothorax | with | phthisis | 81 |
| " | " | empyema | 29 |
| " | " | gangrene | 7 |
| " | " | pulmonary emphysema | 5 |
| " | " | apoplexy | 3 |
| " | " | hepatic fistula | 2 |
| " | " | hydatids | 1 |
| " | " | hæmothorax | 1 |
236 Thèse de Paris, 1841.
Empyema ranks second as a producing cause of pneumothorax. Ordinarily, by direct necrosis of the parietal pleura, an orifice is made through which the pus is evacuated through the bronchi, and air in inspiration enters the pleural cavity by the bronchial fistula. Pyothorax is converted into pyo-pneumothorax. The valvular opening may, however, be closed by inspiration so that air cannot enter, or adhesions may limit a portion of the pleura, and then we have a circumscribed pneumothorax. Empyema, by producing ulceration of the thoracic walls and pointing exteriorly (emphysema necessitatis), leaves fistulæ through which air enters the pleural cavity.
Gangrene of the lung by sloughs allows air to penetrate. Bronchiectasic cavities sometimes become the seat of putrefactive changes and ulcerations through the lungs into the pleura. Infective emboli being arrested in the smaller peripheral branches of pulmonary arteries, air enters the cavity; it is thus that pneumothorax arises in various kinds of surgical diseases when infective emboli pass into the circulation (Fraentzel). Flint237 reports a well-marked case of pneumothorax, lasting less than one month, where there was every reason to suppose that it had been caused by rupture from interstitial emphysema. W. T. Gardner had previously reported a similar case. Saussier found emphysema was a cause in only 5 out of 131 cases. Fraentzel speaks of emphysema as rarely being a cause. Perforation of the oesophagus, ulcerative, cancerous, or traumatic from the use of bougies, produces pneumothorax. Suppurating bronchial glands—a case of which was met with by the author—bursting into the cavity produce pneumothorax. Hydatids of the lungs, abscesses of the abdomen, sometimes coming even from the cæcum and from the liver, burst into the pleural cavity and introduce air. Echinococcus cysts of the liver are occasionally emptied into the pleural cavity.
237 Practice of Medicine, ed. 1881; Series of Amer. Clin. Lectures, article "Pneumothorax," 1875.
Pneumothorax is more than four times as frequent in men as in women. One-third of the whole number of cases occurs in persons between the ages of twenty and thirty years; one-tenth between the ages of ten and twenty; one-twelfth between thirty and forty (Saussier238). Although pneumothorax has a number of exciting causes, yet they are all comparatively rare except pulmonary tuberculosis and purulent pleurisy.
238 Thèse de Paris, 1841.
PATHOLOGICAL ANATOMY.—In traumatic pneumothorax and simple cases, such as from the bursting of emphysematous alveoli, the presence of air is the only pathological product. If the pleura and adjoining organs are not diseased, the rupture or tearing cicatrizes rapidly, and the air disappears in a few days by absorption. If a quantity of air be admitted, the pneumothorax may last for months; yet if the pleura is healthy, the air itself will not produce local changes. If blood or morbid products flow in with the air, then inflammatory changes occur, and we have deleterious products effused. Demarquay and Leconte239 demonstrated the innocuousness of introducing air into healthy pleural sacs of dogs, having injected it repeatedly into the same dogs without any unpleasant result. These observers analyzed the air after it had remained in the chest, and confirm Davy's240 researches as to the changes in its condition. The oxygen diminished gradually, and finally disappeared, while carbonic acid replaced it to nearly the same amount. This air from the pleura approximated in composition to the air of expiration. When blood and bronchial secretions with pus are thrown into the pleura, they promptly produce more serious results, especially intense suppurative pleurisy. Duncan241 found in a case of pyo-pneumothorax a fetid gas to contain 26 parts of sulphuretted hydrogen and carbonic acid and 74 parts of nitrogen. Secondarily, lesions are produced—hydro-pneumothorax and pyo-pneumothorax. In other cases, the pleura having been previously the seat of chronic disease with purulent effusion, this latter undergoes fetid changes and septicæmia results. Under these circumstances the pathological changes are similar to those we have described as found in empyema. We find like increase of tissue-formation, of pus, and of the development of the gases, sulphuretted hydrogen and sulphydrate of ammonia, which give rise to a horrible fetidity. The quantity of air varies very much, as does the amount of fluid: there may be a small quantity of air and much fluid, or the reverse.
239 Gaz. Méd., 1864.
240 Phil. Trans., 1823.
241 Edin. Med. and Surg. Journal, 1827.
The opening into the pleural cavity may be direct or oblique: if direct, it remains open; if oblique, it is generally more or less valvular. The symptoms, prognosis, and treatment vary accordingly. Through a patent orifice the air enters in inspiration, and goes out with the expired air from the lungs. As it cannot accumulate, there can be no positive air-pressure within the pleura. If, however, the orifice be valvular, although the air enters it does not escape, for it presses upon the valve and closes it. If the valvular fold be perfect, the air soon becomes excessive in quantity, and exerts dangerous pressure upon the lung and adjacent organs. By means of a trocar, attached by tubing to a water-pressure gauge, Douglass Powell242 ascertained post-mortem the degree of intra-pleural pressure present in 16 cases of pneumothorax. In 4 out of these cases the pressure was nil. In 12 there was more or less intra-pleural pressure present, varying in degree from 1¾ to 7 inches of water.
242 Medico-Chir. Trans., 1876.
Unless the lung be mechanically prevented, the entrance of air into the pleural cavity at once produces a retraction of the lung, owing to its elasticity. There is no compression of the lung unless the air is increased in quantity by each inspiration, and, having no exit, accumulates; then the lung may be forced against the spinal column and the residual air actually forced out of the alveoli. Powell243 questions whether the intra-thoracic pressure excited in pneumothorax is ever equal to what is sometimes the case in pleurisy: the highest he had ever met with in pneumothorax was 7 inches of water. Garland,244 in repeating Damoiseau's experiments in testing the effects of the introduction of air into the pleural cavity, found that the air did not penetrate between the lung and the lateral chest-walls until the lower border of the lung had retracted upward the distance of several ribs.
243 Loc. cit.
244 Loc. cit.
One of the most pronounced effects constantly observed in pneumothorax is the immediate displacement of the heart to a greater extent than in pleurisy. Gaidy,245 as far back as 1828, described displacement of the heart as an important sign of pneumothorax. He related a case where, at the moment of the perforation, the woman was conscious of the heart's beat having been transferred to the right of the sternum. Powell246 out of 17 cases found the heart displaced in 16: in the seventeenth the unruptured lung was so consolidated that it could not collapse. In pneumothorax of the right side a careful examination is sometimes required to detect the displacement of the heart. The apex can be discovered at a considerable distance to the left of the nipple, with the right ventricle drawn to the left edge of the sternum. It has been generally believed that the cause of this displacement was the intra-pleural pressure of the air, but this does not satisfactorily explain it, for there can be no pressure until the elasticity of the lung has been overcome. In 13 of Powell's cases there was great displacement of the heart with different degrees of intra-pleural pressure. In 3 cases there was great displacement of the heart with no intra-pleural pressure. The same author247 showed, experimentally, that the elastic tension of one lung, when unopposed by that of the other, was sufficient to draw aside the mediastinum, and with it the heart. He thus demonstrated that these displacements are by no means necessarily a sign of intra-pleural pressure, since they may occur to the right of the sternum without there being any pressure. Clinically, we know that the admission of air into the pleural cavity immediately and constantly displaces the heart, unless the opposite lung be consolidated or otherwise injured in its resiliency. This occurs even when the patent orifice of the perforation prevents the accumulation of any quantity of air. There is not enough air to produce direct pressure, but there is enough to impair the elastic traction of the lung, and thus to destroy the equilibrium of traction which keeps the heart in its normal position. The healthy lung by its unimpaired tractile force immediately draws over the heart. Skoda248 maintains that "air does not enter the pleural cavity simply at the cost of the torn and retracted lung, but the sound lung also retracts to such a degree as to move the mediastinum." Garland's experiments249 conclusively demonstrate that the air in pneumothorax is powerless to exert an appreciable lateral displacing force until the lung has completely collapsed; and this does not ordinarily occur. There can be, he says, but one cause of constant and early displacement of the heart—the elastic force of the opposing lung, which draws it over to itself. He adds that "the explanation of the greater displacement of the heart in pneumothorax is that the air, having practically no weight, cannot exert upon the heart the negative pressure which an effusion evidently would."
245 Arch. Gén. de Méd., tome xvii., 1828.
246 Medico-Chirurg. Trans., vol. lix.
247 British Med. Journal and Med. Times and Gazette, July, 1869.
248 Auscultation and Percussion, Eng. trans.
249 Loc. cit.
The fluid in hydro-pneumothorax is very rarely of a serous character. Saussier found but 1 such example in 169 cases. It is almost always purulent pneumothorax, and frequently it has a very offensive fetid odor from putrid decomposition. Mixed with pus there are sometimes found masses of pseudo-membranes, débris of lung, and gangrenous patches, as in purulent pleurisies. The fistulous orifice through which the air has entered is not always easily found, being often hid away among false membranes. It is small and tortuous, and can only be discovered by placing the lung under water and blowing air through the bronchial tubes. Sometimes the orifices close and the air becomes encysted, interlobular, or diaphragmatic. There is sometimes only one opening; again, there may be several. Nolais reports a case where there were six openings. Orifices with lacerated edges are met with, varying in length from one to ten or twelve centimeters. It must be borne in mind that perforation can take place without producing pneumothorax. Saussier found this occurred in 2 out of 74 cases, and in 8 out of 29 resulting from pleurisy. Fériol and Guéneau de Mussey give similar cases.
SYMPTOMS.—The initiatory symptoms of pneumothorax vary according to the cause which produces it. When the effusion of air into the pleural cavity is from perforation of a diseased lung (most frequently tuberculous, more rarely gangrenous or from an abscess), the first symptom is a sudden agonizing pain in the side, accompanied with dyspnoea amounting almost to suffocation. In rare instances, where strong old adhesions limit the pneumothorax, there may be only slight pain, without dyspnoea. The rush of a moderate quantity of air into the cavity causes the lung to collapse; but should the amount of air be excessive, it will render the symptoms of oppression most intense, for it will compress the lung and heart and obstruct the capillary circulation in the lung. Such must be the case, for there is no aspiration of blood from the large veins, and no aëration of blood in the lung. The patient often feels as if the chest were being torn away, and the expression of his countenance betrays distress and alarm. If the orifice be large and valvular, preventing the escape of the air, the air accumulates rapidly and completely forces the air out of the lungs, and death shortly follows, sometimes in a few hours. There is no rise of temperature or fever. On the contrary, the temperature very frequently falls one or two degrees below the normal in consequence of the sudden collapse, the pulse from exhaustion being very frequent and feeble, accompanied by cold sweats. The voice becomes exceedingly feeble and whispering. In many cases the patient does not sink at once from the shock of the perforation, but becomes less oppressed, although he suffers considerably, being unable to lie flat in his bed. Respiration is not only frequent (sometimes 60 per minute), but the dyspnoea is oppressive and distressing to witness. Fever follows invariably, and sometimes with great rapidity, caused by pleuritis. When this occurs, the patient again suffers from dyspnoea as the purulent fluid accumulates in the pleura and gradually dropsy comes on. These cause dyspnoea and cyanosis. The position of the patient, leaning forward, supporting his elbows on his knees, indicates his agony and difficulty in breathing; the pain appears to go through and produce local hyperæsthesia, and the patient dies from the empyema with hectic and oedema of the lungs. The pleurisy excited may be simply serous in its products, even when it is tuberculous in origin. Usually, however, it is purulent, and we must then expect to find the grave symptoms we have enumerated in speaking of empyema with hectic and septicæmia.
PHYSICAL SIGNS.—These are well distinguished and marked, and lead easily to its diagnosis. Inspection shows the side to be immovable and the dilatation permanent; the spaces between the ribs are obliterated and the shoulder raised. There is no rhythmical expansion and contraction of the walls of the chest, the diaphragm is not elevated, and the liver and stomach are kept down. Air continues to enter the cavity, until the quantity is so great that its tension is equal to the atmospheric pressure. The contrast between this condition and that of the healthy side is very great. In the former the breathing is labored, with painful muscular contraction in the walls and whole side. Percussion over the chest gives a hyper-resonant sound, with a graver-pitched tympanitic resonance. There is but little sense of resistance to the finger, owing to the elasticity of the contained air. When fluid is secreted in the second stage we have absolute flatness at the base over a horizontal level, and tympanitic resonance above. The pitch of this last sound varies according to the tension of the gas contained in the chest and the correlative tension of the thoracic walls. If this tension be feeble, the pitch is higher; if it be extreme, the tone will be drum-like, muffled, acute, and the tympanitic character will be less easily perceptible. It may happen that the pitch will be so high that we may be misled and think there is flatness. It is not true flatness, but a clean and high-pitched sound, very different from the tympanitic sound usually found; it is sometimes remarkably metallic in character. With auscultatory percussion, using a solid pleximeter, we have the prolonged metallic resonance which Trousseau appropriately named the bruit d'airain.
The area of hyper-resonance and flatness on percussion is changed with the altered position of the patient. The fluid, obeying the law of gravitation, takes its hydrostatic level, and when the patient's chest is upright is horizontal. Hyper-resonance is often pronounced over the sternum, and sometimes infringes upon the healthy side. When the disease is on the left side it obliterates the normal dulness over the cardiac area.
Palpation.—Thoracic vibrations of the voice are not felt over the portion of the chest containing air, nor over that containing fluid. This absence of vocal fremitus is very characteristic. The hand detects that the heart has been displaced toward the sound side and that the abdominal viscera are pushed down.
Auscultation.—The auscultatory phenomena vary according to the cause of the pneumothorax and the size and direction of the orifice. In tubercular cases, where perforation has produced a large, free opening, as the air passes in and out of this large pleural cavity with firm walls (the lung having collapsed perhaps to one-third or less of its normal size), we have the physical conditions which give marked amphoric and metallic respiratory sounds, with absence of respiratory murmur. The amphoric breathing is of greatest intensity near the point of perforation, which ordinarily is at the mammary or upper scapular region, and is found in both inspiration and expiration. The cough and the whispered voice give the characteristic metallic quality. There is also metallic tinkling produced by droppings of fluid in the cavity, by the shaking of the body, or by vocalization. Even when the orifice in the lung is closed we may have amphoric echo, from sounds produced in the bronchi, and passing through a cavity filled with air. The intensity of these sounds varies in different cases. Sometimes they are very loud; in other cases they are feeble and seem distant from the ear. The fine metallic tinkling may be heard at one moment and disappear at the next. These amphoric and metallic sounds, heard at different points, are characteristic of pneumothorax with free openings. When, however, the orifice from tubercular perforation is small, oblique, or valvular, the respiratory murmur is inaudible, except perhaps at the very apex of the lung, and we cannot perceive any adventitious auscultatory phenomena beyond a faint, distant, hollow sound.
There is, in both kinds of orifices, the well-known splashing Hippocratian succussion sound on shaking the chest. The latter is pathognomonic of hydro-pneumothorax, and is sometimes heard when no other sign is present. The hands applied over the surface of the chest feel the fluctuations of the fluid striking against the interior walls. When pneumothorax follows purulent pleurisy we do not find immediately the pronounced symptoms nor the physical phenomena heretofore described as occurring when it is produced by rupture from the lung into the pleural cavity. The condition of the parts is very different. Pus is present in considerable quantity in the cavity, and the ulceration of the costal pleura and the soft walls of the chest allows the fluid to flow outward and air to enter the cavity. Or there may be necrosis of parietal pleura into a bronchus and consequent discharge of pus through the mouth. The lung is already disabled. The violent pain in the side and the dyspnoea are no longer found. Indeed, the exact time of the rupture and commencement of the discharge is frequently unknown to the patient himself. The symptoms of entrance of air into the pleural cavity may not occur for some time. The patient who has had empyema is made more uncomfortable; the discharge through the mouth is offensive, and its quantity and its character call attention to the chest, in which percussion shows the presence of air; auscultation gives amphoric breathing, and succussion demonstrates the presence of air and fluid in the pleural cavity. Very soon, however, the presence of air produces putridity of the secretion, with loss of appetite, fever, diarrhoea, and the other alarming symptoms of pyo-pneumothorax. In some instances the pleura discharges its contents and heals over. There is another variety of pneumothorax, which is ordinarily attended with only temporary inconvenience, and which may soon disappear, leaving the patient no worse than before the attack. This variety of pyo-pneumothorax may be produced by the sudden rupture of emphysematous vesicles, by coughing, or even without any unusual force in the expiratory effort, the alveoli having become extremely thin and brittle by degeneration of their walls. For the minute the pain is violent and the dyspnoea great, but it soon subsides, and in a few days the gas may be all absorbed, unless it is in large quantity. If the pleura is healthy and the lung not otherwise diseased, the rupture may not cause any inflammatory action, fever, or effusion. The rupture may heal over entirely, or if some inflammatory effusion is produced it will probably be rapidly absorbed. In exceptional cases pleurisy may be excited and the case become prolonged. While the air remains in the pleura we have the physical signs characteristic of pneumothorax—displaced heart, as shown by palpation and auscultation, tympanitic percussion resonance, amphoric breathing, and succussion.
DIAGNOSIS.—Ordinarily, there should be no difficulty in diagnosing pneumothorax, no matter how it is produced. We have simply to consider well the already-mentioned modes of the commencement of the disease, and give due value to the characteristic physical signs, especially displacement of the heart, hyper-resonance on percussion, absence of vocal fremitus, amphoric respiration, succussion, and decided shifting of flatness and resonance on change of position. When all these signs are present, each being in itself almost characteristic, there can be but little question. Obstruction of a large bronchus would be followed by absence of health sounds and intense dyspnoea, but we should not have the other physical signs of pneumothorax. Extensive emphysema would produce some of the signs—exaggerated resonance on percussion and enlargement of the side. Emphysema, however, is bilateral, and the resonance over an emphysematous lung has not the same pronounced tympanitic quality as in pneumothorax. The enlargement in emphysema is more under the clavicle; the breathing not amphoric; the normal murmur, although enfeebled, is never completely annulled; and the heart is not displaced. Large superficial pulmonary cavities with firm but thin walls give us several of the physical signs of localized pneumothorax, such as amphoric respiration and metallic tinkling; but the succussion sound is never heard over them. The tympanitic percussion is rarely so pronounced in a cavity as in pneumothorax, and in the latter there is never the cracked-jar sound. In phthisical cavities of large size there probably would be depression instead of enlargement of the chest. The situation will ordinarily enable us to make the differential diagnosis, for localized pneumothorax is almost always low down in the thorax, and the pulmonary cavities but rarely below its middle third. The progress of the case and clinical history would clear up the diagnosis. If a circumscribed pneumothorax was present with phthisis, the diagnosis might be difficult. Powell calls attention to the similarity of some of the signs of acute congestion rapidly supervening at the base of a comparatively sound lung to those of pneumothorax. But in the former the resonance, although high-pitched, is not truly tympanitic, and the heart is not displaced. There is no other disease of the chest where we find in such close proximity the two extremes of percussion sounds—flatness from the secondary effused fluid, and the tympanitic resonance above. If delicate, slight percussion is used, the line of demarcation can be clearly defined; if, however, the force of the percussion stroke be even of moderate intensity, the flatness is mingled with the tympanitic quality, as it is in percussing from the left lobe of the liver to the stomach.
PROGNOSIS.—The prognosis is unfavorable and always uncertain. During the first few days after the rupture of the pleura it is especially bad, though it becomes less so as time goes by. There are cases where the perforation and its results appear to prolong life. "If the opposite lung be healthy, we may hope that arrest of the pulmonary disease may convert the case into one of chronic empyema" (Powell). But, unfortunately, the rupture often occurs when the patient is emaciated and dying of chronic lung ulceration. Cases of pyo-pneumothorax produced in advanced phthisis or by gangrene of the lung are almost invariably fatal. The most unpromising cases at first sometimes prove the least serious, and, again, those that appear at the commencement slight, contrary to expectation, die. Much depends upon the condition of the other lung and the position of the perforation. If the other lung be healthy and the perforation low down, the chances of recovery are better. The progress is most favorable in the cases where the rupture occurs from emphysema. When from purulent pleurisy the discharge passes through a bronchus, the orifice may heal and in due time plastic material be thrown over it, and the air and fluid be left in the pleura. Cases are reported where the orifice remains open and pneumothorax lasts for a long time. Laennec reported one case where the patient lived six years. Fuller250 reports another where the orifice was open at the end of eleven months, another nineteen months, and another twenty-seven months. We have mentioned Demarquay and Marotte's experiments of the innocuousness of air injected into the pleura. Air is harmless, as they have shown, in the pleura, unless sulphuretted hydrogen or sulphite of ammonia be developed. Fuller says the prognosis is very unfavorable when the effusion is large, with great displacement of the organs. Flint considers pneumothorax occurring as a complication of phthisis as almost hopeless. It is important to ascertain promptly the nature and direction of the opening, whether it be free or valvular.
250 Diseases of Chest.
TREATMENT.—This is in a great measure palliative. Hypodermics of morphia or opiates relieve the agony and lessen the shock caused by the perforation. Alcoholic and diffusible stimulants may sustain the heart in its struggle against the effects of dislocation and impaired circulation. Care must be taken not to depress the powers of reaction by too much morphia. Hot water in india-rubber bags applied to the chest gives great relief. Alcoholic stimulants must be given to prevent sinking from exhaustion. When the distension from air is excessive, paracentesis gives marked relief, the lives of patients having been prolonged for days by it. If the opening is valvular, to prevent the air from accumulating in excessive quantity Reybard's protected gold-beater's skin trocar may be used and kept in the chest. Otherwise fine aspirators may be employed, which would seem to be harmless, and the operation be repeated whenever necessary. Larger points and the trocar should never be used, as there is danger of making a permanent fistulous orifice, as well as of injuring some blood-vessels or the lung itself. After the excess of air has been removed by aspiration the affected side should be strapped to control the inspiratory movements on renewal of positive pressure. Anstie251 recommends drachm ss doses of ether every three or four hours. Fernet252 recommends inhalation of oxygen. If fluid should compress the chest, some of it must be removed by aspiration, but care must be exercised, for the presence of fluid is conservative in its effects. Its pressure stops up the orifice and promotes its healing. If it becomes fetid, pleurotomy, with detersive washes, ought to be resorted to. Food should be frequently administered, with quinine and cod-liver oil, and good hygienic surroundings prescribed.
251 Reynolds's System of Medicine, vol. iv.
252 Nouveau Dict. Méd., vol. xxviii.
Hæmothorax.
DEFINITION.—Accumulation of blood in the thoracic cavity unconnected with inflammation of the pleuræ.
ETIOLOGY.—Hæmothorax may be caused by traumatic injuries, by the bursting of an aneurism, from ulceration through the walls of the aorta of the vena cava, or from the veins of the pleura. It may be caused by laceration of the intercostal arteries in penetrating wounds. In very rare cases a profuse bleeding takes place in caseous pneumonia or in gangrene of the lungs, and bursts into the pleural cavity (Fraentzel). Cancer of the lung or pleura may, by pressure, produce absorption and destruction of the walls of the blood-vessels, and cause discharge of their contents into the pleural cavity. Sir Thomas Watson253 reports a case where enormous hæmothorax caused enlargement of the left side, pushing the heart to the right of the sternum from caries of two ribs with ulceration through an intercostal artery. The blood never escapes from the lung into the pleura when there is considerable pulmonary apoplexy.
253 Practice of Medicine, vol. ii.
PATHOLOGICAL ANATOMY.—Blood is found coagulated to a greater or less degree in the pleural cavity, and the lesion producing the hæmothorax can generally be found; the remains of blood may be found even after it has been some time effused. If the hemorrhage does not prove fatal, it may all be absorbed, or it may by its presence cause local inflammation of the pleural membrane.
SYMPTOMS.—The symptoms are those of perforation into the chest—sudden intense pain on the diseased side, with internal hemorrhage, great pallor, feeble circulation, cold extremities, and syncope. Patients often die in a few minutes. If the hemorrhage is moderate in quantity, they revive and the circulation returns, but they complain of feelings of suffocation and oppression. Slowly the general strength returns and the patient recovers.
SEQUELÆ.—Most modern surgeons admit that serious hemorrhages into the pleura come from the thoracic walls, or from the blood-vessels in the neighborhood of the hilum, or from those which accompany the bronchial diseases of the second or third order. Hæmothorax is always consecutive to some primary lesion. Where it is caused by penetrating wounds or by the bursting of blood-vessels in the lungs, air enters the cavity and becomes mixed with the blood, producing a complication in the form of hæmato-pneumothorax. This frequently gives rise to pyo-pneumothorax with a collection of purulent and ichorous fluid.
DIAGNOSIS.—The previous history of the case, together with the characteristic symptoms we have mentioned, enables us to diagnose hæmothorax from pneumothorax, which commences in a similar way. The only other condition likely to be confounded with it is effusion in pleurisy, the physical signs of which are somewhat the same. If the blood remains uncoagulated we shall have absence of vesicular murmur, with dulness on percussion, absence of fremitus, and no friction sound. The introduction of a fine hypodermic needle enables us to be certain of the nature of the fluid.
The PROGNOSIS is always serious. If the cause of the hemorrhage is the bursting of an aneurism, death supervenes in a short time. Hæmothorax, when caused by penetrating wounds, unless they produce hemorrhage, is not necessarily serious. The blood may entirely disappear in a few weeks. Entrance of air with the blood renders the prognosis more serious. Secondary pleurisy is not ordinarily severe unless pus forms.
TREATMENT.—If time is allowed, every effort must be made by local and general treatment to arrest the hemorrhage—ice-bags and hot-water bags ought alternately to be applied to the chest and between the scapula; the patient to be kept in the horizontal position and made to rest quietly; ice taken by mouth; small doses of morphia and large doses of ergotin must be given promptly hypodermically, as the stomach is in no condition to absorb remedies readily. If the accumulation be excessive and continues to embarrass the respiration very much, we recommend free incisions to take out sufficient blood to relieve the pressure and great dyspnoea. Unless danger is imminent, this is a hazardous experiment, as letting in atmospheric air among blood-clots may seriously complicate the condition. Should pleuritis or other complications occur, they must be rationally treated.
Growths in the Pleural Cavity.
Some authors mention various tumors which are rarely met with in the pleural cavity, and which are not peculiar to the serous membrane of the pleura. Among them may be placed sarcomas, fibro-sarcomas, and epithelioma. Their presence in other organs may assist in the diagnosis. Other varieties exist more or less connected with chronic pleurisies. Among these are fibromas, cartilaginous and osseous formations. Rokitansky speaks of lipomas as deposited on the costal pleura. The only varieties which we think it necessary to call attention to are cancer and hydatids.
CANCER OF THE PLEURA.—Cancer of the pleura is not a very rare disease, but ordinarily it is a secondary formation, coming from cancerous disease of the mediastinum, of the lung, or of some abdominal organ. Some authors doubt whether it is primary even in the lungs and mediastinum. It certainly is not often met with as a primary disease of those organs. Lebert254 had only seen 6 observations, in 447 cases of cancer, involving the mediastinum, the pleura, and the lungs. Walshe255 reported 29 cases of primitive cancer of the respiratory organs; in 18 cases one lung was diseased with its pleura, and in 13 the right lung. Lépine256 in 1869 communicated a very curious case of primary cancer of the pleura in a child ten years of age. The right pleural cavity was filled by a white scirrhous tumor. Darolles257 (1874) reported another example of primary cancer of the pleura, which afterward spread to the lung. Andral, Vidal, and Lebert reported cases where the tumors appeared to develop simultaneously in the pleura and other organs. Primary cancer of the pleura may exceptionally occur, but ordinarily the disease results from its extension step by step, or else distant propagation, from lungs, breast, mediastinum, or the abdominal organs. Most frequently the secondary cancer appears more or less independently of the primitive tumor, and is seen in the form of disseminated points on the surface of one or both folds of the pleura. This propagation of cancer is now generally admitted to be through the intermediary of the lymphatic system; in fact, the lymphatics are themselves attacked by the degeneration, and they are seen, particularly on the surface of the pleura, in the form of white small cords. Some modern pathologists consider that the serous cavities are lymphatic cavities, which can, just as the vessels themselves, serve as ways of generalizing the disease (Cornil and Ranvier, Charcot, Lépine, and Virchow).
254 Traité Prac. Mal. des Cancereuses, Paris, 1851.
255 Nature and Treatment of Cancer, London, 1846.
256 Bull. de la Soc. Anat., 1869.
257 Quoted by Fernet, Nouveau Dict. Méd., vol. xxviii.
PATHOLOGICAL ANATOMY.—Primary cancer of the pleura is ordinarily encephaloid and multiple. Extended infiltration is very rarely found. Lebert reports one case in an infant of seven months. The multiple masses are ordinarily soft and pulpy, varying in volume from the size of a grain of millet-seed to that of a small nut. The aspect is yellowish-white. The juice is rarely pressed out of them. Under the microscope we see large cells and multiple cells with their nuclei. The small granulations or the lenticular masses are flat, resembling drops of wax. We may have solid bodies possessing all the characters of scirrhous, encephaloid, and colloid, grayish, or gelatinous structure. These cancerous productions are generally vascular, especially in the encephaloid variety. Their rupture frequently produces hæmothorax and hemorrhagic pleurisies. The bronchial glands, and finally the cervical glands, often become involved.
SYMPTOMS.—The symptoms of pleural cancer, especially of the smaller and secondary deposits, are often obscure and indefinite. They are not sufficiently definite to attract attention during life. If the masses are scirrhous and large, they press upon the lungs, impede respiration, and give rise to dyspnoea. If the disease is propagated from the lungs or breast, we may suspect cancer where we have a dull pain with some cough. Pain, indeed, is constant, but not violent, unless the nodules excite local inflammation. When scirrhous tumors press upon the intercostal nerves, the pain is very persistent. External pressure over the points gives rise to pain. The dyspnoea increases as the size of the tumor increases. The expectoration is occasionally bloody. The physical signs are sometimes characteristic—dulness on percussion, absence of respiratory murmurs, friction sounds, no vocal fremitus.
DIAGNOSIS.—Generally very difficult. The progress of the disease is ordinarily slow, and follows its development in other portions of the body. Cancerous cachexia, degeneration of the glands above the clavicle, hæmothorax, and hemorrhagic pleurisy, together with dry cough and persistent intercostal neuralgia, are, when present, valuable aids to diagnosis. Extensive caseous pneumonia and pleuritic effusions may be confounded with cancer of the pleura. These tumors may not be at the base, but in the middle of the thorax; dulness may not exist at the base as is invariably the case in pleurisy. The position of the body does not affect the limit of dulness in cancer.
The PROGNOSIS is always very serious, the disease being invariably fatal. In Walshe's cases the duration of the disease was from three and one-half months to twenty-seven months; average duration, thirteen and one-fifth months. One-fourth of his cases occurred between the ages of fifty and sixty years.
The TREATMENT is palliative—opium and other narcotics, and locally chloroform and aconite for the intercostal pains. When effusion results from cancerous inflammation the aspirator may be used to relieve the great oppression caused by the quantity of fluid.
Hydatids of the Pleura.
Trousseau258 considered hydatids of the pleura a comparatively rare disease. He believed that when found in the cavity it was frequently caused by cysts of the lung which had fallen into the pleural cavity. Vigla259 mentions 3 cases. Davaine260 met with 25 cases of hydatids, only 1 of which he believed originated in the pleural cavity. The acknowledged greater frequency of these hydatids in the right inferior lobe of the lung, gives probability to Dolbeau's261 view that "they frequently proceed from cysts on the convex surface of the liver." Hearn262 reports 75 cases collected from various observers as intra-thoracic, 15 of which were in the pleura, in the subserous tissue, between the parietal pleura and thoracic wall.
258 Clin. Med., vol. i., Philada. ed.
259 "Des Hydàtides intrathor.," Arch. gén., 1855.
260 Traité des Entozoaires, etc., Paris, 1860.
261 Thèse de Paris, 1856.
262 Thèse de Paris, 1875.
PATHOLOGICAL ANATOMY.—In the greater number of cases, as examined at autopsies in Hearn's reports, the tumor was formed by a voluminous pocket occupying a large part or the whole of the cavity of the pleura. The walls of the envelope were formed of a transparent or slightly opaline and whitish membrane composed of numerous thin layers, containing on its interior surface the echinococci. In the interior of the cyst there was a limpid hyaline liquid with living parasites. Nothing different was noticed in cysts from those found elsewhere, except the absence of the usual adventitious membrane—a fact previously noticed by Davaine. When the cysts are very large they press upon the lung and adjoining organs just as is the case with large effusions in the pleural cavity. The heart, moreover, is pushed to one side, out of its normal position; the lung is compressed and diaphragm depressed.
SYMPTOMS.—The first appearance of cysts of the pleura causes but little disturbance of the functions of the lung. It is scarcely appreciable until it interferes with the play of the other organs. The three prominent symptoms are the pain, the dyspnoea, and the cough. The pain occupies the exact point where the tumor is situated, and radiates from that point. Once developed, it persists with tenacity throughout the duration of the disease. This persistence of the pain is indeed an important characteristic of the disease, and is a sign of value in the diagnosis between hydatids and pleuritic effusions. The dyspnoea increases progressively with the volume of the tumor. The cough is not heard as frequently as when the cysts occur in the lungs. It is dry, and does not cause hæmoptysis.
DIAGNOSIS.—Physical signs must be marked to enable us to distinguish fluid cysts of the pleura from cysts in the lung or effusions in the pleural cavity. When the hydatid tumor has attained sufficient size to cause pain and dyspnoea it generally presses outward the walls of the chest after the lung has been compressed. It does not occupy the base of the cavity, as the effusions do, and the dilatation has a globular form. Trousseau263 has given several examples in which this shape determined the diagnosis. With this arching of the chest the immobility of the chest is an important sign. Vocal fremitus is diminished or totally abolished, and percussion elicits absolute flatness. These two physical signs assist us in making the diagnosis between hydatids and pleurisy. The auscultatory phenomena, from similar physical conditions, closely resemble those of pleuritic effusions. It must be borne in mind that sometimes hydatid cysts are complicated by pleuritic inflammations, caused by their presence. The diagnosis is unquestionably complicated by difficulties that are not removed unless the cysts burst through a bronchial tube and discharge a transparent and clear fluid in which the microscope shows the presence of echinococci. Such hydatid expectoration is a pathognomonic sign of the existence of an intra-thoracic cyst. Hydatids of the liver may press the diaphragm far up into the pleural cavity without bursting through it. Trousseau maintained that without bursting they may make a passage for themselves through the distended, attenuated fibres of the muscular portion of the diaphragm, for the progress of these cysts is necessarily slow. We must not hesitate to make an exploratory aspiration to determine with certainty the nature of the fluid.
263 Loc. cit.
PROGNOSIS.—The prognosis is certainly very serious, but not so bad as when cysts of the same nature are situated in the lungs. Their spontaneous cure may be effected by bursting through a bronchus or even through the walls of the chest. The patient may, however, die from asphyxia during the discharge through the lungs. When not evacuated they may produce death by compression of the lungs.
TREATMENT.—If the disease is recognized previous to its making an opening through a bronchus, it can be treated safely and effectively by aspiration. Bird264 reports a number of cures by this operation in Australia. Trousseau advises extreme caution, even in regard to exploratory punctures, unless adhesions have taken place between the tumor and the walls of the chest, for he fears the escape of fluid into the cavity of the chest and consequent purulent pleurisy. It is well to remember that this great practitioner was not aware of the innocuousness of capillary punctures and aspiration. If the bronchus has been perforated, we must hope for spontaneous cure. If empyema be caused by the tumor pleurotomy must be used as recommended by Moutard-Martin265 and Vigla,266 and constant washing of the pleuræ must be used. This treatment gives us reasonable assurance of success.
264 Quoted by Hearn.
265 Purulent Pleurisy.
266 Loc. cit.
History of Thoracentesis.
Thoracentesis ([Greek: thôrax], chest, and [Greek: chentein], to pierce) is the operation for the evacuation of collections of fluid, serum, pus, or blood from the pleural cavity.
Among the ancients, dating back to the time of Hippocrates, it was practised, and was known as the operatio empyematis. Hippocrates uses the word [Greek: empyon], signifying, literally, an internal collection of pus just above the cavity of the peritoneum, above the diaphragm. Subsequently he speaks of empyema of blood, empyema of serum, empyema of gas, but not of pus, applying the term to the operation, which he employed principally for empyema necessitatis. Subsequently the name empyema was used, as now, to designate a purulent collection in the pleural cavity.
If we may credit the story which has descended from mythological times, the operation for empyema had its origin in an accident. It is related that a certain Phalereus, who was attacked with what was denominated an ulcer on the lungs, was pronounced by all his physicians to have an incurable disease. In his despair he exposed himself in battle so that he might be slain; the enemy's weapon, however, pierced his side, making an opening through which the pus escaped, and he recovered.267
267 Cicero, De Naturâ Deorum, lib. iii. cap. 28.
It is certain that from the most remote periods the chest was opened when collections of pus were formed. Galen states that the ancients employed actual cautery for that purpose. He reports that Euryphon de Cinde by this means saved the life of Cinesias, son of Evagoras.268 The details into which Hippocrates and his school entered in regard to the operation show that it was frequently performed in their day. It is very remarkable that many of the more important precautions in the operation were observed by Hippocrates. We find from the Aphorisms that the operation was considered the only means of cure,269 and that when these precautions were observed, and the fluid was white and of good quality, the patients recovered.270 The principal precautions were not to delay the operation after the existence of pus was recognized, and to draw off the liquid. He further states that if the serous fluid in dropsy of the chest or pus in empyema should be drawn off too rapidly the patient would die. So impressed were the disciples of Hippocrates by this view that they adopted the operation of perforating a rib instead of cutting through the intercostal space, because they could with more ease stop up the orifice and regulate the outward flow of the fluid. The later Hippocratians preferred cutting instruments to actual cautery. Hippocrates, if unable to discover the locality of the fluid in the thorax by succussion, applied over the walls of the chest a linen compress which he soaked in earth of Eretria and warm water, and concluded that the collection existed at the points where the earth commenced to dry!
268 Comm. in Aphor. Hipp., lib. vii.
269 Aphorisms, lib. vii., Aph. 44.
270 Ibid., lib. vi., Aph. 27.
When these signs failed, he cut through the most prominent rib at the base of the chest and toward the back. He made a large incision through the rib, but only a small one the size of a thumb-nail through the tissue beneath the rib. After allowing a small quantity of pus to escape, he introduced a tent of undressed flax, with a piece of thread attached to it. This he withdrew twice daily, to allow the pus to flow. At the end of two days he permitted the remaining pus to be discharged, and inserted a tent of linen. To prevent the lung, habituated to the presence of fluid, from drying too rapidly he injected wine and oil through a canula. When the excavated fluid was thin (serous?) he replaced the tent by a tube of tin, and when it ceased to secrete fluid he shortened each day the length of the tube, so that the cicatrization of the wound extended from the inner end of the orifice.271 The genius of Hippocrates cannot but excite our admiration, as it did Laennec's, who selected as the subject of his thesis "The Doctrines of Hippocrates as applicable to the Practice of Medicine." Can it have been Hippocrates's modes of physical explanation that suggested to Laennec the idea that led to his great discovery of auscultation?
271 De Morbis, lib. i. p. 448.
Hippocrates's operations were made by boring through the rib or with a red-hot iron or a bistoury cutting through the intercostal space. Galen (A.D. 150) had his pyulcon with which to draw out the fluid. Galen and Roger of Parma bored through the sternum. Many of the ancient surgeons, such as Eumphon of Cnidos, Paul of Ægina, Celsus, Solinger, divided the soft parts by caustics and the knife after laying bare the pleura. Blunt instruments were sometimes used, such as sounds. Celsus in his latter years lost confidence in the operation, and it fell into discredit among the Greeks and the Romans, by whom it seems to have been nearly abandoned. In the Middle Ages the question was discussed whether it was better to open the chest by steel or by fire in traumatic pleurisies. Trousseau states that about the sixteenth century the operation of trepanning the ribs was revived. About the same time the detersive injections which had been recommended by Galen were again advocated, especially by Fabrice d'Aquapendente. The operation was unpopular among the greatest surgeons, and but seldom resorted to except in extreme cases. Notwithstanding the servile obedience to tradition in those days, some important points were advocated in regard to the propriety of allowing the openings for empyema to remain unclosed for an indefinite period. From the seventeenth to the eighteenth century the operation of paracentesis was the topic of many surgical treatises.
Early in the seventeenth century practitioners became less distrustful of puncturing the chest, and were led to believe in the harmlessness of the operation (Trousseau). As a consequence of this tendency, physicians began to study the question of puncturing the chest in hydrothorax. In 1624, Gérome Goulée alleged that he succeeded more frequently in hydrothorax than in abdominal paracentesis. Twenty years later, Zacutus Lucitanus asserted that paracentesis was as necessary in cases of serous effusion into the chest as incision in empyema. In 1663, Robin and Duval recommended thoracentesis as the best treatment for hydrothorax. Some time afterward this practice was put in force by Willis. Lower also mentions a case, and subsequent authors quoted these cases as an encouragement to the performance of paracentesis of the chest for the removal of serous effusions. Jean de Vigo brought out again the pyulcon. Druin about the year 1665 proposed the use of the trocar as a substitute for the actual cautery in opening the chest.
In 1658, Bontius for the first time took up in a precise manner the subject of the introduction of air into the pleural cavity. He declared there was no danger from it. Bartholin maintained the opposite opinion. The indications for the operation were laid down, but they were necessarily very imperfect. In proportion as attention was directed to the question of the admission of air, the manner of operating was modified. In 1669, Scultetus discussed thoracentesis in his work Armamentarium Chirurgicum. He made use of a trocar, with a bladder at the external orifice, principally to prevent the introduction of air, as Reybard later used a piece of cat's intestine and a bladder of gold-beater's skin. Scultetus used the sypho, a common syringe, for injecting the chest, and also the [Greek: pyoulchon] ([Greek: pyon], pus; [Greek: elchô], to draw out), or pyulcon, for drawing out matter, as its name indicates. This was practically the syphon. Scultetus describes the operation by incision with his gladeolo salicet longo, and by puncture with the canula et acus, both figured in his plates; so also his drainage-tubes, with directions for shortening them as the cavity heals, and the long tubes, which probably acted by gravitation after the manner of the syphon. Aspiration was made by the mouth, by cups, and by syringes affixed to a canula or catheter.272
272 These facts were kindly furnished me by Morrill Wyman, who carefully examined Scultetus' work (edition 1672) in the Harvard Library.
It is thus evident that more than two hundred years ago aspiration was used to evacuate fluid from the pleural cavity. Trousseau says that "at that period aspiration and suction were used for this purpose—timidly pursued, in accordance with Scultetus' example; and that it became afterward in vogue with the masters of surgical art."
Palfin preferred the trocar to incision for treatment of hydrothorax. In 1707, Anel wrote a book on the art of sucking wounds without using the mouth. Bourdelin (1742) rejected the trocar for fear of injuring the lung. That Scultetus' practice was continued is evident from the work of Laurence Heister (1742), who described puncture of the chest, with drawings of exhausting syringes for the removal of pus or serum.
In 1765, one hundred years after Druin's use of the trocar, when perforation by actual cautery was abandoned, Lurde timidly advocated it on account of his fear of wounding the lung. He advised the operator to close the canula with the finger at each inspiration, leaving it open during expiration, so as to prevent the entrance of air. Chopart and Desault opposed the use of the trocar as a coarse mode of operation, involving the risk of wounding the intercostal artery and lung (Trousseau). Van Swieten at the end of the last century questioned the advisability of using the trocar. Later, in 1796, Benj. Bell,273 in cases of thoracentesis, used india-rubber bottles fitted to the opening for the same purpose, first compressing them and then allowing them to expand by their elasticity. He strongly recommended paracentesis of the pericardium when the amount was so excessive as to cause death. He gives exact directions how and where to operate.
273 Vol. v.
Isbrand de Diéonerbrock274 plunged a bistoury between the fifth and sixth ribs, and introduced into the wound a silver canula large enough to fit the orifice, and stopped the canula with a tent which he withdrew each day. Jean Scultetus275 recommended several different canulas, some of silver, some of gold. He also invented syringes, straight and curved, to absorb the pus or make injections into the chest. Scultetus operated in the sixth intercostal space; he raised a piece of skin, so that it might lap over the orifice after the operation. He used a tent until the eleventh day, when he inserted a canula. After Scultetus, Lamzweerden276 used suction, and contended that it was very successful. Paul Barbette277 considered thoracentesis as indispensable in empyema and hydrothorax. He maintained that it was less dangerous than the puncture for ascites. F. Hoffmann at the commencement of the eighteenth century278 gave his full and complete approbation to the operation performed according to the accepted rules. Dominique Anel279 was an avowed partisan of the suction of the effused fluids in the chest. He had seen soldiers very successfully suck, with the mouth, wounds of the chest. He invented different syringes and other machines to pump out the effused fluids, some of which were very large, with canulæ whose orifices were very wide and of different shapes.
274 Medic. Morb. Pectoris Hist., 2.
275 Armam. Chir., Paris, vol. i. p. 20, quoted by Sprengel.
276 Appendix ad Sculpt. Armen, 1671, quoted by Sprengel.
277 Chirurgia, lib. iii. cap. 2, Geneva, 1688, quoted by Sprengel.
278 Medicina consultatoma, vol. i., 1721.
279 L'art de Sucer les plaies sans se servir de la bouche d'un Homme, Amst., 1707.
Laurence Heister280 (1742) acknowledged that Anel's syringes were valuable in pumping out the fluid from the middle or lower part of the chest, but not when paracentesis was performed in the higher portions between the second and third ribs. Heister gives281 drawings of exhausting syringes for the removal of pus or serum. C. G. Ludwig published282 a new apparatus invented by a surgeon named Bucer to pump out the fluids contained in the chest. This machine was composed of canulæ, to which was adapted a bowl to receive the liquid as it was withdrawn. Ludwig claimed that the especial advantage of this instrument was that it pumped all the fluid out at one time, without the operator being annoyed by any disagreeable odor. Leber283 proposed a similar instrument which was easier of application. A. T. Richter demonstrated the inutility of all these inventions; the blood, he said, would be drawn out with the fluid and by coagula stop up the canula. Valentin (1772) objected to the use of these pumps as applied to chest fluids.
280 Chirurgie, Th. i. Buch. i. Kap. 10, p. 89.
281 Ibid., p. 72.
282 Diss. de Vul. Pectoris, Leip., 1768.
283 Quoted by Sprengel, p. 60, vol. ix.
In the latter part of the eighteenth century there were numerous English and continental writers on the subject of paracentesis. Among them were J. W. Belquer, Sharp Mohrenheim, Richter, Ponteau, Callisen, Pierre Cooper, Allemoth, Zellar, and Audouard. Some of these preferred the trocar to the bistoury. Some were in favor of prompt action, and others objected to the operation unless there were threatening symptoms. Valentin urged that the presence, on the surface of the chest, of oedema and ecchymosed spots was a certain indication of fluid effusion.
During the first twelve years of this century the operation seems to have fallen into disuse. In 1808, Audouard objected to the Hippocratian method, which had been practised for centuries, of drawing out small quantities at a time, for fear that the sudden withdrawal of a large quantity would produce a vacuum in the chest. He maintained, and proved, that sudden and complete evacuation had no such result. In 1811, Corvisart284 drew attention to thoracentesis. In 1812, Larrey discussed its merits. Charles Bell285 preferred the trocar to the other methods in hydrothorax when he could be positive of the presence of fluid, but he stated that he preferred first to introduce the bistoury. He operated in the sixth intercostal space, but in empyema he preferred to make the puncture higher up. Samuel Cooper286 recommended as small an orifice as possible for the evacuation of serum, but larger and wider ones for pus and blood.
284 Maladies du Coeur, 1811.
285 System of Operative Surgery, vol. ii. p. 194.
286 Dictionary of Surgery, p. 749.
In tracing the history of this important operation we have shown that it has been performed from the time of Hippocrates, and that it has been held in different degrees of estimation by the numerous authors who have discussed it—that sometimes it has been popular, and again regarded unfavorably.
Récamier operated, but unsuccessfully. Up to the period we have now reached (1816) great difficulty of accurate diagnosis existed, and crude notions of physiology prevailed. Errors of diagnosis as to the character of the fluid when present, and still more as to its existence in the chest, frequently led to unpleasant results. Laennec's genius so completely cleared up the differential diagnosis of all diseases of the chest, including pleurisy, that men grew less timid. Laennec287 himself was a strong advocate of the operation; he advised it in acute pleurisy where dyspnoea, threatening life, supervened, and in chronic cases where other remedies failed. He proposed to apply a piston cupping-glass over the wound after the discharge of liquid, and to produce a vacuum in the chest more or less quickly, continuously, and completely according to effects.
287 Traité d'Auscultation mediate, 1818.
As Bowditch288 states, "We should be groping in the same dark way, and perhaps getting into the chest by caustic pastes or by actual cautery, had not Laennec discovered for us auscultation, with all its admirable powers of diagnosis of thoracic affections."
288 Unpublished communication to the writer, 1882.
In 1815, Blondel practised puncture of the chest with a bistoury. Gendrin performed the same operation in acute pleurisy in 1831, but with only bad results. Townsend289 (1833) acknowledged that the operation had fallen into disuse, as much from uncertainty of diagnosis as from any experience of its general danger. He gives the results of Thomas Davies's operations—8 out of 10 successful cases in empyema, with 9 fatal cases in pneumothorax with effusion (probably tubercular), and 3 fatal cases in hydrothorax. Davies used a grooved needle to determine the presence of the liquid, its quality, and the thickness of the walls. After the operation his practice was to inject a weak solution of chloride of lime, which he found to have the effect of diminishing the discharge and correcting its character. Crompton290 (1834) had 3 successful cases out of 10.
289 Cyc. Prac. Med., vol. ii. p. 43.
290 Ibid., vol. iii. p. 400.
Robert Law291 pronounced paracentesis more successful in chronic than in acute pleurisy. Townsend doubts whether the admission of air was hurtful; he quotes Nysten and Spies's experiment, showing that air introduced into healthy pleuræ was invariably absorbed in a few days.
291 Ibid., 1834.
Townsend292 and Law, as well as C. I. B. Williams,293 speak of the different kinds of syringes that have been proposed to draw off the fluids.294 Dupuytren proposed (1814) the introduction of a small canula with a very flexible substance at its outward extremity, such as the bladder of some domestic animal, which would allow fluid to escape, and at the same time would oppose the entrance of air into the chest. Becker (1834) published a work in which he investigated the nature of the false membranes in pleurisy, and showed that the access of air did not produce unpleasant results. He reported 2 successful cases out of 3 of operation.
292 Ibid.
293 Library of Pract. Med., 1841.
294 Boyson, Thèse de Paris, 1814.
R. Townsend295 wrote an elaborate paper in 1833 on empyema, in which he applied the principles of physical diagnosis. He cites numerous cases of thoracentesis, and speaks of the operation as easy of execution, productive of little pain to the patient, generally followed by immediate relief, and as having been in numerous instances crowned with complete success. Robert Law296 (1834) speaks discouragingly of the operation in consequence of the "unavoidable admission of air into the inflamed cavity." He considered the operation of tapping the chest more likely to be successful in chronic than in acute pleurisy.
295 Cyclop. Prac. Med., vol. ii., 1833, London.
296 Ibid., vol. iii., 1834.
In 1835, Faure297 read his paper on thoracentesis before the Academy of Medicine of Paris, which attracted a great deal of attention. Contradictory opinions were given by prominent members as to the value of the operation. The debate was prolonged, and no definite conclusion was reached. Laennec, although he had recommended the operation in excessive effusions and in chronic cases, was yet timid, and his advice had not the overwhelming influence that it should have had. Becker of Berlin in 1834 wrote his paper on chronic pleurisy, in which he also laid down the principles of diagnosis by means of auscultation and percussion. He detailed 5 cases which he had operated upon. To Thomas Davies is due the credit of having in 1835 recommended the use of the exploring-groove needle to ascertain the nature of the pleuritic effusions, but Powell claims that Sir Benj. Brodie first suggested it. Ringer first recommended the use of the hypodermic syringe for that purpose. Stokes298 insisted upon the evils attending paracentesis, among which he mentions the converting of serous into purulent effusions.
297 Bullétin de l'Académie de Médecine, 1838, tome i. p. 62.
298 Dis. of Chest, Dublin.
Watson's lectures on practice, delivered in 1836–37, show that while he was much interested in the operation, the necessity of which he discusses with his characteristic ability, yet his conservatism led him to put prominently forward the dangers and evils connected with it. According to these two prominent English practitioners, only imminent peril to life justified the operation. Guérin299 in 1841 applied his subcutaneous method of operation to empyema. He drew fluids from the chest by a suction-pump applied to a canula, using a curved trocar and canula to prevent injury to the lung.300
299 Essai sur la Méthode Sous-cutanée, Paris, 1841.
300 Drawings of the trocar and canula, with the aspirators, are shown in Jacob and Bongeré, Med. operatoire.
Reybard in 1837 took up Dupuytren's suggestion, and used gold-beater's skin as a valvular means of excluding air at the mouth of the canula; this is now known as Reybard's canula apparatus, and was the one used and highly recommended by Trousseau. Stanski in 1839 invented an apparatus for drawing off air from the chest, working on the principle of aspiration. Bowditch states301 that while in Paris from 1832 to 1835 he never saw a case of pleurisy in Louis's, Chomel's, Andral's, or Trousseau's wards where thoracotomy was performed or even suggested. Medical opinion was either indifferent or in actual opposition at that time. H. I. Bowditch of Boston relates302 that he saw 2 cases of effusion in the pleural cavity in 1839, in which he proposed thoracentesis, but the surgeons would not operate: both of these patients died. He was convinced at the time that their lives might have been saved. Schuh of Vienna published his work on the Influence of Auscultation and Percussion on Practical Surgery, in which he boldly maintained that paracentesis was a radical cure in cases of chronic thoracic effusion, no matter how originating. This work had a great influence in advancing the popularity of the operation of thoracentesis. Subsequently, Schuh and Skoda, both professors at Vienna, published303 a monograph on the treatment of pleurisies, especially by surgical means, which, as Trousseau acknowledged, has become a classical work in Germany, and occupies a distinguished place in the history of paracentesis of the chest. They admitted that when the effusion is not excessive in quantity, and there are no complications, recovery generally takes place. When the effusion is excessive even, it may in time disappear, but it may prove a matter of months or years. They advised that the operation should be performed when there was no marked improvement for three weeks. These authors refuted the arguments urged against the operation, and gave details as to the mode of operating. The Germans were the first to consider the puncture as a means of radical cure in pleuritic effusions: Becker, Schuh, and Skoda gave it a decided impulse. Hope's304 paper endeavored to prove that pleuritic effusions did not require surgical interference, but would yield to general treatment.
301 Unpublished MS., 1883.
302 American Journal Med. Sciences, April, 1852.
303 Medicinische Jahrbücher der K. K. Oesterreich Staates, 1841.
304 "Notes on the Treatment of Chronic Pleurisy," in Medico-Chir. Review, London, 1841.
Thus we see that up to 1841 these unsettled controversies over the dangers and advantages of the operation were still going on. Fred. Bird's results in 1843 proved the possibility of its successful employment, doubted up to that time in England. Trousseau's attention was strongly drawn to the necessity of the operation of thoracentesis as early as 1832, when he attended a case at the Hôtel Dieu that died from excessive pleuritic serous effusion. Louis, from the observation of 150 cases of simple pleurisies that had recovered, had enunciated the law that pleurisy is never the immediate cause of death. This fact, together with Récamier's want of success, had so prejudiced the minds of French practitioners against the operation that it was loudly condemned in acute cases of effusion and in all cases of hydrothorax. Having no fears of fatal termination in pleurisy, they saw naturally no necessity for surgical interference. Trousseau states that it was not until after he had witnessed three patients die from acute pleurisy that he ventured to operate (Sept. 11, 1843). He did not summon a consultation, for fear of being thwarted. It was so successful that he was emboldened to operate without hesitation. After his third operation he read his memoir to the Academy of Medicine in 1843. Trousseau in these memoirs maintained the proposition which extensive observation has now after forty years fully sustained, that dyspnoea and orthopnoea may occur when the effusion is in moderate quantity, and that they may be absent when the effusion is considerable, especially if it has formed slowly. Furthermore, that the signs that constantly indicate the gravity and imminent danger of effusions, and which consequently demand the operation, are the displacement of the heart (whence results syncope), displacement of the mediastinum, depression of the spleen and of the liver, acceleration and feebleness of the pulse, and an anxious countenance.
The next year (1844) Trousseau read another memoir on the same subject. He used the trocar with Reybard's gold-beater's skin at the orifice. While he was popularizing the operation and laying down the indications which called for its performance, several English observers305 were turning their attention in the same direction. The paper by Hughes and Cock306 showed that they had been operating in Guy's Hospital for four or five years, and with great success, using a simple trocar and canula of the diameter of one-twelfth of an inch. They imputed their success to the small size of the instrument used, which allowed the fluid to flow slowly and never permitted air to enter the chest during respiration. They gave a tabular account of 20 operations. Hamilton Roe307 at that time was operating successfully with the trocar. Roe's paper was replete with information and with practical suggestions. He tabulated 39 cases where syncope (one great objection which had been urged against the operation) did not occur even once. He disproved another popular objection, that there was great danger of the admission of air into the pleural sac. Owing to the size of his trocar, a considerable quantity of air entered the pleura during his operations, and in some of them so freely as to produce all the physical signs of pneumothorax, but in none of them did it produce any permanently evil effects. In one instance only was even temporary inconvenience caused. When the fluid was ascertained by the exploring-needle to be purulent, he advised the immediate performance of the operation. In acute cases he recommended a delay of three weeks as the time for testing nature's powers of absorbing the fluid. He advised the closing of the orifice after operation. This author gave an account of his 24 cases. He concluded by stating that the operation is not more dangerous than any other which is performed upon the human body, and that the evil consequences supposed to attend it are imaginary rather than real, inasmuch as it was only fatal in 1 out of 24 cases, and does not produce even temporary inconvenience. Thompson in the same year justly condemns the practice of leaving the canula in the orifice—a proceeding he considers as capable of converting a serous into a purulent fluid. In 1848,308 at the request of H. I. Bowditch of Boston, J. M. Warren operated by the usual method recommended in the works on surgery. Partial relief was obtained, but the amount of suffering undergone by the patient during the operation, and the fact that an aperture was usually left open by this method, decided Bowditch that he would never recommend it unless under very urgent circumstances. Soon after this, Stone operated with the common trocar and canula, by the advice, in consultation, of Bowditch. In 1849, Bowditch saw another death resulting from effusion where he had advised the operation, but the consulting surgeon would not consent.
305 London Medical Gazette, 1847.
306 Guy's Hospital Reports, vol. ii., 1844.
307 London Lancet, 1844, copied into Amer. Journal Med. Sciences, Oct., 1845.
308 Bowditch, Amer. Journal Med. Sciences, April, 1852.
To illustrate the opposition Bowditch found in the United States, he quotes309 a remark of W. W. Gerhard, the distinguished auscultator of Philadelphia, "that he should be as willing to have a bullet shot through his chest as to have paracentesis performed on one of his patients."
309 Unpublished MS., 1882.
About 1850,310 Bowditch saw the paper published by Hughes and Cock, and it determined him in future to try the trocar they had used or something like it.311 "Fortunately, a few weeks before (April 10, 1850) M. Wyman had a sudden and severe case with large effusion and intense orthopnoea. Death was threatening, yet Wyman felt called upon by public opinion, medical and lay, to summon a prominent practitioner from Boston. They both agreed that the patient was in extreme danger, and Wyman urged tapping with an exploring-trocar. It was decided to postpone surgical interference until next day, when another meeting would be held, the consulting physician returning to Boston to advise with the ablest men of the faculty and render their decision the following forenoon. That was done, and it was found that no prominent practitioner in Boston would consent to the idea of tapping. Nevertheless, the oppression was so severe, and death so imminent unless the patient could be relieved by some means, that the country physician agreed to Wyman's proposal that an exploring-trocar should be introduced. The fluid flowed out imperfectly, but some relief and no harm resulted" (Bowditch). Two days after this, Wyman operated again with the exploring-trocar and a suction-pump. Wyman312 demonstrated to John Homans on the 23d of February, 1850, that the chest could be safely punctured with his instrument and the serum evacuated in acute pleurisy.
310 Ibid.
311 Ibid.
312 Private letter to author, 1883.
Although suction, as we have shown, was used as far back, probably, as Galen (second century), by Scultetus in 1662, and was in use in 1707, as shown in Anel's work, in 1742 in Laurence Heister's work, by Ludwig and Lehren in 1768, again in 1796 (Benj. Bell), yet it had been abandoned and lost sight of, with the exception of Laennec's suggestion of its application in the form of a cupping-glass over the orifice of puncture, until Guérin (1841) used it. The author followed Trousseau's clinics in 1849 and 1850, and saw him repeatedly operate with Reybard's canula guarded by gold-beater's skin, but never with Guérin's suction apparatus. The French seemed to have lost sight of it until 1865, when Guérin, at the French Academy, recalled attention to it, showing how he aspirated liquids, instead of allowing them to flow outward after the puncture. His apparatus consisted of a curved trocar, the end of which was made tapering and sharp enough to puncture the thorax through the skin and the muscles; of a pump, the piston of which was perfectly adjusted to produce a vacuum; and of an adjuster at the extremity of the pump, consisting of a stopcock which enabled the operator alternately, without removing the instrument, to aspirate the fluid and evacuate it into a basin. Wyman's pump, invented in 1850, was arranged very much in the same way, only it contained valves which were opened and closed by the movement of the barrel, to enable the operator to suck out the fluid and then force it out of the pump. After the operation the skin, being drawn over and closing the orifice, acted as a valve which prevented at the same time the entrance of air and the escape of fluid. Dieulafoy, in November, 1869, invented his aspirator, which is based upon the same principles as those used by Guérin (1841) and by Wyman and Bowditch (1850)—namely, pneumatic aspiration, which the vacuum of the air-pump supplies. Guérin's instrument was large and costly. Wyman's trocar was of a very small diameter, being only one-twenty-fourth of an inch, and the canula but little larger. This was attached, at first, directly to the aspirating syringe, afterward by means of a flexible tube. With this apparatus Wyman demonstrated that tissues could be safely punctured and cavities evacuated without the admission of atmospheric air, that the wound, causing but a drop or two of blood, was followed by no inflammation, and that no dressing was required. The smallest trocar used previously to Wyman's was that of Roe, which was one-twelfth of an inch in diameter. From 1850, Bowditch appreciated the great value of Wyman's invention, as shown in one of the first operations on a patient of his. He adopted and practised it. His position as professor of diseases of the chest, and his great reputation in that branch, gave him an extensive practice and brought him many cases of pleurisy. He met with great opposition from the surgeons and prominent practitioners of the country, but his results were so favorable that he forced an unwilling and an unbelieving profession to accept, as he expresses it, "the beautiful thought of Wyman of thoracentesis or aspiration with a fine needle." "I considered the operation so simple, and yet so effectual, and never harmful, that I deemed it my duty to print cases illustrative of its value." Bowditch had been for eight or ten years endeavoring to get some effective plan of opening the chest without risk. He readily caught at Wyman's plan, and he operated so frequently and successfully as to demonstrate its value to the medical public both of this country and of Europe. As he states,313 it was, in fact, what he had been for years longing for—viz. a simple and painless, or almost painless, operation for removing fluids from the thorax—one that could be done without danger and leave no open wound. Bowditch relates314 that when he visited Europe, nine years after his first publication of cases, he showed the instrument in England, Scotland, France, and Germany, and that he met with very indifferent recognition of its value. Only W. T. Gardner of Edinburgh and Budd of London seemed to appreciate the plan. They had instruments made after the American pattern. All others had no faith in the operation. In Paris his old master, Louis, smiled incredulously at his enthusiasm for it and doubted its necessity. At Vienna Skoda turned with apparent scorn and left the room as Bowditch was demonstrating its employment. The Parisian authors, Woillez, Peter, Moutard-Martin, Peyrot, and others, do not even mention Bowditch, but give Trousseau alone the credit of popularizing thoracentesis.
313 Unpublished MSS., 1883.
314 Ibid.
Trousseau's first publication was in 1843, and yet in 1859 there was no general adoption of the operation, nor was there until 1869, when Dieulafoy rediscovered Wyman's wonderful improvement of the application of negative force to draw out fluids from the chest.
In estimating the value of the substitution of aspiration for the trocar-and-canula method, we must bear in mind that with the latter there was danger of the introduction of air into the thoracic cavity, of the production of fistulous orifices, and the too rapid, and therefore dangerous, evacuation of the fluid. Moreover, there are cases where the trocar and canula is not effectual, although the quantity effused be considerable—where, indeed, the fluid cannot flow out, although the canula be pushed in actual contact with the fluid. The explanation of this is now understood. The fluid is kept in the pleural sac by a negative pressure of from 4 to 5 inches of water (Stone), 6 millimeters mercury (Donders), 5 millimeters mercury (M. Foster), exercised by the lung in its elastic contraction, and by the passive tension of the arched diaphragm. The fluid has no tendency to flow out, and this suctional pulmonary force must be antagonized by an external suctional force, that of aspiration, before the fluid can be withdrawn.
The invention can best be appreciated from the standpoint reached by modern investigations of the physics of the living mechanism of the chest. The principle of applying suctional force in pleurisy is in imitation of nature's gentle methods in connection with respiration. We have shown that most of the dangers connected with aspiration are caused by not taking into consideration the adjustment of lung-tension with thoracic resilience, and consequently of using too great negative force and withdrawing the fluid too rapidly and in too great quantity.
Thoracentesis by aspiration, with greater or less force as may be necessary, is now placed upon a scientific basis. We claim that this modern method is an American invention—that Morrill Wyman was the discoverer and H. I. Bowditch the utilizer of the discovery. As such they may be regarded as benefactors of the human race.
It is extraordinary that Trousseau never alluded to Bowditch's operations, and that Dieulafoy should never have heard of them. Fraentzel acknowledges that Bowditch was the first to introduce aspiration into practice. The Germans have been very slow in appreciating its value. Fraentzel states that he did not use it until 1871, and that it was not until 1879 that it had in Germany any ardent supporters. Bowditch315 has now operated 387 times upon 246 patients without any unpleasant result.316 The distinctive points in Dieulafoy's ingenious modification of the aspirator are that the needles are very fine, even one-half of a millimeter in diameter; that the barrel of the exhausting pump is of glass; that there is a pre-existing vacuum; that we are not compelled to jar the side of the patient by the process of pumping, and moreover by turning the cock we produce at once a vacuum in the needle itself, and know with certainty the moment the fluid is reached, and can see it flow through the glass index in the tubing, even if it be in drops. We can judge of the nature of the fluid, whether it be serum, pus, or blood. The minuteness of the needle is a great cause of safety, because it allows the fluid to flow so gradually that the lung has time to expand slowly. We can in an instant arrest the flow of the fluid by turning the stopcock, and if necessary by drawing out the needle. By giving the needle a downward direction after it enters the cavity, we prevent the point from pricking the lung. So small an orifice is made that even if the needle does touch the lung, there is no danger, for the orifice closes over at once. As Dieulafoy claims, "the fineness of the needle guarantees the harmlessness of the puncture." Castraux's concealed point (invented in 1873), and Fitch's (of Nova Scotia) protected canula (invented in 1873), are valuable additions to the aspirator-needle. These dome-trocars, as they are called, prevent the possibility of injuring the lung, for the sharp-pointed needle, after it has penetrated the pleural cavity, is at once, by a slight movement, converted into a blunt-pointed needle with an orifice near the end. With these very fine needles the force is sufficient to draw up the thickest fluids. We are compelled to admit that Dieulafoy's instrument is a great advance on any other that has been invented. Its simplicity, its easy application, its safety, have rendered paracentesis a harmless operation and one of great value in serous effusions. While Guérin and Wyman may both claim priority of invention, all must admit that Dieulafoy has improved upon their ideas and given us a beautiful and effective instrument. There have been proposed, since Dieulafoy showed his instrument in 1869, no less than forty other aspirators, modifications in form or dimensions of his apparatus. Of these, to us the most valuable is Potain's bottle aspirator, with which aspiration can be so easily and effectually employed. It is simple and cheap. An india-rubber cork accurately fitting a strong bottle is perforated for two tubes each having a stopcock. One of the tubes fits on the end at the exit in the basin, and the other is adapted to an aspirating syringe.
315 London Lancet, vol. ii., 1879.
316 Letter to author, 1883.
One of the most important of the improvements to the aspirator-canula is the addition—first suggested in 1858 by Charles Thompson,317 and afterward adopted by Potain, Powell, and Fraentzel—of a lateral tube for the outflow connected with the main canula through which the trocar passes. By this improvement, in case the canula is clogged up, the trocar can be pushed down to remove the obstruction without danger.
317 Med. Times and Gazette, 1858.
The principle of aspiration is now well established, and the indications for its use are becoming more defined and more accurate. New applications as a means of diagnosis, as well as of treatment, daily render it more valuable.
To guard against the dangers shown by modern experience to be sometimes attendant upon the operation of aspirating the pleura (see [Dangers of Thoracentesis]), it is now generally admitted that the removal of the contents of the chest should be slow and gradual; and that, ordinarily, it is safest at one operation to remove only a portion of the effused liquid. Our object should be to remove pressure and allow nature by absorption to take away the remainder, for positive pressure is an urgent indication for thoracentesis. It is therefore of primary importance to properly estimate the quantity present, and thus to test the intra-thoracic pressure. Great care and caution must be used, because if we extract too much the operation may be followed by serious results.318 Large-sized canulæ should never be used, for fear of too rapid withdrawal of fluid. It has been demonstrated that even with a capillary perforated needle we can exercise more negative pressure than is safe, especially toward the close of the operation, when there supervenes a negative pressure exerted by the fluid remaining in the pleural cavity. It is from these well-known facts that we recognize the great value of Potain's ingenious addition to the aspirator of a manometer of extreme simplicity, a kind of barometer or cuvette, which is placed along the tube which withdraws the fluid. If we are not satisfied with this new safety improvement of the aspirator, we may adopt Douglass Powell's suggestion (On Consumption, etc.) of fitting into the bottle a pressure-gauge, so as to know at any moment what degree of aspiration is being used.
318 Trans. de l'Assoc. pour l'Adv. des Sciences, 6th Session, 1877.
The syphon method has been of late years very extensively used, especially by Southey, W. H. Stone, and Garland, A. T. H. Waters, Wilks, Oxley, and habitually by Douglass Powell. It is a feeble aspirating force, which has very decided advantages. It is effective, and acts slowly and uninterruptedly with a gentle and uniform negative pressure. Its action allows the lung gradually to expand and the displaced organs slowly to resume their normal position. It thus in many cases furnishes us with a safe means of thoracentesis. (See [Surgical Treatment, in Pleurisy].)
.