Volume 3 — DISEASES OF THE RESPIRATORY SYSTEM. (continued 19)

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.