Chapter XXXIV: Part 34

Jaffé-Duval[23] 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 {495} 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 This excessive congestion, caused by the accumulation of blood occurring when a large quantity of fluid is rapidly withdrawn, produces the syncope, pulmonary congestion, consecutive albuminous expectoration, the pain, and the oppression amounting sometimes to suffocation, and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.

[Footnote 23: _Thèse de Paris_, 1875.]

[Footnote 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 {496} 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.

{497} 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 {498} 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 {499} 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 {500} 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, Garland[25] 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. Powell[26] 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. Garland[27] termed it the dull triangle. Heitler[28] 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. Rosenbach[29] 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.

[Footnote 25: _Loc. cit._]

[Footnote 26: _Med. Times and Gazette_.]

[Footnote 27: _Ziemssen's Supplement_.]

[Footnote 28: _Wien. med. Wochenschr._, 1878, quoted by Garland.]

[Footnote 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 Powell[31] 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.

[Footnote 30: See section on Pathological Anatomy of Pleurisy, distribution line.]

[Footnote 31: _London Med. Times and Gazette_, Oct., 1882.]

{501} 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. Woillez[32] 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.

[Footnote 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 {502} 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. Woillez[36] 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. Williams[37] 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 {503} 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.

[Footnote 33: Avenbrugger, _Ouv._, ed. de Corvisart, 1808, Paris.]

[Footnote 34: _Arch. gén. de Méd._, 1850, t. xxii.]

[Footnote 35: _Ibid._, 1852, t. xxix.]

[Footnote 36: _Mal. Aig. des Org. Resp._, Paris, 1872.]

[Footnote 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 {504} 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. Stokes[38] 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 {505} 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.

[Footnote 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. Powell[39] 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.

[Footnote 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 {506} 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's[42] 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.

[Footnote 40: _Dis. of Resp. Organs_.]

[Footnote 41: J. W. Hunt, _Dub. Med. Journ._, _loc. cit._]

[Footnote 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 {507} 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). Peyrot[43] 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.

[Footnote 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?