Chapter XXXV: Part 35

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 {508} 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, {509} 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 Powell[44] 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.

[Footnote 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 {510} 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 {511} 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.

{512} 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. Négrié[45] 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. Woillez[46] reports 2 cases where death was produced by supervening congestion of healthy lung.

[Footnote 45: _Thèse de Paris_, 1864.]

[Footnote 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. Lacaze[47] reported one case, and that followed thoracentesis; Lugrol reported a similar case.

[Footnote 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 {513} 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. Barth[48] speaks of dilatation of bronchi as a complication of pleurisy. Woillez[49] 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.

[Footnote 48: _Mém. de la Soc. Méd. d'Obs._, Paris, 1856.]

[Footnote 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 {514} 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 {515} 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 {516} 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. Hunt[50] 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.

[Footnote 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.

{517} 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 reported[51] 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. Mercadie[52] 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.

[Footnote 51: _Trans. Int. Med. Cong._, 1881, vol. ii.]

[Footnote 52: _Thèse de Paris_, 1876.]

Thanks to modern investigations, we have in the very fine needle of the {518} aspirator, or that of the hypodermic syringe, a delicate and sure means of accurate diagnosis, not only as to the nature of the fluids, but as to that of tumors and growths which may be confounded with them. We would not use for exploration a trocar and canula. We consider it best to employ a short needle in aspiration, for fear that a delicate hypodermic needle might break. Flint states that he has known several instances of this accident. Aspiration can be performed with perfect safety, and, indeed, without any fears of unpleasant results even if we perforate an aneurism. The orifice made is so small that the tissues close the moment the needle is withdrawn after making the exploratory puncture. If care be taken to cleanse the instrument and to use Listerism that no deleterious germ be introduced, the operation is harmless. (See Purulent Pleurisy.)

Blunders in diagnosis, however, will rarely occur if an examination is conducted with great accuracy, and if we follow the course of the disease with care.

PROGNOSIS.--The prognosis of simple primary pleurisy is generally favorable, unless it is complicated with other diseases or occurs in enfeebled persons. The intrinsic tendency of the disease is to recovery. Laennec considered that the prognosis in acute pleurisy was always favorable. Pleurisy with scanty sero-fibrinous effusion is not in itself serious. Dry pleurisy is free from danger. Subacute pleurisy with large effusions, where the course of the disease is insidious and slow, is more apt to be followed by tuberculosis than the more acute cases. Louis's law, deduced from 150 cases, that patients never died from the effusion in acute pleurisies, was long since disproved by Trousseau. Lacaze du Thiers published in 1873, in his thesis, a number of cases of sudden death from large accumulation of fluid. These deaths were caused by a large amount of effusion being thrown out rapidly, and suddenly compressing the lung before the system had time to accommodate itself to the presence of the effusion. These cases, termed foudroyant, should be very carefully watched. There is danger of death from orthopnoea when the pleural cavity is completely filled, especially in latent pleurisies, where the patient, unaware of the risk, makes, perhaps, unusual physical exertions. Some deaths have been caused by oedema of the lungs and some by syncope; others, again, from thrombosis of the pulmonary artery. We must bear in mind the grave prognostic value of attacks of orthopnoea and severe dyspnoea, because they, more than the mere quantity of the fluid, show the want of tolerance in the organism. These cases demand prompt mechanical interference with the aspirator. The very rapid accumulation of the effused liquid, even if unattended by dyspnoea, is an unfavorable sign, for observation has proved that in such a case its absorption is attended with more difficulty. Bilateral pleurisies attended with considerable effusion are commonly fatal.

If there are complications with other acute diseases, such as pericarditis or pneumonia, the prognosis may be far from favorable, more particularly if pleurisies supervene when the organism has been exhausted by a long continuance of the primary disease.

If absorption begins soon after the acute symptoms subside (and we expect it to do so where the general health and strength are good), and goes on vigorously, we can with confidence predict a favorable result, especially if there be no contraction of the walls. The earlier the reabsorption takes place the more favorable the prognosis. If, however, four or five weeks pass without any perceptible diminution in the extent of the effusion, there is cause for uneasiness. Especially is it dangerous if, in addition, we have those ugly symptoms, emaciation, weakness, and hectic fever, which point to the conversion of the fluid into pus. There is the prospect of protracted formation of pus with its dangerous sequelæ, including tuberculosis from infective absorption.

{519} That these dangers can in a great measure be obviated by prompt thoracentesis ought now to be universally admitted. Anstie predicts that the experience of the next twenty years will enable us to ensure an absolute immunity from fatal results from either of these serious complications. Symptoms of oedema of the lungs or of cyanosis are bad prognostic signs; so is diminution in the amount of urine secreted, which indicates that the arteries are incompletely filled. Still worse are the symptoms of over-distension of the veins, dropsy, and the appearance of albumen, casts, and blood in the urine.

The prognosis in secondary pleurisies is much more serious. In cases where the effusion is purulent at their commencement, the prognosis is graver than when it becomes purulent after remaining some time in the cavity. This is because they are often pyæmic in their origin.

With modern treatment, however, the percentage of recovery is greater than it formerly was. When we have to contend with chronic purulent cases occurring in cachectic constitutions or in those debilitated by other illnesses, especially tubercular, the prognosis is necessarily unfavorable. The most fatal of all secondary pleurisies are those supervening in the course of pyæmia or puerperal infection. Here death is the rule, recovery the rare exception.

Pleurisies supervening on Bright's disease or nephritis, following scarlatina and idiopathic fevers, have a high rate of mortality. The modern employment of the thermometer is of the greatest assistance to us in forming our prognosis. Marked variations of temperature, whether they be below the normal or constantly high or advancingly high, have grave significance. Anstie's valuable results from the use of the sphygmograph, as giving us the favorable and the unfavorable pyrexial pulse-forms, cannot be over-estimated. We fully concur with him, "that in the dangerous secondary pleurisies the combined use, for prognostic purposes, of the thermometer and the sphygmograph is more valuable than all the other modes of observation put together." It is so because they give us accurate physical data by which we can estimate the exact condition of the patients.

Relapses, with a rapid increase in the amount of fluid after reabsorption has been active and convalescence apparent, are frequently attended with danger, because they often denote a tubercular or hemorrhagic development. A very unfavorable sign is the rapid increase in the effusion after spontaneous or artificial discharges, especially if the fluid has become fetid in its character and has the dark appearance of unhealthy, purulent matter.

TREATMENT.--The study of the natural history of acute fibrino-genic pleurisy teaches us that there is always in it a tendency toward recovery unless there is some constitutional weakness behind the disease or a large fibro-serous effusion resulting from it. We have all met with cases where patients have recovered in the course of a month or six weeks spontaneously, without any treatment. Of A. L. Mason's 200 cases, 132 recovered without having to resort to thoracentesis. It is often a harmless disease when left, as far as medical treatment is concerned, entirely to itself. Of course the body-temperature and the physical evidence of the effusion ought always to be carefully observed. The hygienic treatment ought never to be neglected. We should insist upon rest in bed in the most comfortable position to the patient. The temperature of the room should be from 65° F. to 68° F., the approximate in-door winter degree for healthy adults.[53] The body, especially the chest, should be kept quiet; all unnecessary movement should be avoided. The food ought to be nourishing in quality, easy of digestion, and in quantity sufficient to keep up healthy nutrition. Stimulants are unnecessary, but it is a mistake to withdraw water, which contributes so much to the comfort of the patient and {520} cannot injure him in the first stage. We should take care that the patient has enough sleep. If necessary, mild hypnotics should be used. The effusion results from the inflammatory process, and not from simple transudation. If the pain is very severe, we must resort to the administration of opium by mouth or to hypodermics of from one-eighth to one-sixth of a grain of morphia; this, however, should be avoided when possible, as preparations of opium impair the appetite and depress the patient. The pain ordinarily passes off in 48 hours, and can often be relieved by application of hot-water bags, turpentine stupes, or anodyne liniments. Bloodletting, general or local, is rarely necessary. Leeches will give relief to the acute pain, but opium does that more effectively. Depletory remedies are hurtful and retard convalescence, and do not control the amount of the effusion, which in itself is depletory. If the patient is seen at the initiation of the disease, a large dose of quinia (from ten to fifteen grains), especially if the temperature goes to 101° F., often has a marked effect in controlling the temperature and also the tendency to effusion. Smaller doses may be repeated every few hours. Liq. ammonii acetatis, in fluidrachm j to fluidrachm ij doses every two hours, and Apollinaris or other alkaline drinks, relieve vascular tension and promote the action of the skin and kidneys. During the pyrexia, with the effusion increasing, we endeavor to lower arterial pressure within the pleural vessels by aconite, diaphoretics, mild salines, diuretics, with complete rest of the body. Hot applications (not heavy poultices, however) may sometimes be used at short intervals, with a view of dilating the superficial vessels and thus relieving those of the interior.

[Footnote 53: _Boston City Hosp. Reports_, 3d Series, 1882.]

Under this simple treatment many patients are sufficiently well in a few weeks' time to sit up. They ought not to be permitted to move about unless there is a very small amount of effusion. Roberts[54] of University College Hospital applies adhesive strips over the chest in all cases from the beginning. Mason prefers Martin's india-rubber bandage, three or four inches wide, extending from the lower border of the ribs to the axilla, as it adapts itself better to the chest-walls and supplies an easily-regulated elastic pressure. He considers it also useful in promoting absorption after tapping. Generally in three or four weeks, in favorable cases, the effusion has been absorbed and the patient is able to resume his ordinary duties. The writer cordially endorses Anstie and Bartholow's protests against the employment of mercury for any supposed aplastic properties. It really exhausts the recuperative forces of the organism, and probably injures instead of benefiting in pleurisy.

[Footnote 54: Quain's _Medical Dictionary_.]

If the exudation be in considerable quantity, three or four weeks may be required for its absorption. If this process is sluggish, can we by medicines promote it? Mercury has lost its old reputation as a remedy for this purpose. Iodine externally, and iodide of potassium in decided doses, still retain, to a limited extent, the confidence of practitioners. Preparations of iron, especially the muriatic tincture, have had better effects in the hands of the writer than any other remedy. Large blisters cause great discomfort, and their utility is very questionable. Alkalies possess the power of dissolving exudation, and of these the most efficient is ammonia, especially carbonate of ammonium in doses of from five to ten grains. Saline laxatives, by producing watery stools, have some power in reducing the amount of fluid. Some authors recommend highly the acetate and citrate of potassium dissolved in a decoction of scoparium. J. W. Hunt[55] places most reliance upon pilocarpus pinnatus, which has given him most marked and successful results, even where other remedies have failed. He pushes it to the extent of producing extreme diaphoresis. He commences with thirty minims of the fluid extract four times daily, rapidly increasing {521} the quantity and the frequency of the doses to the extent of fluidrachm j every two hours. The one-eighth of a grain of its alkaloid, pilocarpine, given hypodermically, acts very promptly. He admits that the vital forces are so exhausted by this treatment as to require at once the administration of tonics, especially of iron with strong food. Grasset[56] reported 5 cases of effusion treated by jaborandi. They were cases of pleurisy without fever or sign of inflammation--cases which ordinarily require several blisters to produce an effect.

[Footnote 55: _Dublin Journal Med. Sci._, Dec., 1882.]

[Footnote 56: _Journal de Thérapeutique_, Avril, 1876.]

Ernest Wernaere[57] reported 7 cases of acute pleurisy where there was considerable febrile reaction. Jaborandi was effectual in every case, and the effusion rapidly disappeared after two doses of the infusion. The fever at the same time was diminished, and there was no return of it, as frequently occurs in non-inflammatory cases. It has less effect upon children than upon adults. In a case of Wernaere's only one dose was given.

[Footnote 57: _Thèse de Paris_, 1876.]