Chapter XXXVII: Part 37

The needle should be taken out suddenly, the operator having previously turned the stopcock, and the skin allowed at once to fall over the orifice, which is so small that no air can enter. It is indeed obliterated at once. It may be well, however, to put some collodion over it, with a small compress. The patient ought not to be permitted to move for twenty-four hours after the operation. He should lie quietly in bed and partake of simple nourishment. The removal of fluid causes the return of friction sounds and of pleuritic pain. Nature slowly does her work of absorbing the fibrinous bands. The breath-sounds in some cases are not heard for weeks, or even months, after the operation. Complete recovery being slow, and the shock to the organism very serious, the patient should thoroughly re-establish his health and strength before reassuming his active duties. A protracted rest in an invigorating climate or a sea-voyage should be advised. If the lung is slow to expand, the patient should frequently practise long, deep inspirations.

Dangers of and Objections to the Operation.--Thoracentesis as a means of relieving suffering humanity has from time to time been praised and proscribed, even in this century. Boyer operated several times, and never saved a single case. Dupuytren had only 2 successful cases in 50. He said he preferred that his patients should die by the hand of God rather than by the hand of man. Sir Astley Cooper had only 1 successful case, Gendrin not 1 out of 20 cases. Davis saved two-thirds of his cases. The eminent W. W. Gerhard of Philadelphia looked upon the operation as nearly always attended by fatal results. What a contrast to modern views and clinical results! Since Bowditch and Trousseau popularized the operation, and Dieulafoy improved the aspirating instruments, there is now no difference of opinion as to the imperative necessity of operating in cases where there is, from the quantity of fluid, imminent danger to life. Up to Nov., 1882, Bowditch[81] had operated 386 times in 245 cases, without a single fatal result, and with only 1 case in which alarming symptoms supervened. Dieulafoy's[82] cases in 1878 amounted to 150, without the shadow of an accident. My colleague, S. C. Chew, has never met with any unpleasant result from his operations. The author has had 84 cases, with 138 operations, without any unpleasant result beyond temporary cough and slight dyspnoea. Fraentzel[83] had 85 different cases, with 164 operations. A. L. Mason[84] performed 122 operations in 70 cases, with no unfavorable result which could be attributed to the operation in any instance, but usually with great and permanent relief. In 42 of his cases 1 operation was all that was necessary. So common is the operation that cases are not reported unless there is something to attract attention to them. As illustrative of the great interest taken in the operation see the number of writers on the subject and the numberless articles in medical journals, and the modifications of instruments of all kinds connected with aspiration {535} and drainage. Such being the case, we ought not to be surprised that some operators may have used the aspirator-needle when they ought not to have done so--that some should have neglected the simple rules now insisted upon as the result of experience.

[Footnote 81: Unpublished MSS.]

[Footnote 82: _Tho. Pleu. Aig._, 1878.]

[Footnote 83: _Ziemssen's Cyc._, vol. iv.]

[Footnote 84: _Loc. cit._]

Although thoracentesis by aspiration is always a harmless operation in itself, there are dangers and accidents which may follow. They may be slight, serious, and sometimes even fatal. The number of deaths which have been the result of the operation, however, is small compared to that of persons dying from the effusion whose lives might have been saved by the withdrawal of fluid. Thoracentesis was frequently made use of without accident, and was considered a perfectly safe operation until Terrillon[85] called attention to an accident which occurred sometimes after operating, a complication which Pinault[86] had mentioned in 1853--the albuminoid expectoration. Terrillon reported 2 cases of sudden and rapid death with that symptom. Several similar cases, resulting in death, had been previously reported. Dieulafoy has collected from different sources reports of 6 deaths with albuminous expectoration, caused by acute oedema of the lungs brought on apparently by the operation of thoracentesis in twenty-four to thirty-six hours. In one of these cases (Gérard's) death occurred in ten minutes; in another (Gombault's) in fifteen minutes; in another (Bouveret's) in two hours; in Behier's in four hours. Terrillon's cases, where there was this frothy, albuminoid, and sometimes bloody expectoration, numbered 16, of which 6 were fatal. The patient is attacked with cough and oppression, with the characteristic expectoration. Auscultation shows the fine subcrepitant râles of oedema of the lungs, mingled with tubular quality and ægophony. Gradually, in favorable cases, the cough subsides, respiration is re-established, and in one hour the danger has passed. In fatal cases the cough becomes irregular and jerky, the agony increases, and the patient throws up the yellowish and albuminous expectoration in quantity varying from 50 grammes to (in one case reported by Moutard-Martin) 1 liter. The intensity of the dyspnoea and its duration vary very much--from twelve to twenty-four hours.

[Footnote 85: _Thèse de Paris_, 1872.]

[Footnote 86: _Ibid._, 1853.]

There has been considerable discussion among different authors as to what produce this serious condition. The view sustained by Hérard[87] is the one generally admitted to be correct--viz. that it is from rapid congestion and acute oedema of the lung, and not from the passage of serous effusions of the pleura through the bronchi. Foucart[88] relates a similar case of albuminous expectoration occurring in heart disease. This condition could not be produced by perforation of the lung, for the pre-existing vacuum renders the aspirator-needles the safest to introduce, because if there is fluid present it at once flows out and warns the operator not to push the implement farther in. In no autopsy has the orifice made by the needle been found, nor has it ever been known to produce pneumothorax. The quantity of albuminous sputa is out of all proportion to the orifice made. In several cases of reported perforation these symptoms did not occur. After the lung has been a long time compressed by an effusion, and when, in consequence of the expulsion of the liquid, it retakes its normal proportions, there occurs a rush of serum which is expelled by the bronchi. Hérard has seen patients in whom he could not find more than traces of liquid after the puncture, and who at the end of a half hour or an hour expectorated 500 to 1000 grammes of fluid which did not come from the pleura. That oedema of the lungs, or serous exudation from the capillaries into the walls and on the free surface of the alveoli, is a result of hyperæmia and pulmonary congestion is admitted by Robin, Bernard, Niemeyer, Jaccoud, and others. We have first congestion of the lung, then oedema resulting from it, ending in free albuminous expectoration, {536} which comes not only sometimes from the diseased side, but from the healthy side, owing to pressure against the mediastinum and the other lung. This is an accident the possibility of which should be always before us in operating. No precaution ought to be neglected which will ward it off. It is instructive to analyze Terrillon's cases as to the cause of the oedema. As he considers that the aspirator, by draining out the lung, is likely to produce this unfortunate result, it is satisfactory to find that of the 16 cases where this unpleasant symptom was found, 12 were where the old trocar (Reybard's) was used without aspiration, and 4 where aspirators were used. Of the 6 fatal cases collected by Terrillon, 3 were with the trocar and 3 with the aspirator. Five out of the 6 fatal cases are found to have been not simple pleurisies, but pleurisies with complications, such as heart disease, bronchitis, tuberculosis, numerous adhesions, double pleurisy. The same may be said of the benign cases. In addition to these complications, large quantities of fluid had been drawn out at one time. Dieulafoy challenges his confrères to produce an instance of death from this cause when the fluid removed did not exceed 1200 grammes. His rule now is never to withdraw more than 1000 grammes of liquid at one time, and in large effusions to empty the sac by several operations. The older and more complicated the effusion, the more rigorous should be the rule, because there is great danger in thoracentesis when the fluid has existed long enough to have compressed the lung to a serious extent by bands. All careful operators now follow this rule. It is dangerous, and withal unnecessary, to draw off large quantities at a time. The gradual removal of fluid diminishes the risk of syncope where a sudden withdrawal may be serious in its effects. The effect is to suddenly deprive the lung of pressure which has for weeks perhaps made it anæmic. The blood rushes into the empty vessels, the air into the alveoli, and violent congestion and consequent oedema result. If, on the contrary, we draw out moderate quantities at different times with the capillary needle, which is so small that its introduction is harmless, the lung resumes progressively the functions it has lost, and the circulation gradually enters. Thus there is no risk of congestion.

[Footnote 87: _Acad. Méd._, 30 Juillet, 1872.]

[Footnote 88: _Thèse de Paris_, 1875.]

In examining the fatal cases reported by different authors, Foucart, Dieulafoy, Mercier, Lerebenthel, and Gagnet, we find other modes of death in addition to those by oedema of the lung, such as asphyxia and pulmonary emboli, and, as connected with the heart, syncope and cardiac thrombosis. In most of the cases these accidents resulted indirectly from the operation in twenty-four hours or a longer time. In a case reported by Guyot it occurred three days afterward. Congestion by itself may cause sudden and rapid death by determining asphyxia.

There are other lung causes which produce sudden death following thoracentesis, such as atelectasis, consecutive to effusion; secondary pneumonia, caseous or not; pulmonary tubercles. Besnier reports a case of gangrene of the lung following paracentesis. Of the 8 cases collected by Dieulafoy which may be put into this category, we find death from pericarditis, cardiac clot, and from thrombosis of the pulmonary artery. Death from the heart may be due to old lesions, to syncope, or to the presence of clots in the heart or small circulation. Stokes has given fatty degeneration of the heart as a cause of death in simple pleurisy without operation. Syncope, with death after operation, is caused by the sudden return of the heart to its normal position. The heart being pushed out of position, the larger blood-vessels are distorted, and the course of the circulation is severely interfered with. A very slight cause will arrest the circulation. By aspiration the mechanical cause is removed, but a small embolus, may, by the increased force of blood, be carried into the pulmonary circulation. Death by emboli in the capillaries of the lungs is very similar to death {537} from clots in the right side of the heart and at the origin of the pulmonary artery. These clots may be formed in the pulmonary vessels, or may be transported in the small circulation to points more or less distant. Potain in 1861, and Vallin in 1869, reported sudden deaths from effusion in the pleural sac, causing embolism of the cerebral artery. How far aspiration is responsible for accidents of this kind it is difficult to decide. Were they caused by thoracentesis or notwithstanding the operation? They are unquestionably the cause of death without the operation in excessive effusions. The conditions which produce these results ought to be well considered previous to operation. We notice that in most of these cases large quantities of fluid were withdrawn--2000 grammes (Legroux), 3 liters (Vallin), 3500 grammes (Guyot), 1500 grammes (Chaillon and Goquel). The withdrawal in cases of long standing of such large quantities had, beyond a doubt, considerable influence in producing the fatal result. Bowditch[89] addressed letters to 60 physicians, living in 31 of the States and 2 in Canada--representative men--asking if they had ever seen or heard of fatal results following thoracentesis by aspiration. Of this number, 53 replied in the negative, and 7 in the affirmative. "Upon an analysis, however," he states,[89] "of the circumstances under which death occurred in these last, I found nothing to shake my confidence in the operation, provided it be performed with proper precautions during and subsequent to the tapping. In no one of these cases had the operation been the sole cause of the fatal result." "In 4 there was extra motion on the part of the patient after operation, and in the other 3 the disease had been allowed to continue without aid from a surgeon long after the operation was needed. In 1 the operation was a forlorn hope. One patient died on the table from anæsthetics." Bowditch adds: "These cases should not lessen our confidence in the operation, but simply teach us caution on three points--namely: do not delay too long; be very careful to direct the patient not to move, if possible, for twenty-four hours after operation; be cautious of using anæsthetics." Bowditch, from 29 fatal cases collected from Otto Leichtenstein,[90] from his own knowledge, and from European literature, tabulates the causes of death in American and European practice: 7 of these cases were caused by extra-exertion after operation; 3 from cyanosis and coma; 4 from spray injections; only 1 from syncope; and 2 from albuminoid sputa. He quotes the final remark of Leichtenstein: "Death or any serious symptoms are so rare that they ought not to have the least influence upon our estimate of this most benign and blessed operation." Bowditch states that there were only 7 deaths in this country (as far as he could ascertain), and 29, or four times as many, in Europe, although the operation has been done much more frequently here and for a much longer time. Does not this show that in this country, in following Bowditch's precepts of great care and deliberation, the operation has been more successful? He never ceased in his lectures and writings to caution us to suspend the withdrawal of fluid the moment the patient begins to suffer in breathing, even in the slightest degree. Of course there may have been other cases occurring in American practice of fatal results, of which no reports were made to Bowditch.

[Footnote 89: Unpublished MSS., 1882.]

[Footnote 90: _Deutsches Arch. für klin. Med._, vol. xxv., 1880.]

The author has carefully gone over Leichtenstein's collected cases, and he finds a number of deaths mentioned by other European authors which are not included in his list. (The reader is referred to the theses of Terrillon,[91] Foucart,[92] Foster,[93] Dieulafoy,[94] Mercier,[95] Pinault,[96] Wilson Fox,[97] and others.) Terrillon alone reports 6 deaths with symptoms of oedema of the lungs following thoracentesis. Leichtenstein does not mention any deaths from embolism, {538} such as are quoted by Goquel, Chaillon, and Woillez. In his collection he gives only 1 death by syncope, whereas Dieulafoy comments upon 4 as found recorded by Trousseau and other French authorities. Toussaint's[98] statistical tables of 300 cases, collected from other sources, give 14 deaths. Wilson Fox collected between 30 and 40 deaths connected with thoracentesis. Besnier stated in 1876 that the mortality from pleurisy in the French hospitals had greatly increased since the practice of thoracentesis had been largely followed. It is difficult to account for this in the face of the statements made by so many of its innocuousness when properly guarded: it may be explained by the fact that suppurative pleurisies are often confounded with those of a fibro-serous nature and treated by simple aspiration. Many fatal cases of empyema are complicated with phthisis; formerly these were added to the mortality for phthisis; where paracentesis was performed upon them they were added to the pleurisy column. Bearing in mind that chronic pleurisies, serous and purulent, are frequently consecutive to diabetes, Bright's disease, chronic alcoholism, cirrhosis of the liver, and other organic diseases, patients die of the primary lesions, though they have been relieved of the secondary ones. These statistics may record the deaths as resulting from pleurisy, for which there was operative interference, instead of from the organic diseases.

[Footnote 91: _Loc. cit._]

[Footnote 92: _Loc. cit._]

[Footnote 93: _Clin. Obs._]

[Footnote 94: _Loc. cit._]

[Footnote 95: _Thèse de Paris_, 1876.]

[Footnote 96: _Ibid._, 1855.]

[Footnote 97: _Brit. Med. Journ._, Dec., 1877.]

[Footnote 98: _Thèse de Paris_, 1878.]

Formerly, when trocars and canulas of considerable diameters were used, only extreme necessity from peril to life made surgeons consent to operate. We claim that by capillary needles, gentle force, and protected points all the old objections are obviated. As Anstie says, there is no opposition to the modern operation by men who have fairly tried Bowditch's practice. Only theorists who are afraid of its imaginary results and men too timid to act hesitate to make use of it. We have discussed elsewhere (Purulent Pleurisy) the danger of admitting air into the pleural cavity, but we insist that in the close method, with capillary needles, there is no danger whatever of air entering. The puncture is so very small that it closes at once by the elasticity of the structure of the chest, just as the knuckle of the intestine in hernia closes after the needle has drawn gases and fluid out of it.

Another objection urged against puncture of the pleura in such cases is the possibility of perforating the lung by fine needles, thus letting air into the cavity and causing cough.[99] Marotte read a memoir on the subject to the Academy in 1872. He reported 4 cases, in all of which there were only temporary effects, no serious ones. Dieulafoy[100] says: "I have been witness to the puncturing of the lung several times, and I have never seen any accident supervene under any circumstances. I have thoroughly convinced myself that punctures performed with a No. 1 needle, diameter half a millimeter, are harmless, and experiments on animals have given me the same results." He even suggests aspirating a few grammes of blood from a congested lung in the first stage of pneumonia, and thus practising local bloodletting. The author has 3 times pricked the lung in aspirating--twice with a No. 2 needle, diameter 1 millimeter, where a few drops of blood were drawn into the instrument, and they did not even produce a cough or the slightest inconvenience. The third time was with a No. 4 needle (2 millimeters). From this puncture some air escaped into the pleura, and for a few days there was evidence of pneumothorax. It then disappeared entirely, the air being absorbed. The case was a circumscribed empyema, which entirely recovered.

[Footnote 99: Allbutt, _Quain's Dict. Med._, 1883.]

[Footnote 100: _Treatise on Pneumatic Aspiration_, Eng. trans., p. 256.]

It will be noted that throughout the discussion of this important subject liberal use has been made of a valuable communication specially prepared by Henry I. Bowditch for this purpose, and embodying the mature results of his study and experience of thoracentesis. It seems not only to establish conclusively the claim that to him, in conjunction with Wyman, is due the {539} great credit of introducing the principle of aspiration, but also to how great an extent it was through his persevering and skilful advocacy and performance of the operation that it became so firmly established in America upon a true scientific basis.

Purulent Pleurisy.

DEFINITION.--Purulent pleurisy is that disease in which the pleura secretes pus instead of fibro-serous fluid, as in simple pleurisy.

SYNONYMS.--Pyothorax; Empyema; Suppurative pleurisy.

HISTORY.--The term empyema was applied originally to any internal collection of pus--[Greek: en] and [Greek: pyon]. It is now restricted to pus in the pleural sac. The ancients, from the time of Hippocrates, diagnosed and treated empyema by thoracentesis and pleurotomy. They were familiar with the fact that it would sometimes discharge through the bronchi and make an orifice through the walls of the chest, and discharge outwardly. Their views of its pathology and its connection with other forms of pleurisy were necessarily crude and indefinite. Of late years, owing to the aids given by exploratory punctures, purulent pleurisies have been thoroughly investigated. Townsend[101] divided the disease into four varieties, all of which are from degenerations of acute serous pleurisies, from increase of intensity of the inflammatory phenomena, or from modification of the secretion of the serous membrane. More modern researches have shown that frequently such is the case, and that purulent pleurisies often succeed serous pleurisies. The liquid when first thrown out is serous and limpid in character, and afterward becomes cloudy, opaline, then more and more opaque and purulent, owing to the pus being freely secreted and mixing with the fibro-serous effusion. In a certain number of cases, however, the effused liquid has from the first the appearance and anatomical composition of purulent fluid--d'emblée purulente. This has been shown by autopsies in cases of women who died in childbed from suppurating pleurisies, and in persons attacked with pyogenic fever, not simply from deposits of pus, but where an inflammatory period, of longer or shorter duration, preceded the deposit.[102] Dieulafoy[103] showed that in all effused liquids in the pleural sac there were present red globules and leucocytes.[104] Laboulbène[105] has established the fact that the exuded fluid in all pleurisies, even those apparently serous, contained, from the time of their formation, purulent globules. All cases, then, are historically purulent; but clinically serous and purulent pleurisies are distinct in their progress, termination, and treatment. Purulence is not always the sign of chronicity of pleural inflammation. It may, and does, show itself in many instances from the very commencement of the attack. Wilson Fox[106] shows there is but little natural tendency in serous effusions to undergo purulent transformations. He thinks in the vast majority of cases suppurative pleurisies are so at early periods of disease. He states the proportion of primary suppurative pleurisies as from 14 to 20 per cent. It is when the number of leucocytes, from the intensity of the inflammation or modification of the process, discolors the fluid and gives to it its distinctive properties, that we use the name of purulent pleurisy. Verliac[107] states that all chronic cases in infants become purulent.

[Footnote 101: Article "Empyema," _Cyc. Prac. Med._, vol. ii.]

[Footnote 102: _Pleurisie purulente_, (Moutard-Martin), Paris, 1872.]

[Footnote 103: "De l'Examen histologique des Liquides, etc.," _Soc. Méd. des Hôp._, 1878.]

[Footnote 104: See section on Hemorrhagic Pleurisies.]

[Footnote 105: _Traité d'Anatomie path._, Paris, 1872.]

[Footnote 106: _Brit. Med. Journ._, Dec., 1877.]

[Footnote 107: _Thèse de Paris_, 1865.]

ETIOLOGY.--The causes of purulent pleurisies are divided into local or traumatic, which are well ascertained and defined; and the general, the {540} action of which is uncertain. Among the first are wounds of the chest, fractures or caries of the ribs, phlegmonous abscesses of the walls of the chest, effusions of blood, pathological liquids, pulmonary gangrene, rupture of tubercular cavities, and other injuries from adjacent organs, especially of those where pus is discharged into the cavity, for the presence of pus engenders pus. Thoracentesis has been accused of converting serous into purulent pleurisies by the admission of air into the pleural cavity. If the atmosphere admitted is contaminated by germs, we must acknowledge that such a result is possible. By the older methods, previous to the adoption of Reybard's protected canula, such a result may have been produced. We can thus, in a measure at least, account for the great mortality in cases operated upon. But since the adoption of the protected orifices of the small aspirating trocar of Wyman and the capillary perforating needles of Dieulafoy, we question whether, with such an insignificant puncture and the complete exclusion of air, thoracentesis can be justly accused of producing such serious mischief. Trousseau[108] earnestly denied such a deleterious effect of the operation in his day. We have now not only the results obtained by Demarquay, Leconte, and Manotte of injecting air into the pleural cavities of inferior animals, but we have the bold experiments of Matice, who, convinced that air could not have any bad influence, actually had the audacity to perform the operation a number of times, allowing the air to enter freely through the canula. From numerous observations there resulted the fact, unsuspected by many, that air, penetrating freely to replace the liquid extracted, never gave rise to purulence in pleurisy; that, owing to its rapid absorption, it did not in the least interfere with the expansion of the lungs; in short, that it produced no accident whatever. While admitting the force of Matice's conclusions, we think it preferable to avoid the possibility of doing harm.

[Footnote 108: _Loc. cit._]

GENERAL CAUSES.--We have shown that secondary pleurisies frequently occur in the course of convalescence from eruptive diseases, measles, small-pox, and especially scarlet fever, and that they are purulent in their nature. The puerperal condition predisposes to suppurative inflammations of the serous membranes, and pleurisies in lying-in women are almost always purulent. In rheumatism, gout, and delirium tremens, and albuminuria as a rule, the pleuritic effusion is serous. It is purulent in persons suffering from severe injuries and among men exhausted by over-work or by alcoholic excesses, or protracted obscure diseases, such as typhoid fever and pyæmia. Analyses of the cases in which purulent transformation has occurred show that tubercles of the lung have only a minor influence in its production--only 34 per cent. of the whole number. Attimont's[109] observations were founded upon 130 cases, 80 of which recovered; of the remaining 50 that died, he found tubercle in only 9 cases. Sometimes malhygienic conditions and insufficient alimentation may account for them. Men are more subject to this disease than women in the proportion of 8 to 1,[110] and young children oftener suffer from purulent pleurisy than adults. It is not easy to explain the transformation of serum into pus in pleuritic effusions that have existed for some time where there have been no grave symptoms. Imprudent exposure, affecting the general health, may thus produce disastrous results. This occurs so frequently that purulent pleurisies are generally called chronic pleurisies. There are cases where neither local nor general conditions explain the transformation of serous into purulent effusions in the chest.

[Footnote 109: _Thèse de Paris_, 1869.]

[Footnote 110: E. Moutard-Martin.]

PATHOLOGICAL ANATOMY.--This is shown by an examination of the effused liquid, the different solid detritus that it contains, the false membranes, the pleura, the lung, and the thoracic wall itself. The liquid effused is purulent in character. It contains a greater or less number of leucocytes, {541} some red globules, and voluminous granular cells, besides crystals of the fatty acids and plates of cholesterin. The pus is mixed with the serosity in varying quantities. The liquid may be slightly opaline or greenish-yellow, and sometimes gray. It may be thin or thick, with heavy flocculi, so as to pass with difficulty through a canula. The liquid is, ordinarily, inodorous, but it may be strong, and even fetid, where it has been in contact with air. In very few cases of old standing can the pus be regarded as active, the corpuscles being, as a rule, dead or having undergone fatty degeneration. Active suppuration is also more readily set up in a pleura which has already yielded pus.

Purulent effusions, independent of contact with air, may become in a short time the seat of putrid transformations. False membranes undergo alterations which produce fetid gases. The air, with its germs, its humidity, and heat, the three grand factors in putrefaction, is thrown in contact with substances of a putrescible composition. Marshall[111] holds that sero-fibrinous effusions appear to have a greater tendency to quick decomposition when air is admitted into the pleural sac than the sero-purulent or purulent products. Pus, he considers, is more stable and less inclined to rapid putrefaction than sero-albuminous fluid. In quantity it varies from a very small number of grammes to five or even six liters. By examining the fluid first drawn out we can predict, by the number of leucocytes present, whether the pleurisy will continue to be serous or will become purulent. If subjected to the influence of ammonia, it will become thready, just as happens when pus is suspended in water, if the fluid contains many of these pus-elements. The purulent fluid may fill the whole or occupy but a small part of the cavity, or again the interlobular spaces only may contain the fluid, the cavity itself being empty. False membranes are almost constantly present and adherent to the parietal or pulmonary pleura; we find them also floating in the liquid. These false membranes may be more or less voluminous. The flocculi, which may be as large as an egg, undergo transformation when air is admitted, and become horribly fetid. They may give rise to septicæmic symptoms. When we see these enormous masses in the cavity, and are unable to get rid of them by suction, we do not wonder that their presence should poison the patient and the case become incurable. Pleurotomy is the only effective mode of getting rid of these dangerous masses, with sometimes gangrenous portions of pleural or lung-tissue. These false membranes frequently form pouches and divisions for isolated quantities of fluid. The false membranes are partly adherent and partly free, especially in cases where there are pulmonary or thoracic fistula. These false membranes differ in acute purulent pleurisies from those found in pleurisies of long standing. They are but feebly adherent to the pleura, and have a slight rose coloration. In old pleurisies the false membranes are of greater density, sometimes from 6 to 8 mm. in thickness. They are more adherent, and cannot be separated, and have a grayish color. The physical state and position of the lung and disposition of the adjoining structures are very similar to what they are in serous effusions. In but few cases do the false membranes envelop the whole of the lung. They pass over one part, and on to the costal pleura. The pulmonary tissue is condensed, sometimes absolutely impermeable to air, so that it will actually sink when dropped in water, being in a state of atelectasis. In cases of shorter duration it is found crepitant throughout its structure. Brouardet[112] called attention to the inflammation in the under-pleural cellular tissue, as well as in the interlobular connective tissue, forming interstitial pneumonia, which determines condensation of this tissue and its retraction after the manner of cicatrices, and afterward its inextensibility. These explain the retraction of the thoracic walls and the narrowing of the chest.

[Footnote 111: _Loc. cit._]

[Footnote 112: "Interstitielle Pneumonie," _Soc. Méd. des Hôp. Bullétin_, 1872.]

{542} The most serious complication of this disease is the pleuro-bronchial fistula[113] by which the fluid escapes through the lung. The firm adhesions between the lungs and walls, forming enclosed pockets, contribute in no small degree to the incurability of purulent pleurisy. These pockets cannot be emptied thoroughly, nor can the washings be made to penetrate them. The purulent secretion exercises a destructive action over the tissues surrounding it, as well as upon the viscera and walls of the chest: the soft parts become inflamed and abscesses form; the intercostal muscles suffer atrophy and undergo fatty degeneration, external openings occurring from ulceration. The latter are found less frequently than pleuro-bronchial fistula. This external perforation is habitually in front, in the upper intercostal spaces, which, near the sternum, are very wide and not protected by external intercostal muscles. The fifth intercostal is the most frequent locality. There may be one or several openings. They may be caused by the pus ulcerating through the parietal walls, or abscesses may be produced in the walls and burst externally. Exceptionally, the emptying of the liquid is by ulceration of the diaphragm into the abdomen, causing fatal peritonitis. Some years since the author saw, in consultation, a patient where the autopsy proved this condition. Rare cases have been reported where the fluid escaped into the pericardium, into the mediastinum, and into the opposite pleural cavity (Fernet[114]). Bouveret[115] relates a number of cases in which the discharge of pus took place through such unusual channels as the oesophagus, the stomach, the intestines, and the pelvis of kidneys; also where the pus perforated the posterior cul-de-sac of the pleura and appeared in the posterior walls of the abdomen. In the last cases, he states, it may point in the groin, the lumbar region, the buttocks, or even in the thigh.

[Footnote 113: See section on Pneumothorax.]

[Footnote 114: _Loc. cit._]

[Footnote 115: _Journal de Méd._, Dec. 16, 1882; _N.Y. Med. Rec._, March, 1883.]

SYMPTOMS.--In a large number of cases of purulent pleurisy the general symptoms do not differ materially from those of fibro-serous pleurisies. Sometimes, however, they do. This is according to whether they are acute purulent or chronic purulent pleurisies.

In acute purulent pleurisy the disease commences in the same way as the ordinary acute fibro-serous pleurisy. Indeed, the first effusion is ordinarily serous in appearance, and afterward it becomes purulent. We have the initial chilliness more or less marked, accompanied by the characteristic pain in the side and dry cough, the fever keeping up, even as high as 103° to 104° F.; and soon the signs of an effusion supervene. In a few days, ordinarily, in acute fibro-serous pleurisies, the febrile exacerbation disappears. Graves[116] states that the extent of a pleurisy is not augmented after twenty-four hours. In acute purulent pleurisy the fever persists in spite of treatment; the effusion increases, sometimes less rapidly than in the serous variety, but in a continuous manner. If thoracentesis is performed about the eighth or tenth day, we notice that the fluid is opaline and contains a large quantity of pus. After this the fluid is reproduced, and as it forms the fever continues; the skin is hot and dry, the appetite impaired, and sweats appear during the night. In examining carefully the thoracic walls we find oedema of the diseased side. Later on there will probably be oedema of the lower extremities.

[Footnote 116: _Clin. Méd._, edited by Neligan.]

Chronic purulent pleurisy is marked by symptoms somewhat different. It commences in a similar manner to that of acute pleurisy, with fever, but in a few days the fever disappears. In the evenings there may be some febrile action with slight chills. It is remarkable that frequently vast collections of purulent fluid do not give rise to chills. The fluid augments progressively, but sometimes very slowly, and often it appears to remain stationary for a long time. This condition continues sometimes for many months. The {543} patients are pale and feeble, although they may get up and walk until the quantity is increased to such an extent as to impair their breathing capacity. Then the forces of the body by degrees diminish, and the appetite is impaired to a serious extent. The face becomes pale and the lips discolored. From time to time diarrhoea supervenes and oedema of the chest-walls is noticed, and general anasarca comes on without albumen in the urine. If nature does not open an orifice through the parietes of the chest or through the bronchi for the discharge, the patients finally succumb in the last degree of wasting with profuse sweats and fetid colliquative diarrhoea.

PHYSICAL SIGNS.--These, with some modifications, are very similar to those of ordinary sero-fibrinous pleurisy. We have the same dilatation of the chest, but it is more frequently localized. The oedema of the thoracic walls is almost characteristic of the presence of pus in the pleural cavity. We may, however, meet with it in fibro-serous pleurisy and in cachectic subjects on the side of decubitus. Then, again, there are cases of purulent pleurisy where it does not occur. It must be looked for with care, especially at the lateral portion beneath the armpit.

Mensuration and percussion afford especial evidences of purulent pleurisy, and frequently they discover encysted points.

The tubular quality of respiratory sounds is more pronounced, as are also the amphoric characters at the apex, caused by long-continued pressure of the compressed lung around the large bronchi. Ægophony is less frequently heard, the bronchophony is distant and less distinct, and vocal fremitus is more completely abolished. The non-transmission to the ear of the whispered voice through the walls of the chest (Bacelli's sound) in purulent pleurisy is a sign of considerable significance in tracing the transformation from serous fluid into pus. We must, however, bear in mind that when the sero-fibrinous effusion contains fibrinous flocculi, it has the same effect as a purulent fluid in interfering with the passage of the voice. (See article ACUTE PLEURISY.)

DIFFERENTIAL DIAGNOSIS can be but indifferently reached by considering the points mentioned. An exploratory puncture enables us to decide with certainty as to the nature of the fluid. Without this the diagnosis is often very difficult. In acute purulent pleurisy the diagnosis is most difficult, especially at an early period, because the general symptoms and the local signs resemble closely those of ordinary pleurisy. When, however, the disease is further advanced, and we have the earthy aspect of countenance with oedema of the thoracic walls, we can be nearly positive in our opinion. Moutard-Martin[117] speaks of this localized oedema at the level of the fluid as a certain indication of the purulent character of the fluid. But this oedema, as he admits, does not always exist. It is wanting in many cases, and it may be found in cases of sero-fibrinous effusion where the patient has been lying on the side, and in other cases of advanced cachectic disease. Formerly, there were many more errors of diagnosis, which were only discovered at autopsies, but now, thanks to aspiratory punctures, the diagnosis is much more accurate, and indicates to us the rational treatment. In both varieties of purulent pleurisy there is a tendency to discharge by making orifices through the walls of the chest or through the lung. This is nature's mode of spontaneous cure. The most common is the pleuro-bronchial fistula, and the period of the disease at which this accident may occur is very variable. Woillez[118] cites a case where it occurred as early as the twenty-eighth day; ordinarily it occurs at a much later period, sometimes as late as the eightieth day. It comes on early in purulent pleurisy. In infants the perforations take place as early as in fifteen or twenty days, and are favorable to the cure in one-half of the cases. Saussier in 29 {544} perforations of this kind counted 15 cures. The symptoms of this accident are easy of recognition. They vary according as the pleuritic effusion is diffused through the whole pleural cavity or is limited, encysted, or interlobular. In the first variety, where we have the physical evidences of the presence of pus, suddenly, during a paroxysm of coughing, the pus is forced up through the bronchi, and the patient in a very short time expectorates a considerable quantity, varying from a few grammes to a liter or more. The quantity thus thrown off depends upon the diameter of the fistula. It may be excessive, as in a case recently observed by the author where suffocation was produced, causing syncope, asphyxia, and death, the flow being so rapid as to fill up the bronchi to such an extent that the patient could not get rid of it. In many cases the pus is brought up more gradually, with successive coughs or with changes of position. Frequently vomiting is produced by the flow from the vomica. After the first instantaneous evacuation of pus (ordinarily continuous, sometimes intermitting) purulent expectoration takes place. The patient may pass hours without any discharge, when suddenly a severe cough brings up a quantity of pus, and again may spend days without further expectoration. Pleuro-bronchial fistulæ may have a valvular character, so that air may or may not be admitted into the pleural sac as the pus is discharged. With or without the formation of pneumothorax there is a tendency to cause putridity of pus. In cases of children, who swallow their expectoration, it often produces a very troublesome diarrhoea. The course of the disease and its prognosis are necessarily altered according to conditions met with. When the air does not penetrate, we observe that the diseased side becomes depressed and the swelling, previously noticed, disappears. The flatness on percussion diminishes or disappears entirely. On auscultation we have coarse râles, sometimes just inside the fistulous orifices, sometimes at a considerable distance. The general symptoms, as well as the physical signs, improve, and the case advances slowly toward cure. Ordinarily, the pus expectorated from the pleura, when free from contact with the air, is odorless, but it is rarely as unpleasant as in bronchial dilatations, unless it is long retained in the cavity, when putrefaction ensues. When the air enters from the bronchi, it frequently acquires a disgusting odor. If the air enters the pleura and takes the place of the pus, the chest remains enlarged. Indeed, it sometimes increases in size to such an extent as to cause suffocation unless the pus and gas are withdrawn. The valve made by the false membrane allowing the air to enter the cavity, but not to escape from it, causes the fluid to accumulate rapidly, and we have pneumothorax to a very painful degree. The diaphragm is pushed down, and, if the disease is on the right side, the liver is forced down, and descends to a level with the umbilicus.

[Footnote 117: _Purulent Pleurisy_, 1872.]

[Footnote 118: _Traité Clin. des Mal. Aigues des Organes Resp._, 1872.]

The collection of gas and fluid may be in such excess as to produce a concavity of the upper surface of the liver, while the organ is forced down into the abdomen. E. Moutard-Martin[119] explains this extreme condition by the fact that the fistulous orifice being at the superior portion of the lung, the air having equalized the interior pressure with the exterior pressure, the liquid obeys the laws of gravity, and depresses the diaphragm. The fluid thus does not reach the level of the pulmonary fistula. Under these circumstances the expectoration may cease altogether unless the patient, by change of position, allows it to flow outward through the orifice.

[Footnote 119: _Loc. cit._]

The physical signs of this condition of pyo-pneumothorax are very marked and characteristic. Above the level of the fluid there is ordinarily a great exaggeration of resonance on percussion, especially at first. At the end of a few days, however, this resonance is sometimes materially modified, and we have obscurity of the percussion vibrations. Percussion, by itself, may lead {545} us into error of diagnosis which the other modes of physical exploration will correct.

On auscultation we hear the amphoric murmur, which is sometimes of great intensity, and at others so feeble and distant as to require great attention on the part of the auscultator. These varieties of the amphoric respiratory sound appear to depend more upon the position of the pleuro-bronchial fistula, and upon the greater or less free circulation of air through the fistula, than upon the extent of the cavity (E. Moutard-Martin). This sound and the amphoric voice are the two principal auscultatory phenomena. There is also the vibrating metallic tinkling produced always in expiration. Although the physical cause may exist, this latter is by no means a constant sign. It may disappear for hours, and even days together, and then be heard for a short time. Sometimes it is only heard when the patient coughs suddenly and violently. When heard it is a very valuable indication of the presence of a pleuro-bronchial fistula. Auscultatory percussion gives us a still more valuable diagnostic phenomenon--the metallic amphoric reverberation--especially if we percuss with a metallic percussor over a metallic pleximeter. The Hippocratian splashing caused by succussion is a more characteristic sign of pyo-pneumothorax than any other we have mentioned. Other signs may fail, and often this is the only sign present. Almost all the symptoms and signs that have been considered characteristic of the presence of pus may coexist with a perfectly limpid sero-fibrinous effusion. We may even have in serous effusions a high, fluctuating temperature, profuse sweats, and quick pulse lasting several weeks. On the other hand, purulent effusions may be associated with symptoms of so mild a character as to lull suspicion. Previous to the application of exploratory punctures for purposes of accurate diagnosis, purulent pleurisies were confounded with the milder disease until so far advanced as to be too late for effective treatment. Now we can without risk discover purulent pleurisies at their very commencement, and before they reach the point of great danger to the subject we can relieve them by thoracentesis, and afterward pursue the treatment for a radical cure.

Limited, circumscribed pleurisies, such as are found at the base of the surface of the diaphragm and in the interlobular fissures, as well as those involving the pleural cavity itself, may empty their contents through the bronchi. As we have shown, the diagnosis of these forms is often very obscure and difficult. The fine capillary exploring-needle is a safe, and often a reliable, means of diagnosis. It may happen that we can only guess at the nature of the disease until, after a protracted cough, there is ejected by the mouth a quantity of pus, and the diagnosis is made clear. We may perhaps discover a point of flatness at the base or about the centre of the lung, but often this flatness is very incomplete, because the collection of pus does not always reach the thoracic wall. It may, indeed, be separated from it by healthy lung-texture. Auscultation may discover coarse râles or even gurgling with cavernous respiration. The voice sometimes has the character of pectoriloquy, at other times of bronchophony: the cavity is rarely large enough or the walls sufficiently firm to give the amphoric tone. Under these circumstances there is neither metallic tinkling nor Hippocratian succussion. The diagnosis of bronchial fistulas caused by encysted pleurisies may be confounded with tubercular cavities or with dilated bronchi. The exact position, however, of the lesion, the rapid manner of the first purulent expectoration, and the nature of the pus expectorated, will enable us always to arrive at an accurate diagnosis. We must remember that in bronchial dilatation the disease is developed by degrees, and the patients do not expectorate suddenly a notable quantity of pus; tubercular caverns are ordinarily at the summit. The mode of expectoration is different, and the matter expectorated does not present the same purulent and homogeneous characters. {546} The general health is very different where encysted pleurisies exist from what it is in patients suffering from tubercular cavities. In the former case it is comparatively good; there are no profuse night-sweats, diarrhoea, etc. Perforation through the thoracic walls may take place at a period more or less remote from the commencement of the disease. The first indication of this result is, ordinarily, a pain over a limited point of one or two of the intercostal spaces, followed, in a few days or a week, by a raised sensitive point on the surface, without change of color of the covering skin. This may remain a long time in an unchanged condition, but generally it increases gradually until it becomes soft and fluctuating, reducible by pressure, but increased in size by efforts to cough or by forcible expectorations. The skin over the raised point becomes thin with a purplish tinge; suddenly, from some effort to cough or unusual exertion requiring suspension of breath, it bursts and gives exit to a quantity of pus far out of proportion to the size of the small tumor. Sometimes there are several such points in the same subject, appearing simultaneously or consecutively, especially if the discharge is not free through the first one. Ordinarily, there is but one which appears on the anterior portion of the chest about the fifth intercostal space or in the intra-mamillary line. These orifices sometimes close and then reopen. Of 18 cases of empyema necessitatis collected by John Marshall,[120] 1 occurred in the sixth intercostal space and 17 in the fifth, and 6 of his own cases in the fifth, beneath the nipple. This is, as he states, the weak point of the chest, relatively unprotected by the adjacent muscles. The internal intercostal muscle, the weakest portion of the great pectoral, and the thin fascia, are the only coverings at that point. There is valid reason why special bulging and spontaneous perforation should occur there. The spot also corresponds nearly with the middle of the pleural cavity when distended. The fifth intercostal space is wider than those below, and its limiting ribs, held to the sternum, give firmness to its borders--conditions which help the thinness of the walls in determining the place of perforation. In children perforation often takes place in the very wide second intercostal space. The perforation, although it may contract in size, persists and remains a fistulous canal, permitting air to enter and to escape. The fluid rarely becomes fetid unless there is a pleuro-bronchitic fistula or air is otherwise freely admitted. Sometimes when the orifice is oblique, the air does not enter at all. When the purulent effusion escapes through the thoracic walls, the patient experiences at once manifest relief. The respiration becomes better, the fever decreases, the sweats disappear, the appetite improves, and the general condition is decidedly ameliorated. This improvement persists as long as there is free discharge, but if from any cause it ceases, we have a return of serious symptoms. If no air enters, percussion and auscultation show the gradual disappearance of the evidences of disease; but if air enters we have the signs of pyo-pneumothorax, amphoric breathing, metallic and succussion sounds. The diagnosis of parietal openings is comparatively easy: the quantity of pus, its odor, with the physical signs, show its nature. With care this form of pleural opening is distinguishable from a fistula made by caries of the ribs or by vertebral abscesses, and not communicating with the pleura. The existence of a thoracic fistula does not prevent the formation of pleuro-pulmonary fistula, and reciprocally a parietal fistula can be found where the other has been previously formed. The abscesses following purulent pleurisies and empyema have been long recognized. Hippocrates mentioned them as contributing to a favorable prognosis in empyema.

[Footnote 120: _London Lancet_, March, 1882.]

Pulsating empyema is where the lesion is situated in the neighborhood of the heart or of the aorta, which transmit their impulse. They are also sometimes called pulsating tumors, rising and falling with alternate movements of {547} inspiration and expiration (Stokes, Graves, and Aran). These cases strongly simulate aneurisms. According to Fraentzel, the fluid is always purulent. In 1 case reported by him, and in 2 cases seen by Traube, pericarditis with effusion was present. Douglass Powell mentions two well-marked cases of pulsation in the left supra-mammary region where the diagnosis between effusion and aneurism was very difficult, but where paracentesis removed a large quantity of fluid and the signs of pulsation ceased. In these cases there was present neither pus nor pericarditis.