TWO articles appearing recently-the one by Dr. Barrs, in the British Medical Journal, dealing more especially with the dire results of pleuritic effusion, the other by Dr. Lindsay, in the Lancet, touching more on the advisability of early interference in such cases-have brought out very suggestive points for us to consider.
It is, however, with some hesitation that I have undertaken to direct the attention of this Society to so familiar and well nigh hackneyed a subject as pleural effusion and empyema. I feel somewhat at case, though, in doing so, because the disease in question, however familiar, possesses and exceptional clinical interest, and because there are many points in its ultimate pathology, perhaps aetiology-and more especially its treatment- around which much controversy has raged and is still raging. It is out of the question to handle exhaustively so vast a subject as pleural effusion and empyema. I will therefore limit my remarks.
There can be no doubt, in my opinion, that there is a strong and growing tendency to employ operative measures by those who see much pleurisy, and who are able to keep track of these sufferers for months or years after their original attack.
It is only in this collective method that we shall be able to speak pro and con for early operative methods.
As the best thinking and scientific minds of the Old and some of the New School are busying themselves most with preventive medicine, and then with curative medicine, it seems to us that a more fitting field for such investigations does not exist than in the one under discussion.
In orthopaedic surgery much has been learned and discovered within the past ten years-recognizing disease early (by experts), by suitable appliances rectifying deformities, and if they already exist, minimizing them to a marked degree.
In pleurisy a similar picture should the presented.
Unrecognized pleurisy, or pleuritis with effusion, maltreated leads to a maiming of the lung, its disability to perform more than one-third of its proper work, phthisis and lateral curvature of the spine, etc.
Curative medicine, then, in such cases must be looked for in two directions: first, as a power to promote recovery from injury of external origin; secondly, as a power to mitigate or remove diseases arising within the body.
And again, we are led in such cases by our old habits of thought to regard life as a thing of the body alone, and to forget that life lies between the body and the medium, and is, as it were, a play of activities between two surfaces, so that the medium needs as much curative vigilance as the body does, and is far more within our power and comprehension.
Therefore the prominent, and often even exclusive, place given to the administration of medicines and the swallowing of drugs is not only questionable, but positively mischievous, in so far as it leads the public, not to mention ourselves, to attach primary importance to measures at best auxiliary, and in so far as it blinds us to the far greater importance of studying the earlier and lesser deviation of function, and of readjusting the conditions under which the individual lives exist.
Those of us who may have made many post-mortems or witnessed them attentively, must have been impressed with the great frequency with which adhesive pleuritis was met.
And it seems to me that it matters little where these adhesions are found, but that they must represent just so much mechanical interference with the act of respiration and interchange of oxygenation during the act of respiration.
To properly understand the gravity of all pleuritic effusion we should appreciate somewhat the pathology of such cases.
The changes which take place in an inflamed pleura are essentially the same as those met in other serous membranes. The earliest stages are indicated by capillary congestion, and sometimes ecchymotic spots in the subserous tissue, with extravasations of blood into the pleura itself; the membrane then loses its smooth, glossy surface, becoming rough, dull and opaque, and is soon covered by a delicate gray deposit, consisting of fibrin, epithelium and young cells, and as this deposit increases apparently layer by layer, it becomes yellowish in color.
These changes are observed both on the parietal and pulmonary pleura.
In the rare cases in which a more or less diffused pleuritis stops here, and is not followed by liquid effusion, the inflammatory products are either entirely absorbed, or-which occurs most frequently-the opposing surfaces become adherent in whole or in part by organized connective tissue, and the sac is obliterated over the adherent areas.
Complete obliteration over the bases is seen chiefly in severe and long standing cases, where absorption has been left to its own judgment, or after empyema.
Mehu and Laboulbene have justly maintained that the ultimate recovery of the patient will proceed more slowly or more rapidly, according as the exudations are more or less fibrinous.
The next step to congestion and fibrinous exudation is the effusion of fluid.
All pleuritic effusions lead naturally to a number of local and general pathological conditions, partly owing to the quantity and quality of the exudations themselves, and partly in consequence of the changes which these exudations gradually undergo. The amount of the exudation will limit the amount of the compression of the subjacent organs, as the mediastinum, the opposite lung, the great venous, arterial, and nervous trunks, the diaphragm, the chest wall, liver, stomach, etc.
In fibrino-effusions-which frequently met with at the onset of all pleurisies-recovery commences in most cases by the gradual concentration of the exudation. In consequence of this the absorption proceeds much more rapidly at the beginning than it does later on. Finally, the fluid portion of the exudation may entirely disappear, and the pleural surfaces, roughened by deposits, come again in contact and often become fused together.
If the process of absorption sets in sufficiently early, the compressed lung again becomes permeable to air and re-expands.
We must still form an accurate idea of the anatomical changes which arise in those chronic cases in which the exudative deposits become organized into connective-tissue masses.
In the course of the pleuritis we not repeated exudations taking place which undergo organization, harden, and finally are found in layers sometimes an inch in thickness.
The serous and sub-serous tissues are often merged into this new formation, and are hard to distinguish from it.
If the pleura pulmonalis is affected, it always appears thicker on section and shrunk on the surface.
This leads to a shrinking and retraction of the subjacent lung tissue, the hilus of the lung forming the centre of the retraction, while the margins of the lung become rounded by this pleuritis deformans.
This retraction leaves a free space in the pleural cavity which becomes filled with fluid, which has little chance of being absorbed the thicker the two pleural surfaces become. The pleura, in such a state, rapidly loses its absorbent power.
Thus the capability of expansion in such a lung is forever last.
Again, if the pleura becomes covered with thick false membranes while there is still considerable effusion in the pleural cavity, and before its absorption has been possible, this circumstance hinders its further absorption, and the remainder of the exudation may thus remain for months or years encapsulated.
The thicker and more fibrous the false membranes, the less vascular are they.
This organized false membrane sometimes assumes a pyogenic character, from which pus is continuously secreted. When the fluid effused in the earlier stages of the disease becomes absorbed and no new liquid (serous or purulent) effusions are poured out between the layers of exudation, the lung must, in such cases of pleuritis deformans, diminish more and more in size.
The adjacent movable organs, as well as the thoracic walls, must contribute to the filling up of this vacuum.
The different character of the effusions, whether serous, sero-fibrinous, purulent or haemorrhagic, all have their important significance.
Anstie and Wagner, from clinical and microscopical work, have found that these false membranes develop more freely at first when the opposing surfaces are kept apart by the effused liquids. The running of the two pleurae together seem to impede the process of organization.
Wagner betones the fact that these newly-organized and vascular tissues often become the starting-points of fresh inflammatory processes and of new products.
The question, then, now which presents itself to us, after digesting the foregoing opinions of the most reliable authors upon the constant tendency for pleuritis with effusion to leave the lung damaged, is, whether we should be satisfied with remedial measures until the patient is nearly in extremis, or shall we, by a timely and simple operative procedure, speedily restore our patient to perfect health by removing in exudation which is seldom able to leave the organ as it found it.
Professor Nothnagel tells us that “a cure consists in so modifying pathological processes-be they chemical or physical, functional or dynamic-as not only to arrest them, but to restore to a state of physiological and anatomical integrity the organs and tissues that have been deranged. The cure (sometimes) can only take place through vital organic processes, and to medicine belongs the task of determining what outside support can be rendered to the vis medicatrix naturae.”.
The large majority of physicians and surgeons are opposed to operations in pleuritis with effusion during its acme and feverish state. If the orthopnoea becomes intense, the effusion increases rapidly, etc., they may become convinced of the necessity of an immediate relief through aspiration or incision.
In times I feel assured that all pleurisies will be treated by operation where an effusion exists.
The eminent authority on this subject, Dr. Bowditch, of Boston, lays down the rule that if the dyspnoea is excessive, so as to amount to permanent orthopnoea, or if I learn that within a few hours previous to my visit there has been even one attack of momentary orthopnoea, during which the patient felt the breath would be wholly lost, I tap immediately, provided I am sure that there is even a quantity of fluid in the pleural cavity, and that it is, apparently, the chief, or perhaps only, cases of the orthopnoea. “I fear,” he adds, “death may occur before my next visit.” He states, further on, that “when a patient comes under notice in whom a large quantity of fluid has been long effused, I advise thoracocentesis as the first remedy.” .
During the past year I have seen three cases of pleurisy die suddenly for the want of immediate evacuation of the pleural sac.
In such cases, even during the febrile stages, thoracocentesis seems to me the only remedy. Barnes says, “It is my practice to operate at once when the chest is two parts filled with fluid, without waiting for urgent dyspnoea.”.
The propriety of operating in large effusions is being rapidly accepted by the profession generally, but there is considerable difference of opinion, even among enthusiasts for the operation, of the demand or advisability of interfering: 1st, during the febrile stage, and 2d, where moderate effusion remains unabsorbed. During the febrile stage it is maintained by many that the fluid would at once reform, and, furthermore, that the surgical treatment might excite additional inflammatory action. We have very strong evidence to prove that this is not correct.
For example, Castiaux (1873, These de Paris) chains that the operation by aspiration will hasten the cure of acute pleurisy and prevent the formation of the fibrinous deposits and bands which in nearly all cases, even in moderate effusion, impair the expansion of the lungs. He operated 37 cases, and cured them. The pulse and temperature fell within twenty-four hours of the operation, and the patients improved rapidly.
As soon as fluid was detected he operated by aspiration points, feeling that he had at his disposition sure means of relief which are harmless or nearly so, and that it is useless to leave this task to nature, which she so often cannot accomplish even in a half-way satisfactory manner. Medication is often untrustworthy in such conditions.
He operated at the height of the first or inflammatory stage.
In operating thus promptly the relieved the lung of compression, which must impair its expansion; he removed an effusion rich in fibrine and capable of increasing, in time, the thickness of the neo-membranes; he restored the power to the lung to dilate by removing this tendency to false membrane formation, which squeezes the lung tissue.
These membranes cannot become organized, as I have stated before, as long as they are separated by fluid.
He drew off all the fluid he could. The relief to the patient was often most marked. The lung expanded promptly and satisfactorily, as shown by auscultation. In a few cases the effusion returned, with an increased pulse and rise of temperature; another aspiration effectually arrested the process.
The cases treated in this fashion lasted a much shorter time, and apparently no false membrane supervened.
No accident occurred in any of his cases, and he never saw as a result of the operation the transformation of the serosity into pus.
We have nearly as strong testimony in some cases reported by Moutard-Martin. He operated in twelve cases, of about ten days’ standing, with sero-fibrinous effusions, accompanied by fever. In eight there was no reproduction, in four it was very slight, and in none did it become purulent. On the other hand, in cases in existence from twenty to sixty days the fluid was always moderately reproduced.
He insists upon the prompt withdrawal of the fluid as the most successful method, more especially if we suspect the formation of false membranes.
Wedal’s results are even more remarkable than those of Castiaux or Moutard-Martin.
He considered puncture harmless during the acute stage, and claims it shows a hastening of the cure.
He operated seventeen times on seventeen patients form the second to the fifth day, and three times from the eighth to the tenth.
In acute cases, where the patients had no pulmonary or bronchial disease, the cure was not protracted beyond the twelfth day. Some were cured by the sixth. His clients were mostly young, vigorous men.
Dr. J. L. Mason tells us that in one hundred and thirty-two cases, where no operation was performed, the duration of the disease extended over weeks, and, in some cases, months.
What a comparison to draw between Castiaux, Widal, Moutard- Martin, and those cases of Mason.
Wedal thinks the earlier the operation is done, the more successful it is likely to be.
Dieulafoy thinks we should wait until the fever ceases.
According to Wilson Fox, the density of the adhesions and false membranes is determined within the first fortnight of the effusion.
As to the aetiology of pleurisy, we will content ourselves with making the inquiry: It is due to exposure, rheumatism, or tubercle? Dr. Lindsay found, in thirty-five cases, sixteen of them due to a wetting or exposure to cold while the patient was overheated. Rheumatism was present in three instances. In two cases there was a family history of tubercle, and in three haemoptysis of pulmonary origin. In ten cases, or nearly one- third, no cause could be found. Organic heart disease does not seem to induce pleurisy.
The relation of tuberculosis to acute pleurisy is the most important and difficult one.
Dr. Barrs, in a noteworthy article, shows that a very large number of cases of simple pleural effusion are really of tubercular origin.
He hunted up the after-history of seventy-four cases of simple pleural effusion, and found within five years thirty-two of these were dead, twenty-five were living, and seventeen could not be found. Of the thirty-two reported dead, fourteen died of phthisis, four died of other tubercular affections, and several of the others succumbed to some pulmonary affection.
Leaving out those who could not be traced in Dr. Barrs’s report, we have the astounding fact that more than one-half, apparently recovering from a simple pleural effusion, died within five years, and these mainly of some tuberculous affection.
It seems but a fair inference that if these statements are correct and are fairly typical and should be corroborated by others and by wider knowledge and experience, that the ultimate prognosis in simple pleural effusion, so far from being, as it is now commonly regarded, as distinctly favorable, would become most grave.
In Dr. Lindsay’s 35 cases only two instances of a family history of tubercle existed and only three instance of pulmonary haemorrhage. In others the presence of tubercle was suspected, but was not absolutely proven.
The association of pleurisy and tubercle is, therefore. more common than we are in the habit of believing.
The question raised by Dr. Barrs is one of the most important in medicine, and each one of us should sift it to the bottom.
If, then, a patient who has had an attack of acute pleurisy subsequently develops tuberculosis, the question arises whether the pleurisy was originally of tubercular origin or whether the damage suffered by the pleura and lung have not invited a tuberculosis which did not exist prior to the pleuritis.
I incline myself more strongly to the latter opinion.
The method of the treatment of the pleuritic effusion is here often the cause of the dire results we see following such processes.
All my practical knowledge of pulmonary phthisis inclines me to the belief that if a lung be left collapsed and inexpansile and bound down, as the result of pleural effusion, it is very likely to become the seat of tuberculosis, and that the development of tuberculosis under such circumstances is no proof that the underlying process was tubercular from the first.
I must further make the statement that in dealing with the great number of cases of pulmonary phthisis which come under my observation, I have been more and more impressed by the frequency with which pleurisy is found as an antecedent condition.
This is a fact which we cannot and should not ignore.
It is to be much regretted that we have no satisfactory records to show us what is the normal course of pleuritic effusions-moderate and large-without treatment. The tendency is probably to a spontaneous subsidence-quoad the effusion per se- and the great practical question is whether, by the administration of drugs or operative interference, we can materially hasten the cure. It is now generally admitted that many of the methods of elimination formerly in vogue by the Old School are either useless or injurious.
The testimony of those employing early puncture or advocating early operation gives a far different note of hope to the aggressive element in the profession.
The great question, then, for us in this connection to settle is, not whether aspiration should be performed, but how soon must it be done?.
In certain cases where the effusion is large and the dulness ascends as high as the second rib in front, or if the measurement of the affected side be markedly increased, much dyspnoea, etc., the advantage of aspiration cannot for a moment be disputed.
I maintain that we should not allow our patient to come to such a pass.
Those cases which present the most difficulty of decision are where we have a moderate effusion with or without fever and with or without dyspnoea or other disturbing symptoms. In such cases the inquiries arise: 1. Does aspiration lessen the chance of a speedy or remote fatal issue? and 2. Does aspiration shorten the duration of the disease, with the immediate prospects of restoring the affected parts to a condition of perfect physiological action?.
The first question may be somewhat summarily dismissed as to a sudden fatal issue where the effusion is moderate, but as to a remote fatal issue, where the accumulation has been in existence some time, our judgment must be reserved.
The second inquiry is a very interesting one, but the difficulty of absolutely determining it is very great.
It seems to me that the duration of the malady, in answering the second query, must first be taken into consideration.
In cases of several weeks’ standing I believe the lung-and ergo its pleural surface-never returns to a healthy condition.
We must take cognizance, though, in this discussion, of the literature dealing with it. It must shape the judgment of the inexperienced and give a strong support to the man of large experience either pro or con.
One practitioner inclines to tap early in all cases, and to repeat it, if necessary, and his statistics will show the greatest number of recoveries and the shortest duration of illness. His remote results will be the most satisfactory fro a medical, surgical and prognostic point of view.
Another practitioner reserves operation for serious cases with large effusions, or for chronic or semi-chronic cases. His remote results will be the most unsatisfactory from a medical, surgical and prognostic point of view.
In empyema most writers agree that aspiration is not the method to employ, but that free incision, with drainage, is the recognized operation in American and the results quoad vitam are most gratifying.
In children we should note the marked tendency for pleuritic effusions to becomes purulent.
As a summary we would state:.
I. That aspiration carried out antiseptically in any stage of pleuritic effusion is not a dangerous procedure.
II. More people die from a postponed aspiration than from any operative interference.
III. Anstie and Weber have shown that organization of the fibrinous portion of the effusion can proceed very slowly and imperfectly when the two pleural surfaces are allowed to play on each other. Effusion separating the two surfaces hastens the formation of neo-membranes.