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.
