Part 146

In regard to the character of the pus, and its agency in the production of this disease, Billroth says: "The old view, that pyæmia is only induced when decomposed pus (ichor) is reabsorbed, is entirely erroneous. There are cases where decomposed, putrid pus enters the blood, and which present a combination of the symptoms of septicæmia and pyæmia (septo-pyæmia of Hueter)." Dupuytren failed to produce metastasis by injections of pus into the veins of dogs; these results were confirmed by Boyer, who only obtained metastasis when he used ichorous pus in his experiments. The same results are recorded in the works of Günther and Sedillot, based on numerous experiments. Beck made fourteen experiments very carefully, but did not succeed in producing metastasis in a single case. The same results are recorded by a commission of the Physiological Society of Edinburgh. O. Weber has recently shown by extended experiments that carefully filtered pus will not produce metastatic abscesses in the lungs. Therefore, it may be considered as proved that fluid pus injected into the veins of an animal produces no metastatic points of inflammation.

It should not be supposed, however, that because injection of fresh (non-ichorous) pus failed to produce metastatic abscesses, it was therefore without results, as the earlier experimenters thought. Billroth and O. Weber have shown by their recent experiments that these injections are uniformly followed by fever, and, if subcutaneous, by abscess; and further, that injections of fresh pus produce even a higher temperature than do those of ichorous pus; but the pus taken from cold abscesses has apparently very slight effect. The fresh non-ichorous dried pus was found to possess in a similar degree the power to excite inflammation and suppuration; even the removal of the albumen did not change its character or power. It will be observed that these injections caused not only local inflammations, but severe constitutional symptoms, as high temperature, etc. Experiments have thus far completely failed to show the agent that excites the inflammation, although it is generally admitted that it at least exists in the molecular bodies.

Virchow and Panum have shown conclusively by their experiments on living animals that the introduction of foreign bodies into the {957} veins--as powdered coal, wax balls, and quicksilver--fail in all cases to produce metastatic abscesses in the visceral organs or symptoms of pyæmia. These foreign bodies were frequently found blocking up the terminal branches of the pulmonary artery, in some cases encapsulated, frequently resembling miliary tubercles, and occasionally surrounded by evidences of slight local inflammation, but in every instance without suppuration. The same experimenters, however, observed that the introduction of ichorous pus and decomposing animal tissue into the veins was attended with the formation of metastatic abscesses and other symptoms of pyæmia. They therefore conclude that the introduction of putrid animal substances into the veins, and the further transport of the same to the branches of the pulmonary artery, produce metastatic abscesses, and that the origin of these deposits is independent of the mere stopping up of the branches of this artery.

The occlusion of the blood-vessels in this diseased condition is a subject which has given rise to much discussion. Some of the earlier writers supposed this phenomenon constituted the disease pyæmia, while others believed it to be the essential cause. Roser says: "But the thrombus is, as can be easily proved, not the cause, but only a symptom, of pyæmia. If a surgical patient--e.g. one suffering with an injury of the head--is attacked by inflammation, and occlusion of a large vein, as of the common iliac vein, for instance, then there are three different theories for the inflammation of the occluded vessel--viz. Hunter's, Rokitansky's, and Virchow's. According to the old Hunterian phlebitic theory, the coagulation of the blood should be the result of the inflammation of the vein. On account of the circumstances under which the coagulation of the blood in the vein has occurred, one might suppose that the cause must be the oozing of coagulable exudation from the inflamed wall of the vein, but pathological dissections, especially Rokitansky's, would not accord with it. Large veins were found plugged up without the existence of corresponding indications of inflammation, and perfectly clear indications were often present that occlusion had preceded the inflammation. Consequently, the occlusion of the vein was the primary condition, and this must be explained in some other way than by its inflammation. Rokitansky in his theory recognized an independent disease of the blood. Yet it does not appear, on examination of the morbid conditions, that this theory can account for them. If it is recognized as correct that a primary disease of the blood is to be admitted, yet the coagulation of the blood in a large vein has not been traced back to it. It remained wholly unexplained why a single vein, especially one so large and strong as the common iliac, should become the seat of the local coagulation. The necessity of finding a local basis for the local coagulation could not be denied. For that reason it was greeted as a highly desirable advance when Virchow pointed out that the occlusion of such large veins could be dependent on the coagulation of the blood in the concave spaces behind the valves of the veins, or through the coagulation in the small branches--e.g. the hypogastric veins, which is gradually carried forward until it reaches the common iliac, and by continual increase this vein may also be filled up. At the same time, it was demonstrated that not infrequently, much oftener than {958} was formerly supposed, the coagulated masses of blood are broken up and carried farther on in the circulation, in this manner producing occlusion of the pulmonary artery or its branches."

The examination of this subject finally brings Roser to this conclusion: "Contamination of the blood is essentially the primary cause of pyæmia; thrombosis is only a result of this morbid contamination, and cannot, therefore, be regarded as the cause of pyæmia, but only as an apparent part, as one of the symptoms of the same." The opinion here expressed by Roser I believe to be the one generally entertained by the profession at this time.

In cases of pyæmia there are recognized two principal sources of contamination of the blood--viz. the wound itself, and the vitiated condition of the atmosphere surrounding the patient--contamination, in the first place, directly from the wound through the blood-vessels; and in the second, by the passage of disease-germs or of the poisonous elements into the blood along the respiratory tract. E. Wagner says: "The latest examinations in regard to the vegetable parasites have made it very probable not only that these are the active agents, but also--what has been clinically quite generally accepted--that septicæmia and pyæmia owe their origin to different plants (the first to rod bacteria, the latter to globular bacteria); and, finally, that both may combine." These germs may be generated in the wound or be received into it from the surrounding atmosphere. The character of the wound and the conditions surrounding the patient thus become important subjects for the consideration of the surgeon.

It has been observed, and is now generally admitted, that wounds complicated with a fracture of the long bones of the extremities, opening large medullary cavities and accompanied by extensive laceration of the soft parts, always increase the danger of blood-poisoning. This fact may be more thoroughly understood by a brief consideration of the condition of the parts. Frequently in open fractures large quantities of pus constantly remain in contact with the surface of the wound, while detached fragments of bone, which become speedily necrosed, move about with every motion of the injured limb, lacerating more or less the surrounding tissues, and thus exciting inflammation and suppuration. The periosteum becomes inflamed; a widespread suppurative periostitis is the result; necrosis of the bone from insufficient nutrition follows, while mechanical pressure on the pus aids in its absorption. The medulla frequently takes on suppurative inflammation, and here the surgeon fails to receive prompt warning of danger; slowly the suppuration progresses, without pain or other symptoms unless the disease has extended to the other tissues; the medullary cavity at the fractured end of the bone may be completely or partially occluded by a new osseous formation; and in such cases the absorption of pus by the comparatively large venous vessels of this cavity is greatly facilitated.

The soft parts may also be the seat of dangerous trouble. The same force that produced the wound and fracture may have also contused the soft parts, destroying in a greater or less degree their nutrition, thus giving rise to gangrenous sloughs, or in other cases to the formation of abscesses, etc. I will also call attention to the fact that the laudable pus {959} in these cases is most favorably situated for a rapid change into that commonly called ichorous. The heat of the parts and the contact of the pus with the atmosphere will not fail to effect its rapid decomposition.

ETIOLOGY OF SPONTANEOUS PYÆMIA.--It is unquestionable that cases of true pyæmia have been observed in which the etiology was not traceable to a wound; and it is equally certain that this failure to discover such a source of contamination in the majority of cases is no proof that it did not exist. When it is remembered that a large portion of the alimentary canal, the respiratory and the genito-urinary tracts, are so situated that the existence of a contaminating wound might be absolutely undiscoverable, we are compelled to admit the possibility of a local centre of contamination in all these cases. But the question may be asked here with propriety, "Is fatal pyæmia, independent of a wound, ever produced by breathing vitiated air?" The answers to this question must generally be a negative, although it is certainly true that poisoning of the blood does take place to a certain degree, as is abundantly shown by the different symptoms arising in patients thus exposed who are not suffering with wounds. It is said that dogs exposed in this way are found to rapidly emaciate and suffer from severe and constant diarrhoea. The various symptoms arising in patients confined in overcrowded and pus-infected wards, among which may be mentioned loss of appetite, with diarrhoea and emaciation, are too well known to require an enumeration here. Therefore it appears highly probable that living in and breathing a vitiated atmosphere may act as a strongly predisposing cause, only requiring a slight scratch or abrasion of the skin, in which the infection may be said to act as an exciting cause of pyæmia.

In reference to such complications the following questions are asked by Roser: "Is it a specific deleterious material, a miasmatic or contagious disease-poison, or, as it is generally expressed, a zymotic agent? Must we regard each particular typhus-like fever, with its remarkable changes of blood, with its various localizations in all the organs and membranes, with its chills, furred tongue, petechiæ, delirium, etc., as we regard typhus, scarlatina, variola, etc.? or, as Virchow teaches us, is this pyæmia, so greatly feared by all surgeons, only an ontological idea? Is the word pyæmia only a general name for three different conditions--viz. leucocythæmia, thrombosis, and embolism, or ichorrhæmia and septicæmia? or are there, as many have supposed, two ways in which pyæmia may originate? Is there one primary miasmatic pyæmia analogous to the other epidemic, so-called zymotic diseases? and again, a secondary pyæmia arising from suppurative inflammation, wherein the poison is formed in the patient's own body, which is infected by a single organ?"

That this disease is caused by a specific deleterious material in the large majority of cases is no longer a question for discussion. The only question to consider is, whether it always arises from the same cause. Is it possible for pyæmia to originate spontaneously? Are there any cases of sporadic origin, or are they always due to endemic or contagious influences? No definite answer can be given to these questions, although, undeniably, the weight of the argument is strongly opposed to a sporadic origin. The term miasmatic, as {960} used by Roser, probably refers to the vitiated condition of the atmosphere, as seen in the overcrowded surgical and obstetrical wards of hospitals. In no other sense can the word be appropriately used in connection with the subject of pyæmia. It is true, pyæmic diseases are found to prevail at certain seasons and in certain localities much more extensively than under other circumstances. The same, however, is true of cholera, typhus fever, scarlatina, variola, and other contagious diseases. That pyæmia is contagious has been frequently demonstrated. I therefore conclude that the prevalence and spread of this disease must be explained by the same rules as are applied to the existence and propagation of these allied affections.

This inquiry into the etiology of pyæmia brings before us again the four hypotheses which have been given in explanation of the same number of theories. The first and second have been already abandoned by the medical profession, after it was satisfactorily demonstrated that they were based on false theories, and consequently there remain for our consideration only the third and fourth.

The third hypothesis assumes that a chemical poison is developed in the wound-secretions, which when absorbed produces pyæmia. An examination of the subject does not justify us in asserting that this proposition has been proved, although it is certain that the results of experimental inquiry demand for it a more extended investigation. In all the analyses which have thus far been made the investigators have entirely failed to give us an adequate knowledge of this poison, and not a word has ever been said in regard to the agency by which it is produced, although it is universally admitted to have been only obtained from decomposing animal substances. It is therefore pertinent to the continuation of this inquiry to ask, By what agency is the putrefaction of animal substances produced? It has now been fully shown that there can be but one answer given to this question--viz. the putrefaction of albuminoid substances can only be effected by living organisms. We therefore conclude that the fourth hypothesis brings us at least one step nearer the correct explanation of the etiology of pyæmia than the third, since we justly assume that if there is a chemical poison in decomposing albuminoid substances, it is produced through the agency of living organisms.

ETIOLOGY OF SEPTICÆMIA.--The first question which arises in the discussion of the etiology of this morbid condition is entirely dependent on the scope which we give to the word septicæmia. Sternberg says: "The view which is entertained by high authorities, upon clinical and experimental evidence, is that there are two forms of septicæmia--the one a septic toxæmia due to the effects of a chemical poison or poisons evolved during the putrefactive decomposition of certain organic substances, especially of nitrogenous animal products; the other an infective disease produced by the rapid multiplication in the body of the infected animal of a parasitic organism. The best-studied and most widely known form of septicæmia, due to the presence of a parasitic organism, is the disease known as anthrax--charbon of the French, milzbrand of the Germans--but several other varieties are now well established, in which similar symptoms and pathological results are produced by organisms morphologically different from the bacillus anthracis. Among these may {961} be mentioned the form of septicæmia in the mouse, so well studied by Koch, which is due to a minute bacillus, and the form of septicæmia in the rabbit, produced by the subcutaneous injections of human saliva, due to micrococci, which has been studied by Pasteur, Vulpian, and myself independently."

The terms septic toxæmia and septic intoxication are applied indiscriminately to the same disease, and the committee appointed by the London Pathological Society to investigate the nature and cause of those infectious diseases known as septicæmia, etc. further report that "ordinary wound-fever is merely septic intoxication in a very mild form, and it is only necessary for the dose absorbed to be sufficient in quantity for fatal consequences to ensue. Septic intoxication is, therefore, of the commonest possible occurrence as a complication of severe surgical injuries, but it is in so mild a form as to bear but little resemblance to that experimentally produced on animals." The question which now arises is, Shall septic intoxication be classified with septicæmia?

We have been long accustomed to speak of this complication as a surgical or traumatic fever; and consequently any change in this classification must necessarily lead to confusion. Furthermore, it is now generally supposed there is much difference in the etiology of these morbid conditions. It is claimed that septic intoxication arises from the absorption of a chemical poison evolved through the agency of living organisms during the process of putrefaction in a wound, and that the conditions are unfavorable for their development within the blood or tissues of a living animal; but in true septicæmia the organisms are developed in the wound during putrefaction, and then find their way into the blood and tissues of the body, where they rapidly multiply. Consequently, the former condition tends to a rapid recovery--unless the quantity of poison primarily admitted to the system has been excessive--while the latter tends to a fatal termination.

Septic intoxication is regarded as a non-infective disease, and true septicæmia as an infective malady. The only etiological similarity between these morbid conditions is found in the fact that they take their origin in putrefaction, which is effected by the action of different organisms possessing marked morphological differences and requiring essentially different surroundings for the maintenance of life and reproduction. Thus, it is supposed that in cases of septic intoxication the organism by which putrefaction is caused in the wound-secretions can only live in the open air, and that its life is commonly only of a few hours' duration. The brevity of bacterial action in this instance may be due to a failure of the absorptive power or to a changed condition in the wound-fluids, rendering them unfit to support the organism.

It is now a well-recognized fact that all septic absorption ends so soon as the wound-surfaces are covered with healthy granulations, but that septic absorption, which produces septic intoxication, is most commonly of a much shorter duration, and, consequently, that the wound complication, which I prefer to designate traumatic fever, is essentially an acute disease, and can only be lengthened out by unusually favorable circumstances for the continuance of the absorption of the poison by which it is produced. {962} The severity and danger of the disease will necessarily depend on the amount of poison absorbed and the resisting power of the patient; but since there is no multiplication of the materies morbi within the body, a rapid elimination by the natural emunctories may be reasonably expected under favorable circumstances.

It should be observed here that the etiology of septicæmia differs from that of traumatic fever, since the organisms in the former condition are first formed in the wound-secretions, but quickly enter the body, where they rapidly multiply; consequently, Chauvel has defined surgical septicæmia as follows: "The particular intoxication which results from the penetration and multiplication in the body of a specific microbe designated by Pasteur under the name of septic vibrio." The bacterial origin of this disease is now generally accepted, and the only question in the professional mind seems to be whether the organisms are the direct or indirect cause of the malady.

There are also some other interesting questions which have arisen in connection with the study of this subject, and are thought to be of sufficient importance to merit mention here. It has long been known that dissecting wounds are most dangerous when made while examining the body very soon after the death of the subject. Recent observations seem to justify the conclusion that the greatest activity of the septic agent is often, if not always, attained before the odor of putrefaction has become fairly perceptible; and even before this odor has reached its maximum degree of offensiveness the danger from septic poisoning has generally disappeared. In some cases septic intoxication is promptly followed by a slight inflammation in and about the wound, which may entirely disappear within a few hours, but only to reappear after a lapse of eight to fifteen days, with the first vigorous physical exercise of the patient. Two cases of this kind have recently come under my observation. In both instances the wounds were located in the hands, and the exercise which developed the septicæmia consisted in rowing a boat, and while thus engaged the local symptoms reappeared with such severity as to cause the patients to quickly discontinue the labor. The reappearance of the local inflammation in both these instances was quickly followed by a rigor and the rapid development of other constitutional symptoms, although prior to the recurrence there was no pus, nor even marked inflammatory action, in any part of the hands.

Professional attention was first called to the above-stated facts by Panum in 1855, who discovered that the maximum toxic action of putrid substances is generally developed during the first hours of bodily activity. In this stage of incubation in cases of surgical septicæmia, if we admit the bodily action as an etiological factor, we observe a striking resemblance to one of the leading characteristics of all the infectious diseases, which unquestionably depend on some sort of septic poison. Furthermore, this analogy becomes most striking if we contrast the effects arising from dissecting wounds with those of the bites of poisonous serpents and rabid animals.

Further investigation is required to settle the perplexing questions of etiological and pathological differences in these allied morbid conditions, for although much has been accomplished during the last two decades, still much more remains to be done. It has only recently been discovered {963} that the septic material in septicæmia is absorbed by the lymphatics, while in pyæmia the poison enters the body through the veins.

ETIOLOGY OF SEPTO-PYÆMIA.--It is now generally admitted that remittent fever and typhoid may be associated, and this morbid condition is commonly designated by the term typho-malarial fever. The etiology is unquestionably dependent upon the action of the two distinct and entirely dissimilar poisons. Scarlatina is likewise frequently complicated by diphtheria, and here we have the combined action of two poisons, each commonly designated as septic and supposed by many physicians to be similar.

In a like manner, it is believed that septicæmia and pyæmia may be associated, and take their origin in dual poisons; but since the etiology of both these morbid conditions has been already described, it is not deemed necessary to dwell longer on septo-pyæmia under this division of our subject.

PATHOLOGY OF PYÆMIA.--The study of the pathology of pyæmia is advanced by adopting the following classification, which is based on recognized post-mortem lesions. The pathological appearances in these forms of the disease differ widely, although the clinical symptoms are often similar. In pyæmia simplex the pathological conditions are essentially more negative. This variety of the disease can only destroy life by the height and duration of the fever which is maintained in connection with the continued existence of ichorous pus. There is found, as an essential basis of this form of disease, extensive suppuration in the subcutaneous tissues.

The arguments in favor of the admission of pus-corpuscles into the blood are as follows: 1. The blood in pyæmia is known to contain more white granular spherical bodies than are normal. The question has been raised, Are they pus-cells or white blood-corpuscles? The answer is difficult, and has not yet been attained. Virchow, in the mean time, has proved that we cannot differentiate, morphologically, between the blood- and pus-corpuscles. 2. Cohnheim has demonstrated the existence of the wandering corpuscles in cases of inflammation. Therefore it appears probable that in cases of pyæmia the blood may contain the pus-corpuscles, but further investigation is needed to establish this fact. However, the establishment of this point would still leave the more important undetermined.

There are often important changes observed in the blood of patients dead of pyæmia, to which I now desire to direct attention. The red corpuscles of the blood, even in the early stage of the disease, in many cases show signs of disintegrating into molecules, and are observed to be accumulated in masses without showing the slightest tendency to form rouleaux. There is a steady increase in the number of pus- or white corpuscles in the blood of pyæmic patients during the whole course of the disease in fatal cases. The condition of the red corpuscles, already mentioned, becomes more and more marked toward the fatal termination.

In all cases of pyæmia multiplex the increased coagulability of the blood may be observed in the early stages of the disease, and steadily increases as the disease progresses.