A system of practical medicine. By American authors. Vol. 1

by Unknown

In puerperal fever Doléris found the prevailing pathogenic organisms consisted of bacilli or rods, and micrococci or round bacteria in the varieties of micrococci, simple points; diplococci, double points; and chains or wreaths. The bacilli he regarded as the source of acute, rapid septicæmia, while pus-production was associated with the multiplication of the round bacteria, and especially of the diplococci.

4th. The presence of germs in puerperal fever serves not only to fix cases hitherto doubtful in the category of septic diseases, but affords the most satisfactory explanation of the protean phenomena of puerperal fever itself.

We have seen, from both Koch's and Gutmann's experiments upon animals, that death may occur independently of bacteria by the rapid absorption of a chemical poison developed in a putrefying fluid. Clinical experiences, such as the speedy death sometimes observed when retained coagula or portions of placenta undergo decomposition within the uterine cavity, renders it probable that similar cases of putrid intoxication are not unknown in puerperal women, though, so far, the anatomical demonstration of the fact has not been furnished.

In cases, however, where puerperal fever has a distinct period of incubation, and progresses step by step to the fatal ending, bacteria are always found invading the tissues of the genital canal. In rare cases they pass by the Fallopian tube to the peritoneal cavity and excite salpingitis and peritonitis. More commonly from local lesions they enter the canalicular spaces of the connective tissue forming the framework of the genital canal, which is continuous with the subperitoneal connective tissue of the pelvis. From the canalicular space they enter the lymphatics. Cellulitis is excited by their presence, and the lymphatic glands become inflamed and enlarged. In pernicious forms they produce a sero-purulent oedema, which spreads rapidly with a wave-like progress after the manner of erysipelas; or in milder cases the progress of the disease-germs is arrested by the lymphatic glands or the resistance offered by the tissues themselves, and the ordinary circumscribed phlegmon is produced. By the lymphatics which accompany the vessels of the Fallopian tubes they reach the ovaries (puerperal ovaritis), and by the broad ligaments they pass to subperitoneal tissues of the iliac and lumbar regions. Through the same system they are conveyed to the great serous cavities of the body. In the peritoneum they give rise, unless death occurs too speedily, to pyæmic peritonitis, which, unlike the traumatic form, is attended with but little pain, and for which the claim has been set up that it is peculiar to puerperal fever. The wide stomata upon the abdominal surface of the diaphragm allows the facile entrance of the organisms into its lymphatics. Waldeyer found in diaphragmitis the lymphatics of the diaphragm filled with bacteria. And thus, following the lymphatic system, if we only admit that bacteria are the active agents of sepsis, the frequency, in severe types of puerperal fever, of inflammation of the serous membranes of the peritoneum, the pleuræ, the pericardium, the meninges, and the joints finds an easy explanation. Nor is it altogether accident which determines in different cases the precise serous membranes which are affected. The widespread ramifications of the lymphatic system would naturally give rise to eccentric inflammations in place of those following the apparent continuity of tissues.

The ductus thoracicus is the principal channel through which the bacteria enter the blood. It is possible that they may further obtain access into the circulation through the radicles which furnish the communications between the capillaries and the lymphatics. We have seen that bacteria are found with difficulty in the blood during life. A few hours after death they swarm in that fluid. That they do, however, enter the general circulation during life is incontestable. Steurer writes: "As the kidneys are the great filters of the human system, I never neglected to examine them, and almost invariably found micrococci filling the arterioles and glomeruli." This is in correspondence with what occurs in other septic diseases, and accounts for the albuminuria and interstitial nephritis which often supervene in the advanced stages.

The action of the bacilli upon the blood differs materially from that of the round bacteria. So soon as the latter come in contact with the red corpuscles, the corpuscles stick together and form larger or smaller clots in the blood. They then are no longer able to pass through the minute capillary networks, but are arrested in the larger or smaller vessels (Koch). The micrococci in the resulting infarctions multiply, and migrate into the vessels and cellular tissue of the neighborhood. Thus fresh foci of infection are formed. Or by their destructive action they may, when situated near the serous surfaces, penetrate into the serous cavities, and in this way indirectly occasion peritonitis, pleurisy, meningitis, and purulent inflammations of the joints. When the micrococci enter directly into the circulation, they sometimes, in passing through the heart, adhere to the endocardium and the valves, where they cause exudation and ulceration, and give rise to the so-called endocarditis ulcerosa puerperalis.³⁸ The red globules of the blood undergo changes of shape, assume a stellate aspect, and rapidly disappear. The white globules are greatly increased in numbers, and the blood itself becomes nearly colorless. A certain amount of light is thrown upon these blood-changes by Doléris, who added micrococci to the fresh blood of a frog and watched the ensuing changes under the microscope. The micrococci could be seen in the act of penetrating the red globules, which thereupon lost their color and became shrunken, and, following the discharge of the organisms, which meantime had multiplied in an astonishing manner, little or nothing of the original globules remained.

³⁸ Heiberg, Die puerperalen und pyæmischen Processe, Leipzig, 1873, pp. 22 and 34, with references to cases reported by Wiege and Eberth.

In the bacillar form of septicæmia the blood is dark and has a semi-gelatinous appearance, compared by French writers to partially-cooked gooseberry jelly. The red globules, though they exhibit the various stages of deformation, are not diminished in number. The disease is further characterized by ecchymoses and minute apoplectic effusions, and by the absence of pus-formation. In the artificial septicæmia produced by Koch in mice by means of bacilli the rod-like organisms were found to enter the white corpuscles and to compass their destruction. They did not cause the red globules to adhere together, and there was no clogging of the capillary circulation. All the principal structures of the animals subjected to experiment were infiltrated with bacilli. The distribution of the latter was apparently accomplished by the blood-vessels, and not by the lymphatics, the bacilli probably effecting their entrance into the vessels by virtue of their penetrative power, in place of traversing preformed pathways. Possibly it is this action of the bacilli which causes the weakening of the vessel-walls, as evidenced by the large number of red corpuscles which pass out from them.

In puerperal fever it is rare to find either round bacteria or bacilli acting singly as the agent of infection. As a rule, both forms exist together in varying proportions, the predominant form, however, determining in general the character of the symptoms.

Thrombosis of the veins may be a physiological phenomenon, or may be due to an alteration of the blood, to weakness of the heart, or to local influences. So long as the clot remains firm its influence is limited to disturbances of the circulation. The pyæmic symptoms—viz. suppuration of the coagulum, the separation of emboli, and the formation of metastatic abscesses—are always dependent upon the presence of round bacteria. In phlebitis the latter are found in the endothelium and in the sheaths of the veins. The inflammation of the veins is followed by thrombosis. According to Doléris, micrococci derived from the blood are deposited upon the central extremities of the clots; beyond these dépôts a fresh inflammation is set up, followed by fibrinous coagulation. Thus the micrococci become imprisoned between two plugs. The same process may be repeated until a series of abscesses are formed. For a time no mischief may ensue. Finally, however, the resistance of the outworks is overcome, an embolus becomes detached, and an infectious abscess is opened into the blood—an event which is announced by an intense chill and the familiar systemic derangement.