A system of practical medicine. By American authors. Vol. 2

by Unknown

The peritoneal membrane itself has hardly become thickened, certainly not in marked degree, but it has lost its lustrous surface, is, at least in parts, of an opaline color, as if it had absorbed diluted milk, and there is an effusion of serum or slight oedema on its attached surface. Whatever may be the popular opinion regarding the termination of inflammation of the bowels in mortification, whatever the opinion of the older physicians, it is safe to say that gangrene of the peritoneum has never been the result of uncomplicated, diffuse, acute peritonitis. Peritonitis from strangulation of the intestine or analogous causes is of course excepted. But in puerperal peritonitis I have noticed a fact to which I have nowhere seen an allusion. The parietal peritoneum is at two points in the abdomen but loosely attached to the wall. One of these is on the anterior wall, anterior to and a little above the iliac fossa; the other is above and below the kidney on each side of the body. In these parts I have seen the membrane forced off from its attachment to the walls, which with it made a sac containing pus. Such an abscess, if the patient live long enough, would doubtless cause the death of the membrane.

There is in almost every case of peritonitis more or less of serous effusion, commonly not seen at first on opening the abdomen, for it has sunk into the pelvis. It is transparent, of a yellowish hue, and sometimes flocculi of lymph are found in it.

Whether the inflammation of the peritoneum extends to organs covered by it is a question that has been much discussed; but it is admitted that these organs, to a shallow depth on their surface, have an unnatural color; and when it is remembered that the peritoneum is nourished by vessels not exclusively its own, but running along its attached surface, and distributed as well to the surface of the organs it covers, it is easy to admit that to a very limited depth the organs partake of the inflammatory disease. This supposition gives an easy explanation of the constipation which is so prominent a feature among the symptoms of the disease.

The manner in which the false membrane is disposed of in those who recover is an interesting question. Forty or more years ago Vogel described the process by which the new effusion became a living tissue, and the manner in which blood-corpuscles and blood-vessels were formed in it; and another author had found that the time needed to complete this vascularization was twenty days. But now Bauer and most of the German writers inform us that the coagulated fibrin is converted into fatty matter and is absorbed, and that when adhesions occur they result from the coalescence of a new formation of the connective-tissue elements built up into granules. The question, then, arises, Will the chemical constitution of fibrin permit its conversion into oil? If it will, then the further question presents itself, By what chemical action is the change effected within the body? I do not intend to discuss these questions, but propose them by way of expressing some doubt regarding the accuracy of this statement.

I have always supposed that the epithelial layer of the peritoneum was pushed off by the first of the effusions in peritonitis, and that this was one of the causes of the lustreless appearance of the membrane. This opinion I have never attempted to confirm or correct by the microscope. Bauer confounds this idea. He says: "The deposition of fibrin occurs before the endothelium presents any changes. This fibrinous effusion encloses, primarily, hardly any cellular elements, and only a few cast-off endothelial cells are to be found in it. The endothelium itself is swollen and turbid; the cell-body is increased in size; the contents are granular; multiplication of the nuclei is apparent; the cells are, in fact, in active division. In the tissue of the serous membrane itself, soon after the deposition on its surface, an accumulation of indifferent (?) cells takes place, especially around the vessels, so that the spaces between the vessels are thus completely filled up. The fixed connective-tissue corpuscles take part in the inflammatory process."

Delafield says: "If the autopsy is made within a few hours after death, we find the entire peritoneum of a bright-red color from congestion of the blood-vessels; but that is all: there is no fibrin, no serum, no pus; epithelial cells are increased in size and number." For this kind of peritonitis he proposes the term cellular. He finds it in cases of local abscess of the abdominal cavity in which inflammatory action has extended over the whole membrane, and particularly on the omentum also, in the first two days of puerperal peritonitis. "The ordinary form of acute peritonitis is attended with changes in the endothelium and fixed connective tissue, and with the production of serum, fibrin, and pus." He describes the migration of white corpuscles of the blood through the walls of capillaries to become pus-cells, and then says: "Minute examination shows that two distinct sets of changes are going on at the same time: first, a production of fibrin, serum, and pus; second, swelling and multiplication of the endothelial cells. If the inflammation is very intense, the pus and fibrin are most abundant; if milder, the changes in the endothelium are more marked."

I have said above that the epithelium is early washed off by the inflammatory effusions. In opposition—or, perhaps better, in correction—of this idea, Delafield says: "There may be a considerable amount of pus produced, and yet the layer of endothelium remains in place." "If, however, the pus and fibrin are produced in large amounts, the endothelium falls off and leaves the surface of the peritoneum bare." The connective-tissue cells of peritoneum, he says, undergo but little change in the first three days of the inflammation, "but by the seventh day these cells are marked by increase in size and number in all parts of the peritoneum."

Two or three times in my life I have met with a peculiar arrangement of the false membrane and serum of peritoneal inflammation, of which I do not remember to have seen a description. It is this: the serum is enclosed or encysted in bladders, the walls of which are the false membrane. There may be two or three layers of these bladders, one upon another, all more or less flattened, and each holding from two to six ounces of fluid. It would seem that in these cases the inflammatory activity rose and fell in its progress, early reaching the point at which coagulable lymph was effused, then falling to the stage in which serum alone escaped. This serum lifted the false membrane irregularly, so that several pools were formed. After this the inflammation returns to the fibrous exudation stage, and gives to these bladders a floor which blends with the roof at the edges, and thus makes a complete sac. Once more the inflammatory action is changed in its intensity, so that the only effusion is serum; and this serum again raises the new layer of false membrane into bladders—not always or generally in the exact position of the first series. Still again, the inflammation may be so changed as to make a fibrinous flow to this second series of bladders. I am not certain that I have seen a third series of these rare productions. They have doubtless been seen by other persons, and may have been described. I have not been an exhaustive reader on the subject, but I can well understand how they may have been called hydatids on examination of the sacs without looking at the contents. The fluid in the cysts is simply serum, with no echinococcus sacs, and then the number of these inflammatory sacs greatly exceeds the probable number of the fibrous sacs of hydatids.

Pus in large quantity is not often a product of simple acute diffusive peritonitis, although it is frequently found in that form of the disease that attends puerperal fever, septicæmia, or erysipelas. Yet I have seen it a few times. The pus is not generally pure, but is mixed with serum in different proportions, and there will be seen at the same time deposits of lymph attached to the peritoneum or scales of it floating in the fluid effusion, or both. There is reason to believe that in the cases of this class a very large proportion are fatal in the acute stages, but in the cases that live for a few weeks the pus is disposed to collect in pools and become abscesses by adhesions around them at their borders. These abscesses are disposed to find an exit from the body. In one case four abscesses that were found in this way in different parts of the abdominal cavity had each burrowed toward the umbilicus, and were actually discharging their contents at this point when I saw the case. In another case one abscess only was formed, and in four weeks it had perforated the colon. The opening was nearly an inch in diameter.

Kalantarians says, in eight examinations of the solar and hypogastric plexus in persons who had died of acute peritonitis changes which he regards as inflammatory had occurred, with subsequent opaque swelling of the nerve-cells, ultimate fatty degeneration, brown pigmentation, and atrophy. In chronic peritonitis the cells are often converted into amorphous pigment matter, with increase and sclerosis of the ganglionic connective tissue. Still, it is worthy of notice that these changes do not express themselves in symptoms in those that recover.