Part 190

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 {1136} 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.

ETIOLOGY.--Numerous writers have expressed a doubt whether a spontaneous acute peritonitis ever occurs, or if it is ever primary its occurrence in this way is very rare. Habershon has presented the case with more apparent force than any other writer. He studied the record of five hundred autopsies of peritonitis made at Guy's Hospital during twenty-five years, but he "cannot find a single case thoroughly detailed where the disease could be correctly regarded as existing solely in the peritoneal serous membrane."

This statement must be received with some caution. In twenty-five years the records were probably made by a number of different persons, and persons of varying views and varying capacity and judgment. It is possible that the quotation may embrace some of the changes already referred to as the consequences of peritonitis. It does embrace the cases {1137} "when inflammation of the serous membrane occurs in the course of albuminuria, pyæmia, puerperal fever, erysipelas, etc." It also includes "peritonitis caused by general nutritive changes in the system," as seen "in struma, cancer, etc.," "comprising also those cases in which the circulation of the peritoneum has been so altered by continued hyperæmia (modifying its state of growth) that very slight existing causes suffice to excite mischief, as in peritonitis with cirrhosis, disease of the heart, etc."

With these explanations the statement differs widely from what it would seem to mean without them. It is far from saying that peritonitis always follows some abdominal lesion and is caused by that lesion.

Habershon's paper was published twenty-three years ago, and during all these years the curative treatment of peritonitis, to which the paper itself gave currency, has enabled us to study our cases after recovery as well as before the sickness, and it can hardly be doubted that a much larger proportion of the cases are primary and idiopathic than either Louis or Habershon found reason to admit. That a large number are produced by preceding lesions and constitutional conditions no one will be likely to doubt.

Among the 500 post-mortem examinations of peritonitis reported by Habershon, he found preceding disease or injury recognizable in the abdominal cavity in 261. The following is his table, viz.:

From hernia, of which 19 were internal obstruction . . . . . . . 102 From injuries or operations . . . . . . . . . . . . . . . . . . 35 From perforation of the stomach, ileum, cæcum and appendix, colon, etc. (other 13 mentioned with hernia, or with cæcal disease) . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 And leading to fecal abscess (2 otherwise mentioned) . . . . . . 17 From typhoid ulceration without perforation . . . . . . . . . . 5 From disease or operation on bladder and pelvis, viscera, etc. . 42 From disease of the liver and gall-bladder . . . . . . . . . . . 11 From acute disease of the colon (3 others enumerated with perforation) . . . . . . . . . . . . . . . . . . . . . . . . . 3 From disease of the cæcum or appendix (9 others previously mentioned) . . . . . . . . . . . . . . . . . . . . . . . . . . 3 --- 261

Habershon says that in the (his) second and third divisions of the cases the causes were as follows:

From Bright's disease . . . . . . . . . . . . . . . . . . . . . 63 From pyæmia, 13; erysipelas, 5; puerperal fever, 10; with pneumonia, 3 . . . . . . . . . . . . . . . . . . . . . . . . . 31 From strumous disease . . . . . . . . . . . . . . . . . . . . . 70 From cancerous disease . . . . . . . . . . . . . . . . . . . . . 40 From hepatic disease . . . . . . . . . . . . . . . . . . . . . . 27 From heart disease . . . . . . . . . . . . . . . . . . . . . . . 9 --- 240

I have drawn thus liberally from Habershon's paper because it is the only paper that I know, in any language, founded on the analysis of a large number of cases (for five hundred post-mortem examinations is a large number for a disease no more frequent than peritonitis), in the belief that he dealt with facts and that his conclusions must be of great value. He may differ with other physicians regarding what constitutes strumous disease and in the agency of heart disease. He may have mistaken coincidence for consequence, but the paper bears the marks of honesty and good faith from the beginning to the end.

In Habershon's second division, under which he ranks the cases of {1138} peritonitis caused by "a changed condition of the blood," he ascribes 63 to albuminuria. Every physician knows how often meningitis or pericarditis or pleurisy may occur under these circumstances, especially in young persons; but, for myself, I cannot but express surprise at these figures. In one capacity or another I have been connected with large hospitals for forty-eight years, and have seen many cases of albuminuria in private practice, and can recall but few instances in which kidney disease, excepting cancer and other tumors, has terminated in peritonitis. In modification of this statement, however, it is proper to add that the hospital physician cannot know how half the diseases he treats terminate, on account of the American plan of interrupted service, and even less can he know of the mode of death in cases which he sees in consultation. Even with this admission, from my standpoint it is not easy to believe that one-eighth of the cases of peritonitis are caused by albuminuria.

The word pyæmia used by Habershon, it seems to me, ought to be replaced by septicæmia, and it has been by many of the profession. Sédillot many years ago proved that laudable pus injected into the blood-vessels of the dog produced no signs of disease, but that septic pus, so used, was followed by grave symptoms, even death. Among the author's cases thirteen were associated with the septic poison. He also found five which he thinks were independent of erysipelas. One in one hundred is a proportion hardly large enough to establish the relation of cause and effect against the chances of concurrence.

I can make a remark with reference to the inquiry by C. Dubacy in the October number (1881) of the American Journal of Medical Sciences, whether diphtheria produces peritonitis. When diphtheria became epidemic among us in 1860 or 1861 for several years, I saw a great deal of it, but did not recognize any relation between it and peritonitis.

The relations of hernia, injuries, and operations to peritonitis need no commentary.

Perforations of the alimentary canal may require some illustrative statements. These occur most frequently in the vermiform appendix of the cæcum, and are almost invariably caused by some irritating substance imprisoned in its tube. In some cases it is a seed of some fruit, as the orange or lemon; in others, a cherry-pit; in one that I remember it was a small stone, such as is sometimes found in rice; in others, a hard fecal concretion; in one, a child, a singular formation: a strawberry-seed was the centre; around this a layer of fecal matter, around the fecal matter a calcareous layer, on this, again, a fecal layer, and so on to the number of six layers, the external one being calcareous. This body was about one-fourth of an inch in diameter, and may have been years in forming. In this connection I may state, per contra, that I am informed that in a pathological museum in Boston is preserved an appendix that contains, and did contain, a large number of bird-shot, which did no mischief except to enlarge the appendix. This was from the body of a man who had shot and eaten many birds. My observation has led me to the belief that a large proportion of the cases of peritonitis occurring in children are due to perforation of the appendix.

Of the diseases of the liver producing acute diffuse peritonitis, the foremost, I think, is abscess, single or multiple. The different modes in which gall-stones may produce it may be illustrated by the following {1139} cases: (1) A lady died of acute peritonitis. At post-mortem examination a large abscess was found, bounded above by the liver, in other directions by adherent intestines; it contained nearly a quart of pus: at the bottom of the sac was a single gall-stone, very large and very black; the gall-bladder was perforated and very much shrunken. The gall-stone had caused an ulceration of the gall-bladder, but none of the intestines, in this respect differing from the process known as painless transit of a gall-stone. So the calculus caused the abscess, and the abscess caused the general peritonitis. (2) A lady between fifty and sixty years of age had an attack of gall-stone pains; she had had them before. In a few hours symptoms of peritonitis were manifest, and she died. The post-mortem examination showed the ductus cysticus was ulcerated and perforated. Two gall-stones of large size had been formed in the gall-bladder, and had been pushed forward into the duct about halfway to the common duct, leaving it enlarged as they advanced. The foremost one had caused an ulcer on the anterior or lower side of the duct, and bile had escaped, staining all the right half of the abdominal cavity, and throughout this half only the parts were covered with false membrane and stained with bile.

These cases are not so very uncommon. John Freeland of Antigua had a patient, a colored woman sixty-five years of age, who had been suffering from intermittent fever, gastric disorder, and retching. In one of the vomiting spells she experienced great pain, which, being relieved by an opiate, soon returned and was attended by tympanitic and tender abdomen. Death occurred in collapse about eight hours later. The cavity of the abdomen was found filled with blood and bile, the intestines inflamed and gangrenous in spots, and there was general peritonitis. The gall-bladder was empty; the hepatic duct was lacerated, and contained pouches in which gall-stones were encysted. One of these bags was lacerated. This laceration was surrounded by evidences of recent inflammation, and caused the general peritonitis.

The perforations of the stomach which I have seen have been attended by little inflammation of the peritoneum. Death has followed this accident in twenty to thirty-six hours. There has been little pain, little tumefaction of the bowels, little tenderness, but a sense of sinking and a peculiar feeling at the stomach which the patient finds it difficult to describe.

The ulcers of dysentery do at times perforate all the coats of the colon, and yet do not with any uniformity cause general peritonitis; but as the destructive process approaches the outer covering the latter becomes inflamed, and lymph enough is effused to close the opening and prevent the escape of the contents of the intestine; so that, while perforation is not uncommon, I have rarely seen diffuse peritonitis accompanying dysentery.

Habershon reports 5 cases in which incomplete typhoid ulcers of the intestines caused peritonitis, and 15 from the complete perforation. I believe that the physicians of this country and those of France have found the complete perforation much the most common.

I do not remember to have seen fecal accumulation in the intestines produce peritonitis at all general. I did see, years ago, a man of middle {1140} age in whom fecal impaction in the ascending colon had caused destruction of all the layers of the abdominal wall on the right side, so that the contents of the intestine were exposed to view in a space of three inches by two. This implies that there had been peritoneal inflammation enough to seal the intestine to the abdominal wall on all the borders of this extraordinary ulcer. The man recovered in about six months, and returned to his business.

The inconsiderable operation of tapping for abdominal and ovarian dropsy has sometimes been followed by acute peritonitis. In the early part of my professional life I met with several such cases, and have witnessed the same from time to time since. These were mostly cases of dropsy from cirrhosis of the liver. Habershon found 5 such cases, and 7 in the tapping of ovarian cysts.

The rupture of ovarian cysts has produced peritonitis, but in a larger number of cases such rupture, even when the result of violence, has not led to inflammation; but the kidney secretion has been greatly augmented and the fluid absorbed, so that the rupture has been beneficial rather than harmful.

Tumors, particularly those of a malignant character, are apt to grow to the surrounding structures by adhesions the result of chronic inflammation, but now and then they provoke an acute attack which becomes general. Benign tumors may, in rare instances, do this. In one case a man died of acute peritonitis, and the examination showed that a tumor noticed before death, a very large serous cyst standing out of the left kidney, downward-forward, was the only lesion that antedated the inflammation.