Peritonitis from Perforation

There is no part of the gastro-intestinal canal that may not, from one cause or another, become the seat of ulceration. The jejunum is the part of the tube long supposed to be an exception to this rule, but even in it one or two observers have found ulcers. These ulcers often exist without distinctive symptoms, and may go on to cicatrization without announcing themselves. In the stomach, however, there are commonly indications which will admit a conjecture of their existence, and perhaps a diagnosis. Sometimes these ulcers penetrate all the tissues of the tube and allow the contents of the intestine to escape into the peritoneal cavity, or they may have destroyed all but the external layer, and some succussion, as in coughing, sneezing, laughing, or perhaps straining at stool, may make the opening complete, with the same results. In these cases it seems to be inevitable that inflammation should follow, unless it has preceded, the complete opening and sealed it up by adhesions. The tendency of such an inflammation is to be local and limited, but when the contents of intestines escape into the peritoneal cavity it usually becomes general. These accidents are usually attended by the sudden development of local pain, by rapid increase in the frequency of the pulse, paleness, and prostration. The perforation of the vermiform appendix is often a partial exception to this statement, for, while the local symptoms are marked, the sympathy of the general system is not so quickly awakened. The same can be said of perityphlitis. The symptoms are often local for some time—a day or more; sometimes subside, as if the disease were cured, and then return in full form. This is produced by the tendency of the inflammation to limit itself to the immediate neighborhood of its cause. Lymph is effused at a short distance from the point of irritation, and seals the parts together, so as to shut in the offending substance; and though this substance may produce pus in contact with intestine or appendix, that fluid is held for a time, as in abscess. It may be permanently held in its new-made sac till it burrows into some near part, as the intestine or bladder, or remain an abscess till opened by Willard Parker's puncture. On the other hand, the contents of this sac may be increased till it breaks bounds and causes extension of the peritoneal inflammation or general peritonitis. In one particular case this process of setting limits and breaking through them occurred in a young lady four times at intervals of from one to two days. When the limiting adhesions were established symptoms would subside, so as to encourage in her physicians the hope, even the expectation, of recovery; but again and again the fire was rekindled, and she died eight days after the first attack. In the greater number of cases the first breaking of the adhesions is followed by full peritonitis, and this often by death.

The perforations of the stomach which I have seen have not been attended by the severe pain described by most authors, but by a sudden prostration of strength and a feeling of disquiet and sinking at the stomach; more of collapse than of inflammation in the symptoms; no tumefaction of the bowels; almost nothing to indicate the nature of the accident, but a sudden new sensation in the bowels, a rapid increase in the frequency of the pulse, it growing small as it increases in rapidity, and a pale and shrunken countenance, and death in from twelve to thirty hours. Then, on inspection, hardly any signs of peritonitis are found. The peritoneal vessels are fuller and the membrane redder than in health, and its surface covered with the thinnest possible film of lymphy exudation, and some serum in the deeper parts of the cavity.

These ulcerations of the stomach are not always fatal by peritonitis. A few instances are recorded in which adhesions of the outer surface of the organ to adjoining organs have taken place, so as to protect the peritoneum almost wholly from the fatal contact with the gastric fluids, and death has occurred in some other way. I have a remarkable specimen illustrating this fact. It was taken from the body of a woman of about middle age who had long had symptoms of dyspepsia, and had from time to time vomited a little blood. It was not difficult to recognize ulcer, but the extent and peculiarities of it could be learned only by inspection. She died suddenly of copious hæmatemesis. On examination an ulcer two and a half to three inches in its several diameters was found, beginning near the pylorus and extending toward the left, which in this large space had destroyed all the coats of the stomach and exposed an inch and more of the right extremity of the pancreas and about the same extent of the liver. The liver and pancreas were both perceptibly eroded when exposed, and in the latter an artery that would admit the head of a large pin was opened. The stomach, outside of this extraordinary ulcer, was strongly attached to the adjacent organs.

The ulcerations of typhoid fever penetrate the intestine about three times in a hundred cases of the fever. This result is reached by the study of a large number of cases, and appears to be pretty generally admitted. The point where this perforation occurs is in the ileum, near the ileo-cæcal valve—within a foot or eighteen inches of it in the great majority of cases, although it has been known to occur seventy-two inches above the valve, and it has been seen very rarely in the cæcum. The fever itself may be either severe or mild. Suddenly severe pain sets in, oftenest in the lower part of the abdomen, and spreads rapidly; the pulse is quickly accelerated and becomes small; and it has been lately stated that in this and other intestinal perforations the gases of the bowels, escaping into the peritoneal cavity, will give resonance to percussion over the lower part of the liver. Fetid gas found in this cavity after death is not without importance; for example, a distinguished Senator at Washington died not long ago of a very painful abdominal disease which his physicians declined to relieve with opium, though the patient pleaded for it. His family physician at home was summoned. Although the distance he had to travel was many hundred miles, he found the patient alive and still suffering. He at once gave morphine for the relief of the pain, but the patient died. Now, this gentleman had diabetes a year or more before his death, recognized by his physician at home and also by myself. While under my observation the urine ceased to contain sugar and its quantity became normal, but soon after this albumen was occasionally found in it. The quantity was generally small, and casts were only found now and then. This new disease was mild, and seemed to be, within certain limits, manageable. He went to Washington under injunction that he was not to let official and professional labors bear with any weight upon him. This last sickness and the death would naturally enough be supposed to be some new phase or consequence of the previous illness. But, while a post-mortem examination was not permitted, the family wished to have the body embalmed. The family physician accompanied the embalmer, and as the latter made a cut through the abdominal walls there was a gush of air laden with fecal odor, and he through this opening saw the intestines covered with false membrane. He satisfied himself that the intestine was not opened. This fetid gas came from the peritoneal cavity. An ulcer had perforated the intestine somewhere, and caused the death. The final disease could be only remotely dependent on the patient's previous illness, if at all. His impaired health may have made the ulcer possible.

All kinds of perforations in the bowels, except those of the stomach, cæcum, and appendix, even the cancerous, have one history and the same symptoms; and if treatment is ever successful in such occurrences it must all be based on one set of rules—absolute rest, no pressure on the bowels, and no movements of the muscles that will aggravate it; food that will be wholly digested and absorbed by the stomach; complete abstinence from cathartic and laxative medicines, and the free administration of opium or morphine. By these means, I fully believe, numbers have already been saved from the fatal consequences of peritonitis caused by perityphlitis and perforation of the vermiform appendix—some under my own observation and others under that of my friends. A boy fourteen years of age was brought to bed by a pain in the right iliac fossa. After a few hours his father, a physician, desired me to see him. There was already a perceptible fulness, with dulness on percussion, in the fossa, and some febrile excitement. I gave a portion of morphine, and promised to call the next morning. In the morning a message came from the father stating that the boy was better and there was no need of further attendance. In the evening I was recalled. The pain had returned, and had spread over most of the bowels. He had general peritonitis. He took tincture of opium, of which I believe the largest dose was 100 drops, reached after three or four days of gradual but steady increase of dose. From that point the patient got better, and the quantity of the medicine was correspondingly reduced. There were a relapse and a repetition of the treatment, and again the disease yielded. During convalescence, about fourteen days from the attack, the boy, after emptying his bladder, was suddenly pressed to continue the discharge. Now he voided what appeared to be blood, two or three tablespoonfuls. It was, however, pus with blood enough to color it. This purulent discharge from the bladder continued for about three weeks, the boy steadily recovering his health. This occurred twenty or more years ago, and that boy is now a well-known physician. Similar cases could be recited.

In 1850, or thereabout, I attended a physician through an attack of typhoid fever. In the third week there was a sudden outbreak of peritonitis. The opium treatment was resorted to, and he recovered, and had good health for twenty years after. Peritonitis occurs rarely in typhoid fever from any other cause than perforation, and its occurrence in this case at this time, when perforation is more likely to occur, renders it probable, at least, that this attack was produced by that cause.

March 3, 1883, autopsy of Wm. Fletcher, age 59, iron-worker. On Friday last, Feb. 23d, he was attacked with pain in the region of the right iliac fossa; it was severe. There was no chill, but little fever, and only slight acceleration of the pulse. His stomach was a good deal disturbed, and the bowels were soon distended with flatus. I saw him on the Tuesday following, with James D. Elliott. The bowels were a good deal swollen and very resonant on percussion; pulse 84. His stomach was still greatly disturbed, so that he retained no food, yet there was no green vomit, but much flatulency. The movements in respiration were particularly noticeable, being nearly or quite as much abdominal as in health. There was a short friction sound in inspiration, but an entire absence of the sound produced by peristaltic action. There was no dulness on percussing over the iliac fossa, and no pain on pressure over any part of the abdomen. I was careful in examining the right fossa, for the first pain was there, and it was severe; but there was no physical sign by which the perforation could be ascertained. Still, my mind dwelt on the probability of perforation, and I expressed my fears to Elliott regarding it. The respiration was of natural frequency. The bowels had not moved for two or three days.

The next day Flint was added to the consultation. The symptoms had changed but little; the pulse was 102; no pain, no tenderness, no peristaltic action; slight friction at one point only; the abdominal respiration was as marked as before. Frequency of respiration, 18; patient sleepy; pupils only slightly contracted. When we were in consultation I again expressed my fear of perforation, but Flint expressed the most decided opinion as to its absence, because there was dulness to percussion over the liver. I had read his paper on the intrusion of gas between the ribs and liver in cases of intestinal perforation, and felt as if I were almost reproved for entertaining the thought without this physical corroboration.

Thursday, March 1st, the stomach had become much more retentive; there were no pain and no tenderness on pressure; pulse 109; no friction sound, no sound of peristaltic action, no dulness on percussion over right iliac fossa, but resonance over the whole abdomen, excepting over the pubes; there the resonance was not clear; over a small space there was dulness; this was ascribed to moderate fulness of the bladder, and, as there had been no difficulty in emptying it, nothing was said of it. The abdominal respiratory movements were the same as before.

Friday morning, at 3 A.M., no marked change had occurred in the symptoms, but from this time onward there was a steady sinking of the vital powers. The pulse grew small and frequent, the hands became cool, the breathing more frequent, and without any sudden change or new symptom he died early in the morning. At the last visit there was no resonance on percussion over the liver.

Autopsy, Saturday, March 3d, 2 P.M. The bowels were distended, as they mostly are in peritonitis, but not extraordinarily. There was now pretty free resonance over the liver. The section to open the abdominal cavity was carefully made, with the aim of ascertaining whether there was air or gas in the peritoneal cavity. When a half-inch opening was made through the peritoneum, gas was forced out through it for some seconds with an unmistakable noise. The bowels were not opened by this cut. The bowels exposed, a very thin film of false membrane was found on all the middle and upper portions of the intestines, with a fringe of injection where the folds came in contact. But two or three inches above the symphysis pubis the section opened a collection of pus which extended downward into the pelvis. Somewhere hereabout—neither of us could say exactly where—was found a lump of fecal matter, not indurated, as large as a marrowfat pea, the intestine still unopened. Search was made for the vermiform appendix. At first it was not recognized on account of its remarkable shortness. It was found, however, pointing directly toward the median line of the body, and was short because a part had been separated from the rest by slough. The end of what remained was marked by a border, one-eighth of an inch deep, of a very dark-green gangrenous color. We did not attempt to measure the quantity of pus. It was six ounces or more. It was completely bounded and shut in by adhesions.

At no time during life was there resonance over the liver, but there was some at the time of post-mortem examination before the bowels were opened, due perhaps to the fact that at death the relaxation of the muscles allowed the gas to rise higher than it did during life. The unusual median position of the abscess is important in accounting for absence of dulness, when it is usually found in slough or ulcer of the vermiform appendix.

"A Fatal Case of Typhlitis without Recognizable Symptoms." Under this title José M. Fisser published a case of inflammation of the vermiform appendix causing general peritonitis in a young woman nineteen years of age. The peculiarities of the case were that the appendix was not perforated, and consequently there was no tumor in the right iliac fossa—that the symptoms were all referred to the epigastrium, without even tenderness in the fossa. She walked the floor and tossed about in bed; the highest temperature was 103°, and the most frequent pulse was 120, and these continued but a short time. Of tympanitis there was none till near death, and then but little. The obscurity in diagnosis led to the publication of the case. The cause of this disease was fecal matter, not very hard, in the appendix.

Med. Record, Sept. 1, 1883.

As much has been said in this article on the diagnosis of peritonitis, it may be well to introduce a case where that diagnosis was conjectural, and yet quite another state existed. I visited Mrs. H——, when her disease was advanced, twice. My impression was that she had peritonitis, but this opinion was held with grave doubt. After her death, Smith sent me the following record of the autopsy: "Mrs. H—— died Friday evening at ten o'clock; next day, at three in the afternoon, we made an autopsy. No gas or fluid in the peritoneal cavity; the small intestines inflated almost to bursting, with injection of the capillaries. In the left iliac region we at once discovered a portion of the intestine almost black, and on examination found a firm white band encircling and constricting that portion. Upon liberating the gas the intestines collapsed, and the constricted portion was released and easily removed. A further examination showed that two of the epiploic appendages, coming off from the colon above the sigmoid flexure, had united at their extreme points and formed a loop two and a half to three inches long, and through this loop or ring a portion of the ileum had passed, and was there constricted. The constricted intestine was about four feet in length. This examination has been gratifying to me. There was a small quantity of bloody serum in the peritoneal cavity low down in the pelvis. The dark grumous blood that passed the bowels on the second and third days can now be accounted for, and corroborates your remark that the hemorrhage looked like strangulation. This was at your first visit. This must be a new cause of strangulation, and one that we could not anticipate."

There was, before I saw her, a single vomit of a suspicious fluid, but the evidence was not strong enough to enable us to pronounce it stercoraceous. Some of the observers noticed bloody serum in the peritoneal cavity, and perhaps some shreds of lymph, but that was in consequence of the strangulation.