Chapter V: Parasites of the Liver (4)

These facts are stated to show the hesitation and prudence that should control the administration of opium when there is urea in the blood, whether there is peritonitis or not; but a case in which one form of Bright's disease preceded, and perhaps caused, peritonitis will be more instructive: A gentleman sixty-eight years of age was attacked by peritonitis on Thursday evening. There was a moderate chill at the onset (this being one of the few cases in which I have witnessed this occurrence). The diagnosis was then uncertain, and he took quieting doses of Dover's powder, which gave him sleep. The next day the diagnosis was easily made. The urine was examined for albumen, and none found. It was, however, scanty. He took only six-eighths of a grain of sulphate of morphine in the first twenty hours. It was then increased, so that in the next twenty-four hours he took two grains of the sulphate in divided doses--a quantity which has been greatly exceeded in hundreds of cases with the best results; but in this case coma was the result. At 10 A.M. on Sunday he was comatose, but not profoundly; he could be aroused. The breaths were five in the minute, the pulse increasing in frequency; secretion of urine next to none. The galvanic battery was used. After seven hours, while the respiration was growing more natural, the pulse grew more frequent and the stupor increased. At 8.30 P.M. the breathing was fifteen in the minute, and full and perfectly easy, but the pulse was running at 140, and the coma unbroken, and the pupils of good size. The effects of the opiate had passed off, but those of uræmia were profound. He died at 11 P.M. After the alarming symptoms occurred we tried to procure another specimen of the urine for fuller examination, but {1151} could not. It was only after his death that we procured the evidences that he had shown symptoms of contracted kidney for months. The urine contained no albumen at the time of our examination, as very often happens in that disease.

Regarding other points in the opium treatment there is little to be said. Purgatives are entirely inadmissible. The bowels should be left entirely at rest till they recover their muscular tone; then they will expel first the gas, and then the feces; or if, after the inflammation is subdued, they do not move of their own accord, injections are admissible. I have often left the bowels absolutely inactive for fourteen days without any recognizable consequences. If I meet a physician who believes that leeches are essential, I yield him his point, but never advise them. I do this because a moderate bloodletting will do no harm, and little if any good. The same rule I apply to irritating applications to the surface of the abdomen. Mercurials, I think, are harmful, and therefore I object to them. As to food, it should be milk, fresh eggs beaten up with water and pleasantly flavored, peptones, etc. selected from among those that leave no refuse.

The testimony of physicians who have adopted this plan within my own circle is unanimously in favor of it. B. R. Palmer of Woodstock, Vt., afterward of Louisville, Ky., who was the first to test it, told me after a few years' trial that he used to dread peritonitis as he would dread the plague, but with opium in his pocket he met it cheerfully and hopefully, as he did a pneumonia. Chalmers of New York, who is known by many readers of this article, has a very extensive practice, and he told me lately that he had not had a fatal case of peritonitis in twenty-two years. He embraced the plan early.

Now, how did this treatment originate? From whom did the profession adopt it? In 1836-37, I visited daily the hospitals of London, Edinburgh, and Paris, was in frequent intercourse with the physicians of those cities, and never saw a patient anywhere treated by opium, and never heard the least allusion to it. I can safely appeal to any physician who was familiar with the history of the profession before the year 1840, or for two or three years later perhaps, to inquire whether anything was generally known regarding this treatment of peritonitis, or whether he himself ever heard of it. Let the inquiry be made of Willard Parker of New York or Alfred Stillé of Philadelphia--men of a degree of intelligence and learning that has made them leaders in the profession--and of all the profession at that time. I venture to assume that they were as ignorant as I was of what Graves and Stokes had done.

The following fact is significant: In 1843, Graves published _A System of Clinical Medicine_, the preface of which is dated January, 1843. In this he says he had previously published essays, lectures, and articles in several medical journals. In this volume he intends, he says, "to revise what I have written, and to compress the whole within the limits of a single volume." There is nothing in the table of contents or explanatory headings of the several chapters of this volume which alludes to treating peritonitis by opium. It is fair to infer that the cases treated in 1823 had made little impression on his mind, and that he did not think his treatment could take rank as a discovery; and yet Stokes had made favorable mention of it eleven years before this publication. Graves, then, did not {1152} publish his cases, and the first knowledge which the profession could have of them was through Stokes's paper, published in the _Dublin Journal of Medical and Chemical Science_, No. 1, in 1832. Perhaps the reason why Stokes's paper produced so little impression on the profession may be found in the fact that first numbers of journals of every sort have few readers. Anyway, it was not till after the opium treatment had attracted much attention in this country that anybody here knew that Graves or Stokes had ever had anything to do with it. Besides, Graves and Stokes had only used opium in cases of perforation, and they had no plan or symptomatic guide in the use of the drug.

There is something new and strange in the following case copied from the _Medical Record_ of May 12, 1883, under the heading, "Operative Measures in Acute Peritonitis:" "Dr. Reibel relates the case of a child, eight years old, suffering from acute idiopathic peritonitis. The disease had resisted all treatment, and the child being, apparently, about to die, it was determined to open the abdomen with a view to removing the fluid and washing out the peritoneal cavity with a solution of carbolic acid. The meteorism was intense. No fluid was found in the abdominal cavity. In prolonging the incision a loop of the intestine was punctured, as evidenced by the escape of gas and intestinal fluid. The wound was washed with carbolic acid and covered with a layer of antiseptic cotton. The following day the little patient was nearly free from pain, and was able to retain a little milk. The temperature had fallen from 104° to 101°, and the tympanitis was almost entirely gone. The (wounded) loop of intestine was adherent to the abdominal wall, and there had been no escape of fluid into the peritoneal cavity. The patient made an excellent recovery."

If the statements of this abstract are true, and the future supports the practice pursued in this case, acute peritonitis is likely to become a surgical rather than a medical disease. Reibel thinks that opening the intestine in the way he did is a better plan than the punctures with the exploring-needle to relieve the patient of the tympanitis. But it will require more facts than one to persuade the profession that this mishap of the scalpel can grow into a rule of practice. (The _Record_ finds this report in the _Journal de Médecine de Paris_.)

I cannot say that I see the value of a distinction made in 1877 by Gubler between peritonitis and peritonism. By the latter term is meant the total of nervous and other symptoms that arise in the course of peritonitis. Trasour has lately revived this distinction, and thinks it important, and that a light peritonitis may be attended by a grave peritonism. He holds that the distinction is important, because "the treatment of peritonism consists in the administration of alcohol, chloral, and especially of opium in large doses. Of the latter fifteen grains may be given in twenty-four hours." "The symptoms [of peritonism] are produced through the agency of the great sympathetic."[6]

[Footnote 6: _Med. Record_, Aug. 28, 1883.]

I cannot say that I have seen great effects follow small causes, but think that, in general, the effects of peritonitis on the pulse, strength, nervous tone, etc. are, to some extent at least, a measure of its severity.

CONSEQUENCES OF PERITONITIS.--These are usually nothing. When recovery takes place it is commonly complete, but cases have been known {1153} in which the intestines have been left bound to the abdominal wall and to each other, and so made incapable of their natural action. The results of this are a swollen, tympanitic abdomen and impaction of the bowels, but the general health may be very good. A woman at Bellevue was left in this condition, yet she performed the duties of nurse in one of the wards for some years, and finally disappeared from the institution, and I do not know how it ended with her--probably by the breaking up of the adhesions and a return of the bowels to their natural condition.

In some few cases there remains new tissue, which in time is partly broken up and remains partly attached. In this manner strings and bands of considerable strength can be formed, and into these loops the intestine may pass, so as to form an internal hernia of a very dangerous character. In some bands are formed across the intestine, which by contraction flatten the tube and obstruct the fecal movement. There is reason to believe that such bands and bridles are formed by local inflammation of such imperfect manifestation by symptoms that the patient knows nothing about it. A very striking case illustrating the possible sequence of this inflammation came under my observation early in my professional life: A colored woman about twenty-five years of age gave a very clear history of a peritonitis from the consequences of which she had suffered two years before I saw her. About six months after recovery she began to have constipation and to suffer from small and frequent discharges of urine. The latter gradually grew milky and to have a bad odor; the constipation grew more and more, and at length came to be absolute for many days; then would come a diarrhoea of some hours' continuance, after which she would have a feeling of relief. This was her state when I saw her. She was emaciated, and so feeble as hardly able to leave her bed. She vomited occasionally, and her appetite for food was all gone. The urine was heavily loaded with pus, and was ammoniacal. She died after a few weeks. At post-mortem examination a firm membrane was found strained across the upper strait of the pelvis, wholly separating the abdominal cavity from the pelvic. It looked like a drum-head. The left posterior border was drawn very tensely over the colon where it passed into the pelvic cavity, flattening it down completely and making stricture. To the under or lower surface the fundus of the uterus and the base of the bladder were firmly adherent, and in this way both were suspended. The effect of this unnatural suspension of the inactive uterus did not seem to be noticeable, but with the bladder it was very different: it contained three to four ounces of water, ammoniacal and full of pus, and it could never have emptied itself. The explanation is very simple. During the peritonitis a false membrane was effused on the pelvic viscera in situ. When the period of contraction which is common to all such structures came, the new membrane was separated from the greater part of these two organs, but not from their bases. The firm attachment to the brim of the pelvis did the rest. So unusual a sequel of peritonitis I think deserves a record. I should add there were no adhesions above the pelvis. Such a structure as this, found long after the active symptoms of peritonitis have passed, as also the bands and cords before spoken of, does not give support to the doctrine that the false membranes are broken down into fatty matter, and in this condition absorbed.

{1154} The possible remote effects of peritonitis are shown in a case reported by E. A. Mearns to the _Medical Record_, published Sept. 15, 1883: A young man, aged nineteen, four years after he had had acute general peritonitis was attacked with constipation, which was absolute. He had had before occasional attacks of pain in the bowels and constipation, which were overcome. But this was invincible. He had the train of symptoms usual in intestinal obstruction. There was no fever or tympanitis, and this time but little pain. He lived eight days. There was a tangle and a constriction of the intestines at the middle of the ileum, caused by the contraction and hardening of the effusion of the old peritonitis, and the intestine was very much softened.

H. B. Sands reports in another number of the same journal: "The patient was a man about thirty who had suffered from acute obstruction for a week. No exact diagnosis was made. When the abdomen was opened the intestinal coils were found extremely adherent one to another in consequence of a former peritonitis. A careful search failed to discover the nature or seat of the obstruction. The abdominal wound was closed, and the patient died soon after."

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 {1155} 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 {1156} 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 {1157} 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 {1158} 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.[7]

[Footnote 7: _Med. Record_, Sept. 1, 1883.]

{1159} 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.

Local Peritonitis.

This may occur anywhere in the broad extent of the peritoneum, and will be more or less limited in different cases, or may be limited for a time, and then become general. It is either acute or chronic. The product of the diseased action may be serum or lymph or pus, or all of them. The cause of this local inflammation is sometimes very obvious, in other cases wholly unknown. The consequences vary all the way from harmlessness to death; the symptoms are as variable as the consequences, making the diagnosis easy in some cases, in others impossible. Some cases in which it was not difficult to recognize it have already been recorded--those caused by perityphlitis and perforation of the vermiform appendix, for example. In such cases the local pain, the swelling, the dulness or resonance on percussion, depending on whether the tumor is made by inflammatory exudation or gas, together with the general symptoms and the history, leave but little ground for doubt regarding the character of the disease. Perhaps one-half the local abscesses which form between the folds of the peritoneum are recognizable during life by the local, associated with the general, symptoms. When situated in the posterior and upper part of the abdominal cavity, the hand gives little, {1160} perhaps no, assistance, as in the most widely-known case of abscess that has been recorded in all time. While the physicians were giving to the country hopeful reports day by day, thousands of medical men shook their heads and spoke sadly of the prospects. The illustrious patient was losing rather than gaining strength and flesh, his appetite poor, his digestion poor--a strong man growing helpless--and, above all, a pulse that for months never fell below 100. With an adequate cause of abscess, whether there were chills or not, what else could it be? Thus, in peritoneal abscesses that cannot be felt the general symptoms are of great importance to the diagnosis. When abscesses tend to discharge their contents soon or late--sometimes into the intestine, sometimes into the bladder, sometimes externally: in such cases there is a fair chance. Sometimes they burst into the peritoneum: such cases are almost inevitably fatal; even opium will not cure them. The pus of these abscesses often has the fecal odor, which it acquires by the transmission of the intestinal gases through the intestinal walls. I was attending, with the late James R. Wood, a young lady in whom peritoneal abscess had been recognized. It was anterior to the intestines. In the consultation, while we were discussing the propriety of using the trocar, the mother became alarmed at the odor and appearance of the urine just passed, and summoned the doctors back to the chamber. The abscess had opened into the bladder. The urine contained pus which gave off the fecal odor strongly. This patient recovered. It should be added that these abscesses, as well as those of the convex surface of the liver and those that are post-peritoneal, sometimes pierce the diaphragm and produce empyema, or by previous adhesion of the lung to its upper surface find a way into a bronchial tube, and so the pus is expectorated.

The history of local fibrinous exudations is not as easily told as that of the purulent. We find from time to time, on the peritoneum, bands, patches, or cords of false membrane, which were produced in so quiet a way that we can get no information regarding the time when they were formed, and perhaps the subject of them was not aware that anything was wrong with the bowels till he began to have the symptoms of obstruction. These unnatural structures are formed in great variety. The omentum is found thickened and contracted. The mesentery and mesocolon are seen in a similar condition, causing wrinkling and shortening of the bowels. The spleen has on its surface patches or even plates, or one great plate, of firm fibrinous deposit, often cartilaginous in density, sometimes calcareous; and we can rarely fix the time of these occurrences by any symptoms. It is not always so with the liver. We are acquainted with a perihepatitis which is acute, attended by pain in the right side, a febrile movement, and, if the inflammation reaches the under surface of the organ, by jaundice, and have learned to combat this with cups and opiates, the latter in rather free but not heroic doses, and to expect recovery in a few days. This may leave the liver wholly or partly invested with a layer of false membrane which may have a sequel of importance. Then, again, we find the organ invested with a thick contractile membrane, but cannot learn that the symptoms of perihepatitis have ever occurred. The diseased action which produced this bad investment appears to be analogous to that which not only covers the organ with a thinner coat of similar new tissue, but inlays it everywhere with the same material in cirrhosis. This also is {1161} unattended by local pain. The effects that may result from this encasing of the liver in a strong contractile capsule may be illustrated by the following case (the late Buck was the physician): The patient was an unmarried lady of middle age who had consecrated her life to charitable works. In searching for the suffering poor she often had to ascend several flights of stairs. The time came when she found this fatiguing and a tax on her respiration. She observed at the same time that the bowels were enlarged. She called Buck, and he had no difficulty in discovering ascitic fluid. He was surprised, as he knew that her habits were perfectly good, and she had very little the appearance of an invalid. Notwithstanding the proper use of the usual remedies for dropsy, the fluid slowly increased, and at length he was obliged to draw it off. He found it to be a clear, yellowish serum. In the course of about two years she was tapped four times. I saw her, with Buck, after these tappings, when the fluid had again been effused in quantity that half filled the peritoneal cavity. The emaciation was not considerable; there was nothing of the semi-bronzed color of the skin so common in cirrhosis of similar duration; her appetite and digestion were not materially impaired; the temperature was natural; the pulse was increased in frequency only a few beats. The skin over the abdomen was in a soft, natural state, and there was nothing that suggested a hyperæmic or inflammatory dropsy. The liver on percussion appeared to be reduced in size. Taking all things into account, and especially the patient's habits and the absence cancerous cachexia, it seemed probable that the dropsy arose from atrophy of the liver, and that the atrophy was caused by an adventitious capsule of the organ, although the patient had never had symptoms of perihepatitis. From this point the fluid did not increase or diminish, but remained stationary till she died, perhaps two years after, of some other disease. Meanwhile, the lady resumed her favorite charity-work to a limited extent. At the post-mortem examination the capsule was found investing nearly the whole liver, but not materially obstructing the gall-duct. The new membrane was thick and strong, having a thickness of at least one-twentieth of an inch. The remaining liver structure was of natural appearance. The organ was reduced to one-half its natural size. No other cause of dropsy was found.

Chronic Peritonitis.

I have doubted whether any disease deserving this name really exists independent of such low inflammatory action as may arise from the irritations of tumors or heterologous deposits. This statement refers to general not local peritonitis. I have never seen anything that would lead me to believe that acute diffuse peritonitis can be deprived of its acute character and still continue an inflammation. With me it has always been death or cure. I have already referred to a case in which after recovery the bowels were greatly disturbed by tympanitis for years. But this came from adhesions: her general health was good. I have at long intervals met with cases of ascites in which the peritoneal membrane was redder than natural, and in which no obstruction to the portal {1162} circulation was discovered. This, however, I have regarded as hyperæmia rather than inflammation.

Bauer,[8] however, gives to these cases the title latent general peritonitis, especially when after death an abnormal adhesion is found here and there. In the cases that I have seen there was a peculiar state of the surface of the abdomen. The skin there was more or less scaly and dry, but I do not remember whether there were internal adhesions. Bauer regards the diagnosis of this form of disease as difficult, but refers to the constantly present meteorism as well as serous fluid. I have met with three or four instances in which at the time of puberty an abdominal dropsy has rather suddenly occurred, lasting one to three months, and disappearing on the use of diuretics. I have had no reason to attribute this effusion to inflammatory action, except in one case. A lady of extraordinary symmetry and beauty of form, in excellent health, whom I had treated for this disorder twelve years before, applied to know whether there was anything in that disease that would prevent her having children. She had been married seven or eight years, and had not been pregnant. The question then occurred to me, At the time of the dropsy could there have been lymphy exudation that has since confined the ovaries in an unnatural position? The question I could not answer. The treatment which Bauer prefers for his latent peritonitis consists in "painting with iodine, the use of diuretics, and the regulation of diaphoresis by means of Turkish baths."

[Footnote 8: _Cyclopædia of the Practice, etc._, vol. viii. pp. 297-302.]

Another form of general chronic peritonitis is, according to Bauer, that which follows acute peritonitis. He quotes several authorities in support of his views. I must draw on him for a description of it, for, as I have said, practically I know nothing about it.

The symptoms of acute peritonitis are all toned down, but do not all disappear. Vomiting occurs occasionally; tenderness is diminished, but is quite perceptible; meteorism diminishes, but fluctuates greatly; appetite is poor or variable; constipation alternates with diarrhoea or is followed by dysentery; now there is a febrile heat, and then the temperature is normal--this fever is most likely to come in the evening; the pulse is frequent and varying; ultimately extreme emaciation and anæmia. The most striking feature of this condition appears to be sacculation of the fluid in the abdomen, wholly or partially; this fluid then is not freely movable, but will give dulness on percussion, which may contrast well with intestinal resonance in its immediate neighborhood. When the tension of the abdominal wall is diminished these sacs can be felt by the hand as uneven tumors. Colicky pains occur, and in a case cited it was at one time very severe, at another only slight. The majority of the cases terminate, after a protracted course, fatally. Recovery may occur by absorption or external evacuation of the fluid. He gives no special treatment.

Bauer makes still another class of cases of chronic peritonitis--those arising in the course of old ascites; he, however, does not make much out of it. He thinks the cases of this kind occur with cardiac and hepatic disease, and particularly with the nutmeg liver. The symptoms, he admits, are neither well defined nor severe, and the anatomical changes consist "in thickening of the serous membrane by a slight deposit of fibrin, {1163} slight turbidity of the ascitic fluid, and a few flakes of fibrin suspended in it." He then, strangely, gives, as if they were illustrations of such a disease, two cases in which death by acute peritonitis followed the last of many tappings, in one of which a pool of pus was found encysted in front of the intestines. Both are borrowed.

Probably most practitioners who are in the habit of making post-mortem examinations have seen the flakes of lymph in the ascitic fluid, etc., but the German physicians have been the first, I believe, to regard such cases as belonging to separate forms of disease.

William Pepper has published[9] a case observed by himself and G. A. Rex which shows non-malignant chronic peritonitis better than any I can recall to mind. The report forms the sequel to the case of the young woman on whom he successfully performed paracentesis of the pericardium.

[Footnote 9: _Am. Journ. of Med. Sci._, April, 1874.]

This young woman began to have double pleuritic effusion, and this was soon followed by ascites three and a half months after the operation. From that time the ascites was better or worse, but did not wholly leave her, and became considerable before her death. This was sudden, she having some convulsive movements in extremis. Lesions were found in the thoracic cavity like those discovered in the abdominal, showing, it was believed, a special tendency in this person to plastic exudation on the serous membranes. "The lower part of the abdomen was found occupied by an extensive effusion. The intestines were floated upward. There were few if any signs of inflammation of the intestinal peritoneum, but marked changes were observed in the parietal peritoneum and in the capsules of the liver and spleen. The peritonitis was most marked in the upper segment of the abdomen, while the parietal membrane presented large patches of irregular thickening. No tubercles were found on any part of the peritoneum. The capsules of the liver and spleen were greatly thickened, whitish, opaque, and densely fibrous. The liver was enlarged and heavy, and so tightly bound by its thickened capsule that its shape was somewhat altered.

"The diaphragm, especially that part of it underlying the pericardial sacs, had undergone marked fibroid degeneration. The muscular tissue was much atrophied; many fasciculi had evidently disappeared, while many others were markedly narrowed, some of them shading off to a width of less than 1/3000 of an inch, and finally disappearing altogether. They retained, however, even in their narrowest dimensions, their transverse striæ."

(It may be remarked, in passing, that this substitution of fibrous for muscular tissue follows the same law that it does in the heart when that organ is the seat of fibrosis or fibrous degeneration. Here it was supposed to be the consequence of a low grade of inflammatory action. Is it when it occurs in the heart?)

In the abdomen these observers found nothing which suggested the possibility of tubercles or any obscure form of cancer. In the pericardium, on the heart side, were found numerous small nodular roughnesses. Irregularities of the pericardial false membrane are so common that nothing but the close and universal adhesions would raise any question of these relations. But tubercles would hardly be here and nowhere else.

{1164} Delafield says that one form of the chronic disease is the continuance of his cellular peritonitis. In this, he says, the surface of the omentum is covered with cells which look as if they were derived from the endothelium and connective-tissue cells, although they differ from the normal shape of these. The new cells are for the most part polygonal, of different size, with one or several nuclei, and giant-cells--large granular masses filled with nuclei. Although these new cells are produced over the entire surface of the peritoneum, yet, as a rule, they are more numerous in little patches here and there. These little patches may be heaped together in such numbers as to form nodules visible to the naked eye. There is never any stroma between these cells.

This form of peritonitis occurs most frequently with organic heart disease, with cirrhosis of the liver, with chronic pulmonary phthisis, and with acute general tuberculosis. In the two latter diseases he thinks they have been improperly called tubercles.

He describes a form of chronic adhesion of peritoneal surfaces that occurs without the intervention of fibrin, but, as he supposes, by coalescence of the branching cells and a production from them of a fibrillated basement substance, the fibrils crossing in all directions. In the midst of these fibrils he finds the nuclei of these cells. He finds also in the immediate neighborhood of these adhesions thousands of branching cells that are attached one to another and float free in the water, the fixed end being attached to the peritoneum. He regards such a peritonitis with adhesions as a more advanced stage of the forms of cellular peritonitis already described, and the new cells are changed into membrane.

Sayre has published an extraordinary case in the _Transactions of the Pathological Society_. He calls it chronic proliferative peritonitis; it might be called more aptly the consequence of peritonitis.

A large, strong man fell from a hammock, the rope breaking, upon his shoulders, and felt a severe pain in his stomach, and soon developed symptoms of peritonitis. This pain never entirely subsided. The peritonitis was recognized. About one month after he was tapped, and 240 ounces of serum were drawn. He was tapped one hundred and eighty-seven times, and 1203-5/16 pounds of fluid were taken from him during the remainder of his life. At post-mortem examination 3000 cc. of yellow serum were found. The liver and spleen were covered by a thick layer of false membrane, intestines were glued together in the upper part of the abdomen, and the stomach was adherent to the lower surface of the liver. The portal vein was contracted by this membranous coating. There were numerous other lesions in the heart and pleura, but these will account for the dropsy.

This man was unusually strong and hearty until 1876, when he had an attack of double pleuro-pneumonia, and in 1878 he slipped on the front steps and fell, but seemed to recover from the effects of this. The fall from the swing occurred in July, 1879. He died in February, 1884.[10]

[Footnote 10: _Med. Record_, April 19, 1884.]

{1165} Tubercular Peritonitis.

This form of disease is by no means uniform in its first symptoms or in its progress. The only things uniformly attending it are tubercles on the peritoneum and more or less of inflammatory effusion, chiefly lymph and serum; tumor and hardness of the bowels, general or local; deranged function of the stomach and intestines; emaciation; and extreme fatality.

In some cases the invasion is acute and marked--a chill followed by fever, vomiting, early development of meteorism, and in a few days a point or points of resistance to pressure, but not necessarily dulness on percussion. In a few days the febrile action and the meteorism may subside, leaving the symptoms of local peritonitis. But we have not long to wait for a renewal of them and an evident extension of the inflammatory action. Remission and relapse alternate at varying intervals, until the whole extent of the peritoneal surface seems to be involved in inflammation. With this mode of development meteorism may not be renewed in the most common way. The lymphy product of inflammation may so bind the intestines to the posterior walls of the abdomen that they cannot extend forward, but are pushed upward against the liver and diaphragm, and so encroach on the thoracic space. But then the anterior parietes are tense and hard, and do not move in respiration. The febrile heat may not continue more than two or three months, but the pulse will be frequent to the end. There will be a thinning of bowel walls, and here and there a knuckle of adherent intestines may cause some prominence and give some resonance on percussion. There will be also occasional vomiting, and the dejections will be irregular--maybe only deficient or thin; there may be an alternation of constipation and diarrhoea.

Tuberculous ulcerations of the mucous layer of the bowels is not uncommon in tubercular peritonitis, and these ulcers have in rare cases perforated and allowed the fecal matter to accumulate in considerable quantity in a sac limited by previous adhesions. In all forms of tubercular peritonitis death is caused as often by grave complications as by what appears to be the primary disease. The affection occurs in probably every instance in those who had at the beginning, or had acquired in its progress, what we call the tubercular diathesis. We are not surprised, therefore, to find on inspection a wide diffusion of tubercles in the body, particularly on other serous membranes, and in the lungs. Death may occur, then, from phthisis pulmonalis or from pleurisy or meningitis, as well as from the exhaustion and accidents of the peritoneal disease. The effusion serum or turbid serum is very common in tubercular peritonitis, and can be recognized by the dulness it produces in part of the cavity, and sometimes by fluctuation. It is often sacculated, but it is not constantly found after death, it having been absorbed before, and perhaps long before, that event.