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.

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