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.