second a pulsating tumor may suddenly appear in the epigastrium, and
the ordinary indications of hemorrhage--vomiting, fainting fits, cold
extremities, feeble pulse, and general exhaustion--are present. Death
may occur suddenly or the patient may linger on for months. In the
third condition death usually occurs very suddenly, probably from
pressure upon the sympathetic ganglia. There are no symptoms, and the
rapid termination prevents the development of general peritonitis,
which would otherwise occur from the sloughing of the peritoneum.
There are no indications for treatment.
OBSTRUCTION OF THE PANCREATIC DUCT.
Obstruction of the excretory duct is a frequent occurrence in
pancreatic disease, and is due to two classes of causes--namely, 1st,
pressure from without; and, 2d, closure of the canal by catarrhal
swelling of its mucous membrane or by calculi.
In the first class may be placed obstruction depending upon contraction
occurring in sclerosis of the gland, upon carcinoma of the head of the
gland, upon peripancreatic adhesions and indurations, upon the {1130}
presence of large gall-stones in the ductus choledochus, and upon
carcinoma of the pylorus and duodenum and enlargement of the
neighboring lymphatic glands.
In catarrh of the canal of Wirsung the obstruction results either from
simple swelling of the mucous membrane or from the presence of a plug
of tough mucus.
The formation of pancreatic concretions is by no means a rare event,
though these calculi are met with far less frequently than either
gall-stones or salivary concretions. They result from precipitation of
the inorganic ingredients of the pancreatic juice, and are usually
seated in the main duct, although they may be situated in the smaller
branches. They may be single or multiple, as many as twenty having been
counted in one gland. In shape they are spherical, oval, or branched,
with sometimes a smooth, at others a spiculated, surface; their size
varies from that of a minute granule to a small walnut; they are
usually white or grayish-white in color, but may be black; and are
composed of the carbonate of lime or of a combination of the carbonate
and phosphate with oxalate of lime. Coincidently with these calculi it
is common to find concretions in the kidneys and gall-bladder.
Concretions composed of insoluble protein substances have also been
found in the pancreatic ducts (Virchow).
The most probable causes of the formation of pancreatic calculi seem to
be catarrhal conditions of the mucous membrane of the ducts and an
alteration in the chemical composition of the secretion.
Whatever the cause, the obstruction, when complete, leads to retention
of the secretion and the formation of retention cysts.
When the obstruction is situated at the duodenal extremity of the duct,
the canal and its secondary branches are either uniformly dilated or
sacculi are formed. These sacculi are round or oval, vary greatly in
size, sometimes reaching the dimensions of the fist or of a child's
head; they may be single, or several of them may be present, differing
in size and causing irregular projections of the outer surface of the
gland. When the obstruction occurs at some point in the course of the
duct, the dilatations and sacculi are found only behind the point of
occlusion. The small cysts contain a fluid resembling the pancreatic
juice; the larger, a whitish, chalky fluid, which in old cases may
contain white friable concretions composed of carbonate and phosphate
of lime, and become purulent, or be stained bright red or
chocolate-colored from the occurrence of hemorrhage. In such instances
hæmatoidin crystals can be discovered by the microscope. The interior
of the dilated ducts and of the retention cysts is lined by a single
layer of thin flat cells, with irregular edges and with oval flat
nuclei. The walls are thickened, and composed of superimposed layers of
laminated connective tissue separated from one another by flat
nucleated cells. The secreting structure of the gland undergoes atrophy
from pressure, or fatty metamorphosis takes place, and, although the
gland is increased in size from the presence of the cysts, its
functional power is lost.
In addition to causing obstruction of the duct of Wirsung and the
changes mentioned, pancreatic calculi may produce induration, atrophy,
acute inflammation, or even suppuration of the surrounding glandular
tissue.
{1131} SYMPTOMS AND COURSE.--The main feature is the presence in the
epigastrium of a rounded, smooth, fluctuating, painless tumor. There
are also indications of the absence of the pancreatic secretion from
the digestive tract--notably, emaciation, general debility, and the
appearance of fat in the stools. Jaundice resulting from a coincident
obstruction of the bile-duct is a frequent symptom, and melituria has
been noted in some cases. It is probable, too, that the passage of a
calculus along the duct may give rise to pain resembling in character
and distribution the pain of hepatic colic.
The duration is indefinite. Sometimes the termination is sudden from
the rupture of a cyst into the peritoneal cavity or into the stomach or
duodenum, with hemorrhage.
DIAGNOSIS.--The absence of pain, of tenderness, and of cachexia,
together with the physical characters of the tumor, distinguishes it
from carcinoma of the gland.
Though not likely to be confounded with this disease, both hydatid
tumor of the liver and distension of the gall-bladder must be borne in
mind in making the diagnosis of a fluctuating tumor situated in the
upper third of the abdomen.
TREATMENT must be entirely symptomatic. Attention to the general
health, proper regulation of the diet, and the employment of pancreatin
or an infusion of calf's pancreas to supply the place of the deficient
pancreatic juice, are the important steps. Attacks of pancreatic colic
indicate the use of anodynes.
In two reported cases in which the cysts were very large paracentesis
for the removal of the fluid contents was resorted to, and there are
two cases on record in which the cysts were extirpated after abdominal
section. Kulenhampff of Bremen records a case of a man, thirty-nine
years of age, in whom, after a succession of severe blows upon the
abdomen, a tumor appeared in the epigastrium. An exploratory incision
was made, and a few ounces of pancreatic fluid evacuated by aspiration.
Six days afterward the abdomen was opened, the peritoneum united to the
incision, and antiseptic gauze inserted to produce adhesive
inflammation between the sac and the abdominal wall. Adhesion taking
place after four days, the cyst was opened, a liter of fluid evacuated,
a tent inserted, and an antiseptic dressing applied. For sixteen days
fluid constantly escaped in slowly diminishing quantities, and the
tumor disappeared, a fistulous tract remaining. This completely closed
under the use of tincture of iodine and nitrate of silver at the end of
the seventh week. Thiersch opened a pancreatic cyst and evacuated three
liters of chocolate-colored fluid; recovery with a fistula followed.
From a patient supposed to be suffering from ovarian dropsy Rokitansky
partially extirpated a cyst connected with the tail of the pancreas;
death from suppurative peritonitis occurred on the tenth day.
N. Bozeman[4] on December 2, 1880, successfully removed from a woman
forty-one years old a pancreatic cyst weighing, with its contents,
twenty and a half pounds. In this instance also the operation was
undertaken for the removal of a supposed ovarian tumor, the diagnosis
not being established until after the abdomen was opened.
[Footnote 4: _New York Medical Record_, Jan. 14, 1882.]
{1132}
PERITONITIS.
BY ALONZO CLARK, M.D., LL.D.
Italian physicians in the later years of the seventeenth century and in
the early ones of the eighteenth had acquired some knowledge of the
symptoms of the disease we now call peritonitis, but known to them as
inflammation of the intestines. Indeed, it is claimed by some of the
admirers of Hippocrates that there are passages in his writings that
indicate some knowledge of the disease. But this claim will probably be
always received with many doubts as to its validity.
In confirmation of the first statement I will transcribe certain
passages from Morgagni's thirty-fifth letter: In inflammation of the
intestines "Albertini had observed the pulse to be low and rather weak,
such as you will find it to have been in general in the foregoing
letter under Nos. 9, 11, 18, and 25." He also observed the abdomen to
be tense and hard, the face and eyes to have something unusual in their
appearance. "Medical writers, indeed, agree in the tension of the
abdomen, but they add many other symptoms, which prove beyond a doubt
the intestines to be inflamed; yet they mean that evident inflammation
which all may easily ascertain, and not that obscure disorder which we
now speak of, and which few suspect" (gangrene of the intestines). "By
the same writers it is also supposed that there is an obstinate
costiveness and continual vomiting."
Morgagni refers to the assistance rendered by Albertini, Valsala, Van
Swieten, Rosa, and others in elucidating this subject. It is singular,
considering the clearness of his perception of the symptoms of
inflammation of the intestines, that he should be so greatly confused
regarding gangrene and sphacelus of the same parts. He looks on these
as the result of inflammation, and when the two classes of cases are
considered and compared, the result is a contrast and not a
resemblance. Yet he supposes that the differences are to be accounted
for by the different modes in which the same disease may be developed
in different persons.
Another thing obtrudes itself on the attention in these letters: that
while a number of post-mortem examinations are reported of those who
had died of inflammation of the intestines, of gangrene and sphacelus
of the intestines, of hepatic abscess opening into the peritoneal
cavity, there is no record of finding in the abdomen anything
corresponding to what is now known as the inflammatory effusions from
serous membranes.
Sydenham died in 1689. I have searched his works, not for {1133}
peritonitis, for the word was not in use in his day, but for some
account of inflammation of the intestines or of some disease in the
description of which symptoms are named that distinguish or belong to
peritonitis, and with the single exception of pain the search has been
fruitless.
Cullen in 1775 mentions the disease, but says that so little is known
about it that he will not attempt a description of it.
Bichat died in 1802 in the thirty-eighth year of his age. I am not able
at present to lay my hand on his _Pathological Anatomy_; I therefore
quote from Chomel's article on peritonitis in the _Dictionnaire de
Médecine_ to show his claim to important studies regarding that
disease: "For a long time peritonitis was confounded under the name of
inflammation du bas ventre with inflammations of the abdominal viscera;
and it is to Bichat belongs the merit of having proved that
inflammation of the peritoneum is a disease distinct, and that it ought
to be separated from enteritis, gastritis, etc., as pleurisy is
separate from pneumonia. The studies of Gasc and of Laennec soon
confirmed the opinion of Bichat, and assured to peritonitis the
important place which it ought to occupy in all nosological tables. It
has become since then a subject of numerous observations and of
interesting researches regarding the causes de sa marche and the
lesions it causes."
The references are not given by Chomel, but they are probably these:
Laennec, _Histoire des Inflammations du Peritoine_, 1804; and Gasc,
_Dictionnaire des Sciences Méd._, p. 490, 1809.
Gasc says that the twenty years next preceding his publication
witnessed the first stage of the true history of peritonitis. Walther
in 1786 had contributed some facts, and S. G. Vogel in 1795, but the
rounding off and completing their work was left for Bichat.
Acute Diffuse Peritonitis.
MORBID ANATOMY.--The first thing that strikes the observer in the
post-mortem examination of a person who has died of this disease is the
tendency of the intestines to protrude through the cut made in the
abdominal wall. This is produced by their dilatation generally, both
small and large, by gas. No gas, under these circumstances, ever
escapes from the peritoneal cavity unless there has been perforation of
the alimentary canal somewhere. While the intestines are in this manner
dilated, the stomach is small and usually empty.
On the surface of the intestines there will be found a layer of
coagulated fibrin, often very thin and delicate, requiring a scraping
of the surface of the peritoneum to demonstrate it, but commonly
obvious enough, and sometimes quite abundant. This same false membrane
can be found on the viscera covered by the peritoneal membrane, on its
anterior extension, and most at the point of contact of one coil of the
intestine with another. Incorporated with this new membrane or lying
under it will often be seen blood-spots, thin, translucent, diffused,
and having ill-defined boundaries.
The blood-vessels themselves are not remarkably congested. Here and
there may be spots where some redness remains, and the vessels are
larger than natural. But the congestion and redness, which analogy
leads us to {1134} believe belong to the active stages of the disease,
have in great degree disappeared after death.
The peritoneal membrane itself has hardly become thickened, certainly
not in marked degree, but it has lost its lustrous surface, is, at
least in parts, of an opaline color, as if it had absorbed diluted
milk, and there is an effusion of serum or slight oedema on its
attached surface. Whatever may be the popular opinion regarding the
termination of inflammation of the bowels in mortification, whatever
the opinion of the older physicians, it is safe to say that gangrene of
the peritoneum has never been the result of uncomplicated, diffuse,
acute peritonitis. Peritonitis from strangulation of the intestine or
analogous causes is of course excepted. But in puerperal peritonitis I
have noticed a fact to which I have nowhere seen an allusion. The
parietal peritoneum is at two points in the abdomen but loosely
attached to the wall. One of these is on the anterior wall, anterior to
and a little above the iliac fossa; the other is above and below the
kidney on each side of the body. In these parts I have seen the
membrane forced off from its attachment to the walls, which with it
made a sac containing pus. Such an abscess, if the patient live long
enough, would doubtless cause the death of the membrane.
There is in almost every case of peritonitis more or less of serous
effusion, commonly not seen at first on opening the abdomen, for it has
sunk into the pelvis. It is transparent, of a yellowish hue, and
sometimes flocculi of lymph are found in it.
Whether the inflammation of the peritoneum extends to organs covered by
it is a question that has been much discussed; but it is admitted that
these organs, to a shallow depth on their surface, have an unnatural
color; and when it is remembered that the peritoneum is nourished by
vessels not exclusively its own, but running along its attached
surface, and distributed as well to the surface of the organs it
covers, it is easy to admit that to a very limited depth the organs
partake of the inflammatory disease. This supposition gives an easy
explanation of the constipation which is so prominent a feature among
the symptoms of the disease.
The manner in which the false membrane is disposed of in those who
recover is an interesting question. Forty or more years ago Vogel
described the process by which the new effusion became a living tissue,
and the manner in which blood-corpuscles and blood-vessels were formed
in it; and another author had found that the time needed to complete
this vascularization was twenty days. But now Bauer and most of the
German writers inform us that the coagulated fibrin is converted into
fatty matter and is absorbed, and that when adhesions occur they result
from the coalescence of a new formation of the connective-tissue
elements built up into granules. The question, then, arises, Will the
chemical constitution of fibrin permit its conversion into oil? If it
will, then the further question presents itself, By what chemical
action is the change effected within the body? I do not intend to
discuss these questions, but propose them by way of expressing some
doubt regarding the accuracy of this statement.
I have always supposed that the epithelial layer of the peritoneum was
pushed off by the first of the effusions in peritonitis, and that this
was one of the causes of the lustreless appearance of the membrane.
This {1135} opinion I have never attempted to confirm or correct by the
microscope. Bauer confounds this idea. He says: "The deposition of
fibrin occurs before the endothelium presents any changes. This
fibrinous effusion encloses, primarily, hardly any cellular elements,
and only a few cast-off endothelial cells are to be found in it. The
endothelium itself is swollen and turbid; the cell-body is increased in
size; the contents are granular; multiplication of the nuclei is
apparent; the cells are, in fact, in active division. In the tissue of
the serous membrane itself, soon after the deposition on its surface,
an accumulation of indifferent (?) cells takes place, especially around
the vessels, so that the spaces between the vessels are thus completely
filled up. The fixed connective-tissue corpuscles take part in the
inflammatory process."
Delafield says: "If the autopsy is made within a few hours after death,
we find the entire peritoneum of a bright-red color from congestion of
the blood-vessels; but that is all: there is no fibrin, no serum, no
pus; epithelial cells are increased in size and number." For this kind
of peritonitis he proposes the term cellular. He finds it in cases of
local abscess of the abdominal cavity in which inflammatory action has
extended over the whole membrane, and particularly on the omentum also,
in the first two days of puerperal peritonitis. "The ordinary form of
acute peritonitis is attended with changes in the endothelium and fixed
connective tissue, and with the production of serum, fibrin, and pus."
He describes the migration of white corpuscles of the blood through the
walls of capillaries to become pus-cells, and then says: "Minute
examination shows that two distinct sets of changes are going on at the
same time: first, a production of fibrin, serum, and pus; second,
swelling and multiplication of the endothelial cells. If the
inflammation is very intense, the pus and fibrin are most abundant; if
milder, the changes in the endothelium are more marked."
I have said above that the epithelium is early washed off by the
inflammatory effusions. In opposition--or, perhaps better, in
correction--of this idea, Delafield says: "There may be a considerable
amount of pus produced, and yet the layer of endothelium remains in
place." "If, however, the pus and fibrin are produced in large amounts,
the endothelium falls off and leaves the surface of the peritoneum
bare." The connective-tissue cells of peritoneum, he says, undergo but
little change in the first three days of the inflammation, "but by the
seventh day these cells are marked by increase in size and number in
all parts of the peritoneum."
Two or three times in my life I have met with a peculiar arrangement of
the false membrane and serum of peritoneal inflammation, of which I do
not remember to have seen a description. It is this: the serum is
enclosed or encysted in bladders, the walls of which are the false
membrane. There may be two or three layers of these bladders, one upon
another, all more or less flattened, and each holding from two to six
ounces of fluid. It would seem that in these cases the inflammatory
activity rose and fell in its progress, early reaching the point at
which coagulable lymph was effused, then falling to the stage in which
serum alone escaped. This serum lifted the false membrane irregularly,
so that several pools were formed. After this the inflammation returns
to the fibrous exudation stage, and gives to these bladders a floor
which blends with the {1136} roof at the edges, and thus makes a
complete sac. Once more the inflammatory action is changed in its
intensity, so that the only effusion is serum; and this serum again
raises the new layer of false membrane into bladders--not always or
generally in the exact position of the first series. Still again, the
inflammation may be so changed as to make a fibrinous flow to this
second series of bladders. I am not certain that I have seen a third
series of these rare productions. They have doubtless been seen by
other persons, and may have been described. I have not been an
exhaustive reader on the subject, but I can well understand how they
may have been called hydatids on examination of the sacs without
looking at the contents. The fluid in the cysts is simply serum, with
no echinococcus sacs, and then the number of these inflammatory sacs
greatly exceeds the probable number of the fibrous sacs of hydatids.
Pus in large quantity is not often a product of simple acute diffusive
peritonitis, although it is frequently found in that form of the
disease that attends puerperal fever, septicæmia, or erysipelas. Yet I
have seen it a few times. The pus is not generally pure, but is mixed
with serum in different proportions, and there will be seen at the same
time deposits of lymph attached to the peritoneum or scales of it
floating in the fluid effusion, or both. There is reason to believe
that in the cases of this class a very large proportion are fatal in
the acute stages, but in the cases that live for a few weeks the pus is
disposed to collect in pools and become abscesses by adhesions around
them at their borders. These abscesses are disposed to find an exit
from the body. In one case four abscesses that were found in this way
in different parts of the abdominal cavity had each burrowed toward the
umbilicus, and were actually discharging their contents at this point
when I saw the case. In another case one abscess only was formed, and
in four weeks it had perforated the colon. The opening was nearly an
inch in diameter.
Kalantarians says, in eight examinations of the solar and hypogastric
plexus in persons who had died of acute peritonitis changes which he
regards as inflammatory had occurred, with subsequent opaque swelling
of the nerve-cells, ultimate fatty degeneration, brown pigmentation,
and atrophy. In chronic peritonitis the cells are often converted into
amorphous pigment matter, with increase and sclerosis of the ganglionic
connective tissue. Still, it is worthy of notice that these changes do
not express themselves in symptoms in those that recover.
ETIOLOGY.--Numerous writers have expressed a doubt whether a
spontaneous acute peritonitis ever occurs, or if it is ever primary its
occurrence in this way is very rare. Habershon[1] has presented the
case with more apparent force than any other writer. He studied the
record of five hundred autopsies of peritonitis made at Guy's Hospital
during twenty-five years, but he "cannot find a single case thoroughly
detailed where the disease could be correctly regarded as existing
solely in the peritoneal serous membrane."
[Footnote 1: _Medico-Chirurgical Trans._, vol. xliii. p. 5.]