stomach is the appearance of the edges and of the floor of the ulcer.
The edges of recently-formed ulcers (acute ulcers) are clean-cut,
smooth, and not swollen. To use Rokitansky's well-known comparison, the
hole in the mucous coat looks as if it had been punched out by an
instrument. The floor of the ulcer may be smooth and firm or soft and
pulpy. The floor and edges of fresh ulcers are often infiltrated with
blood, but they may be of a pale-grayish color. Usually no granulations
and no pus are to be seen on the surface of the ulcer.[70] In ulcers of
longer duration the margins become thickened, indurated, and abrupt;
the floor acquires a dense fibrous structure.
[Footnote 70: In rare instances granulations may be present, as in a
case of W. Müller's, in which their presence rendered difficult the
diagnosis of simple ulcer from carcinoma (_Jenaische Zeitschrift_, v.,
1870). The microscope may also be required to distinguish the
irregularly thickened margins of old ulcers from scirrhous cancer.]
The floor of the ulcer may be the submucous, the muscular, or the
serous coat, or, if the whole thickness of the stomach be perforated,
it may be some adjacent organ to which the stomach has become adherent,
this organ being usually the pancreas or the left lobe of the liver or
neighboring lymphatic glands.
The microscopic examination of recently-formed ulcers shows that the
tissue immediately surrounding the ulcer is composed of granular
material, disintegrated red blood-corpuscles, pale and swollen
fragments of connective-tissue fibres, and cells unaffected by
nuclear-staining dyes. The red blood-corpuscles are sometimes broken
into fragments of various sizes in about the same way as by the action
of heat. The gastric tubules are separated from each other and
compressed by infiltrated blood, and contain cells which do not stain.
Around this margin of molecular disintegration, which has evidently
been produced by the action of the gastric juice, there is often,
although not constantly, a zone of infiltration with small round cells,
probably emigrated white blood-corpuscles. These cells are most
abundant near the muscularis mucosæ and in the submucosa. Extravasated
red blood-corpuscles extend a variable distance around the ulcer,
farthest as a rule in the submucous coat. Many of the blood-vessels in
the immediate neighborhood of the ulcer appear normal; others,
particularly the arterioles and the capillaries, may be filled with
hyaline thrombi. Clumps of hyaline material may also be seen in the
meshes of the tissue around the ulcer. Fine fatty granules may be seen
in the tissue near the ulcer. The interstices of the loose submucous
tissue and the lymphatic vessels are often filled with fibrillated
fibrin and scattered blood-corpuscles for a considerable distance
around the ulcer.
In the margins of old gastric ulcers there is also a zone of molecular
necrosis. The induration and the thickening of the edges of these
ulcers {506} are caused by a new growth of fibrillated connective
tissue, which blends together all of the coats invaded by the ulcer.
This new tissue is usually rich in lymphoid cells, which are often most
abundant in the lymphatic channels. In the fibrous edges and base of
old ulcers are arteries which are the seat of an obliterating
endarteritis, and which may be completely obliterated by this process.
An interstitial neuritis may affect the nerve-trunks involved in the
fibrous growth. Blood-pigment may be present as an evidence of an old
hemorrhagic infiltration.[71]
[Footnote 71: The histological changes here described are based upon
the examination of typical specimens both of recent and of old gastric
ulcers which have come under my observation.]
Cicatrization is accomplished by the development of fibrous tissue in
the floor and borders of the ulcer. By the contraction of this
new-formed tissue the edges of the mucous membrane are united to the
floor of the ulcer, and may be drawn together so as to close completely
the defect in the mucous membrane. The result is a white stellate
cicatrix, which is usually somewhat depressed and surrounded by
puckered mucous membrane. It is probable that small, superficial ulcers
may be closed so that the scar cannot be detected. The mucous membrane
which has been drawn over the cicatrix is intimately blended with the
fibrous substratum, and is usually itself invaded by fibrous tissue
which compresses and distorts the gastric tubules. Hauser[72] has shown
that the tubular glands grow down into the cicatricial tissue, where
they may branch in all directions. These new-formed tubules are lined
by clear cylindrical or cutical epithelial cells, and may undergo
cystic dilatation. Very irregular cicatrices may result from the
healing of large and irregular ulcers. When the ulcer is large and deep
and the stomach is adherent to surrounding parts, the edges of the
mucous membrane making the border of the ulcer cannot be united by the
contraction of the fibrous tissue in the floor of the ulcer. The
cicatrix of such ulcers consists of fibrous tissue uncovered by mucous
membrane. The closure of the ulcer is incomplete. Such cicatrices are
liable to be the seat of renewed ulceration.
[Footnote 72: _Das chronische Magengeschwür, etc._, Leipzig, 1883. In
the rare instances of carcinoma developing in the borders or in the
cicatrix of gastric ulcer, Hauser believes that the cancerous growth
starts from these glandular growths, which in general have only the
significance of Friedländer's atypical proliferation of epithelial
cells.]
The formation and contraction of the cicatrix may cause various
deformities of the stomach. The character of these deformities depends
upon the situation, the size, and the depth of the ulcer which is
cicatrized. Among the most important of these distortions are stenosis
of the pyloric orifice, followed by dilatation of the stomach, more
rarely stenosis of the cardiac orifice, with contraction of the
stomach, approximation of the cardiac and of the pyloric orifices by
the healing of ulcers on the lesser curvature, and an hour-glass form
of the stomach, produced by the cicatrization of girdle ulcers or of a
series of ulcers extending around the stomach. These abnormalities in
form of the stomach, particularly the constriction of the orifices, may
be attended by more serious symptoms than the original ulcer.
As the ulcer extends in depth a circumscribed peritonitis, resulting in
the formation of adhesions between the stomach and surrounding parts,
is usually excited before the serous coat is perforated, so that the
gravest of all possible accidents in the course of gastric
ulcer--namely, perforation {507} into the peritoneal sac--is
permanently or temporarily averted. It has been estimated that
adhesions form in about two-fifths of all cases of gastric ulcer
(Jaksch). On account of the usual position of the ulcer on the lesser
curvature or on the posterior wall of the stomach, the adhesions are
most frequently with the pancreas (in about one-half of all cases of
adhesion); next in frequency with the left lobe of the liver; rarely
with other parts, such as the lymphatic glands, the diaphragm, the
spleen, the kidney, the suprarenal capsule, the omentum, the colon, and
other parts of the intestine, the gall-bladder, the sternum, and the
anterior abdominal wall. Adhesions cannot readily form between the
anterior surface of the stomach and the anterior abdominal wall, on
account of the constant movement of these parts, so that ulcers of the
anterior gastric wall are those most liable to perforate into the
peritoneal cavity.
It is difficult to include in any description all of the various and
complicated lesions which may result from perforation by gastric ulcer
of all of the coats of the stomach. The consequences of perforation may
be conveniently classified as follows:
1. Some solid organ, usually the pancreas, the liver, or the lymphatic
glands, may close the hole in the stomach.
2. An intra-peritoneal sac shut in by adhesions may communicate through
the ulcer with the cavity of the stomach.
3. A fistulous communication may form either between the stomach and
the exterior (external gastric fistula) or between the stomach and some
hollow viscus (internal gastric fistula).
4. The ulcer may perforate into the general peritoneal cavity.
These lesions may be variously combined with each other. It is to be
noted that in the first three varieties protective adhesions are
present, and that in the last these adhesions are either absent or
ruptured.
When the pancreas, the liver, or the spleen form the floor of the
ulcer, they may be protected from extension of the ulcerative process
by a new growth of fibrous tissue extending from the floor of the ulcer
a variable depth into these organs. Sometimes, however, the ulcerative
process, aided doubtless by the corroding action of the gastric juice,
eats out large excavations in these organs. These excavations
communicate with the cavity of the stomach, and are usually filled with
ichorous pus. The pancreas, unlike the spleen and the liver, possesses
comparative immunity against this invasion by the ulcerative process.
The situation, the form, and the extent of circumscribed peritoneal
abscesses resulting from perforation of gastric ulcer depend upon the
parts with which the stomach has contracted adhesions. Should an ulcer
on the posterior wall of the stomach perforate before the formation of
adhesions, the perforation would of course be directly into the lesser
peritoneal cavity. An interesting example of this rare occurrence has
been communicated by Chiari.[73] In this case, the foramen of Winslow
being closed by adhesions, the lesser peritoneal cavity which
communicated with a gastric ulcer was filled with ichorous pus, and in
this floated the pancreas, which had necrosed in mass and had separated
as a sequestrum. That form of intra-peritoneal abscess known as
subphrenic pneumo-pyothorax has been already described under
Symptomatology. Peritoneal abscesses communicating with the stomach may
open into various places, {508} as into the general peritoneal cavity,
into the pleural cavity, into the retro-peritoneal tissue, through the
abdominal or thoracic walls, etc.
[Footnote 73: _Wiener med. Wochenschr._, 1876, No. 13.]
Gastro-cutaneous fistulæ are a rare result of the perforation of
gastric ulcer.[74] The external opening is most frequently in the
umbilical region, but it may be in the epigastric or in the left
hypochondriac region or between the ribs. Fistulous communications
resulting from the perforation of gastric ulcer have been formed
between the stomach and one or more of the following hollow viscera or
cavities: the colon, the duodenum and other parts of the small
intestine, the gall-bladder, the common bile-duct, the pancreatic duct,
the pleura, the lung, the left bronchus, the pericardium, and the left
ventricle. Gastro-colic fistulæ, in contrast to gastro-cutaneous
fistulæ, are more frequently produced by cancer than by ulcer of the
stomach.[75] In rare instances the peritoneum over ulcers of the lesser
curvature has contracted adhesions with the pyloric portion of the
stomach or with the first part of the duodenum. To accomplish this it
is necessary that a sharp bend in the lesser curvature should take
place. By extension of the ulcerative process abnormal communication is
established between the left and the right half of the stomach or
between the stomach and the duodenum. In either case the right half of
the stomach is often converted into a large blind diverticulum, the
digested food passing through the abnormal opening.[76] Gastro-duodenal
fistulæ are more frequently with the third than with the first part of
the duodenum. In one of Starcke's cases the stomach communicated with
the colon and through the medium of a subphrenic abscess with the left
lung.[77]
[Footnote 74: Of the 25 cases of gastro-cutaneous fistula collected by
Murchison, 18 were the result of disease. In 12 of these cases the
probable cause was simple gastric ulcer (_Med.-Chir. Trans._, vol. xli.
p. 11, London, 1858). Middeldorpf says that among the internal causes
of the 47 cases of external gastric fistula which he tabulated, simple
ulcer of the stomach played an important rôle (_Wiener med.
Wochenschr._, 1860).]
[Footnote 75: Of 33 cases of gastro-colic fistula collected by
Murchison, 21 were from gastric cancer and 9 or 10 probably from simple
ulcer. On the other hand, gastro-cutaneous fistulæ are twice as
frequently the result of simple ulcer as of cancer (_Edinb. Med.
Journ._, vol. iii. 1857).]
[Footnote 76: Thierfelder has made the best study of the complicated
relations existing in these cases (_Deutsches Arch. f. klin. Med._, Bd.
iv. p. 33, 1868).]
[Footnote 77: _Deutsche Klinik_, 1870, No. 39. Habershon also reports a
case in which a subphrenic abscess communicated with the lung, the
stomach, and the colon, but he believes that the ulceration was primary
in the colon (_Guy's Hosp. Rep._, Ser. 3, vol. i. p. 109).]
Four cases of perforation of gastric ulcer into the pericardium,[78]
with the production of pneumo-pericardium, have been reported, and two
cases of perforation into the left ventricle.[79] Müller found
lumbricoid worms in a pleural cavity which had been perforated by
gastric ulcer.[80] Diaphragmatic hernia may result from perforation of
the pleural cavity by gastric ulcer.[81] In one instance the greater
part of the small intestines {509} passed through a hole in the
transverse meso-colon which had been caused by a gastric ulcer.
[Footnote 78: Hallin, _Schmidt's Jahrb._, cxix. S. 37; Säxinger,
_Prager med. Wochenschr._, 1865; Guttmann, _Berl. klin. Wochenschr._,
1880, No. 23. Murchison mentions a specimen in the museum of King's
College, London, of a simple gastric ulcer opening into the pericardium
(_Edinb. Med. Journ._, vol. iii. p. 6). In a case reported by Graves a
liver abscess burst into the stomach and into the pericardium (_Clin.
Lect._, ii. p. 237, Dublin, 1848).]
[Footnote 79: Oser, _Wiener med. Blätter_, 1880, No. 52; Brenner,
_Wiener med. Wochenschr._, 1881, No. 47.]
[Footnote 80: Müller, _Memorabilien_, xvii., Oct., 1872.]
[Footnote 81: Needon, _Wiener med. Presse_, 1869, No. 42. In a case of
Günsburg's the hole in the diaphragm was as large as the hand, and the
left pleural cavity contained the upper half of the stomach and the
spleen (_Arch. f. phys. Heilk._, xi. 3, 1852).]
The various fistulæ which have been mentioned may be either direct or
through the medium of an abscess. While some of them are only
pathological curiosities, others, particularly the communications of
the stomach with the pleural cavity and with the lung, are sufficiently
frequent to be of practical clinical interest.
As has already been explained, ulcers of the anterior wall are the ones
most liable to perforate into the general peritoneal cavity,[82] but on
account of their comparative infrequency perforation occurs oftener in
other situations, particularly in the lesser curvature and near the
pylorus. Except on the anterior wall the perforation is often brought
about by the rupture of adhesions which for a time had prevented this
accident. In a considerable number of cases, particularly of ulcers on
the anterior wall, the ulcer looks as if recently formed (acute
perforating ulcer); in other cases its thickened and indurated margins
indicate long duration. Chiari[83] describes a case in which rupture
into the peritoneal cavity took place through the cicatrix of an old
ulcer, probably in consequence of the distension of the stomach with
gas. The hole in the peritoneum is usually circular, smaller than the
inner surface of the ulcer, and has sharp, well-defined edges. Less
frequently the edges are ragged. Post-mortem digestion may, however, so
change the borders of the opening as to make it difficult or impossible
to tell from their post-mortem appearances alone whether perforation
has occurred before or after death. The peritoneal cavity after death
from perforation is found to contain gas and substances from the
stomach. Usually within a few hours after perforation septic
peritonitis is excited, but in exceptional cases no inflammation of the
peritoneum has occurred even when life has been prolonged twenty-four
hours after perforation.
[Footnote 82: According to Brinton, "the proportion of perforations to
ulcers is such that of every 100 ulcers in each of the following
situations, the numbers which perforate are--on the posterior surface,
about 2; the pyloric sac, 10; the middle of the organ, 13; the lesser
curvature, 18; the anterior and posterior surface at once, 28; the
cardiac extremity, 40; and the anterior surface, 85."]
[Footnote 83: _Wiener med. Blätter_, 1881, No. 3.]
Emphysema of the subcutaneous, subperitoneal, and other loose areolar
tissue of the body is a rare but remarkable result of the perforation
of gastric ulcer. The emphysema is sometimes observed shortly before
death, but it attains its maximum development after death, when it may
spread rapidly over the greater part of the body. The gas consists in
part of hydrogen, as it burns with a blue flame. It is generated, at
least in great part, by fermentation of the contents of the stomach.
The gas may enter the subserous tissue at the edges of the ulcer and
thence spread, or, after perforation of the stomach, it may make its
way from the peritoneal cavity into the loose subserous connective
tissue through some place in the parietal peritoneum which has been
macerated, perhaps by the digestive action of the gastric juice.[84]
[Footnote 84: Roger (_Arch. gén. de Méd._, 1862) and Demarquay (_Essai
de Pneumatologie médicale_, Paris, 1866) deserve the credit of first
calling general attention to the occurrence of subcutaneous emphysema
after rupture of the digestive tract. The following writers have each
reported a case of emphysema following the perforation of gastric
ulcers: Cruveilhier, _Anat. Path._, t. i. livr. xx.; Bell, _Edinb. Med.
Journ._, vol. vi. p. 783; Thierfelder, _Deutsches Arch. f. klin. Med._,
iv., 1868, p. 33; Newman, _The Lancet_, 1868, vol. ii. p. 728;
Poensgen, _Das subcutane Emphysem nach continuitätstrennungen des
Digestionstractus, etc._, Inaug. Diss., Strassburg, 1879, p. 40;
Korach, _Deutsche med. Wochenschr._, 1880 p. 275; {510} Jürgensen,
_Deutsches Arch. f. klin. Med._, Bd. 31, p. 441, 1882. Doubtful cases
are reported by Lefèvre, W. Mayer, and Burggraeve. The fullest
consideration of the subject is to be found in the dissertation of
Poensgen.]
In two cases of sudden death from gastric ulcer Jürgensen found gas in
the veins and arteries of various parts of the body. He believes that
this gas, which certainly was not the result of putrefaction after
death, was derived from the stomach, and that it entered during life
the circulation through vessels exposed in the borders of the ulcer,
thus causing death. In one of the cases a profuse hemorrhage preceded
death, and in the other the ulcer had perforated into the peritoneal
cavity.[85]
[Footnote 85: Jürgensen does not consider whether this gas may not have
made its way into the blood-vessels after death in a manner similar to
its extension through the cellular tissue of the body in the cases of
emphysema just mentioned. In the case which he has reported in full
interstitial and subserous emphysema could be traced from the ulcer
("Luft im Blute," _Deutsches Arch. f. klin. Med._, Bd. 31, p. 441,
1882).]
The source of hemorrhage from gastric ulcer is from blood-vessels
either in the stomach itself or in the neighborhood of the stomach.
Hemorrhages slight or of moderate severity occur from the capillaries
and small arteries and veins in the mucous and submucous coats.
Sometimes profuse and even fatal hemorrhage comes from arteries or from
veins in the submucous coat, especially when these vessels are dilated.
Quickly-fatal hemorrhages take place from the large vessels between the
muscular and the serous coats, particularly from the main trunks on the
curvatures. After the formation of adhesions, followed by the
perforation of all of the coats of the stomach, profuse bleeding may
proceed from the erosion of large vessels near the stomach, such as the
splenic, the hepatic, the pancreatico-duodenal arteries, the portal and
the splenic veins, and the mesenteric vessels. Bleeding may also occur
from vessels in the parenchyma of organs invaded by the ulcer. The most
common source of fatal hemorrhage is from the splenic artery, which
from its position is peculiarly exposed to invasion by ulcers of the
posterior wall of the stomach. The hemorrhage is usually arterial in
origin. It may come from miliary aneurisms of the gastric arteries or
from varicose veins in the wall of the stomach. As Cruveilhier has
pointed out, an ulcer may cicatrize except over one spot corresponding
to an artery from which fatal hemorrhage may occur. Ulcers which give
rise to large hemorrhages are usually chronic in their course. Those
seated on the middle of the anterior wall, although peculiarly liable
to perforate, are comparatively exempt from hemorrhage on account of
the small size of the blood-vessels there.
Changes in the blood-vessels of the stomach have been seen in a
considerable number of cases of gastric ulcer. Instances have been
recorded of the association with gastric ulcer of most of the diseases
to which blood-vessels are subject. An example in all respects
convincing of embolism of the artery supplying the ulcerated region of
the stomach has not been published. Probably the best case belonging
here is one of perforating ulcer of the stomach with hemorrhagic
infiltration in its walls, presented by Janeway to the New York
Pathological Society in 1871.[86] In this case there was in the
gastro-epiploic artery an ante-mortem fibrinous plug which was
continued into the nutrient artery of the ulcerated piece of the
stomach. No source for an embolus could be found. In one case Merkel
found an embolus in a small artery leading to an ulcer {511} of the
duodenum.[87] The arch of the aorta was atheromatous and contained a
thrombus. Patches of hemorrhagic infiltration existed in the stomach.
[Footnote 86: _Trans. of the N.Y. Path. Soc._, vol. ii. p. 1.]
[Footnote 87: _Wiener med. Presse_, vii. p. 30, 1866.]
In many cases thrombosis of the arteries, and especially of the veins
involved in the diseased tissue around an ulcer, has been observed, and
in some the thrombus was prolonged in the vessels for a considerable
distance from the ulcer. It is probable that in most of these cases the
thrombus was secondary to the ulcer. Hyaline thrombosis of the
capillaries near the ulcer is also to be mentioned.
In a certain, but not large, number of cases atheroma with
calcification or with fatty degeneration of the arteries of the stomach
has been found associated with gastric ulcer.[88] Reference has already
been made to the occurrence of obliterating endarteritis in the
thickened edges and floor of gastric ulcer, where it is doubtless
secondary. In one case of gastric ulcer I found a widespread
obliterating endarteritis affecting small and medium-sized arteries in
many parts of the body, including the stomach.[89]
[Footnote 88: For cases in point see Norman Moore, _Trans. of the Path.
Soc. of London_, vol. xxxiv. p. 94.]