can be felt. Under favorable circumstances it can sometimes be
determined that this tumor is smooth, elastic, tympanitic on
percussion, and presents more or less distinctly the contours of the
stomach. By administering effervescing powder it may be possible to
obtain further evidence that the tumor corresponds in its form to the
stomach. The diagnosis of contraction of the cavity of the stomach is
not easy. Some information may be afforded by noting the length to
which the inflexible stomach-tube can be passed. The quantity of water
which can be poured into the stomach until it begins to run out of the
stomach-tube may also bring some confirmatory evidence as to the
existence of contraction of the stomach.
Even should the physical signs suffice to determine that the tumor is
the thickened and contracted stomach, still cancer cannot be excluded,
for this also may grow diffusely in the gastric walls and may cause
contraction of the cavity of the stomach. With our present means of
diagnosis, therefore, the most which can be said is, that a special
combination of favorable circumstances may render probable the
diagnosis of cirrhosis of the stomach, but a positive diagnosis is
impossible.
MORBID ANATOMY.--In most cases of cirrhosis of the stomach the stomach
is contracted. The cavity of the stomach has been found not larger than
would suffice to contain a hen's egg, but such extreme {614}
contraction is very rare. When the stomach in this disease is found
dilated, either the thickening involves only or chiefly the walls of
the pyloric portion, or the morbid process probably began there and was
followed by dilatation.
In typical cases the walls of the entire stomach are thickened, but
frequently the thickening is most marked in the pyloric region. The
walls may measure an inch and even more in thickness. The thickened
walls are dense and firm, so that often upon incision the stomach does
not collapse.
Upon transverse section the different coats of the stomach can be
distinguished. The mucous membrane is least affected, being sometimes
thickened, sometimes normal or atrophied. The muscularis mucosæ is
hypertrophied, and is evident to the naked eye as a grayish band. The
submucous coat is of all the layers the most thickened, being sometimes
ten to fifteen times thicker than normal. It appears as a dense white
mass of fibrous tissue. The main muscular coat is also, as a rule,
greatly hypertrophied; the grayish, translucent muscular tissue is
pervaded with streaks of white fibrous tissue prolonged from the
submucous and subserous coats. This last coat resembles in appearance
the submucous coat, which, however, it does not equal in thickness,
although it is, proportionately to its normal thickness, much
hypertrophied. The free peritoneal surface usually appears opaque and
dense.
To the naked eye it is apparent that the new growth of fibrous tissue
is most extensive in the submucous coat, which it is probably correct
to regard as the starting-point of the disease. The hypertrophy of the
muscular layers is also in most cases an important element in the
increased thickness of the gastric walls.
Microscopical examination[9] shows sometimes a nearly normal mucous
membrane. The tubules, however, are usually more or less atrophied. In
the case reported by Nothnägel tubules could be found only in the
pyloric region of the stomach. The essential lesion is the new growth
of fibrillated connective tissue pervading all of the coats of the
stomach. In an interesting case reported by Marcy and Griffith,[10]
which was believed to be caused by an extensive cicatrized ulcer, a new
formation of smooth muscular tissue was found not only in the main
muscular tunic and the muscularis mucosæ, but also throughout the
submucosa. This peculiarity was probably referable to the cicatrization
of the ulcer.
[Footnote 9: Microscopical examination is always necessary for a
positive diagnosis of cirrhosis of the stomach. In a case which I
examined post-mortem of double ovarian cancer, with multiple secondary
deposits in the peritoneum and with chronic peritonitis, the stomach
presented the typical gross appearances of cirrhosis, but here and
there were to be found nests of cancer-cells in the prevailing new
growth of fibrous tissue in the walls of the stomach.]
[Footnote 10: _Am. Journ. of the Med. Sci._, July, 1884, p. 182.]
Not infrequently adhesions exist between the stomach and surrounding
organs. Exceptionally, a diffuse growth of fibrous tissue may invade
the greater part of the peritoneum, particularly the visceral layer,
and cause a thickening similar to that existing in the stomach. In such
cases ascites is usually a marked symptom.
PROGNOSIS.--The prognosis of cirrhosis of the stomach is grave. The
disease runs a chronic course, and usually terminates in death by
asthenia. There is no reason to believe that the stomach can ever be
restored to its {615} normal condition. Still, cases have been reported
in which it has been supposed that cirrhosis of the stomach has
terminated in recovery.[11] The diagnosis, however, in such cases must
remain doubtful.
[Footnote 11: Lesser, _Cirrhosis Ventriculi_, Inaug. Diss., Berlin,
1876; Smith, "Cirrhosis of the Stomach," _Edinb. Med. Journ._, 1872, p.
521.]
TREATMENT.--The treatment is symptomatic, and is to be guided by the
general principles developed in previous articles concerning the
regulation of the diet and the administration of remedies.
HYPERTROPHIC STENOSIS OF THE PYLORUS.
The various causes of stenosis of the pylorus have already been
mentioned under DILATATION OF THE STOMACH, and the most important of
these causes have received full consideration in connection with ULCER
and with CANCER OF THE STOMACH.
Only one of the varieties of pyloric stenosis can claim consideration
as an independent disease. This variety is the so-called hypertrophic
stenosis of the pylorus (Lebert) or fibroid degeneration of the pylorus
(Habershon[12]). Under the name of hypertrophic stenosis have been
described cases in which the stenosis was due to hypertrophy of only
one of the coats of the stomach, usually either the submucous or the
muscular coat, sometimes only the mucous coat. In most cases, however,
all of the coats of the stomach are involved, and the lesion is similar
to that of cirrhosis of the stomach, but it is confined to the pylorus
or to the pyloric region. In such cases there is new growth of fibrous
tissue, most marked in the submucous coat, and hypertrophy of the
muscular coat. The appearance of the pylorus in some instances of
hypertrophic stenosis has been not inappropriately compared to that of
the cervix uteri.
[Footnote 12: Habershon, _On Diseases of the Abdomen_, London, 1862;
Lebert, _Die Krankh. d. Magens_, Tübingen, 1878; Nauwerk, _Deutsches
Arch. f. klin. Med._, Bd. 21, 1878.]
In the majority of cases the change here described is the result of
cicatrization of a gastric ulcer, and some believe that all cases of
so-called hypertrophic stenosis or fibroid degeneration of the pylorus
are referable to ulcer, although it may be very difficult to discover
the cicatrix of the ulcer. It is certainly not always possible to
detect either ulcer or cicatrix, so that it seems proper to regard the
hypertrophic stenosis in such cases as constituting an independent
affection.
The symptoms are those of dilatation of the stomach, sometimes preceded
by evidences of chronic catarrhal gastritis. The thickened pylorus can
sometimes be felt during life as a small, cylindrical, usually movable
tumor, either stationary in progress or of very slow growth.
In most cases the diagnosis of organic stenosis of the pylorus can be
made. Cancer may sometimes be excluded by the long duration of the
symptoms and the stationary character of the tumor if a tumor can be
felt. The exclusion of ulcer is more difficult and hardly possible, for
ulcer may have existed without producing characteristic symptoms.
The prognosis and treatment have been considered under DILATATION OF
THE STOMACH.
{616} ATROPHY OF THE STOMACH.
Atrophy of the stomach may be the result of stenosis of the cardia or
of the oesophagus. The stomach may participate with other organs in the
general atrophy attending inanition and marasmus. The walls of a
dilated stomach may be very thin.
Especial importance has been attached in recent years to degeneration
and atrophy of the gastric tubules. The glands of the stomach may
undergo degeneration and atrophy in various diseases of the stomach,
such as chronic catarrhal gastritis, phlegmonous gastritis, cirrhosis
of the stomach, and cancer of the stomach. Parenchymatous and fatty
degeneration of the glandular cells of the stomach occurs in acute
infectious diseases, as typhoid fever and yellow fever, also as a
result of poisoning with phosphorus, arsenic, and the mineral acids.
It is claimed by Fenwick that atrophy of the stomach may occur not only
as a secondary change, but also as a primary disease attended by grave
symptoms. Fenwick has described a number of cases in which the gastric
tubules were atrophied without thickening of the walls of the stomach
and without diminution in the size of the cavity of the stomach--cases,
therefore, which cannot be classified with cirrhosis of the
stomach.[13] He attributes in many cases the atrophy of the tubules to
an increase in the connective tissue of the mucous membrane, and draws
a comparison between atrophy of the stomach and the atrophic form of
chronic Bright's disease.
[Footnote 13: _The Lancet_, 1877, July 7 _et seq._]
In 1860, Flint[14] called attention to the relation between anæmia and
atrophy of the gastric glands. He expressed the opinion that some cases
of obscure and profound anæmia are dependent upon degeneration and
atrophy of the glands of the stomach. Since Flint's publication cases
have been reported by Fenwick, Quincke, Brabazon, and Nothnägel, in
which lesions supposed to be due to pernicious anæmia have been found
after death associated with atrophy of the gastric tubules.[15]
Nothnägel's case, which has already been mentioned, was one of
cirrhosis of the stomach.
[Footnote 14: A. Flint, _American Medical Times_, 1860. Further
contributions of Flint to this subject are to be found in the _New York
Medical Journal_, March, 1871, and in his _Treatise on the Principles
and Practice of Medicine_, p. 477, Philada., 1881.]
[Footnote 15: Fenwick, _loc. cit._; Quincke, _Volkmann's Samml. klin.
Vorträge_, No. 100 (case _b_); Brabazon, _British Med. Journ._, 1878,
July 27 (without microscopical examination!); Nothnägel, _Deutsches
Arch. f. kl. Med._, Bd. 24, p. 353.]
The symptoms which have been referred to primary atrophy of the stomach
are severe anæmia and disturbances of digestion, such as anorexia,
eructations, and vomiting. The digestive disturbances are often not
greater than are frequently observed in cases of severe anæmia.
In my opinion, the existence of atrophy of the stomach as a primary and
independent disease has not been established. In many cases which have
been described as primary atrophy the histological investigation of the
stomach has been very defective. Degeneration and atrophy of the
gastric tubules secondary to various diseases of the stomach and to
certain general diseases is an important lesion when it is extensive,
and must seriously impair the digestion, and consequently the
nutrition, of the patient.
{617} ANOMALIES IN THE FORM AND IN THE POSITION OF THE STOMACH.
These anomalies, so far as they have not received consideration in
previous articles, are of more anatomical than clinical interest, and
therefore here require only brief mention.
The stomach may have an hour-glass shape in consequence of a
constriction separating the cardiac from the pyloric half of the organ.
This constriction is sometimes congenital,[16] sometimes caused by
cicatrization of a gastric ulcer, and sometimes caused by spasmodic
contraction of the muscle, which may persist after death, but
disappears when the stomach is artificially distended. Hour-glass shape
of the stomach has been diagnosed during life by administering an
effervescing powder according to Frerichs' method.
[Footnote 16: A careful study of the congenital form of hour-glass
contraction of the stomach has been made by W. R. Williams ("Ten Cases
of Congenital Contraction of the Stomach," _Journ. of Anat. and
Physiology_, 1882-83, p. 460).]
Foreign substances of hard consistence which have been swallowed
sometimes cause diverticula of the stomach.
Sometimes the fundus of the stomach is but little developed, so that
the organ is long and narrow like a piece of intestine.
The stomach may be variously distorted by external pressure, as from
tumors and by adhesions.
The loop-shaped stomach and vertical position of the stomach have been
already considered in connection with DILATATION OF THE STOMACH (page
602).
In transposition of the viscera the stomach is also transposed. In such
a case difficulties may arise in the diagnosis of pyloric cancer, as in
a case described by Légroux.
The stomach may be found in hernial sacs. Mention has already been made
of the presence of dilated stomachs in scrotal hernia. More frequently
the stomach is found in umbilical hernias. In diaphragmatic hernia the
stomach is found more frequently in the thorax than is any other
abdominal viscus. In 266 diaphragmatic hernias collected by Lascher[17]
the stomach was found either wholly or partly in the thorax in 161
cases. The clinical consideration of diaphragmatic hernia, however,
does not belong here.
[Footnote 17: _Deutsches Arch. f. kl. Med._, Bd. 27.]
Furthermore, the stomach may be displaced by tumors, enlargement of
neighboring organs, tight-lacing, adhesions, and the weight of hernias.
These displacements, however, are generally inconsiderable and of
little importance.
In a case described by Mazotti[18] the stomach, of which the pyloric
portion was fixed by adhesions, was twisted around its long axis. Death
was caused by uncontrollable vomiting.
[Footnote 18: _Virchow und Hirsch's Jahresbericht_, 1874, ii. p. 249.]
{618} RUPTURE OF THE STOMACH.
Sufficient attention has already been given to perforation of the
stomach in consequence of diseases of its walls, such as ulcer, cancer,
abscesses, and toxic gastritis.
A healthy stomach may be ruptured by violent injury to the abdomen even
when no external wound is produced. An example of rupture of the
stomach from this cause is that sometimes produced when a person has
been run over by a heavy vehicle.
It has been claimed that a stomach with healthy walls may burst in
consequence of over-distension of the organ with solids or with gas.
The older literature is especially rich in reports of so-called
spontaneous rupture of the stomach. Most of these cases were examples
of perforation of gastric ulcer. In a case of apparently spontaneous
rupture of a stomach which had become abnormally distended with gas,
Chiari[19] found that the rupture was through the cicatrix of a simple
ulcer in the lesser curvature. It is hardly conceivable that rupture of
the healthy stomach from over-distension can occur so long as the
orifices of the organ are unobstructed.
[Footnote 19: _Wiener med. Blätter_, 1881, No. 3.]
Lautschner[20] reports a case of spontaneous rupture of the stomach in
a woman seventy years old with an enormous umbilical hernia which
contained the pyloric portion of the stomach. After drinking eight
glasses of water and two cups of tea and eating meat, she was seized
with vomiting, during which the stomach burst with a report which was
audible to the patient and to those around her. She passed into a state
of collapse and died in thirteen hours. A rent several centimeters long
was found in the posterior wall of the stomach. Lautschner thinks that
the pylorus was bent in the hernial sac so as to be obstructed. In the
walls of the stomach he found no evidence of pre-existing disease.
[Footnote 20: _Virchow und Hirsch's Jahresbericht_, 1881, ii.]
There is no satisfactory proof of the possibility of the occurrence of
rupture of a stomach with healthy walls except as a result of external
violence.
The symptoms and treatment of rupture of the stomach are those of
perforation of the stomach, and have already been described. The
prognosis is fatal.
GASTROMALACIA.
That the subject of gastromalacia should still occupy so much space in
medical works the purpose of which is mainly clinical proves that many
physicians still cling to the belief that this process may occur during
life. It is, nevertheless, certain that the condition which, according
to the ordinary and traditional use of the term, is designated
gastromalacia, is always a post-mortem process and is without the
slightest clinical significance. So long as the circulation of the
blood in the walls of the stomach is undisturbed, self-digestion of
this organ cannot occur. No one doubts {619} that parts of the gastric
walls in which the circulation has been arrested, and which are exposed
to the gastric juice, undergo self-digestion, as has already been set
forth in the article on GASTRIC ULCER. To describe cases of this nature
under the name of gastromalacia, however, is misleading, and can cause
only confusion, for the long-continued discussion as to whether
gastromalacia is a vital or a cadaveric process applied certainly to a
different conception of the term. In some of the cases which have been
published, even in recent years, in support of the vitalistic theory of
gastromalacia, and in which it has been proven that perforation of the
stomach occurred during life, the solution of continuity took place
through parts of the gastric walls in which the circulation had already
been obstructed, particularly by extensive hemorrhagic infiltration.
Some of these cases are probably also examples of perforation of
gastric ulcer or of rupture of cicatrices from over-distension of the
stomach, in which post-mortem digestion of the edges of the ulcer or of
the cicatrix obscured the real nature of the process. The subject of
gastromalacia should be relegated wholly to works on physiology and on
pathological anatomy.
{620}
INTESTINAL INDIGESTION.
BY W. W. JOHNSTON, M.D.
NATURE.--The term indigestion in its most common meaning refers to
gastric indigestion only. This limitation has arisen from the fact that
gastric digestion has been more thoroughly understood than intestinal
digestion, and because the symptoms, flatulence, acidity, eructations
of gas, pyrosis, and vomiting of unaltered food, are readily referred
to the stomach as their source. Intestinal digestion has not been well
known until within a recent date, and its phenomena in disease have
been mistaken for other pathological conditions.
From the important and complex function of the intestinal juices, and
the very great share they take in the solution of food, there must be
many phases of departure from the normal state. The processes of
intestinal digestion are more intricate than those of gastric
digestion, of a higher grade, and the chemical reactions are more
numerous, depending upon the participation of the bile, the pancreatic
juice, and the succus entericus; while intestinal absorption is a more
complex act than that of gastric absorption.
A brief review of the physiology of intestinal digestion will be of aid
in making clear its pathology.
The object of all digestion is to make such a solution of the ingesta
that they may pass through animal membrane and so enter the system.
Mechanical disintegration and simple solution do something toward this,
but for substances insoluble in water a more thorough change is brought
about by ferments which convert insoluble into soluble compounds.
The process of digestion begins in the mouth. Mastication breaks up the
masses of food; the saliva softens them, dissolves soluble substances,
as salt and sugar, and thus the pleasures of the palate are enhanced.
The ferment ptyalin acts upon starch (boiled starch being more rapidly
altered than unboiled), and changes it to dextrin and grape-sugar, both
of which are diffusible through animal membrane, entering lymph-spaces
and blood-vessels. The greater part of the saliva secreted is swallowed
with the food or in the intervals of eating. The amount formed in
twenty-four hours varies from 1500 gm. (Bidder and Schmidt) to 700 gm.
(Tuczek). It must therefore serve some ulterior purpose in the stomach.
Ewald[1] says that saliva converts starch into sugar in acid as well as
in alkaline and neutral solutions. But Langley[2] asserts that the
ferment of {621} saliva is destroyed by the hydrochloric acid of the
gastric juice. The longer food is subjected to mastication and
insalivation, the more thorough is the mouth digestion and the better
prepared is the mass for the action of the gastric and intestinal
juices. It is asserted that fatty matters are emulsified to a certain
extent by the alkaline ferments of the saliva.
[Footnote 1: _Lectures on Digestion_, New York, 1881, p. 37.]
[Footnote 2: "On the Destruction of Ferments in the Alimentary Canal,"
_Journal of Physiology_, London, Jan., 1882, p. 246.]
When the food enters the stomach the nitrogenous (albuminoid) elements
are attacked by the gastric juice, the bundles of muscular fibre are
broken up, the fibrillæ are reduced to a granular mass, but not
completely dissolved (Frerichs), the fat-globules are freed from their
envelopes of connective tissue, milk is coagulated, and the casein is
dissolved.
"The tangible, practical object of this change is to form out of a
little-diffusible body (albumen) one easily diffusible (peptone), which
is capable of absorption through animal membrane in a higher degree
than ordinary albumen" (Ewald). Peptone is formed out of ordinary
albumen, as grape-sugar is formed out of starch, by taking up water; it
is therefore the hydrate of albumen.
The more tardy the digestion in the stomach the more highly charged
with acid is the gastric juice. According to Wright, the degree of
alkalinity of the saliva is in proportion to the acidity of the stomach
fluids, and Bence Jones has observed that during the excretion of acid
in the stomach the total alkalinity of all alkaline digestive fluids is
increased. The lesson is thus learned that a too careful preparation of
food, so as to shorten and lessen gastric labor, diminishes the
activity of the gastric juice as well as that of all other digestive
fluids.
Intestinal digestion begins when the softened mass passes through the
pylorus. This mass (chyme) is composed of (1) the products of gastric
digestion which have not been absorbed--peptone, dextrose, levulose,
peptonized gelatin, with mucus and gastric juice; (2) all matters which
have escaped digestion--the starch of vegetable substances, dissolved
gelatin and albumen which have not been peptonized, and some unaltered
muscle-structure; and (3) fat, fatty acids, and cellulose upon which
neither saliva nor gastric juice has had any influence (Ewald).
This complex semi-fluid mass with an acid reaction enters the duodenum
and comes in contact with fluids and ferments destined to work
remarkable changes in its composition. The first of these fluids is the
bile, which is alkaline and composed of the glycocholate and
taurocholate of sodium, cholesterin, soaps, etc., phosphates and
carbonates of lime and sodium, chlorides of potassium and sodium,
bile-pigment, etc. The outflow of bile is excited by the contact of the
chyme with the orifice of the bile-duct. When the alkaline bile is
mingled with the acid mass in the duodenum, it neutralizes its acidity,
precipitates the peptones, and therefore stops all further action of
the gastric juice. Fats containing free fatty acids are emulsified,
soaps being formed by a combination of the alkalies of the bile with
the fatty acids. Lastly, bile hinders fermentation in the intestine and
acts as a purgative by exciting peristalsis. Absorption is probably
also favored by bile, as it has been found that emulsified fats pass
more readily through an animal membrane which has been wet with
bile.[3]