|
1. Usually preceded by symptoms | 1. Usually preceded by symptoms
of pulmonary or of cardiac | of gastric or of hepatic
disease. Bronchial hemorrhage, | disease, less frequently by
however, without evidence of | other diseases (see Etiology).
preceding disease, is not rare. |
|
2. The attack begins with a | 2. The attack begins with a
tickling sensation in the throat | feeling of fulness in the
or behind the sternum. The blood | stomach, followed by nausea. The
is raised by coughing. Vomiting, | blood is expelled by vomiting,
if it occurs at all, follows the | to which cough, if it occurs, is
act of coughing. | secondary.
|
3. The blood is bright red, fluid| 3. The blood is dark, often
or but slightly coagulated, | black and grumous, sometimes
alkaline, frothy, and frequently | acid, and usually mingled with
mixed with muco-pus. | the food and other contents of
| the stomach.
|
If the blood has remained some | If the blood is vomited at once
time in the bronchi or a cavity, | after its effusion, it is bright
it becomes dark and coagulated. | red and alkaline, or it may be
| alkaline if it is effused into
| an empty stomach.
|
4. The attack is usually | 4. After the attack the physical
accompanied and followed by | examination of the lungs is
localized moist râles in the | usually negative, but there are
chest, and there may be other | generally symptoms and signs of
physical signs of pulmonary or | gastric or hepatic disease.
of cardiac disease. |
|
Bloody sputum continues for some | Black stools follow profuse
time, often for days, after the | hæmatemesis.
profuse hemorrhage ceases. |
As it is important that the patient should be as quiet as possible
during and for some time after the hemorrhage, any physical examination
which disturbs the patient, such as percussing the posterior part of
the chest or palpating the abdomen, should be avoided.
The diagnosis of the many causes of gastric hemorrhage belongs to the
description of the various diseases which have been enumerated under
the etiology.
PROGNOSIS.--It is exceptional for gastric hemorrhage to prove
immediately fatal. According to Fox, such an occurrence is more
frequent with cirrhosis of the liver than with ulcer or cancer of the
stomach. The ultimate result of the hemorrhage depends greatly upon the
previous condition of the patient. If this condition was good, he often
rallies from the most desperate prostration immediately following the
hemorrhage. A previously enfeebled patient is of course more likely to
yield to the further anæmia and exhaustion caused by profuse
hemorrhage. Although the symptoms of gastric ulcer and of cirrhosis of
the liver are sometimes improved after hemorrhage from the stomach,
nevertheless this hemorrhage can never be regarded as a welcome event.
For the treatment of gastric hemorrhage see ULCER OF THE STOMACH.
{586}
DILATATION OF THE STOMACH.
BY W. H. WELCH, M.D.
DEFINITION.--By dilatation of the stomach is understood a condition in
which the stomach is abnormally large and is unequal to the performance
of its normal functions. It will be observed that this definition of
dilatation of the stomach includes an anatomical disturbance and a
physiological disturbance. A stomach which, although unusually large,
performs its functions perfectly well is not, in the clinical sense, a
dilated stomach. The most characteristic functional disturbance in
dilatation of the stomach is delay in the propulsion of the gastric
contents into the intestine in consequence of inability of the muscular
coat of the stomach to perform the work imposed upon it. This muscular
insufficiency, whether primary or secondary, necessarily involves
disorder of the digestive and absorptive powers of the stomach.
SYNONYMS.--Dilatatio ventriculi; Gastrectasia. It has been proposed to
call the early stages of the disease insufficiency of the stomach
(Rosenbach). The condition described by Chomel as dyspepsia of liquids
is undoubtedly dilatation of the stomach.
HISTORY.--Dilatation as a disease of the stomach is not mentioned by
writers of antiquity. Fabricius ab Aquapendente in 1623 was among the
first to record an observation of dilatation of the stomach. During the
following century cases of dilatation of the stomach were recorded more
as curiosities than as of clinical interest. Most cases were attributed
to eating or drinking inordinate quantities. In 1743, Widman clearly
recognized stenosis of the pylorus as a cause of gastric dilatation. In
the works of Van Swieten, Morgagni, Lieutaud, and J. P. Frank, during
the latter half of the last century, different causes of dilatation of
the stomach are recognized. The last writer especially distinguishes
clearly between dilatation due to stenosis and that due to atony. The
data as to the symptoms of the disease were still very imperfect. In
1833, Duplay[1] published an important article in which the main points
in the causation and symptomatology of dilatation of the stomach are
clearly described. After this time the important works on the practice
of medicine or on diseases of the stomach contain, in the main, correct
descriptions of the disease under consideration. Since the publication
in 1869 of Kussmaul's memorable article[2] on the treatment of
dilatation of the stomach by the {587} stomach-pump, much greater
attention has been paid to this disease than ever before, so that the
literature upon this subject during the last fifteen years is very
considerable. In 1875, Penzoldt published an excellent monograph upon
dilatation of the stomach.[3]
[Footnote 1: _Arch. gén. de Méd._, Ser. 2, t. iii. pp. 165, 523.]
[Footnote 2: _Deutsches Arch. f. kl. Med._, Bd. vi., 1869. Kussmaul
first employed the stomach-pump in dilatation of the stomach in 1867,
and in that year he reported a successful result (_Schmidt's Jahrb._,
Bd. 136, p. 386).]
[Footnote 3: _Die Magenerweiterung_, Erlangen, 1875. To this work I am
indebted for most of the historical data in the text.]
ETIOLOGY.--Dilatation of the stomach is the result of inability of this
organ to propel its contents into the intestine within the normal space
of time. In the performance of this mechanical work three factors are
involved--namely, the muscular force of the stomach, the quantity and
quality of the gastric contents, and the size of the opening between
the stomach and the intestine. All causes of dilatation of the stomach
may be referred to abnormalities of one or more of these factors.
The most important group of causes is represented by stenosis of the
pyloric orifice or of the adjacent part of the stomach or of the
intestine.[4] Most cases of hypertrophic dilatation of the
stomach--that is, dilatation with hypertrophy of the muscular walls of
the stomach--are produced by causes belonging to this group.
[Footnote 4: Dilatation of the stomach in consequence of intestinal
obstruction below the duodenum is so rare that no further attention is
given to the subject in the present article. The term pyloric stenosis
is often used in the course of the article to include any obstruction
to the passage of the contents of the stomach into the intestine,
whether the obstruction be in the duodenum, the pyloric orifice, or the
pyloric region.]
The most frequent cause of pyloric stenosis is carcinoma, either in the
form of a diffuse infiltration of the gastric walls in this region or
as a tumor projecting into the cavity of the pyloric portion of the
stomach. Next in frequency are cicatricial growths resulting from
simple ulcer involving the pyloric region. Much less frequent are
similar cicatricial stenoses of the pylorus resulting from ulcers
produced by swallowing corrosive poisons. Simple hypertrophy of the
coats of the stomach in the pyloric region, particularly of the fibrous
and muscular coats, is an occasional cause of dilatation. Obstruction
of the pylorus by mucous polypi or by hypertrophic folds of mucous
membrane is so rare as to have little practical interest. Likewise,
stenosis caused by sarcomata, fibromata, myomata, lipomata, and cysts
need be mentioned only for the sake of completeness.
Narrowing of the pyloric orifice may be caused also by pressure from
outside of the stomach, as by tumors, particularly cancer, of the liver
and of the pancreas, and by the contraction of fibrous adhesions and
thickenings resulting from perigastritis. Obstruction of the duodenum
by tumors growing in its walls, by cicatrices resulting from ulcers,
and by external pressure may also cause dilatation of the stomach.
According to Barker, compression of the duodenum by a wandering right
kidney may induce dilatation of the stomach. The mere association of
dilatation of the stomach and movable right kidney, however, cannot be
considered proof that the former is caused by the latter, for the
subjects of movable kidney (most frequently women with flabby abdominal
walls who have borne many children) are often also favorable subjects
for atonic dilatation of the stomach.
Sometimes with dilatation of the stomach the pyloric orifice is found
abnormally small, without any thickening or other appreciable change in
the walls of the pylorus. These cases in adults have been described by
{588} Landerer under the name of congenital stenosis of the pylorus,
but his conclusions are not free from doubt.[5] Congenital stenosis,
and even complete occlusion of the pylorus, has been observed in
infants.[6]
[Footnote 5: _Ueber angeborene Stenose des Pylorus_, Inaug. Diss.,
Tübingen, 1879. In the ten cases studied by Landerer the patients were
all adults, mostly in advanced life. In only one case is it mentioned
that indigestion existed from childhood; the clinical history in all is
incomplete. With the exception of one case there was no marked
hypertrophy of the muscular coat of the stomach, such as is usually
found with benign pyloric stenosis and would naturally be expected with
a stenosis existing since birth. The pyloric orifice varied from 1½ cm.
to 2 mm. in diameter. Some of the specimens had been in alcohol for a
considerable time. In my opinion, Landerer has not brought forward
sufficient proof that in these cases stenosis of the pylorus existed
since birth.]
[Footnote 6: Wünsche, _Jahrb. d. Kinderheilk._, viii. 3, p. 367.
Andral, Förster, and Bull have found congenital stenosis and atresia of
the pylorus.]
Spasm of the pyloric muscle, which, according to Kussmaul, may be
referable to erosions, ulcers, and inflammations of the adjacent mucous
membrane, can be admitted only as a hypothetical explanation of some
cases of dilatation of the stomach.
Somewhat problematical, although not improbable, is the production of
stenosis of the pylorus or of the duodenum by torsion and by
displacement of these parts. Dilatation of the stomach is sometimes
associated with scrotal hernia, particularly with that containing
omentum or transverse colon. This dilatation Kussmaul explains by the
production of a sharp bend between the movable first part and
comparatively fixed second part of the duodenum, in consequence of the
dragging downward of the stomach by the displaced omentum or transverse
colon. In a similar way Kussmaul believes that the weight of an
over-distended stomach may produce stenosis, and by this mechanism he
explains the occasional occurrence of symptoms of complete pyloric
obstruction when a large quantity of material has accumulated in an
already dilated stomach, and the prompt relief of these symptoms when
the burden of the stomach is removed either by vomiting or by the
stomach-tube.[7]
[Footnote 7: Another explanation given by Kussmaul, and likewise based
upon experiments on the cadaver, is that when the stomach is
over-distended it may rotate upon its own axis, so that the pylorus
acquires a sagittal direction and impinges against the first part of
the duodenum. This rotation of the stomach, however, can occur only
when the abdominal walls are flabby (Kussmaul, "Die Peristaltische
Unruhe des Magens," _Volkmann's Samml. klin. Vortr._, No. 181).]
The manner in which stenosis of the pylorus causes dilatation of the
stomach is sufficiently obvious to require no especial explanation. It
is, however, important to know that stenosis of the pylorus may be
compensated, so that even a very considerable degree of obstruction of
this orifice may exist without any dilatation of the stomach. The
obstruction may be completely counteracted by hypertrophy of the
muscular coat of the stomach, particularly of that in the right half of
the organ. Leube suggests that this increased muscular force, by
increasing the peristaltic movements, may also hasten the digestion and
absorption of the food, so far as these processes take place in the
stomach.[8] The timely removal of the contents of the stomach by
vomiting may also prevent over-distension of the organ. Another
compensatory circumstance may be the reduction of the quantity of solid
and liquid food taken by the patient. Conditions are often present,
however, which oppose the development of these {589} compensatory
circumstances. Such conditions are feebleness of the patient,
degeneration of the muscular coat of the stomach, chronic catarrhal
gastritis, insufficient secretion of gastric juice, and delayed
absorption, causing stagnation and fermentation of the food in the
stomach.
[Footnote 8: Leube, in _V. Ziemssen's Handb. d. spec. Path. u. Ther._,
Bd. vii. 2te Hälfte, p. 211, Leipzig, 1878.]
Dilatation of the stomach may occur without any obstacle to the
evacuation of the gastric contents into the intestine. The cases of
so-called atonic dilatation of the stomach belong to this class. The
degree of dilatation in these cases is rarely so great as when the
dilatation is caused by stenosis. The cause of gastric dilatation in
the absence of stenosis is not always clear, so that a variety of
hypotheses, more or less probable, have been broached to explain these
obscure cases.
Dilatation with unobstructed outlet of the stomach must be referable
either to abnormalities in the quantity or quality of the contents of
the stomach or to weakness of the muscular walls of the stomach. In
most cases both of these causes are combined, and it is not easy to
separate their action.
Abnormal gastric contents may be the result of improper ingesta or of
disturbances in gastric digestion. Although in former times the
frequency of excessive eating and drinking as a cause of dilatation of
the stomach was doubtless exaggerated, nevertheless the efficacy of
this cause cannot be doubted. Dilatation of the stomach is said to be
common in people who live almost exclusively upon a vegetable diet and
therefore require large quantities of food. The habitual drinking of
large quantities of beer may cause dilatation of the stomach. The
occasional association of a dilated stomach with diabetes is referred
to the inordinate appetite and thirst which characterize this disease.
If the food reaches the stomach imperfectly masticated, the process of
digestion is delayed, and as a result the stomach may become dilated.
Indigestible food, particularly that which readily ferments in the
stomach, may be an indirect cause of the disease under consideration. A
similar rôle may be played by swallowing foreign substances either by
accident or by design. It is not proven that dilatation of the stomach
may be referable to exhaustion of its muscular power by the abuse of
agents which at first excite peristalsis, such as emetics, purgatives,
alcoholics, tobacco, spices, etc. Equally doubtful is the production of
dilatation by the misuse of narcotics, such as opium, which restrain
peristalsis.
Of great importance in the production and continuance of gastrectasia
are all circumstances which cause stagnation and fermentation of the
contents of the stomach. These abnormalities of the gastric contents
are referable both to muscular and to chemical insufficiency of the
stomach, but in this connection it is desired to call attention
especially to chemical insufficiency, although in the production of
gastric dilatation this becomes always associated with muscular
insufficiency. In this way chronic catarrhal gastritis is operative in
the causation of gastric dilatation. In consequence of insufficient
secretion of normal gastric juice and of delayed absorption, the food
remains abnormally long undigested in the stomach, and fermentative
changes, with the development of gas, occur. No less important,
however, is the impairment of the muscular power of the stomach in
chronic gastritis. Stagnation and fermentation of the contents of the
stomach occur also in functional or atonic dyspepsia, which is to be
reckoned as a cause of dilatation of the stomach. {590} Naunyn[9]
emphasizes especially the importance of abnormal fermentations in the
stomach (alcoholic, butyric acid, lactic acid, acetic acid
fermentations) both as a cause and as a result of dilatation of the
stomach. Ulcer and cancer of the stomach may cause dilatation by
interfering with the normal digestive processes.
[Footnote 9: _Deutsches Arch. f. kl. Med._, Bd. 31.]
We come now to the third and final group of causes of dilatation of the
stomach--namely, those included under weakness of the muscular walls of
the stomach. In the last analysis all causes of gastric dilatation come
under this heading, for even with pyloric stenosis and with excessive
contents a stomach will not dilate so long as its muscular power is
equal to the proper performance of the work which is demanded. In this
connection, however, reference is had especially to those cases in
which impairment or restraint of the muscular movements of the stomach
may be regarded more or less directly as the primary cause of
dilatation of the stomach.
Clearest of comprehension are those cases in which the muscular power
of the stomach is impaired by organic changes in the muscular coat.
Here may be mentioned partial destruction of the muscular coat,
particularly of that in the pyloric region, by ulcers and by cancers.
Thus, ulcers and cancers which in no way obstruct the outlet of the
stomach may cause dilatation of the organ. Inflammatory infiltration
(inflammatory oedema) of the muscular coat has been adduced as a cause
of its weakness in chronic catarrhal gastritis and in peritonitis.
Whether this is the proper explanation or not, there is no doubt that
the muscular coat of the stomach may become paretic in cases of chronic
catarrhal gastritis, as well as the subjacent muscle in inflammations
of other mucous membranes, as in laryngitis or in cystitis. Our
knowledge of the relation between degeneration of the muscular coat of
the stomach and gastrectasia is very imperfect. Fatty and colloid
degeneration of the muscle of dilated stomachs is probably to be
interpreted as a secondary change. It is probable that amyloid
degeneration may be a cause of atonic dilatation of the stomach.[10]
Oedematous infiltration of the coats of the stomach in cases of
cirrhosis of the liver, pulmonary emphysema, cardiac disease, and
Bright's disease has been assigned as a cause of gastric dilatation,
but without satisfactory evidence. Chronic interstitial gastritis
(cirrhosis of the stomach) is more frequently a cause of contraction
than of dilatation of the stomach.
[Footnote 10: Edinger, _ibid._, Bd. 29.]
The restraint of the muscular movements of the stomach by adhesions and
by dragging downward of the organ in hernia may cause dilatation.
Relaxation of the abdominal walls, as in women who have borne many
children, by removing the normal support of the stomach, has been
thought to cause dilatation.
Atony of the muscular walls of the stomach may be a part of general
muscular weakness and impaired nutrition. Here belong cases of adynamic
dilatation of the stomach secondary to typhoid fever, cholera,
tuberculosis, anæmia, chlorosis, cachexia, senile marasmus,
neurasthenia.
Whether primary paralysis of the stomach can occur or not is wholly
uncertain. We have no positive knowledge as to the occurrence of
paresis of the stomach in consequence of organic or functional changes
{591} in the peripheral or central nervous system. Nor does our meagre
information as to the relation between the nervous system and the
muscular movements of the stomach justify the construction of any
hypotheses as to this point.
For the sake of clearness the various causes of dilatation of the
stomach according to the foregoing classification may be recapitulated
as follows. Some of the more doubtful and of the rarer causes are
omitted:
A. Stenosis of the Pylorus or of the Duodenum.
1. Cancerous;
2. Cicatricial;
3. Hypertrophic (of pylorus);
4. From external pressure;
5. Congenital (of pylorus)?;
6. From torsion of duodenum?
B. Abnormalities in Contents of Stomach.
1. Ingesta:
_a_. Excessive;
_b_. Imperfectly masticated;
_c_. Indigestible.
2. Stagnation and fermentation in consequence of chemical
insufficiency of the stomach, as in chronic catarrhal
gastritis and functional dyspepsia.
C. Impairment of Muscular Force of Stomach.
1. Organic changes in muscular coat:
_a_. Partial destruction by ulcers and cancers;
_b_. Inflammation, as in chronic catarrhal gastritis and
peritonitis;
_c_. Degenerations (fatty, colloid, amyloid);
_d_. Oedema?;
_e_. Cirrhosis of stomach.
2. Mechanical Restraint:
_a_. By adhesions;
_b_. By weight of herniæ.
3. Impaired Nutrition and General Muscular Weakness, Adynamic
dilatation from typhoid fever, tuberculosis, anæmia, etc.
4. Paresis from neuropathic causes?
As a rule, not a single one, but several, of the above-mentioned causes
are operative in the production of dilatation of the stomach, and it is
often impossible to say which is the primary cause. The various gastric
functions are so dependent upon each other that if one is disturbed the
others also suffer. If, for instance, atony of the muscular coat of the
stomach exists, then in consequence of enfeebled peristalsis the
secretion of gastric juice is insufficient, the food is not thoroughly
mingled with the gastric juice, and the absorption of the products of
digestion in the stomach is interfered with; in consequence of which
the accumulating peptones still further hinder the digestive process.
The pylorus remains contracted for an abnormal length of time, as it
naturally is closed until the process of chymification in the stomach
is far advanced, and this process is now delayed. The stagnating
contents of the stomach readily ferment, and the irritating products of
fermentation induce a chronic {592} catarrhal gastritis, which further
impairs the functions of the mucous and muscular coats of the stomach.
Thus, in a vicious circle one cause of dilatation induces another. To
assign to each cause its appropriate share in the production of the
final result is a matter of difficulty, and often of impossibility.
From this point of view the dispute as to whether in atonic dilatation
the most important factor in causation is chemical insufficiency of the
stomach (impaired secretion of gastric juice, fermentations) or
mechanical insufficiency (weakened muscular action, stagnation),
appears of little practical importance.
Of the causes of non-stenotic dilatation of the stomach, the first
place is to be assigned to chronic catarrhal gastritis and to atonic
dyspepsia, as this term is understood by most English and American
writers.
As regards frequency, gastric dilatation is a common result of cancer
of the pylorus. It is less frequently caused by simple ulcer. Other
forms of pyloric stenosis than the cancerous and the cicatricial are
rare.
Opinions differ as to the frequency of non-stenotic or atonic
dilatation of the stomach according to the manner in which one
interprets the cases. Non-stenotic dilatations which are comparable in
degree to those produced by stenosis are rare. The lesser grades of
atonic dilatation, however, are not rare; but here arises the
difficulty of distinguishing these cases from mere chemical or
mechanical insufficiency of the stomach, which often represents the
early stage of the process. Hence it has been proposed to discard
altogether the term dilatation, and to substitute that of insufficiency
of the stomach. But this latter term is applicable to many affections
of the stomach other than dilatation. A typical case of atonic
dilatation of the stomach is a well-defined disease, and because it is
difficult to diagnosticate its early stages is not sufficient reason
for discarding altogether the designation.
Gastrectasia may develop at any age. It is most frequent in middle and
advanced life. The largest number of cases of atonic dilatation is met
with between thirty and forty years of age. The disease is rare in
childhood.[11] The disease occurs in all classes of life. Atonic
dilatation seems to be comparatively more frequent in private practice
and among the favorably situated than in hospitals and among the poor.
Kussmaul says that the largest contingent of patients is furnished by
persons who lead a sedentary life and eat and drink a great deal.