Chapter XXXVI: Front Matter (36)

12. Idiopathic Causes.--Under this unsatisfactory designation are included cases which are aptly described by Flint[1] in the following words: "Hemorrhage sometimes occurs from the stomach, as from the bronchial tubes, the Schneiderian membrane, and in other situations, without any apparent pathological connections, neither following nor preceding any appreciable morbid conditions. It is then to be considered {583} as idiopathic." A person in apparent health has suddenly a hemorrhage, often profuse, from the stomach, which is followed only by symptoms immediately referable to the hemorrhage. The hemorrhage is naturally the source of great anxiety. Ulcer or cancer of the stomach or some other grave disease is usually suspected. But the patient develops no further symptoms, and often never has another hemorrhage. Whatever hypotheses one may construct for these cases of so-called idiopathic hemorrhage, the recognition of the clinical fact of their occurrence is important.

[Footnote 1: Austin Flint, _A Treatise on the Principles and Practice of Medicine_, 5th ed., p. 513, Philada., 1881.]

Inasmuch as hemorrhage from the stomach is usually made manifest by the vomiting of blood, it is important to bear in mind that gastric hemorrhage is not the only cause of hæmatemesis. Blood may gain access to the stomach by being swallowed in cases of hemorrhages from the nose, mouth, throat, bronchi, lungs, and oesophagus. Blood may also enter the stomach from the duodenum in cases of simple ulcer of the duodenum or of typhoid ulcers situated in the upper part of the intestine.

The SYMPTOMS of hemorrhage from the stomach have already been described in connection with ULCER OF THE STOMACH.

MORBID ANATOMY.--As is evident from the enumeration of the causes of gastric hemorrhage, the lesions found after death are manifold. A description of these lesions, however, does not belong here. It is necessary, however, to say a few words concerning the demonstration of the source of the hemorrhage.

The hemorrhage is arterial, venous, or capillary in origin. Ulcerations from the stomach into the heart, which have been mentioned in connection with gastric ulcer, are too infrequent to come into consideration in this connection. If the bleeding is from a large artery or vein or from a medium-sized aneurism or varix, the demonstration of its source is not difficult. Often, however, in cases of fatal gastric hemorrhage the search for the source of the hemorrhage has proved fruitless. It is supposed that in many such cases the hemorrhage is due to diapedesis, and not to rupture of a blood-vessel (rhexis). Doubtless, small gastric hemorrhages, particularly those into the tissues of the stomach, are often the result of diapedesis, but in cases of profuse hemorrhages from the stomach where the source of the hemorrhage is not demonstrable after death, the convenient assumption of hemorrhage by diapedesis, in my opinion, plays too important a rôle. In most cases of profuse gastrorrhagia the symptoms point to a sudden outpouring of blood into the stomach; and our knowledge of diapedesis does not warrant the belief that the red blood-corpuscles can escape through the unsuffused walls of the vessels with that combined rapidity and abundance which would be necessary to explain the sudden and profuse hemorrhage. In these cases hemorrhage by rhexis is altogether more probable even when ruptured vessels cannot be demonstrated. It often requires a long-continued and careful search to find a small vessel which is ruptured. In the case above mentioned of fatal hæmatemesis from miliary aneurism over an hour of continuous searching was required to find the pinhole perforation in the mucous membrane in the bottom of which lay the small aneurism. Chiari[2] has reported a fatal gastric hemorrhage due to rupture of a submucous vein. The erosion of the mucous membrane was not larger than a hempseed. The examination of the mucous membrane is often much impeded by the {584} closely-adherent mucus and blood, which have to be carefully removed. Injection of the vessels of the stomach with fluid may aid in finding a ruptured vessel. It is not intended to assert that in all cases of fatal gastric hemorrhage a painstaking search would reveal the source of the hemorrhage, but it is believed that cases of fatal gastric hemorrhage would less frequently be reported with negative anatomical result as hemorrhages by diapedesis, or by exhalation, or as parenchymatous or capillary hemorrhages, if such a search were made.

[Footnote 2: _Prag. med. Wochenschr._, 1882, No. 50.]

DIAGNOSIS.--Undoubtedly, small hemorrhages into the stomach often occur which are not recognized, and in the absence of vomiting even larger hemorrhages may escape detection unless a careful examination of the stools be made. The patient may die from abundant gastric hemorrhage before any blood has been vomited or has passed by the bowels.

When there is doubt whether the black color of the stools is due to blood or to the administration of iron or of bismuth, it generally suffices to add water to the stools. If blood be present, the water will acquire a reddish color. Should doubt still remain, then the microscope, the spectroscope, or the test for hæmin crystals may be called into requisition (see p. 545).

Whether black, tarry stools are produced by hemorrhage from the stomach or by hemorrhage in the upper part of the intestine can be decided only by the clinical history. If hæmatemesis be likewise present, the presumption is strongly in favor of gastric hemorrhage. The diagnosis, however, between hemorrhage from duodenal ulcer and that from gastric ulcer is very difficult, and can rarely be positively made.

The mere inspection of the vomit is generally sufficient to determine whether it contain blood or not. Color more or less resembling that of altered blood may be produced in the vomit by iron, bismuth, red wine, various fruits, such as cranberries, and by bile. When a careful inspection by the physician leaves doubt as to the presence of blood--which will rarely be the case--then here also recourse may be had to the microscope, spectroscope, and test for hæmin crystals.

Sometimes blood is swallowed and then vomited by hysterical females or by malingering soldiers or prisoners for purpose of deceit. In such cases there are generally no evidences of acute anæmia or of gastric disease. The blood of some animals can be distinguished by the microscope from human blood. When suspicion of deceit exists, there are generally various ways of entrapping the patient.

When blood is vomited by nursing infants the possibility of its coming from the breast of the mother is to be thought of.

Sometimes blood from the nose or throat is swallowed, particularly when the bleeding occurs during the night. This blood may subsequently be vomited. The inspection of the nose or throat will generally reveal the source of the hemorrhage in such cases.

The diagnosis between hemorrhage from the oesophagus and that from the stomach must be based upon the clinical history. The oesophagoscope, however, has been successfully employed for diagnostic purposes. Several cases have been reported of fatal hemorrhage from varices of the oesophagus. Such hemorrhage cannot be distinguished from gastric hemorrhage.

Much more frequently arises the question whether the hemorrhage is from the stomach or from the lungs. Sometimes the decision of this point {585} is very difficult, and it may even be impossible, especially when the physician is obliged to trust only to the statements of the patient or his friends. Difficulty in the diagnosis results mainly from the fact that coughing and vomiting of blood are often associated with each other. With hæmoptysis blood may be swallowed and then vomited, and with hæmatemesis more or less coughing occurs. The diagnosis is to be based upon the points contained in the following table:

HÆMOPTYSIS. | HÆMATEMESIS.
|
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.

[Footnote 11: Kundrat and Widerhofer mention no case of stenotic dilatation of the stomach in children. They say, however, that atonic dilatation due to over-feeding, and particularly to rachitis, is not infrequent in children. Widerhofer reports a case of very large dilatation of the stomach in a girl twelve years old. The cause of the dilatation was not apparent, and the clinical history was imperfect (_Gerhardt's Handb. d. Kinderkrankh._, Bd. iv. Abth. 2). Lafage (_Thèse_, Paris, 1881) reports a case of gastric dilatation at ten years, and another at sixteen years of age. R. Demme (abstract in _Berl. kl. Wochenschr._, 1883, No. 1) reports a case of large dilatation of the stomach in a boy six and a half years old. Cicatricial stenosis was suspected. Pauli (_De Ventriculi Dilatatione_, Frankfurt, 1839) reports an enormous dilatation of the stomach, believed to be due to congenital stenosis.]

SYMPTOMATOLOGY.--Inasmuch as dilatation of the stomach is usually secondary to some other disease, the symptoms of the primary disease have often existed a long time before those of dilatation appear.

The subjective symptoms of gastric dilatation are for the most part directly referable to disturbances of the functions of the stomach. These {593} subjective symptoms alone do not suffice for a positive diagnosis of the disease. Of the greatest diagnostic importance are an examination of the vomit and a careful physical exploration of the stomach.

The appetite with dilatation of the stomach may be normal, diminished, increased, or perverted. In the majority of cases the appetite is diminished, and there may be complete anorexia. Sometimes the appetite is increased even to voracity, which is explicable by the small amount of nutriment which is absorbed. Polyphagia may therefore be a result as well as a cause of dilatation of the stomach.

Often there is excessive thirst in consequence of the small quantity of fluid absorbed.

Dilatation of the stomach in itself does not usually cause sharp epigastric pain, although it is often associated with painful diseases of the stomach.

There is usually in the region of the stomach a sense of fulness and weight, which is often distressing and may be accompanied with dull pain.

Heartburn and eructations of gas and of bitter or of acid fluids are frequently present. The gas is often odorless, but sometimes it is very offensive. It may contain sulphuretted hydrogen. In a number of cases--which, however, are exceptional--the gas has been found inflammable, burning usually with a colorless flame (hydrogen), but rarely, as in a case from Frerichs' clinic, with a bright yellowish-white flame (hydrocarbons). Detonation upon setting fire to the gas has been noted. The analysis of the inflammable gas has shown oxygen and nitrogen in approximately the same proportion as in the atmosphere, in addition to large quantities of carbonic acid and of hydrogen, also marsh gas, and in Frerichs' case olefiant gas in small amount.[12] The oxygen and nitrogen are doubtless simply swallowed, but the carbonic acid and hydrogen are the result of abnormal fermentations in the stomach. The origin of the hydrocarbons in the gas is not clear, but they are probably also produced by fermentation within the stomach.

[Footnote 12: One of the analyses in Frerichs' case gave carbonic acid, 17.40; hydrogen, 21.52; marsh gas, 2.71; olefiant gas, traces; oxygen, 11.91; nitrogen, 46.44. In another analysis were found marsh gas, 10.75, and olefiant gas, 0.20. Sulphuretted hydrogen was also present (Ewald, in _Reichert und Du Bois-Reymond's Archiv_, 1874, p. 222).]

One of the most frequent symptoms, although not a constant one, of dilatation of the stomach is vomiting. This symptom often presents characters which, if not pathognomonic of dilatation, at least raise a strong presumption in favor of its presence. The act of vomiting is sometimes accomplished with such ease that it is hardly more than regurgitation; at other times the act is accompanied with violent and exhausting retching. A feature particularly characteristic of dilatation of the stomach is the abundance of the vomited material. In no other disease is such an enormous quantity evacuated from the stomach at one time. Blumenthal relates a case in which the vomited material amounted to sixteen pounds. Such large quantities can accumulate in the stomach of course only when a considerable time intervenes between the acts of vomiting. The vomiting of gastric dilatation does not generally occur until some hours after a meal. It often presents a certain periodicity, occurring, for instance, at intervals of two or three days, and followed usually by temporary relief. It is often observed that as the stomach {594} becomes larger and larger the vomiting becomes less and less frequent, but at the same time more abundant. Especially toward a fatal termination of the disease the walls of the stomach may become so paralyzed and insensible, and the patient so feeble, that the vomiting ceases altogether. Another valuable diagnostic sign furnished by the vomit is the presence of undigested food which has been taken a considerable time, it may be many days, previously.[13] If the morning vomit habitually contains undigested food which has been eaten the previous day, gastric dilatation either exists or is almost sure to develop.

[Footnote 13: Ritter relates the case of a man who vomited cherry-pits, although he had not eaten cherries for over a year (_Canstatt's Jahresbericht_, 1851, iii. p. 260)!]

The vomited matter is almost always in a condition of fermentation. If the vomit be allowed to stand in a vessel, it will separate into three layers--an upper, frothy; a middle, of turbid fluid, usually yellowish or brownish in color; and a lower layer, composed of solid particles, mostly alimentary débris. The vomit often emits an extremely offensive odor. The reaction is nearly always acid. Different kinds of fermentation--alcoholic, acetous, lactic acid, and butyric acid--are present, usually in combination with each other. The microscope reveals, besides undigested and partly-digested food, crystals of fatty acids, sarcinæ ventriculi, fungus-spores, and various forms of bacteria, particularly rod-shaped ones. The connection between sarcinæ and fermentative processes is not understood. There is no evidence that sarcinæ are capable of causing fermentation. Of greater importance is the recognition by the microscope of the spores of the yeast-fungus (Torula cerevisiæ). These spores are rarely absent, and their constant presence is evidence that fermentation is in progress. Fermentation often exists in undilated stomachs, but, as has already been mentioned, it is an important factor in the production of dilatation, so that its early recognition, if followed by proper treatment (washing out the stomach especially), may ward off the development of dilatation. The article on GASTRIC CANCER is to be consulted with reference to the habitual absence of free hydrochloric acid from the stomach in cases of cancerous dilatation. If cancer or ulcer of the stomach exists, blood is frequently present in the vomit, but even in the absence of ulcer or cancer or other demonstrable source of hemorrhage the vomit in cases of dilatation of the stomach may exceptionally contain blood, even for a considerable length of time. If the dilatation be due to pyloric stenosis, bile is not often found in the vomited material.

It has already been mentioned that vomiting is not a constant symptom of dilatation of the stomach. It remains to add that vomiting may be present without any of the distinctive features which have been described. Gastric dilatation, especially in its early stages, is often accompanied by attacks of acute indigestion (embarras gastrique) after some indiscretion in diet.

Constipation is an almost constant symptom of dilatation of the stomach. This is naturally to be expected when so little substance passes from the stomach into the intestine. The constipation is also to be explained in part by the absence of the usual reflex stimulus which the stomach during digestion normally exerts upon intestinal peristalsis, for the constipation is usually much relieved when the overweighted stomach is systematically washed out.

{595} Occasionally, attacks of diarrhoea occur in cases of dilatation of the stomach. The diarrhoea may perhaps be explained by the sudden discharge of a large quantity of fermenting material from the stomach into the intestine.

With marked dilatation of the stomach, especially when there is profuse vomiting, the urine is often considerably diminished in quantity. Particularly in cases treated by systematic washing out of the stomach, but also in other cases, especially with abundant vomiting, the acidity of the urine is often much reduced. The reaction may be even continuously alkaline (Quincke). Crystals of phosphate of magnesium have been occasionally found in the alkaline urine of gastrectasia (Ebstein). The urine is prone to deposit abundant sediments. It often contains an excess of indican.

The patient may suffer from attacks of dyspnoea and of palpitation of the heart in consequence of flatulent distension of the stomach.

The general condition of the patient will of course depend chiefly upon the character of the primary disease and upon the severity of the gastric symptoms. A moderate degree of dilatation may exist without much disturbance of the general health of the patient. But as the disease progresses and the food stagnates more and more in the stomach, finally to be rejected by vomiting, the patient cannot fail to lose flesh and strength. In extreme cases of gastrectasia, even without organic obstruction, the patient may be reduced to a degree of emaciation and of cachexia indistinguishable from that of cancer. As in so many other gastric diseases, the patient is usually mentally depressed and hypochondriacal. His sleep is disturbed. He suffers much from headache and vertigo. He feels incapable of physical or mental exertion. The skin is dry and harsh; the extremities are cold. Toward the last, cachectic oedema about the ankles can often be recognized.

Kussmaul was the first to call attention to the occurrence of tetanic spasms in cases of dilatation of the stomach.[14] This symptom has been observed almost exclusively in an advanced stage of the disease when the patient has become anæmic and weak. The spasms come on chiefly after attacks of profuse vomiting or after evacuating large quantities by the stomach-tube. The spasms may be preceded by a sense of pain or distress in the region of the stomach, by dyspnoea, by numbness of the extremities, or by great prostration. The tetanic spasms affect especially the flexor muscles of the hand and forearm, the muscles of the calves of the legs, and the abdominal muscles. The spasm may be confined to one or more of these groups of muscles, or there may be general tetanic contraction of the muscles of the body. Sometimes typical epileptiform convulsions with loss of consciousness occur. With general tetanic spasms the pupils are usually contracted, and often irresponsive to light. Sometimes there is abnormal sensitiveness upon pressure over the contracted muscles. The spasms may last for only a few minutes, or they may continue for several hours, or even for days. After their disappearance the patient is left extremely prostrated. Although tetanic spasms increase the gravity of the prognosis, they are not necessarily fatal.

[Footnote 14: _Deutsches Arch. f. kl. Med._, Bd. vi. p. 481.]

Kussmaul considers that these spasms are analogous to those occurring in cholera, and are referable to abnormal dryness of the tissues in consequence of the extraction of fluid. This view is supported by the usual {596} occurrence of the spasms after profuse vomiting or after washing out the stomach. Another explanation, which is perhaps more applicable to the epileptiform attacks, refers the convulsions to auto-infection by toxic substances produced in the stomach by abnormal fermentative and putrefactive changes (Bouchard).[15]

[Footnote 15: Laprevotte, _Des Accidents tétaniformes dans la Dilatation de l'Estomac_, Thèse, Paris, 1884, p. 48.]

Coma, with or without the peculiar dyspnoea of diabetic coma, is a rare occurrence in gastrectasia. (For a description of this form of coma see page 205.)

The temperature in gastric dilatation is generally unaffected. Penzoldt, however, saw two cases with moderate rise of temperature in the evening, which could not be explained by any complication. On the other hand, abnormally low temperature with slow pulse has been observed (Wagner).

Essential to the diagnosis of gastric dilatation is the physical examination of the stomach.

If the stomach be markedly dilated, inspection may reveal an abnormal prominence of the abdominal walls in the epigastric region and extending a variable distance below the level of the umbilicus. This prominence is most marked on the left side. When the abdominal walls are sufficiently thin and relaxed, sometimes the outline of the greater curvature between the umbilicus and pubes, less frequently that of the lesser curvature, can be made out. Sometimes the peristaltic waves of the stomach can be perceived through the thin abdominal walls. By pressure or by passing the hand across the abdomen gastric peristalsis may sometimes be excited. The peristaltic movements of the stomach, however, are rarely perceived except when the dilatation is due to stenosis and the muscular coat of the stomach is hypertrophied. The peristaltic waves generally pass from left to right, rarely in the opposite direction as well. Careful attention to the situation, direction, and extent of these waves is necessary to distinguish them from similar peristaltic movements of the intestine.[16] The diminution in size of the abdominal prominence caused by a dilated stomach after profuse vomiting or after washing out the stomach may aid in the diagnosis.

[Footnote 16: Kussmaul says that vigorous peristaltic movements of the stomach may be perceptible through the abdominal walls even when there is no dilatation of the stomach. Under these circumstances he attributes the peristaltic commotion to an independent neurosis of the stomach ("Die Peristaltische Unruhe des Magens," _Volkmann's Samml. klin. Vorträge_, No. 181).]

An important aid in bringing out the contours of the stomach is the artificial distension of the organ by the generation within it of carbonic acid gas, as first suggested by Frerichs. For this purpose 20-30 grains of bicarbonate of sodium and 15-20 grains of tartaric acid, each dissolved in a little lukewarm water, may be given one after the other. If the stomach be much dilated and relaxed, it may be necessary to give much larger quantities of the powders (up to 2-2½ drachms of the soda and a corresponding quantity of the acid). It is well to have a stomach-tube at hand in order to withdraw the gas in case unpleasant symptoms develop. Sometimes the stomach fails to become distended by this procedure. This is due in some cases to the escape of the gas through the pyloric orifice into the intestine--a condition designated by Ebstein as incontinence of the pylorus. It may be that sometimes the gas produces such firm {597} contraction of the gastric walls that the stomach does not expand by the pressure of the gas. Instead of generating gas, a similar result may be produced by simply injecting air into the stomach through a stomach-tube, as recommended by Oser and by Runeberg. The air may, however, escape along the side of the tube.

Palpation of the distended stomach yields an elastic resistance which has been compared to that of an air-cushion. By palpating carefully from above downward the greater curvature can sometimes be appreciated, but in general it is difficult to distinguish it from the transverse colon. Peristaltic movements may perhaps be appreciated by palpation when they are not evident on inspection. If a dilated stomach contains considerable fluid and the abdominal walls are yielding, fluctuation may be perceived by palpation. The lowest level at which this fluctuation can be felt may afford a clue as to the position of the lower border of the stomach, but not much dependence can be placed upon this sense of fluctuation unless many sources of error in its interpretation are excluded.

By pressing gently and repeatedly against the abdominal walls a splashing sound can usually be heard in cases of well-marked dilatation of the stomach (bruit de clapotement). This sound can best be brought out when the patient is in the recumbent position, with relaxed abdominal walls, by palpating near the left border of the ribs. The same sound can be produced by shaking the patient (bruit de glou-glou). This sound may be heard at a considerable distance from the patient, to whom it may be a source of much annoyance. In itself this splashing sound is without diagnostic significance, as the condition for its production--namely, the simultaneous presence of gas and liquid in the stomach--exists often in healthy persons. By paying attention, however, to the time at which this sound can be produced after eating or drinking, and to its greater or less constancy, some diagnostic importance can be attached to this sign. If the splashing sound can be usually produced two hours or longer after the ingestion of liquid or six hours after an ordinary meal, it generally indicates that dilatation of the stomach exists.[17] It is necessary to exclude somewhat similar sounds which may be produced in the intestines, particularly in the transverse colon and cæcum. The series of gurgling sounds which may sometimes be produced in the intestine by palpation are not likely to be confounded with the single splashing sound produced in the stomach, but under certain circumstances a splashing sound may be produced in the transverse colon which cannot be distinguished from the gastric sound. If a dilated stomach contains a very large quantity of fluid, the splashing sound cannot readily be produced.

[Footnote 17: Baradat, _Étude sur le Bruit de Clapotement stomacal_, Thèse, Paris, 1884. Baradat says that this bruit is also diagnostic of dilatation when it can be produced by palpating below a horizontal line passing through the junction of the ninth and tenth ribs, but it is evident that motion might be transmitted to the stomach even when its greater curvature is above this line by palpating below the level of the umbilicus.]

Leube has pointed out that the end of the stomach-tube (of course the hard tube), after it has been inserted into the stomach, can often be felt through the abdominal walls.[18] He says that if the tube can be felt below a horizontal line passing through the anterior superior spinous processes of the ileum, dilatation of the stomach may be positively diagnosed, {598} and the existence of dilatation is probable if the tube can be felt much below the umbilicus. No force should be used in trying to make the end of the tube palpable. Of course if the abdominal walls are thick or very tense the tube cannot be felt. Leube's method is simple and convenient, and applicable to many cases. As will be explained hereafter, a position of the lower border of the stomach even quite as low as Leube's rule demands cannot be considered by itself positive evidence of dilatation.[19]

[Footnote 18: _Deutsches Arch. f. kl. Med._, Bd. xv. p. 394.]

[Footnote 19: According to Oser, there is a possible source of error in Leube's method--namely, that the sound may slide along the greater curvature of the stomach, and even reach the pylorus, so that the end may be felt higher than the lowest point of the stomach. Considerable objection has been made to Leube's method on the ground of its danger, but this objection is based on the assumption that greater energy is employed in pressing forward the sound than Leube recommends (Oser, article "Magenerweiterung" in _Eulenburg's Real Encyclopädie_, Bd. viii., 1881).]

The length to which the stomach-tube can be inserted before meeting resistance may evidently give some idea as to the size of the stomach. The attempt, however, to establish any general law with reference to this point has not proven successful.

In many cases valuable information as to the size of the stomach is afforded by percussion. Over the greater part of the stomach the percussion note is tympanitic, sometimes with a metallic quality. Over the most dependent part of the stomach a dull sound is produced on percussion in case a sufficient quantity of fluid or solid material is contained in the viscus. In the upright position, therefore, in percussing over the stomach from above downward, the tympanitic note gives place to a dull sound, and this zone of dulness will change with the position of the patient, so that in the recumbent posture the dulness may entirely disappear. In order to prove that the region of dulness belongs to the stomach, Piorry caused the patient to drink a large quantity of water (a pint to a quart). In a healthy empty stomach this quantity of water suffices to produce a zone of dulness which does not descend below the level of the umbilicus. If, however, the dulness be produced below the level of the umbilicus, it is inferred that dilatation exists. Penzoldt's modification of Piorry's method gives more certain results.[20] By withdrawing the fluid from the stomach by the stomach-tube the dulness may be made to disappear, and by injecting more fluid the dulness may be made to reappear at will. By noting the lower limit of the dulness thus produced the position of the lower border of the stomach may be determined. The farther this lies below the umbilicus the greater, presumptively, is the degree of dilatation. The artificial distension of the stomach with gas may also aid in determining its limits by percussion. It must be said that in general the separation of the lower limits of the stomach from the transverse colon by means of percussion is a matter of great difficulty, and sometimes is impossible.

[Footnote 20: Penzoldt, _op. cit._, p. 48.]

Upon auscultation over a dilated stomach sometimes a fine crackling or sizzling sound, like that audible upon first uncorking a bottle of soda-water, can be heard.[21] This is referable to the fermentation which is in progress in the stomach. Eichhorst says that a similar but finer crackling sound can be heard over a stomach in which carbonic acid gas is {599} being artificially generated, and that this sound abruptly ceases when the ear passes below the limits of the greater curvature.[22]

[Footnote 21: Pauli was the first to record this phenomenon (_De Ventriculi Dilatatione_, Frankfurt, 1839).]

[Footnote 22: _Handb. d. spec. Path. u. Ther._, Bd. i. p. 750, 1883.]