[Footnote 89: On the posterior wall of the stomach, midway between the

greater and the lesser curvature and five inches to the right of the

cardiac orifice, was a round ulcer half an inch in diameter, with

smooth, sharp edges. In the floor of the ulcer, which extended to the

muscular coat, was a small perforated aneurism of a branch of the

coronary artery. In addition there were small, granular kidneys,

hypertrophied heart without valvular lesion, and chronic interstitial

splenitis. Small and medium-sized arteries in the kidneys, spleen,

heart, lymphatic glands, and stomach were the seat of a typical

endarteritis obliterans, resulting in some instances in complete

closure of the lumen of the vessel. The patient, who was attended by

Sassdorf, was seized during the night with vomiting of blood, which

continued at intervals for twenty-four hours until his death. The

patient was a man about fifty years of age, without previous history of

gastric ulcer or of syphilis.]

In one case Powell[90] found a small aneurism of the coronary artery in

an ulcer of the lesser curvature of the stomach. Hauser[91] found an

aneurismal dilatation of an atheromatous and thrombosed arterial twig

in the floor of a recent ulcer. In my case of obliterating endarteritis

just referred to there was a small aneurism in the floor of the ulcer.

These miliary aneurisms in the floor of gastric ulcers seem to be

analogous to those in the walls of phthisical cavities. Miliary

aneurisms occur in the stomach independently of gastric ulcer, and may

give rise to fatal hæmatemesis, as in four cases reported by

Galliard.[92]

[Footnote 90: _Trans. of the Path. Soc. of London_, vol. xxix.]

[Footnote 91: _Das chronische Magengeschwür, etc._, p. 11, Leipzig,

1883.]

[Footnote 92: _L'Union méd._, Feb. 26, 1884. Curtis reported a case of

fatal hæmatemesis from an aneurism, not larger than a small pea, seated

in the cicatrix of an old ulcer (_Med. Annals of Albany_, Aug., 1880).]

Gastric ulcer is occasionally associated with waxy degeneration of the

arteries of the stomach.[93] In most of these cases there were multiple

shallow ulcers. Hæmatemesis is generally absent in gastric ulcer

resulting from waxy disease of the gastric blood-vessels. As is well

known, the amyloid material itself resists the action of the gastric

juice.

[Footnote 93: Hauser (_op. cit._) alludes to a case in which, with waxy

degeneration of the stomach, over one hundred small ulcers were found

in different stages of development, from hemorrhagic infiltrations to

complete ulcers. Cases belonging here are reported by Fehr, _Ueber die

Amyloide Degeneration_, Inaug. Diss., Bern, 1866; Merkel, _Wiener med.

Presse_, 1869; Edinger, _Deutsches Arch. f. klin. Med._, Bd. 29, p.

568; Marchiafava, _Atti del Accad. Med. di Roma_, iii. p. 114; and

Mattei, _Deutsche med. Zeitung_, July 5, 1883.]

Finally, varicosities of the veins of the stomach have been once in a

{512} while found with gastric ulcer. In a large number, probably in

the majority, of cases of gastric ulcer no changes have been found in

the blood-vessels of the stomach except such as were manifestly

secondary to the ulcer.

That gastric ulcer is frequently complicated with chronic catarrhal

gastritis has been repeatedly mentioned in the course of this article.

PATHOGENESIS.--Without doubt, the most obscure chapter in the history

of gastric ulcer is that relating to its origin and to its persistence.

Notwithstanding a vast amount of investigation and of discussion,

unanimity of opinion upon these subjects has not been reached. In view

of this uncertainty it is desirable in this article to do little more

than to summarize the leading theories as to the development of gastric

ulcer.

Most observers are agreed that the digestive action of the gastric

juice has some share in the development and the progress of the ulcer,

but as to the first cause of the ulcer there are various hypotheses.

The earliest theory refers the origin of simple ulcer of the stomach to

inflammation. Since its advocacy by Abercrombie and by Cruveilhier this

theory has always had its adherents, particularly among French writers.

It is true that in stomachs which are the seat of simple ulcer

evidences of inflammation can often be found both in the neighborhood

of the ulcer and elsewhere. In recent times the supporters of the

inflammatory origin of gastric ulcer lay especial stress upon the

presence of foci of infiltration with small round cells in the mucous

and the submucous coats.[94] But it is difficult to explain by the

inflammatory theory the usually solitary occurrence and the funnel-like

shape of gastric ulcer.

[Footnote 94: Laveran, _Arch. de Phys. norm. et path._, 1876, p. 443;

Galliard, _Essai sur la Pathogenie de l'Ulcère simple de l'Estomac_,

Thèse de Paris, 1882; Colombo, _Annali univ. di Med._, 1877.]

The theory that gastric ulcer is of neurotic origin has also been

advocated. Some refer the origin to the secretion of an excessively

acid gastric juice under abnormal nervous influence (Günsburg), others

to vaso-motor disturbances, and others to trophic disturbances. Wilks

and Moxon compare simple gastric ulcer to ulcers of the cornea

resulting from paralysis of the trigeminus. The neurotic theory of the

origin of gastric ulcer is altogether speculative and has never gained

wide acceptance.[95]

[Footnote 95: The first to attribute gastric ulcer to nervous influence

was Siebert (_Casper's Wochenschr. f. d. Heilk._, 1842, No. 29, and

_Deutsche Klinik_, 1852). Cf. also Günsburg, _Arch. f. phys. Heilk._,

xi., 1852; Wilks and Moxon, _Lect. on Path. Anat._, 2d ed., Philada.,

1875, p. 386. Osborne in 1845 attributed gastric ulcer to the secretion

of an abnormally acid juice by a circular group of the gastric glands

(_Dublin Journ. of Med. Sci._, vol. xxvii. p. 357).]

The view which has met with the greatest favor is that which attributes

the origin of gastric ulcer to impairment or arrest of the circulation

in a circumscribed part of the wall of the stomach, and to a subsequent

solution by the gastric juice of the part thus affected. Rokitansky

first suggested this view by assigning hemorrhagic necrosis of the

mucous membrane as the first step in the formation of the ulcer; but it

is Virchow who has most fully developed this view and has given it its

main support. The first cause of gastric ulcer, according to Virchow,

is a hemorrhagic infiltration of the coats of the stomach induced by

local disturbances in the circulation. The part the nutrition of which

is thus impaired or destroyed is dissolved by the gastric juice.

{513} The affections of the gastric blood-vessels to which importance

has been attached are (_a_) embolism and thrombosis; (_b_) diseases of

the coats of the vessels, as atheroma, obliterating endarteritis, fatty

degeneration, amyloid degeneration, and aneurismal and varicose

dilatations; (_c_) compression of the veins by spasm of the muscular

coats of the stomach in vomiting and in gastralgia; (_d_) passive

congestion of the stomach by obstruction in the portal circulation.

In support of this view are urged the following facts: First, it has

been proven by the experiments of Pavy that parts of the gastric wall

from which the circulation has been shut off undergo digestion; second,

hemorrhagic infarctions have been observed in the stomach, both alone

(Von Recklinghausen, Hedenius) and associated with gastric ulcer (Key,

Rindfleisch); third, the hemorrhagic infiltration in the walls of

recently-formed ulcers indicates a hemorrhagic origin; fourth, the

funnel-like shape of the ulcer resembles the funnel-shaped area of

distribution of an artery; fifth, gastric ulcers have been

experimentally produced by injecting emboli into the gastric arteries

(Panum, Cohnheim).[96]

[Footnote 96: Pavy, _Philosoph. Trans._, 1763, p. 161; V.

Recklinghausen, _Virchow's Archiv_, Bd. 30, p. 368; Axel Key, _Virchow

und Hirsch's Jahresb._, 1870, Bd. ii. p. 155; Rindfleisch, _Lehrb. d.

path. Gewebelehre_, 5te Aufl., Leipzig, 1878; Panum, _Virchow's

Archiv_, Bd. 25, p. 491; Cohnheim, _Vorles. über allgem. Path._, Bd.

ii. p. 53, Berlin, 1880.]

The main objections to this view are the infrequency with which the

assumed changes in the blood-vessels have been demonstrated, the common

occurrence of gastric ulcer at an age earlier than that at which

diseases of the blood-vessels are usually present, and the absence of

gastric ulcer in the vast majority of cases of heart disease, with

widespread embolism of different organs of the body. To meet some of

these objections, Klebs[97] presupposes in many cases a local spasmodic

contraction of the gastric arteries, causing temporary interruption of

the circulation; Rindfleisch and Axel Key, compression of the gastric

veins, with resulting hemorrhagic infiltration by spasm of the muscular

coat of the stomach in vomiting and in gastralgic attacks. But these

are pure hypotheses.

[Footnote 97: _Handb. d. path. Anat._, Bd. i. p. 185, Berlin, 1869.]

What is actually known concerning diseases of the gastric blood-vessels

in ulcer of the stomach has already been stated under the morbid

anatomy. From this it may be inferred that the origin of gastric ulcer

in diseased conditions of the blood-vessels has been established only

for a comparatively small group of cases.

Böttcher's[98] view that gastric ulcer is of mycotic origin, being

produced by micrococci, has thus far met with no confirmation.

[Footnote 98: _Dorpater med. Zeitschr._, Bd. v. p. 148, 1874.]

There are those who hold an eclectic view concerning the origin of

gastric ulcer. They believe that ulcer of the stomach may be produced

by a variety of causes, such as inflammation, circulatory disturbances,

irritating substances introduced into the stomach, traumatism, etc. The

peculiarities of the ulcer are due not to any specific cause, but to

the solvent action of the gastric juice, which keeps clean the floor

and the sides of the ulcer. These clean edges and floor, which are

incident to all ulcers of the stomach, justify no conclusion as to the

cause of the ulcer. Engel[99] over thirty years ago held that gastric

ulcer might {514} originate in various ways--that there was nothing

specific about it. Brinton was also of similar opinion.

[Footnote 99: _Prager Vierteljahrschr._, 1853, ii.]

Gastric ulcers have been produced experimentally in animals in a

variety of ways, but these experiments have not materially elucidated

the pathenogenesis of ulcer in man. Schiff by lesions of various parts

of the brain, and later Ebstein by lesions of many parts of the central

and peripheral nervous system by injections of strychnine--in fact,

apparently by any means which greatly increased the

blood-pressure--produced in the stomachs of animals ecchymoses and

ulcers. Müller by ligation of the portal vein, Pavy by ligation of

arteries supplying the stomach, likewise produced hemorrhages and

ulcers. The results of Pavy could not be confirmed by Roth and others.

Panum, and afterward Cohnheim, produced gastric ulcers by introducing

multiple emboli into the gastric arteries. Daettwyler under Quincke's

direction caused, in dogs with gastric fistulæ, ulcers of the stomach

by various mechanical, chemical, and thermic irritants applied to the

inner surface of the stomach. Aufrecht observed hemorrhages and ulcers

in the stomachs of rabbits after subcutaneous injections of

cantharidin.[100]

[Footnote 100: Schiff, _De vi motorea baseos encephali_, 1845, p. 41;

Ebstein, _Arch f. exp. Path. u. Pharm._, 1874, p. 183; Müller, _Das

corrosive Geschwür im Magen, etc._, p. 273, Erlangen, 1860; Pavy,

_Guy's Hosp. Rep._, vol. xiii., 1867; Roth, _Virchow's Archiv_, Bd. 45,

p. 300, 1869; Panum, _loc. cit._; Cohnheim, _op. cit._; Daettwyler,

Quincke, _Deutsche med. Wochenschr._, 1882, p. 79; Aufrecht,

_Centralbl. f. d. med. Wiss._, 1882, No. 31.]

The most interesting of these experiments are those of Cohnheim and of

Daettwyler, who demonstrated that in one essential point all of these

experimental ulcers differ from simple gastric ulcer in man--namely, in

the readiness with which they heal. To this ready healing the gastric

juice, much as it has been accused of causing the spread of gastric

ulcers in man, seems to have offered no obstacle. We know that similar

losses of substance in the human stomach heal equally well.[101] Hence

it has been maintained throughout this article that it is unjustifiable

to regard all of the scars found in the human stomach as the result of

simple ulcer.

[Footnote 101: Portions of the mucous membrane of the stomach,

sometimes with some of the submucous coat, have been in several

instances removed with the stomach-pump, but thus far no bad effects

have followed.]

It appears from these experiments, as well as from observations on man,

that it is more difficult to explain why ulcers in the stomach do not

heal than it is to understand how they may be produced. From this point

of view the observation of Daettwyler is of interest, that in dogs

which had been rendered anæmic by repeated abstraction of blood not

only did slighter irritants suffice to produce ulcers of the stomach,

but the ulcers healed much more slowly. Practically, it is important to

learn what are the obstacles to the repair of gastric ulcers, but our

positive knowledge of these is slight. It is probable that such

obstacles are to be found in constitutional causes, such as anæmia and

chlorosis, in abnormal states of the blood-vessels around the ulcer, in

catarrhal affections of the stomach, in irritating articles of food, in

improper modes of living, and in increased acidity of the gastric

juice.

DIAGNOSIS.--In many cases the diagnosis of gastric ulcer can be made

with reasonable certainty; in other cases the diagnosis amounts only to

a suspicion more or less strong, and in still other cases the diagnosis

is impossible.

{515} The diagnostic symptoms are epigastric pain, vomiting, and

gastric hemorrhage. The characteristics of the pain which aid in the

diagnosis are its fixation in one spot in the epigastric region, its

onset soon after eating, its dependence upon the quantity and the

quality of the food, its relief upon the complete expulsion of the

contents of the stomach, its alleviation by changes in posture, and its

increase by pressure. That the pain of gastric ulcer has not always

these characteristics has been mentioned under the Symptomatology.

Vomiting without hæmatemesis is the least characteristic of these

symptoms. It aids in the diagnosis when it occurs after eating at the

acme of a gastralgic attack and is followed by the relief of pain.

Hæmatemesis is the most valuable symptom in diagnosis. The more profuse

the hemorrhage and the younger the individual in whom it occurs, the

greater is the probability of gastric ulcer. It should not be forgotten

that the blood is sometimes discharged solely by the stools.

The simultaneous occurrence of all these symptoms renders the diagnosis

of gastric ulcer easy.[102] In all cases in which gastrorrhagia is

absent the diagnosis is uncertain; but gastric ulcer should be

suspected whenever the ingestion of food is followed persistently by

severe epigastric pain and other causes of the pain have not been

positively determined. When the course of the ulcer is latent and when

the symptoms are only those of dyspepsia, the diagnosis is of course

impossible. In cases previously obscure a diagnosis in extremis is

sometimes made possible by the occurrence of perforation of the

stomach.

[Footnote 102: That even under the most favorable circumstances

absolute certainty in the diagnosis of gastric ulcer is not reached is

illustrated by a case reported with great precision and fulness by

Banti: A female servant, twenty-one years old, had every symptom of

gastric ulcer, including repeated hæmatemesis and the characteristic

epigastric pain. She was nourished by enemata. She died from an

ulcerative proctitis four days after the last hemorrhage from the

stomach. Only a slight catarrhal inflammation of the stomach was found

at the autopsy, without trace of ulcer, cicatrix, or ecchymosis ("Di un

Caso d'Ematemesi," _La Sperimentale_, Feb., 1880, p. 168). It would

seem as if there must have been an ulcer which had healed so completely

as to leave no recognizable scar.]

In making a differential diagnosis of gastric ulcer, as well as of any

disease, reliance should be placed more upon the whole complexion of

the case than upon any fancied pathognomonic symptoms.

The diseases which are most difficult to distinguish from gastric ulcer

are nervous affections of the stomach. Like gastric ulcer, most of

these are more common in women than in men, and especially in chlorotic

women with disordered menstruation and with hysterical manifestations.

These nervous affections are manifold and their leading characteristics

are not yet well defined. The most important of these affections are

nervous dyspepsia, nervous vomiting, nervous gastralgia, and gastric

crises.

The leading symptoms of nervous dyspepsia, as described by Leube,[103]

are the ordinary symptoms of dyspepsia without evidence of anatomical

alteration of the stomach, and with the proof by washing out the

stomach that the process of digestion is not delayed. Nervous dyspepsia

is often associated with other nervous affections, and is caused

especially by influences which depress the nervous system. Epigastric

pain, and especially tenderness on pressure over the stomach, are not

common symptoms in nervous dyspepsia. Only those rare cases of gastric

ulcer in which hemorrhage from the stomach is absent and epigastric

pain is not prominent {516} are likely to be confounded with nervous

dyspepsia. In such cases, although the diagnosis of nervous dyspepsia

is by far the most probable, the patient may be confined to bed and put

upon the strict regimen for gastric ulcer. If in the course of ten days

or two weeks essential relief is not obtained, ulcer may be excluded,

and the proper treatment for nervous dyspepsia with tonics and

electricity may be adopted (Leube).

[Footnote 103: _Deutches Arch. f. klin. Med._, Dec. 18, 1878.]

In nervous vomiting, which occurs most frequently in hysterical women,

other nervous manifestations are present; there are usually less

epigastric pain and tenderness than in ulcer; the nutrition is better

preserved; the vomiting is less dependent upon the ingestion of food

and more dependent on mental states; and there are longer intervals of

relief than in ulcer. Still, it may be necessary to resort to the

therapeutical diagnosis as in the preceding instance.

In this connection attention may be called to the importance of

searching for reflex causes of vomiting, such as beginning phthisis,

ovarian or uterine disease, cerebral disease, and pregnancy; also to

certain cases of chronic Bright's disease in which gastric disturbances

are the main symptoms.

Of all the nervous affections of the stomach, nervous gastralgia is the

one which presents the greatest similarity to gastric ulcer. Its

diagnosis from gastric ulcer is often extremely difficult, and may be

impossible. The points of difference given in the following table may

aid in the diagnosis:

NERVOUS GASTRALGIA. | ULCER OF THE STOMACH.

|

1. Pain is often independent of | 1. Pain is mostly dependent upon

the ingestion of food, and may | taking food, and its intensity

even be relieved by taking food.| varies with the quality and the

| quantity of the food.

|

2. Pain is often relieved by | 2. Pain is increased by pressure.

firm pressure. |

|

3. Pain is rarely relieved by | 3. Pain after a meal is usually

vomiting. | relieved by vomiting.

|

4. Fixed point of tenderness and| 4. These are often present.

of subjective pain not generally|

present. |

|

5. Relief is usually complete | 5. Some pain often continues

between the paroxysms. | between the paroxysms.

|

6. Nutrition frequently well | 6. Nutrition usually affected.

preserved. |

|

7. Usually associated with other| 7. Neuropathic states less

nervous affections, such as | constantly present.

hysteria, neuralgia in other |

places, ovarian tenderness, etc.|

|

8. Benefited less by regulation | 8. Benefited not by electricity,

of diet than by electricity and | but by regulation of diet.

tonic treatment. |

|

9. Not followed by dilatation of| 9. Dilatation of stomach may

stomach. | supervene.

According to Peter,[104] the surface temperature of the epigastrium is

elevated in gastric ulcer, but not in nervous gastralgia.

[Footnote 104: _Gaz. des Hôp._, June, 1883.]

Probably not a single one of the points mentioned in the table is

without exception. Nervous gastralgia may be associated with gastric

ulcer, and if the ulcer is otherwise latent the diagnosis is manifestly

impossible. A diagnosis of purely functional gastralgia has been

repeatedly overthrown by the occurrence of profuse hæmatemesis. There

is no symptom {517} upon which it is more unsatisfactory to base a

diagnosis than upon pain. There is much difference among physicians as

regards the frequency with which they diagnose gastric ulcer in the

class of cases here described. It is probable that the error is

oftenest a too frequent diagnosis of gastric ulcer than the reverse.

Nevertheless, when there is doubt it is well to submit the patient for

a time to the proper treatment for gastric ulcer.

In several instances gastric crises have been mistaken for gastric

ulcer. These gastric or gastralgic crises, as they are called by

Charcot, by whom they have been best described,[105] are most

frequently associated with locomotor ataxia, but they may occur in

connection with other diseases of the spinal cord (subacute myelitis,

general spinal paralysis, and disseminated sclerosis), and an analogous

affection has been described by Leyden[106] as an independent disease

under the name of periodical vomiting with severe gastralgic attacks.

Gastric crises have been most carefully studied as a symptom in the

prodromic stage of locomotor ataxia. The distinguishing features of

these crises are the sudden onset and the atrocious severity of the

gastric pain; the simultaneous occurrence of almost incessant vomiting;

the habitual continuance of the paroxysms, almost without remission,

for two or three days; the normal performance of the gastric functions

in the intervals between the paroxysms, which may be months apart; the

frequent association with other prodromic symptoms of locomotor ataxia,

such as ocular disorders and fulgurating pains in the extremities; and

the development after a time of ataxia. Leyden has observed during the

attacks retraction of the abdomen without tension of the abdominal

walls, obstinate constipation, scanty, dark-colored urine, even anuria

for twenty-four hours, and increased frequency of the pulse (also noted

by Charcot). Vulpian[107] mentions a case in which there was vomiting

of dark-colored blood, and in which naturally the diagnosis of gastric

ulcer had been made. In the autopsies of Leyden and of Charcot no

lesions of the stomach have been found.

[Footnote 105: _Leç. sur les Maladies du Syst. nerveux_, t. ii. p. 32,

Paris, 1877.]

[Footnote 106: _Zeitschr. f. klin. Med._, iv. p. 605, 1882.]

[Footnote 107: _Maladies du Syst. nerveux_, p. 273, Paris, 1879.]

The differential diagnosis of gastric ulcer from gastric cancer will be

considered in the article on GASTRIC CANCER.

It has already been said that a part of the symptoms of gastric ulcer

are due to an associated chronic catarrhal gastritis. Usually other

symptoms are present which render possible the diagnosis of the ulcer.

There is usually some apparent external or internal cause of chronic

catarrhal gastritis, whereas the etiology of ulcer is obscure; in

chronic gastritis gastralgic paroxysms and the peculiar fixed

epigastric pain of gastric ulcer are usually absent; in chronic

gastritis profuse hæmatemesis is a rare occurrence; and in gastritis

the relief obtained by rest and proper regulation of the diet, although

manifest, is usually less immediate and striking than in most cases of

gastric ulcer.

The passage of gall-stones is usually sufficiently distinguished from

gastric ulcer by the sudden onset and the sudden termination of the

pain, by the situation of the pain to the right of the median line, by

the complete relief in the intervals between the attacks, by the

occurrence of jaundice, by the recognition sometimes of enlargement of

the liver and of the gall-bladder, and by the detection of gall-stones

in the feces.

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