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Diseases of the stomach : including dietetic and medicinal treatment

George Roe Lockwood · 1913 · Scanned text · Free in the US

242,175 words · about 16 h 58 min to read

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About this book

Author
George Roe Lockwood
Language
English
Published
1913
Length
242,175 words · about 16 h 58 min
Sections
20 reader sections
Text
Scanned text, read from page scans by OCR; may contain errors
Rights
Public domain in the United States · PD-US by publication date

 

Contents (20)

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Front matter

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COLUMBIA UNIVERSITY

Chapter I

Although acute gastritis is undoubtedly one of the commonest of diseases, the number of cases actually coming under the observation of the physician is relatively small, as in the great majority of instances the symptoms are either transient or of such mild severity that no medical treatment is required. Unfortunatel}^, however, the diagnosis of acute catarrh of the stomach is made far more frequently than is warranted, and often includes cases of acute appendicitis, gall-bladder disease, ulcer, acute onset of cancer of the stomach, neuroses, and even the gastric crises of tabes. The term, strictly speaking, should only be applied to those cases of acute indigestion in which direct evidence of gastric inflammation exists, and not indiscriminately used to include all temporary subjective disturbances that follow dietetic errors. It is, however, extremely difficult to determine, clinically, whether or not a true inflammation exists, as pathognomonic signs of such are usually lacking, except in the infectious forms that are the result of food poisoning.

Acute catarrhal gastritis may be clinically divided into two prominent types :

1. Dietetic or simple gastritis.

2. Infectious gastritis or food poisoning.

I. Dietetic or Simple Gastritis. — Etiology. — Among the causes predisposing to acute catarrhal gastritis may be enumerated lesions of the heart or of the liver, leading to chronic congestion of the stomach. Conditions of depreciated health or of fever that render it difficult for the stomach properly to digest its food, may be considered as contributory causes, although the influence of the general condition of health is far less potent than is ordinarily supposed. It is said that gouty individuals are liable to recurrent attacks of gastric catarrh. 2

The resistance of the stomach to inflammation differs very much in different people — a fact which we recognize by the use of such terms as "strong stomachs" and "weak digestions." There are those whose stomachs, while equal to the ordinary daily task of digestion, are not possessed of any reserve power, but succumb to dietetic errors to which others seem immune.

There are, moreover, individual idiosyncrasies in which some normal and healthy food produces acute gastric irritation, that cannot be ascribed to toxic effects or to bacterial invasion. Thus, some persons suffer from vomiting and urticaria from eating fish in any form, or crabs or lobsters, while in others, beef, pork, and game will produce the same unpleasant results. It is not to be denied, however, that many of these instances are really cases of autosuggestion, from subconscious impressions derived from some previous unpleasant experience with that particular article of food. It is probable that many of these so-called idiosyncrasies may be explained by the recent theory of anaphylaxis. ^

During the earlier years of life the chief cause is found in dietetic errors. In old age the tendency to portal stasis renders the ailment relati\ely common. In these aged subjects the effect of exposure to cold may be sufficient to induce an attack, by causing a sudden increase in the internal congestion. Among other predisposing causes in elderly persons may be mentioned the frecjuency with which achylia is found in those aged over sixty years. The eft'ect of such deficiency of gastric digestion in inducing an attack of acute gastric catarrh can readily be appreciated.

A predisposition to gastric catarrh is present during infectious disease, intestinal parasites, acute renal or cardiac disease, and- often accompanies acute tuberculosis, masking the primary disease in many cases in which the pulmonary symptoms and physical signs are not evident.

Infection of gastric mucous membrane as the result of bacterial invasion is common enough. Gastritis due to streptococcus, typhoid bacillus, or pneumococcus is generally well recognized. These bacteria usually obtain entrance by the blood or lymph channels, and the gastritis is a secondary manifestation of the original infective disease. Pneumococcus infection may occur as a primary form of invasion, and may give rise to gastric ulceration.

Exciting Cause. — The commonest exciting cause for acute gastritis is dietetic error. This may occur in a great variety of ways.

1. Errors in Food. — The food may be too rich, or may be improperly cooked. Overeating is one of the most frequent causes. Drinking of cold liquids or of ice-cream soda when overheated is a common cause for acute gastric catarrh, as is also overindulgence in alcohol. Attacks in children commonly follow the eating of unripe fruit. The influence of idiosyncrasy in diet has already been alluded to.

2. Errors in Eating. — Food may be proper and wholesome, but if imperfectly masticated, or bolted, or eaten when the patient is overtired or under nervous strain, gastric catarrh may ensue.

The form of gastritis that follows the ingestion of infected food is described under a separate heading.

Swallowed secretions from the nasopharynx or bronchi may act as infective agents, especially potent in this regard, being decomposed pus from gangrene of the lung and the alveolar secretions of Rigg's disease.

Pathology. — No one has had a better opportunity of studying the gross appearance of the stomach in this condition than William Beaumont in the course of his prolonged experiments on Alexis St. Martin. He saw the condition as it existed in the living subject without the postmortem changes which render a correct appreciation of the true appearance so difficult. Morbid changes, following errors in eating and drinking, presented themselves several times in St. Martin's stomach during Beaumont's investigations. He thus describes an attack of acute gastritis:

"The coats of the stomach have not appeared in their usual healthy condition for several days past— the color darker; mucous coat unequal, some patches of a purplish color with aphthous edges, surface inclined to be dry, very little secretion of gastric juice, digestion slower and less perfect than usual, bowels inactive."

In another place, under similar conditions, he speaks of the "large proportion of thick, ropy mucus" mixed.with the stomach contents.

This practically represents our conception of the condition at the present time. The stomach is not altered in size or shape. The changes are most marked at the pylorus, the region which bears the brunt of the digestive process. There is diffuse or patchy redness, with swelling of the mucous membrane. At times, there may be minute hemorrhages or superficial erosions. An excessive amount of tenacious mucus, occasionally of brownish tinge from extravasation of blood, covers the surface. The amount of gastric juice secreted is much less than normal, and it contains a diminished amount of hydrochloric acid.

Microscopically the changes are confined almost entirely to the mucosa. The glandular epithelium is swollen and granular, and it is difficult to distinguish between the chief and parietal cells. Goblet cells are numerous. The capillaries and small vessels are dilated and there may be many red blood cells scattered through the mucosa, with some round-celled infiltration between the tubules and extending into the submucosa, which is often edematous. The solitary lymph follicles are often swollen, and leukocytes may be present in the intertubular tissue. The lumina of the glands contain debris of degenerated cells. Leukocytes, red blood cells, and desquamated epithelial cells, in, various stages of degeneration, are mixed with the stringy mucus covering the surface.

Symptoms. — The symptoms begin usually within a few hours after the exciting cause, but may be delayed for twenty-four to thirty-six hours.

In the mild cases, nausea and vomiting may be absent, the chief complaints being headache, mental depression, loss of appetite and coated tongue. The bowels may be constipated or there may be diarrhea. An example of such an attack is as follows:

]\Iale, aged forty-two years.

One week ago he went to a country hotel, where he ate heartily of badly cooked food. Next morning he awoke with a headache, xjoated tongue, and complete anorexia. He felt depresesd and miserable. He remained in bed two days on a milk diet, and gradually improved, although his appetite was a long time in returning. His bowels, though previously regular, became constipated and mo\'ed only after taking calomel.

In the more severe cases the patient com])lains of uneasy feelings in the stomach that merge into nausea. Vomiting soon occurs, the vomited matters consisting of the contents of the stomach, mixed with mucus, and usually offensive from the presence of organic acids. There is almost invarial)ly a reduction or even an absence of hydrochloric acid, although very rarely this form of acidity may be normal or excessive. Acute gastritis, with a total acidity of 40 or over, should arouse our suspicions that more than simple acute catarrh is present. Lactic acid is rarely present.

The tongue is usually dry and coated, and there is apt to be thirst. A diffuse tenderness may be elicited by ])ressure on the ei)igastrium.

In ordinary gastritis the vomitiiuj usuaUy ceases as soon as the stomach is emptied, and is repeated only after ingestion of food. When the vomiting is prolonged, the diagnosis of gastritis should not be made without reservation.

Watery vomiting or the vomiting of large (luantities of fluid containing free hydrochloric acid does not occur in acute gastritis, but suggests some form of pyloric closure, commonly seen with ulcer, more rarely with cancer of the stomach.

Pain as a sym|)toni of acute gastritis is not usually observed exce])t in the attacks that follow a gross dietetic error. In these cases cramp-

ACUTE C'ArARRHAL GASTRITIS 21

like pains in the epif);astrium may occur, later becominjij more generally distributed over the lower abdominal zones, as the undigested ingesta enter the intestinal tract. This is a true "stomach-ache" common in childhood. The following case may be given as an example:

S. (j., male, aged twenty-one years. Admitted May 8, 1909.

Present History. — Always well. On the day of admission he started with friends to " enjoy a day in the city." After visiting several saloons and eating immoderately of pickles and cabbage, he began to feel nauseated and to vomit frequently. He had cramp-like pains in the epigastrium.

Physical Examination. — Tenderness in the epigastrium was present with slight rigidity over the upper right rectus. Otherwise negative. He remained in the hospital for three days and was then discharged cured.

Pain other than this does not appear as a symptom of acute gastritis, despite the fact that many writers mention pain of a burning or lancinating character as not uncommon.

Flatulence does not occur unless it be a preexisting symptom. The urine is usually scanty, highly colored, and cloudy from the precipitation of urates.

In mild cases the temperature is not usually elevated, although predisposition to fever is often peculiar to the individual, and the tendency to develop fever from slight causes may last through adult life. The temperature may be slightly elevated in the more severe cases.

In children, fever may be a prominent symptom and may be continuous for a number of days. To this condition, Eustace Smith has applied the term "acute febrile gastritis of children."

Prostration and headache are common, but are not, as a rule, severe except with food infections. There may be various forms of skin eruptions, chiefly of a roseolar, erythematous, or urticarial character, but these are rare, except after food poisoning, especially by shell-fish.

Diarrhea often appears at the onset, and may be due either to increased intestinal peristalsis or to a complicating ileocolitis. When the stomach alone is involved, constipation is the rule.

As the attack subsides, symptoms of atony often appear, and may protract the course of the disease several days or even weeks. There is lack of appetite or even nausea, though vomiting is rare. A slight amount of gastric flatulence may be present in this atonic stage. These symptoms are transient, however, and no sequelae result.

Duration. — The duration of the attack is short, the acute stage rarely extending over one or two days, although it may be a week or so before the patient regains his appetite and considers himself well.

Cases with nausea and \'omiting extending over two days must be regarded with suspicion. Recurrences are not common, except in those whose life history shows a constant repetition of attacks from individual predisposition, or in those who repeatedly subject themselves to gross dietetic errors. Frequent recurrences without assignahle cause should throw doubt upon the diagnosis.

Diagnosis. — The extreme frequency in which acute appendicitis first manifests itself by pain or distress in the epigastrium and vomiting should always be remembered, and a careful examination should be made, even in cases that seem straightforward examples of acutegastric catarrh. The blood count is of value in doubtful cases.

Exacerbations of chronic appendicitis may be responsible for many cases of apparent gastritis, with pain, nausea, and vomiting, often associated with diarrhea. This is especially the case in children in whom recurring bilious attacks with nausea and vomiting often cease after a frank attack of inflammation of the appendix, and its subsequent removal.

Ulcer of the stomach is often erroneously diagnosticated as gastritis, especially when the former disease assumes the vomiting type. The vomiting of ulcer is, however, more protracted than that of gastritis, is associated with definite pain, and assumes in many instances the acid watery type of vomiting which is never seen in gastric catarrh. jMany cases of cancer begin with vomiting, and it is suspicious of malignancy if, during the age of cancer incidence, protracted vomiting occurs without an apparent exciting cause, especially if the patient has recently been losing somewhat in flesh and strength.

The gastric symptoms of gall-bladder disease are often erroneously diagnosticated as gastritis. Physical examination shows the tenderness located over the gall-bladder area, which should prevent error in diagnosis between these two conditions. It must be remembered that many of the acute infectious diseases may begin with vomiting, as an initial symptom, and that one should be guarded in expressing a definite opinion too soon in the course of the disease, especially in children.

In every case of suspected gastritis, pregnancy, uremia, and the gastric crises of tabes must be excluded. Cyclic vomiting with acidosis in children should not be forgotten.

Treatment. — But little medical treatment is recpiired in the majority of cases of acute gastritis. l{est in bed with abstinence from food until the nausea has disappeared is usually sufficient to effect a speedy cure. When there has been a gross dietetic error, and vomiting has not apparently Ix'cii sufficient to empty the stomach, emesis may be induced either !>> draughts of salt water combined with the tickling of the throat, or, esix-cially in hosjiital cases, hypodermics of apomorphine (grain |) may be employed. Free emesis usually shortens the attack and prevents intestinal complications. If the patient be accustomed to the stomach-tube, the stomach may be washed out by the ordinary method. A tube of fairly large caliber should be used to prevent blocking of the lumen by particles of undigested food.

If the patient is not seen during the early part of the attack, it is generally wise to administer a mild laxative, either calomel, or if the stomach is in a receptive mood, castor oil, magnesium citrate, or other saline aperient. If intestinal cramps and flatulency are present a high saline enema should be given. The nausea is usually relieved promptly after the taking of food has been discontinued. Nausea may also be relieved by small doses of cerium oxalate, or by minim doses of carbolic acid with or without diluted hydrocyanic acid. vSuch a prescription may be given as follows:

I^ — Acid, carbolic, 95 per cent.,

Acid, hydrocyanic, dil aa TTLxyj

Mist, cretse comp ad §ij — M.

Sig. — Teaspoonful in a little water every hour for four doses.

The following may also be employed:

I^ — Acid, carbolic. (Calvert's),

Glycerin aa 5ss

Aq. laurocerasi 5 3

Aq. menth. pip ad giv — M.

Sig. — Teaspoonful in a little water every two hours.

The thirst may be controlled by cracked ice slowly melted in the mouth, or by ^-dram doses of creme de menthe in shaved ice, a remedy which is furthermore of great value in relieving nausea and vomiting.

It is rarely necessary, except in the food-poisoning cases, to continue abstinence from food after twenty-four to thirty-six hours. As soon as the condition of the stomach will permit, peptonized milk or milk with lime water, or cerium oxalate, may be given. In those to whom milk is distasteful, hot broths may be given. Solid food should not be given until nausea has ceased.

During the stage of atony that often follows an attack the bitter stomachics are of service. Of special value is the tincture of nux vomica in 10-minim doses before meals, or the tincture of physostigma in similar doses. As, moreover, a condition of diminished gastric acidity usually follows an attack, diluted hydrochloric acid with the meals may be of service. This after-treatment, together with the limitation of liquids at the time of meals, and with a carefully selected bland diet, is to be continued until food is taken again with relish.

II. Infectious Gastritis (Food Poisoning; Ptomain Poisoning).^ Etiology. — Infectious gastritis may be induced through infected meat, fish or milk, or })y vegetable poisons. Bacteria are largely responsible for the poisoning which follows the ingestion of certain food, because they have been identified in a large proportion of epidemics of food poisoning that have been scientifically investigated. The poisoning may be due to organisms that are present before death in the tissues of the animal from which the food was derived, or to those that have subsequently gained access to such food.

In most instances the infected food has been free from all objectionable odor and taste, and, contrary to the accepted belief, it is rather rare that the ordinary putrefactive organisms or their products are capable of causing poisoning in man.

The most important infecting organism is the Bacillus enteritidis, a bacillus intermediate between the Bacillus typhosus and the Bacillus coli communis, first described by Gartner in 1858, and often associated with his name.

The epidemic investigated by Gartner affected 58 of 93 persons who had eaten the meat of an ox that had been killed because it had diarrhea. Examination of the meat showed that its capillaries contained bacilli identical with those found in the tissues of the fatal cases.

The causative role played by bacteria in the production of gastro-intestinal catarrh is shown by an interesting experiment, made by Poels and Dhont.

A healthy ox was inoculated with a small quantity of pure culture of a variety of Bacillus enteritidis in the jugular vein; twenty-six minutes afterward it was killed and partially bled out. On bacterial examination a few colonies were obtained from the spleen and liver. None were found in cultures from the flesh; a few bacilli were present in the blood. After keeping a piece of the flesh at 20° C. for seventy-two hours the bacilli had become more abundant. The rest of the meat had been kept at a lower temperature, not over 5° C; in this scanty l)acilli were detected. "After we had assured the workers in the slaughter-house that we were convinced from the smallness of the number of bacilli present in the muscle that the danger of eating the meat could not be very great, and that it would probably cause only slight diarrhea, 53 persons resolved to eat it. Of these 53, 15 became ill in consequence; headache, gastro-intestinal catarrh, and abdominal pain came on in from twelve to eighteen hours; in some there was severe diarrhea."

The serum of typhoid fever agglutinates the Gartner bacillus, showing a certain kinship between the two varieties.

Bacillus enteritidis in milk is not uncommon. Klein found this organism in ten out of thirty-nine samples of milk. As boiling does not destroy the toxin, the ordinary methods of sterilization do not render the milk harmless.

Other bacilli, closely resembling Bacillns enteritidis morphologically, but differing from it in agglutinative properties, have been described by other observers.

A paratyphoid bacillus was found by Trautmann to be the cause of one outbreak, and in one epidemic the Bacillus typhosus was found to be the existing cause. In this instance the meat was taken from a cow with a splenic abscess that was found to contain pure culture of this organism.

In many instances infection by Bacillus coli communis has been the cause, less frequently the Bacillus proteus.

Special mention must be made of infection by the Bacillus botulinus, an anaerobic bacillus identified by von Ermengem in 1895, and found in diseased ham. This infection runs somewhat a different course from the Gartner bacillus groups, and usually follows ingestion of diseased sausage meat. To this form of poisoning the name "botulism" is frequently applied. The Bacillus botulinus does not seem to develop to any extent in the human body, so that the symptoms, properly speaking, are not due to an infection, but to an intoxication by the toxin produced by the germ in meat.

In the case of Bacillus botulinus, the toxins are readily destroyed by boiling, but in the case of Bacillus enteritidis the soluble products are not thus affected, and hence meat containing such may be injurious even after it has been cooked.

According to Trautmann, food poisoning represents the acute, whereas paratyphoid fever infection — etiologically due to the same factor and having the same agglutinative reactions — represents the subacute type of infection.

Toxins of which tyrotoxicon, found in various milk products, such as ice-cream, custard, and cheese, by Vaughan is an example, may be the cause for acute gastro-intestinal irritation. A variety of substances belonging to poisonous albumins have been isolated, but about these very little is accurately known.

Fish are infected by the same bacteria as meats. The roe of certain fish at spawning season is also poisonous to man. This is especially the case with Spanish mackerel.

Oysters are commonly infected by contaminated water in which they are placed to whiten them and to render them more palatable.

The ingestion of certain shell-fish, such as crabs and lobsters, are often followed in certain individuals by an attack of severe gastritis, which is, however, hardly to be considered toxic in character.

Symptoms. — The symptoms of food infection are those of a severe gastro-enteritis associated with those of a more or less intense toxemia. The intensity of the symptoms varies according to the quantity of the infecting agent that is taken, its virulence, and the susceptibility of the patient. The result may be anything from a slight passing illness, to a severe or a rapidly fatal attack. The onset may appear within a few minutes of the ingestion of the infected food, or may be delayed twenty-four to thirty-six hours.

Gastro-intestinal symptoms consist of nausea, vomiting, and abdominal pain. The vomiting is usually severe and frequent, and persists long after the stomach has once been emptied — quite a different' picture from that observed in the ordinary forms of acute gastritis, in which vomiting usually ceases soon after the stomach has once been thoroughly emptied of its contents. Nausea and retching are severe and protracted. In rarer instances vomiting is absent, the sj'mptoms being intestinal in character.

Diarrhea is usually present during the early stages, and is accompanied by severe griping pains. The temperature is usually somewhat elevated at the early stages and may be accompanied at its onset by headache, pain in the back and bones, and other manifestations of an acute infection. The duration of the febrile period is usually short, although in many instances fever may persist for days or there may be recrudescences from time to time. In these protracted cases the diagnosis from typhoid fever or paratyphoid may be exceedingly difficult.

Herpetic, urticarial, or erythematous eruptions are not uncommon. In rarer instances desquamation of the hands and feet may occur a number of days after the acute attack. Widely spread petechias have been observed.

Marked prostration accompanies even the milder cases, while severe infections are frequently ushered in by symptoms of collapse that may rapidly prove fatal. In these fulminant cases the collapse may appear before the gastro-intestinal symptoms have time to develop. In these cases the temperature is apt to be subnormal, the pupils dilated.

Pneumonic complications have been noted in a number of epidemics.

The urine is usually scanty and highly albuminous. In some instances there is complete suppression.

Special mention should be made of the infection symptoms of l)otulism. The onset is usually delayed until twenty-four to thirty-six hours after the meal, and is ushered in by nausea, vomiting, and severe abdominal pain. Diarrhea is not as commonly observed as in the cases due to infection by Gartner's bacilli or the Bacillus coli communis.

Visual disturbances are observed in many instances, and consist of cloudiness of vision, dilatation of the pupil with loss of reaction to light, and ptosis. Burning thirst is usually present, but the swallowing of liquids is difficult and often leads to severe choking attacks.

Complete a])honia is not uncommon. The temperature is seldom elevated, and the pulse rarely rises above 90.

Convulsive movements of the muscles of the extremities is commonly observed; in severe cases there may be opisthotonos. Muscular paresis may occur, and dysphagia from paralysis of the esophagus has been observed.

Closely akin to botulism is the clinical course observed in certain cases of poisoning by methyl alcohol. A remarkable epidemic of the latter character has been recently described by Stadelmann,^ in which the symptoms due to methylism seemed identical with those of botulism, except that no motor palsies were observed. Some of the victims died before characteristic symptoms could develop, for, unlike alcohol, the more deadly methyl spirits do not rapidly intoxicate, some twenty-four to thirty-six hours being necessary for the development of the syndrome. In this epidemic 130 cases came under Stadelmann's observation, of whom 58 died.

Treatment. — The treatment of food infections is that of a severe gastro-enteritis in addition to those remedies required to combat the depressive effect of the toxemia.

The stomach should at once be emptied, preferably by washing out its contents by the tube. In the event of the stomach-tube not being at hand, emesis may be produced by any of the 'ordinary means. Apomorphine, so commonly given in the cases of single gastritis, should be given with caution, if at all, because of its depressing effect.

Free bowel evacuations should be produced by salines, elaterium, or calomel. As these remedies take time for the desired effect, or may be vomited, colon irrigations or high enemas should be given at the earliest opportunity.

Collapse should be averted as far as possible by the judicious use of hypodermic stimulation. Camphor injections, caffeine-sodiumbenzoate, and the preparations of digitalis are the most desirable forms of such stimulation. Strychnine should be given with caution in the cases that are complicated by convulsions or muscular contractions. Hypodermoclysis should be employed in the collapsed patients who suffer from repeated vomiting and severe diarrhea.

Albumen water, broths, and similar mild fluid may be given after nausea and vomiting have ceased, but not without caution even then, as relapses from premature feeding are not uncommon.

1 Berlin, klin. Woch., Janiiaiy 29, 1912.

Convalescence is re^jularly protracted — the general strength is not apt to return for three to six weeks. The general management of these cases of protracted convalescence is practically that of typhoid fever.

MEMBRANOUS GASTRITIS (CROUPOUS GASTRITIS- DIPHTHERITIC GASTRITIS)

Etiology. — Membranous gastritis due to infection by the Klebs- Loeffler bacillus is of rare occurrence. Leary found but two instances, of diphtheritic infection of the stomach in 136 cases of fatal diphtheria at the Boston City Hospital. Primary invasion is still more uncommon, as diphtherial gastritis is almost regularly secondary to a similar invasion of the esophagus, throat, or upper respiratory passages.

The lesion may be produced by infective agents other than the diphtheritic bacillus. It has t)ccurred during the course of typhus fever, tyi)hoid, puerperal fever, pyemia, and a variety of other infections.

Foulerton^ reports a case secondary to quinsy, in which the infecting agents were the pneumococcus and the Bacillus mesentericus vulgatus. Dieulafoy reports similar cases due to the dij)lococcus. Other observers have found streptococci in the shreds of false membrane vomited by the patient.

Membranous gastritis may also occur when chemical irritants are taken accidentally or with suicidal intent. While no age is exempt, the disease is commonly obser^'ed in young children.

Pathology. — The changes produced in the stomach in this condition are not essentially different from those of diphtheritic inflammation of other mucous membranes.

The mucosa is, at first, the seat of an acute inflammation which leads to degeneration and desquamation of the superficial epithelium. These degenerated and descjuaniated cells l)ecome mixed with fibrin, leukocytes, and red blood cells, all being fused together into a more or less homogeneous mass — the so-called false membrane — by the process of coagulative necrosis. In the mild cases this inflammatory exudate rests upon a fairly well-preserved mucosa and can be removed from it without much injury. When the process is more severe there is more or less extensive involvement of the mucosa, so that it is fused with the overlying membrane and the latter cannot be removed without injury to the former.

(ienerally the membrane occurs in irregular strips or patches. It may iinoKe only the crests of the ruga*. On the other hand, cases

' Tran.sactions of Piithol()fi;i''.'il Sof-iciy "f liondoii, 1902, p. 2S6.

MEMBRANOUS GASTRITIS have been reported where the inenibrane formed a more or less perfeet cast of the interior of the stomach. The membrane is grayish in color or brownish from hemorrhage. The mucosa of the rest of the stomach

FlQ. 1

M

MM ( S

Membranous gastritis. A, membrane, adherent to the mucosa at the left and dipping down into it at B. To the right the membrane has separated from the mucosa and appears coiled upon itself; M, mucosa showing dilated vessels X, X, X, and cellular infiltration to the right; MM, muscularis mucosae; S, submucosa; Y, muscularis.

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