fibers are separated, and the muscular fiber is degenerated or disintegrated. The abscess may open into the stomach, or the peritoneal cavity, or the pleural cavity; or may burrow through adhesions into adjacent organs.

Clinical Description. The disease usually begins suddenly, with a severe chill, though in some of the cases there have been, for two or three days preceding the commencement, symptoms of digestive disorder or symptoms of the primary disease of which the purulent gastritis is a secondary infection. The chill is accompanied by high fever, which is usually remittent, ranging from 102° to 105° F.; and the rigor may be several times repeated during the evolution of the disease. There are great prostration and extremely severe epigastric pains, which may not be increased by pressure; and the stomach may be retracted in the commencement, but soon relaxes, and is distended with gas. There is nausea, repeated vomiting, pinched countenance, prostration, and the symptomgroup may suggest acute poisoning. Sooner or later peritonitis develops and adds its local and general signs to those given by the intense cellulitis. The peritonitis may remain localized or may become general, and in the pyemic cases the pericardium and the pleura may also be affected. The brutal beginning is sometimes followed by a short period of calm, after which the symptoms become continuous or remittent, and usually subside again before the fatal termination in collapse or in coma. Vomiting may not appear until the second day; it becomes frequent, and finally diminishing in frequency, subsides during the calm preceding death. The vomit consists of undigested food, mucus, inflammatory products, blood, and bile, but little or no pus, except toward the end, when the abscess may have opened into the stomach. The bowels may be obstinately constipated, but diarrhea is more common. Where circumscribed, the abscess may present a palpable tumor, which is usually tender on pressure. In the circumscribed form the pain and fever may subside for a few days when the tumor appears, to be followed a few days later by hectic fever and the signs of peritonitis or of perforation into the stomach or into some other cavity.

The general symptoms are even more intense than the local signs-extreme prostration, anxious and pinched countenance, frequent, small, irregular pulse, delirium with suicidal impulses. Tetany may also develop.

The duration of the disease varies from three or four days to as many weeks. Where the suppuration is circumscribed, the local and the general symptoms are less intense, the fever

becomes ultimately hectic, and the duration is much longer than in the violent, rapid, and diffuse form. The average duration is about one week.

The disease ends fatally in 95 per cent. of the cases. That complete recovery is possible has been demonstrated by anatomical preparations (Dittrich, Deininger).

Diagnosis. The disease has no characteristic sign; the evolution and the combination of symptoms are not distinctive. The diagnoses of intestinal obstruction, of peritonitis, of abscess formation in other parts of the abdomen, have been made. Epigastric resistance to palpation or a tumor which becomes less and disappears after the vomiting of pus may be supposed to be characteristic; but this combination of signs is rare, and might be due to an abscess which had burrowed and opened into the stomach. Corrosive poisoning is easily excluded by the absence of the distinctive effects of such poisons on the mouth and throat.

The development of the symptoms in the course of one of the infectious diseases which it sometimes complicates may create a suspicion. It may be confounded with acute pancreatitis or pancreatic abscess, with perigastritis developing in the course of perforating ulcer of the stomach, with hepatic abscess, and with purulent cholelithiasis.

Treatment. The treatment is purely symptomatic so far as the medical management is concerned. Where the disease is suspected and attributable to pus formation and to local peritonitis, an exploratory laparotomy is indicated. Surgical treatment might be successful where the pus is collected in abscesses, and a tumor, developing with the symptoms of acute purulent inflammation, should be explored with a needle, with a view to operative intervention.

The disease usually goes undiagnosed before death, and the treatment has been that of the disease for which it was mistaken. Functional rest, opium to relieve pain, control of the excessive fever, stimulants-summarize the symptomatic treatment. Some recommend quinin.

(2) GASTRIC FEVER.

The existence of this form of infectious gastritis is denied by some authors, who do not admit that the disease is specific, but contend that the cases reported as such are either food intoxications, severe forms of common gastritis, or abortive attacks of well-known infectious diseases, such as typhoid fever and cholera.

While the specific nature of the disease awaits the discovery of its pathogenic germ, clinically the gastritis is neither simple, nor fermentative, nor toxic; but in its pathology and evolution is distinct, and analogous to the bacterial infections. It occurs in persons who have already been affected with typhoid fever, from which it is clinically clearly distinct. The fever is continuous, the spleen is not palpable, and the course is uninfluenced by quinin, the administration of which increases the gastric symptoms-which is not the case where the plasmodium malariæ exists in the blood. It bears a close resemblance to the gastric form of influenza, but in our experience usually occurs isolated in families and is not contagious. The disease is more frequent in spring and in autumn, and occurs more often in the middle period of life than in infancy, childhood, and old age. It occurs isolated, and endemics have been reported.

Clinical Description.—The beginning is like that of most infectious diseases of mild type-general discomfort, a slight chill, fever, headache, and pains in the extremities, in the back, and in the epigastrium. The general precede the gastric symptoms, and develop independently and out of proportion to the gastritis. Several hours after the commencement there are pains in the stomach, epigastric tenderness, nausea, and vomiting. The vomit consists of an alkaline fluid containing mucus, and, incidentally, sometimes bile and undigested food. The bile is usually absent, except after retching, and the development of the gastric symptoms is in no relation with the diet or with the period of digestion, and there is no gastric fermentation.

The fever attains its highest point within forty-eight hours, and oscillates between 100° and 103° F., with a morning remission of about 1° F.; it continues, uncontrolled by quinin, for ten or twelve days, and drops, with a greater morning remission, in two or three days to the normal point.

In addition to the initial chill, slight rigors may occur in the course of the disease. The bowels may be constipated, but there are usually a few diarrheal movements, which have none of the characteristics of the typhoid stool. The pulse is rapid, the patient restless, and delirium may occur in the course of the disease. Insomnia is the rule. The nervous symptoms, apart from the often severe initial pains, continue more or less throughout the disease-headache, restlessness, insomnia, vertigo, tinnitus aurium, prostration, and, with the high temperature, sometimes delirium.

Diagnosis. This form of infectious gastritis may be con

founded with typhoid fever. But the step-like rise of the temperature during the first week, and its slow remittent decline during the third or fourth week, the enlarged spleen, the characteristic stool, the ileocecal stagnation and gurgling, the Widal serum sign, and the eruption are all absent. A few bronchial râles may exist, as in typhoid fever; but the gastritis is an essential and distinctive sign, and the spleen is never palpable.

From the fermentation form of gastritis and the severe form of simple acute gastritis it differs in the absence of fermentation and of a relation with alimentation and digestion, and in the predominance of the general symptoms. In gastric fever the disturbance of the system is much greater than the disease of the stomach would naturally produce, and the general and the local symptoms bear no close relation to each other. The evolution of the disease, which is in itself distinctively characteristic, is not controlled by treatment.

Treatment.-The treatment is that of an infectious disease the course of which can not be abridged by drugs. Tepid sponging, the compress, and a fluid diet are indicated to control the fever and the gastric symptoms. Calomel may be given in the beginning, and often exercises a good influence on the symptoms and the temperature. The nervous symptoms may require phenacetin, but it is best not to disturb the stomach with drugs oftener than can be avoided.

III. ACUTE TOXIC GASTRITIS.

Acute toxic gastritis is an inflammation of the mucous membrane of the stomach excited by the action of certain poisons introduced into the stomach from without.

The poisons which produce an injurious effect on the stomach may be formed within the body or may be introduced from without. The endogenous poisons are brought to the stomach by the blood. We have nothing to do here with the diseases of the stomach (among which may be gastritis) due to the retention or the excessive formation of normal nutritive or secretory products, or due to the abnormal substances formed by disease or by bacteria within the body.

Acute toxic gastritis may be produced by alcohol, by tobacco, and by many of the drugs extensively used in the treatment of disease. The essential oils and resins, the iodids, the preparations of mercury, the bromids, the salicylates, arsenic, purgatives, iron and its compounds, and a large

number of other drugs, when given improperly, or for a long time, produce gastritis. But it would not be wise to say more of the serious injury which is often done while conscientiously endeavoring to do good. Acute toxic gastritis is, however, often produced by poisons which have been taken by accident or for suicidal purposes, or which have been administered with forethought and malice. Some of the most common forms of it will be briefly described.

All poisons are not capable of exciting an acute gastritis. As regards their action on the stomach, poisons may be divided into three classes.

I. Those which enter into chemical combination with the tissues, either dissolving the cells, as do the caustic alkalies, or coagulating the protoplasm, as does alcohol, or uniting with their constituents, as do phosphorus and the mineral acids. These are chemically destructive poisons.

2. Those which irritate and excite inflammation of the glandular layer.

3. Those which produce no anatomical change in the mucous membrane perceptible during life or visible after death. This class consequently plays no part in the etiology of toxic gastritis.

(a) Poisonous Acids.-The stronger acids brought in contact with the mucous membrane of the stomach directly, produce death of the tissues by dehydrating, coagulating, or combining with the constituents of the cells, for which they have strong chemical affinities; and by irritation of the adjacent parts they excite inflammation, which may be so intense as to lead to local death. The separation of the necrosed tissues is a reactive process, which may be followed by cicatricial healing, or by regeneration, if the action has been superficial.

Pathological Anatomy.-The stomach is the center of the destructive changes produced by swallowing corrosive acids, being the place where they are first arrested, and where they long remain. The action on the stomach is conditioned by the quality, the concentration, and the chemical affinities of the acid, and by the quantity and the nature of the contents of the stomach at the time when the poison is swallowed. In small quantities the action is most intense and may be confined to the region about the cardia and the lesser curvature, along which the acid flows to and around the pylorus. Consequently a very small quantity, after recovery by cicatrization, is likely to leave serious and obstructive deformity of the orifices. In larger quantity, the action is more diffused