to the kidneys by their local action alone, with the exception, possibly, of the unassimilable albumin.

But indirectly, by their influence on the liver, on the blood, on the cardiovascular system, and on the nourishment of the body, the diseases of the stomach may initiate changes in the glomeruli and the tubules. The process may be degenerative, congestive, or inflammatory. Chronic degeneration may result from subnutrition in conjunction with auto-intoxication. The epithelium lining the cortex tubes is swollen and infiltrated with granular matter and fat. There is little albumin in the urine, and only a few casts (there being no changes in the blood-vessels or in arterial tension, no hypertrophy of the left ventricle, and no uremia), the patient's strength and nutrition gradually or progressively failing. But besides the chronic degeneration, an exudative or even productive inflammation of the glomeruli or of the cortex tubes may result indirectly from the diseases of the stomach. The diseases of the stomach undoubtedly influence the evolution of chronic nephritis, and a therapeutic rule may be drawn from this clinical fact. But the part which the diseases of the stomach play in the causation of the diseases of the kidneys is not definitely known, and it is very likely that their pathogenic influence may easily be exaggerated.

CHAPTER II.

THE SECONDARY DISEASES OF THE STOMACH.

THE secondary diseases of the stomach are produced by the diseases of a large number of other organs, and, as a rule, but not always, bear no marks which would reveal or suggest their origin. When once established, they are capable of an independent existence, and may have their usual evolution. They may, however, be more obstinate than is ordinarily the case, and their cure requires the cure or control of the causative disease or its natural advance to another stage in which it has not the same influence on the stomach.

The disease of the stomach may be an accidental association, developing before the beginning or during the course of the disease of the other organ, and as the effect of the same or of totally different causes. They exist together, but the one is not produced by the other.

In order that the disease of the stomach be considered secondary, it must be connected in its origin and evolution with a primary disease. What precedes can not be a result. Its course must be influenced by the primary disease, and it must be observed to follow the primary disease with sufficient frequency to be considered an order of sequence. Naturally, the probability of the etiological relation is greater when an explanation can be given of the mode of genesis.

In order to throw light on the often obscure relation, it is necessary to know the age and nature of the stomach trouble with more exactness than can be learned from the clinical history, from the physical signs, and from autopsies. Diseases of the stomach are too often latent, are too often ill-defined or similar in their subjective manifestations, too often escape a physical search, too often leave no traces perceptible after death, and too often change their nature during their terminal period, to have their age and nature revealed without the use of the modern methods of examination.

I. DISEASES OF THE INTESTINES.

Clinical observation establishes the fact that a disease (except obstruction) of one of the divisions of the digestive tube affects the divisions of the alimentary tract below it much more frequently than those above it. Consequently, secondary disease of the stomach does not often result from intestinal disease, although the stomach is not exempt from intestinal pathogenic influences.

Symptomatic disturbances-loss of appetite, nausea, vomiting, excessive or diminished secretion-of the stomach are very common in diseases of the intestines. Active abdominal plethora may result from the active hyperemia of intestinal irritation or inflammation. Active plethora is as frequent as portal congestion, and in this manner intestinal disease may produce congestion of the stomach or gastritis.

Duodenal obstruction or chronic stenosis in the upper intestinal tract may produce gastric retention and secondary dilated hypertrophy of the stomach. If the obstruction is below the opening of the common duct, there is regular reflux of bile and of pancreatic juice into the stomach, and there is accompanying hyperchlorhydria or hypochlorhydria according to the functional power of the gastric glands. In intestinal obstruction there is antiperistalsis and excessive gastro

intestinal secretion above the obstruction, with nausea, vomiting, and hydrothionemia.

Intestinal auto-intoxication may produce paroxysmal or digestive adenohypersthenia gastrica. The paroxysmal attacks may be very severe-nausea, vomiting, cramps, severe headache, anxiety, depression of spirits, collapse, and even stupor. The stools are very foul, there are HS flatus and indicanuria, and sometimes HS can be detected in the breath and in the urine. Chronic intestinal auto-intoxication may produce chronic gastritis by its direct and indirect influ

ences.

Intestinal neurasthenia and the hypersthenic chronic affections of the intestines may produce neurasthenia gastrica, and duodenitis may extend by continuity of structure to the gastric mucous membrane. Enteroptosis, also, may produce gastroptosis, but in our opinion the particular pathological influence of enteroptosis has been somewhat exaggerated by Glénard. The enteroptosis is as frequently the result as it is the cause of the displacements of the other abdominal organs, and all these displacements are more frequently the result of a common cause-emaciation and lack of proper support.

II. DISEASES OF THE LIVER.

In the diseases of the liver secondary diseases of the stomach are common and have not received the study and recognition which their frequency and clinical importance demand.

The chemistry of digestion may be disturbed by the reflux of bile into the stomach, which may excite excessive secretion, nausea, and vomiting. In all our cases of chronic reflux of bile into the stomach there has been constant hyperchlorhydria, and such is probably the rule, unless there be antecedent asthenic gastritis or gastric atrophy.

Simple enlargement of the liver may produce vertical displacement of the stomach and interfere with the performance of its motor work. Obstructive stagnation is not seldom produced in this manner, the evacuation of the stomach having been delayed in a little more than half of our cases, accompanied by noteworthy enlargement of the liver from various

causes.

In catarrhal icterus and in infectious cholangitis hyperchlorhydria is the rule, and in only a few of our cases have we found secretion normal. But we have studied too few of

N!

these cases to do more than emphasize the desirability of further investigations.

Hypertrophic cirrhosis produces hyperchlorhydria with more or less stagnation (13 of 18 cases). The chronic hypersthenic gastritis (9 of 18) may have been due to the same cause as the hypertrophic cirrhosis, but it is important, at least, to remember the frequency of the association. severe cases of atrophic cirrhosis we have always found hypochlorhydria, the result probably of portal congestion or of chronic gastritis.

In

It is often stated that hyperchlorhydria is an important differential sign between gastric ulcer and cholelithiasis. We have found hyperchlorhydria in 17 of 23 cases of gallstones, and 3 of the 6 remaining ones had chronic asthenic gastritis. Hyperchlorhydria occurs as frequently in cholelithiasis as in ulcer, but in 5 of the 17 cases it disappeared in the interval between the attacks. The hyperchlorhydria is cured by the passage or removal of the stone, and its persistence after an attack of gall-stone colic should excite suspicion of stones still remaining in the ducts or in the gallbladder.

Pyloric or duodenal stenosis may result from carcinoma of the gall-bladder or from gall-stones. The inflammatory complications of gall-stones may produce cicatricial obstruction, but the pylorus may also be obstructed by the presence of a gall stone in the common duct. If, under such circumstances, there be gastric retention, pain, vomiting, and supersecretion, ulcer with pyloric obstruction would probably be the diagnosis erroneously made. Or if there be pain, vomiting, gastric stagnation or retention, emaciation, and absence of free HCl, carcinoma would be suspected, and the erroneous suspicion would become a belief if, as often happens, a tumor (the stone) should be felt in the pyloric region.

III. DISEASES OF THE HEART AND ARTERIES. So long as the valvular diseases of the heart are compensated the functions of the stomach are not disturbed by them in any manner, and the heart may become moderately or temporarily insufficient without producing an appreciable or more than evanescent diminution of secretion. But in the asystolic stage of chronic valvular disease the passive congestion of the stomach causes secretion to become insufficient or the free hydrochloric acid may entirely disappear

from the contents obtained after the test-breakfast. If gastritis has not resulted from the congestion of the stomach, the secretion will become normal after the integrity of the circulation is restored by proper medication. If gastritis, on the other hand, has been produced, the gastric secretion will be permanently under the influence of the anatomical changes of the mucous membrane. After cyanosis and dropsy are well established, no medication, in our experience, restores the lost or impaired secretion. The examination in 18 cases during the period of compensation revealed no disease of the stomach nor disturbance of secretion which could not be readily explained by the action of other causes than the disease of the heart. In compensated heart disease gas often accumulates in the stomach, although secretion be normal and no signs of fermentation can be detected. Seven of these 18 cases complained greatly of the flatulency. Twentythree cases examined when the signs of heart insufficiency were marked showed normal secretion (5), diminished secretion (13), and the complete absence of free HCl (5). The ferments do not diminish so rapidly as the free HCl, and in none of the cases of valvular disease examined by us during the stage of broken compensation have we found hyperchlorhydria or myasthenia.

Arteriosclerosis and cardiosclerosis, or aortic valvular disease secondary to chronic disease of the arteries, produce three forms of stomach trouble. In eleven cases we found the digestion of the test-breakfast normal, but there was no free HCl after the Riegel test-dinner, albumin digestion being proportionately defective. The stomach is capable of doing a small task, but soon becomes exhausted if prolonged work is required of it. Again, we have observed six cases of arteriosclerosis which presented, from time to time, a peculiar form of gastralgia or gastrospasm. These attacks occur during the digestion of a meal (usually large and somewhat excitant in its physiological action), and resemble the muscle cramps of arteriosclerosis. It is probable that they are due to anemia, produced by the gastric localization of the arteriosclerosis, and are not associated in any regular manner with disturbances of secretion. Again, arteriosclerosis may produce chronic interstitial and atrophic gastritis (eight cases), and it is a noteworthy fact that this form of secondary gastritis is sometimes accompanied by motor insufficiency. The relative secretory insufficiency, the digestive gastrospasm, and the mixed gastritis may develop at different periods during the course of the arterial disease. In only three of the cases of